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CARDIOVASCULARY SYSTEM DISORDERS
Anatomy and Physiology

Cardiovascular Physiology
Circulatory system includes a pump (the heart), interconnected tubes (blood vessels or vascular system), and
extracellular fluid and cells (blood)
Heart and heart wall layers

! The heart is located in the left side of the mediastinum.
The Layers of the Heart Wall

Essential layer of the heart
Epicardium
Coronary arteries are found in this layer
(visceral
pericardium)
Middle and thickest layer of the heart
Myocardium
(CBQ)
Responsible for contraction of the heart
Innermost layer of the heart
Endocardium Lines the inside of the myocardium
Covers the heart valves
"
"
"
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The layer that covers the heart is the PERICARDIUM
There are two parts- parietal and visceral pericardium
The space between the two pericardial layers is the

pericardial space
Chambers of heart
Right atrium: collecting chamber for incoming systemic venous system
Right ventricle: propels blood into pulmonary system
Left atrium: collects blood from pulmonary venous system
Left ventricle: largest thick-walled muscle that acts as a high-pressure pump which propels
blood into the systemic arterial system
The heart chambers are guarded by valves

- The atrio-ventricular valves- Tricuspid and bicuspid
- The semi-lunar valves- Pulmonic and aortic valves
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The Blood supply of the heart comes from the Coronary arteries
- Right coronary artery
- Left coronary artery
Blood supply for the heart:
Coronary arteries supply blood to myocardium
Coronary blood flow blood flowing through the coronary arteries
Coronary sinus drainage area for the blood; empties into right atrium
The main functions of this system are:
- to transport oxygen, hormones and nutrients to the tissues
- and to transport waste products to the lungs and kidneys for excretion
The CONDUCTING SYSTEM OF THE HEART
Consists of the
1. SA node- the pacemaker
2. AV node- slowest conduction
3. Bundle of His branches into the Right and the Left bundle branch
4. Purkinje fibers- fastest conduction
The Heart sounds
1. S1- due to closure of the AV valves
2. S2- due to the closure of the semi-lunar valves
3. S3- due to increased ventricular filling
4. S4- due to forceful atrial contraction
Heart rate
- Normal range is 60-100 beats per minute
- Tachycardia is greater than 100 bpm
- Bradycardia is less than 60 bpm

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- Sympathetic system INCREASES HR

- Parasympathetic system (Vagus) DECREASES HR (CBQ)
The Heart: Physiology
- The amount of blood the heart pumps out in each beat is called the STROKE VOLUME
- When this volume is multiplied by the number of heart beat in a minute (heart rate), it becomes the CARDIAC
OUTPUT
- When the Cardiac Output is multiplied by the Total Peripheral Resistance, it becomes the BLOOD PRESSURE
Blood pressure = Cardiac output X Peripheral resistance
Blood pressure
- Control is neural (central and peripheral) and hormonal
- Baroreceptors in the carotid and aorta
- Hormones - ADH, Adrenergic hormones, Aldosterone and ANF
The Heart: Physiology
- The PRELOAD is the degree of stretching of the heart muscle when it is filled-up with blood
- The AFTERLOAD is the resistance to which the heart must pump to eject the blood
Vascular System
- The vascular system consists of the arteries, veins and capillaries
- The arteries are vessels that carry blood away from the heart to the periphery
- The veins are the vessels that carry blood to the heart
- The capillaries are lined with squamos cells, they connect the veins and arteries
- The lymphatic system also is part of the vascular system and the function of this system is to collect the extravasated
fluid from the tissues and returns it to the blood
Cardiac Assessment
1. Health History
- Obtain description of present illness and the chief complaint

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- Chest pain, SOB, Edema, etc.

- Assess risk factors
2. Physical examination
- Vital signs- BP, PP, MAP
- Inspection of the skin
- Inspection of the thorax
- Palpation of the PMI, pulses
- Auscultation of the heart sounds
3. Laboratory and diagnostic studies

- CBC
- Cardiac catheterization
- Lipid profile
- arteriography
- Cardiac enzymes and proteins
- CXR

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CVP
ECG
Holter monitoring
Exercise ECG
Laboratory Test Rationale

- To assist in diagnosing MI
- To identify abnormalities
- To assess inflammation
- To determine baseline value
- To monitor serum level of medications
- To assess the effects of medication
CKCK- MB (creatine kinase)
- Indicates myocardial damage
- Elevates in MI within 4-6 hours
- peaks in 18 hours and then declines till 3 days
- 0-5% of total CK (26-174U/L)
- Normal value is 0-7 U/L
Lactate Dehydrogenase (LDH)
- Elevates in MI in 24 hours
- peaks in 48-72 hours
- Normally LDH1 is greater than LDH2
- MI- LDH2 greater than LDH1 (flipped LDH pattern)
- Normal value is 70-200 IU/L
Myoglobin
- Oxygen binding protein
- Found in both skeletal and cardiac
- Level rises 1 hour after cell death
- Peaks in 4-6 hours
- Returns to normal w/in 24-36 hours
- Not used alone
- Muscular and RENAL disease can have elevated myoglobin
Troponin I and T
- Troponin I has a high affinity for myocardial injury
- Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks!
- Troponin I - <0.6 ng/mL
- Troponin T 0-0.2ng/mL
- REMEMBER to AVOID IM injections before obtaining blood sample!
- Early and late diagnosis can be made!
SERUM LIPIDS
- Lipid profile measures the serum cholesterol, triglycerides and lipoprotein levels
- Cholesterol= 200 mg/dL
- Triglycerides- 40- 150 mg/dL
- LDL- 130 mg/dL
- HDL- 30-70- mg/dL
- NPO post midnight (usually 12 hours)

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ELECTROCARDIOGRAM (ECG)
- A non-invasive procedure that evaluates the electrical activity of the heart
- Electrodes and wires are attached to the patient
- Tell the patient that there is no risk of electrocution
- Avoid muscular contraction/movement
Holter Monitoring
- A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period
of 24 hours
- Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop
Echocardiogram
Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound
No special preparation is needed

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Stress Test
A non-invasive test that studies the heart during activity and detects and evaluates CAD
Exercise test, pharmacologic test and emotional test
Treadmill testing is the most commonly used stress test
Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise
Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and
caffeine
Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of breath
Instruct client to avoid taking a hot shower for 10-12 hours after the test
Pharmacological stress test
! Use of dipyridamole
! Maximally dilates coronary artery
! Side-effect: flushing of face
! Pre-test: 4 hours fasting, avoid alcohol, caffeine
! Post test: report symptoms of chest pain
Cardiac Catheterization
Insertion of a catheter into the heart and surrounding vessels
Obtains information about the structure and performance of the heart valves and surrounding vessels
Used to diagnose CAD, assess coronary artery patency and determine extent of atherosclerosis
PRE PROCEDURE
# Ensure Consent
# assess for allergy to seafood and iodine
# Withhold solid food 6-8 hours and liquids for 4 hours
# document weight and height, baseline VS, blood tests and document the peripheral pulses
# inform client that a local anesthetic will be administered before insertion
# Client may feel fatigued because of the need to lie for 2 hours
# Prepare IV line if prescribed
# Prepare insertion site by shaving and cleaning with an antiseptic solution if prescribed
# Administer pre medication
INTRATEST
# inform patient of a fluttery feeling as the catheter passes through the heart
# inform the patient that a feeling of warmth and metallic taste may occur when dye is administered.

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POST TEST
# Monitor VS and cardiac rhythm
# Monitor dysrrhytmia and chest pain
# Monitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion site
# Apply sandbag or compression device to insertion site if required to maintain pressure
# Maintain strict bed rest for 6-12 hours
# Client may turn from side to side but bed should not be elevated more than 15 degrees
# Notify physician if client complains of tingling, cool, pale, cyanosis and loss of peripheral pulses
# Keep the leg straight to prevent occlusion
# Monitor for bleeding and hematoma formation
# Encourage fluid intake to flush out the dye
# Immobilize the arm if the antecubital vein is used
# Monitor for dye allergy
# Encourage fluid intake to promote renal excretion of dye
# Monitor nausea, vomiting, rash and other sign of HPS rxn
CVP
The CVP is the pressure within the SVC
Reflects the pressure under which blood is returned to the SVC and right atrium
is measured with a central venous line in the SVC and balloon flotation catheter in the pulmonary artery
Normal CVP is 3 to 8 mmHg/ 4-10 cm H2O
Increased CVP
1. increase in blood volume as a result of Na and water retention, excessive IVF or heart/renal failure
Decreased CVP
2. May indicate decrease in circulating blood volume and may be to hypovolemia, hemorrhage and severe vasodilatation
Measuring CVP
1. Position the client supine with bed elevated at 45 degrees (CBQ)
2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL, 4th ICS
3. Instruct the client to be relaxed and avoid coughing and straining.
! note disease that activity that increases intra-thoracic pressure such as coughing and straining
! If the client is on the ventilator reading should be taken at the point of end expiration

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Cardiac Implementation
Implementation
1. Assess the cardio-pulmonary status
- VS, BP, Cardiac assessment
2. Enhance cardiac output
- Establish IV line to administer fluids
3. Promote gas exchange
- Administer O2
- Position client in SEMI-Fowlers
- Encourage coughing and deep breathing exercises
4. Increase client activity tolerance
- Balance rest and activity periods
- Assist in daily activities
- Provide strict bed rest if indicated
- Soft foods
- Assistance in self-care
5. Promote client comfort
- Assess the clients description of pain and chest discomfort
- Administer medication as prescribed
! Morphine for MI
! Nitroglycerine for Angina
! Diuretics to relieve congestion (CHF)
6. Promote adequate sleep
7. Prevent infection
- Monitor skin integrity of lower extremities
- Assess skin site for edema, redness and warmth
- Monitor for fever
- Change position frequently
8. Minimize patient anxiety
Encourage verbalization of feelings, fears and concerns
Answer client questions. Provide information about procedures and medications
CARDIOVASCULAR DISORDERS
Cardiac Diseases
$ Coronary Artery Disease
$ Myocardial Infarction

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$ Congestive Heart Failure

$ Infective Endocarditis
$ Cardiac Tamponade
Vascular Diseases
$ Hypertension
$ Buergers disease
$ Aneurysm
$ Varicose veins
$ Deep vein thrombosis
Cardiac Diseases
Coronary Artery Disease (CAD)

(CAD)
- results from the focal narrowing of the large and medium-sized coronary arteries due to deposition of atheromatous
plaque in the vessel wall
Risk Factors
1. Age above 45/55 and Sex- Males and post-menopausal females
2. Family History
3. Hypertension
4. DM
5. Smoking
6. Obesity
7. Sedentary lifestyle
8. Hyperlipedimia
Most important MODIFIABLE factors:
- Smoking
- Hypertension
- Diabetes
- Cholesterol abnormalities
Pathophysiology
- There is decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply
- If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, this becomes significant
- Potential for Thrombosis and embolism
Artery walls have three layers.
1. The inner layer provides a slippery surface.
2. The middle layer is strong, elastic and muscular.
3. The outer, fibrous, layer adds strength and contains tiny blood vessels that supply blood to the arteries themselves.
Narrowing or obstruction of the coronary arteries is the main cause of a group of disorders known as ischaemic heart
disease.
Coronary Artery Disease.
- Acute Coronary Syndrome (ACS) is the phrase used when referring to any cardiac condition involving the coronary
arteries.
- Angina is a feeling of tightness or pain across the chest that may spread outwards to the shoulders, upper arms and
back.

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May occur with exercise or strong emotion and can be worse after a meal or in cold weather. Symptoms usually disappear
after 1-2 minutes rest.
- Heart attack (myocardial infarction or MI)
MI is when part of the heart muscle dies. This is usually caused by a blood clot
(coronary thrombosis), which has blocked one of the coronary arteries supplying the heart and depriving the tissues of
oxygen.
Coronary Artery Disease treatment

$Angioplasty & Stent
$Coronary Artery Bypass Graft.
- Treatment for C.A.D involves the removal or treatment of risk factors.
- Sometimes procedures to enlarge or bypass coronary artery narrowing are required.
- If Coronary Disease is not treated and the coronary artery becomes blocked the result may be a heart attack.
Angioplasty
- Coronary angioplasty involves inserting a balloon into a diseased (blocked/narrowed) coronary artery through an
artery in the groin or arm.
- Commonly a metal support (stent) is inserted into the artery to help keep it open.
C. A. B. G.
- Veins and sometimes arteries are grafted from the aorta to a point on the coronary artery beyond the area of disease.
This enables an adequate blood supply to reach those parts of the heart suffering from ischaemia
Valve Replacements
- Aortic Valve Replacement (AVR)
- Mitral Valve Replacement (MVR)

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Angina Pectoris
- Chest pain resulting from coronary atherosclerosis or myocardial ischemia
Angina Pectoris: Clinical Syndromes

Three Common Types of Angina
1. Stable Angina
- The typical angina that occurs during exertion, relieved by rest and drugs and the severity does not change
2. Unstable angina
- Occurs unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by
rest and drug
3. Variant angina
- Prinzmetal angina, results from coronary artery VASOSPASMS, may occur at rest
ASSESSMENT FINDINGS
1. Chest pain - ANGINA
- The most characteristic symptom
- PAIN is described as mild to severe retrosternal pain, squeezing, tightness or burning sensation
- Radiates to the jaw and left arm
- Precipitated by Exercise, Eating heavy meals, Emotions like excitement and anxiety and Extremes of temperature
- Relieved by REST and Nitroglycerin
2. Diaphoresis
3. Nausea and vomiting
4. Cold clammy skin
5. Sense of apprehension and doom
6. Dizziness and syncope
LABORATORY FINDINGS
1. ECG may show normal tracing if patient is pain-free. Ischemic changes may show ST depression and T wave
inversion
2.
3.
-
Cardiac catheterization
Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions
Decreased cardiac output
Impaired gas exchange
Activity intolerance
- Anxiety

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Nursing Management
1. Administer prescribed medications
! Nitrates- to dilate the venous vessels decreasing venous return and to some extent dilate the coronary arteries
! Aspirin- to prevent thrombus formation
! Beta-blockers- to reduce BP and HR
! Calcium-channel blockers- to dilate coronary artery and reduce vasospasm
2. Teach the patient management of anginal attacks
! Advise patient to stop all activities
! Put one nitroglycerin tablet under the tongue
! Wait for 5 minutes
! If not relieved, take another tablet and wait for 5 minutes
! Another tablet can be taken (third tablet)
! If unrelieved after THREE tablets% seek medical attention
3. Obtain a 12-lead ECG
4. Promote myocardial perfusion
! Instruct patient to maintain bed rest
! Administer O2 @ 3 lpm
! Advise to avoid valsalva maneuvers
! Provide laxatives or high fiber diet to lessen constipation
! Encourage to avoid increased physical activities
5. Assist in possible treatment modalities
! PTCA- percutaneous transluminal coronary angioplasty
! To compress the plaque against the vessel wall, increasing the arterial lumen
! CABG- coronary artery bypass graft
! To improve the blood flow to the myocardial tissue
6. Provide information to family members to minimize anxiety and promote family cooperation
7. Assist client to identify risk factors that can be modified
8. Refer patient to proper agencies
Myocardial infarction
- Death of myocardial tissue in regions of the heart with abrupt interruption of coronary blood supply
FIGURE 13-1 Different degrees of damage occur to the heart muscle after a myocardial infarction. The diagram

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shows the zones of necrosis, injury, and ischemia.
ETIOLOGY and Risk factors

1. CAD
2. Coronary vasospasm
3. Coronary artery occlusion by embolus and thrombus
4. Conditions that decrease perfusion- hemorrhage, shock
Risk factors
1. Hypercholesterolemia
2. Smoking
3. Hypertension
4. Obesity
5. Stress
Pathophysiology
- Interrupted coronary blood flow% myocardial ischemia % anaerobic myocardial metabolism for several hours %
myocardial death % depressed cardiac function % triggers autonomic nervous system response % further imbalance
of myocardial O2 demand and supply
Assessment Findings
1. Chest Pain
- Chest pain is described as severe, persistent, crushing substernal discomfort
- Radiates to the neck, arm, jaw and back
- Occurs without cause, primarily early morning
- NOT relieved by rest or nitroglycerin
- Lasts 30 minutes or longer
2. Dyspnea
3. Diaphoresis
4. cold clammy skin
5. N/V
6. restlessness, sense of doom
7. tachycardia or bradycardia
8. hypotension
9. S3 and dysrhythmias
Laboratory Findings
1. ECG- the ST segment is ELEVATED, T wave inversion, presence of Q wave
2. Myocardial enzymes- elevated CK-MB, LDH and Troponin levels

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3. CBC- may show elevated WBC count

4. Test after the acute stage - Exercise tolerance test, thallium scans, cardiac catheterization
Pain
-

Impaired gas exchange
Activity intolerance
Altered tissue perfusion
Constipation
Nursing Intevention
1. Provide Oxygen at 2 lpm, Semi-fowlers
2. Administer medications
- Morphine to relieve pain
- Nitrates, thrombolytics, aspirin and anticoagulants
- Stool softener and hypolipidemics
3. Minimize patient anxiety
- Provide information as to procedures and drug therapy
- Allow verbalization of feelings
- Morphine can be administered
4. Provide adequate rest periods
- Bed rest during acute stage
5. Minimize metabolic demands
- Provide soft diet
- Provide a low-sodium, low cholesterol and low fat diet
6. Assist in treatment modalities such as PTCA and CABG
7. Monitor for complications of MI- especially dysrhythmias, since ventricular tachycardia can happen in the first few
hours after MI
8. Provide client teaching
Medical Management
1. Analgesic
- The choice is MORPHINE
- It reduces pain and anxiety
- Relaxes bronchioles to enhance oxygenation
2. ACE inhibitors
- Prevents formation of angiotensin II
- Limits the area of infarction
3. Thrombolytic therapy

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- Streptokinase, Alteplase
- Dissolve clots in the coronary artery allowing blood to flow
Nursing Interventions After Acute Episode
1. Maintain bed rest for the first 3 days
2. Provide passive ROM exercises
3. Progress with dangling of the feet at side of bed
4. Proceed with sitting out of bed, on the chair for 30 minutes TID
5. Proceed with ambulation in the room % toilet % hallway TID
6. Cardiac rehabilitation
- To extend and improve quality of life
- Physical conditioning
- Patients who are able to walk 3-4 mph are usually ready to resume sexual activities
Infective endocarditis
- Infection of the heart valves and the endothelial surface of the heart
Can be acute, sub-acute or chronic
Etiologic factors
1. Bacteria- Organism depends on several factors
2. Fungi
Risk factors
1.
2.
3.
4.
5.
Prosthetic valves
Congenital malformation
Cardiomyopathy
IV drug users
Valvular dysfunctions
Assessment findings
1. Intermittent high grade fever
2. anorexia, weight loss
3. cough, back pain and joint pain
4. splinter hemorrhages under nails
5. Oslers nodes- painful nodules on fingerpads
6. Roths spots- pale hemorrhages in the retina
7. Heart murmurs
8. Heart failure= usually acute heart failure
Prevention
- Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy, surgery, etc.
- Any invasive procedure that is associated with transient bacteremia may cause the microrganism to lodge in the
damaged, irregular valves
Laboratory Exam
- Blood Cultures to determine the exact organism
! Usually, 3 culture specimens are obtained and antibiotic sensitivity done
Nursing management
1. Regular monitoring of temperature, heart sounds
2. Manage infection

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3. Long-term antibiotic therapy is given to ensure eradication of bacteria

Medical management
1. Pharmacotherapy
- IV antibiotic for 2-6 weeks
- Antifungal agents are given amphotericin B
2. Surgery
3. Valvular replacement
Congestive Heart Failure (CHF)

(CHF)
- A syndrome of congestion of both pulmonary and systemic circulation caused by inadequate cardiac function and
inadequate cardiac output to meet the metabolic demands of tissues
- Inability of the heart to pump sufficiently
- The heart is unable to maintain adequate circulation to meet the metabolic needs of the body
This can happen acutely or chronically

- Acute% in Myocardial infarction
- Chronic % cardiomyopathies
Classified according to the major ventricular dysfunction
1. Left Ventricular failure
2. Right ventricular failure
Etiology of CHF
1. CAD
2. Valvular heart diseases
3. Hypertension
4. MI
5. Cardiomyopathy
6. Lung diseases
7. Post-partum
8. Pericarditis and cardiac tamponade
Class 1
- Ordinary physical activity does NOT cause chest pain and fatigue
- No pulmonary congestion
- Asymptomatic
- NO limitation of ADLs
Class 2
- SLIGHT limitation of ADLs
- NO symptom at rest
- Symptoms with INCREASED activity
- Basilar crackles and S3
Class 3
- Markedly limitation on ADLs
- Comfortable at rest BUT symptoms present in LESS than ordinary activity
Class 4
- SYMPTOMS are present at rest

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PATHOPHYSIOLOGY
LEFT Ventricular pump failure
back up of blood into the pulmonary veins
increased pulmonary capillary pressure
pulmonary congestion (edema)
Pulmonary manifestations
LEFT ventricular failure
Decreased perfusion to the brain, kidney and other tissues
Cerebral anoxia, fatigue, oliguria, dizziness

RIGHT ventricular failure
blood pooling in the venous circulation
increased hydrostatic pressure
peripheral edema
RIGHT ventricular failure
Venous blood pooling
venous congestion in the kidney, liver and GIT

Left Sided CHF Assessment Findings
1. Dyspnea on exertion, activity intolerance
2. PND
3. Orthopnea
4. Pulmonary crackles/rales
5. Cough with Pinkish, frothy sputum
6. Tachycardia
7. Cool extremities
8. Cyanosis
9. decreased peripheral pulses
10. Fatigue
11. Oliguria
12. signs of cerebral anoxia
Right Sided CHF Assessment Findings
1. Peripheral dependent, pitting edema
2. Weight gain
3. Distended neck vein
4. hepatomegaly

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5.
6.
7.
8.
9.
Ascites
Body weakness
Anorexia, nausea
Pulsus alternans
Nocturia= urination at night at frequent intervals as the blood moves from interstitial space to the intravascular
space and is excreted
Laboratory Findings
1. CXR may reveal cardiomegaly
2. ECG may identify Cardiac hypertrophy
3. Echocardiogram may show hypokinetic heart
4. ABG and Pulse oximetry may show decreased O2 saturation
5. PCWP is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF
Nursing Interventions
1. Assess patient's cardio-pulmonary status
2. Assess VS, CVP and PCWP. Weigh patient daily to monitor fluid retention
3. Administer medications- usually cardiac glycosides are given- DIGOXIN or DIGITOXIN, Diuretics, vasodilators and
hypolipidemics are prescribed
Cardiotonics
To increase cardiac contractility
Diuretics
Low Sodium Diet
Hypolipidemics
To decrease the intravascular volume in the circulation

To minimize water retention
To decrease the lipid levels of high risk patients
Positive inotropic agents
Digoxin Health teaching

- Oral tablet usually once a day
- Increases force of contraction
- DECREASES heart rate
- Assess: Apical pulse, ECG, hypokalemia
- Withhold the drug if apical pulse is less than 60
- Note for early signs of toxicity: NAVDA
- Provide potassium supplements
4. Provide a LOW sodium diet. Limit fluid intake as necessary
5. Provide adequate rest periods to prevent fatigue
6. Position on semi-fowlers to fowlers for adequate chest expansion
7. Prevent complications of immobility
Nursing Intervention after the Acute Stage
1. Provide opportunities for verbalization of feelings
2. Instruct the patient about the medication regimen- digitalis, vasodilators and diuretics
3. Instruct to avoid OTC drugs, Stimulants, smoking and alcohol
4. Provide a LOW fat and LOW sodium diet
5. Provide potassium supplements
6. Instruct about fluid restriction
7. Provide adequate rest periods and schedule activities
8. Monitor daily weight and report signs of fluid retention
CARDIAC TAMPONADE

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- A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial
effusion)
- This condition restricts ventricular filling resulting to decreased cardiac output
- Acute tamponade may happen when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac
Causative factors
1. Cardiac trauma
2. Complication of Myocardial infarction
3. Pericarditis
4. Cancer metastasis
Assessment Findings
1. BECKs Triad- Jugular vein distention, hypotension and distant/muffled heart sound
2. Pulsus paradoxus
3. Increased CVP
4. decreased cardiac output
5. Syncope
6. anxiety
7. dyspnea
8. Percussion- Flatness across the anterior chest
Laboratory Findings
1. Echocardiogram= shows accumulate fluid in the pericardial sac
2. Chest X-ray
1. Assist in PERICARDIOCENTESIS
2. Administer IVF
3. Monitor ECG, urine output and BP
4. Monitor for recurrence of tamponade
Pericardiocentesis
- Patient is monitored by ECG
- Maintain emergency equipments
- Elevate head of bed 45-60 degrees
- Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration and myocardial trauma
Vascular Diseases
General Measures to Improve Peripheral Circulation
1. Implement Regular Physical Activity to facilitate movement of venous blood
2. Eliminate cigarette smoking- to prevent vasoconstriction
3. Control hyperlipidemia and cholesterol levels- to prevent the progression of atherosclerosis
4. Avoid cold environmental temperature
5. Teach clients to assess fingers and toes daily for circulatory adequacy: Check the peripheral pulses, capillary refill and
temp
6. Report break in the skin
Hypertension
- A systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg over a sustained period, based on
two or more BP measurements.
Types of Hypertension

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1.
2.
-
Primary or Essential
Most common type
Secondary
Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushings, Conns , SIADH
CLASSIFICATION OF BP FOR ADULTS 18 YRS AND OLDER (PHIL. SOCIETY OF HPN)

Optimal
o <120 mmHg / <80 mmHg
Recheck in 2 years.
Normal
o 120-129 mmHg / 80-84 mmHg
Recheck in 2 years.
High normal
o 130-139 mmHg / 85-89 mmHg
Recheck in 1 year.
Stage 1 (mild) HPN
o 140-159 mmHg / 90-99 mmHg
Confirm in 2 months.
Stage 2 (moderate) HPN
o 160-179 mmHg / 100-109 mmHg
Evaluate within a month.
Stage 3 (severe) HPN
o 180-209 mmHg / 110-119mmHg
Evaluate within a week.
Stage 4 (very severe) HPN
o 210 mmHg / >/=120 mmHg Evaluate
Pathophysiology
- Multi-factorial etiology
o BP= CO (SV X HR) x TPR
Any increase in the above parameters will increase BP
Risk factors for
for Cardiovascular Problems in Hypertensive patients
Major Risk factors
1. Smoking
2. Hyperlipidemia
3. DM
4. Age older than 60
5. Gender- Male and post menopausal women
6. Family History

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Any increase in the above parameters will increase BP

1. Increased sympathetic activity
2. Increased absorption of Sodium, and water in the kidney
3. Increased activity of the RAAS
4. Increased vasoconstriction of the peripheral vessels
5. Insulin resistance
Assessment Findings
1. Headache
2. Visual changes
3. chest pain
4. dizziness
5. N/V
Diagnostic Studies
1. Health history and PE
2. Routine laboratory- urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS
3. Other lab- CXR, creatinine clearance, 24-huour urine protein
Medical Management
1. Lifestyle modification
2. Diet therapy
3. Drug therapy
MEDICAL MANAGEMENT
Drug therapy
- Diuretics
- Beta blockers
- Calcium channel blockers
- ACE inhibitors
- A2 Receptor blockers
- Vasodilators
1. Provide health teaching to patient
- Teach about the disease process
- Elaborate on lifestyle changes
- Assist in meal planning to lose weight
- Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day
- Limit alcohol intake to 30 ml/day
- Regular aerobic exercise
- Advise to completely Stop smoking
2. Provide information about anti-hypertensive drugs
- Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition
- Instruct to avoid over-the-counter drugs that may interfere with the current medication
3. Promote Home care management
- Instruct regular monitoring of BP
- Involve family members in care
- Instruct regular follow-up
4. Manage hypertensive emergency and urgency properly

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Aneurysm
- Dilation involving an artery formed at a weak point in the vessel wall

- Saccular= when one side of the vessel is affected
- Fusiform= when the entire segment becomes dilated
Risk Factors
1. Atherosclerosis
2. Infection= syphilis
3. Connective tissue disorder
4. Genetic disorder= Marfans Syndrome
Pathophysiology
- Damage to the intima and media% weakness %outpouching of vessel wall
- Dissecting aneurysm% tear in the intima and media with dissection of blood through the layers
Assessment
1. Asymptomatic
2. Pulsatile sensation on the abdomen
3. Palpable bruit
Laboratory:
- CT scan
- Ultrasound
- X-ray
- Aortography
Medical Management:
- Anti-hypertensives
- Synthetic graft
Nursing Management:
- Administer medications
- Emphasize the need to avoid increased abdominal pressure
- No deep abdominal palpation
- Remind patient the need for serial ultrasound to detect diameter changes.
Peripheral Arterial Occlusive Disease
- Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis.
- Usually found in males age 50 and above
- The legs are most often affected
Risk factors for Peripheral Arterial occlusive disease
Non-Modifiable
1. Age
2. gender
3. family predisposition
Modifiable
1. Smoking
2. HPN
3. Obesity
5. DM
6. Stress

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Assessment Findings
1. INTERMITTENT CLAUDICATION- the hallmark of PAOD
- This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same degree of
exercise or activity
- This pain is RELIEVED by REST
- This commonly affects the muscle group below the arterial occlusion
2. Progressive pain on the extremity as the disease advances
3. Sensation of cold and numbness of the extremities
4. Skin is pale when elevated and cyanotic and ruddy when placed on a dependent position
5. Muscle atrophy, leg ulceration and gangrene
Diagnostic Findings
1. Unequal pulses between the extremities
2. Duplex ultrasonography
3. Doppler flow studies
Medical Management
1. Drug therapy
- Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles
- Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation
2. Surgery- Bypass graft and anastomoses
1. Maintain Circulation to the extremity
- Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time
- Administer post-operative care to patient who underwent surgery
- Administer heat modalities to the leg cautiously to promote vasodilatation
2. Monitor and manage complications
- Note for bleeding, hematoma, and decreased urine output
- Elevate the legs to diminish edema
- Encourage exercise of the extremity while on bed
- Teach patient to avoid leg-crossing
3. Promote Home management
- Encourage lifestyle changes
- Instruct to AVOID smoking
- Instruct to avoid leg crossing
BUERGERS DISEASE
Thromboangiitis obliterans
- A disease characterized by recurring inflammation of the medium and small arteries and veins of the lower
extremities
- Occurs in MEN ages 20-35
- RISK FACTOR: SMOKING!
Pathophysiology
Pathophysiology
- Cause is UNKNOWN
- Probably an Autoimmune disease
- Inflammation of the arteries and veins% thrombus formation % occlusion of the vessel
Assessment Findings
1. Leg PAIN
- Foot cramps in the arch

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- (INSTEP CLAUDICATION) after exercise

- Relieved by rest
- Aggravated by smoking, emotional disturbance and cold chilling
2. Digital rest pain not changed by activity or rest
3. Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances
4. Paresthesias
Diagnostic Studies
1. Duplex ultrasonography
2. Contrast angiography
1. Assist in the medical and surgical management
- Bypass graft
- amputation
2. Strongly advise to AVOID smoking
3. Manage complications appropriately
PostPost-operative care: after amputation
- Elevate stump for the FIRST 24 HOURS to minimize edema and promote venous return
- Place patient on PRONE position after 24 hours several times a day
- Assess skin for bleeding and hematoma
- Wrap the extremity with elastic bandage
Raynauds Disease
- A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain and pallor of the fingertips or toes
- Cause : UNKNOWN
- Most commonly affects WOMEN, 16- 40 years old
Assessment Findings
1. Raynauds phenomenon
- A localized episode of vasoconstriction of the small arteries of the hands and feet that causes color and temperature
changes
W-B-R is the acronym for the color change
- Pallor- due to vasoconstriction, then %
- Blue- due to pooling of Deoxygenated blood
- Red- due to exaggerated reflow or hyperemia
2. Tingling sensation
3. Burning pain on the hands and feet
Medical management
- Drug therapy with the use of CALCIUM channel blockers
! To prevent vasospasms
1. Instruct patient to avoid situations that may be stressful
2. Instruct to avoid exposure to cold and remain indoors when the climate is cold
3. Instruct to avoid all kinds of nicotine
4. Instruct about safety. Careful handling of sharp objects
Venous diseases

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Varicose Veins
- THESE are dilated veins usually in the lower extremities
Predisposing Factors
! Pregnancy
! Prolonged standing or sitting
! Incompetent venous valves
Pathophysiology
Factors % venous stasis %increased hydrostatic pressure% edema
Assessment findings
- Tortuous superficial veins on the legs
- Leg pain and Heaviness
- Dependent edema
Laboratory findings
- Venography
- Duplex scan pletysmography
Medical management
- Pharmacological therapy
- Leg vein stripping and ligation
- Anti-embolic stockings
Nursing management
1. Advise patient to elevate the legs with pillow to increase venous return
2. Caution patient to avoid prolonged standing or sitting
3. Provide high-fiber foods to prevent constipation
4. Teach simple exercise to promote venous return
5. Caution patient to avoid constrictive clothing
6. Apply anti-embolic stockings as directed
7. Avoid massage on the affected area
DVTDVT- Deep Vein Thrombosis
- Inflammation of the deep veins of the lower extremities and the pelvic veins
- The inflammation results to formation of blood clots in the area
Predisposing factors
- Prolonged immobility
- Varicosities
- Traumatic procedures
- Increased age
- Malignancy
- Estrogen therapy
- Smoking
Complication
- PULMONARY thromboembolism
Assessment findings
- Leg tenderness
- Leg pain and edema
- Positive HOMANs SIGN

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HOMANs SIGN
The foot is FLEXED upward (dorsiflexed) , there is a sharp pain felt in the calf of the leg% indicative of venous
inflammation
Laboratory findings
- Venography
- Duplex scan
Medical management
- Antiplatelets- aspirin
- Anticoagulants
- Vein stripping and grafting
- Anti-embolic stockings
Nursing management
1. Provide measures to avoid prolonged immobility
- Repositioning Q2
- Provide passive ROM
- Early ambulation
2. Provide skin care to prevent the complication of leg ulcers
3. Provide anti-embolic stockings
4. Administer anticoagulants as prescribed
5. Monitor for signs of pulmonary embolism% sudden respiratory distress
Blood disorders
$Anemia
$Nutritional anemia
$Hemolytic anemia
$Aplastic anemia
$Sickle cell anemia
Anemia
- A condition in which the hemoglobin concentration is lower than normal
Three broad categories

1. Loss of RBC- occurs with bleeding
2. Decreased RBC production
3. Increased RBC destruction
Hypoproliferative Anemia
Iron Deficiency Anemia
- Results when the dietary intake of iron is inadequate to produce hemoglobin

Etiologic Factors
1. Bleeding- the most common cause

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2. Mal-absorption
3. Malnutrition
4. Alcoholism
Pathophysiology
- The body stores of iron decrease, leading to depletion of hemoglobin synthesis
- The oxygen carrying capacity of hemoglobin is reduced% tissue hypoxia
Assessment Findings
1. Pallor of the skin and mucous membrane
2. Weakness and fatigue
3. General malaise
4. Pica
5. Brittle nails
6. Smooth and sore tongue
7. Angular cheilosis
Laboratory findings
1. CBC- Low levels of Hct, Hgb and RBC count
2. Low serum iron, low ferritin
3. Bone marrow aspiration- MOST definitive
Medical management
1. Hematinics
2. Blood transfusion
Nursing Management
1. Provide iron rich-foods
- Organ meats (liver)
- Beans
- Leafy green vegetables
- Raisins and molasses
2.
-
Administer iron
Oral preparations tablets- Fe fumarate, sulfate and gluconate
Advise to take iron ONE hour before meals
Take it with vitamin C
Continue taking it for several months
Oral preparations- liquid
It stains teeth
Drink it with a straw
Stool may turn blackish- dark in color
Advise to eat high-fiber diet to counteract constipation
IM preparation
Administer DEEP IM using the Z-track method
Avoid vigorous rubbing
Can cause local pain and staining
Aplastic Anemia
- A condition characterized by decreased number of RBC as well as WBC and platelets
Causative Factors

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1.
2.
3.
4.
Environmental toxins- pesticides, benzene

Certain drugs- Chemotherapeutic agents, chloramphenicol, phenothiazines, Sulfonamides
Heavy metals
Radiation
Pathophysiology
Toxins cause a direct bone marrow depression
Acellular bone marrow
decreased production of blood elements

PANCYTOPENIA
Assessment Findings
- fatigue
- pallor
- dyspnea
- bruising
- splenomegaly
- retinal hemorrhages
Laboratory Findings
1. CBC- decreased blood cell numbers
2. Bone marrow aspiration confirms the anemia- hypoplastic or acellular marrow replaced by fats
Medical Management
1. Bone marrow transplantation
2. Immunosupressant drugs
3. Rarely, steroids
4. Blood transfusion
Nursing management
1. Assess for signs of bleeding and infection
2. Instruct to avoid exposure to offending agents
Megaloblastic Anemias
- Anemias characterized by abnormally large RBC secondary to impaired DNA synthesis due to deficiency of Folic acid
and/or vitamin B12
Folic Acid deficiency
Causative factors
1. Alcoholism
2. Mal-absorption
3. Diet deficient in uncooked vegetables
Pathophysiology of Folic acid deficiency

Decreased folic acid
impaired DNA synthesis in the bone marrow
Impaired RBC development, impaired nuclear maturation but CYTOplasmic maturation continues
large size

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Vitamin B12 deficiency

deficiency
Causative factors
1. Strict vegetarian diet
2. Gastrointestinal mal-absorption
3. Crohn's disease
4. Gastrectomy
Vitamin B12 deficiency: Pernicious Anemia
- Due to the absence of intrinsic factor secreted by the parietal cells
- Intrinsic factor binds with Vit. B12 to promote absorption
Assessment findings
1. weakness
2. fatigue
3. listless
4. neurologic manifestations are present only in Vit. B12 deficiency
Assessment findings
Pernicious Anemia
- Beefy, red, swollen tongue
- Mild diarrhea
- Extreme pallor
- Paresthesias in the extremities
Laboratory findings
1. Peripheral blood smear- shows giant RBCs, WBCs with giant hyper-segmented nuclei
2. Very high MCV
3. Schillings test
4. Intrinsic factor antibody test
Medical Management
1. Vitamin supplementation
2. Folic acid 1 mg daily
3. Diet supplementation
4. Vegetarians should have vitamin intake
5. Lifetime monthly injection of IM Vit B12
Nursing Management
1. Monitor patient
2. Provide assistance in ambulation
3. Oral care for tongue sore
4. Explain the need for lifetime IM injection of vit B12
Hemolytic Anemia: Sickle Cell

Cell
- A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene.
Causative factor
- Genetic inheritance of the sickle gene- HbS gene
Pathophysiology
Decreased O2, Cold, Vasoconstriction can precipitate sickling process
Factors % cause defective hemoglobin to acquire a rigid, crystal-like C-shaped configuration % Sickled RBCs will adhere to
endothelium % pile up and plug the vessels % ischemia results% pain, swelling and fever
Assessment Findings

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1. jaundice (hemolytic jaundice)

2. enlarged skull and facial bones
3. tachycardia, murmurs and cardiomegaly
- Primary sites of thrombotic occlusion: spleen, lungs and CNS
- Chest pain, dyspnea
Assessment Findings
1. Sickle cell crises
- Results from tissue hypoxia and necrosis
2. Acute chest syndrome
- Manifested by a rapidly falling hemoglobin level, tachycardia, fever and chest infiltrates in the CXR
Medical Management
1. Bone marrow transplant
2. Hydroxyurea
3. Increases the HbF
4. Long term RBC transfusion
Nursing Management
1. manage the pain
Support and elevate acutely inflamed joint
Relaxation techniques
analgesics
2. Prevent and manage infection
Monitor status of patient
Initiate prompt antibiotic therapy
3. Promote coping skills
- Provide accurate information
- Allow patient to verbalize her concerns about medication, prognosis and future pregnancy
4. Monitor and prevent potential complications
- Provide always adequate hydration
- Avoid cold, temperature that may cause vasoconstriction
- Leg ulcer
! Aseptic technique
- Priapism
! Sudden painful erection
! Instruct patient to empty bladder, then take a warm bath
Polycythemia
! Refers to an INCREASE volume of RBCs

! The hematocrit is ELEVATED to more than 55%
! Classified as Primary or Secondary
Primary Polycythemia
- A proliferative disorder in which the myeloid stem cells become uncontrolled
Causative factor
- unknown
Pathophysiology
- The stem cells grow uncontrollably
- The bone marrow becomes HYPERcellular and all the blood cells are increased in number

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- The spleen resumes its function of hematopoiesis and enlarges

- Blood becomes thick and viscous causing sluggish circulation
- Overtime, the bone marrow becomes fibrotic
Assessment findings
- Skin is ruddy
- Splenomegaly
- headache
- dizziness, blurred vision
- Angina, dyspnea and thrombophlebitis
Laboratory findings
1. CBC- shows elevated RBC mass
2. Normal oxygen saturation
3. Elevated WBC and Platelets
Complications
1. Increased risk for thrombophlebitis, CVA and MI
2. Bleeding due to dysfunctional blood cells
Medical Management
1. To reduce the high blood cell mass- PHLEBOTOMY
2. Allopurinol
3. Dipyridamole
4. Chemotherapy to suppress bone marrow
Nursing Management
1. Primary role of the nurse is EDUCATOR
2. Regularly asses for the development of complications
3. Assist in weekly phlebotomy
4. Advise to avoid alcohol and aspirin
5. Advise tepid sponge bath or cool water to manage pruritus
RESPIRATORY SYSTEM DISORDERS

GENERAL RESPIRATORY ANATOMY AND PHYSIOLOGY
I.
General Respiratory Anatomy and Physiology

A.
The respiratory system is comprised of the upper airway and lower airway structures.
B.
The upper respiratory system filters, moistens and warms air during inspiration.

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C.
II.
The lower respiratory system enables the exchange of gases to regulate serum PaO2, PaCO2 and Ph.
Upper Respiratory
A.
Nose and sinuses
1. Filters, warms and humidifies air
2. First defense against foreign particles
3. Inhalation for deep breathing is to be done via nose
4. Exhalation is done through the mouth
B.
Pharynx
1. Behind oral and nasal cavities
2. Nasopharynx
a.
behind nose
b.
soft palate, adenoids and eustachian tube
3. Oropharynx
a.
from soft palate to base of tongue
b.
palatine tonsils
4. Laryngopharynx
a.
base of tongue to esophagus
b.
where food and fluids are separated from air
c.
bifurcation of larynx and esophagus
C.
Larynx
1. Between trachea and pharynx
2. Commonly called the voice box
3. Thyroid cartilage - Adam's apple
4. Cricoid cartilage
a.
contains vocal cords
b.
the only complete ring in the airway
5. Glottis - opening between vocal cords
6. Epiglottis - covers airway during swallowing

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III.
Lower Respiratory and Other Structures
A.
B.
C.
D.
E.
Trachea
1. Anterior neck in front of esophagus
2. Carries air to lungs
Mainstem bronchi
1. Right and left
2. Right is more vertical, so right middle lobe is more likely to receive aspirate into it with the result
of aspiraton pneumonia, which is more commonly found in elderly populations
Conducting airways
1. Lobar bronchi
a.
surrounded by blood vessels, lymphatics, nerves
b.
lined with ciliated, columnar epithelial cell
c.
cilia move mucus or foreign substances up to larger airways
2. Bronchioles
a.
no cartilage; collapse more easily
b.
no cilia
c.
do not participate in gas exchange
Alveolar ducts and alveoli
1. Lungs contain approximately 300 million alveoli
2. Alveoli surrounded by capillary network
3. Gas exchange area (blood takes O2, gives off CO2)
4. Gas exchange happens at alveolar-capillary membrane (al-cap memb)
5. Held open by surfactant which decreases surface tension to minimize alveolar collapse
Accessory muscles of respiration

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1.
2.
3.
4.
IV.
Scalene muscles - elevate first two ribs

Sternocleidomastoid - raise sternum
Trapezius and pectoralis - stabilize shoulders
Abdominal muscles - puts power into cough and used most often with chronic respiratory
problems and acute severe respiratory distress
Physiology
A.
Basic gas-exchange unit of the respiratory system is the alveoli.
B.
Alveolar stretch receptors respond to inspiration by sending signals to inhibit inspiratory neurons in the
brain stem to prevent lung over distention.
C.
During expiration stretch receptors stop sending signals to inspiratory neurons and inspiration is ready to
start again.
D.
Oxygen and carbon dioxide are exchanged across the alveolar capillary membrane by process of diffusion.
E.
Neural control of respirations is located in the medulla. The respiratory center in the medulla is stimulated
by the concentration of carbon dioxide in the blood.
F.
Chemoreceptors, a secondary feedback system, located in the carotid arteries and aortic arch respond to
hypoxemia. These chemoreceptors also stimulate the medulla.
G.
Ph regulation
1. Blood Ph (partial pressure of hydrogen in blood): a decrease in blood Ph stimulates respiration
hyperventilation, both through the neurons of the brain's respiratory center and through the
chemoreceptors in carotid arteries and aortic arch.
2. Blood PaCO2 (partial pressure of carbon dioxide in arterial blood): an increase in the PaCO2 results
in decreased blood Ph, and stimulates respiration.
3. Blood PaO2 (partial pressure of oxygen in arterial blood): a decrease in the PaO2 results in a
decreased blood Ph, stimulating respiration.
4. When arterial Ph rises or the arterial PaCO2 falls, hypoventilation occurs.
FUNCTION
A. Primary functions of the respiratory system
1. Provides oxygen for metabolism in the tissues
2. Removes carbon dioxide, the waste product of metabolism
B. Secondary functions of the respiratory system
1. Facilitates sense of smell
2. Produces speech
3. Maintains acid-base balance
4. Maintains body water levels
5. Maintains heat balance
ASSESSMENT OF RESPIRATORY FUNCTION
A. DIAGNOSTIC STUDIES
"
Chest x-ray film (radiograph)

> Provides information regarding the anatomical location and appearance of the lungs
Nursing Responsibilities
Preprocedure
a. Remove all jewelry and other metal objects from the chest area.

Page 35
"
"
"
b. Assess the client's ability to inhale and hold his or her breath.
c. Question women regarding pregnancy or the possibility of pregnancy.
Sputum specimen
> Specimen obtained by expectoration or tracheal suctioning to assist in the identification of organisms or
abnormal cells
Preprocedure
a. Determine specific purpose of collection
b. Obtain an early morning sterile specimen
c. Instruct the client to rinse the mouth with water before collection.
d. Obtain 15 mL of sputum.
e. Instruct the client to take several deep breaths and then deeply to obtain sputum.
f. Always collect the specimen before the client begins antibiotic therapy.
3. Postprocedure
a. If a culture of sputum is prescribed, transport the specimen to the laboratory immediately.
b. Assist the client with mouth care.
Bronchoscopy
> Direct visual examination of the larynx, trachea, and bronchi with a fiberoptic bronchoscope
Preprocedure
a. Obtain informed consent.
b. NPO post midnight
c. Obtain vital signs.
d. Remove dentures or eyeglasses.
e. Prepare suction equipment.
Postprocedure
a. Monitor vital signs.
b. Maintain the client in a semi-Fowler's position.
c. Assess for the return of the gag reflex.
d. Maintain NPO status until the gag reflex returns.
e. Have an emesis basin readily available for the client to expectorate sputum.
f. Monitor for bloody sputum.
g. Monitor respiratory status
h. Monitor for complications
i. Notify the physician if fever, difficulty in breathing, or other signs of complications occur following the
procedure.
Pulmonary angiography
> An invasive fluoroscopic procedure in which a catheter is inserted through the antecubital or femoral
vein into the pulmonary artery or one of its branches
> Involves an injection of iodine or radiopaque contrast material
Preprocedure
b. Assess for allergies to iodine, seafood, or other radiopaque dyes.
c. NPO for 8 hours before the procedure.
d. Monitor vital signs.
e. Assess results of coagulation studies.
f. Establish an intravenous access.
g. Administer sedation as prescribed.
h. Instruct the client to lie still during the procedure.
i. Instruct the client that he or she may feel an urge to cough, flushing, nausea, or a salty taste following
injection of the dye.
j. Have emergency resuscitation equipment available.
Postprocedure

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"
"
"
"
"
"
"
"
"
"
"
"
"
"
b. Avoid taking blood pressures for 24 hours in the extremity used for the injection.
c. Monitor peripheral neurovascular status of the affected extremity.
d. Assess insertion site for bleeding.
e. Monitor for delayed reaction to the dye.
Thoracentesis
> Removal of fluid or air from the pleural space via a transthoracic aspiration
Preprocedure
b. Obtain vital signs.
c. Assess results of coagulation studies.
d. Place client in sitting position, with the arms and shoulders supported by a table at the bedside during
the procedure.
e. If the client cannot sit up, the client is placed lying in bed toward the unaffected side, with the head of
the bed elevated.
f. Instruct the client not to cough, breath deeply, or move during the procedure.
Postprocedure
b. Monitor respiratory status.
c. Apply a pressure dressing, and assess the puncture site for bleeding and crepitus.
d. Monitor for signs of pneumothorax, air embolism, and pulmonary edema.
Lung biopsy
> A percutaneous lung biopsy is performed to obtain tissue for analysis by culture or cytological
examination.
Preprocedure
b. Maintain NPO status of the client before the procedure.
c. Inform the client that a local anesthetic will be
d. Administer analgesics and sedatives as prescribed.
Postprocedure
b. Apply a dressing to the biopsy site and monitor for drainage or bleeding.
c. Monitor for signs of respiratory distress.
d. Monitor for signs of pneumothorax and air emboli, and notify the physician if they occur.
Pulse Oximetry
& measures oxygen saturation of hemoglobin
& 90-100%
Arterial Blood Gas Analysis
& measures concentrations of blood gases and identifies acid base balance of the body
& use of arterial blood
Pulmonary Function Test
& Measures lung volumes and capacity
& Done by respiratory therapists; painless; client will breath into a machine
Tidal volume (VT)- volume of inhaled and exhaled during normal and quiet breathing
Inspiratory reserve volume (IRV)- maximum amount of air that can be inhaled over and above the normal
breath
Expiratory reserve volume maximum amount of air that can be exhaled following a normal exhalation
Residual volume (RV)- amount of air remaining in the lungs after maximal exhalation
Total lung capacity (TLC)- total volume of lungs at maximum inflation; VT + IRV + ERV + RV
Vital capacity (VC)- total amount of air that can be exhaled after a maximal inspiration; VT+ IRV + ERV
Inspiratory capacity- total amount of air that can be inhaled following normal quiet respiration; VT + IRV
Functional residual capacity (FRC)- volume left in the lungs after normal exhalation; ERV +RV
Minute volume (MV)- total amount of air breathed in one minute

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B. COMMON SIGNS AND SYMPTOMS:

"
"
"
"
"
"
"
"
"
"
"
"
"
"
"
"
"
Cough
& Most common sign of respiratory disease
& Caused by irritation of mucous membranes
& Chief protection against accumulation of secretions and foreign body
Chest pain: may indicate hypoxia or damage to lungs
Cyanosis and Clubbing of fingers: indicates hypoxia
Hemoptysis: blood expectorated from the respiratory tract; caused by trauma or break in the continuity of
respiratory tract
Effort in breathing: Dyspnea or Orthopnea
Sputum production
Reaction of lungs to constantly recurring irritation
Thoracic sounds
Crackles: loud, low pitched bubbling sound; results from air passing through fluid
Wheezes: musical sound; caused by air passing through narrowed airways
Stridor: loud, high pitched crowing sound
Friction rub: grating, loud harsh sound
Ronchi: sounds likes snores or moans
Chest Configuration- AP: L= 1:2
Barrel chest- increase in AP diameter
Pigeon chest- increase in AP diameter; results from sternal displacement
Funnel chest- depression of lower portion of sternum
C. HISTORY:
1. Current respiratory problems:
" Changes in breathing pattern
" Activities that may cause symptoms
" How many pillows used at night
2. History of respiratory disease
" Any respiratory diseases or infections
" Frequency of occurrence
" Exposure to pollutants
3. Lifestyle
" Smoking history
" Exposure to smoke and other respiratory irritants
" Alcohol use
" Exercise pattern
4. Presence of cough
" How often
" When does it occur
" Productive or dry
5. Description of sputum
" When it is produced
" Amount, color, thickness, odor
" Presence of blood
6. Presence of chest pain
" Location
" Description
" Does it occur with inspiration or expiration
" How long does it affect breathing

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" Aggravating and alleviating factors

7. Presence of risk factors
" History of respiratory diseases in the family
8. Medication History
" OTC prescriptions for breathing e.g. bronchodilators
UPPER RESPIRATORY DISEASES
RHINITIS
Allergic Rhinitis
Definition:
is a group of disorders characterized by inflammation and irritation of the mucous

membranes of the nose.
It may be classified as nonallergic or allergic.
Rhinitis may be an acute or chronic condition.
Cause:
pollen, flowers, grasses and occur in spring/fall; last several weeks while allergens are high.
.
Signs/Symptoms:
rhinorrhea (excessive nasal drainage, runny nose)

nasal congestion
nasal discharge (purulent with bacterial rhinitis)
nasal itchiness
sneezing
Headache may occur, particularly if sinusitis is also present.
Treatment:
Identify and avoid triggers

Antihistamines
Decongestants
Desensitization
Acute Viral Rhinitis

Definition:
Common cold (acute coryza).

Page 39
used when referring to an upper respiratory tract infection that is self-limited and caused
by a virus (viral rhinitis).
Cause:
Virus that invades the upper respiratory tract. Is the most prevalent infectious disease in
the world and is spread by airborne droplets.
Signs/Symptoms:
malaise
fever/chills
headache
nasal discomfort
dry, sore throat
cough (either productive or nonproductive)
mild leukocytosis
*Complications:
Treatment:
laryngitis, sinusitis, otitis media, tonsillitis, and lung infection.

no specific treatment for the common cold or influenza.
Symptomatic therapy.
Some measures include
! providing adequate fluid intake
! encouraging rest
! increasing intake of vitamin C
! using expectorants as needed.
! Warm salt-water gargles soothe the sore throat
! nonsteroidal anti-inflammatory agents (NSAIDs) such as aspirin or ibuprofen relieve
the aches, pains, and fever in adults.
! Antihistamines are used to relieve sneezing, rhinorrhea,
! Nasal congestion. Topical (nasal) decongestant agents
! Echinacea, an herbal therapy, stimulates immune system and has antibacterial and antiinflammatory properties. Considered safe when taken at recommended doses for 10
to 14 days. Do not take for more than 8 weeks. Patients with immune disorders
should not use Echinacea.
INFLUENZA
Definition:
Flu
Cause:
Three groups of viruses (A, B & C, though C has little pathogenic effects)
Signs/Symptoms:
Abrupt onset of cough, fever, and myalgia often accompanied by headache and sore
throat. Symptoms of uncomplicated flu usually subside within 7 days. Some experience
weakness and lassitude, hyperactive airways and chronic cough that may persist for weeks
(older adults, especially).
PNEUMONIA is the most common complication of flu.
Diagnostic Tests:
Viral cultures or throat or nasal swabbings

Culture and Sensitivity Test
Treatment:
Vaccine is 70 to 90% effective in preventing flu when given in the fall (mid-Oct) before
exposure occurs.
Treatment is primarily symptomatic
Acetaminophen is given for fever, headache, and myalgia
Rest and increase fluid intake

Page 40
Antiviral Zanamivir(Relenza) and Oseltamivir (Tamiflu)

Amantadine (Symmetrel)
Other viral infection
Bird Flu
SARS
aH1N1
LOWER RESPIRATORY DISEASES
ACUTE BRONCHITIS
Definition:
Inflammation of the bronchi in the lower respiratory tract usually due to infection.
Cause:
Usually occurs as a complication of an upper respiratory tract infection brought on by a

virus (rhinovirus, influenza, corona virus, respiratory synctial virus (RSV), adenovirus,
influenza A and B, parainfluenza).
Bacterial infections are also common
Signs/Symptoms:
Chilliness
Malaise
Soreness and constriction behind the sternum-worse patient cough
Slight fever
Cough, at first dry and painful; later, green or yellowish sputum with pus cells
Persistent cough following an acute upper airway infection (rhinitis/pharyngitis)
Diagnosis:
When symptoms are severe, chest x-rays can differentiate acute bronchitis from
pneumonia (acute bronchitis has no evidence of consolidation or infiltrates).
Treatment:
Usually self-limiting; treatment is supportive
Fluids
Rest
Anti-inflammatory agents
Antiviral medications
Cough suppressant or bronchodilators for symptomatic treatment of nocturnal

cough/wheezing
Other symptom relief to reduce complaints
PNEUMONIA
Definition:
An acute inflammation of the lung parenchyma that commonly impairs gas exchange.
Cause:
Pneumonia may be viral, bacterial, fungal, protozoal (parasitic), or chemical in origin.

Bacterial pneumonia:

Page 41
Infection initially triggers alveolar inflammation and edema, which produces an

area of low ventilation with normal perfusion.
Capillaries become engorged with blood, causing stasis.
As alveolocapillary membrane breaks down, alveoli fill with blood and exudate,
resulting in atelectasis (lung collapse)
Lungs look heavy and liver-like.
Viral pneumonia:
The virus first attacks bronchiolar epithelial cells, which causes interstitial
inflammation and desquamation.
The virus also invades bronchial mucous glands and goblet cells.
It spreads to the alveoli, which fill with blood and fluid.
Aspiration pneumonia:
Types & Classifications:
Inhalation of gastric juices or hydrocarbons trigger inflammation and inactivates

surfactant over a large area.
Decreased surfactant leads to alveolar collapse.
Acidic gastric juices may damage the airways and alveoli. Particles containing
aspirated gastric juices may obstruct the airways and reduce airflow, leading to
secondary bacterial pneumonia.
Community-Acquired Pneumonia (CAP)
A lower respiratory tract infection of the lung parenchyma with onset in the
community or during the first 2 days of hospitalization.
Highest incidence in winter months
Smoking is a high risk factor
Hospital-Acquired Pneumonia (HAP)
Pneumonia occurring 48 hours or longer after hospital admission and not

incubating at the time of hospitalization.
Risk for HAP in mechanically ventilated patients is 6 to 20 times higher than other
patients.
Inpatient mortality rates much higher than mortality for CAP (1-5% vs. 12%)
Aspiration Pneumonia
The sequelae occurring from abnormal entry of secretions or substances into the
lower airway. Usually follows aspiration of material from the mouth or stomach
into the trachea and subsequently the lungs.
Usually patient has a history of loss of consciousness (seizure, anesthesia, head

injury, stroke, alcohol intake), with gag and cough reflex depression or is on tube
feedings.
Opportunistic Pneumonia
Affects patients with compromised immune systems.

Page 42
Pneumocystis carinii = HIV/AIDS.
Cytomegalovirus (type of herpes virus) = organ transplant patients.
Chest x-ray shows diffuse bilateral

alveolar pattern of infiltration. In widespread disease, lungs are massively
consolidated. Treat with Bactrim.
Gives rise to latent infections and reactivation with virus shedding. May
be mild or can be fulminant and produce pulmonary insufficiency leading
to death. In pneumonia, may be combined with other bacteria and fungi.
Treat with Cytovene.
Signs/Symptoms:
Diagnosis:
Chest x-ray
Sputum cultures
For drug-resistant pathogens
Organisms not responsive to empiric treatment (broad-spectrum antibiotics)
Should be done before administration of antibiotics
Blood tests
Treatment:
For seriously ill patients, collect two cultures before treatment
ABGs usually reveal hypoxemia
Leukocytosis found in bacterial pneumonia (>15,000/microliter)
Supportive measures:
Oxygen therapy (hypoxemia)
Analgesics for chest pain
Antipyretics (aspirin/Tylenol) for fever
Restrict activity and encourage rest
Viral pneumonia

Page 43
No definitive treatment is recommended
Prevent or treat flu

o
Flu vaccine
Empiric treatment of flu includes amantadine, rimantadine or a

neuraminidase inhibitor
Pneumococcal vaccine
For people at risk

o Chronic illness (lung/heart disease; diabetes)
o
o
Recovering from severe illness

65 years or older
Living in a long-term care facility
Nutritional therapy
Role of Nurse:
Fluid intake of at least 3 L per day to support treatment; may need to be

administered by IV
Minimum of 1500 calories per day
Goals
Eat small, frequent meals.
Clear breath sounds
Normal breathing patterns
No signs of hypoxia
Normal chest x-ray
No
complications
related
to
pneumonia
TUBERCULOSIS
Definition:
An infectious disease caused by Mycobacterium tuberculosis. Usually involves the lungs,

but may occur in the larynx, kidneys, bones, adrenal glands, lymph nodes and meninges
and can be disseminated throughout the body.
Cause:
M. tuberculosis is a gram-positive, acid-fast bacillus that is spread from person to person

via airborne droplets, which are produced when the infected individual with pulmonary
or laryngeal TB coughs, sneezes, speaks or sings.
Risk factors:
Poor, under-served minorities
Homeless people
Residents of inner-city neighborhoods
Foreign-born people
Older adults
Institutionalized people
IV/injection drug users

Page 44
Socioeconomically disadvantaged
Medically underserved of all races
Immunosuppressed people (HIV, cancer, organ transplant)
Health care workers
TB is not highly infectious and transmission usually requires close, frequent or prolonged
exposure.
Signs/Symptoms:
Diagnosis:
Tuberculin Skin Testing
o
o
o
Antigen/Antibody reaction testuses purified protein derivative (PPD) of

tuberculin to detect TB antibodies from a previous immune response.
Once acquired, sensitivity to TB persists throughout life.
Reaction of >5 mm induration is positive for patients with
o
o
Recent close contact with person diagnosed with infectious TB

Chest x-ray with fibrotic lesions likely to be healed TB
Known or suspected HIV infection
o Organ transplants and other immunosuppressive conditions

Reaction of >10 mm induration is positive for patients
o
With other medical risk factors known to substantially increase risk of TB

once infection has occurred (diabetes, renal disease, cancer)

Page 45
Who recently immigrated from (in past 5 years) from areas of high
prevalence
Who are medically under-served or homeless
o
o
o
Who reside in long-term care facilities and prisons

Who use IV drugs
Who are health care workers
o Who are low risk for TB

Reaction of >15 mm induration is positive for all others at low risk.
Chest X-ray
Bacteriologic Studies
o
o
True diagnosis can only be made by demonstrating the presence of tubercle bacilli.
Stained sputum smear for acid-fast bacilli is usually the first bacteriologic evidence
of infection.
o
Three consecutive sputum specimens collected on different days are

tested.
Treatment: Outpatient Treatment

o
o
Patient may continue to work and maintain lifestyle

Hospitalization is only for diagnosis or for severe illness, adverse drug reactions or
treatment failures.
Drug Therapy
o
Active Disease
o
o
Treatment usually consists of a combination of at least four drugs.

Five primary drugs currently used are:
'
Isoniazid (INH)
'
'
Rifampin (Rifamate)
Pyrazinamide
'
'
Streptomycin
Ethambutol (Myambutol)
Fixed-dose combo drugs (INH/rifampin and INH/rifampin/pyrazinamide)

are available and may enhance compliance to treatment
o
o
Therapy must be continued for 6 to 9 months.

Monitor the effectiveness of drugs and the development of toxic side
effects.
Follow-up care ensures adherence to the treatment regimen with Directly
Observed Therapy (DOT) with patients known to be at risk for
noncompliance.
The major side effect of INH, rifampin and pyrazinamide is HEPATITIS.
o
Vaccine
o
Immunization with bacilli Calmette-Guerin (BCG) vaccine prevents.
Role of Nurse: Goals:

Page 46
Patient will comply with therapeutic regimen
o
o
Patient will have no recurrence of disease

Patient will have normal pulmonary function
Patient will take appropriate measures to prevent the spread of disease.
Interventions:
o
Assess symptomatic patient for exposure to persons with TB.
Patients strongly suspected of having TB should
o
o
Be placed on respiratory isolation

Receive four-drug therapy
Receive an immediate medical work-up, including chest x-ray, sputum

smear and culture
Use a negative pressure isolation room that offers six or more exchanges
per hour to isolate patient.
Teach patient to cover the nose and mouth with paper tissue every time he or she
coughs, sneezes or produces sputum. The tissues should be burned, flushed down
the toilet or thrown into a paper bag and disposed of with the trash.
Instruct the patient about certain factors that could reactivate TB such as
immunosuppressive therapy, malignancy and prolonged debilitation.
OBSTRUCTIVE PULMONARY DISEASE

The most common chronic lung diseases and are characterized by increased resistance to airflow as a result of
airway obstruction or airway narrowing.
Includes four conditions:
o
Asthma (allergic reaction)
Emphysema (COPD)
Chronic Bronchitis (COPD)
ASTHMA
Definition:
An obstructive pulmonary disease characterized by airway inflammation, and non-specific

hyperirritability or hyper-responsiveness of the tracheobronchial tree (bronchospasm). The
hyper-responsiveness seen in asthma is caused by bronchoconstriction in response to physical,
chemical and pharmacological agents.
Cause:
Allergens
Exaggerated allergic response (IgE) to environmental factors (dust, pollen, grass, mites,
roaches, mold, dander, etc.).
Exercise
Exercise-Induced Asthma
Occurs within several minutes of vigorous exercise

Page 47
Respiratory Infections
Most common precipitating factor of an acute asthma attack.
Bacterial infections cause inflammatory changes
Nose, Sinuses and Drugs/Food Additives
Asthma-Triad.Nasal polyps, asthma, sensitivity to aspirin and NSAIDS
Nose and Sinus Problems
Allergic rhinitis (seasonal or perennial) and nasal polyps contribute to asthma

problems
Treat/prevent sinusitis and remove large nasal polyps
Drug Allergies
o
Exposure to ASA/NSAIDS = wheezing within 2 hours
Avoid Beta blockers (propranolol, timolol, other -olol drugs)
Avoid ACE inhibitors
Food Allergies
o
Avoid exposure to Tartrazine (yellow dye #5 found in many foods)
Avoid vitamins
Avoid sodium metabisulfite (food preservative in fruit, beer/wine and salad

bars).
Emotional Stress
Psychological or emotional stress may be a trigger
Panic and anxiety during an attack may exacerbate and prolong the attack
Signs/Symptoms:

Page 48
Early-Phase Response
'
bronchospasm
'
inflammatory response.
'
Immediate response that peaks within 30 to 60 minutes of exposure to the trigger.
'
Symptoms: wheezing, chest tightness, dyspnea and cough.
Late-Phase Response
'
Characterized by inflammation,
inflammation constriction of bronchioles and excess mucus.
mucus
'
Late-phase response peaks 5 to 6 hours after exposure and may last for days.
'
WBC infiltration
'
This activity increases airway reactivity which worsens the symptoms of future attacks, and
makes them easier to trigger.
'
increased work of breathing.
'
airway remodeling.
Clinical Manifestations of asthma:
Recurrent episodes of wheezing, breathlessness, dyspnea, chest tightness and cough

(particularly at night and in the early morning) after exposure to a trigger
Characterized by prolonged expiration (wheezing upon expiration, air trapping and

hyperinflation).
Diminished or absent breath sounds during attack is an ominous sign
Person may sit upright or slightly bent forward using the accessory muscles of respiration
to try to get enough air.
Attacks may last a few minutes to several hours.

Page 49
Symptoms of hypoxia occur: restlessness, anxiety, inappropriate behavior, increased pulse

and blood pressure, significantly increased respiratory rate (>30 breaths per minute) with
use of accessory muscles.
* Status Asthmaticus
Severe, life-threatening attack that does not respond to usual treatment.
The longer it lasts, the worse it gets and the worse it gets, the longer it lasts.
Caused by viruses; aspirin/NSAIDS; stress; environmental pollutants; allergens; abrupt

discontinuation of drug therapy (corticosteroids); abuse of aerosol medication; use of
beta-blockers.
Symptoms same as asthma, but more severe and more prolonged with extreme anxiety,
fear of suffocation, diaphoresis and severely increased work of breathing.
Chest remains in hyperinflated state; hypertension, sinus tachycardia and ventricular

arrhythmias may occur (related to hypoxemia).
History and physical examination
Pulmonary function studies including response to bronchodilator therapy
Peak expiratory flow monitoring
Chest X-Ray
Measurement of ABGs or Oximetry
Allergy skin testing (if indicated)
Blood level of eosinophils and IgE.
Diagnosis:
Treatment:
Acute Episode:
Oxygen therapy immediately with pulse oximetry and ABGs
Inhaled B2-agonists by metered-dose inhaler (MDI) with spacer or nebulizer

every 20 minutes to 4 hours as necessary.
If no response in 30 to 60 minutes, use oral corticosteroids, or if severeIV

corticosteroids. IV aminophylline may be considered, but effectiveness is
questionable.
Continue treatment until patient breathes comfortably, wheezing has stopped

and pulmonary function results are near baselines.
Status Asthmaticus:
o
Correct hypoxemia and improve ventilation
Same interventions as for acute asthma (above), but may need to increase the
frequency and dose of inhaled bronchodilators to 2 to 6 puffs every 5 to 20
minutes (depending upon medication).
Continuous monitoring of patient is critical.
If B2-agonists do not work, use IV corticosteroids (methylprednisolone) every 4

to 6 hours (peaks in 12 hours).

Page 50
IV mag sulfate and subcutaneous epinephrine may act as bronchodilators. If

administered, monitor BP and EKG closely.
Oxygen therapy and IV fluids (for hydration) are usually required.
Severe, non-responsive attacks may require mechanical ventilation.
Even after bronchospasm resolves, inflammation, edema, and viscous mucus plugs
remain for several days.
Drug classifications
o
Two categories:
'
Long-term control (achieve/maintain control of persistent asthma)
'
Role of Nurse:
Coricosteroids (anti-inflammatory)
Quick-relief (treat symptoms and exacerbations)
Mast cell stailizers (cromolyn, nedocromil)
Bronchodilators
o
B2-agonists (albuterol)
Anticholinergics (Atrovent)
methylxanthine derivatives (theophylline)
Interventions
Administer oxygen
Administer bronchodilators
Perform chest physiotherapy
Administer medications as ordered
Continuously monitor patients condition
Monitor effectiveness of treatments
Decrease the patients sense of panic; encourage slow breathing using pursed lips for
prolonged exhalation
Provide rest and a quiet, calm environment for the patient
COPD/EMPHYSEMA & CHRONIC BRONCHITIS

Definition:
Group of diseases with the major characteristic of airflow obstruction and hyper-reactivity of
airway. Symptoms include difficulty with exhalation caused by airway obstruction from edema
or excessive mucus production. Lung hyperinflation causes alveolar air trapping and leads to
frequent pulmonary infections. Symptoms are usually progressive and irreversible.
Emphysema:
Emphysema an abnormal, permanent enlargement of the airspaces distal to the terminal
bronchioles, accompanied by destruction of their walls and without obvious fibrosis.
Chronic Bronchitis:
Bronchitis the presence of a chronic productive cough for 3 months in each of 2
successive years in a patient in whom other causes of chronic cough have been excluded.

Page 51
Cause:
Cigarette Smoking.
Infection
Heredity
Aging
Signs/Symptoms: Emphysema:
Emphysema
Two typesbut may overlap in some patients

Page 52
Centrilobular
'
Involves central part of the lobule
'
Bronchioles enlarge, walls are destroyed and bronchioles become

confluent (merge together)
Panlobular
'
Involves distention and destruction of the whole lobule.
'
Bronchioles, alveolar ducts and sacs, and alveoli are affected
'
Progressive loss of lung tissue and decreased alveolar-capillary surface

area results
Barrel chest;
Underweight
Hypoxemia (early sign) and hypercapnia (late sign)
Chronic Bronchitis
Hyperplasia of mucus-secreting glands in the trachea and bronchi
Increase in goblet cells
Disappearance of cilia
Chronic inflammatory changes and narrowing of small airways
Altered function of alveolar macrophages, leading to increased bronchial infections

Page 53
High colonization with microorganisms = increased infection risks
Chronic inflammation causes narrowing of the airway lumen = diminished airflow
Hypoxemia and hypercapnia develop more frequently than in emphysema
Diminished respiratory drive (hypoventilation and retention of CO2)
Symptoms
Diagnosis:
H & P; chest x-ray; pulmonary function tests; sputum specimens for culturing; ABGs; EKGs;
exercise testing with oximetry; cardiac nuclear scans
Treatment:
Goals:
Improve ventilation
Promote secretion removal
Prevent complications and progression of symptoms
Promote patient comfort and participation in care
Improve quality of life as much as possible
Avoid environmental pollutants
Treat infections immediately

Page 54
Stop smoking
Drug therapy:
Bronchodilators (as a maintenance therapy, not for acute symptoms)

o
Beta-2 agonists are commonly used
MDI or nebulizer
Anticholinergics are more effective in emphysema
Oxygen therapy
o
Raises the partial pressure of O2 in inspired air to treat hypoxemia
Humidification and nebulizers

'
O2 is dry and irritating and must be humidified before delivery
Complications of O2 Therapy
'
Combustion
'
CO2 Narcosis (Oxygen-Drive for breathing may get eliminated if

oxygen is administered)
'
O2 Toxicity (from prolonged exposure to O2; may inactivate pulmonary

surfactant and lead to ARDS (acute respiratory distress syndrome).
'
Infection (humidity encourages growth of bacteria in lungs)
Respiratory Therapy
Breathing retraining (pursed lip breathing; diaphragmatic/abdominal; practice 8 -10 reps;

3-4 x per day )
Effective coughing techniques
Chest physiotherapy
Exercise; pulmonary conditioning; smoking cessation and COPD support groups
Nutritional Therapy
Maintain weight
Rest for 30 minutes before eating
Use bronchodilator before meals
Eat five to six small meals (avoid bloating which puts pressure on diaphragm)
Liquid/pureed diets may be helpful
Avoid foods that require a lot of chewing
Avoid exercise within 1 hour of eating
Bloating/early satiety may be related to swallowing air, position of diaphragm or side

effects of meds
High calorie/high protein recommended for emphysema
High carbs metabolize into high CO2, and should be avoided

Page 55
Fluid intake should be at least 3 L per day unless contraindicated, and between meals
rather than with meals
ENDOCRINE SYSTEMS DISORDERS
Scope
Physiology
Disorders
PITUITARY DISEASES
ADH DISEASES
ADRENAL GLANDS DISEASES
THYROID DISEASES
PARATHYROID DISEASES
PANCREAS DISEASES
Major Hormone Secreting Glands

Page 56
The Sequence
Hypothalamus
Pituitary
Anterior
Posterior
Target
Gland
or
Hypophysis
Adenohypophysis
Neurohypophysis
or
or
Glands
The ANATOMY of the Endocrine System

The Hypothalamus
- This part of the DIENCEPHALON is located below the thalamus and is connected to the pituitary gland by a stalk
Physiology
- Secretes RELEASING HORMONES for the pituitary gland
- Releasing hormones= hypothalamus
The Pituitary Gland
- Is a gland located below the hypothalamus at the base of the brain.
APG
Adenohypophysis
- TSH - target % thyroid gland
- ACTH - target % adrenal gland
- ICSH - target % testes (maturation of spermatozoa)
- GH - target % epiphyseal plate (bone growth)
- FSH target % ovary-estrogen (maturation of graafian follicles to release mature ovum)
- LH target % graafian follicle (formation of corpus luteum to maturation of ova)
- MSH skin (pigmentation)
- PROLACTIN (maturation of mammary gland and production of milk)
PPG
Neurohypophysis
- ADH
target
(H2O reabsorption)
- OXYTOCIN uterine contraction and ejection of milk
kidney
tubules

Page 57
Pituitary Gland and Its Hormones
Target Glands
Thyroid
Adrenal
Mammary
Skin
Bone plates
Ovaries
Testes
Kidney tubules
Uterus
Thyroid and Parathyroid
The THYROID gland
Anatomy
- Located in the anterior neck lateral to the trachea
- Contains two lobes connected by the isthmus
- Microscopically composed of thyroid follicles where the hormones are produced and stored
The PARAthyroid glands

Anatomy
- Located at the back of the thyroid glands
- Four in number
Follicular Cells- T3, T4- BMR, and

CHON and bone turnover
T3- metabolism, growth
T4- catabolism, body heat production
C Cells- Calcitonin - calcium & phosphate levels
Parathormone -calcium & phosphorus regulation, osteoclast
The Physiology
Parathyroid Hormone is released
in HYPOCALCEMIA
- calcium level
Parathyroid hormone is NOT
secreted in HYPERCALCEMIA
Calcitonin
is
stimulated
HYPERCALCEMIA
-calcium level
Calcitonin
is
inhibited
HYPOCALCEMIA
by
by

Page 58
The Adrenal Glands

Anatomy
- Located above the kidneys
- Composed of two parts- the outer Adrenal Cortex and the inner Adrenal medulla
Cortex
! Mineralocorticoid:Aldosterone -Na & water reabsorption, K loss
! Glucocorticoid: Cortisol - blood glucose regulation
! Androgen: DHEA - sex hormones testosterone
Medulla (catecholamines)
! stress or sympathetic effect
! Epinephrine and Nor-epinephrine
- neurotransmitters
The GONADS
Anatomy
Ovaries
These two almond-shaped glands are found in the pelvic cavity attached to the uterus by the ovarian ligament
Testes
These two oval-shaped glands are found in the scrotum
Physiology
Ovary
estrogen
affects
devt
of
female
sex
organs
and
secondary
sexual
- progesterone- influences menstrual cycle, stimulates the growth of uterine wall, and maintains pregnancy
Testes
- testosterone- affects the devt of male sex organs and secondary sexual characteristics
Pineal
characteristics
Gland
Melatonin (dec skin pigmentation, inhibit gonadotropic hormone)
The Pancreas
- This retroperitoneal organ has both endocrine and exocrine functions
Anatomy
- The endocrine function resides in the ISLETS of Langerhans
- The islets have three types of cells- alpha, beta and delta cells
Physiology
- The ALPHA cells secrete GLUCAGON
- The BETA cells secrete INSULIN
- The DELTA cells secrete SOMATOSTATIN

Page 59
Placenta
- HCG- maintains pregnancy
- estrogen, progesterone, human placental lactogen
! Pancreas:
Islet
of
langerhans
Alpha- glucagon- blood sugar (hyperglycemia) by stimulating glycogenolysis & gluconeogenesis
! Beta- insulin - blood sugar (hypoglycemia) by facilitating transport of glucose across cell membranes of muscle, liver,
adipose tissue, inhibits breakdown of proteins
DISORDERS OF THE ENDOCRINE GLAND

Disorders are generally grouped into:
1. HYPER- when the gland secretes excessive hormones
2. HYPO- when the gland does not secrete enough hormones
Hyper and Hypo can be classified as PRIMARY when the Gland itself is the problem or SECONDARY when the pituitary or
the hypothalamus is causing the problem
PITUITARY GLAND DISORDERS
$HYPOPITUITARISM
$HYPERPITUITARISM
$PITUITARY TUMORS
Hypopituitarism
- Hypofunction of the pituitary gland
Caused by:
- trauma, tumor at the hypothalamus or pituitary gland
- complication from radiation therapy (head and neck)
- Panhypopituitarism (Simmonds Disease)- total absence of pituitary secretions
- Sheehans Syndrome postpartum pituitary necrosis (bleeding)
Manifestations:
- Related to hypofunction of:
! thyroid hypometabolism
! gonads amenorrhea, impotence
! adrenal glands - adrenal insufficiency
! growth hormone dwarfism, hypoglycemia
- Hemianopsia and headache (if due to tumor)
- Increased ICP (if due to tumor)
Assessment Findings
- Retarded physical growth due to decreased GH% dwarfism
- Low intellectual development
- poor development of secondary sexual characteristics

Page 60
Management:
- Surgical removal of tumor
- Radiation
- HRT hormonal replacement therapy
Pituitary Tumors
- Usually benign
- 3 Types
! Eosinophilic Tumors
! Basophilic Tumors
! Chromophobic Tumors (most common)
Eosinophilic Tumors
- Gigantism (before puberty)
- Acromegaly (after puberty)
- Visual disturbance (compression from tumor)
Hyperpituitarism
- hyper-secretion of the gland
- ACROMEGALY-after 15-16 yo
- Gigantism-before 15-16 yo
Causes: tumor, congenital disorder

Page 61
Assessment Findings
1. Increased growth% Gigantism or Acromegaly
2. large and thick hands and feet
3. Visual disturbances
4. Hypertension, hyperglycemia
5. Organomegaly
Pituitary Tumors
Basophilic Tumors
- Cushings Syndrome
- Musculinization and amenorrhea (female)
Chromophobic Tumors (COMMON)
- Destroy the rest of the pituitary gland
- No hormones except for prolactin (galactorrhea)
- Blindness
- Increased ICP
Diagnostic:
- CT scan
- MRI
- Assessment Findings
Management:
- Drug
Bromocriptine (Parlodel) to lower GH and Prolactin
- Radiation
- Surgery
(transsphenoidal
Octreotide (Sandostatin) = preop drug to reduce tumor

hypophysectomy)
Page 62
Post op Care: HYPOPHYSECTOMY

- Head elevation for 2 weeks/ Semi- Fowlers position
- Nasal packing, Avoid sneezing, coughing
Oral care
- Monitor LOC and neurologic status
- No activity that will increase ICP
- Watchout Diabetes Insipidus, Monitor I & O
- Observe for CSF leakage
- Administer prescribed medications
DISORDERS OF THE POSTERIOR PITUITARY GLAND: ADH Abnormality

$SIADH
$DI
SIADH Syndrome of Inappropriate Anti Diuretic Hormone
- Increased secretion of ADH
- Increased
tubular
reabsorption
of
= water intoxication and increased blood volume (hypervolemia): (low Hct, hypoosmolality, edema)
- Decreased
urine
=
concentrated
(high S.G., dark urine)
- Watch out for manifestations of Fluid Volume Excess
- Cause: over medication of vasopressin and benign pituitary tumor
water
output
urine
ASSESSMENT findings
- Signs of Hypervolemia
1. Mental status changes
2. Abnormal weight gain
3. DISORDERS OF the PITUITARY GLAND: Posterior gland
4. ASSESSMENT findings
5. Hypertension
6. Anorexia, Nausea and Vomiting
7. HYPOnatremia
Diagnostic Test
- Urine specific gravity is increased (concentrated)
- Hyponatremia
- CBC shows hemodilution
- SIADH
Management:
- FVE intervention
- Stop vasopressin
- Surgery (tumor excision)
Critical conditions:
- Pulmonary edema

Page 63
Cerebral edema
Heart failure
Hypertension
Renal Failure
1. Monitor VS and neurologic status
2. Provide safe environment
3. Restrict fluid intake (less than 500cc/day)
4. Monitor I and O and daily weight
5. Administer Diuretics and IVF carefully
6. Administer prescribed Demeclocycline to inhibit action of ADH in the kidney
DI Diabetes Insipidus
- Decreased ADH secretion
- Decreased
tubular
reabsorption
of
=
decreased
blood
(high Hct, hyperosmolality, thrombosis)
- Increased
urine
= diluted urine (low S.G., clear urine)
- Watch out for manifestations of Fluid Volume Deficit
- Cause: trauma or injury to pituitary gland, resection of hypophysis, insensitivity of kidney to ADH
water
volume
output
Assessment findings
1. Polyuria of more than 4 liters of urine/day
2. Polydipsia
3. Signs of Dehydration
4. Muscle pain and weakness
5. Postural hypotension and tachycardia
Diagnostic Test
1. Urinary Specific gravity % very low, 1.006 or less
2. Serum Sodium levels % high
Management:
- FVD intervention
- Synthetic ADH administration (vasopressin)
- Desmopressin (DDAVP) spray intranasal OD or BID
- Vasopressin tannate in oil = IM OD or every 4 days
- Thrombosis thromboembolism pulmonary embolism
- Ischemia
- Infarction
- Necrosis (CVA, MI, RF)
1. Monitor VS, neurologic status and cardiovascular status
2. Monitor Intake and Output
3. Monitor urine specific gravity
4. Provide adequate fluids
5. Administer Chlorpropamide or Clofibrate as prescribed to increase the action of ADH if decreased
6. Administer VASOPRESIN. Desmopressin or Lypressin are given intranasal. Pitressin is given IM
Abnormalities of Adrenal Gland

Page 64
$Conns
$Cushings Disease
$Cushings Syndrome
$Addisons Disease
$Pheochromocytoma
Conns Disease or Primary Hyperaldosteronism

- Adrenal cortex disorder
- Over secretion of aldosterone or mineralocorticoid
- Increased Na and H2O reabsorption=FVE
- Increased K urinary excretion=hypokalemia
- Watch out for manifestations of:
# SIADH
# Hypervolemia or FVE / Hypertension
# Hypokalemia (arrhythmias)
# Hypernatremia
Caused:
- tumor and trauma of the adrenal cortex
Conns Management:
- FVE intervention
- Stop sodium intake
- Critical conditions:
- Arrhythmias
- Hypertension
- Same with SIADH
1. Monitor VS, I and O and urine sp gravity
2. Monitor serum K and Na
3. Provide Potassium rich foods and supplements
4. Administer prescribed diuretic- Spironolactone- K sparer
5. Maintain sodium-restricted diet
6. Prepare patient for possible surgical interventions
Cushings Disease (Primary)
! Adrenal cortex disorder/ tumor, pituitary tumor
! Over secretion of
! Mineralocorticoid: Aldosterone = Na and H2O retention, K excretion
! Glucocorticoid = hyperglycemia
! Androgen
! Female: hoarseness of voice, hirsutism, clitoris
! Steroids = buffalo neck, trunkal obesity
Pathophysiology
Normal functions
Glucocorticoids:
Cortisol
1. Gluconeogenesis
of
Exaggerated functions
HYPERGLYCEMIA

Page 65
2. Protein breakdown
OSTEOPOROSISS,
delayed wound healing
Purplish striae , Bleeding
Muscle wasting
THIN extremity, Truncal
deposition
IMMUNOSUPPRESSION
3. Fat breakdown
4. Decreased WBC
Functions
Mineralocorticoids
1. Sodium Retention
of
Exaggerated functions
Hypernatremia
2.Secondary
water
retention
3. Potassium excretion
HypervolemaHypertension
HYPOKALEMIA
Function of
Hair growth
HIRSUTISM
androgen:
Assessment
1. Generalized muscle weakness and wasting
2. Truncal obesity
3. Moon-face
4. Buffalo hump
5. Easy bruisability
6. Reddish-purplish striae on the abdomen and thighs

7. Hirsutism and acne
8. Hypertension
9. Hyperglycemia
10. Osteoporosis
11. Amenorrhea

Page 66
Management:
! Diet: Low Sodium, High Potassium
! FVE intervention
! Replace potassium
! Insulin administration
! Hypertension
! Surgery is adrenalectomy
! Arrhythmias due to hypoK
! Hypertensive crisis
! Fluid overload
! Hyperglycemia
Cushings Syndrome (Secondary)
- Pituitary gland disorder
- Same with Cushings Disease
- Surgery is hypophysectomy
Addisons Disease
- Adrenal cortex disorder/ tumor, idiopathic
- Hyposecretion of:
! Mineralocorticoid: Aldosterone=Na and H2O excretion (hyponatremia, hypovolemia, hypotension), K reabsorption
(hyperkalemia)
! Glucocorticoid=hypoglycemia
! Androgen=decreased libido
MSH=bronzing of the skin (primary)
Management
- FVD intervention
- Increase potassium excretion
- Glucagon or simple sugar administration
- Steroid medication
- Monitor VS especially BP
- Monitor weight and I and O
- Monitor blood glucose level and K
- Administer hormonal agents as prescribed
- Observe for ADDISONIAN crisis
- Educate the client regarding lifelong treatment, avoidance of strenuous activities, stress and seeking prompt consult
during illness
- Provide a high-protein, high carbohydrate and increased sodium intake
Addisonian crisis
- A life-threatening disorders caused by acute severe adrenal insufficiency

Page 67
Causes:
- Severe stress
- infection
- trauma or surgery
Pathophysiology
- Overwhelming stimuli % mobilize body defense % decreased stress hormones % inadequate coping
ASSESSMENT Findings for Addisonian Crisis= severe lahat
- Severe headache
- Severe pain
- Severe weakness
- Severe hypotension
- Signs of Shock
- Addisons Disease
Critical Conditions:
- Addisonian crisis cyanosis, with signs of circulatory shock: pallor, apprehension, rapid and weak pulse,
- RR, and acute hypotension
- Dehydration
- Arrhythmias due to hyperkalemia
- Hypoglycemia
- Same with DI
- Administer IV glucocorticoids, usually hydrocortisone
- Monitor VS frequently
- Monitor I and O, neurological status, electrolyte imbalances and blood glucose
- Administer IVF
- Maintain bed rest
- Administer prescribed antibiotics
Steroid
- Dose is variable
- Best time to give between 7-8 AM (active gland) to prevent side effects
- Steroid-induced adrenal insufficiency = TAPERING the DOSE
- Pituitary adrenal suppresion = DOSAGE CONTROL
-
Steroid
Hypertension, thromboembolism
Prone to infection
Glaucoma, corneal ulceration
Muscle wasting, poor wound healing
Osteoporosis,
Hyperglycemia
Weight gain, moon face, trunkal obesity, buffalo hump
Acne
MEDIC-ALERT CARD
Addisons Disease
Critical Conditions
- Dehydration
- Arrhythmias due to hyperK
- Hypovolemic shock
- Hypoglycemia
- Same with DI
- inc ACTH, inc cortisol = pituitary problem (benign tumor)
- normal ACTH, inc cortisol = adrenal problem (benign tumor)
- dec ACTH, dec cortisol = atrophy of the pituitary gland
- normal ACTH, dec cortisol = atrophy of the adrenal gland
Pheochromocytoma
- Hyperfunction of adrenal medulla
- Cause: Tumor usually benign
- catecholamines (nor E and E)
Sign and Symptoms:
- 5 H: HPN, Headache, Hypermetabolism
- Hyperglycemia, Hyperhidrosis(sweat),, n&v, anorexia, dilated pupils, weight loss, tremors, cold extremities, CHF and
cerebral bleeding.

Page 68
Diagnosis
- VMA vanilly mandelic acid (urine specimen)
- catecholamines (blood specimen)
- blood sugar and glycosuria
- Monitor VS esp BP
- Give antihypertensive drugs:Phentolamine
- Provide high calorie foods
- Prepare pt forSurgical Intervention (adrenalectomy)
Abnormalities
of
the
Thyroid
Gland
GOITER
- Iodine-deficient
- Goitrogenic = cabbage, beans
- Compensatory hypertrophy
- No s/sx, compression of the trachea
- SSKI to suppress pituitarys TSH secretions
- Less than 40 fg/day of iodine = goiter
- Iodized salt = 1:100,000
- PREVENTION = iodized salt
$Hypothyroidism
$Hyperthyroidism
Note:
! inc T3, inc T4, dec TSH = thyroid problem
! inc T3, inc T4, inc TSH = pituitary tumor (benign)
Hypothyroidism
Caused by:
- Autoimmune Disease (Hashimotos Thyroiditis)
- Use of radioactive iodine
- Destruction or removal of thyroid tissue
- Overtreatment of antithyroid drug

Page 69
! MYXEDEMA- Adults
! CRETINISM- Children
3 Basic Concepts:
- Decreased metabolic rate due to hyposecretion of T3
- Decreased body heat production due to hyposecretion of T4
- Hypercalcemia due to hyposecretion of calcitonin
Assessment
1. Lethargy and fatigue
2. Weakness and paresthesia
3. COLD intolerance
4. Weight gain
5. Bradycardia, constipation
6. Dry hair and skin, loss of body hair
7. Generalized puffiness and edema around the eyes and face
Cont of s/sx
- SQ swelling, puffy skin, puffy eyelids
- Thinning of hair, loss of lateral 1/3 of the eyebrow
- Menorrhagia or amenorrhea, decreased libido, abortions
- Myxedema = severe complication leads to coma
Management
- Symptomatic
- Monitor VS and daily weights
- Provide warm environment
- Diet: low calorie, high fiber
- Thyroid hormone replacement
- T4 Synthroid, Levothyroid
- T3 Cytomel
- T3 & T4 Proloid
- T3 given NGT, faster than T4
- T4 given parenterally(S.E. adrenal insuf.)
- Note: 3-12 wks S/Sx must disappear
Hyperthyroidism
Caused by:
! Graves Disease: Autoimmune
! TSAb thyroid stimulating antibody duplicate

Page 70
! TSH, which increases thyroid hormone secretion ( T3 and T4)

! Toxic nodular goiter (benign, hot spot)
! Overmedication of thyroid hormone
! Severe emotional stress
3 Basic Concepts:
! Increased metabolic rate due to hypersecretion of T3
! Increased body heat production due to hypersecretion of T4
! Hypocalcemia due to hypersecretion of calcitonin
Manifestations:
! Nervousness, tremors, emotional lability
! Weight loss, emaciated
! Flushed skin, warm and moist
! Increased temp and palpitation to atrial fibrillation
! Heat intolerance
! Hypertension
! Difficulty in sitting quietly
! Thyroid gland may be palpable and a (+) bruit
! Diarrhea
! Bulging eyes (exophthalmus), startled expression
! Amenorrhea, oligomenorrhea, decreased libido
! Delirium, disorientation, extreme nervousness
! Arrhythmias
! Thyroid storm = hyperpyrexia, diarrhea, dehydration,
! tachycardia, arrhythmias, delirium, coma, shock, death
Exophthalmus
Thyroid Scan

Page 71
MANAGEMENT
! Beta blockers- Metoprolol: Inderal
! to control tachycardia and hypertension
! Thiomides- PTU (propylthiouracil) and Tapazole ( Methimazole)
! to inhibit synthesis of thyroid hormone side effects: Agranulocytosis and neutrpenia
! Radioactive Iodine isolation for a few days, body secretions are radioactive contaminated
! Surgery:Thyroidectomy: 5/6 of the gland is removed
! SSKI (Lugols) is given preop to dec thyroid vascularity & to inhibit release of thyroid hormone
! Given with juice to disguise taste
! Given with straw to prevent staining of teeth
! Postop:
! Position: Semi-fowlers, neck at the midline
! Monitor for bleeding, prevent hemorrhage by placing ice collar over the neck
! Monitor blood pressure- to assess for TROUSSEAUS Sign ( hypocalcemia)
! Check for tetany and monitor for signs of hypocalcemia (parathyroid gland is severed)
! give calcium gluconate
! Hoarseness of voice-laryngeal nerve damage- ask the client to speak every hour
! Watchout thyroid crisis
THYROIDECTOMY
! Removal of the thyroid gland
NURSING INTERVENTIONS
1. Provide adequate rest periods in a quiet room
2. Administer anti-thyroid medications that block hormone synthesis- Methimazole and PTU
3. Provide a HIGH-calorie diet, HIGH protein
4. Manage diarrhea
5. Provide a cool and quiet environment
6. Avoid giving stimulants
7. Provide eye care
! Hypoallergenic tape for eyelid closure
8. Administer PROPRANOLOL for tachycardia
9. Administer IODIONE preparation- Lugols solution and SSKI to inhibit the release of T3 and T4
10. Prepare clients for Radioactive iodine therapy
11. Prepare patient for thyroidectomy
12. Manage thyroid storm appropriately
DISORDERS OF the THYROID GLAND
Thyroid storm
! An acute LIFE-threatening condition characterized by excessive thyroid hormone
CAUSE: Manipulation of the thyroid during surgery causing the release of excessive hormones in the blood
ASSESSMENT Findings for Thyroid Storm
1. HIGH fever
2. Tachycardia and Tachypnea
3.
4.
5.
6.
Systolic HYPERtension
Delirium and coma
Severe vomiting and diarrhea
Restlessness, Agitation, confusion and Seizures
1. Maintain PATENT airway and adequate ventilation
2. Administer anti-thyroid medications such as Lugols solution, Propranolol, and Glucocorticoids
3. Monitor VS
4. Monitor Cardiac rhythms

Page 72
5.
6.
7.
8.
Administer PARACETAMOL
( not Aspirin) for FEVER
Manage Seizures as required.
Provide a quiet environment
Parathyroid
Gland
Abnormalities
$Hypoparathyroidism
$Hyperparathyroidism
Parathyroid Gland
- produce parathyroid hormone/parathormone which regulates calcium and phosphorus balance
dec serum Ca level
PTH release
withdraws Ca from bones
serum Ca levels
Therefore: Hyperparathyroidism: Hypercalcemia
Hypoparathyroidism: Hypocalcemia
Hypoparathyroidism
Caused:
- Accidental removal or destruction of parathyroid gland
- Thyroidectomy
- Radical neck dissection
- Idiopathic
- Autoimmune
Diagnostic:
- Decreased PTH
- Decreased serum Ca (7.5 mg/100 ml)
- Increased PO4
Manifestation:
- Hypocalcemia
- Tetany
- Numbness of fingers
- +Chvosteks sign
- +Trousseaus sign
- +Laryngeal spasm
- Severe anxiety and apprehension
- Muscle cramps
- Cardiac dysrhythmias

Page 73

Page 74
Management:
- Treat the cause
- IV calcium gluconate -Syringe and ampule of Ca sol. on bedside
- Oral Ca with Vit. D
Hyperparathyroidism
Caused:
! Primary
! Tumor/adenoma
! hyperplasia
Diagnostic:
- Increased vit D
- Increased PTH
- Increased serum Ca (11 mg/100 ml)
- Decreased PO4
Manifestation:
- Hypercalcemia
- Decalcification of bone
- Fracture
- Deep bone pain
- Depression of neuromuscular function
- Generalized fatigue
- Memory loss
- Dec LOC, stupor coma
Management:
- Treat the cause
- Hydration (IV saline)
- Diuretics (Ca excretion)
- Calcitonin (inhibits bone resorption)
- Dietary Ca restriction
- Avoid thiazide and vit D (may increase Ca)
- Dialysis
- Digitalis is withdrawn (may increase Ca)
Pancreas:
Islet
of
Alpha- glucagon- blood sugar (hyperglycemia) by stimulating glycogenolysis & gluconeogenesis
langerhans
Beta- insulin- blood sugar (hypoglycemia) by facilitating transport of glucose across cell membranes of muscle, liver,
adipose tissue, inhibits breakdown of proteins, requires Na for transport of CHO and requires K for production
Diabetes Mellitus

Page 75
- DM is a disorder of glucose intolerance caused by a deficiency in insulin production and action resulting in
hyperglycemia and abnormal CHO, CHON and fat metabolism.
Types
$Type
no
diseased pancreas (beta cell)
$Type
decreased
inadequate insulin
or
II
IDDM
insulin
NIDDM
insulin
IDDM- Juvenile Onset DM, Brittle DM, Unstable DM

- Genetic and hereditary
- Zero insulin
- Coxsackie virus
- Onset: Young age before 30 y/o
- 5-10% of persons with diabetes
- 3 Ps with weight loss
- Thin
- DKA
Management
- Diet
- Activity/Exercise
- Insulin
NIDDM- Maturity Onset DM, Stable DM, Ketosis Resistant DM
- Adult onset
- Genetic
- 90-95% of persons with diabetes
- Insulin resistance
- Obesity
- 3 Ps
- HHNK Coma or HONK Coma
Manifestations
- Polyuria- glucose exert high osmotic pressure w/in the renal tubules, osmotic diuresis occurs, hypovolemia, ECF/ICF
dehydration
- Polydipsia- results from ECF/ICF dehydration
- Polyphagia- the cells are starved
- Glycosuria- glucose level exceed renal threshold (180mg/dl)
- Inc Blood Viscosity- sluggish circulation, microorganism proliferation, infection
- Ketonuria
- Tissue wasting
- Weight Loss
Complications
- Macroangiopathies
! brain: CVA
! heart: Myocardial Infarction
! peripheral arteries: peripheral vascular disease
- Microangiopathies
! kidneys: renal failure
! eyes: retinopathy/cataract
- Neuropathy
! spinal cord/ ANS

Page 76
! paralysis
! peripheral neuropathy
! numbness/tingling sensation
! neurogenic bladder
Management
- Diet
- Activity/Exercise
- Oral Hypoglycemic Agents
- Insulin- in case of stress, surgery, infection, pregnancy---these conditions trigger stress response and stimulate the
secretion of epi, norepi, glucocorticoids thereby causing hyperglycemia
- DIET- CHO 50%, Fats 30%, CHON 20%
- calorie specially if obese
- ACTIVITY/EXERCISE- CHO uptake by the cells, insulin requirements, maintains ideal body weight
! done 1-2 hours after meals to prevent hypoglycemia
! regular pattern
- MEDICATIONS: Oral Hypoglycemic Agents- indicated only in type II DM
- INSULIN
OHA = oral hypoglycemic agents
- Sulfonylureas - stimulates insulin secretions and increases tissue sensitivity to insulin (Glipizide, Euglucon)
- Biguanides decreases intestinal uptake and hepatic production of glucose and increases tissue sensitivity
(Glucophage) Alpha
- Glucosidase Inhibitor slows CHO carbohydrate absorption (Glucobay)
- Thiazolidinediones insulin sensitizer, increases tissue sensitivity to insulin (Avandia)
TYPES OF INSULIN
Immediate
Acting,
Lispro
Rapid
Acting
clear insulin
Humulin R,
Regular,
Semilente
Actrapid
Intermediate
ActingActingcloudy NPH
Lente,
Humulin N
Monotard
Long Acting
cloudy
UltraLente
ONSET
PEAK
DURATION
5-15 min
3030-90 min
hours
3030-60min
2-4 hours
6-8 hours
1-2 hours
6-8 hours
1818-24 hours
3-4hours
161620hours
3030-36 hours
Mixture of NPH and Regular

Humulin 70/30
Novolin 70/30
Humulin 50/50
Onset 2 hours

Page 77
- Peak 8-12 hours

- Duration 12-16 hours
About
Insulin!
- Hyperinsulinism
tremors,
hunger
and
diaphoresis will manifest
- Somogyi
Phenomenon
rebound
hyperglycemia
after
insulin
administration
(gradual reduction of insulin is the key to manage it)
- Lipodystrophy is a complication if the site of injection is not rotated properly, it can also alter the rate of insulin
absorption.
- Insulin
Pump
external
battery
operated,
needle
is
inserted
SQ
that
delivers
regular insulin (monitor hypokalemia)
- Site
abdomen
(best
site),
upper buttocks- rotate the site of injection
- Route SQ, only REGULAR insulin can be given as IV bolus
(flush the line first it will absorb insulin)
- IV bolus mixed with D5W if hypoglycemic, or PNSS ideal for DKA and HONKS
- Subcutaneous-Pinch or 45 for thin patient, 90 for regular client
- Good site must be supple skin.
- Mixed Insulin regular (clear) first to be drawn followed by NPH (cloudy)
- Administer at room temp- cold insulin leads to lipodystrophy
- Refrigerate after use.
Diagnostic Evaluation
- Fasting Blood Sugar 80-120mg/dl
140 mg/dl for 2 readings
- 2H Postprandial Blood Sugar Test
200 mg/dl
100
gm
of
then check after 2H
- OGTT - 200 mg/dl
blood is withdrawn initially
150-300
gm
of
every hour bloos specimen is taken (1H,2H,3H after)
done when results of FBS and 2H PPBS are borderline
- Random
Blood
200 mg/dl for 2x + 3 Ps blood is withdrawn anytime
- Glycosylated
Hg
can
detect
glucose
level
2-3
months
Adult 2.2%-4.0%
Children 1.8%-4.0%
upper
esp
sugar
CHO/sugar
Sugar
A1C
average
over
(most
in
arms,
case
of
DKA
orally
PO
serum
preceding
reliable)
FLUIDS AND ELECTROLYTES

Fluids and Electrolytes
INTRODUCTION

Page 78
#
#
#
#
!
!
To maintain good health, a balance of fluids and electrolytes, acids and bases must be normally regulated for metabolic
processes to be in working state.
A cell, together with its environment in any part of the body, is primarily composed of FLUID.
Thus fluid and electrolyte balance must be maintained to promote normal function. Potential and actual problems of fluid
and electrolytes happen in all health care settings, in every disorder and with a variety of changes that affect homeostasis.
The nurse therefore needs to FULLY understand the physiology and pathophysiology of fluid and electrolyte alterations so
as to identify or anticipate and intervene appropriately.
Fluids
a solution of solvent and solute
Solvent
a liquid substance where particles can be dissolved
Solute
a substance, either dissolved or suspended in a solution
!
!
Solution
a homogeneous mixture of 2 or more substances of dissimilar molecular structure
usually applied to solids in liquids but applies equally to gasses in liquids
A.
1.
2.
3.
4.
5.
Body Fluids
Function
Transporter of nutrients , wastes, hormones, proteins and etc
Medium or milieu for metabolic processes
Body temperature regulation
Lubricant of musculoskeletal joints
Insulator and shock absorber
B. Body Fluid Compartments

Intracellular
Within Cells
Extracellular
Outside cells
55% or 2/3 TBW
42.5% or 1/3 TBW

Transport system of our body
Potassium*
Phosphates
Magnesium
Sodium*
Bicarbonates
Chloride
Interstitial
Fluid surrounding
the cells
20%TBW or 2/3
of ECF
Intravascular
Within the blood
vessels
1/3 of ECF Plasma
7.5%
Higher
content
C. Body Compartment Volumes

Normal values
Premature
TBW
Male:
80%
Female:
Transcellular
Contained
in
body
cavities
2.5%
Not readily utilized by
the body
CSF,
Pleural
fluid,
Synovial
Fluid
and
peritoneal fluid
Secreted by epithelial
cells
Term
75%
protein
Bound
Bone
and
Cartilage 7.5%
Dense
Connective
tissues 7.5%
25 yrs
60%
50%
45 yrs
55%
47%

65 yrs
50%
45%
Page 79
ECF
ICF
Blood Volume
!
!
!
A.
B.
C.
45%
35%
90-100 ml/kg
40%
35%
85 ml/kg
20%
40%
70 ml/kg
neonates reach adult values by 2 yrs and are about half-way by 3 months
average values ~ 70 ml/100g of lean body mass
percentage of water varies with tissue type,
lean tissues ~ 60-80%
bone ~ 20-25%
fat ~ 10-15%
D. Tonicity of Body Fluids

! Tonicity refers to the concentration of particles in a solution
! The normal tonicity or osmolarity of body fluids is 250-300 mOsm/L
1. Isotonic
! Same as plasma
2. Hypotonic
! have a lesser or lowers solute concentration than plasma
3. Hypertonic
! higher or greater concentration of solutes
Common Intravenous Solutions

Solution
Na
ClClD5W
0
0
NaCl 0.9%
150
150
NaCl 3.0%
513
513
D4W/NaCL 0.18% 30
30
Hartmans
129
109
Plasmalyte
140
98
Haemaccel
145
145
Mannitol20%
0
0
Dextran 70
154
154
!
!
!
!
!
!
#
#
K+
0
0
0
0
5
5
5.1
0
0
Ca
0
0
0
0
0
Glu
278
0
0
222
0
6.25
0
0
0
0
0
Osm.
Osm.
253
300
855
282
274
294
293
108
300
pH
5
5.7
5.7
3.5 5-5
6.7
5.5
7.3
6.2
4- 7
Lact
0
0
0
0
28
27
0
0
0
kJ/l
840
0
0
672
37.8
84
0
0
0
Osmole
the weight in grams of a substance producing an osmotic pressure of 22.4 atm. when dissolved in 1.0 litre of solution
(gram molecular weight) / (no. of freely moving particles per molecule)
Osmolality
the number of osmoles of solute per kilogram of solvent
Osmolarity
the number of osmoles of solute per litre of solution
Mole
that number of molecules contained in 0.012 kg of C12, or,
the molecular weight of a substance in grams = Avogadro's number
= 6.023 x 1023
Molality
the number of moles of solute per kilogram of solvent
Molarity
is the number of moles of solute per litre of solution
THE Normal DYNAMICS OF BODY FLUIDS

Page 80
The methods by which electrolytes and other solutes move across biologic membranes are Osmosis, Diffusion, Filtration
and Active Transport. Osmosis, diffusion and filtration are passive processes, while Active transport is an active process.
1.
!
!
!
2.
!
!
!
OSMOSIS
This is the movement of water/liquid/solvent across a semi-permeable membrane from a lesser concentration to a higher
concentration
Osmotic pressure is the power of a solution to draw water across a semi-permeable membrane
Colloid osmotic pressure (also called oncotic pressure) is the osmotic pull exerted by plasma proteins
DIFFUSION
Brownian movement or downhill movement
The movement of particles/solutes/molecules from an area of higher concentration to an area of a lower concentration
This process is affected by:
a. The size of the molecules- larger size moves slower than smaller size
b. The concentration of solution- wide difference in concentration has a faster rate of diffusion
c. The temperature- increase in temperature causes increase rate of diffusion
Facilitated Diffusion is a type of diffusion, which uses a carrier, but no energy is expended. One example is fructose and
amino acid transport process in the intestinal cells. This type of diffusion is saturable.
3. FILTRATION
! This is the movement of BOTH solute and solvent together across a membrane from an area of higher pressure to an area
of lower pressure
! Hydrostatic pressure is the pressure exerted by the fluids within the closed system in the walls of the container
4. ACTIVE TRANSPORT
! Process where substances/solutes move from an area of lower concentration to an area of higher concentration with
utilization of ENERGY
! It is called an uphill movement
! Usually, a carrier is required. An enzyme is utilized also.
a.
!
!
b.
!
!
Types of Active Transport:

Primarily Active Transport
Energy is obtained directly from the breakdown of ATP
One example is the Sodium-Potassium pump
Secondary Active Transport
Energy is derived secondarily from stored energy in the form of ionic concentration difference between two sides of the
membrane.
One example is the Glucose-Sodium co-transport; also the Sodium-Calcium counter-transport
THE REGULATION OF BODY FLUID BALANCE
To maintain homeostasis, many body systems interact to ensure a balance of fluid intake and output. A balance of body
fluids normally occurs when the fluid output is balanced by the fluid input
A. Systemic Regulators of Body Fluids

1.
#
#
#
Renal Regulation (RAS)

This system regulates sodium and water balance in the ECF
The formation of urine is the main mechanism
Substance released to regulate water balance is RENIN. Renin activates Angiotensinogen to Angiotensin-I, A-I is
enzymatically converted to Angiotensin-II ( a powerful vasoconstrictor)
2. Endocrine Regulation
# The primary regulator of water intake is the thirst mechanism, controlled by the thirst center in the hypothalamus
(anterolateral wall of the third ventricle)
# Anti-diuretic hormone (ADH) is synthesized by the hypothalamus and acts on the collecting ducts of the nephron

Page 81
#
#
#
ADH increases rate of water reabsorption

The adrenal gland helps control F&E through the secretion of ALOSTERONE- a hormone that promotes sodium retention
and water retention in the distal nephron
ATRIAL NATRIURETIC factor (ANF) is released by the atrial cells of the heart in response to excess blood volume and
increased wall stretching. ANF promotes sodium excretion and inhibits thirst mechanism
3. Gastro
Gastro--intestinal regulation
# The GIT digests food and absorbs water
# The hormonal and enzymatic activities involved in digestion, combined with the passive and active transport of electrolyte,
water and solutions, maintain the fluid balance in the body.
B.
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Fluid Intake
Healthy adult ingests fluid as part of the dietary intake.
90% of intake is from the ingested food and water
10% of intake results from the products of cellular metabolism
Usual intake of adult is about 2, 500 ml per day
The other sources of fluid intake are: IVF, TPN, Blood products, and colloids
C.
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Fluid Output
The average fluid losses amounts to 2, 500 ml per day, counterbalancing the input.
The routes of fluid output are the following:
SENSIBLE LOSS- Urine, feces or GI losses, sweat
INSENSIBLE LOSS- though the skin and lungs as water vapor
URINE- is an ultra-filtrate of blood. The normal output is 1,500 ml/day or 30-50 ml per hour or 0.5-1 ml per kilogram per
hour. Urine is formed from the filtration process in the nephron
FECAL loss- usually amounts to about 200 ml in the stool
Insensible loss- occurs in the skin and lungs, which are not noticeable and cannot be accurately measured. Water vapor goes
out of the lungs and skin.
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Water Metabolism
Daily Balance: turnover ~ 2500 ml
a. Intake
i. drink ~ 1500 ml
ii. food ~ 700 ml
iii. metabolism ~ 300 ml
b. Losses
i. urine ~ 1500 ml
ii. skin ~ 500 ml
insensible losses ~ 400 ml
sweat ~ 100 ml
iii. lungs ~ 400 ml
iv. faeces ~ 100 ml
Minimum daily intake ~ 500 ml with a "normal" diet
Minimum losses ~ 1500 ml/d
Losses are increased with;
a. increased ambient T
b. hyperthermia ~ 13% per C
c. decreased relative humidity
d. increased minute ventilation
e. increased MRO2
Fluid Imbalances
Imbalances
FLUID VOLUME DEFICIT or HYPOVOLEMIA

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Definition: This is the loss of extra cellular fluid volume that exceeds the intake of fluid. The loss of water and electrolyte is
in equal proportion. It can be called in various terms- vascular, cellular or intracellular dehydration. But the preferred term
is hypovolemia.
# Dehydration refers to loss of WATER alone, with increased solutes concentration and sodium concentration
Pathophysiology of Fluid Volume Deficit
# Etiologic conditions include:
a. Vomiting
b. Diarrhea
c. Prolonged GI suctioning
d. Increased sweating
e. Inability to gain access to fluids
f. Inadequate fluid intake
g. Massive third spacing
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Risk factors are the following:

Diabetes Insipidus
Adrenal insufficiency
Osmotic diuresis
Hemorrhage
Coma
Third-spacing conditions like ascites, pancreatitis and burns
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PATHOPHYSIOLOGY:
Factors
inadequate fluids in the body
decreased blood volume
decreased cellular hydration
cellular shrinkage
weight loss, decreased turgor, oliguria, hypotension, weak pulse, etc.
The Nursing Process in Fluid Volume Deficit
ASSESSMENT:
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Physical examination
Weight loss, tented skin turgor, dry mucus membrane
Hypotension
Tachycardia
Cool skin, acute weight loss
Flat neck veins
Decreased CVP
Subjective cues
Thirst
Nausea, anorexia
Muscle weakness and cramps
Change in mental state
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Laboratory findings
Elevated BUN due to depletion of fluids or decreased renal perfusion
Hemoconcentration
Possible Electrolyte imbalances: Hypokalemia, Hyperkalemia, Hyponatremia, hypernatremia
Urine specific gravity is increased (concentrated urine) above 1.020
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NURSING DIAGNOSIS

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Fluid Volume deficit

PLANNING
To restore body fluids
IMPLEMENTATION
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ASSIST IN MEDICAL INTERVENTION

Provide intravenous fluid as ordered
Provide fluid challenge test as ordered
NURSING MANAGEMENT
1. Assess the ongoing status of the patient by doing an accurate input and output monitoring
2. Monitor daily weights. Approximate weight loss 1 kilogram = 1liter!
3. Monitor Vital signs, skin and tongue turgor, urinary concentration, mental function and peripheral circulation
4. Prevent Fluid Volume Deficit from occurring by identifying risk patients and implement fluid replacement therapy as
needed promptly
5.
Correct fluid Volume Deficit by offering fluids orally if tolerated, anti-emetics if with vomiting, and foods with
adequate electrolytes
6.
Maintain skin integrity
7.
Provide frequent oral care
8.
Teach patient to change position slowly to avoid sudden postural hypotension
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FLUID VOLUME EXCESS: HYPERVOLEMIA

Refers to the isotonic expansion of the ECF caused by the abnormal retention of water and sodium
There is excessive retention of water and electrolytes in equal proportion. Serum sodium concentration remains NORMAL
Pathophysiology of Fluid Volume Excess
Etiologic conditions and Risks factors
Congestive heart failure
Renal failure
Excessive fluid intake
Impaired ability to excrete fluid as in renal disease
Cirrhosis of the liver
Consumption of excessive table salts
Administration of excessive IVF
Abnormal fluid retention
PATHOPHYSIOLOGY
Excessive fluid
expansion of blood volume
edema, increased neck vein distention, tachycardia, hypertension.
The Nursing Process in Fluid Volume Excess
ASSESSMENT
Physical Examination
Increased weight gain
Increased urine output
Moist crackles in the lungs
Increased CVP
Distended neck veins
Wheezing
Dependent edema
Subjective cue/s

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1. Shortness of breath
2. Change in mental state
Laboratory findings
1. BUN and Creatinine levels are LOW because of dilution
2. Urine sodium and osmolality decreased (urine becomes diluted)
3. CXR may show pulmonary congestion
NURSING DIAGNOSIS
o Fluid Volume excess
IMPLEMENTATION
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Administer diuretics as prescribed

Assist in hemodialysis
Provide dietary restriction of sodium and water
NURSING MANAGEMENT
Continually assess the patients condition by measuring intake and output, daily weight monitoring, edema assessment and
breath sounds
Prevent Fluid Volume Excess by adhering to diet prescription of low salt- foods.
Detect and Control Fluid Volume Excess by closely monitoring IVF therapy, administering medications, providing rest
periods, placing in semi-fowlers position for lung expansion and providing frequent skin care for the edema
Teach patient about edema, ascites, and fluid therapy. Advise elevation of the extremities, restriction of fluids, necessity of
paracentesis, dialysis and diuretic therapy.
Instruct patient to avoid over-the-counter medications without first checking with the health care provider because they
may contain sodium
ELECTROLYTES
Electrolytes are charged ions capable of conducting electricity and are solutes found in all body compartments.
1. Sources of electrolytes
Foods and ingested fluids, medications; IVF and TPN solutions
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2. Functions of Electrolytes
Maintains fluid balance
Regulates acid-base balance
Needed for enzymatic secretion and activation
Needed for proper metabolism and effective processes of muscular contraction, nerve transmission
3. Types of Electrolytes
CATIONS- positively charged ions; examples are sodium, potassium, calcium
ANIONS- negatively charged ions; examples are chloride and phosphates]
The major ICF cation is potassium (K+); the major ICF anion is Phosphates
The major ECF cation is Sodium (Na+); the major ECF anion is Chloride (Cl-)
DYNAMICS OF ELECTROLYTE BALANCE
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1. Electrolyte
Electrolyte Distribution
ECF and ICF vary in their electrolyte distribution and concentration
ICF has K+, PO4-, proteins, Mg+, Ca++ and SO4ECF has Na+, Cl-, HCO3-
2. Electrolyte Excretion
These electrolytes are excessively eliminated by abnormal fluid losses

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Routes can be thru urine, feces, vomiting, surgical drainage, wound drainage and skin excretion
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3. Regulation of Electrolytes
a) Renal Regulation
occurs by the process of glomerular filtration, tubular reabsorption and tubular secretion
b) Endocrine Regulation
Regulation
hormones play a role in this type of regulation:
AldosteroneAldosterone- promotes Na retention and K excretion
ANFANF- promotes Na excretion
PTHPTH- promotes Ca retention and PO4 excretion
CalcitoninCalcitonin- promotes Ca and PO4 excretion
c) GIT Regulation
electrolytes are absorbed and secreted
some are excreted thru the stool
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THE CATIONS
SODIUM
The most abundant cation in the ECF
Normal range in the blood is 135-145 mEq/L
A loss or gain of sodium is usually accompanied by a loss or gain of water.
Major contributor of the plasma Osmolality
Sources: Diet, medications, IVF. The minimum daily requirement is 2 grams
Imbalances- Hyponatremia= <135 mEq/L; Hypernatremia= >145 mEq/L
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Functions:
Participates in the Na-K pump
Assists in maintaining blood volume
Assists in nerve transmission and muscle contraction
Primary determinant of ECF concentration.
Controls water distribution throughout the body.
Primary regulator of ECF volume.
Sodium also functions in the establishment of the electrochemical state necessary for muscle contraction and the
transmission of nerve impulses.
8. Regulations: skin, GIT, GUT, Aldosterone increases Na retention in the kidney
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SODIUM DEFICIT: HYPONATREMIA

Refers to a Sodium serum level of less than 135 mEq/L. This may result from excessive sodium loss or excessive water gain.
Pathophysiology
Etiologic Factors
Fluid loss such as from Vomiting and nasogastric suctioning
Diarrhea
Sweating
Use of diuretics
Fistula
Other factors
Dilutional hyponatremia
Water intoxication, compulsive water drinking where sodium level is diluted with increased water intake
SIADH
Excessive secretion of ADH causing water retention and dilutional hyponatremia
Hyponatremia% hypotonicity of plasma% water from the intravascular space will move out and go to the intracellular
compartment with a higher concentration% cell swelling
Water is pulled INTO the cell because of decreased extracellular sodium level and increased intracellular concentration

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The Nursing Process in HYPONATREMIA

ASSESSMENT
Sodium Deficit (Hyponatremia)
Clinical Manifestations
Clinical manifestations of hyponatremia depend on the cause, magnitude, and rapidity of onset.
Although nausea and abdominal cramping occur, most of the symptoms are neuropsychiatric and are probably related to
the cellular swelling and cerebral edema associated with hyponatremia.
As the extracellular sodium level decreases, the cellular fluid becomes relatively more concentrated and pulls water into
the cells.
In general, those patients having acute decline in serum sodium levels have more severe symptoms and higher mortality
rates than do those with more slowly developing hyponatremia.
Features of hyponatremia associated with sodium loss and water gain include anorexia, muscle cramps, and a feeling of
exhaustion.
When the serum sodium level drops below 115 mEq/L (SI: 115 mmol/L), thee ff signs of increasing intracranial pressure
occurs:
lethargy
Confusion
muscular twitching
focal weakness
hemiparesis
papilledema
convulsions
In summary:
Altered mental status
Vomiting
Lethargy
Muscle twitching and convulsions (if sodium level is below 115 mEq/L)
Focal weakness
Subjective Cues
Nausea
Cramps
Anorexia
Headache
Laboratory findings
Serum sodium level is less than 135 mEq/L
Decreased serum osmolality
Urine specific gravity is LOW if caused by sodium loss
In SIADH, urine sodium is high and specific gravity is HIGH
NURSING DIAGNOSIS
Altered cerebral perfusion
Fluid volume Excess
IMPLEMENTATION
Provide sodium replacement as ordered. Isotonic saline is usually ordered.. Infuse the solution very cautiously. The serum
sodium must NOT be increased by greater than 12 mEq/L because of the danger of pontine osmotic demyelination
Administer lithium and demeclocycline in SIADH
Provide water restriction if with excess volume
NURSING MANAGEMENT

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Provide continuous assessment by doing an accurate intake and output, daily weights, mental status examination, urinary
sodium levels and GI manifestations. Maintain seizure precaution
2. Detect and control Hyponatremia by encouraging food intake with high sodium content, monitoring patients on lithium
therapy, monitoring input of fluids like IVF, parenteral medication and feedings.
3. Return the Sodium level to Normal by restricting water intake if the primary problem is water retention. Administer sodium
to normovolemic patient and elevate the sodium slowly by using sodium chloride solution
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SODIUM EXCESS: HYPERNATREMIA

Serum Sodium level is higher than 145 mEq/L
There is a gain of sodium in excess of water or a loss of water in excess of sodium.
Pathophysiology:
Etiologic factors
Fluid deprivation
Water loss from Watery diarrhea, fever, and hyperventilation
Administration of hypertonic solution
Increased insensible water loss
Inadequate water replacement, inability to swallow
Seawater ingestion or excessive oral ingestion of salts
Other factors
Diabetes insipidus
Heat stroke
Near drowning in ocean
Malfunction of dialysis
Increased sodium concentration
hypertonic plasma
water will move out form the cell outside to the interstitial space
CELLULAR SHRINKAGE
then to the blood
Water pulled from cells because of increased extracellular sodium level and decreased cellular fluid concentration
The Nursing Process in HYPERNATREMIA
A.. Sodium Excess (Hypernatremia)
primarily neurologic
Presumably the consequence of cellular dehydration.
Hypernatremia results in a relatively concentrated ECF, causing water to be pulled from the cells.
Clinically, these changes may be manifested by:
restlessness and weakness in moderate hypernatremia
disorientation, delusions, and hallucinations in severe hypernatremia.
Dehydration (hypernatremia) is often overlooked as the primary reason for behavioral changes in the elderly.
If hypernatremia is severe, permanent brain damage can occur (especially in children). Brain damage is apparently due to
subarachnoid hemorrhages that result from brain contraction.
A primary characteristic of hypernatremia is thirst. Thirst is so strong a defender of serum sodium levels in normal people
that hypernatremia never occurs unless the person is unconscious or is denied access to water; unfortunately, ill people may
have an impaired thirst mechanism. Other signs include dry, swollen tongue and sticky mucous membranes. A mild
elevation in body temperature may occur, but on correction of the hypernatremia the body temperature should return to
normal.
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ASSESSMENT
Restlessness, elevated body temperature

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Disorientation
Dry, swollen tongue and sticky mucous membrane, tented skin turgor
Flushed skin, postural hypotension
Increased muscle tone and deep reflexes
Peripheral and pulmonary edema
Subjective Cues
Delusions and hallucinations
Extreme thirst
Behavioral changes
Laboratory findings
Serum sodium level exceeds 145 mEq/L
Serum osmolality exceeds 295 mOsm/kg
Urine specific gravity and osmolality INCREASED or elevated
IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1. Administer hypotonic electrolyte solution slowly as ordered
2. Administer diuretics as ordered
3. Desmopressin is prescribed for diabetes insipidus
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NURSING MANAGEMENT
Continuously monitor the patient by assessing abnormal loses of water, noting for the thirst and elevated body temperature
and behavioral changes
Prevent hypernatremia by offering fluids regularly and plan with the physician alternative routes if oral route is not
possible. Ensure adequate water for patients with DI. Administer IVF therapy cautiously
Correct the Hypernatremia by monitoring the patients response to the IVF replacement. Administer the hypotonic solution
very slowly to prevent sudden cerebral edema.
Monitor serum sodium level.
Reposition client regularly, keep side-rails up, the bed in low position and the call bell/light within reach.
Provide teaching to avoid over-the counter medications without consultation as they may contain sodium
POTASSIUM
The most abundant cation in the ICF
Potassium is the major intracellular electrolyte; in fact, 98% of the bodys potassium is inside the cells.
The remaining 2% is in the ECF; it is this 2% that is all-important in neuromuscular function.
Potassium is constantly moving in and out of cells according to the bodys needs, under the influence of the sodiumpotassium pump.
Normal range in the blood is 3.5-5 mEq/L
Normal renal function is necessary for maintenance of potassium balance, because 80-90% of the potassium is excreted
daily from the body by way of the kidneys. The other less than 20% is lost through the bowel and sweat glands.
Major electrolyte maintaining ICF balance
Sources- Diet, vegetables, fruits, IVF, medications
Functions:
Maintains ICF Osmolality
Important for nerve conduction and muscle contraction
Maintains acid-base balance
Needed for metabolism of carbohydrates, fats and proteins
Potassium influences both skeletal and cardiac muscle activity.
For example, alterations in its concentration change myocardial irritability and rhythm.
Regulations: renal secretion and excretion, Aldosterone promotes renal excretion acidosis promotes K exchange for
hydrogen
Imbalances:
Hypokalemia= <3.5 mEq/L
Hyperkalemia=> 5.0 mEq/L

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POTASSIUM DEFICIT: HYPOKALEMIA

Condition when the serum concentration of potassium is less than 3.5 mEq/L
Pathophysiology
Etiology
Gastro-intestinal loss of potassium such as diarrhea and fistula
Vomiting and gastric suctioning
Metabolic alkalosis
Diaphoresis and renal disorders
Ileostomy
Other factor/s
Hyperaldosteronism
Heart failure
Nephrotic syndrome
Use of potassium-losing diuretics
Insulin therapy
Starvation
Alcoholics and elderly
Decreased potassium in the body% impaired nerve excitation and transmission% signs/symptoms such as weakness, cardiac
dysrhythmias etc..
The Nursing Process in Hypokalemia
Potassium Deficit (Hypokalemia)
Potassium deficiency can result in widespread derangements in physiologic functions and especially nerve conduction.
Most important, severe hypokalemia can result in death through cardiac or respiratory arrest.
Clinical signs rarely develop before the serum potassium level has fallen below 3 mEq/L (51: 3 mmol/L) unless the rate of
fall has been rapid.
Manifestations of hypokalemia include fatigue, anorexia, nausea, vomiting, muscle weakness, decreased bowel motility,
paresthesias, dysrhythmias, and increased sensitivity to digitalis.
If prolonged, hypokalemia can lead to impaired renal concentrating ability, causing dilute urine, polyuria, nocturia, and
polydipsia
ASSESSMENT
Physical examination
Muscle weakness
Decreased bowel motility and abdominal distention
Paresthesias
Dysrhythmias
Increased sensitivity to digitalis
Subjective cues
Nausea , anorexia and vomiting
Fatigue, muscles cramps
Excessive thirst, if severe
Laboratory findings
Serum potassium is less than 3.5 mEq/L
ECG: FLAT T waves, or inverted T waves, depressed ST segment and presence of the U wave and prolonged PR
interval.
Metabolic alkalosis
IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1.
Provide oral or IV replacement of potassium

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2. Infuse parenteral potassium supplement. Always dilute the K in the IVF solution and administer with a pump. IVF with
potassium should be given no faster than 10-20-mEq/ hour!
3. NEVER administer K by IV bolus or IM
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NURSING MANAGEMENT
Continuously monitor the patient by assessing the cardiac status, ECG monitoring, and digitalis precaution
Prevent hypokalemia by encouraging the patient to eat potassium rich foods like orange juice, bananas, cantaloupe,
peaches, potatoes, dates and apricots.
Correct hypokalemia by administering prescribed IV potassium replacement. The nurse must ensure that the kidney is
functioning properly!
Administer IV potassium no faster than 20 mEq/hour and hook the patient on a cardiac monitor. To EMPHASIZE:
Potassium should NEVER be given IV bolus or IM!!
A concentration greater than 60 mEq/L is not advisable for peripheral veins.
POTASSIUM EXCESS: HYPERKALEMIA
HYPERKALEMIA
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Serum potassium greater than 5.5 mEq/L

Pathophysiology
Etiologic factors
Iatrogenic, excessive intake of potassium
Renal failure- decreased renal excretion of potassium
Hypoaldosteronism and Addisons disease
Improper use of potassium supplements
Other factors
Pseudohyperkalemia- tight tourniquet and hemolysis of blood sample, marked leukocytosis
Transfusion of old banked blood
Acidosis
Severe tissue trauma
Increased potassium in the body
Causing irritability of the cardiac cells
Possible arrhythmias!!
The Nursing Process in Hyperkalemia
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Potassium Excess (Hyperkalemia)

By far the most clinically important effect of hyperkalemia is its effect on the myocardium.
Cardiac effects of an elevated serum potassium level are usually not significant below a concentration of 7 mEq/L (SI: 7
mmol/L), but they are almost always present when the level is 8 mEq/L (SI: 8 mmol/L) or greater.
As the plasma potassium concentration is increased, disturbances in cardiac conduction occur.
The earliest changes, often occurring at a serum potassium level greater than 6 mEq/ L (SI: 6 mmol/L), are peaked narrow T
waves and a shortened QT interval.
If the serum potassium level continues to rise, the PR interval becomes prolonged and is followed by disappearance of the P
waves.
Finally, there is decomposition and prolongation of the QRS complex. Ventricular dysrhythmias and cardiac arrest may
occur at any point in this progression.
Note that in Severe hyperkalemia causes muscle weakness and even paralysis, related to a depolarization block in muscle.
Similarly, ventricular conduction is slowed.
Although hyperkalemia has marked effects on the peripheral neuromuscular system, it has little effect on the central nervous
system.
Rapidly ascending muscular weakness leading to flaccid quadriplegia has been reported in patients with very high serum
potassium levels.
Paralysis of respiratory muscles and those required for phonation can also occur.

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Gastrointestinal manifestations, such as nausea, intermit tent intestinal colic, and diarrhea, may occur in hyperkalemic
patients.
ASSESSMENT
Diarrhea
Skeletal muscle weakness
Abnormal cardiac rate
Subjective Cues
Nausea
Intestinal pain/colic
Palpitations
Laboratory Findings
Peaked and narrow T waves
ST segment depression and shortened QT interval
Prolonged PR interval
Prolonged QRS complex
Disappearance of P wave
Serum potassium is higher than 5.5 mEq/L
Acidosis
IMPLEMENTATION
1. Monitor the patients cardiac status with cardiac machine
2. Institute emergency therapy to lower potassium level by:
a. Administering IV calcium gluconate- antagonizes action of K on cardiac conduction
b. Administering Insulin with dextrose-causes temporary shift of K into cells
c.
Administering sodium bicarbonate-alkalinizes plasma to cause temporary shift
d. Administering Beta-agonists
e. Administering Kayexalate (cation-exchange resin)-draws K+ into the bowel
NURSING MANAGEMENT
Provide continuous monitoring of cardiac status, dysrhythmias, and potassium levels.
Assess for signs of muscular weakness, paresthesias, nausea
Evaluate and verify all HIGH serum K levels
Prevent hyperkalemia by encouraging high risk patient to adhere to proper potassium restriction
Correct hyperkalemia by administering carefully prescribed drugs. Nurses must ensure that clients receiving IVF with
potassium must be always monitored and that the potassium supplement is given correctly
6. Assist in hemodialysis if hyperkalemia cannot be corrected.
7. Provide client teaching. Advise patients at risk to avoid eating potassium rich foods, and to use potassium salts sparingly.
8. Monitor patients for hypokalemia who are receiving potassium-sparing diuretic
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CALCIUM
Majority of calcium is in the bones and teeth
Small amount may be found in the ECF and ICF
Normal serum range is 8.5 10.5 mg/dL
Sources: milk and milk products; diet; IVF and medications
Functions:
1. Needed for formation of bones and teeth
2. For muscular contraction and relaxation
3. For neuronal and cardiac function
4. For enzymatic activation
5. For normal blood clotting

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Regulations:
1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to increase absorption
2. Renal regulation- Ca+ is filtered in the glomerulus and reabsorbed in the tubules:
3. Endocrine regulation:
Parathyroid hormone from the parathyroid glands is
released when Ca+ level is low. PTH causes release of calcium
from bones and increased retention of calcium by the kidney but PO4 is excreted
Calcitonin from the thyroid gland is released when the calcium level is high. This causes excretion of both calcium and PO4
in the kidney and promoted deposition of calcium in the bones.
Imbalances- Hypocalcemia= <8.5 mg/dL; Hypercalcemia= >10.5 mg/dL
THE ANIONS
CHLORIDE
The major Anion of the ECF
Normal range is 95-108 mEq/L
Sources: Diet, especially high salt foods, IVF (like NSS), HCl (in the stomach)
Functions:
1. Major component of gastric juice
2. Regulates serum Osmolality and blood volume
3. Participates in the chloride shift
4. Acts as chemical buffer
Regulations: Renal regulation by absorption and excretion; GIT absorption
Imbalances: Hypochloremia= < 95 mEq/L; Hyperchloremia= >108 mEq/L
PHOSPHATES
The major Anion of the ICF
Normal range is 2.5 to 4.5 mg/dL
Sources: Diet, TPN, Bone reserves
Functions:
1. Component of bones, muscles and nerve tissues
2. Needed by the cells to generate ATP
3. Needed for the metabolism of carbohydrates, fats and proteins
4. Component of DNA and RNA
Regulations: Renal glomerular filtration, endocrinal regulation by PTH-decreases PO4 in the blood by kidney excretion
Imbalances- Hypophosphatemia= <2.5 mg/dL; Hyperphosphatemia >4.5 mg/dL
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BICARBONATES
Present in both ICF and ECF
Regulates acid-base balance together with hydrogen
Normal range is 22-26 mEq/L
Sources: Diet; medications and metabolic by-products of the cells.
Function: Component of the bicarbonate-carbonic acid buffer system
Regulation: Kidney production, absorption and secretion
Imbalances: Metabolic acidosis= <22 mEq/L; Metabolic alkalosis= >26 mEq/
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ACID BASE BALANCE

Acids
substances that can donate or release protons or hydrogen ions (H+); examples are HCl, carbonic acid, acetic acid.
Bases or alkalis
substances that can accept protons or hydrogen ions because they have low H+ concentration. The major base in the body
is BICARBONATE (HCO3)
Carbon dioxide is considered to be acid or base depending on its chemical association
When assessing acid-base balance, carbon dioxide is considered ACID because of its relationship with carbonic acid.

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!
Because carbonic acid cannot be routinely measured, carbon dioxide is used.

pH- is the measurement of the degree of acidity or alkalinity of a solution. This reflects the relationship of hydrogen ion
concentration in the solution.
The higher the hydrogen ion concentration, the acidic is the solution and pH is LOW
The lower the hydrogen concentration, the alkaline is the solution and the pH is HIGH
Normal pH in the blood is between 7.35 to 7.45
SUPPLY AND SOURCES OF ACIDS AND BASES
Sources of acids and bases are from:
1. ECF, ICF and body tissues
2. Foodstuff
3. Metabolic products of cells like CO2, lactic acids, and ammonia
DYNAMICS OF ACIDACID-BASE BALANCE
Acids are constantly produced in the body
Because cellular processes need normal pH, acids and bases must be balanced continuously
CO2 and HCO3 are crucial in maintaining the balance
A ratio of HCO3 and Carbonic acid is maintained at 20:1
Several body systems (like the respiratory, renal and GIT) together with the chemical buffers are actively involved in the
normal pH balance
The major ways in which balance is maintained are the process of acid/base secretion, production, excretion and
neutralization
1. REGULATION OF ACIDACID-BASE BALANCE BY THE CHEMICAL BUFFER
Buffers are present in all body fluids functioning mainly to prevent excessive changes in the pH.
Buffers either remove/accept H+ or release/donate H+
The major chemical buffers are:
1. Carbonic acid-Bicarbonate Buffer (in the ECF)
2. Phosphate buffer (in the ECF and ICF)
3. Protein buffer (in the ICF)
The action of the chemical buffer is immediate but limited
2. REGULATION OF ACIDACID-BASE BALANCE BY RESPIRATORY SYSTEM
The respiratory center in the medulla is involved
Carbon dioxide is the powerful stimulator of the respiratory center
The lungs use CO2 to regulate H+ ion concentration
Through the changes in the breathing pattern, acid-base balance is achieved within minutes
Functions of the respiratory system in acid-base balance:
1. CO2 + H2O% H2CO3
2. CO2%activates medulla%RR%CO2 is exhaled% pH rises to normal
3. HCO3%depresses RR%CO2 is retained%Bicarbonate is neutralized% pH drops to normal
3. REGULATION OF ACIDACID-BASE BALANCE BY THE KIDNEY
Long term regulator of the acid-base balance
Slower to respond but more permanent
Achieved by 3 interrelated processes
1. Bicarbonate reabsorption in the nephron
2. Bicarbonate formation
3. Hydrogen ion excretion
When excess H+ is present (acidic), pH falls%kidney reabsorbs and generates Bicarbonate and excretes H+
When H+ is low and HCO3 is high (alkalotic). pH rises% kidney excretes HCO3 and H+ is retained.

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1.
2.
3.
4.
5.
6.
Normal Arterial Blood Gas Values

pH 7.35-7.45
pO2 80-100 mmHg
pCO2 35-45 mmHg
Hco3 22-26 mEq/L
Base deficit/Excess (+/-)2
O2 saturation 98-100%
FACTORS AFFECTING BODY FLUIDS, ELECTROLYTES
ELECTROLYTES AND ACIDACID-BASE BALANCE
!
!
!
1. AGE
Infants have higher proportion of body water than adults
Water content of the body decreases with age
Infants have higher fluid turn-over due to immature kidney and rapid respiratory rate
1.
!
!
GENDER AND BODY SIZE

Women have higher body fat content but lesser water content
Lean body has higher water content
2. ENVIRONMENT AND TEMPERATURE

! Climate and heat and humidity affect fluid balance
3.
!
!
!
4.
!
!
DIET AND LIFESTYLE

Anorexia nervosa will lead to nutritional depletion
Stressful situations will increase metabolism, increase ADH% causing water retention and increased blood volume
Chronic Alcohol consumption causes malnutrition
ILLNESS
Trauma and burns release K+ in the blood
Cardiac dysfunction will lead to edema and congestion
5. MEDICAL TREATMENT, MEDICATIONS AND SURGERY

! Suctioning, diuretics and laxatives may cause imbalances
Acid Base Imbalances
!
!
!
!
!
!
Metabolic Alkalosis
A base bicarbonate excess
A result of a loss of acid and the
accumulation of bases
S/S - serum pH > 7.45, increased serum
HCO3, serum K level less than 4, tetany, confusion and convulsions
Nursing Interventions - watch for s/s of hypokalemia, LOC and seizure precautions
!
!
!
!
Metabolic Acidosis
A base bicarbonate deficit
Comes from too much acid from metabolism and loss of bicarbonate
S/S - Serum pH <7.35, Increased K+ level, DKA (Kussmauls Respirations), Shock, stupor, coma
Nursing Intervention - Give HCO3/Monitor K+ levels
!
!
!
Respiratory Alkalosis
A deficit of carbonic acid caused by hyperventilation
S/S - decreased levels of CO2 and increased levels of pH, HCO3 near normal
Nursing Interventions - monitor for anxiety and observe for signs and symptoms of tetany

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Respiratory Alkalosis
A carbonic acid excess
Caused by an condition that interferes with the release of CO2 from the lungs (sedatives, COPD, narcotics etc.)
S/S - serum pH < 7.35, increased serum CO2 levels> 45 mm Hg, serum K increased, cyanosis
Nursing Interventions - Provide O2, Semifowlers position, seizure precautions
Interpretation Arterial Blood Gases
!
!
!
!
!
!
!
!
!
!
!
!
!
!
!
!
!
If acidosis the pH is down

If alkalosis the pH is up
The respiratory function indicator is the PCO2
The metabolic function indicator is the HCO3
Step 1
Look at the pH
Is it up or down?
If it is up - it reflects alkalosis
If it is down - it reflects acidosis
Step 2
Look at the PCO2
Is it up or down?
If it reflects an opposite response as the pH,
then you know that the condition is a respiratory imbalance
If it does not reflect an opposite response as the pH - move to step III
Step 3
Look at the HCO3
Does the HCO3 reflect a corresponding
response with the pH
If it does then the condition is a metabolic imbalance
NEURO
Overview of the Structures & Functions of Nervous System
Central NS
PNS
ANS
Brain & spinal cord
31 spinal & cranial
sympathetic NS
Parasypathatic NS
Somatic NS
C- 8
T- 12
L- 5
S- 5
C- 1
ANS (or adrenergic of parasympatholitic response)
SNS involved in fight or aggression response
Release of norepinephrine (adrenaline cathecolamine)
Adrenal medulla (potent vasoconstrictor)
Increases body activities
VS = Increase
Except GIT decrease GITmotility
* Why GIT is not increased = GIT is not important!
Effects of SNS ((anti-cholinergic/adrenergic)

1. Dilate pupil to aware of surroundings
- medriasis
2. Dry mouth
3. BP & HR= increased
bronchioles dilated to take more oxygen
4. RR increased
5. Constipation & urinary retention

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Increase blood flow to skeletal muscles, brain & heart.

I. Adrenergic Agents Epinephrine (adrenaline)
SE: SNS effect
II. PNS: Beta adrenergic blocking agents (opposite of adrenergic agents) (all end in lol)
- Blocks release of norepinephrine.
- Decrease body activities except GIT (diarrhea)
Ex. Propanolol, Metopanolol
SE:
B broncho spasm (bronchoconstriction)
E elicits a decrease in myocardial contraction
T treats HPN
A AV conduction slows down
Given to angina & MI beta-blockers to rest heart
Anti HPN agents:
1. Beta blockers (-lol)
2. Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL
3. Calcium antagonist
ex CALCIBLOC or NEFEDIPINE
Peripheral nervous system: cholinergic/ vagal or sympatholitic response
- Involved in fly or withdrawal response
- Release of acetylcholine (ACTH)
- Decrease all bodily activities except GIT (diarrhea)
4. RR decrease broncho constriction
I Cholinergic agents
ex 1. Mestinon
Antidote anti cholinergic agents Atropine Sulfate S/E SNS
Effect of PNS: (cholinergic)

(
1. Meiosis contraction of pupils
2. Increase salivation
3. BP & HR decreased
5. Diarrhea increased GI motility
6. Urinary frequency
S/E- of anti-hpn drugs:

1. orthostatic hpn
2. transient headache & dizziness.
-Mgt. Rise slowly. Assist in ambulation.
CNS (brain & spinal cord)
I. Cells A. neurons
Properties and characteristics
a. Excitability ability of neuron to be affected in external environment.
b. Conductivity ability of neuron to transmit a wave of excitation from one cell to another
c. Permanent cells once destroyed, cant regenerate (ex. heart, retina, brain, osteocytes)
Regenerative capacity
A. Labile once destroyed cant regenerate
- Epidermal cells, GIT cells, resp (lung cells). GUT
B. Stable capable of regeneration BUT limited time only ex salivary gland, pancreas cells cell of liver, kidney cells
C. Permanent cells retina, brain, heart, osteocytes cant regenerate.
3.) Neuroglia attached to neurons. Supports neurons. Where brain tumors are found.
Types:
1. Astrocyte
2. Oligodendria
Astrocytoma 90 95% brain tumor from astrocyte. Most brain tumors are found at astrocyte.
Astrocyte maintains integrity of blood brain barrier (BBB).
BBB semi permeable / selective

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-Toxic substance that destroys astrocyte & destroy BBB.

Toxins that can pass in BBB:
1. Ammonia-liver cirrhosis.
2. 2. Carbon Monoxide seizure & parkinsons.
3. 3. Bilirubin- jaundice, hepatitis, kernicterus/hyperbilirubenia.
4. 4. Ketones DM.
OLIGODENDRIA Produces myelin sheath wraps around a neuron acts as insulator facilitates rapid nerve impulse
transmission.
No myelin sheath degenerates neurons
Damage to myelin sheath demyellenating disorders
DEMYELLENATING DSE
1.)ALZHEIMERS
ALZHEIMERS DISEASE
DISEASE atrophy of brain tissue due to a deficiency of acetylcholine.
S&Sx:
A amnesia loss of memory
A apraxia unable to determine function & purpose of object
A agnosia unable to recognize familiar object
A aphasia
- Expressive broccas aphasia unable to speak
- Receptive wernickes aphasia unable to understand spoken words
Common to Alzheimer receptive aphasia
Drug of choice ARICEPT (taken at bedtime) & COGNEX.
Mgt: Supportive & palliative.
Microglia stationary cells, engulfs bacteria, engulfs cellular debris.
II. Compositions of Cord & Spinal cord
80% - brain mass
10% - CSF
10% - blood
MONROE KELLY HYPOTHESIS: The skull is a closed vault. Any increase in one component will increase ICP.
Normal ICP: 0-15mmHg
Brain mass
1. Cerebrum largest -
Connects R & L cerebral hemisphere

- Corpus collusum
Rt cerebral hemisphere, Lt cerebral hemisphere
Function:
1. Sensory
2. Motor
3. Integrative
Lobes
1.) Frontal
a. Controls motor activity
b. Controls personality development
c. Where primitive reflexes are inhibited
d. Site of development of sense of umor
e. Broccas area speech center
Damage - expressive aphasia
2.) Temporal
a. Hearing

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3.)
4.)
5.)
6.)
b. Short term memory

c. Wernickes area gen interpretative or knowing Gnostic area
Damage receptive aphasia
Parietal lobe appreciation & discrimation of sensory imp
- Pain, touch, pressure, heat & cold
Occipital - vision
Insula/island of reil/ Central lobe- controls visceral fx
Function: - activities of internal organ
Rhinencephalon/ Limbec
- Smell, libido, long-term memory
Basal Ganglia areas of gray matte located deep within a cerebral hemisphere
- Extra pyramidal tract
- Releases dopamine- Controls gross voluntary unit
Decrease dopamine (Parkinsons) pin rolling of extremities & Huntingtons Dse.
Decrease acetylcholine Myasthenia Gravis & Alzheimers
Increased neurotransmitter = psychiatric disorder
Increase dopamine schizo
Increase acetylcholine bipolar
MID BRAIN relay station for sight & hearing
Controls size & reaction of pupil 2 3 mm
Controls hearing acuity
CN 3 4
Isocoria normal size (equal)
Anisocoria uneven size damage to mid brain
PERRLA normal reaction
DIENCEPHALON- between brain
Thalamus acts as a relay station for sensation
Hypothalamus (thermoregulating center of temp, sleep & wakefulness, thirst, appetite/ satiety center, emotional
responses, controls pituitary function.
BRAIN STEM- a. Pons or pneumotaxic center controls respiration
Cranial 5 8 CNS
MEDULLA OBLONGATA- controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus
Vasomotor center, spinal decuissation termination, CN 9, 10, 11, 12
CEREBELLUM lesser brain
- Controls posture, gait, balance, equilibrium
Cerebellar Tests:
a.) R Rombergs test- needs 2 RNs to assist
- Normal anatomical position 5 10 min
(+) Rombergs test (+) ataxia or unsteady gait or drunken like movement with loss of balance.
b.) Finger to nose test
(+) To FTNT dymetria inability to stop a movement at a desired point
c.) Alternate pronation & supination
Palm up & down . (+) To alternate pronation & supination or damage to cerebellum dymentrium
Composition of brain - based on Monroe Kellie Hypothesis
- Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP

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Normal ICP 0 15 mmHg

Foramen Magnum
C1 atlas
C2 axis
(+) Projectile vomiting = increase ICP
Observe for 24 - 48 hrs
CSF cushions the brain, shock absorber
Obstruction of flow of CSF = increase ICP
Hydrocephalus posteriorly due to closure of posterior fontanel
CVA partial/ total obstruction of blood supply
INCREASED ICP increase ICP is due to increase in 1 of the Intra Cranial components.
Predisposing factors:
1.) Head injury
2.) Tumor
3.) Localized abscess
4.) Hemorrhage (stroke)
5.) Cerebral edema
6.) Hydrocephalus
7.) Inflammatory conditions - Meningitis, encephalitis
B. S&Sx
change in VS = always late symptoms
Earliest Sx:
a.) Change or decrease LOC Restlessness to confusion
Wide pulse pressure: Increased ICP
- Disorientation to lethargy
Narrow pp: Cardiac disorder, shock
- Stupor to coma
Late sign change in V/S
1. BP increase (systolic increase, diastole- same)
2. Widening pulse pressure
Normal adult BP 120/80 120 80 = 40 (normal pulse pressure)
Increase ICP = BP 140/80 = 140 80= 60 PP (wide)
3. RR is decreased (Cheyne-Stokes = bet period of apnea or hyperpnea with periods of apnea)
4. Temp increase
Increased ICP: Increase BP
Shock decrease BP
Decrease HR
Increase HR
CUSHINGS EFFECT
Decrease RR
Increase RR
Increase Temp
Decrease temp
b.) Headache
Projectile vomiting
Papilledima (edema of optic disk outer surface of retina)
Decorticate (abnormal flexion) = Damage to cortico spinal tract /
Decerebrate (abnormal extension) = Damage to upper brain stem-pons/
c.) Uncal herniation unilateral dilation of pupil. (Bilateral dilation of pupil tentorial herniation.)
d.) Possible seizure.
Nursing priority:
1.) Maintain patent a/w & adequate ventilation
a. Prevention of hypoxia (decrease tissue oxygenation) & hypercarbia (increase in CO2 retention).
Hypoxia cerebral edema - increase ICP
Hypoxia inadequate tissue oxygenation
Late symptoms of hypoxia B bradycardia

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E extreme restlessness
D dyspnea
C cyanosis
Early symptoms R restlessness
A agitation
T tachycardia
Increase CO2 retention/ hypercarbia cerebral vasodilatation = increase ICP
Most powerful respiratory stimulant increase in CO2
Hyperventilate decrease CO2 excrete CO2
Respiratory Distress Syndrome (RDS) decrease Oxygen
Suctioning 10-15 seconds, max 15 seconds. Suction upon removal of suction cap.
Ambu bag pump upon inspiration
c. Assist in mechanical ventilation
1. Maintain patent a/w
2. Monitor VS & I&O
3. Elevate head of bed 30 45 degrees angle neck in neutral position unless contra indicated to promote venous drainage
4. Limit fluid intake 1,200 1,500 ml/day
(FORCE FLUID means:Increase fluid intake/day 2,000 3,000 ml/day)- not for inc ICP.
6. Prevent increase ICP by:
a. Maintain quiet & comfy environment
b. Avoid use of restraints lead to fractures
c. Siderails up
d. Instruct patient to avoid the ff:
-Valsalva maneuver or bearing down, avoid straining of stool
(give laxatives/ stool softener Dulcolax/ Duphalac)
- Excessive cough antitussive
Dextrometorpham
-Excessive vomiting anti emetic (Plasil Phil only)/ Phenergan
- Lifting of heavy objects
- Bending & stooping
e. Avoid clustering of nursing activities
7. Administer meds as ordered:
1.) Osmotic diuretic Mannitol./Osmitrol promotes cerebral diuresis by decompressing brain tissue
Nursing considerations: Mannitol
1.
2.
3.
4.
Monitor BP SE of hypotension
Monitor I&O every hr. report if < 30cc out put
Administer via side drip
Regulate fast drip to prevent formation of crystals or precipitate
2.) Loop diuretic - Lasix (Furosemide)

Nursing Mgt: Lasix
Same as Mannitol except
- Lasix is given via IV push (expect urine after 10-15mins) should be in the morning. If given at 7am. Pt will urinate at 7:15
Immediate effect of Lasix within 15 minutes. Max effect 6 hrs due (7am 1pm)
S/E of Lasix
S&Sx
Hypokalemia
Hypokalemia (normal K-3.5 5.5 meg/L)
1.
Weakness & fatigue

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2. Constipation
3. (+) U wave in ECG tracing
Nursing Mgt:
1.) Administer K supplements ex Kalium Durule, K chloride
Potassium Rich food:
ABCs of K
Vegetables
A - asparagus
B broccoli (highest)
C carrots
Fruits
A apple
B banana green
C cantalope/ melon
O orange (highest) for digitalis toxicity also.
Vit A squash, carrots yellow vegetables & fruits, spinach, chesa
Iron raisins,
Food appropriate for toddler spaghetti! Not milk increase bronchial secretions
Dont give grapes may choke
S/E of Lasix:
1.) Hypokalemia
Tetany:
2.) Hypocalcemia (Normal level Ca = 8.5 11mg/100ml) or Tetany
S&Sx
weakness
Paresthesia
(+) Trousseau sign pathognomonic or carpopedal spasm. Put bp cuff on arm=hand spasm.
(+) Chevosteks sign
Arrhythmia
Laryngospasm
Administer Ca gluconate IV slowly
Ca gluconate toxicity:
toxicity Sx seizure administer Mg SO4
Mg SO4 toxcicity
toxcicity administer Ca gluconate
B BP decrease
U urine output decrease
R RR decrease
P patellar reflexes absent
3.) Hyponatremia Normal Na level = 135 145 meg/L
Hypotension
Signs of Dehydration: dry skin, poor skin turgor, gen body malaise.
Early signs Adult: thirst and agitation / Child: tachycardia
Mgt: force fluid
Administer isotonic fluid sol
S/Sx
4.) Hyperglycemia increase blood sugar level

P polyuria
P polyphagia
P polydipsia
Nsg Mgt:
a. Monitor FBS (N=80 120 mg/dl)
5.) Hyperurecemia increase serum uric acid. Tophi- urate crystals in joint.
Gouty arthritis
Cool moist skin
kidney stonesstones renal colic (pain)

Sx joint pain & swelling usually at great toe.

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Nsg Mgt of Gouty Arthritis

a.) Cheese (not sardines, anchovies, organ meat)
(Not good if pt taking MAO)
b.) Force fluid
c.) Administer meds Allopurinol/ Zyloprim inhibits synthesis of uric acid drug of choice for gout
Colchicene excretes uric acid. Acute gout drug of choice.
Kidney stones renal colic (pain). Cool moist skin
Mgt:
1.) Force fluid
2.) Meds narcotic analgesic
Morphine SO4
SE of Morphine SO4 toxicity
Respiratory depression (check RR 1st)
Antidote for morphine SO4 toxicity Narcan (NALOXONE)
Naloxone toxicity tremors
Increase ICP meds:
3.) Corticosteroids - Dexamethsone decrease cerebral edema (Decadrone)
4.) Mild analgesic codeine SO4. For headache.
5.) Anti consultants Dilantin (Phenytoin)
Question: Increase ICP what is the immediate nsg action?
a. Administer Mannitol as ordered
b. Elevate head 30 45 degrees
c. Restrict fluid
d. Avoid use of restraints
Nsg Priority ABC & safety
Pt suffering from epiglotitis. What is nsg priority?
a. Administer steroids least priority
b. Assist in ET temp, a/w
c. Assist in tracheotomy permanent (Answer)
d. Apply warm moist pack? Least priority
Rationale: Wont need to pass larynx due to larynx is inflamed. ET cant pass. Need tracheostomy onlyMagic 2s of drug monitoring
Drug
N range
D digoxin
.5 1.5 meq/L
L - lithium
.6 1.2 meq/L
A aminophylline
10 19 mg/100ml
D Dilantin
10 -19 mg/100 ml
A acetaminophen
10 30 mg/100ml
Toxicity
2
2
20
200
Classification
cardiac glycosides
antimanic
bronchodilator
20
anticonvulsant
narcotic analgesic
Indication
CHF
bipolar
COPD
seizures
osteoarthritis
Digitalis increase cardiac contraction = increase CO

Nursing Mgt
1. Check PR, HR (if HR below 60bpm, dont giveDigoxin)
Digitalis toxicity antidote - Digivine
a. Anorexia
-initial sx.
b. n/v
GIT
c. Diarrhea
d. Confusion

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e. Photophobia
f. Changes in color perception yellow spots
(Ok to give to pts with renal failure. Digoxin is metabolized in liver not in kidney.)
L lithium (lithane) decrease levels of norepinephrine, serotonine, acetylcholine
Antimanic agent
Lithium toxicity
S/Sx a.) Anorexia
b.) n/s
c.) Diarrhea
d.) Dehydration force fluid, maintain Na intake 4 10g daily
e.) Hypothyroidism
(CRETINISM the only endocrine disorder that can lead to mental retardation)
A aminophyline (theophylline) dilates bronchioles.
Take bp before giving aminophylline.
S/Sx : Aminophylline toxicity:
1. Tachycardia
2. Hyperactivity restlessness, agitation, tremors
Question: Avoid giving food with Aminophylline
a. Cheese/butter food rich in tyramine, avoided only if pt is given
MAOI
b. Beer/ wine c. Hot chocolate & tea caffeine CNS stimulant tachycardia
d. Organ meat/ box cereals anti parkinsonian
MAOI antidepressant
m AR plan
n AR dil
can
lead
to
CVA
p AR nate
3 4 weeks - before MAOI will take effect
Anti Parkinsonian agents Vit B6 Pyridoxine reverses effect of Levodopa
or
hypertensive
crisis
D dilatin (Phenytoin) anti convulsant/seizure

Nursing Mgt:
1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate
- Do sandwich method
- Give NSS then Dilantin, then NSS!
2. Instruct the pt to avoid alcohol bec alcohol + dilantin can lead to severe CNS depression
Dilantin toxicity:
S/Sx:
G gingival hyperplasia swollen gums
i. Oral hygiene soft toothbrush
ii. Massage gums
H hairy tongue
A - ataxia
N nystagmus abnormal movement of eyeballs
A acetaminophen/ Tylenol non-opoid analgesic & antipyretic febrile pts
Acetaminophen toxicity :
1. Hepato toxicity
2. Monitor liver enzymes

Page 104
SGPT (ALT) Serum Glutamic Piruvate Tyranase

SGOT- Serum Glutamic Acetate Tyranase
3. Monitor BUN (10 20)
Crea (.8-1)
Acetaminophen toxicity can lead to hypoglycemia
T tremors, Tachycardia
I irritability
R restlessness
E extreme fatigue
D depression (nightmares) , Diaphoresis
Antidote for acetaminophen toxicity Acetylcesteine = causes outporing of secretions. Suction.
Prepare suctioning apparatus.
Question: The following are symptoms of hypoglycemia except:
a. Nightmares
b. Extreme thirst hyperglycemia symptoms
d. Diaphoresis
c. Weakness
PARKINSONS DSE (parkinsonism) - chronic, progressive disease of CNS char by degeneration of dopamine
producing cells in substancia nigra at mid brain & basal ganglia
- Palliative, Supportive
Function of dopamine: controls gross voluntary motors.
Predisposing Factors:
1. Poisoning (lead & carbon monoxide). Antidote for lead = Calcium EDTA
2. Hypoxia
3. Arteriosclerosis
4. Encephalitis
High doses of the ff:
a. Reserpine (serpasil) anti HPN, SE 1.) depression - suicidal 2.) breast cancer
b. Methyldopa (aldomet)
- promote safety
c. Haloperidol (Haldol)- anti psychotic
d. Phenothiazide
- anti psychotic
SE of anti psychotic drugs Extra Pyramidal Symptom
Over meds of anti psychotic drugs neuroleptic malignant syndrome char by tremors (severe)
S/Sx: Parkinsonism
1. Pill rolling tremors of extremities early sign
2. Bradykinesia slow movement
3. Over fatigue
4. Rigidity (cogwheel type)
a. Stooped posture
b. Shuffling most common
c. Propulsive gait
5. Mask like facial expression with decrease blinking eyes
6. Monotone speech
7. Difficulty rising from sitting position
8. Mood labilety always depressed suicide
Nsg priority: Promote safety
9. Increase salivation drooling type
10. Autonomic signs:
- Increase sweating
- Increase lacrimation
- Seborrhea (increase sebaceous gland)
- Constipation
- Decrease sexual activity
Nsg Mgt

Page 105
1.) Anti parkinsonian agents

- Levodopa (L-Dopa), Carbidopa (Sinemet), Amantadine Hcl (Symmetrel)
Mechanism of action
Increase levels of dopa relieving tremors & bradykinesia
S/E of anti parkinsonian
- Anorexia
- n/v
- Confusion
- Orthostatic hypotension
- Hallucination
- Arrhythmia
Contraindication:
1. Narrow angled closure glaucoma
2. Pt taking MAOI (Parnate, Marplan, Nardil)
Nsg Mgt when giving anti-parkinsonian
1. Take with meals to decrease GIT irritation
2. Inform pt urine/ stool may be darkened
3. Instruct pt- dont take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg
- Cause B6 reverses therapeutic effects of levodopa
Give INH (Isoniazide-Isonicotene acid hydrazide.) SE-Peripheral neuritis.
2.) Anti cholinergic agents relieves tremors
Artane
mech inhibits acetylcholine
Cogentin
action , S/E - SNS
3.) Antihistamine Diphenhydramine Hcl (Benadryl) take at bedtime
S/E: adult drowsiness, avoid driving & operating heavy equipt. Take at bedtime.
Child hyperactivity CNS excitement for kids.
4.) Dopamine agonist
Bromotriptine Hcl (Parlodel) respiratory depression. Monitor RR.
Nsg Mgt Parkinson
1.)
Maintain siderails
2.)
Prevent complications of immobility
- Turn pt every 2h
Turn pt every 1 h elderly
3.)
Assist in passive ROM exercises to prevent contractures
4.)
Maintain good nutrition
CHON in am
CHON in pm to induce sleep due Tryptopan Amino Acid
5.)
Increase fluid in take, high fiber diet to prevent constipation
6.)
Assist in surgery Sterotaxic Thalamotomy
Complications in sterotaxic thalmotomy- 1.) Subarachnoid hemorrhage 2.) aneurism 3.) encephalitis
MULTIPLE SCLEROSIS (MS)
Chronic intermittent disorder of CNS white patches of demyelenation in brain & spinal cord.
- Remission & exacerbation
- Common women, 15 35 yo
cause unknown
Predisposing factor:
1. Slow growing virus
2. Autoimmune (supportive & palliative treatment only)
Normal Resident Antibodies:
Ig G can pass placenta passive immunity. Short acting.
Ig A body secretions saliva, tears, colostrums, sweat
Ig M acute inflammation

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Ig E allergic reactions
IgD chronic inflammation
S & Sx of MS: (everything down)
1. Visual disturbances
a. Blurring of vision
b. Diplopia/ double vision
c. Scotomas (blind spots) initial sx
2. Impaired sensation to touch, pain, pressure, heat, cold
a. Numbness
b. Tingling
c. Paresthesia
3. Mood swings euphoria (sense of elation )
4. Impaired motor function:
a. Weakness
b. Spasiticity tigas
c. Paralysis major problem
5. Impaired cerebellar function
Triad Sx of MS
I intentional tremors
N nystagmus abnormal rotation of eyes
Charcots triad
A Ataxia
& Scanning speech
6. Urinary retention or incontinence
7. Constipation
8. Decrease sexual ability
Dx MS
1. CSF analysis thru lumbar puncture
- Reveals increase CHON & IgG
2. MRI reveals site & extent of demyelination
3. Lhermittes response is (+). Introduce electricity at the back. Theres spasm & paralysis at spinal cord.
Nsg Mgt MS
- Supportive mgt
1.) Meds
a. Acute exacerbation
ACTH adenocorticotopic
Steroids to reduce edema at the site of demyelination to prevent paralysis
Spinal Cord Injury
Administer drug to prevent paralysis due to edema
a. Give ACTH steroids
b. Baclopen (Lioresol) or Dantrolene Na (Dantrene)
To decrease muscle spasticity
c. Interferone to alter immune response
d. Immunosuppresants
2. Maintain siderails
3. Assist passive ROMexercises promote proper body alignment
5. Encourage fluid intake & increase fiber diet to prevent constipation
6. Provide catheterization die urinary retention
7. Give diuretics
Urinary incontinence give Prophantheline bromide (probanthene)
Antispasmodic anti cholinergic
8. Give stress reducing activity. Deep breathing exercises, biofeedback, yoga techniques.
9. Provide acid-ash diet to acidify urine & prevent bacteria multiplication
Grape, Cranberry, Orange juice, Vit C

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MYASTHENIA GRAVIS (MG) disturbance in transmission of impulses from nerve to muscle cell at neuro muscular
junction.
Common in Women, 20 40 yo, unknown cause or idiopathic
Autoimmune release of cholenesterase enzyme
Cholinesterase destroys ACH (acetylcholine) = Decrease acetylcholine
Descending muscle weakness
(Ascending muscle weakness Guillain Barre Syndrome)
Nsg priority:
1) a/w
2) aspiration
3) immobility
S/ Sx:
1.) Ptosis drooping of upper lid ( initial sign)
Check Palpebral fissure opening of upper & lower lids = to know if (+) of MG.
2.) Diplopia double vision
3.) Mask like facial expression
4.) Dysphagia risk for aspiration!
5.) Weakening of laryngeal muscles hoarseness of voice
6.) Resp muscle weakness lead respiratory arrest. Prepare at bedside tracheostomy set
7.) Extreme muscle weakness during activity especially in the morning.
Dx test
1. Tensilon test (Edrophonium Hcl) temporarily strengthens muscles for 5 10 mins. Short term- cholinergic. PNS
effect.
Nsg Mgt
1. Maintain patent a/w & adequate vent by:
a.) Assist in mechanical vent attach to ventilator
b.) Monitor pulmonary function test. Decrease vital lung capacity.
2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, 5/5, etc)
3. Siderails
4. Prevent complications of immobility. Adult-every 2 hrs. Elderly- every 1 hr.
5. NGT feeding
Administer meds
a.) Cholinergics or anticholinesterase agents
Mestinon (Pyridostigmine)
Neostignine (prostigmin) Long term
- Increase acetylcholine
s/e PNS
b.) Corticosteroids to suppress immune resp
Decadron (dexamethasone)
Monitor for 2 types of Crisis:
Myastinic crisis
A cause 1. Under medication
2. Stress
3. Infection
B S&Sx 1. Unable to see Ptosis & diplopia
2. Dysphagia- unable to swallow.
3. Unable to breath
C Mgt adm cholinergic agents
Cholinergic crisis
Cause: 1 over meds
S/Sx - PNS
Mgt. adm anti-cholinergic

- Atropine SO4
- SNS dry mouth
7. Assist in surgical proc thymectomy. Removal of thymus gland. Thymus secretes auto immune antibody.
8. Assist in plasmaparesis filter blood

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9. Prevent complication respiratory arrest

Prepare tracheostomy set at bedside.
GBS Guillain Barre Syndrome
- Disorder of CNS
- Bilateral symmetrical polyneuritis
- Ascending paralysis
Cause unknown, idiopathic
- Auto immune
- r/t antecedent viral infection
- Immunizations
S&Sx
Initial :
1. Clumsiness
2. Ascending muscle weakness lead to paralysis
3. Dysphagia
4. Decrease or diminished DTR (deep tendon reflexes)
- Paralysis
5. Alternate HPN to hypotension lead to arrhythmia - complication
increase sweating, increase salivation.
6. Autonomic changes
Increase lacrimation
Constipation
Dx most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON (same with MS)
Nsg Mgt
1. Maintain patent a/w & adequate vent
a. Assist in mechanical vent
b. Monitor pulmonary function test
2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia
3. Siderails
4. Prevent compl immobility
5. Assist in passive ROM exercises
6. Institute NGT feeding due dysphagia
7. Adm meds (GBS) as ordered: 1. Anti cholinergic atropine SO4
2. Corticosteroids to suppress immune response
3. Anti arrhythmic agents
a.) Lidocaine /Xylocaine SE confusion = VTach
b.) Bretyllium
c.) Quinines/Quinidine anti malarial agent. Give with meals.
- Toxic effect cinchonism
Quinidine toxicity
S/E anorexia, n/v, headache, vertigo, visual disturbances
8. Assist in plasmaparesis (MG. GBS)
9. Prevent comp arrhythmias, respiratory arrest
Prepare tracheostomy set at bedside.
INFL CONDITONS OF BRAIN
Meninges 3-fold membrane cover brain & spinal cord
Fx:
Protection & support
Nourishment
Blood supply

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3 layers
1. Duramater
2. Arachmoid matter
3. Pia matter
sub dural space

sub arachnoid space
where CSF flows L3 & L4. Site for lumbar puncture.
MENINGITIS inflammation of meningitis & spinal cord

Etiology Meningococcus
Pneumococcus
Hemophilous influenza child
Streptococcus adult meningitis
MOT direct transmission via droplet nuclei
S&Sx
- Stiff neck or nuchal rigidity (initial sign)
- Headache
- Projectile vomiting due to increase ICP
- Photophobia
- Fever chills, anorexia
- Gen body malaise
- Wt loss
- Decorticate/decerebration abnormal posturing
- Possible seizure
Sx of meningeal irritation nuchal rigidity or stiffness
Opisthotonus- rigid arching of back
Pathognomonic sign (+) Kernigs & Brudzinski sign
Leg pain
neck pain
Dx:
1. Lumbar puncture lumbar/ spinal tap use of hallow spinal needle sub arachnoid space L3 & L4 or L4 & L5
Aspirate CSF for lumbar puncture.
Nsg Mgt for lumbar puncture invasive
1. Consent / explain procedure to pt
- RN dx procedure (lab)
- MD operation procedure
2. Empty bladder, bowel promote comfort
3. Arch back to clearly visualize L3, L4
Nsg Ngt post lumbar
1. Flat on bed 12 24 h to prevent spinal headache & leak of CSF
2. Force fluid
3. Check punctured site for drainage, discoloration & leakage to tissue
4. Assess for movement & sensation of extremeties
Result
1. CSF analysis:
a. increase CHON & WBC

b. Decrease glucose
Confirms meningitis c. increase CSF opening pressure
N 50 160 mmHg
d. (+) Culture microorganism
2. Complete blood count CBC reveals increase WBC
Mgt:
1. Adm meds
a.) Broad-spectrum antibiotic penicillin
Content of CSF:
CSF Chon, wbc, glucose

Page 110
S/E
1. GIT irritation take with food
2. Hepatotoxicity, nephrotoxcicity
3. Allergic reaction
4. Super infection alteration in normal bacterial flora
- N flora throat streptococcus
- N flora intestine e coli
Sx of superinfection of penicillin = diarrhea
b.) Antipyretic
c.) Mild analgesic
2. Strict resp isolation 24h after start of antibiotic therapy
A Cushings synd reverse isolation - due to increased corticosteroid in body.
B Aplastic anemia reverse isolation - due to bone marrow depression.
C Cancer anytype reverse isolation immunocompromised.
D Post liver transplant reverse isolation takes steroids lifetime.
E Prolonged use steroids reverse isolation
F Meningitis strict respiratory isolation safe after 24h of antibiotic therapy
G Asthma not to be isolated
3.
4.
5.
6.
7.
Comfy & dark room due to photophobia & seizure

Prevent complications of immobility
Maintain F & E balance
Monitor vs, I&O , neuro check
Provide client health teaching & discharge plan
a. Nutrition increase cal & CHO, CHON-for tissue repair. Small freq feeding
b. Prevent complication hydrocephalus, hearing loss or nerve deafness.
8. Prevent seizure.
Where to bring 2 yo post meningitis
- Audiologist due to damage to hearing- post repair myelomeningocele
- Urologist -Damage to sacral area spina bifida controls urination
9. Rehab for neurological deficit. Can lead to mental retardation or a delay in psychomotor development.
CEREBRO VASCULAR ACCIDENT stroke, brain attack or cerebral thrombosis, apoplexy
- Partial or complete disruption in the brains blood supply
- 2 largest & common artery in stroke
Middle cerebral artery
Internal carotid artery
- Common to male 2 3x high risk
Predisposing factor:
1. Thrombosis clot (attached)
2. Embolism dislodged clot pulmo embolism
S/Sx: pulmo embolism
embolism
Sudden sharp chest pain
Unexplained dyspnea, SOB
Tachycardia, palpitations, diaphoresis & mild restlessness
S/Sx: cerebral embolism
Headache, disorientation, confusion & decrease in LOC
Femur fracture complications: fat embolism most feared complication w/in 24hrs
Yellow bone marrow produces fat cells at meduallary cavity of long bone
Red bone marrow provides WBC, platelets, RBC found at epiphisis
2.)
Hemorrhage

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3.)
Compartment syndrome compression of nerves/ arteries
Risk factors of CVA: HPN, DM, MI, artherosclerosis, valvular heart dse - Post heart surgery mitral valve replacement
Lifestyle:
1. Smoking nicotine potent vasoconstrictor

3. Hyperlipidemia genetic
4. Prolonged use of oral contraceptives
- Macro pill has large amt estrogen
- Mini pill has large amt of progestin
- Promote lipolysis (breakdown of lipids/fats) artherosclerosis HPN - stroke
5. Type A personality
a. Deadline driven person
b. 2 5 things at the same time
c. Guilty when not dong anything
6. Diet increase saturated fats
7. Emotional & physical stress
8. Obesity
S & Sx
1. TIA- warning signs of impending stroke attacks
- Headache (initial sx), dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or plegia
(monoplegia 1 extreme)
Increase ICP
2. Stroke in evolution progression of S & Sx of stroke
3. Complete stroke resolution of stroke
a.) Headache
b.) Cheyne-Stokes Resp
c.) Anorexia, n/v
d.) Dysphagia
e.) Increase BP
f.) (+) Kernigs & Brudzinski sx of hemorrhagic stroke
g.) Focal & neurological deficit
1. Phlegia
2. Dysarthria inability to vocalize, articulate words
3. Aphasia
4. Agraphia diff writing
5. Alesia diff reading
6. Homoninous hemianopsia loss of half of field of vision
Left sided hemianopsia approach Right side of pt the unaffected side
Dx
1. CT Scan reveals brain lesion
2. Cerebral arteriography site & extent of mal occlusion
- Invasive procedure due to inject dye
- Allergy test
All graphy invasive due to iodine dye
Post
1.) Force fluid to excrete dye is nephrotoxic
2.) Check peripheral pulses - distal
Nsg Mgt
1. Maintain patent a/w & adequate vent
- Assist mechanical ventilation
- Administer O2
2. Restrict fluids prevent cerebral edema
3. Elevate head of bed 30-45 degrees angle. Avoid valsalva maneuver.

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4. Monitor vs., I&O, neuro check

5. Prevent compl of immobility by:
a. Turn client q2h
Elderly q1h
- To prevent decubitus ulcer
- To prevent hypostatic pneumonia after prolonged immobility.
b. Egg crate mattress or H2O bed
c. Sand bag or foot board- prevent foot drop
6. NGT feeding if pt cant swallow
7. Passive ROM exercise q4h
8. Alternative means of communication
- Non-verbal cues
- Magic slate. Not paper and pen. Tiring for pt.
- (+) To hemianopsia approach on unaffected side
9. Meds
Osmotic diuretics Mannitol
Loop diuretics Lasix/ Furosemide
Corticosteroids dextamethazone
Mild analgesic
Thrombolytic/ fibrolitic agents tunaw clot. SE-Urticaria, pruritus-caused by foreign subs.
Streptokinase
Urokinase
Tissue plasminogen activating
Monitor bleeding time
Anticoagulants Heparin & Coumadin sabay
Coumadin will take effect after 3 days
Heparin monitor PTT partial thromboplastin time if prolonged bleeding give Protamine SO4- antidote.
Coumadin Long term. monitor PT prothrombin time if prolonged- bleeding give Vit K Aquamephyton- antidote.
Antiplatelet PASA aspirin paraanemo aspirin, dont give to dengue, ulcer, and unknown headache.
Health Teaching
1. Avoidance modifiable lifestyle
- Diet, smoking
2. Dietary modification
- Avoid caffeine, decrease Na & saturated fats
Complications:
Subarachnoid hemorrhage
Rehab for focal neurological deficit physical therapy
1. Mental retardation
2. Delay in psychomotor development
CONVULSIVE Disorder (CONVULSIONS)
(CONVULSIONS)- disorder of the CNS char. by paroxysmal seizures with or without loss of
consciousness, abnormal motor activity, alteration in sensation & perception & change in behavior.
Can you outgrow febrile seizure?
Febrile seizure Normal if < 5 yo
Pathologic if > 5 yo
Difference between:
Seizure- 1st convulsive attack

Epilepsy 2nd and with history of seizure
Predisposing Factor
Head injury due birth trauma
Toxicity of carbon monoxide
Brain tumor
Genetics

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Nutritional & metabolic deficit

Physical stress
Sudden withdrawal to anticonvulsants will bring about status epilepticus
Status epilepticus drug of choice: Diazepam & glucose
S & Sx
I. Generalized Seizure
a.) Grand mal / tonic clonic seizures
With or without aura warning symptoms of impending seizure attack- Epigastric pain- associated with olfactory, tactile,
visual, auditory sensory experience
- Epileptic cry fall
- Loss of consciousness 3 5 min
- Tonic clonic contractions
- Direct symmetrical extension of extremities-TONIC. Contractions-CLONIC
- Post ictal sleep -state of lethargy or drowsiness - unresponding sleep after tonic clonic
b.) Petimal seizure (same as daydreaming!) or absent seizure.
- Blank stare
- Decrease blinking eye
- Twitching of mouth
- Loss of consciousness 5 10 secs (quick & short)
II. Localized/partial seizure
a.) Jacksonian seizure or focal seizure tingling/jerky movement of index finger/thumb & spreads to shoulder &
1 sideof the body with janksonian march
b.) Psychomotor/ focal motor - seizure
-Automatism stereotype repetitive & non-purposive behavior
- Clouding of consciousness not in control with environment
- Mild hallucinatory sensory experience
HALLUCINATIONS
1. Auditory schitzo paranoid type
2. Visual korsakoffs psychosis chronic alcoholism
3. Tactile addict substance abuse
III. Status epilecticus continuous, uninterrupted seizure activity, if untreated, lead to hyperprexia coma death
Seizure: inc electrical firing in brain=increased metabolic activity in brain=brain using glucose and O2=dec glucose,
dec O2.
Tx:Diazepam (drug of choice), glucose
Dx-Convulsion- get health history!
1. CT scan brain lesion
2. EEG electroencephalography
- Hyperactivity brain waves
Nsg Mgt
Priority Airway & safety
1. Maintain patent a/w & promote safety
Before seizure:
1. Remove blunt/sharp objects
2. Loosen clothing
3. Avoid restraints
4. Maintain siderails
5. Turn head to side to prevent aspiration
6. Tongue guard or mouth piece to prevent biting of tongue-BEFORE SEIZURE ONLY! Can use spoon at
home.
7. Avoid precipitating stimulus bright glaring lights & noises
8. Administer meds
a. Dilantin (Phenytoin) ( toxicity level 20 )

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Ginguial hyperplasia
H-hairy tongue
A-ataxia
N-nystagmus
A-acetaminophen- febrile pt
Mix with NSS
- Dont give alcohol lead to CNS depression
b. (Tegretol) Carbamasene- given also to Trigeminal Neuralgia. SE: arrythmia
c. Phenobarbital (Luminal)- SE: hallucinations
SE
2. Institute seizure & safety precaution. Post seizure: Administer O2. Suction apparatus ready at bedside
3. Monitor onset & duration
- Type of seizure
- Duration of post ictal sleep. The longer the duration of post ictal sleep, the higher chance of having status epilepticus!
4. Assist in surgical procedure. Cortical resection
5. Complications: Subarachnoid hemorrhage and encephalitis
Question: 1 yo grand mal immediate nursing action = a/w & safety
a. Mouthpiece 1 yr old little teeth only
b. Adm o2 inhalation post!
c. Give pillow safety (answer)
d. Prepare suction
Neurological assessment:
1. Comprehensive neuro exam
2. GCS - Glasgow coma scale obj measurement of LOC or quick neuro check
3 components of ECS
M motor
6
V verbal resp 5
E eye opening 4
15
15 14 conscious
13 11 lethargy
10 8 stupor
7 coma
3 deep coma lowest score
Survey of mental status & speech (Comprehensice Neuro Exam)
1.) LOC & test of memory
2.) Levels of orientation
3.) CN assessment
4.) Motor assessment
5.) Sensory assessment
6.) Cerebral test Romhberg, finger to nose
7.) DTR
8.) Autonomics
Levels of consciousness (LOC)
1. Conscious (conscious) awake levels of wakefulness
2. Lethargy (lethargic) drowsy, sleepy, obtunded
3. Stupor (stuporous) awakened by vigorous stimulation
Pt has gen body weakness, decrease body reflex
4. Coma (Comatose) light (+) all forms of painful stimulations

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Deep (-) to painful stimulation

Question: Describe a conscious pt ?
a. Alert not all pt are alert & oriented to time & place
b. Coherent
c. AwakeAwake- answer
d. Aware
Different types of pain stimulation
- Dont prick
1. Deep sternal stimulation/ pressure 3x fist knuckle
With response light coma
Without response deep coma
2. Pressure on great toe 3x
3. Orbital pressure pressure on orbits only below eye
4. Corneal reflex/ blinking reflex
Wisp of cotton used to illicit blinking reflex among conscious patients
Instill 1-drop saline solution unconscious pt if (-) response pt is in deep coma
5. Test of memory considered educational background
a.) Short term memory
- What did you eat for breakfast?
Damage to temporal lobe (+) antero grade amnesia
b.) Long term memory
(+) Retrograde amnesia damage to limbic system
6. Levels of orientation
Time
Place
Person
Graphesthesia- can identify numbers or letters written on palm with a blunt object.
Agraphesthesia cant identify numbers or letters written on palm with a blunt object.
CN assessment:
I
II
III
IV
V
VI
VII
VIII
IX
X
XI
XII
Olfactory
Optic
Oculomotor
Trocheal
Trigeminal
Abducens
Facial
Acustic/auditory
Glassopharyngeal
Vagus
Spinal accessory
Hypoglossal
s
s
m
m
b
m
b
s
b
b
m
m
smallest CN
largest CN
longest CN
I. Olfactory dont use ammonia, alcohol, cologne irritating to mucosa use coffee, bar soap, vinegar, cigarette tar
- Hyposmia decrease sensitivity to smell
- Diposmia distorted sense of smell
- Anosmia absence of sense of smell
Either of 3 might indicate head injury damage to cribriform plate of ethmoid bone where olfactory cells are located or
indicate inflammation condition sinusitis
II opticoptic test of visual acuity Snellens chart central or distance vision
Snellens E chart used for illiterate chart
N 20/20 vision distance by w/c person can see letters- 20 ft
Numerator distance to snellens chart
Denominator distance the person can see the letters
OD Rt eye
20/2020/200 blindness cant read E biggest

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OS left eye
OU both eye
2.
a.
b.
c.
d.
20/20
20/20
Test of peripheral vision/ visual field
Superiority
Bitemporally
Inferiorly
Nasally
Common Disorders see page 85-87 for more info on glaucoma, etc.
1. Glaucoma Normal 12 21 mmHg pressure
- Increase IOP - Loss of peripheral vision tunnel vision
2. Cataract opacity of lens - Loss of central vision, Blurring or hazy vision
3. Retinal detachment curtain veil like vision & floaters
4. Macular degeneration black spots
III, IV, VI tested simultaneously
- Innervates the movementt of extrinsic ocular muscle
6 cardinal gaze EOM
Rt eye
IO
SO
LR
MR
N
O
S
E
left eye
SR
3 4 EOM
IV sup oblique
VI lateral rectus
Normal response PERRLA (isocoria equal pupil)
Anisocoria unequal pupil
Oculomotor
1. Raising of eyelid Ptosis
2. Controls pupil size 2 -3 cm or 1.5 2 mm
V Trigeminal Largest consists of - ophthalmic, maxillary, mandibular
Sensory controls sensation of the face, mucus membrane; teeth & cornea reflex
Unconscious instill drop of saline solution
Motor controls muscles of chewing/ muscles of mastication
Trigeminal neuralgia diff chewing & swallowing extreme food temp is not recommended
Question: Trigeminal neuralgia, RN should give
a. Hot milk, butter, raisins
b. Cereals
c. Gelatin, toast, potato all correct but
d. Potato, salad, gelatin salad easier to chew
VI Facial:
Facial Sensory controls taste ant 2/3 of tongue test cotton applicator put sugar.
-Put applicator with sugar to tip to tongue.
-Start of taste insensitivity: Age group 40 yrs old
Motor- controls muscles of facial expression, smile frown, raise eyebrow
Damage Bells palsy facial paralysis

Page 117
Cause bells palsy pedia R/T forcep delivery

Temporary only
Most evident clinical sign of facial symmetry: Nasolabial folds
VIII Acoustic/
Acoustic vestibule cochlear (controls hearing) controls balance (kenesthesia or position sense)
- Movement & orientation of body in space
- Organ of Corti for hearing true sense organ of hearing
Outer tympanic membrane, pinna, oricle (impacted cerumen), cerumen
Middle hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media
- Eustachean ear
Inner ear- meniere dse, sensory hearing loss (research parts! & dse)
Remove vestibule menieres dse disease inner ear
Archimedes law buoyancy (pregnancy fetus)
Daltons law partial pressure of gases
Inertia law of motion (dizziness, vertigo)
1.) Pt with multiple stab wound - chest
- Movement of air in & out of lungs is carried by what principle?
- Diffusion Daltons law
2.) Pregnant check up ultrasound reveals fetus is carried by amniotic fluid
- Archimedes
3.) Severe vertigo due- Inertia
Test for acoustic nerve:
- Repeat words uttered
IX Glossopharyngeal controls taste posterior 1/3 of tongue
X Vagus controls gag reflex
Test 9 10
Pt say ah check uvula should be midline
Damage cerebral hemisphere is L or R
Gag reflex place tongue depression post part of tongue
' Dont touch uvula
XI Spinal Accessory - controls sternocleidomastoid (neck) & trapezius (shoulders and back)
- Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia
XII Hypoglossal controls movement of tongue say ah. Assess tongue position=midline
L or R deviation
- Push tongue against cheek
- Short frenulum lingue
Tongue tied bulol
ONCOLOGY NURSING
ONCOLOGY / CANCER NURSING

Page 118
THE CELL
Definition of Related Terms
Cell
- The basic unit of living organism; can reproduce itself
Cancer a disease process whereby cells proliferate abnormally, ignoring growth
regulating signals in the environment surrounding the cells.
Carcinoma
a new growth or malignant tumor that originates from epithelial cells, the skin, GIT, Lungs, Uterus, breast
and other organs.
Benign usually a reference to growths that are encapsulated, remain localized, and are slow growing
Malignant
- terms for growth that is encapsulated but metastasize and grow. These growths are cancerous lesions
having the characteristics of disorderly, uncontrolled proliferation of the cell
Tumor - Abnormal swelling usually from inflammation, or from morbid enlargement.
- They are uncontrolled tissue growth that in which cell rapidly multiplies
Oncology
- The study of cancer
Staging - a method of classifying malignancies based on the presence and extent of the tumor on the body
Metastasis
- the transfer of disease from one organ or apart to another not directly connected to it.
Undifferentiated cells cells that lost the capacity for specialized functions
Carcinogenesis
Carcinogenesis process of transforming normal cells into malignant cells
Carcinogens
- agents that initiate or promote cellular transformation.
Oncogene
- cancer gene that alters the normal cell
Carcinoma
- usually solid tumors arising from epithelial cell
Sarcoma
- from muscle, bone, fat and other connective tissue
Sarcoma
Lymphoma
- malignant tumors in lymphatic system
Leukemia
- cancer of the blood
Nadir - lowest point of WBC depression after therapy that has toxic effects on the bone marrow
Metastasis
- spread of cancer cells from the primary tumor to distant sites.
Review of Anatomy and Physiology: Cell
Centrioles
- self-replicating organelles made of
o nine
bundles of microtubules and
are found only in animal cells
Cilia and Flagella essential for locomotion (singlecelled). Cilia function to move fluid
or materials past an immobile cell as well as moving
a cell
or group of cells.
Endoplasmic Reticulum a network of sacs
that manufactures processes and transports
chemical compounds for use inside and outside of
the
cell.
Provides a pipeline between the nucleus
and
the
Cytoplasm.
Golgi apparatus The distribution and Shipping
department for the cells
chemical products
Lysozymes
- Main function is digestion. Breaks down cellular waste products and debris from outside the cell into
simple compounds, which are transferred to the cytoplasm as new cell-building materials.
Mitochondria - are oblong shaped. The main power generators, converting oxygen and
nutrients into energy
Nucleus - Serves as the information processing and administrative center of the
cell.
- Stores DNA
- Coordinates cell activities
o Growth
o Intermediary metabolism
o Protein synthesis
o Reproduction (cell division)

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- found inside the cytoplasm

Perixosomes
Plasma membrane encloses cell contents. Selectively
Permeable.
Ribosomes
- comprised of approx. 60% RNA and 40%
protein
Cell Division
Overview
of
Mitosis
Cell division is an elegant process that enables organisms to grow and reproduce. Through a sequence of steps, the
replicated genetic material in a parent cell is equally distributed to two daughter cells. While there are some subtle
differences, mitosis is remarkably similar across organisms.
Before a dividing cell enters mitosis, it undergoes a period of growth called interphase. Interphase is the "holding" stage or
the stage between two successive cell divisions.
In this stage, the cell replicates its genetic material and organelles in preparation for division.
Mitosis
Prophase
is
composed
of
several
stages:
In prophase, the chromatin condenses into discrete chromosomes. The nuclear envelope breaks down and spindles form at
opposite
"poles"
of
the
cell.
Metaphase
In metaphase, the chromosomes are aligned at the metaphase plate (a plane that is equally distant from the two spindle
poles).
Anaphase
In
anaphase,
the
paired
chromosomes
(sister
chromatids)
move
to
opposite
ends
of
the
cell.
Telophase
In this last stage, the chromosomes are cordoned off in distinct new nuclei in the emerging daughter cells. Cytokinesis is
also
occurring
at
this
time.
At the end of mitosis, two distinct cells with identical genetic material are produced.
Before a dividing cell enters mitosis, it undergoes a period of growth called interphase. Some 90 percent of a cell's time in
the
normal
cellular
cycle
may
be
spent
in
interphase.
Stages of Interphase
G1 phase: The period prior to the synthesis of DNA. In this phase, the cell increases in mass in preparation
for cell division. Note that the G in G1 represents gap and the 1 represents first, so the G1 phase is the first gap
phase.
S phase: The period during which DNA is synthesized.

In most cells, there is a narrow window of time during which DNA is synthesized. Note that the S represents synthesis.

Page 120

G2 phase: The period after DNA synthesis has occurred but prior to the start of prophase. The cell
synthesizes proteins and continues to increase in size. Note that the G in G2 represents gap and the 2 represents
second, so the G2 phase is the second gap phase.
In the latter part of interphase, the cell still has nucleoli present.
The nucleus is bounded by a nuclear envelope and the cell's chromosomes have duplicated but are in the
form of chromatin.
In animal cells, two pair of centrioles formed from the replication of one pair are located outside of the
nucleus.
Pathogenesis of Cancer
a. Cellular Transformation & Derangement Theory

-
Conceptualizes that normal cells may be transformed into cancer cells due to exposure to some
etiologic agents.
b. Failure of the Immune Response Theory

-
Advocates that all individuals possess cancer cells. However, the cancer cells are recognized by the
immune response system. So, the cancer cell undergoes destruction. Failure of the immune response
system leads to inability to destroy the cancer cells.
ROLE OF THE IMMUNE SYSTEM

-
malignant cells are capable of developing on a regular basis

Immune system can detect the development of malignant cells and destroys them before cell growth
becomes uncontrolled.
Clinical cancer develops when the immune system fails to identify and stop the growth of malignant
cells.
Normal Immune Response

- recognizes as foreign certain antigens(tumor associated antigens) on the cell membrane of cancer cells
- macrophages, T lymphocytes, soldiers of the cellular immune response
- T-lymphocytes has cytotoxic properties
- Lymphokines produced by lymphocytes, capable of killing or damaging various types of malignant
cells
- Interferon (IFN) produce by the body in response to viral infection, possesses anti tumor properties.
- Natural Killer
Killer Cells subpopulation of lymphocytes, producing lymphokines and certain enzymes that
kills tumors
Immune System Failure
- Body fails to recognize malignant cells as different from self
- Immune response may not be activated
- Tumor antigens combine with antibodies produced by the immune system and hides/disguise
themselves from normal immune defense mechanism.
ASSESSMENT
ETIOLOGY:
A. VIRUSES & BACTERIA viruses incorporate themselves in the genetic structure of cells, altering future generation of
that cell population perhaps leasing to Cancer.
e.g. Epstein-Barr Virus Highly suspect as a cause in
- Burkitts lymphoma
- Nasopharyngeal Ca
- some types of non-Hodgkins Lymphoma
- Hodgkins Disease
Herpes Simplex II, CMV, HPV 16, 18, 31, 33

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o
o
Dysplasia
Ca of the cervix
Hepatitis B virus
o Liver Ca
Human T cell lymphotropic Virus
o lymphocytic leukemia
o lymphomas
HIV
o Kaposis Sarcoma
Helicobacter pylori (bacteria)
o Gastric Malignancy
B. PHYSICAL AGENTS
a. Exposure to UV rays of the sun
b. Exposure to Ionizing radiation
c. Chronic inflammation or Irritation
d. Tobacco use
C. CHEMICAL AGENTS
- 75 % of all Ca are thought to be related to the environment
- Tobacco smoke single most lethal chemical carcinogen 30% of Ca deaths
- Chemical substances found in workplace (amines, aniline dyes, pesticides and formaldehydes, arsenic,
tars, asbestos, benzene, Cadmiun, Nickel and Zinc ores, PVCs etc.)
- Chemical agents alters DNA structure in body sites distant from chemicalexposure (liver, lungs and
kidneys are most commonly affected)
D. GENETIC & FAMILIAL FACTORS
- genetics, shared environments, cultural or lifestyle factors, chance.
E. DIETARY FACTORS
- Proactive (protective) substances High fiber, cruciferous vegetables, carotenoids,, Vit. E & C, Zinc and
Selenium
- Cacinogenic
Cacinogenic & Co-Carcinogenic substances High fat, Low Fiber, Alcohol, Salt-cured or smoked meats,
foods w/ nitrates & nitrites, High Caloric.
F. HORMONAL AGENTS
- Endogenous vs. Exogenous hormones
- DES (Diethylstilbestrol) vaginal carcinomas
- Oral contraceptives and prolonged estrogen replacement therapy
Predisposing Factors
Age
- Older individuals are more prone to cancer, they have been exposed to carcinogens longer, they may have
developed immune system alteration.
Sex
- Women = more prone to breast, uterus, cervical cancer
Men = more prone to prostate, lung cancer
Residence
- Urban dwellers are more prone to cancer than Rural dwellers.
Geographic distribution
- Japan = cancer of the stomach
- US = cancer of the breast
- Due to influence of environmental factors such as, national diet, ethnic customs, type of pollutions
Occupation
- Chemical factory workers, farmers, radiology department person
Heredity
- Greater risk with positive family history
Stress
- Depression, grief, anger, aggression, despair or life stresses decreases
immunocompetence (affect hypothalamus and pituitary gland)
- immunodeficiency may spur the growth and proliferation of cancer cells
Precancerous lesions
- May undergo transformation into Ca lesions and tumors.
- E.g. pigmented moles, burn scars, senile keratosis, leoukoplakia, benign polyps/adenoma of the colon
or stomach, fibrocystic disease of the breast
Obesity - Studies have linked obesity to breast and colorectal Ca

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American Cancer Society 7 Warning Signs (CAUTION)

CAUTI
ON-
Change in bowel or bladder HABITS

A sore that does not heal
Unusual bleeding or discharges
Thickening or a lump in the breast or elsewhere
Indigestion and difficulty of swallowing
Obvious change in a wart or a mole
Nagging cough or hoarseness of the voice
Cancer Classification
1. Solid Tumors Associated with the organs from which they develop. Such as breast cancer or lung cancer
2. Hematological Cancer Originate from blood cell-forming tissues, such as the Leukemia sans the Lymphomas
Characteristic
Characteristic of Malignant vs. Benign neoplasm
CHARACTERISTICS
Rate of growth
BENIGN
Usually slow
Mode of growth
Grows by expansion; does not

infiltrate surrounding tissues; usually
encapsulated
Well differentiated cells that resembles
normal cells of the tissues from which
the tumor originated
Not spread by metastasis
Cell characteristics
Metastasis
General effects
Tissue destruction
Ability to cause death
Usually a localized phenomenon that

does not cause generalized effects
unless its location interferes with
blood flow
Does not usually cause tissue damage
unless its location interferes with
blood flow
Does not usually cause death unless its
location interferes with vital functions
MALIGNANT
Variable
and
depends
on level
of
differentiation; the more anaplastic the tumor,
the faster its growth
Grows at he periphery and sends out processes
that infiltrate and destroy surrounding tissues
Undifferentiated and often bear little
resemblance to the normal cells of the tissue
from which they arose
Gains access to the blood and lymphatic
channels and metastasizes to other areas of the
body
Often causes generalized effects such as
Anemia, Weakness, and weight loss
Often causes extensive tissue damage as the
tumor outgrows its blood supply or
encroaches on blood flow to the area; may
also produce substances that cause cell damage
Usually causes death unless growth can be
controlled
Grading and Staging of Tumors
Staging determines the size of the tumor and the existence of metastasis
TNM system most frequently used system in classifying the extent of disease.
T Extent of Primary Tumor
N Lymph node involvement
M extent of mmetastasis
Primary Tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis carcinoma in situ

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T1, T2, T3, T4 increasing size and / or local extent of the primary tumor
Regional Lymph Node (N)
NX Regional lymph nodes cannot be assessed
N0 No regional Lymph node metastasis
N1,N2,N3 Increasing involvement of regional lymph nodes
STAGING
Stage 0
Stage I
Stage II
Stage III
Stage IV
Carcinoma in situ
Tumor limited to the tissue of origin; localized tumor growth
Limited local spread
Extensive local and regional spread
Metastasis
Distant Metastasis
Metastasis (M)
MX distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
Grading refers to the classification of the tumor cells.

GRADING
Grade I
Grade II
Grade III
Grade IV
Cells
Cells
Cells
Cells
seeks to define the type of tissue from which the tumor originated and the degree to which the tumor
cells retain the functional and histologic characteristics of the tissue of origin.
done through Cytology, Biopsy, Surgical Excision.
differ slightly from normal cells and are well differentiated (mild dysplasia)
are more abnormal and are moderately differentiated (moderate dysplasia)
are very abnormal and are poorly differentiated (severe dysplasia)
are immature (anaplasia) and undifferentiated; cell of origin is difficult to determine
PRIMARY AND SECONDARY PREVENTION

Primary prevention concerned with reducing the risk of cancer in healthy people
- Client Education and counseling. (Avoidance of Carcinogens and
dietary and lifestyle changes).
Secondary Prevention involves detection and screening to achieve early diagnosis and
prompt intervention to halt cancer process.
EARLY DETECTION
1.
2.
3.
4.
5.
6.
7.
Mammography
Papanicolaous (Pap) smear
Stools for occult blood
Sigmoidoscopy: colonoscopy
Breast self-examination
Testicular Self Examination
Skin inspection
DIAGNOSTIC TESTS
TESTS
1. Blood analysis- an unestablished diagnostic test used by some health care
practitioners to determine a course of treatment

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RBC, WBC, Platelets
2. Bone Marrow Examination refers to the pathologic analysis of samples of bone

marrow obtained by bone marrow biopsy (Trephine) and bone marrow aspiration.
Bone Marrow Biopsy removal of soft tissue from inside of the bone. Bone
marrow grows inside some larger bones in the body. It produces platelets and red and white blood cells.
3. Radiographic / imaging tests
TEST
Tumor
identification
DESCRIPTION
DIAGNOSTIC USES
Analysis of substances found in blood or other Breast, colon, lung, ovarian,
body fluids that are made by the tumor or by testicular, prostate Cancer
the body in response to the tumor.
MRI
Use of magnetic fields and radiofrequency signals Neurologic, pelvic, abdominal,
to create sectioned images of various body thoracic cancers
structures
CT scan
Use of Narrow beam x-ray to scan successive Neurologic, pelvic, skeletal,
layers of tissues for cross-sectional views
abdominal, thoracic cancers
Fluoroscopy
Use of x-rays that identify contrasts in body Abdominal and pelvic cancers
tissue densities; may use contrast agents
Endoscopy
Direct visualization of a body cavity or Bronchial, GI cancer
passageway by insertion of an endoscope into a
body cavity or opening; allowing tissue biopsy,
fluid aspiration and excision of small tumors;
both diagnostic and therapeutic
PET scan
Computed cross-sectional images of increased Lung, colon, liver, pancreas,
concentration of radioisotopes in malignant cells breast,
esophagus
cancer;
provide information about biologic activity of Hodgkins and non-Hodgkins
malignant cells; helps identify if malignant or just lymphoma and Melanoma.
benign
Radioimmunoconjugates
Monoclonal antibodies are labeled with a Colorectal,
breast,
ovarian,
radioisotope and injected intravenously into the head
and
neck
cancers;
patient; antibodies aggregate at the tumor site lymphoma and melanoma
then visualized with scanners
3. Biopsy the definitive means of diagnosing cancer and provides histological proof of malignancy
- involves surgical incision of a small piece of tissue for microscopic examination
marker
Types:
a. Needle
- Aspiration of cells
b. Incisional
- Removal of a wedge of suspected tissue from a larger mass
c. Excisional
- Complete removal of the entire lesion
d. Staging
- Multiple needle or incisional biopsies in tissues where metastasis
is suspected or likely.
***
> procedure is usually performed in an outpatient surgical setting

> Prepare Client Physically and psychologically and following physicians
Instructions
> Obtain an Informed consent
Pathophysiologic Basis of Malignant Neoplasm
Cancer is a disease process that begins when an abnormal cell is transformed by the genetic mutation of the cellular
DNA. This abnormal cell forms a clone and begins to proliferate abnormally, ignoring growth regulating signals in the
environment surrounding the cell. The cells acquire invasive characteristics, and changes occur in surrounding tissues. The
cells infiltrate these tissues and gain access to lymph and blood vessels, which carry the cells to other areas of the body. This
phenomenon is called Metastasis.

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Cancer is not a single disease with a single cause; rather, it is a group of distinct diseases with different causes,
manifestations, treatments and prognoses.
Proliferative patterns
Hyperplasia
Increase in the number of cells of a tissue; most often associated
with periods of rapid body growth
Metaplasia
conversion of one type of mature cell into another type of cell
Dysplasia
bizarre cell growth resulting in cells that differ in size, shape, or
arrangement from other cells of the same type of tissue.
Anaplasia
cells that lack normal cellular characteristics and differ in shape
and organization with respect to their cells of origin; usually, anaplastic cells are malignant
Neoplasia
Uncontrolled cell growth that follows no physiologic demand.
Invasion and Metastasis

Metastatic Mechanism
a. Lymphatic spread
- most common. Through the lymphatic circulation.
b. Hematogenous spread
- malignant cells are disseminated through the
bloodstream. Directly related to the vascularity of
the tumor.
c. Angiogenesis
- Ability of malignant cells to induce growth of new
capillaries from the host tissue to meet their needs for nutrients and oxygen.
Carcinogenesis
- a.k.a. Malignant transformation; has three-step cellular process
a. Initiation Carcinogens escape normal enzymatic mechanisms and alter the genetic structure of the cellular DNA
(Permanent cellular mutations)
b. Promotion repeated exposure to co-carcinogens causes the expression of abnormal or mutant genetic
information even after long latency periods.
Cellular oncogenes responsible for the vital cellular functions of growth and
differentiation.
Cellular ProtoProto-oncogenes acts as an ON switch for cellular growth.
Cancer Suppressor genes turn OFF or regulate unneeded cellular proliferation
- when mutated, rearranged, amplified, or lose their regulatory
capabilities, malignant cells reproduce.
P53 gene
- tumor suppressor gene that is frequently mutated in many human
cancers.
- regulates whether cells will repair or die after DNA damage.
c. Progression Cellular changes exhibit increased malignant behavior.
- cells shows propensity to invade adjacent tissues and to
metastasize.
Cellular Aberration
1. Ca Cell Proliferation disrupts normal cell growth and interfere with tissue function
Manifestation:
- Pressure
- Obstruction
- Pain
- Effusion

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Ulceration
Vascular Thrombosis, Embolus, Thrombophlebitis
2. Paraneoplastic Syndrome Malignant cells produce enzymes, hormones and other

substances.
Manifestation:
- Anemia
- Hypercalcemia
- Edema
- DIC
3. Anorexia Cachexia Syndrome
Manifestation:
- Tissue wasting
- Severe weight loss
- Severe Debilitation
!
Paradigm (Carcinogenesis and cellular aberration)
THERAPEUTIC MODALITIES FOR CANCER

A. SURGERY
- used to diagnose, stage and treat cancer
Approaches:
a.
Local excision warranted if the mass is small

- removal of the mass and a small margin of normal tissue that is easily accessible
b . Wide or Radical excision (en bloc dissection) removal of primary tumors,
lymph nodes, adjacent involved structures, and surrounding tissues that may be at high risk for tumor spread.
- considered if the tumor can be removed completely and the chances of cure or control are good.
!
!
!
!
!
!
TYPES:
Salvage Surgery uses an extensive surgical approach to treat the local recurrence of the cancer after a less
extensive primary approach is used. E.g. mastectomy to treat recurrent breast Ca after primary lumpectomy and
radiation
Electrosurgery makes use of electrical current to destroy the tumor cells
Cryosurgery uses liquid nitrogen to freeze tissue to cause cell destruction
Chemosurgery uses combined topical chemotherapy and layer-by-layer surgical removal of abnormal tissue
Laser surgery makes use of light and energy aimed at an exact tissue location and depth to vaporize cancer cells
Stereotactic Radiosurcegy (SRS) single and highly precise administration of high dose radiation therapy used in
some types of brain and head and neck cancers.
a.
Prophylactic Sx performed in clients with an existing premalignant condition or a known family history that
strongly predisposes the person to the development of cancer
- an attempt is made to remove the tissue or organ at risk and thus prevent the development of cancer
b. Curative Sx all gross and microscopic tumor is removed or destroyed
c. Control (Cytoreductive) Sx a debulking procedure that consist of removing part of the tumor
- Sx decreases the number of cancer cells and increases the chance that other therapies will be successful
d. Palliative Sx performed to improve quality of life during the survival time.
- to reduce pain, relieve airway obstruction, relieve obstructions in
the GI or Urinary tract, relieve pressure on the brain or spinal cord, prevent hemorrhage, remove infected or ulcerated
tumors, or drain abscesses.
e. Reconstructive / Rehabilitative Sx performed to improve quality of life by restoring maximal function and
appearance suh as breast reconstruction after Mastectomy
Side Effects:

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1.
2.
3.
4.
Loss or loss of function of a specific body part

Reduced function as a result or organ loss
Scarring or disfigurement
Grieving about altered body image or imposed change in lifestyle
Nursing Management:
!
!
!
!
!
!
general perioperative nursing care

Education and emotional support
o Assessing Pt. and Family needs, fears, coping mechanisms
o Encourage to take an active role in decision making when possible
o Explain laboratory findings based on information the physician previously conveyed to them when the Pt.
and the family asks.
Asses Pts response to the Sx
Monitor for possible complications ( Infection, bleeding, thrombophlebitis, wound dehiscence, F & E imbalance,
and organ dysfunction )
Provide comfort
Provide post-op teaching (wound care, activity, nutrition, medication information)
BONE MARROW TRANSPLANTATION

to treat leukemia in clients who have closely matched donors and who are experiencing temporary remission
with chemotherapy
TYPES:
a. Allogenic Marrow donor is sually a sibling or parent with a similar tissue type
b. Syngeneic from an identical twin
c. Autologous most common type
- marrow donor is also the recipient
- marrow is harvested during disease remission and is stored frozen to be infused later
PROCEDURE:
1. Harvest
2. Conditioning
3. Transplantation
4. Engraftment
COMPLICATIONS:
1. Failure to engraft
2. Graft-versus-Host disease
3. Venoocclusive disease
B. RADIATION THERAPY
-
Side Effects:
!
!
!
!
destroys cancer cells with minimal exposure of normal cells to the damaging effects of radiation. The
cells damaged die or become unable to divide
effective on tissues directly within the path of the radiation beam.
Skin changes and irritation

Alopecia
Fatigue
Altered taste sensation
Types:
a. External ( Teletherapy) also called beam radiation; radiation source is external to

client.

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client does not emit radiation and does not pose a hazard to anyone else
wash area with mild soap and water using hand rather than washcloth
rinse thoroughly and pat dry
do not remove radiation markings from the skin
no powders, ointments, lotions or creams on the areas unless prescribed
avoid sun and heat exposure
monitor for moist desquamation (weeping of the skin)
if moist desquamation occurs, cleanse the area with warm water ad pat dry, apply antibiotic ointment
as prescribed.
Client education:
b. Internal (Brachytherapy) radiation source comes in direct, continuous contact with tumor tissues for a specific time
- radiation source is within the client, for a period of time, client emits radiation and can pose hazard to
everybody
- Sealed vs. Unsealed source
- Unsealed -via ORAL, IV or instillation to body cavities
- eliminated in various excreta which are radioactive and harmful to others
- Sealed
- solid, temporary or permanent, is implanted within the
tumor target tissues
- client emits radiation while the implant is in place, but the excreta are not radioactive
Care of the client with a sealed radiation Source:

-
Private room with a private bath

Caution sign on the door
Minimize exposure to the radiation source
Limit time to 30 mins per care provider per shift
Wear docimeter badge
Principles of Timing Distance and Shielding
Limit Visitors
C. CHEMOTHERAPY
Chemotherapy,
Chemotherapy in its most general sense, refers to treatment of disease by chemicals that kill cells, specifically those of
micro-organisms or cancer. In popular usage, it will usually refer to antineoplastic drugs used to treat cancer or the
combination of these drugs into a standardized treatment regimen.
In its non-oncological use, the term may also refer to antibiotics (antibacterial chemotherapy). In that sense, the first
modern chemotherapeutic agent was Paul Ehrlich's arsphenamine, an arsenic compound discovered in 1909 and used to
treat syphilis. This was later followed by sulfonamides discovered by Domagk and penicillin discovered by Alexander
Fleming.
Other uses of cytostatic chemotherapy agents (including the ones mentioned below) are the treatment of autoimmune
diseases such as multiple sclerosis and rheumatoid arthritis and the suppression of transplant rejections
Objectives:
-
To destroy all malignant tumor cells without excessive destruction of normal cells
To control tumor growth if cure is no longer possible
Used as adjuvant therapy
Contraindications:
Infection. The anti-tumor drugs are immunosuppresives
Recent surgery. The drugs may retard healing process
Impaired renal / hepat
hepatic
ic function. The drugs are nephrotoxic & hepatotoxic
Recent Radiation Therapy. Also immunisuppresive
Pregnancy. The drugs may cause congenital defects

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Bone Marrow Depression. The drugs may aggravate the condition. The WBC level must be within normal
limits.
AntiNeoplastic Medications
- Kills or inhibit the reproduction of neoplastic cells
- Normal cells are also affected
- Cell cycle phase specific medications
o Affects cells only during a certain phase of the reproductive cycle
- Cell cycle phase nonnon-specific medications
medications
o Affects cells in any phase of the reproductive cycle
- Can use combination medications or with other treatment modalities
Side Effects:
1. G.I. System Nausea & Vomiting, Diarrhea, constipation, anorexia
2. Integumentary System
a. Pruritus, urticaria & systemic signs
b. Stomatitis
c. Alopecia
d. Skin pigmentation
e. Nail changes
3. Hematopoetic system
a. Anemia
b. Neutropenia
c. Thrombocytopenia
4. Genito Urinary system
a. Hemorrhagic cystitis
b. Urine color changes
5. Others
a. Pain
b. Malnutrition
c. Memory loss
d. Weight loss or gain
e. Hemorrhage
f. Secondary neoplasms
g. Cardiotoxicity
h. Hepatotoxicity
i. Nephrotoxicity
j. Ototoxicity
k. tumor lysis syndrome
l. post-chemotherapy cognitive impairment("chemo brain")
m. Infertility
Interventions:
-
Monitor V/S and lab values

Bleeding precaution
Neutropenic precaution
Nutrition (High calorie with protein supplements)
Antiemetics (12-48 hours before)
Hydration
Administer Allopurinol for increased Uric Acid
Health care provider safety
Advise purchase of wig
Hair growth occurs several months after the final treatment
Contraception = teratogenic effects of meds

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Classifications
Classification
I. ALKYLATING MEDS
Cell cycle
nonspecific
II.ANTI-TUMOR
ANTIBIOTICS
Cell cycle
nonspecific
III. ANTIMETABOLITES
IV. MITOTIC INHIBITORS

(Vinca Alkalopids)
V. HORMONAL MEDS /
ENZYMES
VI. OTHERS
Side effects
Gonadal
Suppression,
Hemorrhagic
cystitis,
Alopecia,
Hematuria
Examples
Nitrogen Mustards Cyclophosphamide (Cytoxan)
Ifosfamide(Ifex)
Nitrosoureas
Streptozocin(Zanosar)
Carmustine(BiCNU)
Alkylating-like
Cisplatine(Platinol)
Thiotepa
(Thioplex)
Bleomycin
Sulfate(Blenoxane)
Daunorubicin
(Cerubidine)
Doxorubicin(Adriamycin)
Plicamycin(Mithracin) Dactinomycin(Actinomycin
D)
Bone
Marrow
depression,
Gonadal
Suppression,
Vesication
Cell cycle Bone
marrow 5-Fluouracil (Adrucil)
6specific (S suppression,
Mercapturine(Purinethol) Methotrexate (Folex)
Phase)
stomatitis,
photosensitivity,
hepatotoxicity
Cell cycle Neurotoxicity,
Vincristine Sulfate(Oncovin) Teniposide(Vamon)
specific (M Leukopenia, Ptosis,
Phase)
Constipation,
Peripheral
Neuropathy
Slows
Leukopenia,
ESTROGEN:Diethylstilbestrol ANTI-ESTROGEN:
growth
gynecomastia, hot Tamoxifen citrate ANDROGENS:Testosterone
rate
of flashes,
sex ANTI-ANDROGENS:Flutamide
tumors
characteristic
PROGESTINS:Medroxyprogesterone(Depoalterations
provera) OTHERS: Asparginase,Mitotane
Immunomodulator agents = Interleukins / Interferon
Colony-stimulating factors = Erythropoietin (Epogen)
CANCER TYPES
BREAST CANCER
Invasive when it penetrates the tissue surrounding the mammary duct &
grows in an irregular patter
Metastasis
via lymph nodes to Bones, lungs, brain and liver
Precipitating factors:
1. family History
2. Early menarche / late menopause
3. Previous Ca of Breast, Uterus or ovaries
4. Nulliparity
5. Obesity

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6. High dose exposure of radiation to chest

Assessment:
BSE
- Mass felt ( Upper outer quadrant / beneath the nipples )
- Fixed, irregular, non-encapsulated
- Painless (except in late stages)
- Nipple retraction / elevation
- Assymetry (affected breast higher)
- Discharges (bloody / clear)
- Edema / paeu dorange sin
- Lymphedema/lymphadenopathy
- Lesion seen on mammography
Diagnosis:
1. Breast biopsy (needle aspiration)
2. Surgical removal of tumor (for microscopic examination)
Intervention:
NON-SURGICAL
SURGICAL
-Chemotherapy
-Lumpectomy
- Radiation Therapy
-Simple mastectomy
-Hormonal manipulation
-MRM
-Halstead radical Mastectomy
-Oophorectomy (for estrogen receptor (+)tumor)
-Ablative therapy w/ adrenalectomy or chemical
ablation (blocks the production of cortisol / androstenedione / aldosterone)
Post-op:
1.
2.
3.
4.
5.
6.
Monitor v/s
positioning - (Semifowlers ,Back to unaffected side, affected arm elevated above the level of the heart)
Deep breathing and coughing exercise
Monitor operative site for infection/swelling/drainage
No IV, Injection, BP taking, venipuctures in affected arm
diuretics & low salt diet
CERVICAL CANCER
- Pre invasive Ca (Cervical intraepithelial neoplasia)
o I Mild dysplasia
o II Moderate dysplasia
o III severe dysplasia to carcinoma in situ
-
Metastasis confined to the pelvis but may have lymphatic spread
Precipitating factors:
- low social economic groups
- early first marriage
- early & frequent intercourse
- multiple sex partners
- high parity
- poor hygiene
Assessment:
-
Painless vaginal bleeding postmenstrually & post coitally

Foul smelling / serosanguinous vaginal discharge
Pelvic / lower back/leg/groin pain
Anorexia & wt. loss

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Diagnosis:
-
Leakage of urine & feces from the vagina

Dysuria
Hematuria
(cytological changes) on Pap Smear
Management:
NON-SURGICAL
SURGICAL
-Chemotherapy
- Conization
- Hysterectomy
- External radiation
- Pelvic exenteration
- Internal radiation implants (intracavitary)
- laser therapy
- cryosurgery
OVARIAN CANCER
- Grows rapidly / spreads fast / often bilateral
- Prognosis usually is poor (tumor detected late)
Assessment:
-
Abdominal discomfort / swelling

GI disturbances
Dysfunctional vaginal bleeding
Abdominal mass
Diagnosis:
-
Exploratory Laparotomy (to diagnose & to stage tumor)
Intervention:
1. External Radiation
2. Chemotherapy (Post-op / for all stages)
3. Intraperitoneal Chemotherapy (abdominal Cavity)
4. Immunotherapy
5. TAHBSO
HODGKINS DISEASE
- (Lymphoma) malignancy of the lymph nodes
- Metastasis to other lymph nodes and eventually nonlymphoid tissues
- Usually affects lymph nodes, spleen and bone marrow
- Distinguishing sign : ReedReed-sternberg cell
Etiology:
- viral infection
- previous exposure to alkylating chemical agents
Assessment:
-
Fever
Malaise, fatigue, weakness
Night sweats
Loss of appetite and significant wt. loss
Enlarged lymph nodes, spleen & liver
Anemia & thrombocytopenia
STAGING in HODGKINs DISEASE

I involvement of a single lymph node region or in extra lymphatic organ / site
II two or more lymph node regions on the same side of diapraghm or localized
involvement of an extralymphatic organ / site

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III lymph node regions on both side of the diapraghm

IV diffuse or disseminated involvement of one or more extralymphatic organs
w/ or w/o associated lymph node involvement
Diagnosis:
- Biopsy (cervical nodes affected first) (+) and with REED-STERNBERG CELL
- CT SCAN (Liver & spleen)
Intervention;
1. for stage I & II extensive external radiation of the involved lymph node regions
2. radiation with multi-agent chemotherapy
3. Maintain infection & bleeding precaution
4. Inform male clients about possibility of sterility (discuss options like sperm banking)
MULTIPLE MYELOMA
- malignant proliferation of plasma cells and tumors within the bone
- plasma cells % tumors % destroys bones
- abnormal plasma cells produce abnormal antibody (myeloma protein or the BenceBence-Jones protein) found in
blood and urine.
- Causes decrease production of (immunoglobulins & antibodies)
- Causes increase levels of (Uric acid & calcium) leading to RENAL FAILURE
Etiology:
- unknown
Assessment:
1.
2.
3.
4.
5.
6.
7.
Skeletal pain (pelvis, spine, ribs)

weakness & fatigue
Recurrent infections
Anemia
Osteoporosis
Renal failure
Spinal cord compression & paraplegia
Diagnosis:
-
Blood tests (elevated serum protein, thrombocytopenia, granulocytopenia, elevated uric acid & calcium levels)
Urine exams (presence of Bence-Jones protein)
Intervention:
1. Chemotherapy
2. Supportive care (to control symptoms & prevent complications)
3. Maintain Neutropenic & Bleeding precautions
4. Fluids 3-4 L/day
5. Monitor for signs of Renal Failure
6. Encourage ambulation
7. IV Fluids & diuretics, blood transfusion, analgesics, antibiotics as prescribed
LEUKEMIA
- Leukemia or leukaemia (Greek leukos , "white"; aima , "blood") is a cancer of the blood or bone marrow
and is characterized by an abnormal proliferation (production by multiplication) of blood cells, usually white blood cells
(leukocytes). Leukemia is clinically and pathologically subdivided into several large groups. The first division is between its
acute and chronic forms:
Acute leukemia is characterized by the rapid increase of immature blood cells. This crowding makes the bone
marrow unable to produce healthy blood cells. Acute forms of leukemia can occur in children and young adults. (In

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fact, it is a more common cause of death for children in the US than any other type of malignant disease).
Immediate treatment is required in acute leukemias due to the rapid progression and accumulation of the malignant
cells, which then spill over into the bloodstream and spread to other organs of the body. Central nervous system
(CNS) involvement is uncommon, although the disease can occasionally cause cranial nerve palsies.
Chronic leukemia is distinguished by the excessive build up of relatively mature, but still abnormal, blood cells.
Typically taking months or years to progress, the cells are produced at a much higher rate than normal cells,
resulting in many abnormal white blood cells in the blood. Chronic leukemia mostly occurs in older people, but
can theoretically occur in any age group. Whereas acute leukemia must be treated immediately, chronic forms are
sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy.
Four major kinds of leukemia

Cell type
Acute
Lymphocytic
(or "lymphoblastic")
leukemia Acute lymphocytic leukemia (ALL)

Onset: <15y.o.
Chronic
Chronic lymphocytic leukemia (CLL)

Onset: >50y.o
Chronic myelogenous leukemia (CML)
Myelogenous
leukemia Acute myelogenous leukemia (AML)
Onset:>50 y.o.
(also "myeloid" or "nonlymphocytic") Onset: 15-39 y.o.
(mostly granulocytes)
Cause:
- Unknown
- Gene damage of cells(suspect)
Risk Factors:
- Genetic
- Viral
- Environmental
- Immunological
- Exposure to Radiation, Chemicals, Medications
Signs / Symptoms:
-
people with leukemia may become bruised, bleed excessively, or develop pinprick bleeds (petechiae).
Immunosuppression
anemia
dyspnea.
Fever, chills, night sweats and other flu-like symptom

Weakness and fatigue
Swollen or bleeding gums
Neurological symptoms (headaches)
Enlarged liver and spleen
Frequent infection
Bone pain
Joint pain
Dizziness
Nausea
Swollen tonsils
Diarrhea
Paleness
Malaise
Unintentional weight loss
Diagnosis

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Diagnosis requires blood tests to look for an abnormal number of white blood cells, and a bone marrow examination
to look for abnormal numbers or forms of cells in the bone marrow.
Management:
- Induction chemotherapy to bring about bone marrow remission.
- Consolidation therapy to eliminate any remaining leukemia cells.
- CNS prophylaxis (preventive therapy) to stop the cancer from spreading to the brain and nervous system.
- Maintenance treatments with chemotherapeutic drugs to prevent disease recurrence once remission has been
achieved.
- Alternatively, allogeneic bone marrow transplantation may be appropriate for high-risk or relapsed
patients.
- Single agent chemotherapy
- Combination Chemotherapy
- Protective isolation
- Bleeding precaution
- Monitor v/s & lab values
- Nutrition
- Radiation Therapy
LIVER CANCER
- Associated with Chronic liver disease / Hepa-B/ Hepa-C / Cirrhosis
Risk Factors:
- Cigarette Smoking
- Alcohol Use
Metastasis:
- Portal Circulation
- Lymphatic changes
- Direct extension
Signs / Symptoms:
- Pain (RUQ/ Epigastrium/ Bask)
- Wt. Loss / Anorexia
- Loss of strength
- Anemia
- Enlarged liver
- Ascites
- Jaundice
Diagnosis:
- Lab Exams
- Increased serum levels of Alpha FetoProtein (AFP)
- X-rays
- Liver scans
- CT Scan
- UTZ
- MRI
- Arteriography
- Laparoscopy
- PET Scans
- BIOPSY
Management:
NON-SURGICAL:
SURGICAL:
- Radiation Therapy
- Hepatic Resection
- Chemotherapy
- Lobectomy
- Immunotherapy
- Cryosurgery
- Percutaneous Billiary Drainage
- Liver Transplantation

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Laser Hyperthermia
LUNG CANCER
- Can be Primary or Metastatic
- Bronchogenic Carcinoma spreads thru direct extension & lymphatic dissemination
4 major types:
1. Small Cell (Oat cell)
2. Epidermal (Squamous cell)
3. Adenocarcinoma
4. Large cell anaplstic carcinoma
Diagnosis:
- CXR
- Bronchoscopy
- Sputum Studies
Causes:
- Cigarette smoking
- Exposure to Environmental pollutants
- Exposure to Occupational pollutants
Signs / Symptoms:
- Cough
- Dyspnea
- Hoarseness
- Hemoptysis
- Chest pain
- Anorexia / Wt. loss
- Weakness
Interventions:
- Monitor v/s
- Position : High Fowlers position
- Assess for tracheal deviation
- Oxygen with humidifier
- Pulse oximeter
- Meds: Analgesics, Bronchodilators, corticosteroids
- Nutrition: High calorie, protein, vitamins
NON-SURGICAL
SURGICAL
- Radiation therapy
- Laser Therapy
- Chemotherapy
- Thoracentesis / Pleurodesis
- Immunotherapy
- Thoracotomy with pneumonectomy
o Thoracotomy with lobectomy
o Thoracotomy with segmental resection
PROSTATE CANCER
- SLOW GROWING
- Usually androgen dependent type of adenocarcinoma
- Risk = increases in men each decade after 50 y/o
- Metastasis= direct invasion, bloodstream & lymphatics, to bone (a concern)
Diagnosis:
- DRE
- PSAT
- Confirmed if with increased in Serum acid phosphatase
Signs/Symptoms:
- Early stage = asymptomatic
- Hard, peas sized nodule
- Hematuria
- Urinary obstruction

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Pain (Radiating from lumbosacral area down the leg)
Intervention:
NON-SURGICAL
SURGICAL
- Hormone manipulation therapy
- orchiectomy(palliative)
- Radiation Therapy
= decreased testosterone
- Chemotherapy (Hormone resistant tumors) - TURP
o Prostatectomy
o Cryosurgical Ablation
BRAIN TUMOR
- LOCALIZED / INTRACRANIAL LESION
- Effects are due to compression & infiltration of tissues
- Primary vs. secondary
o Primary = Originated from cells & structures within the brain
o Secondary = Metastatic / develops from structures outside the brain
Cause:
- Unknown
Risk Factor:
- Exposure to ionizing radiation
- Greater in men than in women
Signs / Sypmtoms:
1. Increased ICP / Cerebral Edema
2. Seizure activity / focal neurologic signs
3. Hydrocephalus
4. Altered pituitary function
Classification:
I.
INTRACEREBRAL TUMORS
a. GLIOMAS infiltrate any portion of the brain; most common type of brain tumors
i. ASTROCYTOMAS
ii. GLIOBLASTOMA MULTIFORME
iii. OLIGODENDROCYTOMA
iv. EPENDYMOMA
v. MEDULLOBLASTOMA
II.
ARISING FROM SUPPORTING STRUCTURES
a. Meningiomas
b. Neuromas
c. Pituitary Adenomas
III.
DEVELOPMENTAL TUMORS
a. Angiomas
b. Dermoid, Epidermoid, Teroma, craniopharyngioma
IV.
METASTATIC LESIONS
Diagnosis:
- CT SCAN
- MRI
- PET scan
- EEG
- Cytologic Studies
Management:
NON-SURGICAL
- Chemotherapy
- Radiation therapy
SURGICAL
- craniotomy
- Laser / Radiotion (Iodine 131)

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- Gamma Knife
Brachytherapy
Corticosteroids
Photodynamic therapy33699
MUSCULOSKELETAL SYSTEM
The musculo-skeletal system consists of the muscles, tendons, bones and cartilage together with the joints
The primary function of which is to produce skeletal movements
Three types of muscles exist in the body
1. Skeletal Muscles
Voluntary and striated
2. Cardiac muscles
Involuntary and striated
3. Smooth/Visceral muscles
Involuntary and NON-striated
Tendons: Bands of fibrous connective tissue that tie bones to muscles
Ligaments: Strong, dense and flexible bands of fibrous tissue connecting bones to another bone
Bones: Variously classified according to shape, location and size
Functions
1. Locomotion
2. Protection
3. Support and lever
4. Blood production
5. Mineral deposition
Joints: The part of the Skeleton where two or more bones are connected
Cartilages: A dense connective tissue that consists of fibers embedded in a strong gel-like substance
Bursae: Sac containing fluid that are located around the joints to prevent friction
1. BONE MARROW ASPIRATION
Usually involves aspiration of the marrow to diagnose diseases like leukemia, aplastic anemia
Usual site is the sternum and iliac crest

Pre-test: Consent
Intratest: Needle puncture may be painful
Post-test: maintain pressure dressing and watch out for bleeding
2. Arthroscopy
A direct visualization of the joint cavity
Pre-test: consent, explanation of procedure, NPO
Intra-test: Sedative, Anesthesia, incision will be made
Post-test: maintain dressing, ambulation as soon as awake, mild soreness of joint for 2 days, joint rest for a few days, ice
application to relieve discomfort
BONE SCAN
Imaging study with the use of a contrast radioactive material
Pre-test: Painless procedure, IV radioisotope is used, no special preparation, pregnancy is contraindicated

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Intra-test: IV injection, Waiting period of 2 hours before X-ray, Fluids allowed, Supine position for scanning
Post-test: Increase fluid intake to flush out radioactive material
DXA- Dual-energy XRAY absorptiometry
Assesses bone density to diagnose osteoporosis
Uses LOW dose radiation to measure bone density. Painless procedure, non-invasive, no special preparation. Advise to
remove jewelry
PAIN
These can be related to joint inflammation, traction, surgical intervention
1. Assess patients perception of pain
2. Instruct patient alternative pain management like meditation, heat and cold application, TENS and guided imagery
3. Administer analgesics as prescribed
Usually NSAIDS
Meperidine can be given for severe pain
4. Assess the effectiveness of pain measures
IMPAIRED PHYSICAL MOBILITY
1. Instruct patient to perform range of motion exercises, either passive or active
2. Provide support in ambulation with assistive devices
3. Turn and change position every 2 hours
4. Encourage mobility for a short period and provide positive reinforcements for small accomplishments
SELF-CARE DEFICITS
1. Assess functional levels of the patient
2. Provide support for feeding problems
Place patient in Fowlers position
Provide assistive device and supervise mealtime
Offer finger foods that can be handled by patient
Keep suction equipment ready
3. Assist patient with difficulty bathing and hygiene
Assist with bath only when patient has difficulty
Provide ample time for patient to finish activity
Traction
A method of fracture immobilization by applying equipments to align bone fragments
Used for immobilization, bone alignment and relief of muscle spasm
Skin traction- Buck, Bryant
Skeletal traction
Balanced Suspension traction
Running/Straight traction
Pulling force exerted on bones to reduce or immobilize fractures, reduce muscle spasm, correct or prevent deformities
TO decrease muscle spasms
TO reduce, align and immobilize fractures
To correct deformities
Traction: General principles
1. ALWAYS ensure that the weights hang freely and do not touch the floor
2. NEVER remove the weights
3. Maintain proper body alignment
4. Ensure that the pulleys and ropes are properly functioning and fastened by tying square knot
Traction: General principles
5. Observe and prevent foot drop
Provide foot plate

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6. Observe for DVT, skin irritation and breakdown

7. Provide pin care for clients in skeletal traction- use of hydrogen peroxide
8. Promote skin integrity
Use special mattress if possible
Provide frequent skin care
Assess pin entrance and cleanse the pin with hydrogen peroxide solution
Turn and reposition within the limits of traction
Use the trapeze
CAST
Immobilizing tool made of plaster of Paris or fiberglass
Provides immobilization of the fracture
1.
CAST: types
Long arm, Short arm, Short leg, Long leg, Spica , Body cast
Plaster of Paris
Drying takes 1-3 days
If dry, it is SHINY, WHITE, hard and resistant
Fiberglass
Lightweight and dries in 20-30 minutes
Water resistant
Cast Application:
1. TO immobilize a body part in a specific position
2. TO exert uniform compression to the tissue
3. TO provide early mobilization of UNAFFECTED body part
4. TO correct deformities
5. TO stabilize and support unstable joints
CAST: General Nursing Care
1. Allow the cast to air dry (usually 24-72 hours)
2. Handle a wet cast with the PALMS not the fingertips
3. Keep the casted extremity ELEVATED using a pillow
4. Turn the extremity for equal drying. DO NOT USE DRYER for plaster cast
Encourage mobility and range of motion exercises
5. Petal the edges of the cast to prevent crumbling of the edges
6. Examine the skin for pressure areas and Regularly check the pulses and skin
7. Instruct the patient not to place sticks or small objects inside the cast
8. Monitor for the following: pain, swelling, discoloration, coolness, tingling or lack of sensation and diminished pulses
CAST: General Nursing Care
Hot spots occurring along the cast may indicate infection under the cast
Osteoporosis
A disease of the bone characterized by a decrease in the bone mass and density with a change in bone structure
Normal homeostatic bone turnover is altered rate of bone RESORPTION is greater than bone FORMATION reduction in
total bone mass reduction in bone mineral density prone to FRACTURE
Osteoporosis: TYPES
1. Primary Osteoporosis- advanced age, post-menopausal
2. Secondary osteoporosis- Steroid overuse, Renal failure
RISK factors for the development of Osteoporosis
2. Age
3. Diet- caffeine, alcohol, low Ca and Vit D

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4. Post-menopausal
5. Genetics- caucasian and asian
6. Immobility
ASSESSMENT FINDINGS
1. Low stature
2. Fracture Femur
3. Bone pain
LABORATORY FINDINGS
1. DEXA-scan
Provides information about bone mineral density
T-score is at least 2.5 SD below the young adult mean value
2. X-ray studies
Medical management of Osteoporosis
1. Diet therapy with calcium and Vitamin D
2. Hormone replacement therapy
3. Biphosphonates- Alendronate, risedronate produce increased bone mass by inhibiting the OSTEOCLAST
4. Moderate weight bearing exercises
5. Management of fractures
Osteoporosis Nursing Interventions
1. Promote understanding of osteoporosis and the treatment regimen
Provide adequate dietary supplement of calcium and vitamin D
Instruct to employ a regular program of moderate exercises and physical activity
Manage the constipating side-effect of calcium supplements
Take calcium supplements with meals
Take alendronate with an EMPTY stomach with water
Instruct on intake of Hormonal replacement
2. Relieve the pain: Instruct the patient to rest on a firm mattress. Suggest that knee flexion will cause relaxation of back
muscles. Heat application may provide comfort. Encourage good posture and body mechanics .Instruct to avoid twisting
and heavy lifting
3. Improve bowel elimination. Constipation is a problem of calcium supplements and immobility. Advise intake of HIGH
fiber diet and increased fluids
4. Prevent injury. Instruct to use isometric exercise to strengthen the trunk muscles. AVOID sudden jarring, bending and
strenuous lifting. Provide a safe environment
Juvenile Rheumatoid Arthritis: Definition: AUTO-IMMUNE inflammatory joint disorder of UNKNOWN cause. SYSTEMIC
chronic disorder of connective tissue
Diagnosed BEFORE age 16 years old PATHOPHYSIOLOGY : unknown Affected by stress, climate and genetics. Common in
girls 2-5 and 9-12 y.o.
Systemic JRA: fever, salmon pink rash, five or more joints, anorexia, anemia, and fatigue.
Pauci-articular: Mild joint pain and swelling, iridocyclyitis, less than 4 joints, very good prognosis
POlyarthritis: Moming joint and stiffness and fever. Weight bearing joints, five or more joints, poor prognosis
JRA: Symptoms may decrease as child enters adulthood. With periods of remissions and exacerbation.
Medical Management: Aspirin and NSAIDS - mainstay treatment; slow acting anti rheumatic drugs, corticosteroids
Nsg Management: Encourage normal performance of ADL; Assist child in ROM exercises; Administer Medications;
encourage social and emotional development.
Nsg Management: during acute attact: splint the joints. Neutral positioning, Warm or cold packs.
Osteoarthritis: the most common form of degenerative joint disorder

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Osteoarthritis: Patho: Injury, genetic, obesity, advanced age--> stimulate the chondrocytes to release chemicals-> chemicals
will cause cartilage degeneration reactive inflammation of the synovial lining and bone stiffening
Risk factors: Increased age, obesity, repetitive use of joints with previous joint damage, anatomical deformity, genetic
susceptibility
Assessment Findings: joint pain, joint stiffness, functional joint impairment limitation. The joint involvement is assymetrical.
This is not systemic, there is no fever, no severe swelling. Atrophy of unused muscles. Usual joint are the weight bearing
joints.
Joint Pain: caused by inflamed cartilage and synovium, stretching of the joint capsule. irritation of nerve endings.
Stiffness. Commonly occurs in the morning after awakening. Lasts only for less than 30 minutes. Decreases with movement,
but worsens after increased weight bearing activity. Crepitation may be elicited.
Dx Findings: 1. X-ray: narrowing of the joint space, loss of cartilage, osteophytes. 2. Blood tests will show no evidence of
systemic inflammation and are not useful.
Medical Management: 1. Weight reduction. 2. Use of splinting devices to support joints. 3. Occupational and physical
therapy. 4. Pharmacologic management: use of paracetamol, nsaids, use of glucosamine and chondroitin; topical analgesics,
intra-articular to decrease inflammation
Nsg Intervention: 1. Provide relief of Pain: Administer prescribed analgesics; Application of heat modalities. ICE packs may
be used in the early acute stage. Plan daily activitites when pain is less severe. Pain meds before exercising. 2. Advise pt to
reduce weight: aerobic exercise and walking. 3. Administer prescribed meds: NSAIDS. 4. Position the client to prevent
flexion deformity: Use of foot board, splints, wedges, and pillows.
Rheumatoid Arthritis: A type of chronic systemic inflammatory arthritis and connective tissue disorder affecting more
women ages 35-45 than men.
Factors: Genetics: autoimmune connective tissue disorders. Fatigue, emotional stress, cold, infection.
Patho: Immune reaction in the synovium-- attracts neutrophils -- releases enzymes -- breakdown of collagen -- irritates the
synovial lining -- causing synovial inflammation edema and pannus formation and joint erosions and swelling.
Assessment: Pain; Joint Swelling and stiffness: symmetrical, bilateral; Warthm, erythema and lack of function; Fever, weight
loss, anemia, fatigue; Palpation of joint reveals spongy tissues; hesitancy in joint movement.
Assessment Findings: Joint involvement is symmetrical and bilateral: characteristically beginning in the hands, wrists, and
feet. Joint stiffness occurs early morning last more than 30 minutes, not relieved by movement, dimishes as the day
progresses. Joints are swollen and warm. Painful when moved. Deformities are common in the hands and feet causing
misalignment. Rheumatoid nodules may be found in the subcutaneous tissues.
Dx test: 1. xray shows bony erosion. Blood studies reveal positive rheumatoid factor, elevated ESR and CRP and anti
nuclear antibody. Arthrocentesis shows synovial joint that is cloudy, milky, or dark yellow containing numerous WBC and
inflammatory proteins.
Medical ManagementL: Therapeutic dose of NSAIDS and Aspirin to reduce inflammation. Chemotherapy with
methotrexate, antimalarials, gold therapy, and steroids. For advanced cases - arthroplasty, synovectomy. Nutritional
therapy.
Gold therapy: IM or Oral preparation. takes severals months 3-6 months before effects can be seen. Can damage the
kidney and causes bone marrow depression.
Nsg Management:
1.
Relieve pain and discomfort: use splints to immobilize the affected extremity during acute stage of the disease and
inflammation to reduce deformity. Administer prescribed medications. Suggest application of Cold packs during the
acute phase of pain, then Heat application as the inflammation subsides.
2. Decrease patient fatigue: schedule activity when pain is less severe, provide adequate periods of rests.
3. Promote restorative sleep.
4. Increase pt mobility: advise proper posture and body mechanics. support joint in function position. advise Active
ROM.

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5.
Provide Diet therapy: pts experiences anorexia, nausea and weight loss. Regular diet with caloric restrictions
because steroids may decrease appetite. Supplements of vitamins, iron, and proteins.
6. Increase Mobility and prevent deformity: lie flat on a firm mattress. Lie prone several times to prevent HIp flexion
contractures. Use on pillow under the head because of risk of dorsal kyphosis. No pillow under the joints because
this promotes flexion contractures.
Hot application: use to relieve joint stiffness, pain and muscle spasm. after acute attacks.
COld: use to control inflammation and pain. Acute attacks.
RA: onset is early, chronic systemic disease, involves the synovium, involved joints are symmetrical-fingers, cervical spine;
malaise, fever, anemia.
OA: onset is late. degenerative disease. involves the cartilages. involved joints are unilateral-weight bearing knee, hips,
spine. no other systemic s/sx
Gouty arthritis: A systemic disease caused by deposition of uric acid crystals in the joint and body tissues. Causes: 1. primary
gout: disorder of purine metabolis. 2. Secondary gout: excessive uric acid in the blood like leukemia.
Assessment" Fever low grade occasionaly. Pain on the knees, fingers, ankles, toes. Joints stiff and deformed, and tender to
touch. SKIN appears red, shiny, swollen and hot skin over affected joints. Tophi deposits - urate leaking (advanced) Other:
racing heart, chills, malaise, and tendon inflammation.
Assessment: 1. Severe pain in the involved joints initially the big toel. 2. Swelling and inflammation of the joint. 3. TOPHI yellowish-whitish irregular deposits in the skin that break open and reveal a gritty appearance. 4. PODAGRA- a big toe. 5.
Fever, malaise. 6. Body weakness and headache. 7. Renal stones.
Dx tests: Elevated levels of uric acid in the blood. Uric acid stones in the kidneys. Positive urate crystals in the synovial fluid.
Medical Management: 1. Allupurinol - take it with food. Rash signifies allergic reaction. 2. Colchicine: for acute attack. 3.
Probenecid: for uric acid excretion in the kidney.
Nsg Intervention. 1. Provide a diet with Low Purine: avoid organ meats, age and processed foods. Strict dietary restrictions
is not necessary. 2. Encourage an increased fluid intake (2-3L/day) to prevent stone formation. 3. Instruct the pt to avoid
alcohol. 4. Provide alkaline ash diet to increase urinary pH. 5. Provide bed rest during early attack of gout. 6. Position the
affected extremity in mild flexion. 7. Administer anti gouty meds and analgesics.
Fracture: a break in the continuity of the bone and is defined according to its type and extent.
Severe mechanical stress to bone - - bone fracture. Direct blows. crushing forces. sudden twisting motion. extreme muscle
contraction.
Types: 1. Complete: involves a break across the entire cross section. 2. Incomplete fracture: the break occurs through only a
part of the cross-section.
1. Comminuted: a fracture that involves production of several bone fragments. 2. Simple fracture: a fracture that involves
break of bone into two parts or one.
Assessment: Pain or tenderness over the involved area, loss of function, deformity, shortening, crepitus, swelling, and
discoloration.
PAIN: continuous and increases in severity. Muscle spasm accompanies the fracture is a reaction of the body to immobilize
the fractured bone. 2. Loss of function: abnormal movement and pain can result to this manifestation. 3. Deformity:
displacement, angulation or rotation of fragments causes deformity. 4. Crepitus: a grating sensation produced when the
bone fragments rub each other.
Emergency Management of Fracture: 1. Immobilize any suspected fracture. 2. Support the extremity above and below
when moving the affected part from a vehicle. 3. Suggested temporary splints: hard board, stick, rolled sheets. 4. Apply
sling if forearm fracture is suspected or the suspected fractured arm maybe bandaged to the chest. 5. Open fracture is
managed by covering a clean / sterile gauze to prevent contamination. 6. Do not attempt to reduce the fracture. \
Medical Management: 1. Reduction of fracture either open or closed, immobilization and Restoration of function. 2.
Antibiotics, muscle relaxants and pain medications.
For Closed Fracture: 1. Assist in reduction and immobilization. 2. Administer pain medication and muscle relaxants. 3.
Teach patient to care for the cast. 4. Teach pt about potential complication of fracture and to report infection, poor

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alignment and continuous pain.

For Open Fracture: 1. Prevent wound and bone infection. Administer prescribed antibiotics. Administer tetanus prophylaxis.
Assist in serial wound debridement. 2. Elevate the extremity to prevent edema formation. 3. Administer care of traction
and cast.
Early complication: shock, fat embolism, compartment syndrome, infection, dvt.
Late complication: 1. Delayed union, avascular necrosis, delayed reaction to fixation devices, complex regional syndrome.
Fat Embolism: occurs usually in fractures of the long bones. Fat globules may move into the blood stream because the
marrow pressure is greater than capillary pressure. Fat globules occlude the small blood vessels of the lungs, brain, kidneys,
and other organs. Onset is rapid, within 24-72 hours
Assessment findings: sudden dyspnea and respiratory distress, tachycardia, chest pain, crackles, wheezes and cough,
petechial rashes over the chest, axilla, and hard palate.
Nsg management: 1. Support the respiratoty function. Respiratory failure is the most common cause of death. Admister o2
in high concentration. Prepare for possible intubation and ventilator support. 2. Administer drugs: corticosteroids,
dopamine. and morphine. 3, Institue preventive measures: immediate immobilization of fracture, minimal fracture
manipulation. adequate support for fractured bone during turning and positioning. Maintain adequate hydration and
electrolyte balance.
Compartment Syndrome: A complication that develops when tissue perfusion in the muscles is less than required for tissue
variability.
Assessment: 1. Pain: deep, throbbing and unrelieved by pain by opoiod. Pain is due to reduction in the size of the muscle
compartment by tight cast. Pain is due to increased mass in the compartment by edema, swelliung or hemorrhage.
Medical and Nsg Management: 1. Assess frequently the neurovascular status of the casted extremity. 2. Elevate the
extremity above the level of the heart. 3. Assist in cast removal and fasciotomy.
Strains: excessive stretching of a muscles or tendon.
Nsg Management: immobilize the affected part. Apply cold packs initially then heat packs. Limit joint activity. administer
NSAIDS and muscle relaxants.
Sprains: excessive stretching of the ligaments
nsg management: immobilize extremity and advise rest. Apply cold packs initialy and heat packs. Compression bandage
may be applied to relieve edema. Assist in cast application. Administer NSAIDS.
Historical Background of Orthopedic Nursing
The word orthopedics was derived from the Greek words; orthos meaning straight or free of deformity and pais
meaning child.
Orthopedics also called orthopedic surgery medical specialty concerned with the preservation and restoration of
function of the skeletal system and its associated structures, i.e., spinal and other bones, joints, and muscles.
Nicolas Andry, a professor of medicine at the University of Paris published a textbook in Orthopedics in 1741
concerning the following;
1. Maintaining a straight child
2. Straightening a deformed child
3. Finding new ways to straighten deformed child
In 1728-1793, John Hunter contributed to the advancement of understanding fractures and other musculo-skeletal
injuries.
Orthopedics began in the 18th century with the pioneering efforts of Jean Andr Venet, who established an
institute in Switzerland for the treatment of crippled children's skeletal deformities.
In 1834-1891, Hugh Owen Thomas, an Englishman specialized in the treatment of chronic joint disease, fractures
and dislocations.

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In 1867-1948, Agnes Hunt, referred to as the Florence of Nightingale of Orthopedic Center in Great Britain.
The efforts of Sir Robert Jones and the massive casualties of World War I led to the founding of many orthopedic
training centers in the early 20th century.
In 1840, William Little established the Royal Orthopedic Infirmary in Great Britain.
In 1857, Anthonius Methyson of Holland described the plaster bandage.
In 1866, the New York Orthopedic Dispensary was formed.
A vastly increased knowledge of muscular functions and of the growth and development of bone was gained in the
19th century. Significant advances at this time were the new operation of tenotomy (the cutting of tendons, which made
correcting deformities easier), the surgical correction of clubfoot, the invention of the Thomas splint (which provided better
support for fractures of long bones in the limbs), and the introduction of quick-setting plaster of Paris for use in orthopedic
bandages.
Modern orthopedics has extended beyond the treatment of fractures, broken bones, strained muscles, torn
ligaments and tendons, and other traumatic injuries to deal with a wide range of acquired and congenital skeletal
deformities and with the effects of degenerative diseases such as osteoarthritis. A specialty that originally depended on the
use of heavy braces and splints, orthopedics now utilizes bone grafts and artificial plastic joints for the hip and other bones
damaged by disease, as well artificial limbs special footwear, and braces to return mobility to disabled patients. Orthopedics
uses the techniques of physical medicine and rehabilitation and occupational therapy in addition to those of traditional
medicine and surgery.
History of the Philippine Orthopedic Center
POC started in February 9, 1945 by PCAU General Hospital. The US Army established the hospital in
Mandaluyong, Rizal. It was then called as Mandaluyong Emergency Hospital. Its main purpose is to help take care of the
civilian casualties of war. But its function was not only as emergency basis seeing not only victims of wars but also all cases.
In May 1945, the hospital was turned over to the Phil. Government. In August 1945, the Bureau of Health took
over and only fracture cases and bone joint condition remained.
The hospital kept functioning during those difficult years and it is attributed to the skill, ingenuity, dedication and
foresight of the staff lead by Dr. Jose V. delos Santos.
The hospital finally transferred to its present site in Quezon City.
Review of Structure and Function of the MusculoMusculo-skeletal System
I The Bones
A. The human skeleton consist of two main division:
1. Axial body upright structure
a) Skull
b) vertebral column
2. Appendicular the body appendages
a) Arms
b) hips
c) ribs
c) legs
B. Four major bone type

1. Long bones - length exceeds breadth and thickness
2. Short bones - equal in main dimensions
3. Flat bones primary made up of cancellous bone tissue
4. Irregular bones
C. Long Bones:
1. Structure

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a) Diaphysis shaft provides strength resist bending

b) Metaphysis flared portion between diaphysis and epiphysis
c) Epiphysis end
- Primary cancellous bone
- Assist with bone development
d) Epiphyseal plate/line between metaphysis and epiphysis
- Cartilage growth in length of diaphysis and metaphysis
e) Periosteum connective tissue covering bone
- continues at the end of bone with joint capsule but does not cover articular cartilage
2. Blood supply
a) Nutrient artery tunnel in the diaphysis of long bone
b) Periosteal vessels supply compmact bones with nutrients
c) Metaphyseal and epiphyseal vessels supply the spongy bone and narrow of the epiphysis
D. Functions
1. Provides framework for the body
2. Serves as lever for skeletal muscles
3. Protects vital organs such as the brain, heart and lungs
4. Stores calcium and release it to the blood stream according to the body requirement
5. Manufactures new blood cells in the red bone marrow
II Cartilage
1) Fibrocartilage greatest tensile strength
- occurs in the intervertebral dics and in the symphysis pubis
2) Elastic cartilage possesses firmness and elasticity
- occurs in the external air and in the Eustachian tube
3) Hyaline cartilage cushions most of the joints to help soften any impact
- firm yet flexible
- occurs also in the part of the nasal system, larynx, trachea and in the bronchial ring
III Ligaments and Tendons
Ligaments strong cords of fibrous tissue
- joint capsule provides the primary connection between the bones, but ligament bind the joints more
firmly
Tendons firm cords of fibrous tissue that extend from the muscle to the periosteum
- connects muscle to each other to other tissue
IV Skeletal muscle
a.
b.
c.
Muscles can be long and tapered, short and blunt, triangular, quadrilateral or irregular.
Muscle fiber arrangement varies
1. In some muscles, the fiber runs parallel to the muscles long axis
2. In others, the fibers are oblique and bipennate like the feather of a quill pin
3. Fibers curve cut from a narrow attachment at the muscles and to form a triangle
Main functions
1. Prime mover directly brings about a desired motion
2. Antagonist muscles that directly opposes the movement under consideration
3. Fixation generally stabilizes a joint or its part thereby maintaining position while prime mover acts
V Joints
3 Basic Joint Types

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1.
Fibrous composed of fibrous tissue, tightly, connecting the articular surfaces of two bones
2 types
a) sutures permits no movement
b) syndesmosis permits minimal movement between bones
2. Cartilagenous joints connect two bones with cartilage, allowing only slight movement.
3. Synovial joints, the most common joint type, have the most complex structure and permit maximum mobility.
These joints include the following
a) joint capsule
b) synovial membrane
c)
articular cartilage
d) synovial cavity
FRACTURES
A. Fracture is a break in the continuity of the bone. In adults this break is usually complete in that the periosteum and the
cortical tissue on both sides are completely severed.
In pathology, a break in a bone, caused by stress. Certain normal and pathological conditions may predispose bones to
fracture. Children have relatively weak bones because of incomplete calcification, and older adults, especially women past
menopause, develop osteoporosis, a weakening of bone concomitant with aging. Pathological conditions involving the
skeleton, most commonly the spread of cancer to bones, may also cause weak bones. In such cases very minor stresses may
produce a fracture. Other factors, such as general health, nutrition, and heredity, also have effects on the liability of bones
to fracture and their ability to heal.
An incomplete break or greenstick fracture is mere common in children. Bone broken is bent but securely hinged at one
side.
A complete fracture occurs when periosteum and cortical tissue completely severed on both sides of bone.
B. Fracture bone fragments are labeled according to relationship to the cortex of the body.
1.
distal away from
2. proximal here to
C. Causes of fracture
1.
In normal bones, fracture occurs when more stress is placed upon a bone that is able to absorb such as:
a) Direct blow or crushing form
b) Twisting force (torsion a severe twisting of a broken bone at a side different from where the force was
actually applied.
c)
Powerful contractions highly developed muscles contract so violently that muscles tear from bone
sometimes pulling a small piece of bone with it.

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d) Fatigue and stress bone breaks after repeated stress

2. Bones weakened by a disease or tumors and subject to pathological fractures
Classification of fractures
Broad classification
1.
Open fracture
2. Closed fracture
Principles of Fracture Treatment
A. Reduction or realignment of bone fragments
B. Maintenance or realignment by immobilization
C. Restoration of function
A. Reduction
Reduction
1.
Closed reduction is accompanied by application of plaster cast after the fracture4 have been aligned with
or without the use of anesthesia, to include the joint above and below the fracture line.
2. Open reduction immobilization is done by nails, screws, pins, wires or rods which are inserted with or
without plates. Such devices stay in the patient indefinitely unless they produce symptoms after healing
takes place.
B. Immobilization
The most important phase in obtaining the union of fracture fragments.
a. Cast
b. Traction
c. Brace
d. Fixation devices
a. Internal fixation devices
b. External fixation devices
CARE OF PATIENT IN CAST
Plaster Cast is temporary immobilization device, which is made of gypsum sulfate, rendered anhydrous by calcification
when mixed with water swells and forms into hard cement.
FUNCTIONS
1.
2.
3.
4.
To immobilize
To prevent or correct deformity
To support, maintain and protect realigned bone
To promote healing and early weight bearing
* Cast can be applied to the extremities, to the trunk and to the extremity and trunk as in spicas.
It can be applied to encase the whole area where it should be applied or it can be applied as a splint or mold.
*Complications of cast
1. Neurovascular compromise
2. Incorrect fracture alignment
3. Cast syndrome, superior mesenteric artery
a. Occurs with body cast
b. Traction on superior mesenteric artery causes decrease in blood supply to bowel
c. Signs and symptoms, abdominal pain, nausea and vomiting

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4. Compartment syndrome is a condition in which increases pressure within limited space, compromises circulation and
function of the tissue within that space.
Principle in application of plaster cast
1.
A cast is applied with padding first

Padding materials include the following wadding sheet, roll cotton, stockinet felt.
It can be applied as a combination like stockinet and wadding sheet.
2. Apply it to the joint above and joint below the injured part.
3. Apply it in circular motion and mold it as you do the procedure by the palm.
4. Support it with the palm
Contraindications
Contraindications of plaster cast application
1. Pregnancy
2. Skin diseases
For Circular Cast Application
1. Check for doctors orders
2. Inform and prepare the patient for the procedure.
Explain to the patient and his relatives the need for placing the affected part of the body cast. Show an illustration
of the type of cast to be applied to help them visualize HOW IT IS and WHAT IT IS.
They are also made aware of the approximate duration for the body to
remain in cast, the limitation and the
discomfort arising from immobilization less boredom and frustrating.
If possible, a good cleaning bath and shampoo be given to the patient. The affected part be cleansed thoroughly
with soap and water or with detergent and dried. If there is a wound dress it accordingly.
3. Ready all things needed for the application.
4. Position the extremity (by the doctor)
5. Apply padding including the joints above and below the fracture line with thicker pads on the bony prominences
6. Soak the plaster cast into a bucket with water; leave it undisturbed until bubble ceases, one after the other.
7. Grasp both ends, when bubbles cease, towards the center without squeezing it.
8. Free the end of the cast and hand it to operator.
9. Apply cast in CIRCULAR MOTION until the whole area is covered and mold it during the process of application by
the palm.
10. Support the cast while applying.
11. Handle the cast with care.
Moving patients or transferring with wet cast must be avoided as much as possible. If this is necessary, care must be
taken to maintain the integrity of the cast.
The excess plaster cast is trimmed by means of a trimming knife. Cast spilled on the skin is easily removed by
wiping it with a damp cloth.
To hasten drying of the cast, several ways can be used
1. Exposure to open air or electric fan
2. Exposure to heat lamp
3. Placing the patient in a warm room
Care should be taken in protecting the patient form rapid drying of the cast, as this will result to a dry outer layer while the
inner layer remains wet. Complaints of discomfort should be investigated and appropriate measures be given to bring
comfort.
Patients in body cast or spica cast is turned every 4-6 hours to promote even drying of the cast.
Finishing touches on the dried cast.

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Edges that are extremely rough should be trimmed and smoothened very slightly with a knife.
Rough edges can be covered with adhesive petals, especially if there is no stockinet underneath the plaster and wadding
sheet.
Care of the Patient in Cast
The duration of keeping the body or part of it in cast is at least 1 month. Though, it varies among patients. Factors that
influence the duration are
1. Age of the patient
2. Part of the e body affected
3. The degree of injury the affection of the part
*During the
a.
b.
c.
d.
entire period that the patient is in cast, the nurse responsibility is focused on the following:
Neurovascular check
Preservation of the efficiency of the cast
Maintenance and promotion of the integrity of the system of the body
Maintenance of the cleanliness of the cast
A. Neurovascular checks
In all casted patient, COLOR, MOTION, TEMPERATURE AND SENSATION OF TOES/FINGERS should be observed
every 30minutes for several hours. After cast application, longer if there is edema, and then regularly every 3 hours.
Circulatory impairment results in symptoms of coldness, edema, cyanosis, pain and finally numbness in the toes or
fingers. The blanching sign will indicate whether or not there is an adequate circulation. When the nail of the thumb or
great toes is compressed and immediately released, the color should go from white to pink with the same speed/. If not, the
circulation is slow and the toes or fingers need closer observation.
Patients in arm or leg casts should be able to move and feel each toe or finger, because the same nerve does not
innervate each other. All toes and fingers should be checked.
Nerve Function Test
Nerve
Action by the nurse

- Test for Sensory Function
Radial
Prick web part between thumb

and index finger
Median Prick distal surface of index

finger
Action by the patient

- Test for Motor Function
Hyperextend the thumb
Oppose thumb and little
finger flex wrist
Ulna
Prick distal end of the small

finger
Abduct all fingers
Peroneal
Prick lateral surface of the great toes

extend toes
Dorsiflex ankle
Tibial
Prick medial and lateral surface

of sole of foot
Psychological Implications and Going Home In Cast
second toe
Plantar flex ankle and

flex toes
To relieve patients apprehension and anxieties that crowd their minds with their cast on, the nurse can help the [patient
make a start toward resolving some of the problems by helping them become to remain as independent as possible.
Instruction regarding cast care need to be received and patient can be reminded that frequent rest periods for the entire
body are necessary. Discussing plans with the patient before discharge will make the transition from the hospital to another
facility much smoother and add to her peace of mind.

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What to observe/remarks
Cast of the upper extremities

1.
Signs of impaired circulation/circulation of fingers such as

a. cyanosis of the skin
b. coldness of the skin
c. loss of function
d. numbness
e. pulselessness of the extremity
f. severe pain
g. marked swelling
2. Nerve damage due to pressure on the nerve as it passes over bony prominences
a. pain increasing in persistence
b. anesthesia
c. feeling of deep pressure
d. paresthesia
e. motor weakness and paralysis
3. Infections, tissue necrosis due to skin breakdown
a. musty, unpleasant odor over the cast or edges of the cast
b. drainage through cast or windows
c. sudden unexplained rise in temperature
d. hot spot felt on cast over lesion
4. Pressure on the elbows, axilla, wrists, metacarpals and iliac crest
Remarks
1. Avoid insertions of foreign bodies in cast
2. Avoid soiling of the cast
3. Report signs of cracks and weakness of the cast
4. Maintain proper alignment of casted extremity
5. Proper support of the cast
Cast of the Lower Extremities
1. Observe for impaired circulation as manifested by
a. Cyanosis or bluish discoloration of the skin
b. coldness of sensation
c. loss of function of the affected extremity
d. numbness
e. absence of pulse
f. marked swelling
2. Nerve damage due to pressure on the nerve as it passes over bony prominences
a. increasing persistent localized pain
b. numbness in the extremity
c. feeling of deep pressure
d. paresthesia
e. motor weakness or paralysis
3. Infections, tissue necrosis due to skin breakdown
a. drainage through casts
b. sudden, unexplained rise in temperature
c. hot spot felt on cast over the lesion
d. pressure on the groins, knee, ankle and metatarsals
Spica Casts
1. Signs of respiratory distress
2. Signs of cast syndrome
a. Prolonged nausea
b. Repeated vomiting

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3.
4.
5.
6.
c. Distention
d. Vague abdominal pain
e. Absence of bowel sounds
Pressure on the jaws, ears, face, clavicle area, anterior superior iliac crest, groin, buttocks, and above the knee.
Urinary and bowel disturbances
Signs of plaster cast
a. itchiness/burning sensation
b. severe pain
c. rise in the body temperature
d. disturb sleep
e. night cries among babies
f. restlessness
Signs of infections and tissue necrosis
Turning Patient In Cast

Turning casted trunk and lower extremities must be done carefully. The Patient must be lifted and not rolled or
dumped. Support should be provided to the encased part and the whole body.
The first changing of the patients position is dependent on the condition of the cast and the body area involved. The
first turning usually is to dry the posterior surface of the cast as well as to provide comfort and protect against respiratory
complications.
There should be no attempt to turn the patient alone if one estimates that one is physically unable without the patients
assistance.
Turning Patient in Hip Spica 1 - 1
A. Supine to lateral
With 2-3 members working together the patient is gently pulled toward the unaffected side. Member remains on this
side to give the patient the sense of security while the other member moves to the opposite side of the bed where the
affected leg is to arrange the pillow along the entire length of the casted leg and back.
B. Supine to prone
One member places his hands on the patient shoulder and hips, while the other support the thighs and extremities. The
member of the opposite side pulls the shoulder and thighs as the patient is gently teased on his front. After the patient has
been turned, observe the following points:
a. Toes should not dips against the mattress
b. Body section of the cast plaster should not press the back, chest and abdomen
c. Heels should be maintained in correct angulations and should be allowed to extend beyond the mattress
Placing Patient in Bedpan
In bowel or bladder elimination, the buttocks should be lower than the head and toward the breast. This can be
achieved by:
a.
Elevating the head part slightly and placing a small pillow under the back of the patient.
b. Placing a folded cloth on the posterior aspect of the bedpan. This will absorb moisture and this prevents
spoiling the cast.
Adult patients are usually placed in their good side first. The bedpan is placed so that the buttocks are on the
posterior section of the bedpan. Pillows, blankets are then arranged to support the legs and back so that there
will no be back flow.
If patient can support himself by lifting with the aid of the overhead trapeze, the bedpan is slipped under the
buttocks.

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Bladder and bowel elimination in children with hip spica if placed in headboard frame is not difficult if the
bedpan is kept constantly in the spica under the buttocks.
Instrument for Cast Removal
1. Cast cutter (manual electric)
2. Spreader
3. Trimming knife
4. Bandage scissors
5. Plaster sears
Points to Remember
1. After the cast is removed, support the part with pillow maintaining the same position that existed in the cast.
2. Move the extremity gently.
3. Observe the skin for any abrasions and plaster sore.
4. Wash skin with mild soap followed by application of oil or lanolin.
TRACTION
Traction is the application of a pulling force to a part of the body. It is used to align and immobilize fractured bones, to
relieve muscle spasms and to correct flexion contractures, deformities and dislocations.
For traction to be effective, there must be also a pull in the OPPOSITE DIRECTION (COUNTER TRACTION) by using
the body or by elevating part of the bed toward the traction.
PRINCIPLES OF TRACTION
1. MAINTAIN THE ESTABLISHED LINE OF PULL
Weights should hang freely, not hitting the bed or resting on the floor. The position of the weights should be
rechecked if the level of the bed is altered.
AVOID
1. Bumping against the weights when walking near the bed.
2. Allowing the weights to sway.
Both movements can cause pain for the patient in traction. It is preferred that the weights should not hang over
the patient, if necessary, the nurse should tape the weights so they will not fall on the patient.
2. PREVENT FRICTION
Traction rope should rest in the groove of the pulley and move easily. The rope should not be frayed. The nurse
should TIE securely knots in the traction rope and tape the rope ends. The rope knots should not lodge against the pulley
because this will interfere with the line of pull. For the same reason, the nurse should ensure that the pulley, spreader bar
and footplate do not rest against the foot of the bed.
3. MAINTAIN COUNTER TRACTION
To provide traction, the nurse must ensure that counter traction is maintained. If the weight of the patient body is to
provide the counter traction, HIS BODY should not interfere with the DIRECTION OF PULL. For instance, the feet of the
patient in BUCK traction should not touch the foot of the bed, or if the patient is in cervical traction, his head should not
touch the head of the bed.
4. MAINTAIN CORRECT BODY ALIGNMENT
The patient should have correct BODY alignment while lying centered in the bed. The nurse must ensure that the
patient does not angle his body or lean off the side of the bed because the line of traction pull would then be changed or
interrupted.
Types of Traction
1.
SKIN TRACTION
Skin traction is accomplished by weights that pull on tape, sponge rubber or plastic materials attached to the skin.
TRACTION on the SKIN, TRANSMITS traction to the musculoskeletal structures.

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Forms
1.
Buck Extension
A form of skin traction in which the pull is exerted in one plane when partial or temporary
immobilization is desirable. In Bucks extension, strips of adhesive, moleskin or perforated flex foam are
applied smoothly to each side of the affected extremity and attached to a spreader block at the foot. The
extremity is wrapped with elastic bandage to improve adherence of the tape to the skin and prevent
slipping. A traction rope is attached to the spreader block then over the pulley, thence to a weight hung
over the side of the bed.
2. Russells Traction
Russell traction when properly applied in good mechanical

working efficiency is a comfortable device for the patient.
The equipment required is not elaborated. A single section of
common Balkan frame can be attached to the bed with overhead
bar directly above the injured limb. Four pulleys are used. These
pulleys are arranged so that one is on the overhead bar at a level
directly above the tubercle of the tibia of the fractured leg, another
is attached to the footplate and two are attached to a crossbar at
the foot of the bed and are placed at about the level of the
mattress. A hammock which is used from the knee sling and
traction tapes form the BASIS OF TRACTION.
Important points in the nursing care of patient in Russell Traction

1.
The knee sling should be smooth and its edges must not cause pressure on the soft tissue over the
peroneal nerve.
2. The heel of the foot in traction should just clear the bed.
Firm pillows should support the thigh and the calf along the
entire length, leaving the heel free of the bed.
3. The popliteal space must be watched for ridging and skin denudation. Elevation of the backrest is
permitted and few difficulties are encountered in giving nursing care because the fractured leg is not at
the mercy of the gravity and will not be altered in position.
4. Encourage active dorsiflexion and plantar flexion of the feet.
Important features
1.
A piece of felt should be inserted between the sling and the patients skin to prevent wrinkling of the
sling under the popliteal area. This will assist in eliminating pressure sores that sometimes form at this
point.
2. The heel should clear the bed. The ideal position for the heels of the patient in Russell traction is that
of a person standing with his heels four inches apart. Abduction is to be avoided.
3. Two pillows are usually placed under the limb in traction. One under the thigh to maintain the
desired angle and the other under the calf down and including the Achilles tendon.
2. SKELETAL TRACTION
Method of traction used most frequently in the treatment of fracture of the femur, humerus and the tibia. The traction
is applied directly to the bones by use of a metal pin or wire (Kirschnerwire, Steimann pin), inserted into and through a
bone distal to the fracture. Usually the skin is made under local anesthesia. The pin or wire is sterilized with all the aseptic
precaution of an operation. Following insertion of pins, the wound is covered with a small gauze squares. If the wire or pin
extends back to the caliper, a cork placed over the end of the pin prevents the tearing of lines and other more serious
accidents.
Skeletal traction is applied by weights and pulleys as described for skin traction. The Thomas Splint with the Pearson
attachment is usually used with skeletal traction in fractures of the femur. It may be used with skin traction and other
balanced suspension apparatus. Because upward traction is required for these fractures, the patient is placed on a fracture
bed.
Inasmuch as fracture occurs under varying circumstances and involves individuals of different ages, weights and body
builds, NO TWO FRACTURES ARE ALIKE and every fractured patient require individual treatment. By same token, traction

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may be modified in many ways to meet a variety of special requirements, as exemplified by so called BALANCED
SUSPENSION TRACTION and the RUNNING TRACTION.
3. MANUAL TRACTION
Means the application of traction to a part of the body by the hands of the operator. When assisting with the
application of traction or a cast, the nurse may be asked to apply a manual traction. This calls a firm smooth grip on the
extremity and the avoidance of sudden jerking movements.
BALANCED SUSPENSION
Balanced suspension traction is used primarily for femoral fractures in adults by means of the Thomas splint with a
Pearson attachment. Balanced suspension provides counter traction by its own system of weights and pulleys. Therefore
when the patient lifts, the splint should also lift so that traction is maintained.
The Thomas splint has a sling that supports the thigh. The nurse should check for irritation from the ring to the groin,
inner thigh and ischium. The Pearson attachment is connected to the splint by the knee and supports the calf in a position
parallel to and above the bed. A Steimann pin or Kirschner wire is inserted through the distal end of the femur or through
the proximal or distal end of the tibia.
The nurse teaches the patient and family that the tractions main purpose is to provide sling, this allows the leg to rest
comfortably and provides freedom to move without disrupting traction pull or alignment.
By using the overhead trapeze, the patient can lift the shoulders and upper body. This movement allows for change of
linen from the top to the bottom of the bed. Similarly, the nurse can apply lotion to the patients back because the
individual is not allowed to turn for back care.
UPPER EXTREMITY TRACTION
Skin/Skeletal
Sidearm traction is used to immobilized fracture of the humerus and may be applied either a skin or skeletal traction. There
is outward pull on the upper arm and an upward pull on the forearm. For this reason, two separate set-ups of adhesive
strips and elastic bone wraps are needed. In addition, if skeletal traction is used, a Kirschnerwire is usually inserted trough
the olecranon.
If the traction equipment is attached to the bed frame under the mattress, elevating the head of the bed will not disrupt
the traction pull. However, if the frame is attached so that it moves when the bed position changes, the nurse should keep
the head of the bed flat. Placing a folded blanket under the mattress near the traction frame can provide COUNTER
TRACTION.
Skeletal
Overhead 90-90 traction, there is an upward pull on the upper arm, which is at a 90degree to the body. The elbow is
flexed at a 90degree that the forearm is suspended in a sling and rest above and across the body. Weight is attached to the
sling and to the Kirschner wire that is usually inserted through the olecranon.
Because the arm is elevated, the patient should have less edema. This will be the case as long as the nurse ensures the
patient keeps the involved hand supported in the sling and does not allow it to hang freely.
CERVICAL TRACTION
Skin Cervical Halter
Skin traction is frequently used for patients with sprains or strains to the cervical spine and ruptured cervical discs. It is
applied to the cervical spine by a halter with straps that go under the chin and around the head of the base of the skull.
After the halter is placed, the spreader bar and attached weights are connected. The patient may have small pillow under
his head and should rest the back against the bed. Because cervical traction is usually ordered intermittently for a specified
period, the nurse should teach the patient how to remove and reapply it. This information is especially important for the
patient because there may be the need to remove the halter if vomiting or choking occurs. Any severe headache or pain in
the area of the traction should be reported.

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Skeletal Cervical Tong

Skeletal traction to the cervical spine is used to immobilize and reduce fractures of the cervical spine that may injure the
spinal cord. This type of traction is always continuous and is applied by Gardner, Vinki or crutchfield tongs inserted into the
skull.
There should be little bleeding after the first 24hours should be reported. If the tongs loosened or slip out, emergency
measures include immobilizing the patients head with sandbags and notifying the physician immediately.
With the skeletal traction to the cervical spine, there is a straight line of pull and the head of the bed may be elevated 6
inches to provide counter traction. An overhead trapeze must not be used with either skin or skeletal traction because it is
use could strain the individuals neck.
The physician determines the degree of stability of the spine and writes
specific orders for the patient to turn. If turning is allowed, the nurse should use
the LOGROLLING. Technique that is, the patient is rolled as a unit so that the
spine stays aligned and is not twisted.
PELVIC TRACTION
Types
1. Pelvic belt is primarily for relief of lower back pain to the lumbar spine
whereas the pelvic sling is used to treat a pelvic fracture.
Pelvic belt traction is applied to the lumbar spine by a pelvic belt with straps attached to weights. It is used to
reduce muscle spasms and in the conservative management of low back pain and herniated lumbar disc. This traction
may be ordered for intermittent periods. However, patients cooperation is crucial to success.
The nurse should place the patient in Williams position, in which both the hips and knees are flexed at a 30degree
angle and the head of the bed is slightly elevated. This position relieves pressure from the lower back by decreasing the
lumbar curve. It also provides counter traction. If traction increases pain to the back or legs, the nurse should report this
to the physician.
2. Pelvic sling
It is used continuously to stabilize and immobilize fractures of the pelvis. A
large canvas sling attached to weights suspends the patients buttocks just off
the bed. The pelvic sling may also be used to compress the entire pelvis (by
applying pressure along each side), if there is a pelvic ring separation.
Compression is achieved when the physician repositions the rods from the
attachment edges of the sling to grooves that are closer together toward the
patients midline.
Strict immobilization is required to maintain the traction force. The nurse
should give back care every 4 hours by sliding her hands between the sling
and the patients back. However, it is difficult to reach the buttocks for skin
care and bathing and the patient may generally uncomfortable. For these
reasons an external fixator may be inserted into each iliac crest to stabilize
unstable fractures of the pelvis. External fixation can reduce the patients pain,
allow for his early ambulation and facilitate nursing care.
NURSING PRIORITIES FOR PATIENTS IN TRACTION
1. Frequently inspection of the fracture dressing in the first 24hours after application. A bandage that appears loose
when applied may in a very few hours cause constriction which if not relieved may lead to gangrene of the
extremity.
2. Dressing is applied in such a way as to leave the tips of the fingers and toes exposed. Any cyanosis, loss of
temperature, tingling sensation in these parts should warn the nurse that the dressings are too tight. If the condition
is caused by a single turn of the bandage, the turn may be divided with scissors, but it is usually advisable to notify
the surgeon.
3. After the first 24 hours, the fracture dressing should be inspected at least 3-4 times daily. Evidences of constriction
should be noted and pressure points checked heel on the bedclothes resting on toes.
4. It is also important to ask the patient if there are any painful areas.
5. If traction is in used, the apparatus should be checked to see the ropes are in the wheel of the groove of the pulleys
that the supporting apparatus is free of the pulleys, that the weights hang freely and that the patient has not slipped
down in the bed.

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6. The foot must be in natural position; rotation outward or inward should be reported. FOOT DROP is to be
avoided and the patients foot must be maintained in the neutral position supported by appropriate orthopedic
devices. The rope sometimes frays; therefore, it too must be inspected at least daily.
7. Weights are necessary to provide constant force and may be ordinary metal traction weights or bags of water, hot
or cold. It is especially important that the knots on the traction rope be tied securely. Enough weight is applied at
first to overcome shortening tendency of the injured limb, but is gradually lessened as the fracture becomes more
fixed. Weights should never be removed from a patient with fracture unless a life-threatening situation arises.
Weight and pulley is applied to secure constant corrective extension.
8. WHEN THERE IS PULL IN ONE DIRECTION, THERE MUST BE AN EQUAL PULL IN THE OPPOSITE DIRECTION.
Counter traction is supplied by either the patients body and friction against the bed (fracture of the upper
extremity) or by elevating the foot of the bed (fracture of the lower extremity).
9. When traction frames are used, a trapeze may be suspended overhead within easy reach of the patient. This
apparatus is of great help in assisting the patient to move in bed and on and off the bedpans.
NURSING CARE OF PATIENT IN TRACTION
Nursing principles and implications
implications
The purposes of traction regardless how it is achieved are
1. To reduce and to immobilize a fracture
2. To lessen or to eliminate muscle spasms
3. To prevent fracture deformity
PERCETION AND COORDINATION

Part 1 EYES
!
!
A.
An eye is a round-shaped organ that works with the brain to provide us with vision. The shape of the eye is
maintained by the pressure of the aqueous humor.
The main function of the eye is to work with the brain to provide us with vision. The eye and brain translate light
waves into a sensation we call vision.
External Structures of the Eye
Ocular Adnexa
! Are the accessory structures of the eyes that support and protect it.
Ocular Muscles
! Eyeball is moved by 6 ocular muscles, which are attached to the surface of the globe.
! 4 Rectus muscles move eyes vertically & horizontally
(medial, lateral, superior, inferior)
! 2 Oblique muscles rotate the eye in circular movements (superior, inferior)
Eyelids
elastic folds of skin that close to protect anterior eyeball.
Protect the eye from foreign particles.
distribute tears to prevent evaporation & drying of its surface.

Palpebral Fissure
elliptic space between the two open lids

Canthi
the corners of the fissure
Medial or Inner Canthus next to the nose
Lateral or Outer Canthus the outside corner

Meibomian Glands
are embedded in both upper and lower lids
oil secreting glands.

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B.
External Structures of the Eye
1. OUTER LAYER
- fibrous coat that supports the eye
SCLERAE
- Tough, white connective tissue white of the eye
- located anteriorly & posteriorly
CORNEA
- Transparent tissue through which light enters the
eye.
- Located anteriorly.
2. MIDDLE LAYER
- second layer of the eyeball
- vascular & highly pigmented
CHOROID
- a dark brown membrane located between the
sclera & the retina
- it lines most of the sclera & is attached to the
retina but can easily detach from the sclera
- contains blood vessels that nourishes the retina
- located posteriorly.
CILIARY BODY
- connects the choroid with the iris
- secretes aqueous humor that helps give the eye its
Shape.
IRIS
- the colored portion of the eye
- located in front of the lens
- it has a central opening called the pupil.
3. INNER LAYER (RETINA)
- a thin, delicate structure in which the fibers of the optic nerve
are distributed
- bordered externally by the choroid & sclera and internally by the
vitreous
- contains blood vessels & photoreceptors (cones & rods)
- light sensitive layer.
CONTAINS THE FOLLOWING STRUCTURES
1. CONES
- Specialized for fine discrimination, central vision & color
vision
- Functions at bright levels of illumination
2. RODS
RODS
- More sensitive to light than cones
- Aid in peripheral vision
- Functions at reduced levels of illumination.
AQUEOUS HUMOR
- Clear, watery fluid that fills the anterior &
posterior chambers of the eye
- produced by the ciliary processes, & the fluid
drains in the Canal of Sclemm

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- The anterior chamber lies between the cornea &

iris
- the posterior chamber lies between the iris & lens
- serves as refracting medium & provides nutrients
to lens & cornea
- contributes to maintenance of IOP
VITREOUS HUMOR
- Clear, gelatinous/jell-like material that fill the posterior cavity of
the eye
- Maintains the form & shape of the eye
- Provides additional physical support to the eye
- It is produced by the vitreous body
VITREOUS BODY
- contains a gelatinous substance that occupies the
vitreous chamber which is the space between the lens & retina
- transmits light & gives shape to the posterior eye.
OPTIC DISK
- a creamy pink to white depressed area in the retina
- the optic nerve enters & exits the eyeball in this area
- Referred to as the BLIND SPOT
- contains only nerve fibers
- lack photoreceptors
- insensitive to light
MACULA LUTEA
- Small, oval, yellowish pink area located lateral & temporal to the
optic disk
- the central depressed part of the macula is the FOVEA
CENTRALIS which is an area where acute vision occurs
CANAL OF SCHLEMM
- a passageway that extends completely around the eye
- permits fluid to drain out of the eye into the systemic circulation
so that a constant IOP is maintained
LENS
- A transparent circular structure behind the iris & in front of the
vitreous body
- Bends rays of light so that the light falls on the retina
PUPILS
- Control the amount of light that enters the eye & reaches the
retina
- Darkness produces dilation while light produces constriction.
EYE MUSCLES
- Muscles do not work independently but work in
conjunction with the muscle that produces the
opposite movement.
A. RECTUS MUSCLES
- Exert their pull when the eye turns temporally
B. OBLIQUE MUSCLES
- Exert their pull when the eye turns nasally
NERVES
A. CRANIAL NERVE II
- Optic nerve (nerve of sight)

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B. CRANIAL NERVE III

- Oculomotor
C. CRANIAL NERVE IV
- Trochlear
D. CRANIAL NERVE VI
- Abducens
BLOOD VESSELS
A. OPTHALMIC ARTERY
- Major artery supplying the structures in the eye
B. OPTHALMIC VEINS
- Venous drainage occurs through vision
ASSESSMENT OF VISION
VISUAL ACUITY TEST
- measures the clients distance & near vision
SNELLEN CHART
CHART
- simple tool to record visual acuity
- the client stands 20 ft from the chart & covers 1 eye and uses the
other eye to read the line that appears more clearly
- this procedure is repeated for the other eye
- the findings are recorded as a comparison between what the
client can read at 20 ft and the no. of feet normally required by
an individual to read the same line
EXAMPLE: 20/50
- The client is able to read at 20 ft from the chart what a healthy
eye can read at 50 ft
EXTRAOCULAR MUSCLE FUNCTION
- tests muscle function of the eyes
- tests 6 cardinal positions of gaze
1. Clients right (lateral position)
2. Upward & right (temporal position)
3. Down & right
4. Clients left (lateral position)
5. Upward & left (temporal position)
6. Down & left
- client holds head still & asked to move eyes & follow a small
object
- the examiner looks for any parallel movements of the eye or for
nystagmus
- an involuntary rhythmic rapid twitching of the eyeballs
COLOR VISION TEST
- Tests for color vision which involve picking nos. or letters out of a
complex & colorful picture
ISHIHARA CHART
- consists of nos. that are composed of colored dots located within a circle
of colored dots
- client is asked to read the nos. on the chart
- each eye is tested separately
- the test is sensitive for the diagnosis of red/green blindness but not
effective for the detection of the discrimination of blue
PUPILS

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- Normal: round & of equal size

- Increasing light causes pupillary constriction
Decreasing light causes pupillary dilation
- the client is asked to look straight ahead while the examiner quickly
brings a beam of light ( penlight) in from the side & directs it onto the side.
- Constriction of the eye is a direct response to the light shining into the
eye; constriction of the opposite eye is known as CONSENSUAL
RESPONSE
FLUORESCEIN ANGIOGRAPHY
- detailed imaging & recording of ocular circulation by a series of
photographs after administration of the dye
COMPUTED TOMOGRAPHY
- a beam of x-ray scans the skull & orbits of the eye
- a cross-sectional image is formed by the use of a computer
- contrast material is not usually administered
SLIT LAMP
- allows examination of the anterior ocular structures under
microscopic magnification
- the client leans on a chin rest to stabilize the head while a
narrow beam of light is aimed so that it illuminates only a narrow
segment of the eye.
TONOMETRY
- the test is primarily used to assess for an increase in IOP and
potential glaucoma
- NORMAL IOP: 8-21 mm Hg
OPTHALMIC MEDICATIONS
PARASYMPATHOLYTIC DRUGS
- used pre-op or for eye examinations to produce mydriasis
- C/I in clients with glaucoma because of the risk of increased IOP
Classification
MYDRIATICS
- dilate the pupils (mydriasis)
CYCLOPLEGIA
- relax the ciliary muscles
ANTICHOLINERGICS
- block responses of the sphincter muscle in the
ciliary body, producing mydriasis
Example:
Atropine sulfate (Isopto-Atropine, Ocu-Tropine, Atropair, Atropisol)
Scopolamine hydrobromide (Isopto-Hyoscine)
Cyclopentolate hydrochloride (Cyclogyl, AK-Pentolate, Pentolair)
Homotropine hydrobromide (Isopto Homatrine, AK-Homatropine,
Spectro-Homatrine)
Tropicamide (Mydriacyl, I-Picamide, Tropicacyl)
Phenylephrine hydrochloride (AK-Dilate, Dilatair, Mydfrin, Ocu-Phrin)
Nursing
Nursing care:
Assess for constipation & urinary retention
Instruct the client that a burning sensation may occur
on installation

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Instruct the client not to drive or operate machine for 24 hrs

after
installation of the medication unless
otherwise directed by the physician
Instruct the client to wear sunglasses until the effects of the medication wear of
Instruct to notify MD if blurring of vision, loss of sight, difficulty in breathing, sweating or flushing occur
Instruct the client to report eye pain to the physician
PARASYMPATHOMIMETIC
Miotics
- reduce IOP by constricting the pupil & contracting the ciliary muscle,
thereby increasing the blood flow to the retina & decreasing retinal
damage & loss of vision
-open the anterior chamber angle & increase the outflow of aqueous
humor
- used for chronic open-angle glaucoma or acute & chronic closed-angle
Glaucoma
Example of miotic drugs
Acethylcholine Cl (Miochol)
Carbachol (Miostat)
Pilocarpine HCl (Isopto Carpine, Pilocar)
Pilocarpine nitrate (Pilofrin, Liquifilm, Pilagan)
Echothiophate iodide (Phospholine iodide)
Demecarium bromide (Humorsol)
Isoflurophate (Floropr
Nursing Care:
Assess breath sounds for rales & rhonchi

- cholinergic meds cause bronchospasms & increased bronchial secretions
Maintain oral hygiene
- due to increased salivation
Have Atropine sulfate available as antidote for Pilocarpine
Instruct the client not to stop the meds suddenly
Instruct to avoid activities such as driving while vision is impaired
Instruct clients with glaucoma to read labels on OTC meds & to avoid
Atropine-like meds
- Atropine increase IOP
BETABETA-ADRENERGIC BLOCKING EYE MEDICATIONS

- IOP by decreasing sympathetic impulses & decreasing aqueous humor production w/o
pupil size
- Used to treat chronic open-angle glaucoma
- C/I in the client with asthma
affecting
accommodation
or
EXAMPLES
Betaxolol HCl (Betoptic)
Carteolol HCl (Ocupress)
Levobunolol HCl (Betagan)

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Metipranolol (Optipranolol))
Timolol maleate (Timoptic)
Nursing Care
If the pulse is below 60 or if systolic BP is below 90 mm Hg, withhold the
medication & contact MD
Instruct to change positions slowly to avoid orthostatic hypotension
ADRENERGIC EYE MEDICATIONS
Decrease the production of aqueous humor & lead to a decrease in IOP

-Used to treat glaucoma
ADRENERGIC MEDICATIONS
Apraclonidine HCl (Iopidine)
Brimonidine tartrate (Alphagen)
Dipivefrin HCl (Propine)
Epinephrine borate (Epinal, Eppy)
Epinephrine HCl (Epifrin, Glaucon

CARBONIC ANHYDRASE MEDICATIONS
- Interfere with the production of carbonic acid which leads to
decreased aqueous humor formation & decreased IOP
- Used for long-term treatment of open-angle glaucoma
- C/I in the client allergic to sulfonamides
EXAMPLES
ACETAZOLAMIDE ( DIAMOX)
DICHLORPHENHAMIDE (DARANIDE, ORATROL)

ETHOXYZOLAMIDE (CARDRASE, ETHAMIDE)
METHAZOLAMIDE (NEPTAZANE)
OSMOTIC MEDICATIONS
Lower IOP
Used in emergency treatment
treatment of acute closedclosed-angle glaucoma
Used pre-op & post-op to decrease vitreous humor volume
EXAMPLES
Glycerin (Glyrol, Osmoglyn)
Mannitol (Osmitrol)
Urea (Ureaphil)
EYE LUBRICANTS
- Replace tears or add moisture to the eyes
- Moisten contact lenses or an artificial eye
- Protect the eyes during surgery or diagnostic procedures
- Used for keratitis, during anesthesia or in a disorder that results in
unconsciousness or decreased blinking
EXAMPLES
Hydroxypropyl methylcellulose
methylcellulose (Lacril, Isopto Plain)
PetroleumPetroleum-based ointment (Artificial Tears, Liquifilm Tears)

NURSING CARE
Inform the client that burning may occur on installation
Be alert to allergic responses to the preservatives in the lubricants

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ANESTHETICS FOR THE EYE

TOPICAL ANESTHETICS
-Produce corneal anesthesia
Used for anesthesia for eye examinations, surgery, or to remove
foreign bodies from the eye
EXAMPLES
Proparacaine HCl (Ophthaine, Opthenic)
Tetracaine HCl (Pontocaine)

NURSING CARE
Note that the medications should not be given to the client for home use & are not to be self-administered by the
client
Note that the blink reflex is temporarily lost & that the corneal epithelium needs to be protected
Provide an eye patch to protect the eye from injury until the corneal reflex returns
ANTIANTI-INFLAMMATORY EYE MEDICATIONS
EXAMPLES
Dexamethasone (Maxidex)
Diclofenac (Voltaren)
Flurbiprofen Na (Ocufen)
Suprofen (Profenal)
Ketorolac tromethamine (Acular)
Prednisone acetate (Predfor

(Predforte,
te, Econopred)
Prednisolone Na phosphate (AK(AK-Pred, Inflamase)
Rimaxolone (Vexol
ANTIANTI-INFECTIVE EYE MEDICATIONS
ANTIBACTERIAL
Chloramphenicol (Chloromycetin, Chloroptic)
Ciprofloxacin hydrochloride (Cipro)
Erythromycin (Ilotycin)
Gentamicin sulfate (Garamycin, Genoptic)
Norfloxacin (Chibroxin)
Tobramycin (Nebcin, Tobrex)
Silver nitrate 1%
ANTIFUNGAL
Natamycin (Natacyn Opthalmic)

ANTIVIRAL
Idoxuridine (Herplex(Herplex-Liquifilm)
Trifluridine (Viroptic)
Vidarabine (Vira(Vira-A Opthalmic)

DISORDERS OF THE EYE
EYE
A. LEGALLY BLIND
Anyone with vision worse than 20/200 that cannot be improved with
corrective lenses is considered legally
blind.
A legally blind person with vision of 20/200 has to be as close as 20 feet to identify objects that people with
normal vision can spot from 200 feet.
Legal blindness is very common in older people because eyesight tends to worsen with time and age.
The leading causes of blindness are accidents, diabetes, glaucoma, and macular degeneration.
Nursing Care:
! When speaking to a client who has limited sight or blind, the nurse uses a normal tone of voice.

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! Alert the client when approaching.

! Orient the client to the environment.
! Use a focal point & provide further orientation to the environment from the focal point.
! Allow the client to touch objects in the room.
! Use the clock placement of foods on the meal tray to orient the client.
! Promote independence as much as possible
Provide radios, TVs, & clocks that give the time orally or provide a
Braille watch.
When ambulating, allow the client to grasp the nurses arm at the
Elbow the nurse keeps his or her arm close to the body so that the client
can detect the direction of movement
Instruct the client to remain one step behind the nurse when
ambulating.
People may use talking thermometers, enlarged or marked oven dials, talking watches, talking clocks, talking
scales, talking calculators, talking compasses and other talking equipment.
A small number of people employ guide dogs to assist in mobility.

General Care For Eye surgeries
Preoperative CARE
If both eyes are to be covered after surgery, the patient needs to be oriented to the staff and the
physical envinment prior to surgery
The child should practice having the eyes covered to decrease postoperative fear and restlessness
If both eyes are covered or if vision is greatly restricted, the call light should be placed within the
reach of the patient
The preparation of the eye on the day of the surgery may include the instillation of combination
of drugs into the eye at various intervals to dilate the pupil
POST OPERATIVE CARE
! General goal of Post operative care
o To prevent
o Increased IOP
o Stress on the suture line
o Hemmorage into the anterior chmabe (hyphema)
o Infection
Immediately after operative, the patiet must keep still the head still and try to avoid coughing,
vomiting, sneezing or moving suddently
The patient should lie with unoperated side down to prevent pressure on the operated eye and to
prevent possible contamination of the dressing with vomiting
A burning sensation about one hour after surgery usually means that the anesthethic is wearing off
The patient is instructed to avoid lifting the head or hips, straining at stolol or squeezing the eyelid
o If sneezing or coughinh occurs, the patient should follow through with open mouth
o If vomiting occurs, the eyelids should be kept open
o Cough medicines and antiemetics can be givenb for cough and vomiting, stool softener
and laxatives for constipation
To prevent stress on the suturebline, bending forward is avoided
o Sudden jerky movement may result in hemorrhage into the hyphema
Side rails are placed on the bed immediately postoperatively and are kept on while both eyes are
covered or as long as necessary for protection
The bedside table should be placed on the side of the unoperated eye so that the patient can see it
without excessive movement of the head
Care is taken that the dressing is not looased or removed
o Bleeding and serous fluid should be minimal
o Edema of the eyelids subside within 3 to 4 days

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The feeling of something in the eye 4 to 5 days post op usually is because of sutures and
is normal
o Sensation of pressure within the eye ad sharp pain are quickly reported to the surgeon.
These indicate bleeding
Supervision and assistance on ambulation should be given by the nurse to avoiding sustain injury
The patient is advised not to bend,or lift objects for several weeks post op, to prevent increasing
intraocular pressure
o
B.
CATARACT
- an opacity of the lens that distorts the image projected onto the
retina & that can progress to blindness.
- Intervention is indicated when visual acuity has been reduced to
a level that the client finds to be unacceptable or adversely
affecting lifestyle
Risk Factors
# Normal aging (90%)
# long-term exposure to ultraviolet light, exposure to radiation
# exposure to infrared radiation such as glassblowers, microwave radiation
# Drugs Coticosteroids, Haloperidol, Miotics
$ Denatured proteins can exhibit a wide range of characteristics, from loss of solubility to communal aggregation.
Types of cataracts;
1. Senile Cataracts: age-related begin around age of 50 years
Classified into three:
a. Cortical
-opacification found in the periphery of the lens
-progree slowly, infrequenly involve the visual axis, often do not cause severe loss of vision
b. Nuclear sclerotic cataracts- progressive and hardening of the central lens
c. Posterior subcapsular cataracts- occur centrally on the posterior lens capsule and cause visual loss early in their
development because they lie directly on the visual axis
2. Traumatic: those associated with injury
3. Congenital; Those associated at birth
4. Secondary: Those which occur following other eye or systemioc diseases
ASSESSMENT
# Opaque or cloudy white pupil
# Gradual loss of vision
# Blurred vision or hazy
hazy vision
# Decreased color perception
# Vision that is better in dim light with pupil dilation
# Photophobia
# Absence of red reflex - reddish-orange reflection from
the eye's retina that is observed when using an
ophthalmoscope.
MEDICAL MANAGEMENT
! No known medical treatment that either prevents or reduces cataract formation.
! OBJECTIVE: To remove the opacified lens.
EXTRACAPSULAR EXTRACTION ECCE
# removing the lens & anterior portion of lens capsule, the posterior lens capsule is left intact.
# allow insertion of lens implant w/ fewer post-op complication.
INTRACAPSULAR EXTRACTION ICCE
# removing the lens including the lens capsule.
PHACOEMULSION 2 to 3 mm
- the lens is broken up by ultrasonic vibrations & extracted.

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Cryoextraction: The cataract is lifted from the eye by a small probe that has been cooled to a temperature below zero and
Cryoextraction
adheres to the wet surface of the cataract
PREPRE-OP NURSING CARE
Instruct measures to prevent or decrease IOP
Administer pre-op eye medications including mydriatics & cycloplegics as prescribed

POSTPOST-OP NURSING CARE
Elevate the head of the bed 30-45 degrees
Turn the client to the back or un-operative side
Position the clients personal belongings on the un-operative side
Use side rails for safety.

Assist with ambulation.
Protective eye patch for 24 hours after surgery followed by eyeglasses worn during the day and metal shield worn
at night for 1 to 4 weeks
CLIENT EDUCATION AFTER CATARACT SURGERY
Avoid eye straining
Avoid rubbing or placing pressure on the eyes
Avoid rapid movements, straining, sneezing, coughing, bending,

vomiting, or lifting objects over 5 lbs
Teach measures to prevent constipation
Wipe excess drainage or tearing with a sterile wet cotton ball from
the inner to the outward canthus
Use an eye shield at bedtime

Contact the MD for any decrease in vision, severe eye pain or increase in eye discharge.
*After removal of the lens, the patientis referred to as aphakic (without lens)
Lens Replacement:
Intraocular lenses
Lens implanted at the time of cataract extraction
Held position either suture to the iris or by implanting it into the capsular sac
Better binocular vision (ability of both eyes to focus on one subject and fuse the two images into
one)
If an eye implant is not performed, the eye cannot accommodate &
glasses must be worn at all times
Note: Temporary glasses may be prescribed 1-4 weeks after surgery.USUALLY WITHIN 6-12 weeks healing has been
sufficient for fitting of permanen glasses or contact lenses
Aphakic Eyeglasses
Safest least expensive method
Very thick lenses magnify object 25%,m making them appear closer than they are actually
are
Cataract glasses act as magnifying glasses & replace central vision only
Cataract glasses magnify, & objects appear closer therefore teach
client to judge distance & climb stairs carefully
Contact lenses
Contact lenses provide sharp visual acuity and must have the manual dexterity to
handlethe lenses, cleaning, insertion of lenses, replacement of lenses and the dasnger of
corneal abrasion
If an eye implant is not performed, the eye cannot accommodate &

glasses must be worn at all times

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Cataract glasses act as magnifying glasses & replace central vision only
Cataract glasses magnify, & objects appear closer therefore teach

client to judge distance & climb stairs carefully
Contact lenses provide sharp visual acuity but dexterity is needed to

insert them
C.
GLAUCOMA
Ocular condtions characterized by optic nerve damage that will lead to irreversible blindness
blindness related to
increased IOP due to congestion of aquuenous humor in the eye
Glaucoma is the second leading cause of blindness in the world, according to the World Health
Organization.
Aquenous Humor
Flows in the anterior and posterior chamber of the eyes, nourishing the cornea and lens
90% of fluid flows out the anterior chamber, draining through the spongy trabecular meshwork into the
canal of schlemn and the episcleral veins
10% of fluids exits through the ciliary body into the suprachoridalspace and then drains into the venous
circulation of the ciliary body, choroid and sclera
Outflow of aquenous humor depends on an intact drainage system and an open angle ( 45 degrees)
between the iris and the cornea.
IOP
NormalNormal- 1010-21 mmhg
When A.H is inhibited from flowing out, the pressure builds up within the eye ( Increase IOP)
Increase IOP----damages the optic nerve---blindness
Two theories regarding how IOP damages the optic nerve
Direct mechanicasl theory
' High IOP damages the retinal layer as it passess through the optic nerve head
Indirect ischemic theory
' High IOP compresses the microcirculation in the optic nerve head, resulting in cell injury
and death
STAGES in the development of Glaucoma
1. Initiating events
PF= illness, emotional stress, congenital narrow angles, long term corticosteroid,
mydriatics
2. Structural altrertaion in the aquenous outflow system
`
Tissue and cellular changes
3.Functional alterations: :conditions such as increased IOP or impaired blood flow create functional changes
4. Optic nerve damage: atrophy of the optic nerve is characterized by loss of nerve fibers and blood supply
5. Visual loss: progressive loss of vision is characterized by visual field effect
Classification
Terms:
Primary and secondary glaucoma refer whether the cause is the disease alone or another condition
Acute and chronic refer to the onset and duration of the disorder
Open ( wide) and closed ( narrow- describe the width of the angle between cornea and the iris .Narrower angle places the
iris closer to the trabecular meshwork =impeded the outflow of A.H
Types of glaucoma:
I.
Primary OpenOpen-Angle Glaucoma POAG
! Often referred to as thief in the night.

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The pressure in the eye slowly rises and the cornea adapts without swelling
is the most common type of glaucoma.
slow damage to the nerve in the back of the eye (optic nerve) causes gradual loss of eyesight.
has been called simple glaucoma
glaucoma, chronic glaucoma,
glaucoma and widewide-angle glaucoma..
glaucoma.
The most common cause is degenerative change in the trabecular meshwork, rresulting
esulting in decrease outflow of
aqueous humor.
! IOP= 3030-50 mmhg
Risk Factors:
a. Age. The risk for glaucoma increases rapidly after age 40.
b. Race. Blacks are 4 times more likely than whites to have glaucoma.
c. Family history of glaucoma
d. Prior loss of vision in one eye from glaucoma
e. Diabetes. People with diabetes are also at risk for a type of secondary glaucoma where new blood vessels grow
into and block the drainage angle of the eye (trabecular meshwork).
!
!
!
!
!
II.Close
II.Close angle glaucoma
An acute attack can develop only in an eye in which the anterior chamber angle is
anatomically narrow.
Attack occurs due to sudden blockage of the anterior angle by the base of the iris.
When Aqueous flow is obstructed >>> IOP becomes markedly elevated >>> severe
pain & blurred vision >>> Blindness
This sudden rise in pressure can occur within a matter of hours and become very
painful. If the pressure rises high enough, the pain may become so intense that it can
cause nausea and vomiting.
The eye becomes red,
clouds, and the patient may see haloes
red the cornea swells and clouds
around lights and experience blurred vision.
IOP= 50-70 mmhg
Risk Factors:
a. Race. People from East Asia or with East Asian ancestry, as well as Canadian, Alaskan
b. Age. People over age 40 are at increased risk for closed-angle glaucoma.
c. Sex. Older women are more likely than older men to develop closed-angle glaucoma.
d. Birth defects - born with narrow drainage angles in the eyes.
e. Physical injuries. Severe trauma, such as being hit in the eye, can result in increased eye pressure. Injury can also
dislocate the lens, closing the drainage angle.
f. Farsightedness, Family history, Having closed-angle glaucoma in one eye .
III.
!
!
!
!
!
Congenital glaucoma
is a rare form of glaucoma that is present in babies at birth.
often caused by a birth defect
defect that can cause abnormal development of structures in the eye.
usually diagnosed by the end of the first year of life.
Glaucoma that develops between birth and age 3 is called infantile glaucoma
glaucoma.
People between the ages of 3 and young adulthood can develop another type of developmental glaucoma called
juvenile glaucoma.
glaucoma.
Symptoms:
# Watery eyes, sensitivity to light
# eyes that look cloudy
# Eyes look larger than normal
# Rubbing the eyes or keeping the eyes closed much of the time.
IV.
LowLow-Tension Glaucoma
Resembles Primary Open-Angle Glaucoma
The angle is normal, optic nerves are cupped, & show peripheral vision deficits.
IOP is within normal range.

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V.
Treatment is indicated to lower the pressure even further, to avoid progressive optic nerve damage and visual field
loss.
Secondary Glaucoma
Glaucoma may develop after an eye injury, after eye surgery, from the growth of an eye tumor, or as a
complication of a medical condition such as diabetes - cause new blood vessels to grow into the drainage angle
of the eye.
Certain medicines : corticosteroids
Pigmentary glaucoma - is a form of secondary glaucoma caused by pigment granules being released from the
back of the iris. These granules can block the drainage of aqueous humor.
Phacomorphic glaucoma - Cataract that causes swelling of the lens can cause glaucoma.
Primary OpenOpen-angle Glaucoma:

# Peripheral vision loss objects to the side are ignored ( tunnel vision)
# Insiduous onset-generally no discomfort
# Patient may bump into other person in the street or fail to see passing vehicles, yet not realize that the fault lies on
their own vision
# The loss of peripheral vision ( TUNNEL VISION) CAN PROGRESS until the person is legally blind, yet the person
may be able to see well straight ahead
# Persistent dull eye pain in the morning
# Frequent changes of glasess, difficulty in adjusting to darkness, failure to detect changes in color accurately
AngleAngle- closure Glaucoma:
# Sudden, severe blurring of vision
# Severe eye pain
# Colored halos around lights
# Redness of the eye
# Nausea and vomiting
Diagnostic Assessment:
$ Ophthalmoscopy - it is used to examine the area where the optic nerve leaves the eye (optic disc). Damage to the
optic nerve related to glaucoma can be diagnosed by ophthalmoscopy.
$ Tonometry - measures the pressure in the eye (intraocular pressure, or IOP). Normal intraocular pressure is usually
between 10 and 21 millimeters of mercury (mm Hg). People with glaucoma sometimes have above-normal IOP.
$ Gonioscopy - is done to see if the drainage angle of the eye is closed or nearly closed.
! This helps your doctor see which type of glaucoma you have. Gonioscopy can also find scarring or other damage
to the drainage angle.
! Treat glaucoma. During gonioscopy, laser light can be pointed through a special lens at the drainage angle. Laser
treatment can decrease pressure in the eye and help control glaucoma.
! Check for birth defects that may cause glaucoma.
Nursing Care:
( Remove contact lenses
( Eyedrops are used to numb the eye so that you will not feel the lens touching your eye during this painless
examination.
( ask client to lie down or to sit in a chair & look straight ahead.
( A special lens is placed lightly on the front of the eye, and a narrow beam of bright light is pointed into the eye.
( the drainage angle is checked & measured.
( The examination takes less than 5 minutes.
( If pupils were dilated, vision may be blurred for several hours after the test - (do not rub the eyes for 20 minutes
after the test, or until the medicine wears off).
Perimetry test (visual field testing)
! Measures all areas of eyesight, including peripheral vision.
! Regular perimetry tests can be used to see if treatment for glaucoma is preventing further vision loss.
! It may take more than 45 minutes when both eyes are tested.

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To do the test, you sit and look inside a bowl-shaped instrument called a perimeter. While you stare at the center
of the bowl, lights flash. You press a button each time you see a flash. A computer records the spot of each flash
and if you pressed the button when the light flashed in that spot.
At the end of the test, a printout shows if there are areas of your vision where you did not see the flashes of light.
Medical Management: OPEN ANGLE GLAUCOMA

GOAL: to reduce IOP and keep it at a safe level
o
o
o
o
o
o
Diet: no caffeine, low sodium

Patient is advised tto
o avoid fatigue or stress and to avoid drinking large quantities of fluids
Instruct the client the need for lifelife-long medication use
Instruct the client to avoid antianti-cholinergic medications
Instruct the client to report eye pain, halos around eyes & changes
changes of vision to the physician
Instruct the client that when maximal medical therapy has failed to halt the progression of visual field loss & optic
nerve damage, surgery will be recommended
o Pharmocologic therapy
Topical Miotics Pilocarpine hydrochloride
o causes pupillary constriction to open canal of schlemm
o constricts pupil & increase outflow
Topical epinephrine also increase outflow
Topical beta-blockers or alpha-adrenergics Timolol Maleate
o Decreases production of aqueous humor
Oral carbonic anhydrase inhibitors acetazolamide/Diamox
o Inhibits production of aqueous humor
$
When medical management is no longer effective, surgical intervention may be indicated.
Surgical Management:
Laser Trabeculoplasty
! Laser is used to create an opening in the trabecular meshwork to allow increased outflow of aqueous.
! IOP is reduced in about 80% of cases.
! Effect of laser treatment decreases over time & procedure may need to be repeated.
! Tx with medications is usually continued.
Filtering Procedures
! Goal is to create an outflow channel from the anterior chamber into the subconjunctival space.
Example:
Trabeculectomy-remove
the part of trabecular meshwrok to allow drainage of aqueous humor into the conjuctival
Trabeculectomy
spaces
SclerotomySclerotomy surgical incision of sclera
Iridectomyridectomy portion of the iris is excised to facilitate outflow of aquenuos humor
*25% of cases, the opening closes because of scar formation
Ways to prevent scar tissue formation
o Topical corticosteroid used post op antiinflammtory action inhibits proliferation of fibroblast at the
surgical site
o Injection subconjunctival of 5-FU, mitomycin and other anti-metabolites
Cyclodestructive Procedure
Procedure- destroying part of ciliary by
cyclocryotherapy ( application of freezing tip) or
cyclophotocoagulation
Medical Management: Close ANGLE GLAUCOMA
Treat as medical emergency
Maintain bed rest in quiet, darkened room, elevate head 30 degrees

Administer miotics eyedroips

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D.
!
!
!
Administer acetazolamide, glycerol orally as ordered

Assess patient;s ability to see
Prepare for eye examination as ordered
Avoid atropine preparation and other mydriatics as these drugs dilate pupils
Administer anti emetics as ordered for nausea
Provide diet as tolerated
Prepare for surgery if ordered
RETINAL DETACHMENT
Occurs when 2 retinal layers separate because of either fluid accumulation or contraction of the vitreous body.
Most often occurs between ages 50-70.
CAUSES:
sudden severe physical exertion,
post cataract extraction,
myopia, hemorrhage, & tumor
TYPES
! PARTIAL RETINAL DETACHMENT
DETACHMENT
- becomes complete if left untreated
! COMPLETE RETINAL DETACHMENT
- when detachment is complete, blindness may occur.
$ there is a hole or a tear in the retina. Fluid that normally fills the inside of the eye can go through these retinal
holes or tears and get behind the retina. This separates the retina from the back of the eye, causing a detachment.
$ Retina is separated from the choroid >>> avascular necrosis >>> interrupts the transmission of visual images
from retina to the brain >>> progressive loss of vision >>> COMPLETE BLINDNESS.
Clinical Manifestations:
# Shadow or curtain falling across the field of vision-part of detachment in the retina
# Painless onset is usually sudden
# Black spots/Floaters- these are blood and retinal cells that are freed at the time of the tear and cast shadows on the
retina as they seem to drift about the eye
# Flashes of light the light that enters the yes is not absorbed by the detached melanin epithelial pigment
Ep the patient
Diagnostic Tests:
Ophthalmoscopy
o used to evaluate the extent and source of detachment.
o Areas of detachment appears bluish gray.
gray
Immediate nursing care: to prevent further detachment
Provide bedrest
Cover both eyes with patches to prevent further detachment
Speak to the client before approaching
The head is positioned so that the retinal hole is in the lowest part of the eye ( dependent position)
Protect the client from injury
Avoid jerky head movements
Minimize eye stress
Prepare the client for surgical procedure as prescribed

$ SURGERY
- is required to repair detached retina.
$ GOAL:
To place retina back in contact with the choroid and to seal accompanying holes & breaks.
Cryopexy
! Use of freezing probe or laser photocoagulation to seal the hole & stimulate adhesion formation.

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Diathermy
! The use of electrode needle and heat through the sclera stimulate an inflammatory response leading to adhesions
Laser therapy
! To stimulate an inflammatriy response to seal small retinal tears before detachment occurs
Sceral Buckling
! Used to splint and hold the retina & choroid together.
! A silicone sponge implant is placed over the tear and held in place with an encircling band.
Pre op Nsg. Care:
# Place on activity restrictions based on the size & location of detachment.
# General anesthesia is used & pupil must be dilated before the operation.
Post op Nsg. Care:
# Observe eye patch for any drainage.
# Narcotics needed during first 24 hours.
# Nausea & vomiting may require management.
# IOP monitoring for first 24 hours.
# Resume regular diet & fluids as tolerated.
# Antibiotic-steroid combination drop
# Cycloplegic agents
# Redness & swelling of lids & conjunctiva should be expected.
# Clean eyes with warm tap water & clean wash cloth.
# Glasses worn during the day & eye shield should be worn at night.
# Avoid vigorous activities and heavy lifting.
# Healing takes place over weeks & months, vision may improve gradually. (Warm & cold compress for comfort).
E.
Macular Degeneration
Is an atrophic degenerative process that affects the macula and surrounding tissues, resulting in central visual
deficits.
Found in most adults over age 65. Incidence increases with each decade over 50.
It may also be hereditary.
There is no known medical treatment or prevention for age-related macular degeneration.
Client may notice blurred scotoma or decreased central visual acuity.
Amsler Grid
! a simple device to test the early and progressive effects of age-related macular degeneration.
! patients can test their own vision by posting the grid on the refrigerator or somewhere else at home.
! Then patients can report any changes they detect.
F.
Diabetic Retinopathy
A progressive disorder of the retina characterized by microscopic damage to the retinal vessels.
As a result of inadequate blood supply , sections of the retina deteriorate & vision is permanently lost.
All diabetics are prone to develop retinopathy.
Clients who have had diabetes for 15-20 years have an 80-90% chance of developing retinopathy.
Clinical Manifestations:
# Gradual or sudden loss of vision
# Floaters or shadows
Management:
# tight control of diabetes.
# tight control of diabetes.
# avoiding smoking,
# keeping regular appointments with your doctor and the eye specialist.
# Community referrals for rehabilitation & low vision aids.
Eye infection
Conjunctivitis
$ Conjunctivitis is an inflammation or infection of the conjunctiva.

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Three types:
A. Infectious commonly known as Pink eye.
B. Allergic
C. Chemical
Clinical manifestation:
o Hyperemia redness
o Tearing & exudation
o Psuedoptosis drooping of the upper lid
o Sandy or scratchy feeling in the eyes
o Blurred vision
It is important to prevent spreading conjunctivitis. If contagious, measures can be taken to prevent spreading conjunctivitis
to others.
# Keep your hands away from your eyes;
# Thoroughly wash hands before and after applying eye medications;
# Do not share towels, washcloths, cosmetics or eye drops with others;
# Seek treatment promptly.
Infectious conjunctivitis
# treated with antibiotic eye drops and/or ointment.
Allergic conjunctivitis
# avoid contact with any animal if it causes an allergic reaction.
Chemical conjunctivitis
# Wear swimming goggles if chlorinated water irritates your eyes.
Blepharitis
! Is a common chronic bilateral inflammation of the eyelid margins.
! Signs & Symptoms:
itching & burning of the eyes.
red eyelid margins,
scales or granulations along lashes.
lashes.
In view of the longlong-term nature of the condition, strict lid hygiene is necessary. The following regimen may be useful:
# Fill a small glass with warm water.
# Add three drops of baby shampoo.
# Take a clean cotton ball and soak it in the solution.
# While th
the
e eyes are closed, gently scrub both eyelids for two minutes .
# Rinse with cool tap water.
# Gently dry with a clean towel.
# Use medications as directed.
$ Infected blepharitis may be treated with antibiotic ophthalmic ointment.
Hordeolum
! Stye is an infection
infection of the glands of the eyelids.
! Caused by staphylococcus infections.
! Signs & Symptoms:
redness & pain; localized swelling; may be filled with purulent material.
! Management:
Warm compress
Antibiotics
Incision & drainage as indicated.
Chalazion
! Is a sterile chronic granulomatous inflammation of a meibomian gland.
! Meibomian Cysts
! Usually characterized by painless localized swelling along the lid margin without redness.
! If large enough to distort vision or to be a cosmetic blemish, it may be surgically
surgically excised.
Extraocular Muscle Disorrders
Strabismus : called SQUINT EYE or LAZY EYE

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-a condition in which the eyes are not aligned because of lack of

muscle coordination of the extraocular muscles
- most often results from muscle imbalance or paralysis of
extraocular muscles, but may also result from conditions such as
brain tumor, myasthenia gravis or infection
- normal in young infant but should not be present after about age
4 months
ASSESSMENT
# Amblyopia if not treated early
# Permanent loss of vision if not treated early
# Loss of binocular vision
# Impairment of depth perception
# Frequent headaches
# Squints or tilts head to see
#
Medical Management:
Corrective lenses as indicated
Instruct the parents regarding patching (occlusion therapy) of the good eye
- to strengthen the weak eye
Prepare for botulinum toxin (Botox) injection into the eye muscle
- produces temporary paralysis
- allows muscles opposite the paralyzed muscle to strengthen the eye
Inform the parents that the injection of botulinum toxin wears off in about 2
months & if successful, correction will occur
Prepare for surgery to realign the weak muscles as Rx if nonsurgical

interventions are unsuccessful
Instruct the need for follow-up visits

HYPHEMA
- the presence of blood in the anterior chamber
- occurs as a result of injury
- condition usually resolves in 5-7 days
NURSING CARE
Encourage rest in semi-Fowlers position
Avoid sudden eye movements for 3-5 days to decrease bleeding
Administer cycloplegic eye drops as prescribed

- to place the eye at rest
Instruct in the use of eye shields or eye patches as prescribed
Instruct the client to restrict reading & watching TV

Trauma to the eye and related structure
CONTUSIONS
- bleeding into the soft tissue as a result of an injury
- causes a black eye & the discoloration disappears in
approximately 10 days
- pain, photophobia, edema & diplopia may occur
NURSING CARE
Place ice on the eye immediately
Instruct the client to receive an eye examination

Intraocular FOREIGN BODIES
- an object such as dust that enters the eye
NURSING CARE
Wash hands thoroughly before touching the eye
Have the client look upward, expose the lower lid, wet a cotton-

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tipped applicator with sterile NSS & gently twist the swab over
the particle & remove it
If the particle cannot be seen, have the client look downward,

place a cotton applicator horizontally on the outer surface of
the upper eye lid, grasp the lashes, & pull the upper lid outward
& over the cotton applicator, if the particle is seen, gently twist
over it to remove
If foreign body is lodged into the cornea, do not attempt to remove it, see a physician
Avoid pressure on the eye, do not touch , do not rub the eye
Use sterile technique, when treating the eyes
CHEMICAL BURNS
- an eye injury in which a caustic substance enters the eye
NURSING CARE
Treatment should begin stat
Flush the eyes at the site of injury with water for at least 15-20 mins
At the site of injury, obtain a small sample of the chemical involved
At the ER, the eyes is irrigated with NSS or an opthalmic irrigation

solution
The solution is directed across the cornea & toward the lateral canthus
Prepare for visual acuity assessment
Apply an antibiotic ointment as prescribed
Cover the eye with a patch as prescribed

PENETRATING OBJECTS
- an injury that occurs to the eye in which an object
penetrates the eye
NURSING CARE
Never remove the object because it may be holding ocular
structures in place, the object must be removed by MD
Cover the object with a cup
Dont allow the client to bend
Dont place pressure on the eye
Client is to be seen by MD stat

Refraction errors:
! Emmetropia: normal refractive state
! Ammetropia: sight not in proper measure
o Hyperopia
' Farsightedness
' Parallel rays of light focus behind the retina
' Corrected with convex lens
o Myopia
' Nearsightedness
' Paraleel rays of light focus in front of retina
' Corrected with concave lens
' Radial keratomy ( rk surgery)
Presbyopia
' old sight
' Lessening of the effective powers of accommodation, occurs because of hardening of the lens due
to aging process
' Blurring of near object or visual fatigue when doing
doing close eye work
' Convex reading glasses are recommended

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Astigmatism
' distorted vison
' Caused by variation in refractive power along different meridians of the eye
' Optical distortion is most often caused by irregular caorneal curvature which prevents clear
clear focus
of light from any point
Corneal Inflammation ( keratitis)

Assessment
Pain
Phaotophobia
Lacrimation
Blepharospasm
Decreased vision
Treatment
Trifuridine ( Viroptic), Idoxuridine (IDU)
Mechanical/chemical debridement
Corneal UlcerationUlceration-medical emergency
May result to corneal perforation, scarring or intraocular infection, permanent impairment of vision
Causes
Trauma
Exposure
Allergy
Vit deficiency
Lowered resistance
Bacterial, viral, fungal infection
Corneal OpacityOpacity- lack of corneal transparency
transparency dur to inflammation, ulceration or injury
Corneal Transplantation ( keratoplasty)
To repair corneal opacity, perforation of corneal ulcer
Donor eyes for corneal transplantations come from cadavers
Ideally, a donated eye is transplanted immediately or is
is removed form the bidy within 2 4 hours of death. Cornea
may still be viable within 12 hours after death if the body has been refrigerated; may be trabsplanted up to 48 hours
after death if it kept in a sterile container, on a piece of gauzed soaked in NSS at 4 degrees celcius
Eye Surgery
ENUCLEATION
- removal of the entire eyeball
EXENTERATION
- removal of the eyeball & surrounding tissues
Performed for the removal of ocular tumors
After the eye is removed, a ball implant is inserted to provide a firm

base for socket prosthesis & to facilitate the best cosmetic result
A prosthesis is fitted approximately 1 month after surgery

EVISCERATION
-removal of the entire eyeball contents and cornea, except the sclera
PREPRE-OP NURSING CARE
Provide emotional support to the client
Encourage the client to verbalize feelings related to loss

POSTPOST-OP NURSING CARE
Monitor V/S
Assess pressure patch or dressing

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Report changes in V/S or the presence of bright red drainage on the
pressure patch or dressing

ORGAN DONATION
DONOR EYES
Obtained from cadavers
Must be enucleated soon after death due to rapid endothelial

cell death
Must be stored in a preserving solution
Storage, handling & coordination of donor tissue with surgeons

is provided by a network of state eye bank associations across
the country
CARE OF THE DECEASED CLIENT AS A POTENTIAL EYE DONOR
Discuss the option of eye donation with MD & family
Raise the head of the bed 30
Instill antibiotic eye drops as RX

Close the eyes & apply a small ice pack to the closed eyes
PRE-OP CARE OF THE RECIPIENT
Recipient may be told of the tissue availability only several hrs

to 1 day before surgery
Assist in alleviating client anxiety
Assess for signs of eye infection
Report the presence of any redness, watery or purulent

drainage or edema around the eyes to MD
Instill antibiotic drops into the eyes as Rx to reduce the no. of

microorganisms present
Administer IV fluids & medications as Rx

POSTPOST-OP CARE TO THE RECIPIENT
Eye is covered with a pressure patch and protective shield that

are left in place until the next day
Dont remove or change the dressing without the MDs order
Monitor V/S, LOC & assess dressing
Position the client on unoperative side to reduce IOP
Orient
Orient the client frequently
Monitor for complications of bleeding, wound leakage, infection

& graft rejection
Instruct the client in how to apply the patch & eye shield
Instruct the client to wear the eye shield at night for 1 month &
whenever around
around small children or pets
GRAFT REJECTION
Can occur at anytime
Inform the client of signs of rejection
Signs include redness, swelling, decreased vision, & pain
Treated with topical steroids

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GASTROINTESTINAL SYSTEM DISORDERS

FUNCTION OF GIT SYSTEM
SYSTEM:
TEM:
! To break down food particles into the molecular form for digestion.
! To absorb into the bloodstream the small molecules produced by digestion.
! To eliminate undigested and unabsorbed foodstuffs and other waste products from the body.
The GIT is composed of two general parts
The main GIT starts from the mouth%Esophagus Stomach SI LI
The accessory organs are the
Salivary glands
Liver
Gallbladder
Pancreas
The Mouth
Contains the lips, cheeks, palate, tongue, teeth, salivary glands, masticatory/facial muscles and bones
Anteriorly bounded by the lips
Posteriorly bounded by the oropharynx
Important for the mechanical digestion of food
The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of carbohydrates
The Esophagus
A hollow collapsible tube
Length- 10 inches
Made up of stratified squamos epithelium
The upper third contains skeletal muscles
The middle third contains mixed skeletal and smooth muscles
The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found here
$ Functions to carry or propel foods from the oropharynx to the stomach
The stomach
J-shaped organ in the epigastrium
Contains four parts- the fundus, the cardia, the body and the pylorus
The cardiac sphincter prevents the reflux of the contents into the esophagus
The pyloric sphincter regulates the rate of gastric emptying into the duodenum
Capacity is 1,500 ml!
PARTS OF A STOMACH:
Cardia (holding area for food in the top of stomach)
Fundus (upper left part of stomach)
Body (holding area for food and the main area of stomach)
Antrum (lower stomach, where food mixes with gastric juices and chyme is formed
FUNCTION OF THE STOMACH:
Serving as a temporary storage area for food.
Beginning digestion.
Breakdown of food into chyme, a semifluid substance
Moving the gastric contents into the small intestine.
Stomach:
1. Parietal cells- HCl acid and Intrinsic factor
2. Chief cells- pepsin% digestion of PROTEINS!

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3. Antral G-cells- gastrin ( stimulates gastric secretion & motility)

4. Argentaffin cells- serotonin (enhances intestinal motility)
5. Mucus neck cells- mucus
GI HORMONES & FUNCTIONS
GASTRIN ( Produced in pyloric antrum &duodenal mucosa)----- stimulates secretion of gastric acid& pepsinogen, increases
gastric blood flow, stimulates gastric smooth muscle contraction.
GASTRIC INHIBITORY PEPTIDES ( produced in duodenal & jejunal mucosa)--- inhibits gastric secretion & motility.
SECRETIN (produced in duodenal & jejunal mucosa)- stimulates secretion of bile and alkaline pancreatic fluid.
CHOLECYSTOKININ ( produced in duodenal & jejunal mucosa) stimulates gallbladder contraction and secretion of
enzyme-rich pancreatic fluid), slows down gastric emptying.
The Small intestine

Grossly divided into the Duodenum, Jejunum and Ileum
The duodenum contains the two openings for the bile and pancreatic ducts
The ileum is the longest part (about 12 feet)
FUNCTION OF THE SMALL INTESTINE:
Finalized digestion of all food stuff
Absorbing food molecules through its wall into the circulatory system , which delivers them to body cells.
Secreting hormones that help control secretion of bile , pancreatic fluid, & intestinal fluid.
The Large intestine
Approximately 5 feet long, with parts:
1. The cecum% widest diameter, prone to rupture
2. The appendix
3. The ascending colon
4. The transverse colon
5. The descending colon
6. The sigmoid% most mobile, prone to twisting
7. The rectum- holds fecal material until urge to defecate occurs
8. Anus- opening through which stool leaves the body, anal sphincter provides closure of anus.
FUNCTION OF THE LARGE INTESTINE:
Absorbs water
Eliminates wastes
Bacteria in the colon synthesize Vitamin K
Appendix participates in the immune system
SYMPATHETIC
Generally INHIBITORY!
Decreased gastric secretions
Decreased GIT motility
But: Increased sphincteric tone and constriction of blood vessels
PARASYMPATHETIC
Generally EXCITATORY!
Increased gastric secretions
Increased gastric motility
But: Decreased sphincteric tone and dilation of blood vessels
The Liver
The largest internal organ

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Located in the right upper quadrant

Contains two lobes- the right and the left
The hepatic ducts join together with the cystic duct to become the common bile duct
FUNCTION OF THE LIVER:

Functions to store excess glucose, fats and amino acids
Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12
Produces the BILE for normal fat digestion
The Von Kupffer cells remove bacteria in the portal blood
Detoxifies ammonia into urea & eliminated to the urine.
The gallbladder
Located below the liver
The cystic duct joins the hepatic duct to become the bile duct
The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum
FUNCTION OF THE GALLBLADDER:
Stores and concentrates bile
Contracts during the digestion of fats to deliver the bile
Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder and relaxation of the
sphincter of Oddi
The pancreas
A retroperitoneal gland
Functions as an endocrine and exocrine gland
The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi
FUNCTION OF THE PANCREAS:
The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates, fats and proteins
Pancreatic amylase% carbohydrates
Pancreatic lipase (steapsin) fats
Trypsin, Chymotrypsin and Peptidases proteins
Bicarbonate% to neutralize the acidic chyme. Stimulated by SECRETIN!
The ABDOMINAL examination
The sequence to follow is:
Inspection
Auscultation
Percussion
Palpation
COMMON LABORATORY PROCEDURES
FECALYSIS
Examination of stool consistency, color and the presence of occult blood.
Special tests for fat, nitrogen, parasites, ova, pathogens and others
FECALYSIS: Occult Blood Testing
Instruct the patient to adhere to a 3-day meatless diet
No intake of NSAIDS, aspirin and anti-coagulant, vit c, iron
Screening test for colonic cancer
Upper GIT study: barium swallow
Examines the upper GI tract

Barium sulfate is usually used as contrast

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Upper GIT study: barium swallow

Examines the esophagus & stomach
Pre-test: NPO post-midnight
Post-test: Laxative is ordered (constipation), instruct that stools will turn white, monitor for obstruction
Lower GIT study: barium enema
Gastric
Examines the lower GI tract, large colon
Pre-test: Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test
Lower GIT study: barium enema
Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn white, monitor for
obstruction -(inform MD if bowel movement doe not occur in 2days.)
analysis
Aspiration of gastric juice to measure pH, appearance, volume and contents
HOW?
Insertion of nasogastric tube to examine fasting gastric contents for acidity & volume.
o CONT
PRETEST:
KEEP NPO 6-8 HOURS PRETEST
ADVICE CLIENT ABOUT NO SMOKING, ANTICHOLINERGIC MEDICATION, ANTACIDS FOR 24 HOURS
BEFORE THE TEST.
INFORM CLIENT THAT TUBE WILL BE INSERTED INTO THE STOMACH VIA THE NOSE, & INSTRUCT TO
EXPECTORATE SALIVA TO PREVENT BUFFERING OF SECRETIONS.
POSTTEST:
PROVIDE FREQUENT MOUTH CARE.
EGD
(esophagogastroduodenoscopy
! Visualization of the upper GIT by endoscope
! Pre-test: ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
! Intra-test: position : RIGHT lateral to facilitate salivary drainage and easy access
! Post-test:
! NPO until the gag reflex return
! Sims position until the client awakens.
! Monitor for signs of perforation (bleeding, pain, unusual difficulty swallowing , elevated temp.
! Maintain bedrest for the sedated client until alert.
! Lozenges, saline gargles, or oral analgesics can relieve minor sore throat , after the gag reflex returns.
Lower GI- scopy
! Use of endoscope to visualize the anus, rectum, sigmoid and colon
! Pre-test: consent, clear liquid diet at noon before the test, NPO 8 hours, cleansing enema until return is clear
!
!
!
Lower GI- scopy

Intra-test: position is LEFT lateral, right leg is bent and placed anteriorly
Post-test: bed rest, monitor for complications like bleeding and perforation
Cholecystography
! Examination of the gallbladder to detect stones, its ability to concentrate, store and release the bile
! Pre-test: ensure consent, ask allergies to iodine, seafood and dyes; contrast medium is administered the night prior,
NPO after contrast administration
!
!
Post-test: Advise that dysuria is common as the dye is excreted in the urine, resume normal activities.
A normal diet may be resumed( fatty meal may enhance excretion of the contrast agent.)

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Paracentesis
Removal of peritoneal fluid for analysis & for the relief of difficulty of breathing (ascitis)
Pre-test: ensure consent, instruct to VOID and empty bladder, measure abdominal girth
Intra-test: Upright on the edge of the bed, back supported and feet resting on a foot stool
POSTPROCEDURE:
1. MONITOR THE VS
2. MEASURE ABDOMINAL GIRTH & WEIGHT
3. MONITOR FOR HYPOVOLEMIA, ELECTROLYTE LOSS, MENTAL STAUS CHANGES & ENCEPHALOPATHY
4. MONITOR FOR HEMATURIA CAUSED BY BLADDER TRAUMA.
5. EVALUATE EFFECTIVENESS BY: ABDOMINAL GIRTH, WEIGHT, RESPIRATORY RATE.
Liver biopsy
Pretest: Consent, NPO, Check for the bleeding parameters (platelet count, PT, PTT)
Intratest Position: Semi fowlers LEFT lateral to expose right side of abdomen or supine.
Post-test: position on RIGHT lateral with pillow underneath, monitor VS and complications like bleeding, perforation.
Instruct to avoid lifting objects for 1 week
CONSTIPATION- An abnormal infrequency and irregularity of defecation

Pathophysiology
Interference with three functions of the colon
1. Mucosal transport
2. Myoelectric activity
3. Process of
of defecation
1. Assist physician in treating the underlying cause of constipation
2. Encourage to eat HIGH fiber diet to increase the bulk
3. Increase fluid intake
4. Administer prescribed laxatives, stool softeners
5. Assist in relieving stress
DIARRHEA- Abnormal fluidity of the stool excessively frequent passage of stools
Multiple causes
Gastrointestinal Diseases
Hyperthyroidism
Food poisoning
Drugs
Food intolerance
Infectious organisms
1. Increase fluid intake- ORESOL is the most important treatment! (water is not sufficient)
2. Determine and manage the cause (antibiotics if bacteria is the cause)
3. Anti-diarrheal drugs ( not initially used if bacteria is the cause)

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4. Avoid carbonated, caffeinated, and high-sugar drinks (osmotic pull) increases diarrhea ---NCLEX
5. Diet should progress, as tolerated. As the symptoms begin to subside, bland foods (cream soups, crackers, toast, rice,
yogurt, custards) can be introduced into the diet. Spicy foods, dairy products, vegetables, fruits, high-sugar foods, and
alcohol should be avoided for the first 2 to 3 days
6. Check VS, Monitor for shock due to dehydration.
DUMPING SYNDROME
A condition of rapid emptying of the gastric contents into the small intestine usually after a gastric surgery
Symptoms occur 30 minutes after eating
ASSESSMENT FINDINGS: early symptoms
1. Nausea and Vomiting
2. Abdominal fullness
3. Abdominal cramping
4. Palpitation
5. Diaphoresis
6. Drowsiness
7. Weakness and Dizziness
8. Hypoglycemia
DOS NURSING INTERVENTIONS
1. Advise patient to eat LOW-carbohydrate HIGH-fat and HIGH-protein diet
2. Instruct to eat SMALL frequent meals, include MORE dry items.
3. Instruct to AVOID consuming FLUIDS with meals
4. Administer anti-spasmodic medications to delay gastric emptying
PERNICIOUS ANEMIA
Results from Deficiency of vitamin B12 due to autoimmune destruction of the parietal cells, lack of INTRINSIC
FACTOR or total removal of the stomach
PERNICIOUS ANEMIA ASSESSMENT
Signs and Symptoms
Severe pallor
Fatigue
Weight loss
SMOOTH BEEFY-RED TONGUE
Mild jaundice
Paresthesia of extremities
Balance disturbance
Diagnostic test:
Schillings test:
test: measures the absorption of radioactive vitB12 both before & after parenteral administration of intrinsic
factor.
Fasting client is given radioactive vit B12 by mouth & non radioactive vit B12 IM to saturate tissue binding sites & to permit
some excretion of radioactive vitamin B12 in the urine if it is absorbed.
24 hour urine collection is obtained.
8%-40% is excreted in 24 hours is normal.
More than 40% indicates pernicious anemia.
NURSING INTERVENTION for Pernicious Anemia Lifetime injection of Vitamin B 12 weekly initially, then MONTHLY
Check up twice a year is recommended. Why? Prone to gastric cancer
STOMATITIS

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Stomatitis is an inflammation of the mucous membranes of the mouth, involving the cheeks, gums, tongue, lips, and roof or
floor of the mouth, and affecting all age groups. The two primary types of stomatitis are aphthous (also called a canker
sore) and herpes simplex virus type 1 (also called a cold sore).
CAUSES
TRAUMA TO MUCOUS MEMBRANES
IRRITATION
HERPES SIMPLEX VIRUS
Signs and symptoms
PAIN
ULCERATIONS, LESIONS
SWOLLEN LYMPH NODES
TREATMENT:
1. Practice good oral hygiene.
2. Appropriate dental care. ( soft bristled toothbrush, toothettes, poorly fitting dentures should be corrected.)
3. Avoid irritating beverages & spicy foods. Avoid hot food & drinks. No to tortilla chips & nuts.
4. Topical anesthetics can be used to decrease pain. ( lidocaine mouthwash.)
5. Oral meds may be prescribed: acyclovir ( herpes), tetracycline, corticosteriods, Nystatin ( fungal)
HIATAL HERNIA
Portion of your stomach herniates to the weakened esophageal hiatus of your diaphragm.
Two types- Sliding hiatal hernia
( most common) and Axial hiatal hernia
CAUSES
MALFORMATIONS
MUSCLE WEAKNESS OF THE ESOPHAGEAL HIATUS
ESOPHAGEAL SHORTENING
OBESITY
ASSESSMENT Findings in Hiatal hernia
1. Heartburn
2. Regurgitation
3. Dysphagia
4. 50%- without symptoms
DIAGNOSTIC TEST
Barium swallow and fluoroscopy
1. Provide small frequent feedings (bland)
2. AVOID supine position for 1 hour after eating
3. Elevate the head of the bed on 8-inch block
4. Provide pre-op and post-op care
5. Avoid carbonated beverages & anticholinergic drugs.- CBQ
6. Avoid heavy lifting- CBQ
7. Avoid tight constricted clothing.- CBQ
8. Importance of treating persistent cough.
9. Adherence to weight reduction plan.
Esophageal Varices
Dilation and tortuosity of the submucosal veins in the distal esophagus
ETIOLOGY: commonly caused by PORTAL hypertension secondary to liver cirrhosis
This is an Emergency condition!

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ASSESSMENT findings for EV

1. Hematemesis
2. Melena
3. Ascites
4. jaundice
5.hepatomegaly/splenomegaly
DIAGNOSTIC PROCEDURE: Esophagoscopy
NURSING INTERVENTIONS FOR EV
1. Monitor VS strictly. Note for signs of shock
2. Monitor for LOC
3. Maintain NPO
4. Monitor blood studies
5. Administer O2
6. prepare for blood transfusion
7. prepare to administer Vasopressin and Nitroglycerin
8. Assist in NGT and Sengstaken-Blakemore tube insertion for balloon tamponade
9. Prepare to assist in surgical management:
Endoscopic sclerotherapy
Variceal ligation
Shunt procedures
PEPTIC ULCER DISEASE
! An ulceration of the gastric and duodenal lining
! May be referred as to location as Gastric ulcer in the stomach, or Duodenal ulcer in the duodenum
! Most common Peptic ulceration: anterior part of the upper duodenum
GASTRIC ULCER
Ulceration of the gastric mucosa, submucosa and rarely the muscularis
Risk factors:
Stress,
smoking,
NSAIDS abuse,
Alcohol,
Helicobacter pylori infection,
type A personality
History of gastritis
Incidence is high in older adults
Acid secretion is NORMAL
ASSESSMENT (Gastric Ulcer)
Epigastric pain
Characteristic: Gnawing, sharp pain in the mid-epigastrium 1-2 hours AFTER eating, often NOT RELIEVED by food intake,
sometimes AGGRAVATING the pain!
ASSESSMENT (Gastric Ulcer)
Nausea
Vomiting is more common
Hematemesis
Weight loss
DIAGNOSTIC PROCEDURES

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1. EGD to visualize the ulceration

2. Urea breath test for H. pylori infection
Avoid antibiotics for 1 month
Avoid sucralfate, omeprazole 1 week before the test -CBQ
3. Biopsy- to rule out gastric cancer
1. Give DAT / BLANDdiet, small frequent meals during the active phase of the disease-CBQ
2. Administer prescribed medications- H2 blockers, PPI, mucosal barrier protectants and antacids
3. Monitor for complications of bleeding, perforation and intractable pain
4. provide teaching about stress reduction and relaxation techniques
5. Avoid acid producing substances ( caffeine, alcohol, highly seasoned foods, spicy foods ( irritant).)
6. Plan for rest periods after mealtime.
DUODENAL ULCER
Ulceration of duodenal mucosa and submucosa
Usually due to increased gastric acidity
DUODENAL ULCER ASSESSMENT
PAIN characteristic:
Burning pain in the mid-epigastrium 2-4 HOURS after eating or during the night, RELIEVED by food intake
DIAGNOSTIC TESTS
EGD and Biopsy
1. Same as for gastric ulceration
2. Patient teaching-avoid alcohol, smoking, caffeine and carbonated drinks
Take NSAIDS with meals
Adhere to medication regimen
CROHNS DISEASE
Also called Regional Enteritis
An inflammatory disease of the GIT affecting usually the small intestine
ETIOLOGY: unknown
The terminal ileum thickens, with scarring, ulcerations, abscess formation and narrowing of the lumen
ASSESSMENT findings for CD
1. Fever
2. Abdominal distention
3. Diarrhea
4. Colicky abdominal pain
5. Anorexia/N/V
6. Weight loss
7. Anemia
ULCERATIVE COLITIS
Ulcerative and inflammatory condition of the GIT usually affecting the large intestine
The colon becomes edematous and develops bleeding ulcerations
Scarring develops overtime with impaired water absorption and loss of elasticity
ASSESSMENT findings for UC
1. Anorexia
2. Weight loss
3. Fever

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4. SEVERE diarrhea with Rectal bleeding

5. Anemia
6. Dehydration
7. Abdominal pain and cramping
NURSING INTERVENTIONS for CD and UC
1. Maintain NPO during the active phase
2. Monitor for complications like severe bleeding, dehydration, electrolyte imbalance
3. Weigh daily, record the number & characteristics of stools daily.
4. Monitor bowel sounds, stool and blood studies
5. Restrict activities, promote rest, good perineal care with frequent washing & adequate drying after each bowel
movement.
6. Administer IVF, electrolytes and TPN if prescribed
7. Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and
vegetables especially SPINACH, pepper, alcohol and caffeine-----LOCAL ALERT!!
8. Diet progression- clear liquid% LOW residue, high protein diet
9. Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/iron supplements
APPENDICITIS
! Inflammation of the vermiform appendix
! ETIOLOGY: usually fecalith, lymphoid hyperplasia, foreign body and helminthic obstruction
ASSESSMENT FINDINGS for Appendicitis
1. Abdominal pain: begins in the umbilicus then localizes in the RLQ (Mc Burneys point)
2. Right side lying with left hip flex ( psoas sign)
3. Rovsing sign-palpation on the LLQ can paradoxically have pain on RLQ
4. Fever, anorexia, N/V
5. Rebound tenderness and abdominal rigidity (if perforated)
6. Constipation or diarrhea
1. Preoperative care
Monitor bowel sounds, fever and hydration status
POSITION of Comfort: RIGHT SIDELYING in a low FOWLERS

Avoid Laxatives, enemas & HEAT APPLICATION LOCAL ALERT!!!
2. Post-operative care
Monitor VS and signs of surgical complications
Maintain NPO until bowel function returns
If rupture occurred, expect drains and IV antibiotics
2. Post-operative care
POSITION post-op: RIGHT side-lying, semifowlers to decrease tension on incision, and legs flexed to promote drainage
Administer prescribed pain medications
HEMORRHOIDS
Congestion & dilation of the veins of the rectum & anus; usually result from impairment of flow of blood through
the venous plexus.
May be internal ( above the anal sphincter) or external ( outside the anal sphincter)
Most commonly occur between ages 20-50
Predisposing factors:
Occupation that requires prolonged standing
Increased intra-abdominal pressure or caused by prolonged constipation such as: pregnancy, heavy lifting, obesity, straining
at defecation, portal hypertension
Internal hemorrhoids
! These dilated veins lie above the internal anal sphincter

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!
!
!
!
Usually, the condition is PAINLESS

External hemorrhoids
These dilated veins lie below the internal anal sphincter
Usually, the condition is PAINFUL
ASSESSMENT findings for Hemorrhoids

1. Internal hemorrhoids- cannot be seen on the peri-anal area
2. External hemorrhoids- can be seen
3. Bright red bleeding with each defecation
4. Rectal/ perianal pain
5. Rectal itching
6. Constipation
DIAGNOSTIC TEST
1. Anoscopy
2. Digital rectal examination
1. Advise patient to apply cold packs to the anal/rectal area followed by a SITZ bath
2. Apply astringent like witch hazel soaks
3. Encourage HIGH-fiber diet and fluids (no to nuts, coffee, spicy foods)IRRITATING!!!--- CGFNS!
4. Administer stool softener as prescribed
Post-operative care for hemorrhoidectomy
1. Maintain dressing over the surgical site
2. Monitor for bleeding
3. Administer analgesics and stool softeners
4. Advise the use of SITZ bath 3-4 times a day
5. limit sitting to short periods of time
DIVERTICULOSIS AND DIVERTICULITIS

! Diverticulosis
! Abnormal out-pouching of the intestinal mucosa occurring in any part of the LI most commonly in the sigmoid
! Diverticulitis
! Inflammation of the diverticulosis
ASSESSMENT findings for D/D
1. Left lower Quadrant pain
2. Flatulence
3. Bleeding per rectum
4. nausea and vomiting
5. Fever
6. Palpable, tender rectal mass
DIAGNOSTIC STUDIES
1. If no active inflammation, COLONOSCOPY and Barium Enema
2. CT scan is the procedure of choice!
3. Abdominal X-ray
BED REST DURING ACUTE PHASE
NPO/ CLEAR LIQUIDS DURING ACUTE PHASE

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AVOID LIFTING, STRAINING, COUGHING, BENDING--- to avoid increased intra-abdominal pressure

AVOID GAS FORMING FOODS, HIGH ROUGHAGE FOODS, SEEDS, NUTS
AVOID HIGH FIBER DURING INFLAMMATION
AVOID BARIUM ENEMA!!!
AVOID MORPHINE!!!! GIVE DEMEROL FOR PAIN
NO TO LAXATIVE!!!!!!!
Liver Cirrhosis
! A chronic, progressive disease characterized by a diffuse damage to the hepatic cells
! The liver heals with scarring, fibrosis and nodular regeneration
ETIOLOGY:
Post-infection, Alcohol, Cardiac diseases, Schisostoma, Biliary obstruction
Types:
Laennecs Cirrhosis- most common, alcoholic cirrhosis, scar tissue surrounds the portal area, chronic
chronic disease
Postnecrotic Cirrhosis-- a sequelae of viral hepatitis
Biliary Cirrhosis - due to chronic biliary obstruction and infection
Cardiac Cirrhosis due to right-sided heart failure
ASSESSMENT FINDINGS
1. Anorexia and weight loss
2. Jaundice
3. Fatigue
ASSESSMENT FINDINGS
4. Early morning nausea and vomiting
5. RUQ abdominal pain
6. Ascites
7. Signs of Portal hypertension
1. Monitor VS, I and O, Abdominal girth, weight, LOC and Bleeding
2. Promote rest. Elevated the head of the bed to minimize dyspnea
3. Provide Moderate to LOW-protein (1 g/kg/day) and LOW-sodium diet to prevent hep enceph
4. Provide supplemental vitamins (especially K) and minerals
5. Administer prescribed
Diuretics= to reduce ascites and edema
Lactulose= to reduce NH4 in the bowel
Antacids and Neomycin= to kill bacterial flora that cause NH production
6. Avoid hepatotoxic drugs
Paracetamol
Anti-tubercular drugs
7. Reduce the risk of injury
Side rails reorientation
Assistance in ambulation
Use of electric razor and soft-bristled toothbrush
8. Keep equipments ready including Sengstaken-Blakemore tube, IV fluids, Medications to treat hemorrhage
Cholelithiasis
Formation of GALLSTONES in the biliary apparatus
Predisposing FACTORS
F
Female

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Fat
Forty
Fertile
Fair
1. Maintain NPO in the active phase
2. Maintain NGT decompression
3. Administer prescribed medications to relieve pain. Usually Demerol (MEPERIDINE)
Codeine and Morphine may cause spasm of the Sphincter% increased pain. Morphine cause MORE PAIN
4. Instruct patient to AVOID HIGH- fat diet and GAS-forming foods
5. Assist in surgical and non-surgical measures
6. Surgical procedures- Cholecystectomy, Choledochotomy, laparoscopy
CONDITION OF THE GALLBLADDER
PHARMACOLOGIC THERAPY
Analgesic- Meperidine
Chenodeoxycholic acid= to dissolve the gallstones
Antacids
Anti-emetics
Post-operative nursing interventions
1. Monitor for surgical complications
2. Post-operative position after recovery from anesthesia- LOW FOWLERs
3. Encourage early ambulation
4. Administer medication before coughing and deep breathing exercises
5. Advise client to splint the abdomen to prevent discomfort during coughing
6. Administer analgesics, antiemetics, antacids
7. Care of the biliary drainageor T-tube drainage
8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed
Pancreatitis
Inflammation of the pancreas
Can be acute or chronic
Pancreatitis
Etiology and predisposing factors
Alcoholism
Hypercalcemia
Trauma
Hyperlipidemia
Etiology and predisposing factors
Biliary tract disease
- cholelithiasis
Bacterial disease
PUD
Mumps
ASSESSMENT findings
1. Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake
2. Abdominal guarding
3. Bruising on the umbilicus (cullen sign), Bruising on the flanks ( grey turners spots)---CGFNS!!!
4. N/V, jaundice

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5. Hypotension and hypovolemia

6. HYPERGLYCEMIA, HYPOCALCEMIA
7. Signs of shock
DIAGNOSTIC TESTS
1. Serum amylase and serum lipase
2. Ultrasound
3. WBC
4. Serum calcium
5. CT scan
6. Hemoglobin and hematocrit
1. Assist in pain management. Usually, Demerol is given. Morphine is AVOIDED CGFNS ALERT!!
2. Assist in correction of Fluid and Blood loss
3. Place patient on NPO to inhibit pancreatic stimulation ( NO ICE CHIPS & HARD CANDIES)---NCLEX!
4. NGT insertion to decompress distention and remove gastric secretions
5. Maintain on bed rest
7. Position patient in SEMI-FOWLERs to decrease pressure on the diaphragm
8. Deep breathing and coughing exercises
9. Provide parenteral nutrition
10. Introduce oral feedings gradually- HIGH carbo, LOW FAT
11. Maintain skin integrity
12. Manage shock and other complications
GENITOURINARY SYSTEM DISORDERS

MANAGEMENT OF PATIENT WITH URINARY DISORDERS
INFECTIONS OF THE URINARY TRACT ( Acute and Chronic )
Caused by pathologic microorganism (the normal urinary tract is sterile above the urethra)
Lower UTI (structure below the bladder)
Cystitis (inflammation of the bladder)
Prostitis (inflammation of the prostate gland)
Urethritis (inflammation of the urethra)
Upper UTI (ureters and kidney)
Pyelonephritis (inflammation of renal pelvis)
Interstitial nephritis (inflammation of kidney)
Renal abcess
Mechanism that maintain sterility of the bladder
Physical barrier of the urethra
Urine flow (downward)
Uretero vesical junction (prevents urine reflux)
Various antibacterial enzymes and antibodies

Anti-adherent effect mediated by mucosal cell of the bladder
PATHOPHYSIOLOGY OF LOWER URINARY TRACT INFECTION
Bacterial invasion
- Body Defense : shedding of bladder epithelial (remove bacteria)

- GAG (Glycosaminoglycan) hydrophilic protein exerts protective

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effect against bacteria.

- NORMAL BACTERIAL flora of vagina & urethra interferes with
adherence of e-coli
-IgA in urethra provides a barrier to bacteria
REFLUX
-due to obstruction to urine flow urethra to bladder (urethrovesical reflux)
- Body defense:
- Cough,sneeze, straining
-increase bladder pressure force urine from
bladder to urethra
BACTERURIA:
Define:
Bacteria normally present- urethral area
CAUSATIVE AGENTS
E. coli - 54.7%
Pseudomonas
Enterococcus
ROUTES OF INFECTION
1.Ascending (up the urethra)= transurethral (fecal contamination)
-sexual intercourse/ massaging of urethra forces the bacteria up in bladder
2.Hematogenous
3. Direct extension( (+) fistula from intestine)
CLINICAL MANIFESTATION
LOWER UTI: over 50% with bacteruria have no symptoms
- others: frequent pain & burning sensation on urination; urgency, increase in frequency,
nocturia,incontinence & suprapubic or pelvic pain, hematuria, backpain
UPPER UTI: fever, chills, flank and low back pain
Nausea and vomiting, painful urination
(+) tenderness @ cortovertebral angle (+)kidney punch
ASSESMENT AND DIAGNOSTIC FINDING
TEST: colony count
Cellular studies
Urine culture
*ACOG=recommend pregnant for bacteruria

( in pregnant state bladder does not
empty as it normally does)
COLONY COUNT: 10 to the 5th power CFU/ml urine

- clean catch midstream
- catheterization
- suprapubic needle aspiration
CELLULAR STUDIES:
Microscopic hematuria: greater than 4 RBC/ hpf
PYURIA: greater than 4 WBC/ hpf
URINE CULTURE
Recommended for all men and Diabetic with 3 episodes of UTI for the past year ,
Post-menopausal, Pregnant, women who are sexually active, have new partners

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And who undergo instrumentation ( catheterization)

TESTING METHODS
MULTISTRIP DIPSTICK testing for WBC
- leukocytes esterase test: ( (+) Patient has pyuria )
- nitrate testing (Griess nitrite reduction test)
(+) if nitrate is reduce to nitrite
Test or evaluation for STD
Intravenous Pyelography (IVP) for high risk and recurrent history of UTI
CT scan and Ultrasound
MEDICAL MANAGEMENT
-Pharma & Px education (infection prevention)
-CRANBERRY extract /juice
NURSING Dx
Deficient knowledge related to factor predisposing the patient to infection
Ex) Cancer, DM
NURSING INTERVENTION: Relieving pain
Management/ monitoring & managing potential complication (RF/ Sepsis)
Teaching patient self care = hygiene, fluid intake, voiding habit, complication
Recognition and management
UPPER URINARY TRACT INFECTION
PYELONEPHRITIS Bacterial invasion of the renal pelvis, tubules & interstitial tissue of one or both
Kidneys.
- Route of Infection: Ascending ( from urethra to the kidneys)
- causes: ureterovesical reflux
Urinary tract obstruction
Bladder tumors
Strictures (infant)
BPH
Stones
Acute Pyelonephritis
- kidney becomes enlarge with interstitial infiltration of inflammatory cell and abscess are
noted.
Chronic Pyelonephritis
- Scarred, contracted, non- functioning
CLINICAL MANIFISTATION
ACUTE: Patient appear ill and with chill, fever, pyuria, bacteruria, flank pain & CVA tenderness,
Dysuria, frequency in voiding
ASSESMENT AND DIAGNOSTIC FINDINGS
Ultrasound/ CT/ IVP
Urine culture
MEDICAL MANAGEMENT
Antibiotic ( TMP- SMZ ,CIFROFLOXACIN,LEVOFLOXACIN for 10 to 14 days
CHRONIC : Usually none unless in acute exacerbation
- fatigue/ poor appetite/ polyuria/ thirst/ weight loss
Persistence & recurrent infection---- progressive scarring of kidneys--- Renal Failure
ASSESSMEN T AND DIGNOSTIC FINDINGS
Intravenous Pyelography
Blood Urea Nitrogen and Creatinine

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COMPLICATIONS
-End Stage Renal Disease
- Hypertension , \formation of Kidney stones
MANAGEMENT
- Antimicrobial drugs, Teaching patient on bladder emptying, Perineal hygiene
ACUTE GLOMERULONEPHRITIS
- Inflammation of the glomerullar capillaries
- Primarily a disease of older children 2 years or at any age
CAUSATIVE AGENTS; Group A Beta Hemolytic Streptococcos infection of the throat
Infection of the skin Impetigo ( Staphylococcos). Viral, Mumps
Chickenpox, EVB virus, HepB, HIV/AIDS
CLINICAL MANIFESTATIONS:
-primary presenting features : hematuria (micro/gross, cola-colored urine)
Proteinuria
Increased BUN and creatinine as urine output decreased
Anemia
Edema
HPN( Hypertension)
Flank pain
ASSESSMENT & DIAGNOSTIC FINDINGS
-Elevated ASO titer: kidneys are swollen, enlarged & congested
COMPLICATIONS:
-Hypertensive encephalopathy, heart failure, pulmonary edema, End stage renal disease
MANAGEMENT:
-Treat symptoms, preserve kidney function, treat complications
-pharma
pharma drugs depend on causative agent : Penicillin for streptococcal infection
Steroids for inflammation & edema
Diuretics
Anti-hypertensive
Diet:
Diet Decrease dietary protein when BUN is elevated
Sodium restriction when with HPN, Edema & heart failure
CHRONIC GLUMERULONEPHRITIS
-Due to repeated episodes of AGN, hypertensive nephrosclerosis, hyperlipidemia, chronic
injury
-the kidney is reduced to as little as 1/5 of its normal size
tubulointerstitial
Signs and symptoms of renal insufficiency= periorbital edema
anemia
HPN
Retinal findings
Cardiopulmonary findings
ASSESSMENT & DIAGNOSTIC FINDINGS:
-Falling
Falling GFR below 50ml/min. (normal GFR= 100-200ml/min.)
-Hyperkalemia
Hyperkalemia due to decrease potassium excretion
-Metabolic
Metabolic acidosis due to decrease acid secretion of kidney
-Anemia
Anemia due to decrease erythropoeisis
-Hypoalbuminemia
Hypoalbuminemia with edema due to protein loss through the damaged glumerular membrane

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NEPHROTIC SYNDROMES
-Primarily a Glumerular disease characterized by:
Proteinuria (increased protein in urine)- markedly
Hypoalbuminimia
Edema
Hyperlipidemia (high serum cholesterol & low density lipoprotein)
CAUSE:
-Any intrinsic renal disease or systemic disease that affect glumerulus (DM)
-Generally considered a disease of childhood, may also occur at any age
-Causes includes CGN, DM, SLE
Edema (periorbital, sacrum, ankles,hand, ascitis)
Malaise
Headache
Irritability
DIAGNOSTIC FINDINGS:
Proteinuria greater than 3.5g/day
Increased WBC
COMPLICATIONS:
-Accelerated atherosclerosis due to hyperlipidemia
-infection due to deficient immune (proteinuria)
MEDICAL MANAGEMENT:
-The objective is to preserve renal function
-diuretics
-ACE inhibitor- reduce degree of proteinuria
-coticosteroids
-antineoplastic agents
Diet: protein 0.85/kg/day with emphasis on high biologic protein such as dairy products,
meats
Low in saturated fats
egg &
ACUTE RENAL FAILURE (ARF)

-sudden and almost complete loss of renal function over a period of hours to days
-manifested by oliguria (less
than 400ml/day)
(
Anuria (less than 50ml/day)
Rising BUN & creatinine
Retention of other metabolic waste (azotemia
azotemia)
azotemia
3 MAJOR CATEGORIES OR CONDITION CAUSING ARF
1.. PrePre-renal occurs as a result of impaired blood flow that leads to hypoperfussion of the kidney and a
drop of GFR. Ex. Gastrintestinal losses, vasodilation (shock,sepsis)
2. IntraIntra-renal occur in actual parenchymal damage to the glumeruli or kidney. Ex. Burns, crash injuries,
infection, nephrotoxic agents
acute tubularnecrosis----loss of kidney function
3. PostPost-renalrenal occurs from obstruction somewhere distal to the kidney.
4 PHASES OF ACUTE RENAL FAILURE
1.Initiation: begins with initial insults and ends with oliguria
2.Oliguria- period is accompanied by increase serum concentration usually
(Urea, BUN, creatinine, uric acid, k, magnesium , organic acid(< 400 ml)
3. diuresis- pt. gradually increases urine output (sign of GFR recovery)
4. recovery- takes 3-4 months ( witch result returns to normal)

excreted by
the kidney
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CLINICAL MANIFESTATIONS
Lethargy, appears very ill, nausea, vomiting, diarrhea , dry mucous membrane
Uremic factor , CNS s/sx
Management
Identify cause and damage--- treat accordingly
PHARMA: hyperkalemiatreated by cation exchange resin
( kayexalate)kayexalate work by exchanging Na to K in the GIT
(sorbitol)(sorbitol)- induce diarrhea type or water Loss effect
-- RETENTION ENEMA by rectal catheter (kayexalate)
CHRONIC RENAL FAILURE
(ESRD)- progressive, irreversible deterioration in renal function in which the kidney s ability to maintain fluid and
electrolyte falls results to uremia or acoismia (retention of urea and nitrogen waste product in the blood)
Cause: DM, GN, Hypertensive vascular disease, Polycystic kidney
Clinical Manifestations: CVD signs and symptoms, Dermatologic signs, GIT s/sx, CNS s/sx
Assessment: GFR. Electrolyte analysis, Anemia
Management; Pharmacologic
SURGERY: kidney transplant
Nrsg. MNGT: pre op/ intra-op, and during postoperative period
IMMUNOSUPRESSIVE TREATMENT
- the survival of transplanted kidney depends on the ability to BLOCK THE BODYS immune response for the transplanted
kidney and to overcome or minimize bodys defense mechanism, immunosuppresive agents such as,immuran, azathiopine,
cyclosporan are administered
OTHER URINARY SYSTEM DISORDER
UROLITHIASIS ( gravel,sand) bladder stone
--refer to stones (calculi) in urinary tract
--formed when urinary concentration of substances are increased ( due to stasis/obstruction/inability to excrete.
-- ( calcium oxalate, calcium phosphate, uric acid.
OTHER CONDITIONS: excessive intake of vit.D, milk and alkali, Hyperthyroidism, Calcium
CLINICAL MANIFESTATIONS: S/SX of obstruction, infection, edema (RF)
DIAGNOSIS: by X-ray of KUB or Ultrsound
MANAGEMENT: Pain mgt. (NSAID)= hot bath apply to the flank
Surgical: by cystoscopy and by ESWL.
URINARY TRACT CANCER
(Ca.of the Bladder) = predominant cause cigarette smoking.
=metastasis-colon, rectum
=50-70 yrs. Old
= painless visible hematuria, alteration in voiding
NEPROSCLEROSIS
= hardening or sclerosis of the arteries of the kidney due to prolonged Hypertension
= decreased blood flow---glumeruli destruction
URETHRITISinflammation of urethra --- ascending infection-- Gonoccocal or Non-gonoccocal Uritritis or due Sexually
transmitted disease
ASSESSMENT OF RENAL AND URINARY TRACT FUNCTION
Summarized and lecture by Dr. G. Flores
Urinary System Comprises: Kidneys, ureters, bladder and urethra
Structures of which precisely maintain the internal chemical environment of the body perform various
excretory, regulatory and secretory functions.

Page 198
KIDNEYS
Pain located retroperitoneally (behind and outside the peritoneal cavity) on the posterior wall of the
abdomen from 12th thoracic vertebrae to 3rd lumbar vertebrae (adult)
Wt. 120-170gram: right kidney lower the left
size : 12 X 6 X 2.5cm
protected by ribs, muscle, fascia, perirenal fat and renal capsule
Region:
o Parenchyma divided into:
' cortex contain the glomeruli tubules collecting ducts peritubular capillaries
' Medulla contain the pyramid which drain into calices renal pelvis
o Renal pelvis
Each contain about 1 million nephrons - cortical nephron (located at the cortex)
- juxtemedulla nephron (located at the medulla)
Glumerulus compose of three filtering layers:
1. Capillary endothelium filters fluid and small molecules, limit
passages of large molecules such as blood (RBC) and albumin
(protein)
2. Basement membrane
3. Epithelium
Function decreases at a rate of 1% each year by age 30 years old.
URETERS
- fibromuscular tube that connects kidney and bladder
- passage of urine
-24-30 cm long; originate to renal pelvis and ends in the bladder wall; left slightly shorter
Three narrowed areas in the ureter:
1. Uretero pelvic junction
2. Sacroiliac junction
3. Ureterovesical junction the angling provides antegrade or downward movement
- prevents vesicourethral reflux or retrograde, backward movement of urine
URINARY BLADDER
A muscular hollow sac behind the pubic bone (true pelvis)
Capacity (adult): 300-600mL
Has 2 inlets (ureters) and 1 outlet (urethrovesical junction)
4 layers of Urinary Bladder:
1. Adventitia (outermost)
2. Detrusor smooth muscle
3. Lamina propia (smooth muscle)
4. Urothelium (innermost) specialized transitional cell epithelium, containing a membrane that is
impermeable to water (prevent reabsorption of urine stored in bladder)
Bladder neck contain: portion of internal sphincter (involuntary smooth muscle) urethral sphincter and
external sphincter under voluntary control at the anterior urethral
URETHRA
Arises from the base of the bladder
Male: it passes to the penis
Female: it open just anterior to the vagina
In male the prostate gland which lies just below the bladder neck, surround the urethra posteriorly and laterally.
Function of the Urinary System
Urine Formation

Page 199
- urine is formed in the nephrons through a complex 3 steps process

Glomerular Filtration blood flow to kidneys 1200mL/min , normally 20% of blood passing through the
glomeruli are filtered into the nephron
filtrate consist of water/electrolytes, small molecular substances ---amounting to about 180L/day
efficient filtration depends on adequate blood flow (Pressure, obstruction, Hypotension, decrease Oncotic
pressure)
2. Tubular reabsorption in tubular reabsorption, a substance moves free in the filtrate back to vasa recta in tubular
secretion, a substance moves from vasa recta into tubular filtrate.
3. Tubular secretion- substances move from the filtrate back to vasa recta
1.
Of the 180L/day (45 gallon) of filtrate that the kidney produce each day, 99% is reabsorb in the bloodstream
resulting to 1000-1100 urine each day
Reabsorption and secretion frequently involve passive and active transport and may require use of energy.
Filtrates in the collecting ducts become concentrated under the influence of ADH and becomes urine and enters the
renal pelvis.
Excretory of Waste Products

-major waste product of protein metabolism and urea 25-30g is produce and excreted daily all must be exacted
accumulate
- other waste eliminated / excreted: Creatinine, Phosphate, Sulfates
- Purine Metabolism : Uric Acid
- Excrete drug metabolites
REGULATION OF ELECTROLYTE EXCRETION
- Normal: Amount of energy excreted per day is exactly equal to the amount of ingested
- Example: Diet: 6-8 g/day of NaCl (salt) and Protein, Chlorides = Nearly all are excreted in urine
Water from the filtrate follows the reabsorbed sodium to maintain osmotic balance
If more Na is excreted than ingested = dehydration
If less Na is excreted than injected = fluid retention
The regulation of Na volume excreted depends on ALDOSTERONE, a hormone synthesized and released from the
Adrenal Cortex.
Increased Aldosterone in blood, less sodium excreted in urine (Increased Renal Reabsorption of Na)
The release of Aldosterone is under the control of ANGIOTENSIN II. Angiotensin II is controlled by RENIN, an
enzyme that is released from specialized cell in the kidney.
Ex, activating RAA in fall of pressure in renal arterioles such as HYPOTENSION, SHOCK, DEHYDRATION
Aldosterone causes the kidney to excrete potassium = retention is the life threatening effect of renal failure.
REGULATION OF ACID EXCRETION
! Sulphuric and Phosphoric acids are non-volatile. This cannot be eliminated by the lungs = excreted by kidney
accumulation result / lower blood pH (Acidic) and this inhibits cell functions
! Kidney excrete acid directly to urine until the urine pH reaches 4.5. utilize chemical buffers so that the pH will not
futher decrease (Phosphate ions, Amonia ammonium)
! Acids are excreted in bound forms =will not lower pH of urine
REGULATION OF WATER EXCRETION
Low intake = low urine
High fluid intake= large diluted urine
Example: person normally ingested 1.2L/day. All is excreted but 500ml in urine; other routes lung, feces
OSMOLALITY : the degree of dilution or concentration of urine
: the number of particles (electrify and other molecules) dissolved per kilogram of urine
Normal: 300milliosmo/L
Diluted urine: low osmolality
Concentrated : high osmolality
Test is valuable to determine kidneys ability to concentrate and dilute urine
SPECIFIC GRAVITY
! A measurement of kidneys ability to concentrate urine
! Compares the weight of (particles) urine to weight of distilled water which has a specific gravity of 1.000

Page 200
Normal Specific Gravity: 1.010 1.025 when fluid intake is normal

Specific Gravity increases when intake decreases; decreases specific gravity when intake increases
Example:
Disease cause to decrease specific gravity = Diabetes Insipidus, Glumerulonephritis, renal
failure
Disease cause to increase specific gravity = DM, nephrosis, excessive fluid loss (dehydration)
ANTI-DIURETIC HORMONE (VASOPRESSIN)
- regulate water excretion and urine concentration in the tubules
- secreted by posterior pituitary gland in response to change in osmolality of blood (same as urine)
Decrease water intake = increase blood osmolality = stimulates ADH release = increase reabsorption of water =
minimizes osmolality of blood
Increase water intake = decrease blood osmolality = suppress secretion or inhibits ADH = less water reabsorption
= diuresis (increase urine volume)
Early signs of kidney disease is its inability to dilute and concentrate urine.
AUTO REGULATION OF BLOOD PRESSURE
Vasa recta constantly monitor BP as blood begins its passage in the kidney
When BP decreases juxtaglomerular cells secrete rennin convert angiotensin (in liver) to angiotensin I = Angiotensin
II (powerful vasoconstriction) increase BP
o Failure of feedback mechanism = primary care of Hypertension ACE decrease BP stimulate secretes ,
aldosterone (Adrenal cortex) = increase BPdue to poor perfusion or increase osmolality
RENAL CLEARANCE
! Refers to the ability of the kidney to clear solute from plasma
! A 24hr collection is the primary test of the renal clearance use to evaluate how well the kidney perform the
excretory function
CREATININE CLEARANCE
! Endogeneous waste of skeletal muscle excreted in urine
! Good measure of the glomerular filtration rate (N:100-200mL/min)
! To calculate creatine clearance a 24hr urine specimens is collected
Formula:[ Volume of urine(mL/min) x urine creatine (mg/dL) ] / serum creatinine (mg/dL)
*midway through the collection serum creatinine is measured
REGULATION OF RBC PRODUCTION
! When kidney sense a decrease in oxygen tension in renal blood flow, they release erythropoietin = stimulate the
bone marrow to produce RBC = thereby increase the amount haemoglobin available to carry oxygen.
VITAMIN D SYNTHESIS
! Kidney are responsible for the final conversion of inactive Vit. D to its active form, 1.25-dihydroxycholecalciferon
! Vit. D is necessary for maintaining normal calcium balance in the body
SECRETION OF PROSTAGLADIN
! Kidney also produces PGE and prostacycline (PGI) which have vasodilator effect and are important in maintaining
renal blood flow
URINE STORAGE
! Bladder is the reservoir of urine
! In adult bladder filling and emptying is modified by conducted sympathetic and parasympathetic NS control
mechanism involving the destrusor muscle and bladder outlet
! In infants : mediated by micturation center in the pons area of the brain stem
! By 3-4yrs old : the cerebral cortex is mature enough to cause awareness of bladder filling
*stretch receptor in the bladder wall activate to cause desire to void
! First sensation of bladder fullness is transmitted to CNS when capacity reaches to 200-300mL in adult =mitral
desire to void
! Strong desire ; functional capacity = 300mL
;anatomic capacity 1000-1500mL when under anesthesia= pressure 60mmHg

Page 201
Can store urine 2-4hrs at a time during the day = 6-8hrs at night due to the release ADH (vasoregulator) due to
less intake = concentrated urine
BLADDER EMPTYING
! MICTURATION : Normal: approximately 8xaday
! Normal residual urine : less than 50mL (middle age adult)
50 100mL (older adult)
ASSESSMENT FOR GUT DYSFUNCTION
! Unexplained anemia, manifested by fatigue, SOB, exercise intolerance
! Pain due to obstructed urine flow, inflammation and swelling of tissue
! Changes in voiding, frequency, urgency, dysuria, hesitancy, incontinence, eneuresis, polyuria, oliguria, hematuria
! GIT symptoms: occur because of shared autonomic and sensory innervation
: Nausea/Vomiting/Diarrhea, abdominal pain/ discomfort/distention
PHYSICAL EXAMINATION
(Head-to-toe assessment)
Emphasis in abdomen, suprapubic region, genitalia, lower back and lower extremities
! Direct palpation of kidney: determines size and mobility
! Tenderness of the costovertebral angle
! Auscultation for bruits (low pitch murmurs that indicate renal artery stenosis or an aortic aneurism)
! Presence of peritoneal fluid
! Percussion of bladder and residual urine (from midline umbilicus downward)
! DRE for BPH (yearly exam to men greater than 50yrs old = PSH level
! Inguinal area palpated = (+) enlarged nodes/ hernia/ varicocoele
! Look/papate:: Urethrocoele (bulging of anterior vaginal wall into urethra)
: Cystocoele ( herniation of the bladder wall into vaginal vault)
: Pelvic prolapsed (Cervix bulging in the vaginal vault)
: Enterocoele (hernation bowel into the posterior vaginal wall)
: Rectocoele (herniation of rectum into the vaginal wall)
! Edema/ change in body weight (face independent part of the body, ankle, scrotum)
! 1kg increase= 1000mL of fluid retension
DIAGNOSTIC EXAMINATION
! Urinalysis (+) hematuria (+) pyuria, (+) bacteriuria
! Urine culture
! Renal function test: serum creatinine, BUN, creatinine clearance
! X-ray (KUB delinate size, shape, position of the kidney, abnormalities and calculi
! Ultrasound
! CT/MRI provide cross section views of kidney, urinary function
Example: nephrolithiasis,metastatic disease
! Nuclear scan use to evaluate acute renal function, renal masses, pre and post-renal transplant
! Urography, cystography
! Biopsy
DYSFUNCTIONS OF URINARY TRACT: Management
1.Urinary
Urinary Incontenence
a. Risk Factor: Pregnancy/vaginal delivery/ episiotomy
:stroke, age-related change in urinary tract, medication,diuretic,immobility,sedation
Management: anti cholinergic agent: Oxybutymin; Tx is according to the underlying
cause
Dicycloverine
Treatment : fluid management
Standard voiding frequency
:time and voiding
:habit retraining
:bladder retraining (drill)
:PME (Kegels exercise)

Page 202
2.. Neurogenic bladder

! a dysfunction that result from a lesion of NS
! cause by spinal cord injury, multiple sclerosis, congenital anomalies (spina bifida) myelomeningomyecoelo,
infection, DM,
! Patho: loss of conscious sensation and cerebral motor control bladder muscle does not contract
! Management: pharmacologic: urecholine increase force of contraction in the bladder
: surgical
:catheterization
DIALYSIS
Hemodialysis
Peritoneal Dialysis
! Acute dialysis
! Chronic dialysis / maintenance dialysis indicated for ESRD
- patient with no renal function can be maintained by dialysis for years
Hemodialysis (6-8hrs)
Used to: Patient acutely ill and require short term dialysis (days to weeks)
: Patient with ESRD to require long term and maintenance therapy
Dialyzer: (artificial kidney) serves as synthetic semi-permeable membrane, replacing the glomeruli and tubules
PRINCIPLE OF HEMODIALYSIS
! Objective: to extract toxic nitrogeneous substances from blood and to remove excess fluid (water)
! Diffusion, osmosis, ultrafiltration
ultrafiltration are the principle in which hemodialysis is base.
! Diffusion movement of solute from area of high concentration to low concentration in the dialysate
! Toxins of waste in the blood is remove by diffusion
(dialysate is a solution is made by of all important electrolyte on the ideal extracellular concentration)
! Osmosis excess water is remove by osmosis in which the water move from area of higher concentration to an
area (blood) to an area of lower solute concentration ( the dialysate bath)
! Ultrafiltration define as water moving under high pressure to an area of low pressure
Peritoneal Dialysis (36-48hrs)
! Principles : the peritoneum as the semi-permeable membrane
: dialysate fluid is introduce into the abdominal cavity by catheter
: waste (urea/creatinine) are cleared by diffusion and osmosis
high concentration (peritoneal blood supply) across the semi-permeable membrane(peritoneum) =
peritoneal cavity
: ultrafiltration (removal of water) is through osmotic gradient created by using a dialysate fluid with a
higher glucose concentration
COMPLICATION OF PERITONEAL DIALYSIS
1. Peritonitis
2. Bleeding
3. Leakage
4. Low term : hypertriglycerimia, abdominal hernia
NURSING MANAGEMENT
! Directed on financial job related, waning sexual desire and impotency, depression from being clinically ill, fear of
dying, burden to family
! Meeting psychosocial needs
o Expression of feeling
o Counselling
o Referral to specialist
o Help in effective coping

Page 203

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