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CIRCULATORY

SYSTEM
Review of Ana-Phy
FUNCTIONS
– Primary function: transportation of hormones,
nutrients, wastes, respiratory gases, vitamins,
minerals, enzymes, water, leukocytes, antibodies,
and buffers
MEDICAL-SURGICAL
NURSING

Prepared by:
Cherry Ann G. Garcia, RN

• Secondary function: contributes directly


Structures
of the
Circulatory System
BLOOD VESSELS

BLOOD

HEART
HEART
Functions:
Pumps blood throughout the
body
Routes blood
Ensures one-way blood flow
Regulates blood supply
HEART
 Location: in mediastinum
 Structure:
Pericardium – covering of the heart
Heart wall: myocardium – cardiac
muscle cells; endocardium –
endothelial inner lining
4 Cavities: Left and Right Atria; Left
and Right Ventricles
Valves: Tricuspid valve, Mitral valve,
Aortic valve, Pulmonic Valve
HEART
Arrange the following to form the correct path of the blood
through different organs starting with the superior and
inferior vena cava
SUPERIOR
VENA CAVA

INFERIOR
VENA CAVA
HEART
BLOOD CIRCULATION
SUPERIOR
VENA CAVA RIGHT TRICUSPID RIGHT
INFERIOR ATRIUM VALVE VENTRICLE
VENA CAVA

PULMONARY PULMONIC
LUNGS VALVE
PULMONARY ARTERY
VEIN

LEFT MITRAL LEFT AORTIC


ATRIUM VALVE VENTRICLE VALVE

SYSTEMIC AORTA
CIRCULATION
Memory Tip

TRIGHT
 Tricuspid on the Right

MITRALEFT
 Mitral on the Left
Conduction System of
the Heart
INTERNODAL
SA NODE PATHWAY
AV NODE

RIGHT AND BUNDLE


PURKINJE LEFT OF HIS
FIBERS BUNDLE
BRANCHES

Pathway of Depolarization
BLOOD
Plasma Formed Elements
Liquid/ Water portion of A. ERYTHROCYTES – red blood
the blood cells; lives for 120 days
principal component:
HEMOGLOBIN – O2 carrier of
ALBUMIN – major the blood
plasma protein
B. LEUKOCYTES – white blood
cells
- antibody synthesis
- phagocytosis
C. THROMBOCYTES – platelets
- blood coagulation
BLOOD VESSELS
• Transport system of the circulatory
system
• 3 major types:
Arteries
Veins
Capillaries

Comparison of the 3 types of blood vessels


MAJOR DISORDERS
OF THE
CIRCULATORY
SYSTEM
Hypertension
DEFINITION

A common disorder characterized by


sustained elevation of blood pressure;
exists when BP is greater than or equal
to 140/90 mm Hg
Hypertension
PATHOPHYSIO CLINICAL FINDINGS

 Increased renin release  Headache, light-headedness,


tinnitus, easy fatigability, visual
 Increased blood
disturbances, palpitations
volume
 BP greater than 140/90mmHg
 Increased peripheral
obtained on 3 separate
vascular resistance
occasions, retinal changes,
epistaxis, cardiac hypertrophy
Hypertension
RISK FACTORS INTERVENTION
 F – family history
 A – age  Lifestyle modification
 S – stress; sedentary
living
 H – hyperlipidemia
 I – increased blood
volume
 O - obesity
 N - nutrition
ISCHEMIC HEART DISEASES
ATHEROSCLEROSIS

Deposition of fatty plaques and fibrous


tissue along inner wall of coronary arteries
that leads to inflammation, narrowing and
possible obstruction
Atherosclerotic Plaque
Formation
– Narrowing of lumen
• plaque formation -
related to Risk Factors
• results in decreased
myocardial perfusion
– Poor tissue perfusion
causes:
– tissue damage
(ischemia)
– tissue death
(infarction)
ISCHEMIC HEART DISEASES
ARTERIOSCLEROSIS

Endothelial lining of blood vessels are


damaged causing the thickening of the
walls
ISCHEMIC HEART DISEASES

ANGINA PECTORIS

Episodic pain experienced when


oxygen supplied by the blood
cannot meet the metabolic
demands of the muscle
Angina Pectoris
“Choking in the chest”

• Angere - to choke
• Myocardial oxygen
demand exceeds
supply during
periods of increased
activity, exercise,
or stressful event
Angina Pectoris
• During stress, the
myocardium demands
more O2
• Coronary arteries
would normally
dilate to supply
more blood and O2
• In Angina Pectoris,
the coronary
arteries are unable
to dilate
sufficiently to
increase perfusion
Symptoms -Angina Pectoris

• Pain usually associated with


3E’s
– Exercise
– Eating
– Emotion
Symptoms -Angina Pectoris

• Great anxiety/Fear
• Fixation of the body
• Pale, ashen, or livid face
• Dyspnea (SOB) may be
associated
Symptoms -Angina Pectoris

• Nausea
• Diaphoresis
• BP usually up during
attack
• Dysrhythmia may be
present
Forms of Angina Pectoris

• Stable Angina
– Occurs with exercise
– Predictable
– Relieved by rest or
Nitroglycerin
Forms of Angina Pectoris

• Unstable Angina
– More frequent/severe
– Can occur during rest
– May indicate impending MI
– Requires immediate
treatment and transport
to appropriate facility
PAIN ASSESSMENT

(PQRST)
P – Position/Provocation
Q – Quality/Quantity
R – Radiation/Relief
S – Severity/Symptoms
T – Timing
ISCHEMIC HEART DISEASES
MYOCARDIAL INFARCTION

Acute necrosis of the heart muscles


caused by interruption of oxygen supply to
the area (ischemia), resulting in altered
function and decreased cardiac output
Acute Myocardial Infarction
“Heart Attack”

Inadequate perfusion
of myocardium

– Death of myocardium
•Infarct
– Damage to myocardium
•Ischemia
Acute Myocardial Infarction
CLINICAL FINDINGS

 For MI:
 Increased Cardiac troponin T within 21 days
 Elevated CPK-MB for 4-6 hrs after pain, peak at
24 hours and goes back to normal after 72 hours
 Elevated myoglobin for 1-3 hrs and goes back to
normal after 12 hours
 ECG: presence of Q wave
 Elevated temperature and WBC
ISCHEMIC HEART DISEASES
INTERVENTIONS
 Angina:
 Nitroglycerin
 O2
 Pulse oximeter
 Vital signs monitoring
 MI:
 ASA administration on the way to the hospital
 Analgesics: morphine sulfate
 O2
 Thrombolytic therapy within 6 hours of MI; anticoagulants
 Cardiac monitoring
 NPO on the first 24 hours
 Complete bed rest
Acquired Valvular Disorders

The valves of the heart control the flow


of blood through the heart into the
pulmonary artery and aorta by
opening and closing in response to
the blood pressure changes as the
heart contracts and relaxes through
the cardiac cycle.
MITRAL VALVE PROLAPSE

• A portion of a mitral valve leaflet


balloons back into the atrium during
systole
• Ballooning stretches the leaflet to the
point that the valve does not remain
closed during systole (ie, ventricular
contraction).
• Blood then regurgitates from the left
ventricle back into the left atrium
MITRAL REGURGITATION

• Blood regurgitates back into the LEFT


atrium during systole.

• With each beat of the left ventricle,


some of the blood is forced back into
the left atrium. Because this blood is
added to the blood that is beginning
to flow in from the lungs, the left
atrium must stretch. It eventually
hypertrophies and dilates.
MITRAL REGURGITATION
• The backward flow of blood from the
ventricle diminishes the volume of blood
flowing into the atrium from the lungs.

• As a result, the lungs become


congested, eventually adding extra strain
on the right ventricle. Mitral regurgitation
ultimately involves the lungs and the right
ventricle.
MITRAL STENOSIS
• Obstruction of blood flowing from the
left atrium into the left ventricle.

• Most often caused by rheumatic


endocarditis, which progressively
thickens the mitral valve leaflets
causing them to fuse together.
• Eventually, the mitral valve orifice
narrows and progressively obstructs
blood flow into the ventricle.
AORTIC REGURGITATION

• Aortic regurgitation is the flow of


blood back into the left ventricle from
the aorta during diastole.

• It may be caused by inflammatory


lesions that deform the leaflets of the
aortic valve, preventing them from
completely closing the aortic valve
orifice.
AORTIC STENOSIS
• Narrowing of the orifice between the
left ventricle and the aorta.
• The stenosis may involve congenital
leaflet malformations or an abnormal
number of leaflets (ie, one or two
rather than three), or it may result
from rheumatic endocarditis or cusp
calcification of unknown cause.
• The leaflets of the aortic valve may
fuse.
Can valvular diseases lead to
heart failure?

HOW?
Acquired Valvular Disorders

INTERVENTIONS

• Valvuloplasty – repair of valves

• Commissurotomy – surgical
opening to separate the leaflets
Inflammatory Diseases of the
Heart
PERICARDITIS

Acute or chronic inflammation of the


pericardium that can cause loss of
pericardial elasticity, build up of fluid within
the sac, heart failure, or cardiac
tamponade
Inflammatory Diseases of the
Heart
MYOCARDITIS

Inflammation of the myocardium that can


cause impaired contractility of the heart,
myocardial ischemia or necrosis
Inflammatory Diseases of the
Heart
INFECTIVE ENDOCARDITIS

Inflammation of the inner lining of the heart


and valves that can cause structural
damage to the valves, pump failure or
embolization
Inflammatory Diseases of the
Heart
CLINICAL FINDINGS INTERVENTIONS

 Precordial or substernal  P – pericardectomy –


pain; dyspnea, chills, surgical removal of the
fatigue, and malaise scar tissues in the
 Dysrhythmias, increased pericardium
cardiac enzyme, fever,  A – antibiotics for
positive blood cultures, underlying infection
friction rubs on  C – cardiac monitoring
auscultation  O – oxygen therapy and
bed rest
Congestive Heart Failure
Congestive Heart Failure

DEFINITION

Inability of the heart to meet the oxygen


demands of the body that can be caused by
cardiac abnormalities or activities that
increases the demand to the heart
Congestive Heart Failure

Causes of CHF:
 Coronary Artery Disease
 Chronic hypertension (high blood
pressure)
 AMI
 Valvular heart disease
Congestive Heart Failure
 Usually begins with left-sided failure.
– Left ventricle fails
– Blood “stacks up” in lungs
– High pressure in capillary beds
– Fluid forced out of capillaries into alveoli
Congestive Heart Failure
 Right-sided failure most commonly
caused by Left-sided failure. Blood
“backs up” into systemic circulation
– Distended neck veins
– Fluid in abdominal cavity
– Pedal edema
HEART FAILURE
LEFT-SIDED HF RIGHT-SIDED HF
(PULMONARY) (CIRCULATORY
CONGESTION)
 Crackles, Cheyne-  Bloating
Stokes respiration  Pitting edema
 Orthopnea  Ascites
 Paroxysmal nocturnal  Jugular vein distention
dyspnea  Ankle edema (1st sign of
 Frothy, blood-tinged RHF)
sputum  Hepatomegaly
 Cyanosis
HEART FAILURE

INTERVENTIONS
(ADD 02)
 Assume semi-recumbent position
 Daily weight, abdominal girth, intake and
output and V/S monitoring; diuretics therapy
 Decrease cardiac workload; Digoxin
 O2 therapy
Vascular Diseases

• Involves both arteries and veins


• Includes: Buerger’s disease,
Raynaud’s, Thrombophlebitis, DVT,
and Varicose Veins
Vascular Diseases
Signs and Symptoms
Vascular Diseases
BUERGER’S DISEASE

 Thromboangiitis Obliterans
 Impairment in the peripheral circulation
due to inflammatory occlusions of the
arteries
 Occurs in male smokers
Vascular Diseases
RAYNAUD’S DISEASE

 Spasm of digital arteries caused by


abnormal response of the sympathetic
nervous system to cold or emotional stress
 Occurs in young females
Vascular Diseases

THROMBOPHLEBITIS

 Clot in the vein with inflammation of the walls of


the vein manifested by unilateral leg edema with
positive Homan’s sign
 Called DEEP VEIN THROMBOSIS if the clot
formation happened deeper in the veins
Deep Vein Thrombosis

Etiology and Pathophysiology


Virchow’s triad

Venous stasis

↑Blood coagulation Damage to vein


Deep Vein Thrombosis
Risk Factors
■ ↑Age, obesity, immobility, oral contraceptives
■ Varicose veins, popliteal pressure, fractures
Signs and Symptoms
■ Edema, ache, calf pain on foot dorsiflexion
(Homan’s sign)
■ ↑P, dyspnea, chest pain if thrombus dislodges →
pulmonary embolism
Deep Vein Thrombosis
Treatment
■ Meds: Thrombolytic, anticoagulants
■ Thrombectomy, insertion of vena cava filter to
prevent PE
Nursing
■ Prevention: Antiembolism stockings, sequential
compression device, exercise, ↑fluids;
prophylactic anticoagulant
■ Acute phase: BR, ↑extremity, warm soaks if
ordered
Vascular Diseases
Vascular Diseases
VARICOSE VEINS

 Occurs when veins in the lower extremities


become dilated, congested and tortuous
as a result of weakness of valves or loss
of elasticity of the vessel walls
Vascular Diseases
INTERVENTION INTERVENTION
(RAYNAUD’S & (VARICOSE VEINS)
BUERGER’S)
 SCLEROTHERAPY –
 Advise client to stop injecting a chemical
smoking irritant into the vein
 Sympathectomy  Ligation of the vein above
 Limb amputation if the varicosity
severely impaired  Avoid crossing legs;
 Avoid cold weather prolonged standing or
sitting
Vascular Diseases
INTERVENTION
(THROMBOPHLEBITIS)

 Prophylactic antiembolytic stockings


 Moist heat as ordered to promote
vasodilation
 Anticoagulants to prevent recurrence
 Thrombolytics to dissolve clot
 No ambulation
ANEURYSMS

DEFINITION

Distention at the site of a weakness


in the arterial wall that can be
caused by trauma, atherosclerosis,
syphillis or congenital weakness
ANEURYSMS

Etiology and Pathophysiology


■ Weakness in vessel → protrusion
and possible rupture

Risk Factors
■ Atherosclerosis, trauma, congenital
weakness, infection, inflammation
■ HTN, smoking
Types of ANEURYSM

Dissecting Saccular
Aneurysm
False aneurysm aneurysm
Fusiform
Normal artery True aneurysm aneurysm
(A) Normal artery
(B) False aneurysm—actually a pulsating hematoma. The
clot and connective tissue are outside the arterial wall.
(C) True aneurysm. One, two, or all three layers of the artery
may be involved.
(D) Fusiform aneurysm—symmetric, spindle-shaped
expansion of entire circumference of involved vessel.
(E) Saccular aneurysm—a bulbous protrusion of one side of
the arterial wall.
(F) Dissecting aneurysm—this usually is a hematoma that
splits the layers of the arterial wall.
ANEURYSMS

Signs and Symptoms


■ May be symptom-free; may be able
to palpate a pulsating mass
■ Dissecting aneurysm: Sudden
severe chest pain extending to
back, shoulder, epigastrium,
abdomen; diaphoresis; ↑PR
ANEURYSMS
Treatment
■ Confirm diagnosis with CT, MRI, sonogram
■ Repair with graft
■ ↓BP with antihypertensives to ↓risk of rupture
or extension
Nursing
■ Monitor BP, Hgb/Hct
■ Assess for sudden ↑pain (may signal impending
rupture)
■ Teach to avoid activities that ↑intra-abdominal
pressure (sneezing, coughing, vomiting,
straining at stool)
PERICARDIAL EFFUSION

 Refers to the accumulation of fluid in


the pericardial sac

 Normally, the pericardial sac contains


less than 50 mL of fluid, which is
needed to decrease friction for the
beating heart
PERICARDIAL EFFUSION
 Increase in pericardial fluid raises the
pressure within the pericardial sac and
compresses the heart.
 This has the following effects:
– Increased right and left ventricular end-
diastolic pressures
– Decreased venous return
– Inability of the ventricles to distend
adequately and to fill
PERICARDIAL EFFUSION
MANIFESTATIONS:
3 F’s
 Feeling of fullness/pressure within the chest
 Fluctuating BP
 Fully distended neck veins

* Pulsus paradoxus – systolic blood pressure


that is detected during exhalation but not heard
with inhalation
Cardiac Tamponade

DEFINITION

 Refers to the compression of the heart


 Caused by rapid accumulation of blood
in the pericardium or pericardial effusion
Cardiac Tamponade
Signs and Symptoms
Beck’s Triad
Increased central venous
pressure

Small quiet heart Hypotension


(decreased heart unresponsive to
sounds) treatment
Signs
And
Symptoms
Cardiac Tamponade

Management
• Secure airway
• High concentration O
2

• Rapid transport
• Definitive treatment:
• PERICARDIOCENTESIS
Types of Shock and Their Causes
Cardiogenic Shock
 Pump failure
 Heart’s output depends on
 How often it beats (heart rate)
 How hard it beats (contractility)

 Occurs when the heart cannot pump enough


blood to supply the amount of oxygen needed
by the tissues
Cardiogenic Shock
 Causes
 Acute myocardial infarction
 Very low heart rates (bradycardias)

 Very high heart rates (tachycardias)

Why would a high heart rate caused decreased output?

Hint: Think about when the heart fills.


Cardiogenic Shock Pathophysiology
Neurogenic Shock

 Loss of peripheral resistance


 Spinal cord injured
 Vessels below injury dilate

What happens to the pressure in a


closed system if you increase its size?
Hypovolemic Shock
 Loss of blood volume
 Causes
 Blood loss: trauma

 Plasma loss: burns

 Water loss: Vomiting, diarrhea, sweating, increased


urine, increased respiratory loss

If a system that is supposed to be closed


leaks, what happens to the pressure in it?
Psychogenic Shock

 Simple fainting (syncope)


 Caused by stress, pain, fright
 Heart rate slows, vessels dilate
 Brain becomes hypoperfused
 Loss of consciousness occurs

What two problems combine to produce


hypoperfusion in psychogenic shock?
Septic Shock
 Results from body’s response to bacteria in
bloodstream
 Vessels dilate, become “leaky”

What two problems combine to produce


hypoperfusion in septic shock?
Anaphylactic Shock
 Results from severe allergic reaction
 Body responds to allergen by releasing
histamine
 Histamine causes vessels to dilate and become
“leaky”

What two problems combine to produce


hypoperfusion in anaphylaxis?
Shock:
Signs and Symptoms
 Restlessness, anxiety  Nausea, vomiting
 Decreasing level of  Thirst
consciousness
 Diminished urine
 Dull eyes
output
 Rapid, shallow
respirations

Why are these signs and symptoms present?


Hint: Think hypoperfusion
Shock:
Signs and Symptoms

 Hypovolemia will cause  Neurogenic shock will


 Weak, rapid pulse cause:
 Weak, slow pulse
 Pale, cool, clammy skin
 Dry, flushed skin
 Cardiogenic shock may
cause:  Sepsis and
 Weak, rapid pulse or weak, anaphylaxis will
slow pulse cause:
 Weak, rapid pulse
 Pale, cool, clammy skin
 Dry, flushed skin
Shock:
Signs and Symptoms
 Patients with anaphylaxis will:
 Develop hives (urticaria)
 Itch

 Develop wheezing and difficulty breathing


(bronchospasm)

What chemical released from the body during an


allergic reaction accounts for these effects?
Shock:
Signs and Symptoms

Shock is NOT the same thing


as a low blood pressure!

A falling blood pressure


is a LATE sign of shock!
Treatment

 Secure, maintain airway


 Apply high concentration oxygen
 Assist ventilations as needed
 Keep patient supine
 Control obvious bleeding
 Stabilize fractures
 Prevent loss of body heat
Treatment

 Elevate lower extremities 8 to 12 inches in


hypovolemic shock
 Do NOT elevate the lower extremities in
cardiogenic shock

Why the difference in


management?
Hematologic
Disorders
Anemia
Types of Anemia: (FIPS)
• Folic acid Deficiency Anemia
• Iron Deficiency Anemia
• Pernicious Anemia
• Sickle cell Anemia
Folic Acid Deficiency Anemia
Main Problem:
Depletion of folate, which results to
progressive anemia. It occurs in:
• infants
• adolescents
• pregnant women
• lactating women
• alcoholics
Folic Acid Deficiency Anemia
Manifestations:
• Fatigue
• Weakness
• Pallor
• Light headedness
• Lack of appetite
• Difficulty in concentrating
• Cracked lips and smooth tongue
Folic Acid Deficiency Anemia
Interventions:
• Teach the client to increase sources of
folic acid in the diet like: (GOLFY)
• Green vegetables (asparagus,
broccoli and spinach)
• Organ meats
• Liver
• Fresh fruits (do not overcook foods)
• Yeast
Iron Deficiency Anemia

Main Problem:
• Decreased oxygen carrying capacity
of the blood. The condition is usually
associated with:
• nutritional deficiency of iron.
• increased milk intake in infants
• females
Iron Deficiency Anemia
Manifestations:
• Easy fatigability
• Poor sucking (infants)
• Chubby but pale babies (milk babies)
• Dyspnea on exertion
• Pallor
• Fatigue
• Irritability
• Tachycardia
• Spoon shaped, brittle nails
Iron Deficiency Anemia
Interventions:
• Instruct the client to have frequent
rest periods.
• Increase iron in the diet (organ
meat, egg yolk).
• Milk (breast or cow’s) is a poor
source of iron.
• Administer oral iron supplements
as ordered.
Pernicious Anemia
Main Problem:
• Reduced Vitamin B12 absorption
due to the absence of the intrinsic
factor, related to:
• gastrectomy
• atrophy of gastric mucosa in
elderly clients.
Pernicious Anemia
Manifestations:
• Fatigue
• Beefy red tongue or glossitis
• Pallor
• Paresthesia
• Weakness
• Sore mouth
• (+) Romberg’s test
Pernicious Anemia
Diagnostics:

• Schilling’s test reveals more than 40


% urinary excretion of ingested
Vitamin B12
Pernicious Anemia
Interventions:

• Teach the client that monthly IM


Vitamin B12 replacement therapy is
lifelong. Report tingling sensation in
the lower extremities as this
indicates a complication (peripheral
neuropathy)
Sickle Cell Anemia
Main Problem

• Severe chronic, hemolytic anemia


characterized by episodes of pain
due to the occlusion of small blood
vessels by sickled RBC’s. It is
transmitted by autosomal recessive
pattern
Sickle Cell Anemia
Manifestations:

• Growth retardation
•  Dyspnea on exertion
• Joint swelling
• Aching bones
• Generalized pain
• Leg ulcers
Sickle Cell Anemia
Interventions:

• Priorities are hydration and pain


relief
• Report signs and symptoms of
vaso-occlusion, MI or CVA
• Refer the parents to a geneticist
Thalassemia
Main Problem:
• Genetically transmitted disorder
characterized by decreased and defective
production of hemoglobin

Two types:
• Alpha - thalassemia  alpha chains of
hemoglobin are affected
• Beta thalassemia  beta chains of
hemoglobin are affected
Thalassemia
Manifestations:
• Initial: fatigue/shortness of breath
• Other manifestations:
• jaundice
• splenomegaly
• hepatomegaly
• hemosiderosis  accumulation of iron
in the tissues
Thalassemia
Interventions:

• Prevent bleeding and provide rest


• Administer the drug: Deferoxamine
(chelation therapy) to decrease iron in
the body
• Prepare for bone marrow transplant
Anemia
GLUCOSE-6-PHOSPHATE
DEHYDROGENASE DEFICIENCY

• Abnormality in this disorder is in the G-6-PD


gene; this gene produces an enzyme within the
RBC that is essential for membrane stability
• Results in hemolysis only when the RBCs are
stressed by certain situations, such as fever or
the use of certain medications
Anemia
Aplastic Anemia
■ Etiology and pathophysiology: Bone marrow stem
cells destroyed → ↓RBCs, ↓WBCs (neutropenia)
and ↓platelets (thrombocytopenia); idiopathic or
caused by radiation, infection, or chemicals
■ Signs and symptoms: MCV 100fl; no reticulocytes;
↓WBCs, ↓platelets; infection; bleeding (purpura,
retinal hemorrhage)
■ Treatment: Bone marrow transplant; peripheral
blood stem cell transplant; immunosuppressants
(cyclosporine)
Anemia
Normal Ranges
Anemia
Normal Ranges
LEUKEMIA
ETIOLOGY AND PATHOPHYSIOLOGY

■ Unrestricted proliferation of immature


WBCs in blood forming tissues
■ Leukocyte count is low and immature cells
(blasts) are high
■ Blast cells compete for and deprive normal
cells of nutrients essential for
metabolism → anemia from ↓RBCs, infection
from ↓neutrophils, and bleeding from
↓platelets
■ Leukemic cells may infiltrate other organs
(e.g., spleen, liver, lymph nodes, CNS)
LEUKEMIA
SIGNS AND SYMPTOMS
■ Pallor, fatigue, irritability, ↑T,
anorexia, ↓wt
■ Bleeding tendencies (bruising, bleeding
from mucous membranes, petechiae,
hemorrhage)
■ Bone and joint pain; enlarged liver,
spleen, lymph nodes
■ CNS involvement
■ Usually occurs 2–6yr old; onset is
insidious to acute
LEUKEMIA
TREATMENT

■ IV and intrathecal chemotherapy given via 4


phase protocol to achieve remission, ↓tumor
burden, ↓CNS involvement and preserve remission
■ Bone marrow transplant
■ Monitor VS particularly T and BP; provide
balance between rest and activity
■ Teach infection prevention (e.g., hand
washing, avoiding crowds and
people with an infection)
■ Support patient coping with side effects of
meds (e.g., soft toothbrush, bland foods, small
frequent fluid intake, hat to cover hair loss)

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