The Gastro

Medical Surgical Nursing
The GASTRO-INTESTINAL system

By: Maricel S. Jose MD,RN
The Gastro-Intestinal System
Review of the GIT Anatomy and Physiology

The GIT System: Anatomy and Physiology
Review of • The GIT is composed of two general parts
• The main GIT starts from the mouthEsophagus
Review of Common Symptoms and their Stomach  SI  LI  Rectum
nursing interventions • 23-26 foot-long
• The accessory organs are the
- Salivary glands
Review of common disorders of the:
- Liver
- Gallbladder
- Esophagus
- Stomach - Pancreas
- Small intestine
- Large Intestine The Mouth
- Gallbladder
- exocrine pancreas
- liver • Anatomy
- Contains the lips, cheeks, palate, tongue, teeth, salivary
 Organs of the Digestive System glands, masticatory/facial muscles and bones
- Anteriorly bounded by the lips
- Posteriorly bounded by the oropharynx
• Physiology
- Important for the mechanical digestion of food
- The saliva contains SALIVARY AMYLASE or PTYALIN that
starts the INITIAL digestion of carbohydrates
The Esophagus
• Anatomy
- A hollow muscular tube
- Length- 25 cm
- Made up of stratified squamos epithelium
- Located in the mediastinum, anterior to the
spine,posterior to the trachea and heart
- The upper third contains skeletal muscles, contains the
upper esophageal or hypopharyngeal sphincter
- The middle third contains mixed skeletal and smooth
muscles
- The lower third contains smooth muscles and the
esophago-gastric/ cardiac sphincter is found here
• Physiology
- Functions to carry or propel foods from the oropharynx
to the stomach
- Swallowing or deglutition is composed of three phases:
Upper 3rd
Miidle 3rd
Lower 3rd
The stomach
• Anatomy
- J-shaped organ in the LUQ
- Contains four parts- the fundus, the cardia, the body and
the pylorus
- The cardiac sphincter prevents the reflux of the contents
into the esophagus(entrance)
- The pyloric sphincter regulates the rate of gastric
emptying into the duodenum(exit)
- Capacity is 1,500 ml!
 Decreased gastric secretions

 Decreased GIT motility
 Sphincters and blood vessels constrict
- Parasympathetic
Generally EXCITATORY!
• Physiology  Increased gastric secretions
 Increased gastric motility
- The functions of the stomach are generally to digest the  Sphincters relax
food (proteins) and to propel the digested materials into Terms
the SI for final digestion
- The Glands and cells in the stomach secrete digestive • Digestion: phase of the digestive process that occurs when
enzymes: enzymes mix with ingested food and when proteins, fats,
1. Parietal cells- HCl acid and Intrinsic factor and sugars are broken down into their component molecules
2. Chief cells- pepsin digestion of PROTEINS! • Absorption: phase of the digestive process that occurs when
3. Antral G-cells- gastrin small molecules, vitamins, and minerals pass through the
4. Argentaffin cells- serotonin walls of the small and large intestine and into the
5. Mucus neck cells- mucus bloodstream
• Elimination: phase of the digestive process that occurs after
The Small intestine digestion and absorption, when waste products are
eliminated from the body
• Anatomy
- Longest segment, about 2/3 of the total length Functions of the GIT
- Grossly divided into the Duodenum (proximal),
Jejunum(middle) and Ileum(distal) • The breakdown of food particles into the molecular form for
- Duodenum w/ampulla of vater-common bile duct empties, digestion
passage of bile and pancreatic secretions • The absorption into the bloodsteam of small nutrient
- The ileum is the longest part (about 12 feet) molecules produced by digestion
• The elimination of undigested unabsorbed foodstuffs and
other waste products
• Physiology
- The intestinal glands secrete digestive enzymes that
finalize the digestion of all foodstuffs Digestive Processes
- Enzymes for carbohydrates  disaccharidases
• Chewing
- Enzymes for proteins  dipeptidases and aminopeptidases
- 1.5ml of saliva is secreted daily from the parotid,
- Enzyme for lipids  intestinal lipase submaxillary and sublingual glands
- PTYALIN or SALIVARY AMYLASE is an enzyme that begins
the digestion of starches
The Large intestine
• Swallowing begins as a voluntary act, w/c is regulated by
• Anatomy the swallowing center in the medulla oblongata of the CNS
- Approximately 5 feet long, with parts:
1. The cecum widest diameter, prone to rupture • Gastric Function
2. The appendix - stomach-secretes a highly acidic fluid in response to the
3. The ascending colon presence of ingested food
4. The transverse colon - fluid can total as 2.4L/day can have a ph as low as 1 and
5. The descending colon derives its acidity from hydrochloric acid (HCl)
a. to breakdown food into more absorbable components
6. The sigmoid most mobile, prone to twisting
b. to aid in the destruction of ingested bacteria
7. The rectum
8. The Anus Gastric Enzymes
Secreted by zymogens or chief cells
BLOOD SUPPLY Amylase=for starch digestion
- GIT recieves blood from arteries that originate along the Lipase=for fat digestion
entire length of the thoracic and abdominal aorta Pepsin=for protein digestion
- The portal venous system is composed of 5 large veins: Rennin=for milk and protein digestion
superior mesenteric, inferior mesenteric, gastric, splenic,
and cystic veins w/c form the vena portae that enters the Secreted by parietal cells
liver HCl - maintains acidity 1.0 pH destroy some bacteria
- Oxygen and nutrients are supplied to the stomach by the ingested aids also in digestion of food
gastric artery and to the intestines by the mesenteric Intrinsic factor - aids in absorption of vit B12
arteries. * pernicious anemia
• Physiology Secreted by endocrine cells

- Sympathetic Gastrin, somatostatin and serotonin
Generally INHIBITORY!
• Small Intestine Function

- duodenal secretions come from the accessory digestive • Upper GIT study: Barium swallow
organs- pancreas, liver and gallbladder and the glands on - Examines the upper GI tract
the intestinal walls - Barium sulfate is usually used as contrast
- pancreatic secretions have alkaline pH due to the high - Pre-test: NPO post-midnight
concentration of bicarbonate- this neutralizes the acid
entering the duodenum from the stomach
- Post-test: Laxative is ordered, increase pt fluid intake,
instruct that stools will turn white, monitor for
obstruction
Digestive enzymes secreted by the pancreas:
- trypsin aids in digesting protein
- amylase aids in digesting starches
- lipase aids in digesting fats
pancreatic secretions  pancreatic duct  ampulla of vater
2 Types of contractions in the small intestines

a. segmental contractions- mixing waves that move
the intestinal contents back and forth in a churning motion
b. intestinal peristalsis- propels the contents towards
the colon
* both movements are stimulated by the presence of
chyme
Finger like projections/villi are present throughout the small
intestines- absorption-begins in the jejunum by active
transport and diffusion
• Colonic Function
- bacteria make up a major component of the contents of
the large intestine, assist in completing the breakdown of
waste material esp undigested and unabsorbed proteins
and bile salts
2 types of colonic secretions:

a. electrolyte solution- is chiefly bicarbonate solution that
act to neutralize the end products formed by the colonic
bacterial action
b. mucus- protects the colonic mucosa
• Waste Products of Digestion

- Feces - undigested foodstuff, inorganic materials, water
and bacteria
- 75% fluid 25% solid material • Lower GIT study: Barium enema
- brown color results from the breakdown of bile - Examines the lower GI tract
- gases- methane, hydrogen sulfide and ammonia - Pre-test: Clear liquid diet and laxatives, NPO post-
- Elimination begins with distention of the rectum w/c midnight, cleansing enema prior to the test
initiates contractions of the rectal musculature and
relaxes the closed internal anal sphincter
- Post-test: Laxative is ordered, increase patient fluid
- internal anal sphincter- autonomic nervous system intake, instruct that stools will turn white, monitor for
- external anal sphincter- cerebral cortex; maintained in obstruction
tonic contraction
Gastrointestinal Assessment
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
- Screening test for colonic cancer
• Gastric analysis
- Aspiration of gastric juice to measure pH, appearance,
volume and contents
- Pre-test: NPO 8 hours, avoidance of stimulants, drugs and
smoking
- Post-test: resume normal activities
• EGD - esophagogastroduodenoscopy
- Visualization of the upper GIT by endoscope
- Pre-test: ensure consent, NPO 8 hours, pre-medications
like atropine and anxiolytics
Gastroscopy
• 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
- Intra-test: position : LEFT lateral to facilitate salivary

drainage and easy access
- Post-test: NPO until gag reflex returns, place patient in
SIMS position until he awakens, monitor for
complications, saline gargles for mild oral discomfort
• Lower GI- scopy

- Use of endoscope to visualize the anus, rectum, sigmoid
and colon
- Pre-test: consent, NPO 8 hours, cleansing enema until
return is clear • Cholecystography
- Examination of the gallbladder to detect stones, its ability
• Colonoscopy 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
• Paracentesis
- Removal of peritoneal fluid for analysis
- 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
• Liver biopsy
- Pretest
Consent
NPO
Check for the bleeding parameters
- Intratest
Position: Semi fowler’s LEFT lateral to expose right side of
abdomen
- Post-test: position on RIGHT lateral with pillow
underneath, monitor VS and complications like bleeding,
perforation. Instruct to avoid lifting objects for 1 week Quadrants of the Abdomen
The NURSING PROCESS in GIT Disorders
Assessment
- Health history Nursing History
- PE
- Laboratory procedures
Assessment: History
- Include all information related to GI function

• Abdominal pain, dyspepsia, gas, nausea and vomiting,
constipation, diarrhea, fecal continence, change in bowel
patterns, characteristics of stool, jaundice, history of GI
surgery or problems, appetite and eating patterns, teeth, and
nutritional assessment, including weight patterns
- Psychosocial, spiritual, and cultural factors
- Assess knowledge; need for patient education
Common Sites of Referred Abdominal Pain
COMMON GIT SYMPTOMS AND MANAGEMENT

CONSTIPATION
DIARRHEA
DUMPING SYNDROME
• Constipation
An abnormal infrequency and irregularity of defecation
Multiple causations
Pathophysiology
Interference with three functions of the colon
1. Mucosal transport
2. Myoelectric activity
3. Process of defecation
The ABDOMINAL examination
The sequence to follow is:
Nursing Interventions
- Inspection
1. Assist physician in treating the underlying cause of
- Auscultation
constipation
- Percussion
2. Encourage to eat HIGH fiber diet to increase the bulk
- Palpation
3. Increase fluid intake
4. Administer prescribed laxatives, stool softeners
5. Assist in relieving stress
Examination of the Abdomen
• Diarrhea Chronic - slowly progressive, a fully formed abscess

- Abnormal fluidity of the stool may occur w/o the pt’s knowledge, leads to a “blind
- Multiple causes dental abscess” w/c is a periapical granuloma,
 Gastrointestinal Diseases discovered on X-ray, treated w/ root canal therapy
 Hyperthyroidism
 Food poisoning - Clinical Manifestations - dull, gnawing, continuous
pain w/ surrounding cellulitis and edema of the
adjacent facial structures and mobility of the involved
- Nursing Interventions tooth, difficult to open the mouth, fever, malaise
1. Increase fluid intake- ORESOL is the most important
treatment! - Management- needle aspiration or drill an opening
2. Determine and manage the cause into the pulp chamber to relieve pressure and pain,
3. Anti-diarrheal drugs drainage thru an incision in the gingiva to the
jawbone, antibiotics
PERNICIOUS ANEMIA
- Results from Deficiency of vitamin B12 due to autoimmune - Nursing Management- assess the pt for bleeding,
destruction of the parietal cells, lack of INTRINSIC FACTOR instruct to use warm saline, take medications, follow
or total removal of the stomach up
- Assessment
 Severe pallor 3. Malocclusion
 Fatigue - Misalignment of the teeth of the upper and lower dental arcs
 Weight loss when the jaws are closed
 Smooth BEEFY-red tongue - Inherited or acquired
 Mild jaundice - Makes the teeth difficult to clean and can lead to decay, gum
 Paresthesia of extremities disease
 Balance disturbance - Corrections requires an orthodontist, treatments begins when
the pt has shed the last primary tooth and the last permanent
- Nursing Intervention successor has erupted
 Lifetime injection of Vitamin B 12 weekly initially, then
MONTHLY
Disorders Of The Jaw
Conditions of the GIT Categorized as follows:
a. myofascial pain- discomfort in the muscle
• UPPER GI system controlling jaw function and neck and shoulder
Conditions of the Oral Cavity muscles
Disorders Of The Teeth b. internal derangement of the joint- dislocated jaw,
1. Dental Plaque and Caries displaced disc, or injured condyle
- tooth decay is an erosive process that begins w/ the c. degenerative joint disease- rheumatoid arthritis or
action of bacteria on fermentable CHO in the osteoarthritis of the jaw
mouth, w/c produces acid that dissolve tooth
enamel Clinical Manifestations - dull, throbbing, debilitating pain
- the extent of damage to the teeth depends on the ff: that can radiate to the ears, teeth, neck muscle, facial
 presence of dental plaque- gluey, gelatin like sinuses, restricted jaw motion, locking of the jaw, difficult
substance that adheres to the teeth chewing and swallowing
 strength of the acid and ability of the saliva to
neutrlize Assessment and Diagnostic Findings- diagnosis is based on
 the length of time the acids are in contact the pt’s report of pain, limitation of motion, dysphagia,
 susceptibility of the teeth to decay difficulty in chewing, difficulty w/ speech, hearing
- Prevention difficulties.
 Mouth Care- brushing and flossing, normal Management- stress reduction, range of motion exercises,
mastication (chewing), normal flow of saliva pain management w/ NSAIDS, muscle relaxants, if
 Diet- ↓ the amount of sugar & starch irreversible- surgery
 Fluoridation
 Pit and Fissure Sealants- special coating to fill and
Disorders of The Salivary Glands
seal pits and fissures, can last to 5-10 years
 1. PAROTITIS- inflammation of the parotid gland
2. Dentoalveolar abscess or Periapical Abscess MUMPS- epidemic parotitis, a communicable disease
- Collection of pus in the apical dental periosteum caused by a viral infection mostly affect children
(fibrous membrane supporting the tooth structure) - elderly, acutely ill, debilitated people w/ decreased
and the tissue surrounding the apex (in the jaw bone) salivary flow from dehydration or medications are at
- May be acute or chronic higher risk
Acute - secondary to a suppurative pulpitis that arises - organism is usually staphylococcus aureus
from an infection from a dental caries
- onset is sudden, fever, the gland swells and becomes

tense and tender, pain, difficult swallowing,
- management- adequate nutrition and fluid intake,
good oral hygiene, antibiotics, analgesic, parotidectomy
2. SIALADENITIS- inflammation of the salivary gland
- caused by dehydration, radiation therapy, stress,
malnutrition, salivary gland calculi, improper oral
hygiene
- organisms: Staph.aureus, Strep. viridans
- manifestation- pain, swelling, purulent discharge
- treatment- antibiotics, massage, hydration, warm
compresses, corticosteroids, surgical drainage of the
gland or excision
3. SALIVARY CALCULUS (SIALOLITHIASIS)
- occurs in the submandibular glands
- formed mainly from calcium phosphate
- PE- gland is swollen, tender, palpable w/ stone
-Tx - extraction, lithotripsy
Aphthous Stomatitis
- Canker Sore
- Shallow ulcer w/ white or yellow center and red border; seen
on the inner side of the lip, cheek or on the tongue
- Begins w/ burning or tingling sensation and slight swelling;
painful
- Lasts 7-10 days and heals w/o a scar
- Assoc w/ emotional or mental stress, fatigue, hormonal
factors, minor trauma, allergies, acidic foods and juices,
dietary deficiencies
- Assoc w/ HIV infection
- Instruct pt on comfort measures, soft or bland diet
CANCER OF THE ORAL CAVITY
- Give prescribed antibiotics or corticosteroids
- Often assoc w/ use of alcohol and tobacco
- 95% occur among 40 y/o and older affecting more men
Stomatitis
than women
- Regardless of the stage of cancer at diagnosis, the 5 yr
survival rate is 56% and the 10 yr survival rate is 41%
- Usually squamous cell cancers, affects lips, lateral
aspects of the tongue, floor of the mouth
- S/SX- painless sore or mass that does not heal,
difficulty in chewing, swallowing and speaking
- DX- assessment of oral cavity, biopsy,
- MX- chemotx, radiationTx, surgical resection
Condition Of The Esophagus

Hiatal Hernia
- The opening in the diaphragm through w/c the esophagus
passes becomes enlarged and part of the upper stomach
tends to move up
- More common among women
- Two types- Sliding or type I hiatal hernia (most common-
90%) and Paraesophageal hiatal hernia: type II, III and IV
( IV- greatest herniation)
- Assessment Findings
1. Heartburn
2. Regurgitation
3. Dysphagia
4. 50%- without symptoms
 implicated in reflux
 hemorrhage, obstruction, strangulation
Sliding Esophageal and Paraesophageal Hernia

3. Ascites
4. jaundice
5. hepatomegaly/splenomegaly
Signs of Shock- tachycardia, hypotension, tachypnea, cold
clammy skin, narrowed pulse pressure
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
- Diagnostic Test 6. Prepare for blood transfusion
Barium swallow and fluoroscopy 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
Gastro-esophageal reflux
- Backflow of gastric contents into the esophagus
- Usually due to incompetent lower esophageal sphincter ,
pyloric stenosis or motility disorder
- Symptoms may mimic ANGINA or MI
- Incidence increase w/ aging
- Assessment (For Gerd)

 Heartburn / Pyrosis
 Dyspepsia / Indigestion
 Regurgitation
 Odynophagia
 Dysphagia / Difficulty swallowing
 Excessive salivation
- Diagnostic test
 Endoscopy or barium swallow
 Gastric ambulatory pH analysis
 Note for the pH of the esophagus, usually done for 24
hours
 The pH probe is located 5 inches above the lower
esophageal sphincter
 The machine registers the different pH of the refluxed
material into the esophagus
- Nursing Interventions
1. Instruct the patient to AVOID stimulus that increases
stomach pressure and decreases LES pressure
Nursing Interventions 2. Instruct to avoid spices, coffee, tobacco and carbonated
1. Provide small frequent feedings drinks
3. Instruct to eat LOW-FAT, HIGH-FIBER diet
2. AVOID supine position for 1 hour after eating
4. Avoid foods and drinks TWO hours before bedtime
3. Elevate the head of the bed on 8-inch block 5. Elevate the head of the bed with an approximately 8-
4. Provide pre-op and post-op care inch block
6. Administer prescribed H2-blockers, PPI and prokinetic
Esophageal Varices meds like cisapride, metochlopromide
Dilation and tortuosity of the submucosal veins in the distal 7. Advise proper weight reduction
esophagus
ETIOLOGY: commonly caused by PORTAL hypertension
secondary to liver cirrhosis
This is an Emergency condition!
Conditions of the Stomach
Gastritis
ASSESSMENT findings for EV
1. Hematemesis
- Inflammation of the gastric mucosa
2. Melena
- May be Acute or Chronic
- Etiology:
Acute - irritating foods, highly seasoned or contaminated
w/ disease causing microorganism, NSAIDS, alcohol, bile
reflux and radiationTx
Chronic- Ulceration, bacteria (Helicobacter pylori),
Autoimmune disease (pernicious anemia), diet
(caffeine),alcohol, smoking, bile reflux
- Pathophysiology of Gastritis
Insults cause gastric mucosal damage  inflammation,
hyperemia and edema  superficial erosions  decreased
gastric secretions of gastric juice (very little acid more
mucus),  ulcerations and bleeding
- ASSESSMENT
(Acute)
 Abdominal discomfort
 Headache
 Anorexia
 Nausea/Vomiting
(Chronic)
 Pyrosis
 Singultus
 Sour taste in the mouth
 Dyspepsia
 N/V/anorexia
 Pernicious anemia
- Diagnostic Procedure
 EGD- to visualize the gastric mucosa for inflammation
 Absent (Achlorhydria) or Low levels of HCl - NURSING INTERVENTIONS
(hypochlorhydria) or High Levels of HCl
(hyperchlorhydria)
 Biopsy to establish correct diagnosis whether acute or
1. Give BLAND diet
chronic 2. Monitor for signs of complications like bleeding,
obstruction and pernicious anemia
Erosive Gastritis 3. Instruct to avoid spicy foods, irritating foods, alcohol
and caffeine, NSAIDS,
4. Conditions of the Stomach
5. Administer prescribed medications- H2 blockers,
antibiotics, mucosal protectants
6. Inform the need for Vitamin B12 injection if deficiency
is present
Peptic Ulcer Disease
- An ulceration of the esophageal, gastric and duodenal

lining
- May be referred as to location as Gastric ulcer in the
pylorus of the stomach, or Duodenal ulcer in the
duodenum, or in the esophagus
- Most common Peptic ulceration: anterior part of the
upper duodenum
- Common between 40-60 y/o, blood type O
- Causes: H.pylori infection, excessive secretion of HCl,

stress, alcohol, smoking, caffeinated beverage, spicy
foods
- PATHOPHYSIOLOGY of PUD
 Disturbance in acid secretion and mucosal protection
 Increased acidity or decreased mucosal resistance
erosion and ulceration
 Zollinger-Ellison Syndrome- severe peptic ulcer,
extreme gastric hyperacidity, and gastrin secreting benign or
malignant tumors of the pancreas-resistant to standard Relieved by food, Commonly Accompanied

medical treatment antacids, H2 blockers; is by nusea, vomiting with
 Stress ulcer - occurs after physiological stressful not associated with food intake, and a
events such as burns, shock, sepsis, trauma, ventilator vomiting (if atypical variable response to
assisted pt, features occur think of medication
complications) Low gastric acid levels
 Cushing’s ulcer - common in pts w/ head injury and High gastric levels
brain trauma, more penetrating and deeper than stress ulcer, H. pylori+++ H. pylori+++
involves esophagus, stomach and duodenum Does not represent a Malignancy+
 Curling’s ulcer - observed about 72 hours after malignancy
extensive burns, involves stomach and duodenum Usually not accompanied 25% of GU will be
by a high complication accompanied by
- Duodenal Ulcer rate; when complications significant bleeding
do occur it is usually higher mortality and
 Age: 30-60 y/o M/F=3:1 ploric stenosis or morbididty than DUs
 80% of peptic ulcers are duodenal posterior penetration
 Weight Gain
 Hypersecretion of HCL acid
 Pain occurs 2-3 h after meal
 Ingestion of food relieves pain - Clinical Manifestations - dull, gnawing pain or a burning
 Vomiting uncommon sensation in the midepigastrium or in the back, pyrosis,
 Hemorrhage less likely vomiting, constipation or diarrhea, bleeding (melena-
 Melena more common than hematemesis black tarry stool)
 Most likely to perforate
 Possibility of Malignancy is rare - Assessment and Diagnostic Findings
 Risk Factors: H.pylori, alcohol, smoking, stress  epigastric tenderness or abdominal distention
- Gastric Ulcer  endoscopy is the preferred procedure bec of direct
 Usually 50 and over visualization and biopsy can be done
 Male:Female = 1:1  stool exam
 Weight Loss  gastric secretory studies, urea breath test
 Pain occurs ½ to 1 hour after meal
 Ingestion of food does not help, causes pain
 Vomiting common
 Hemorrhages more likely
 Hematamesis more common than melena
 Possibility of Malignancy: occasional
 Risk Factors: H.pylori, alcohol, smoking, NSAID
- Gastric Ulcer
 Usually 50 and over
 Male:Female = 1:1
 Weight Loss
 Pain occurs ½ to 1 hour after meal
 Ingestion of food does not help, causes pain
 Vomiting common
 Hemorrhages more likely
 Hematamesis more common than melena
 Possibility of Malignancy: occasional
 Risk Factors: H.pylori, alcohol, smoking, NSAID
Duodenal Ulcer Gastric Ulcer

Pain occurs 90 min to 3h Commonly pain occurs
after meals; wakes up within a short time of
patient midnight to 3AM food intake
- Diagnostic Tests
 EGD and Biopsy
- Medical Management
 Pharmacologic therapy- combination of antibiotics,
proton pump inhibitors and bismuth salt to
eradicate H.pylori for 10-14 days, Histamine-2 (H2)
receptor antagonist and PPI are used to treat
NSAID induced ulcers
 Stress reduction and rest
 Smoking cessation
 Dietary modification
Surgical Management
 Pharmacotherapy
 Histamine-2 (H2) receptor antagonists (PO/IV)
 Action: ↓ HCl production
 taken with meals or at H.S., cigarettes reduces
its action
 SE: headache, dizziness, nausea/vomiting &
urticaria
 8 weeks medication (if s/sx does not improve,
start antibiotics)
 Cimetidine (Tagamet)
 Ranitidine (Zantac)
 Famotidine (Pepcid)
 Nizatidine (Axid)
 Antibiotics
 Action: antibacterial to eradicate H. pylori
 Amoxicillin (Amoxil)
 Clarithromycin (Biaxin)
 Metronidazole (Flagyl)
 Tetracycline
 Can be combined with other drugs Vagotomy
 Mucosal Barrier
 Action: forms protective barrier, adheres to ulcer
surface
 30 min interval before taking antacids
 SE: constipation, and nausea/vomiting
 Give 1-2 hour after meal or during bedtime on an
empty stomach
 5 hours duration
 Sucralfate (Carafate)
 Pharmacotherapy
 Antacids (non absorbable)
 Action: ↓ gastric acidity
 Chew then swallow, taken 1 hr after meals or at
H.S.
 Aluminum Hydroxide SE: constipation
 Don’t give other drugs w/in 1-2 hrs after the
antacids
Pyloroplasty
 Magnesium Oxide SE: diarrhea
 Taken in between meals or at bedtime
 May increase serum Magnesium level in RF client
 Chew follow with water
 Calcium Carbonate SE: ↑ uric acid
 Taken in between meals or at bedtime with milk
 NaHCO3 SE: metabolic alkalosis and tetany
 Proton Pump Inhibitor
 Action: ↓ gastric acid secretion of the parietal
cells
 4-8 weeks medications
 Esomeprazole (Nexium)
 Omeprazole (Prilosec)
 Lansoprazole (Prevacid)
 Pantoprazole (Protonix)
- Surgical Procedures For Pud

- Total gastrectomy, vagotomy, gastric resection, Billroth
I and II, pyloroplasty
Billroth I-Gastroduodenostomy Nursing Interventions

1. Give BLAND diet, small frequent meals
during the active phase of the disease
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
Nursing Interventions For Bleeding

1. Maintain on NPO
2. Administer IVF and medications
3. Monitor hydration status, hematocrit and
hemoglobin
4. Assist with SALINE lavage
5. Insert NGT for decompression and lavage
6. Prepare to administer blood transfusion
7. Prepare to give VASOPRESSIN to induce
vasoconstriction to reduce bleeding
Billroth II-Gastrojejunostomy 8. Prepare patient for SURGERY if warranted
Surgical Procedures For Pud

Post-operative Nursing management
1. Monitor VS
2. Post-op position: FOWLER’S
3. NPO until peristalsis returns
4. Monitor for bowel sounds
5. Monitor for complications of surgery
6. Monitor I and O, IVF
7. Maintain NGT
8. Diet progress: clear liquid  full liquid  six
bland meals
9. Manage DUMPING SYNDROME
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
Pathophysiology
- Foods high in CHO and electrolytes must be diluted in
- Vagotomy – severing of the vagus nerve the jejunum before absorption takes place.
- Decreases gastric acid
- Diminishing cholinergic stimulation to the parietal - The rapid influx of stomach contents will
cells- less responsive to gastrin - cause distention of the jejunum early
- Billroth I – Gastroduodenostomy
- symptoms
- Removal of the lower portion of the antrum
- Antrum contains the cells that secretes gastrin
- The hypertonic chyme will draw fluid from the blood
- Small portion of duodenum and pylorus
vessels to dilute the high concentrations of CHO and
- Remaining portion is anastomosed to the duodenum
electrolytes
- Billroth II – Gastrojejunostomy
- Remaining portion is anastomosed to the jejunum
- Later, there is increased blood glucose
- Billroth I
- stimulating the increased secretion of insulin
 Feeling of fullness
 Dumping syndrome
 Diarrhea
- Then, blood glucose will fall causing reactive
 Recurrence rate is <1% hypoglycemia
− Billroth II
 Dumping syndrome Assessment Findings:
 Anemia - Early symptoms
 Malabsorption 1. Nausea and Vomiting
 Weight loss 2. Abdominal fullness
 Recurrence rate of ulcer is 10-15% 3. Abdominal cramping
4. Palpitation
5. Diaphoresis
6. Weakness - Abnormal hardening of stools

7. Diarrhea - Irregularity of elimination
- Retention of stool for a prolonged period
- Late symptoms:
8. Hypoglycemia
9. Weakness and Dizziness
10.Drowsiness Caused by:
11.Perspiration - Medications
12.Palpaitation  Iron, antacids with aluminum
13.Pallor - Hemorrhoids
- Cancer of the bowel
Nursing Interventions - Endocrine disorders
- Clinical Manifestation
1. Advise patient to eat LOW-carbohydrate
- Abdominal distention
HIGH-fat and HIGH-protein diet
- Borborygmus
2. Instruct to eat SMALL frequent meals, - gurgling sound caused by passage of gas in the intestine
include MORE dry items. - Pain and pressure
3. Instruct to AVOID consuming FLUIDS with - Indigestion
meals - Sensation of incomplete emptying
4. Instruct to LIE DOWN after meals - Straining
5. Administer anti-spasmodic medications to delay - Hard, dry stools
gastric emptying
Medical Management
Gastric Cancer - Bowel habit training
- Increased fiber and fluid intake
- 40-70 y/o, more common among men - Discontinue laxative abuse
- Diet high in smoke foods, low in fruits and vegetables - Exercise to strengthening abdominal muscles
- Chronic inflammation of the stomach
- Pernicious anemia Diarrhea
- Gastric ulcers - Increased frequency of bowel movement more than 3x a
- H. Pylori infections day
- Chronic Smoking - Increased amount of stool
- Previous Subtotal Gastrectomy - Altered consistency
- Genetics
Clinical Manifestations
Pathophysiology - Abdominal cramps, Distention
- Adenocarcinomas w/c occur anywhere in the stomach - Intestinal rumbling/borborygmus
affecting the gastric mucosa - Anorexia and thirst
- Asymptomatic in the early stage
- Pain relieved with antacids
- Anorexia, dyspepsia, weight loss Assessment and Diagnostic Findings
- Constipation, anemia - CBC count
- Nausea and vomiting - Chemical profile
- Urinalysis
Assessment and Diagnostic Findings - Stool exam
- Advanced Gastric Ca- palpable mass Medical Management
- Ascites and Hepatomegaly- if cancer cells metastasized - Control symptoms
to the liver - Treat the underlying disease
- Sister Mary Joseph’s Nodule- palpable nodules around
the umbilicus Fecal Incontinence
- EGD/Endoscopy w/ biopsy and cytology - Involuntary passage of stool from the rectum
- Barium x-ray exam - Inability of the rectum to sense and accommodate stool
- CT Scan, Bone Scan, Liver Scan - Amount and consistency of the stool
- Medical Management - Integrity of the anal spinchter
- Removal of the tumor - Rectal motility
- Chemotherapy
Clinical Manifestation
Soiling
Conditions of the Lower Tract Occasional urgency and loss of control
Small and Large Intestine Complete incontinence
Poor control of flatus
CONDITIONS OF THE SMALL INTESTINE
Medical Management
Abnormalities of Fecal Elimination Biofeedback therapy
Constipation Bowel training programs
Surgical reconstruction, spinchter repair or fecal diversion - Barium enema

- MRI and CT scan
Complications
- toxic megacolon, perforation, bleeding, osteoporotic
Crohn’s Disease fracture
- Also called Regional Enteritis
- An inflammatory disease of the GIT affecting usually the
distal ileum and colon
- Usually first diagnosed in adolescents and young adults Nursing Interventions For Cd And Uc
- More often seen among smokers 1. Maintain NPO during the active phase
2. Monitor for complications like severe bleeding,
- Etiology: unknown dehydration, electrolyte imbalance
- The terminal ileum thickens w/ edema formation, with
3. Monitor bowel sounds, stool and blood studies
scarring, ulcerations, abscess formation and narrowing of 4. Restrict activities= rest and comfort
the lumen
- The clusters of ulcers- classic cobblestone appearance 5. Administer IVF, electrolytes and TPN if prescribed
Monitor complications of diarrhea
Clinical Manifestations of Crohn’s Dse 6. Instruct the patient to AVOID gas-forming foods, MILK
1. Fever products and foods such as whole grains, nuts, RAW
2. Abdominal distention fruits and vegetables especially SPINACH, pepper,
3. Diarrhea alcohol and caffeine
4. Crampy RLQ abdominal pain 7. Diet progression- clear liquid LOW residue, high
5. Anorexia/N/V protein diet
6. Weight loss 8. Administer drugs- anti-inflammatory, antibiotics,
7. Anemia steroids, bulk-forming agents and vitamin/iron
supplements
Assessment and Diagnostic Findings
- Proctosigmoidoscopy initially
- stool exam- maybe (+) for occult blood and steatorrhea Appendicitis
- barium study of the upper GI tract- is confirmatory w/c - Inflammation of the vermiform appendix
shows the classic string sign on x-ray film indicating
constriction the segment involved
- CBC, ESR (↑), Albumin and protein (↓)
Complications
- intestinal obstruction,strictures, perianal dse, fluid and
electrolyte imbalances, malnutrition
CONDITIONS OF THE LARGE INTESTINE
Ulcerative Colitis
- Recurrent ulcerative and inflammatory condition of the
mucosal and submucosal layers of the colon and rectum
- The colon becomes edematous and develops bleeding
ulcerations
- Scarring develops overtime with impaired water
absorption and loss of elasticity
SEVERE diarrhea (10-20 liquid stools/day) with Rectal
bleeding
1. Weight loss
2. Fever Etiology: usually fecalith, lymphoid hyperplasia, foreign body
3. Anorexia and helminthic obstruction
4. Anemia and Hypocalcemia
5. Dehydration Pathophysiology
6. LLQ Abdominal pain and cramping
- Obstruction of lumen increased pressure  decreased
7. Tenesmus
blood supply  bacterial proliferation and mucosal
inflammation  ischemia  necrosis  rupture
Assessment and Diagnostic Findings
- assess for tachycardia, tachypnea, hypotension, fever Assessment Findings
and pallor, level of hydration and nutritional status 1. Abdominal pain: begins in the umbilicus then localizes in
- stool exam- (+) for blood the RLQ (Mc Burney’s point)
- ↓ hematocrit and hemoglobin and albumin 2. Anorexia
- ↑ WBC 3. Nausea and Vomiting
4. Fever
- Sigmoidoscopy, colonoscopy
5. Rebound tenderness and abdominal rigidity (if

perforated)
6. Constipation or diarrhea
ASSESSMENT findings for Hemorrhoids

- Internal hemorrhoids- cannot be seen on the peri-anal
area
- External hemorrhoids- can be seen
- Bright red bleeding with each defecation
- Rectal/ perianal pain
- Rectal itching
- Skin tags
Diagnostic Test
- Anoscopy
- Digital rectal examination
Trearments
- Nonsurgical treatments
 Infrared photocoagulation
 Laser therapy
- Conservative surgical treatment
Diagnostic Tests  rubberband ligation procedure
- CBC- reveals increased WBC count  cryosurgical hemorrhoidectomy
- Ultrasound - Hemorrhoidectomy
- Abdominal X-ray  For advance thrombosed vein
Nursing Interventions Nursing Interventions

- Preoperative care - Advise patient to apply cold packs to the anal/rectal
- NPO area followed by a SITZ bath
- Consent - Apply astringent like witch hazel soaks
- Monitor for perforation and signs of shock - Encourage HIGH-fiber diet and fluids
- Monitor bowel sounds, fever and hydration status - Administer stool softener as prescribed
- POSITION of Comfort: RIGHT SIDELYING in a low
FOWLER’S Post-operative care for hemorrhoidectomy
- Avoid Laxatives, enemas & HEAT APPLICATION
- Position: Prone or Side-lying
- Post-operative care
- Maintain dressing over the surgical site
- Monitor VS and signs of surgical complications
- Monitor for bleeding
- Maintain NPO until bowel function returns
- Administer analgesics and stool softeners
- If rupture occurred, expect drains and IV antibiotics
- Advise the use of SITZ bath 3-4 times a day
- POSITION post-op: RIGHT side-lying, SEMI- FOWLER’S to
decrease tension on incision, and legs flexed to promote
drainage DIVERTICULOSIS AND DIVERTICULITIS
- Administer prescribed pain medications Diverticulosis
- Abnormal out-pouching of the intestinal mucosa
Hemorrhoids occurring in any part of the LI most commonly in the
- Abnormal dilation and weakness of the veins of the anal sigmoid
canal
- Variously classified as Internal or External, Prolapsed, Diverticulitis
Thrombosed and Reducible - Inflammation of the diverticulosis
PATHOPHYSIOLOGY Diverticular Disease

- Increased pressure in the hemorrhoidal tissue due to - Diverticulum: sac-like herniations of the lining of the
straining, pregnancy, etc dilatation of veins bowel that extend through a defect in the muscle layer
- May occur anywhere in the intestine, but are most
Internal hemorrhoids common in the sigmoid colon
- These dilated veins lie above the internal anal sphincter - Diverticulosis: multiple diverticula without inflammation
- Usually, the condition is PAINLESS - Diverticulitis: infection and inflammation of diverticula
- Diverticular disease increases with age and is associated
External hemorrhoids with a low-fiber diet
- These dilated veins lie below the internal anal sphincter - Diagnosis is usually by colonoscopy
- Usually, the condition is PAINFUL
PATHOPHYSIOLOGY
- Increased intraluminal pressure, LOW volume in the

lumen and Decreased muscle strength in the colon
wall herniation of the colonic mucosa
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 - Volvulus

1. If no active inflammation, COLONOSCOPY and Barium Enema
2. CT scan is the procedure of choice!
3. Abdominal X-ray
NURSING INTERVENTIONS
1. Maintain NPO during acute phase
2. Provide bed rest
3. Administer antibiotics, analgesics like meperidine (morphine is
not used) and anti-spasmodics
4. Monitor for potential complications like perforation,
hemorrhage and fistula
5. Increase fluid intake
6. Avoid gas-forming foods or HIGH-roughage foods containing
seeds, nuts to avoid trapping
7. introduce soft, high fiber foods ONLY after the inflammation
subsides
8. Instruct to avoid activities that increase intra-abdominal
pressure
Intestinal Obstruction
- Partial or complete blockage prevents the flow of intestinal
contents thru the intestinal tract
- Hernia (Inguinal)
Mechanical Obstruction
- Intraluminal obstruction or mural obstruction from
pressure on the intestinal wall occurs
 Stenosis, adhesions, hernias
Functional obstruction
- The intestinal musculature cannot propel the contents
along the bowel
 Muscular dystrophy, endocrine disorders or
neurologic disorders
Mechanical
- Adhesions – fibrous band of scar tissue from surgery
- Hernias – incarcerated or strangulated
- Volvulus – twisting of bowel
- Intussusception – telescoping of the bowel upon itself
- Tumors
- Hematoma
- Fecal impaction
- Intraluminal obstruction
- Intussusception
Neurogenic
- Paralytic ileus
- Adynamic ileus Nursing Management
- intestinal tube insertion (miller abott, cantor tube) for
Vascular decompression
- Occlusion of arterial blood supply - fluid and electrolyte replacement
- Mesenteric thrombosis - prophylactic antibiotic
- Abdominal angina - v/s, I&O
- Small Bowel Obstruction - stool exam
- Intestinal contents, fluids and gas accumulate above the - surgery
intestinal obstruction
- Reduce the absorption of fluids and stimulate more gastric Conditions of the GIT accessory organs
secretion
- Pressure within the intestinal lumen increases
Liver
- Decrease in venous and arteriolar capillary pressure
- Edema, congestion, necrosis, and rupture or perforation of Anatomy
intestinal wall → peritonitis - The largest internal organ
- Reflux vomiting leads to ↓K+, ↓Clˉ in blood, with fluid - Located in the right upper quadrant
losses resulting to shock - Contains two lobes- the right and the left, covered w/
- Clinical Manifestations connective tissue
- Crampy pain, wavelike and colicky - The hepatic ducts join together with the cystic duct to
- May pass blood and mucous, but no fecal matter and become the common bile duct
flatus; vomiting occurs Liver and Biliary System
- If obstruction is complete, vigorous peristalsis, and
assume a reverse direction with the intestinal content
propelled toward the mouth
- If obstruction is in the ileum, fecal vomiting takes place
- Dehydration: thirst, drowsiness, malaise, and a parched
tongue and mucous membranes
- The lower the GI obstruction, the more marked the
abdominal distention
- Uncorrected obstruction leads to shock
- Diagnostics and Management
- Abdominal X-ray and CT Scan
- Electrolyte studies and CBC
- Medical Management
- Decompression of the bowel through a nasogatric or small
bowel tube
- Surgical treatment, if completely obstructed
 Removal, repair, and anastomosis
Large Bowel Obstruction

Liver
- Accumulation of intestinal contents, fluid, and gas
proximal to the obstruction
- Right and left lobe separated by falciform ligament
- If blood supply is cut off, intestinal strangulation and
- Caudate lobe near the IVC
necrosis occur
- Quadrate lobe between left lobe and gall bladder
- Dehydration occurs more slowly
- Receives oxygenated blood from hepatic artery
- Caused by adenocarcinoid tumors
- Receives food-laden blood from GIT
- Symptoms develop slowly, constipation, bloody stool → - Blood from both sources mix in the liver sinusoids
iron deficiency anemia - Oxygen, nutrients and certain toxic substances are
- Distented abdomen and crampy lower abdominal pain extracted by hepatic cells
- Fecal vomiting develops
- Shock may occur FUNCTIONS OF THE LIVER
- Glucose Metabolism and Regulation of blood glucose
Medical Management concentration
- IV therapy, NGT aspiration & decompression - Ammonia Conversion- amino acids from protein for
- Colonoscopy: untwist and decompress the bowel gluconeogenesis results in ammonia formation as a
- Cecostomy: surgical opening made into the cecum, urgent byproduct. Liver converts to urea and excreted in the
relief from obstruction urine
- Surgical resection: remove the obstruction - Protein Metabolism- synthesizes all of the plasma proteins
- A temporary or permanent colostomy (except gamma globulins), including albumin, alpha &
- Ileoanal anastomosis, if necessary to remove the entire beta globulins, blood clotting factors, transport proteins
large bowel and plasma lipoproteins. Vit K is required by the liver for
- Rectal tube used to decompress area lower in the bowel the synthesis of clotting factors. Amino acids serve as
building blocks for CHON synthesis
- Fat Metabolism- fatty acids are broken down for the

production of ketone bodies, esp occurs during starvation
and uncontrolled DM
- Vitamin and Iron storage- Vit A, B, D, several B complex,
iron, copper
- Drug Metabolism- results in the loss of activity of the
medication, one impt pathway is conjugation
- Bile Formation- formed in the hepatocytes, composed
mainly of water and electrolytes bile is collected & stored
in the gallbladder is emptied into the intestines for
digestion
- Bilirubin Excretion- bilirubin is a pigment derived from the
breakdown of Hgb by the REC including the Kupffer cells of
the liver
Liver Function Studies

- Serum aminotransferases: AST(SGOT=4.8-19U/L), Jaundice
ALT(SGPT=2.4-7U/L), GGT, GGTP, LDH - Yellow- or greenish yellow-tinged body tissues, sclera,
- Serum protein studies and skin due to increased serum bilirubin levels
- Pigment studies: direct and indirect serum bilirubin, urine - Levels exceed 2.5mg/dl
bilirubin, and urine bilirubin and urobilinogen - Types
- Prothrombin time - Hemolytic
- Serum alkaline phosphatase - Hepatocellular
- Serum ammonia - Obstructive
- Cholesterol - Hereditary hyperbilirubinemia
- Hepatocellular and obstructive jaundice types are most
Additional Diagnostic Studies associated with liver disease.
- Liver biopsy
- Ultrasonography Hemolytic Jaundice
- CT due to:
- MRI - rapid RBC destruction increased in indirect,
- Other unconjugated or B2
- due to hemolytic transfusion reaction and other
Hepatic Dysfunction hemolytic disorders
- Acute or chronic (more common) - Do not experience symptoms or complications unless
- Cirrhosis of the liver extreme hyperbilirubinemia
- Predisposes to pigment stones in the Gallbladder, and in
- Causes: extremely severe jaundice poses a risk for brain stem
Most common cause is malnutrition related to alcoholism. damage
 Infection
 Anoxia Obstructive Jaundice
 Metabolic disorders due to:
 Nutritional deficiencies - occlusion of the bile duct
 Hypersensitivity states - gallstone
- biliary atresia
Manifestations - inflammation of the biliary tract
- Jaundice- increased bilirubin conc. in blood - tumors
- Portal hypertension, ascites, and varices -results from
circulatory changes w/in the diseased liver & produces
- cholestatic agent- antithyroid, phenothiazines,
sulfonylureas, tricyclic antidepressants, nitrofurantoin,
severe GI hge, marked sodium & fluid retention
androgens and estrogens
- Hepatic encephalopathy or coma -accumulation of
- total bilirubin is increased
ammonia in the serum
- Nutritional deficiencies-results from inability to metabolize - bile is dammed into the liver and reabsorbed into the
vitamins circulation
s/sx:
- deep orange, foamy urine
- dark tea colored urine
- clay colored stool
- severe itchiness
- steatorrhea
Hepatocellular Jaundice
due to:
- Diseased liver (hepatitis or cirrhosis)
- Inability of the liver to clear normal amount of bilirubin
from the blood
- Increased bilirubin and albumin
- Bed rest during acute stage

Signs and Symptoms Associated with Hepatocellular and - Nutritional support
Obstructive Jaundice
- Hepatocellular
 Patient may appear mildly or severely ill. Hepatitis B (HBV)
 Lack of appetite, nausea, weight loss - Transmitted through blood, saliva, semen, and vaginal
 Malaise, fatigue, weakness secretions, sexually transmitted, transmitted to infant at
 Headache, chills, and fever if infectious in origin the time of birth
- Obstructive - A major worldwide cause of cirrhosis and liver cancer
 Dark orange-brown urine and light clay-colored stools
 Dyspepsia and intolerance of fats, impaired digestion • At Risk: surgeons, nurses, lab workers
 Pruritus - Mortality rate: 10%
- Has a carrier state and can develop to chronic state and
Jaundice Management: hepatocellular injury
- Long incubation period: 1-6 months
- Control pruritus
 calamine • Manifestations: insidious and variable
 baking soda - similar to hepatitis A:
 NaHCO3  anorexia, dyspepsia
 Antihistamine  abd’l pain
 Soothing baths  generalized itching
- Drug  malaise
Cholestyramine = it binds bile salts in the intestine and  weakness
eliminated via feces.  w/ or w/o jaundice
 Look for the cause and manage it
- The virus has antigenic particles that elicit specific
Hepatitis antibody markers during different stages of the disease.
- Viral hepatitis: a systemic viral infection that causes
necrosis and inflammation of liver cells with characteristic • ASSESSMENT AND DIAGNOSTIC FINDINGS
symptoms and cellular and biochemical changes - HBV is a DNA virus composed the ff antigenic
A particles:
B  HBcAg- hep B core antigen
C  HBsAg- hep B surface antigen
D  HBeAg- independent CHON circulating in the blood
E  HBxAg- gene product of X gene of HBV/DNA
 Hepatitis G and GB virus-C - Each antigen elicits its specific antibody and is marker
- Nonviral hepatitis: toxin- and drug-induced for the diff stages of the disease process:
- Hepatitis A and E- fecal-oral route  Anti-HBc- persists during acute illness, may indicate
- Hepatitis B, C, D share many characteristics continuing HBV in the liver
Hepatitis A (HAV)  Anti-HBs- detected during late convalescence and
- 20-25% of clinical hepatitis, infectious hepatitis indicates recovery and devt of immunity
- Fecal-oral transmission  Anti-HBe- usually signifies reduced infectivity
- Spread primarily by poor hygiene; hand-to-mouth
contact, close contact, or through food and fluids • Management
- Prevention
• Incubation:  Vaccine: for persons at high risk, routine
 15-50 days vaccination of infants
 Illness may last 4-8 weeks.  Passive immunization for those exposed
 Standard precautions/infection control measures
- Mortality is 0.5% for younger than age 40 and 1-2% for  Screening of blood and blood products
those over age 40. - Bed rest
- Nutritional support
• Manifestations: - Medications for chronic hepatitis type B include alpha
1. mild flu-like symptoms interferon and antiviral agents: lamivudine (Epivir), adefovir
2. low-grade fever (Hepsera).
3. anorexia
4. later jaundice and dark urine
5. indigestion and epigastric distress Hepatitis C
6. enlargement of liver and spleen - Transmitted by blood and sexual contact, including
needlesticks and sharing of needles
- Anti-HAV antibody in serum after symptoms appear - The most common bloodborne infection
- A cause of 1/3 of cases of liver cancer and the most
• Management common reason for liver transplant
- Prevention
- Good handwashing, safe water, and proper sewage disposal
- Vaccine
- Immunoglobulin for contacts to provide passive immunity
• Risk factors - Liver physiology and Pathophysiology

 Incubation period is variable. Normal Function Abnormality in function
1. Stores glycogen = Hypoglycemia
- Symptoms are usually mild.
- Chronic carrier state frequently occurs. 2. Synthesizes proteins = Hypoproteinemia
3. Synthesizes globulins = Decreased Antibody
• Management formation
- Prevention 4. Synthesizes Clothing = Bleeding tendencies
- Screening of blood factors
- Prevention of needlesticks for health care workers 5. Secreting bile = Jaundice and pruritus
- Measures to reduce spread of infection as with hepatitis
6. Converts ammonia to = Hyperammonemia
B
urea
- Alcohol encourages the progression of the disease, so
7. Stores Vit and =Deficiencies of Vit and
alcohol and medications that affect the liver should be
minerals min
avoided.
- Antiviral agents: interferon and ribavirin (Rebetol) 8. Metabolizes estrogen = Gynecomastia, testes
atrophy
Hepatitis D and E
Hepatitis D
- Only persons with hepatitis B are at risk for hepatitis D.
- Transmission is through blood and sexual contact.
- Symptoms and treatment are similar to hepatitis B, but
patient is more likely to develop fulminant liver failure
and chronic active hepatitis and cirrhosis.
Hepatitis E
- Transmitted by fecal-oral route
- Incubation period 15-65 days
- Resembles hepatitis A and is self-limited, with an abrupt
onset. No chronic form.
- Other Liver Disorders
- Nonviral hepatitis
- Toxic hepatitis
- Drug-induced hepatitis
- Fulminant hepatic failure
Liver Cirrhosis
- A chronic, progressive disease characterized by a diffuse
damage to the hepatic cells
- The liver heals with scarring, fibrosis and nodular
regeneration
Assessment Findings
ETIOLOGY: 1. Anorexia and weight loss
2. Jaundice
Post-infection, Alcohol, Cardiac diseases, 3. Fatigue
Schisostoma, Biliary obstruction
- Types:
• Laennec’s Cirrhosis
 most common
 alcoholic cirrhosis
 scar tissue surrounds the portal areas
 chronic disease
• Postnecrotic Cirrhosis
 a sequelae of viral hepatitis
 Biliary Cirrhosis
 due to chronic biliary obstruction and infection
- Pathogenesis:
• repeated destruction of hepatic cell
→ scar tissue formation (fibrotic) → regeneration of liver cell
follows → another destruction will occur → cycle (scarring and 4. Early morning nausea and vomiting
regeneration) will be repeated until hepatocytes becomes 5. RUQ abdominal pain
fibrotic and liver function is compromised 6. Ascites
7. Signs of Portal hypertension
Cancer of the Liver

- Primary liver tumors
- Few cancers originate in the liver.
- Usually associated with hepatitis B and C
- Hepatocellular carcinoma (HCC)
- Liver metastasis
- Liver is a frequent site of metastatic cancer.
Manifestations
- Pain, dull continuous ache in RUQ, epigastrium, or back
- Weight loss, loss of strength, anorexia, anemia may
occur.
- Jaundice if bile ducts occluded, ascites if obstructed
portal veins
Nonsurgical Management of Liver Cancer

- Underlying cirrhosis, which is prevalent in patients with
liver cancer, increases risks of surgery.
- Major effect of nonsurgical therapy may be palliative.
- Radiation therapy
- Chemotherapy
- Percutaneous biliary drainage
- Other nonsurgical treatments
Surgical Management of Liver Cancer

- Treatment of choice for HCC if confined to one lobe and
liver function is adequate
- Liver has regenerative capacity.
NURSING INTERVENTIONS - Types of surgery
1. Monitor VS, I and O, Abdominal girth, weight, LOC and  Lobectomy
Bleeding  Cryosurgery
2. Promote rest. Elevated the head of the bed to minimize  Liver transplant
dyspnea
3. Provide Moderate to LOW-protein (1 g/kg/day) and LOW- Nursing Care of the Patient Undergoing a Liver Transplant
sodium diet - Preoperative nursing interventions
4. Provide supplemental vitamins (especially K) and minerals - Postoperative nursing interventions
5. Administer prescribed - Patient teaching
 Diuretics= to reduce ascites and edema
 Lactulose= to reduce NH4 in the bowel The Gallbladder
 Antacids and Neomycin= to kill bacterial flora that Anatomy
cause NH production - The gallbladder
6. Avoid hepatotoxic drugs - Located below the liver
 Paracetamol - The cystic duct joins the hepatic duct to become the
 Anti-tubercular drugs common bile duct
7. Reduce the risk of injury - The common bile duct joins the pancreatic duct in
 Side rails reorientation the sphincter of Oddi in the first part of the
 Assistance in ambulation duodenum
 Use of electric razor and soft-bristled toothbrush
8. Keep equipments ready including Sengstaken-Blakemore tube, Liver, Biliary System, and Pancreas
IV fluids, Medications to treat hemorrhage
Nursing Interventions Rationale

1. Low sodium Diet To reduce edema
2. Low protein diet To reduce NH production
3. Benadryl and mild soap To relieve pruritus
4. Pressure onto injection To prevent bleeding
site
5. Assist in paracentesis Done to relieve abdominal
pressure
6. Administer Medications:
• Diuretics, Neomycin,
Lactulose
• Albumin, Amino acid
• Vitamin K
(Menadione)
Physiology ASSESSMENT findings for cholecystitis

- Stores and concentrates bile 1. Indigestion, belching and flatulence
- Contracts during the digestion of fats to deliver the 2. Fatty food intolerance
bile 3. Epigastric pain that radiates to the scapula or
- Cholecystokinin-pancreozymin is a hormone localized at the RUQ
released by the duodenal cells, causing the 4. Mass at the RUQ
contraction of the gallbladder and relaxation of the 5. Murphy’s sign
sphincter of Oddi 6. Jaundice
7. dark orange and foamy urine
Cholecystitis
- Inflammation of the gallbladder DIAGNOSTIC PROCEDURES
- Can be acute or chronic 1. Ultrasonography- can detect the stones
- Acute cholecystitis usually is due to gallbladder stones 2. Abdominal X-ray
- Chronic cholecystitis is usually due to long standing 3. Cholecystography
gall bladder inflammation 4. WBC count increased
5. Oral cholecystography cannot visualize the
gallbladder
6. ERCP: revels inflamed gallbladder with gallstone
NURSING INTERVENTIONS
1. Maintain NPO in the active phase
2. Maintain NGT decompression
3. Administer prescribed medications to relieve
pain. Usually Demerol (MEPERIDINE)
4. Codeine and Morphine may cause spasm of
the Sphincter increased pain. Morphine cause
MOREPAIN
5. Instruct patient to AVOID HIGH- fat diet and
GAS-forming foods
6. Assist in surgical and non-surgical measures
7. Surgical procedures- Cholecystectomy,
Choledochotomy, laparoscopy
PHARMACOLOGIC THERAPY
1. Analgesic- Meperidine
2. Chenodeoxycholic acid= to dissolve the gallstones
3. Antacids
4. Anti-emetics
- Formation of GALLSTONES in the biliary apparatus
Predisposing FACTORS
- “F”
 Female
 Fat
 Forty
 Fertile
 Fair
- Pathophysiology
 Supersaturated bile, Biliary stasis
↓
- Stone formation
↓
- Blockage of Gallbladder
↓
- Inflammation, Mucosal Damage and WBC infiltration
The pancreas: Exocrine function

The pancreas
Anatomy
 A retroperitoneal gland
 Functions as an endocrine and exocrine gland
 The pancreatic duct (major) joins the common bile
duct in the sphincter of Oddi
Physiology
- 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!
Pancreatitis
- Inflammation of the pancreas
- Can be acute or chronic
- Pancreatitis
- A severe disorder that can lead to death. Acute
pancreatitis does not usually lead to chronic
pancreatitis.
- Acute pancreatitis: pancreatic duct becomes
obstructed and enzymes back up into the pancreatic
duct, causing autodigestion and inflammation of the
pancreas
- Chronic pancreatitis: a progressive inflammatory
disorder with destruction of the pancreas. Cells are
replaced by fibrous tissue, and pressure within the
pancreas increases. Mechanical obstruction of the
pancreatic and common bile ducts and destruction of
- Cholesterol Gallstones and Pigment Gallstones the secreting cells of the pancreas occur.
-
Etiology and predisposing factors
- Alcoholism
- Hypercalcemia
- Trauma
- Hyperlipidemia
- Biliary tract disease - cholelithiasis
- Bacterial disease
- PUD
- Mumps
PATHOPHYSIOLOGY of acute pancreatitis

- Self-digestion of the pancreas by its own digestive
enzymes principally TRYPSIN
- Spasm, edema or block in the Ampulla of Vater
reflux of proteolytic enzymes  auto digestion of the
pancreas  inflammation
- Autodigestion of pancreatic tissue
Post-operative nursing interventions
- Monitor for surgical complications ↓
- Post-operative position after recovery from - Hemorrhage, Necrosis and Inflammation
anesthesia- LOW FOWLER’s ↓
- Encourage early ambulation - KININ ACTIVATION will result to increased
- Administer medication before coughing and deep permeability
breathing exercises ↓
- Advise client to splint the abdomen to prevent
- Loss of Protein-rich fluid into the peritoneum
discomfort during coughing
- Administer analgesics, antiemetics, antacids ↓
- Care of the biliary drainageor T-tube drainage - HYPOVOLEMIA
- Fat restriction is only limited to 4-6 weeks. Normal
diet is resumed
Quick Summary
Manifestations • Peptic Ulcer
• Acute - Ulceration of mucosa; In the stomach or duodenum
- Severe abdominal pain - Outstanding Symptom: PAIN
- Patient appears acutely ill. - Nursing Goal: Allow ulcer to heal, prevent complication
- Abdominal guarding - Rest: physical and Mental
- Nausea and vomiting - Eliminate certain foods
- Fever, jaundice, confusion, and agitation may occur. - Medications: antacid, H2 blockers, Proton Pump
- Ecchymosis in the flank or umbilical area may occur. inhibitors, antibiotics, mucosal protectants
- Patient may develop respiratory distress, hypoxia, renal - Surgery: Vagotomy, Billroth 1 and 2
failure, hypovolemia, and shock. - Quick Summary
- Liver Cirrhosis
• Chronic - Destruction of liver with replacement by scars
- Recurrent attacks of severe upper abdominal and back pain - Common causes: alcoholism, post-hepatitic
accompanied by vomiting - Manifestations related to liver derangements
- Weight loss - Jaundice, Ascites, splenomegaly, bleeding, enceph
- Steatorrhea - Nursing goal: Control manifestations and maximize liver
function
Assessment Findings • Liver Cirrhosis

1. Abdominal pain- acute onset, occurring after a - Encourage rest
heavy meal or alcohol intake - Avoid hepatotoxic drugs
2. Abdominal guarding - Diet: HIGH calorie, Restricted protein, LOW Na
3. Bruising on the flanks and umbilicus - Weight client and measure abdominal girth daily
4. N/V, jaundice - Provide skin care for jaundice and edema
5. Hypotension and hypovolemia - Assess for bleeding: esophageal, rectal, cutaneous
6. Signs of shock - DRUGS: Antacids, Diuretics, Albumin, Neomycin and
Lactulose
Diagnostic Tests
1. Serum amylase and serum lipase • Cholecystitis
2. Ultrasound - Inflammation of the gallbladder commonly caused by
3. WBC cholelithiasis (Female, Fat, Forty, Fertile, Fair)
4. Serum calcium - Manifestations: Fat intolerance, RUQ pain, Nausea and
5. CT scan vomiting, Jaundice, Murphy’s sign
6. Hemoglobin and hematocrit - Nursing Goal: Relieve symptoms and assist in stone
removal
Nursing Interventions - Administer MEPERIDINE, avoid morphine
1. Assist in pain management. Usually, Demerol is - Maintain Fluid and electrolyte balance
given. Morphine is AVOIDED - Maintain a LOW fat diet
2. Assist in correction of Fluid and Blood loss - Semi-fowler’s position
3. Place patient on NPO to inhibit pancreatic - Assist in surgery
stimulation - Care of the T-tube
4. NGT insertion to decompress distention and
remove gastric secretions • Pancreatitis
5. Maintain on bed rest - Inflammation of the pancreas brought about by the
digestion of the organ by the enzyme it produces
6. Position patient in SEMI-FOWLER’s to decrease - Common causes: Alcoholism, stone
pressure on the diaphragm - Manifestations: Extreme upper abdominal pain radiating
7. Deep breathing and coughing exercises into the back, vomiting, nausea, Abdominal distention,
8. Provide parenteral nutrition Steatorrhea and weight loss
9. Introduce oral feedings gradually- HIGH carbo, - Laboratory: ELEVATED lipase and amylase
LOW FAT
- Nursing Goal : relieve symptoms, maintain blood
10.Maintain skin integrity
volume and GIT rest
11.Manage shock and other complications
- NPO
- Provide IVF and Parenteral nutrition
- Drugs: MEPERIDINE, never morphine, Antacids,
anticholinergics
- After Acute phase: LOW fat diet, avoid alcohol, fat and
vitamin replacements

The Gastro

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The Gastro

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Medical Surgical Nursing

The GASTRO-INTESTINAL system

The Gastro-Intestinal System

Review of the GIT Anatomy and Physiology

 Decreased gastric secretions

• Physiology Secreted by endocrine cells

• Small Intestine Function

2 Types of contractions in the small intestines

2 types of colonic secretions:

• Waste Products of Digestion

• FECALYSIS: Occult Blood Testing

• Lower GI- scopy

- Intra-test: position : LEFT lateral to facilitate salivary

• Lower GI- scopy

- Post-test: Advise that dysuria is common as the dye is

- Include all information related to GI function

Common Sites of Referred Abdominal Pain

COMMON GIT SYMPTOMS AND MANAGEMENT

• Diarrhea Chronic - slowly progressive, a fully formed abscess

- onset is sudden, fever, the gland swells and becomes

Condition Of The Esophagus

Sliding Esophageal and Paraesophageal Hernia

- Assessment (For Gerd)

- May be Acute or Chronic

Peptic Ulcer Disease

- An ulceration of the esophageal, gastric and duodenal

- Causes: H.pylori infection, excessive secretion of HCl,

malignant tumors of the pancreas-resistant to standard Relieved by food, Commonly Accompanied

Duodenal Ulcer Gastric Ulcer

- Surgical Procedures For Pud

Billroth I-Gastroduodenostomy Nursing Interventions

Nursing Interventions For Bleeding

Surgical Procedures For Pud

6. Weakness - Abnormal hardening of stools

Surgical reconstruction, spinchter repair or fecal diversion - Barium enema

CONDITIONS OF THE LARGE INTESTINE

5. Rebound tenderness and abdominal rigidity (if

ASSESSMENT findings for Hemorrhoids

Nursing Interventions Nursing Interventions

PATHOPHYSIOLOGY Diverticular Disease

- Increased intraluminal pressure, LOW volume in the

ASSESSMENT findings for D/D

DIAGNOSTIC STUDIES - Volvulus

Large Bowel Obstruction

- Fat Metabolism- fatty acids are broken down for the

Liver Function Studies

- Bed rest during acute stage

• Risk factors - Liver physiology and Pathophysiology

Cancer of the Liver

Nonsurgical Management of Liver Cancer

Surgical Management of Liver Cancer

Nursing Interventions Rationale

Physiology ASSESSMENT findings for cholecystitis

The pancreas: Exocrine function

PATHOPHYSIOLOGY of acute pancreatitis

Assessment Findings • Liver Cirrhosis

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