Professional Documents
Culture Documents
Nursing of Clients With Gastrointestinal Disorders
Nursing of Clients With Gastrointestinal Disorders
Nursing of Clients With Gastrointestinal Disorders
WITH GASTROINTESTINAL
DISORDERS
Rhenier S. Ilado, RN
Gastrointestinal System
I. Upper alimentary canal - function for digestion
Mouth – mechanical and chemical digestion, deglutition
Pharynx (throat)
Esophagus – passage of bolus by peristalsis, contains
UES and LES
Stomach- mechanical and chemical digestion, secretion
of gastric juice, gastric emptying
1st half of duodenum
Gastrointestinal System
II. Middle Alimentary canal – Function: for absorption
-Complete absorption – large intestine
2nd half of duodenum - for digestion/absorption of most
nutrients
Jejunum
Ileum
1st half of ascending colon
Gastrointestinal System
III. Lower Alimentary Canal – Function:
elimination/defecation
2nd half of ascending colon
Transverse
Descending colon
Sigmoid
Rectum
Gastrointestinal System
IV. Accessory Organ
Salivary gland
Vermiform appendix
Liver
Pancreas – auto digestion
Gallbladder – storage of bile
DIAGNOSTIC EXAMS
Stool for Occult Blood (Guaic Stool Exam)
• used to check stool samples for hidden (occult) blood.
• detects GI bleeding
• Nursing Intervention before exam:
High fiber diet for 48-72 hours
Avoid Red meats, poultry, fish and dark colored foods
No Iron – because it causes blackish discoloration of
stool
No steroids causes GI irritation
3 stool specimen will be collected
+ Guaic stool exam means peptic ulcer or gastric cancer
Gastric Analysis
• This test measures acid content of
stomach collected through a
nasogastric (stomach) tube.
• Measures secretion of HCL and
pepsin
• NPO for 12 hours
• NGT is inserted
• Gastric contents collected for every
15minutes to 1 hour
• Results: Increase HCL means
duodenal ulcer
Decrease HCL means gastric
cancer, Pernicious anemia
Radiographic Tests
UGIS (Upper GI Series/Barium Swallow) – to
visualize the esophagus, stomach, duodenum
and jejunum
Nursing Interventions Before procedure:
a. NPO for 6-8 hours
b. Barium sulfate (BaSO4) per Orem
c. X-ray will be taken
After procedure:
a. laxative
b. increase fluid intake
c. inform client that the stool is white
for 24-72 hours
d. observe Ba impaction: distended
abdomen, constipation
Radiographic Tests
LGIS (Lower GI Series/Ba Enema) – to
visualize the colon
Before procedure:
a. low residue/clear liquid diet for 2
days
b. laxative for cleansing the bowel
c. cleansing enema in AM
d. BaSO4 per rectum
After procedure:
a. laxative
b. increase fluid intake
c. inform client that the stool is white
for 24-72 hours
d. observe Ba impaction: distended
abdomen, constipation
Endoscopy
UGI Endoscopy – direct visualization of esophagus, stomach and
duodenum
Before procedure:
a. Consent
b. NPO for 6-8 hours
c. Anticholinergic - atropine sulfate. To reduce mucus secretion
d. Sedatives, narcotics, tranquilizers. To relax the client
(Diazepam/Meperidine HCL)
e. Remove dentures. To prevent airway obstruction.
f. local anesthetic spray on posterior pharynx. To depress gag
reflex.
After Procedure:
a. Side-lying position. To prevent aspiration
b. NPO until gag reflex returns (2-4 hours)
c. monitor VS
d. NSS gargle. To soothe the throat
e. assess: bleeding, fever, neck/throat pain, dyspepsia, dysphagia
f. advice to avoid driving for 12 hours. If sedative was used
LGI Endoscopy
Proctosigmoidoscopy (Sigmoid, rectum)
Before procedure:
a. clear liquid diet 24 hours before
b. laxative
c. cleansing enema
d. knee chest /lateral position
After procedure:
a. supine position. To prevent postural
hypotension.
b. assess for signs of perforation – bleeding, pain,
fever
c. hot sitz bath for discomfort in anorectal area.
LGI Endoscopy
Colonoscopy
• Preparation is the same with
proctosigmoidoscopy
• Sedation is done to relax the
client
• Patient is placed in left lateral
position
After procedure
• Monitor VS – bradycardia
(vasovagal response)
• assess for signs of perforation –
bleeding, pain, fever
Liver Biopsy
Before procedure:
1. Consent
2. NPO 2-4 hours
3. Vit K injection; monitor PT
4. Position in left side or supine with pillow under
right shoulder
5. Instruct the patient to exhale deeply, hold breath for
5-10 seconds, during needle insertion to prevent trauma to
diaghpram.
After procedure:
1. Turn to right side for 4 hours to apply pressure and
prevent bleeding
2. Bed rest for 24 hours
3. Monitor VS 30 min.
Liver Biopsy
Paracentesis
• aspiration of fluid in the peritoneal cavity
Indications
• to relieve abdominal pressure from ascites
• to diagnose spontaneous bacterial peritonitis and other infections
• to diagnose metastatic cancer
• to diagnose blood in peritoneal space in trauma
Before procedure:
1. consent
2. check initial VS
3. empty bladder to prevent puncture
4. place in sitting or supine pos.
After procedure:
1. assess VS
2. Assess rigidity of the abdomen (peritonitis) and
hypovolemic shock
Paracentesis
Endoscopic Retrograde
Cholangiopancreatography (ERCP)
• direct visualization with radiographic examination of the liver,
gallbladder and pancreas.
• Contrast medium is introduced via the endoscope, x-ray are taken
simultaneously.
Before procedure:
1. Consent
2. NPO 10-12 hours
3. Check allergy to iodine/seafoods
4. VS
5. AtSO4, valium
6. Local anesthetic spray into the throat
7. pos. in left side
After procedure:
1. NPO until gag returns
2. Turn to sides to prevent aspiration
3. VS
4. monitor for signs of perforation and sepsis
Endoscopic Retrograde
Cholangiopancreatography (ERCP)
Nasogastric Tube Feeding (NGT)
Nursing responsibilities:
1. Assist patient in semi to high Fowler’s position
2. Assess tube placement and patency
a. Auscultation –introduced 10 ml of air in NGT and auscultate at
epigastric area for gurgling sound
b. Aspiration – gastric contents is aspirated which is
yellowish/greenish in color
c. Immersion – immerse the tip of the tube in the water, no
bubbles should be produced
3. the most effective – X- ray
4. Assess residual feeding contents. To assess absorption of the last
feeding. If 100 or more, verify if the feeding will be given
5. Height of feeding is 12 inches above point of insertion.
6. Instill 30-60 ml of water into NGT after feeding. To cleanse the lumen of
the tube
7. Have client remain in semi to high- Fowler’s position 30-60 minutes after
feeding. To prevent gastric reflux and aspiration
Tube Feeding (NGT)
Administering ENEMA
• Purposes:
To relieve constipation
To relieve flatulence
To administer medication
To evacuate feces in
preparation for diagnostic
procedure or surgery
Administering ENEMA
Non- retention Enema/Cleansing Enema – stimulates peristalsis by irritating the colon
and rectum
• Solutions:
a. Tap water (500-1000ml)
b. Soap suds
c. NSS (9 ml of NaCl to 1000ml of water)
d. Hypertonic solution/fleet enema (90-120 ml)
Retention Enema – introduces oil into the rectum and sigmoid colon, oil retained in 1 to 3
hours
• act to soften the feces and to lubricate the rectum and anal canal facilitating the passage of
feces
Nursing responsibilities:
1. Check doctor’s order
2. Provide privacy
3. position – left lateral position. To facilitate flow of solution by gravity
4. Lubrication 2 inches of the rectal tube. To prevent trauma to anorectal mucosa
5. Insert 3-4 inches while asking to inhale deeply
6. If abdominal cramps occur, temporarily stop the flow by clamping the tube.
7. Ask the client who is using the toilet not to flush it. The nurse should actually assess the
return flow of the solution
GASTROINTESTINAL
DISORDERS
GASTROESOPHAGEAL
REFLUX DISEASE (GERD)
Gastroesophageal Reflux Disease
(GERD)
• Backward flow of gastric or duodenal contents into the
esophagus
• Affects 15 to 20% of adults; increasing incidence with
aging
• Etiology:
Reflux results from transient relaxation or incompetence of the
lower esophageal sphincter; pyloric stenosis
Increased gastric volume (after meals)
Positions pushing gastric contents close to gastroesophageal
juncture (i.e. bending or lying down)
Increased gastric pressure (obesity or tight clothing)
Pathophysiology
• A weak or incompetent LES allows backward movement
of gastric contents into esophagus
• Decreased esophageal peristalsis and salivary function
impair clearance of the refluxed acid, resulting in mucosal
injury to the esophagus
Gastroesophageal Reflux Disease
(GERD)
• Signs and Symptoms:
Pyrosis – burning sensation in the esophagus
Dyspepsia – indigestion
Regurgitation
Dysphagia – difficulty on swallowing
Odynophagia – pain on swallowing
Hypersalivation
Esophagitis
Complications:
Esophageal strictures progressing to dysphagia
Increased risk for esophageal cancer
Diagnostic Test
• Diagnosis may be made from history of symptoms
• Barium Swallow – evaluation of esophagus, stomach
and small intestine
• Upper endoscopy – for direct visualization
Collaborative Management
• Life style changes
• Diet modifications
Elimination of acid foods or irritants (tomatoes, spicy, citrus foods,
coffee)
Avoiding foods which relax esophageal sphincter or delay gastric
emptying (fatty foods, chocolate, alcohol)
Maintain ideal body weight
Eat small meals and stay upright for 2 hours after eating; client
should not eat 3 hours prior to going to bed
Elevate the head of bed on 6 to 8 blocks to decrease reflux
Eat a low fat, high fiber diet
Collaborative Management
• Medications
Antacids: mild to moderate symptoms e.g. Maalox,
Gaviscon
H2 receptor blockers: decrease acid production; given
BID or more often e.g. cimetidine, ranitidine
Proton pump inhibitors; reduce gastric secretions,
promote healing of esophageal erosion e.g. omeprazole
Pro-motility agent; enhances esophageal clearance and
gastric emptying e.g. metoclopramide
Collaborative Management
• Surgical Management
Nissen Fundoplication – suture fundus around the esophagus;
wrapping a portion of the gastric fundus around the sphincter area
of the esophagus
HIATAL HERNIA
(DIAPHRAGMATIC HERNIA)
HIATAL HERNIA (Diaphragmatic Hernia)
• Part of the stomach protrudes through the esophageal hiatus
of the diaphragm into thoracic cavity
• Most cases are asymptomatic; incidence increases with age
• Types:
Sliding Hiatal Hernia
o protrusion of the esophageal junction into the thoracic cavity and back
into the abdominal cavity in relation to position changes
o Primary cause is muscle weakness in the esophageal hiatus (opening
between the domes of the diaphragm where the esophagus enters the
abdominal cavity)
o Due to aging process, congenital muscle weakness, obesity, trauma,
surgery, prolonged increased in intra-abdominal pressure i.e. heavy
lifting
HIATAL HERNIA (Diaphragmatic
Hernia)
HIATAL HERNIA (Diaphragmatic
Hernia)
Paraesophageal hernia or rolling hernia
o Protrusion of the fundus of the stomach and the greater curvature
into the thorax next to the esophagus
o Gastric junction remains below the diaphragm
o Due to anatomic defect
HIATAL HERNIA (Diaphragmatic
Hernia)
HIATAL HERNIA (Diaphragmatic
Hernia)
• Clinical Manifestations:
Heartburn due to gastroesophageal reflux
Dysphagia (difficulty swallowing) – due to compression of
the esophagus
Dyspnea – due to compression of the lungs
Abdominal pain due to compression of the protruding
portion of the stomach
Nausea and vomiting
Gastric distention, belching, flatulence due to
accumulation of gas in the stomach and abdomen caused
by impaired motility
Collaborative Management
• Modify diet
High protein diet to enhance LES pressure and prevent esophageal
reflux
Small frequent feedings to prevent gastric distention (this prevents
further protrusion of the stomach into the thoracic cavity)
Instruct client to eat slowly and chew food properly. To reduce gastric
motility
The client should avoid foods and beverages that decreases LES
pressure like fatty foods, cola beverages, coffee, tea, chocolate, alcohol
The client should assume upright position before and after eating for 1
to 2 hours (this prevents protrusion of the stomach into the thoracic
cavity)
Instruct the client to avoid eating at least 3 hours before bedtime (to
prevent night time reflux)
Collaborative Management
• Administer medications as ordered:
Antacids to relieve heartburns
Antiemetics to releive nausea and vomiting e.g. phenergan
(promethazine HCL), Reglan (Metochlopromide)
Histamine H2 receptor antagonists to suppress secretion of gastric
acid e.g. ranitidine, cimetidine
• Advise client to reduce body weight if obese
• Advise client to promote lifestyle changes
Elevate head of bed 6-12 inches for sleep
Avoid factors that increase abdominal pressure like use of
constrictive clothing, straining at stool, heavy lifting, bending,
stooping, vigorous coughing
Avoid cigaratte smoking. Smoking causes rapid and significant
drop in LES pressure
Collaborative Management
• Surgical Management
Nissen Fundoplication – suture fundus around the esophagus;
wrapping a portion of the gastric fundus around the sphincter area
of the esophagus
GASTRITIS
GASTRITIS
• localized inflammation of the gastric mucosa
which is normally protected from gastric acid
and enzymes by mucosal barrier
• Types:
Acute Gastritis
• short inflammatory process due to ingestion
of chemical agents or food products that
irrigate and erode gastric mucosa
• Disruption of mucosal barrier allowing
hydrochloric acid and pepsin to have contact
with gastric tissue
• Self-limiting
• Erosive Gastritis – a form of acute gastritis,
stressed-induced, complication of a life-
threatening condition i.e. Curling’s ulcer with
burns, gastric mucosa becomes ischemic
and tissue is injured by stomach acid
GASTRITIS
Chronic Gastritis
• Progressive disorder beginning with superficial
inflammation and leads to atrophy of gastric tissues
• Type A – autoimmune component; loss of hydrochloric
and pepsin secretion; patient develops pernicious anemia
• Type B – more common and occurs with aging; caused by
chronic infection of mucosa by helicobacter pylori;
associated with rick of peptic ulcer disease and gastric
cancer
Etiology
• Irritants include aspirin and other NSAIDS,
corticosteroids, alcohol, caffeine
• Ingestion of corrosive substances; alkali or acid
• Effects from radiation therapy, certain chemotherapeutic
agents
GASTRITIS
• Signs and Symptoms:
Acute Gastritis
Mild – anorexia, mild epigastric discomfort, belching
More severe – abdominal pain, nausea, vomiting,
hematemesis, melena
Erosive – not associated with pain; bleeding occurs 2 or more
days post-stress event
Chronic Gastritis
Vague gastric distress, epigastric heaviness not relieved by
antacids
Fatigue associated with anemia; symptoms associated with
pernicious anemia i.e. paresthesia
Diagnostic Tests
• Gastric analysis – assess hydrochloric acid secretion
(les with chronic gastritis)
• Hemoglobin, hematocrit, RBC – anemia including
pernicious anemia or iron deficiency
• Serum vitamin B12 levels – determine presence of
pernicious anemia
• Upper endoscopy – visualizes mucosa; identify areas of
bleeding; obtain biopsies
Collaborative Management (Acute Gastritis)
• NPO status to rest GI tract for 6 to 12 hours; reintroduce clear
liquids gradually; give IV fluid and electrolytes if indicated
• Medical treatment: proton-pump inhibitor (omeprazole) or H2-
receptor blocker (Ranitidine); sucralfate (carafate) acts locally
to coat and protect the gastric mucosa
• Type B: eradicate H. Pylori infection with combination therapy of
two ATBC – (Metronidazole and clarithromycin or tetracycline)
and proton-pump inhibitor
• Teach food safety measures to prevent acute gastritis from food
contaminated with bacteria
• Management of acute gastritis with NPO state and then gradual
reintroduction of fluids with electrolytes and glucose then
advanced to solid foods
• Teach regarding use of prescribed medications, smoking
cessation and alcohol abuse
PEPTIC ULCER DISEASE (PUD)
PEPTIC ULCER DISEASE (PUD)
• excoriation / erosion of
submucosa & mucosal
lining of the
esophagus, stomach
and intestine due to:
Hypersecretion of acid –
pepsin
Decrease resistance of
mucosal barrier
• Types:
Duodenal ulcers
Gastric Ulcers
Types:
Postoperative
If spinal anesthesia was used, position patient flat on bed for 6 to
8hours (to prevent spinal headache)
Maintain NPO until peristalsis returns. Return of bowel sounds and
passing out of flatus indicate return of peristalsis
Ambulate client 24 hours to prevent postop complications
In ruptured appendicitis – client should be placed in semi-fowler’s
position to promote drainage and to localize inflammation within the
pelvic area (at risk for peritonitis)
PERITONITIS
Peritonitis
• Inflammation of peritoneum, lining that covers wall
(parietal peritoneum) and organs (visceral peritoneum) of
abdominal cavity
• Caused by contamination of normal sterile peritoneal
cavity with infections or chemical irritants
• Etiology:
Ruptured appendicitis
Perforated peptic ulcer
Pelvic inflammatory disease
UTI
Trauma
Bowel obstruction
Peritonitis
• Inflammatory process may lead to the following problems:
Adhesions, abscess formation and intestinal obstruction
Decreased peristalsis leading to the following:
o Fluid shifting into the abdominal cavity (300 to 500 ml/hr) – third
spacing
o Bowel distention with gas and fluid
o Hypovolemia, electrolyte imbalance, dehydration and shock
Peritonitis
• Diagnostic Tests:
Elevated WBC to 20,000
Blood culture: to identify bacteria in the blood
Abdominal x-rays – detect intestinal distention, air-fluid
levels (sign of perforation)
Diagnostic paracentesis
Peritonitis
• Clinical manifestations:
Abdominal pain and rebound tenderness
Board like or abdominal rigidity
Abdominal distention (accumulation of gas and fluid in the
abdomen)
Paralytic ileus; diminished to absent bowel sounds
(decrease peristalsis)
Fever, elevated wbc (20,000/mm3) – due to inflammatory
process
Restlessness, tachycardia, tachypnea, weakness,
oliguria, pallor (signs of shock)
Peritonitis
• Complications:
Abscess leading to SEPTICEMIA
Hypovolemic shock (fluid loss into abdominal cavity)
Paralytic ileus (intestinal obstruction)
Collaborative Management
• Monitor VS, I & O (to assess fluid balance)
• Assists in NGT insertion for intestinal decompression to
relieve abdominal distention
• Bed rest in semi-fowler’s position (to localize inflammatory
process in pelvic cavity)
• Intravenous fluids and electrolytes to maintain vascular
volume and electrolyte balance
• Encourage deep breathing to prevent respiratory
complications (abdominal distention and pain may inhibit
the client from deep breathing)
• Administration of broad spectrum ATBCs an analgesics
• Surgical management: Laparotomy to treat the cause
and remove inflamed tissue
DIVERTICULAR DISEASE
Diverticular disease
Diverticulum – is a single outpouching of the mucosal
lining of the GIT, commonly in the colon
Diverticula (diverticulosis) – are multiple outpouchings
of the mucosal lining of the GIT, especially in the colon
Diverticulitis – is an acute inflammation and infection
caused by trapped fecal material and bacteria in an
outpouching of the mucosal lining of the colon
• Incidence increases with age
• Muscle in bowel wall thickens narrowing bowel lumen and
increasing intraluminal pressure
Diverticular disease
• Etiology: (related to weakening of the bowel wall and
increased intraluminal pressure leading to formation of
diverticula)
Low fiber diet (most common cause)
Decreased activity levels
Postponement of defecation
Pathophysiology
Low fecal volume in the colon
Increased muscular
contraction to push
Increased intraluminal pressure feces
Perforation
peritonitis
Clinical Manifestations
• Crampy abdominal pain in the left lower
quadrant worsen with movement,
coughing or straining
• Chronic constipation with episodes of
diarrhea (due to obstruction in the colon)
• Low grade fever (due to inflammation)
• Nausea and vomiting
• Abdominal distention and tenderness
(due to accumulation of gas and fecal
waste)
• Palpable LLQ mass
• Occult bleeding
• Signs and symptoms of peritonitis (due
to perforation)
Diverticular disease
• Diagnostic Tests
• Barium enema—reveals inflammatory process,
confirmatory
• CBC reveals: decreased hematocrit and hemoglobin
• WBC count – leukocytosis
• Guaiac test – determine presence of occult blood
Collaborative Management
• High fiber diet – to increase bulk of the feces and promote
peristalsis
• Liberal fluid intake of 2,500-3000ml/day – to prevent constipation
• Avoid nuts and seeds – these can become trapped in the diverticula
• Bulk-forming laxatives (to promote peristalsis and defecation) e.g.
metamucil, fibercon (calcium polycarbophil)
• During acute episodes:
Bed rest (to reduce peristalsis and relieve pain)
NPO then clear liquids to rest the bowel
Avoid high fiber foods to prevent further irritation of the colon
IV fluids to replace fluid and electrolyte losses due to vomiting, fever
Broad-spectrum ATBCs to treat infection
Antispamosdics/anticholinergics – to rest the bowel bowels and relieve pain
e.g. Probanthine
NGT insertion to releive abdominal distention
CHRONIC INFLAMMATORY
BOWEL DISORDERS
CHRONIC INFLAMMATORY BOWEL
DISORDERS
• Includes two chronic inflammatory gastrointestinal disorders:
Ulcerative colitis and Crohn’s disease (Regional Enteritis)
• Etiology – unknown
Run in families
Related to infectious agent
Altered immune response
Exacerbations can be precipitated by
o Pesticides
o Food additives
o Tobacco
o Radiation expsure
• Peak incidence occurs between the ages of 15 to 35; second
peak is between ages 60 to 80
• Characterized by exacerbations and remissions
Ulcerative Colitis
• Inflammatory process usually starts to rectum and
sigmoid colon, then ascends until entire lower colon is
affected
• Rectal involvement is 100%
• Inflammation is continuous
• Inflammation leads to mucosal hemorrhages and
abscess formation – leading to necrosis and sloughing
of bowel mucosa
• Mucosa becomes red and ulcerated – bleeding
• Signs and symptoms:
Diarrhea with stool containing pus, blood and mucus; 20-30
watery stools/day)
Fecal urgency; LLQ cramping
Fatigue, anorexia, weakness
Abdominal pain
Weight loss
Crohn’s disease (regional enteritis)
• Can affect any portion of the GI tract, but ileum and
ascending colon are commonly affected
• inflammation is discontinuous (regional)
• Inflammatory lesion of mucosa and sub mucosa
develops into ulcers involving the entire bowel wall
(transmural inflammation)
• Fistula formation – abnormal opening that
connects small and large intestine (contamination
of small intestine content – septicemia); bowel and
bladder fistula
• Absorption problems leading protein loss and
anemia
• Signs and symptoms:
Diarrhea (5-6 soft stool/day) – semi-formed or liquid with
pus and mucus
Abdominal pain
Tenderness in RLQ relieved by defecation
Fever, fatigue, malaise, weight loss
anemia
Complications
• Ulcerative Colitis:
Hemorrhage
Toxic megacolon – usually involves transverse colon which
dilates and lacks peristalsis (charac. by fever, tachycardia,
hypotension, dehydration, abdominal cramping)
Colon perforation leading to peritonitis (15% mortality rate)
Increased risk for colorectal cancer (20 to 30 times) – need
yearly colonoscopies
Complications
• Crohn’s disease
Intestinal obstruction cause by repeated inflammation and
scarring/fibrosis
Fistulas
Perforation of bowel with peritonitis
Massive hemorrhage
Increased risk of bowel cancer (5-6 times)
Diagnostic Tests
• Colonoscopy, sigmoidosopy – determine area and
pattern of involvement; visualize ulcerations
• Upper GI series, Barium enema – most conclusive test;
shows mucosal irregularities; shortening of the bowel and
dilation of bowel loops
• Stool examination and stool culture to rule out infections
and blood
• CBC – anemia, leukocytosis from inflammation and
abscess formation
• low Serum albumin due to mal-absoprtion
Collaborative Management
• Low fiber diet/low residue, high protein, high
calorie – to rest the bowel
• Promote nursing care for a client who is NPO,
receiving IV fluids or TPN during acute
exacerbations to provide nutritional support
• Total parenteral nutrition –feeding a person
intravenously, bypassing the usual process of
eating and digestion; if severe malnutrition is
present
• Assess for fluid and electrolyte imbalance;
administer IV fluids and electrolytes as ordered
Collaborative Management
• Medical treatments:
Corticosteroids – to relieve inflammation
Sulfasalazine (Azulfidine) – sulfonamide ATBC with
topical effect in the colon
Metronidazole (Flagyl) and Ciprofloxacin to control
secondary bowel inflammation and infection
• Surgical Management
Chron’s Disease
o Total colectomy with ileostomy (stoma is found in
the right lower quadrant of the abdomen)
o Segmental colectomy with anastomosis
Ulcerative Colitis
o Proctocolectomy with ileostomy
ANATOMY & PHYSIOLOGY OF
THE LIVER, GALL BLADDER
AND PANCREATIC SYSTEM:
Liver
• Largest glandular organ
• Has 2 lobes
• Located in the RUQ of the abdomen
• 2/3 of blood supply comes from
portal vein (receives mostly
unoxygenated blood)
• Blood supply are portal vein and
hepatic artery
• Functional unit is hepatic lobule
• Contain Kupffer cells – phagocytic
cells which cleansed blood of
bacteria and other foreign
substances
• Contain hepatocytes – liver cells
Liver
• Major Functions:
Metabolism of carbohydrates, proteins and fats
Carbohydrate metabolism
o Glycogenesis (formation of glycogen from glucose)
o Glycogenolysis (breakdown of glycogen to form glucose)
o Gluconeogenesis (production of glucose from non-carbohydrate substance)
Protein metabolism
o Protein catabolism
o Synthesize plasma proteins i.e. albumin, clotting factors, enzymes, globulins
Fat metabolism
o Synthesis of cholesterols and phospholipids
o Formation of lipoproteins
o Ketone formation (from breaking down fatty acids)
Liver
Production of bile salts (hepatocytes) – produces 1L/day;
BILE comprises of water, electrolytes, phospholipids,
cholesterol and bile salts
Bilirubin metabolism; breakdown product of hemoglobin;
being conjugated to be secreted into the bile
Detoxification of endogenous and exogenous substances
e.g. ammonia, steroids and drugs
Converts AMMONIA to urea
Storage of minerals and vitamins – vitamin A, D, E, K,
B12, Iron
Excretion of adrenal cortex hormones e.g. glucocorticoid,
mineralocorticoid i.e. aldosterone, sex hormone
Phagocytosis by Kupffer cells
Liver
• Physiologic changes of the liver with aging:
Decrease in size of the liver
Decrease in enzymes involved in the metabolism with
drugs
Increased propensity to drug toxicity
Gallbladder
• Stores and concentrate bile produced by the liver
• Liver produces 600 to 1200 mls of bile at a time. 90% of this volume
is water, which is absorbed by the mucous membrane lining of
gallbladder
• Stores 50-70 ml of concentrated bile
• Bile is greenish liquid composed of water, cholesterol, bile salts,
electrolytes and phospholipids
• Functions of BILE:
Bile is important in fat emulsification and intestinal absorption of fatty acids,
cholesterol and other lipids
Aids in excretion of conjugated bilirubin from liver and prevent jaundice
• Presence of fat in the acidic chyme transported into duodenum
causes secretion of cholecystonin
• Cholecystonin causes gallbladder contraction and relaxation of
sphincter of Oddi, Releasing bile into the common bile duct for
delivery in the duodenum
Pancreas
• A heterocrine gland – perform both
exocrine and endocrine functions
• Exocrine function: secrete
pancreatic juice containing
pancreatic amylase, lipase and
trypsin
• Amylase completes digestion of
carbohydrates; lipase completes
digestion of fats; trypsin completes
digestion of proteins
• Endocrine function: involves the
Islet of Langerhans
• Islet of Langerhans has two types of
cells: Beta and Alpha cells
• Beta cells secrete insulin to promote
carbohydrate metabolism
• Alpha cells secrete glucagon, which
stimulates glycogenolysis in the liver
LIVER CIRRHOSIS
Liver Cirrhosis
• A chronic progressive disease of the liver characterized
by replacement of normal liver tissue with diffuse fibrosis
that disrupts the structure and function of the liver
• Repeated destruction of hepatic cells causes the
formation of scar tissue
• Incidence is twice as high among men than women
• Peak incidence occurs between the ages of 40 and 60
years
Liver Cirrhosis
• Types:
Laennec’s Cirrhosis (alcohol-induced)
o most frequent type caused by chronic alcoholism and chronic
nutritional deficiencies;
o cellular necrosis causes wide spread scar tissue surrounding
portal areas
Posthepatic cirrhosis
o occurs after massive liver necrosis
o occurs as a complication of acute viral hepatitis or exposure to
hepatotoxins;
o scar tissue causes destruction of liver lobules and entire lobes
Biliary cirrhosis
o scarring occur in the liver around the bile ducts and results from
chronic biliary obstruction and infection
Liver Cirrhosis
• Causes:
Alcohol abuse (most common cause)
Malnutrition
Infection
Drugs
Biliary obstruction
Right-sided congestive heart failure
Fibrosis/Scarring
Inflammation
Bile stasis
Hepatocellular damage