Alterations of

Digestive Function

Adapted by: Bridget Miranda, DNP, MBA, FNP-C

Copyright © 2017, Elsevier Inc. All rights reserved.
Structure and Function

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 Clinical Manifestations of
Gastrointestinal Dysfunction
˜ Anorexia
Ø A lack of a desire to eat despite physiologic stimuli that would
normally produce hunger
˜ Vomiting
Ø The forceful emptying of the stomach and intestinal contents through
the mouth.
Ø Vomiting center: postrema, lies in the medulla oblongata
˜ Nausea
Ø Subjective
Ø Specific neural pathways have not been identified for nausea.
Hypersalivation and tachycardia are common associated symptoms
Ø Retching, Nonproductive vomiting
˜ Projectile vomiting
Ø Spontaneous vomiting -does not follow nausea or retching

Copyright © 2017, Elsevier Inc. All rights reserved. 3

 Clinical Manifestations of Gastrointestinal
Dysfunction: Constipation
Bristol Stool Chart
Ø Defined as infrequent or difficult defecation
Ø Primary condition
• Normal transit (functional)
• Slow transit
• Pelvic floor or outlet dysfunction
Ø Secondary condition
• Different factors such as diet, medications,
various disorders, aging
• Neurotransmitters or neural pathways are
diseased or degenerated, resulting in delayed
colon transit time.

Indicators of constipation include two of the following for at least 3 months:

[Link] with defecation at least 25% of the time
[Link] or hard stools at least 25% of the time
[Link] of incomplete emptying at least 25% of the time
[Link] maneuvers to facilitate stool evacuation for at least 25% of defecations
[Link] than three bowel movements per week.
4
Clinical Manifestations of Gastrointestinal
Dysfunction: Diarrhea
Ø Presence of loose, watery stools
Ø Large-volume diarrhea
• Caused by excessive amounts of water or secretions or both in
the intestines
Ø Small-volume diarrhea
• Volume of feces is not increased, usually results from excessive
intestinal motility
Ø Major mechanisms of diarrhea
• Osmotic, Secretory or Motility diarrhea
Ø Systemic effects
• Dehydration, Electrolyte imbalance, Weight loss
Ø Associated with malabsorption syndromes
Ø Treated with fluid restoration, antimotility or water-absorbent
medications, treatment of causal factors

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 Abdominal pain

Ø Mechanical, inflammatory, or ischemic

Ø Usually associated with tissue injury and
inflammation
Ø Parietal (Somatic) pain
• localized, more intense
Ø Visceral pain
• In organs
Ø Referred pain
• Often from visceral pain
Ø Biochemical mediators of inflammation
• histamine, bradykinin and serotonin stimulate
organic nerve ending and produce abd. Pain

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 Gastrointestinal bleeding

Ø Obvious manifestations of gastrointestinal bleeding are hematemesis (vomiting of blood),

melena (dark, tarry stools), and hematochezia (frank bleeding from the rectum).
7
Ø Physiologic response depends on rate and amount of blood loss
 Disorders of Motility:
Dysphagia
Ø Difficulty swallowing
• Mechanical obstructions: Tumors, strictures, diverticular herniations or outpouching
• Functional disorders: neuronal or muscular disorders interfere with voluntary
swallowing or peristalsis – disorders of striated muscles of hypopharyngeal area
and upper esophagus interfere with oropharyngeal (voluntary) phase of swallowing
(CVA, PD, MS, MD, or achalasia)
Ø Achalasia
• Functional dysphagia caused by loss of esophageal innervation.
• Related to loss of inhibitory neurons in the myenteric plexus with smooth muscle
atrophy in the middle and lower portions of the esophagus
Ø Manifestations
• Stabbing pain at the level of obstruction
• Discomfort after swallowing
• Regurgitation of undigested food
• Unpleasant taste sensation
• Vomiting
• Aspiration
• Weight loss 8
 Disorders of Motility:
Gastroesophageal reflux disease
GERD
Abnormalities in LES function, motility, or emptying cause reflux of acid
and pepsin from the stomach to the esophagus à esophagitis.

Ø Resting tone of the LES tends to be lower

than normal from either transient relaxation or
weakness of the sphincter
Ø Delayed gastric emptying contributes to reflux
esophagitis by
• Lengthening the period during which
reflux is possible
• Increasing the acid content of chyme.
• Conditions that increase abdominal
pressure or delay gastric emptying can
contribute to the development of reflux
esophagitis Copyright © 2017, Elsevier Inc. All rights reserved. 9
 Disorders of Motility:
Gastroesophageal reflux disease
Ø Risk factors • Severe Reflux Esophagitis : If
• Obesity, hiatal hernia, and drugs the gastric content is highly
or chemicals that relax the LES acidic or contains bile salts and
(anticholinergics, nitrates, pancreatic or intestinal enzymes
calcium channel blockers,
• Increases exposure à mucosal
nicotine).
injury and inflammation with
• GERD may trigger asthma,
chronic cough, or sinusitis.
hyperemia, increased capillary
permeability, edema, tissue
Ø Manifestations fragility, erosions, and
• Heartburn ulceration.
• Acid regurgitation
• Dysphagia
• Barrett esophagus: Fibrosis
• Chronic cough
and thickening may developà
• Asthma attacks
Precancerous lesions
• Laryngitis
• Upper abdominal pain within 1 Why are Proton pump inhibitors are the agents
hour of eating of choice for controlling symptoms and healing
esophagitis? 10
 Disorders of Motility: Hiatal hernia

Ø Diaphragmatic hernia with protrusion of the upper

part of the stomach through the diaphragm and into
the thorax
• Type 1: Sliding hiatal hernia
† proximal portion of the stomach moves into the
thoracic cavity through the esophageal hiatus, an
opening in the diaphragm for the esophagus and
vagus nerves.
• Type 2: Paraesophageal hiatal hernia
† herniation of the greater curvature of the stomach
is through a secondary opening in the diaphragm
• Type 3: Mixed hiatal hernia
† occur in conjunction with GERD, PUD,
cholecystitis, cholelithiasis chronic pancreatitis,
and diverticulosis.
11
Disorders of Motility: Gastroparesis
Ø Delayed gastric emptying in the absence of mechanical gastric
outlet obstruction
Ø Associated with diabetes mellitus, surgical vagotomy, or
fundoplication
Ø Pathophysiology is not well understood but involves abnormalities
of the autonomic nervous system, smooth muscle cells, enteric
neurons, and gastrointestinal hormones.

Ø Symptoms include nausea, vomiting, abdominal pain, and

postprandial fullness or bloating

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 Disorders of Motility:
Pyloric obstruction
Gastric outlet obstruction is the narrowing or blocking of the
opening between the stomach and the duodenum.

Ø Congenital or Acquired
Ø Manifestations
• Epigastric pain and fullness
• Nausea
• Succussion splash
• Vomiting
• With a prolonged obstruction,
malnutrition, dehydration, and
extreme debilitation

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 Disorders of Motility:
Intestinal obstruction and paralytic ileus
Ø An intestinal obstruction is any condition that prevents the
flow of chyme through the intestinal lumen
• Simple obstruction
† Mechanical blockage of the lumen
† Preserved blood flow if not strangulated
• Functional obstruction (paralytic ileus)
† Failure of intestinal motility
† Often occurs after intestinal or abdominal surgery, pancreatitis, or
hypokalemia
† Anesthetic agents, local inflammatory reactions, use of opioid
analgesia, and hyperactivity of the sympathetic nervous system
contribute to postoperative ileus.
• Most severe consequences are fluid and electrolyte losses,
hypovolemia, shock, intestinal necrosis, and perforation of the
intestinal wall. 14
 Intestinal Obstruction
• Small intestinal obstruction
• Colicky pains
• Nausea and vomiting
• Large intestine obstruction
• Hypogastric pain
• Abdominal distention

15
 Gastritis

Inflammatory disorder of the gastric mucosa due to regurgitation of bile

˜ Acute gastritis

Ø injury of the protective mucosal barrier

Ø NSAIDs Inhibit the action of cyclooxygenase-1 (COX-1) à gastritis because they inhibit
prostaglandin synthesis (stimulates the secretion of mucus and suppresses inflammation).

˜ Chronic gastritis – Most severe

Ø Gastric atrophy and decreased secretion of hydrochloric acid, pepsinogen, and IF
• Chronic fundal gastritis (type A, immune) Autoantibodies against parietal cells
or IF) à Pernicious Anemia
• Chronic antral gastritis (type B, nonimmune) – More common
† Chronic use of alcohol, tobacco, and nonsteroidal anti-inflammatory drugs
are contributing factors.
† There are high levels of hydrochloric acid secretion with an increased risk of
duodenal ulcers.
† *H. pylori INFECTION may trigger the immune response à autoimmune
atrophic gastritis and involves the fundus, thus becoming pangastritis.
16
 Therefore, comfort yourselves
together, and edify one another,
even as also you do.
1 Thessalonians 5:11
 Peptic Ulcer Disease
PUD: single or multiple breaks, or ulcerations, in the
protective mucosal lining of the lower esophagus, stomach, or
duodenum.
˜ Acute and chronic ulcers
Ø H. Pylori, habitual aspirin, NSAIDs, alcohol….
˜ Superficial
Ø Erosions to the mucosa but do not penetrate the muscularis mucosae
˜ True
Ø Extends through the muscularis mucosae and damage blood vessels,
causing hemorrhage or perforating the gastrointestinal wall.
˜ Zollinger-Ellison syndrome
Ø Gastrin-secreting neuroendocrine tumor or multiple tumors (gastrinoma) of
the pancreas or duodenum.
Ø Gastrin stimulates a proliferation of gastric parietal cells and chronic
secretion of gastric acid.
18
 Peptic Ulcer Disease:
Duodenal Ulcer

Ø Most common of the peptic ulcers

Ø Developmental factors:
• Helicobacter pylori infection
• Hypersecretion of stomach acid and pepsin
• Use of NSAIDs
Ø Characterized by intermittent pain in the epigastric area
• Relieved rapidly by ingestion of food or antacids
Ø Management aimed at relieving the causes and effects of
hyperacidity and preventing complications

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 Gastric Ulcer

˜ Gastric ulcers tend to develop in

the antral region of the stomach,
adjacent to the acid-secreting
mucosa of the body
˜ Pathophysiology
Ø The primary defect is an increased
mucosal permeability to hydrogen
ions
Ø Gastric secretion tends to be
normal or less than normal
˜ Manifestations and treatment
similar to duodenal ulcers except
food cause pain

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 Stress-Related Mucosal Disease

˜ Acute form of peptic ulcer that is related to

physiologic stress due to severe illness or
major trauma
Ø Ischemic ulcers
• Within hours of trauma, burns, hemorrhage, heart failure,
or sepsis
Ø Curling ulcers
• Ulcers that develop as a result of burn injury
Ø Cushing ulcers
• Ulcers that develop as a result of a brain injury or brain
surgery

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 Surgical Treatment of Ulcer

˜ Most common indications

Ø Recurrent or uncontrolled bleeding and perforation
of the stomach or duodenum
˜ Objectives
Ø Reduce stimuli for acid secretion, decrease the
number of acid-secreting cells in the stomach
Ø Correct complications of ulcer disease

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 Postgastrectomy Syndromes

˜ Alkaline reflux gastritis is stomach inflammation

caused by the reflux of bile and pancreatic
secretions from the duodenum into the stomach.
These substances disrupt the mucosal barrier and
cause inflammation.

˜ Afferent loop obstruction is an obstruction of the

duodenal stump on the proximal side of a
gastrojejunostomy. Biliary and pancreatic secretions
accumulate in the stump, causing distention,
intermittent pain, and vomiting.

˜ Dumping syndrome is the rapid emptying of

chyme into the small intestine. It causes an osmotic
shift of fluid from the vascular compartment to the
intestinal lumen, which decreases plasma volume. 23
 Malabsorption Syndromes

˜ Maldigestion
Ø Failure of the chemical processes of digestion
˜ Malabsorption
Ø Failure of the intestinal mucosa to absorb digested nutrients
˜ Maldigestion and malabsorption frequently occur together

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 Malabsorption Syndromes

˜ Pancreatic exocrine insufficiency

Ø Insufficient pancreatic enzyme production
• Lipase, amylase, trypsin, or chymotrypsin
Ø Causes
• Pancreatitis
• Pancreatic carcinoma
• Pancreatic resection
• Cystic fibrosis
Ø Fat maldigestion is the main problem, so the
patient will exhibit fatty stools and weight loss

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 Malabsorption Syndromes

˜ Lactase deficiency
Ø Inability to break down
lactose into
monosaccharides and
therefore prevent
lactose digestion and
absorption
Ø Fermentation of lactose
by bacteria causes gas
(cramping pain,
flatulence, etc.) and
osmotic diarrhea
Copyright © 2017, Elsevier Inc. All rights reserved. 26
 Malabsorption Syndromes

˜ Bile salt deficiency

Ø Conjugated bile salts
needed to emulsify and
absorb fats
Ø Bile salts are conjugated in
the bile that is secreted from Fat-soluble vitamin deficiencies:
the liver Vitamin A
Night blindness
Ø Can result from liver disease Vitamin D
and bile obstructions Decreased calcium absorption
Bone pain
Ø Poor intestinal absorption of Osteoporosis

lipids causes fatty stools Fractures

Vitamin K
(steatorrhea), diarrhea, and Prolonged prothrombin time
loss of fat-soluble vitamins Purpura
Petechiae
(A, D, E, K) Vitamin E
Uncertain
27
 Inflammatory Bowel Disease
˜ Ulcerative colitis and Crohn disease
Ø Chronic, relapsing inflammatory bowel disorders
• Genetics
• Environmental factors
• Alterations of epithelial barrier functions
• Altered immune reactions to intestinal flora

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Copyright © 2017, Elsevier Inc. All rights reserved. 29
 Ulcerative Colitis
˜ Chronic inflammatory disease that causes ulceration of the colonic
mucosa
Ø Sigmoid colon and rectum
Ø Begins in the rectum and may extend proximally to the entire colon
Ø Intermittent periods of remission and exacerbation
˜ Symptoms:
Ø Diarrhea (10 to 20/day)
Ø Urgency
Ø Bloody stools
Ø Cramping
˜ Treatment
Ø Mild to moderate disease is treated with 5-aminosalicyclate therapy followed
by steroids
Ø Thioprine and immunomodulatory agents or vedolizumab are used for
serious disease
Ø Surgery for severe disease
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 Crohn Disease

˜ Granulomatous colitis, ileocolitis, or regional enteritis

˜ Idiopathic inflammatory disorder; affects any part of the
digestive tract, from mouth to anus
˜ Causes “skip lesions”
˜ One side of the intestinal wall may be affected and not the
other
˜ Ulcerations can produce fissures that extend into the
lymphatics
˜ Symptoms similar to ulcerative colitis
˜ Anemia may result from malabsorption of vitamin B12 and
folic acid
˜ Treatment similar to ulcerative colitis
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 Microscopic Colitis

˜ Relatively common cause of diarrhea

˜ Primarily in females and older adults
˜ Two forms
Ø Lymphocytic
• more than 20 intraepithelial lymphocytes per 100
epithelial cells.
Ø Collagenous
• thickened (10 to 20 µm) subepithelial collagen band,
alteration of the vascular mucosal pattern, and mucosal
nodularity.
˜ Cause unknown
˜ Results in chronic daily watery diarrhea, Abd pain, weight loss
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 Irritable Bowel Syndrome

IBS: characterized by abdominal pain with altered bowel

habits
˜ Symptom-based disease characterized by recurrent abdominal
pain with altered bowel habits
˜ Alterations in the brain-gut axis, gut microflora, gut immune
responses, gut neuroendocrine cell function, genetic
susceptibility, and epigenetic factors contribute à intestinal
hypersensitivity, intestinal inflammation, increased permeability,
and symptoms caused by alterations in motility and secretion
˜ More common in females, Youth and Middle age
˜ Associated with anxiety, depression, and reduced quality of life

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 Irritable Bowel Syndrome

˜ Cause unknown but mechanisms proposed

* May be related to pain and a dysregulation of the bidirectional
“brain-gut axis”
Ø Visceral hypersensitivity w/ rectum and gut distension
Ø Abnormal intestinal permeability, motility, and secretion
Ø Postinflammatory
Ø Alteration in gut microbiota
Ø Food allergy/intolerance
Ø Psychosocial factors
˜ Manifestations
Ø Lower abdominal pain or discomfort and bloating
˜ Symptoms are usually relieved with defecation and do not interfere with sleep
˜ No cure, and treatment is individualized

34
 Diverticular Disease of the Colon

˜ Diverticula
Ø Herniations of mucosa
through the muscle layers of
the colon wall, especially the
sigmoid colon
˜ Diverticulosis
Ø Asymptomatic diverticular
disease
˜ Diverticulitis
Ø The inflammatory stage of
diverticulosis
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 Diverticular Disease of the Colon

˜ Diverticula can occur

anywhere in the
gastrointestinal tract,
particularly at weak points in
the colon wall
˜ Complicated diverticulitis
includes abscess, fistula,
obstruction, bleeding, or
perforation
˜ Symptoms of uncomplicated
diverticular disease may be
vague or absent

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 Appendicitis

˜ Inflammation of the vermiform

appendix
˜ Possible causes:
Ø Obstruction, foreign bodies,
infection
˜ Gastric or periumbilical pain
Ø Rebound tenderness to RLQ
˜ Perforation, peritonitis, and
abscess formation are the
most serious complications

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 Mesenteric Vascular Insufficiency

˜ Blood supply to the stomach and intestine

Ø Celiac artery, Superior and inferior mesenteric arteries
˜ Mesenteric venous thrombosis - Least common
Ø Risk Factors: Hypercoagulability, endothelial injury, malignancies, right-
sided HF, and DVT Acute mesenteric artery insufficiency - More common
in elderly
Ø Significant reduction in mucosal blood flow to the large and small
intestines. Preexisting dissecting aortic aneurysms and arterial thrombi.
˜ Chronic mesenteric ischemia – Most Common
Ø Secondary to Cardiac Alterations: atherosclerotic stenosis (most
common); congestive heart failure, acute MI, etc (if it decreases arterial
blood flow).

38
ALTERATIONS IN GI
ACCESSORY ORGANS

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Structure and Function

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 Alcoholic Liver Disease

˜ Related to toxic effects of alcohol and

coexisting liver disease
Ø Alcoholic fatty liver
Ø Alcoholic steatohepatitis
Ø Alcoholic cirrhosis
˜ Anorexia, nausea, jaundice, and edema
develop with advanced fatty infiltration or the
onset of alcoholic steatohepatitis

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Nonalcoholic Fatty Liver Disease and
Nonalcoholic Steatohepatitis
˜ Nonalcoholic fatty liver
disease (NAFLD)
Ø Infiltration of hepatocytes
with fat occurring in the
absence of alcohol intake
Ø May progress to
nonalcoholic steatohepatitis,
which may progress to
cirrhosis and end-stage liver
disease

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 Liver Disorders: Cirrhosis

˜ Irreversible inflammatory, fibrotic

liver disease
˜ Biliary channels become
obstructed and cause portal
hypertension
˜ Severity and rate of progression
depend on the cause
˜ Many causes

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 Liver Disorders: Portal hypertension

Ø Abnormally high blood pressure in the portal venous system

caused by resistance to portal blood flow
• Intrahepatic
• Posthepatic
Ø Varices
• Lower esophagus
• Stomach
• Abdominal wall
• Rectum
Ø Splenomegaly
• Hepatopulmonary syndrome
• Portopulmonary syndrome
Ø Vomiting of blood from bleeding esophageal varices is the most
common clinical manifestation
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 Liver Disorders: Ascites
Ø Accumulation of fluid in the peritoneal
cavity
Ø Most common cause is cirrhosis
Ø Development associated with
• Portal hypertension
• Decreased synthesis of albumin by the
liver
• Splanchnic vasodilation
• Renal sodium and water retention
Ø 25% mortality in 1 year if associated with
cirrhosis
Ø Causes abdominal distention and
increased abdominal girth and weight
gain
Ø Paracentesis

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 Liver Disorders:
Hepatic encephalopathy
A neurologic syndrome of impaired behavioral, cognitive,
and motor function due to biochemical alterations that affect
neurotransmission
• Liver dysfunction and collateral vessels that shunt blood around
the liver to the systemic circulation permit neurotoxins and
other harmful substances absorbed from the gastrointestinal tract
to accumulate and circulate freely to the brain.
† Substances include inflammatory cytokines, short-chain fatty
acids, serotonin, tryptophan, and false neurotransmitters.
• Ammonia, cannot be converted to urea by the
diseased liver.
† Digested blood from leaking or ruptured varices adds to the
amount of ammonia present in systemic blood, as does the
action of ammonia-forming bacteria in the colon.
 Liver Disorders:
Hepatic encephalopathy
Ammonia à brain à metabolized to glutamine, with osmotic
disturbances and alterations in cerebral blood flow that interfere
with neurotransmitters à cytotoxic edema and oxidation.

Permeability of the BBB also may be increased (vasogenic

edema), à brain edema, and intracranial hypertension.
Excessive amounts GABA, may contribute to reduced levels of
consciousness. Infection, hemorrhage, inflammation, electrolyte
imbalance, sedatives, and analgesics also can precipitate stupor
and coma in the presence of liver disease

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 Liver Disorders:
Hepatic encephalopathy
Ø Early symptoms
• Subtle changes in personality, memory loss, irritability,
disinhibition, lethargy, and sleep disturbances
Ø Later symptoms
• Confusion, disorientation to time and space, flapping
tremor of the hands (asterixis), slow speech,
bradykinesia, stupor, convulsions, and coma

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Liver Disorders: Jaundice (icterus)

Ø Caused by
hyperbilirubinemia
Ø Obstructive jaundice
• Extrahepatic obstruction
• Intrahepatic obstruction
Ø Hemolytic jaundice
• Prehepatic jaundice
• Excessive hemolysis of red
blood cells
Ø Characterized by dark urine, Total bilirubin: 0.3 to 1.9 mg/dL

yellow discoloration of Direct bilirubin (Conjugated) : 0.0 to 0.3

mg/dL - Liver
sclera and skin, and light-
colored stools Indirect (Unconjugated) _the difference
between Total and Direct. - Hemoglobin

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 Liver Disorders: Acute Liver Failure

˜ Rare clinical syndrome resulting in severe impairment

or necrosis of liver cells without preexisting liver
disease or cirrhosis
˜ Acetaminophen overdose is leading cause in the
United States

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 Liver Disorders: Viral Hepatitis

˜ Systemic viral disease that

primarily affects the liver
˜ 5 types (A, B, C, D, and E)
Ø Can cause acute, icteric
illness
˜ Spectrum of manifestations
ranges from absence of
symptoms to fulminating
hepatitis, with rapid onset of
liver failure and coma

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 Viral Hepatitis

˜ Phases
Ø Incubation
Ø Prodromal
• 2 weeks after exposure and ends with the appearance of
jaundice.
Ø Icteric
• 1 to 2 weeks after the prodromal phase and lasts 2 to 6 weeks.
Individuals who develop chronic HBV infection do not become
jaundiced and may not be diagnosed
Ø Recovery
• The posticteric or recovery phase begins with resolution of
jaundice, about 6 to 8 weeks after exposure.
• Chronic hepatitis may begin at this point and is associated with
HBV, HCV, and HDV infection.
52
Copyright © 2017, Elsevier Inc. All rights reserved. 53
Cirrhosis

54
 Biliary Cirrhosis

˜ Damage and inflammation leading

to cirrhosis begin in bile canaliculi
and bile ducts
Ø Primary
• Chronic, autoimmune, cholestatic liver
disease. It is caused by natural-killer T
lymphocytes and highly specific
antimitochondrial antibody destruction of
the small intrahepatic bile ducts.
Ø Secondary
• Prolonged partial or complete
obstruction of the common bile duct or
its branches. The obstruction may be
caused by gallstones, tumors, fibrotic
strictures, or chronic pancreatitis.
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Copyright © 2017, Elsevier Inc. All rights reserved. 56
 Disorders of the Gallbladder:
Cholecystitis
˜ Prolonged partial or complete obstruction of the
common bile duct or its branches. The obstruction
may be caused by gallstones, tumors, fibrotic
strictures, or chronic pancreatitis.
Ø Almost always caused by a gallstone lodged in
the cystic duct
Ø Pain is similar to that caused by gallstones
Ø Fever, leukocytosis, rebound tenderness, and
abdominal muscle guarding are common
findings

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 Disorders of the Gallbladder:
Cholelithiasis
Ø Gallstones are formed from impaired
metabolism of cholesterol, bilirubin, and
bile acids.
Ø Type depends on chemical composition
• Cholesterol – 70% of Gallstones
† Formed from bile that is
supersaturated with cholesterol
produced by the liver Ø Often asymptomatic
or vague
• Pigmented brown
† Formed from calcium bilirubinate and fatty Ø Epigastric and right
acid soaps that bind with calcium hypochondrium
• Black pain
† Composed of calcium bilirubinate with Ø Intolerance to fatty
mucin glycoproteins foods
† Associated with chronic liver disease and
hemolytic disease
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 Disorders of the Pancreas:
Pancreatitis
Ø Inflammation of the pancreas
Ø Develops because of obstruction to
the outflow of pancreatic digestive
enzymes caused by bile and
pancreatic duct obstruction
Ø Risk factors include obstructive
biliary tract disease (particularly
cholelithiasis), alcoholism, peptic
ulcers, abdominal trauma,
hyperlipidemia, smoking, certain
drugs, and genetic factors (hereditary
pancreatitis, cystic fibrosis).

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 Disorders of the Pancreas:
Acute Pancreatitis
Ø Usually mild and
resolves
spontaneously
Ø May result from direct
cellular injury from
alcohol, drugs, or viral
infection
Ø Cardinal manifestation
is epigastric or
midabdominal constant
pain

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Disorders of the Pancreas:
Chronic Pancreatitis
Ø Process of progressive fibrotic
destruction of the pancreas
Ø Related to chronic alcohol abuse
Ø Continuous or intermittent
abdominal pain and weight loss
are common
Ø Risk factor for pancreatic cancer

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CANCER OF THE
GASTROINTESTINAL TRACT

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 Cancer of the Esophagus

˜ Carcinoma of the esophagus is a

rare
˜ Squamous cell carcinomas are
more common in the thoracic and
cervical areas of the esophagus.
˜ Adenocarcinoma is found in the
distal one-third of the esophagus
and is associated with risk factors
that include reflux esophagitis,
Barrett esophagus, abdominal
obesity, drugs that decrease lower
esophageal pressure, sliding hiatal
hernia, and smoking.

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 Gastric Adenocarcinoma:
Cancer of the Small Intestine
˜ Most cases are
adenocarcinoma.
˜ Squamous cell
carcinoma is very
rare
˜ Most important risk
factors:
Ø H. Pylori

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Cancer of the Colon and Rectum
˜ CRC is third most common cause of
cancer and cancer death
˜ Genetic and environmental factors
˜ If Polyp is neoplastic or cancerous
à progress into adenocarcinomas.
˜ When polyps are larger than 2 cm,
more numerous (greater than 20),
and have a villous architecture, they
have the most malignant potential.
˜ The adenomatous polyp forms in an
area of epithelial cell
hyperproliferation and crypt
dysplasia.

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 Cancer of the Liver

˜ A leading cause of
cancer death worldwide
˜ Primary hepatocellular
carcinoma is increasing
significantly as a result
of chronic hepatitis C
infection
˜ Cancer in the liver is
usually caused by
metastatic spread from
a primary site
elsewhere in the body.
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Cancer of the Gallbladder
˜ Rare but lethal disease
˜ Adenocarcinomas and, less
commonly, squamous cell
carcinomas.
˜ Infiltrative tumors are
associated with gallstones, and
invasion of the liver and lymph
nodes occurs early.
˜ Spreading extends to the
pancreas and retroperitoneal
lymph nodes. Direct invasion of
the stomach and the duodenum
can cause pyloric obstruction.
˜ Infection often accompanies
cancer of the gallbladder.

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 Cancer of the Pancreas

˜ Most pancreatic tumors (95%)

arise from metaplastic exocrine
cells in the ducts and are called
ductal adenocarcinomas
˜ There is significant expansion
of the extracellular matrix
(stroma) from activation of
pancreatic stellate cells, a type
of fibroblast in the pancreas,
which also promotes
inflammation, angiogenesis,
and tumor growth.

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