Chapter 42

Alterations of Digestive Function

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 Clinical Manifestations of
Gastrointestinal Dysfunction
⬤Anorexia (loss of appetite)
⮚ Lack of desire to eat, despite physiologic stimuli that
would normally produce hunger
⬤Vomiting
⮚ Forceful emptying of the stomach and intestinal
contents through the mouth
⮚ Vomiting center: Medulla oblongata
⮚ Several types of stimuli initiate the vomiting reflex.

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Vomiting (cont.)
⮚ Antiemetic medications: For nausea and vomiting
• Zofran
• Metoclopramide
• Olanzapine
• Corticosteroids
• Can lead to fluid, electrolyte, and acid-base disturbances,
hyponatremia, hypokalemia, hypochloremia, and metabolic
alkalosis.

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Nausea
⮚ Subjective experience associated with a number of
conditions
⮚ Common symptoms: Hypersalivation and tachycardia
⬤Retching
⮚ Vomiting without the expulsion of vomitus
⬤Projectile vomiting
⮚ Spontaneous vomiting that does not follow nausea or
retching

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Constipation
⮚ Infrequent or difficulty defecation
⮚ Normal: Two or three per day to three per week
⮚ Pathophysiology
• Normal transit (functional) constipation: Normal rate of stool
passage, but difficulty with stool evacuation from low-residue,
low-fluid diet and sedentary lifestyle
• Slow-transit constipation: Impaired colonic motor activity with
infrequent bowel movements; straining, abdominal distension,
palpable stool
• Pelvic floor dysfunction: Failure of the pelvic floor muscles or
anal sphincter to relax with defecation
• Secondary: From an actual disease processes, diet,
medications
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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Constipation (cont.)
⮚ Clinical manifestations
• Two of the following for at least 3 months
⮞ Straining with defecation at least 25% of the time
⮞ Lumpy or hard stools at least 25% of the time
⮞ Sensation of incomplete emptying at least 25% of the time
⮞ Manual maneuvers to facilitate stool evacuation for at least
25% of defecations
⮞ Fewer than three bowel movements per week
• Fecal impaction: Hard, dry stool retained in rectum

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Constipation (cont.)
⮚ Treatment
• Bowel retraining
• Moderate exercise
• Increased fluid and fiber intake
• Enemas (should not be habitually used)
• Drugs
⮞ Methylnaltrexone (relistor): For opioid-induced constipation
in individuals who are terminally ill
⮞ Stool softeners and laxatives

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Diarrhea
⮚ Increased frequency of bowel movements
• Three or more per day
⮚ Increased volume, fluidity, weight of feces

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Diarrhea (cont.)
⮚ Clinical manifestations
• Dehydration, electrolyte imbalance (hyponatremia,
hypokalemia)
• Metabolic acidosis and weight loss
⮚ Treatment
• Restore fluid and electrolyte balance.
• Medications: Antimotility (loperamide [an opiate] or atropine
[Lomotil]) and/or water absorbent (attapulgite and
polycarbophil)
• Mild diarrhea: Natural bran and psyllium
• Clostridium difficile–associated diarrhea: Probiotics
• Fecal transplantation

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Systemic manifestations of diarrhea
⮚ Manifestations of acute bacterial or viral infection
• Fever, with or without vomiting or cramping pain
⮚ Manifestations of inflammatory bowel disease
• Fever, cramping pain, bloody stools
⮚ Manifestations of malabsorption syndromes
• Steatorrhea (fat in the stools), bloating, and diarrhea

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤Abdominal pain
⮚ Symptom of a number of gastrointestinal (GI) disorders
⮚ From mechanical, inflammatory, or ischemic
⮚ Parietal (somatic) pain: In the peritoneum
⮚ Visceral pain: In the organs themselves
⮚ Referred pain: Felt in another area
⬤Biochemical mediators of the inflammatory
response (histamine, bradykinin, and serotonin)
stimulate pain nerve endings, producing
abdominal pain.

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤GI bleeding
⮚ Upper GI bleeding
• From the esophagus, stomach, or duodenum
• Frank, bright red bleeding in emesis or dark, grainy digested
blood (coffee grounds) in stool
⮚ Lower GI bleeding
• From the jejunum, ileum, colon, or rectum
⮚ Treatment: Blood products

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 Clinical Manifestations of
Gastrointestinal Dysfunction (Cont.)
⬤GI bleeding (cont.)
⮚ Hematemesis: Bloody vomit
⮚ Hematochezia: Bloody stools
⮚ Melena: Black, tarry stools
⮚ Occult bleeding: Not visible

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 Disorders of Motility
⬤Dysphagia
⮚ Difficulty swallowing
⮚ Types
• Mechanical obstructions of esophagus
• Functional obstructions of esophageal motility
⮚ Achalasia
• Denervation of smooth muscle in the esophagus and lack of
lower esophageal sphincter relaxation
• Propensity for esophageal cancer

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 Disorders of Motility (Cont.)
⬤Dysphagia (cont.)
⮚ Clinical manifestations
• Upper esophageal obstruction: Discomfort occurring 2–
4 seconds after swallowing
• Lower esophageal obstruction: Discomfort occurring 10–15
seconds after swallowing
• All types: Retrosternal pain, regurgitation of undigested food,
unpleasant taste, vomiting, and weight loss

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 Disorders of Motility (Cont.)
⬤Dysphagia (cont.)
⮚ Treatment
• Eating slowly, eating small meals, taking fluid with meals,
and sleeping with the head of the bed elevated
• Oral medications: May need to be formulated to facilitate
swallowing.
• Tube feedings, particularly after a stroke
• Dilation or surgical myomotomy of the lower esophageal
sphincter
• Botulinum toxin

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 Disorders of Motility (Cont.)
⬤Gastroesophageal reflux disease (GERD)
⮚ Acid and pepsin reflux from the stomach into the
esophagus, causing esophagitis.
⮚ Resting tone of the lower esophageal sphincter tends
to be lower than normal from either transient
relaxation or weakness of the sphincter.
⮚ Conditions that increase abdominal pressure can
contribute to GERD.
• Vomiting, coughing, lifting, bending, obesity, or pregnancy

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 Disorders of Motility (Cont.)
⬤GERD (cont.)
⮚ Clinical manifestations
• Heartburn from acid regurgitation, chronic cough, laryngitis,
asthma attacks, sinusitis
• Upper abdominal pain within 1 hour of eating
⮚ Evaluation
• Biopsy: Dysplastic changes (Barrett esophagus)
⮚ Treatment
• Proton pump inhibitors: Most effective (protonix)
• Histamine type 2 (H2) receptor antagonists (pepcid) ,
prokinetic (reglan) agents, and antacids; pain medication
• Elevate head of the bed 6 inches; reduce weight; stop
smoking. Avoid Caffeine, chocolate.
• Surgery: Laparoscopic fundoplication
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 Disorders of Motility (Cont.)
⬤Hiatal hernia
⮚ Protrusion (herniation) of the upper part of the stomach
through the diaphragm and into the thorax

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 Disorders of Motility (Cont.)
⬤Hiatal hernia (cont.)
⮚ Clinical manifestations
• Asymptomatic
• Heartburn, regurgitation, dysphagia, and epigastric pain

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 Disorders of Motility (Cont.)
⬤Hiatal hernia (cont.)
⮚ Treatment
• Small, frequent meals; avoidance of recumbent position
after eating
• Avoidance of abdominal supports and tight clothing;
weight control for obese individuals
• Proton-pump inhibitors
• Contraindicated agents (delay gastric emptying): Drugs
that relax the lower esophageal sphincter
(anticholinergics, nitrates, calcium channel blockers)
• Paraesophageal: Laparoscopic surgery (fundoplication)

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 Disorders of Motility (Cont.)
⬤Pyloric (gastric outlet) obstruction
⮚ Blocking or narrowing of the opening between the
stomach and duodenum
⮚ Acquired or congenital
⮚ Clinical manifestations
• Epigastric pain and fullness, nausea, succussion splash,
vomiting; if prolonged, malnutrition and dehydration
⮚ Treatment
• Gastric drainage; intravenous (IV) fluid and electrolytes
• IV nutrition
• Proton pump inhibitors or histamine type 2 (H2) receptor
antagonists
• Surgery or stenting
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 Disorders of Motility (Cont.)
⬤Intestinal obstruction and ileus
⮚ Intestinal obstruction: Any condition that prevents the
flow of chyme through the intestinal lumen or failure of
normal intestinal motility in the absence of an
obstructing lesion
⮚ Clinical manifestations
• Small intestine obstruction: Colicky pains caused by
intestinal distention, followed by nausea and vomiting
• Large intestine obstruction: Hypogastric pain and abdominal
distention

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 Disorders of Motility (Cont.)
⬤Intestinal obstruction and ileus (cont.)
⮚ Treatment
• Replacement of fluid and electrolytes
• Gastric or intestinal suction
• Adhesions: Laparoscopic procedures
• Strangulation and complete obstruction: Immediate surgical
intervention
• Malignant obstruction: Colonic stent
• Colonic pseudo-obstruction: Neostigmine, a
parasympathomimetic and colonoscopic decompression
• Intestinal perforation: IV antibiotics, fluid resuscitation,
surgery

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 Disorders of Motility (Cont.)
⬤Intestinal obstruction and ileus (cont.)
⮚ Type of vomitus: Can indicate the location of the
obstruction
Location
of Obstruction Type of Vomitus
Pylorus Early, profuse vomiting of clear gastric fluid

Proximal small Mild distention and vomiting of bile-stained fluid

intestine
Lower in small More pronounced distention because a greater
intestine length of intestine is proximal to the obstruction.
Vomiting may not occur or may occur later and
contain fecal material.

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 Disorders of Motility (Cont.)
⬤Intestinal obstruction and ileus (cont.)
⮚ Simple obstruction
• Presence of a lesion
⮚ Functional obstruction: Paralytic ileus
• Failure of motility, especially after surgery

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 Disorders of Motility (Cont.)
⬤Small intestinal obstruction
⮚ Most common: Fibrous adhesions
⬤Large bowel obstruction
⮚ Most common: Colorectal cancer, volvulus (twisting),
and strictures related to diverticulitis
⮚ Acute colonic pseudo-obstruction (Ogilvie syndrome):
Massive dilation of the large bowel; patients who are
critically ill and older adults who are immobilized

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 Gastritis
⬤Inflammatory disorder of the gastric mucosa
⬤Acute gastritis
⮚ Associated with Helicobacter pylori, nonsteroidal
antiinflammatory drugs (NSAIDs), drugs, chemicals,
metabolic disorders
⮚ Clinical manifestations
• Vague abdominal discomfort, epigastric tenderness, and
bleeding
⮚ Treatment
• Healing usually occurs spontaneously within a few days.
• Discontinue injurious drugs.
• Administer antacids.
• Decrease acid secretion with a histamine type 2 (H2)
receptor antagonist and a proton pump inhibitor.
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 Gastritis (Cont.)
⬤Chronic gastritis
⮚ Clinical manifestations
• Manifestations do not often correlate with the severity of the
disease.
• Anorexia, fullness, nausea, vomiting, epigastric pain, and
gastric bleeding.
⮚ Treatment
• Smaller meals; soft, bland diet; avoidance of alcohol and
NSAIDs
• Administration of combination antibiotics
• Vitamin B: For pernicious anemia

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 Peptic Ulcer Disease
⬤Break or ulceration in the protective mucosal lining
of the lower esophagus, stomach, or duodenum
⬤Acute vs. chronic ulcers
⬤Superficial (erosions) vs. deep
⬤Risk factors
⮚ Genetic predisposition
⮚ H. pylori infection
⮚ Habitual use of NSAIDs and aspirin
⮚ Excessive use of alcohol, smoking, acute pancreatitis, chronic
obstructive pulmonary disease, obesity, cirrhosis, socioeconomic
status, and over 65 years of age

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 Peptic Ulcer Disease (Cont.)
⬤Chronic peptic ulcer

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 Peptic Ulcer Disease (Cont.)
⬤Duodenal ulcers
⮚ Most common of the peptic ulcers
⮚ Developmental factors
• Altered mucosal defenses
• High gastrin levels
• Rapid gastric emptying
• Acid production caused by cigarette smoking
⮚ Clinical manifestations
• Chronic intermittent pain in the epigastric area.
• Pain begins 30 minutes to 2 hours after eating when the
stomach is empty.
• Pain is relieved by food and antacids.

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 Peptic Ulcer Disease (Cont.)
⬤Duodenal ulcers (cont.)
⮚ Treatment
• Antacids: To neutralize gastric contents, elevate pH,
inactivate pepsin, and relieve pain
• Proton pump inhibitors, H-2 receptor blockers,
anticholinergics: To suppress acid secretion
• Sucralfate and colloidal bismuth: To coat ulcer
• Surgical resection
⮚ Risk of duodenal ulcer may be reduced with a diet
high in vitamin A, vitamin C, zinc, selenium, and fiber.

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 Gastric Ulcer
⬤Tends to develop in the antral region of the
stomach, adjacent to the acid-secreting mucosa
of the body.
⬤Pathophysiology
⮚ Frequent cause: H. pylori
⮚ Primary defect: Increased mucosal permeability to
hydrogen ions

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 Gastric Ulcer (Cont.)
⬤Pathophysiology

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 Gastric Ulcer (Cont.)
⬤Clinical manifestations
⮚ Pain occurs immediately after eating.
⮚ Tends to be chronic.
⮚ Anorexia, vomiting, and weight loss
⬤Treatment
⮚ Same as the treatment for duodenal ulcers

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 Zollinger-Ellison Syndrome
⬤Associated with a gastrinoma
⬤Chronic secretion of gastric acid
⬤Gastric and duodenal ulcers
⬤Clinical manifestations
⮚ Gastroesophageal reflux with abdominal pain and
diarrhea
⬤Treatment
⮚ Proton pump inhibitors: To reduce gastric acid
secretion
⮚ Surgical removal of tumors: To limit metastasis

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 Stress-Related Mucosal Disease
⬤Is a peptic ulcer related to a severe illness, multisystem
organ failure, or major trauma.
⮚ Clinical manifestations
• Bleeding: Most common
⮚ Treatment: Prophylactic therapy

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 Dumping Syndrome
⬤Rapid emptying of hypertonic chyme from the
stomach into the small intestine
⬤Complication of partial gastrectomy, bariatric
procedure, or pyloroplasty
⬤Developmental factors for early dumping
⮚ Loss of gastric capacity, loss of emptying control, and
loss of feedback control by the duodenum when it is
removed
⬤Clinical manifestations
⮚ Diarrhea, cramping, feeling of epigastric fullness, pain,
nausea, and vomiting
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 Dumping Syndrome (Cont.)
⬤Late dumping syndrome (1–3 hours after eating)
⮚ Clinical manifestations
• Weakness, diaphoresis, and confusion
⬤Treatment for early and late dumping
⮚ Consuming frequent small meals high in protein and low in
carbohydrates
⮚ Drinking fluids between meals instead of at mealtime
⮚ Reclining on the left side after eating
⮚ Reconstructing the pylorus or a gastrojejunostomy
⮚ Administering Octreotide: To inhibit insulin release and
slow intestinal transit time

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 Malabsorption Syndromes
⬤Interfere with nutrient absorption
⬤Maldigestion
⮚ Failure of the chemical processes of digestion
⬤Malabsorption
⮚ Failure of the intestinal mucosa to absorb (transport)
the digested nutrients

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 Malabsorption Syndromes (Cont.)
⬤Pancreatic insufficiency
⮚ Insufficient pancreatic enzyme production
• Lipase, amylase, trypsin, or chymotrypsin
⮚ Causes: Pancreatitis, pancreatic carcinoma,
pancreatic resection, and cystic fibrosis
⮚ Fat maldigestion: Primary problem
⮚ Most common signs: Fatty stools (steatorrhea);
weight loss
⮚ Treatment: Lipase supplements

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 Malabsorption Syndromes (Cont.)
⬤Lactase deficiency
⮚ Congenital defect in the lactase gene
⮚ Inability to breakdown lactose into monosaccharides
and thus prevent lactose digestion and
monosaccharide absorption
⮚ Fermentation of lactose by bacteria, causing gas
(cramping pain, flatulence) and osmotic diarrhea
⮚ Treatment
• Avoidance of milk products; adherence to a lactose-free diet
• Maintenance of adequate calcium intake to decrease risk of
osteoporosis
• Lactase enzyme replacement

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 Inflammatory Bowel Diseases
⬤Chronic, relapsing inflammatory bowel disorders
of unknown origin
⮚ Genetics
⮚ Environmental factors
⮚ Alterations of epithelial barrier functions
⮚ Immune reactions to intestinal flora
⮚ Varying phenotypes
⬤Examples
⮚ Ulcerative colitis
⮚ Crohn’s disease

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 Ulcerative Colitis
⬤Is a chronic inflammatory disease that causes
ulceration of the colonic mucosa.
⮚ Sigmoid colon and rectum
⬤Is common in those 20–40 years of age.
⬤Pathophysiology
⮚ Lesions are continuous with no skipped lesions, are limited
to the mucosa, and are not transmural.

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 Ulcerative Colitis (Cont.)
⬤Clinical manifestations
⮚ Large volumes of watery diarrhea, bloody stools,
cramps, pain, urge to defecate
⮚ Remission and exacerbations
⬤Treatment
⮚ First-line therapy: 5-aminosalicylic acid (mesalazine)
⮚ Steroids and salicylate
⮚ Immunosuppressive agents
⮚ Broad-spectrum antibiotics
⮚ Surgery: Resection of the colon or a colostomy
⬤Increased risk for colon cancer is demonstrated.
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 Crohn’s Disease
⬤Granulomatous colitis, ileocolitis, or regional
enteritis
⬤Idiopathic inflammatory disorder; affects any
part of the digestive tract, from mouth to anus
⬤Difficult to differentiate from ulcerative colitis
⮚ Similar risk factors and theories of causation
⬤Strong association
⮚ Nucleotide-binding oligomerization domains
(CARD15/NOD2) gene mutations

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 Crohn’s Disease (Cont.)
⬤Causes “skip” lesions.
⬤Inflamed areas mixed with uninflamed areas,
noncaseating granulomas, fistulas, deep
penetrating ulcers
⬤Clinical manifestations
⮚ Rectal bleeding and diarrhea are the most common
signs; abdominal tenderness, anemia.
⮚ Anemia may develop as a result of malabsorption of
vitamin B12 and folic acid.

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 Crohn’s Disease (Cont.)
⬤Treatment
⮚ Similar to ulcerative colitis
⮚ Immunomodulatory agents
⮚ Tumor necrosis factor–alpha (TNF-α) blocking agents:
To treat fistulas and maintain remission
⮚ Surgery
• Complication: Short bowel syndrome with malabsorption,
diarrhea, and nutritional deficiencies

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 Crohn’s Disease (Cont.)
⬤Crohn’s disease vs. normal bowel

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 Comparison of Ulcerative Colitis and
Crohn’s Disease

Feature Ulcerative Colitis Crohn’s Disease

Location of lesions Colon and rectum; no “skip” All of GI tract—mouth to anus;
lesions “skip” lesions common
Area affected Mucosal layer Entire intestinal wall
Granuloma Rare Common “cobblestone”
appearance
Abdominal pain Occasional Common
Bloody stools Common Less common
Steatorrhea Rare Common

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Comparison of Ulcerative Colitis and
Crohn’s Disease (Cont.)

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 Irritable Bowel Syndrome
⬤Functional gastrointestinal disorder with no
specific structural or biochemical alterations
⬤Pathophysiology
⮚ Visceral hypersensitivity or hyperalgesia
⮚ Abnormal gastrointestinal permeability, motility,
secretion, and sensitivity
⮚ Postinflammatory irritable bowel syndrome
⮚ Alteration in gut microbiota
⮚ Food allergy or food intolerance
⮚ Psychosocial factors

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 Irritable Bowel Syndrome (Cont.)
⬤Clinical manifestations
⮚ Lower abdominal pain
⮚ Diarrhea-predominant, constipation-predominant, or
alternating diarrhea and constipation
⮚ Gas, bloating
⮚ Nausea

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 Irritable Bowel Syndrome (Cont.)
⬤Treatment
⮚ No available cure
⮚ Laxatives, soluble fiber
⮚ Restriction of gluten, FODMAPs
⮚ Antidiarrheals
⮚ Antispasmodics
⮚ Pro-secretory drugs
⮚ Visceral analgesics
⮚ Low-dose antidepressants
⮚ Serotonin agonists/antagonists
⮚ Antibiotics
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 Diverticular Disease
of the Colon
⬤Diverticula
⮚ Herniation of mucosa through the muscle layers of the
colon wall
⬤Diverticulosis
⮚ Asymptomatic diverticular disease
⬤Diverticulitis
⮚ Inflammatory stage of diverticulosis
⬤Predisposing factors
⮚ Older age, genetics, obesity, smoking, diet, lack of physical
activity, and medications

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 Diverticular Disease
of the Colon (Cont.)
⬤Anatomy

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 Diverticular Disease
of the Colon (Cont.)
⬤Clinical manifestations
⮚ Low cramping abdominal pain, diarrhea, constipation,
distension, flatulence
⮚ Diverticulitis: Fever, leukocytosis
⬤Treatment
⮚ Increase of dietary fiber intake to increase stool
weight, lower colonic pressures, improve transit times,
and relieve symptoms
⮚ Uncomplicated diverticular disease: Bowel rest and
antibiotic administration
⮚ Surgical resection

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 Appendicitis
⬤Inflammation of the vermiform appendix
⬤Possible causes
⮚ Obstruction, ischemia, increased intraluminal
pressure, infection, inflammation
⬤Clinical manifestations
⮚ Epigastric and periumbilical pain, rebound
tenderness
⮚ Nausea, vomiting, fever, anorexia
⮚ Complications: Perforation, peritonitis, abscess
formation
⬤Treatment
⮚ Antibiotics and appendectomy
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 Intestinal Vascular
Insufficiency
⬤Blood supply to the stomach and intestine
⮚ Celiac artery; superior and inferior mesenteric arteries
⬤Mesenteric venous thrombosis
⬤Acute mesenteric ischemia
⬤Chronic mesenteric insufficiency

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 Intestinal Vascular
Insufficiency (Cont.)
⬤Clinical manifestations
⮚ Abdominal pain, fever, bloody diarrhea, hypovolemia,
leukocytosis, shock
⬤Treatment
⮚ Antibiotics, anticoagulation, vasodilators, and
inhibitors of reperfusion injury
⮚ Rehydration
⮚ Surgery

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 Portal Hypertension
⬤Abnormally high blood pressure in the portal
venous system primarily caused by resistance to
portal blood flow
⮚ Increase to above 5 mmHg (normal is 3–5 mmHg)
⬤Causes
⮚ Prehepatic
⮚ Intrahepatic
⮚ Posthepatic
⬤Can cause fatal consequences.

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 Portal Hypertension (Cont.)
⬤Consequences
⮚ Varices
• Distended, tortuous, collateral veins
• Lower esophagus, stomach, rectum, abdominal wall, spleen
• If rupture: Life-threatening
⮚ Splenomegaly
• Enlargement of the spleen
• Thrombocytopenia: Increased risk for bleeding

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 Portal Hypertension (Cont.)
⬤Consequences (cont.)
⮚ Hepatopulmonary syndrome
• Respiratory complications with portal hypertension
• Intrapulmonary vasodilation
• Intrapulmonary shunting and hypoxia
• Portopulmonary hypertension (pulmonary vasoconstriction
and vascular remodeling)

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 Portal Hypertension (Cont.)
⬤Clinical manifestations
⮚ Vomiting blood from bleeding esophageal varices
⬤Treatment
⮚ No definite treatment
⮚ Beta-blockers: To prevent variceal bleeding
⮚ Bleeding varices
• Fluid resuscitation
• Administration of prophylactic antibiotics, vasoactive drugs
(nonselective β-receptor antagonists and octreotide)
• Endoscopic vein ligation, endoscopic variceal band
ligation, compression of the varices with an inflatable tube
or balloon, and injection
of a sclerosing agent
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 Portal Hypertension (Cont.)
⬤Varices

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 Ascites (Cont.)
⬤Accumulation of fluid in the peritoneal cavity
⬤Most common cause: Cirrhosis
⬤Clinical manifestations
⮚ Abdominal distention, increased abdominal girth, and
weight gain
⬤Evaluation
⮚ Serum-ascites albumin gradient (SAAG): Most
specific diagnostic indicator

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 Ascites (Cont.)
⬤Mechanisms

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 Ascites (Cont.)
⬤Person with ascites

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 Ascites (Cont.)
⬤Treatment
⮚ Dietary salt restriction
⮚ Potassium-sparing diuretics
⮚ Strong diuretics, such as furosemide or ethacrynic
acid
⮚ Vasopressin receptor 2 antagonists: For dilutional
hyponatremia
⮚ Possible administration of albumin
⮚ Monitor serum electrolytes, especially sodium and
potassium

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 Ascites (Cont.)
⬤Treatment (cont.)
⮚ Paracentesis: Removal of 1 or 2 L of ascitic fluid and
relief of respiratory distress
• Removing too much fluid too fast relieves pressure on the
blood vessels, causing arteriolar vasodilation and carries the
risk of hypotension, shock, or death.
• Ascitic fluid reaccumulates in individuals with irreversible
disease.
• Is likely to cause peritonitis.
⮚ Transjugular intrahepatic portosystemic shunt or
peritoneovenous shunt: For refractory ascites
⮚ Liver transplant: Best treatment option
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 Hepatic Encephalopathy
⬤ Complex neurological syndrome characterized by
impaired behavioral, cognitive, and motor function
⬤ Clinical manifestations
⮚ Personality changes
⮚ Confusion
⮚ Irritability
⮚ Lethargy
⮚ Sleep disturbances
⮚ Flapping tremor (asterixis)
⮚ Stupor, coma, death

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 Hepatic Encephalopathy (Cont.)
⬤Treatment
⮚ Correct fluid and electrolyte imbalances.
⮚ Withdraw depressant drugs metabolized by the liver.
⮚ Restrict dietary protein intake.
⮚ Hypertonic saline, mannitol, hypothermia
⮚ Eliminate intestinal bacteria.
• Neomycin
• Lactulose
• Glutamase inhibitors
• Rifaximin

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 Jaundice
⬤Called icterus
⬤Yellow or greenish pigmentation of the skin
caused by hyperbilirubinemia (total plasma
bilirubin concentrations >2.5–3 mg/dL)
⬤Causes
⮚ Extrahepatic obstruction to bile flow (gallstones)
⮚ Intrahepatic obstruction (hepatocellular disease such
as cirrhosis or hepatitis)
⮚ Prehepatic obstruction: Excessive production of
bilirubin (excessive hemolysis of red blood cells)

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 Jaundice (Cont.)
⬤Pathophysiology

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 Jaundice (Cont.)
⬤Clinical manifestations
⮚ Dark urine
⮚ Clay-colored stools
⮚ Yellow discoloration possibly occurring first in the
sclera of the eye and then progressing to the skin
⮚ Skin xanthomas (cholesterol deposits) and pruritus
⮚ Anorexia, malaise, fatigue
⬤Treatment
⮚ Correct the cause: Jaundice is only a sign of an
underlying disorder.

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 Hepatorenal Syndrome
⬤Renal failure demonstrating oliguria,
hypotension, and peripheral vasodilation as a
result of advanced liver disease
⬤Usually associated with alcoholic cirrhosis
⬤Treatment
⮚ Manage fluid and electrolyte disorders, bleeding,
infections, and encephalopathy.
⮚ Administer systemic vasoconstrictors (α-adrenergic
agonists and octreotide) and albumin.
⮚ Liver transplantation

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 Acute Liver Failure
⬤Severe impairment or necrosis of liver cells
without preexisting liver disease or cirrhosis
⬤Leading cause: Acetaminophen overdose
⬤Pathophysiology
⮚ Hepatocytes become edematous.
⮚ Patchy areas of necrosis and inflammatory cell
infiltrates disrupt the parenchyma.
⮚ Hepatic necrosis is irreversible.

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 Acute Liver Failure (Cont.)
⬤Clinical manifestations
⮚ Anorexia, vomiting, abdominal pain, and progressive
jaundice
⬤Treatment
⮚ N-acetylcysteine: For acetaminophen poisoning
⮚ Antiviral therapy: To improve survival in cases of viral
hepatitis
⮚ Lowering blood ammonia levels
⮚ Liver transplantation

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 Autoimmune Hepatitis
⬤Rare, chronic, and progressive autoimmune
inflammatory liver disease
⬤Clinical manifestations
⮚ No symptoms
⮚ Jaundice, fatigue, loss of appetite, amenorrhea,
acute liver failure
⬤Treatment
⮚ Immunosuppressive drug therapy (e.g.,
corticosteroids or in combination with azathioprine)
with remission within 24 months
⮚ Relapses common with treatment withdrawal
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 Hepatitis A
⬤Can be found in the feces, bile, and sera of
infected individuals.
⬤Is usually transmitted by the fecal-oral route.
⬤Risk factors
⮚ Crowded, unsanitary conditions
⮚ Food and water contamination
⬤Prevention
⮚ Handwashing
⮚ Administration of immunoglobulin before exposure or
early in the incubation period
⮚ Administration of vaccines
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 Hepatitis B
⬤Parenterally and sexually transmitted
⬤Maternal transmission occurs if the mother is
infected during the third trimester.
⬤Hepatitis B vaccine prevents the transmission
and development of hepatitis B.
⬤Hepatitis B immunoglobulin provides post-
exposure prophylaxis against hepatitis B.

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 Hepatitis C
⬤Is responsible for most cases of posttransfusion
hepatitis.
⬤Is also implicated in infections related to IV drug
use and human immunodeficiency viral (HIV)
infection.
⬤Coinfection with hepatitis B is common.
⬤Approximately 80% of those with hepatitis C
develop chronic liver disease.
⬤No vaccine is available.
⬤Administer antiviral medications.
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 Hepatitis D and E
⬤Hepatitis D
⮚ Dependent on hepatitis B for replication
⮚ Treatment: Pegylated interferon alpha
⬤Hepatitis E
⮚ Fecal-oral transmission
⮚ Contaminated water or uncooked meat
⮚ Most common in Asian and African countries
⮚ Vaccine in China but not in other countries

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 Cirrhosis
⬤Is an irreversible inflammatory fibrotic disease that
disrupts liver function and even liver structure.
⬤Most common causes are alcohol abuse and HCV.
⬤Hepatic function from nodular and fibrotic tissue
synthesis (fibrosis) decreases.
⬤Biliary channels become obstructed and cause portal
hypertension.
⬤Because of the hypertension, blood is shunted away
from the liver, and hypoxic necrosis develops.

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 Cirrhosis (Cont.)
⬤Alcoholic liver disease
⮚ Oxidation of alcohol, causing damage to hepatocytes
⮚ Steatosis (alcoholic fatty liver)
• Is the mildest form.
• Is reversible if drinking is stopped.
⮚ Alcoholic hepatitis (steatohepatitis)
• Is characterized by inflammation.
• Degeneration and necrosis of the hepatocytes occur.
⮚ Alcoholic cirrhosis (fibrosis)
• Toxic effects of alcohol metabolism on the liver,
immunologic alterations, oxidative stress from lipid
peroxidation, and malnutrition occur.

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 Cirrhosis (Cont.)
⬤Alcoholic liver disease (cont.)
⮚ Impairs the hepatocytes’ ability to oxidize fatty acids,
synthesize enzymes and proteins, degrade hormones, and
clear portal blood of ammonia and toxins.
⮚ Clinical manifestations
• Nausea, anorexia, fever, abdominal pain, and jaundice
⮚ Treatment
• Cessation of alcohol
• Rest, a nutritious diet
• Corticosteroids, antioxidants, drugs that slow fibrosis
• Management of complications: Ascites, gastrointestinal bleeding,
infection, and encephalopathy

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 Cirrhosis (Cont.)
⬤Clinical manifestations

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 Disorders of the Gallbladder
⬤Cholelithiasis
⮚ Gallstone formation
⮚ Cholesterol stone formation in bile that is
supersaturated with cholesterol
• Enzyme defect: Increased cholesterol synthesis
• Decreased secretion of bile acids to emulsify fats
• Decreased resorption of bile salts from the ileum
• Gallbladder smooth muscle hypomotility, stasis
• Increased secretion of biliary calcium
• Genetic predisposition
• Combination of any or all of the above

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Disorders of the Gallbladder (Cont.)
⬤Cholelithiasis (cont.)
⮚ Clinical manifestations
• Epigastric and right hypochondrium pain
• Intolerance to fatty foods
• Biliary colic: Lodging of stones in the cystic or common duct
• Jaundice: Stone in the common bile duct
• Abdominal tenderness and fever: Cholecystitis

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Disorders of the Gallbladder (Cont.)
⬤Cholelithiasis (cont.)
⮚ Treatment
• Laparoscopic cholecystectomy: Preferred treatment
• Transluminal endoscopic surgery: Rapidly advancing
• Endoscopic retrograde cholangiopancreatography and
sphincterotomy with stone retrieval
• Large stones: Lithotripsy
• Alternative treatment: Drugs that dissolve smaller stones
such as bile acid chenodeoxycholic acid (CDCA) and
ursodeoxycholic acid

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Disorders of the Gallbladder (Cont.)
⬤Cholecystitis
⮚ Inflammation of the gallbladder
⮚ Acute vs. chronic
⮚ Clinical manifestations
• Fever, leukocytosis, rebound tenderness, and abdominal
muscle guarding
⮚ Treatment
• Pain control
• Replacement of fluids and electrolytes
• Fasting
• Antibiotic administration
• Laparascopic cholecystectomy

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 Disorders of the Pancreas
⬤Pancreatitis
⮚ Inflammation of the pancreas
⮚ Associated with several clinical disorders (alcohol
intake and cholelithiasis)
• Is caused by injury or damage to pancreatic cells and ducts,
causing a leakage of pancreatic enzymes into the pancreatic
tissue.
• These enzymes cause autodigestion of pancreatic tissue and
leak into the bloodstream to cause injury to blood vessels
and other organs.
⮚ Acute vs. chronic

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 Acute Pancreatitis
⬤Resolves spontaneously
⬤Clinical manifestations
⮚ Epigastric or midabdominal pain; nausea and vomiting
⮚ Fever and leukocytosis
⬤Evaluation
⮚ Elevated serum lipase: Primary diagnostic marker
⬤Treatment
⮚ Narcotics, NSAIDs, acetaminophen
⮚ Nasogastric suctioning
⮚ IV fluids

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 Acute Pancreatitis (Cont.)
⬤Pathophysiology

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 Chronic Pancreatitis
⬤Repeated exacerbations of acute pancreatitis
can lead to chronic changes.
⮚ Destroys acinar cells and the islets of Langerhans.
• Pancreatic parenchyma is destroyed and replaced by fibrous
tissues, strictures, calcification, ductal obstruction, ischemia,
and pancreatic cysts.
⬤Chronic alcohol abuse and smoking: Most
common cause.
⮚ Is a risk factor for pancreatic cancer.

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 Chronic Pancreatitis (Cont.)
⬤Clinical manifestations
⮚ Continuous or intermittent abdominal pain
⬤Treatment
⮚ Oral lipase and insulin
⮚ Corticosteroidal agents: For autoimmune pancreatitis
⮚ Cessation of alcohol use and smoking
⮚ Analgesics, endoscopic therapy, nerve block, and
surgical drainage of cysts or partial resection of the
pancreas

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