Download Clinical manifestations

Alterations of Digestive Function
Part 1
Chapter 34
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Clinical Manifestations of
Gastrointestinal Dysfunction
Anorexia
 A lack of a desire to eat despite
physiologic stimuli that would normally
produce hunger.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Vomiting (emesis)
 The forceful emptying of the stomach and
intestinal contents through the mouth
 Stimuli that initiate vomiting reflex include:



Severe pain
Distention or chemical irritation of the stomach
or duodenum
Activation of the chemoreceptor trigger zone in
the medulla.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Vomiting (cont.)
 Vomiting is usually preceded by nausea
and retching.


Retching - nonproductive vomiting; begins
movement of gastric and duodenal contents up
through the esophagus toward the mouth.
Projectile vomiting - spontaneous vomiting
that is not preceded by nausea or retching.

Associated with direct stimulation of the
vomiting center in the brain
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Clinical Manifestations of
Gastrointestinal Dysfunction
Constipation
 Constipation is defined as infrequent or
difficult defecation.
 Causes - low fiber diet; dehydration; lack
of exercise; drugs or disorders that impair
intestinal motility or obstruct the intestinal
lumen; hypothyroidism.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Diarrhea
 Increased frequency of bowl movements with
increased volume, fluidity, and weight of
feces.
 More than three stools per day is considered
abnormal.
 Stool volume and consistency is determined
by water content of the colon and the
presence of unabsorbed food, unabsorbable
material, and intestinal secretions.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Diarrhea (cont.)
 Large-volume diarrhea - caused by excessive
amounts of water or secretions in the
intestines.
 Small-volume diarrhea - results from
excessive intestinal motility, usually from
inflammation.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Diarrhea (cont.)
 Major mechanisms of diarrhea:

Osmotic diarrhea - nonabsorbable substance
draws excess water into the intestine and
increases stool weight and volume.
• Causes - inability to digest lactose due to
lactase and pancreatic enzyme deficiency;
excessive ingestion of synthetic,
nonabsorbable sugars.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Diarrhea (cont.)
 Major mechanisms of diarrhea:

Secretory diarrhea - excessive mucosal secretion of
fluid and electrolytes.
• Causes - bacterial enterotoxins, exotoxins, or
neoplasms.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Diarrhea (cont.)
 Major mechanisms of diarrhea:

Motility diarrhea - food is not mixed properly,
digestion is impaired, and motility is increased.
• Causes - resection of the small intestine, fistula
formation between loops of intestine and
excessive motility of the intestine caused by
diabetic neuropathy.
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ACTIVITY
Explain why factors that slow movement of
feces through the colon cause constipation,
whereas factors the speed up movement of
feces through the colon cause diarrhea.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Abdominal Pain
 Abdominal pain is caused by stretching,
inflammation, or ischemia.
 Originates in the organs themselves (visceral
pain) or in the peritoneum (parietal pain).
Visceral pain is often referred to the back.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Abdominal Pain (cont.)
 Parietal
pain - localized and intense pain from
irritation of the parietal peritoneum.
 Visceral pain - from the organs themselves; it
is poorly localized with a radiating pattern.
 Referred pain - visceral pain felt at some
distance from a diseased or affected organ;
felt in skin or deeper tissues that share a
sensory pathway with the affected organ.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Gastrointestinal Bleeding
 Upper gastrointestinal bleeding - from the
esophagus, stomach, or duodenum.


Causes - most commonly from bleeding varices in
the esophagus; also peptic ulcers, or a MalloryWeiss tear at the esophageal gastric junction from
severe retching.
Hematemesis - bright red bleeding or dark “coffee
ground” material (affected by stomach acids).
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Clinical Manifestations of
Gastrointestinal Dysfunction
Gastrointestinal Bleeding (cont.)
 Lower gastrointestinal bleeding - from the
jejunum, ileum, colon, or rectum.




Causes - polyps, inflammatory disease, cancer, or
hemorrhoids.
Melena - Black, sticky, tarry, foul-smelling stools
caused by digestion of blood.
Hematochezia - fresh, bright red blood passed
from the rectum.
Occult bleeding - traces of blood in normalappearing stools; detectable only with guaiac test.
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Clinical Manifestations of
Gastrointestinal Dysfunction
Gastrointestinal Bleeding (cont.)
 Acute, severe gastrointestinal bleeding is life
threatening, depending on volume and rate of
loss.
 Chronic gastrointestinal bleeding can cause
iron-deficiency anemia.
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GI Bleeding
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Disorders of Motility
Dysphagia
 Dysphagia is difficulty swallowing.
 Results from mechanical obstruction of the
esophagus or a disorder that impairs its
motility.
 Mechanical obstructions - tumors, strictures,
and diverticular herniations (outpouchings).
 Functional obstructions - neurological or
muscular disorders that interfere with
voluntary swallowing or peristalsis.
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Disorders of Motility
Dysphagia (cont.)
 Achalasia - form of functional dysphagia
caused by denervation of smooth muscle in
the esophagus; results in loss of esophageal
peristalsis and failure of the lower esophageal
sphincter (LES) to relax.
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Achalasia
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Disorders of Motility
Gastroesophageal Reflux Disease (GERD)
 GERD - reflux of chyme from the stomach
to the esophagus.
 Reflux esophagitis - inflammation of the
esophagus due to repeated exposure to
acids and enzymes.
 Normally the lower esophageal sphincter
(LES) prevents reflux of acidic chyme.
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Gastroesophageal Reflux
Disease
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Disorders of Motility
Gastroesophageal Reflux Disease (cont.)
 Causes - loss of muscle tone in LES or
increased abdominal pressures.
 Manifestations - heartburn, dysphagia, and
upper abdominal pain within 1 hour of
eating.
 Sequealae - GERD may cause
esophageal ulcerations and strictures, and
possibly cancer.
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Disorders of Motility
Hiatal Hernia



Protrusion of the upper part of the stomach through
the diaphragm at the gastroesophageal junction.
Sliding hiatal hernia - stomach slides into the
thoracic cavity through the esophageal hiatus.
Paraesophageal hiatal hernia - greater curvature of
the stomach herniates through a secondary
opening in the diaphragm and lies alongside the
esophagus.
 Strangulation of the hernia is a major
complication.
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Hiatal Hernia
Sliding hiatal hernia
Paraesophageal
hiatal hernia
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Disorders of Motility
Hiatal Hernia
 Manifestations - may be asymptomatic; but
often exhibit gastroesophageal reflux,
dysphagia, heartburn, and epigastric pain;
regurgitation and substernal discomfort after
eating.
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Disorders of Motility
Pyloric Obstruction
 Blocking or narrowing of the opening
between the stomach and the duodenum.
 Causes - congenital defect, inflammation
and scarring secondary to a gastric ulcer, or
tumor growth.
 Manifestations - epigastric pain and fullness
after eating, nausea, succussion splash,
vomiting, and, with a prolonged obstruction,
malnutrition, dehydration, and extreme
debilitation.
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Disorders of Motility
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.
 Ileus - an obstruction of the intestines.
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Disorders of Motility
Intestinal Obstruction and Ileus
 Simple obstruction - mechanical blockage
of the lumen, often by torsion, herniation,
or a tumor.
 Functional obstruction - failure of motility
(paralytic ileus), often occurring after
abdominal surgery.
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Intestinal Herniation
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Disorders of Motility
Intestinal Obstruction and Ileus
 Intussusception - telescoping of a section
of small intestine into the distal portion of
the bowel.
 Volvulus (torsion)- twisted loop of intestine
and mesentery.
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Intussusception
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Volvulus (Torsion)
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Volvulus and Intussusception
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Disorders of Motility
Intestinal Obstruction and Ileus
 Pathophysiology:
 Fluid
and gas accumulate upstream of
blockage, causing distension of the intestinal
wall.
 Pressure from distension reduces blood flow,
resulting in ischemic damage, which allows
intestinal contents and bacteria to leak into
peritoneum; fluids shift into peritoneal cavity.
 Blockage reduces absorption of fluids and
electrolytes.
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Disorders of Motility
Intestinal Obstruction and Ileus
 Manifestations - colicky pain that occurs
intermittently as a peristaltic wave of
muscle contraction meets the obstruction;
vomiting; and abdominal distension.
 Sequealae - fluid and electrolyte losses
cause acidosis, hypokalemia, dehydration,
hypovolemia, hypotension and shock;
ischemia causes necrosis, perforation of
intestinal wall and peritonitis.
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Intestinal
Obstruction
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Gastritis

Acute or chronic inflammation of the
gastric mucosa.
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Gastritis
Acute gastritis
 Inflammation that erodes the surface
epithelium in a diffuse or localized pattern.
 Usually due to injury of the protective
mucosal barrier caused by drugs or
chemicals.
 NSAIDs
cause gastritis by inhibiting
prostaglandins, which stimulate secretion
of mucus.
 Alcohol, histamine, digitalis, and metabolic
disorders can contribute.
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Gastritis
Acute gastritis (cont.)
 Manifestations - vague abdominal
discomfort, epigastric tenderness, and
bleeding.
 Treatment - healing usually occurs
spontaneously within a few days.
Discontinuing injurious drugs, using
antacids, or decreasing acid secretion with
cimetidine (Tagamet®, a histamine H2receptor antagonist) facilitates healing.
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Gastritis
Chronic gastritis
 More complex and serious than acute
gastritis.
 Characterized by atrophy of the gastric
mucosa.
 Most commonly a result of chronic
infection by H. pylori bacteria; also
autoimmune conditions.
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Gastritis
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H. pylori Infection
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Gastritis
1. Chronic fundal gastritis (atrophic gastritis)
 Affects fundus and body.
 Most severe form.
 Can
result in gastric atrophy and
decreased secretion of hydrochloric acid,
pepsinogen, and intrinsic factor, which can
lead to pernicious anemia.
 This is a risk factor for developing gastric
carcinoma.
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Gastritis
2. Chronic antral gastritis
 Affects pyloric antrum
 Most common type
 Not usually associated with impaired
secretion or gastric atrophy.
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Gastritis
Chronic gastritis
 Manifestations - symptoms often do not
correlate with the severity
 Symptoms
are often vague, including
anorexia, fullness, nausea, vomiting, and
epigastric pain
 Clinical signs include diminished secretion
of hydrochloric acid (achlorhydria) and
gastric bleeding.
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Gastritis
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ACTIVITY

What treatments would be appropriate for
treating chronic gastritis (including its
sequelae)?
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Peptic Ulcer Disease


Break or ulceration in the protective mucosal
lining of the lower esophagus, stomach, or
duodenum.
Caused by excessive secretion of gastric
acid, disruption of the protective mucosal
barrier, or both.
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Peptic Ulcer
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Peptic Ulcer Disease

Risk factors - smoking, advanced age,
habitual use of nonsteroidal anti-inflammatory
drugs (NSAIDs), alcohol, psychological
stress, and Helicobacter pylori infection,
chronic diseases such as emphysema,
rheumatoid arthritis, cirrhosis, and diabetes.
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Peptic Ulcer Disease
Duodenal ulcers
 Ulceration of the duodenal mucosa and
submucosa layers.
 Most common of the peptic ulcers.
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Duodenal Ulcer
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Peptic Ulcer Disease
Duodenal ulcers
 Causes:
 Infection
with H. pylori - releases toxins and
enzymes that promote inflammation and
ulceration.
 Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit mucosal prostaglandin synthesis.
 Hypersecretion of acid and pepsin by stomach due to high gastrin levels and smoking.
 Inadequate secretion of bicarbonate by the
duodenal mucosa.
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Peptic Ulcer Disease
Duodenal ulcers



Clinical manifestations - epigastric pain that begins
2 to 3 hours after eating, most often at night.
 Ingestion of food or antacids usually relieves
pain.
Complications - perforation of the duodenal wall
with development of peritonitis.
Treatment - avoidance of smoking, NSAIDs, and
alcohol; antibiotics to treat the H. pylori infection;
and proton pump inhibitors (PPIs) to prevent
gastric acid production.
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Peptic Ulcer Disease
Gastric Ulcers
 Tend to develop in the antral region of
stomach, adjacent to the acid-secreting
mucosa of the body.
 Less common than duodenal ulcers.
 Causes are similar to those of duodenal
ulcers, including chronic H. pylori infection
and NSAID use.
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Gastric Ulcers
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Peptic Ulcer Disease
Gastric Ulcers
 Pathophysiology:




The primary defect is reduced mucus secretion
an increased mucosal permeability to H+ ions.
Gastric secretion tends to be normal or less
than normal.
Clinical manifestations - epigastric pain
immediately after eating, anorexia,
vomiting, and weight loss.
Treatment - same as for duodenal ulcers.
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Gastric Ulcers
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Peptic Ulcer Disease
Stress Ulcers
 Peptic ulcers that result from severe
physiologic stress such as burns, head
injury, multiple trauma, severe infection,
and mechanical ventilation.
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Stress Ulcers
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Peptic Ulcer Disease
Stress Ulcers
Types:
1. Ischemic ulcers - develop suddenly after severe
illness, systemic trauma, or neural injury.

Ulceration follows mucosal damage caused by
decreased blood flow to the gastric mucosa.
2. Curling ulcers – ischemic ulcers that develop as a
result of burn injury.
3. Cushing ulcers - caused by head trauma or brain
surgery.

Ulceration follows hypersecretion of gastric acid
due to overstimulation of the vagal nuclei.
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Peptic Ulcer Disease
Stress Ulcers
 Clinical manifestations - often form multiple
painless ulcers in the stomach and duodenum
which present as occult bleeding in fecal
tests.
 Life-threatening
hemorrhage may be the first
indication of their presence.
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Peptic Ulcer Disease


Ulcer surgery - peptic ulcers may be treated
surgically if the patient suffers recurrent or
uncontrolled bleeding or perforation of the
stomach or duodenum.
Gastrectomy - resection of all or part of the
stomach.
 Anemia
can result due to decreased
production of intrinsic factor (which decreases
B12 absorption).
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Malabsorption Syndromes

Malabsorption syndromes result in
impaired digestion or absorption of
nutrients.



Maldigestion - failure of the chemical
processes of digestion.
Malabsorption - failure of the intestinal mucosa
to absorb digested nutrients.
Maldigestion and malabsorption frequently
occur together.
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Malabsorption Syndromes
Pancreatic Insufficiency
 Insufficient pancreatic enzyme production
causes malabsorption associated with
impaired digestion.
 The
pancreas does not produce sufficient
amounts of the enzymes that digest protein,
carbohydrates, and fats into components that
can be absorbed by the intestine.
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Malabsorption Syndromes
Pancreatic Insufficiency
 Causes - pancreatitis, pancreatic carcinoma,
pancreatic resection, and cystic fibrosis.
 Clinical manifestations - fatty stools, diarrhea,
weight loss, and failure to thrive.
 Treatment - oral replacement of pancreatic
enzymes during meals.
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Pancreatic Insufficiency
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Malabsorption Syndromes
Lactase deficiency
 Deficient lactase production in the brush
border of the small intestine results in lactose
intolerance.



Inhibits the breakdown of lactose (milk sugar) and
prevents its absorption.
Fermentation of lactose by bacteria causes gas
(cramping, pain, flatulence, etc.).
Excess lactose in lumen draws fluid in and
increases gut motility, causing osmotic diarrhea.
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Malabsorption Syndromes
Lactase deficiency
 Causes - can be genetic (more common in
certain ethnic groups) or caused by diseases
of the intestine such as gluten-sensitive
enteropathy.
 Generally

does not develop until adulthood.
Treatment - avoidance of lactose-containing
foods.
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Malabsorption Syndromes
Bile Salt Deficiency
 Bile salts are needed to emulsify and absorb
fats and fat-soluble vitamins.



Synthesized from cholesterol in the liver.
Bile salt deficiency causes fat malabsorption
and steatorrhea (fatty stools).
Causes - liver disease, obstruction of the
bile duct, intestinal hypomotility, and Crohn
disease.
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Malabsorption Syndromes
Bile Salt Deficiency
 Clinical manifestations:
 Poor
intestinal absorption of lipids causes
fatty stools and diarrhea.
 Malabsorption of fat-soluble vitamins causes
vitamin deficiencies.
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Malabsorption Syndromes
Bile Salt Deficiency
 Clinical manifestations of vitamin deficiencies:




Vitamin A - night blindness
Vitamin D - decreased calcium absorption, bone
pain, osteoporosis, fractures.
Vitamin K - prolonged prothrombin time, purpura,
and petechiae
Vitamin E - uncertain; may cause testicular
atrophy and neurologic defects in children.
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Malabsorption Syndromes
Bile Salt Deficiency
 Treatment - increase medium-chain
triglycerides in the diet (coconut oil); oral
bile salts; injections of Vitamins A, D, and K.
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Inflammatory Bowel Diseases

Chronic, relapsing inflammatory bowel
disorders of unknown origin.
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Ulcerative Colitis


Chronic inflammatory disease that causes
ulceration of the colonic mucosa, usually in
the rectum and sigmoid colon.
Possible causes - although the specific cause
is unknown it is related to a number of factors:


Genetics - runs in families and more common
is certain ethnic groups (Caucasians, Jews).
Autoimmunity - associated with other
autoimmune diseases such as systemic lupus
erythematosus (SLE); immune cells cause
inflammation of mucosa.
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Ulcerative Colitis
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Ulcerative Colitis

Pathophysiology:

Injury to the colon is mediated by macrophages, T
cytotoxic cells, and the production of anticolon
antibodies.
 These cause inflammatory ulceration in the large
intestine with mucosal erythema and edema.
 Ulceration and swelling cause narrowing of the
colonic lumen, diarrhea, and significant bleeding
(hematochezia).
 Process begins in the rectum and advances up
through the colon in a continuous manner and does
not "skip" parts of the mucosa.
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Ulcerative Colitis

Clinical manifestations:







Most often presents in early adulthood.
Usually of sudden onset, with severe signs and
symptoms.
Frequent loose bowel movements (10 to 20 stools
per day) with bloody stools.
Crampy abdominal pain and dehydration.
Bleeding can cause iron-deficiency anemia.
A course of frequent remissions and exacerbations
is common.
Increased risk of infection, perforation, strictures,
and colon cancer.
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Ulcerative Colitis

Treatment - anti-inflammatory drugs;
colonic resection with colostomy
placement may be necessary.
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Crohn Disease

http://www.youtube.com/watch?v=k0kRSF80
PJ0

4:21 min
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Crohn Disease

Similar to ulcerative colitis, but it affects both
the large and small intestines.




Most often involves ascending and transverse
colon and distal ileum; rarely involves rectum.
Ulceration tends to involve all the layers of the
intestinal wall (not just the mucosa).
“Skip lesion” fissures (affected areas
separated by normal ones) and granulomas
are characteristic.
Similar risk factors and theories of causation
as ulcerative colitis.
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Crohn Disease
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Crohn Disease
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Crohn Disease

Clinical manifestations - symptoms vary
considerably from person to person.

Usually develops slowly.
 Diarrhea, abdominal pain, and weight loss are typical.
 Anemia due to deficiency of vitamin B12 and folic acid
absorption.
 Weight loss due to inadequate absorption of nutrients.
 Fistulae formation.
 Bloody diarrhea is less common than in ulcerative
colitis.

Treatment - similar to ulcerative colitis.
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Crohn vs. Ulcerative Colitis
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Diverticular Disease of the Colon

Diverticula - outpouchings of colonic
mucosa through the muscle layers of the
colon wall.


Most common in sigmoid colon.
Diverticulosis - asymptomatic condition
characterized by presence of diverticula.

Associated with a diet low in fiber and high in
refined foods, constipation, and increased
pressure on weakened colon walls.
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Diverticular Disease of the Colon
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Diverticular Disease of the Colon

Diverticulitis - inflammation of the
diverticula.

Caused by a fecolith (impacted fecal matter)
that blocks the opening of a diverticulum,
causing irritation and bacterial growth.
 Clinical manifestations - lower left quadrant
abdominal pain (since sigmoid colon is usually
involved), fever, and episodes of diarrhea
and/or constipation.
 Sequelae - bleeding, necrosis of wall,
perforation, peritonitis, fistula formation, and
stenosis of the colon causing obstruction.
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Appendicitis



Inflammation and infection of an outpouching
of the vermiform appendix.
Usually develops during early adulthood,
although it can occur in children.
Cause - obstruction of the appendix with fecal
matter causes inflammation, infection,
edema, and ischemia of the appendix.
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Appendicitis
Normal
appendix
Inflamed
appendix
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Appendicitis

Clinical manifestations:

Initially pain is in epigastric or umbilical region, but
swelling causes contact with the sensitive parietal
peritoneum, causing pain to move to lower right
quadrant.
 Anorexia (from pain), nausea and vomiting.
 Low grade fever.
 Leukocyte count moderately elevated.

Treatment - surgical removal of the appendix
and administration of antibiotics.

Without surgical resection, inflammation may
progress to gangrene, perforation, and peritonitis.
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ACTIVITY

What are some similarities between
appendicitis and diverticulitis?
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Irritable Bowel Syndrome



IBS is a functional disorder with no known
structural or biochemical alterations
“Spastic colon”
Involved in up to half of the GI problems for
which people seek help.
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Irritable Bowel Syndrome

Symptoms vary, but can include cramping,
fatigue, and constipation alternating with
diarrhea.
 Diarrhea
symptoms are due to increased
intestinal motility, reducing the time for fluid
absorption.
 Cramping is due to a loss of peristaltic
coordination with conflicting waves of
peristalsis.
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Irritable Bowel Syndrome

Factors involved:
 Alterations
in the brain-gut axis with intestinal
hypersensitivity
 Abnormal GI motility and secretion
 Intestinal infection
 Changes in composition of intestinal flora
 Food allergy or intolerance
 Psychosocial factors such as emotional stress
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Irritable Bowel Syndrome

Treatment - no cure; treatments aim at easing
the symptoms, including antidepressants,
antispasmotics, visceral analgesics,
antidiarrheals, laxatives, and fiber.
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