Transcript Gastrointestinal Diseases   Esophageal mucosa is lined by non-keratinized stratified squamous epithelium Gastric mucosa is lined by columnar glandular epithelium.

Gastrointestinal
Diseases
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Esophageal mucosa is lined by non-keratinized stratified
squamous epithelium
Gastric mucosa is lined by columnar glandular epithelium
Disorders of the esophagus
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Motor disorders: Achalasia
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Mechanical injury: Lacerations
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Varices
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Esophagitis: Reflux, infections, drugs,
irradiation
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Malignant neoplasms
Achalasia (failure to relax)
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Incomplete relaxation of lower sphincter
during swallowing leading to functional
obstruction and proximal dilatation
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Aperistalsis, incomplete relaxation, increased
resting tone
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Clinical picture: dysphagia, regurgitation and
aspiration
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Histology: Inflammation in the area of
autonomic nerve supply.
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Hypotheses: autoimmune, viral infections
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May occur secondary to Trypanosoma cruzi
infection.
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5% develop squamous cell carcinoma, at
younger age.
Esophageal lacerations
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Longitudinal tears at the gastroesophageal
junction
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Clinical setting: chronic alcoholics after a severe
vomiting
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Tear may be superficial or deep affecting all
layers
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Clinical picture: Pain, bleeding, superimposed
infection.
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Hiatus hernia is found in 75% of patients
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Most often bleeding stops without intervention,
but life-threatening hematemesis may occur.
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Supportive therapy and balloon tamponade.
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Healing is prompt with minimal or no residue
Hiatal hernia
95%
5%
•Dilatation of the space between the diaphragmatic muscles which
permits a dilated segment of the stomach to protrude above the
diaphragm.
•1-20% of adult subjects; only 9% of those affected suffer from
heartburn and reflux esophagitis; complications may include
ulceration and bleeding
Esophagitis
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Reflux esophagitis
Infections
Prolonged gastric intubation
Ingestion of irritant substance
Chemotherapy and irradiation
Reflux esophagitis
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Reflux of gastric contents into
esophagus
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Possible etiologies:
inadequate function of lower
sphincter; sliding hiatal hernia
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C\P: “heart burn”
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Complications: ulceration,
bleeding, stricture
Barrett esophagus
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A complication of long standing reflux esophagitis
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Replacement of squamous epithelium by columnar
epithelium with goblet cells
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30- to 40-fold greater risk to develop adenocarcinoma
Esophageal varices
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Tortuous dilated veins in the submucosa of distal
esophagus
Esophageal varices
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Etiology: portal hypertension secondary to liver
cirrhosis
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Asymptomatic until they rupture leading to massive
hemorrhage
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50% subsides spontaneously
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20-30% die during the first attack
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Rebleeding occurs in 70% of cases within one year
Esophageal carcinoma
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Squamous cell carcinoma
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More prevalent worldwide
Risk factors: longstanding esophagitis,
achalasia, smoking,
alcohol, genetics
50% in middle 1/3
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Adenocarcinoma
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More common
Occurs on top of
Barrett esophagus
More in distal 1/3
Stomach
2
1
3
1) Cardia
2) Body: Parietal and Chief cells
3) Antrum: Mucin secretion and G-cells
that secrete gastrin
Chronic Gastritis
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Infiltration of the mucosa by chronic
inflammatory cells (lymphocytes and plasma
cells)
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Causes:
 Helicobacter
pylori: G-ve bacilli; is present in
70-90% of patients with gastric and duodenal ulcers,
respectively
 Autoimmune:
autoantibodies to parietal cells
(decreased acid and intrinsic factor)
Helicobacter pylori and associated disorders
H. pylori
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Gastric ulcer
Gastritis (chronic and acute), peptic (gastric and
duodenal) ulcers
Gastric adenocarcinoma
Gastric lymphoma
Acute gastritis “gastropathy”
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Injury to the gastric mucosa (erosions) with no
significant participation of inflammatory cells
Causes include:
Non-steroidal antiinflammatory drugs
 Alcohol
 Hypo-volemia
 Shock
 Stress
 Uremia
 Enterogastric reflux
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Peptic ulcer
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Location: stomach or first portion of duodenum
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More frequent in patients with alcoholic cirrhosis,
chronic obstructive pulmonary disease, chronic renal
failure and hyperparathyroidism.
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Causes include: Helicobacter pylori and causes of acute
gastritis (especially NSAID)
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Clinical features: Epigastric pain (worse at night and
relieved by food), bleeding (30%) and perforation (5%;
accounts for 2/3 of deaths).
Gastric cancer
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Intestinal-type:
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Risk factors: diet (nitrites,
smoked food, increased
salt), chronic gastritis,
altered anatomy after
resection
On top of intestinal
metaplasia
Decreasing in incidence
Glandular morphology
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Diffuse-type:
Undefined risk factors
( no known relation to H.
pylori)
 Signet cell morphology
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Macroscopic (growth patterns) of gastric
adenocarcinoma
Mass
Ulcer
Lintis plastica
Clinical picture:
asymptomatic or abdominal
discomfort, weight loss,
anemia
Small and large bowel
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Developmental: Meckel diverticulum
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Diarrheal disease:
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Infections: viruses, bacteria, protozoa
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Idiopathic inflammatory bowel disease
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Malabsorption
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Diverticular disease
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Tumors
Types and causes of diarrheal illness
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Secretory diarrhea: loss of intestinal fluid that is
isotonic with plasma and persists during fasting.
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Viruses: rotavirus: destroy the absorptive surface,
common in children 6-24 month of age, 130 million
cases per year.
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Toxin-mediated: Vibrio cholera, E.coli (need time)
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Preformed toxin: Stapylococcus aureus (immediate
effect)
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Excessive laxatives
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Exudative diarrhea: pruluent bloody stool
(inflammation of the mucosa and/or hemorrhage)
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Infections causing tissue damage: Shigella,
Salmonella, Entamoeba histolytica
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Infections causing both tissue damage and toxins:
Clostridium difficile; with antibiotic therapy, leading
to pseudo-membranous colitis
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Idiopathic inflammatory bowel disease
Parasites
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Entamoeba histolytica: Invasive, amebic colitis and
amebic liver abscesses
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Giardia lamblia: non-invasive, duodenum and jejunum,
diarrhea and malabsorption
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Cryptosporidium: self-limited diarrhea in immuno-
competent individuals; long course in AIDS patients
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Worms:
Pseudomembranous colitis
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Membranes made of neutrophils and fibrin
Seen in Clostridium difficile infection and in ischemia
Idiopathic inflammatory bowel disease
Crohn disease
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Small bowel and colon
Patchy involvement
Transmural inflammation
Non-caseating granulomas
Poor response to surgery
Increased risk for cancer
Ulcerative colitis
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Colon only
Continuous involvement
Superficial inflammation
No granulomas
Good response to surgery
Increased risk for cancer
Malabsorption syndromes
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Defective intraluminal digestion:
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pancreatic insufficiency
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Defective bile secretion
Mucosal abnormalities:
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Disaccharide deficiency (lactose intolerance)
Reduced surface area
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Celiac disease
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Surgical resection
Infections: Tropical infection
Clinical features of malabsorption
syndromes
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Hematopietic system:
 Anemia: iron, folate and B12 deficiency
 Bleeding: vitamin K deficiency
Musculoskeletal system:
 Osteopenia: calcium and vitamin D deficiency
Skin:
 Purpura: vitamin K deficiency
 Dermatitis: vitamin A deficiency
Nervous system:
 Peripheral neuropathy: folate and B12 deficiency.
Meckel diverticulum
Meckel
diverticulum
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A blind pouch located in distal small bowel
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The most common congenital anomaly of the small intestine; results from failure
of the involution of the omphalomesenteric (vitelline) duct
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The rule of 2’s:
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2% of the population, 2 inches in length, 2 feet proximal to the ileocecal
valve, 2 types of heterotopic tissue (pancreas and stomach); 2% are
symptomatic.
Symptoms are rare:
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Overgrowth of bacteria that depletes vitamin B12 leading to anemia
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“Peptic” ulcer and bleeding
Diverticulosis
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Herniation of the mucosa and submucosa
through the muscle wall
50% after age 50
Related to low-fiber diet, increased intraluminal
pressure and focal defects in muscular layer
Mostly in sigmoid colon
Asymptomatic unless infected
Tumors of the large bowel
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Hyperplastic polyps: not precancerous
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Adenomatous polyps: precancerous
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Familial polyposis syndrome: 500-2500 polyps, 100%
risk for developing cancer
Colonic adenocarcinoma:
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Always arises from adenomatous polyp
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Risk factors: low fiber, high fat, decreased vit A, C, E,
idiopathic inflammatory bowel disease, familial
adenomatous polyposis
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Several hits to different genes: APC, k-ras, p53; or DNA
mismatch repair genes
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Survival depends on stage (depth of invasion and node
metastasis)
Colonic adenocarcinoma
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Clinical picture:
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Asymptomatic or fatigue, weakness and iron
deficiency anemia in tumors of right side.
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Left sided tumors may produce bleeding, change in
bowel habits and crampy pain
Colonic adenocarcinoma
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Course: tumor invades bowel wall and lymphatics/blood
vessels with metastasis to lymph nodes, liver, lungs, and
bones. 25% of patients have metastatic disease at
presentation
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Diagnosis is based on endoscopy and biopsy
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Prognosis depends on stage (depth of invasion, nodal and
distant metastasis), and 5-year survival varies from >90%
in stage I, to 4% with distant metastasis.