1. Gastrointestinal Diseases

2. Esophageal mucosa is lined by non-keratinized stratified squamous epithelium
Gastric mucosa is lined by columnar glandular epithelium

3. Disorders of the esophagus
Motor disorders: Achalasia
Mechanical injury: Lacerations
Varices
Esophagitis: Reflux, infections, drugs, irradiation
Malignant neoplasms

4. Achalasia (failure to relax)
Incomplete relaxation of lower sphincter during swallowing leading to functional obstruction and proximal dilatation
Aperistalsis, incomplete relaxation, increased resting tone
Clinical picture: dysphagia, regurgitation and aspiration
Because it is a mechanical disorder, I have no picture for it, it is detected by the clinical picture and pressure measurement of the lower sphincter. T.Cruzi infection is a parasite that is transmitted by mosquito and leads to destruction of myenteric plexus in esophagus, stomach, colon and ureter

5. Histology: Inflammation in the area of autonomic nerve supply.
Hypotheses: autoimmune, viral infections
May occur secondary to Trypanosoma cruzi infection.
5% develop squamous cell carcinoma, at younger age.

6. Esophageal lacerations
Longitudinal tears at the gastroesophageal junction
Clinical setting: chronic alcoholics after a severe vomiting
Tear may be superficial or deep affecting all layers
Clinical picture: Pain, bleeding, superimposed infection.

7. Hiatus hernia is found in 75% of patients
Most often bleeding stops without intervention, but life-threatening hematemesis may occur.
Supportive therapy and balloon tamponade.
Healing is prompt with minimal or no residue

8. Hiatal hernia 5%
95%
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

9. Esophagitis Reflux esophagitis Infections Prolonged gastric intubation
Ingestion of irritant substance
Chemotherapy and irradiation

10. Reflux esophagitis Reflux of gastric contents into esophagus
Possible etiologies: inadequate function of lower sphincter; sliding hiatal hernia
C\P: “heart burn”
Complications: ulceration, bleeding, stricture

11. Barrett esophagus A complication of long standing reflux esophagitis
Replacement of squamous epithelium by columnar epithelium with goblet cells
30- to 40-fold greater risk to develop adenocarcinoma

12. Esophageal varices
Tortuous dilated veins in the submucosa of distal esophagus

13. Esophageal varices
Etiology: portal hypertension secondary to liver cirrhosis
Asymptomatic until they rupture leading to massive hemorrhage
50% subsides spontaneously
20-30% die during the first attack
Rebleeding occurs in 70% of cases within one year .

14. Esophageal carcinoma Squamous cell carcinoma Adenocarcinoma
More prevalent worldwide
Risk factors: long-standing esophagitis, achalasia, smoking, alcohol, genetics
50% in middle 1/3
Adenocarcinoma
More common
Occurs on top of Barrett esophagus
More in distal 1/3

15. Stomach 2 1 3 1) Cardia 2) Body: Parietal and Chief cells
3) Antrum: Mucin secretion and G-cells that secrete gastrin P
Parietal cells secrete acid and intrinsic factor; while Chief secrets digestive enzymes like pepsin
Gastrin stimulates the secretion of acid from parietal cells

16. Chronic Gastritis
Infiltration of the mucosa by chronic inflammatory cells (lymphocytes and plasma cells)
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)

17. Helicobacter pylori and associated disorders
H. pylori
Gastric ulcer
Gastritis (chronic and acute), peptic (gastric and duodenal) ulcers
Gastric adenocarcinoma
Gastric lymphoma

18. Acute gastritis “gastropathy”
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
It is a major cause for hematemesis especially in alcoholics. 25% of presons who take daily aspirin for Rh arthritis develop acute gastritis at one point. Erosions are breach of the superficial mucosa and can heal rapidly as opposed to ulceration

19. Peptic ulcer Location: stomach or first portion of duodenum
More frequent in patients with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure and hyperparathyroidism.
Causes include: Helicobacter pylori and causes of acute gastritis (especially NSAID)
Clinical features: Epigastric pain (worse at night and relieved by food), bleeding (30%) and perforation (5%; accounts for 2/3 of deaths).
Cirrhosis: alcohol; smoking: decrease blood flow and healing, CRF and HPTH increase Ca and acid

20. Gastric cancer Intestinal-type: Diffuse-type:
Risk factors: diet (nitrites, smoked food, increased salt), chronic gastritis, altered anatomy after resection
On top of intestinal metaplasia
Decreasing in incidence
Glandular morphology
Diffuse-type:
Undefined risk factors
( no known relation to H. pylori)
Signet cell morphology

21. Macroscopic (growth patterns) of gastric adenocarcinoma
Mass
Ulcer
Lintis plastica
Clinical picture: asymptomatic or abdominal discomfort, weight loss, anemia

22. Small and large bowel Developmental: Meckel diverticulum
Diarrheal disease:
Infections: viruses, bacteria, protozoa
Idiopathic inflammatory bowel disease
Malabsorption
Diverticular disease
Tumors

23. Types and causes of diarrheal illness
Secretory diarrhea: loss of intestinal fluid that is isotonic with plasma and persists during fasting.
Viruses: rotavirus: destroy the absorptive surface, common in children 6-24 month of age, 130 million cases per year.
Toxin-mediated: Vibrio cholera, E.coli (need time)
Preformed toxin: Stapylococcus aureus (immediate effect)
Excessive laxatives
These organisms need time to proliferate within the bowel to produce their toxin, so if the symptoms appear right after eating, one should not think of those kinds of bacteria

24. Exudative diarrhea: pruluent bloody stool (inflammation of the mucosa and/or hemorrhage)
Infections causing tissue damage: Shigella, Salmonella, Entamoeba histolytica
Infections causing both tissue damage and toxins: Clostridium difficile; with antibiotic therapy, leading to pseudo-membranous colitis
Idiopathic inflammatory bowel disease

25. Parasites
Entamoeba histolytica: Invasive, amebic colitis and amebic liver abscesses
Giardia lamblia: non-invasive, duodenum and jejunum, diarrhea and malabsorption
Cryptosporidium: self-limited diarrhea in immuno-competent individuals; long course in AIDS patients
Worms:

26. Pseudomembranous colitis
Membranes made of neutrophils and fibrin
Seen in Clostridium difficile infection and in ischemia

27. Idiopathic inflammatory bowel disease
Crohn disease
Small bowel and colon
Patchy involvement
Transmural inflammation
Non-caseating granulomas
Poor response to surgery
Increased risk for cancer
Ulcerative colitis
Colon only
Continuous involvement
Superficial inflammation
No granulomas
Good response to surgery
Increased risk for cancer

28. Malabsorption syndromes
Defective intraluminal digestion:
pancreatic insufficiency
Defective bile secretion
Mucosal abnormalities:
Disaccharide deficiency (lactose intolerance)
Reduced surface area
Celiac disease
Surgical resection
Infections: Tropical infection

30. Clinical features of malabsorption syndromes
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.

31. Meckel diverticulum Meckel diverticulum
A blind pouch located in distal small bowel
The most common congenital anomaly of the small intestine; results from failure of the involution of the omphalomesenteric (vitelline) duct
The rule of 2’s:
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:
Overgrowth of bacteria that depletes vitamin B12 leading to anemia
“Peptic” ulcer and bleeding

32. Diverticulosis
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

33. Tumors of the large bowel
Hyperplastic polyps: not precancerous
Adenomatous polyps: precancerous
Familial polyposis syndrome: polyps, 100% risk for developing cancer

34. Colonic adenocarcinoma:
Always arises from adenomatous polyp
Risk factors: low fiber, high fat, decreased vit A, C, E, idiopathic inflammatory bowel disease, familial adenomatous polyposis
Several hits to different genes: APC, k-ras, p53; or DNA mismatch repair genes
Survival depends on stage (depth of invasion and node metastasis)

35. Colonic adenocarcinoma
Clinical picture:
Asymptomatic or fatigue, weakness and iron deficiency anemia in tumors of right side.
Left sided tumors may produce bleeding, change in bowel habits and crampy pain

36. Colonic adenocarcinoma
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
Diagnosis is based on endoscopy and biopsy
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.