1. Acute (erosive): stress, shock, food, exogenous chemicals, drugs • Erosions: shallow mucosal defects in the epithelium • Ulcerations: deeper and entire mucosal thickness 2. Chronic atrophic gastritis with and without intestinal metaplasia • Helicobacter pylori related → antibiotics • Leads to gastric atrophy, reduced HCL, pepsin.

Gastrointestinal System Disorders Flashcards by Kristen Van Kampen

Main functions of the GI tract

• Ingestion
• Mastication (chewing)
• Deglutition (swallowing)
• Digestion
• Absorption
• Excretion

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Developmental abnormalities of the oral cavity

Cleft lip
• Congenital abnormality
• Inherited as a polygenic trait (multi-gene inheritance)
• Lack of fusion of the fetal nasal and maxillary process that
form the upper lip
Cleft palate
• Fissure forms between mouth and nasal cavity

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Dental and periodontal disease

Bacterial infection leads to:
1. Dental caries (tooth decay)
• Oral saprophytic bacteria
2. Periodontal disease (gums)
3. Stomatitis (oral mucosa

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Oral cancer

• Often related to tobacco smoking/chewing, alcoholism
• Most tumours histologically classified as squamous cell carcinomas
Morphologically present as:
• Leukoplakia (white mucosal lesion)
• Erythroplakia (red mucosal lesion)
• Ulcer
• Crater
• Nodule

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Diseases of the esophagus clinical presentations

• Dysphagia – difficulty swallowing
• Esophageal (retrosternal) pain
• Aspiration or regurgitation

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Developmental abnormalities of the esophagus

• Atresia (lack of lumen), upper and lower sections don’t connect.
With or without esophageal-tracheal fistula (the two are connected)

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Hiatal hernia

Displacement of cardiac portion of the stomach from the
abdominal cavity to the thoracic cavity through the diaphragmatic hiatus
Sliding: the whole thing goes up
Paraesophageal: only one bulge sneaks out

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Achalasia (disease of esophagus)

• motility disorder
• Stenosis = abnormal narrowing
• Spasms of the lower esophageal sphincter
• Dilation of esophagus proximal to the site of spasm
• Inability to swallow food

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Esophageal varices

• Circulatory disturbances
• Can rupture leading to bleeding
• Hematamesis (vomiting blood)

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Esophagitis

Inflammation of the esophagus
1. Reflux of gastric juice (“peptic esophagitis”)
2. Infection: viruses, fungi (immunosuppressed individuals) bacterial
super infection
3. Chemical irritants: exogenous chemicals, drug

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Carcinoma of the esophagus

• Accounts for 4% of all cancers: 8000 cases per year in the United States
• Correlates with alcohol, tobacco abuse
• More common in men than women
• Poor prognosis: average survival = 2 years
• Tumors grow into the lumen or infiltrate the wall
• Esophagus is usually indurated and ulcerated
• Pain, dysphagia, bleeding
• Locally invasive
• Spread through the adventitia, to the lymph nodes and surrounding tissues/organs

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Disease of the stomach and duodenum symptoms

Pain: midline, upper abdomen
Vomiting
Bleeding: acute with hematemesis or chronic with melena
Dyspepsia: inability to digest food
Systemic consequences: iron deficiency anemia caused by chronic blood loss, vitamin B12 malabsorption

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Developmental abnormalities of the stomach

Congenital hypertrophic pyloric stenosis
• 3-5 weeks after birth, 4:1 boys:girls
• Unknown etiology
• Hypertrophy of the stomach wall of the pyloris
• Prevents emptying of the stomach
• Results in projectile vomiting

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Gastritis

Acute (erosive): stress, shock, food, exogenous chemicals, drugs
• Erosions: shallow mucosal defects in the epithelium
• Ulcerations: deeper and entire mucosal thickness
Chronic atrophic gastritis with and without intestinal metaplasia
• Helicobacter pylori related → antibiotics
• Leads to gastric atrophy, reduced HCL, pepsin.

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Peptic ulcers

• Chronic and multifactorial etiology
• Mucosal ulceration extending through the entire gastric epithelial layer into the muscularis
Contributing factors:
1. Gastric juices: HCL, pepsin → no acid no ulcer
2. Mucosal barrier defects: stress, shock, NSAIDs, smoking
3. H. Pylori: found in stomach or duodenum of most patients.
Antibiotics can eradicate bacterial infection

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Complications of peptic ulcers

Hemorrhage (most common) hematemesis, melena, iron deficiency anemia
Penetration: ulcers of the duodenum can erode the wall and penetrate into the pancreas (acute pancreatitis)
Perforation: duodenal ulcers through the intestinal wall forming holes peritonitis
Cicatrization: healing of ulcers leads to excessive scarring and stenosis

Carcinoma of the stomach

• Common, affects 25,000 persons, accounts for ~14,000 deaths yearly
• Incidence has decreased over the past 70 years
Etiology is unknown:
• Suspect nitrosamines in food
• nitrosamines are produced when nitrates and amines combine in
acidic places like the stomach
• Potential role of H. pylori
Macroscopic features
Forms:
1. Superficial – early preinvasive stage
2. Polypoid – protrudes into lumen
3. Ulcerated – irregular shape
4. Diffusely infiltrative into the gastric wall

Developmental abnormalities of the intestines

Hirschsprung Disease
• Congenital abnormality in the
innervation of the of the rectum and
sigmoid colon
• Intramural ganglions do not develop
• Permanent spasm
• megacolon

Diverticulitis

• Characterized by the formation of diverticula
• Protrusions of the mucosa through a hole in the weakened wall
• Solitary or multiple throughout
• Congenital or acquired
• Mostly localized in the sigmoid colon
• More prominent in individuals >60 years old

Inflammatory bowel disease: Crohn’s

More common than ulcerative colitis
• Often involves the terminal ileum and colon
• Apthous ulcers: shallow mucosal defects overlying Peyer’s patches
• Inflammation extends entire wall of the intestine (transmural),
typically segmental
• Granulomas, fibrosis of muscularis and seros

Inflammatory bowel syndrome: Ulcerative colitis

• Often large intestine and rectum
• Inflammation spreads proximally
• Diffuse but does not extend into the ileum
• Early lesions are flat edematous patches, entire circumference of the rectum, prone to bleeding
• Crypt abscess, inflammatory
pseudopolyps

Gastrointestinal infections

• Food poisoning: bacterial toxins
• Viral infections
• Infectious diarrhea
• Small-intestine infection: E. coli, Vibrio cholera, rotavirus
• Large intestine infection: E. coli, Norwalk virus

Causes of diarrhea

• Ingested toxin
• Toxins formed by bacteria colonize the
intestine
• Bacteria invade the wall of the
intestine
• cAMP signaling = watery diarrhea

Acute appendicitis

• Bacterial infection of the appendix
• Requires surgical intervention
• More common in children and adolescents
• Clinical features: sudden-onset fever, leukocytosis and abdominal pain

Acute peritonitis

• Inflammation of peritoneal lining of the abdominal cavity Bacterial invasion of the abdominal cavity due to: • Rupture of the stomach (peptic ulcer) or intestines • Spread of infection from fallopian tubes • Rupture of abscess • Infection of preexisting ascites (cirrhosis)

Intestinal obstructions

• Paralytic ileus: neuromuscular paralysis • Mechanical (obstructive) ileus: hernia (part bulges into another area), intussection (sides create a little dead end), volvulus (a twist)

Malabsorption

Abnormalities in 1. Intraluminal digestion of food 2. Uptake & processing of nutrients with intestinal cells 3. Transport of nutrients from intestine to liver Can result from: Defective intraluminal digestion • Deficiency of gastric juices: post gastrectomy conditions, atrophic gastritis • Deficiency of bile: biliary obstruction, liver disease, Crohn’s disease • Deficiency of pancreatic juices: chronic pancreatitis • Pathogen overgrowth: Giardia lamblia (parasite) Defective uptake of nutrients: • Celiac sprue/disease – loss of villi, flat • Tropical sprue - flattening of villi • Infectious enteritis (e.g., E. coli, rotavirus) • Crohn’s disease • Congenital abetalipoproteinemia – fat and fat soluble vitamins • Short bowel syndrome (after surgical resection) Defective transport of nutrients: • Gastrointestinal lymphoma • Congestive heart failure with intestinal ischemia • Scleroderma (autoimmune) • Amyloidosis

Intestinal neoplasms

• Colon most often affected • May be sporadic or familial (S:F = 8:2) • May be benign or malignant (B:M = 3:1) • May be solitary or multiple • Epithelial tumors (adenomas, carcinomas): account for 90% of all tumors; more common than lymphomas or mesenchymal tumors (benign soft tissue tumor, e.g., lipoma, leiomyoma, sarcomas

Colon cancer: etiology

• Mostly unknown etiology • Genetic factors (play important role) • Familial polyposis coli • Hereditary nonpolyposis colorectal cancer • Dietary factors (“Western diet”: low fiber, high carbohydrate, high fat content) • Interaction of carcinogens, oncogenes, tumor suppressor gene

Classification of intestinal tumours

1. Non-neoplastic polyps: hyperplastic polyp, inflammatory polyp, juvenile polyp, Peutz-Jeghers polyp, lymphoid polyp 2. Benign neoplasms: tubular adenoma, villous adenoma, tubulovillous adenoma, benign stromal tumors (e.g., leiomyoma) 3. Malignant neoplasms: adenocarcinoma, carcinoid, lymphoma, sarcoma

Intestinal polyps appearance

Can be stalk-like (tubular adenoma) or finger-like (villous adenoma)

Adenocarcinoma of the colon

Ulcerating masses Napkin-ring stenotic lesions Localized crater-like ulcer

Adenocarcinoma of the sigmoid colonç

Sigmoid colon – diffusely infiltrated the entire circumference of the intestine

Gastrointestinal carcinoids

• Carcinoid: neuroendocrine tumour • 90% occur in intestines • Appendix: most common site of origin • Smaller than 2 cm = benign; larger can metastasize • May be multiple, especially in terminal ileum, stomach cancers • Composed of neuroendocrine cells that contain granules visible by electron microscopy, polypeptide hormones

Clinical features of gastrointestinal carcinoids

• Tumors secrete serotonin, polypeptide hormones; cause diarrhea, hypermotility of intestines • Tumors metastasizing to liver cause carcinoid syndrom