1. Digestion Carbohydrates
    • Mouth: salivary amylase splits starch into smaller segments of dextrins, monosaccharides, and oligosaccharides
    • Small intestine: pancreatic amylase continues breakdown of starches by splitting them into lactos, maltose, and sucrose
    • Small intestine: Brush border enzymes of small intestines further breakdown sugars into galactose, glucose and fructose then the monosacharides are absorbed by carrier proteins into intestinal epithelium
  2. Digestion: Proteins
    • Stomach: pepsin (active form of enzyme pepsinogen)
    • Duodenum: pancreatic enzymes trypsin, and chymotrypsin, break down proteins further into small peptides
    • Small intestine: Brush border enzymes break down small peptides into amino acids which are absorbed through the action of protein carriers by active transport
  3. Digestion: Lipids
    • Fats are unemulsified when first digested, agents help to make an emulsion of fat with liquid
    • bile salts (micelles)
    • Micelles: are transport mechanisms for fats into the epithelium, contain a core that holds fat soluble vitamins and cholesterol
    • Small intestine (exclusively): through actions of pancreatic lipase which breaks them into fatty acids and monoglycerides
  4. Peptic ulcer disease
    • A break (ulceration) in the protective lining of the lower esophogus, stomach (gastric), or duodenum (duodenal)
    • generally occur next to acid-secreting mucosa of body
    • Primary defect: abnormality that increases mucosa barriers permeability to hydrogen ions
  5. factors of peptic ulcer disease
    • Decreased formation of mucus
    • Decreases formation of protaglandin
    • Reflux of bile and pancreatic enzymes from duodenum
    • use of ulcerogenic drugs
  6. destructive factors Peptic ulcer disease
    • Acid: from parietal cells
    • Increased by histamin caffeine acetylcholin gastrin
    • Decreased by prostaglandins and hormones that inhibit acid production
    • Pepsin: cheif enzyme of gastric juice
  7. Protective factors Peptic Ulcer disease
    • Mucus (^ prostaglandins)
    • bicarbonate secretion (^ by prostaglandins)
    • blood flow
    • epithelial cell turnover
  8. Factors of Peptic ulcer disease causing disruption in barrier
    • Helicobacter Pylori: gram negative bacillus that live in unstirred layers, present 95% of Duodenal Ulcers & 70% of gastric
    • Aspirin, NSAIDS, glucocorticoids: inhibit prostaglandins
    • Smoking: decrease HCO3 and increase gastric emptying
    • Stress: increases acid secretion and glucocorticoid secretion
    • Genetics: mostly duodenal ulcers
    • Duodenal gastric reflux
  9. Symptoms of Duodenal ulcers
    • Epigastric pain 2-3 hours after meal: chronic intermittent sharp burning gnawing
    • Pain-food or pain-antacid relief
    • complications: bleeding (hematemesis or melena), perforation, obstruction of outlet
  10. Symptoms of Gastric ulcers
    • Epigastric pain immediately after eating: chronic, up to 2-4 hours after meal
    • Pain-antacid-relief
    • anorexia, weight loss, vomiting
  11. % of ulcers with symptoms
    • 10-30% no symptoms
    • 30-50% have symptoms but no ulcer
  12. Management of peptic ulcers
    • Relieve cause of hyperacidity
    • Administer antacid drugs that suppress acid secretion:
    • acid lowering agents: antacids, histamine blocker, proton pump inhibitors
    • antibiotic for H.pylori
    • mucosal protective agents: sulcralfate, PGE1 analog misoprostol
  13. Esophageal sphicters
    • Upper esophageal sphincter: Skeletal muscle
    • Lower esophageal sphincter: smooth muscle just below diaphragm
    • relaxation occurs intermittently and with swallowing
    • normally LES exerts more pressure than UES keeping food where it belongs
  14. GastroEsophageal Reflux Disease
    • Hernia: LES slides into thorax
    • LES relaxes more often
    • Pressure in stomach
  15. Signs & symptoms GastroEsophageal Reflus Disease
    • Early: postprandial and nocturnal heartburn, waterbrash (regurgitation on bending or lying down)
    • Middle: reactive airway disease, hoarseness or cough, dysphagia
    • Late: strictures, bleeding from esophageal ulcer or varices
  16. Management of GERD
    • decrease # of episodes, increase protective lining, decrease acidity of reflux, increase clearance of esophageal contents
    • Dietary: smal meals, no bedtime snack, high protein/low fat diet
    • Avoid: high-acid foods, chocolate, fat, ETOH, smoking, tight abdominal clothing
    • Elevate head of bed, lose weight
    • Decrease acid
    • Increase LES pressure, protect mucosa (prostaglandins)
  17. Ulcerative Colitis
    • Starts in rectum progresses up through colon
    • Continuous involvement
    • mucosa and submucosa affected
    • hyperemic and hemorrhagic ulcerations (blood in stool)
  18. Crohns Disease
    • "Regional enteritis"
    • Anywhere in GI but most terminal ileum
    • stress worsens condition
    • skips sections
    • transmural involvement (fistulas common)
    • granulomas (nodules of inflammatory cells) in 50%
    • Narrow lumen (especially terminal ileum): string sign
  19. chron's disease etiology
    • Genetic: 30-50% of twins
    • autoimmune: misdirected immunity to common intestinal organisms or contents
  20. Symptoms of ulcerative colitis
    • diarrhea, chronic
    • rectal bleeding
    • abdominal pain and cramping
    • increased risk of colon cancer
    • toxic megacolon: massive dilation of colon, may cause perforation septicemia or death
  21. Symptoms of Chrons Disease
    • Diarrhea: steatorrhea (fat in stool)
    • Abdominal pain
    • Fistulas
    • Intestinal obstruction and perforation
    • abscess formation
  22. Inflammatory bowel diseases
    • 10-15% cant tell diff
    • both labels may represent multiple diseases
    • both have genetic basis
    • chrons and ulceritive colitis
  23. Managment of Inflammatory Bowel diseases
    • Corticosteroids
    • immunomodulators
    • Antibiotics for CD (flagyl), decreases effects of abscesses
    • Surgery
    • diet
  24. Liver: normal function of hepatocytes
    • Bilirubin conjugation and excretion and bile secretion
    • albumen synthesis
    • coagulation factor synthesis
    • urea formation
    • vitamin storage
    • inactivation of steroid hormones, toxins, and drugs
    • glycogen storage and gluconeogenesis
  25. Liver: hepatitis
    • Inflamation of liver
    • can lead to cirrhosis (scarring)
    • viral hepatitis and ETOH account for most
    • sequelae: Cirrhosis (chronic liver failure), Jaundice (yellow), Fulminant liver failure, hepatocellular carcinoma
  26. symptoms of acute hepatitis
    • fatigue and malaise
    • low grade fever
    • RUQ pain
    • jaundice
    • elevated liver enzymes
  27. Hepatitis A
    • Common in developing countries
    • Fecal-oral spread
    • Incubation 2-6 weeks
    • vaccine available
  28. Hepatits B
    • Approximately 4-5% progress to chronic state: cirrhosis and cancer
    • parenteral contact
    • incubation 4-26 weeks
    • can cause acute fulminating disease with acute liver failure
    • vaccine available
  29. Hepatitis C
    • parenteral transmission at very high rate
    • At least 80% becomes chronic: cirrhosis and hepatic cancer
    • no vacine
  30. Hepatits D
    • Must have Hep B present to replicate
    • increases severity of Hepatitis
  31. Hepatits E
    • Fecal-oral route (associated with contaminated water)
    • no chronic state
    • more severe than Hep A
    • no treatment, no vaccine
  32. Liver: Cirrhosis
    • End-stage fibrosis of the liver: nodules due to regeneration and scarring, disruption of sinusoids and bile ducts
    • ETOH causes 60-70% of cases
    • Viral causes 10%
  33. Clinical manifestations of Cirrhosis
    • Arise from: direct & acute hepatocyte dysfuntion, Portal hypertension (vascular dysfunction)
    • 10% found on autopsy
    • Jaudice: bilirubin accumulation
    • Ascites: lack of albumin, 3rd spacing, portal HTN, anorexia
    • Coagulopathy: loss of clotting factors
    • Gynocomastia (Testicular atrophy): Increase in circulating estrogen
    • Encephalopathy: ammonia build-up in bloodstream
    • Anemia: lac of and inability to store vitamins
  34. Portal HTN complications
    • Ascites: can lead to spontaneous bacterial peritonitis
    • Esophageal varices: Often catastrophic upper GI bleed common cause of death in cirrhosis patients
    • Caput medusae: cutaneous veins radiating from the umbilicus
    • Splenomegaly
  35. Liver: Jaundice
    • Normal hemoglobin breakdown produces bilirubin that liver cells make water soluble for excretion in the feces: Unconjugated bilirubin increases with liver disease as liver loses function: It deposits in brain (brain damage), and the skin/sclera (deep yellow color)
    • Overproduction of RBC because of chronic destruction (hemolytic anemia)
    • Decreased excretion of RBC due to decreased transport into liver cells, decreased conjugation, dcreased secretion into bile
Card Set
GI disorders