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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
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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
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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
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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
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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
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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
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Protective factors Peptic Ulcer disease
- Mucus (^ prostaglandins)
- bicarbonate secretion (^ by prostaglandins)
- blood flow
- epithelial cell turnover
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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
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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
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Symptoms of Gastric ulcers
- Epigastric pain immediately after eating: chronic, up to 2-4 hours after meal
- Pain-antacid-relief
- anorexia, weight loss, vomiting
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% of ulcers with symptoms
- 10-30% no symptoms
- 30-50% have symptoms but no ulcer
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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
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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
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GastroEsophageal Reflux Disease
- Hernia: LES slides into thorax
- LES relaxes more often
- Pressure in stomach
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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
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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)
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Ulcerative Colitis
- Starts in rectum progresses up through colon
- Continuous involvement
- mucosa and submucosa affected
- hyperemic and hemorrhagic ulcerations (blood in stool)
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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
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chron's disease etiology
- Genetic: 30-50% of twins
- autoimmune: misdirected immunity to common intestinal organisms or contents
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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
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Symptoms of Chrons Disease
- Diarrhea: steatorrhea (fat in stool)
- Abdominal pain
- Fistulas
- Intestinal obstruction and perforation
- abscess formation
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Inflammatory bowel diseases
- 10-15% cant tell diff
- both labels may represent multiple diseases
- both have genetic basis
- chrons and ulceritive colitis
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Managment of Inflammatory Bowel diseases
- Corticosteroids
- immunomodulators
- Antibiotics for CD (flagyl), decreases effects of abscesses
- Surgery
- diet
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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
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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
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symptoms of acute hepatitis
- fatigue and malaise
- low grade fever
- RUQ pain
- jaundice
- elevated liver enzymes
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Hepatitis A
- Common in developing countries
- Fecal-oral spread
- Incubation 2-6 weeks
- vaccine available
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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
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Hepatitis C
- parenteral transmission at very high rate
- At least 80% becomes chronic: cirrhosis and hepatic cancer
- no vacine
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Hepatits D
- Must have Hep B present to replicate
- increases severity of Hepatitis
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Hepatits E
- Fecal-oral route (associated with contaminated water)
- no chronic state
- more severe than Hep A
- no treatment, no vaccine
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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%
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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
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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
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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
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