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90 Cards in this Set
- Front
- Back
Gastroesophageal reflux: 3 mechanisms involving the LES (lower esophageal sphincter)
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1) Weak basal LES pressure
2) Inadequate LES response to increased abdominal pressure 3) Transient relaxation of the LES without peristalsis |
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Antireflux barrier: Anatomy
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-lower esophageal sphincter
-crural diaphragm -phrenoesophageal ligament |
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Reflux esophagitis
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esophageal injury that is due to reflux of acidic gastric contents into the esophagus
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Pill-induced esophagitis
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Caustic injury from lingering in the esophagus
Examples -KCl -FeSO4 -quinidine -NSAIDS -tetracycline |
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Infectious esophagitis (causes, host factors)
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Causes
-Candida -HSV -CMV Host factor: Immunocompromised |
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Barrett's Esophagus
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-patch or patches of metaplastic columnar epithelium (specialized intestinal metaplasia) in the lower esophagus, often due to severe reflux esophagitis
-increased prevalence of adenocarcinoma |
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GERD: External factors
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-Diet (eg high fat foods)
-Smoking -Medication |
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GERD: Mucosal pathophysiology
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Impaired esophageal mucosal resistance
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GERD: Reasons for diminished esophageal clearance
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-Peristalsis
-Body position -Saliva |
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GERD: Gastric factors
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-Acid
-Bile acids -Gastric emptying -Gastric distention |
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Heartburn: Indications of severe disease
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-Age > 40
-Symptoms > 3 years -Alarming symptoms --Dysphagia --Weight loss --Anemia |
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Heartburn: differential diagnosis
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-Esophagitis
-Stricture -Barrett's esophagus |
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Approach to patient with dysphagia
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Algorithm image
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Spastic esophageal motility disorders: Syndromes
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-DES (Diffuse esophageal spasm)
-Nutcracker esophagus -Hypertensive LES (lower esophageal sphincter_ -Nonspecific |
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Spastic esophageal motility disorders: Symptoms
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-Chest pain
-Dysphagia |
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Spastic esophageal motility disorders: Manometric features
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-Some normal peristalsis
-Contractions (simultaneous/spontaneous/repetitive/high-amplitude) -High LES pressure |
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Achalasia manometry
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-Incomplete relaxation
-Aperistalsis -Lower esophageal sphincter hypertension |
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Scleroderma manometry
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-Weak contractions
-LES hypotension |
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Parietal cell function
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In: Ca, ACh, Gastrin.
Out: HCl |
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Evidence for H. Pylori's role in gastric ulcer
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1. Colonization precedes ulcer
2. Eradication of H. Pylori ends cycle of recurrent ulcers |
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How are peptic ulcers named?
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By location:
-Gastric -Duodenal -Esophageal |
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Percentage of ulcers caused by H. Pylori
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Duodenal: 70% (if not used NSAIDs to excess)
Gastric: 65-95% (45% if NSAID related) |
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Testing for H. Pylori
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Noninvasive
-serology (rare) -Urease breath test Invasive (biopsy) -rapid urease test –special stains |
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Difference between ulcers in NSAID related disease and H. Pylori related disease
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NSAIDS: less surrounding inflammation
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NSAID related injury: Preventive factors in normals
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i. mucus
ii. superoxide scavengers in mucosa (e.g. glutathione) iii. bicarbonate iv. high blood supply of stomach (promoting repair and cellular metabolic functions) |
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Risk factors for NSAID-induced damage
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-history of ulcer disease, dyspepsia, gastritis
-age (lower gastric perfusion) -high/prolonged NSAID dose -corticosteroids -anticoagulants |
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Typical location of gastrinoma
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Pancreas
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Causes of diarrhea
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-Osmotic-lactose intolerance (High fecal osmotic gap: > 125)
-Malabsorption/fatty -Inflammatory -Secretory (Low fecal osmotic gap: <50) -Altered motility |
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Fecal osmotic gap: calculation
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290 - 2(Na + K)
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Causes of diarrhea by location
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Picture
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Celiac Sprue: antibodies
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-Tissue transglutaminase
-Anti-gliadin -Anti-endomysial |
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Celiac Sprue: MHC
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HLA-DQ2 associated
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Celiac Sprue: Triggers and manifestations
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Trigger: gluten
Manifestations: -Abdominal symptoms -Malnutrition -Low nutrients (Iron, Vit. D, Vit. K) |
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Ulcerative Colitis: Major features
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Symptoms: Bloody diarrhea
Inflammation -continuous (no skip lesions) -Rectum involved |
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Crohns Disease: Major features
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Symptoms:
-Diarrhea (not necessarily bloody) -RLQ pain -Fever -Weight loss Inflammation: -Transmural -Large ulcers -Skip lesions Fistulae and Strictures |
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IBD: Medical Treatment
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Induce and maintain remission
Drugs: 1) 5-amino-salicylates (inhibit COX and 5-Lipox --> anti-inflammatory) 2) Corticosteroids 3) Antibiotics 4) Immune modulators (6-MP, azathoprine) |
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IBD: Surgical therapy
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Ulcerative colitis: Total colectomy: curative
Crohn's Disease: Usually recurs after surgery |
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Ulcerative Colitis: Complications
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Massive hemorrhage
Fulminant colitis Colonic stricture (rare) Colon cancer |
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Crohn's Disease: Complications
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Bile acid malabsorption
-Secretory diarrhea: bile acids on colon -Gallstones: bile more lithogenic -Steatorrhea: vitamins ADEK malabsorption -Nephrolithiasis: steatorrhea causes more oxalate absorption leading to calcium oxalate stones --- NOT uric acid stones Malignancy: -colon cancer -small bowel cancer (lymphoma or adenocarcinoma – very rare) |
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Benign colon disorders: Differential
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-Constipation
-Diverticula -Hemorrhoids -Anorectal fistula -Anal fissure |
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Gallstones: Epidemiology
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-women
-people over age 60 -Native Americans -Mexican Americans -overweight men and women -people who fast or lose a lot of weight quickly -hormonal women |
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Gallstones: Types
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-Cholesterol stones (90% of US gallstones)
-Pigment stones |
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Gallstones: Cholesterol stone causes
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-Hypersecretion of cholesterol into bile (Obesity, OCPs, estrogen, rapid weight loss)
-Hyposecretion of bile acids (Impaired synthesis, intestinal loss (t.i.resection), progesterone) -Gallbladder stasis (Progesterone, pregnancy, total parenteral nutrition) |
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Gallstones: Pigment stones
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Black pigment
–cirrhosis -hemolytic anemia --hemoglobinopathy --red cell disorders Brown pigment -Asian patients (infection) |
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Gallstones: Diagnosis
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ultrasound
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Gallstones: Treatment
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Laparoscopic cholecystectomy
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Gallstones: Symptoms/Manifestations
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-Asymptomatic (in gallbladder) (75%)
-Intermittent biliary colic (floating in and out of cystic duct) (20%) -Acute pain/cholecystitis (impacted in cystic duct) (10%) -Jaundice/biliary colic (impacted in distal common bile duct) (5%) |
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Pancreatitis: Most common etiologies
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Image
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Pancreatitis: Local effects of enzymes
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-Inflammation
-Third space losses -Fat necrosis -Pancreatic/peripancreatic necrosis |
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Pancreatitis: Signs and Symptoms
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-Abdominal pain/tenderness
-Nausea/vomiting -Fever -Tachycardia |
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Pancreatitis: Lab tests
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-Increased WBC
-Increased serum amylase -Increased serum lipase |
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Pancreatitis: Differential diagnosis
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-Choledocholithiasis (gallstone in common bile duct)
-Perforated ulcer -Mesenteric ischemia -Intestinal obstruction -Salpingitis -Ectopic pregnancy |
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Chronic Pancreatitis: Most common etiologies
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Alcohol: 70%
Idiopathic: 12.5% |
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ALT levels: Vary with?
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-BMI
-Elevated lipids -Glucose |
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High AST/ALT ratio
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Alcoholic liver disease
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Level for AST for 95% chance of hepatocellular liver disease
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>300 IU
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Elevated alkaline phosphatase indicates:
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1. Liver disease – overproduction of alkaline phosphatase by liver and regurgitation into blood. Highest values in bile duct obstruction and some drug toxicities.
2. Bone disease – overproduction by bone |
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Difference between direct and indirect bilirubin
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Direct: conjugated with glucouronides. water soluble. excreted in urine
Indirect: unconjugated bilirubin, insoluble in water and not excreted in urine |
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Direct bilirubin: normal
Indirect bilirubin: elevated Bilirubinuria: none |
Increased production: Hemolysis, PA, Thal
Decreased conjugation: Gilbert's syndrome, Crigler-Najjar Syndrome |
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Direct bilirubin: elevated
Indirect bilirubin: elevated Bilirubinuria: positive |
Decreased excretion: All types of liver disease
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Normal albumin levels + liver symptoms = ?
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Possibly acute liver disease
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Low albumin levels + liver symptoms = ?
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Possibly chronic liver diseasse
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Prolonged PT (prothrombin time)
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Vitamin K deficiency: Administer vitamin K and recheck --> if PT normalizes, it's Vit K deficiency
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Which coagulation factor is not made in the liver?
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Factor VIII – made vascular endothelium and R-E cells
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Hep A IgM antibody
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acute infection
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Hep A IgG antibody
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prior infection
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Hep B surface Ag: +
Hep B surface Ab: - Hep B core IgM Ab: + Hep B core IgG Ab: - Hep B e Ag: + Hep B e Ab: - HBV-DNA: + |
Acute
(only time Hep B core IgM Ab is positive) |
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Hep B surface Ag: -
Hep B surface Ab: + Hep B core IgM Ab: - Hep B core IgG Ab: + Hep B e Ag: - Hep B e Ab: + HBV-DNA: - |
Resolved acute infection
(Hep B core IgM is negative --> Hep B surface Ab is positive --> Hep B e Ab is positive --> Resolved Acute infection) |
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Hep B surface Ag: -
Hep B surface Ab: + Hep B core IgM Ab: - Hep B core IgG Ab: - Hep B e Ag: - Hep B e Ab: - HBV-DNA: - |
Vaccinated
(Hep B core IgM is negative --> Hep B surface Ab is positive --> Hep B e Ab is negative OR nothing else is positive --> Vaccinated) |
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Hep B surface Ag: +
Hep B surface Ab: - Hep B core IgM Ab: - Hep B core IgG Ab: +/- Hep B e Ag: - Hep B e Ab: + HBV-DNA: - |
Chronic carrier state
(Hep B core IgM is negative --> Hep B surface Ab is negative --> Hep B e Ab is positive --> HBV DNA is negative --> Chronic carrier state) |
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Hep B surface Ag: +
Hep B surface Ab: - Hep B core IgM Ab: - Hep B core IgG Ab: +/- Hep B e Ag: + Hep B e Ab: - HBV-DNA: + |
Chronic active hepatitis
(Hep B core IgM is negative --> Hep B surface Ab is negative --> Hep B e Ab is negative --> Chronic active hepatitis) |
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Hep B surface Ag: +
Hep B surface Ab: - Hep B core IgM Ab: - Hep B core IgG Ab: +/- Hep B e Ag: - Hep B e Ab: + HBV-DNA: - |
Chronic active hepatitis pre-core mutant
(Hep B core IgM is negative --> Hep B surface Ab is negative --> Hep B e Ab is positive --> HBV DNA is positive --> Chronic active hepatitis pre-core mutant) |
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HVPG < 12
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Normal
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HVPG > 12
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Portal hypertension - Intrahepatic. Due to sinusoidal arteries (due to cirrhosis)
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Portal hypertension, Pre-hepatic
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Portal or splenic vein thrombosis
AV fistulas in the splanchnic bed or spleen |
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Portal hypertension, Intrahepatic, normal HVPG
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Pre-sinusoidal --> Normal HVPG
Sarcoid, Schistosomiasis Post-sinusoidal --> Budd Chiari – can’t get into hepatic veins (clot in veins) |
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Portal hypertension, Post hepatic
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Webs in IVC
Cardiac disease --> constrictive pericarditis, right heart failure |
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Complications of cirrhosis
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Varices
Ascites Hepatic encephalopathy Hepatorenal syndrome |
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Prokinetic Agents - Subbclasses
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-Cholinergic agents
-Serotonin receptor modulators -Dopamine receptor blockers -Motilin-like agents |
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Drugs for constipation - subclasses
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-Bulk forming agents
-Softeners/surfactants -Osmotic agents -Stimulants -Miscellaneous |
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Prokinetic agents - Cholinergic agents
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Bethanechol
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Prokinetic agents - Serotonin receptor modulators
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-Metoclopramide
-Cisapride -Tegaserod |
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Prokinetic agents - Dopamine receptor blockers
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-Domperidone
-Metoclopramide |
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Constipation drugs - Bulk-forming agents - Toxicities and examples
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Toxicity
-Bloating Natural -Psyllium (Metamucil) Semi-synthetic -Methylcellulose -Polycarbophil |
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Constipation drugs - Softeners/Surfactants - Mechanism, toxicities and examples
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Mechanism: Lowers surface tension of stool
Toxicities: -Impaired absorption of fat soluble agents -Oil leakage -Lipid pneumonitis Examples -Docusate -Mineral oil |
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Constipation drugs - Osmotic agents - Mechanism, toxicities and examples
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Mechanism
-Osmotically-mediated water retention stimulates peristalsis Toxicities -Abdominal distention, flatulence -Saline: caution if renal/cardiovascular disease or electrolyte disorder. Monitor electrolytes. Examples -Saline-based -Sugar/alcohol-alcohol based -Other (PEG solutions) |
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Constipation drugs - Stimulant Laxatives - Mechanism, toxicities and examples
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Mechanism: Migrating colonic contractions
Concern: Overuse Examples: -Diphenylmethanes -Anthraquinones -Castor oil |
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Constipation drugs - Lubiprostone - Mechanism, toxicities
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Mechanism: Activates Cl channels within GI tract --> increasing intestinal fluid secretion
Toxicities: Nausea Abdominal distention and pain Diarrhea and flatulence Headache Avoid in pregnancy |
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Anti-diarrheals - Bulk-forming & binding agents - Examples
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Natural
-Psyllium Semi-synthetic -Methylcellulose -Polycarbophil Other agents -Cholestyramine -Bismuth subsalicylate |
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Anti-diarrheals - classes
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-Bulk-forming/binding agents
-Antimotility agents -Antisecretory agents -Miscellaneous |