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90 Cards in this Set

  • Front
  • Back
Gastroesophageal reflux: 3 mechanisms involving the LES (lower esophageal sphincter)
1) Weak basal LES pressure
2) Inadequate LES response to increased abdominal pressure
3) Transient relaxation of the LES without peristalsis
Antireflux barrier: Anatomy
-lower esophageal sphincter
-crural diaphragm
-phrenoesophageal ligament
Reflux esophagitis
esophageal injury that is due to reflux of acidic gastric contents into the esophagus
Pill-induced esophagitis
Caustic injury from lingering in the esophagus

Infectious esophagitis (causes, host factors)

Host factor: Immunocompromised
Barrett's Esophagus
-patch or patches of metaplastic columnar epithelium (specialized intestinal metaplasia) in the lower esophagus, often due to severe reflux esophagitis
-increased prevalence of adenocarcinoma
GERD: External factors
-Diet (eg high fat foods)
GERD: Mucosal pathophysiology
Impaired esophageal mucosal resistance
GERD: Reasons for diminished esophageal clearance
-Body position
GERD: Gastric factors
-Bile acids
-Gastric emptying
-Gastric distention
Heartburn: Indications of severe disease
-Age > 40
-Symptoms > 3 years
-Alarming symptoms
--Weight loss
Heartburn: differential diagnosis
-Barrett's esophagus
Approach to patient with dysphagia
Algorithm image
Spastic esophageal motility disorders: Syndromes
-DES (Diffuse esophageal spasm)
-Nutcracker esophagus
-Hypertensive LES (lower esophageal sphincter_
Spastic esophageal motility disorders: Symptoms
-Chest pain
Spastic esophageal motility disorders: Manometric features
-Some normal peristalsis
-Contractions (simultaneous/spontaneous/repetitive/high-amplitude)
-High LES pressure
Achalasia manometry
-Incomplete relaxation
-Lower esophageal sphincter hypertension
Scleroderma manometry
-Weak contractions
-LES hypotension
Parietal cell function
In: Ca, ACh, Gastrin.
Out: HCl
Evidence for H. Pylori's role in gastric ulcer
1. Colonization precedes ulcer
2. Eradication of H. Pylori ends cycle of recurrent ulcers
How are peptic ulcers named?
By location:
Percentage of ulcers caused by H. Pylori
Duodenal: 70% (if not used NSAIDs to excess)
Gastric: 65-95% (45% if NSAID related)
Testing for H. Pylori
-serology (rare)
-Urease breath test

Invasive (biopsy)
-rapid urease test
–special stains
Difference between ulcers in NSAID related disease and H. Pylori related disease
NSAIDS: less surrounding inflammation
NSAID related injury: Preventive factors in normals
i. mucus
ii. superoxide scavengers in mucosa (e.g. glutathione)
iii. bicarbonate
iv. high blood supply of stomach (promoting repair and cellular metabolic functions)
Risk factors for NSAID-induced damage
-history of ulcer disease, dyspepsia, gastritis
-age (lower gastric perfusion)
-high/prolonged NSAID dose
Typical location of gastrinoma
Causes of diarrhea
-Osmotic-lactose intolerance (High fecal osmotic gap: > 125)
-Secretory (Low fecal osmotic gap: <50)
-Altered motility
Fecal osmotic gap: calculation
290 - 2(Na + K)
Causes of diarrhea by location
Celiac Sprue: antibodies
-Tissue transglutaminase
Celiac Sprue: MHC
HLA-DQ2 associated
Celiac Sprue: Triggers and manifestations
Trigger: gluten

-Abdominal symptoms
-Low nutrients (Iron, Vit. D, Vit. K)
Ulcerative Colitis: Major features
Symptoms: Bloody diarrhea

-continuous (no skip lesions)
-Rectum involved
Crohns Disease: Major features
-Diarrhea (not necessarily bloody)
-RLQ pain
-Weight loss

-Large ulcers
-Skip lesions

Fistulae and Strictures
IBD: Medical Treatment
Induce and maintain remission

1) 5-amino-salicylates (inhibit COX and 5-Lipox --> anti-inflammatory)
2) Corticosteroids
3) Antibiotics
4) Immune modulators (6-MP, azathoprine)
IBD: Surgical therapy
Ulcerative colitis: Total colectomy: curative

Crohn's Disease: Usually recurs after surgery
Ulcerative Colitis: Complications
Massive hemorrhage
Fulminant colitis
Colonic stricture (rare)
Colon cancer
Crohn's Disease: Complications
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

-colon cancer
-small bowel cancer (lymphoma or adenocarcinoma – very rare)
Benign colon disorders: Differential
-Anorectal fistula
-Anal fissure
Gallstones: Epidemiology
-people over age 60
-Native Americans
-Mexican Americans
-overweight men and women
-people who fast or lose a lot of weight quickly
-hormonal women
Gallstones: Types
-Cholesterol stones (90% of US gallstones)
-Pigment stones
Gallstones: Cholesterol stone causes
-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)
Gallstones: Pigment stones
Black pigment
-hemolytic anemia --hemoglobinopathy
--red cell disorders

Brown pigment
-Asian patients (infection)
Gallstones: Diagnosis
Gallstones: Treatment
Laparoscopic cholecystectomy
Gallstones: Symptoms/Manifestations
-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%)
Pancreatitis: Most common etiologies
Pancreatitis: Local effects of enzymes
-Third space losses
-Fat necrosis
-Pancreatic/peripancreatic necrosis
Pancreatitis: Signs and Symptoms
-Abdominal pain/tenderness
Pancreatitis: Lab tests
-Increased WBC
-Increased serum amylase
-Increased serum lipase
Pancreatitis: Differential diagnosis
-Choledocholithiasis (gallstone in common bile duct)
-Perforated ulcer
-Mesenteric ischemia
-Intestinal obstruction
-Ectopic pregnancy
Chronic Pancreatitis: Most common etiologies
Alcohol: 70%
Idiopathic: 12.5%
ALT levels: Vary with?
-Elevated lipids
High AST/ALT ratio
Alcoholic liver disease
Level for AST for 95% chance of hepatocellular liver disease
>300 IU
Elevated alkaline phosphatase indicates:
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
Difference between direct and indirect bilirubin
Direct: conjugated with glucouronides. water soluble. excreted in urine

Indirect: unconjugated bilirubin, insoluble in water and not excreted in urine
Direct bilirubin: normal
Indirect bilirubin: elevated
Bilirubinuria: none
Increased production: Hemolysis, PA, Thal

Decreased conjugation: Gilbert's syndrome, Crigler-Najjar Syndrome
Direct bilirubin: elevated
Indirect bilirubin: elevated
Bilirubinuria: positive
Decreased excretion: All types of liver disease
Normal albumin levels + liver symptoms = ?
Possibly acute liver disease
Low albumin levels + liver symptoms = ?
Possibly chronic liver diseasse
Prolonged PT (prothrombin time)
Vitamin K deficiency: Administer vitamin K and recheck --> if PT normalizes, it's Vit K deficiency
Which coagulation factor is not made in the liver?
Factor VIII – made vascular endothelium and R-E cells
Hep A IgM antibody
acute infection
Hep A IgG antibody
prior infection
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: -

(only time Hep B core IgM Ab is positive)
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: +
Resolved acute infection

(Hep B core IgM is negative --> Hep B surface Ab is positive -->
Hep B e Ab is positive --> Resolved Acute infection)
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: -

(Hep B core IgM is negative --> Hep B surface Ab is positive --> Hep B e Ab is negative OR nothing else is positive --> Vaccinated)
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: +
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)
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: -
Chronic active hepatitis

(Hep B core IgM is negative --> Hep B surface Ab is negative --> Hep B e Ab is negative --> Chronic active hepatitis)
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: +
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)
HVPG < 12
HVPG > 12
Portal hypertension - Intrahepatic. Due to sinusoidal arteries (due to cirrhosis)
Portal hypertension, Pre-hepatic
Portal or splenic vein thrombosis

AV fistulas in the splanchnic bed or spleen
Portal hypertension, Intrahepatic, normal HVPG
Pre-sinusoidal --> Normal HVPG
Sarcoid, Schistosomiasis

Post-sinusoidal --> Budd Chiari – can’t get into hepatic veins (clot in veins)
Portal hypertension, Post hepatic
Webs in IVC

Cardiac disease --> constrictive pericarditis, right heart failure
Complications of cirrhosis


Hepatic encephalopathy

Hepatorenal syndrome
Prokinetic Agents - Subbclasses
-Cholinergic agents
-Serotonin receptor modulators
-Dopamine receptor blockers
-Motilin-like agents
Drugs for constipation - subclasses
-Bulk forming agents
-Osmotic agents
Prokinetic agents - Cholinergic agents
Prokinetic agents - Serotonin receptor modulators
Prokinetic agents - Dopamine receptor blockers
Constipation drugs - Bulk-forming agents - Toxicities and examples

-Psyllium (Metamucil)

Constipation drugs - Softeners/Surfactants - Mechanism, toxicities and examples
Mechanism: Lowers surface tension of stool

-Impaired absorption of fat soluble agents
-Oil leakage
-Lipid pneumonitis

-Mineral oil
Constipation drugs - Osmotic agents - Mechanism, toxicities and examples
-Osmotically-mediated water retention stimulates peristalsis

-Abdominal distention, flatulence
-Saline: caution if renal/cardiovascular disease or electrolyte disorder. Monitor electrolytes.

-Sugar/alcohol-alcohol based
-Other (PEG solutions)
Constipation drugs - Stimulant Laxatives - Mechanism, toxicities and examples
Mechanism: Migrating colonic contractions

Concern: Overuse

-Castor oil
Constipation drugs - Lubiprostone - Mechanism, toxicities
Mechanism: Activates Cl channels within GI tract --> increasing intestinal fluid secretion

Abdominal distention and pain
Diarrhea and flatulence
Avoid in pregnancy
Anti-diarrheals - Bulk-forming & binding agents - Examples
Other agents
-Bismuth subsalicylate
Anti-diarrheals - classes
-Bulk-forming/binding agents
-Antimotility agents
-Antisecretory agents