Step 1 - GI 3

denniskwinn's version from 2015-04-25 16:01


Question Answer
Hepatic steatosisShort-term change with moderate alcohol intake. Macrovesicular fatty change that may be reversible with alcohol cessation
Alcoholic hepatitisRequires sustained, long-term consumption . Swollen and necrotic hepatocytes with neutrophilic infiltration. Mallory bodies (intracytoplasmic eosinophilic inclusions) are present
Alcoholic cirrhosisFinal and irreversible form . Micronodular, irregularly shrunken liver with "hobnail" appearance. Sclerosis around central vein (zone III). Has manifestations of chronic liver disease (e .g., jaundice, Hypoalbuminemia)
Nutmeg liverDue to backup of blood into liver. Commonly caused by right~sided heart failure and Budd-Chiari syndrome The liver appears mottled like a nutmeg. If the condition persists, centrilobular congestion and necrosis can result in cardiac cirrhosis
Hepatocellular carcinoma/hepatomamost common primary malignant tumor of the liver in adults. ↑ incidence is associated with hepatItis B and C. Wilson's disease, hemochromatosis, alpha1-antitrypsin deficiency, alcoholic cirrhosis, and carcinogens (e.g., aflatoxin in peanuts).
Hepatocellular carcinoma/hepatoma FindingsJaundice, tender hepatomegaly, ascites, polycythemia, and hypoglycemia. . Commonly spread by hematogenous dissemination - - ↑ alpha fetoprotein - may lead to Budd-Chiari syndrome
Budd-Chiari syndromeOcclusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease (hepatomegaly, ascites, abdominal pain, and eventual liver failure). May develop varices and have visible abdominal and back veins. Absence of JVD. Associated with polycythemia vera, pregnancy, and hepatocellular carcinoma
Α1 antitrypsin deficiencyMisfolded gene product protein accumulates in hepatocellular ER. ↓ elastic tissue In lungs → panacinar emphysema. PAS-positive globules in liver. Codominant trait
Physiologic neonatal jaundiceAt birth, immature UDP-glucuronyl transferase → unconjugated hyperbilirubinemia → jaundice/kernicterus.
Neonatal janudice Treatment phototherapy (converts UCB to water-soluble form).
Hepatocellular jaundice characterizationHigh conjugated/unconjugated bilirubin, high urin bilirubin, normal or low urine urobilinogen
Obstructive jaundiceHigh conjugated bilirubin, High urine bilirubin, low urine urobilinogen
Hemolytic jaundiceHigh unconjugated bilirubin, Absent urine bilirubin (acholuria), High urine urobilinogen
Gilbert’s syndromeMildly ↓ UDP-glucuronyl transferase or ↓ bilirubin uptake. Asymptomatic. Elevated unconjugated bilirubin without overt hemolysis. Associated with stress.
Crigler-Najjar syndrome, Type IAbsent UDP-glucuronyl transferase (problem with bilirubin conjugation). Presents early in life; patients die within a few years - Type II is less sever and responds to phenobarbital which ↑ liver enzyme synthesis. . Both = unconjugated bilirubinema
Crigler-Najjar syndrome findingsjaundice, kernicterus (bilirubin deposition in brain), ↑ unconjugated bilirubin
Dubin-Johnson syndromeConjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver, Benign. (problem with excretion of conjugated bilirubin) = conjugated bilirubinemia
Rotor syndromesimilar but even milder and does not cause black liver - mild hyperbilirubinemia due to defective liver excretion - milder than Dubin-johnson (conjugated bilirubinemia)
Wilson’s disease (hepatolenticular degeneration)Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin →copper accumulation, especially in liver, brain, cornea, kidneys and joints. - Autosomal recessive
Wilson’s disease characteristicsAsterixis, Basal ganglia degeneration (parkinsonian symptoms), Ceruloplasmin ↓, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular), Choreiform movements, Dementia, Hemolytic anemia
Wilson’s disease treatmentpenicillamine
HemochromatosisHemosiderosis is the deposition of hemosiderin (iron); hemochromatosIs is the disease caused by this iron deposition. Results in CHF and ↑ risk of hepatocellular carcinoma. Disease may be 1 ° (autosomal recessive) or 2° to chronic transfusion therapy (e.g., β thalassemia major). ↑ ferritin , ↑ iron, ↓ TIBC→↑ transferrin saturation. - Total body iron may reach 50 g, enough to set off metal detectors at airports. Associated with HLA-A3
Hemochromatosis classic triadMicronodular Cirrhosis, Diabetes mellitus, and skin pigmentation → " bronze" diabetes.
Hereditary hemochromatosis treatmentrepeated phlebotomy, deferoxamine
Gallstones (cholelithiasis)form when solubilizing bile acids and lecithin are ovewhelmend by cholesterol and or bilirubin or gallbladder stasis - can cause ascending cholangitis, acute pancreatitis, bile stasis, cholecycstitis. Can caus fistula between gallbladder and SI
Gallstone ileusgallstone obstructing ileocecal valve - happens when gall stones go through fistula in gallbladder and then travel through SI.
Types of gall stonesCholesterol stones (radiolucent with 10- 20% opaque due to calcifications)-80% of stones. Associated with obesity, Crohn's disease, cystic fibrosis, advanced age, clofibrate, estrogens, multi parity, rapid weight loss, and Native American origin . 2. Pigment stones (radiopaque)-seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection
Charcot's Triad of cholangitis1. Jaundice, 2. Fever, 3. RUQ pain
Biliary colicgallstones interfere with bile flow, causing bile duct contraction. May present without pain
Cholelithiasis diagnosis/treatmentDiagnose with US, treat with cholecystectomy
CholecystitisInflammation of gallbladder. Usually from gallstone; rarely ischemia or infectious (CMV) ↑ Alkaline phosphatase if bile duct becomes involved (e.g ascending cholangitis)
Acute pancreatitis CausesGallstones, Ethanol, Trauma, Steroids, Mumps, Autoimillune disease, Scorpion sting, Hypercalcemia/Hyperlipidemia, ERCP, Drugs (e.g., sulfa drugs). - GET SMASHED
Acute pancreatitisAutodigestion of pancreas by pancreatic enzymes - Can lead to DIC, ARDS, diffuse fat necrosis, hypocalcemia (Ca2+ collects in pancreatic caIicium soap deposits), pseudocysl formation, hemorrhage, Infection, and multiorgan failure
Acute pancreatitis clinical presentationepigastric abdominal pain radiating to back, anorexia, nausea
Acute pancreatitis labselevated amylase, lipase (higher specificity)
Chronic pancreatitis can lead topancreatic infufficiency → steatorrhea, fat-soluble vitamin deficiency, and DM
Chronic calcifying pancreatitisstrongly associated with alcohol with increased risk of pancreatic cancer
Pancreatic adenocarcinomaPrognosis avcrages 6 months or Iess; very aggressive; usually already metastasized at presentation; tumors more common in pancreatic head (=obstructive jaundice). ↑ risk in Jewish and African-American males. CEA and CA-19-9 tumor markers. Associated with cigarettes but not EtOH
Pancreatic adenocarcinoma often presents with1. Abdominal pain radiating to back 2. Weight loss (due to malabsorption and anorexia) 3. Migratory thrombophlebitis-redness and tenderness on palpation of extremlties (Trousseau's syndrome) 4. Obstructive jaundice with palpable gallbladder (Courvoisier's sign)