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Hepatology_UW Flashcards

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1
Q

What is non-alcoholic fatty liver disease? It is further classfied by histology into what?

A

Hepatic steatosis on imaging or biopsy (resembles alcohol-induced liver injury on histology). Exclusion of significant alcohol use. Exclusion of other causes of fatty liver. Further classified into 1) fatty liver disease and 2) nonalcoholic steatohepatitis (which progresses further into fibrosis/cirrhosis)

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2
Q

What is the pathophysiology of non-alcoholic fatty liver disease?

A

Likely due to peripheral insulin resistance => increased lipolysis, TAG synthesis and hepatic uptake of fatty acids => intra-hepatic FA oxidation => increases oxidative stress and proinflammatory cytokines (like TNF-alpha) => liver inflammation, increased fat accumulation and fibrosis/cirrhosis.

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3
Q

What are the major risk factors for non-alcoholic steatohepatitis (NASH)?

A

Top 3 risk factors - obesity, diabetes mellitus, hypertriglyceridemia. Other risk factors (certain medications, corticosteroids, HAART, tamoxifen, diltiazem, amiodarone), TPN, endocrinopathies.

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4
Q

What is the criteria for initiating tx for chronic hepatitis C?

A

1) Age > 18 2) detected HCV RNA in serum 3) liver biopsy with bridging fibrosis (or worse) and chronic hepatitis 4) compensated liver disease (i.e., albumin greater than 3.4mg/dL, no ascities, bilirubin

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5
Q

What are the contraindications for HCV tx?

A

Ongoing alcohol or drug abuse, major uncontrolled depression.

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6
Q

What is the initial treatment for treatment-naïve HCV patients? What additional tx do patients with HCV genotype 1 receive?

A

pegylated interforon + ribavirin. Additional protease inhibitor (telaprevir + boceprevir).

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7
Q

Chronic HBV tx is recommended for?

A

1) Patients with acute liver failure 2) Clinical complications of cirrhosis 3) Advanced cirrhosis wih high serum HBV DNA levels 4) patients without cirrhosis but with positive HBeAg, HBV DNA >20,000 IU/mL and serum ALT >2x upper limit level 5) patients during chemotherapy or immunosuppression so as to prevent HBV reactivation.

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8
Q

What are the available treatments for HBV?

A

Interferon (usually just short-term treatment and used for younger patients with compensated liver disease), Lamivudine (is showing high levels of resistance to this drug), Entecavir, Tenofovir. Last two most potent, there’s least drug resistance to these.

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9
Q

Medical control of bleeding may be accomplished by what kind of drugs?

A

vasoconstrictors like Terlipressin (synthetic analogue of vasopression), octeotride, or somatostatin.

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10
Q

All patients with newly diagnosed Hep C infection should be evaluated for?

A

Antiviral treatment with the goal of eradication HCV RNA and to prevent progression of hepatitis to cirrhosis.

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11
Q

Why should liver biopsy be offered to patients with newly diagnosed HCV infection?

A

Offers best clinical predictor of disease progression, and helps assess likely response to tx. Patients with moderate to severe inflammation and some fibrosis have higher chance of progression to cirrhosis and respond better. Liver biopsy also determines the stage of the disease, rule other other concomitant liver disease (like hemochromatosis), and guide tx decisions.

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12
Q

Having a detectable level of HCV RNA means?

A

You have chronic hepatitis C

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13
Q

What is hepatic encephalopathy? What is the pathophysiology?

A

Alteration in CNS function due to liver’s inability to convert ammonia to urea. Although other toxins may be responsible. These toxins stimulate the inhibitory (GABA) and impair the excitatory pathways in the brain.

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14
Q

What are the sx of hepatic encephalopathy?

A

Hepatic encephalopathy can be graded in stages. Stage 1 can be altered sleep patterns (diurnal sleep patterns) to Stage 4 (stupor and coma).

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15
Q

What is the treatment for hepatic encephalopathy?

A

1) Supportive care (such as volume repletion) 2) treatment of the underlying problem/precipitating cause (meds, hypovolemia, infection xs nitrogen, or electrolyte abnormalities such as HYPOKALEMIA), and 3) lowering serum ammonia. TX: 1) non-absorbable disaccharides such as LACTULOSE. Colonic bacteria metabolize lactulose to short-chain FA which acidifies the colon and stimulates the conversion of absorbable ammonia to non-absorbable ammonia and also causes a catharsis. 2) Antibiotics such as Rifaximin can decrease the number of ammonia producing bacteria in the colon. Usually added to lactulose if no improvement with lactulose is seen within 48 hours. 3) Laxatives that cause catharsis.

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16
Q

What is the clinical presentation of Hep C?

A

Asymptomatic or develop fatigue (most common), can show other non-specific signs like arthralgias, myalgias, weakness, weight loss, nausea, serum transaminases can be elevated or normal, can progress to cirrhosis in up to 20% of patients, increased risk of hepatocellular carcinoma

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17
Q

What are the common extrahepatic manifestations of chronic HCV?

A

1) heme: essential mixed cryoglobulinemia which is due to circulating immune complexes that deposit in small and medium vessels. May be a/w with low serum complement levels. Patients can develop palpable purpura, arthralgias and 2) renal complications (usually MPGN) 3) Skin: porphyria cutanea tardea (PCT) - fragile sensitive skin, photosensitivity, vesicles and erosions on dorsum of hands, lichen planus 4) endocrine: inreased risk of diabetes.

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18
Q

What is porcelain gallbladder? How does it present? What does it look like on x-ray and CT? and what is usually recommended in this patient population?

A

WHAT: Calcium-laden gall bladder with bluish discoloration that can develop in patients with chronic cholecystitis. Thought that calcium salts deposit intramurally secondary to chronic inflammation from gallstones or the natural progression of chronic inflammation. PPT: Can be asymptomatic or present with RUQ pain or a firm, non-tender mass in the RUQ. IMAGING: x-ray - calcification, CT - calcification with central bile filled dark area. RECOMMENDATION: Cholecystectomy because up to 33% of patients with develop gallbladder carcinoma (mostly adenocarcinoma).

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19
Q

Gallstones (choleithiasis) are common in what? (phrase)

A

Fat, forty, female fertile women.

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20
Q

What are the major types of gallstones and which are the most common?

A

1) Cholesterol 2) pigment 3) mixed. Cholesterol and mixed gallstones are the most common type of gallstones in the US and cholelithiasis is more common in the west compared to the east.

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21
Q

Which gallstones are radiolucent?

A

Cholestserol and mixed gallstones.

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22
Q

What is primary biliary cirrhosis?

A

Chronic liver disease that is characterized by auto-immune destruction of intrahepatic bile ducts and cholestasis.

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23
Q

What is the ppt of primary biliary cirrhosis (age, onset, first sx, physical findings)

A

Usually in middle aged WOMEN with insidious onset. First sx is usually pruritus and it may be very severe, especially at night. PE findings: hepatosplenomegaly, xanthomatous lesions in the eyelids or in the skin/tendons. With disease progression, patient may get jaundice, portal HTN, steatorrhea, osteopenia.

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24
Q

How is primary biliary cirrhosis dx confirmed?

A

Anti-mitochondrial antibodies in the serum.

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25
What other conditions is primary biliary cirrhosis a/w
Sjogren's syndrome, Raynaud's syndrome, scleroderma, autoimmune thyroid disease, hypothyroidism, and celiac disease. Hepatobiliary malginancy risk is elevated in PBC patients.
26
What is the drug of choice in treating primary biliary cirrhosis?
Ursodeoxycholic acid is the drug of choice. Relieves symptoms and also lengthens transplant free survival time. Methotrexate and colchicine have also shown to be of moderate benefit.
27
Whats more common - liver mets or HCC?
Liver mets (20x more common than HCC). Also, AFP is elevated with HCC.
28
How should acute pancreatitis be managed?
Conservative treatment - analgesis (meperidine over morphine), IV fluids, and nothing by mouth to avoid further inflammation of the pancreas.
29
Anti-1 antitrypsin deficiency is a/w?
Panacinar emphysema and liver cirrhosis.
30
How is the diagnosis of A1AT deficiency established?
Measurement of A1AT serum level, followed by confirmatory genetic testing.
31
In the liver, hepatocytic inclusions of A1AT stains with what agent
Stain with Periodic-Acid Schiff reaction and also resists digestion by elastase.
32
What is the hallmark of ischemic hepatopathy?
Huge increases in AST and ALT with milder associated increases in total bilirubin and and alkaline phosphatase.
33
What is the serology of patients that have had the Hep B vaccine?
Anti-HBsAg (positive) but negative for HBsAg and all other markers.
34
What are the serologic markers for Hepatitis B virus?
HBsAg: First virological marker after inoculation, precedes elevation of serum aminotransferases and onset of clinical sx. Remains detectable during the entire symptomatic phase of acute Hep B and suggests infectivity.
35
An elevated biliary sphincter pressure is highly specific for?
Sphincter of Oddi dysfunction
36
What is the tx of choice for sphincter of oddi dysfunction?
ERCP with sphincterectomy
37
Development of a palpable mass in the epigastrium with pain radiating to the back, 4 weeks after an episode of acute pancreatitis is highly suggestive of?
Pancreatic pseudocyst
38
What is a pancreatic pseudocyst?
It is not a true cyst as it doesn't have a epithelial lining, rather it is encapsulated by a thick fibrous wall. It contains enzyme rich fluid, tissue, and debris that accumulates within the pancreas and creates an inflammatory response.
39
How is pancreatic pseudocyst best diagnosed?
Ultrasound and tends to resolve spontaneously.
40
Pancreatic carcinoma with tumors in the pancreatic body/tail present what way vs. tumors in the head?
Body/tail = pain and weight loss. Head = steatorrhea, jaundice.
41
What is Courvoisier's sign? (possible sign of pancreatic cancer)
Nontender but palpable gallbladder at the right costal margin in a jaundiced patient.
42
What is Virchow's node (possible sign of pancreatic cancer)
Left supraclavicular adenopathy in a patient with metastatic disease.
43
What is the initial imaging test for patients with jaundice? What next if the first test is non-diagnostic?
U/S. Abdominal CT next.
44
What is the presentation of Gilbert's syndrome? Which part of the Bilirubin uptake process has the defect?
Icterus secondary to a mild, predominantly unconjugated hyperbilirubinemia (normal levels in these patients are
45
Which part of the Bilirubin uptake process has the defect?
Familial disroder of bilirubin glucoronidation - production of UDP glucuronyl transferase is reduced. (therefore problem of conjugating the bilirubin)
46
Dx of Gilbert's is suggested by? Presumptive diagnosis is made by?
No apparent liver disease with mild uncongugated hyperbilirubinemia thought to be provoked by class trigger (hemolysis, fat free diet, physical exertion, febrile illness, stress, fatigue, fasting.) Presumptive dx made when uncongjuated hyperbilirubinemia persists with repeat testing, but LFTs, blood count, blood smear and retic count look normal.
47
What is the Tx for Gilberts?
Generally considered unnecessary but mode of inheritance should be discussed with patietns to prevent needless testing in family.
48
What is Criggler Najjar syndrome type 1? Where is the defect in bilirubin uptake/metabolism?
Autosomal recessive disorder of bilirubin metabolism with absent UDP glucuronyl transferase and therefore high levels of indirect biliruin levels (20-25mg/dl to as high as 50mgldl)
49
What are the findings of Criggler Najjar syndrome type 1?
In infants, severe jaundice and neurologic impairment due to kernicterus (bilirubin encephelopathy). Liver enzymes and histology are normal.
50
What is the tx for Criggler Najjar syndrome type 1?
Plasmapheresis or phototherapy helpful in short term. Only curative option is liver transplant
51
What is Criggler Najjar syndrome type 2? Liver enzymes and histology are?
Milder autosomal recessive disorder of bilirubin metabolism with lower serum bilirubin levels
52
If IV phenobarbital is administered in Criggler Najjar types 1 and 2, what happens?
Type 1 = Serum bilirubin level does not go down. Type 2 = Serum bilirubin levels go down.
53
Acute bleeding in patients (coagulopathy) with liver failure is best treated with?
Fresh frozen plasma which has all the clotting factors.
54
What clotting factor does the liver not synthesize?
Factor 8
55
What are the Vit K dependent clotting factors?
Factor 2, 7, 9 and 10
56
What are the two familial disroders of hepatic bile secretion that result in conjugated hyperbilirubinemia?
Dubin-Johnson syndrome and Rotor Syndrome.
57
What is Dubin-Johnson syndrome? What part of the bilirubin uptake/metabolism process is there a defect?
Rare syndrome with predominantly conjugated hyperbilirubinemia not a/w hemolysis. Benign condition found in Sephardic Jews but also in all races/men and women. Basically there is a problem with excretion of conjugated bilirubin.
58
What is the clinical ppt of Dubin-Johnson? What are the routine lab values of blood count and liver funcion profile?
Icterus is evident but can be so mild and only appear after a trigger like illness, pregnancy, or OCP use. Most patients are asymptomatic or present with very nonspecific complaints. Routine lab tests are all normal. Serum bilirubin levels usually range 2-5 can be very eelvated to 20-25. Additional insight lab values for Dubin-Johnson is that they have normal amounts of total urinary coproporphyrin but over 80% is coproporphyrin 1 (vs. normal ppl have similar majority of coproporphyrin III)
59
How is the dx of Dubin-Johnson made? How is confirmation obtained?
Conjugated hyperbilirubinemia with a direct bilirubin fraction of at least 50%, otherwise normal liver function profile. Confrimation through high levels of coproporphyrin I.
60
What is Rotor syndrome?
Benign condition with defect in hepatic storage of conjugated bilirubin, resulting in leakage into plasma. Chronic and mild hyperbilirubinemia of both unconjugated and conjugated forms develop - no hemolysis. LFTs are normal.
61
What is the difference in hepatocytes between Rotor and Dubin-Johnson?
Dubin-Johnson syndrome = Liver is strikingly black, histological features are normal but dense pigment composed of epinephrine metabolists wtihin lysosomes seen. Rotor syndrome - no pigmented granules in hepatocytes.
62
For all patients with symptomatic gallstones that are medically stable, what is indicated?
Cholecystectomy
63
Hepatitis A is what kind of virus? Where is it common? Transmission route? What is the nature of the onset of disease? What/are there long term complications?
RNA picornavirus with average incubation period of 30 days. Common in areas of poor sanitation and overcrowding. Transmission route: fecal-oral. Acute onset. Self limiting disease that does not typically lead to chronic hepatitis, cirrhosis or hepatocellular carcinoma.
64
Amebiasis is caused by?
Protozoal disease - entamoeba Histolytica
65
Hx of travel to endemic area (like mexico), dystentery, followed by RUQ pain with single cyst in right lobe of liver is indicative of?
Amebic liver disease
66
Where are amebic liver abscesses generally located and what kind of symptoms can they cause?
Generally single. Located on right lobe. Abscess on superior surface of liver can cause a pleuritic like pain that radiates to the shoulder.
67
What is the usual tx for amebic liver abscess?
Metronidazole. Usually cures >90% of patients within 7-10 days.
68
Patients with liver mass who have traveled to an endemic area should be evaluted for what, txed for what, tested for what?
Evaluated for amebic abscesses, txed with empiric metronidazole and tested serologically for antibodies. Aspiration is NOT recommended due to risks such as bleeding, amebic peritonitis, puncture of an undiagnosed echinococcal cyst, and secondary bacterial infection.
69
Ascites is most commonly caused by?
Cirrhosis
70
Cirrhosis is msot commonly caused by?
Alcohlic liver disease and hepatitis C
71
New-onset ascites requires what procedure?
Paracentesis to determine the cause.
72
What is cholangitis?
Infection of the common bile duct
73
What is Charcot's triad? This is indicative of?
Fever, severe jaundice, and RUQ pain. Acute ascending cholangitis.
74
What is the tx for acute ascending cholangitis?
Acute condition - need immediate supportive care and broad spectrum antibiotics. If patients don't respond to this tx, then ERCP for biliary decompression should be done. This significantly decreases mortality and morbidity.
75
Wilson's disease is also known as?
Hepatolenticular degeneration (what happens in the basal ganglia due to copper deposits)
76
What is Wilson's disease? What age group does it typically occur in?
Rare autosomal reccessive disease. Typically occurs in younger indiividuals 5-40 yo.
77
What is the pathophysiology of Wilson's disease?
Genetic mutation that results in reduced copper secretion into the biliary system (reduces and decreases the formation and secretion of ceruloplasmin). Copper accumulates in the liver (pro-oxidant), free radicals cause damage in hepatic tissue. Copper leaks out of the hepatocytes and starts depositing in other organs (cornea, basal ganglia)
78
How does Wilson disease usually present in children/adolescent vs. adults
Children/adolescents = liver disease ranging from asymptmomatic aminotransferase elevatiosn to FHF. Young adults = neuropsychiatric disease.
79
Wilson's disease is a/w which other diseases?
Fanconi syndrome, hemolytic anemia, and neuropathy.
80
How is Wilson's disease diagnosed?
Low serum ceruloplasmin (
81
In alcoholic liver disease, what are the levels of GGT and ferritin, usually?
GGT (gamma-glutamyl transferase), an enzyme present in the liver and other cells and ferritin (acute phase reactant) likely elevated in liver disease.
82
The absolute values of ALT and AST is usually what in alcoholic liver disease.
Usually less than 300 IU/L but almost always
83
What is emphysematous cholecystitis? What population (age and conditions) does it typically occur in?
common form of acute cholecystitis that occurs due to secondary infection of gallbladder wall by gas producing bacteria. Males, typically 50-70. Pre-disposing factors DIABETES MELLITUS, immunosuppresion, gall stones, vascular compromise (obstruction or stenosis of cystic artery).
84
How do you diagnose emphysematous cholecystitis?
Abdominal radiograph: Airfluid levels in the gall bladder, U/S showing curvilinear gas in gallbladder.
85
What is acute acalculous cholecystitis?
Acute inflammation of the gallbladder in the absence of gallstones. Most commonly seen in severely ill hospitalized patients (such as extensive burns, trauma, prolonged tPN, fasting, mechanical ventilation).
86
What is the initital testing of choice for acute acalculous cholecystitis? What testing is more sensitive and specific?
Ultrasonogram = shows signs of cholecsystitis and no gallstones. CT and HIDA scan more sensitive and specific.
87
All patients with chronic liver disease should be immunized against?
Hepatitis A and Hepatitis B since they are at high risk for hepatic failure or cirrhosis upon infection with viral hepatitis.
88
Elevated serum alk phos is indicative of what? What imaging should be done?
Cholestatisis.RUQ Abdominal ultrasound to assess for intra or extra-hepatic causes of biliary obstruction.
89
Eruptive xanthomas in a patient with symptoms of acute pancreatitis should raise suspicion for what etiology?
Hypertriglyceridemia. It can lead to acute pancreatitis if triglycerides are over 1000mg/dL.
90
Dx of hypertriglyceridemia in patient with acute pancreatitis can be confirmed by what test?
Fasting serum lipid profile.
91
Person who has been exposed to blood that contains hepatitis B should receive what?
HB immune globin as soon as possible and if unvaccinated against Hep B, should receive the vaccine as soon as possible as well.
92
What is fulminant hepatic failure?
Hepatic encephalopathy that develops within 8 weeks of onset of acute liver failure.
93
What is the only effective treatment for fulminant hepatic failure?
Orthotopic liver transplantation, regardless of etiology. Pat
94
What is the prognosis for acute hepatitis B infection?
90% of adults with acute hep B will recover completely. Minority will develop crhonic hep B, and 0.1-0.5% will develop fulminant hepatic failure.
95
Hyperestrogenism in cirrhosis leads to?
Gynecomastia, spider angiomas, palmar erythema, testicular atrophy, decreased body hair in males.
96
Liver functions can be divided into three distinct categories
1) Synthetic (cholestesrol, proteins, clotting factors; 2) Metabolic (metabolism of drugs and toxins;) 3) Excretory (bile secretion
97
Why does hyperestrogenism occur in cirrhosis?
Liver has decreased ability to metabolize circulating estrogens.
98
What is the pathophysiology of caput medusae?
Dilatation of superficial veins in anterior abdominal wall secondary to portal hypertension. Portal HTN results due to increased resistance to portal flow at the sinusoids, leading to increased pressure at portosystemic collateral veins in anterior abdomen, lower rectum, and lower end of esophagus where the portal and systemic circulations meet. Responsible for esophageal varices, hemorrhoids and caput medusae
99
What is the pathophysiology of cirrhotic ascites?
Complex - includes sinusoidal hypertension => seepage of hepatic lymph into peritoneal cavity, leakage of intestinal fluid, and renal retention of sodium and water.
100
What is the pathophysiology of pitting edema in liver disease?
Bad liver - poor liver function, i.e., synthesis of albumin. Hypoalbuminemia leads to decrease in intravascular oncotic pressure. Fluid then moves to extravascular space and pitting edema results.
101
Cirrhosis due to alcohol or hemochromatosis can be a/w?
Hypogonadism, likely due to primary gonadal injury or hypothalamic-pituitary dysfunction.
102
What is Murphy's sign?
Worsening of RUQ pain with inpsiration that sometimes causes the patient to suddenly hold their breath
103
Acute cholecystitis is usually due to?
Gallstone formation in 90% of cases, most commonly arising when a gallstone impacts in the cystic duct.
104
Pathophysiology of acute cholecystitis?
Gallstone impacts cystic duct => duct tissue behind gallstone becomes infected from bacterial overgrowth in stasis => subsequent ischemic changes most commonly lead to gangrene and performation, generatlized peritonitis, or a well-circumscribed abscennes. Other complications include cholangititis and choledocholithiasis.
105
What is the presenation of acute cholecystitis?
Sudden onset of RUQ pain, fever, vomiting and leukocytosis.
106
In evaluating asymptomatic elevation of aminotransferases, the first step is to do what?
Take thorough history to rule out common hepatitis risk factors (sexual practices, travel outside country, alcohol and drug use)
107
What are hepatic adenomas and what population is it generally seen in?
Uncommon benign epithelial tumor sof the liver usually arise as a solitary mass in the right hepatic lobe. Found predominantly in young and middle-aged women who have been using OCP for a long time.
108
Histologically, what do hepatic adenomas look like?
Enlarged adenoma cells that contain glycogen and lipid. Nuclei are small and regular, but normal hepatic architecture is absent.
109
What are the most dreaded complications of hepatic adenomas
Intra-tumor hemorrhag eand malignant transformation.
110
What is the most common cause of ductopenia?
Primary biliary cirrhosis. Other causes include failing liver transplant, Hdogkin's disease, GVHD, sarcoid, CMV invection, HIV and medication toxicity.
111
P-ANCA is a/w?
Churg-Strauss synrome and microscopic polyangiitis
112
Anti-smith antibodies are highly specific for?
SLE but only found in 30-50% of SLE cases
113
Anti-smooth muscle antibodies and anti-LKM antibodies are a/w?
Acute and chronic hepatitis.
114
Anti-nuclear antibodies are strongly a/w?
SLE and type 1 autoimmune hepatitis.
115
What is the best screening test for acute hep B infection?
HBsAg and anti-HBc
116
Hyatid cysts in the liver are due to infection with?
Echinococcus granulosus.
117
Eggshell classification of a hepatic cyst on CT scan is highly suggestive of?
Hyatid cyst.
118
Aspiration of hyatid cysts is generally not indicuted due to?
Risk of anaphylactic shock secondary to spilling of cyst contents.
119
What is the tx of hyatid cyst?
Surgical resection under cover of alebendazole
120
1) What kind of virus is Hep E? 2) Mode of transmission? 3) risk for pregnant women?
1) RNA virus 2) fecal-oral. Mostly found in poor areas/countries (India, Africa, Asia, Central America etc) 3) high rate of progression to fulminant hepatitis, especially in third trimester.
121
What is choledocholithiasis?
Gallstones in the common bile duct.
122
What is hepatic hydrothorax?
Transudative pleural effusions in patients with cirrhosis who have no underlying cardiac or pulmonary disease to account for the pleural effusion.
123
What side does hepatic hydrothorax generally occur?
Right side
124
What is the treatment for hepatic hydrothorax?
Initial tx: Diuretics and salt restricted diet, refractory hepatic hydrothorax: transjugular intrahepatic portosystemic shunt (TIPS)
125
Ursodeoxycholic acid is used when in cholelithiasis? How does it work? Disadvantage of this medication?
When patients don't want to undergo cholecystectomy/are poor surgical candidates. Basically a bile salt that when given, decreases hepatic secretion and intestinal absorption of cholesterol. Used to dissolve radiolucent gallstones in patients with normal, functional gallbladders. Very costly, and patients relapse after stopping medication.
126
What is the normal liver span?
6-12 cm in the midclavicular line.
127
What are the three major pathological stages of alcoholic liver disease? What is reversible?
1) Fatty liver 2) Alcoholic hepatitis 3) Alcoholic fibrosis/cirrhosis. Reversible up to early cirrhosis.
128
True fibrosis in alcoholic liver disease is characterized by?
Regenerative nodules
129
What histologic findings are there in alcoholic hepatitis?
Mallory bodies, neutrophilic infiltrates, liver cell necrosis, perivenular inflammation.
130
Gallbladder carcinoma is a rare malignancy that generally occurs in what patient population?
Hispanic and Southwestern native americans. Usually female with a history of gallstones. (typically diagnosed intraoperatively or after cholecystectomy)
131
Isoniazid can cause what kind of liver injury? Histologic features are similar to?
Idiosyncratic liver injury (i.e., not dose dependent and with variable latent periods). Viral hepatitis.
132
Within the first few weeks, approximately 10-20% of patients taking isoniazid will develop what?
Mild aminotransferase elevation. The hepatic injury is isually self limited and will resolve without intervention.
133
What is cryoglobulinemia?
Immune complex disorder (IgM against anti-hepatitis virus C IgG) most commonly due to chronic hepatitis C.

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