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DEMS I > liver disease > Flashcards

liver disease Flashcards

1
Q

acute vs chronic liver injury

A

acute injury can lead to liver failure, resolution or chronic injury. Chronic injury can lead to cirrhosis then liver failure, cirrhosis then resolution, or directly to resolution

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2
Q

signs of liver failure

A

jaundice, icterous, acites (hypoalbuminemia), spyder angiometa, palmar erythema, gynecomastia, coagulopathy, encephalopathy, and renal failure

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3
Q

What is Cirrhosis

A

scarred liver, end point to many chronic liver diseases. Result of chronic recurring death of hepatocytes, deposition of extracellular matrix, and architectural and vascular reorganization. Can be compensated (functional) or decompensated (failing functions)

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4
Q

Cirrhosis histology

A

diffuse fibrous septation that divides the liver parenchyma into nodules

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5
Q

signs of liver cirrhosis

A

portal hypertension due to vascular reorganization in liver and increased sinusoidal pressure. Ascites, hemorrhoids, splenomegaly, esophageal varices, hepatic encephalopathy

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6
Q

Causes of jaundice and cholestasis

A

excessive extrahepatic bilirubin production, reduced hepatocyte uptake, impaired conjugation, decreased hepatocellular excretion and impaired bile flow

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7
Q

common causes of chronic liver disease in US adults

A

viral hepatitis C > alcoholic liver dz > non-alcohol fatty liver disease > viral hepatitis B

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8
Q

What is hepatitis

A

•Inflammatory injury and death of hepatocytes resulting from steatohepatitis or viral causes

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9
Q

Hepatitis histology

A

swelling/degeneration of hepatocytes, apoptosis/lobular cells with a clear interface separating apoptotic and non-apoptotic cells, bridging necrosis, coagulative necrosis,

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10
Q

Types of inflammation in hepatitis

A

Lymphocytes – many hepatitides; common in viral. Neutrophils – common in steatohepatitis (fatty liver). Eosinophils – common in drug injury. Plasma cells – common in autoimmune hepatitis

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11
Q

•Be able to compare and contrast acute and chronic hepatitis time course

A

acute: New onset (< 6 months) of symptomatic disease and laboratory evidence of hepatocyte injury. Chronic: hepatocyte injury and inflammation >6 months.

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12
Q

•Be able to compare and contrast acute and chronic hepatitis time causes

A

acute: Common causes include acute viral hepatitis and drug injury. Chronic: Caused by chronic viral hepatitis, autoimmune hepatitis and drug injury

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13
Q

•Be able to compare and contrast acute and chronic hepatitis microscopic findings

A

acute: Micrscopic findings include lobular disarray, marked inflammation throughout, widespread hepatocyte injury and necrotic hepatocytes, no fibrosis. Chronic: Microscopic findings include less prominent inflammation and injury (lymphoid aggregates), preponderance of portal tract-based inflammation, fibrosis

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14
Q

Cytoplasmic accumulations in liver injury

A

Fat – Steatosis. Bile (yellow inclusions) – Cholestasis. Iron – Hemosiderosis/ genetic hemochromatosis. Copper – Wilson Disease / chronic cholestasis. Viral particles (ground glass) – Viral hepatitis

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15
Q

Regeneration and fibrosis cycle in liver injury

A

Chronic injury and regeneration > activated stellate cells deposit collagen > architectural and vascular reorganization > cirrhosis

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16
Q

How is disease progression tracked in chronic hepatitis

A

liver biopsies: grade indicates amount of inflammation and injury. Stage indicates amount of fibrous tissue deposition

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17
Q

Stages of liver fibrosis

A

no fibrosis (stage 0) > portal fibrosis (stage 1) > periportal fibrosis (stage 2) > bridging fibrosis (stage 3) > cirrhosis (stage 4)

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18
Q

grades of liver inflammation and injury

A

grade 1: focal inflammation, no necrosis. Grade 2: focal necrosis with mild inflammation. Grade 3: confluent necrosis without bridging and moderate inflammation. Grade 4: bridging necrosis with severe inflammation

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19
Q

Hepatitis A transmission, frequency of chronic liver dz, diagnosis

A

fecal oral contaminated food or water, NEVER causes chronic liver dz only causes acute hepatitis, detection of serum IgM Abs

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20
Q

Hepatitis B type of virus, transmission, frequency of chronic liver dz, diagnosis

A

Partially dsDNA (only hepatic virus that can integrate into host genome), parenteral, sexual contact or perinatal. 10% develop chronic liver dz. Diagnosed with HBsAg or Ab to HBcAg

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21
Q

Hepatitis C transmission, frequency of chronic liver dz, diagnosis

A

Parenteral (blood and body fluids), intranasal cocaine use is risk factor. 80% develop chronic liver dz. PCR for HCV RNA, or 3rd generation ELISA for Ab detection

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22
Q

Hepatitis D diagnosis and transmission

A

Detection of IgM and IgG Abs. HDV RNA serum. HDAg in liver. IV drug use most common mode

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23
Q

Hepatitis E transmission, frequency of chronic liver dz, diagnosis

A

Fecal-oral. Never causes chronic liver dz, only causes acute hepatitis. PCR for HEV RNA, detection of serum IgM and IgG Abs

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24
Q

hepatitis C antibodies

A

Hep C is geneticall unstable with multiple genotypes and subtypes. Anti-HCV Abs are made, but antibodies are not neutralizing

25
Q

Outcomes of Hep C

A

85% develop chronic hepatitis, 15% resolve and rarely fulminant hepatitis results.

26
Q

Discuss appearance of important Hep B Abs and Ags

A

Hep Be Ag and HBV-DNA signifies active disease and viral replication. Hep B surface Ag appears before onset of symptoms and peaks during overt dz. IgM Abs rise before IgG

27
Q

compare serum markers of Hep B in infection with recovery compared to chronic carrier

A

Infection with recovery: HBeAg, HBV-DNA and HBsAg reach peak during active disease, then drop to zero in 4-12 weeks. IgM anti-HBc and anti-Hbe rise immediately then decrease in 4-20 weeks. Anti-HBs and anti-HBc IgG rise over period of years. Chronic: HBeAg, HBV-DNA and HBsAg all rise and stay elevated. IgM rises and stays elevated. IgG rises later and stays elevated

28
Q

Hepatitis B histology

A

ground glass hepatocytes, sanded nucleus

29
Q

Hepatitis D viral infection

A

•Replication incompetent, completely dependent on HBV coinfection. Potentiates effects of HBV with : increased risk of fulminant hepatitis, increased activity, and faster progression to end stage liver disease.

30
Q

Autoimmune hepatitis presentation and serology, histology

A

78% women. Indolent to severe. Presents with other autoimmune dz. Serology: autoantibodies (ANA, ASMA, anti-LKMB) and elevated IgG. Histology: plasma cell rich, centrolobular necroinflammation

31
Q

Primary biliary cirrhosis cause, presentation, serology, prognosis

A

•Immune-mediated attack of intrahepatic small caliber bile ducts. Pruritus, middle aged women, elevated ALP, GGT and bilirubin, jaundice. Serology: anti-mitochondrial Ab and elevated IgM. 25% have liver failure in 10 yrs

32
Q

primary biliary cirrhosis histology

A

lymphocyte mediated bile duct damage, granulomatous duct destruction

33
Q

primary sclerosing cholangitis cause, presentation, diagnosis and prognosis

A

•Presumed immune-mediated obliterative fibrosis of intrahepatic and extrahepatic bile ducts (generally large caliber bile ducts). Men > women, 70% have ulcerative colitis, ALP elevation, progressive fatigue, pruritis and jaundice. Diagnosis: cholangiography shows alternating biliary strictures and dilation. Increased risk for cholangiocarcinoma

34
Q

primary sclerosing cholangitis histology

A

periductal onion-skin fibrosis, fibrous obliteration of bile ducts

35
Q

intrinsic vs idiosyncratic drug induced liver injury

A

intrinsic is dose related, idiosyncratic is unpredictable

36
Q

acetaminophen liver injury

A

major cause of acute liver failure. Acetaminophen is an intrinsic hepatotoxin that causes centrilobular necrosis in zone 3

37
Q

list metabolic liver dz

A

steatosis, hereditary hemochromatosis, wilsons dz and alpha-1-antitrypsin deficiency

38
Q

What is steatosis

A

•Accumulation of fat in hepatocytes. Metabolic derangement of hepatocytes

39
Q

causes of steatosis

A

•metabolic syndrome, alcohol, drug effect, Wilson disease, viral infection. Lipid influx is greater than lipid clearance

40
Q

Steatohepatitis definition and causes

A

•Hepatocellular injury in association with steatosis, +/- overt inflammation. Triad of steatosis, lobular inflammation and hepatocyte ballooning degeneration. Causes: alcohol, metabolic syndrome, drug injury

41
Q

steatohepatitis histology

A

ballooning degeneration, inflammation and steatosis. Pericentral and pericellular fibrosis

42
Q

What causes alcohol steatosis/steatohepatitis

A

Defects in beta oxidation of hepatic lipids into CO2 and ketones, and defects in generation of VLDL.

43
Q

Alcoholic steatohepatitis histology

A

neutrophilic infiltrates, mallory bodies,

44
Q

What is non-alcoholic steatosis/steatohepatitis

A

fatty liver dz associated with obesity, diabetes type II, hypertriglyceridemia. Increased lipolysis and decreased beta oxidation/VLDL production

45
Q

Hereditary hemochromatosis cause and presentation

A

genetic iron overload dz throughout body manifests as liver disease, diabetes, heart failure in middle age. AR inheritance, HFE gene mutations lead to abnormal regulation of iron absorption resulting in increased absorption

46
Q

hereditary hemochromatosis histology

A

progressive iron deposition within the cytoplasm of hepatocytes, beginning in the periportal region first. Over time, iron acts as an oxidant and results in hepatocyte injury and fibrosis.

47
Q

Wilson disease

A

genetic copper overload throughout body causing liver dz and neuropsych problems. Due to mutations in ATP7B gene involved in bile excretion of copper.

48
Q

alpha-1-antitrypsin deficiency

A

•Alpha-1-antitrypsin is a protease inhibitor that prevents actions of proteases released by neutrophils and limits tissue damage. PiMM is normal genotype; PiZZ is the common disease and most people have pulmonary emphysema, 10% develop liver dz.

49
Q

alpha-1-antitrypsin deficiency histology

A

PASD stain shows intracytoplasmic accumulation,

50
Q

Abnormalities of blood flow affecting liver

A

impaired blood inflow causes intestinal congestion. Impaired intrahepatic blood flow causes ascites, hepatomegaly and elevated aminotransferases. Hepatic vein outflow obstruction causes ascites, hepatomegaly, elevated aminotransferases and jaundice

51
Q

malignant and benign liver masses in adults

A

malignant: hepatocellular carcinoma and cholangiocarcinoma. Benign: hemangioma, focal nodular hyperplasia and hepatocellular adenoma.

52
Q

Hepatocellular carcinoma cells, risks, prognosis

A

Malignant neoplasm of hepatocytes. Most common 1° malignant liver tumor. Occurs mostly in patients with chronic liver disease (HCV, HBV, alcohol) and cirrhosis. In general, dismal long-term survival

53
Q

hepatocellular carcinoma gross and microscopic appearance

A

gross: Invasion of main branch of portal vein or hepatic artery. May have green-yellow color (bile). Micro: Thickened hepatic plates, Endothelialization of sinusoids, Invasion of fibrous tissue/vessels, Unpaired arteries, No true portal areas

54
Q

Cholangiocarcinoma cells affected, risk factor, prognosis

A

Malignant neoplasm of bile ducts, May be intrahepatic or extrahepatic, Major risk factor is primary sclerosing cholangitis, In general, dismal long-term survival

55
Q

Cholangiocarcinoma gross and microscopic appearance

A

gross: -Densely fibrotic mass in the hilar region with infiltrative edges, Tan-white in color. Micro: Invasive gland forming tumor with abundant desmoplastic response

56
Q

Hemangioma structures affected, presentation

A

Benign neoplasm of dilated vascular spaces. Most common primary hepatic tumor. Small and asymptomatic usually, but can cause vague RUQ pain, early satiety, nausea, vomiting

57
Q

Focal nodular hyperplasia structures affected, Sx

A

•Benign mass-like proliferation of hepatocytes. Arises due to local vascular flow anomaly. Usually asymptomatic

58
Q

Hepatocellular adenoma structures affected, risk, Sx

A

Benign neoplasm of hepatocytes. Occurs mostly in women of child-bearing age and associated with oral contraceptive use. Asymptomatic or RUQ abd pain. Low risk of malignant transformation

DEMS I (28 decks)

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