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GI Week 6 > Liver Pathology 2 > Flashcards

Liver Pathology 2 Flashcards

1
Q

Define cirrhosis

A

hepatic disease characterized by widely distributed (diffuse, not focal) interconnecting fibrous scars with nodular parenchymal regeneration

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2
Q

State the most common cause of cirrhosis

A 
1. alcoholic liver disease
viral hepatitis (B,C,D)
biliary diseases
hereditary hemochromatosis
Wilson's disease
A1At deficiency
cryptogenic cirrhosis (non-alcholic fatty liver disease)
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3
Q

List the 3 main causes of death associated with cirrhosis

A

hepatic failure
portal hypertension
hepatocellular carcinoma

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4
Q

List the key causes of hepatic failure

A

acute liver failure: massive hepatic necrosis from hepatitis, reye’s syndrme, acute fatty liver of pregnancy. most common cause if acetaminophen overdose

chronic liver failure: usually due to cirrhosis

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5
Q

What are some of the clinical manifestations of hepatic failure

A 
jaundice
hypoalbuminemia
coagulopathy
hyperammonemia
fetor hepaticus
increased liver enzymes
hypoglycemia
endocrine changes
hepatorenal syndrome
hepatic encephalopathy and coma
hepatopulmonary syndrome
portppulmonary hypertension
portal hypertension
decreased metabolism of drugs
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6
Q

State the most common cause of portal hypertension

A

cirrhosis

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7
Q

State the four main complications of portal hypertension

A

ascites
portosystemic shunts like esophageal varices
splenomegaly
hepatic encephalopathy

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8
Q

Describe the pathologic finginds on liver biopsy of alcoholic steatosis

A

in the earlystages of alcohol abuse, the liver accumulates lipid and is enlarged

note - this is reversible with cessation of alcohol consumption

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9
Q

Describe the pathologic findings of alcoholic hepatitis

A

you get the fatty deposits AND evidence of hepatocyte injury or inflammation

lver cell swelling and necrosis, mallory bodies, neurophilic inflammation

can be accompanied by perivenular and pericellular fibrosis (steatofibrosis) which is a precursor to cirrhosis

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10
Q

What are mallory bodies?

A

aggregates of cytokeratin - can be seen in other liver diseases though (not specific for alcoholic liver disease

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11
Q

Describe the typical gross appearance of alcoholic cirrhosis

A

progressive fibrosis and liver cell necrosis resulting in bridging fibrosis with intervening hepatocytes regeneration in nodules

liver can be fatty and enlarged

late stages it will be shrunken though and cholestasis is uusally present

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12
Q

List the major causes of death in alcoholic cirrhosis

A

hepatic encephalopathy and coma
massive GI tract hemorrhage from esophageal varices
infections (spontaneous bacterial peritonitis)
hepatorenal syndrome
hepatocellular carcinoma

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13
Q

Define non-alcoholic fatty liver disease

A

it’s pathology similar to alcoholic steatosis and steatohepatitis but they don’t drink

patholoyg is virtually identical

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14
Q

What patient populations can get non-alcoholic fatty liver disease

A

patient with metabolic syndrome - obesity, type 2 diabetes, dyslipidemia, and insulin resistance

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15
Q

Define PBC

A

it’s an autoimmune destruction of the small and medium-sized intrahepatic bile ducts (but NOT the extraheptaic bile ducts)

can lead to cirrhosis

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16
Q

What type of patient typically gets PBC?

A

middle aged females, especially people of northern european ancestry (me)

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17
Q

What symptoms may be exhibited by a patient with PBC?

A

fatigue and ANICTERIC puritis - they just itch all the time

often discovered incidentally with lab tests for other disorders

later on xanthomas steatorrhea, vitamin D malabsorption with osteomalacia and osteoporosis

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18
Q

State a key diagnostic lab test for PBC.

A

elevated alkaline phosphatase

positive anti-mitochondrial antibodies (that target the E2 component of the mitochondrial pyruvate dehydrogenase complex)

note there are cases of AMA negative autoimmune cholangitis - they’ll be ANA positive and anti-smooth muscle like in AIH

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19
Q

What are the findings on liver biopsy in PBC?

A

stage 1: lymphocytic/granulomatous cholangitis around the portal tracts (may have loss of bile ducts)

2: periportal hepatitis with periportal fibrosis
3. briding necrosis and bridging fibrosis
4. cirrhosis

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20
Q

Define secondary biliary cirrhosis.

A

cirrhosis secondary to any disorder that cuasea a prolonged extrahepatic bile duct obstruction

it produces bile stasis, and bile is an irritating substance

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21
Q

What are some possible causes of secondary biliary cirrhosis?

A

stones, tumor, biliary atresia, cystic fibrosis, choledochal cysts

anything that blocks bile movement

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22
Q

Defome PSC

A

autoimmune cholangiopathy characterized by fibroinflammatory obliteration of BOTH intra and extrahepatic bile ducts (makes is different from PBC)

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23
Q

What is a key patient population that PSC can occur in?

A

men who have ulcerative colitis , middle age

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24
Q

How do you diagnose PSC?

A

key diagnostic test is cholangiography, which will demonstrate stricutres and dilations of the extrahepatic and intrahepatic bile ducts

looks like a beaded appearance

25
Q

Describe the key pathologic findings on liver biopsy in PSC?

A

you get inflammation obliteration of the bile ducts - jus tplugs

on cholangiography you see a beaded appearance

26
Q

Define hereditary hemochromatosis and describe the underlying pathogenesis.

A

disorder of excessive iron absorption resulting in the accumulation of iron in tissues

27
Q

State some of the clinical manifestations of hemachromatosis.

A

classic clinical triad is cirrhosis, diabetes and skin pigemtation (bronze diabetes)

can have arthralgias, lethary, hypogonadism, abdominal pain, cardiomyopathy

28
Q

What are the findings on liver biopsy in hemochromatosis?

A

iron accumulates in the hepatocytes of the periportal region initially

iron is directly cytotoxic, s you get fibrosis and micronocular cirrhosis

29
Q

How is hemochromatosis diagnosed?

A

clinical diagnosis, and liver biopdsy can be used where there is uncertainty about diagnosis

Iron will be high. Serum ferritin will be high. Very high transferrin staturation.

30
Q

What test would you use to screen for hemochromatosis?

A

fasting transferrin saturation

if elevated, repeat transferrin sturation with serum ferritin

if both elevated, order HFE gene test

31
Q

How is hemochromatosis treated?

A

phlebotomy or iron chelating agents

32
Q

Define secondary hemochromatosis.

A

build up of iron not form the genetic defect

33
Q

What are some causes of secondary hemochromatosis?

A

parenteral iron overload form transfusion

ineffective erythropoiesis with increased erythroid activity

increased oral intake of iron

chronic alcoholic liver dsiesase redistributes iron to the liver

34
Q

How does the liver biopsy of secondary hemochromatosis differ from hereditary hemochromatosis?

A

the iron will initially accumulate in the Kupffer cells and then only secondarily in hepatocytes

35
Q

Define Wilson’s disease

A

autosomal recessive disorder of copper etabolism resultin gin accumulation of toxic levels fo copper in tissues

mutation of ATP7B

36
Q

What are the abnormalities on key diagnostic tests in Wilson’s disease?

A

ceruloplasmin will be low because it can’t enter circulation

copper will accumulate in the liver and spill over into the blood for deposit in other tissues. also can be excreted by the kidneys, so they’ll have high copper in urine

overall serum copper levels are LOW because of the lack of ceruloplasmin

37
Q

What can be seen on eye exam in Wilson’s?

A

RIng of copper deposit at the limbus of the cornea - kayser Fleischer ring

38
Q

When should you consider Wilson’s disease as a diagnostic possibility?

A

In anyone less than 30 years of age with hepatitis and liver failure

39
Q

What is increase on the liver biopsy in Wilson’s?

A

liver pathology is not distinctive - can be steatosis, acute hepatitis, chronic hepatitis, cirrhosis or massive liver necrosis

liver biopsy will have inccreased hepatic copper - do quantitative because the copper stains can be negative

40
Q

Define alpha-1-antritryppin deficiency

A

autosomal codominant disorder with abnormally low levesl fo alpha-1-antitrypsin which is a protease inhibitor

41
Q

Describe and contrast the pathogenesis of the lung injury from the liver injury in alpha-1-antitrypsin deficiency

A

Risk for emphysema is directly related to the A1At level. DUe ot the imbalance of A1At and the elastase in the lung - without A1At, the elastase will break down the alveolar walls

Liver damage is NOT linked o the level of A1At - it’s independent. Mostly associated with Z and Mmalton - it’s due to the accumulation of mutant A1At in the hepatocytes. unfolded protein response triggers cell death.

42
Q

What test would you order to screen for alpha-1-antitrypsin deficiency>

A

alpha-1 antitrupsin level and phenotype

43
Q

What key findings can be seen on liver biopsy in alpha-1-antitrypsin deficiency?

A

globular inclusions of te protein in hepatocytes

You can stain it with PAS stain to see it better

44
Q

Describe the two main categories of drug=induced liver injury.

A

Direct hepatotoxicity: toxic to the liver in a predictable dose dependnet fashion (tylenol, muschroom poisoning)

Unpredictable (idiosyndratic) hepatotoxicity: produces injury in an unpredictable manner and not everyone gets the damage

45
Q

Define Reye’s syndrome

A

acute postviral illness with liver injury and encephalopathy

probably due to widespread mitochondrial injury

46
Q

What is the typical population that gets Reye’s syndrome?

A

children and teenagers following a viral infection, especially if they took aspirin

47
Q

How is Reye’s syndrome avoided?

A

don’t give aspirin for fevers

48
Q

What is the main finding on liver biopsy in Reye’s syndrome?

A

MICROvesicular steatosis and not macro….

49
Q

Define neonatal cholestasis

A

groups of disorders characterized by prolonged conjugated hyperbilirubinemia in the neonate because of impaired secretion of bile

two causes: biliary atresia and neonatal hepatitis

50
Q

Define biliary atresia

A

complete or partial obstruciton of the lumen of the extrahepatic bile ducts within the first 3 months of life

51
Q

Define neonatal hepatitis

A

hepatitis occuring in early infanty from many different disorders like biliary atresia, inherited metabolic disorders, tyrosinemia, etc.often idiopathic.

whole different beast than neonatal jaundice (which is physiologic)

52
Q

List com causes of granulomatous hepatitis.

A 
idiopathic (50%)
sarcoidosis
drug related
TB
PBC< Histo, Lymphoma
53
Q

List the four major types of the “liver funciton tests”

A
  1. Thins that look for hepatocellualr damage (AST, ALT)
  2. Markers of cholestasis (alk phos and GGT)
  3. Hepatic synthesis function tests (albumin and PT)
  4. Test to determine a specific etiology
54
Q

How can one use AST and ALT ?

A

AST is not specific to liver
ALT is mostly specific to the liver - so better than AST

Can use to help differentiate what’s the cause of the liver damage

80% of AST is in mitochondria, so ETOH abuse will hurt the mitochondria and release high levels of AST. Hense, AST:ALT is over 2.

55
Q

How can one use alkaline phosphatase?

A

increase usually due to eithe rbone or liver disease

in liver disease, it’s becaus eof increased synthesis of hepatic ALP which is found in the Canalicular membrane of hepatocytes,

the primary stimulus for this is bile duct obstruction

56
Q

How can one use GGT?

A

elevated GGT means the high alk phos is from the liver, not the bone

57
Q

How can you differentiate a hepatocellular injury pattern from a cholestasi injury pattern?

A

hepatocellular will have higher transaminases and lower alk phos

cholestasic injury will have higher alk phos and lower transaminases

58
Q

State the two reasons for doing a liver biopsy.

A
  1. Determine the cause of the liver disease

2. determine the extent of damage

59
Q

Define what grade and stage mean on a liver biopsy performed for chronic hepatitis infection.

A

grade is the severity of the necro-inflammatory activity

stage is the degree of fibrosis

GI Week 6 (14 decks)

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