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GI- Week 6 > Nelson: Liver 2 > Flashcards

Nelson: Liver 2 Flashcards

1
Q

What is cirrhosis?

A

Hepatic disease characterized by widely distributed (diffuse) interconnecting fibrous scars with nodular parenchymal regeneration.

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2
Q

What is the MC cause of cirrhosis?

A

i. Alcoholic liver disease
ii. Viral hepatitis
iii. Biliary disease
iv. Hereditary hemochromatosis
v. Wilsons disease A1AT deficiency
vi. Cryptogenic cirrhosis (non-alcoholic fatty liver)

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3
Q

What are the 3 main causes of death associated w/ cirrhosis?

A

Progressive liver failure
complications of portal hypertension
hepatocellular carcinoma

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4
Q

What is hepatic failure?

A

Fibrosis destroying and impairing the normal vascular interconnection in the liver resulting in decreased hepatic profusion. May be the result of acute or (more commonly) chronic liver failure.

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5
Q

What causes Acute hepatic failure? What is the MCC?

A

secondary to massive hepatic necrosis (active Hep. A or B, drug/toxin). Most common cause is acetaminophen.

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6
Q

What causes chronic hepatic failure?

A

chronic liver disease associated with cirrhosis

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7
Q

How does hepatic failure manifest?

A

jaundice

Albumin/bleeding/ammonia/glucose/endocrine/drug metabolism changes

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8
Q

What are the MC causes of portal HTN?

A

Cirrhosis

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9
Q

What are the 4 main complications associated w/ portal htn?

A

ascites
portosystemic shunts (esophageal varices)
splenomegaly
hepatic encephalopathy

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10
Q

What is steatosis?

A

fatty liver

In early stages liver accumulates macro vesicular steatosis (large lipid vacuoles). Reversible with cessation of alcohol consumption.

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11
Q

What is steatohepatitis (alcoholic hepatitis)?

A

steatosis and evidence of hepatocyte injury and inflammation

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12
Q

Liver cell injury (swelling, necrosis), mallory bodies and neutrophillic inflammation are all signs of…

A

Steatohepatitis

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13
Q

What are mallory bodies?

A

cytokeratin aggregates that can also be seen in NADFLD and PBC

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14
Q

Describe the typical gross appearance of alcoholic cirrhosis in the early and late stages.

A

Early stages- liver is ENLARGED, FATTY and micronodular.

Late stages- SHRUNKEN, NONFATTY with variable size nodules and cholestasis is usually present.

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15
Q

What are the major causes of death in alcoholic cirrhosis?

A

Hepatic encephalopathy and coma
Massive GI tract hemorrhage (esophageal varices). Pic to right
Infection
Hepatorenal syndrome
Hepatocellular carcinoma (1-6% annual risk)

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16
Q

What is non-alcoholic fatty liver disease? What pt population can get this disease?

A

Hepatocyte injury similar to alcoholic steatosis and non-alcoholic steatohepatitis. (hepatocyte lipid accumulation and oxidative injury resulting in necrosis and inflammatory reaction)

Pts w/:
metabolic syndrome
obesity
type 2 diabetes
dyslipidemia
insulin resistance.
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17
Q

What is non-alcoholic fatty liver disease? What pt population can get this disease?

A

Hepatocyte injury similar to alcoholic steatosis and non-alcoholic steatohepatitis. (hepatocyte lipid accumulation and oxidative injury resulting in necrosis and inflammatory reaction)

Pts w/:
metabolic syndrome
obesity
type 2 diabetes
dyslipidemia
insulin resistance.
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18
Q

What is PBC?

A

Autoimmune cholangiopathy

Characterized
by:
progressive inflammatory destruction of small and medium intrahepatic bile ducts>
may lead to cirrhosis. Extrahepatic ducts spared.

Believed to be autoimmune, most patient have circulating antimitochondrial antibodies (AMA)

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19
Q

What pt typically gets PBC?

A

middle aged F of N european ancestry

*most have other autoimmune diseases

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20
Q

What lab findings are associated w/ PBC?

A

elevated alkaline phosphatase
GGT (cholestatic injury pattern)
positive AMA.

Biopsy determines loss of ducts and stage.

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21
Q

What are the 4 stages of PBC?

A

Stage 1 lymphocytic/granulomatous cholangitis in portal tracts. More commonly on change is loss of intrahepatic bile ducts with protal hepatitis
Stage 2 periportal hepatitis with periportal fibrosis
Stage 3 bridging necrosis with bridging fibrosis
Stage 4 cirrhosis (micronodular with bile stasis)

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22
Q

What are the 4 stages of PBC?

A

Stage 1 lymphocytic/granulomatous cholangitis in portal tracts. More commonly on change is loss of intrahepatic bile ducts with protal hepatitis
Stage 2 periportal hepatitis with periportal fibrosis
Stage 3 bridging necrosis with bridging fibrosis
Stage 4 cirrhosis (micronodular with bile stasis)

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23
Q

What are possible causes of secondary biliary cirrhosis?

A

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

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24
Q

What are possible causes of secondary biliary cirrhosis?

A

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

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25
Q

What is PSC?

A

Autoimmune cholangiopathy, progressive random and uneven fibroimflammatory obliteration of extrahepatic and intrahepatic bile ducts

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26
Q

What key pt population does PSC often occur in?

A

Male age 40.

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27
Q

How does a 40 y/o M w/ PSC present?

A

fatigue
pruritis
jaundice

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28
Q

How do you dx PSC?

A
  1. cholangiography>
    demonstrates strictures and dilation of extrahepatic and intrahepatic ducts (appears beaded)
  2. Biopsy> demonstrates focal fibrosing cholangitis (used for staging)
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29
Q

What is hereditary hemochromatosis? Inheritance pattern?

A

Hereditary = due to deceased synthesis of hepcidin>

excessive absorption of Fe

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30
Q

What is the pathogenesis of hereditary hemochromatosis?

A

Excessive iron absorption>
accumulation of iron in tissues>
tissue injury

31
Q

What are the clinical manifestations of hereditary hemochromatosis?

A
  1. Liver- iron accumulation in hepatocytes (periportal initially), directly toxic leads to fibrosis and micronodular cirrhosis.
  2. Pancreas- hemosiderin deposits in acinar and islets- diffuse fibrosis and atrophy
  3. Heart- hemosiderin deposits can have interstitial fibrosis
  4. Skin- hemosiderin in macrophages and fibroblasts and increased melanin may get slate gray skin.
  5. Endocrine- deposits in thyroid, adrenal, pituitary glands, may get atrophic testis.
  6. Joint synovium- deposits.
32
Q

What findings are found on liver biopsy in a pt w/ hereditary hemochromatosis?

A

Iron deposits in hepatocytes

33
Q

How is hereditary hemochromatosis dx?

A

Classic triad:
cirrhosis
diabetes
skin pigmentation

*Can also present with arthralgias, lethargy, hypogonadism, ab pain and cardiomyopathy.

34
Q

What test would you use to screen for hereditary hemochromatosis?

A

fasting transferrin saturation

35
Q

How is hemochromatosis treated?

A

phlebotomy or iron chelating agents

36
Q

What is secondary hemochromatosis?

A

Excessive iron accumulation in tissues from a non-hereditary source.

37
Q

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

A

HH= iron accumulates in hepatocytes

S= iron accumulates in Kupffer cells

38
Q

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

A

HH= iron accumulates in hepatocytes

S= iron accumulates in Kupffer cells

39
Q

What is Wilson’s disease? Inheritance?

A

AR

Disorder of copper metabolism resulting in accumulation of toxic levels in tissues (liver, brain eye).

40
Q

What abnormalities are present in a pt w/ wilson’s disease on key diagnostic tests?

A

LOW circulating ceruloplasmin levels (copper complexed to apoceruloplasmin, how it circulates in blood)

Increased 24 hour urine copper excretion.

Low serum copper levels.

41
Q

What can be seen on an eye exam of a pt w/ Wilsons disease?

A

deposits of iron at limbus of cornea (Kayser-Fleischer ring)

42
Q

What is increased on the liver biopsy in a pt w/ Wilsons disease?

A

biopsy will show increased hepatic copper which may present as negative stain but will be raised on quantitative testing

43
Q

What is increased on the liver biopsy in a pt w/ Wilsons disease?

A

biopsy will show increased hepatic copper which may present as negative stain but will be raised on quantitative testing

44
Q

What is alpha 1 antitrypsin def?

A

Codominant autosomal disorder

LOW levels of alpha-1-antitrypsin (protease inhibitor). Inhibits neutrophil elastase.

Liver produces A1AT glycoprotein at low levels

45
Q

How does lung injury differ from liver injury cuased by alpha-1-antitrypsin def?

A

Lung- imbalance between A1AT and neutrophil elastase (anti-protease/protease imbalance)> emphysema
Null-Null most severe

Liver- accumulation of A1AT in hepatocytes and not protease/anti-protease imbalance. Null-Null have no liver manifestation

46
Q

What key finding can be seen on liver biopsy of a pt w/ alpha 1 antitrypsin def?

A

cytoplasmic globular inclusions and PAS stain

47
Q

What key finding can be seen on liver biopsy of a pt w/ alpha 1 antitrypsin def?

A

cytoplasmic globular inclusions and PAS stain

48
Q

What are the two main categories of drug induced liver injury?

A
  1. Direct hepatotoxicity

2. Unpredictable hepatotoxicity

49
Q

What is unpredictable hepatotoxicity?

A

produce liver injury in an unpredictable manner

Not all exposed develop injury.

May be due to rate of metabolism or propensity for immune response.

50
Q

What is unpredictable hepatotoxicity?

A

produce liver injury in an unpredictable manner

Not all exposed develop injury.

May be due to rate of metabolism or propensity for immune response.

51
Q

What is Reye’s syndrome?

A

Rare acute POSTVIRAL illness with liver injury (microvesicular steatosis) and encephalopathy.

Also present with widespread mitochondrial injury.

52
Q

What pt population does Reye’s syndrome usually affect?

A

Usually in children and teens following viral infection.

95% having received salicylates (asprin).

53
Q

What is found on a liver biopsy in pts w/ reye’s syndrome?

A

Microvesicular steatosis, with small lipid vacuoles within hepatocytes.

*Can also be seen in acute fatty liver of pregnancy and tetracycline toxicity

54
Q

What is found on a liver biopsy in pts w/ reye’s syndrome?

A

Microvesicular steatosis, with small lipid vacuoles within hepatocytes.

*Can also be seen in acute fatty liver of pregnancy and tetracycline toxicity

55
Q

What is neonatal choletasis?

A

group of disorders with prolonged conjugated hyperbilirubinemia in neonates

56
Q

What is neonatal hepatitis?

A

cause of neonatal cholestasis

Hepatitis during early infancy (1-2mo).

57
Q

What is neonatal hepatitis?

A

cause of neonatal cholestasis

Hepatitis during early infancy (1-2mo).

58
Q

What are some causes of granulomatous hepatitis?

A

a. Idiopathic
b. Sacroidosis
c. Drug related
d. TB
e. Other

59
Q

What are the 4 major types of liver function tests?

A

AST
ALT
ALP
GGT

60
Q

ALT

A

alanine aminotransferase only small amount in other tissues.

More specific indicator of HEPATOCELLULAR injury

61
Q

AST

A

aspartate aminotransferase
present in other TISSUES elevation NOT liver specific.

80% found in mitochondria,

ETOH is mitochondrial toxin so AST:ALT ratio over 2 suggests ALCOHOLIC LIVER DISEASE disease.

62
Q

ALP

A

Alkaline phosphatase

increase usually indicates bone or liver disease

Increase in liver disease due to increased synthesis of ALP.

Found in canalicular membrane. Stimulus is BILE DUCT OBSTRUCTION.

63
Q

GGT

A

associated with biliary epithelium, assists in determining if ALP rise is due to BONE OR LIVER

64
Q

What tests are used to determine viral hepatitis?

A

serology, nuclear testing DNA/RNA

65
Q

What tests are used to determine AIH?

A

ANA

anti-smooth muscle ABs

66
Q

What tests are used to dtermine Wilsons?

A

ceruloplasmin

67
Q

What tests are used to determine a-1-a def?

A

a1at level

phenotype

68
Q

What tests are used to determine hemochromatosis?

A

Fe
TIBC
transferrin saturation
genetics

69
Q

What tests are used to determine primary biliary cirrhosis?

A

AMA-M2

70
Q

How do liver fxn tests distinguish a hepatocellular injury pattern from a cholestatic injury pattery?

A

AST and ALT- do not measure hepatic fxn. Elevations of these enzymes reflect HEPATOCELLULAR DAMAGE

Alkaline phosphatase and GGT (gamma glutamyl transpeptidase)- reflect INJURY TO BILE DUCTS epithelium/canailicular membrane markers of cholestasis.

71
Q

What reflects global hepatic synthesis fxn?

A

albumin
PTT
CF (factor V)

72
Q

What are the two reasons for doing a liver biopsy?

A

determine cause of liver disease

determine extent of liver damage

73
Q

What does grade mean on a liver biopsy for chronic hepatitis?

A

Severity of necro-inflammatory activity
i. Based on amount of lymphocytic piecemeal and lobular necrosis and inflammation present, also assessed with ALT elevation

74
Q

What does stage mean on a liver biopsy for chronic hepatitis?

A

degree of fibrosis

GI- Week 6 (14 decks)

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