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Gastrointes 2 > 011215 hepatic inflam and fibrosis > Flashcards

011215 hepatic inflam and fibrosis Flashcards

1
Q

in fibrosis, where is periportal fibrosis?

A

around portal triad and extending a bit beyond

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2
Q

what stage is cirrhosis called?

A

stage 4

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3
Q

hepatic necrosis

A

ACUTE cell death

can lead to acute liver failure

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4
Q

fulminant liver failure

A

acute liver failure complicated by coagulopathy and encephalopathy

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5
Q

most common causes of acute and fulminant liver failure

A 
meds (acetaminophen)
viral hepatitis (causes fibrosis, which takes longer, and necrosis, which is acute)
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6
Q

pathophysiology of alcoholic liver disease

A 
increased NADH 
increased acetaldehyde (activates stellate cells to form collagen, microfilaments that maintain intracellular skeleton are sheared causing ballooning, Kupffer cells produce TNFalpha)
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7
Q

what changes do you see at the microscopic level with alcoholic liver disease?

A

dense extracellular matrix laid down in the space of Disse

loss of fenestrations in the sinusoids

loss of microvilli on hepatocytes

activated Kupffer cell

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8
Q

what are the 3 complications of alcoholic liver disease

A

steatosis/fatty liver
alcoholic hepatitis
cirrhosis

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9
Q

alcoholic hepatitis

A

fat plus inflammatory cells

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10
Q

risk factors for alcoholic liver dis

A

more than 30g alcohol/day in men, 20g/day in women

alcohol outside of meals
binge drinking

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11
Q

lab abnormalities in ALD

A 
AST/ALT ratio greater than 2
ALT usually under 300 IU/mL
rarely raised alk phos
low albumin
increased INR (advanced disease)
increased bilirubin

thrombocytopenia (advanced dis)
macrocytosis/anemia

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12
Q

tx for alcoholic HEPATITIS

A

abstinence, nutritional support

anti-inflammatory drugs (glucocorticoids, Pentoxifylline)

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13
Q

jaundice can be attributable to

A

many conditions

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14
Q

alcoholic liver disease is histoliogically like

A

non-alcoholic fatty liver dis

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15
Q

most common cause of elevated transaminases in the US

A

NAFLD

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16
Q

NAFLD is histologically categorized into 2 categories

A

non alcoholic fatty liver (NAFL)–abnormal liver tests, no ballooning of hepatocytes

non alcoholic steatohepatitis (NASH)–steatosis and inflam present. with hepatocellular injury (ballooning of hepatocytes) with or without fibrosis

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17
Q

prevalence of chronic liver disorders in US–what is most common?

A

nonalcoholic fatty liver, then
nonalcoholic steatohepatitis
then chronic hep C
then alcoholic liver dis

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18
Q

risk factors for non alcoholic liver disease

A

abdominal OBESITY
hypertriglyceridemia
high fasting glucose/diabetes

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19
Q

causes of steatosis and steatohepatitis

A

alcohol
meds
nutritional (TPN, etc)
insulin resistance

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20
Q

therapeutic strategies for NAFLD

A

WEIGHT LOSS

for NASH:
vitamin E (first line)
pioglitazine

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21
Q

HFE gene

A

mutated in hereditary hemochromatosis

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22
Q

what does HFE doe?

A

downregulates transferrin when iron supplies are adequate so that iron is not absorbed from small intestine

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23
Q

hemochromatosis occurs most commonly in what population?

A

Europeans

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24
Q

clinical presentation of hereditary hemochromatosis

A

liver fxn abnormalities
SKIN HYPERPIGMENTATION-BRONZE
DIABETES

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25
Q

what gene combination results in hereditary hemochromatosis

A

C282Y/C282Y (homozygous recessive)

C282Y is the mutant form of the wildtype gene

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26
Q

C282Y/H63D suggests

A

10% chance of developing hereditary hemochromatosis

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27
Q

tx for C282Y/C282Y hereditary hemochromatosis

A

if older than 40 or if elevated ALT/AST, consider biopsy to assess for cirrhosis

and phlebotomy

28
Q

two defects in Wilson’s disease

A

gene mutation in ATB7B

also can’t make enough ceruloplasmin

29
Q

pathophysiology of Wilson’s dis

A

due to mutation in ATB7B, liver can’t transport copper into biliary excretion to be fecally excreted

also, ceruloplasmin is reduced. so non-ceruloplasmin-bound copper deposits in liver

30
Q

what is one of the few diseases that can cause necrosis and fibrosis

A

Wilson’s disease

31
Q

damage in Wilson’s dis occurs mainly to

A

liver and brain

32
Q

ceruplasmin test for Wilson’s dis

A

not the best test b/c high levels will occur in inflam and may lead to false negatives

33
Q

Kayser Fleischer rings

A

Wilson’s disease

34
Q

tx for Wilson’s dis

A

Trientine (binds unbound copper to excrete in urine)

zinc (prevents copper absorption from GI tract)

35
Q

alpha1anti trypsin

A

inhibitor of the proteolytic enzyme elastase

36
Q

M gene

A

normal gene for alpha1anti trypsin. this gene produces normal amts of the protein

37
Q

the most common mutant form for alpha1 anti trypsin deficiency

A

Z

38
Q

what organs are involved in alpha1anti trypsin deficiency

A

lungs

liver

39
Q

the mechanisms for alpha1 anti trypsin deficiency disease

A

lung: loss of fxn mutation
liver: gain of fxn in that the small amts of A1AT are abnormal so they accumulate in liver and induce toxicity

40
Q

what form of A1AT deficiency causes lung disease only?

A

PiSZ

and Pi null-null

41
Q

what form of A1AT deficiency causes both lung and liver dis

A

PiZZ

42
Q

what do you find in the serum of autoimmune hepatitis pts?

A

autoantibodies against hepatocytes (IgG)

43
Q

the few things that have ALT, AST elevation over 1000

A

autoimmune hepatitis
viral hepatitis A, B
meds
ischemic

44
Q

interface hepatitis

A

around the portal triad

seen in autoimmune hepatitis

45
Q

plasma cell infiltrate

A

autoimmune hepatitis

46
Q

ANA, ASMA are positive in

A

type 1 autoimmune hepatitis

47
Q

anti liver kidney microsomal antibody is postive in

A

type 2 autoim hepatitis

48
Q

associated conditions of autoim hepatitis

A

THYROID DISEASE
RA
other autoimmune diseases

49
Q

tx for autoim hepatitis

A

prednisone and azathioprine combo

50
Q

primary biliary cirrhosis is a misnomer b/c

A

the disease can actually have stage 1-4 of fibrosis (only 4 is cirrhosis)

51
Q

PBC

A

chronic, progressive, cholestatic liver disease

destruc of intrahepatic ducts (the very small bile ducts)

52
Q

AMA +

A

PBC

53
Q

what markers do you see for PBC?

A

AMA positive

elevated IgM

54
Q

AMA targets what?

A

PDC E2 on the membrane of biliary epithelial cells

55
Q

symptoms of PBC

A

asymptomatic or

FATIGUE
PRURITUS

56
Q

itching-think?

A

bile duct problem

57
Q

xanthelasma (fat deposits)

A

PBC

58
Q

consequences of PBC?

A

steatorrhea

deficiency of vit A,D,E,K

59
Q

florid duct lesion

A

PBC

60
Q

florid duct lesion-define

A

lymphocytes and mononuclear cells causing inflam changes around bile ducts

61
Q

tx for PBC

A

ursodeoxycholic acid (a hydrophilic bile acid that balances the ratio of excessive hydrophobic bile acid accumulation in PBC)

for pruritis-use benadryl at night and cholestyramine during day

62
Q

Wilson’s dis pt-what ages?

A

3-40

63
Q

if synthetic fxn is intact, don’t think

A

cirrhosis

64
Q

meds can cause hepatocellular injury or cholestatic injury?

A

both

65
Q

can you burn out the bile ducts?

A

no (you can however burn out hepatocytes)

Gastrointes 2 (15 decks)

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