Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what stage is cirrhosis called?

A

stage 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hepatic necrosis

A

ACUTE cell death

can lead to acute liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

fulminant liver failure

A

acute liver failure complicated by coagulopathy and encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 3 complications of alcoholic liver disease

A

steatosis/fatty liver
alcoholic hepatitis
cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

alcoholic hepatitis

A

fat plus inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

tx for alcoholic HEPATITIS

A

abstinence, nutritional support

anti-inflammatory drugs (glucocorticoids, Pentoxifylline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

jaundice can be attributable to

A

many conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

alcoholic liver disease is histoliogically like

A

non-alcoholic fatty liver dis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

most common cause of elevated transaminases in the US

A

NAFLD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

risk factors for non alcoholic liver disease

A

abdominal OBESITY
hypertriglyceridemia
high fasting glucose/diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

causes of steatosis and steatohepatitis

A

alcohol
meds
nutritional (TPN, etc)
insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

therapeutic strategies for NAFLD

A

WEIGHT LOSS

for NASH:
vitamin E (first line)
pioglitazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

HFE gene

A

mutated in hereditary hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does HFE doe?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hemochromatosis occurs most commonly in what population?

A

Europeans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

clinical presentation of hereditary hemochromatosis

A

liver fxn abnormalities
SKIN HYPERPIGMENTATION-BRONZE
DIABETES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what gene combination results in hereditary hemochromatosis

A

C282Y/C282Y (homozygous recessive)

C282Y is the mutant form of the wildtype gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

C282Y/H63D suggests

A

10% chance of developing hereditary hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions