Liver- Cirrhosis & Neoplasms Flashcards Preview

Unit 6: Pathology > Liver- Cirrhosis & Neoplasms > Flashcards

Flashcards in Liver- Cirrhosis & Neoplasms Deck (43)
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1
Q

what mediates (what cytokine) fibrosis in cirhosis

A

TGF-B from stellate cells which lie beneath the endothelial cells that line the sinusoids

2
Q

what are 4 things that portal HTN leads to?

A
  1. ascitis
  2. congestive splenomegaly/hypersplenism
  3. portosystemic shunts
  4. hepatorenal syndrome
3
Q

what are the 3 classical portosystemic shunts

A

esophageal varices, hemorrhoids and caput medusae

4
Q

what is hepatorenal syndrome

A

rapidly developing renal failure secondary to cirrhosis

5
Q

what causes the eventual coma in cirrhosis

A

increased serum ammonia levels

6
Q

what are some SE that can be seen because the loss of the liver’s ability to metabolize estrogen

A

gynecomastia
spider angiomata
palmar erythema

7
Q

how do you follow the degree of coagulation factor deficiency caused by hepatic cirrhosis?

A

follow the PT

8
Q

what is the most common cause of liver disease in the west?

A

alcohol related liver disease

9
Q

what is the appearance of the liver in alcohol related liver disease

A

heavy, greasy liver (resolves with abstinence)

10
Q

what metabolite of alcohol mediates the cell damage?

A

acetaldehyde

11
Q

what are mallory bodies and when are they seen?

A

they are damaged cytokeratin filaments and they are seen in alcohol related liver disease

12
Q

what liver enzyme is more elevated in alcoholic related liver disease?

A

both AST and ALT are elevated but AST it more markedly elevated

13
Q

so some one has fatty liver disease and they sayyyy they dont drink but you know that sometimes people hide that shitttt so how do you tell if his fatty liver is due to alcohol or not

A

NONalcoholic fatty liver disease is a diagnosis of exclusion.. so you gotta have some faith in da patient

but also their ALT will be “more elevated” than their AST (and its opposite in alcoholic related fatty liver)

14
Q

what word..

“ excess body iron leading to deposition in tissues”

A

hemosiderosis

15
Q

what word..

“ excess body iron leading to deposition in tissues and organ damage”

A

hemachromatosis

16
Q

what is technically causing the damage in hemachromatosis

A

formation of free radicals

17
Q

what causes primary hemachromatosis?

A

due to mutation in HFE gene (usually C282Y)

18
Q

what causes secondary hemachromatosis?

A

chronic transfusions

19
Q

what is the classic triad of symptoms seen in hemachromatosis

A

cirrhosis, secondary DM and bronze skin

20
Q

what are some other signs/symptoms that can be see in hemachromatosis (besides the triad)

A

dilated cardiomyopathy
cardiac arrhythmias
gonadal dysfunction (due to testicular atrophy)

21
Q
what do the labs show in hemachromatosis
ferritin
TIBC
serum iron
% saturation
A

ferritin- increase
TIBC- decrease
serum iron- increase
% saturation- increase

22
Q

soooo normal aging of the liver will show brown spots (lipofuscin), but you’re telling me that in hemachromatosis there is also brown spots in the liver, so when i get a tricky question how am i suppose to know what the cause is

A

prussian blue stain distinguishes iron (blue) from lipofuscin

23
Q

you have a recessive defect in ATP7B, what disease do you have? what does this gene encode for?

A

wilsons disease

gene encodes for an ATP mediated hepatocyte copper transport

24
Q

how does wilsons disease present

A

presents in childhood with cirrhosis, neurologic manifestations and kayser fleisher rings in cornea

25
Q

what do the labs show in wilsons disease
urinary copper
serum ceruloplasmin
copper on liver biopsy

A

urinary copper- increase
serum ceruloplasmin- decrease
copper on liver biopsy-increase

26
Q

what is the treatment for wilsons (im just asking this bc its a pharm tie in and we gotta start thinking about that shiz)

A

D-penicillamine (chelates copper)

27
Q

what disease

“autoimmune granulomatous destruction of intrahepatic bile ducts”

A

primary biliary cirhosis

28
Q

what population does primary biliary cirrhosis present in?

A

woman, average age 40

29
Q

how does primary biliary cirrhosis present?

A

obstructive jaundice

30
Q

what disease

“inflammation and fibrosis of intrahepatic and extrahepatic bile ducts”

A

primary sclerosing cholangitis

31
Q

how does primary sclerosing cholangitis appear?

A

periductal fibrosis with “onion skin” appearance

uninvolved regions are dilated–“beaded appearance”

32
Q

what GI disease is primary sclerosing cholangitis associated with?

A

ulcerative colitis

YOU BETTER KNOW THIS. I BET $$ ITS GONNA BE A QUESTION

33
Q

what marker is often + in primary sclerosing cholangitis

A

p-ANCA

34
Q

what cancer are people with primary sclerosing cholangitis at an increased risk for?

A

cholangiocarcinoma

35
Q

what disease

“fulminant liver failure and encephalpathy in children with viral illness who take aspirin”

A

reye syndrome

36
Q

how does reye syndrome present

A

hypoglycemia, elevated liver enzymes, N/V

can progress to coma and death

37
Q

hepatic adenoma is associated with..

A

oral contraceptives

38
Q

hepatic adenomas are benign but carry some risks, what are these

A

rupture and intraperitoneal bleeding (esp during prego because the tumors grow in response to estrogen)

39
Q

what are the 3 risk factors for hepatocellular carcinoma

A

chronic hepatitis (HBV, HCV)
cirrhosis
aflatoxins from aspergillus

40
Q

what do aflatoxins from aspergillus do

A

induce p53 mutations

41
Q

what is the serum tumor marker for hepatocellular carcinoma

A

alpha fetoprotein

42
Q

how does budd chiari syndrome present (a complication of hepatocellular carcinoma)

A

painful hepatomegaly and ascitis

43
Q

what is the most common cancer in the liver

A

metastases

most common locations are colon, pancreas, lung and breast