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liver disease Flashcards

1
Q

causes of jaundice

A

medical doctors aren’t very happy
surgeons aren’t much better

Malignancy
Drugs
Antibiotics 
Viruses
Haematological
Stones 
Alcohol
Malignancy of pancreatic head
better
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2
Q

acute liver disease classified as ?

A

less than 6 months

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3
Q

what is acute liver disease/

A

the rapid development of hepatic dysfunction without prior liver disease causing encephalopathy and prolonged coagulation

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4
Q

investigations for liver disease?

A

LFTs, prothrombin time, history and examination , ultrasound, virology, rarely liver biopsy

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5
Q

tereatment of liver disease?

A

rest
NO ALCOHOL
increase calories

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6
Q

which kind of foods are poorly tolerated in liver disease?

A

high fat foods

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7
Q

what can you do for itch symptoms ?

A

sodium bicarbonate bath
cholestyramine
orseodeoxycholic acid

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8
Q

how long would hepatic drug reactions take?

A

6 weeks from exposure to effect

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9
Q

what is the definition of fulminant hepatic failure?

A

jaundice and encephalopathy in a patient with a previously normal liver

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10
Q

what is wilsons disease?

A

build up of copper in the body

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11
Q

what sign do you get in the eyes in wilsons?

A

kaiser Fleischer rings

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12
Q

causes of fulminant hepatic failure?

A

paracetamol, viral, drugs,

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13
Q

treatment of FHF?

A

inotropes and fluid, renal replacement, management of raised ICP

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14
Q

chronic liver failure time frame?

A

> 6months

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15
Q

what are the stages leading to cirrhosis

A

Inflamation –> fibrosis –> cirrhosis

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16
Q

PBC - what antibodies associated with it?

A

IgM and AMA

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17
Q

who typically gets PBC?

A

women, middle aged presenting with itch

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18
Q

In PBC, what would you expect to be up ?

A

GGT and ALP (bile)

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19
Q

In late disease in PBC, what would happen to bilirubin, prothrombin time and albumin?

A

bilirubin up, PT up, albumin down

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20
Q

in liver disease, when does albumin drop?

A

late

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21
Q

tx of PBC?

A

urseodeoxycholic acid and transplant

can give cholestyramine for itch

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22
Q

on histology, what would you see in PBC?

A

granulomas and bile duct loss (mum gran)

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23
Q

what would bile ducts look like in PBC?

A

chronic portal inflammation, bile ducts inflamed

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24
Q

ultimately, what could PBC progress to

A

cholestasis liver injury, inflammation, fibrosis and cirrhosis

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25
Q

who gets autoimmune hepatitis more? women or men?

A

women

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26
Q

what would you expect on examination in AIH?

A

hepatomegaly, splenpmegaly, jaundice

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27
Q

AIH - what markers are up? (AIG)

A

AST, ALT, IgG

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28
Q

Interface hepatitis, with marked piecemeal necrosis and lobular involvement, plasma cells?

A

autoimmune hepatitis

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29
Q

hw may yes of autoimmune hepatitis are there?

A

3

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30
Q

which one would be more common in children and young adults?

A

2

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31
Q

primary sclerosing cholangitis, big association with?

A

UC

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32
Q

what do you get destruction of in PSC?

A

destruction of large/medium sized bile ducts

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33
Q

how do you describe the appearance of fibrosis of bile ducts in PSC?

A

periductal ONION SKINNING fibrosis, jaundice, and fibrosis

34
Q

male or female patients more likely to get PSC?

A

male

35
Q

which kind of carcinoma is heavily associated with PSC(15%)

A

cholangiocarcinoma

36
Q

antibodies in PSC?

A

AMA -ve, ANA, SMA, ANCA may be positive

37
Q

sexual dysfunction in haemachromatosis?

A

men can’t get erection

38
Q

where is iron deposited in the liver?

A

portal connective tissue –> this stimulates fibrosis

39
Q

haemochromotosis - how long can it take to develop?

A

years - iron is deposited in the liver for years

40
Q

in haemochromotosis, what would you do in terms of the heart?

A

an ECG/echo - iron can be deposited in heart

41
Q

what is the treatment of haemochromotosis ?

A

venesection - continual removal of blood

42
Q

wilsons - what is the mode of inheritance?

A

autosomal recessive, same as haemochromotosis

43
Q

what is the copper binding protein called in which you get a loss of function in wilsons ?

A

caeruloplasmin

44
Q

where does copper accumulate in the body?

A

liver and the brain (basal ganglia)

45
Q

what kind of movements do you get in wilsons and what can it do to personality ?

A

chorea-athetoid movements

depression, mania, labile emotions, changed libido, personality change

46
Q

what would you see in eyes in wilsons?

A

kaiser Fleischer rings

47
Q

treatment of wilsons?

A

copper chelating drugs

48
Q

alpha 1 anti trypsin deficiency. as well as emphysema, what can this cause in liver?

A

liver damage through deposition of A1A

49
Q

what is budd chiari?

A

thrombosis of hepatic veins

50
Q

presentation of bud chiari?

A

jandice and ascites

51
Q

diagnosis of bud chiari?

A

hepatic vein ultrasound

52
Q

how could the heart cause cirrhosis?

A

secondary to high right heart pressure

53
Q
  • Final, irreversible common endpoint for liver disease
A

cirrhosis

54
Q

micronodular and macronodular cirrhosis. which one is alcoholic ?

A

micronodular mick

55
Q

complications of cirrhosis

A

portal hypertension, oesophageal varices, caput medusa, haemarrhoids

56
Q

what is encephalopathy?

A

brain damage, disease or malfunction

57
Q

why do you get encephalopathy in liver disease?

A

a build up of ammonia (liver removes ammonia from your body)

58
Q

classification to predict liver dysfunction /

A

child pugh (grade A -> C(most severe)

59
Q

causes of portal hypertension?

A 
pre hepatic (portal vein thrombosis or occlusion)
intrahepatic - presinusoidal (schistisomiasis) 
post sinusoidal (cirrhosis, alcoholic hepatitis, congeital fibrosis)
post hepatic  - bile problems
60
Q

intrahepatic causes of portal hypertension (pre and post sinusoidal)

A

pre sinusoidal - schistisomiasis and non cirrhotic portal hypertension
post sinusoidal - cirrhosis

61
Q

what is SBP?

A

spontaneous bacterial peritonitis

62
Q

what is SBP?

A

translocated bacterial infection of ascites

63
Q

what should you do in all ascites to investigate?

A

tap - neutrophil count (>250)

64
Q

treatment of ascites?

A

antibiotics and alba, terlipressin

65
Q

prevention of variceal bleeding?

A

BBlockers (propranolol and ligation)

66
Q

causes of jaundice ?

A

medical doctors aren’t very happy
surgeons are not much better

malignancy 
drugs
alcohol
viral
haematological 
stones
antibiotics 
malignancy of pancreatic head
67
Q

how would you identify biliary problems ?

A

us scan

68
Q

what is the treatment for hepatitis?

A

acute - supportive

chronic - interpheron alpha or antiviral/tenofovir etc)

69
Q

haematological what do you get in all infectious individuals in hep B?

A

HBsAG

70
Q

how is hep C spread?

A

by blood

71
Q

what is the progression of Hep C ?

A

acute and becomes chronic

72
Q

what does the presence of anti hb sag indicate?

A

clinical recovery and immunity

73
Q

Hep C is only an RNA vaccine, how do you test for it?

A

by PCR -> there is no vaccine

74
Q

is there a vaccine available for hep B?

A

yes

75
Q

markers of acute infection and chronic infection in hep B

A

♣ IgM antiHBc – acute infection

♣ IgG antiHBc – chronic infection

76
Q

how do you get hepatitis E?

A

undercooked, contaminated food

77
Q

what is the muscle in the cheek that moves during food mastication?

A

buccinator

78
Q

why do you need to be careful when using ferritin values for iron?

A

ferritin is an acute phase protein - may be synthesised in increased quantities during inflammation.

79
Q

how do you measure iron overload?

A

transferrin saturation (less than 50% in males and 45% in females)

80
Q

when would ferritin levels be decreased?

A

in iron deficiency anaemia

81
Q

what are both duputryens contracture and parotitis signs of?

A

alcoholic liver disease

GI (22 decks)

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