Chemical Pathology - Liver disease CPC Flashcards

1
Q

What is the inheritance pattern of Gilbert’s?

A

Autosomal recessive

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2
Q

What test measures bilirubin, and how does it work?

A

van den Bergh test
Fractionation
A direct reaction shows the conjugated bilirubin
Additional of methanol shows total bilirubin
Therefore you can calculate uncojugated bilirubin

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3
Q

How can normal paediatric jaundice be distinguished from pathological paediatric jaundice?

A

physiological jauncide in neonates- the bilirubin will be unconjugated and it is just due to liver immaturity

if not or doesnt go away - look for rare causes like congenital hypothyroidism

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4
Q

How can normal paediatric jaundice be treated?

A

phototherapy

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5
Q

What would make jaundice worse in Gilbert’s?

A

Fasting

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6
Q

What is the abnormally-functioning protein that causes Gilbert’s?

A

UDP glucoronyl transferase - it is reduced to 30% activity

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7
Q

What increases in Gilbert’s - conjugated bilirubin, unconjugated bilirubin or both?

A

ONLY unconjugated bilirubin

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8
Q

What is the best marker of liver function in acute liver injury?

A

Prothrombin time

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9
Q

How can you tell that a paracetamol OD is bad enough to need transplant?

A

PT in seconds is > hours since OD

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10
Q

How does acute alcoholic hepatitis present?

A

Nausea, abdominal pain and jaundice
Pain is due to inflammation

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11
Q

What are 3 key histological findings that is pathognemonic for alcoholic hepatitis?

A

Mallory denk bodies
Megamitochondria
Fibrosis

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12
Q

Which antibody to hep A will be the first to be produced, and for what time period post-exposure to the virus will it be present in serum?

A

IgM
Initial production at 3 weeks
Peaks at 5 weeks
Gone by 13 weeks

note in hep A virus will be in faecaes from 2-4 weeks

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13
Q

Which immunoglobulin class provides long-term hep A immunity, and how soon after exposure is it produced?

A

IgG
From 5 weeks

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14
Q

From when, and for how long, does hep A cause jaundice in an infected person?

A

From 4 weeks, potentially until 8 weeks, post-exposure

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15
Q

What are the 2 markers of hep B infection that can first be identified in an infected person,

A

HbS antigen - infectivity or vaccinatin

and HbE antigen- infectivity

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16
Q

Which hepatitis antigen is most infectious?

A

HbE antigen

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17
Q

In a patient who successfully fights off Hep B, for how long are HbS and HbE present in serum?

A
HbS = 4 months 
HbE = 2 months
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18
Q

what does anti-HBc or HBcAb mean in hep B

A

past or current hepatitis B infection.

core antibody does not provide any protection against the hepatitis B virus unlike the surface antibody

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19
Q

What are the 3 key signs of portal hypertension?

A

Caput medusae
Splenomegaly
Ascites

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20
Q

What sign may be indicative of liver failure?

A

Asterixis - flapping tremor

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21
Q

If a patient has scratch marks, what does this tell you about their jaundice?

A

It must be post-hepatic, as itching is called by bile salts and bile acids

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22
Q

What is courvoisier’s law?

A

If gallbladder is palpable but painless, it is almost always pancreatic cancer causing the jaundice

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23
Q

give 5 genetic causes of cirrhosis

A

haemochromastosis
wilsons
A1AT def
galactosemia
glycogen storage disease

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24
Q

what drug can cause cirrhosis

A

methotrexate

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25
Q

the 3 main alcoholic liver diseases that cause cirrhosis

A

hepatic steatosis (fatty liver)
alcoholic hepaitits
alcoholic cirrhosis

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26
Q

micronodular cirrhosis is seen in

A

alcoholic cirrhosis

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27
Q

steatosis is seen in

A

fatty liver

(fully reversible if alcohol avoided)

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28
Q

who is autoimmune hep more common in? what is the associated HLA

A

78% female
HLA DR3
linked to the other autoimmune’s

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29
Q

2 types of autoimmune hep and the antibodies

A

type 1 = ANA (antinuclear Ig), anti SMA etc
type 2 = anti LKM (liver, kidney, microsomal) Ig

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30
Q

2 biliary causes of cirrhosis

A

PBC AND PSC

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31
Q

outline the main differences between PBC & PSC

A

PBC = inflammation of intrahepatic bile ducts, PSC = intra & extra hepatic bile ducts, structure formation
PBC = 10X more in F, PSC = M> F
PBC scan = no bile duct dilation, PSC = bile duct dilation
PBC = treat w ursodeoxycholic acid, PSC = linked to IBD (UC)

PSC - linked to chalngiocarcinoma, histology shows onion skinning fibrosis

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32
Q

PSC increases risk of what cancer

A

cholangiocarcinoma

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33
Q

histology of PBC vs PSC

A
PBC = bile duct loss w granulomas 
PSC = onion skinning (concentric) fibrosis
34
Q

are strictures are formed in PBS or PSC

A

strictures are in PSC, giving ending appearance of bile ducts

35
Q

outline 3 zones of the liver

A

zone 1 - closest to portal triad - peri portal hepatocytes
zone 2 - mid zone
zone 3- close to terminal hepatic vein, perivenular hepatocytes are most mature and metabolically enzyme. most liver enzymes.

36
Q

spotty necrosis on histopathology signifies

A

acute hepatitis (due to viruses a to e or drugs)

37
Q

piecemeal necrosis on histology indicates

A

chronic hepatitis

38
Q

is alcoholic hepatitis macro or micro nodular

A

micronodular

39
Q

give 3 macronodular causes of hepatitis

A

viral hepatitis
Wilsons
A1AT

40
Q

outline the 3 alcoholic liver diseases

A
  1. hepatic steatosis - fat droplets in hepatocytes
  2. alcoholic hepatitis - ballooning, mallory denk bodies
  3. alcoholic cirrhosis - micro nodular fibrosis

can reverse steatosis if alcohol avoided

41
Q

which hepatitis virus tends to cause chronic infection more commonly

A

HCV> HBV

42
Q

4 histopathological signs of cirrhotic liver

A

hepatocyte necrosis
fibrosis
nodules of regenerating hepaatocytes
disturbance of vascular architecture

43
Q

what score indicated prognosis in liver cirrhosis

A

modified Childs Pugh score
higher score = worse
under 7 = child Pugh A = HALF SURVIVE 5 YEARS
7-9 = child Pugh B = 20% SURVIVE 5 YEARS
10+ = child Pugh C = UNDER 20% SURVIVE 5 YEARS

total out of 15, 3 points for each indicator

44
Q

what are the 5 components of the child Pugh score

A

albumin
bilirubin
PT
ascites
encephalopathy

45
Q

what are 3 genetic causes of cirrhosis & inheritance

A

haemachromatosis - AR
Wilsons - AR
A1AT def - AD

46
Q

what gene is affected in haemachromatosis

A

HFE gene

47
Q

what gene is affected in Wilsons

A

ATP7B on chromosome 13

48
Q

histolgoical finding of haemochromatosis

A

iron deposits in liver stain w Prussian blue

49
Q

main histo finding of Wilsons

A

copper stains w rhodaNine

50
Q

histolgoical findings of A1AT def & what stain used

A

intracytopalmsic inclusions of A1AT which stain with periodic acid Schiff

51
Q

3 main signs in haemochromatosis

A

skin bronzing (melanin deposition)
diabetes
hepatomegaly

52
Q

triad of Wilsons signs

A

liver disease
neuro disease (basal ganglia involvement)
Kayser flesicher rings

53
Q

presentation of A1AT in children vs adults

A
children = neonatal jaundice 
adults = emphysema and chronic liver disease
54
Q

3 iron results in haemochromatosis

A

iron and ferritin increased
transferrin saturation over 45%
TIBC decreased

55
Q

3 blood results in Wilsons

A

serum careuloplasmin decerased
serum copper decreased
urinary copper Increased

56
Q

2 results of investigations in A1AT def

A

A1AT decreased
absent alpha globulin band on electrophoresis

57
Q

2 treatments for haemochromatosis

A

venesection
desferrioxamine

58
Q

drug for Wilsons

A

life long penicillamine

59
Q

state 2 benign liver tumours? which is most common

A
haaemangioma (most common, no treatment needed) 
hepatic adenoma (linked to COCP)
60
Q

state 4 malignant liver tumours

A

hepatocellular carcinoma
cholangiocarcinoma
haemangiosarcoma
hepatoblastoma

61
Q

what is deposited in the space of disse in liver injury

A

collagen

62
Q

what are liver macrophages called

A

kupffer cells

63
Q

biomarker for HCC?

A

alpha fetoprotein

64
Q

which malignant tumour tends to arise in those w chronic liver disease

A

HCC

65
Q

which malignant tumour presents as an abdominal mass, originating from immature liver precursor cells

A

hepatoblastma

66
Q

which malignant liver tumour is highly invasive

A

haemoangiosarcoma
cancer of vascular epithelium

67
Q

what is the most common cause of malignant liver lesions

A

usually multiple secondary tumours from GIT, breast or bronchus

68
Q

transmission of hep A & hep E plus type of infection

A

BOTH =
acute
fAeco-oral -
food (shellfish) or men or men sex
hep A - contaminated water
hep B- also uncooked pork

69
Q

treatment of hep A

A

after jaundice and fever symptoms IgG is produced so cured and immune

70
Q

hepatitis D requires co infection with

A

hepatitis B

71
Q

what antigens are typically measured in hep B? what do they signify

A

HBsAg - Hepatitis B surface antigen = infected
HBeAg = infected & can spread

HBsAb - indicates that a person is protected/immune against the hepatitis B virus througb vaccination or naturally.

if vaccinated you’ll have anti HBs but NOT HBe

72
Q

what % of hep B go on to be chronic compared to hep C

A

hep B only 10% go on to be chronic
hep C up to 80% go on to be chronic

73
Q

HBV & HCV are associated w what liver cancer

A

HCC

74
Q

give a risk factor for HCV

A

thalsscemia due to recurrent transfusions
transfusions/blood product spread are a MAJOR risk factor for HCV (much less so in HBV)

75
Q

what types of viruses are hep B & C

A

hep B - DNA
hep C - RNA

76
Q

is hep B or hep C more commonly transmitted through unprotected sex

A

hep B more so

77
Q

give a drug that can cause chronic hep

A

methotrexate

78
Q

3 signs of portal hypertension

A

caput medusae
ascites
spelnomegaly

79
Q

4 signs of chronic stable (alcoholic) liver disease

A

palmar erythema
gynaecomastia (liver can’t break oestrdiol down)
spider nave > 5
duputryens contracture

80
Q

3 vitamin to give in alcoholic hep

A

B1 - thiamine - beri beri
B3 -niacin - pellagra
B12 - cobalamin - B12 def/SCDC

81
Q

what does courvoiseirs law state

A

if gallbladder is palpable in jaundiced patient, unlikely to be gallstones (ie probs pancreatic cancer which foot mets to liver)

82
Q

itching is a sign of what type of jaundice

A

obstructive