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Leila's Yr 5 Pathology > Chem path 4s - Liver disease CPC > Flashcards

Chem path 4s - Liver disease CPC Flashcards

1
Q

What does the portal triad consist of?

A

Hepatic portal vein
Hepatic artery
Bile duct

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2
Q

What does the portal triad consist of?

A

Hepatic portal vein
Hepatic artery
Bile duct

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3
Q

Why is the liver epithelium unique?

A

Fernestrated, means bloods comes in to contact with all the liver enzyme so by the time it reaches the central vein to be drained, all toxins have been removed.

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4
Q

What is the name given to the space between the hepatocytes and the endothelium?

A

Space of Disse

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5
Q

Which areas are zones 1 and zones 3?

A

Zone 1 = periportal

Zone 3 = Centrilobular (around central vein - least oxygenated)

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6
Q

Which zone most likely to become ischaemic?

A

Zone 3

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7
Q

Damage to zone 1 leads to a rise of which liver enzxyme?

A

ALP (portal triad close to bile ducts)

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8
Q

If you suspect a diagnosis of Gilbert’s, what investigaiton should you do?

A

Fasted bilirubin (Causes a further increase in bilirubin levels)

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9
Q

What investigations do you need to do for a pre-hepatic cause of jaundice?

A

Blood film + FBC

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10
Q

How do you measure the split bilirubin?

A

Using the van den Bergh reaction

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11
Q

What is the Van den Bergh reaction?

A

A direct reaction measures the conjugated Br
Then add methanol, allows you to measure total bilirubin
The difference between these two values is the unconjugated bilirubin (indirect)

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12
Q

Gilbert’s mode of inheritance and population prevalence who carry the gene?

A

Autosomal recessive

50% carry the gene

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13
Q

What % of the population actually have Gilbert’s?

A

6%

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14
Q

Pathophysiology of Gilbert’s

A

UDP glucuronyl transferase is reduced to 30%

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15
Q

Do you normally find bilirubin in the urine in Gilbert’s?

A

NO, unconjugated bilirubin is tightly bound to albumin and does not enter urine

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16
Q

What bilirubin product is found in the urine of normal people and what does the absence of this suggest?

A

Urobilinogen, sign of intact enterohepatic circulation

Absence suggests obstruction of biliary tree

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17
Q

What do bacteria in the bowel convert bilirubin in to?

A

Stercobilinogen and urobilinogen

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18
Q

Which marker is most representative of liver function?

A

Prothrombin time

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19
Q

What is a general rule regarding PT and time since paracetamol OD?

A

If the PT is higher than the hours since overdose, the patient should be trasnferred to a liver unit for transplant

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20
Q

Which three markers are representative of liver function?

A

Clotting factors (PT, aPTT
Albumin
Bilirubin

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21
Q

3 main features of hepatitis

A

Fever, jaundice and raised AST/ALT

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22
Q

Of the hepatitis viruses, which is the only DNA virus?

A

Hep B

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23
Q

When do you have onset of symptoms in hepA?

A

~2-6 weeks after exposure

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24
Q

Can you be infected by hepA more than once in your life?

A

NO

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25
Q

Is there a hepA vaccine?

A

Yes (havrix)

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26
Q

What % of pts go on to have chronic hepB?

A

~10%

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27
Q

When do you have onset of symptoms in hepB?

A

2-6 months followign ifnection

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28
Q

Which 2 antigens are measured in acute hepB infection?

A

HbSAg

HbEAg

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29
Q

Which antigen cannot be measured?

A

Core antigen

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30
Q

What is the presence of E antigen suggestive of?

A

That you are highly infectious

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31
Q

Which 3 anitbodies can be detected once you have fought HepB?

A

Anti-HbS
Anti-HbE
Anti-HbC

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32
Q

Hep B chronic carriers blood status

A

They never clear the virus but infectivity decreases with time.
HbSAg, anti-HbC, anti-HbE

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33
Q

Why is the liver epithelium unique?

A

Fernestrated, means bloods comes in to contact with all the liver enzyme so by the time it reaches the central vein to be drained, all toxins have been removed.

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34
Q

What % of people infected with Hep C develop chronic infection?

A

60-80%

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35
Q

Which areas are zones 1 and zones 3?

A

Zone 1 = periportal

Zone 3 = Centrilobular

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36
Q

Which zone most likely to become ischaemic?

A

Zone 3

37
Q

Damage to zone 1 leads to a rise of which liver enzxyme?

A

ALP (portal triad close to bile ducts)

38
Q

If you suspect a diagnosis of Gilbert’s, what investigaiton should you do?

A

Fasted bilirubin (Causes a further increase in bilirubin levels)

39
Q

What investigations do you need to do for a pre-hepatic cause of jaundice?

A

Blood film + FBC

40
Q

How do you measure the split bilirubin?

A

Using the van den Bergh reaction

41
Q

What is the Van den Bergh reaction?

A

A direct reaction measures the conjugated Br
Then add methanol, allows you to measure total bilirubin
The difference between these two values is the unconjugated bilirubin (indirect)

42
Q

Gilbert’s mode of inheritance and population prevalence who carry the gene?

A

Autosomal recessive

50% carry the gene

43
Q

What % of the population actually have Gilbert’s?

A

6%

44
Q

Pathophysiology of Gilbert’s

A

UDP glucuronyl transferase is reduced to 30%

45
Q

Do you normally find bilirubin in the urine in Gilbert’s?

A

NO, unconjugated bilirubin is tightly bound to albumin and does not enter urine

46
Q

What bilirubin product is found in the urine of normal people and what does the absence of this suggest?

A

Urobilinogen, sign of intact enterohepatic circulation

Absence suggests obstruction of biliary tree

47
Q

What do bacteria in the bowel convert bilirubin in to?

A

Stercobilinogen and urobilinogen

48
Q

Which marker is most representative of liver function?

A

Prothrombin time

49
Q

What is a general rule regarding PT and time since paracetamol OD?

A

If the PT is higher than the hours since overdose, the patient should be trasnferred to a liver unit for transplant

50
Q

Which three markers are representative of liver function?

A

Clotting factors (PT, aPTT
Albumin
Bilirubin

51
Q

3 main features of hepatitis

A

Fever, jaundice and raised AST/ALT

52
Q

Of the hepatitis viruses, which is the only DNA virus?

A

Hep B

53
Q

When do you have onset of symptoms in hepA?

A

~2-6 weeks after exposure

54
Q

Can you be infected by hepA more than once in your life?

A

NO

55
Q

Is there a hepA vaccine?

A

Yes (havrix)

56
Q

What % of pts go on to have chronic hepB?

A

~10%

57
Q

When do you have onset of symptoms in hepB?

A

2-6 months followign ifnection

58
Q

Which 2 antigens are measured in acute hepB infection?

A

HbSAg

HbEAg

59
Q

Which antigen cannot be measured?

A

Core antigen

60
Q

What is the presence of E antigen suggestive of?

A

That you are highly infectious

61
Q

Which 3 anitbodies can be detected once you have fought HepB?

A

Anti-HbS
Anti-HbE
Anti-HbC

62
Q

Hep B chronic carriers blood status

A

They never clear the virus but infectivity decreases with time.
HbSAg, anti-HbC, anti-HbE

63
Q

Hep B vaccinated antibody status

A

Anti-HbS but NO HbEAg or Anti-HbE

64
Q

Treatment of acute and chronic hepB

A 
Acute = supportive
Chronic = antivirals
65
Q

Hx of jaundice, hepatomegaly, weight loss, raised AFP

A

HCC

66
Q

Major risk factor for HCV

A

Blood transfusions (less of a risk factor for hepB), “history of thalassaemia”

67
Q

HCV commonly symptomatic or asymptomatic?

A

Asymptomatic presentation

68
Q

Increased risk of hep E infection in…

A

Expectant mothers

Immunocompromised

69
Q

What do balloon cells on liver histology suggest?

A

Alcoholic hepatitis

70
Q

Defining histology findings of alcoholic hepatitis

A

Liver cell damage - Ballooning degeneration + mallory hyaline (MALLORY-DENK BODIES)
Inflammation
Fibrosis

71
Q

What is the most common cause of liver disease in the western world?

A

Non-alcoholic steatohepatitis (NASH)

72
Q

Nutmeg liver?

A

Suggests venous congestion i.e. budd-chiari or congestive heart failure

73
Q

Features of chronic STABLE alcoholic liver disease

A

Palmar erythema
Duputyren’s contracture
Gynaecomastia
Caput medusa (>5)

74
Q

Signs of portal HTN

A

Ascites
Caput medusa/visible veigns
Splenomegaly

75
Q

Liver failure is defined by…

A

o Failed synthetic function
o Failed clotting factor and albumin production
o Failed clearance of bilirubin
o Failed clearance of ammonia (leads to encephalopathy)
 Flapping tremor (asterixis) = manifestation of hepatic encephalopathy

76
Q

What kind of fibrosis is seen in cirrhosis?

A

Micronodular fibrosis (small nodules)

77
Q

Appearance of a fatty liver

A

Pale, micronodular cirrhosis

78
Q

Sites of port-systemic anastamoses in liver disease

A

oesophageal varices
rectal varices
umbilical vein recanalising
spleno-renal shunt

79
Q

What makes you itchy in jaundice?

A

bile acids and bile salts

80
Q

Courvoisier’s law

A

Jaundice in presence of painless palpable gall bladder unlikely to be gall stones

81
Q

Where does pancreatic cancer typically metastasise to?

A

Liver

82
Q

Causes of macronodular liver changes

A

Viral hepatitis, Wilson’s disease, A1AT

83
Q

Autoimmune hepatitis type I

A

ANA, anti-SMA, Anti actin Ig, anti-soluble liver antigen Ig

84
Q

Autoimmune hepatitis type II

A

Anti-LKM Ig

85
Q

Drugs which cause chronic hepatitis

A

Methotrexate

86
Q

PBC associations

A

AMA, NO BILE DUCT DILATATION, bile duct loss

87
Q

PSC associations

A

pANCA, bile duct dilatation, BEADS ON A STRING, Cholanigocarcinoma, UC

88
Q

What score is used to determine prognosis in liver cirrhosis?

A

Child-Pugh

Leila's Yr 5 Pathology (100 decks)

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