Diseases of the Hepatobiliary System 1 Flashcards Preview

Year 2 Clinical Pathology > Diseases of the Hepatobiliary System 1 > Flashcards

Flashcards in Diseases of the Hepatobiliary System 1 Deck (79)
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1
Q

At what level of bilirubin is jaundice visible?

A

> 40micromol/l

2
Q

What is the commonest sign of liver disease?

A

Jaundice

3
Q

What is the cause of pre-hepatic jaundice?

A

Haemolytic uraemia

4
Q

What is the general principle cause of hepatic jaundice?

A

Too few functioning liver cells

5
Q

Give 3 causes of hepatic jaundice?

A

1) Acute diffuse liver cell injury
2) End stage chronic liver disease
3) Inborn errors

6
Q

What is the cause of post hepatic jaundice?

A

Bile duct obstruction - eg. stone stricture or tumour (nb. could be in liver or pancreas)

7
Q

What kind of bilirubin is produced by red cell breakdown?

A

Unconjugated

8
Q

Where is bilirubin conjugated?

A

In the liver

9
Q

Pre-hepatic jaundice is raised levels of what kind of bilirubin?

A

Unconjugated, bound to albumin, not exctreted

10
Q

What are the 2 symptoms a patient notices with pre hepatic jaundice?

A

Yellow sclera
Yellow skin
ie. doesnt reach anywhere else as it is in soluble and cant be excreted

11
Q

What kind of bilirubin is raised in hepatic jaundice, is it soluble?

A

Mainly conjugated, soluble

12
Q

What are the 2 main symptoms that a patient notices with hepatic jaundice?

A

1) yellow eyes
2) dark urine
(Soluble so can get in urine)

13
Q

What kind of bilirubin is raised in post hepatic jaundice?

A

Conjugated - it is soluble but cant be excreted

14
Q

What 3 symptoms does a patient notice with post hepatic jaundice?

A

1) Pale stool
2) Yellow eyes
3) Dark urine

15
Q

What 2 liver enzymes leak from hepatocytes, how would there levels in acute and chronic liver disease differ?

A

AST and ALT
Chronic - mild increase over time
Acute - severe acute liver disease

16
Q

What enzyme leaks from bile ducts?

A

Alkaline Phosphate

17
Q

Is albumin raised or lowered in chronic liver disease?

A

Lowered

18
Q

Does albumin have a long or short half life?

A

Long half life

19
Q

Are clotting factors raised or reduced in liver disease?

A

Low in liver disease

20
Q

Do clotting factors have a long or short half life?

A

Short

21
Q

What is the first histopathological sign of obstructive jaundice?

A

Bile in the liver parenchyma (hence patient is yellow)

22
Q

As time goes on what are the 4 other histopathological signs of obstructive jaundice?

A

1) Portal tract expansion
2) Oedema
3) Ductular reaction - proloferation of duictules aroudn the edge
4) Bile salts and copper cant get out - accumulated in hepatocytes and patient gets itchy as bile salts accumulate in skin

23
Q

What are most non obstructive cases of jaundice due to?

A

Hepatitis

24
Q

What is the process of investigation of jaundice?

A

USS to check for dilated ducts in obstruction

Only in no dilated ducts then do a liver biopsy to look for cause of jaundice

25
Q

What is hepatitis?

A

Inflammation of the liver - essentially any liver disease that is non neoplastic

26
Q

What happens to liver enzymes in hepatitis?

A

Raised

27
Q

What is the broad difference between causes of acute hepatitis and chronic hepatitis?

A

Acute - caused by something which goes away

Chronic - caused by something which doesnt go away

28
Q

Doe hepatitis always have symptoms?

A

No - its commonly asymptomatic

29
Q

What are the 2 milder symptoms of hepatitis?

A

1) Malaise

2) Jaundice

30
Q

What can be the haematological effect of hepatitis?

A

Coagulopathy

31
Q

What are the 2 most serious presentations of hepatitis?

A

1) Encephalopathy

2) death

32
Q

What 2 things does the severity of the symptoms of hepatitis depend on?

A

1) The number of liver cells damaged

2) How good the liver regeneration is

33
Q

What are the 2 broad classes of causes of acute hepatitis?

A

1) Inflammatory - viral, drugs, autoimmune, unknown (sero negative)
2) Toxic/metabolic injury - alcohol, drugs, paracetemol

34
Q

Why can lobular disarray be seen in an acute hepatitis biopsy?

A

Lobular disarray = disordered appearance of the liver cell plates
Due to the injury and death of individual liver cells

35
Q

What are the 5 causes of chronic hepatitis?

A

1) Immunological injury
2) Toxic/metabolic injury - fatty liver disease, alcohol, NAFLD, drugs
3) Genetic inborn errors - iron, copper, alpha 1 anti-trypsin
4) Biliary disease
5) Vascular disease - clotting disorders, drugs

36
Q

What is the basic pathology of chronic liver disease?

A

1) Injury to liver cells
2) inflammation
3) Formation of scar tissue and regeneration of hepatocytes

37
Q

What are the 2 uses of biopsy in diagnosis of liver disease?

A

1) To determine the cause of damage - some causes have specific pathological features
2) To assess the stage of the disease - ie. how much scarring and where does it lie on the spectrum from normal to cirrhosis

38
Q

What is the pattern of scarring from normal liver to cirrhosis?

A

1) Scarring starts around portal tracts - this is portal fibrosis
2) Scarring then links portal tracts - bridging fibrosis
3) Scarring then links all vascular structures (portal tracts and central veins) - cirrhosis

39
Q

In addition to viruses hepatitis A, B and C, in which people is hepatitis D seen in?

A

Only people with heaptitis B

40
Q

How is hepatitis E transmitted, is it seen in the uk?

A

Waterborne - increasingly seen in the UK, zoonosis

41
Q

In addition to the hepatitis viruses what 3 other viruses can cause hepatitis as part of systemic disease?

A

1) EBV
2) CMV
3) HSV

42
Q

What is the route, of transmission, treatment and vaccine for Hep A?

A

Faecal-oral
No treatment
Ig Vaccine

43
Q

Can Hep A infection ever cause chronic hepatitis?

A

No

44
Q

What is the route, of transmission, treatment and vaccine for Hep b?

A

Parenteral
IFN and IV Iamivudine
Ig Vaccine

45
Q

What is the route, of transmission, treatment and vaccine for Hep C?

A

Parenteral
IFN and IV ribavirin
No vaccine

46
Q

Can hep b evolve to chronic hepatitis?

A

Yes in 10% of adults

47
Q

Can hep c evolve to chronic hepatitis?

A

Yes in over 70% of adults

48
Q

What are the 3 steps of the spectrum of alcoholic liver disease?

A

1) Fatty change
2) Steatohepatitis
3) Cirrhosis
(depends on dose and susceptibility)

49
Q

What is steatohepatitis?

A

Get fatty change (steatosis) = fatty deposits in the liver
Get inflammatory cells and ballooned hepatocytes with mallory bodies
Get fibrosis in portal tracts and around hepatocytes (pericellular fibrosis)

50
Q

What is non-alcoholic fatty liver disease?

A

Same spectrum as fatty liver disease but is associated not with alcohol but metabollic syndrome (type 2 DM, hyperlipidaemia and also some drugs)

51
Q

What is the commonest cause of liver disease?

A

NAFLD

52
Q

What is the treatment for NAFLD?

A

Address the cause of metabolic syndrome

53
Q

What is DILI?

A

Drug induced liver injury

54
Q

What is the broad causes of DILI?

A

iatrogenic

55
Q

In which 2 ways is DILI classified?

A

1) Intrinsic - anyone taking this drug is likely to get it

2) Idiosyncratic - depends on individual susceptibility, rare

56
Q

What ratio is used to classify the type of acute liver injury in DILI into hepatic, cholestatic or mixed?

A

Ratio of ALT:alk phos

57
Q

What is the most common symptoms of DILI?

A

Jaundice

58
Q

Does DILI tend to cause acute or chronic liver disease?

A

Acute as improves on stopping the drug but can sometimes cause chronic

59
Q

What are the 3 standard criteria for diagnosing DILI?

A

1) Onset of LFTs after intake of drugs
2) Improvement (reduction of 50%) in LFTs after stopping the drug
3) Alternative causes excluded, including by biopsy

60
Q

What is the basic mechanism of paracetemol toxicity?

A

1) Too much paracetemol exceeds the safe metabolic pathways (glucuronyl transferase and sulphotransferase)
2) Paracetemol then gets metabolised by P53 to a taxc metabollite NAPQ1
3) NAPQ1 binds covalently to heptocytes membrane proteins and causes necrosis

61
Q

What chemical can bind NAPQ1 to make it safe and stop it causing hepatocyte damage?

A

Glutathione

62
Q

What is the treatment for paracetemol toxicity, how does it work?

A

IV N acetyl-cysteine - restores glutathione

63
Q

how is cirrhosis defined?

A

Diffuse hepatic process characterised by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules - liver cells still present but cant perform function due to loss of hepatic lobules

64
Q

Why does portal hypertension occur in cirrhosis?

A

Increased blood flow to a stiff liver, pressure within the liver increases and in the portal vein - nb this can also lead to oesophageal varices

65
Q

What is the end point of chronic liver disease?

A

Cirrhosis

66
Q

What are the 5 common causes of cirrhosis?

A

1) Alcohol
2) NAFLD
3) Chronic viral hepatitis - C and B
4) Autoimmune liver disease - autoimmune hepatitis
5) Metabolic - iron, copper, alpha 1 antitrypsin

67
Q

Why are patients with cirrhosis vulnerable to infection?

A

Because the liver is an important sight of the immune response

68
Q

Cirrhosis can cause symptoms due to fewer hepatocytes through what 4 mechanisms?

A

1) Lack of synthesis - oedema, bruising, muscle wasting
2) Lack of detoxification - encephalopathy
3) Ascites - due to low albumin, portal hypertension, hormone fluid retention (aldosterone)
4) Lack of excretion - bilirubin = jaundice, bile salts = itching

69
Q

Alpha 1 anti trypsin deficiency is a metabolic disorder which can cause liver disease, how does it do so?

A

Abnormal anti protease made in the liver which cannot be exported from the hepatocyte - accumulates in the liver and injures them causing cirrhosis

70
Q

In alpha 1 anti trypsin deficiency the low levels of alpha 1 anti trypsin in the serum make patients vulnerable to which lung disease?

A

Emphysema

71
Q

In haemachromatosis, iron accumulates in what 5 organs, causing what conditions?

A

1) Liver - cirrhosis
2) Pancreas - diabetes
3) Skin - pigmented
4) Joints - arthritis
5) Heart - cardiomyopathy

72
Q

What is Wilson’s disease?

A

An inborn error of copper metabolism

73
Q

What 3 organs does copper accumulate in Wilson’s disease?

A

1) Liver -cirrhosis
2) Eyes - Kayser-Faisher rings
3) Brain - ataxia

74
Q

What is the treatment for Wilsons disease?

A

Chelate copper and enhance its excretion

75
Q

What is the therapy for haemachromatosis?

A

Venesection - to deplete iron stores to normal

76
Q

What are the 6 physical signs of cirrhosis?

A

1) Ascites
2) Muscle wasting
3) Bruising
4) Gynaecomastia
5) Spider Naevi
6) Caput medusae - varices from umbilical vein collaterals

77
Q

What is the definition of portal hypertension?

A

increased pressure of blood in the portal veins >12mmHg

78
Q

What are the 4 main complications of portal hypertension?

A

1) Splenomegaly - low platelets
2) Oesophageal varices - haemorrhage
3) Piles - perianal vairces but nb. most arent to do with portal hypertension
4) Part of cause of ascites

79
Q

Into which 3 categories can the causes of portal hypertension be classified?

A

1) Post sinusoidal - hepatic vein thrombosis
2) Sinusoidal - cirrhosis
3) Pre sinusoidal - portal fibrosis in cirrhosis and non cirrhotic portal hypertension such as sarcoid, schistosomiasis, portal vein thrombus

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