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Clinical Pathology > 59 - Diseases of the hepatobiliary system > Flashcards

59 - Diseases of the hepatobiliary system Flashcards

1
Q

Jaundice is visible when bilirubin is >?

A

> 40umol/l

Commonest sign of liver disease

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2
Q

Jaundice has 3 types

A

Pre-hepatic - too much bilirubin made e.g. haemolytic anaemia, Gilbert’s syndrome

Hepatic - too few functioning liver cells

Post hepatic - bile duct obstruct

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3
Q

Bilirubin pathway

A

Bilirubin produced by RBC breakdown = uncojugated

Metabolised in liver - conjugated and excreted in bile

Some bilirubin is re-absorbed from gut

Also bile salts

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4
Q

Pre-hepatic is…

A

unconjugated

Bound to albumin, insoluble, not excreted - less dangerous

Yellow skin/dark eyes ONLY

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5
Q

Hepatic is…

A

Conjugated

Soluble = yellow eyes and dark urine

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6
Q

Post hepatic is…

A

Conjugated - soluble, excreted but can’t get into gut

Yellow eyes, pale stool and dark urine

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7
Q

LFTs test what

A 
ALT
AST
Alk Phos
Bilirubin
Albumin
Clotting factors
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8
Q

ALT, AST

A

Leak from hepatocytes due to injury

Mild increase over time = chronic liver

Very high levels = severe acute

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9
Q

Alk Phos

A

Leak from bile ducts

High in obstructive jaundice and chronic biliary disease

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10
Q

Histopathological features in liver with obstructive jaundice

A

Bile in liver parenchyma - jaundice in skin

Increasing with time: portal tract expansion, oedema, ductular rxn, bile salts and copper can’t get out, which accumulates in hepatocytes

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11
Q

Where would obstructive jaundice occur?

A

Bile pigment forms bile plugs that block intracellular canaliculli.

Swelling and irregularity of hepatocytes + increased Kupffer cells phagocytosis increases the issue

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12
Q

Obstructive jaundice long term effects pathogenesis

A

The portal tract gets larger - due to swelling (oedema with tissue looking pale), then ductular rxn (more small bile ducts around periphery of tracts).

More inflammatory cells inc. neurophils. Over time, liver sorts itself out, but the features combine to have characteristic biliary Gestalt.

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13
Q

Jaundice - investigation

A

USS for dilated ducts

Only if no dilated ducts is biopsy done

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14
Q

Cause of most non-obstructive cases of jaundice

A

Acute hepatitis

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15
Q

what is hepatitis?

A

inflammation of liver - any liver disease not neoplastic

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16
Q

Acute hepatitis - clinical presentation

A 
asymptomatic
malaise
jaundice
coagulopathy
encephalopathy
death
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17
Q

Acute hepatitis - causes

A

any dmg to hepatocytes

inflammation - viral, drugs, autoimmune, unknown

toxic - e.g. -OH, drugs (paracetamol)

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18
Q

Injury and death of hepatocytes is called what on a slide

A

lobular disarray

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19
Q

severe acute hepatitis with confluent necrosis

A

severe end of spectrum acute hep

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20
Q

acute hepatitis with bridging necrosis

A

Between portal tract and hepatic vein is bridge

intermediate severity

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21
Q

Chronic hepatitis - causes

A

immunological
toxic/metabolic - fatty liver disease, -OH, non-alcoholic fatty liver disease (NAFLD), drugs

Genetic in born errors - Fe, Cu, alpha1antitrypsin
Biliary disease
Vascular disease

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22
Q

Chronic hepatitis - pathology

A

Injury to liver cells, inflammation, scar tissue and regeneration of hepatocytes

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23
Q

Chronic hepatitis - progression

A

Scarring gradually increases and starts to link vascular structure (bridging)

Transform liver tissue into separate nodules - end-stage cirrhosis

24
Q

Viral hepatitides

A

Hepatotrophic viruses - A, B, C
D = delta, only in people with B
E = waterbourne, increasingly recognised in last few years - zoonosis

EBV
CMV
HSV - in immunocomp

25
Q

Table of slide 24

A

worth looking at

26
Q

-OH and liver

A

Spectrum of fatty change, alcoholic steatohepatitis and cirrhosis

Depends on dose and susceptibility

27
Q

-OH and liver biopsy

A

Features of steatohepatitis if long term alcoholic liver disease

if fatty change this is reversible

28
Q

Steatohepatitis

A

Van Gieson stain for collagen

Chicken wire appearance increases as well as portal tract fibrosis

-OHic characteristically very fibrotic with small nodules of hepatocytes

29
Q

NAFLD stands for

A

Non-alcoholic fatty liver disease

30
Q

NAFLD - presentation

A

steatosis
steatohepatitis
cirrhosis
HCC

31
Q

NAFLD - associated with

A

metabolic syndromes: obesity, T2DM, hyperlipidaemia and some drugs

32
Q

Hepatotoxic drugs -

A

Iatrogenic - induced inadvertently by a doctor, medical treatment or diagnostic procedures.

33
Q

Intrinsic hepatoxocity

A

e.g. paracetamol - every time, predictable

34
Q

Idiosyncratic hepatoxicity

A

Rare, unpredictable - metabolic, immunological

35
Q

Criteria for DILI

A

Onset of abnormal LFTs
50% reduction in LFTs after stopping drug
Alternative causes researched
Increase in LFTs by 100% if rechallenged

36
Q

Slide 38

A

look at paracetamol mechanism toxicity

37
Q

Paracetamol toxicity - treatment

A

IV - N-acetyl cystein

Restores - glutathione

Avoids liver cell damage

38
Q

Cirrhosis - defined

A

Histologically as a diffuse hepatic process characterised by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules

39
Q

Cirrhosis - pathogenesis

A

Liver cells still present, but portal vein blood bypasses sinusoids so liver cell cannot perform functions. Pressure in liver increases = portal hypertension

40
Q

Cirrhosis - causes

A

-OH
No-alcoholic steatohepatitis (metabolic syndrome)
Chronic viral hep - B, C
Autoimmune - primary biliary cirrhosis, primary sclerosing cholangitis
Metabolic - Fe, Cu, alpha1antitrypsin

41
Q

Cirrhosis - complications

A

Structural changes, fibrosis -> portal hypertension, increased blood flow, stiff liver, pressure rises in portal vein —–> oesophageal varices

Liver cell failure

Excretion

Reticulo-endothelial cells - vulnerable to infection

42
Q

Cirrhosis - liver cell failure complication

A

Fewer hepatocytes +/- blood bypass

Synthetic - oedema, bruising, muscle wasting

Detoxifying - drugs, hormones, encephalopathy

Ascites - low albumin, portal hypertension, hormone fluid retention (aldosterone)

43
Q

Cirrhosis - excretion complication

A

Bile - jaundice

Bile salts - itching

44
Q

Liver biopsy tests

A

Stage
Cause of disease
Current activity
Response to treatment

45
Q

Alpha-1-antitrypsin deficiency

A

Abnormal anti-protease which cannot be exported from hepatocyte - PAS +ve globules in hepatocytes

Accumulates in liver cells and injures them - cirrhosis

Insufficient in blood failure to inactivate neurophil enzymes - emphysema

46
Q

Haemochromotosis

A

Inborn error of iron metabolism - bronzed diabetes

Fe accumulates in liver - cirrhosis, pancreas - diabetes, skin - pigmented, joints - arthritis, heart - cardiomyopathy

Rx venesection to deplete iron stores to normal (take blood)

Also have high [transferrin] in serum

47
Q

Wilson disease

A

Inborn error of copper metabolism

Copper accumulates in liver - cirrhosis, eyes - Kayser-Fleischer rings, brain - ataxia

Treatment to chelate copper and enchance its excretion

48
Q

Systemic effects of liver failure

A 
Ascites
Muscle wasting
Bruising
Gynaecomastia
Spider naevi

Caput medusae - varices from umbilical vein collaterals

49
Q

Ascites is

A

Abnormal swelling due to fluid accumulating in the peritoneal cavity

50
Q

Spider naevi is

A

Small clusters of dilated capillary vessel in the skin due to hormone imblaance

51
Q

Caput medusae

A

Dilated veins radiating around the umbilicus in patients with severe portal hypertension due to recanalisation of the embryonic vitelline vein to the umbilicus

52
Q

Portal hypertension - definition

A

Increased pressure in portal veins

53
Q

Portal hypertension - main causes

A

Pre-sinusoidal, sinusoidal and post-sinusoidal

54
Q

Portal hypertension - complications

A

Splenomegaly - low platelets
Oesophageal varices - haemorrhage
Piles - perianal varices (most aren’t due to portal hypertension)
Part of cause of ascites

55
Q

Post-sinusoidal

A

Hepatic vein thrombosis = Budd Chiari syndrome

56
Q

Sinusoidal -

A

Cirrhosis

57
Q

Pre-sinusoidal

A

Portal fibrosis in cirrhosis

Non-cirrhotic portal hypertension caused by sarcoid, schistosomiasis, portal vein thrombosis

Clinical Pathology (65 decks)

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