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CLINICAL PATHOLOGY > Medical liver diseases > Flashcards

Medical liver diseases Flashcards

1
Q

Bilirubin metabolism

A

Produced by red blood cell breakdown in the spleen

It is then conjugated in the liver with glucuronic acid to make it soluble

It is excreted via bile

Bacteria in the gut make it unconjugated again

It is not absorbed - passed out of faeces

but a small amount is reabsorbed from gut and bile acids are secreted then reabsorbed

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2
Q

Jaundice and bilirubin

A

Jaundice is visible when bilirubin is >40umol/l

It is the commonest sign of liver disease

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3
Q

Pre-hepatic jaundice

A

too much bilirubin produced

haemolytic anaemia

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4
Q

hepatic jaundice

A

too few functioning liver cells

acute diffuse liver cell injury

end stage of chronic liver disease

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5
Q

post hepatic jaundice

A

bile duct obstruction by a stone, structure or tumour

usually in the bile duct of the pancreas

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6
Q

symptoms and signs of jaundice

A

Yellowing of skin and eyes for pre-hepatic

Yellow eyes, skin and dark urine for hepatic

Yellow eyes dark urine and pale stool for post hepatic

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7
Q

diagnostic pathway for jaundice

A

Ultra sound to check for dilation of ducts in obstruction

If no dilation, take a liver biopsy

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8
Q

Liver function tests for jaundice

A

increase of Alanine aminotransferase (ALT) and/or Aspartate aminotransferase (AST

Raised conjugated bilirubin without extrahepatic duct obstruction indicates disease of hepatocytes

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9
Q

Histopathology of jaundiced liver

A

First sign:
Bile in the liver parenchyma
(jaundice in the skin, patient is yellow)

Increasing with time:
Portal tract expansion, 
Oedema
Ductular reaction – proliferation of ductules around the edge of portal tracts
Bile salts and copper can’t get out
Accumulate in hepatocytes 
Bile salts in skin = itch
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10
Q

How is bile visible histologically?

A

Bile pigment is visible in the bile plugs which represent the bile that has been excreted by hepatocytes into intracellular canaliculi

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11
Q

Hepatitis - the different causes (8)

A 
Viral
Alcohol
Obesity
Drugs
Inherited haemochromatosis 
Wilson's disease
Alpha-1 antitrypsin deficiency
Autoimmune
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12
Q

Acute vs chronic hepatitis

A

Acute and Chronic refer to the time frame – acute hepatitis has a recent onset, and will resolve back to normal as long as the cause does not persist.

Chronic hepatitis has by definition been present for over 6 months, and results in ongoing liver cell injury and progressive structural liver damage of scarring and remodelling.

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13
Q

Causes of acute hepatitis

A 
things that damage hepatocytes, short term
Inflammatory injury (hepatitis) –
Viral, drugs, autoimmune, unknown (‘seronegative’)
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14
Q

Clinical presentation of acute hepatitis

A 
Asymptomatic, 
malaise, 
jaundice, 
coagulopathy, encephalopathy, 
death
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15
Q

Causes of chronic hepatitis

A

Immunological injury – virus, autoimmune, drugs

Toxic/metabolic injury – fatty liver disease,

Alcoholic or non- alcoholic fatty liver disease (NAFLD)
Drugs

Genetic inborn errors – iron, copper, alpha 1 antitrypsin

Biliary disease – autoimmune, duct obstruction, drugs,

Vascular disease – clotting disorders, drugs

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16
Q

progression of chronic liver disease

A

scarring gradually increases

starts to link vascular structures (bridging)

eventually transforming the liver tissue into separate nodules – end stage = cirrhosis.

A normal
B portal fibrosis
C bridging fibrosos
D cirrhosis

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17
Q

Types of hepatotrophic viruses

A

A, B, C
D = delta, only in people with B
E waterborne, increasingly recognised in UK in last few years, zoonosis, pigs

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18
Q

What viruses can cause Hepatitis?

A

EBV, CMV, HSV – usually immunocompromised host

Epstein barr
cytomegalovirus
herpes simplex

19
Q

Vaccines for Viral Hep

A

A and B have one but C does not

20
Q

Hepatitis A

A

Picorna RNA

21
Q

Hepatitis B

A

Hepadna DNA

22
Q

Hepatitis C

A

Flavivirus RNA

23
Q

As hepatitis progresses, the amount of fibrosis…

A

Increases
Portal areas become short and fibrous
Bridging occurs
Ending in cirrhosis

24
Q

Alcohol and the liver

A

1 Fatty change (steatosis)
2 Alcoholic steatohepatitis
3 Cirrhosis

Depends on dose and susceptibility

Significant driver of mortality from liver disease

25
Q

Histological signs of steatohepatitis

A

Fatty change
Ballooned hepatocyte with Mallory Body
Inflammatory cells

Fibrosis in portal tracts and around hepatocytes

26
Q

NAFLD - none fatty acid liver disease

what is it caused by and what is the Tx?

A

Same pathological spectrum as alcoholic liver disease

Associated with “Metabolic syndrome” – obesity, type 2 diabetes, hyperlipidaemia, also some drugs
Now recognised to be the commonest cause of liver disease
Treatment – address the causes of metabolic syndrome

27
Q

Steatosis vs. Steatohepatitis

A 
Steat = fatty change
Steatohepatitis = fatty change plus hepatocyte injury
28
Q

Hepato toxic drugs - Iatrogenic

A

induced inadvertently
by a doctor
or by medical treatment
or diagnostic procedures

29
Q

Classification of drug induced liver injury (DILI)

A

Intrinsic
every time, predictable
e.g. paracetamol

Idiosyncratic
- rare, unpredictable
metabolic or immunological

30
Q

Acute liver failure due to paracetamol

A

Metabolised in liver
5% toxic intermediary
Conjugated with Glutathione

Overdose:
Run out of glutathione
Antidote n-acetylcysteine if < 8 hours replenishes

0-24h Mild symptoms
Nausea, vomiting , sweating
24-72h Increasing liver cell death

3-5 days Massive necrosis, liver failure and death

31
Q

Haemochromatosis - what is it?

A 
Inborn error of iron metabolism
‘bronzed diabetes’
Iron accumulates in 
Liver - cirrhosis 
Pancreas - diabetes
Skin - pigmented
Joints – arthritis
Heart - cardiomyopathy
32
Q

What is inherited wilson’s disease?

A

Inborn error of copper metabolism
Usually presents at a younger age

Copper accumulates in
Liver – Cirrhosis
Eyes – Kayser-Fleischer rings
Brain – Ataxia, etc.

Treated by chelate copper and enhancement of its extraction using penicillamine

33
Q

What is alpha 1 antitrypsin deficiency?

A

Abnormal anti-protease which cannot be exported from hepatocyte

Accumulates in liver cells and injures them – cirrhosis

Insufficient in blood, failure to inactivate neutrophil enzymes: emphysema

34
Q

Autoimmune liver disease- autoimmune hepatitis

A

Mostly female patients

Auto-antibodies (anti-nuclear, smooth muscle, etc.), raised IgG, ALT, other autoimmune diseases

Liver biopsy – plasma cells, “interface” hepatitis

Can cause severe acute liver failure (needing transplant) or chronic disease (cirrhosis)

Treatment by immune suppression

35
Q

Primary biliary cholangitis - how does it present?

A

Anti-mitochondrial antibodies

Elevated alkaline phosphatase

Bile duct granulomas at early stage,

Then ductopenia (loss) and cirrhosis

36
Q

Primary sclerosing cholangitis (PSC) - how does it present?

A

Associated with ulcerative colitis, high alk phos
‘pruned tree’ on biliary imaging
Periductal “onion skin” fibrosis
then ductopenia and cirrhosis

37
Q

What is cirrhosis?

A

Diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.

Liver cells still present, but portal vein blood bypasses the sinusoids so the hepatocytes cannot perform their function

And often fewer liver cells (240 billion –> 172 billion)

Pressure inside the liver increases causing portal hypertension.

38
Q

Causes of cirrhosis

A

Alcohol
Non-alcoholic steatohepatitis (metabolic syndrome)

Chronic viral hepatitis – B, C

Autoimmune liver disease – autoimmune hepatitis,
primary biliary cirrhosis, primary sclerosing cholangitis

Metabolic – iron, copper, alpha 1 antitrypsin

39
Q

How does cirrhosis appear microscopically?

A

Regenerative nodules of hepatocytes

Surrounded by sheets of fibrous tissue

40
Q

Structural cell changes due to cirrhosis

A

fibrosis causing portal hypertension:

Increased blood flow, stiff liver

Pressure rises in portal vein

Oesophageal varices / haemorrhoids/ caput medusa

41
Q

Liver cell failure due to cirrhosis

A

fewer hepatocytes and blood bypasses sinusoids

Synthetic - oedema, bruising, muscle wasting

Detoxifying – drugs, hormones, encephalopathy

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

Failure of excretion:
Bile > Jaundice
Bile salts > Itching

42
Q

What is hepatic failure? How does it present in acute vs. chronic?

A

acute is just severe rapid liver injury

chronic leads to:
Ascites

Muscle wasting

Bruising

Gynaecomastia

Spider naevi

Varices, Caput medusae =

variceal umbilical vein collaterals

43
Q

Liver biopsy in chronic liver disease

A 
Can provide Information on:
Cause of disease
Current activity
Stage of disease
Response to treatment

CLINICAL PATHOLOGY (56 decks)

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