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Year 3 > Case 3 - Liver Disease > Flashcards

Case 3 - Liver Disease Flashcards

1
Q

What is the definition of acute hepatitis?

A

Liver disease presenting with feeling generally unwell with jaundice
Can progress to fulminant, chronic or recovery
Increased ALT/AST/ALP/Bilirubin
Severe cases will show coagulopathy and encephalopathy when fulminant has set in, also renal failure

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2
Q

What is the definition of chronic hepatitis?

A

Low grade inflammation of the liver which is often asymptomatic
There is fibrosis then cirrhosis
Damage is reversible at the fibrosis level if the trigger is removed, but not at the cirrhosis level
Usually only present when cirrhosis has set in
Mild increase in ALT seen

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3
Q

What is the definition of fulminant hepatitis?

A

The onset of hepatic encephalopathy within 28 days of jaundice due to an acute hepatitis episode
High mortality - often needs transplant

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4
Q

What is the definition of alcoholic liver disease?

A

The liver undergoes steatosis due to alcohol, DM and increase in weight
Can skip straight to alcoholic hepatitis in a large binge and skip the fatty liver stage

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5
Q

What is the definition of cirrhosis?

A

The point at which the chronic liver disease fibrosis is non-reversible
The only end point is death, cannot reverse the progress now

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6
Q

What are the causes of liver disease?

A

Lifestyle:

  • Obesity
  • DM
  • Alcohol excess

Hereditary:

  • Hereditary haemochromatosis
  • Alpha-1-antitrypsin deficiency
  • Wilson’s disease

Drugs:

  • Methotrexate
  • Rifampicin
  • Paracetamol
  • Anti-epileptics
  • Flucloxacillin

Infective:

  • Hep A, B, C
  • EBV
  • CMV

Extrahepatic:

  • Gallstones
  • Ca of head of the pancreas

Autoimmune:

  • Autoimmune hepatitis
  • PBC
  • PSC
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7
Q

What is hep A?

A

Causes acute hepatitis
Usually self-limiting, can become fulminant
Spread F-O and endogenous in the developing world
Can immunise those who are travelling/have liver disease
The body’s Ig rise in accordance with the virus - IgM first and then IgG

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8
Q

What is hep B?

A 
Causes acute and chronic hepatitis
Preogression to chronic more likely with:
-Low age
-Immunosuppressed
-Route of infection 
-Genotype

Carcinogenic virus, with no definite cure
Can be vaccinated against though
Rate of fibrosis and viral load determine the progression

Can be passed through vertically/sexually/blood e.g. MSM, IVDU
Treat with interferons and antivirals (entecavir/tenofavir), but these do not interfere with the cell cycle and therefore do not cure

HBsAg = infected acutely/chronically
Anti-HBs = could indicate a previous infection or vaccine
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9
Q

What is hep C?

A

Causes acute and chronic hepatitis
Can be treated, but there is no vaccination
Test for antibodies, then PCR for viral RNA
Can be transmitted through blood and bodily fluids e.g. unsterile medical equipment, can be transmitted vertically/sexually, but this is rare
Treat with protease inhibitors and ribavirin
Should screen donors, MSM, HIV positive or those with deranged LFTs

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10
Q

What is hep delta?

A

Can only replicate in the presence of hep B

Worsens prognosis of hep B

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11
Q

What is hep E?

A

Causes acute hepatitis

High mortality in pregnant women

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12
Q

What are the signs of chronic liver disease?

A 
Gynaecomastia
Hair loss
Spider naevi
Dupuytrens Contracture
Palmar Erythema
Caput medusa
Leukonychia
Varices
Piles
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13
Q

What are the signs of liver decompensation?

A 
Ascites
Jaundice
Encephalopathy i.e. liver flap
Oedema
Bleeding
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14
Q

What could be the triggers for decompensation?

A 
Constipation
Infection
Alcoholic binge
Drugs
GI bleed
Metabolic
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15
Q

What is the physiology of jaundice?

A

Bilirubin is a breakdown product of RBC
Haem > Biliverdin > Bilirubin
Therefore when there’s more haemolysis (pre-hepatic), there will be increased bilirubin
Increased bilirubin > jaundice

Bilirubin converted using the enzyme glucuronyl transferase to become conjugated - making it more soluble
It is extricated in the bile
Flows into GI tract, where it becomes reabsorbed
Flow back to liver to become metabolised

Pre-hepatic > more unconjugated, same conjugated as the enzyme is saturated

Hepatocellular damage > can lead to either conjugated/unconjugated hyperbilirubinaemia

Post-hepatic (obstructive) > increase in conjugated, low unconjugated as the less soluble unconjugated cannot escape the liver

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16
Q

What signs would pre-hepatic liver disease show?

A

Increased bilirubin
Increased unconjugated bilirubin
No change in ALT or ALP
No change in stool or urine colour

17
Q

What signs would hepatocellular liver disease show?

A 
Increased bilirubin
Increased unconjugated bilirubin
V high ALT
Normal/slightly high ALP
May show change in stool and urine colour - if conjugated high and present in urine
18
Q

What signs would obstructive liver disease show?

A 
Increased bilirubin
Increased conjugated bilirubin
V high ALP
Normal ALT
Pale stools
Dark urine
19
Q

What investigations could you do for liver disease?

A

Bloods:

  • LFTs to compare ALT and ALP, bilirubin
  • GGT
  • AFP (liver tumour marker)
  • Clotting

USS:

  • To look for duct dilatation
  • If there’s no dilatation, then it’s hepatocellular or pre-hepatic
  • If there’s dilatation, do CT to look for stones

For alcoholic liver disease:

  • Liver biopsy
  • Assess for transplant if they still have compensation after 3 months of best treatment and abstinence
20
Q

What is alcohol withdrawal?

A

Can lead to delirium tremens - seizures, tremor, sweatyencephalopathy etc.
Stop drinking gradually
For symptoms use lorazepam or carbemazepine
Should be treated with oral lorazepam > IV lorazepam > IV haloperidol
Use lorazepam for seizures

21
Q

What would an ascitic tap show?

A

Albumin-ascites gradient (Serum albumin - ascites albumin)
>1.1 g/dL=transudate. Due to portal HTN ie. cirrhosis, nephrotic syndrome etc.
<1.1 g/dL = exudate. Due to peritoneal disease e.g. TB, cancer

> 500 WBC/mm3 = SBP

22
Q

Pathophysiology of cirrhosis and the signs of chronic liver disease

A

Regenerative noduels in the liver
Stellate cells are in the perisinusoidal space (between hepatocyte and sinusoid), usually dormant
Hepatocyte damage > stellate activation > loss of vitamin A
There is replication of TGF-beta and collagen
Fibrotic tissue builds up > compresses sinusoids > portal HTN
Fluid leaks out = ascites
Back flow from the portal vein > splenomegaly and renal failure

Year 3 (23 decks)

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