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CR/MET PBLs > PBL2: Liver Disease > Flashcards

PBL2: Liver Disease Flashcards

1
Q

What is cirrhosis?

A

The end stage of chronic liver disease characterised by fibrosis, scarring and nodular degeneration.

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2
Q

What are the causes?

A 
Hepatitis B and C
Wilson's disease
Alcohol haemochromatosis
Autoimmune liver disease
Primary biliary cirrhosis
Recurrent biliary obstruction
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3
Q

How can hepatitis B and C cause liver disease?

A

Cause hepatocellular carcinoma which goes on to form cirrhosis

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4
Q

How is hepatitis B and C spread?

A

Spread through blood tranfusion/body fluids/ contaminated instruments/sexual contact/surgery/tatoos/needles

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5
Q

What is alcohol haemachromatosis?

A

High iron levels

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6
Q

What is Wilson’s disease?

A

Disorder in metabolism of copper

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7
Q

What is primary biliary disease?

A

Inflammatory disease on bile ducts so get infiltration of lymphocytes/macrophages/plasma cells cells/eosinophils
- leads to expansion of portal tract, proliferation of bile ductule, granulomas

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8
Q

What are the features of compensated cirrhosis?

A

ASYMPTOMATIC

  • liver still functions
  • pathological
  • fibrous circles
  • increased risk of decompensation and liver cancer
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9
Q

What are the features of decompensated cirrhosis?

A

LIVER CANNOT FUNCTION

  • ascites, bleeding, encephalopathy
  • caused by: liver cancer, infections, haemorrhage, portal vein clot
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10
Q

What are the main effects of liver disease on the cardiovascular system?

A

Portal hypertension
Low INR
Thrombocytopenia

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11
Q

How does liver disease reduce coagulation factors?

A 
Cannot produce proteins
Bile reduction (cholestasis) so vitamin K is malabsorped and is needed for clotting factor synthesis
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12
Q

What are the effects of thrombocytopenia?

A

Haemorrhage
Bruising
Slow clotting post injury

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13
Q

Why is there a low INR?

A

Prothrombin, clotting factors, albumin reduction as hepatocytes synthesis

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14
Q

What does portal hypertension result in?

A

Increased hydrostatic pressure in capillaries detected by the baroreceptors in the carotid arteries and so RAAS system is activated as well as the SNS to reduc preoload and release ADH
- Also porto-systemic collaterals are used so may get backflow if hypertension increases causing varices

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15
Q

How does liver disease affect metabolic state?

A

Glucose levels are low as the damaged liver cannot respond to insulin and stores cannot be broken down and released into the blood = hypolgycaemic

Ketones are high as in a starved state
Fats are the main source of energy supply

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16
Q

What are the complications of liver disease?

A
  • oedema and ascites (albimun deficiency)
  • Pulmonary hypertension causes vasodilation of the splanchnic circulation as all blood flow as gone to the abdomen
  • hepatic encephalopathy
  • bacterial peritonitis
  • splenomegaly
17
Q

How does portal hypertension occur?

A
  • Kidney impairment due to ascites and cirrhosis = ADH release = hyponatremia and water retention
  • hypoalbuminemia = redcued colloid pressure = water into vessels
18
Q

Why are haemoglobin and platelets low?

A
  • anaemia of chronic disease
  • portal hypertension so lots of blood flow to spleen which breaks down blood cells
  • GI blood loss
19
Q

Why is bilirubin high?

A

Liver cannot conjugate bilirubin from broken RBCs so less excretion leads to jaundice

20
Q

Why is urea increased?

A

GI bleeding = protein in blood breaks down = urea main product of this

21
Q

What is AST and how is affected in liver disease?

A

Aspartate aminotransferase

  • mitchondrial enzyme
  • increases in hepatic necrosis, MI, muscle injury
22
Q

What is ALT and how is it affected in liver disease?

A

Alanine aminotransferase

  • cystolic enzyme
  • specific to liver
  • increased in liver disease
23
Q

What does AST:ALT tell you?

A

If <1 there is a liver disease as ALT would be greater than AST

24
Q

What is ALP and how is it affected in liver disease?

A

Alkaline phosphate

Found in alkaline canaliculi and sinusoidal membranes

25
Q

What is Gamma GT and how is it affected in liver disease?

A

Gamma glutamultranspeptidase
microsomal enzyme
induced by drugs and alcohol
can determine alcohol intake if ALP normal

26
Q

Why is ALP, AST, ALT and GGT high?

A

Hepatocyte necrosis so enzymes leak out

Not extremely high as had previous Hep C damage

27
Q

What is the main treatment for liver disease?

A
  • Thiamine (deficiency)
  • Pabrinex (vitamins, cofactors, sugar energy - refeeding)
  • DIeurectis (spironolactone) - for oedema
  • Nutritional therapy
  • Terlipressin (lowers blood pressure and relieved PH and vasoconstriction for splanchnic circulation)
  • Lactulose
  • banding of varices
28
Q

What is Pabrinex

A 
Refeeding
Vitamins, cofactors, sugar
2 forms:
1) B1, B2 (carbs to sugar), B6 (amino acid breakdown)
2) C, B3, glucose
29
Q

Why is nutritional therapy given

A

Carbs and proteins so not malnourished

- branched chain amino acids preventing encephalopathy, muscle wasting and increases albumin

30
Q

What does lactulose do?

A

Reduces fluid uptake from the gut (osmotic laxative)

Acidifies gut contents so less ammonia reabsorbed = less encephalopathy

31
Q

What is hepatic encephalopathy?

A

Neuropsychiatric abnormalities with liver disease as toxins not removed

32
Q

How does hepatic encephalopathy occur?

A

LACTATE BUILD UP:

  • ammonia exposure as liver does not clear and increased bleeding increases levels when blood is broken down
  • thiamine deficiency
33
Q

What is thiamine required for? How does this cause hepatic encephalopathy?

A
  • Cofactor for pyruvate to acetyl-coA conversion so reduction = lactate build up = Wernicke-Korsakoffs
  • impaired branched chain amino acid metabolism so increased aromatic amino acid uptake = distrubred neurotransmission
34
Q

Why does bacterial peritonitis occur?

A

Build up of fluid due to ascites, intenstine gram negative bacteria
- kupffer and sinuosoidal cells usually help clear bacteria

CR/MET PBLs (15 decks)

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