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
What is Gamma GT and how is it affected in liver disease?
Gamma glutamultranspeptidase microsomal enzyme induced by drugs and alcohol can determine alcohol intake if ALP normal
26
Why is ALP, AST, ALT and GGT high?
Hepatocyte necrosis so enzymes leak out | Not extremely high as had previous Hep C damage
27
What is the main treatment for liver disease?
- 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
What is Pabrinex
``` Refeeding Vitamins, cofactors, sugar 2 forms: 1) B1, B2 (carbs to sugar), B6 (amino acid breakdown) 2) C, B3, glucose ```
29
Why is nutritional therapy given
Carbs and proteins so not malnourished | - branched chain amino acids preventing encephalopathy, muscle wasting and increases albumin
30
What does lactulose do?
Reduces fluid uptake from the gut (osmotic laxative) | Acidifies gut contents so less ammonia reabsorbed = less encephalopathy
31
What is hepatic encephalopathy?
Neuropsychiatric abnormalities with liver disease as toxins not removed
32
How does hepatic encephalopathy occur?
LACTATE BUILD UP: - ammonia exposure as liver does not clear and increased bleeding increases levels when blood is broken down - thiamine deficiency
33
What is thiamine required for? How does this cause hepatic encephalopathy?
- 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
Why does bacterial peritonitis occur?
Build up of fluid due to ascites, intenstine gram negative bacteria - kupffer and sinuosoidal cells usually help clear bacteria