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liver failure Flashcards

1
Q
  • What bilirubin concentration [BR] will lead to yellow sclera and a persons skin turning yellow respectively?
A

Yellow sclera and mucous membrane: >30 micromol/L

Skin turns yellow: >34 micromol/L
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2
Q
  • Define cholestasis
A

Slow/cessation of bile flow, which normally results in jaundice

(Jaundice doesn't necessarily mean there is cholestasis)
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3
Q
  • List and explain the causes of pre-hepatic jaundice
A

Haemolysis- from haemolytic anaemia, toxins and massive blood transfusion-
Transfused short-lived erythrocytes

Haematoma - Collection of erythrocytes deep to skin → Degradation and haemolysis of erythrocytes increases levels of unconjugated bilirubin for resorption

ineffective erythropoiesis- more RBC to break down

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4
Q
  • List and explain the intrahepatic causes of jaundice
A

Reduced uptake of BR into hepatocytes → increased serum unconjugated BR levels within sinusoidal space and systemic circulation eg Gilbert Syndrome

Decreased conjugation of BR → Enters into systemic circulation and passes through BBB eg Crigler-Najjar Syndrome

Reduced BR secretion into biliary canaliculi → Black liver eg Dubin-Johnson and Rotor Syndrome

Intrahepatic cholestasis- Sepsis TPN (total parenteral nutrition) feeding, drugs

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5
Q
  • What are the post-hepatic causes of jaundice?
A

Gallstones and tumours

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6
Q
  • Define acute LF
A

Fulminant epatic failure leading to rapid development (<8 weeks) of severe acute liver injury:

- Impaired synthetic function (clotting factors, albumin)
- Encephalopathy
- Previously normal liver or well-compensated liver disease

Sub-fulminant: <6 months

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7
Q
  • Define chronic LF
A

Failure persisting over years , concerned with liver cirrhosis

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8
Q
  • Outline the pathophysiology of liver failure (LF)
A

Rate of hepatocyte death > regeneration

Hepatocyte death is attributed with a combination of apoptosis (acetaminophen=paracetamol) and necrosis (ischaemia)

Within a hepatic acinus, Zone 3 (central vein region) is sensitive to necrosis and ischaemia due to its relative distance to oxygenated blood supply

Clinically, LF is concerned with coma/death due to multi-organ failure. (catastrophic)
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9
Q
  • What are the commonest causes of acute LF?
A

Toxins (West) - paracetamol, amanita phalloides, bacillus cereus

Inflammation (East) - exacerbations of chronic Hep-B (Hong Kong) and Hep-E (India)
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10
Q
  • What are the other causes of acute LF and give examples of each?
A

Diseases of pregnancy
- Acute fatty liver of pregnancy (AFLP), HELLP syndrome, hepatic infarction, Hepatitis-E Virus (HEV), Budd-Chiari

Idiosyncratic drug reactions

- Single agent - isoniazid, NSAIDs, valproate
- Combinations of drugs

Vascular diseases
- Ischaemic hepatitis, post Orthotopic Liver Transplantation hepatic artery thrombosis, post-arrest, veno-occlusive disease (VOD)

Metabolic diseases - Wilson’s disease , Reye’s disease

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11
Q
  • What are the causes of chronic LF?
A

Inflammation - chronic persistent viral hepatitis.
Alcohol abuse
Side effects of drug (folic acid antagonists e.g. phenylbutazone)
CV causes - decreased venous return (right HF)
Inherited diseases - glycogen storage disease, Wilson’s disease, galactosaemia, haemochromatosis, A1AT deficiency
Non-alcoholic steatohepatitis (NASH)
Autoimmune hepatitis, primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC)

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12
Q
  • Outline the pathophysiology of cirrhosis
A

1) Necrosis concerned with ischaemia results in hepatocyte degradation
2) Releasing intracellular enzymes, in addition to cytokine release.
3) Intracellular contents stimulate chemotaxis of inflammatory cells. (neutrophils and monocyte differentiation into macrophages)
4) Cytokines activate Kupffer cells → Growth factor and cytokine release → Activation of hepatic stellate cells
5) Hepatic stellate cells and macrophages undergo fibroblast proliferation, depositing ECM
6) Increased collagen, proteoglycans and matrix glycoprotein deposition → Fibrosis of hepatic tissue

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13
Q
  • What are the main hepatocyte functions?
A

Metabolic and catabolic - synthesis/ use of carbohydrates, lipids and proteins

Secretory and excretory - excretion of bile and waste products 

Detoxification and immunological- process drugs, breakdown of pathogens
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14
Q
  • List the causes of death as a consequence of LF
A

Bacterial and fungal infections - due to loss of immunological ability

Circulatory instability - lack of homeostasis

Cerebral oedema - encephalopathy

Renal failure 

Respiratory failure 

Acid-base and electrolyte disturbance 

Coagulopathy- as loss of clotting factors
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15
Q
  • Which vitamin is lacking due liver failure and what does this lead to?
  • Why is it lacking?
A

Vitamin K essential cofactor for the carboxylation for glutamic acid residues for the synthesis of factors II, VII, IX, X → coagulopathy & bleeding

lack of bile salts, decreased micelles and absorption of vitamin K

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16
Q
  • Why does ascites occur in liver failure?
A

Reduction in serum albumin
reduces the oncotic pressure within the capillaries
therefore this will reduce the water retention ability for interstitial fluid to be drawn into the capillaries
so water deposited to abdominal spaces

17
Q
  • What does the decreased plasma volume lead to as a result of liver failure?
A

Secondary hyperaldosteronism → Hypokalaemia and alkalosis

18
Q

name the consequence to liver failure that corresponds with the liver function

  • production of clotting factors
  • protein synthesis
  • detoxification
  • glycogen storage
  • production of globulins/ immunological function
  • maintenance of homeostasis
A 
coagulopathy and bleeding
ascites
encephalopathy and cerebral odema
hypoglycaemia
increased susceptibility to infection
circulatory collapse and renal failure
19
Q
  • Explain the some pathogenesis of cholestasis
A

Biliary transporters are incorrectly positioned, insertion of carriers will reduce bile salt secretion into the biliary canaliculi, transporters may be present on the basolateral membrane

Bile salts increase tight junction permeabilty → increasing amount of bile passing through sinusoidal space → reducing bile flow in canaliculi

Canalicular dilation - reduction in bile flow pressure and fluid mechanics

Decreased cell membrane fluidity

Decreased mitochondrial ATP synthesis - reduces ability for active transport of bile salts and xenobiotics into hepatocyte

Deformed brush border
20
Q
  • Why might pruritis be a consequence of cholestasis?

- What is the general cause of portal hypertension?

A

Bile salts secreted into circulation are deposited as crystals deep to the skin resulting in irritation

Fibrotic portal veins coupled with obstruction to venous supply to the liver leads to hypertension
21
Q
  • Explain how thrombocytopenia, oesophageal varices and exudative enteropathy are all consequences of portal hypertension?
A

Thrombocytopenia - when too many platelets are destroyed or accumulate within an enlarged spleen

Oesophageal varices-   Blood flow through the liver slows, the pressure in the portal vein goes up, pushes blood into vessels of oesophagus 

Exudative enteropathy - Increased ascites → Loss of albumin from plasma into intersititial fluid and GIT → Favours colonic bacteria → NH4+ compound liberation → Encephalopathy
22
Q
  • Why might splenomegaly result from portal hypertension?
A

blood backs up into the spleen- cant get out, causes an enlarged spleen, leading to breakdown of red blood cells (anaemia) white blood cells (leukopenia) and platelets (thromocytopenia)

23
Q
  • What is a pre-hepatic cause of portal hypertension?

- What are the post-hepatic causes of portal hypertension?

A

Portal vein thrombosis

Right heart failure - causes backwards pressure within venous system due to insufficient contractility of right atria

Constrictive pericarditis - inflammation and reduced elasticity of the pericardium
24
Q
  • What are the intrahepatic causes of portal hypertension?
A

Presinusoidal - chronic hepatitis, primary biliary cholangitis, granulomas

Sinusoidal - acute hepatitis, alcohol, fatty liver, toxins, amyloidosis

Post-sinusoidal - venous occlusive disease of venules and small veins: Budd-chiari
25
Q
  • How does hepatic encephalopathy present?

- How can hyperammonaemia lead to hepatic encephalopathy?

A

Apathy, memory gaps, tremor and liver coma

exudative enteropathy
when less albumin in plasma, colonic bacteria is fed proteins
liberation of ammonia (hyperammonaemia)
toxic to brain

26
Q
  • What 3 ways can toxins lead to encephalopathy?
A

toxins bypass liver → not extracted or detoxified → passes blood brain barrier → encephalopathy

False transmitters from aromatic amino acids in brain → encephalopathy

exudative enteropathy

27
Q
  • What is hepato-renal syndrome?
A

portal hypertension leads to arterial vasodilation through decreased vascular resistance → activating vasoconstrictor factors (RAAS, SNS, vasopressin ) → renal vasoconstriction decreased glomerular filtration rate

28
Q
  • What does the Child-Pugh score assess?

- what are the five areas assessed?

A

Disease severity for end-stage liver disease, and a prognosticator for peri-op death

bilirubin, serum albumin, INR/PT, ascites, hepatic encephalopathy

29
Q
  • How do you treat encephalopathy?
A

Reduce protein intake

Phosphate enemas/lactose

No sedation
30
Q
  • How do you treat hypoglycaemia, hypocalcaemia and renal failure?
A

Hypoglycaemia - Infusion 10-50% dextrose

Hypocalcaemia - 10ml 10% calcium gluconate

Renal failure - Hemofiltration
31
Q
  • How do you treat respiratory failure, hypotension and infection?
A

Respiratory failure - Ventilation

Hypotension - Albumin and Vasoconstrictors

Infection - Frequent cultures and antibiotics
32
Q
  • How do you treat bleeding?
A

Vitamin K

Fresh Frozen Plasma

Platelets
33
Q

how does portal hypertension cause malnutrition

how does portal hypertension cause vasodilators to be released

A

nutrient filled blood cant get into liver, nutrients cant be processed

vasodilators (eg glucagon, VIP , substance P, prostacyclin and NO) released to decrease blood pressure, increased cardiac output, causes hyperperfusion of abdominal organs and varices

BRS (41 decks)

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