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GI - Y2 > L16 - Liver disease and liver failure > Flashcards

L16 - Liver disease and liver failure Flashcards

1
Q

Summarise functions of liver

A

Synthesis - proteins, clotting factors, vit D, bile
Breakdown - waste removal, NH3
Storage - Vit B12, Vit A, iron, copper
Immune system: Kupffer cells

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2
Q

Liver stores:

A 
Vitamin A (1-2) years supply.
Vitamin D (1-4) months 
Vitamine B12 (1-3) years 
Iron 
Copper
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3
Q

Liver and angiotensinogen

A

Liver synthesises angiotensinogen, a hormone that is responsible for raising the BP when activated by renin.

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4
Q

State some causes of acute liver failure?

A

Infection: Hep A, B, E
Drugs: paracetamol, halothane (anaesthetic)
Poisoning: amanita phalloides (mushrooms)
Immune and metabolic: autoimmune hepatitis, Wilson’s disease. acute fatty liver or pregnancy

Other:
Budd Chiari
Ischaemic hepatitis
Trauma

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5
Q

Budd Chiari

A 
Caused by occlusion of the hepatic veins that drain the liver.
Presents with triad of:
- abdominal pain 
- ascites 
- liver enlargement
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6
Q

Hepatic hydrothorax

A

Presence of a pleural effusion in a patient with cirrhosis who do not have any other reasons to have pleural effusion.

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7
Q

What is hepatic encephalopathy?

A

Brain dysfunction caused by liver insufficiency.

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8
Q

Sarcopenia

A

Syndrome characterised by progressive and generalised loss of skeletal muscle mass, strength and it strictly correlated with physical disability, poor quality of life and death.

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9
Q

Describe how hereditary haemochromatosis occurs?

A
  • Mutations in HFE gene
  • HFE product invovled in intestinal iron uptake
  • caused excessive intestinal absorption of iron
  • accumulation of iron in liver and pancreas
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10
Q

Describe how Wilson’s disease occurs?

A
  • Mutation in ATP7B
  • ATP7B is metal iron transporter
  • accumulation of copper in liver, brain (esp. basal ganglia) and eyes (Kayser-Fleischer rings)
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11
Q

Summarise the degradation of haemoglobin?

A
  1. Haem —-(haem oxygenase)—-Biliverdin—-(biliverdin reductase)—-Bilirubin
  2. Bilirubin bound to serum albumin, transported to liver
  3. Carrier mediated bilirubin uptake at sinusoidal membrane
  4. Conjugation with 1 or 2 molecules of glucuronic acid by bilirubin uridine disphosphate glucuronyl transferase (RER)
  5. Excretion of water soluble non-toxic bilirubin glucuronides into bile
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12
Q

What occurs to bilirubin glucuronoids once they reach the gut lumen?

A

De-conjugated in gut lumen by bacterial B-glucuronidases.

- Degraded to colourless urobilinogen

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13
Q

Briefly compare unconjugated and conjugated bilirubin?

A

Unconjugated

  • virtually insoluble
  • exists in tight complexes with serum albumin
  • cannot be excreted in urine

Conjugated

  • water soluble
  • non-toxic
  • loosely albumin bound
  • can be excreted in urine
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14
Q

Describe why neonatal jaundice may occur?

A
  • hepatic machinery for conjugating and excreting bilirubin does not occur until 2 weeks of age.
  • jaundice may be reduced when breast feeding as breast milk contains bilirubin deconjugating enzymes
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15
Q

What mode of inheritance causes Wilson’s disease?

A

Autosomal recessive

  • mutation in ATP7B gene
  • impaired copper excretion into bile
  • failure to incorporate copper into ceruloplasmin
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16
Q

Where does most copper absorption take place?

A

Proximal small intestine.

Duodenum.

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17
Q

How does copper travel in body to liver ?

A
  • absorbed in duodenum and prox. small intestine
  • transported portal circulation complexed with albumin and histidine.
  • free copper dissociated
  • taken up by hepatocytes
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18
Q

What happens to the copper at liver?

A
  • Binds to a2-globulin to form ceruloplasmin, then secreted into blood.
  • circulates through blood
  • eventually de-sialylated and endocytosised by liver
  • degraded with liver lysosomes
  • released copper excreted into bile
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19
Q

Deficiency in ATP7B would result in?

A
  • decreased copper transport into bile
  • impaired incoporation into ceruloplasmin
  • inhibits ceruloplasmin secretion into blood.
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20
Q

Increased non ceruloplasmin bound copper from liver may result in?

A

Haemolysis

Haemolytic anaemia as copper is toxic o cell memrbanes

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21
Q

Age of onset of Wilson’s disease?

A

Variable.
Average age 11.4 years/

Movement disorders: tremors, poor coordination, chorea, gait disturbances.

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22
Q

Biocemical diagnoses of Wilsons

A
  • decrease in serum ceruloplasmin
  • increase in hepatic copper content
  • increased urinary excretion of copper
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23
Q

Describe the appearance of Kayer-Fleischer rings?

A
  • green to brown depositions of copper in descemet membrane in limbus of cornea
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24
Q

Green brown deposits in cornea are known as

A

Kayer-Fleishcer rings

25
Q

What kind of therapy might be used in Wilson’s?

A
  • Zinc based therapy

- blocks uptake of copper in gut

26
Q

Describe how drug induced liver disease may occur from ingestion of acetaminophen?

e.g. paracetamol

A
  • Cytochrome P450 produces toxic metabolite in acinus of zone 3 hepatocytes.
  • h.cytes will die, zone 2 h.cytes will take over and also become injured
27
Q

Appearance of liver in Budd Chiari syndrome?

A
  • liver swollen, red-purple, has tense capsule

- affected hepatic parenchyma reveals severe centrulolobular congestion and necrosis

28
Q

Summarise jaundice

A
  • clinical manifestation of an increased concentration of bilirubin in plasma
  • bile salts causing itching
  • detectable in sclerae, level >35
  • affects skin, mucous membranes, stained yellow
29
Q

Pre-hepatic jaundice

A

Haemolytic.

  • Increased haemolysis
  • excess unconjugated bilirubin produced faster than liver able to conjugate it
  • bilirubin in plasma unconjugated
  • not excreted by kidney
  • resulting in acholuric jaundice
30
Q

Acholuric jaundice

A

Circulating blood has excessive amounts of unconjugated bilirubin and no bile pigments

31
Q

Hepatic jaundice

A

Congenital. Defect of h.cyte function.

  • Hepatocecllular injury / infection
  • disorder liver cell during stages of uptake
  • intrahepatic cholestasis, failure to excrete conjugated bilirubin into canaliculi in liver
32
Q

Post-hepatic jaundice

A

Obstruction of bile duct.
Biliary atresia, bile duct carcinoma, extrinsic compression.

  • relatively intact h.cyte
  • conjugated bilirubin released back into plasma and excreted in kidney.
  • dark urine and pale stools
33
Q

Why is ALP used as a marker of liver disease?

A
  • cells of collecting system predominantly secrete ALP

- cells of collecting system proliferate in presence of obstruction

34
Q

How may transferases be used as a marker of liver disease?

A
  • transferases are a constituent of h.cytes

- serum transferase concentration increases when there is hepatocellular damage.

35
Q

Process of conjugation

A

Hydrophilicity of bilirubin is increased by esterification

36
Q

Describe the formation of stercobilinogen ?

A

Conjugated bilirubin in gut is catabolised by bacteria to form stercobilinogen also known as fecal urobilinogen.

37
Q

Describe Phase 1 and 2 of drug metabolism?

A
  1. Addition of polar group
    - polarity of drug increased by oxidation or hydroxylation. Catalysed by cytochrome p450 oxidases.
  2. Conjugation
    - cytoplasmic enzyme conjugate the functional groups introduced in first phase
38
Q

Idiosyncratic drug toxicity

A

Drug may be toxic in some individual at one level and the normally tolerated by most other patients

39
Q

When therapeutically taken paracetamol normally conjugated with?

A

Glucuronic acid or sulfate - which is then excreted by kidneys

40
Q

What occurs during paracetamol overdose?

A
  • capacity of conjugation pathways are overwhelmed
  • acetaminophen oxidised by liver P450 cytochrome CYP3A4 to n-acetyl benzoquinoneimine.
  • causes free radical peroxidation of membrane lipids
  • hepatocellular damage
41
Q

Describe accumulation of unconjugated bilirubin in neonates brain?

A

Very toxic to immature brain.

Causes a condition known as kernicterus.

42
Q

What might be done is plasma bilirubin too high in neonates?

A
  • Phototheraphy with blue white light, isomerises bilirubin to more soluble pigment that might be excreted with bile
  • exchange blood transfusion to remove excess bilirubin
43
Q

Signs of post hepatic jaundice

A
  • pale coloured stool
  • absence of fecal bilirubin
  • dark urine
44
Q

Role of ceruloplasmin

A
  • major copper containing protein of liver and plasma
  • function as an iron oxidising enzyme
  • necessary for mobilisation of stored iron
45
Q

Briefly describe some genetic disorders impairing bilirubin conjugation or secretion?

A
  1. Gilberts syndrome: causes mild unconjugated hyperbilirubinaemia
  2. Crigler-Najjar syndrome: causes severe uncojugated hyperbilirubinaemia
46
Q

Why is caudate lobe spared of Budd chiari syndrome?

A
  • independent blood supply

- venous drainage

47
Q

Describe liver disease in pregnancy?

A

Hyperemesis gravidarum: pathological vomiting during pregnancy, associated with liver dysfunction and jaundice

48
Q

Acute liver failure may lead to

A

Encephalopathy.

Mental changes progressing from delerium to coma

49
Q

Examples of causes of acute liver failure

A
  • acute viral hepatitis
  • paracetamol toxicity
  • amanita phalloided (mushroom poisoning)
50
Q

Clinical manifestations of acute liver failure?

A
  • cerebral disturbance
  • subtle at first: reduced alterness, poor concentration, restlessness, drowsiness and coma
  • cerebral oedema due to increased ICP.
51
Q

Signs of acute liver failure

A
  • abnormally reacting pupil
  • fixed pupil
  • bradycardia
  • hyperventilation
  • profuse sweating
52
Q

Fatty liver

A

Accumulation of triglycerides and other fats in liver cells. May be accompanied by hepatic inflammation and liver cell death (steatohepatitis)

53
Q

Describe action of alcohol on lipolysis

A

Increase of alcohol results in increase lipolysis through direct stimulation of adrenal pituitary axis.

Chronic ethanol ingestion inhibits oxidation of fatty acids in liver and release of VLDL into blood.

54
Q

State some complications of chronic liver failure?

A
  • portal hypertension
  • SBP: spontaneous bacterial peritonitis
  • HCC: hepatocellular carcinoma
55
Q

Cirrhosis

A

Replacement of normal liver tissue by scar tissue.

56
Q

Summarise the role of ET-1 and No in the pathogenesis of portal hypertension and oesophageal varices?

A

ET-1 : powerful vasoconstrictor synthesized by sinusoidal endothelial cells that have been implicated in increased hepatic vascular resistance of cirrhosis and in the development of liver fibrosis.

NO: vasodilator also made by SEC. Cirrhotic liver: production NO decreased, resulting in vasoconstriction.

57
Q

Spontaneous bacterial peritonitis

A

Acute bacterial infection of ascitic fluid.

58
Q

Factors predisposing peritoneal inflammation and bacterial growth in ascitic fluid

A
  • Intestinal bacterial overgrowth
  • along impaired phagocytic function
  • decreased activity of the reticuloendothelial system contributes to an increased number of microorganisms and decreased capacity to c

GI - Y2 (18 decks)

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