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Yr 3 Med 2 > Hepatology - Liver Function Tests > Flashcards

Hepatology - Liver Function Tests Flashcards

1
Q

Explain the role of the liver

A
  • Macronutrient metabolism
  • Blood volume regulation
  • Immune system support
  • Endocrine control of growth
  • Signalling pathways
  • Lipid and cholesterol homeostasis
  • Breakdown of xenobiotic compounds
  • Glucose metabolism
  • Lipid metabolism
  • Amino acid and protein metabolism → Urea cycle
  • Secretion → Bile
  • Storage → Vit A, D, B12, Cu, Fe
  • Hematological function → phagocytosis, hemopoeisis
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2
Q

What are the zones in the liver?

A
  • Endothelial cells have more space between = GAS EXCHANGE
  • Hepatocyte - most common cell in liver
  • If Zone 1 switches off → Zone 2 → Zone 3
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3
Q

What are the cells in the liver (what do they do)?

A
  • Hepatocytes are the primary epithelial cell
  • Cholangiocytes (biliary epithelial) are the second most abundant epithelial
  • Stellate cells can exist in a quiescent (Vit A store) or activated state (injury response lays collagen → fibrosis)
  • Kupffer cells are the resident macrophage
  • Sinusoidal cells are a specialized endothelial → barrier functions
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4
Q

What is glycolysis?

A
  • Glycolysis is the metabolic pathway that converts glucose C₆H₁₂O₆, into pyruvic acid, CH₃COCOOH. The free energy released in this process is used to form the high-energy molecules adenosine triphosphate (ATP)
  • Glycolysis is a sequence of ten reactions catalyzed by enzymes.
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5
Q

What is gluconeogenesis?

A
  • Gluconeogenesis is a metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates.
  • Happens in the liver and kidneys
  • Made from glycerol, lactate, amino acids
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6
Q

What is glycogenolysis?

A
  • Glycogenolysis is the breakdown of glycogen to glucose-1-phosphate
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7
Q

What is neo-glucogenesis?

A

s

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8
Q

What happens in normal vs diabetic state with glucose (management in body)?

A
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9
Q

Explain the role of lipids

A
  • Uptake
  • Synthesis
  • Packaging
  • Secretion of lipoproteins
  • Chylomicrons assembled from lipoproteins and digested lipids from gut
  • Fatty acids extracted from Chylomicrons
  • Assemble fatty acids/glycerol into triglycerides, VLDL which secreted through hepatocytes
  • Lipid soluble vitamin absorption
  • Fatty acids - Oxidative pathways - ketogenic products (reduces TCA toxic end-products)
  • Cholesterol Homeostasis – HMG-CoA Pathway
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10
Q

What is the most common protein?

A

Albumin (55% synthesis from anabolism)

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11
Q

How can we dispose of nitrogenous waste?

A

Urea cycle (add diagram)

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12
Q

What is a substrate of gluconeogenesis?

A

Amino acids

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13
Q

What is the mechanism of fat lipolysis, hepatic triglyceride secretions and gluconeogenesis?

A

A:

Insulin secreted from the pancreas suppresses fat lipolysis, hepatic triglyceride (TG) secretion, and gluconeogenesis. Insulin also acts on the brain, which independently suppresses lipolysis by suppression of sympathetic outflow and increases TG secretion from the liver through an unknown mechanism.

B:

In diabetes, decreased insulin action on the brain and fat results in increased lipolysis. This increases the delivery of free fatty acids (FFAs) to the liver, increasing TG synthesis. Impaired insulin action at the liver results in increased gluconeogenesis. Increased blood glucose and decreased insulin action at the brain suppress TG secretion from the liver.

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14
Q

Talk through the coagulation pathway

A
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15
Q

Explain some common coagulation pathway problems

A

Factor 8 - vWF, HemoA (haemophilia)

Factor 9 - HemoB

Factor 11 - HemoC

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16
Q

Where are most of the coagulation factors synthesised?

A

Most are synthesised by the liver

17
Q

What are the Vitamin K dependent clotting factors?

A
  • 2
  • 7
  • 9
  • 10
  • (Protein C & S)
18
Q

List some natural anticoagulants

A
  • Protein C
  • Protein S
  • Heparin
  • Antithrombin
19
Q

What is Disseminated intravascular coagulation (DIC)?

A
  • Condition in which blood clots*** form throughout the body, ***blocking small blood vessels
  • In a severe systemic illness dying cells release procoagulant agents that activate coagulation, resulting in fibrin generation that occludes small vessels. Platelets and clotting factors are used up and result in bleeding elsewhere. Blood tests reveal thrombocytopenia, increased PT/INT and APTT, and raised D-dimer and fibrin degradation products. Treat by removing cause and supportive therapies (blood, platelets, FFP, cryoprecipitate)
20
Q

What can liver failure lead to?

A

Result in a global decline in clotting factors which affects both the intrinsic*** and ***extrinsic clotting pathways

21
Q

What can hypersplenism cause?

A

For platelets to be LOW

22
Q

What can coagulation impairment be caused by?

A
  • Chronic Liver disease → Cirrhosis/ Malnutrition
  • Acute Liver failure
  • Biliary Pathology → Cholestatic Liver Disease
23
Q

Explain thrombocytopenia in liver disease

A
  • Alcohol is toxic to megakaryocytes
  • Splenomegaly is a consequence of portal hypertension
  • Reduced thrombopoietin
  • Platelet dysfunction – signalling error, endothelial dysregulation
  • Overall cirrhosis is thrombogenic – 5-10% PVT, 8% extrahepatic VTEs
24
Q

What are the advantages & disadvantages of LFTs?

A

Advantages

  • Quick screening test
  • Follow certain pattern of liver dysfunction
  • Some diagnostic and prognostic value

Disadvantages

  • Lacks specificity
  • May be normal in liver cirrhosis and hence interpretation requires clinical context
25
Q

What does an LFT show?

A
  • Bilirubin - product of heme degredation
    • 2 types:
      • Conjugated (direct) → makes bilirubin water soluble
      • Unconjugated(indirect)
  • ALT and AST → integrity of hepatocytes
  • Albumin and PT → Synthetic function
  • AlkP and GGT → outflow flow
26
Q

Explain trans-aminases in LFTs

A
  • ALT (Alanine amino-transaminase)
    • More hepatocyte (systolic) specific. Elevated levels reflect liver damage
  • AST (Aspartate amino-transaminase)
    • Non-specific to liver. Found in liver(cytosolic + mitochondrial),pancreas, muscle, intestine.
    • Hence its value is important in context of alcoholic/Non-alcoholic liver disease where the ratio of ALT/AST is reversed, i.e.<2

OVERALL checks integrity of hepatocytes

27
Q

What are the causes of raised ALT and how high would it be?

A

ALT > 1000

  • Ischemia – Vascula → shock
  • Drugs – paracetamol toxicity
  • Infection – Hepatitis (A - E) , HSV

Leptospirosis (Weil’s Disease)

  • Autoimmune hepatitis
  • Shock/acute liver injury
28
Q

How to check synthetic function in an LFT?

A
  • Prothrombin Time:Factors II, IV, VII, IX and X.
    • PT is a good marker of coagulation because coagulation factors have a short half-life → easy to see if coagulation factors have gone wrong straight away
  • Albumin: Non-specific, used in clinical context Causes of low albumin could be:
    • Infection
    • Nephrotic syndrome
    • Severe Malnutrition
    • Burns etc.
29
Q

How to check outflow function?

A
  • Alkaline Phosphatase: (AlkP) Non specific to liver. However iso-enzymes are specific
    • In hepatitis it will RISE
  • Gamma-glutamyltransferase (GGT): marker for cholestasis. Raised GGT in isolation is suggestive of Alcohol intake( ~40u/wk) or antiepileptic use(phenytoin)
30
Q

What are the signs and symptoms someone would get with a gall stone?

A
  1. Pain
  2. Jaundice
  3. Temperature (pyrexia)

Yr 3 Med 2 (8 decks)

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