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Liver and Gallbladder

Anna Hogarth Metabolism English 28 cards

Liver and Gallbladder

Cards in this deck (28)

  1. 1What are the key functions of the liver and gallbladder?1) Carbohydrate metabolism
    2) Protein metabolism
    3) Lipid metabolism
    4) Production of bile
  2. 2Describe the blood supply to the liver.75% of the blood supply is the portal vein - the rest is arterial blood. Mixes in the sinusoid within the hepatic lobule. Non-useful substances drain into the hepatic portal vein, biliary system runs in the counter direction.
  3. 3What are sucrose, lactose and starches made of? What does the liver do to these components?1) Fructose and glucose
    2) Galactose and glucose
    3) Maltose and glucose
    4) Converts fructose and galactose to glucose.
  4. 4What effect does insulin have on the liver? What opposes this?1) Promotes glycogen synthesis, suppresses gluconeogenesis, accelerates glycolysis, increases fatty acid synthesis.
    2) Glucagon
  5. 5What substances can be fed into gluconeogenesis?Lactate, pyruvate, amino acids and glycerol.
  6. 6What does the presence of alanine and aspartate aminotransferases in the urine indicate?Liver damage - they are responsible for transamination (part of protein metabolism) reactions in the liver, their presence suggests that hepatocytes may be damaged.
  7. 7What does deamination of glutamate result in? Why is this potentially bad/what can it lead to?1) Production of an a-ketoglutarate and ammonia. Note that gut bacteria are also a significant cause of NH3+.
    2) Excess ammonia depletes the cell of a-ketoglutarate (buffer) which can impair the TCA cycle. NH3 in astrocytes leads to excess glutamine which can cause an increase in osmotic pressure and astrocyte swelling (encephalopathy).
  8. 8How is ammonia excreted?Converted into ammonium (more soluble in water), which can then reduced to urea and excreted in the urine.
  9. 9What does high serum urea indicate?Usually kidney failure - could be due to bleeding into stomach.
  10. 10What is plasma vs serum?Same thing but serum lacks clotting factors.
  11. 11Where do the majority of plasma proteins arise from? What happens when this organ is diseased?1) 90% arise from the liver
    2) Loss of plasma proteins leads to oedema (reduced oncotic pressure)
  12. 12What are fatty acids broken down into? What are these parts used for?1) Glycerol and fatty acids.
    2) Fatty acids are converted into acetyl CoA which can be used in respiration to produce energy or in cholesterol production. Glycerol can be used in gluconeogenesis.
  13. 13What does insulin resistance in type II diabetes lead to?1) Increased glucose (ChREBP) - de novo lipogenesis, non-alcoholic fatty liver disease.
    2) Inappropriate gluconeogenesis (normally switched off by insulin)
    FOXO1-mediated
    3) Impaired glycogen synthesis
    4) Impaired suppression of lipolysis in adipocytes
    -Increased glycerol and FFA
  14. 14What does the liver do to lipids?1) Converts excess glucose to fatty acids (SREBP-1c and ChREBP)
    2) Synthesises phospholipids
    3) Ketogenesis
  15. 15What effect does insulin have on ketogenesis? What is used to produced ketone bodies?1) Switches it off
    2) Lipids and proteins
  16. 16—1) Left lobe of liver
    2) Hepatic duct
    3) Common bile duct
    4) Stomach
    5) Duodenum
    6) Gallbladder
    7) Cystic bile duct
    1) Left lobe of liver 2) Hepatic duct 3) Common bile duct 4) Stomach 5) Duodenum 6) Gallbladder 7) Cystic bile duct
  17. 17How much bile is produced every day? Where is bile secreted from? How is bile modified/why? Where does the common bile duct open up onto?1) 800 ml
    2) Hepatocytes in canaliculi
    3) Modified by cholangiocytes - addition of HCO3- to neutralise the acidic chyme
    4) Ampulla overta of the duodenum
  18. 18What role does cholecystokinin play in bile secretion? Secretin?1) Fatty acids in lumen of duodenum, CCK causes gallbladder contraction and relaxation of the sphincter of Oddi.
    2) Helps to neutralise the acid chyme in the duodenum and stimulates biliary ductal cells.
  19. 19What is the composition of bile? Where is bile made, stored, secreted into and reabsorbed from?1) Water (>90%), bile salts, bilirubin, cholesterol, fatty acids, lecithin and electrolytes.
    2) Made in the liver, stored in the gallbladder, secreted into the duodenum , reabsorbed from the terminal ileum.
  20. 20What are the function of bile salts? What can they be conjugated to and what are they secreted as?1) Detergents and aid in the absorption of lipophilic substances e.g. fat soluble vitamins. Signalling molecules - can activate FXR to affect cholesterol metabolism, gluconeogenesis and metabolic processes.
    2) Glycine or taurine, secreted as sodium salts.
  21. 21What is obeticholic acid?Semi-synthetic bile acid which selectively activates FXR.
  22. 22What are sources of cholesterol? What is it used for?1) Exogenous (diet) and endogenous (liver)
    2) Cell membranes, steroid hormones, skin and bile salts (80%)
  23. 23What happens if the flow of bile is blocked? What are the different causes? (3)Jaundice
    1) Pre-hepatic (too much breakdown of RBC)
    2) Hepatic (liver failure)
    3) Post-hepatic (gallstones, cancer)
  24. 24What is bilirubin?RBC are broken down in the spleen (damaged after 90 days). Need to recycle the haem and globin. This can then be conjugated in the liver, some of it is reused but some is excreted.
  25. 25What are the storage functions of the liver?1) Vitamins (A, D and B12)
    2) Iron: apoferritin - ferritin (reversible); hemosiderin.
  26. 26What are the three components of drug metabolism which happen in the liver?1) Phase I - modification (hydroxylation by cytochrome P450)
    2) Phase II - Conjugation
    3) Phase III - Further modification/excretion
  27. 27What is responsible for the toxicity of the paracetamol overdose? In which patient group will this be worse? How is it treated?1) Paracetamol has to be conjugated to a sulphate or a glucuronide - with overdose this doesn't happen and you get a toxic build-up of NAPQI.
    2) Alcoholics and the malnourished
    3) Infuse with glutathione to promote the conversion of NAPQI to cysteine and mercapturic acid conjugates
  28. 28What symptoms arise from liver failure?1) Oedema (low protein)
    2) Chronic encephalopathy (high ammonia due to failure to enter into urea cycle etc.)
    3) Hypoglycaemia
    4) Jaundice
    5) Impaired clotting (results in bleeding)

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Dr. Alazawi
Created by
Anna Hogarth · Jan 2018
Updated
Jan 24, 2018
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