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GI > W2 P+P of Liver > Flashcards

W2 P+P of Liver Flashcards

1
Q

what are the metabolic functions of the liver

A

regulation of metabolism of carbohydrates, amino acids and lipid

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2
Q

Describe the metabolism of carbohydrates by the liver and in what way it is regulated

A

This is hormonally regulated

  • Gluconeogenesis: glucose produced from AA
  • Glycolysis: to form pyruvate then acetyl coA (aerobic) or lactate (anaerobic)
  • Glycogenesis: glucose to glycogen
  • Glycogenolysis: to release glucose
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3
Q

Describe fat metabolism by the liver

A

chylomicrons are processed, synthesis of cholesterol and lipoproteins, ketogenesis in starvation (for neural function)

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4
Q

Describe protein metabolism by the liver

A

plasma proteins are synthesised
transamination and deamination of AA
Conversion of ammonia to urea

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5
Q

Which hormones are deactivated by the liver

A

insulin, glucagon, ADH, steroid hormones

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6
Q

Which hormones are activated by the liver

A
  • vitamin D –> 25-hydroxyvitamin D2 (further activated to 1,25- dihydroxyvitamin D3 in kidneys)
  • conversion of thyroid hormone
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7
Q

State the 4 Major functions of the liver

A
  • Storage
  • Synthesis of proteins
  • Detoxification
  • Protection
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8
Q

What does the liver store

A
  • Fat soluble vitamins ADEK in hepatocytes
  • Water soluble vitamin B12 (hydroxycoblamin)
  • iron, copper
  • glycogen
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9
Q

what proteins does the liver process

A
  • Coagulation factors II, VII, IX, X and Proteins C,S,Z
  • Albumin
  • complement proteins
  • apolipoproteins
  • carrier proteins
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10
Q

how does the liver provide protection

A
  • Kupffer cells (liver macrophages) digest old RBC and bacteria
  • immune factors eg acute phase proteins
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11
Q

detoxification by liver

A
  • Endogenous substances eg bilirubin for Hb breakdown

- Exogenous substances like xenobiotics (drugs, ethanol)

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12
Q

What secretes bile

A

liver and bile duct cells (cholangiocytes)

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13
Q

where is bile before a meal

A

Stored and concentrated in the gall bladder (sphincter of oddi closed)

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14
Q

Describe release of bile

A
  • smooth muscle in gall bladder contracts due to presence of chyme in duodenum via CCK and vagal impulses causing the sphincter of Oddi to open
  • bile enters duodenum via cystic duct and common bile duct
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15
Q

what does the bile being slightly alkaline help?

A

neutralisation of chyme
pH adjustment for enzymes
protection of mucosa
micelle formation

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16
Q

Contents of hepatocyte juices

A
  • primary bile acids
  • water and electrolytes (Na+, K+, HCO3-, Ca2+, Cl-)
  • lipids and phospholipids
  • cholesterol
  • IgA
  • Bilirubin
  • Metabolic wastes and conjugated drug metabolites
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17
Q

what is bilirubin

A

Breakdown product of porphyrin of Hb, makes urine yellow and faeces brown

18
Q

what is cholelithiasis

what is it caused by

A

Gall Stones

Concentration of bile in GB due to reabsorption of water, excess cholesterol relative to bile acids and lecithin

19
Q

Best treatment for cholelithiasis

A

Laparoscopic cholecystectomy if causing symptoms

20
Q

Treatment for cholelithiasis with impaired renal function and small/medium bile stones and side effects of treatment

A

Ursodeoxycholic acid

Diarrhoea

21
Q

What is biliary colic

Symptoms

A

symptomatic cholelithiasis
colic (sudden pain) occurs due to a gallstone temporarily blocking the cystic duct.
Pain in right upper part of the abdomen, lasts from 15 minutes to a few hours.

22
Q

Treatment of Biliary colic and what can make it worse

A

Analgesia
Morphine can make it worse (SOO constricts)
Buprenorphine, pethidine

23
Q

Treatment for biliary spasm

A

Atropine, GTN

24
Q

how are bile salts reabsorbed

A

By active transport in the terminal ileum

25
Q

how do bile salts return to the liver from the SI

A

hepatic portal circulation

via active and passive transport

26
Q

how does body compensate for loss of small amount of bile acid via colon

A

resynthesis using hepatic cholesterol

27
Q

Name primary and secondary bile salts and how 1 is converted to 2

A

Cholic and chenodeoxycholic are dehydroxylated by bacteria to deoxycholic and lithocholic

28
Q

what happens to secondary bile acids

A

Return to liver, turned into bile salts

29
Q

Name the three Bile acid sequestrants

A

Colveselam
Colestipol
Colestyramine

30
Q

Action of bile acid sequestrants

A

Bind to bile acids, preventing their reabsorption

31
Q

How do bile acid sequestrants lower LDL

A
  • conversion of cholesterol to bile salts in liver
  • increased LDL receptors on hepatocytes
  • increase LDL cholesterol clearance from plasma
32
Q

Clinical uses of bile acid sequestrants

A

hyperlipidaemia
cholestatic jaundice (itch)
bile acid diarrhoea

33
Q

Limitations and adverse effects of bile acid sequestrants

A

large doses, diarrhoea, reduced absorption of fat soluble vitamin and some drugs (thiazide diuretics)

34
Q

Main organ of drug metabolism

A

Liver

35
Q

Phase I of drug metabolism

A

Oxidation, Reduction, Hydrolysis

makes drug more polar by adding a reactive group, allowing for conjugation

36
Q

Phase II of drug metabolism

A

Conjugation of chemically reactive groups

37
Q

Where do phase I oxidation reactions occur

A

haem groups in ER of hepatocytes

38
Q

where do phase II reactions occurs and do they result in

A

Liver

Inactive products

39
Q

Glucouronidation

A

Part of phase II

transfer of glucouronic acid to electron rich atoms of substrate

40
Q

What is hepatic encephalopathy

Symptoms

A

In hepatic failure, detoxification of ammonia to urea fails so blood NH3 levels rise, having a toxic effect on CNS

Drowsiness, incoordination, coma, death due to cerebral oedema

41
Q

Treatment of hepatic encephalopathy

A
  • Lactulose (acidifies stoo, converts NH3 to NH4 which isnt absorbed)
  • antibiotics :neomycin, rifamixin (suppress colonic flora therefore ammonia production)

GI (7 decks)

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