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PA10315 2nd semester > Liver function > Flashcards

Liver function Flashcards

1
Q

why is cholesterol important

A

synthesis of cell membranes and contributes to fluidity
lipid rafts- patches of fluidity
precursor for synthesis of several molecules eg vit D

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2
Q

cholesterol synthesis

A

80% production in the liver
from Acetyl CoA
Multi step pathway

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3
Q

cholesterol synthesis step 2/3

A

squalene synthesised from isopentenyl pyrophosphate
cyclization of squalene to form lanosterol
lanosterol goes through several steps to form cholesterol

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4
Q

statins

A

inhibit HMG CoA-reductase in cholesterol synthesis pathway

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5
Q

how is cholesterol transported in the body and why

A

lipophilic so does not dissolve well in water.
Packaged with phospholipids and apolipoproteins to form a series of different lipoproteins (have a lipid core and hydrophlic outer surface with phospholipids, free cholesterol and apolipoproteins.
include LDLs and HDLs

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6
Q

How to treat atherosclerosis

A

Inhibit cholesterol synthesis, because high LDL levels associated with atherosclerosis

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7
Q

HDL vs LDL

A

Ldl risk factor of CVD and athersclerosis, HDL protective

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8
Q

Bile salt production recap

A

Primary bile salts formed in the liver, go into GI tract, where modified by gut bacteria to form secondary bile salts
dehydroxylation

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9
Q

bile contains

A 
bile salts
lecithin
HCO3-
cholesterol
bile pigments
trace metals
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10
Q

Bile production

A

Hepatocytes secrete hepatic bile into canaliculi

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11
Q

hepatic bile

A

bile salts, bile pigments, cholesterol and lecithin

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12
Q

what do epithelial cells that line the bile ducts secrete

A

a bicarbonate rich fluid that increases the volume of the bile

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13
Q

what are precursors of bile salts

A

bile acids synthesized from cholesterol

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14
Q

Primary bile acids

A

cholic acid and chenodeoxycholic acid

synthesised in the hepatocytes

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15
Q

secondary bile acids

A

deoxycholic and lithocholic- are formed inthe intestine by the dehydroxylating action of bacteria flora

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16
Q

conjugation

A

in the liver, primary or secondary bile acids are conjugated to amino acids to generate water soluble bile salts

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17
Q

bile salts have

A

hydrophobic and hydrophilic regions that aggregate to form micelles at a critical concentration
Important for the emulsification of fats

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18
Q

where are the majority of bile salts reabsorbed

A

by a sodium dependent pathway in the ileum (last segment of the small intestine)

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19
Q

how do bile salts get recycled back to the liver from the intestine

A

portal vein

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20
Q

how does uptake of bile salts from portal blood into hepatocytes occur

A

active transport

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21
Q

enterohepatic circulation

A

recycling from the GI tract to the liver

22
Q

sphincter of oddi

A

ring of smooth muscle where common bile enters small intestine

23
Q

Cholecystokinin (CCK)

A

peptide hormone
produced by small intestine
stimulus for release- AAs, fatty acids in the intestine

24
Q

What does increased CCK lead to

A

gallbadder contraction, increased bile flow into common bile duct
relax sphincter of oddi, incr bile flow into duodenum

25
Q

what happens when the sphincter of oddi is closed

A

bile diverted to gall bladder

26
Q

what does the gall bladder do with bile stored for digestion

A

concentrates it by removal of salts and water

27
Q

bile pigments

A

breakdown product of heme portion of haemoglobin from erythrocytes broken down in the liver and spleen
major pigment is bilirubin found in bile and secreted into duodenum
pigments responsible for characteristic bile colour

28
Q

what else does the liver secrete

A

plasma proteins

29
Q

albumin

A

plasma protein, transport lipids and steroid hormones

30
Q

Globulins

A

approx 40% total plasma proteins

a-globulins and B-globulins also transport lipids and steroid hormones

31
Q

clotting factors

A

most produced by the liver

32
Q

IGF- insulin like growth factors

A

Important mediator of growth hormone action
Liver synthesises IGF 1 and 2 in response to growth hormone
structurally similar to pro-insulin

33
Q

IGF-1

A

levels low in infancy, peak in puberty during growth and declines in adult

34
Q

IGF 2

A

more important in fetal and neonatal growth

35
Q

Phase 1 reactions drug metabolism

A

Cytochrome p450 enzymes important
Population variation in these is important in terms of therapeutics
Naturally occurring dietary substances can inhibit or induce p450 enzymes with impact on drug metabolism

36
Q

clopidogrel

A

anti-thrombotic agent that inhibits platelet activation

pro drug that requires oxidation

37
Q

what is a pro drug

A

a biologically inactive compound which can be metabolized in the body to produce a drug.

38
Q

metabolism of clopidogrel

A

2 step, using hepatic P450 enzymes to generate the active thiol metabolite that reacts with platelets
Binds selectively and irreversibly to P2Y12 receptor on platelet membranes

39
Q

What happens to majority of clopidogrel

A

inactivated by blood esterases so only 15 % metabolised by hepatic P450 enzymes

40
Q

What are mutations in P450 enzymes associated with

A

reduced response to clopidogrel treatment

41
Q

Phase 2 reactions

A

conjugation step that leads to pharmacologically inactive or less soluble lipid product that is eliminated in urine or bile

42
Q

groups often associated with conjugation

A

glucuronyl, sulphate, methyl, acetyl etc

43
Q

what is paracetamol

A

non-narcotic analgesic-antipyretic agent

44
Q

paracetamol peak plasma conc

A

30-60 mins

45
Q

paracetamol inactivated in liver by

A

conjugation to glucuronide or sulphate

46
Q

Toxic dose causes

A

hepatotoxicity and renal toxicity

47
Q

what happens with paracetamol toxic dose

A

normal conjugation pathways saturated and drug metabolised by mixed function oxidases to form N-acetyl-p-benzoquinone imine (NAPBQI)- toxic to cells

48
Q

kupffer cells function

A

phagocytize pathogens from entering blood circulation

first line of defence against particulates and immunoreactive material from GI tract via portal circulation

49
Q

cholesterol synthesis 1st step

A

Acetyl CoA is joined to acetoacyl CoA to form HMG CoA. This product is converted to melvalonate by HMG-CoA reductase.
Mevalonate is phosphorylated by three kinases sequentially utilizing three ATPs and is then decarboxylated to form isopentenyl diphosphate.

50
Q

cholic forms

A

deoxycholic

51
Q

chenodeoxycholic forms

A

lithocholic

52
Q

phase 1 reaction processes

A 
Oxidation
Hydroxylation
Dealkylation
Deamination 
hydrolysis

involve the creation of a functional group or the modification of an existing one by oxidation, reduction, or hydrolysis.

PA10315 2nd semester (27 decks)

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