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exam revision > biochem > Flashcards

biochem Flashcards

1
Q

what are PGs metabolised by

A

lung endothelial cells

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2
Q

actions of PGE2

A

vasodilation
hyperalgesic
pyrogenic
angiogenic

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3
Q

what leads to reddening and oedema in inflammation (what mediators)

A

PGE2 - vasodilation

bradykinin - increases permeability

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4
Q

what enhances the pain response of bradykinin

A

PGE2

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5
Q

mechanism for fever

A

peripheral inflammation - mac activation - cytokines - circulate to hypothalamus (outside BBB) - induce COX2 - produce PGE2 - cAMP - increase temperature set point and behavioural mechanisms

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6
Q

how do NSAIDS supress fever

A

good access to brain, suppress COX2 induction in hypo

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7
Q

how is PGE2 gastroprotective

A

increase blood flow
angiogenesis
mucous secretion
decrease gastric acid secretion

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8
Q

what do aspirin triggered lipoxins bind to, and what do they cause

A

FPR2 Rs - suppress neut recruitment

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9
Q

what is better omega 3 or 6

why

A

omega 3 - replaces arachidonic acid in membrane, retains ability to produce PGI2, but TXA produced in much lower quantities due to substrate preference of thromboxane synthase

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10
Q

oxy state of haemoglobin

A

R = relaxed

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11
Q

does 23BPG increase or decrease in altitude training

A

increases - to increase O delivery to tissues

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12
Q

how is CO2 carried in blood

A

carbamate on N terminal of deoxy Hb

HCO3 converted by carbonic anhydrase - soluble in plasma

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13
Q

4 fates of cholesterol

A

membrane stability
bile acids
vitamin D and steroid hormones
transport

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14
Q

how do we carry cholesterol, what do you have to do to it first

A

esterify to make more hydrophobic (cholesterol is amphipathic), incorporate into lipoproteins

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15
Q

where is HDL made

A

liver adn intestines

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16
Q

where is ACAT and what does it do

A

in liver, helps VLDL form

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17
Q

where is LCAT and what does it do

A

in plasma, helps HDL scavenge cholesterol from membranes

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18
Q

define dyslipidaemia

A

disorder of lipid metabolism

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19
Q

where is CYP450 found

A

liver and intestines in ER (and mitochondria)

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20
Q

where are main CYPs for detoxification

A

ER

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21
Q

what are xenobiotics

A

hydrophobic toxins

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22
Q

most common CYP for drug metabolism

A

CYP3A4

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23
Q

CYP polymorphisms for codeine

A

CYP2D6

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24
Q

structure of CYP

A

haem prosthetic group, cysteine anchor - bind FE to anchor haeme, hydrophobic foot - anchors CYP to ER

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25
Q

what does grapefruit juice inhibit

A

CYP3A4

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26
Q

what do cruciferous vegies do

A

induce CYP1A2

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27
Q

name of system of blood vessels in spleen to facilitate removal of old/damaged RBCs

A

red pulp

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28
Q

how are old/damaged RBCs removed

A

carried to spleen by macs and removed by macs

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29
Q

free Hb is bound to __

A

haptoglobin

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30
Q

free heme is bound to__

A

hemopexin, albumin

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31
Q

free iron bound to __

A

transferrin

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32
Q

what does decrease in haptoglobin indicate

A

haemolytic anaemia

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33
Q

haeme recycling

A

haeme converted to bilivirdin by haeme oxygenase I and II

bilivirdin converted to bilirubin by bilivirdin reductase

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34
Q

which haeme oxygenase is inducible, which is constitutive

A

haeme oxygenase 1 - inducible

haeme oxygenase II - constitutive

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35
Q

what binds bilirubin in plasma

A

albumin

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36
Q

what conjugates bilirubin

A

bilirubin UDP- glucoronyltransferase

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37
Q

what is deficient in crigler-Najjar syndrome

A

bilirubin UDP-glucoronyltransferase

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38
Q

what is treatment for crigler-Najjar

A

blue light therapy

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39
Q

e.g.s of some phase I enzymes

A

CYP450

haeme oxygenase I

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40
Q

what makes bile pigments

A

conjucated bilirubin

41
Q

what is deficient in dubin johnson syndrome

A

cMOAT

42
Q

alcohol water or lipid soluble

A

water soluble

43
Q

where is absorption of alchy faster, stomach or duo/SI

A

duo/SI

44
Q

what oxidises ethanol, into what

A

alcohol dehydrogenase, into acetaldehyde

45
Q

what are superior alcohol dehydrogenases

A

ADH1B2 and ADH1B3 (better than ADH1B*1)

46
Q

what converts acetaldehyde, into what

A

aldehyde dehydrogenase into acetate

47
Q

what is main aldehyde dehydrogenase responsible, and where in a cell

A

ALDH2, in mitochondria

48
Q

what is ALDH found in asians

A

ALDH2*2

49
Q

is ADH inducible?

A

nope

50
Q

What are the 3 ways to metabolise alcohol

A

main - ADH and ALDH
CYP2E1 - MEOS
catalase

51
Q

what metabolism pathways does alcohol induce

A

CYP2E1 and MEOS

52
Q

what is MEOS, what does it do

A

microsomal enzyme oxidising system - CYP2E1 converts ethanol to acetaldehyde

53
Q

problem with alcoholics and vit a

A

vit a is oxidised to active metabolites by ADH and ALDH - competitive inhibition by alchy

54
Q

what is catalase system, where is it, when mainly used

A

haeme containing enzyme in liver peroxisomes, minor pathway, mainly used in fasting state

55
Q

why do you get fatty liver in alcoholics

A

breakdown of alcohol produced acetate then acetyl-CoA
ADh and ALDH reactions produce large quantities of NADH - inhibits gluconeogenesis, inhibits Cori cycyel, favours lactate to pyruvate, inhibits B-oxidation adn crebs cycle
so environment favours fatty acid synthesis

56
Q

how do alcoholics damage their liver

A

for one, fatty liver BUT
decreased intake of antioxidatnts - from dietary neglect and alcohol consumption
interferes with glutathione transport through membranes leading to depletion in mitochondria
MEOS pathway produces ROS that are not mopped up by glutathione

57
Q

wernicke korsakoff syndrome

A

result of thiamine deficiency from chronic alcohol abuse - leading to alcoholic dementia

58
Q

drug to treat alcoholics, what does it do

A

disulfram - irreversible ALDH inhibitor

59
Q

cells that make up exocrine pancreas

A

acinar cells - zymogen granules

duct cells - line duct, secrete mucous and bicarb

60
Q

how do duct cells secrete bicarb

A

uptake bicarb through basolateral side with bicar/Na transporter
CO2 and H2O diffuse in - carbonic anhydrase adds to bicarb pool
bicarb is secreted into lumen via bicar/Cl transporter
water and Na secretion through paracellular route - follows bicarb

61
Q

what regulates bicarb secretion

A

secretin

62
Q

what form is pancreatic amylase secreted in

A

active form

63
Q

what is a zymogen

A

enzyme secreted in inactive form

64
Q

what starts of cleavage cascade of pancreatic enzymes

A

enteropeptidase from intestinal mucosal epithelial cells

65
Q

what does enteropeptidase do, what does it lead to

A

enteropeptidase cleaves trypsinogen to trypsin, which cleaves procolipase to colipase

66
Q

where are enzymes for protein digestion from

A

gastric, pancreatic, brush border

67
Q

what are most bile acids conjugated to, to form what, why

A

conjugated to glycine or taurine to form bile salts, become neg charged molecules with increased solubility

68
Q

bile acids/salts form ___ with __ and __ to maintain___

A

form mixed micelles with cholesterol and phospholipids to maintain cholesterol solubility

69
Q

what happens if cholesterol > bile salt solubilization

A

gallstones

70
Q

bile release stimulated by

A

CCK

71
Q

bile reabsorbed in

A

ileum

72
Q

what does CCK release cause

A

gall bladder contraction
pancreatic enzyme release
satiety signal
insulin release

73
Q

why is CO in breath a measure of haeme destruction

A

bc haeme oxygenase converts haem to bilivirdin and CO

74
Q

where is haeme oxygenase found

A

microsomal enzyme in macs and kupfer cells of liver

75
Q

where is bilivirdin reductase found

A

cytosol

76
Q

where is bilirubin conjugated

A

smooth ER of hepatocytes

77
Q

how does unconjugated bilirubin accumulate in hepatocytes

A

binds to ligandin on hepatocytes - higher affinity for bilirubin than albumin

78
Q

how much bilirubin do you have to have to have jaundice

A

> 35um (normal is 17)

79
Q

what is HO-I polymorphism resulting in jaundice

A

decrease in GT repeats in promoter, increases HO-I expression - so increases bilirubin production resulting in jaundice

80
Q

extrinsic cause of prehepatic jaundice

A

malaria

81
Q

intrinsic cause of prehepatic jaundice

A

sickle cell

82
Q

if you have prehepatic jaundice, what colour is your urine and stools

A

normal coloured, bc increase in unconjugated bilirubin

83
Q

if have post-hepatic jaundice, what colour is urine and stools

A

pale stools and dark urine (less conjugated bilirubin is getting to stools bc blockage - so decreased colour, and more is leaking into the blood - so increase urine colour)

84
Q

what type of bilirubin increases in cirrhosis

A

increase in unconjugated bc liver can’t process

85
Q

how many newborns have jaundice in days 1-3

A

> 80%

86
Q

why do neonates get jaundice

A
  1. neonatal RBCs have shorter lifespan so increased turnover and more bilirubin produced
  2. transient deficiency in conjugation and therefore clearance of bilirubin
87
Q

where does neonatal jaundice start, where does it spread

A

starts at head, spreads to feet

88
Q

why is prolonged jaundice in neonates bad

A

can lead to neurological problems

89
Q

breasfeeding jaundice

A

jaundice due to problems breastfeeding

90
Q

breast milk jaundice

A

jaundice DUE TO THE BREAST MILK

91
Q

two genetic mutations that could result in neonatal jaundice

A

G6PD - glucose 6 phosphate dehydrogenase

galactosaemia due to galactose-1-phosphatase deficiency

92
Q

why does deficiency in glucose 6 phosphate dehydrogenase result in jaundice

A

RBCs have no mitochondria, so rely on pentose phosphate pathway for NADPH to preserve reduced glutathione levels to counteract oxidative stress
G6PD is the first step in the pentose phosphate pathway
without this, oxidative damage accumulates in RBCs, leading to increased destruction

93
Q

what does galactosaemia cause

A

deficiency in galactose 1 phosphase means inability to break down galactose, leading to jaundice
toxic levels of galactose IP accumulate leading to brain damage and cirrhosis

94
Q

what is name for bilirubin encephalopathy

A

kernicterus

95
Q

what is kernicterus due to, where does it primarily occur in brain

A

due to increases in unconjugated biliurubin, primarily in basal ganglia

96
Q

what is bilirubin induced neurologic dysfunction

A

clinical signs of bilirubin toxicity - acute and chronic phases

97
Q

why is high unconjugated bilirubin levels a problem

A

bc lipid soluble, can cross BBB and penetrate neurons and glia

98
Q

what are the greatest risk factors for bilirubin induced brain injury

A

prematurity and low birth weight

exam revision (15 decks)

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