Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

exam revision > biochem > Flashcards

biochem Flashcards

(98 cards)

Start Studying
1
Q

what are PGs metabolised by

A

lung endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

actions of PGE2

A

vasodilation
hyperalgesic
pyrogenic
angiogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

PGE2 - vasodilation

bradykinin - increases permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what enhances the pain response of bradykinin

A

PGE2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do NSAIDS supress fever

A

good access to brain, suppress COX2 induction in hypo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how is PGE2 gastroprotective

A

increase blood flow
angiogenesis
mucous secretion
decrease gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

FPR2 Rs - suppress neut recruitment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

oxy state of haemoglobin

A

R = relaxed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

does 23BPG increase or decrease in altitude training

A

increases - to increase O delivery to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is CO2 carried in blood

A

carbamate on N terminal of deoxy Hb

HCO3 converted by carbonic anhydrase - soluble in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

4 fates of cholesterol

A

membrane stability
bile acids
vitamin D and steroid hormones
transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where is HDL made

A

liver adn intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where is ACAT and what does it do

A

in liver, helps VLDL form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where is LCAT and what does it do

A

in plasma, helps HDL scavenge cholesterol from membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

define dyslipidaemia

A

disorder of lipid metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

where is CYP450 found

A

liver and intestines in ER (and mitochondria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where are main CYPs for detoxification

A

ER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are xenobiotics

A

hydrophobic toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

most common CYP for drug metabolism

A

CYP3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

CYP polymorphisms for codeine

A

CYP2D6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

structure of CYP

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what does grapefruit juice inhibit
CYP3A4
26
what do cruciferous vegies do
induce CYP1A2
27
name of system of blood vessels in spleen to facilitate removal of old/damaged RBCs
red pulp
28
how are old/damaged RBCs removed
carried to spleen by macs and removed by macs
29
free Hb is bound to __
haptoglobin
30
free heme is bound to__
hemopexin, albumin
31
free iron bound to __
transferrin
32
what does decrease in haptoglobin indicate
haemolytic anaemia
33
haeme recycling
haeme converted to bilivirdin by haeme oxygenase I and II | bilivirdin converted to bilirubin by bilivirdin reductase
34
which haeme oxygenase is inducible, which is constitutive
haeme oxygenase 1 - inducible | haeme oxygenase II - constitutive
35
what binds bilirubin in plasma
albumin
36
what conjugates bilirubin
bilirubin UDP- glucoronyltransferase
37
what is deficient in crigler-Najjar syndrome
bilirubin UDP-glucoronyltransferase
38
what is treatment for crigler-Najjar
blue light therapy
39
e.g.s of some phase I enzymes
CYP450 | haeme oxygenase I
40
what makes bile pigments
conjucated bilirubin
41
what is deficient in dubin johnson syndrome
cMOAT
42
alcohol water or lipid soluble
water soluble
43
where is absorption of alchy faster, stomach or duo/SI
duo/SI
44
what oxidises ethanol, into what
alcohol dehydrogenase, into acetaldehyde
45
what are superior alcohol dehydrogenases
ADH1B*2 and ADH1B*3 (better than ADH1B*1)
46
what converts acetaldehyde, into what
aldehyde dehydrogenase into acetate
47
what is main aldehyde dehydrogenase responsible, and where in a cell
ALDH2, in mitochondria
48
what is ALDH found in asians
ALDH2*2
49
is ADH inducible?
nope
50
What are the 3 ways to metabolise alcohol
main - ADH and ALDH CYP2E1 - MEOS catalase
51
what metabolism pathways does alcohol induce
CYP2E1 and MEOS
52
what is MEOS, what does it do
microsomal enzyme oxidising system - CYP2E1 converts ethanol to acetaldehyde
53
problem with alcoholics and vit a
vit a is oxidised to active metabolites by ADH and ALDH - competitive inhibition by alchy
54
what is catalase system, where is it, when mainly used
haeme containing enzyme in liver peroxisomes, minor pathway, mainly used in fasting state
55
why do you get fatty liver in alcoholics
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
how do alcoholics damage their liver
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
wernicke korsakoff syndrome
result of thiamine deficiency from chronic alcohol abuse - leading to alcoholic dementia
58
drug to treat alcoholics, what does it do
disulfram - irreversible ALDH inhibitor
59
cells that make up exocrine pancreas
acinar cells - zymogen granules | duct cells - line duct, secrete mucous and bicarb
60
how do duct cells secrete bicarb
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
what regulates bicarb secretion
secretin
62
what form is pancreatic amylase secreted in
active form
63
what is a zymogen
enzyme secreted in inactive form
64
what starts of cleavage cascade of pancreatic enzymes
enteropeptidase from intestinal mucosal epithelial cells
65
what does enteropeptidase do, what does it lead to
enteropeptidase cleaves trypsinogen to trypsin, which cleaves procolipase to colipase
66
where are enzymes for protein digestion from
gastric, pancreatic, brush border
67
what are most bile acids conjugated to, to form what, why
conjugated to glycine or taurine to form bile salts, become neg charged molecules with increased solubility
68
bile acids/salts form ___ with __ and __ to maintain___
form mixed micelles with cholesterol and phospholipids to maintain cholesterol solubility
69
what happens if cholesterol > bile salt solubilization
gallstones
70
bile release stimulated by
CCK
71
bile reabsorbed in
ileum
72
what does CCK release cause
gall bladder contraction pancreatic enzyme release satiety signal insulin release
73
why is CO in breath a measure of haeme destruction
bc haeme oxygenase converts haem to bilivirdin and CO
74
where is haeme oxygenase found
microsomal enzyme in macs and kupfer cells of liver
75
where is bilivirdin reductase found
cytosol
76
where is bilirubin conjugated
smooth ER of hepatocytes
77
how does unconjugated bilirubin accumulate in hepatocytes
binds to ligandin on hepatocytes - higher affinity for bilirubin than albumin
78
how much bilirubin do you have to have to have jaundice
>35um (normal is 17)
79
what is HO-I polymorphism resulting in jaundice
decrease in GT repeats in promoter, increases HO-I expression - so increases bilirubin production resulting in jaundice
80
extrinsic cause of prehepatic jaundice
malaria
81
intrinsic cause of prehepatic jaundice
sickle cell
82
if you have prehepatic jaundice, what colour is your urine and stools
normal coloured, bc increase in unconjugated bilirubin
83
if have post-hepatic jaundice, what colour is urine and stools
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
what type of bilirubin increases in cirrhosis
increase in unconjugated bc liver can't process
85
how many newborns have jaundice in days 1-3
>80%
86
why do neonates get jaundice
1. neonatal RBCs have shorter lifespan so increased turnover and more bilirubin produced 2. transient deficiency in conjugation and therefore clearance of bilirubin
87
where does neonatal jaundice start, where does it spread
starts at head, spreads to feet
88
why is prolonged jaundice in neonates bad
can lead to neurological problems
89
breasfeeding jaundice
jaundice due to problems breastfeeding
90
breast milk jaundice
jaundice DUE TO THE BREAST MILK
91
two genetic mutations that could result in neonatal jaundice
G6PD - glucose 6 phosphate dehydrogenase | galactosaemia due to galactose-1-phosphatase deficiency
92
why does deficiency in glucose 6 phosphate dehydrogenase result in jaundice
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
what does galactosaemia cause
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
what is name for bilirubin encephalopathy
kernicterus
95
what is kernicterus due to, where does it primarily occur in brain
due to increases in unconjugated biliurubin, primarily in basal ganglia
96
what is bilirubin induced neurologic dysfunction
clinical signs of bilirubin toxicity - acute and chronic phases
97
why is high unconjugated bilirubin levels a problem
bc lipid soluble, can cross BBB and penetrate neurons and glia
98
what are the greatest risk factors for bilirubin induced brain injury
prematurity and low birth weight

exam revision (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions