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PHARMACOGENOMICS > PG > Flashcards

PG Flashcards

1
Q

Her2+ gene treatment?

A

Trastuzumab or herceptin

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2
Q

treatment of oncogene V600E BRaf melanoma?

A

vemurafenib

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3
Q

treatment of myelogenous leukaemia

A

gleevec or imatinab

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4
Q

is haemophilia a simple disease and what does it affect?

A

simple genetic disease only affecting on gene - Factor 8 decrease in co-ag cascade

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5
Q

whats the gene that causes late onset alzhiemers called?

A

apolipoprotein E

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6
Q

how many variants of apolipoprotein?

A

E2,E3,E4

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7
Q

How much of a risk do you have to develop alzhiemers if you have one parent with E4 variant

A

4x

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8
Q

how much of a risk do you have of developing late onset alzheimers if you have both parents with the E4 variant

A

10x

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9
Q

difference between the variant (alleles) E4 and E2 apolipoprotein genes

A

E2 decreases risk of Azmrs

E4 increases risk of Azmrs

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10
Q

How are the variants caused?

A

SINGLE NUCLEOTIDE POLYMORPHISM

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11
Q

which genes that code for cytochrome p450 enzymes help treatment with warfarin? (anticoagulant)

A

CYP2C9

VKORC1 (vitamin k reductase)

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12
Q

which cytochrome p40 enzyme gene codes for anti-platelet drugs? and what are antiplatelet drugs called?

A

CYP2C19

and clopidogrels

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13
Q

what is the main component of coagulation?

A

fibrin

fluid converted into gel/like fibrin mixture

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14
Q

fibrous network/wall is responsible for what?

A
  • trapping and stopping microorganisms from entering the body
  • stopping bleeding by forming platelet plug
  • forming a bases for initiation of repair
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15
Q

What are co-agulation factors

A

plasma proteins that are inactive in the liver but become active once they are faced with vessel injury which causes them to undergo proteolytic cleavage - become active

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16
Q

phospholipids

A

found on the membrane of the platelets which are ACTIVATED

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17
Q

calcium ions

A

help coagulation factors to be activated

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18
Q

what does thrombin (factor 2 produce)

A

fibrinogen is activated (soluble) which is converted to fibrin (insoluble)

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19
Q

describe extrinsic pathway of coagulation

A

Factor 3 is converted into factor 3a
then factor 7 is converted into 7a which activates factor 10a from factor 10
then thrombin is activated (2a)
thrombin causes fibrinogen to be converted into fibrin
factor 13 causes the formation of fibrin polymer

20
Q

describe the intrinsic pathway of coagulation

A

factor 12 into 12 a then 11 into 11a then causes 9 into 9 a which causes 8 into 8a
8a and 9a activate 10a from 10
causes thrombin to be activated (factor 2 to 2a)
causes thrombin to cause fibrinogen to convert into fibrin
factor 13 a causes fibrin polymer to be formed

21
Q

intrinsic pathway caused by:

A

exposure to endothelial collegen

22
Q

extrinsic pathway caused by

A

exposure to tissue factor (released during injury)

extrinsic occurs first

23
Q

what is deep vein thrombosis?

venous thrombosis

A

thrombus formed in deep veins such as legs due to sluggish flow - this causes clots to form
this causes the venous thromboembolism to bud off into pulmonary ciruculation and block pulonary artery

24
Q

treatment for deep vein thrombosis

A

anticoagulants such as warfarin

25
Q

what is arterial thrombosis?

diseases associated?

A

platelets start to aggregate and form clots in the arteries which may cause myocardial infarction and ischaemic stroke

26
Q

treatment of arterial thrombosis

A

anticoagulants long term/prophylaxis

fribrinolytics - clot busters (short term)

27
Q

which four diseases does warfarin treat

A 
DVT
pulmonary embolisms
arterial fibrillation 
heart valve receivers
and can be used as aprophylactic drug (days before opperation)
28
Q

whats a narrow therapeutic range

A

small changes in the dose can cause major changes so have to administer dose carefully

29
Q

side effects of warfarin

A

haemorrhage and bleeding

30
Q

what does vitamin K? reductase do?

A

VKR is cofactor for GGCX (gamma glutamyl carboxylase)

which activates factor 2,7,9 and 10 by binding calcium

31
Q

what does warfarin do to vitamin k reductase

A

acts as an antagonist - inhibits it
inhibiting doesnt allow it to co-factor for GGCX which prevents activation of factor 2,7,9 and 10 by calcium binding not happening

DECREASES COAGULATION

32
Q

dosing depends on what?

A

genetics, weight, other medications and diseases and diet

33
Q

which enzymes cause variability in pharmacokinetics of warfarin?

A

CYP2C9(liver enzyme) and VKORC1 (site of warfarin action - antagonist)

34
Q

what are the two stereoisomers of warfarin?

A

R and S at chiral centre 9

S is 5x more effective at breaking down cytocrhome p450 in the liver to produce metabolites

35
Q

what metabolites of CYP2C9 are formed?

A

6 and 7 hydroxy metabolites

36
Q

which variant of CYP2C9 is more effective?

A

variant 3

37
Q

what causes the variant CYP2C9 2

A

arginine replaced with cystine at 144 position

38
Q

what causes variant cyp2c9 3

A

isoleucine replaced with leucine at 359 position

39
Q 
warfarin dose in lower in patients with what phenotype?
a. TT
b.CC
c.CT
why?
A

a.TT because people with this genotype have a rare recessive bleeding disorder (deficiency of vitamin K reductase)
affected in INTRON 1

40
Q

Highest sensitivity to dosage?

A

variant 3 (more effective breakdown)

41
Q

highest resistance to warfarin?

A

VKORC1 - coding region cause warfarin resistance

42
Q

which ethnicity has more CYP2C9 3 and 2?

A

caucasians more than asians and africans

43
Q

which ethnicty has more noncoding (C) VKORC1?

A

asians

44
Q

which ethnicity has more coding TVKROC1?

A

cacasians more than africans

45
Q

whats the function first approach or genomic first approach?

A

genes should be analysed first before drug administration to find the best match of drug to suit the variations in each individual

46
Q

why percision medicine now?

A

we have the human genome project
we have better technologies (biomed analysis) now
we have better datasets to record information in

47
Q

ethical and legal issues with percision medicine

A

confidentiality of genetic info
fairness (insurance, employers)
- psychological impact
- reproductive use (having kids)
- clinical issues (doctors need to know how to handle patient - quality control)
- uncertanities with complex diseases (just cause you have succeptibility doesnt mean you have disease)
-expensive

PHARMACOGENOMICS (3 decks)

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