Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IDT Winter > Anticoag Medchem > Flashcards

Anticoag Medchem Flashcards

1
Q

how is a fibrin clot formed?

A

a protease converting an inactive precursor protein (zymogen) into another catalytically-active protease

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

describe the process of turning the inactive Factor X into an insoluble fibrin clot

A

Factor X (inactive) is activated by the tissue factor pathway and the contact activation pathway which are vitamin K dependent to become Factor Xa (active). Factor Xa then activates Prothrombin (Factor II, inactive) to Thrombin (Factor IIa, active) which is also vitamin K dependent. Factor IIa then activates Fibrinogen to Fibrin. Fibrin Stabilizing Factor (Factor XIIIa) then activates Fibrin to a fibrin clot

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

what is the mechanism of vitamin K-dependent clotting factor activation? where does warfarin interfere?

A

Vitamin K epoxide is reduced by Vitamin K oxido-reductase (VKOR) into reduced vitamin K. This reduced vitamin K is used by vitamin k-dependent carboxylate to activate prothrombin to thrombin.
warfarin blocks VKOR which will ultimately block the process of forming a fibrin clot

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

warfarin is converted to 7-hydroxywarfarin via which enzyme?

A

CYP2C19

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

why does warfarin have slow onset?

A

functional coagulation cofactors are not affected by warfarin, so normal protein catabolism slowly breaks them down

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

for warfarin: normal genotype is cyp2C91/1. how do the following mutations affect warfarin dosing?
CYP2C92/1
CYP2C93/1
CYP2C93/3

A

CYP2C92/1: 19% lower dose
CYP2C93/1: 34% lower dose
CYP2C93/3: 78% lower dose

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

Tecarfarin is a prodrug that functions similarly to warfarin. It is converted to it’s active metabolite via?

A

esterase

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

dabigatran etexilate (pradaxa) is a prodrug converted to dabigatran via?
what is it mainly used for?

A

esterase
preventing VTE after knee or hip surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which factor IIa inhibitor was taken off the market due to concerns over potential liver toxicity?

A

ximelagatran (Exanta)

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

what routes of metabolism does Rivaroxaban (Xarelto) have?
what is it used for?
which drugs are strong inducers of cyp3A4 that we need to use caution for?

A

Cyp3A4 and oxidation
prevention of VTE after knee or hip surgery
rifampicin and phenytoin

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

what is apixaban (eliquis) used for?

A

prevention of VTE after knee or hip surgery, and reducing the risk of stroke and systemic embolism in pts with afib

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

what is edoxaban (savaysa) used for?

A

afib, DVT, and pulmonary embolism

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

what is betrixaban (bevyxxa) used for?

A

reversal agent for inhibiting Xa drugs causing bleeding or when emergency surgery is required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the structuring of heparin?

A

a large polysaccharide chain of alternating D-glucuronic acid and N-Ac-D-glucosamine units. It is heavily O- and N-sulfated

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

Heparin is considered a key pentasaccharide that’s recognized by?

A

antithrombin III

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

why is heparin no longer isolated from bovine lung?
what is it isolated from instead?
how can it be administered?

A

due to bovine spongiform encepalopathy aka mad cow disease
porcine
IV or SC

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

what is heparins mechanism of action?

A

heparin binds to antithrombin III and induces a conformational change to ATIII that promotes binding to thrombin. Thrombin then binds to the heparin ATIII complex which inactivates the thrombin. the thrombin ATIII complex is released from heparin and it can bind again

18
Q

what is low molecular weight heparins mechanism of action?

A

ATIII binds to LMWH and induces a conformational change. Factor Xa then binds to ATIII and becomes inactivated. the Xa ATIII complex is released and LMWH can bind again

19
Q

how is fondaparinux sodium different from heparins and LMWH?

A

it is more selective for inhibiting factor Xa. it is more effective in preventing VTE after surgery

20
Q

Idrabiotaparinux is a derivative of fondaparinux, what is its main advantage?

A

it is easily suppressed with IV administration of avidin

21
Q

what are the SEs of heparin?

A

heparin induced thrombocytopenia (HIT) which is divided into 2 types:
HIT type I is a non-immunologic response to heparin which causes transient thrombocytopenia but little increase in thrombosis risk
HIT type II results in formation of antibodies that activate platelets. its a main complex of heparin with platelet factor 4 causing thrombocytopenia and excessive thrombin generation with increased risk of thrombosis. this requires immediate stopping of heparin use and administration of a direct thrombin inhibitor

22
Q

if a patient hemorrhages from using heparin, what do we use to inactivate it?

A

protamine sulfate

23
Q

what is lepirudin?

A

a recombinant hirudin that works as a direct thrombin inhibitor that does not require antithrombin III

24
Q

what is argatroban?
what metabolizes it?
how is it administered?

A

a reversible direct thrombin inhibitor for prophylaxis and treatment of thrombosis in pts with HIT
Cyp3A4
IV or SC

25
Q

describe the process of platelet activation/aggregation

A

Arachidonic acid is converted to Thromboxane A2 via COX1 which causes phospholipase C activation. Then platelet calcium levels increase causing a conformational change in glycoproteins IIb/IIIa which increases its affinity for fibrinogen leading to increased platelet aggregation

26
Q

what drugs can we use to inhibit COX1 to prevent platelet aggregation? what step in specific do they block?

A

aspirin and sulfinpyrazone
thromboxane A2 synthesis

27
Q

how does adenylate cyclase decrease platelet calcium to prevent platelet aggregation?

A

it converts ATP to cAMP which blocks calcium from binding to platelets

28
Q

how does PDE3 increase platelet calcium to promote platelet aggregation?

A

converts cAMP to AMP to prevent cAMP from blocking calcium

29
Q

how do the antiplatelet drugs clopidogrel and prasugrel inhibit platelet aggregation?

A

they bind and block the P2Y12 receptor (aka ADP receptor antagonist), an inhibitor of adenylate cyclase, to increase cAMP and inhibit platelet aggregation

30
Q

how do the antiplatelet drugs dipyridamole and cilostazol inhibit platelet aggregation? when do we use these drugs?

A

they inhibit PDE3 to increase cAMP and inhibit platelet aggregation
to prevent thrombus formation on prosthetic heart valves

31
Q

what was the first generation drug that was an ADP receptor antagonist and what was the issue with it?

A

ticlopidine: had GI effects and risk of neutropenia

32
Q

clopidogrel is a prodrug that is metabolized to its active metabolite by?

A

CYP2C19 and 3A4

33
Q

in regards to clopidogrel, in CYP2C19 loss-of-function carriers, what enzyme’s activity seems to be correlated with responsiveness to clopidogrel activity?

A

paraoxonase-1, a lactonase

34
Q

what metabolizes prasugrel?
what polymorphism causes increased thrombosis?
what is it used for?
is it faster or slower than clopidogrel? more or less bleeding risk?

A

esterase and cyp2B6
2B6*2
preventing atherothrombotic complications in pts undergoing percutaneous coronary intervention
faster, more bleeding risk

35
Q

what is ticagrelors mechanism of action?
what does it treat?\
metabolism?

A

a reversible inhibitor of P2Y12 receptor
acute coronary syndrome
O-deethylation

36
Q

what drug class is Abciximab?
what is it used for?

A

GP IIb/IIIa receptor antagonist
percutaneous coronary intervention

37
Q

what drug class is tirofiban?
what does it treat?
how is it administered?
what is an adverse effect?

A

GP IIb/IIIa receptor antagonist
unstable angina
as an injection
can cause bleeding

38
Q

what drug class is eptifibatide?`
what does it treat?
how is it administered?
what is an adverse effect?

A

GP IIb/IIIa receptor antagonist
unstable angina and during percutaneous transluminal angioplasty
can cause bleeding

39
Q

what is our bodies natural way to break up clots?

A

Tissue plasminogen activator activates plasminogen to plasmin which can turn an insoluble fibrin clot into soluble fibrin fragments

40
Q

what drug class is streptokinase?
what is it used for?
what are the issues with it?

A

indirect plasminogen activator
acute pulmonary embolism, DVT, acute MI
activates antibodies, so it can’t be used for several months. it also can cause bleeding

41
Q

what is Anistreplase?
what does it treat?

A

anisoylated plasminogen streptokinase activator complex
pulmonary embolism and DVT

42
Q

what is urokinase used to treat?

A

pulmonary embolism and DVT

IDT Winter (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions