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IHO Week 5 > Thrombolytics, Anticoagulants and Anti-Platelets > Flashcards

Thrombolytics, Anticoagulants and Anti-Platelets Flashcards

1
Q

What does aspirin do?

A

It’s an irreversible COX1 inhibitor that permanently takes COX1 out of the equation for the life of a platelet

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2
Q

How does aspirin fight clotting?

A

Without COX1, the platelet can’t form TXA2, which it uses to attract and activate more platelets for the clot

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3
Q

What are the adverse effects of aspirin?

A

bleeding
GI disturbances
Tinnitus at high doses

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4
Q

What are three ADP receptor antagonists?

A

Clopidogrel
Prasugrel
Ticlopidine

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5
Q

How do the ADP receptor antagonists work against clotting?

A

ADP, like TXA2, is used by the platelet to activate additional platelets

By irreversibly binding to the ADP receptor, it blocks that activation

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6
Q

When are the ADP receptor antagonists used most often?

A

during stenting and for patients that can’t tolerate aspirin

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7
Q

What’s the downside of using an ADP receptor antagonist

A

it takes a while for them to work

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8
Q

What are the side effects of the ADP receptor antagonists?

A

bleeding!!!

nausea, diarrhea, rash, severe leukopenia, TTP

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9
Q

Of the three ADP receptor antagonists, which one has the worst side effects?

A

ticlopidine

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10
Q

Which of the ADP receptor antagonists do you really need to worry about for drug drug interactions? Why?

A

Clopidogrel

Because it may requires activation by CYP2C19 - so any drug that impairs that isoform (like omeprazole) whould be used with caution

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11
Q

How does dipyridamole work?

A

It is a phosphpdiesterase 3 inhibitor, which means you increase cAMP by preventing it’s breakdown to 5’ AMP

also inhibits platelet uptake of adenosine, so you increase cAMP even further

This inhibits platelet activation

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12
Q

What’s the main side effect of dipyridamole? why?

A

headaches 0 because it’s also a vasodilator

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13
Q

What are the three GPIIa-IIIb inhibitors?

A

abciximab
eptifibatide
tirofiban

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14
Q

How do the GPIIa-IIIb inhibitors work?

A

By binding to the receptor (which isn’t present until the platelet is activated), you prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets, so you don’t get clot formation

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15
Q

How does Abciximab differ from the other two: eptifibatide and tirofiban?

A

Abciximab is an antibody against the receptor while the other two are fibrinogen analogues that can bind the receptor with high affinity

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16
Q

What’s perk about the GPIIa-IIIb inhibitors stemsf rom the fact that they inhibit the final common pathway?

A

It means that they’ll work regardless of what activated the platelet in the first place

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17
Q

How are the GPIIa-IIIb inhibitors given?

A

IV (with aspirin and heparin during angioplasy or for acute coronary syndroms)

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18
Q

What are the adverse effects of the GPIIa-IIIb inhibitors?

A

bleeding and thrombocytopenia with chornic use

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19
Q

What is the most important thrombin inhibitor?

A

heparin

20
Q

What are the four DIRECT thrombin inhibitors?

A

lepirudin
bivalirudin
argatroban
dabigatran etexylate

21
Q

What are the three indirect thrombin inhibitors?

A

unfractionated heparin (HMW heparin)
low molecular weight heparin
Fondaparinux

22
Q

The indirect thrombin inhibitors work by helping what molecule? What do they help it do?

A

antithrombin

Heparin, LMWH and Fondaparinux all enhance its inactivation of factor Xa

Heparin and some LMWH also enhance antithrombin’s inactivation of thrombin IIa

either way…the end result is that Factor Xa and IIa don’t work, so you don’t get clotting

23
Q

Which requires mroe monitoring? unfracitonated heparin or low molecular weight heparin?

A

unfractionated - it’s pharmacokinetics are harder to predict, so you need to what the activated partial thromboplastin time closely (INR)

24
Q

What are the adverse effects of heparin, LMW heparin and Findaparinux?

A

bleeding and heparin-induced thrombocytopenia

25
Q

What is heparin-induced thrombocytopenia probalby the result of?

A

development of IgG antibodies against complexes of heparin with platelet factor 4 (also hwy it’s more common in women)

26
Q

Of the indirect thrombin inhibitors, which ones can be reversed?

A

Heparin you can reverse
LMWH can be partially reversed
Findaparinux cannot be reversed

27
Q

What drug do you give to reverse heparin?

A

protamine

28
Q

How does protamine work?

A

It’s a highly basic, positively charged peptide that combines with negatively charged heparin and to some extend LMWH) to form a stable complex that lacks anticoagulant activity

29
Q

What’s the most important ORAL anticoagulant?

A

Warfarin (coumadin)

30
Q

How does warfarin work?

A

It inhibits the conversion of oxidized vitamine K epoxide into its reduced form, vitamin K hydroquinone, which in turn inhibits vitamin-K dependent gamma-carbozylation of factors 2, 7, 9, 10 and protein C, so they don’t work

31
Q

Does warfarin work right away?

A

nope - takes a while

32
Q

Why is warfarin HYPERcoagulable before the INR increases?

A

Because it inhibits protein C and S before Factors 2, 7, 9 and 10. That’s why you have to give heparin early on.

33
Q

What are the adverse effects of warfarin?

A

bleeding
flatulence and diarrhea
cutaneous necrosis
chrondodysplasia punctata (birth defect)

34
Q

Warfarin is a racemic mixture of R- and S- forms. Which one is more active?

A

S is the active enantiomer

35
Q

What are two examples of genetic polymorphisms that affect sensitivity to warfarin?

A
  1. polymorphism in CYP2C9, which metabolizes S-warfarin
  2. polymorphism in the C1 subunit of vitamin K reductase which affects the susceptibility of the enzyme to inhibition by warfarin
36
Q

What pharmacokinetic changes woul increase the effects of warfarin?

A

inhibition of CYP450 metabolism

Decreased plasma protein binding

37
Q

What pharmacodynamic changes would increase the effects of warfarin?

A

decreased platelet/clotting factor function

decreased availability of vitamin K

38
Q

What are two pharmacokinetic changes that would decrease the effects of warfarin?

A

induction of CYP450 metabolism

Decreased absorption

39
Q

What are two pharmacodynamic changes that would decrease the effects of warfarin?

A
  • increased clotting factor concentration

Increased vitamin K concentrations

40
Q

What do you do if someone’s bleeding because of twoo much warfarin?

A
  1. stop the warfarin

2. give them vitamin K

41
Q

What are some of the ways you can add vitamin K?

A
  • phytonadione - vitamin K1
  • prothrombin complex concentrations
    Recombinant factor Ia
42
Q

What do we use as fibrinolytic drugs?

A

the Tissue Plasminogen activators (tPAs)
alteplase
reteplase
tenecteplase

43
Q

How do the fibrinolytic drugs work?

A

they activate plasminogen that is bound to fibrin, converting it to plasmin which will break the fibrin down

(this means it can’t break down fibrin systemically)

44
Q

How are the fibrinolytic drugs administered?

A

IV - they have a narrow spectrum of use

45
Q

What are the adverse effects of the tPAs?

A

bleeding and cost

IHO Week 5 (8 decks)

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