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IHO Week 5 > Regal- Thrombolytics, Anticoagulants, and Antiplatelet Drugs > Flashcards

Regal- Thrombolytics, Anticoagulants, and Antiplatelet Drugs Flashcards

1
Q

When do we interfere w/ hemostasis?

A

Prevent and treat thrombosis

  1. Venous thrombosis
  2. Arterial thrombosis–platelet activation is central
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2
Q

What agents do we use to control blood fluidity?

A

Antiplatelet agents
Parenteral anticoagulant heparin and its derivatives (Thrombin inhibitors direct/indirect)
Oral Coumadin anticoagulants (inhibitors of vit K)
Fibrinolytic agents to lyse pathological thrombi

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3
Q

What does aspirin do mechanistically?

A

It is an irreversible inhibitor of COX

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4
Q

Do platelets have Cox2?

A

NO

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5
Q

Can platelets make more COX

A

NO they don’t have a nucleus

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6
Q

What does aspirin do clinically?

A

Antipyretic, analgesic, anti-inflamatory

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7
Q

What are the adverse effects of aspirin?

A

Bleeding
GI disturbances
Tinnitus

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8
Q

What is the difference between low and high doses of aspirin?

A

LOW- antiplatelet

HIGH- inhibits COX1 and 2 in epithelial cells (anti-inflammatory)

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9
Q

What are the three ADP receptor antagonists?

A

Clopidogrel
Ticlopidine
Prasugrel

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10
Q

How do ADP antagonists work?

A

Irreversible ADP receptor antagonists that prevent activation of ADP receptor that would ultimately lead to platelet aggregation

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11
Q

How long do ADP receptor antagonists last?

A

days

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12
Q

When are ADP receptor antagonists commonly used?

A

Stenting

Recommended for pts that don’t tolerate aspirin

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13
Q

What are the adverse effects of ADP receptor antagonists?

A

BLEEDING

nausea, diarrhea, rash
severe leukopenia
TTP (very rare–ticlodipine)

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14
Q

Which ADP R Antag has the worst side effects?

A

Ticlodipine

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15
Q

Which ADP drug requires activation?

A

Clopidogrel via CYP2C10

**drugs that impair this isoform should be used w/ caution (omeprazole)

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16
Q

What does dipyridamole do?

A

Increases cAMP and inhibits platelet activation by inhibiting PDE3 (preventing the break down of cAMP) and inhibiting platelet uptake of adneosine, thus increasing adenosine interaction w/ adensoine receptor and increasing cAMP

PDE 3 inhibitor

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17
Q

What adverse effect is associated w/ dipyridamole?

A

Headache

b/c it’s a vasodilator

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18
Q

How is dipyridamole commonly prescribed? Why?

A

In combination w/ aspirin or warfarin

No beneficial effect by itself

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19
Q

What do GPiiB/IIIa receptor inhibitors do?

A

Prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets

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20
Q

How do abciximab, eptifibatide and tirofiban differ?

A

abciximab-Humanized MAB a against receptor
eptifibatide- fibrinogen analoguse
tirofiban- non-peptide competitive inhibitor

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21
Q

What are the three GPIIb/IIIa receptor inhibitors?

A

abciximab
eptifibatide
tirofiban

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22
Q

What is the one disadvantage of GpIIb/IIIa receptor inhibitors?

A

they have to be given IV

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23
Q

What are GpIIb/IIIa receptor inhibitors commonly used for?

A

w/ aspirin and heparin during angioplasty

for acute coronary syndromes

24
Q

What are the adverse effects of GpIIb/IIIa receptor inhibitors?

A

Bleeding

thrombocytopoenia

25
Q

What are the two types of thrombin inhibitors?

A

Direct and indirect?

26
Q

What are the 4 types of direct thrombin inhibitors?

A

Lepirudin
Bivalirudin
Agratroban
Dabigatran (ORAL)

27
Q

What are the three types of indirect thrombin inhibitors?

A

Unfractionated heparin
LMW heparin
Fondaparinux

28
Q

What do lepirudin, bivalirudin and argatroban and dabigatran do? How is dabigatran different?

A

bind directly to thrombin and inhibit the enzyme

dabigatrin is ORAL

29
Q

Which indirect thrombin inhibitors interact w/ antithrombin and enhance/accelerate its inactivation of Factors Xa?

A

Heparin
LMWH
Fondaparinux

30
Q

Which indirect thrombin inhibitors enhance/accelerate antithrombin’s inactivation of thrombin (IIa)?

A

Heparin and LMWH

31
Q

What is the end effect of indirect thrombin inhibitors?

A

Factor Xa and thrombin IIa don’t work so clotting doesn’t happen

32
Q

Unfractionated heparin requires close monitoring of…?

A

aPTT–activated partial thromboplastin time

33
Q

Does LMW heparin require monitoring?

A

No, it has more predictable pharamacokinetics

34
Q

What are the adverse effects of indirect thrombin inhibitors?

A

Bleeding

Heparin induced thrombocytopenia

35
Q

What causes Heparin induced thrombocytopenia?

A

Probably the development of IgG antibodies against complexes of heparin w/ platelet factor 4

**twice as likely in women than men

36
Q

Which indirect thrombin inhibitors only targets Xa?

A

Fondaparinux

37
Q

Which indirect thrombin inhibitors has no antidote effect?

A

Fondaprinux

LMWH has only parital
Heparin is full

38
Q

What does protamine do?

A

Combines w/ negatively charged heparin to form a stable complex that lacks anticoagulant activity

39
Q

What does protamine do to LMWH?

A

incompletely reverses its activity

40
Q

What are the two oral anticoagulant drugs?

A

Warfarin

Vitamin K

41
Q

What does Warfarin do?

A

Inhibits conversion of oxd vit K epoxide into it’s reduced form, vit K hydoquinone>

this inhibits vit K dependent gamma carboxylation of factors II, VII, IX and X and Prot C

42
Q

What’s important to know about the pharmakokinetics of warfarin?

A

Delayed hypothrombic effect

narrow TI–need enough so that you don’t clot and not enough that you don’t bleed all over

43
Q

What are the adverse effects of warfarin?

A

Bleeding
flatulence and diarrhea
cutaneous necrosis
chondrodysplasia

44
Q

What is the difference between R and S warfarin and which is the more active enantiomer?

A

S is more active enantiomer

S- metabolized by cyp2c9
R- metabolized by cyps1a1, 1A2, 3A4

45
Q

What is one of the worst things about warfarin?

A

It interacts with MANY drugs

46
Q

What are the effects of warfarin pharmacokinetically?

A

Inhibition of cyt450
Metabolism-> more warfarin
Decreased plasma protein binding

47
Q

What are the effects of increased warfarin on pharmacodynamics?

A

decreased platelet/clotting factor function

Decreased availabilty of vit K–>warfarin increases

48
Q

What are the effects of decreased warfarin pharmacokinetically and pharmacodynamically?

A

pharmacokinetically- induction of CYT p450 metabolism, decreased absorption

pharmacodynamically- increased clotting factor/vit K concentrations

49
Q

What do you do if a pt has been given TOO much warfarin and is bleeding uncontrollably?

A

STOP the drug

Add vit K–so enzyme can do it’s thing and make the right clotting factors (phytonodione)

50
Q

What are urokinases?

A

kidney enzymes that directly converts plasminogen to plasmin

51
Q

What are the three tPAs?

A

Alteplase
reteplase
tenecteplase

52
Q

What do tPAs do?

A

Preferentially activate plasminogen that is bound to fibrin which confines it to the thrombus rather than systemic activation.

53
Q

What do Fibrinolytic Drugs do?

A

Dissolve EXISTING life threatening thrombi

activate plasminogen

54
Q

How are fibrinolytic drugs given?

A

IV

Narrow spectrum of use

55
Q

What are the adverse effects of fibrinolytic drugs?

A

Bleeding

cost

56
Q

What is the MOA of alteplase, reteplase, tenecteplase?

A

Selective activation of fibrin bound plasminogen

IHO Week 5 (9 decks)

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