Strokes And Venous Thromboembolism Flashcards Preview

Pharm Block 11 > Strokes And Venous Thromboembolism > Flashcards

Flashcards in Strokes And Venous Thromboembolism Deck (58):
1

What is the most common type of stroke

Ischemic

2

What are the two types of strokes

Ischemic and hemorrhagic

3

Risk factors for strokes

HTN
Smoking
DM
A fib
Dyslipidmeia

4

Clinical presentation of stroke

Weakness on one side of the body, inability to speak, loss of vision, vertigo, and falling

5

pathophysiology of VTE (venous thromboembolism)

Potentially fatal
Clot formation from deep veins and/or pulmonary embolism

6

Clinical presentation of VTE

DVT=leg swelling, pain, warmth
PE= cough, chest pain, shortness of breath, hemoptyiss

7

Which is more fatal, DVT or PE

PE

8

What category of drugs do we use to prevent strokes

Antiplatelet drugs

9

What are the antiplatelet drugs we use to prevent strokes

-Aspirin
-ADP receptor blockers (clopidogrel)
-glycoprotein IIa/IIIb inhibitors (abciximab)
-PDE III inhibitors (dioyramidole)

10

what is the most important antiplatelet drug used to prevent strokes

Aspirin

11

MOA of aspirin

Irreversibly inhibits cyclooxygenase to prevent synthesis of TXA2 (which causes platelet aggregation)
-because platelets dont have a nucleus, they cant synthesize more COX so the drop in TXA2 levels persists for the life of the platelet (10 days)

12

Use of aspirin

Prevent TIAs and ischemic stroke

13

Side effect of aspirin

Bleeding

14

Which drug used to prevent strokes inhibits platelet aggregation

Aspirin

15

MOA of ADP receptor blockers (clopidogrel)

Irreversibly inhibit ADP receptors preventing ADP-mediates platelet activation

16

Use of clopidogrel

Prevent TIAs and strokes in patients who cannot tolerate aspirin, sometimes combined with aspirin in high risk parents

17

Side effects of clopidogrel

Bleeding

18

If a patient cannot tolerate aspirin, which drug should they be switched to

Clopidogrel

19

Glycoprotein IIa/IIIb inhibitors

Abciximab
Prevents strokes
Antiplatelet

20

MOA of abciximab

Block the binding of fibrinogen with its receptor (IIa/IIIb) preventing platelet activation and cross-linking

21

Use of abciximab

Coronary angioplasty to prevent clots

22

Side effect of abciximab

Bleeding

23

PDEIII inhibitor MOA

Block the breakdown of cAMP; more cAMP prevents platelets from aggregating

24

Use of PDE III inhibitors

Combined with aspirin for antiplatelet benefits

25

Adverse effects of PDEIII inhibitors

Bleeding

26

What is PDEIII inhibitor similar too

Inamrinole for acute CHF

27

What are the two most common antiplatelet used to prevent strokes

Aspirin and clopidogrel

28

What is used for immediate treatment of strokes

Thrombocytes (fibrinolytics or clot busters)

Alteplase

29

What is the name of the thromblytic used to immediately treat a stroke

Alteplase (AKA tissue plasminogen activator or tPA)

30

When should alteplase be given to a stroke patient

Within 3 hours to decrease mortality and preserve organ failure

31

MOA of alteplase

Thrombolytic

Binds to fibrin-bound plasminogen to catalyze the conversion of plasminogen to plasma. Plans in readily breaks the color

Breaks up the clot pretty much

32

Side effects of alteplase (thrombolytics)

Bleeding

33

What are the anticoagulants used to prevent VTE

Heparin
enoxaparin
Warfarin
Direct thrombin inhibitors: dabigatran
Direct factor Xa inhibitors: rivaroxaban

34

What are the clotting factors affected by warfarin

2,7,9,10

35

What are the clotting factors affected by heparin

2a,9a,10a,12a

36

What are clotting factors?

Protease

37

What is the final step in the clotting cascade?

Fibrinogen to fibrin

38

What’s the difference between fibrinogen and fibrin

Fibrinogen is so;lube and fibrin is insoluble (forms the clot)

39

How does alteplase break up the clot

Takes plasminogen to fibrin and turns it into plasmin

40

Are heparin and enoxaparin acute or chronic treatments

Acute

41

MOA of heparin

Catalyze the binding to antithrombin III (a serine protease inhibitor) to factors 2a, 9a, 10a, and 12a resulting in their rapid inactivation

42

Use of heparin

Give IV for rapid anticoagualtion for VTE

43

Side effects of heparin

Bleeding, heparin induced thrombocytopenia
-this is problem if taking more than 5 days

44

Antidote for heparin

Protagonist sulfate (chemical antagonism)
-binds to theheparin and immediately stops it

45

Which is faster, heparin or enoxaparin

Heparin

46

MOA of enoxaparin

Low molecular weight heparin that binds ATIII with primary activity against factor 10a (rapid inactivation)

47

What anticoagulant is specific to factor 10a

Enoxaparin

48

why is warfarin dangerous

Because it takes a long time to show up on labs, must watch for 3 days to see benefit

49

MOA of warfarin

Decreases hepatic synthesis of vitamin K dependent factors 2, 7, 9, 10. Specifically blocks witamin K epoxied reductase prevention the regeneration of vitamin K

50

Use of warfarin

Oral for long term anticoagulation for VTE prevention; a fib

51

Side effects of warfarin

Bleeding; lots of drug interactions

52

Antidote for warfarin

Vitamin K
-takes a long time though
Fresh frozen plasma
-rapid treatment
-already has clotting factors in it

53

Vitamin K dependent factors

2,7,9,10

54

MOA of direct thrombin inhibitors: dabigatran

Directly inhibits thrombin (doesn’t work via ATIII)

55

Side effects of direct thrombin inhibitors :dabigatran

Blooeding, not need to monitor PT or INR

56

What is a good alternative to warfarin

Direct thrombin inhibitors: dabigatran

Rapid

57

MOA of direct factor 1Xa inhibitors: rivaroxaban

Directly inhibits factor Xa (doesn’t work via ATIII)

58

Side effects of direct factor Xa inhibitors: rivaroxaban

Bleeding
No need to monitor PT or INR