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Pharm Block 11 > Strokes And Venous Thromboembolism > Flashcards

Strokes And Venous Thromboembolism Flashcards

1
Q

What is the most common type of stroke

A

Ischemic

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2
Q

What are the two types of strokes

A

Ischemic and hemorrhagic

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3
Q

Risk factors for strokes

A 
HTN
Smoking 
DM
A fib 
Dyslipidmeia
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4
Q

Clinical presentation of stroke

A

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

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5
Q

pathophysiology of VTE (venous thromboembolism)

A

Potentially fatal

Clot formation from deep veins and/or pulmonary embolism

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6
Q

Clinical presentation of VTE

A

DVT=leg swelling, pain, warmth

PE= cough, chest pain, shortness of breath, hemoptyiss

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7
Q

Which is more fatal, DVT or PE

A

PE

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8
Q

What category of drugs do we use to prevent strokes

A

Antiplatelet drugs

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9
Q

What are the antiplatelet drugs we use to prevent strokes

A
  • Aspirin
  • ADP receptor blockers (clopidogrel)
  • glycoprotein IIa/IIIb inhibitors (abciximab)
  • PDE III inhibitors (dioyramidole)
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10
Q

what is the most important antiplatelet drug used to prevent strokes

A

Aspirin

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11
Q

MOA of aspirin

A

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)

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12
Q

Use of aspirin

A

Prevent TIAs and ischemic stroke

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13
Q

Side effect of aspirin

A

Bleeding

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14
Q

Which drug used to prevent strokes inhibits platelet aggregation

A

Aspirin

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15
Q

MOA of ADP receptor blockers (clopidogrel)

A

Irreversibly inhibit ADP receptors preventing ADP-mediates platelet activation

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16
Q

Use of clopidogrel

A

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

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17
Q

Side effects of clopidogrel

A

Bleeding

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18
Q

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

A

Clopidogrel

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19
Q

Glycoprotein IIa/IIIb inhibitors

A

Abciximab
Prevents strokes
Antiplatelet

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20
Q

MOA of abciximab

A

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

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21
Q

Use of abciximab

A

Coronary angioplasty to prevent clots

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22
Q

Side effect of abciximab

A

Bleeding

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23
Q

PDEIII inhibitor MOA

A

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

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24
Q

Use of PDE III inhibitors

A

Combined with aspirin for antiplatelet benefits

25
Q

Adverse effects of PDEIII inhibitors

A

Bleeding

26
Q

What is PDEIII inhibitor similar too

A

Inamrinole for acute CHF

27
Q

What are the two most common antiplatelet used to prevent strokes

A

Aspirin and clopidogrel

28
Q

What is used for immediate treatment of strokes

A

Thrombocytes (fibrinolytics or clot busters)

Alteplase

29
Q

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

A

Alteplase (AKA tissue plasminogen activator or tPA)

30
Q

When should alteplase be given to a stroke patient

A

Within 3 hours to decrease mortality and preserve organ failure

31
Q

MOA of alteplase

A

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
Q

Side effects of alteplase (thrombolytics)

A

Bleeding

33
Q

What are the anticoagulants used to prevent VTE

A 
Heparin 
enoxaparin 
Warfarin
Direct thrombin inhibitors: dabigatran
Direct factor Xa inhibitors: rivaroxaban
34
Q

What are the clotting factors affected by warfarin

A

2,7,9,10

35
Q

What are the clotting factors affected by heparin

A

2a,9a,10a,12a

36
Q

What are clotting factors?

A

Protease

37
Q

What is the final step in the clotting cascade?

A

Fibrinogen to fibrin

38
Q

What’s the difference between fibrinogen and fibrin

A

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

39
Q

How does alteplase break up the clot

A

Takes plasminogen to fibrin and turns it into plasmin

40
Q

Are heparin and enoxaparin acute or chronic treatments

A

Acute

41
Q

MOA of heparin

A

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

42
Q

Use of heparin

A

Give IV for rapid anticoagualtion for VTE

43
Q

Side effects of heparin

A

Bleeding, heparin induced thrombocytopenia

-this is problem if taking more than 5 days

44
Q

Antidote for heparin

A 
Protagonist sulfate (chemical antagonism)
-binds to theheparin and immediately stops it
45
Q

Which is faster, heparin or enoxaparin

A

Heparin

46
Q

MOA of enoxaparin

A

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

47
Q

What anticoagulant is specific to factor 10a

A

Enoxaparin

48
Q

why is warfarin dangerous

A

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

49
Q

MOA of warfarin

A

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
Q

Use of warfarin

A

Oral for long term anticoagulation for VTE prevention; a fib

51
Q

Side effects of warfarin

A

Bleeding; lots of drug interactions

52
Q

Antidote for warfarin

A 
Vitamin K
-takes a long time though 
Fresh frozen plasma
-rapid treatment 
-already has clotting factors in it
53
Q

Vitamin K dependent factors

A

2,7,9,10

54
Q

MOA of direct thrombin inhibitors: dabigatran

A

Directly inhibits thrombin (doesn’t work via ATIII)

55
Q

Side effects of direct thrombin inhibitors :dabigatran

A

Blooeding, not need to monitor PT or INR

56
Q

What is a good alternative to warfarin

A

Direct thrombin inhibitors: dabigatran

Rapid

57
Q

MOA of direct factor 1Xa inhibitors: rivaroxaban

A

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

58
Q

Side effects of direct factor Xa inhibitors: rivaroxaban

A

Bleeding

No need to monitor PT or INR

Pharm Block 11 (7 decks)

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