Strokes And Venous Thromboembolism Flashcards
What is the most common type of stroke
Ischemic
What are the two types of strokes
Ischemic and hemorrhagic
Risk factors for strokes
HTN Smoking DM A fib Dyslipidmeia
Clinical presentation of stroke
Weakness on one side of the body, inability to speak, loss of vision, vertigo, and falling
pathophysiology of VTE (venous thromboembolism)
Potentially fatal
Clot formation from deep veins and/or pulmonary embolism
Clinical presentation of VTE
DVT=leg swelling, pain, warmth
PE= cough, chest pain, shortness of breath, hemoptyiss
Which is more fatal, DVT or PE
PE
What category of drugs do we use to prevent strokes
Antiplatelet drugs
What are the antiplatelet drugs we use to prevent strokes
- Aspirin
- ADP receptor blockers (clopidogrel)
- glycoprotein IIa/IIIb inhibitors (abciximab)
- PDE III inhibitors (dioyramidole)
what is the most important antiplatelet drug used to prevent strokes
Aspirin
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)
Use of aspirin
Prevent TIAs and ischemic stroke
Side effect of aspirin
Bleeding
Which drug used to prevent strokes inhibits platelet aggregation
Aspirin
MOA of ADP receptor blockers (clopidogrel)
Irreversibly inhibit ADP receptors preventing ADP-mediates platelet activation
Use of clopidogrel
Prevent TIAs and strokes in patients who cannot tolerate aspirin, sometimes combined with aspirin in high risk parents
Side effects of clopidogrel
Bleeding
If a patient cannot tolerate aspirin, which drug should they be switched to
Clopidogrel
Glycoprotein IIa/IIIb inhibitors
Abciximab
Prevents strokes
Antiplatelet
MOA of abciximab
Block the binding of fibrinogen with its receptor (IIa/IIIb) preventing platelet activation and cross-linking
Use of abciximab
Coronary angioplasty to prevent clots
Side effect of abciximab
Bleeding
PDEIII inhibitor MOA
Block the breakdown of cAMP; more cAMP prevents platelets from aggregating
Use of PDE III inhibitors
Combined with aspirin for antiplatelet benefits
Adverse effects of PDEIII inhibitors
Bleeding
What is PDEIII inhibitor similar too
Inamrinole for acute CHF
What are the two most common antiplatelet used to prevent strokes
Aspirin and clopidogrel
What is used for immediate treatment of strokes
Thrombocytes (fibrinolytics or clot busters)
Alteplase
What is the name of the thromblytic used to immediately treat a stroke
Alteplase (AKA tissue plasminogen activator or tPA)
When should alteplase be given to a stroke patient
Within 3 hours to decrease mortality and preserve organ failure
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
Side effects of alteplase (thrombolytics)
Bleeding
What are the anticoagulants used to prevent VTE
Heparin enoxaparin Warfarin Direct thrombin inhibitors: dabigatran Direct factor Xa inhibitors: rivaroxaban
What are the clotting factors affected by warfarin
2,7,9,10
What are the clotting factors affected by heparin
2a,9a,10a,12a
What are clotting factors?
Protease
What is the final step in the clotting cascade?
Fibrinogen to fibrin
What’s the difference between fibrinogen and fibrin
Fibrinogen is so;lube and fibrin is insoluble (forms the clot)
How does alteplase break up the clot
Takes plasminogen to fibrin and turns it into plasmin
Are heparin and enoxaparin acute or chronic treatments
Acute
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
Use of heparin
Give IV for rapid anticoagualtion for VTE
Side effects of heparin
Bleeding, heparin induced thrombocytopenia
-this is problem if taking more than 5 days
Antidote for heparin
Protagonist sulfate (chemical antagonism) -binds to theheparin and immediately stops it
Which is faster, heparin or enoxaparin
Heparin
MOA of enoxaparin
Low molecular weight heparin that binds ATIII with primary activity against factor 10a (rapid inactivation)
What anticoagulant is specific to factor 10a
Enoxaparin
why is warfarin dangerous
Because it takes a long time to show up on labs, must watch for 3 days to see benefit
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
Use of warfarin
Oral for long term anticoagulation for VTE prevention; a fib
Side effects of warfarin
Bleeding; lots of drug interactions
Antidote for warfarin
Vitamin K -takes a long time though Fresh frozen plasma -rapid treatment -already has clotting factors in it
Vitamin K dependent factors
2,7,9,10
MOA of direct thrombin inhibitors: dabigatran
Directly inhibits thrombin (doesn’t work via ATIII)
Side effects of direct thrombin inhibitors :dabigatran
Blooeding, not need to monitor PT or INR
What is a good alternative to warfarin
Direct thrombin inhibitors: dabigatran
Rapid
MOA of direct factor 1Xa inhibitors: rivaroxaban
Directly inhibits factor Xa (doesn’t work via ATIII)
Side effects of direct factor Xa inhibitors: rivaroxaban
Bleeding
No need to monitor PT or INR
