Anticoagulation I Dr. Covert Flashcards
Dr. Covert EXAM IV
What factors contribute to Thrombosis?
Virchow’s Triad
-Endothelial Injury
-Abnormal Blood flow (long travel)
-Hypercoagulability (contraceptives, pregnancy, cancer therapy)
What tests assess clotting disorders?
intrinsic: PTT (play table tennis - inside)
normal: 25-35 sec
extrinsic pathway: PT (play tennis - outside)
normal: 12 sec
Reasons for prophylactic anticoagulation therapy
Some risk of clot
-Immobility in hospitalized patients (some) changes in blood
Reasons for full-dose anticoagulation
Big Risk of clot:
-Atrial fibrillation: change in blood flow, risk of stroke
-Mechanical heart valves: platelets will stick to it, endothelial injury, change in blood flow
-certain clotting disorder: hypercoagulable state
Presence of clot:
-Deep vein thrombosis
-Pulmonary embolism
What are the available Anticoagulants and MOA?
MOA: inhibit clotting or deplete clotting factors
Drugs:
-Warfarin blocks the reduction of Vitamin K -> which is needed for the carboxylation of factors
-DOACS ( direct oral anticoagulants): like apixaban
-heparin
-enoxaparin (LMWH)
Indication for Anticoagulants
-DVT
-PE
-Atrial fibrillation
-red clot: fibrin rich
What is the MOA of Antiplatelets?
MOA: inhibit platelet aggregation
drugs: Aspirin, P2Y12 inhibitors (clopidogrelel, prasugrel, ticagrelor)
white clot: platelet-rich
Indication of Antiplateteltes
-prevents platelet clots, makes the blood slippier
Indication:
-Ischemic stroke (preventing platelet clot -> stroke)
-coronary artery disease (CAD)
-peripheral artery disease
What are the injectable Anticoagulants?
-Unfractionated Heparin (UFH)
-Enoxaparin (LMWH)
MOA Heparin
-Potentiates antithrombin III (ATII) activity à Inactivates thrombin (Factor II) MOA and Factor Xa
Onset and duration:
IV: immediately (quick ON, quick OFF - useful right before surgery to turn OFF the anti coag state for surgery)
SQ: 20-30 min, OFF: 1-2h
How is heparin cleared?
Reticuloendothelial system (binds to endothelial cells)
NOT hepatically or renally cleared
Which tests are used to assess the activity of heparin?
Therapeutic drug monitoring
-heparin works on the intrinsic pathway
-aPTT, anti-Xa
What are the side effects of heparin and how can it be reversed?
ADE: Heparin-induced-thrombocytopenia (immune cells activate platelet-clotting), bleeding
-reverse agent: Protamine
Heparin-induced-thrombocytopenia
-platelets release PF4
-PF4 binds to the long tail of heparin -> the body reacts and release IgG -> IgG binds to PF4/heparin-complex -> the complex binds to endothelial cells
-> causing release of tissue factor -> tissue factor increases thrombin generation -> CLOTTING
all platelets are bound to the complex, patients have low platelets but still activate the clotting cascade
Platelet level in patients with HIT
low platelets
-high risk of clotting
-HIT is diagnosed based on the 4T score (likelihood of HIT, Lexicomp calculator)
-> if at risk -> DC heparin/enoxaparin and change to argatroban (direct thrombin inhibitor)
MOA Enoxaparin (LMWH)
Lovenox
Potentiates ATIII activity; Inactivates Factor Xa more than Factor II due to the short tail