antiplatelets Flashcards
(26 cards)
thrombophilias
- deficiency of antithrombin or proteins C or S
- the presence of activated protein C resistance (eg factor V Leiden gene mutation)
- the prothrombin gene mutation (20210A)
- antiphospholipid antibodies—it is reasonable to test for antiphospholipid syndrome in all patients with an unprovoked VTE.
irreversible cyclooxyrgenase inhibitors
aspirin
adverse effects of aspirin
Reye syndrome
Aspirin exacerbated respiratory disease
GI upset
Salicylate toxicity
Affects the kidneys in a dose-dependent manner
Low doses → uric acid retention
High doses → uric acid excretion
P2Y12 receptor antagonists
Clopidogrel
Prasugrel
Ticagrelor
Ticlopidine
Cangrelor
P2Y12 receptor antagonist adverse effects
Allergic reactions
Hemorrhage
GI upset
Glycoprotein IIb/IIIa inhibitors
Abciximab
Eptifibatide
Tirofiban
Glycoprotein IIb/IIIa inhibitor adverse effects
Acute thrombocytopenia
Hemorrhage
Reye syndrome
a rare type of hepatic encephalopathy that is associated with aspirin use for viral illness in children < 19 years
What are NOACs?
Non-vitamin K antagonist oral anticoagulants like dabigatran and rivaroxaban
NOACs have gained popularity due to their ease of use and fewer interactions.
How do vitamin K antagonists work?
eg. warfarin and phenprocoumon.
They inhibit the enzyme vitamin K epoxide reductase
This inhibition blocks hepatic synthesis of the active, reduced form of vitamin K.
What coagulation factors are affected by vitamin K antagonists?
- Factors II, VII, IX, and X
- Protein C
- Protein S
How are vitamin K antagonists metabolized?
By C-P450 (CYP) enzymes
This metabolism leads to interactions with various foods and drugs.
What is the mechanism of action for NOACs
NOACs act selectively via inhibition of thrombin (dabigatran) or factor Xa (rivaroxaban, apixaban, edoxaban).
What are the advantages of NOACs over vitamin K antagonists?
- Comparatively short half-life
- Fewer interactions
- Easier to control and administer
- Do not require regular monitoring
disadvantages of NOACs
Costly
Limited clinical experience with these drugs
Not recommended, and partially contraindicated, in patients with artificial cardiac valves
Not suited for patients with valvular atrial fibrillation
antidotes for NOACs
Antidotes available in the case of life-threatening bleeding
Dabigatran: idarucizumab (monoclonal antibody)
Apixaban and rivaroxaban: andexanet alfa
antidotes for coumarins
In cases of life-threatening bleeding:
Direct reversal by replacement (e.g., with prothrombin complex concentrate, FFP)
Indirect/delayed reversal by increasing production of coagulation factors (e.g., with vitamin K substitution)
coumarins are
vit K antagonists
What condition is associated with high doses of warfarin within the first few days of treatment?
Warfarin-induced skin necrosis
This condition occurs due to the rapid depletion of anticoagulants protein C and S compared to procoagulants.
Which vitamin K-dependent coagulation factors are inhibited by warfarin?
Factors II, VII, IX, and X
What is the consequence of the depletion of protein C and S compared to procoagulants?
Increased factor V and VIII activity, leading to an initial hypercoagulable state
This hypercoagulable state results in the formation of microthrombi.
List the symptoms of warfarin-induced skin necrosis.
- Painful purpura
- Hemorrhagic blisters
- Large areas of necrosis
These symptoms primarily affect subcutaneous adipose tissue.
What is a risk factor for developing warfarin-induced skin necrosis?
Underlying hereditary protein C deficiency
Patients with this deficiency are at increased risk due to reduced levels of anticoagulant activity.
What is a preventive measure for warfarin-induced skin necrosis?
Temporary bridging anticoagulation with heparin until warfarin has started to act
This helps to bridge the initial hypercoagulable state.
