anti thrombotics Flashcards
unfractionated heparin moa
binds to and inactivates Xa and IIa via antithrombin
reversible w/ protamine
LMWH moa
Xa and IIa via antithrombin, smaller than heparin and less risk
inhibit Xa and IIa to different degrees
fondaparinux moa
inactivates Xa via anti thrombin
indirect thrombin inhibitor delivery
heparins given IV and sub Q (LMWH and fonda)- large molecules and not orally absorbed
heparin toxicities
HIT- low platelets and thrombosis risk
parenteral direct thrombin inhibitors
argatroban and bivalirudin
use for parenteral direct thrombin inhibs
argatroban and bival are alternatives to heparins for ppl w/ HIT
what are the oral direct acting anti coags?
thrombin: dabigatran
Xa: apixaban, riveroxaban, edoxaban
warfarin moa
oral vit K inhib (vit K reductase enzyme inhib)- blocks carboxylation of II, VII, IX, X, C and S
PK issues w/ warfarin
slow onset, must have current coag factors degrade first- dealt with thru heparin bridging
warfarin drug interaction in blood
NSAIDs and drugs (like FADs) compete for albumin binding increasing the free warfarin in blood
genetic issues w/ warfarin PK
VKORC1 and CYP2C9 polymorphisms affect dosing: CYP2C9 metabolizes warfarin and VKORC1 is the target
diet issues w/ warfarin
variability in vit K intake from diet affects warfarin
pregnancy issues w/ warfarin
fetal warfarin syndrome: bone defects, facial defects, shortened fingers, etc
warfarin drug interaction in liver
amiodarone and cimetidine inhibit cyp2c9 which metabolizes warfarin
CV aspirin uses
unstable angina, MI, stroke
P2Y12 inhib CV uses
MI and stroke
GPIIb/IIIa CV uses
angioplasty and stent placement
cox 1/2 inhib toxicities
gastric damage
P2Y12 inhib examples and moa
clopidogrel, prasugrel, ticagralor
irreversibly block ADP receptor and platelet activation
PK issues for clopidogrel
it is a prodrug, must be activated by cyp2c19
some ppl are slow metabolizers w/ cyp2c19
gpIIb/IIIa inhib examples and moa
block receptor for fibrin on platelets
abciximab, eptifibitide, tirofiban
fibrinolytics general moa
stimulate activity of plasmin to break down clots
fibrinolytics examples
t-PA, alteplase, streptokinase
moa of atleplase and streptokinase
convert inactive plasminogen to plasmin
uses for fibrinolytics
immediate therapy for STEMIs, if no cath lab available
other uses for streptokinase and alteplase
both for immediate PE if pt is in shock,
alteplase also for immediate stroke tx
drugs for initial ACS
anti platelet and anti coag
drugs for secondary ACS prevention
dual anti platelet- ASA and P2Y12
drugs for acute VTE
anti coag w/ NOAC if low risk, fibrinolytics if in shock
drugs for chronic VTE
anti coag (NOAC unless has active cancer)
VTE prophylaxis for ill pts
anti coag like NOACs or VKA, enoxaparin is preferred over both but VKA good for renal disease
anti thrombotics for ppl w/ mechanical valve
VKA
heparin if procedure is needed