Venous Thromboembolisms Flashcards
where do fibrinolytics work?
convert plasminogen to plasmin
what can an arterial occlusion lead to
MI
stroke
peripheral ischemia
what can a venous occlusion lead to
DVT or PE
intravascular clot that floats within the blood
Emboli
are proximal or distal DVTs more concerning
distal DVTs due to associated w/ pulmonary embolism
what is our natural fibrinolytic that our body makes
tPA
what stabilizes the clot?
Fibrin
what dissolves the fibrin network as injury heals
Fibrinolysis
what likes to stick to clots
Cholesterol, so when the clot tries to break away it is stuck due to the cholesterol coating it
what is the extrinsic pathway for blood coagulation?
Tissue injury expressed tissue factor which complex and converts factor VII to VIIa which converts IX to IXa and X to Xa
what does Facto XA convert prothrombin to?
Thrombin which helps stabilize the clot
what removes small peptides from fibrinogen converting it to fibrin monomer which polymerizes to give the fibrin clot.
thrombin
what composes Virchow’s Triad
Venous stasis (sx, MI, varicose veins, CHF) venous endothelial injury (mechanical/ chemical) hypercoaguability (genetics)
gold standard for DVT diagnosis
Venography
what is useful in proximal DVTs
IPD (impedance plethysmography)
what can you test for in the blood that comes from fibrin-derived fragment that is released into circulation and broken down by the fibrinolytic system. Not super specific but can help rule out
D-Dimer
If non-invasive tests are negative for DVT but clinically suspicious what should you do?
Perform serial tests on days 5-7 and again on days 10-14
If noninvasive tests are negative and suspect PE what should be done?
V/Q scan
3 main medications for DVT
platelet aggregation inhibitors
anticoagulants
fibrinolytics (thrombolytics)
what are platelet aggregation inhibitors
aspirin
dipyridamole
clopidogrel
glycoprotein IIb/IIIa inhibitions
what are glycoprotein IIb/IIIa inhibitors
Abciximab
tirofiban
eptifabtide
aspirin C/I
children under 12
breast feeding
hemophilia
PUD
what must you combine dipyridamole with?
aspirin
MOA of dipyridamole
Increase cAMP levels result in decreased thromboxane A2 synthesis and thus platelet aggregation.
ADRs with dipyridamole
HA
GI bleed
Contraindications w/ aspirin
patients w/ sever HYPOTN
caustions in patients w/ serious CAD
is dipyridamole superior to aspirin alone
NO
MOA of ticlopidine
Blocks ADP-induced platelet-fibrinogen and platelet-platelet binding.
indications for ticlopidine
prevention of stroke
coronary artery stinting
C/I with ticlopidine
Liver dysfunction
blood disorders
PUD
internal bleeding
MOA of clopidogrel and ROA
inhibits activation of the glycoprotein IIb\IIIa receptor on the surface of platelets, which is required for aggregation to occur.
(oral med)
what is often added to aspirin to obtain better platelet inhibition and is safer than ticlopidine.
Clopidogrel
MOA of abciximab and ROA
antibody fragment directed towards the glycoprotein IIb/IIIa receptor of platelets. Binding & Blocking the receptor prevents platelet aggregation.
IV drug
indications for abciximab
prevention of ischemic cardiac complications in patients undergoing PCI
short term prevention of MI in patients w/ unstable angina
contraindications for abciximab
active bleeding
ADRs of abciximab
hemorrhage
N/V
HPOTN
concern with tirofiban and eptifabitide
potentially antigenic so should only be used once
MOA for heparin
Binds to antithrombin III and accelerates inactivation of coagulation factors
Binds to thrombin (inhibit activity)
binds and inhibits Factor Xa which converts prothrombin to thrombin
What does antithrombin III do?
Inhibits the binding of fibrinogen to thrombin and hence is an anticoagulant
what does Low molecular weight heparin inactivate?
Factor Xa (doesn't bind as well to thrombin)
what is the route of administration for low molecular weight heparin?
Sub Q