PC3 MOD 5.1

ACS (rupture of a plaque→ thrombus formation→ blood occlusion)

• unstable angina

• MI (blood has stopped flowing to a part of the heart)

  • ST- segment elevated MI (STEMI)

  • non-ST segment elevated MI (NSTEMI)

VTE

• blood clot in the lower or upper extremity veins

primary MI

• spontaneous presentation d/t atherothrombosis or an alt acute coronary pathology (spontaneous coronary artery dissection or coronary embolism)

secondary MI

• secondary to an acute condition where supply-demand imbalance unmasks obstructive coronary artery disease or results, new ventricular impairment

• w/out acute coronary syndrome

procedure-related MI

• is a complication from stent or graft failure or as a result of cardiac surgery

• w/in 30 days of procedure

platelet activation

damage (injury)→ collagen from vessel wall is exposed which causes the vessel to vasoconstrict→ platelets activated→ platelets release ADP, Ca, sertonin, & thrombaxane→ plug

take home on clotting factors

• stepwise fashion diff clotting factors are going to activate other clotting factors until factor II (prothrombin) is to converted to clotting factor IIA (prothrombin)

• thrombin activates fibrinogen to form fibrin

• fibrin strings help reinforce the platelet plug

proteins C & S

• our body’s own natural anticoags

what are the two important clotting factors

1. Factor X

2. Factor II

important players on the platelet side

1. thromboxane (TXA2)

2. P2Y12 receptor

3. GP IIb/IIIa receptor complex

ALL IMPORTANT TARGETS FOR DRUG Txs

virchows triad

circulating factors (hypercoagulable state)

vessel integrity (endothelial injury)

blood flow (circulatory stasis)