Pharmexam2pt3.txt

chronic stable angina, acute coronary syndrom (which includes unstable angina, SNTEMI, and STEMI)

• characterized by chest pain
• results from MI or imbalance of oxygen supply and demand
• cell dealth occurs with MI

reproducible pattern of pain following a given amount of exertion

• new onset of angina, worsening of angina, angina at rest
• this is a medical emergency

• results from plaque rupture leading to cell death
• limited to subendocardial myocardium
• less extensive than STEMI

• results from plaque rupture that leads to cell death
• extends the thickness of myocardial wall
• Q waves commonly seen

• caused by coronary artery vasospasm resulting in ischemia
• uncommon
• pain occurs at rest

troponin I and CPK-MB

• pressure equales tension in wall divided by radius of ventricle
• therefore, a dilated heart needs more oxygen to do the same work
• decreasing pressure decreases oxygen demand

coronary atherosclerosis (fixed obstruction)

• increase supply of oxygen (improve pulmonary function, treat anemia, improve O2 extraction by not smoking, prevent platelet adhesion with aspirin)
• decrease oxygen demand (reduce HR, wall tension, force of contraction)
• morphine sulfate (to relieve pain and decrease preload)

• treatment for chest pain
• M - morphine sulfate (given last)
• O - oxygen (given first)
• N - nitroglycerine (given second)
• A - aspirin (given first)

• alteplace, reteplace, streptokinase
• given to STEMI pts only

fibinolytic

aspirin, thienopyridines (ticlid, plavix)

• permanently inhibits COX1
• reduces risk of MI
• chew 325mg after chest pain
• antiplatlet therapy following MI/chest pain

• used as antiplatlet therapy in pts who cannot tolerate aspirin
• requires 3 days to see max effect

• glycoprotein receptor inhibitors
• given in combo with ASA and heparin
• bleeding is the main toxicity

• anticoagulant
• aPTT, Hgb/Hct, platelets to monitor

• low molecular weight heparin
• decreases mortality, MI, and recurrent angina after acute coronary syndrome
• bleeding is main toxicity

• anticoagulant
• first line therapy for pts with STEMI receiving thrombolytics
• do not use with patients with renal probs

nitroglycerine, isosorbide dinitrate, isorbide mononitrate

• causes venous and arterial dilation resulting in decrease preload and afterload (primarily venodilation)
• oral admin for prophylaxis, sublingual for acute attacks or prophylaxis (5-10 min b/f activity); also given trnsmucosally, topically, IV
• large first pass effect
• toxicity: burning under tongue, syncope, HA, tachycardia
• drug interaction: sildenafil citrate, cialis; causes decreased myocardial flow and ischemia

propanolol, atenolol, metoprolol

• beta blockers
• decrease O2 demand by decreasing HR, contractility, BP
• decreases r/o arrhythmias and infaction size, imroves survival after MI
• contraindication: cocain use (can use labetolol)
• minimizes HR therefore helping a pt to avoid aerobic threshold
• abrupt d/c may increase frequency, duration, severity of anginal attacks; taper over 2 weeks
• Patient related variables: raynauds, variant angina, DM, unstable HF, asthma, hearblock, bradycardia

verapamil, diltiazem, nifedipine

• decrease O2 demand by causing arteriolar dilation and by increasing inotropic state (diltiazem, verapamil)
• prevent and reverse coronary artery spasm, useful in variant angina
• can cause reflex tachycardia (esp nifedipine)
• toxicity: constipation, edema
• patient related variables: preexisting heart block, systolic HF, concurent use of beta-blockers, hypovolemia

• calcium channel blocker
• dyhodropyradine
• increases vasodilation, renin activation, HR

• calcium channel blockers
• nondyhydropyradines
• direct effects on heart
• decrease HR, contractility

• ASA
• clopidogrel
• beta blockers
• ACEI/ARBs
• aldosterone antagonists
• statins

• ASA
• statins
• ACEI/ARBs
• nitrates
• beta blockers
• calcium channel blockers