Pharm - CAD Flashcards
(11 cards)
Anticoagulant Agents (Goal, Types)
G: anti-thrombotics
T: UH, LMWH, Penta (Fondaparinux), DOACs (Hirudin)
Aspirin - ASA
Mechanism, Effect, Side Effect
M: blocks TxA2 synthesis from arachidonic acid to prevent TxA2 from activating other platelets
E: anti-platelet = anti-thrombotic
SE: dyspepsia (indigestion)
ADP Receptor Antagonists
Mechanism, Effect, Types
M: block P2Y12 receptor from binding ADP (which activates platelets)
E: anti-platelet = anti-thrombotic
Clopidogrel: irreversible P2Y12 binding, pro-drug, slow onset, quick offset
Prasugrel: irreversible P2Y12 binding, pro-drug, fast onset and lasts longer
Ticagrelor: reversible P2Y12 binding, active drug, fast onset, and shortest duration
GpIIb/IIIa Inhibitors
Mechanism, Effect, Types
M: prevent platelet aggregation by inhibiting receptor
E: Anti-platelet = anti-thrombotic
ReoPro/Abciximab: mAb, longest platelet-bound half-life and shortest plasma half-life
Eptifibitide/Tirofiban: small mLc, cyclic peptides, need to be continuously administered due to short platelet bound half life and longer plasma half life
Fibrinolytic Agents (mechanism, types)
Disrupt clots = anti-thrombotic
Streptokinase: antigenic, indirect plasmin activation (requires cofactor), non-specific
Alteplase (tPA): direct Pla activation, specific, requires continuous infusion
Tenecteplase (TNK-tPA): can be given as single bolus with HIGH specificity
Beta Blockers (Mechanism, Types, Clinical Use, Side Effects)
M: block cardiac beta-adrenergic receptors = reduce HR, Contractility, BP = reduce O2 demand = anti-ischemic
beta-1 specific: Nebivolol, METOPROLOL, atenolol, esmolol
B-1 & B-2: Propanolol, Nadolol, Carvediol
Carvediol: mixed alpha and beta inhibition - good for LV dysfunction by further dropping BP
CU: Angina, arrythmia, BP, HF
SE: bradycardia, asthma (b-2), sex dysfunction, fatigue, AV conduction delay, peripheral vascular disease
Nitrates
Mechanism, Side Effects
M: increase cGMP in SMC = activate MLC phosphatase = SMC relaxation = VD & decreased preload = increase O2 supply and decrease O2 demand
SE: AS, headache, syncope, hypotension, bradycardia
Calcium Channel Blockers
Mechanism, Types, Side Effects, Tx
M: decrease VC, increase VD - decrease O2 demand and increase O2 supply
Dihydropyridines (Amlodipine, ‘-ipines’): most potent VDs, also decrease contractility (bad for HF patients), increase CBF
Diltiazem & Verapamil: increase diastole and VD
SE: bradycardia, HF, LV dysfunction, Peripheral Edema, SSS, Flushing, Dizziness, Hypotension
Tx: angina, HTN, SVT
Late Sodium Channel Inhibitors
Mechanism, type
M: Ischemia/HF naturally increases late I(na) - sodium overload - calcium overload (more ATP consumption = ischemia; contractile dysfunction, and electrical instability)
RANOLAZINE: inhibits late I(na) = less ATP consumption = anti-ischemia & more contractility; more contractility/relaxation = treats HF, decreases arrhythmias
ACE Inhibitors (Mechanism, Type, Tx, Side Effects)
M: block conversion of AngI to AngII and block bradykinin degradation
AngII: more aldosterone = water retention = high BP; VC = high BP; Symp Activation = high BP
T: ‘-prils’
Tx: HTN, CHF, prevent atherosclerotic complications, reno-protective
SE: cough/skin rxns/angioedema due to more bradykinin; renal dysfunction
Angiotensin Receptor Blockers
Mechanism, Type, Tx, Side Effects
M: block AT1 receptor for AngII (same as ACE-Is except no buildup of bradykinin)
T: ‘artans’ (angiotensin receptor antagonist)
Tx: HTN, HF, maybe CAD progression
SE: very infrequent, least amount of SE for anti-HTN meds
