Exam 2- Integration of Chronic Ischemic Heart Disease Flashcards
Angiotensin Coverting Enzyme Inhibitors (ACE-I)
Drugs: Captopril Enalapril Lisionpril "Pril"
MOA: prevents conversion of angiotension I to angiotensin II
ADE: hyperkalemia, reduced renal filtration
Contraindications: pregnancy, ACE-I induced angioedema
May promote persistent cough and angioedema
May try ARB if ACE-I not tolerated except in worst cases of angioedema
Angiotensin Receptor Blockers (ARBs)
Drugs:
Losartan
“Sartan”
MOA: angiotensin II receptor antagonist
ADE: hyperkalemia, reduced renal filtration (especially with NSAIDs), no cough
Contraindications: pregnancy, severe ACE-I angioedema
Alpha-1 Blockers
Drugs: Doxazosin Prazosin Terazosin "Azosin"
MOA: competeitively inhibits a1 which results in vasodilation of veins and arterioles and decrease in total peripheral resistance and BP
ADE: postural hypotension (1st dose), reflex tachycardia, edema
Alpha-2 Agonists
Drugs:
Clonidine
Methyldopa
MOA: stimulates a2
ADE: drowsiness, dizziness, depression, and orthostatic hypotension (not as much as a1 blockers)
Clonidine has disadvantage of rebound hypertension with noncompliance
Methyldopa is pregnancy category B and can cause positive Coombs test, hemolytic anemia, and SLE-like syndrome
Direct Arterial Vasodilators
Drugs:
Hydralazine
Minoxidil
MOA: direct vasodilation of arterioles
Hydralazine ADE: Lupus-like syndrome especially in slow acetylators, edema, reflex tachycardia, and orthostatic hypotension
Minoxidil ADE: ECG changes, edema, hair growth
Nitrates
Drugs:
Isosorbide Dinitrate
Isosorbide Mononitrate
Nitroglycerin
MOA: vasodilate by increasing nitric oxide in vascular smooth muscle, increase in cGMP and smooth muscle relaxation
ADE: reflex tachycardia, hypotension, flushing, headache, development of tolerance
Interactions: PDE5 inhibitors may enhance vasodilation
Digoxin
MOA: acts as adenosine agonist to increase vagal tone at SA and AV nodes; inhibits Na/K ATPase which indirectly increase intracellular free Ca (more info on slides)
ADE: bradycardia, bronchoconstriction, proarrhythmic, hypokalemia increases risk of arrhythmia, N/V, visual disturbance (yellow halo), hyperkalemia
Ranolazine
MOA: blocks late Na current, which reduces Ca
Small prolongation of QTc interval
Last-line agent for chronic angina
Tissue Plasminogen Activator (tPA)
Drugs:
Alteplase (for ischemic stroke)
MOA: works by dissolving the clot and improving blood flow to the blood-deprived part of the brain
Antidotes: Aminocaproic acid and tranexamic acid
Unfractionated Heparin (UFH)
MOA: anticoagulation effect by binding to antithrombin, which inhibits IXa, Xa, XIIa, and thrombin; prevents growth and propagation of formed thrombus and allows for endogenous thrombolytic systems to degrade the clot
Monitoring of UF heparin with aPTT
ADE: bleeding, osteoporosis, reversible alopecia, mineralocorticoid deficiency, and HIT
If HIT suspected, all heparin must be discontinued
Antidote: protamine
Low-Molecular-Weight Heparin (LMWH)
Drugs:
Enoxaparin
Dalteparin
Tinzaparin
“Parin”
MOA: similar to UFH but reduced activity against thrombin vs factor Xa, less affinity for plasma proteins, and longer duration of action
ADE: bleeding
Avoid in patients with history of HIT (100% cross reactivity with heparin antibodies)
Pros: better bioavailability, predictable, less monitoring, ease of self-administration
Cons: cost, no reliable reversal agent
Fondaparinux
MOA: binds specifically (but reversibly) to antithrombin and selectively inhibits factor Xa activity
CBC should be monitored
Contraindication: when CrCl
Direct Thrombin Inhibitors
Drugs:
Bivalirudin
Dabigatran
MOA: reversible direct thrombin inhibitors that inhibit both free and fibrin bound thrombin
Dabigatran ADE: bleeding, dyspepsia
