Exam 3 Flashcards
K+ channel openers
Minoxidil, hydralazine, diazoxide
Main uses: HTN uncontrolled by other drugs, HTN emergencies, severe HTN, research
Main problems: strong inducers of the reflexes to vasodilation, can reveal myocardial ischemia
Calcium channel blockers
Several drugs approved in the U.S., all selectively inhibit L-type Ca2+ channels, these channels are present in both vascular and cardiac muscle cells, dihydropyridines are more vascular selective than other CCB’s
Uses: mild to moderate HTN, to reduce TPR, cardiac ischemia
Nifedipine
Calcium channel blocker/anti hypertensive drug
Dihydropyridines (“…dipines”)
Highly smooth muscle selective vs cardiac; evokes reflex tachycardia (because don’t bind to heart much at all)
2.5 fold increased risk of sudden death with short acting dihydropyridines. Do not use this specific class in HTN patients with ischemic heart disease
Diltiazem
Calcium channel blocker/anti hypertensive drug
Benzothiazepine
Slightly smooth muscle selective vs cardiac
Cause little to no reflex tachycardia because they block it by binding to cardiac L-type channels
Verapamil
Calcium channel blocker/anti hypertensive drug
Phenylalkylazmine
Non-selective for smooth vs cardiac
Cause little to no reflex tachycardia because they block it by binding to cardiac L-type channels
Sodium nitroprusside
Inorganic nitrate/anti hypertensive drug
Nitric oxide donor
Uses: Hypertensive emergencies, reduce bleeding during surgery (bc lower BP), cardiac ischemia (reduces pre-load and after-load and thus cardiac work)
Nitroglycerin
Organic nitrate/anti hypertensive drug
Nitric oxide donor
Uses: angina (reduces cardiac work)
Methyldopa (Aldomet)
Sympatholytic anti hypertensive drug
Centrally acting, direct alpha2-adrenergic receptor selective agonist
Inhibits sympathetic outflow from the brainstem
Uses: for HTN resistant to other treatments, decrease TPR and reduce CO
Bad side effects: nausea, withdrawal syndrome, sedation
Clonidine (Catapres)
Sympatholytic anti hypertensive drug
Centrally acting, alpha2-adrenergic receptor selective agonist (it is a prodrug)
Inhibits sympathetic outflow from the brainstem
Uses: for HTN resistant to other treatments, decrease TPR and reduce CO
Bad side effects: nausea, withdrawal syndrome, sedation
Trimethaphan (Arfonad)
Anti hypertensive drug
Peripherally acting sympatholytic ganglionic blocker
Non-depolarizing inhibitor of ganglionic nicotinic cholinergic receptor
Uses: controlled hypotension (dissecting aneurysm and reduce surgical bleeding), dampen spinal autonomic reflexes (spinal cord injury)
Prazosin (Minipress)
Alpha-1 adrenergic antagonist
Blocks the vasoconstrictor of sympathetic tone
Reduces TPR
Causes vasodilation commensurate with degree sympathetic activity is involved in vasoconstriction
Use: symptomatic prostate hypertrophy
Propranolol (Inderal)
Non-selective beta adrenergic receptor antagonist. Anti hypertensive drug
Mechanism: inhibit inotropic and chronotropic effects of asanas in the heart. Reduces cardiac output
Uses: gold standard for anti-HTN
Side effects: exercise intolerance, impotence
Metoprolol (Lopressor)
Selective Beta-1 adrenergic receptor antagonist. Anti hypertensive drug
Mechanism: inhibit inotropic and chronotropic effects of asanas in the heart. Reduces cardiac output
Uses: better for asthmatics than non selective
Side effects: exercise intolerance, impotence
Aliskrien (Tekturna)
Renin inhibitor. Anti hypertensive drug
Lisinopril (Prinivil)
ACE inhibitor. Anti hypertensive drug
Losartan (Cozaar)
AT1-Receptor antagonist. Anti hypertensive drug
Minoxidil
Vasodilator drug/anti hypertension
K+ channel openers
Open K channel leads to K efflux, cell hyperpolarization; which inhibits voltage sensitive L-type Ca2+ channels, which reduces Ca2+ and causes relaxation
IOW, indirect inhibition of L-type Ca2+ channels
Diuretics
Diuretics in HTN
Thiazide: ‘gold standard’ proven in mild HTN, reduces TPR
K+ sparing: use as adjuvants
Loop: only in refractory HTN, “big guns”
Glyceryl trinitrate (GTN, Nitroglycerin)
Nitrovasodilator. Anti-anginal drug
Sublingual administration avoids the first-pass effect and produces rapid (3-5 min) onset and short duration (2-30 min). transdermal administration prolongs onset and duration of action
Mechanism: nitric oxide donor. Reduces venous return, reduction in preload reduces ventricular wall stress and myocardial oxygen demand
Adverse effects: orthostatic hypotension, reflex tachycardia, severe throbbing headache, dizziness. Cross potentiation with PDE-5 inhibitors (viagra)
Calcium channel blockers
Anti-anginal drugs
Verapamil, Diltiazem, nifedipine
Block L-type “slow” calcium channels
Reduce influx of extra cellular Ca into vascular and cardiac muscle
Preferential arteriolar vasodilators vs veins
Drugs have differing selectivity for Ca channels in vascular vs cardiac tissue
Ranolazine
Anti anginal drug
It inhibits the late inward sodium current in heart muscle which leads to reduction in intracellular calcium
Uses: anti-anginal effects independent of reductions in BP and/or HR. Useful as adjunct or alternative anti-anginal therapy. For chronic angina, not useful for Acute Coronary Syndrome
Adverse effects: prolongs QTc. CYP3A4 substrate
Epinephrine, Dobutamine
Positive inotropic agents for acute, severe heart failure
Beta adrenergic receptor agonists: induce cAMP
Administered IV, active beta-adrenergic receptors
Milrinone (cardiac PDE-3)
Positive inotropic agents for acute, severe heart failure
Phosphodiesterase inhibitors: protect cAMP
Administered IV, short term inotropic support
Atorvastatin (Lipitor), Rosuvastatin (Crestor)
Treatment of hyperlipidemia
Inhibitor is cholesterol synthesis
“Statins”
HMG-CoA reductase inhibitor - reversibly competitive
First line agents in most patients with increased LDL
Movement of SCAP/SREBP complex to golgi is stimulated
