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34 Cards in this Set
- Front
- Back
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Methyldopa- Class, Tox, PK
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Class: Centrally acting sympathoplegic
Tox: sedation, lactation, POSITIVE coombs test if pt on drug for more than 12 monthes PK: enters BRAIN via aromatic amino acid transporter, delayed effect (in like 4-6 hrs) b/c drug must go through gut and brain, effects persist for 24 hrs b/c accumulate in vesicles |
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Methylodopa- Use, MOA
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Use: Most commonly used in pregnancy
MOA: •Converted to α-methyldopamine & α-methylnorepinephrine (false analogs of DA, NE) •Stimulates CENTRAL α2 receptors leading to ↓PVR, ↓HR/CO, ↓renal vascular resistance |
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Clonidine- Class, Tox, PK
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Class:Centrally acting sympathoplegic
Tox: Dry mouth, sedation, withdrawal after long term use may lead to life threatening Htn crisis. Rash at site of patch PK: Lipid solubility allows entry to brain, oral (2x/day), transdermal patch 1x/7days |
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Clonidine, Use, MOA, CI
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Use: Htn
MOA: PARTIAL agonist at alpha2 in MEDULLA leads to decreased PVR and decrease HR. Decreases BP while maintaining renal blood Q unlike methyldopa. Decreases catecholamine levels. CI: do not use in severe Htn b/c will act as partial agonist at arterioles leading to vasoconstriction |
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Guanethidine- Class, PK, Tox
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Class: Peripheral adrenergic neuronal blocker
PK: long acting-- t1/2= 5 DAYS, gradual onset, long acting after stop of use Tox: sympathectomy--postural hypotension, delayed ejaculation CI: pheochromocytoma |
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Guanethidine- MOA, Use, CI
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MOA: guan will enter peripheral nerve ending concentrate vesicles and displaces NE leading to decreased release of NE from sympathetic nerve endings-- decreases CO and decreases PVR. Will lead to compensatory SEVERE reflexive RAAS.
Use: NOt really used any more--old drug used for severe Htn CI: Pheochromocytoma and drug intxn |
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Reserpine- Class, Tox, Use, MOA
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Class: Peripheral adrenergic neuronal blocker
Tox: minimal postural hypotension, DEPRESSION Use: not used frequently MOA: decreases uptake of biogenic amines into transmitter vesicles, IRREVERSIBLLY depleting stores. Occurs throughout body, affecting NE, DA, serotonin. Result--hypotensive effects with possible sedation, mental depression, etc |
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Beta blockers (-olols)- MOA, Tox, CI
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MOA: decrease BP by competitively blocking beta receptors in heart and kidneys to reduce binding of catecholamines. Dec HR, card contractility, and CO. Blocks binding to JGA in kidneys to DECREASE renin secretion. Do not reduce bp in ppl without htn.
Tox: Bradycardia, bronchospasm, increase triglycerides, worsen acute heart failure, impotence CI: asthma, heart block, or peripheral vasc disease with loss of B2 |
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Propanolol- Class, Use, PK
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Use: Hypertension, ischemic heart disease (1st one effective in these)
Class: NON SELECTIVE beta blocker- so may cause a problem with obstructive lung disease. PK: very lipid soluble (can enter brain)- hepatic metabolism, large vol of dist. |
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Metoprolol- Class, Use, PK
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Class: Cardioselective-beta 2 blocker
Use: asthmatics, if worried about bronchoconstriction with propanolol PK: very lipid soluble (can enter brain)- hepatic metabolism, large vol of dist. |
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Esmolol- Class, Use, PK
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Class: selective beta blocker, metab by CIRCULATING esterases
PK: IV infusion, extremely short half life (9-10 minutes)-- good for critical control Use: intraoperative/postoperative htn and emergencies |
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Labetolol- Class, Use, PK
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Class: NON selective beta blocker-- is also an alpha 2 blocker- reduces sys vasc resistance w/o changing HR or CO
Use: orally for severe htn, IV to treat Htn crisis. Alpha 1 block relaxes vessels and beta block prevents tachycardia seen with alpha 1 blockers alone |
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Carvediol- Use, Class, PK
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Use: orally treat severe Htn and also in heart failure Tx (DOC)-- b/c decreases mortality
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Pindolol, acebutolol, penbutolol- Class, Use
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PARTIAL agonists-- so do have some sympathomimetic activity - so will decrease vascular resistance via beta 2 agonism but does NOT reduce CO as much
Use: Htn with CHF (b.c the fact that CO does not increases decreases the load on the heart) |
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Prazosin, terazosin, doxazosin- Class, Use, MOA, Tox
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Class: SELECTIVE alpha 1 blocker
MOA: sel alpha 1 block in arts/venules (no CNS or cardiac), while NE just acts on alpha 2-- negative feedback, dilates both resistance and capacitance vessels, may improve lipid profiles Tox: INCREASE risk of HF if used as monotherapy, postural hypotension, salt and water retention via RAAS, FIRST dose phenomenon- so should start at bedtime Use: most effective when used with beta blocker and diuretic- avoid reflexive tachycardia and RAAS |
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Phentolamine, phenoxybenzamine- Class, Use
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Class: NON selective alpha blockers
Use: pheochromocytoma- dx with phentolamine, and Tx with phenoxybenzamine |
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Hydralazine- Class, MOA, PK, Use, Tox
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Class: vasodilator
MOA: unknown mech, in which only arterioles are vasodilated- decrease PVR PK: RAPIDLY metab in first pass (low bioavailability), variation b/c of acetylation Tox: LUPUS like syndrome--dose dep and reversible, angina from reflex tachycardia (mediated by baroreceptors then through sympathetic beta blockers) Use: can be used in pregnancy |
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Minoxidil- Class, Tox, MOA, Use
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Class: vasodilator
MOA: opens K+ channels in SM membrane-- hyperpolarizes the cell so less likely to contract-- arterioles ONLY Tox: reflex responses: tach, angina, pericardial effusion, hisuitism, postural hypotension Use: for SEVERE htn, used with loop diuretics and beta blockers to avoid reflex responses |
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Sodium nitroprusside- Class, PK, Use
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Class: vasodilator
PK: rapid metab- RBC uptake and release of CN, CN metab into thiocynate which is cleared by the kidney Use: Htn emergencies (IV) and severe heart failure (will dilate veins) , start on oral meds at same time so time on nitroprusside is minimized |
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Sodium nitroprusside- MOA, Tox
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MOA: release of NO activates guanylyl cyclase-- which increase cGMP-- relaxation of vascular SM
Tox: thiocynate build up which would lead to cyanide poisoning |
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Diazoxide- MOA, Class, PK
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Class: Vasodilator
MOA: Opens K channels, thus hyperpolarizing and relaxing SM in arterioles (thiazide derivative, but no diuretic activity) PK: long half life |
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DIazoxide- Tox, Use
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Tox: profound hypotension, salt/watr retention
Use: IV, not used long term b/c of htn |
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Fenoldopam- Class, MOA, Tox, Use
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Class: vasodilator
MOA: D1 agonist, causing dilation of peripheral arts and natiuresis Tox: reflex tach CI: pts with glaucoma b/c will increase intraocular pressure Use: htn emergencies and post operative htn |
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Calcium channel blockers- Use, MOA, Tox
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Use: monotherapy, works for new Htn only. when combines w/ ace inhibitor and diuretic will block RAAS effects and inappropriate vasodilation (edema). Advantages of cal channel blockers is that it will reverse LVH, lipid neutral, helps vasc disesae, preserves cerebral blood Q, and preserves GFR
MOA: slows calcium influx in SM-- specifically L type channel so only reserved for cardiac and vascular effects. most abund in cardiac muscle, most active in vasc smooth muscle Tox: cardiac arrest (SA), car block (AV), CHF (neg ionotropism). Inapprop vasodilation-- edema, postural hypotension |
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Calcium channel blockers- drug interactions
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- β-blockers: worsen the inappropriate cardiac effects of Diltiazem & Verapamil
- Digitalis (slows heart): levels are increased with use of Diltiazem & Verapamil |
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Nelfidipine, amlodipine, felodipine, isradipine, nicardipine, nisoldipine (DIHYDROpyridines)- Class, MOA, Tox, Use
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Class: calcium channel blockers
MOA: have more vascular effects then cardiac effects Tox: Besides normal CA+2 blocker side effects also-- Nifedipine: reflex tachycardia & gum hypertrophy- not a good choice for DHP-CCB (best is Amlodipine) Use: Monotherapy: only effective for new hypertension, Combined with ACE inhibitor & diuretic: blocks RAAS effects & inappropriate vasodilation (ie edema) Advantages: reverses LVH, lipid neutral, helps vascular disease, preserves cerebral flow, preserves GFR |
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Verapamil- Class, MOA, Tox, Drug Intrxns
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Class: Ca+2 channel blockers
MOA: primarily cardiac effects - used for cardiac arrythmias Tox: constipation b/c of effects on non vasc SM Drug Intrxns: • β-blockers: worsen the inappropriate cardiac effects of Diltiazem & Verapamil •Digitalis (slows heart): levels are increased with use of Diltiazem & Verapamil |
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Diltiazem- Class, MOA, Tox, Drug Intxn, Use
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Class: calcium channel blocker
MOA: intermed effects -- both vascular and cardiac Use: ischemic conditions, htn, angina Drug intrxn: beta blockers-- will worsen inapprop cardiac effects of diltiazem, digitalis-- levels will be increased with diltizem |
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Ace inhibitors- Use, MOA, Tox, CI
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Use: htn, decreases morbidity and mortality in heat failure and LV dysfunction after MI, delays progression of diabetic nephropathy
MOA: •Blocks conversion of AT I to AT II (↓AT II effects) •Inhibits degradation of bradykinin, thus ↑vasodilation from bradykinin (Note: may cause cough & angioedema) •Overall: ↓systemic vascular resistance, without ↑HR, and promotes natriuresis Tox: gen well tolerated, sulfa allergy rash, taste probs, hypotension, renal failure, hyperkalemia b/c decrease ald prod, cough due to bradykinin CI: PREGNANCY, chronic renal failure and SLE (will lead to bone marrow suppression), hyperkalemia, angioedema |
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Captopril- PK, Class
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Class: Ace inhibitors
PK: active w/o conversion in the liver--NOT A PRO DRUG |
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Lisinopril-PK, Class
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PK: active, w/o conversion in the liver, not a pro drug
Class: ACE inhibitors |
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Losartan, Valsartan, Candesartan- MOA, CI, Class
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Class; Angiotensin receptor blockers
MOA: •Competitive antagonist of AT1 receptor isoform, which mediates vasoconstriction & aldosterone secretion •More complete block of AT II effects, but no bradykinin dilation -- equal in efficacy of ACE-I CI: PREGNANCY, bilateral renal stenosis, hyperkalemia, lupus |
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Losartan, Valsartan, Candesartan- Tox, Use, Class
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Class: angiotensin receptor blockers
Use: used only when coughing is a problem with ACE inhibitors Tox: sim to ace inhibitors BUT DOES NOT CAUSE COUgh/angioedema b/c bradykinin is not influenced |
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Aliskiren, clonidine, propranolol- Class
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Class: Renin inhibitors
Aliskiren- reduces plasma renin Clonidine (rem is centrally acting sympathoplegic)- affects renin by affecting renal symp activity Propranolol- beta blocker which affects JG cells renin secretion |
