Term
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Definition
Transmitter depleter
Crosses BBB so central effects as well as depleting NE in SNS
Many SEs including depression
Long acting |
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Term
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Definition
Transmitter depleter
Depletes NE peripherally
Potent
Many SEs |
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Term
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Definition
Centrally-acting alpha-2 agonist
MOA: act on post-synaptic alpha-2A receptors in NTS and Imidazoline receptors in RVLM
SE: sedation, dry mouth, decreased libido, no CNS SEs like alpha-methyl-DOPA, some minimal ortho-hypo, rebound HT (abrupt withdrawal)
USE: drug and nicotine plans
Reduce left-ventricle hypertrophy and lower total cholesterol w/o reducing HDL |
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Term
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Definition
Centrally-acting alpha-2 agonist
MOA: prodrug metabolized to alpha-methyl-NE intra-neuronally -> released as false NT
Activity @ alpha-2A receptor > alpha-1 receptor
USE: decreases SNS, moderately potent anti-HT, can be used safely during pregnancy
SE: dry mouth, nasal congestion, + Coombs test (resolves), sedation, EPS, lactation, decreased libido, ortho-hypotension
Reduce left-ventricle hypertrophy and lower total cholesterol w/o reducing HDL |
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Term
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Definition
Alpha-1 antagonists
MOA: alpha-1 and alpha-2B selective
SE: syncope (during 1st admin and dose increases), minimal ortho-hypo, headaches, priapism
USE: more severe HT, usually in combo
Decreases total cholesterol w/o effect on HDL
Caution: arrythmias -> sudden death |
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Term
Propanolol and Labetolol (nonselective)
Acebutolol, Atenolol, Metoprolol (beta-1 cardioselective) |
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Definition
Beta-blockers
MOA: decrease renin, decrease CO, block presynaptic beta receptors?
May produce rapid drop in BP, or have more slowly developing anti-HT effect
Used for mild to moderate HT, and in combo for more severe HT
SE: myocardial depression, bronchial constriction, potentiation of hypoglycemia, withdrawal rebound, impaired exercise tolerance, increase TGs and decrease HDLs
DI: NSAIDs may block or reduce anti-HT effect of beta-blockers
Not good at preventing stroke like ACE inhibitors, ARBs, Ca2+ channel blockers -> use other first unless pt has cardiac issues for which you need to use beta-blockers |
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Term
| Hydrochorothiazide, Chlorthalidone, Spironolactone, Amiloride |
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Definition
thiazides
MOA: mild diuretic effect, possibly reduce Na+ in VSM to reduce contractility
Very well tolerated, very inexpensive, as good/better than more expensive agents for mild HT and in combo for more severe HT
Chlorthalidone as effective as Ca2+ channel blocker or ACE inhibitor in preventing fatal CHD or non-fatal MI, also more effective in preventing heart failure
No orthostatic hypotension
Many options available
Hydrochlorthiazide: overall anti-HT effect is mild and plateaus (ceiling effect-efficacy maxed out at 15mmHg)
Does not lower BP in normotensive, high sodium intake can reverse anti-HT effects
SE: hypokalemia, hyperglycemia, hyperuricemia, increased cholesterol and TGs |
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Term
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Definition
Smooth muscle vasodilator
MOA: increased NO, increased K+ permeability
SEs (if used alone): tachycardia, headache, fluid retention, edema, nausea, lupus-like syndrome (resolves with DQ)
USE: generally used with severe HT in combo
Reflexes intact, little or no otho-hypo
-give with beta blocker to counter tachycardia |
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Term
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Definition
Smooth muscle vasodilator
MOA: increased K+ channel opening
USE: very potent, used in severe HT-usually in combo
SEs like hydralazine, also hirsutism and edema
-give with diuretic and beta blocker |
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Term
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Definition
Smooth muscle vasodilator
MOA: metabolized to NO
Very potent, unstable compound, prepared fresh and given IV
SE: headache and nausea
Used for HT crisis, gives moment to moment control of BP, cheap |
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Term
| Captopril, Enalapril, Fosinopril |
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Definition
ACE inhibitors
MOA: prevent conversion of A1 to A2, increase bradykinin, increase PGI and NO
USE: mild or moderate HT, well tolerated
Do not interfere with reflexes -> no ortho-hypotension
SE: cough, bronchospasm, ageusia (mainly captopril), renal complications (long term, kidney excretion), hypotension with volume depletion, fetal mortality (2nd and 3rd trimesters), birth defects seen in 1st trimester, angioedema: rare -> DQ drug, resolves in hours
DI: dangerous hyperkalemia if combined w/ K+ sparing agent, oral contraceptives increase A1 levels, NSAIDs can reduce anti-HT and may increase kidney complications, increase Li2+ retention (bipolar pts)
In heart failure -> slow progession of disease and prolong survival
In diabetics -> decrease development of glomerulopathies
Less effective in African Americans |
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Term
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Definition
Angiotension receptor blockers (ARBs)
In terms of efficacy, patient tolerance, and SEs -> similar to ACE-Is
Advantage: no cough
SE: dizziness, fetal toxicity, hyperkalemia
Less effective in African Americans |
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Term
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Definition
Renin inhibitor
MOA: binds renin, inhibits cleaving of angiotensinogen to produce angio-1
Does not increase plasma renin activity
BP reduction similar to ARBs
Expect other effects similar to ACE-Is and ARBs (heart, kidney) -> but not known
No or little cough
Long ½ life=24 hrs
SE: rash, increased uric acid , gout (low incidence)
Do not use during pregnany
-sometimes see unexpected beneficial effects or deleterious effects |
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Term
Nifedipine (arteriolar)
Verapamil and Diltiazem (arteriolar and cardiac) |
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Definition
Calcium channel blockers
MOA: reduce VSM tone to decrease PR
Numerous SEs including adverse cardiac events including sudden death (more common in short acting)
Nifedipine-good vasodilation with little cardiac depression, but significant reflex tachycardia
Verapamil and Diltiazem-little reflex tachycardia, but do produce cardiac depression
Works well in African Americans |
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Term
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Definition
PDE5 inhibitor
MOA: prolongs cGMP presence, vasodilation
USE: pulmonary arterial HT
Danger: unexpected presence of NO
Limitation: requires cognitive activation
SE: retinal cGMP |
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