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Renal II Final > Vasodilators And Sympathoplegics DSA > Flashcards

Vasodilators And Sympathoplegics DSA Flashcards

1
Q

List the calcium channel blockers: dihydropyridines (DHPS) (vasodilators)

A 
*Amlodipine
Clevidipine
Felodipine
Isradipine
Nicardipine
*Nifedipine
Nisoldpine
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2
Q

List calcium channel blockers: non-dihydropyridines (vasodilators)

A

Diltiazem

Verapamil

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3
Q

List potassium channel openers (vasodilators)

A

Diazoxide

Minoxidil

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4
Q

List dopamine agonist (vasodilator)

A

Fenoldopam

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5
Q

List NO modulators (vasodilators)

A

*Hydralazine
*Nitroprusside
Organic nitrates
-isosorbide dinitrate
-nitroglycerin

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6
Q

List the beta-adrenergic antagonists (beta-blockers) (sympathoplegics)

A 
Acebutolol
*Atenolol
Betaxolol
Bisoprolol
Carteolol
*Carvedilol
Esmolol
*Labetalol
*Metoprolol
Nadolol
Nebivolol
Penbutolol
Pindolol
*Propranolol
Timolol
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7
Q

List the alpha1-adrenergic antagonists (alpha1-blockers) (sympathoplegics)

A

Doxazosin
*Prazosin
Terazosin

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8
Q

List the centrally acting alpha2 agonists (sympathoplegics)

A

*Clonidine
Guanabenz
Guanfacine
*Methyldopa

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9
Q

Describe the general MOA of vasodilators

A

All vasodilators that are useful in HTN relax smooth muscle of arterioles, thereby decreasing peripheral vascular resistance and thus arterial blood pressure. Sodium nitroprusside and nitrates also relax veins
Intact sympathetic reflexes prevent orthostatic hypotension and sexual dysfunction in response to vasodilators used as monotherapy
Vasodilators work best when used in combo with other antihypertensive drugs that oppose compensatory CV responses (diuretic or beta-blocker). But potentially dangerous combo of non-DHP CCBs and beta-blockers

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10
Q

What are the two major subclasses of calcium channel blockers, their prototypes, and MOA?

A

Dihydropyridines (DHPs)
Prototypes: nifedipine, amlodipine
MOA: blocks L-type calcium channels in vasculature > cardiac channels

Non-DHPs
Prototypes: verapamil, diltiazem
MOA: nonselective block of vascular and cardiac L-type calcium channels

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11
Q

Describe pharmacodynamics of calcium channel blockers

A

All CCBs block L-type calcium channels (voltage-gated), which are responsible for Ca flux into smooth muscle cells, cardiac myocytes, and SA and AV nodal cells in heart
All CCBs bind to L-type calcium channels, but DHPs and non-DHPs bind to different sites on channel proteins. This leads to differences in effects on vascular vs cardiac tissue responses and different kinetics of actions at receptor
CCBs bind more effectively to open channels and inactivated channels and reduce frequency of opening in response to depolarization

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12
Q

Describe effects of CCBs on smooth muscle

A

Cause vasodilation, which decreases peripheral resistance
Arterioles are more sensitive than veins
Orthostatic hypotension is not usually a problem
Relaxation of arteriolar smooth muscle leads to decreased afterload and decreased O2 demand by heart

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13
Q

Describe effects of CCBs on cardiac muscle

A

Reduced contractility throughout heart and decreases in SA node pacemaker rate and AV node conduction velocity
Non-DHPs exhibit more cardiac effects than DHPs
DHPs do have effects on cardiac muscle, but they block channels in smooth muscle at much lower concentrations
Thus, cardiac effects are negligible at effective therapeutic concentrations

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14
Q

Describe pharmacokinetics of CCBs

A

Orally active but have high-first pass metabolism
Have high degree of plasma protein binding and are extensively metabolized
Nifedipine, clevidipine, verapamil, and diltiazem are also used IV
Amlodipine has a long elimination half-life of 35-50 hrs, relative to 2-12 hrs half-life for most other CCBs
Extended release preparations are available for many of CCBs

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15
Q

Describe adverse effects/contraindications of DHPs

A

Excessive hypotension, dizziness, headache, peripheral edema, flushing, tachycardia, rash, and gingival hyperplasia
Some studies: increased risk of MI, stroke, or death in pts receiving short-acting nifedipine for HTN
Therefore, short-acting DHPs should not be used for management of chronic HTN
Slow-release and long-acting DHPs are preferred to minimize reflex cardiac effects

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16
Q

Describe adverse effects/contraindications of non-DHPs

A

Dizziness, headache, peripheral edema, *constipation (esp verapamil), AV block, bradycardia, HF, lupus-like rash with diltiazem, pulmonary edema, coughing, and wheezing
(Verapamil>diltiazem): slow heart rate can slow atrioventricular conduction, can cause heart block, and are contraindicated in pts also taking a beta-blocker
-DHP nifedipine does not decrease AV conduction and therefore can be used more safely than non-DHPs in presence of AV conduction abnormalities

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17
Q

Describe CCBs and heart failure

A

Initial studies suggested CCBs (especially cardiac-selective non-DHPs) could cause further worsening of HF as a result of negative ionotropic effect
Later studies demonstrated neutral effects of vasoselective CCBs amlodipine and felodipine on mortality
As a result, CCBs are not indicated for use in HF, but amlodipine or felodipine can be used if necessary for another indication, such as angina or HTN

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18
Q

Describe drug-drug interactions of CCBs

A

Verapamil may increase digoxin blood levels through a pharmacokinetic interaction
DHPs: additive with other vasodilators
Non-DHPs: additive with other cardiac depressants and hypotensive drugs

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19
Q

Describe clinical uses of CCBs

A

Long-term outpatient therapy of HTN, hypertensive emergencies, angina

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20
Q

Describe MOA/pharmacodynamics of diazoxide (potassium channel opener)

A

MOA: opens potassium channels in smooth muscle
Increased potassium permeability hyperpolarizes smooth muscle membrane, reducing probability of contraction
Arteriolar dilator resulting in reduced systemic vascular resistance and mean arterial pressure

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21
Q

Describe pharmacokinetics of diazoxide (potassium channel openers)

A

Relatively long-acting (4-12 hrs after injection)
Exhibits high protein binding
Typically administered as 3-4 injections, 5-15 minutes apart as needed. Sometimes administered by IV infusion

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22
Q

Describe adverse effects/contraindications of diazoxide (potassium channel opener)

A

Excessive hypotension resulting in stroke and myocardial infarction
Hypotensive effects are greater in pts with renal failure (due to reduced protein binding) and in pts pretreated with beta-blockers to prevent reflex tachycardia. Smaller doses should be administered to these pts
Hyperglycemia, particularly in pts with renal insufficiency
Should be avoided in pts with ischemic heart disease due to propensity for angina, ischemia, and cardiac failure
In contrast to structurally related thiazide diuretics, diazoxide causes sodium and water retention. Rarely a problem due to typical short duration of use

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23
Q

What is the clinical use of diazoxide (potassium channel openers)?

A

Hypertensive emergencies (diminishing use)

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24
Q

Describe MOA/pharmacodynamics of minoxidil (potassium channel opener)

A

MOA: active metabolite (minoxidil sulfate) opens potassium channels in smooth muscle
Increased potassium permeability hyperpolarizes smooth muscle membrane, reducing probability of contraction
Dilation of arterioles but not veins. More efficacious than hydralazine

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25
Q

What are the adverse effects/contraindications of minoxidil (potassium channel opener)?

A

Common: headache, sweating, hypertrichosis (abnormal hair growth)
Even more than with hydralazine, use is associated with reflex sympathetic stimulation and sodium and fluid retention resulting in tachycardia, palpitations, angina, and edema
Minoxidil must be used in combination with beta-blocker and loop diuretic in order to avoid these effects

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26
Q

What are the clinical uses of minoxidil (potassium channel opener)?

A 
Long-term outpatient therapy of severe hypertension
Topical formulations (rogaine) are used to stimulate hair growth
27
Q

What are the MOA, pharamcodynamics, and pharmacokinetics of fenoldopam?

A

MOA: agonist at dopamine D1 receptors

Peripheral arteriolar dilator, natriuretic

Administered by continuous IV infusion due to rapid metabolism and short half-life (10 min)

28
Q

What are the adverse effects/contraindications of fenoldopam?

A

Tachycardia, headache, and flushing

Should be avoided in patients with glaucoma due to increases in intraocular pressure

29
Q

What are the clinical uses of fenoldopam?

A

Hypertensive emergencies, peri- and postoperative hypertension

30
Q

Describe MOA, pharmacodynamics, and pharmacokinetics of hydralazine (NO modulator)

A

MOA: stimulates release of NO from endothelium resulting in increased cGMP levels

Dilation of arterioles but not veins.
Reflex tachycardia

Well absorbed, but high first-pass effect results in low bioavailability
Metabolism occurs in part via acetylation, so bioavailability is variable among individuals dependent on rate of acetylation

31
Q

What are the adverse effects/contraindications of hydralazine (NO modulator)?

A

Common: headache, nausea, anorexia, palpitations, sweating, and flushing
In pts with ischemic heart disease, reflex tachycardia and sympathetic stimulation may provoke angina or ischemic arrhythmias
Rare: peripheral neuropathy, drug fever

32
Q

What are the clinical uses of hydralazine (NO modulator)?

A

Long-term outpatient therapy of hypertension
Combination with nitrates is effective in heart failure and should be considered in pts, especially African-Americans, with both hypertension and heart failure
First-line therapy for hypertension in pregnancy, with methyldopa
Parenteral formulation is useful in hypertensive emergencies

33
Q

Describe MOA and pharmacodynamics and pharmacokinetics of sodium nitroprusside (NO modulator)?

A

MOA: drug metabolism releases nitric oxide resulting in increased cGMP levels

Powerful dilation of arterial and venous vessels reduces peripheral vascular resistance and venous return
In absence of heart failure, blood pressure decreases and cardiac output does not change (or decreases slightly)
When cardiac output is alreadly low due to heart failure, cardiac output often increases due to afterload reduction

Rapid metabolism results in rapid onset and short duration of effect
Should be administered by IV infusion with continuous monitoring of arterial blood pressure

34
Q

What are the adverse effects of sodium nitroprusside (NO modulator)?

A

Excessive hypotension

Cyanide and thiocyanate are released during metabolism.

  • This is typically not problematic because nitroprusside is used only briefly.
  • Cyanide poisoning (metabolic acidosis, arhythmias, excessive hypotension, and death) can occur if infusions are administered for several days
35
Q

What are the clinical uses of sodium nitroprusside (NO modulator)?

A

Hypertensive emergencies, acute decompensated HF

36
Q

What is the prototype for organic nitrates (NO modulator)? What are other agents?

A

Nitroglycerin

Isosorbide dinitrate, isosorbide mononitrate

37
Q

Describe the MOA of organic nitrates (NO modulator)

A

MOA: release of NO via enzymatic metabolism
Relaxes most types of smooth muscle (veins>arteries). Virtually no direct effect on cardiac or skeletal muscle
Increases venous capacitance, decreases ventricular preload, reduces pulmonary vascular pressures and heart size
In absence of heart failure, cardiac output is reduced
Decreases platelet aggregation

38
Q

Describe pharmacokinetics of organic nitrates (NO modulator)

A

High first-pass effect results in low bioavailability.
-sublingual route of administration is typically used to avoid first-pass

Therapeutic blood levels are reached within minutes and last 15-30 minutes

Oral, transdermal, and buccal preparations are available when longer duration of action is needed

Toleraance may occur following continuous exposure, especially with nitroglycerin
-a nitrate-free period of at least 8 hrs between doses is required to prevent tolerance

39
Q

Describe the adverse effects/contraindications of organic nitrates (NO modulator)

A

Common: orthostatic hypotension, syncope, throbbing headache

Mech of tolerance:
Diminished release of NO due to reduced bioactivation
Reduced availability of sulfhydryl donors
Increased generation of oxygen free radicals
Diminished availability of calcitonin gene-related peptide (CGRP)
Compensatory responses contributing to development of tolerance: tachycardia, increased cardiac contractility, retention of salt and water

Glaucoma was previously thought to be contraindication, but nitrates can be used safely in presence of intraocular pressure

Contraindicated if intracranial pressure is elevated

Transdermal patches should be removed before use of external defibrillators

40
Q

Describe drug-drug interactions of organic nitrates (NO modulator)

A

Synergistic hypotension with phosphodiesterase type 5 inhibitors (sildenafil, tadalafil, vardenafil)

41
Q

What are clinical uses of organic nitrates (NO modulator)?

A

Hypertensive emergencies, angina, heart failure

42
Q

Describe generalities of sympathoplegic agents

A

Alter sympathetic nervous system function
Can elicit compensatory effects through mechanisms independent of adrenergic nerves (efficacy may be limited by sodium retention and expansion of blood volume)
Most effective when used concomitantly with a diuretic

43
Q

What are beta-blockers useful for?

A

Especially useful in preventing refelx tachycardia that often results from treatment with direct vasodilators in severe hypertension
Reduce mortality after MI. Some reduce mortality in pts with HF

44
Q

What are the MOA and pharmacodynamics of beta-blockers?

A

MOA: non-selective beta-blocker
Non-selective agents primarily decrease blood pressure by decreasing cardiac output
Other beta-blockers may decrease cardiac output and/or decrease peripheral vascular resistance depending on cardioselectivity and partial agonist activities
Some agents exhibit vasodilating activity mediated by variety of molecular mechs
These agent do not usually cause hypotension in healthy, normotensive pts
Blockade of beta1 receptors in kidney inhibits renin release
Several beta-blocker exhibit local anesthetic action due to blockade of sodium channels and resultant membrane stabilization. These effects are usually not apparent at plasma concentrations achieved after systemic administration

45
Q

What is the prototype for beta-blockers?

A

Propranolol

46
Q

What are the pharmacokinetics of beta-blockers?

A

Except for esmolol, all are available as oral preps
Carvedilol, metoprolol, and propranolol are available as extended-release tablets
Atenolol, esmolol, labetalol, metoprolol, and propranolol are available as parenteral preps
Wide range of half-lives
Most exhibit low-to-moderate lipid solubility. Exceptions are propranolol and penbutolol, which are quite lipophilic and readily cross BBB

47
Q

What are adverse effects/contraindications of beta-blockers?

A

Asthma/COPD
Diabetes
Most common side effects are bradycardia and fatigue
Sexual dysfunction and depression sometimes occur
Chronic use has been associated with unfavorable plasma lipid profiles (increased VLDL and reduced HDL)
Sudden withdrawal may cause rebound HTN, angina, and possibly MI. Mech may involve upregulation of receptor synthesis

48
Q

Describe adverse effects of beta-blockers in asthma/COPD pts

A

Blockade of beta2 receptors in bronchial smooth muscle may lead to increase in airway resistance
No currently available beta1 selective agents are specific enough to completely avoid beta blockade
These agents should be avoided in asthmatics
Pts with COPD may tolerate these drugs, and the benefits may outweight the risks, especially in cases of concurrent ischemic heart disease

49
Q

Describe adverse effects of beta-blockers in diabetes pts

A

Glycogenolysis is partially inhibited by beta2 blockade
May mask signs of hypoglycemia and delays recovery from insulin-induced hypoglycemia
Use with caution in insulin-dependent diabetics (benefits may outweigh risks in diabetics after MI)

50
Q

What are the drug-drug interactions with beta-blockers?

A

Can cause heart block, especially if combined with CCBs verapamil or diltiazem, which also slow conduction

51
Q

What are clinical uses of beta-blockers?

A

HTN: metoprolol and atenolol most widely used. Not commonly used for initial monotherapy in absence of specific indication

HF: administration may worsen acute congestive HF.

  • Even in stable, compensated HF, cardiac decompensation may occur if cardiac output is dependent on sympathetic drive, but careful, long-term use with gradual dose increases may prolong life.
  • Specifically, carvedilol, bisoprolol, and metoprolol reduce mortality.

Ischemic heart disease: beta-blockers reduce the frequency of angina episodes and improve exercise tolerance in many pts
-timolol, metoprolol, and propranolol prolong survival after MI

Cardiac arrhythmias: often effective in treatment of supraventricular and ventricular arrhythmias

Glaucoma: topical drops of timolol, betaxolol, carteolol, and others reduce intraocular pressure (agents with local anesthetic action are not used topically on eye)

Beta1-selectivity may be advantageous in treating pts with comorbid asthma, diabetes, or peripheral vascular disease

Agents with partial beta2-agonist activity may be advantageous in pts with bradyarrhytmias or peripheral vascular disease

52
Q

What is the prototype of alpha1-blockers?

A

Prazosin

53
Q

What are the MOA and pharmacodynamics of alpha1-blockers?

A

MOA: reversible antagonists at alpha1receptors
Prevent vasoconstriction of both arteries and veins. BP is reduced by lowering peripheral vascular resistance
Relaxes smooth muscle in prostate
Retention of salt and water occur when used without a diuretic
Associated with either no change or improvement (increased HDL) in plasma lipid profiles. Mech unknown

54
Q

What are adverse effects/contraindications of alpha1-blockers?

A

Generally well tolerated
Orthostatic hypotension, dizziness (especially first dose syncope), palpitations, headahce, lassitude
Less incidence of reflex tachycardia than non-selective alpha adrenergic blockers because alpha2 receptor inhibition of NE release from nerve endings is unaffected

55
Q

Describe drug-drug interactions with alpha1-blocerks

A

Most effective when used in combo with other agents (beta-blocker and diuretic)

56
Q

What are clinical uses of alpha1-blockers?

A

Primarily used in men with concurrent HTN and BPH

57
Q

What are the prototypes for centrally acting agents alpha2-agonists?

A

Clonidine, methyldopa

58
Q

What are the general MOA of centrally acting agents alpha2-agonists?

A

Reduce sympathetic outflow from vasomotor centers in brainstem but allow these centers to retain or even increase their sensitivity to baroreceptor control
Agonists at central alpha2 receptors
Slight variations in hemodynamic effects of clonidine and methyldopa suggest that these two drugs may act at different populations of central neurons

59
Q

What are the clinical uses of centrally acting agents alpha2-agonists?

A

With exception of clonidine, these agents are rarely used today
Methyldopa is used for HTN during pregnancy

60
Q

Describe pharmacodynamics of clonidine

A

centrally acting agents alpha2-agonists
Lowers blood pressure by reducing cardiac output (decreased HR and relaxation of capacitance vessels) and reducing peripheral vascular resistance

61
Q

What are adverse effects of clonidine?

A

centrally acting agents alpha2-agonists
Sedation, dry mouth, depression, sexual dysfunction
Transdermal preparation is associated with less sedation than oral but may cause skin reaction
Abrupt withdrawal can lead to life-threatening hypertensive crisis

62
Q

What are the pharmacodynamics and pharmacokinetics of methyldopa?

A

centrally acting agents alpha2-agonists
Lowers BP by reducing peripheral vascular resistance. Variable reduction in HR and cardiac output
Methyldopa is analog of L-dopa. Converted to alpha-methylnorepinephrine by an enzymatic pathway that directly parallels synthesis of NE from L-dopa

63
Q

What are adverse effects of methyldopa?

A

Sedation, dry mouth, lack of concentration, sexual dysfunction

Renal II Final (8 decks)

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