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Renal II Final > Vasodilators and sympathoplegics > Flashcards

Vasodilators and sympathoplegics Flashcards

1
Q

Calcium channel blockers

A

Dihydropyridines and non-dihydropyridines

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2
Q

Dihydropyridines (DHPs)

A 
Amlodipine
Clevidipine
Felodipine
Isradipine
Nicardipine
Nifedipine
Nisoldipine
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3
Q

Non-dihydropyridines

A

Diltiazem

Verapamil

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4
Q

K channel openers

A

Diazoxide

Minoxidil

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5
Q

Dopamine agonist

A

Fenoldopam

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6
Q

Nitric oxide modulators

A 
Hydralazine
Nitroprusside
Organic nitrates:
Isosorbide dinitrate
Nitroglycerin
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7
Q

B-blockers

A 
Acebutolol
Atenolol
Betaxolol
Bisoprolol
Carteolol
Carvedilol
Emolol
Labtalol
Metoprolol
Nadolol
Nebivolol
Penbutolol
Pindolol
Propranolol
Timolol
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8
Q

a1-adrenergic antagonists

A

Doxazosin
Prazosin
Terazosin

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9
Q

Centrally acting a2 agonists

A

Clonidine
Guanabenz
Guanfacine
Methyldopa

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10
Q

Vasodilators general MOA

A
  • Relax smooth muscle of arterioles, decreasing peripheral vascular resistance and thus arterial blood pressure
  • Nitros relax veins too
  • Intact sympathetic reflexes prevent orthostatic hypotension and sexual dysfunction
  • Work best when used in combo with other antihypertensives to prevent compensatory responses
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11
Q

Dihydropyridines MOA

A
  • Prototypes: nifedipine, amlodipine

- Blocks L-type Ca channels in the vasculature > cardiac channels

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12
Q

Non-dihydropyridines MOA

A
  • Prototypes: verapamil, Diltiazem

- Nonselective block of vascular and cardiac L-type Ca channels

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13
Q

Ca-channel blockers pharmacodynamics

A
  • Block L-type Ca channels (voltage gated) responsible for Ca influx into smooth muscle, cardiac myocytes, and SA and AV nodal cells
  • CCBs bind more effectively to open channels and inactivated channels and reduce frequency of opening in response to depolarization
  • All CCBs cause vasodilation, decreasing peripheral resistance; arterioles more sensitive than veins - decreased after load and decreased O2 demand by heart
  • Reduced contractility throughout the heart and decreases in SA node pacemaker rate and AV node velocity (non-DHPs more cardiac effects than DHPs)
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14
Q

Ca-channel blockers pharmacokinetics

A
  • All orally active but have high first-pass metabolism, high plasma protein binding, extensively metabolized
  • nifedipine, clevidipine, verapamil, and diltiazem have IV forms
  • Amlodipine has a long half-life (35-50 hr, most others 2-12 hrs)
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15
Q

Ca-channel blocker contraindications

A

-Generally well-tolerated

  • DHPs: excessive hypotension, dizziness, headache, peripheral edema, flushing, tachycardia, rash and gingival hyperplasia.
  • -nifedipine: increased risk for MI, stroke, death; short acting should not be used for chronic HTN
  • Non-DHPs: Dizziness, headache, peripheral edema, constipation (verapamil), AV block, bradycardia, heart failure, lupus-like rash (diltiazem), pulmonary edema, coughing and wheezing. Contraindicated in individuals taking a B-blocker - verapamil > diltiazem; slow heart rate, can slow AV conduction causing heart block
  • Nifedipine does not decrease AV conduction, use in AV conduction abnormalities
  • Non-DHP negative ionotropic effect may worsen heart failure; amlodipine or felodipine can be used in angina or HTN
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16
Q

CCBs drug-drug interactions

A
  • Verapamil may increase digoxin blood levels
  • DHPs: additive w/ other vasodilators
  • Non-DHPs: additive w/ other cardiac depressants and hypotensive drugs
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17
Q

CCB clinical uses

A

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

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18
Q

K channel openers (Diazoxide) MOA

A

-Opens K channels in smooth muscle

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19
Q

K channel openers (Diazoxide) pharmacodynamics

A
  • Increased K permeability hyper polarizes the smooth muscle membrane, reducing the probability of contraction
  • arteriolar dilator resulting in reduced systemic vascular resistance and MAP
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20
Q

K channel openers (Diazoxide) pharmacokinetics

A
  • Relatively long-acting
  • High protein binding w/ unknown metabolism
  • administered as 3-4 injections 5-15 minutes apart, sometimes IV
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21
Q

K channel openers (Diazoxide) adverse effects and contraindications

A
  • Excessive hypotension resulting in stroke and MI
  • Hypotensive effects are greater in those with renal failure (reduced protein binding) and those pre-treated with B-blockers to prevent tachycardia (administer smaller doses)
  • Hyperglycemia - renal insufficiency
  • Should be avoided in patients with ischemic heart disease and cardiac failure
  • diazoxide causes Na and water retention but not normally a problem due to short duration of use
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22
Q

K channel openers (Diazoxide) clinical uses

A

-Hypertensive emergencies

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23
Q

K channel openers (Minoxidil) MOA

A

-Active metabolite opens K channels in smooth muscle

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24
Q

K channel openers (Minoxidil) Pharmacodynamics

A
  • Increased K permeability hyper polarizes the smooth muscle membrane, reducing the probability of contraction
  • Dilation of arterioles but not veins, more efficacious than hydralazine
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25
Q

K channel openers (Minoxidil) contraindications

A
  • Headache, sweating, hypertrichosis (abnormal hair growth)
  • Reflex sympathetic stimulation and Na and fluid retention resulting in tachycardia, palpitations, angina, and edema
  • Must be used in combo with B-blocker and loop diuretic to avoid these effects
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26
Q

K channel openers (Minoxidil) clinical uses

A
  • Long-term outpatient therapy of severe HTN

- Topical formulas (Rogaine) for hair growth

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27
Q

K channel openers (Fenoldopam) MOA

A

Agonist at D1 receptors

28
Q

K channel openers (Fenoldopam) Pharmacodynamics

A

Peripheral arteriolar dilator, natriuretic

29
Q

K channel openers (Fenoldopam) Pharmacokinetics

A

-Continuous IV infusion due to rapid metabolism and short half life

30
Q

K channel openers (Fenoldopam) adverse effects and contraindications

A
  • Tachycardia, headache, flushing

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

31
Q

K channel openers (Fenoldopam) clinical uses

A

Hypertensive emergencies, peri- and postoperative hypertension

32
Q

NO modulators (hydralazine) MOA

A

-Stimulates the release of NO from endothelium resulting in increased cGMP levels

33
Q

NO modulators (hydralazine) Pharmacodynamics

A
  • Dilation of arterioles but not veins

- Reflex tachycardia

34
Q

NO modulators (hydralazine) Pharmacokinetics

A
  • Well-absorbed with high first pass metabolism

- Metabolism occurs in part via acetylation, bioavailability varies among individuals

35
Q

NO modulators (hydralazine) adverse effects and contraindications

A
  • Headache, nausea, anorexia, palpitations, sweating and flushing
  • In patients with ischemic heart disease, reflex tachycardia, and sympathetic stimulation, it may provoke angina or ischemic arrhythmias
  • peripheral neuropathy or drug fever - rare
36
Q

NO modulators (hydralazine) clinical uses

A
  • long-term outpatient HTN
  • combination with nitrates effective in heart failure
  • first line therapy for HTN in pregnancy with methyldopa
  • parenteral formulation in HTN emergencies
37
Q

NO modulators (Na nitroprusside) MOA

A

-Release NO resulting in increase cGMP levels

38
Q

NO modulators (Na nitroprusside) pharmacodynamics

A
  • Powerful dilation of arterial and venous vessels, reduces peripheral vascular resistance and venous return
  • in absence of heart failure, BP decreases and cardiac output doesn’t change
  • When CO is already low due to heart failure, CO often increases due to after load reduction
39
Q

NO modulators (Na nitroprusside) pharmacokinetics

A
  • Rapid metabolism with rapid onset and short duration

- IV infusion with continuous monitoring of BP

40
Q

NO modulators (Na nitroprusside) adverse effects

A

-Excessive hypotension
-Cyanide and thiocyanate are released during metabolism
Cyanide poisoning can occur if infusions administered for several days - metabolic acidosis, arrhythmias, excessive hypotension, death

41
Q

NO modulators (Na nitroprusside) clinical uses

A

-hypertensive emergencies, acute decompensated heart failure

42
Q

Organic nitrates (nitroglycerin) MOA

A
  • Release of NO via enzymatic metabolism
  • Relaxes most types of smooth muscle (veins > arteries), no direct effect on cardiac or skeletal muscle
  • Increases venous capacity, decrease ventricular preload, pulmonary vascular pressures and heart size reduced
  • Decreases platelet aggregation
43
Q

NO modulators (Na nitroprusside) pharmacokinetics

A
  • High first pass, sublingual route typically used
  • Therapeutic levels reached within minutes, last 15-30
  • Oral, transdermal, and buccal allow for longer release
  • tolerance may occur with continuous exposure; 8 hours between doses to prevent tolerance
44
Q

NO modulators (Na nitroprusside) adverse effects and contraindications

A
  • Orthostatic HTN, syncope, throbbing headache
  • Tolerance (diminished release of NO due to reduced bioactivation; reduced availability of sulfhydryl donors; increased generation of ROS; diminished ability of calcitonin gene-related peptide (CGRP); compensatory responses - tachycardia, increased cardiac contractility, retention of salt and water)
  • Contraindicated with increased intracranial pressure
  • transdermal patches must be removed before use of defibrillators
45
Q

NO modulators (Na nitroprusside) drug-drug interactions

A

-synergistic hypotension with PDE5 inhibitors (sildenafil, tadalafil, vardenafil)

46
Q

NO modulators (Na nitroprusside) clinical uses

A

hypertensive emergencies, angina, heart failure

47
Q

B-blockers facts

A
  • Useful in preventing the reflex tachycardia that results from tx with direct vasodilators in severe HTN
  • Reduce mortality after MI and some reduce mortality in pts with heart failure
48
Q

B-blockers MOA

A

-non-selective B-blocker but others are more specific

49
Q

Non-selective, Non-ISA B-blockers

A

Propranolol, carvedilol

50
Q

Non-selective, ISA B-blockers

A

Labetalol

51
Q

B1 selective, Non-ISA B-blocker

A

Metoprolol, Atenolol

52
Q

B-blocker pharmacodynamics

A
  • Non-selective agents that decrease BP by decreasing cardiac output
  • May decrease peripheral vascular resistance depending on cardioselectivity and partial agonist activities
  • Some exhibit vasodilating activity
  • Do not usually cause hypotension in healthy, normotensive individuals
  • Blockade of B1 receptors inhibits renin release
  • Several B-blockers exhibit local anesthetic action due to blockade of Na channels and resultant membrane stabilization
53
Q

B-blocker pharmacokinetics

A
  • Except esmolol, all are available as oral preps
  • cavedilol, metoprolol, and propranolol available as extended release tablets
  • Atenolol, esmolol, labetalol, metoprolol, and propranolol available parenterally
  • Wide range of half-lives
  • Low to moderate lipid solubility (except propranolol and penbutolol)
  • Propranolol and penbutolol cross the BBB
54
Q

B-blocker adverse effects and contraindications

A
  • Asthma/COPD: blockade of B2 receptors may lead to increase in airway resistance. None of the B1 specific are specific enough to avoid B2 blockade - avoid in asthmatics
  • Diabetes: glycogenolysis is partially inhibited after B2 blockade; mask signs of hypoglycemia and delays recovery from insulin-induced hypoglycemia - caution in insulin-dependent DM - benefit outweighs risk after MI
  • Most common side effects are bradycardia and fatigue, sexual dysfunction and depression
  • Chronic use causes poor lipid profiles (increased VLDL and reduced HDL)
  • Sudden withdrawal causes rebound HTN, angina, and possibly MI - up regulation of receptor synthesis
55
Q

B-blocker drug-drug interactions

A

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

56
Q

B-blocker clinical uses

A
  • HTN: metoprolol and atenolol are most widely used
  • Heart failure: administration may worse acute CHF, even if stable compensated HF, cardiac decompensation if CO is dependent on sympathetic drive; gradual increase in dose may prolong life in CHF: carvedilol, bisoprolol, and metoprolol reduce mortality
  • Ischemic heart disease: may reduce frequency of angina episodes, improve exercise tolerance. Timolol, metoprolol, and propranolol prolong survival after MI
  • Cardiac arrhythmias: effective in treatment of supra ventricular and ventricular arrhythmias
  • Glaucoma: topical drops of timolol, betaxolol, carteolol and others reduce pressure
  • B1 selectivity advantageous in pts w/ comorbid asthma, diabetes, or peripheral vascular disease
  • Agents w/ partial B2-agonist activity may be advantageous in pts w/ bradyarrhythmias or peripheral vascular resistance
57
Q

a1-blockers (prazosin) MOA

A

reversible antagonists at a1 receptors

58
Q

a1-blockers (prazosin) pharmacodynamics

A
  • Prevent vasoconstriction of both arteries and veins, BP reduced by lowering peripheral vascular resistance
  • Relaxes smooth muscle of the prostate
  • Retention of salt and water occur when used w/o a diuretic
  • Associated w/ no change or improvement (increased HDL) in lipid profiles
59
Q

a1-blockers (prazosin) adverse effects and contraindications

A
  • Generally well-tolerated
  • Orthostatic hypotension, dizziness (1st dose), palpitations, headache, lassitude
  • less increase in reflex tachycardia than non-selective alpha adrenergic blockers (alpha2 receptor inhibition of NE release from nerve endings is unaffected)
60
Q

a1-blockers (prazosin) drug-drug interactions

A

-most effective when used in combination with other agents (B-blocker and diuretic)

61
Q

a1-blockers (prazosin) clinical uses

A

-primarily used in men with concurrent HTN and BPH

62
Q

a2-agonists (clonidine, methyldopa) MOA

A
  • reduce sympathetic outflow from vasomotor centers in the brainstem allow the centers to retain or increase sensitivity in baroreceptor control
  • Agonists at central a2 receptors
63
Q

a2-agonists (clonidine, methyldopa) Clinical uses

A
  • methyldopa is used for HTN in pregnancy

- clonidine is still commonly used but not the others

64
Q

Clonidine

A

-Pharmacodynamics: lowers BP by reducing cardiac output (decreased HR and relaxation of capacitance vessels) and reducing peripheral vascular resistance

  • Adverse effects: sedation, dry mouth, depression, sexual dysfunction
  • Transdermal prep has less sedation than oral but may cause skin reaction
  • Abrupt withdrawal can lead to life-threatening HTN crisis
65
Q

Methyldopa

A
  • Pharmacodynamics: lowers BP by reducing peripheral vascular resistance, variable reduction in heart rate and cardiac output
  • Pharmacokinetics: methyldopa is analog of L-dopa, converted to a-methylnorepinephrine by an enzymatic pathway that directly parallels synthesis of NE from L-dopa
  • Adverse effects: sedation, dry mouth, lack of concentration, sexual dysfunction

Renal II Final (5 decks)

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