ANS sympatholytics Flashcards
Sympathetic NTs
-norepinephrine
-epinephrine
-adrenergic
veins and arteries only controlled by
SNS
Cardiac muscle receptors
-B1
Vasc smooth muscle receptors
-a1
CNS receptors
-a1 and a2
BP=
CO x TPR
CO=
SV x HR
SV determined by
-cardiac contractility
-venous return to heart (preload)
-resistance to left ventricle to eject blood into aorta (afterload)
selectivity of adrenergic receptor agonists
-
Baroreceptor reflex when BP decreases
-activates sympathetic fibers that feed back and innervate heart (B1)
-inc HR - reflex tachycardia
-a1 constricts bloodvessels
-inhibits vagus PSNS!
=inc blood pressure
Baroreceptor reflex when BP increases
-inhibits sympathetic
-activates vagus (PSNS)
-dec HR - reflex bradycardia
-no direct effect on blood vessels
=dec BP
Phenylephrine
-act a1
-inc systolic pressure
-vasoconstriction
-DEC HR
-activate baroreceptor to decrease HR
Epinephrine
-B and a receptors
-inc pressure and HR
-a1 vasoconstriction
-B2 vasodilation
-B1 positive inotropic and chronotropic effects
-ACTIVATE baroreceptor reflex that mitigates direct effects
Isoproterenol
-B receptors
-dec diastolic pressure, inc pulse pressure HR
-vasodilation
-positive I and C effects
-activate baroreceptors
if patient stands up really fast what is the baroreceptor response
-activated to inc CO, and vascular resistance to raise BP
Classes of anti-HTNs
-diuretics
-sympatholytics
-vasodilators
-renin-angiotensin antagonists
B-blocker action
-dec HR, contractility, renin secretion
a and b blockers
–dec HR, contractility, renin secretion
-smooth muscle relaxation
central a2 agonist action
-dec sympathetic tone
peripheral a1 antagonists
-vasc smooth muscle relaxation
a1 ANTAgonist drugs
-prazosin
-terazosin
-doxazosin
-double ring and piperazine ring
a1 Antagonist
-excreted in bile
-vasodilators
-relax smooth muscle and enlarge prostate
-NO reflex tachycardia
Prazosin vs phentolamine
-dec TPR via a1
-activate baroreceptor
-inc NE release
-phentolamine blocks a2 tho so no negative feedback = cardiac overstimulation = reflex tachycardia
Prazosin and terazosin action
-a1 ANTAgonist arterioles and venules
-dec TPR
-less tachycardia than nonselective a
-renin release )consider diuretic)
Prazosin and Terazosin use
-BPH
-HTN (not first line)
-Reynaud;s disease (mrs pairitz)
a1 antagonist problems
-minor
-first dose: orthostatic hypotension and syncope
Direct acting a2 agonists
-reduce BP by reducing output from brain
-inhibit NE
=DEC HR, contractility, renin release, vasoconstriction
direct acting a2 agonist drugs
-clonidine
-guanabenz
-guanfacine
-methyldopa
clonidine
-a2
-activation of presynaptic a2 receptor in CNS to dec SNS
-dichlorophenyl ring = lipophilic
-HTN, neuropathic pain/opiate withdrawal
-ADHD
Clonidine problems
-HYPOtension
-sedation
-dry mouth
-withdrawal after long time use (HTN, tachycardia, angina, MI)
Guanabenz and Guanfacine
-a2 agonists
-open ring imidazolines
-ring w chlorine
-nonionized at phy pH
-HTN
-guanfacine for ADHD
Methyldopa
-a2 agonist
-prodrug
-dec SNS outtflow
-displaces NE
-esterases
-oral, parenteral (dopate)
-HTN in pregnancy
B-blockers use
-angina (reduce O2 demand bc dec HR and contractility)
-arrhythmia (slow AV conduction)
-Post MI (reasons above
-HTN (dec CO and renin)
-HF (dec overstimulation and catecholamine toxicity)
non-selective B-Blockers
-Propranolol and nadolol (HTN, angina, arr, HD, prophylaxis migraines)
-Timolol (glaucoma, dec aq humor)
-minor probs, rebound HTN taper dose
propranolol effects
-dec CO and HR
-inc VLDL, dec HDL
-inhibit lipolysis
-inhibit response to hypoglycemia
-inc bronchial airway resistancw
Nonselective B-bloxkers w Intrinsic sympathomimetic activity
-pindolol (angina, migraine)
-carteolol (glaucoma)
-less likely to cause bradycardia and lipid probs
-HTN
selective B1 blockers
-metoprolol
-bisoprolol
-atenolol
-esmolol (very short acting, tachycardia, afib)
-nebivolol (NO production)
-less bronchoconstriction
-admin oral and parenteral
-use HTN, anigina, arr, HF
B-blocker side effects
-bradycardia
-AV block
-sedation
-mask hypoglycemia sx
-withdrawal syndrome
B-blocker contraindications
-asthma
-copd
-congestic HF type IV
mixed a1 B1 and B2 antagonists
-labetolol (HTN emergency, pheochromocytoma)
-carvedilol (HF)
-dec TPR via a (prevent tachycardia)
-b-blocking prevents tachycardia)
-a1 vasodilation mitigates bradycardia from B-blocking
Mixed adrenergic antagonist probs
-similar to B-blockers
-taper dose
Fenoldopam
-dopamine receptor agonist
-does not activate a1 or B receptors
-severe HTN
-dont use in glaucoma
-good for renal impairment
if B-blocker can produce vasodilation it is
-3rd gen
renin
-aspartic acid protease that converts to angiotensin I
ACE
-converts angiotensin I to II
-inactivate bradykinin that promotes vasodilation
renin inhibitor drug
-direct inhibitor of renin and dec formation of angiotensisn I from angioteninogen
-expensive HTN tx
B1 blockers inhibit
-renin release
ACE inhibitors (-pril) classes
- sulfhydryl-containing
-dicarboxyl-containing
-phosphorus containing
Dicarboxyl-containing ACEi
-lisinopril
-enalapril (prodrug)
-quinapril (prodrug)
ring chain
Sulfhydryl ACEi
-captopril
-not prodrug
-short acting
phsophorus containing ACEi
-fosinopril (monopril)
-prodrug
ACE inhibitor action
-inhibit ACE
-reduce vasoconstriction
-reduce myocardial mitogenic activity = dec hypertrophy
-reduce Na and water retention
-reduce TPR
ACEi use
-first line monotherapy for HTN, HF
-works better in whites
-good for pt w HF and CKD
-better for pt w diabetes than thiazides
-better for pt w ischemic HD than vasodilators
ACEi probs
-cough
-angioedema (lips and tongue, worse in black pt)
-hyperkalemia (dec production of aldosterone_
-NOT in preg
-dont use if GFR<30%
-NSAIDs may reduce effectiveness (dec bradykinin)
bradykinin
-produces vasodilation
-mediated by prostaglandins
ARBs SAR
-acidic group
-simidazole
-carboxylic acid group
ARB drugs
-Sartans
-block angiotensin II w higher affinity for AT1 than AT2
ARB action
-competitive inhibition of AT1
-reduce vasoconstriction
-dec TPR
-dec afterload
-dec preload
-dec SNS
-dec remodling
ARB use
-usually pt that cant tolerate ACE
-better in diabetes than TZDs
-better in ischemic HD
-better in pt w CKD
ARB side effects
-HYPOtension
-hyperkalemia
-angioedema
-fetal pathologies
-reduced GFR
-no cough tho (dont breakdown bradykinin)
-less effecgtive in black pt
Aldosterone ANTAgonist (MRA)
-spirinolactone and eplerenone
-block reabsorption of sodium and dec bBP
MRA use
-heart failure
-reduce mortality
0not monotherapy for HTN but used to reduce hypokalemia
Thiazides
-block NaCl transporter on DCT
-diuretic effect dec BP
-long term effect on contractility
-first line HTN
-better for black pt
-not drug of choice for diabetes, hyperlipidemia, gout
thiazide probs
-hypokalemia
-alkalosis
-hyperuricemia
-hypercalcemia
-hyperglycemia
-hyperlipidemia
other diuretics
-loop not recommended first line, potent but short acting
-K+ spaing not recommended first line bc week and hyperkalemia risk
HTN in pregnancy
-methyldopa
-labetalol, metoprolol
-avoid ACE/ARBs/renin inhibitors, and MRAs