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Therapeutics II > ANS sympatholytics > Flashcards

ANS sympatholytics Flashcards

1
Q

Sympathetic NTs

A

-norepinephrine
-epinephrine
-adrenergic

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2
Q

veins and arteries only controlled by

A

SNS

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3
Q

Cardiac muscle receptors

A

-B1

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4
Q

Vasc smooth muscle receptors

A

-a1

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5
Q

CNS receptors

A

-a1 and a2

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6
Q

BP=

A

CO x TPR

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7
Q

CO=

A

SV x HR

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8
Q

SV determined by

A

-cardiac contractility
-venous return to heart (preload)
-resistance to left ventricle to eject blood into aorta (afterload)

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9
Q

selectivity of adrenergic receptor agonists

A

-

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10
Q

Baroreceptor reflex when BP decreases

A

-activates sympathetic fibers that feed back and innervate heart (B1)
-inc HR - reflex tachycardia
-a1 constricts bloodvessels
-inhibits vagus PSNS!
=inc blood pressure

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11
Q

Baroreceptor reflex when BP increases

A

-inhibits sympathetic
-activates vagus (PSNS)
-dec HR - reflex bradycardia
-no direct effect on blood vessels
=dec BP

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12
Q

Phenylephrine

A

-act a1
-inc systolic pressure
-vasoconstriction
-DEC HR
-activate baroreceptor to decrease HR

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13
Q

Epinephrine

A

-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

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14
Q

Isoproterenol

A

-B receptors
-dec diastolic pressure, inc pulse pressure HR
-vasodilation
-positive I and C effects
-activate baroreceptors

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15
Q

if patient stands up really fast what is the baroreceptor response

A

-activated to inc CO, and vascular resistance to raise BP

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16
Q

Classes of anti-HTNs

A

-diuretics
-sympatholytics
-vasodilators
-renin-angiotensin antagonists

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17
Q

B-blocker action

A

-dec HR, contractility, renin secretion

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18
Q

a and b blockers

A

–dec HR, contractility, renin secretion
-smooth muscle relaxation

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19
Q

central a2 agonist action

A

-dec sympathetic tone

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20
Q

peripheral a1 antagonists

A

-vasc smooth muscle relaxation

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21
Q

a1 ANTAgonist drugs

A

-prazosin
-terazosin
-doxazosin

-double ring and piperazine ring

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22
Q

a1 Antagonist

A

-excreted in bile
-vasodilators
-relax smooth muscle and enlarge prostate
-NO reflex tachycardia

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23
Q

Prazosin vs phentolamine

A

-dec TPR via a1
-activate baroreceptor
-inc NE release

-phentolamine blocks a2 tho so no negative feedback = cardiac overstimulation = reflex tachycardia

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24
Q

Prazosin and terazosin action

A

-a1 ANTAgonist arterioles and venules
-dec TPR
-less tachycardia than nonselective a
-renin release )consider diuretic)

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25
Prazosin and Terazosin use
-BPH -HTN (not first line) -Reynaud;s disease (mrs pairitz)
26
a1 antagonist problems
-minor -first dose: orthostatic hypotension and syncope
27
Direct acting a2 agonists
-reduce BP by reducing output from brain -inhibit NE =DEC HR, contractility, renin release, vasoconstriction
28
direct acting a2 agonist drugs
-clonidine -guanabenz -guanfacine -methyldopa
29
clonidine
-a2 -activation of presynaptic a2 receptor in CNS to dec SNS -dichlorophenyl ring = lipophilic -HTN, neuropathic pain/opiate withdrawal -ADHD
30
Clonidine problems
-HYPOtension -sedation -dry mouth -withdrawal after long time use (HTN, tachycardia, angina, MI)
31
Guanabenz and Guanfacine
-a2 agonists -open ring imidazolines -ring w chlorine -nonionized at phy pH -HTN -guanfacine for ADHD
32
Methyldopa
-a2 agonist -prodrug -dec SNS outtflow -displaces NE -esterases -oral, parenteral (dopate) -HTN in pregnancy
33
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)
34
non-selective B-Blockers
-Propranolol and nadolol (HTN, angina, arr, HD, prophylaxis migraines) -Timolol (glaucoma, dec aq humor) -minor probs, rebound HTN taper dose
35
propranolol effects
-dec CO and HR -inc VLDL, dec HDL -inhibit lipolysis -inhibit response to hypoglycemia -inc bronchial airway resistancw
36
Nonselective B-bloxkers w Intrinsic sympathomimetic activity
-pindolol (angina, migraine) -carteolol (glaucoma) -less likely to cause bradycardia and lipid probs -HTN
37
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
38
B-blocker side effects
-bradycardia -AV block -sedation -mask hypoglycemia sx -withdrawal syndrome
39
B-blocker contraindications
-asthma -copd -congestic HF type IV
40
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
41
Mixed adrenergic antagonist probs
-similar to B-blockers -taper dose
42
Fenoldopam
-dopamine receptor agonist -does not activate a1 or B receptors -severe HTN -dont use in glaucoma -good for renal impairment
43
if B-blocker can produce vasodilation it is
-3rd gen
44
renin
-aspartic acid protease that converts to angiotensin I
45
ACE
-converts angiotensin I to II -inactivate bradykinin that promotes vasodilation
46
renin inhibitor drug
-direct inhibitor of renin and dec formation of angiotensisn I from angioteninogen -expensive HTN tx
47
B1 blockers inhibit
-renin release
48
ACE inhibitors (-pril) classes
1. sulfhydryl-containing -dicarboxyl-containing -phosphorus containing
49
Dicarboxyl-containing ACEi
-lisinopril -enalapril (prodrug) -quinapril (prodrug) ring chain
50
Sulfhydryl ACEi
-captopril -not prodrug -short acting
51
phsophorus containing ACEi
-fosinopril (monopril) -prodrug
52
ACE inhibitor action
-inhibit ACE -reduce vasoconstriction -reduce myocardial mitogenic activity = dec hypertrophy -reduce Na and water retention -reduce TPR
53
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
54
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)
55
bradykinin
-produces vasodilation -mediated by prostaglandins
56
ARBs SAR
-acidic group -simidazole -carboxylic acid group
57
ARB drugs
-Sartans -block angiotensin II w higher affinity for AT1 than AT2
58
ARB action
-competitive inhibition of AT1 -reduce vasoconstriction -dec TPR -dec afterload -dec preload -dec SNS -dec remodling
59
ARB use
-usually pt that cant tolerate ACE -better in diabetes than TZDs -better in ischemic HD -better in pt w CKD
60
ARB side effects
-HYPOtension -hyperkalemia -angioedema -fetal pathologies -reduced GFR -no cough tho (dont breakdown bradykinin) -less effecgtive in black pt
61
Aldosterone ANTAgonist (MRA)
-spirinolactone and eplerenone -block reabsorption of sodium and dec bBP
62
MRA use
-heart failure -reduce mortality 0not monotherapy for HTN but used to reduce hypokalemia
63
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
64
thiazide probs
-hypokalemia -alkalosis -hyperuricemia -hypercalcemia -hyperglycemia -hyperlipidemia
65
other diuretics
-loop not recommended first line, potent but short acting -K+ spaing not recommended first line bc week and hyperkalemia risk
66
HTN in pregnancy
-methyldopa -labetalol, metoprolol -avoid ACE/ARBs/renin inhibitors, and MRAs

Therapeutics II (55 decks)

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