Sympathetic Nervous System Pharmacology Flashcards by Kajal Khatri

CPCRs

activate second messengers and exnymes within the cell

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catecholamines

dopamine
NE
Epi
(all derived from tyrosine)

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release from sympathetic neurons

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NE and Epi

relatively equivalent, except NE has low potency for B2 rec

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sympathomimetic

enhance signalling

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sympatholytic

decrease signaling

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adrenergic receptors in the brain

central noradrenergic system that originate in the brain stem and release NE to activate adrenergic receptors thorughout brain

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effects of adrenergic receptors in brain

attention, arousal, wakefulness, anxiety, memory formation

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can peripheral NE and EPi cross BBB?

but many adrenergic drugs do. therefore, can regulate brain adrenergic receptors to produce therapeutic and unwanted side effects

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reflex bradycardia

low HR is compensation, reflex response to drug administered (response to vasoconstriction)

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reflex tachycardia

histamine –> decrease BP –> increase HR for compensation (response to dilation)

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alpha 1 receptors

-cause Ca2+ release
-stimulate smooth muscle contraction
-vasoconstriction
-mydriasis

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Alpha 2 receptors

-presynaptic
-inhibits Nt release
-reduce BP
-decrease in sympathetic outflow

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beta 1 receptors

increase HR and contractibility

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beta 2 receptors

-dilate / relax smooth muscle along respiratory tract and BV (bronchodilation)
-vasodilation in skeletal msucles

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beta 3 receptors

-lipolysis in adipocytes (release energy reserves)

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4 alpha adrenergic agonists

epinephrine
phenylephrine
oxymetazoline
clonidine

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epinephrine

-vasoconstrictor with local anesthetic

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phenlyephrine

-a1 selective
-decongestant

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oxymetazoline

-a1 selective
-decongestant

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overuse of oxymetazoline in short term

rhinitis medicamentosa

rebound congestion (more congestion than before)

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overuse of oxymetazoline in long term

turbinate hypertrophy

enlargement of bone and tissue in airway

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clonidine

a2 selective
-decrease sympathetic outflow, reduce BP
-decrease NE release because autoreceptor on presynaptic terminal

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2 types of alpha adrenergic antagonists

prozosin
tamsulosin

prozosin

-a1 selective -antihypertensive (relaxation of smooth muscle)

amsulosin

-a1 selective -relaxation of prostatic smooth muscle in BPH

side effects of A1 blockers (3)

1. orthostatic hypotension 2. reflex tachycardia 3. nasal congestion

orthostatic hypotension

BP from sitting to standing

reflex tachycardia

increase in HR and CO to compensate for decrease in TPR

nasal convestion

relaxation of vessels - more fluid for congestion

3 beta adrenergic agonsits

1. dobutamine 2. albuterol 3. salmeterol

dobutamine

b1 agonist -increase CO in acute heart failure

albuterol

b2 selective -used for acute asthma

salmeterol

b2 selective -longer lasting asthma

nonselective or B1 selective B blockers

-decrease cardiac work -treat heart failure -dec glaucoma

is there any use for b2 selective b blockers?

side effects of B1 blockade

hypotension heart failure

side effects of B2 blockade

hypoglycemia bronchoconstricion

non-selective b blocker

propranolol

-decrease CO by blocking B1 rec in heart -bronchoconstriction by blocking B2 rec in lungs -impair glucose metabolization -inexpensive

b1 selective.b blockers

metaprolol

-similar to propranolol -avoids bronchoconstriction and hypoglycemia

two other types of beta blockers

acebutolol labetalol

ebutalol

-has intrinsic sympathomimetic activity (partial agonist of B rec, not full agonist) -avoids bradycardia

labetalol

-blocks B1, B2, and A1 -useful in hypertension

unopposed alpha stimulation

-potential contraindication for use of epi in pt taking beta blocker -b rec blocked while alpha rec stimulated -leads to large increase in vascular resistance, reflex bradycardais

mixed acting sympathomimetics

abuse potential increase

why is there an increase in abuse potential for mixed acting sympathomimetics?

-drugs enter CNS readily -drugs that block dopamine reuptake

toxic effects of sympathomimetics

-avoid individuals with pre-existing CVD -risk highest with indirect acting symp drugs -risk for toxicity is additive

sympathomimetic toxidrome

MATHS

cocaine

inhibits NE transporter and NE reuptake

amphetamine

enhances NE release and blocks reuptake

ephedrine / pseudoephedrine

enhance release and direct agonist activity decongestant effect

atropine and mydriasis

stimulate alpha rec on dilator msucle

drugs to treat glaucoma

1. cholinomimetics 2. beta blocker 3. prostaglandins

cholinomemetics and glaucoma

facilitate drainage through trabecular meshwork by contractign iris and ciliary muscle pilocarpine and physostigmine

beta blockers and glaucoma

reduce aqueous humor production timolol

prostaglandins and glaucoma

increase permeability of trabecular meshwork

angle of glaucoma between

cornea and iris