Sympathetic Nervous System Pharmacology Flashcards

1
Q

CPCRs

A

activate second messengers and exnymes within the cell

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2
Q

catecholamines

A

dopamine
NE
Epi
(all derived from tyrosine)

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3
Q

NE

A

release from sympathetic neurons

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4
Q

NE and Epi

A

relatively equivalent, except NE has low potency for B2 rec

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5
Q

sympathomimetic

A

enhance signalling

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6
Q

sympatholytic

A

decrease signaling

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7
Q

adrenergic receptors in the brain

A

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

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8
Q

effects of adrenergic receptors in brain

A

attention, arousal, wakefulness, anxiety, memory formation

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9
Q

can peripheral NE and EPi cross BBB?

A

no

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

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10
Q

reflex bradycardia

A

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

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11
Q

reflex tachycardia

A

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

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12
Q

alpha 1 receptors

A

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

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13
Q

Alpha 2 receptors

A

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

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14
Q

beta 1 receptors

A

increase HR and contractibility

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15
Q

beta 2 receptors

A

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

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16
Q

beta 3 receptors

A

-lipolysis in adipocytes (release energy reserves)

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17
Q

4 alpha adrenergic agonists

A

epinephrine
phenylephrine
oxymetazoline
clonidine

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18
Q

epinephrine

A

-vasoconstrictor with local anesthetic

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19
Q

phenlyephrine

A

-a1 selective
-decongestant

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20
Q

oxymetazoline

A

-a1 selective
-decongestant

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21
Q

overuse of oxymetazoline in short term

A

rhinitis medicamentosa

rebound congestion (more congestion than before)

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22
Q

overuse of oxymetazoline in long term

A

turbinate hypertrophy

enlargement of bone and tissue in airway

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23
Q

clonidine

A

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

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24
Q

2 types of alpha adrenergic antagonists

A

prozosin
tamsulosin

25
Q

prozosin

A

-a1 selective
-antihypertensive (relaxation of smooth muscle)

26
Q

amsulosin

A

-a1 selective
-relaxation of prostatic smooth muscle in BPH

27
Q

side effects of A1 blockers (3)

A
  1. orthostatic hypotension
  2. reflex tachycardia
  3. nasal congestion
28
Q

orthostatic hypotension

A

BP from sitting to standing

29
Q

reflex tachycardia

A

increase in HR and CO to compensate for decrease in TPR

30
Q

nasal convestion

A

relaxation of vessels - more fluid for congestion

31
Q

3 beta adrenergic agonsits

A
  1. dobutamine
  2. albuterol
  3. salmeterol
32
Q

dobutamine

A

b1 agonist
-increase CO in acute heart failure

33
Q

albuterol

A

b2 selective
-used for acute asthma

34
Q

salmeterol

A

b2 selective
-longer lasting asthma

35
Q

nonselective or B1 selective B blockers

A

-decrease cardiac work
-treat heart failure
-dec glaucoma

36
Q

is there any use for b2 selective b blockers?

A

no

37
Q

side effects of B1 blockade

A

hypotension
heart failure

38
Q

side effects of B2 blockade

A

hypoglycemia
bronchoconstricion

39
Q

non-selective b blocker

A

propranolol

40
Q

propranolol

A

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

41
Q

b1 selective.b blockers

A

metaprolol

42
Q

metaprolol

A

-similar to propranolol
-avoids bronchoconstriction and hypoglycemia

43
Q

two other types of beta blockers

A

acebutolol
labetalol

44
Q

ebutalol

A

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

45
Q

labetalol

A

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

46
Q

unopposed alpha stimulation

A

-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

47
Q

mixed acting sympathomimetics

A

abuse potential increase

48
Q

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

A

-drugs enter CNS readily
-drugs that block dopamine reuptake

49
Q

toxic effects of sympathomimetics

A

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

50
Q

sympathomimetic toxidrome

A

MATHS

51
Q

cocaine

A

inhibits NE transporter and NE reuptake

52
Q

amphetamine

A

enhances NE release and blocks reuptake

53
Q

ephedrine / pseudoephedrine

A

enhance release and direct agonist activity

decongestant effect

54
Q

atropine and mydriasis

A

stimulate alpha rec on dilator msucle

55
Q

drugs to treat glaucoma

A
  1. cholinomimetics
  2. beta blocker
  3. prostaglandins
56
Q

cholinomemetics and glaucoma

A

facilitate drainage through trabecular meshwork by contractign iris and ciliary muscle

pilocarpine and physostigmine

57
Q

beta blockers and glaucoma

A

reduce aqueous humor production

timolol

58
Q

prostaglandins and glaucoma

A

increase permeability of trabecular meshwork

59
Q

angle of glaucoma between

A

cornea and iris