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Pharm #2 > L14-16 adrenergic agonists and antagonists > Flashcards

L14-16 adrenergic agonists and antagonists Flashcards

1
Q

pre-ganglionic fibers release

A

Ach

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2
Q

post-ganglionic fibers release

A

parasympathetic : Ach

sympathetic : Norepinephrine (adrenergic)

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3
Q

adrenal medula releases

A

Mostly Epi and some NE into the circulation

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4
Q

post-ganglionic sympathetic fivers that innervate the sweat glands release

A

Ach (exception)

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5
Q 
Main functions of the parasympathetic NS on:
eye
heart
bronchioles
GI tract
Bladder
A

eye - constrict the circular (sphincter) muscles of the pupil (miosis)

heart - innervates the sinoatrial node to reduce HR, and the AV node to slow conduction

bronchioles - constricts smooth muscle of the bronchi

GI tract - promotes secretions and motility

Bladder - causes constriction of the detrusor muscle and emptying

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6
Q

Main functions of the sympathetic NS on:
eye
heart
bronchioles

A

eye - innervates the radial(dilator) muscle causes mydriasis and the ciliary body to stimulate production of aqueous humor

heart - accelerated sinoatrial node pacemaker depolarization (increases HR)

bronchioles - relaxation of the smooth muscle lining

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7
Q

How does sympathetic innervation affect HR

A

increases the inward calcium current to promote faster spontaneous depolarization (phase 4)

lowers the threshold for activation

stimulates a greater calcium influx into myocytes increasing the contractile force of depolarization.

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8
Q 
Main functions of the sympathetic NS on:
Blood vessels
GI tract
Bladder
metabolic fuctions
A

Blood vessels - contraction and relaxation depending on the receptor

GI tract - decreased motility

Bladder - inhibits emptying by contracting sphincters

metabolic functions - increase blood sugar

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9
Q

factors determining the response to NT receptor binding

A
  1. type of receptor
  2. secondary messenger system
  3. cell machinery (cell type)
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10
Q

effects of inhibition of re-uptake

A

potent sympathomimetic effects - signifies the importance of re-uptake in termination of the normal NTs affects

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11
Q

Sympathomimetic drugs

A

stimulate the sympathetic system

interact with adrenergic receptors directly

endogenous ligands for adrenergic receptors are epinephrine, norepinephrine, and dopamine

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12
Q

alpha1 receptors where they are found and what they do

A

contracts vascular smooth muscle

contracts pupillary dilator muscle (mydriasis)

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13
Q

Beta1 receptors where they are found and what they do

A

heart - stimulates rate and force

juxtaglomerular cells - stimulates renin release

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14
Q

Beta2 receptors where they are found and what they do

A

respiratory, uterine, and vascular smooth muscle - relaxes

somatic motor nerve terminals (voluntary muscle) - causes tremor

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15
Q

Dopamine1 receptors where they are found and what they do

A

renal and other splanchnic blood vessels - relaxes/ reduces resistance.

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16
Q

process of vascular smooth muscle contraction

A
  1. NE or EPI (or another a1-agonist) binds the a1-adrenergic receptor on vascular smooth muscle
  2. Gaq subunit activates PLC which liberates IP3 and DAG
  3. IP3 activates IP3 receptor opening a Ca release channel from the SR and allowing the release of Ca- stimulation smooth muscle contraction
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17
Q

alpha2 receptors in nerve terminals

A

pre-synaptic alpha2 receptor activation decreases NT release.

  1. binding of alpha2 inhibits adenylyl cyclase > reduces cAMP
  2. reduced activation of PKA
  3. reduced calcium influx during membrane depolarization
  4. reduced vesicular release of NT
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18
Q

how does B1 receptors have a positive chronotrophic effect

A

activation of adenylyl cyclase and increase of cAMP can activate PKA– promoting phosphorylation of Ca channels leading to increased inward Ca current and faster nodal depolarization to the firing threshold

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19
Q

how does B1 receptors have positive inotrophic effects

A

increased cAMP > increased PKA > phosphorylation of L-type Ca channels > more Ca influx > larger trigger signal for release of Ca from the SR

more Ca also gets stored in the SR increasing the Ca release for the next trigger.

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20
Q

how does B2 receptors cause vascular smooth muscle relaxation?

A

cAMP activates PKA which phosphorylates and INACTIVATES myosin light chain kinase (MLCK).

Phosphorylated MLCK has a lower affinity for Ca-calmodulin decreasing its ability to phosphorylate myosin and allow cross-bridge formation.

overall: reduced smooth muscle contraction

highly expressed on bronchi and some vascular beds and therefore regulates the degree of airway constriction and peripheral vascular resistance

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21
Q

role of peripheral a2-adrenergic receptors

A

produce peripheral vasoconstriction (opposite mechanism of B2 receptors- inhibits adenylyl cyclase and cAMP)

inhibition of PKA leads to activation of MLCK and vascular smooth muscle constriction

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22
Q

isoproterenol (ISO)

A

synthetic catecholamine with large substitution that gives it increased affinity for beta receptors

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23
Q

efficacy at the a1-adrenergic receptors

A

epi > (or =) NE&raquo_space;isoproterenol

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24
Q

efficacy at the a2-adrenergic receptors

A

epi > (or =) NE&raquo_space;isoproterenol

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25
Q

efficacy at the B2-adrenergic receptors

A

isoproterenol > EPI&raquo_space; NE

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26
Q

efficacy at the B1-adrenergic receptors

A

Isoproterenol > EPI = NR

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27
Q

systolic pressure is mostly affected by

A

CO (adrenergic receptors in the heart)

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28
Q

diastolic pressure is mostly affected by

A

TPR (arterial vasoconstriction, adrenergic receptors on the vasculature)

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29
Q

epinephrine at low doses

A

B-receptor effects predominate

B2 receptor activations causes peripheral vasodilation–decreasing diastolic BP

B1 receptor activation has positive inotrophic (force) and chronotropic (HR) effects — increasing CO and systolic BP

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30
Q

epinephrine at high doses

A

a1 receptor activation predominates (more receptors) – peripheral vasoconstriction

= elevated systolic and diastolic pressures

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31
Q

epinephrines effect on mean blood pressure

A

low dose- slight increase (bigger pulse pressure)

high dose- large increase

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32
Q

epinephrines affect on bronchiles

A

B2 receptors - bronchodilation

a1 receptor - decrease in bronchiole secretions

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33
Q

epinephrines toxicities

A

arrhythmias (a1 due to potential for very high BP)

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34
Q

epinephrine stimulates which receptors

A

a1, a2, B1, B2

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35
Q

Norepinephrine stimulates

A

a1, a2, B1

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36
Q

NE effects

A

Cardiovascular - due mostly to a1 activation: vasoconstriction (increased TPR and diastolic BP). B1 positive inotropic and chronotropic effects (increase systolic BP)

large rise in BP leads to baroreceptor response and DECREASE in HR (dominates over the direct chronotropic effects)

Overall: MAP increases (NE has a limited affinity for B2 receptors so there is little change in bronchiole smooth muscle)

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37
Q

NE toxicities

A

ischemia (preexisting could become gangrene)

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38
Q

contraindication for NE

A

pre-existing excessive vasoconstriction and ischemia

39
Q

dopamine receptor affinities

A

stimulates D1 at low concentrations but can also stimulate B1 and a1 and a2 receptors at higher concentrations

40
Q

domamine effects

A

low infusion rates : D1 receptor - decreased TPR

medium : actives B1 receptors leading to increased cardiac contractility and HR

high: stimulates alpha receptors leading to increased BP and TPR

41
Q

dopamine toxicity

A

low infusion rate: hypotension

high infusion rates: ischemia

42
Q

dopamine contraindication

A

uncorrected tachyarrhythmias

43
Q

advantage of dopamine vs Epi

A

dopamine vasodilates blood vessels to certain organs such as the kidneys which can protect them from ischemia in shock while constricting other vessels to raise BP

44
Q

example of non-selective B-adrenergic agonist

A

isoproterenol

45
Q

effects of non-selective B-adrenergic agonist

A

CV: B1- positive inotrophic and chronotrophic. B2 peripheral vasodilation. Overall- slight decrease in MAP (may have small increase in systolic initially followed by decrease)

Bronchioles: dilation (B2)

46
Q

toxicity effects of B-adrenergic agonis (Isoproterenol)

A

tachyarrhythmias

47
Q

contraindications of non-selective B-adrenergic agonist (isoproterenol)

A

arrhythmias

48
Q

example of a selective B1 agonist

A

Dobutamine (receptor affinity is B1>B2>a)

49
Q

Selective B1 receptor agonist effects

A

CV: increased CO– unique in that positive inotropic effect (contractility) > positive chronotropic (HR) effect (due to lack of B2 mediate vasodilation and reflex tachycardia)

high doses- B2 activation could lead to hypotension with reflex tachycardia

50
Q

dobutamine toxicity (B1 selective agonist)

A

hypotension (especially at doses activating B2)

51
Q

effects of selective B2 adrenergic agonists

A

CV: negligible usually but can cause some B1 agonist-like response

Bronchioles- bronchiodilation

52
Q

toxicity

A

B1 activation- tachycardia, tolerance (long term use)
B2-skeletal muscle tremor (activation of B2 receptors on pre-synaptic nerve terminals of cholinergic somatomotor neurons)

53
Q

therapeutic uses of selective B2 agonist

A

bronchospasms (acute asthma) and obstructive airway disease

54
Q

examples of selective B2 adrenergic agonists

A

terbutaline and albuterol

55
Q

example of selective a1 adrenergic agonist

A

phenylephrine

56
Q

effects of selective a1 adrenergic agonists

A

CV: peripheral vasoconstriction and increased BP, activates baroreceptor reflex decreasing HR

Ophthalmic: dilates pupil

Bronchioles: decrease bronchial (and upper airway) secretions

57
Q

contraindication of selective a1 agonists

A

pre-existing excessive vasoconstriction ans ischemia

58
Q

benefits of phenylephrine

A

longer half life (not a catecholamine therefore not degraded by COMT) allowing it to be applied directly to where it is needed– topically or inhaled

IV during surgery to increase BP

59
Q

toxicity of a1 adrenergic agonists

A

hypertension

60
Q

Selective a2 adrenergic agonists example

A

clonidine

61
Q

clonidine effects

A

CV: peripheral vasoconstriction and slight increase in BP, crosses the BBB to cause reduced sympathetic outflow which reduces vasoconstriction and BP. OVERALL: reduction in BP

reduces tonic excitatory input to the sympathetic cells reduces sympathetic output to vascular smooth muscle

62
Q

toxicity of clonidine

A

Dry mouth, withdrawal after chronic use can lead to life-threatening hypertensive crisis

63
Q

function of indirectly acting sympathomimetics

A

increase the concentration of endogenous catecholamines in the synapse and circulation via either:

  1. release of cytoplasmic catecholamines
  2. blockade of re-uptake transporters
64
Q

examples of releasing agents

A

amphetamine, methamphetamines, methylphenidate, ephedrine, pseudoephedrine, tyramine

65
Q

amphetamine like drugs method of action

A

are taken up by re-uptake proteins
reverse the re-uptake mechanism
causes release of NT in a calcium-independent manor

easily cross the BBB- high abuse potential due to reinforcing effects of central dopamine release

66
Q

effects of releasing agents

A

CV: due to NE release, a receptor- peripheral vasoconstriction. B-receptor positive inotropy and contractility

CNS: stimulant, anorexia agent

67
Q

toxicity of releasing agents

A

tachycardia

68
Q

therapeutic uses of releasing agents

A

ADD, narcolepsy, nasal congestion

69
Q

contraindications of releasing agents

A

rx with NAO inhibitors within the previous 2 weeks (will increase the effects)

70
Q

3 categories of beta blockers

A 
non selective (B1 and B2)
cardiac selective (B1)
partial agonist (B1 and B2)
71
Q

examples of non-selective B-Blockers

A

propranolol, nadolol, timolol

72
Q

disadvantage of non-selective B-Blockers

A

potentially harmful side effects for patients with respiratory disease

73
Q

Effects of non-selective B-Blockers

A

CV: reduced HR and contractility, reduced renin release leads to reduced vasoconstriction

Bronchioles: bronchiole constriction in those with asthma or chronic obstructive pulmonary disease

74
Q

uses of non-selective B-blockers

A

hypertension, angina, glaucoma, heart failure, arrhythmia

75
Q

toxicity associate with non-selective B-blockers

A

bronchospasm asks symptoms of hypoglycemia, CNS effects including insomnia and depression, some can raise triglycerides, bradycardia

76
Q

contraindications with non-selective B-blockers

A

Bronchial Asthma***

sinus bradycardia, heart block, cariogenic shock

77
Q

examples of cardioselective B1-blockers

A

metoprolol, atenolol, esmolol

78
Q

effects of cardioselective B1-blocker

A

CV: same as nonselective: reduced HR and contractility, reduced renin release leads to reduced vasoconstriction

79
Q

toxicity of cardioselective B-blockers

A

typically mild and transient- depression, insomnia, hypotension*, bradycardia

80
Q

contraindications for cardioselective B-Blockers

A

heart block, cardiogenic shock

81
Q

partial agonists B-blockers example

A

pindolol

82
Q

pindolol acts on which receptors

A

B1 and B2

83
Q

benefits to pindolol

A

good when hypertension is due to high sympathetic output- they have less bradycardic effect bc some B signal still remains

used when patients are less tolerant of bradycardia effects

84
Q

effects of partial agonist B-blocker

A

CV: reduced HR and contractility, reduced renin release leads to reduced vasoconstriction (same as others)

85
Q

therapeutic uses

A

hypertension in those who are less tolerant of bradycardia and reduced exercise capacity cause by other beta blockers

86
Q

toxicity of partial agonist B-blockers

A

bronchospasm asks symptoms of hypoglycemia, CNS effects including insomnia and depression, some can raise triglycerides, bradycardia(less severe)

87
Q

non selective alpha-adrenergic antagonists example

A

phenoxybenazamine (irreversable)

phentolamine (reversible)

88
Q

characteristics of a reversible antagonist

A

Emax remains the same but ED50 increases

89
Q

effects of nonselective a-receptor antagonists

A

CV: inhibit vasoconstriction (decreases BP), increased inotropy and chronotropy due to blockade of pre-synaptic a2 receptor. reflex increase in NE release- unmasks vasodilatory effect of EPI

90
Q

toxicity of nonselective alpha antagonists

A

prolonged hypotension, reflex tachycardia, nasal congestion

91
Q

examples of selective a1-receptor blockers

A

prazosin, doxazosin, terazosin

92
Q

effects of selective a1-receptor blockers

A 
inhibit vasoconstriction (decreased BP)
less cardiac stimulation than non-selective a-blockers due to preservation of a2 adrenergic function
93
Q

therapeutic uses of selective a1-antagonists

A

hypertension, benign prostatic hyperplasia (relaxes the muscle to help with urination)

Pharm #2 (13 decks)

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