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Pharmacology > Week 12 ANS > Flashcards

Week 12 ANS Flashcards

1
Q

You can stimulate the parasympathetic NS w/drugs that act as an agonist to _______ receptors, or inhibit _____________ enzyme.

A

nicotinic receptors

acetylcholinesterase enzyme

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2
Q

describe nicotinic receptors

A
  • “nicotinic cholinergic receptors”
  • in sympathetic ganglia & skeletal mm., nicotine mimics stimulatory actions of Ach
  • vs. muscarinic which act in smooth mm. & glands via muscarine stimulation
  • ligand-gated ion channels
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3
Q

describe nicotinic receptors

A
  • “nicotinic cholinergic receptors”
  • in sympathetic ganglia & skeletal mm., nicotine mimics stimulatory actions of Ach
  • vs. muscarinic which act in smooth mm. & glands via muscarine stimulation
  • ligand-gated ion channels (do not use 2nd messengers)
  • signal for muscular contraction upon a chemical stimulus
  • triggered by binding of Ach & nicotine
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4
Q

Which adrenergic receptors (a, b1, b2) affect vascular system?

A

alpha

Alpha-adrenoceptor agonists (α-agonists) bind to α-receptors on vascular smooth muscle and induce smooth contraction and vasoconstriction, thus mimicking the effects of sympathetic adrenergic nerve activation to the blood vessels.

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5
Q

Which adrenergic receptors (a, b1, b2) affect heart?

A

beta 1

antagonists increase cardiac output

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6
Q

Which adrenergic receptors (a, b1, b2) affect lungs?

A

beta 2

agonists cause smooth mm relaxation

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7
Q

what side effects would you expect from a substance that blocks b2 receptors?

A
  • respiratory problems (bronchospasm)
  • however no isolated b2 blocker is used clinically
  • b1 antagonists are also b2 blockers => CV depression, nausea, diarrhea, diabetes, etc)
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8
Q

what is the difference between miosis and mydriasis?

A

mydriasis: pupil dilation
miosis: pupil contraction

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9
Q

Which adrenergic receptors (a, b1, b2) affect heart?

A

beta 1
antagonists increase cardiac output

remember: 1 heart

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10
Q

Which adrenergic receptors (a, b1, b2) affect lungs?

A

beta 2
agonists cause smooth mm relaxation

remember: 2 lungs

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11
Q

what autonomic receptors do you want to target for asthma

A

beta 2

want agonists

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12
Q

what autonomic receptors do you want to target for BPH

A

a1

want antagonists

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13
Q

what autonomic receptors do you want to target for urinary incontinence

A

muscarine

want antagonists

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14
Q

what autonomic receptors do you want to target for glaucoma

A

muscarine - agonist

b1 - antagonist

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15
Q

s/e assoc. with b1 antagonists

A 
hypotension
fatigue
nausea
diarrhea
diabetes
erectile dysfunction
bronchospasm
decreased circulation
insomnia
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16
Q

s/e assoc. with b2 agonists

A

insomnia
anxiety
tremors
CV sxs

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17
Q

s/e assoc. with a1 agonists

A

rebound congestion

freq. application causes ischemia

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18
Q

s/e assoc. with a1 antagonists

A

retrograde ejaculation

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19
Q

s/e assoc. with a2 antagonist

A

fatigue

dry mouth

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20
Q

s/e assoc. with muscarinic receptor agonists

muscarine, pilocarpine, Ach

A
  • increased secretions (saliva, urine, lacrimation, defecation), mitosis,smooth mm contraction & peristalsis (Cramping)
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21
Q

What is the difference between epinephrine & ephedra with regards to how long it remains active in the body?

A
  • epinephrine: short T1/2 (MAO & COMT enzymes)

- ephedra: more intense reaction, longer acting

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22
Q

How does an a2 agonist lower BP?

A
  • a2 receptors located in brain

- SE: inhibits NE release by negative feedback

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23
Q

what are b1 blockers used to treat? what is the most common side effect?

A
  • tx: heart problems & glaucoma

- s/e: decreased heart function, fatigue, dizziness

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24
Q

what are b2 agonists used to treat? what is the most common side effect?

A
  • asthma, pulmonary conditions

- s/e: insomnia, anxiety, tremors, CV problems

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25
Q

what are a1 blockers used to treat? what is the most common side effect?

A
  • tx: BPH, HTN

- s/e: retrograde ejaculation

26
Q

what are s/e of cholinesterase inhibitors? what would you use it to treat?

A
  • dementia of Alzheimer’s
  • s/e: SLUDGE
    salivation/lacrimation/urination/defecation/GI upset/emesis)
27
Q

if someone was poisoned with a nerve gas or a mushroom was causing severe GI distress (vomiting, diarrhea), what class of drugs could help?

A

anticholinergics

e.g. atropine, oxybutynin, tolterodine

28
Q

what class of drugs decrease nocturnal melatonin levels & decrease HDL cholesterol & elevate blood sugar?

A

b1 blockers

29
Q

what receptors do confine and curare target? agonist or antagonist?

A
  • conine: nicotinic early agonist, and late antagonist

- curare: nicotinic antagonist

30
Q

epinephrine binds to which receptors?
adrenergic
muscarinic
nicotinic

A

adrenergic
alpha & beta
(not selective - binds to all)

31
Q

indications for administering epinephrine?

A

anaphylaxis
sepsis (can cause BP to drop)
cardiac arrest
asthma - when other drugs ineffective or unavailable

32
Q

MOA of ephedrine?

A
  • releases stored NE from storage vesicles

- directly stimulates both alpha & beta receptors

33
Q

compare epinephrine & norepinephrine

A

The actions of epinephrine and norepinephrine are generally similar, although they differ from each other in certain of their effects. Norepinephrine constricts almost all blood vessels, while epinephrine causes constriction in many networks of minute blood vessels but dilates the blood vessels in the skeletal muscles and the liver. Both hormones increase the rate and force of contraction of the heart, thus increasing the output of blood from the heart and increasing the blood pressure. The hormones also have important metabolic actions. Epinephrine stimulates the breakdown of glycogen to glucose in the liver, which results in the raising of the level of blood sugar. Both hormones increase the level of circulating free fatty acids.

34
Q

indications for ephedra/pseudoephedrine/synephrine?

A

asthma
sinusitis
weight loss
allergies

35
Q

MOA of caffeine?

A
  • inhibits adenosine receptors = increases release of catecholamines
  • inhibits phosphodiesterase enzyme (increases cAMP)
36
Q

MOA of caffeine?

A
  • inhibits adenosine receptors = increases release of catecholamines
  • inhibits phosphodiesterase enzyme (increases cAMP; cAMP is inactivated by phosphodiesterase) => results of epinephrine are sustained
  • coffee doesn’t bind to adrenergic receptors, it just prevents the breakdown of the signal
37
Q

what sympathetic effects does cAMP result in?

A
  • relaxation of smooth mm
  • enhanced contractility of cardiac mm
  • glycogenolysis
  • lipolysis
38
Q

caffeine inhibits which enzyme?

A

phosphodiesterase

which breaks down cAMP

39
Q

what is the MOA of a1 agonist as a decongestant?

A

a1 agonist = vasoconstriction

topical application avoids systemic s/e

40
Q

what do a-agonists do?

A

Alpha-adrenoceptor agonists (α-agonists) bind to α-receptors on vascular smooth muscle and induce smooth contraction and vasoconstriction, thus mimicking the effects of sympathetic adrenergic nerve activation to the blood vessels.

41
Q

what is the difference between a1 and a2 receptors?

A

α1-adrenoceptors are the predominant α-receptor located on vascular smooth muscle.

α2-adrenoceptors located on the sympathetic nerve terminals that inhibit the release of norepinephrine and therefore act as a feedback mechanism for modulating the release of norepinephrine.

42
Q

what is the MOA of a2 agonist as an antihypertensive?

A

α2-adrenoceptors located on the sympathetic nerve terminals that inhibit the release of norepinephrine and therefore act as a feedback mechanism for modulating the release of norepinephrine.

a2 agonists decrease release of EP/ND

43
Q

what is the MOA of a1 agonist as a decongestant?

A

a1 agonist = vasoconstriction
sympathoMIMETIC

topical application avoids systemic s/e

44
Q

what is the MOA of a2 agonist as an antihypertensive?

A

α2-adrenoceptors located on the sympathetic nerve terminals that inhibit the release of norepinephrine and therefore act as a feedback mechanism for modulating the release of norepinephrine.

a2 agonists decrease release of EP/ND

sympathoLYTIC

45
Q

what is the MOA of a1 antagonist as an antihypertensive or as tx for BPH?

A

sympathoLYTIC

  • vasodilator
  • relax smooth mm & sphincters (prostate & bladder)
46
Q 
which class of adrenergic drugs end in "-zosin"?
which ends in "-zoline"?
A

zosin: alpha blockers
zoline: alpha agonist

47
Q

describe beta blockers in general

A

Beta-blockers are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors. Therefore, beta-blockers are sympatholytic drugs. Some beta-blockers, when they bind to the beta-adrenoceptor, partially activate the receptor while preventing norepinephrine from binding to the receptor. These partial agonists therefore provide some “background” of sympathetic activity while preventing normal and enhanced sympathetic activity.

48
Q

describe beta blockers in general

A

Beta-blockers are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors. Therefore, beta-blockers are sympatholytic drugs. Some beta-blockers, when they bind to the beta-adrenoceptor, partially activate the receptor while preventing norepinephrine from binding to the receptor. These partial agonists therefore provide some “background” of sympathetic activity while preventing normal and enhanced sympathetic activity.

Beta-blockers prevent the normal ligand (norepinephrine or epinephrine) from binding to the beta-adrenoceptor by competing for the binding site.

49
Q

blood vessels have b1 or b2 receptors?

A

b2

50
Q

heart has predominantly which beta receptor type? b1 or b2?

A

b1

51
Q

heart has predominantly which beta receptor type? b1 or b2?

A

b1

Compared to their effects in the heart, beta-blockers have relatively little vascular effect because β2-adrenoceptors have only a small modulatory role on basal vascular tone. Nevertheless, blockade of β2-adrenoceptors is associated with a small degree of vasoconstriction in many vascular beds. This occurs because beta-blockers remove a small β2-adrenoceptor vasodilator influence that is normally opposing the more dominant alpha-adrenoceptor mediated vasoconstrictor influence.

52
Q

b1 blockers MOA in cardiac arrhythmias, angina pectoris, HTN, glaucoma (topical)

A
  • b1 receptor antagonist
  • selectively block EP/NE from binding to b-receptors
  • physiological effects: decrease CO, decrease HR, decrease BP (unclear)
53
Q

what effect do b1 blockers have on sleep?

A

insomnia - decreases nocturnal melatonin levels

54
Q

b2 agonists are indicated for tx in which 2 conditions?

A

asthma

pulmonary conditions

55
Q

b2 adrenergic receptors react with with hormone/NT?

A

adrenaline (epinephrine)

56
Q

what is the action of b2 receptors?

A
  • smooth mm relaxation (uterus, GI tract [decreases motility], seminal tract, bronchi)
  • dilation of blood vessels
  • increase mass & contraction speed of striated muscle [fight/flight]
  • glycogenolysis (produce fuel)
57
Q

side effects of b2 agonists?

A 
(less common w/inhalers)
insomnia
anxiety
tremors
CV symptoms
58
Q

name 6 effects that stimulation of the parasympathetic NS has?

A

pupil constriction (myosis)
bronchoconstriction
decrease HR & force
increase gastric peristalsis & digestion
increase secretions (tears, sweat, saliva, bile)
allows for urination

59
Q

Ach binds to which 2 receptors?

A

nicotinic

muscarinic

60
Q

where are muscarinic receptors located in the body?

A
  • target organs of PNS (heart, lungs, glands, organs)

- CNS (involved in reward & neuroplasticity)

61
Q

where are nicotinic receptors located in the body?

A
  • autonomic ganglions (sympathetic & PNS)

- neuromuscular junction: somatic NS

Pharmacology (5 decks)

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