Autonomics Flashcards

1
Q

what neurotransmitters are released at presynaptic and postsynaptic sites in the ANS?

A

presynaptic autonomic motor: acetylcholine

postsynaptic parasympathetic: acetylcholine

postsynaptic sympathetic: acetylcholine

sympathetic ganglionic neurons: norepinephrine

adrenal medulla: epi/NE

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2
Q

what types of cholinergic receptors are found in ANS ganglia?

A

muscarinic (M1, M2, M3, M4, M5)- postsynaptic parasympathetics, sympathetics to sweat glands

nicotinic (Nn, Nm)- presynaptic parasympathetics

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3
Q

for the sympathetic NS, what types of cholinergic and adrenergic receptors respond to the release of neurotransmitter in the target tissues?

A

adrenergic receptors: a1- smooth muscle, glands

a2- nerve endings, some smooth muscle

B1- cardiac muscle

B2- smooth muscle, liver, heart

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4
Q

for the parasympathetic NS, what types of cholinergic and adrenergic receptors respond to the release of NTs in the target tissues?

A

cholinergic: muscarinic, nicotinic

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5
Q

how does sympathetic innervation of eccrine (thermoregulatory) sweat glands differ from the sympathetic innervation of other tissue targets?

A

acetylcholine is released by sympathetic neurons innervating sweat glands- the receptor is muscarinic. in other sympathetic innervations, primarily norepinephrine is released to adrenergic receptors.

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6
Q

what do specific enzymes in catecholamine synthesis have to do with instances when postsynaptic sympathetics release DA and Epi rather than NE?

A

absence of dopamine beta hydroxylase determines if dopamine is released

presence of phenethanolamine-N methyltransferase determines if adrenal Epi is released

if DBH is present, NE is released; if PNMT is present, NE is NOT released

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7
Q
definitions/differences between:
adrenergic
cholinergic
cholinoceptor
adrenoceptor
cholinomimetic
sympathomimetic
parasympatholytic
sympatholytic
sympathoplegic
A

cholinomimetic- mimics action of endogenous NT

sympathomimetic- mimicking adrenaline, etc.

parasympatholytic- blocks action of endogenous NT

sympatholytic/sympathoplegic- blocks action of endogenous NT

the cholinergic, adrenergic are terms to describe the neruons/terminals

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8
Q

list the types of receptors located within each of the target end organs: sweat glands, suprarenal glands, everything involving parasympathetics, everything else in sympathetics

A

sweat glands- preganglionic sympathetic cholinergic; post ganglionic sympathetic cholinergic

suprarenal glands: preganglionic cholinergic (direct innervation)

parasympathetics: preganglionic cholinergic; post ganglionic cholinergic
sympathetics: preganglionic cholinergic; postganglionic adrenergic

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9
Q

what special role is played by a2 adrenergic receptors in the CNS and PNS?

A

the 2nd messenger effect is to LOWER the cAMP levels; located in nerve endings

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10
Q

explain how baroreceptor reflex functions as a compensatory mechanism

A

changes in peripheral resistance changes BP which activates baroreceptors, which through CNS centers regulate both sympathetic and parasympathetic outflow; provides QUICK, HOMEOSTATIC RESPONSES so BP doesn’t shift normally

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11
Q

why might a drug that contracts peripheral vessels result in bradycardia?

A

contracted peripheral vessels will cause BP to rise, resulting in bradycardia due to the baroreceptor reflex

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12
Q

why might a drug that relaxes peripheral vessels cause tachycardia?

A

relaxed peripheral vessels will lower BP, causing tachycardia due to the baroreceptor reflex

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13
Q

what are the smooth muscle and epithelial targets for ANS drugs in the eye? what are the autonomic receptors involved?

A

dilator pupillary muscle (sympathetic), sphinter pupillary muscle (para), ciliary muscle (para), ciliary epithelium

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14
Q

how is pupil diameter and aqueous humour flow altered by specific autonomic related drugs?

A

pupil diameter: sympathetics contract the dilator pupil muscle (a1 receptor)

aqueous humor: a agonist (phenylephrine) facilitates outflow

b blockers reduce synthesis of aqueous humor

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15
Q

why would a muscarinic agonist be useful in treatment of glaucoma?

A

a muscarinic agonist would help to increase outflow of aqueous humor; relaxes vessels, so reduces intraocular pressure.

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16
Q

what are the symptoms of muscarinic agonist toxicity? what do the symptoms reflect?

A

SLUDGE: salivation, lacrimation, urination, defecation, GI upset, emesis

they reflect the role of muscarinic receptors in various target tissues.

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17
Q

what is the difference in the way that acetylcholine and catecholamines are cleared from the synaptic cleft?

A

acetylcoline is degraded by AChE enzyme; catecholamines are diffused away, reuptake or metabolized

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18
Q

what is the difference between a direct-acting and indirect-acting cholinomimetic? what about sympathomimetics?

A

direct-acting: act like acetylcholine

indirect-acting: cholinesterase inhibitors- compete with ACh for the enzyme

sympathomimetics: direct-acting: a or B agonists

indirect-acting: increase the conc of endogenous catecholamines in the synaptic cleft by increasing release of NT or inhibiting reuptake

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19
Q

list the 5 classes of ANS drugs and specific examples of what drugs fall into each class (blue)

A

direct-acting cholinomimetics- bethanecol

cholinoceptor blockers- atropine, scopolamine (anti-muscarinic)

indirect-acting cholinesterase inhibitors- neostigmine, organophosphates

sympathomimetics (direct/indirect)- direct: epi, NE, phenylephrine, albuterol; indirect: tyramine, amphetamine, cocaine, tricyclic antidepressants

adrenoceptor blockers- prazosin, propanolol

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20
Q

how do cholinergic agonists effect changes in peripheral vascular vessel diameter when these vessels lack direct autonomic fiber inputs?

A

vasodilation from cholinomimetics even when parasympathetic fibers don’t innervate the blood vessels, because muscarinic receptors are located in endothelial cells, receptor activation leads to release of NO, which diffuses to adjacent vascular smooth muscle, relaxes the vessels

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21
Q

what specific types of receptors do ganglionic blockers work on?

A

nicotinic receptors

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22
Q

why were drugs that fall into ganglionic blocker class once used but are now NOT used to treat hypertension?

A

too many side effects: they block sympathetic and parasymp. outflow; not tolerated well.

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23
Q

what type of autonomic drugs would result in bronchodilation versus bronchoconstriction in the lungs?

A

bronchodilation: anti-muscarinic

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24
Q

what type of autonomic drugs would exacerbate or relieve the urinary retention seen in patients with benign prostatic hyperplasia? what receptors are involved?

A

alpha blockers (adrenoceptor blocker)

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25
Q

some drugs like the tricyclic antidepressants have side effects that reflect the action of….

A

anti-muscarinic action

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26
Q

how do indirect-acting cholinomimetics differ from direct acting cholinomimetics?

A

indirect-acting cholinomimetics inhibit the enzymes that breakdown ACh

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27
Q

explain in a general sense how neostigmine works to augment the conc of acetylcholine in the synaptic cleft?

A

neostigmine inhibits AChE activity by binding to it and undergoing hydrolysis (competes with ACh for the active site)

28
Q

how do sympathetic fibers constrict cutaneous blood vessels while dilating skeletal blood vessels?

A

different receptors: cutaneous blood vessels have alpha receptors, skeletal blood vessels have B2 receptors

29
Q

compare and contrast the mechanism underlying the sympathomimetic effects of tyramine, amphetamine, cocaine, and tricyclic antidepressants

A

tyramine and amphetamine: induce release of stored catecholamines from terminal

cocaine- blocks reuptake at the NE or DA transporter

tricyclic antidepressants- blocks reuptake at the NE transporter

30
Q

why are sympathomimetic drugs sometimes added to local anesthetics?

A

they cause local vasoconstriction, which controls spread of anesthesia from the site and causes hemostasis

31
Q

what is the functional difference in the activation of a and B adrenergic receptors with respect to smooth muscle in the walls and sphincters of the GI tract?

A

the B2 receptor relaxes smooth muscle (walls)

the a2 receptor causes contraction (sphincters)

32
Q

what specific drugs have the potential to alter the level of thermoregulatory sweating?

A

anti-muscarinic drugs

33
Q

The ANS is under the control of….

A

supraspinal centers

34
Q

what is the role of the hypothalamus with respect to regulation of the ANS? what part of the hypothalamus is the regulating center for parasympathetics? for sympathetics?

A

principal CNS integration center for ANS; separate parasympathetic and sympathetic regulating areas; except the area for cholinergic sweating is located in anterior hypothalamus with parasympathetics; the rest of sympathetics are located in the posterior hypothalamus

35
Q

what receptors are used by the parasympathetic and sympathetic innervation of the bladder?

A

sympathetics inhibit bladder wall: activate B receptors, decreasing the presynaptic a2 receptors from parasympathetics

sympathetics excite internal urethral sphincter via a1 receptors (constrict)

parasympathetics excite bladder wall through activation of muscarinic receptors

36
Q

what are two ways in which the sympathetic input to the bladder inhibits the tone of the detrussor muscle?

A

relaxes the detrussor muscle via B2 receptors

37
Q

distinguish the type of neurogenic bladder seen after different CNS lesions. what type of lesion would be seen after a bilateral lesion of the sacral spinal cord?

A

LMN type; areflexic, flaccid bladder, incontinence, severe urinary retention could result in renal damage

38
Q

what type of lesion would be seen between the lumbar cord and the pons? above the pons?

A

between lumbar spinal cord and pons: UMN; loss of voluntary control; hyperreflexia; spastic bladder, doesn’t empty fully; incontinence

above the pons: no desire to control micturition or urgency to urinate but can’t delay; uninhibited reflex bladder (infantile)

39
Q

parasympathetics release ___ at the postsyn site

A

acetylcholine

40
Q

presynaptic receptor of parasympathetics is what type of receptor? the post synaptics of parasympathetics?

A

nicotinic

muscarinic

41
Q

sympathetics that go to sweat glands are this type of receptor

A

muscarinic

42
Q

presynaptic adrenergic autoreceptors are what type of receptor?

A

a2 - for negative feedback control of NT release

43
Q

muscarinic receptor blocker (used clinically to block postgang parasympathetics)

A

atropine

44
Q

blocks release of acetylcholine

A

botulinum toxin

45
Q

blocks monoamine reuptake at synapse to prolong action of neurotransmitters

A

cocaine

46
Q

blocks binding of ACh to its nicotinic receptor on skeletal muscle

A

curare

47
Q

inhibits AChE activity, prolonging, ACH activity

A

neostigmine

48
Q

irreversibly inactivates AChE

A

organophosphates

49
Q

blocks monoamine reuptake

A

tricyclic antidepressants

50
Q

varenicline is what type of drug?

A

direct-acting cholinoceptor agonist

51
Q

donepezil, neostigmine, physostigmine, pyridostigmine: what type of drugs?

A

indirect-acting cholinoceptor agonists

52
Q

atropine, scopolamine, solifenacin: what type of drugs?

A

muscarinic cholinoceptor antagonists

53
Q

albuterol, amphetamine, ephedrine, epi, methamphetamine, methylphenidate, norepi, phenylephrine, pseudoephedrine: what class of drugs?

A

sympathomimetic drugs

54
Q

tamsulosin: what class of drugs?

A

adrenergic receptor antagonists

55
Q

direct-acting cholinomimetic

A

bethanecol

56
Q

mushroom poisoning is synonymous with..

A

cholinomimetic toxicity (SLUDGE)

57
Q

how does vasodilation from cholinomimetics occur when parasympathetics do not innervate blood vessels?

A

there are muscarinic receptors on endothelial blood vessel cells; when activated, they release NO, diffuses to adjacent smooth muscle, increases cAMP, relaxation of vessels– causes sweating, tachycardia, vasodilation

58
Q

prototypical cholinesterase inhibitor

A

neostigmine

59
Q

what’s unique about neostigmine?

A

doesn’t work if injected into plasma; more stable, longer half life; doesn’t enter CNS

60
Q

direct acting sympathomimetics (prototype?)

A

epi (prototype), norepi, phenylephrine, albuterol

61
Q

two modes of action of indirect acting sympathomimetics

A
  1. increase release of NT

2. inhibit reuptake, thereby increasing action

62
Q

-zosin indicates

A

a1 blocker

63
Q

prototypical non-selective B blocker

A

propranolol

64
Q

beta blockers: what affect do they have on secretion of aqueous humor?

A

decrease secretion of aqueous humor

65
Q

location of lesion for spastic bladder. for flaccid bladder?

A

spastic bladder-between lumbar spinal cord and pons

flaccid bladder: sacral spinal cord/cauda equina