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Cardiovascular Unit > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

Where (generally) is autonomic outflow to the CV system regulated?

A

medulla

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2
Q

Where is afferent baroreceptor information received?

A

nucleus tract solitarii (NTS)

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3
Q

Where is parasympathetic outflow regulated?

A

dorsal motor nucleus of the vagus

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4
Q

Where is sympathetic outflow regulated?

A

rostral ventrolateral medulla (RVLM)

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5
Q

Which neurotransmitter is used in inhibitory neurons in the ventrolateral medulla?

A

GABA

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6
Q

How does efferent parasympathetic outflow reach the CV system?

A

vagus nerve

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7
Q

Where does sympathetic outflow from the RVLM to the CV system travel?

A

IML of the spinal cord

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8
Q

What is the major neurotransmitter of both sympathetic and parasympathetic preganlionic neurons?

A

ACh

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9
Q

What is the major NT of postganglionic sympathetic fibers?

A

NE

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10
Q

What is the major exception to postganglionic sympathetic fiber regulation?

A

Sweat glands (ACh)

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11
Q

What NT mediates parasympathetic postganglionic fibers?

A

ACh

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12
Q

Where is epi found?

A

adrenal medulla, CNS, para-aortic bodies

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13
Q

How is ACh synthesized?

A

acetyl CoA + choline, catlayzed by choline acetyltranferase

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14
Q

What is usually the rate-limiting step in ACh synthesis?

A

transport of choline into the cell

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15
Q

What agent blocks the neuronal release of ACh?

A

botulinum toxin

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16
Q

Which enzyme catalyzes the rapid hydrolysis of ACh in the synaptic cleft?

A

acetylcholinesterase, ACh->choline + acetic acid

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17
Q

What is pseudocholinesterase?

A

non-specific cholinesterase found in plasma but not in RBCs or cholinergic neurons

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18
Q

How are catecholamines (NE, Epi, Dopamine) synthesized?

A
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19
Q

How do people with dopamine ß-hydroxylase deficiency present?

A

lifelong orthostatic hypotension, ptosis, exercise intolerance

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20
Q

How do local synaptic concentrations of catecholamines modulate their own release?

A

Interact with presynpatic α2-receptors to reduce release of NE

Interact with presynaptic β2-receptors to increase release of NE

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21
Q

What happens to released catecholamines (termination of action)?

A
  1. retaken up into the neuron via NE transporter
  2. taken up by extraneuronal tissue
  3. washed into the extracellular fluid and into the circulation
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22
Q

How are catecholamines broken down?

A

MAO converts them into their corresponding aldehydes

COMT converts epi and NE into metanephrine and normetanephrine

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23
Q

Describe the action of carbidopa

A

inhibits peripheral dopa decarboxylase to prevent formation of peripheral dopamine when treating Parkinson’s

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24
Q

What intracellular mechanisms result from β-adrenoreceptor stimulation?

A

Gs activates adenylyl cyclase to synthesize cAMP

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25
Q

What intracellular mechanisms result from alpha 2 adrenoreceptor or muscarinic M2 stimulation?

A

Gi binds to GTP, inhibiting adenylyl cyclase

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26
Q

What intracellular mechanisms result from alpha1 adrenoreceptor stimulation?

A

activation of membrane-bound phospholipase C

PLC hydrolyzes PIP2, resulting in the formation of DAG and IP3

IP3 causes release of Ca2+ from intracellular stores

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27
Q

α1 adrenoreceptor effects of NE

A

mydriasis

arteriolar constriction (vasoconstriction)

viscous salivary secretion

pilomotor erection

bladder sphincter contraction

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28
Q

α2 adrenoreceptor effects of NE

A

reduced sympathetic outflow (medulla oblongata)

vasoconstriction

viscous salivary secretion

platelet aggregation

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29
Q

β1 adrenoreceptor effects

A

increase HR

increase contractility

increase renin release

30
Q

β2 adrenoreceptor effects

A

arteriolar dilation

bronchial relaxation

uterine relaxation

31
Q

What are the major α1 agonists?

A

phenylephrine

NE

(epinephrine, dopamine)

32
Q

What are the indications for phenylephrine use?

A

hypotension

nasal congestion

33
Q

What are the α1 antagonists?

A

phentolamine

phenoxybenzamine

prazosin

34
Q

What are the characteristics of phentolamine?

A

competitive, short-acting α-antagonist

35
Q

What are the indications for phentolamine?

A

to determine whether a given level of HTN is catecholamine-mediated

help diagnose pheochromocytoma

36
Q

Major side effects of phentolamine

A

arrythmias

angina pectoris

hypotension

abdominal cramping

37
Q

What are the characteristics of phenoxybenzamine?

A

noncompetitive, long-acting α-antagonist

38
Q

Indication for phenoxybenzamine

A

medical management of pheochromocytoma

39
Q

Major side effect of phenoxybenzamine

A

hypotension

40
Q

What class of drugs is prazosin?

A

α1-selective antagonist

41
Q

Prazosin indications

A

hypertension

CHF

42
Q

Which adrenoreceptor mediates feedback-inhibition of NE release?

A

presynaptic α2 receptors

43
Q

α2 agonists

A

clonidine

methyldopa (α-methylnorepinephrine)

44
Q

Vascular effects of high and low doses of α2 agonists

A

Low: Redcuce sympathetic outflow to the CV system

High: May stimulate peripheral postsynaptic vascular α2-receptors, vasoconstriction

45
Q

α2 antagonist

A

yohimbine

46
Q

yohimbine effects

A

block α2-receptors in the medulla: increase sympathetic outflow

block α2-receptors in the periphery: enhance NE release

47
Q

Isoproterenol drug class

A

non-selective β agonist

48
Q

Isoproterenol effects

A

increased contractility

increased HR

dilate arterioles

increased likelihood of premature beats/arrythmias

49
Q

Dobutamine drug class

A

relatively β1-selective agonist

50
Q

Dobutamine indications

A

pulmonary edema

coronary bypass post-op

51
Q

What is ephedrine used for?

A

weight loss, therapy of asthma, nasal decongestant, adjunct therapy for myasthenia gravis

52
Q

Where are muscarinic receptors located?

A
  • tissues innervated by postganglionic parasympathetic neurons
  • presynaptic noradrenergic and cholinergic nerve terminals
  • vascular endothelium
  • CNS
53
Q

Where are nicotinic receptors located?

A
  • sympathetic and parasympathetic ganglia
  • adrenal medila
  • neuromuscular junction of skeletal muscle
  • CNS
54
Q

Important selectivity of muscarinic receptor subtypes

A

M2: heart

M3: bladder, GI tract

55
Q

What are the subtypes of nicotinic receptors?

A

NM mediates skeletal muscle stimulation

NN mediates stimulation of the ganglia of the ANS

56
Q

muscarinic agonists

A

ACh, bethanechol, methacholine, pilocarpine

57
Q

Muscarinic effects of ACh

A

contraction of iris sphincter (miosis) and ciliary muscle (accomodation)

bradycardia (SA node)

reduced conduction velocity (AV node)

bronchial muscle contraction

increased GI motility and secretion

bladder contraction

58
Q

What are the clinical uses of muscarinic agonists?

A

open-angle glaucoma (pilocarpine)

urinary retention

gastroparesis

Sjögren’s syndrome

diagnosstic testing of pulmonary function (methacholine)

59
Q

What is the classical muscarinic antagonist?

A

atropine

60
Q

What is atropine derived from?

A

Deadly nightshade, Jimson weed

61
Q

What are the clinical uses of muscarinic agonists?

A

bradycardia
excessive secretion
pupillary dilatation
preanesthetic medication (intubation)

neurocardiogenic syncope

62
Q

Side effects of muscarinic agonists

A

constipation, xerostomia, hyphidrosis, mydirasis, glaucoma, tachycardia, etc.

63
Q

Effects of nicotine

A

stimulates ganglionic nicotinic receptors, enchancing both sympathetic and parasympathetic neurotransmission (low doses)

64
Q

What effect does nicotine have at high doses?

A

some antagonism at nicotinic receptors

65
Q

NM blockers

A

tubocararine (nondepolarizing)

succinylcholine (depolarizing)

66
Q

reversible cholinesterase inhibitors

A

physostigmine (enters CNS)

neostigmine (does not enter CNS)

parathion

malathion

67
Q

physostigmine muscarinic side effects

A

nausea, pallor, sweating, bradycardia

(add anticholinergic drugs which do not cross BBB)

68
Q

uses of cholinesterase inhibitors

A

myasthenia gravis
• open-angle glaucoma
• overdose reversal
• Insecticide
• Poor GI motility
• parasympathetic failure • chemical warfare

69
Q

What is pralidoxime used for?

A

counteracts cholinesterase inhibtor intoxication by reactivating the cholinesterase enzyme

70
Q

irreversible cholinesterase inhibitors

A

insecticides (organophosphates), sarin (war gas)

71
Q

Clinical manifestations of cholinesterase inhibitor intoxication

A

SLUDGE

Cardiovascular Unit (4 decks)

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