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Cardiovascular Unit > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

(71 cards)

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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
What intracellular mechanisms result from alpha 2 adrenoreceptor or muscarinic M2 stimulation?
Gi binds to GTP, inhibiting adenylyl cyclase
26
What intracellular mechanisms result from alpha1 adrenoreceptor stimulation?
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
27
α1 adrenoreceptor effects of NE
**mydriasis** **arteriolar constriction (vasoconstriction)** viscous salivary secretion pilomotor erection **bladder sphincter contraction**
28
α2 adrenoreceptor effects of NE
reduced sympathetic outflow (medulla oblongata) **vasoconstriction** viscous salivary secretion platelet aggregation
29
β1 adrenoreceptor effects
increase HR increase contractility increase renin release
30
β2 adrenoreceptor effects
arteriolar dilation bronchial relaxation uterine relaxation
31
What are the major α1 agonists?
phenylephrine NE (epinephrine, dopamine)
32
What are the indications for phenylephrine use?
hypotension nasal congestion
33
What are the α1 antagonists?
phentolamine phenoxybenzamine prazosin
34
What are the characteristics of phentolamine?
competitive, short-acting α-antagonist
35
What are the indications for phentolamine?
to determine whether a given level of HTN is catecholamine-mediated help diagnose pheochromocytoma
36
Major side effects of phentolamine
arrythmias angina pectoris hypotension abdominal cramping
37
What are the characteristics of phenoxybenzamine?
noncompetitive, long-acting α-antagonist
38
Indication for phenoxybenzamine
medical management of pheochromocytoma
39
Major side effect of phenoxybenzamine
hypotension
40
What class of drugs is prazosin?
α1-selective antagonist
41
Prazosin indications
hypertension CHF
42
Which adrenoreceptor mediates feedback-inhibition of NE release?
presynaptic α2 receptors
43
α2 agonists
clonidine methyldopa (α-methylnorepinephrine)
44
Vascular effects of high and low doses of α2 agonists
Low: Redcuce sympathetic outflow to the CV system High: May stimulate peripheral postsynaptic vascular α2-receptors, vasoconstriction
45
α2 antagonist
yohimbine
46
yohimbine effects
block α2-receptors in the medulla: increase sympathetic outflow block α2-receptors in the periphery: enhance NE release
47
Isoproterenol drug class
non-selective β agonist
48
Isoproterenol effects
increased contractility increased HR dilate arterioles increased likelihood of premature beats/arrythmias
49
Dobutamine drug class
relatively β1-selective agonist
50
Dobutamine indications
pulmonary edema coronary bypass post-op
51
What is ephedrine used for?
weight loss, therapy of asthma, nasal decongestant, adjunct therapy for myasthenia gravis
52
Where are muscarinic receptors located?
* tissues innervated by postganglionic parasympathetic neurons * presynaptic noradrenergic and cholinergic nerve terminals * vascular endothelium * CNS
53
Where are nicotinic receptors located?
* sympathetic and parasympathetic ganglia * adrenal medila * neuromuscular junction of skeletal muscle * CNS
54
Important selectivity of muscarinic receptor subtypes
M2: heart M3: bladder, GI tract
55
What are the subtypes of nicotinic receptors?
NM mediates skeletal **_m_**uscle stimulation NN mediates stimulation of the ganglia of the A**_N_**S
56
muscarinic agonists
ACh, bethanechol, methacholine, pilocarpine
57
Muscarinic effects of ACh
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
What are the clinical uses of muscarinic agonists?
open-angle glaucoma (pilocarpine) urinary retention gastroparesis Sjögren’s syndrome diagnosstic testing of pulmonary function (methacholine)
59
What is the classical muscarinic antagonist?
atropine
60
What is atropine derived from?
Deadly nightshade, Jimson weed
61
What are the clinical uses of muscarinic agonists?
bradycardia excessive secretion pupillary dilatation preanesthetic medication (intubation) neurocardiogenic syncope
62
Side effects of muscarinic agonists
constipation, xerostomia, hyphidrosis, mydirasis, glaucoma, tachycardia, etc.
63
Effects of nicotine
stimulates ganglionic nicotinic receptors, enchancing both sympathetic and parasympathetic neurotransmission (low doses)
64
What effect does nicotine have at high doses?
some antagonism at nicotinic receptors
65
NM blockers
tubocararine (nondepolarizing) succinylcholine (depolarizing)
66
reversible cholinesterase inhibitors
physostigmine (enters CNS) neostigmine (does not enter CNS) parathion malathion
67
physostigmine muscarinic side effects
nausea, pallor, sweating, bradycardia (add anticholinergic drugs which do not cross BBB)
68
uses of cholinesterase inhibitors
myasthenia gravis • open-angle glaucoma • overdose reversal • Insecticide • Poor GI motility • parasympathetic failure • chemical warfare
69
What is pralidoxime used for?
counteracts cholinesterase inhibtor intoxication by reactivating the cholinesterase enzyme
70
irreversible cholinesterase inhibitors
insecticides (organophosphates), sarin (war gas)
71
Clinical manifestations of cholinesterase inhibitor intoxication
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Cardiovascular Unit (4 decks)

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