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N929 Pharmacology II > Autonomic Drugs Lecture 2 > Flashcards

Autonomic Drugs Lecture 2 Flashcards

1
Q

Cholinergic drugs can be either

A

direct-acting (receptor agonists) or indirect acting (ACHe-inhibitors)

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2
Q

Direct-acting receptor agonists include

A

muscarinic agonist such as acetylcholine, pilocarpine or nicotinic agonist such as succinylcholine or varenicline

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3
Q

Indirect-acting receptor agonists include

A

reversible acetylcholinesterase inhibitors (Edrophonium, neostigmine) and irreversible acetylcholinesterase inhibitors (nerve gases)

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4
Q

Acetylcholinesterase inhibitor drugs mechanism of action

A

binding to active site and inhibiting acetylcholinesterase
undergoes hydrolysis; acidic portion slowly released, prevents acetylcholine from binding which increases the ACh concentration

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5
Q

Irreversible vs. reversible AChE inhibitors

A

Irreversible means requires synthesis of new AChE to overcome
Reversible includes short & medium duration and it latches on, slowly hydrolyzes and moves acetylcholinesterase

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6
Q

Clinical uses of acetylcholinesterase inhibitors include

A 
reversal of NM blockade by non-depolarizing drug
myasthenia gravis tx & diagnosis
glaucoma
GI-ileus
postop urinary retention
Alzheimer's disease
non-therapeutic-insecticide
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7
Q

Effect of acetylcholinesterase inhibitor

A

increases acetylcholine
amplifies effects @ cholinergic synapses; indirect stimulant of nicotinic and muscarinic receptors by increased acetylcholine

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8
Q

Cholinergic crisis

A

DUMBELSS: Diarrhea, diaphoresis, urination, miosis, bradycardia, excitation (CNS; skel musc) ((paralysis follows initial excitation)), Lacrimation, Salivation, Sweating

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9
Q

Edrophonium is considered to be a

A

acetylcholinesterase inhibitor, alcohol, quaternary amine

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10
Q

Edrophonium works by

A

causing a reversible blockade of acetylcholinesterase

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11
Q

Edrophonium onset & duration

A

onset: 30-60 seconds
duration: 10 minutes

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12
Q

Edrophonium is used to

A

reverse nondepolarizing NM block

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13
Q

Neostigmine is considered to be a

A

acetylcholinesterase inhibitor, carbamate, quaternary amine

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14
Q

Neostigmine works by

A

hydrolyzed by acetylcholinesterase

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15
Q

Neostigmine is used for

A

reversal of NDMB

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16
Q

Neostigmine onset & duration

A

Onset: 10-30 minutes
Duration: 2-4 hours

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17
Q

Physostigmine is considered to be

A

a acetylcholinesterase inhibitor, carbamate, tertiary amine (crosses BBB)

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18
Q

Physostigmine works by

A

hydrolyzing acetylcholinesterase

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19
Q

Physostigmine is used for

A

treatment of anticholinergic toxicity

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20
Q

Physostigmine onset & duration

A

onset: 3-8 min.
duration: 1 hr.

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21
Q

AChE inhibitor drug effects autonomic

A

increased secretions (salivary, lacrimal, bronchial, GI), increased GI motility, bronchoconstriction, bradycardia, hypotension, miosis

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22
Q

AChE inhibitor drug affects NMJ

A

reverses NM block by non-depolarizing blocker, improves transmission-myasthenia gravis, large doses-depolarizing block

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23
Q

AChE inhibitor drug affects CNS

A

therapeutic- dementia Tx

toxicity- excitation (possibly convulsions) and then depression (unconscious)

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24
Q

The antidote for cholinergic toxicity includes

A

atropine

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25
Q

Pralidoxime can be given to

A

regenerate active AChE enzyme (helpful in cholinergic toxicity)

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26
Q

Muscarinic agonist drug effects are known as

A

“parasympathomimetic”

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27
Q

Muscarinic agonist drug effects include

A

CV: decreased HR, decreased CO & arterial pressure, vasodilation
GI: increased motility
Bladder: contracts
Lungs: bronchoconstriction
Secretions: increased sweat, lacrimation, salivation, bronchial
Eyes: miosis, accommodation for near vision, decreased intraocular pressure

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28
Q

Muscarinic agonist clinical uses include

A

Glaucoma, contract ciliary body & increase outflow of aqeous humor
GU/GI: postop ileus, postop urinary retention, xerostomia

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29
Q

What is the effect of muscarinic agonists on vascular smooth muscle

A

vasodilation via nitrous oxide

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30
Q

Muscarinic agonists include

A

acetylcholine, muscarine, pilocarpine, bethanechol

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31
Q

The “SLUDGE” mnemonic applies to

A

muscarinic agonists and includes salivation, lacrimation, urination, diarrhea, GI upset, and emesis

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32
Q

What drug is a nicotinic agonists?

A

succinylcholine

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33
Q

What drugs are nicotinic antagonists?

A

pancuronium, vecuronium, atracurium, cisatricurium, rocuronium

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34
Q

Nicotinic N receptor agonists uses include

A

smoking cessation

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35
Q

Nicotinic N agonists effects include

A

stimulation of post-ganglionic neuronal activity (autonomic NS) and CNS stimulation

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36
Q

Nicotinic N agonists adverse effects include

A

CNS stimulation (excitatory), Skeletal muscle depolarizing/blockade, HTN, increased HR, N/V, diarrhea

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37
Q

Nicotinic M agonists effects include

A

Activation of NM endplates

contraction

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38
Q

Nicotinic M agonists clinical uses include

A

depolarizing skeletal muscle paralysis

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39
Q

Nicotinic M agonists adverse include

A

paralysis

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40
Q

Cholinergic drugs should not be given in patients with

A

GI/GU obstruction, CV disease, Respiratory disorder (COPD, asthma)

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41
Q

Nonselective muscarinic antagonists include

A

atropine, glycopyrrolate, scopolamine

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42
Q

Clinical uses of muscarinic receptor antagonists include

A

motion sickness (scopolamine), Parkinson’s, exam requiring eyes, decreases secretions, COPD, asthma, GI hypermotility, urinary urgency, anesthetic premed to decrease secretions and for sedation, cholinergic poisoning, AChE inhibitor toxicity

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43
Q

The effects of muscarinic receptor antagonists include

A

increased heart rate, bronchodilation, decreased GI, GU & Glands; decreased sweat glands, mydriasis, sedation

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44
Q

Would you expect to see effects of muscarinic receptor antagonists at blood vessels & skeletal muscle?

A

No b/c there is only nicotinic receptors present in these areas

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45
Q

Medication classes with anticholinergic activity include

A

antihistamines, antispasmodics, antiparkinson drugs, skeletal muscle relaxants, antipsychotics, antidepressants, antimuscarinics for urinary incontinence

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46
Q

Who is most susceptible to anticholinergic toxicity?

A

elderly

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47
Q

Potential concerns with anti-muscarinic drugs include

A

hyperthermia risk d/t decreased sweating, glaucoma, GU obstruction, prostatic hypertrophy, GI-ileus, ulcerative colitis, etc., CV especially MI, HF, arrhythmias, HTN

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48
Q

Memory aid for anticholinergic effects is:

A

dry as a bone, hot as a pistol, red as a beet, blind as a bat, mad as a hatter

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49
Q

The drug class of atropine is

A

muscarinic antagonists & it crosses BBB

50
Q

The drug class of scopolamine is

A

muscarinic antagonists and it crosses BBB causing CNS effects of amnesia & sedation

51
Q

The drug class of glycopyrrolate is

A

muscarinic antagonists and it has decreased CNS effects

52
Q

The half-life of atropine is

A

4 hours (elderly ~10 hours)

53
Q

Atropine can be administered

A

IV, IM, Ophthalmic

54
Q

Atropine is used for

A

ophthalmic, bradycardias, preop, inhibit secretions, adjunct to NM block reversal

55
Q

Scopolamine half life, onset & duration is

A

half-life: 1-4 hours

onset: 10 min.
duration: 2 hours

56
Q

Scopolamine can be administered

A

transdermal patch, IV, or IM

57
Q

Scopolamine uses include

A

motion sickness, postop N/V, preop for amnesia, sedation, anti-emetic, decreasing secretions

58
Q

Glycopyrrolate half-life, onset, and duration includ

A

half-life: 1 hour
Onset: 1 min
Duration: 7 hour

59
Q

Glycopyrrolate is used for

A

pre-op; cardiac dysrhythmia (vagal reflex association), adjunct- reversal NM blockade

60
Q

The mechanism of action for NM blocker competitive agonists is

A

binding to nicotinic receptor at NMJ and preventing acetylcholine from thus binding

61
Q

What are the effects of nicotinic M receptor antagonists?

A

competitive antagonism at skeletal muscle

non-depolarizing

62
Q

The clinical uses of nicotinic M receptor antagonists include:

A

skeletal muscle relaxation for surgical intubation, ventilation control

63
Q

What drugs are able to counteract a nicotinic M receptor antagonist neuromuscular blockade?

A

acetylcholinesterase inhibitors

64
Q

What are the effects of nicotinic N receptor antagonists?

A

it blocks ganglionic output

65
Q

What are the clinical uses of nicotinic N receptor antagonists?

A

Historically used for hypertensive emergency

66
Q

Adrenergic agonists may also be called

A

sympathomimetics

67
Q

Direct acting adrenergic agonists can act on

A

alpha, beta or mixed alpha/beta

68
Q

Indirect acting adrenergic agonists work by

A

increasing NT release, inhibiting NE reuptake, or decreasing metabolism of NT (MAO inhibitor)

69
Q

Adrenergic drug types can include

A

indirect, direct receptor agonist and mixed-multiple sites of action
mixed work by release NE from nerve terminal and activate adrenergic receptors

70
Q

Tyramine works by

A

displacing/releasing stored catecholamines

not a drug, in fermented foods; role in drug-food interactions of MAO inhibitors

71
Q

Cocaine works by

A

blocks NE reuptake; blocks sodium channels so has local anesthetic actions

72
Q

Amphetamine works by

A

displaces/releases stored catecholamines NT

secondary inhibits catecholamine reuptake

73
Q

Amphetamine is used in

A

ADHD, narcolepsy, & appetite suppression

74
Q

Indirect acting adrenergic agonists include

A

amphetamine, cocaine, SNRI, tranylcypromine

ephedrine is mixed

75
Q

Ephedrine & pseudoephedrine are (class & MOA)

A

indirect acting mixed adrenergic agonists and work by displacing/releasing stored catecholamine NT, have some agonists activity on alpha and beta adrenergic receptors

76
Q

What herbal source contains ephedrine?

A

ma huang

77
Q

When catecholamines are administered as drugs:

A

rapid onset, brief duration, don’t give PO (b/c won’t cross) and have poor CNS penetration for the same reason

78
Q

Most adrenergic drugs are

A

non-catecholamines, longer acting, and have PO administration

79
Q

Receptor affinity of Epi. vs. Norepi. vs. Isoproterenol for alpha adrenoreceptors:

A

High to low: epi, norepi, isoproterenol

80
Q

Receptor affinity of Epi. vs. norepi vs. isoproterenol for beta adrenoreceptors:

A

High to low: isoproterenol, epi, norepi

81
Q

Epinephrine has an affinity for

A

alpha 1, alpha 2, beta 1, beta 2, and beta 3 receptors
low dose: beta effects
high doses: alpha effects

82
Q

Epinephrine is used for

A

anaphylaxis, local anesthetics, and cardiac arrest

83
Q

Norepinephrine has an affinity for

A

alpha 1 and beta 1 (little effect on beta 2)

84
Q

Norepinephrine is used to treat

A

shock (extravasation can result d/t vasoconstriction) q

85
Q

Isoproterenol has affinity for

A

beta 1 and beta 2

86
Q

Isoproterenol is used to treat

A

acute asthma (now obsolete) and cardiac stimulant

87
Q

Dopamine has an affinity for

A

low dose: D1 in renal, mesenteric, coronary vascular beds
medium doses: beta 1
higher doses: alpha 1

88
Q

Dopamine is used to treat

A

shock, HF, increase blood flow to kidneys

89
Q

Dobutamine has an affinity for

A

beta 1 primarily

90
Q

Dopamine is used to treat

A

acute HF

91
Q

The predominant effects of adrenergic receptor agonists on alpha 1

A

vasoconstriction (skin/splanchnic beds)
Smooth muscle- contracts (except GI) & trophic effect (BPH)
GI/GU sphincters- contract
Eye-mydriasis

92
Q

The predominant effects of adrenergic receptor agonists on alpha 2

A

decrease NE release (presynaptic)
CNS-inhibit sympathetic outflow
Platelet aggregation
Pancreas: decrease insulin

93
Q

The predominant effects of adrenergic receptor agonists on beta 1

A

increased HR, contractility
effects on rhythm
kidney- renin release
Trophic effect- hypertrophy

94
Q

The predominant effects of adrenergic receptor agonists on beta 2

A 
Bronchodilation
vasodilation (esp. skel m beds)
most smooth muscle relaxes
skeletal muscle contracts- tremor (hypokalemia/increase K+ uptake)
GI/GU- relax
Uterine smooth muscle relax
Glycogenolysis
95
Q

Indirect acting adrenergic agonists include

A

tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors- block NE reuptake
Monamine oxidase inhibitors (MAOIs)- prevent breakdown of catecholamines in presynaptic terminal–catecholamines accumulates in vesicles

96
Q

The effects on alpha 1 receptor agonists include

A

Increased vascular tone, increased PVR, increased BP and mydriasis

97
Q

The clinical uses of alpha 1 receptor agonists include

A

shock

OTC: as decongestants & ophthalmic hyperemia

98
Q

An example of an alpha 1 receptor agonists includes

A

phenylephrine

99
Q

An adverse effect of alpha 1 receptor agonists is

A

increased BP (seen even w/ nasal spray)

100
Q

The effects on alpha 2 receptors agonists include

A

decreased NE release

101
Q

The clinical uses of alpha 2 receptor agonists include

A

hypertension (central effects)

102
Q

The adverse effects of alpha 2 receptor agonists include

A

sedation because we’re decrease NE which is excitatory in the brain

103
Q

An example of an alpha 2 receptor agonists is

A

clonidine

104
Q

Dexmedetomidine (class & MOA)

A

selective alpha 2 receptor agonist- CNS actions

suppresses sympathetic NS activity

105
Q

The effects of dexmedetomidine include

A

Sedative effects via locus coeruleus and activates endogenous sleep pathways; analgesic effects (spinal cord)

106
Q

Adverse effects of dexmedetomidine include

A

decrease HR, decreased SVR, hypotension, transient HTN w/ bolus, bradycardia & decreases RR w/ some decrease in tidal volume

107
Q

Potential concerns with adrenergic agonists include

A

CV disease, cerebrovascular disease, diabetes (increased blood sugar), IV extravasation risks, thyroid disease

108
Q

Nonselective beta blocker includes

A

propranolol (contraindicated in someone with asthma because it can trigger bronchoconstriction)

109
Q

Selective beta 1 blocker includes

A

metoprolol & esmolol

110
Q

Effects of alpha 1 receptor antagonists include

A

smooth muscle relaxation, decreased PVR, decreased BP

111
Q

Clinical uses of alpha 1 receptor antagonists include

A

hypertension, BPH, pehochromocytoma

112
Q

Adverse effects of alpha 1 receptor antagonists include

A

reflex tachycardia, orthostatic hypotension (severe)

113
Q

An example of an alpha 1 receptor antagonists is

A

prazosin

114
Q

An example of a beta 1 (B2) receptor antagonists

A

propranolol

115
Q

The effects of nonselective beta receptor antagonists include

A

decreased HR, decreased force of contraction, decreased renin, and anti-dysrhythmic effects

116
Q

The clinical uses of beta receptors antagonists include

A

hypertension, angina pectoris, arrhythmia, myocardial infarction, thyrotoxicosis, heart failure- chronic, stable; other- infantile hemangioma, glaucoma, migraine, prophylaxis, anxiety

117
Q

The adverse effects of beta antagonists include

A

bronchoconstriction, creation of arrhythmias, bradycardia, sedation, decreased sexual function, blocking ability to raise sugar w/ typical symptoms of hypoglycemia obscured

118
Q

Potential concerns with adrenergic antagonists include

A

respiratory disease, cardiovascular, diabetes (beta blockers may potentiate hypoglycemia & mask signs/symptoms), thyroid disease

119
Q 
A beta 2 receptor agonist would not:
A. increase glycogenolysis
B. relax uterine smooth muscle
C. Relax bronchiolar smooth muscle
D. Stimulate renin release
A

D.

120
Q

The effects of isoproterenol could be blocked by a/an:
A. alpha 1 adrenergic receptor antagonist
B. muscarinic receptor antagonist
C. Nonselective beta adrenergic receptor antagonist
D. Nicotinic N receptor antagonist
E. alpha 2 adrenergic receptor antagonist

A

C.

121
Q

Which would be expected upon administration of a muscarinic agonist drug, but NOT with parasympathetic nerve stimulation?
A. increased bronchial secretion
B. vasodilation
C. contraction of smooth muscle in urinary bladder wall
D. Increased GI Motility

A

B.

122
Q 
Cholinergic receptors would be found at all of the following sites, EXCEPT:
A. adrenal medullary cells
B. Juxtaglomerular cells
C. Neuromuscular junction
D. Sympathetic ganglia
E. Sweat glands
A

B.

N929 Pharmacology II (16 decks)

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