Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MS 2 - Unit 2 > Pharmacology - Autonomics I > Flashcards

Pharmacology - Autonomics I Flashcards

1
Q

Postganglionic PS fibers release:

A

Aceytlcholine

“cholinergic”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Postganglionic symptathetic fibers generally release:

A

Norepinephrine

“adrenergic”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

T/F: Not all postganglionic sympathetic fibers are adrenergic - other NTs can be used.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

All preganglionic neurons, both sympathetic and parasympathetic, release:

A

ACh and stimulate nicotinic receptors on postganglionic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

All preganglionic neurons, both sympathetic and parasympathetic, release ACh and stimulate ______ receptors on postganglionic neurons.

A

Nicotinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

All postganglionic PS neurons release ACh and stimulate _____ ACh receptors on target tissues.

A

Muscarinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Postganglionic symptathetic fibers to sweat glands release:

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Postganglionic sympathetic fibers to renal vessels release:

A

Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

____ blocks ACh and, when, injected, can locally inhibit muscle contraction.

A

Botulinim Toxin A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Drugs that block NE synthesis, storage or release, for example, guanethidine, are useful in several diseases like hyptertension, because they block _____ function

A

sympathetic, but NOT parasympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the physiologic effect of cocaine?

A

To block NE uptake –> increase adrenergic transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cholinoceptors include:

A

Muscarinic

Nicotinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where are M1 receptors found?

A

Location:
CNS
sympathetic PG neurons

Effects:
formation of IP3 and DAG
increased intracellular Ca
**same as M3 receptors (exocrine glands, CNS, vessels)
**same as M5 receptors (vascular endothelium esp cerebral vessels, CNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where are M2 receptors found?

A

Location:
Myocardium
Smooth muscle
CNS

Effects:
open K channels
inhibit Adenyl cyclase
**same as M4 receptors (CNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Nicotinic receptors, both Nn (N2) and Nm (N1) have what effect?

A

Opening of Na and K channels, depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where are Nm (N1) receptors found?

A

Skeletal muscle neuromuscular end plates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the effect of Alpha 1 adrenergic receptors?

A

Effects:
Formation os IP3 and DAG
increased intracellular Ca

Location:
Postsynaptic effector cells esp smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the effect of Alpha 2 (adrenoreceptors) receptors?

A

Effects:
Inhibition of adenyl cyclase
decreased cAMP

Location:
Presynaptic adrenergic nerve terminals, 
platelets
lipocytes
smooth muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

All beta (adrenoreceptors) receptors have what function?

A

stimulate AC
increase cAMP

all found in heart, beta-1 found most widespread in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

All muscarinic receptors (M1-M5) are

A

GPCRs
M2, M4 –> Gi (decrease cAMP, hyperpolarize) –> inhibition of neurotransmitter release

M1, M3, M5 –> Gq (increase IP3 and DAG)

**enables ACh to have specific effects, depending on the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Class: Bethanechol

A

Direct acting carbamic acid ester

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MOA: Bethanechol

A

Direct-acting muscarinic cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Uses: Bethanechol

A 
Post-operative and neurogenic ileus; 
urinary retention (bowel and bladder smooth muscle ACh-innervated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Side Effects: Bethanechol

A

SLUDGE
Salivation: stimulation of the salivary glands
Lacrimation: stimulation of the lacrimal glands
Urination: relaxation of the internal sphincter muscle of urethra, and contraction of the detrusor muscles
Diaphoresis
Gastrointestinal upset: Smooth muscle tone changes causing gastrointestinal problems, including diarrhea
Emesis: Vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Class: Pilocarpine

A

Direct acting non-ester alkaloid

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MOA: Pilocarpine

A

Direct-acting muscarinic cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Uses: Pilocarpine

A

Glaucoma (ACh activates sphincter and ciliary muscles of eye)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Side Effects: Pilocarpine

A

SLUDGE
Salivation: stimulation of the salivary glands
Lacrimation: stimulation of the lacrimal glands
Urination: relaxation of the internal sphincter muscle of urethra, and contraction of the detrusor muscles
Diaphoresis
Gastrointestinal upset: Smooth muscle tone changes causing gastrointestinal problems, including diarrhea
Emesis: Vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Class: Cevimeline

A

Direct acting non-ester alkaloid

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MOA: Cevimeline

A

Direct-acting muscarinic cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Uses: Cevimeline

A

Dry mouth/xerostomia (in, e.g., Sjogren’s, post-radiation therapy; via increased salivation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Side Effects: Cevimeline

A

SLUDGE
Salivation: stimulation of the salivary glands
Lacrimation: stimulation of the lacrimal glands
Urination: relaxation of the internal sphincter muscle of urethra, and contraction of the detrusor muscles
Diaphoresis
Gastrointestinal upset: Smooth muscle tone changes causing gastrointestinal problems, including diarrhea
Emesis: Vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Class: Nicotine

A

Direct acting non-ester alkaloid

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

MOA: Nicotine

A

Direct-acting muscarinic cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Uses: Nicotine

A

Smoking cessation/reduces craving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Class: Physiostigmine

A

Indirect acting carbamate

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

MOA:
Physostigmine
Echothiophate

A

AChE inhibitor (short acting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Uses:
Physostigmine
Echothiophate

A

Glaucoma (ACh activates papillary sphincter and ciliary muscles of eye)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Side Effects: Physostigmine

A

SLUDGE
general increase in cholinergic neurotransmission;
paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q 
Class:
Muscarine
Pilocarpine
Cevimeline
Nicotine
A

Direct acting non-ester alkaloid

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Uses:
Pilocarpine
Physostigmine
Echothiophate

A

Glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Class: Edrophonium

A

Indirect acting non-ester

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

MOA: Edrophonium

A

AChE inhibitor (v. short acting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Uses:
Edrophonium
Pyridostigmine
Neostigmine

A

Myasthenia Gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Side Effects: Edrophonium

A

SLUDGE
general increase in cholinergic neurotransmission;
paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Class: Neostignmine

A

Indirect acting carbamate

cholinomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Class:
Neostigmine
Physostigmine

A

Indirect acting carbamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MOA: Neostigmine

A

AChE inhibitor (short acting)

49
Q

Uses: Neostigmine

A

Post-operative and neurogenic ileus; urinary retention; myasthenia gravis; reversal of neuromuscular blockade

50
Q

Side Effects: Neostigmine

A

SLUDGE
general increase in cholinergic neurotransmission;
paralysis

51
Q

Class: Muscarine

A

Direct acting non-ester alkaloid

cholinomimetic

52
Q

MOA: Muscarine

A

Direct-acting muscarinic cholinomimetic

53
Q

Side Effects: Muscarine

A

SLUDGE

54
Q

Class: Donepezil

A

Indirect acting non-ester

cholinomimetic

55
Q

MOA: Donepezil

A

AChE inhibitor

56
Q

Uses: Donepezil

A

Alzheimer’s (amplifies endogenous ACh in brain)

57
Q

Side Effects: Donepezil

A

SLUDGE
general increase in cholinergic neurotransmission;
paralysis

58
Q

Class:
Donepezil
Edrophonium

A

Indirect acting non-ester

cholinomimetic

59
Q 
Side Effects:
Neostigmine
Physostigmine
Donepezil
Sarin
Edrophonium
Echothiophate
Pralidoxime
A

SLUDGE
general increase in cholinergic neurotransmission;
paralysis

60
Q 
Side Effects:
Bethanechol
Muscarine
Pilocarpine
Cevimeline
A

SLUDGE

61
Q

Class: Echothiophate

A

Indirect acting organophosphate

cholinomimetic

62
Q

MOA: Echothiophate

A

AChE inhibitor (long acting)

63
Q

Uses: Echothiophate

A

Glaucoma (ACh activates papillary sphincter and ciliary muscles of eye)

64
Q

Side Effects: Echothiophate

A

SLUDGE
general increase in cholinergic neurotransmission;
paralysis

65
Q

Class: Sarin

A

Very potent indirect acting organophosphate

cholinomimetic

66
Q

MOA: Sarin

A

AChE inhibitor

67
Q

Uses: Sarin

A

volatile nerve gas

68
Q

Side Effects: Sarin

A

SLUDGE
general increase in cholinergic neurotransmission;
paralysis
DEATH

69
Q

Class: Pralidoxime

A

Strong nucleophile

cholinomimetic

70
Q

MOA: Pralidoxime

A

AChE inhibitor

71
Q

Uses: Pralidoxime

A

Poisoning by nerve gas, insecticide

72
Q

Class: Atropine

A

Tertiary amine antimuscarinic

cholinergic receptor inhibitor

73
Q 
Class:
Atropine
Scopolamine
Dicyclomine
Tropicamide
Tolterodine
Benztropine
A

Tertiary amine antimuscarinic

cholinergic receptor inhibitor

74
Q

MOA: Atropine

A

Blocks muscarinic receptors

75
Q 
MOA: 
Atropine
Scopolamine
Dicyclomine
Tropicamide
Tolterodine
Benztropine
Ipratroprium
Tiotropium
A

Blocks muscarinic receptors

76
Q 
Side Effects:
Atropine
Scopolamine
Dicyclomine
Tropicamide
Tolterodine
Benztropine
Ipratroprium
Tiotropium
A

General block of muscarinic functions

77
Q

Uses:
Atropine
Tropicamide

A

To cause:
Mydriasis
Cycloplegia is paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation

*Tropicamide has a short half life

78
Q

Uses: Scopolamine

A

Motion sickness

79
Q

Uses: Dicyclomine

A

Reduce transient hypermotility of GI tract

80
Q

Uses: Tolterodine

A

Treat transient cystitis;
postoperative bladder spasms;
incontinence

81
Q

Uses: Benztropine

A

To prevent manifestations of Parkinson’s disease

82
Q

Class:
Ipatroprium
Tiotropium

A

Quarternary amine antimuscarinic

cholinergic receptor inhibitor

83
Q

Uses:
Ipatroprium
Tiotropium

A

Bronchodilation in asthma or COPD

84
Q

Class: Succinylcholine

A

Depolarizing blocker

cholinergic receptor inhibitor

85
Q

MOA: Succinylcholine

A

Overstimulation of nicotinic receptor, leading to desensitization of muscle unit to further ACh stimulation

86
Q

Uses: Succinylcholine

A

Brief procedures (e.g., tracheal intubation, reset dislocated joints)

87
Q

Side Effects:
Succinylcholine
Tubocurarine
Mivacurium

A

Respiratory paralysis;

disturbance of autonomic function

88
Q

MOA:
Tubocurarine
Mivacarium

A

Blocks nicotinic (Nm) receptor

89
Q

Class:
Tubocurarine
Mivacarium

A

Nondepolarizing blocker

cholinergic receptor inhibitor

90
Q

Uses:
Tubocurarine
Mivacarium

A

Muscle relaxant for surgery w/o deep anesthesia

91
Q

Class: Botulinum Toxin A

A

local paralytic

92
Q

MOA: Botulinum Toxin A

A

Blocks vesicle fusion and ACh release on presynaptic terminal by degrading SNAP-25

93
Q

Uses: Boltulinum Toxin A

A

Reduce frown lines and wrinkles;
achalasia;
strabismus;
oromandibular dystonia

94
Q

Class:
Hexamethonium
Mecamylamine

A

Ganglionic blocker

cholinergic receptor inhibitor

95
Q

MOA:
Hexamethonium
Mecamylamine

A

Blocks ganglionic (Nn) receptor and sympathetic tone

96
Q

Uses:
Hexamethonium
Mecamylamine

A

Hypertensive crisis; “Bloodless” field surgery

97
Q

Clinical Uses:
Ipratroprium
Tiotroprium

A

to cause bronchodilation in asthma and COPD

98
Q

What kind of amine is atropine?

A

Tertiary - can interact with CNS AND peripheral muscarinic receptors well - good for nerve gas exposure

99
Q

Mnemonic for atropine overdose

A

Dry as a bone - no glandular secretions
Blind as a bat - blockade of accomodation and excessive dilation
Red as a beet - atropine flush - dilation of cutaneous blood vessels AND inhibition of sweat glands (inhibition alpha-1 mediated vasoconstriction)
–also atropine fever from lack of sweating
Mad as a hatter - delirium - CNS

100
Q

Atropine fever can be lethal in:

A

infants and small children
Sweat glands are sympathetic but utilize cholinergic post-ganglionic fibers
symptom managament to treat, do not use a cholinesterase inhibitor ie physostigmine

101
Q

Prazosin

A

alpha-blocker

alpha-1 selective antagonist

102
Q

Phenoxybenzamine

A

alpha-blocker

Antagonist: α1, α2; non-competitive blocker (covalent bond to receptor)

103
Q

Therapeutic Use: Prazosin

A

Raynaud’s
BPH
Primary HTN

104
Q

Therapeutic Use: Phenoxybenzamine

A

Pheochromocytoma, Raynaud’s, frostbite

105
Q

MOA Tyramine

A

Increases NE release

gets uptaken into cleft like NE

106
Q

Best way to adrenergically increase HR:

A

Epinephrine

Beta-1 effects greater than NE

107
Q

MOA Terbutaline

A

beta-2 selective agonist

Uses: Prevent or reverse exercise-induced bronchospasm; mild asthma; COPD; early labor

108
Q

Glaucoma is treated with muscarinic agonists or antagonists?

A

muscarinic agonists, which facilitate the outflow of aqueous humor

109
Q

An alpha agonist vasodilates or vasocontricts?

A

Vasoconstricts

110
Q

Parasympathetic control of salivation is mediated by:

A

M3 receptors found in salivary glands; these receptors elevate calcium concentration and activate the secretory process.

111
Q

T/F: Although MAO may contribute to the ultimate metabolism of NE, it does not assist in the termination of NE neurotransmission.

A

True

Termination of NE neurotransmission:
Uptake by non-neuronal cells.
Diffusion out of the synaptic cleft.
Uptake by neuron plasma membrane.

112
Q

Phenylephrine MOA

A

alpha-1 agonist
decongestant
vasoconstriction → increase in total peripheral resistance → increase in blood pressure → activation of a baroreceptor response to decrease sympathetic outflow and increase parasympathetic outflow, resulting in a decrease in heart rate.

113
Q

For prevention of migraines, consider:

A

Propranolol, methysergide, and calcium channel blockers have all been shown to be prophylactic in migraine therapy.

114
Q

For treatment of an acute migraine, consider:

A

Ergotamine and the several “triptans” (e.g. sumatriptan [Imitrex]) are effective in the acute treatment of a migraine headache.

115
Q

T/F: Activation of α2 receptors which are presynaptic can reduce subsequent release of norepinephrine from post-ganglionic fibers.

A

True

116
Q

MOA Succinylcholine

A

Succinylcholine (diacetylcholine) activates Nm persistently because it is poorly hydrolyzed at the NMJ. This hyperactivation causes persistent depolarization at the endplate, blocking Nm function and leading to flaccid paralysis.

117
Q

Side effects: Prazosin

A

Orthostatic HTN;

Tachycardia

118
Q

How would metoprolol decrease renin release?

A

blocking beta receptors on juxtaglomerular apparatus cells

MS 2 - Unit 2 (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions