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Pharmacology > Sem 2 Block 1 > Flashcards

Sem 2 Block 1 Flashcards

1
Q

muscarinic receptors are __
nicotinic receptors are __
GPCR vs ligand gated

A

muscarinic= GPCR
nicotinic= ligand gated

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2
Q

what is the result of muscarinic receptor binding

A

formation of IP3= increased intracellular calcium

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3
Q

what is the result of nicotinic receptor binding

A

opening of Na+ and K+ channels leading to depolarization

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4
Q

are somatic motor neurons cholinergic or adrenergic

A

cholinergic

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5
Q

what is the effect of the drug hemicholinium

A

inhibit choline carrier

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6
Q

what is the effect of the drug vesamicol

A

inhibition of vesicle associated transporter

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7
Q

what is the effect of botulinum toxin

A

inhibition of release of acetylcholine by inhibiting specific SNARE proteins required for exocytosis

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8
Q

what is the effect of neostigmine

A

it’s an antiacetylcholinesterase which as a result, increases ACh at the neuromuscular junction

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9
Q

M1 and M3 are what class of GPCR

A

Gq= increases phospholipase C= increase IP3= increase Ca2+

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10
Q

M2 is what class of GPCR

A

Gi= decreases adenyly cyclase= decreased cAMP

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11
Q

muscarinic receptors are blocked by __

A

atropine

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12
Q

gastric glands have M_ receptors while the rest of the GIT has M_

A

gastric glands= M1
rest= M3

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13
Q

parasympathetics have the greatest effect on M2 receptors at what location of the heart

A

SA and AV node

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14
Q

what are the 2 classes of cholinesterases

A

acetyl cholinesterase= true
butyryl cholinesterase= pseudo

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15
Q

what is the difference in function between acetyl cholinesterase and butyryl cholinesterase

A

acetyl= termination of ACh action
butyryl= hydrolysis of ingested esters

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16
Q

in the cardiovascular system, ACh activates __ receptors on vascular endothelium resulting in the production of __ which causes __

A

M3
NO/endothelial derived growth factor
vasodilation

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17
Q

ACh with muscarinic receptors causes increased tone and peristalsis through M_ and increased secretions of the GIT glands through M_

A

M3
M1

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18
Q

dilator pupillae has what sympathetic receptor

A

alpha1

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19
Q

sphincter pupillae has what parasympathetic receptor

A

M3

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20
Q

what adrenergic sympathetic receptor is found on the ciliary muscle

A

beta2

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21
Q

what is the difference between miosis and mydriasis

A

miosis= pupil constriction
mydriasis= pupil dilation

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22
Q

what is the effect of pupil contraction on intraocular pressure

A

intraocular pressure decreases (there is increased access to the trabecular network)

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23
Q

contraction of what muscle allows for near vision by making the suspensory ligaments loose

A

ciliary muscle

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24
Q

ACh causes contraction of the circular muscle of the iris leading to widening of the iridocorneal angle. this __ outflow of aqueous humor and __ intraocular pression

A

increased outflow
decreases intraocular pressure

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25
Q

what is the effect of mydriasis on aqueous humor flow

A

mydriasis narrows the iridocorneal angle, blocking the passage of aqueous humor from the posterior chamber to the anterior chamber

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26
Q

voiding of urine can occur as muscarinic agonists cause contraction of __ and relaxation of __

A

contract detrusor (M3)
relax trigone/internal sphincter

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27
Q

besides acetylcholine, what are 2 examples of a choline ester

A

bethanechol
carbachol

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28
Q

bethanechol primarily affects what 2 tracts

A

urinary
GI

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29
Q

bethanechol stimulates atonic bladder (bladder muscles don’t fully contract), particularly in what 4 situations

A

post-partum
post-operative
non-obstructive urinary retention
megacolon

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30
Q

what is carbachol, a cholinergic drug, used for

A

topically in the eye as a miotic agent to treat glaucoma

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31
Q

what is the methacholine challenge test used to diagnose

A

bronchial asthma

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32
Q

what are some adverse effects of cholinergic drugs such as bethanechol and carbachol

A

flushing, sweating, decreased BP, abdominal pain, diarrhea, bronchospasms

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33
Q

what type of receptor does cevimeline activate

A

M3 receptors on lacrimal and salivatory glands

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34
Q

what is pilocarpine used for

A

pupil constriction for emergency lowering of intraocular pressure

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35
Q

are neostigmine and physostigmine direct or indirect acting cholinergic drugs

A

indirect

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36
Q

are neostigmine and physostigmine reversible or irreversible acting cholinergic drugs

A

reversible

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37
Q

acetylcholinesterase hydrolyzes ACh very rapidly in 2 steps. these steps are

A
  1. initial step
    acetylcholine-_>choline+acetylated AChE
  2. hydrolysis
    acetylated AChE+H2O –>AChE+acetate
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38
Q

what is the effect of neostigmine and physostigmine on AChE and the rate of drug-enzyme complex hydrolysis

A

there is temporary inhibition of AChE
drug enzyme complex is freed at a slower rate

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39
Q

is physostigmine, an indirect reversible AChE inhibitor:
charged or uncharged
lipid or water soluble
cross or doesn’t cross BBB

A

uncharged
lipid soluble
cross BBB

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40
Q

what reversible AChE inhibitor is used to treat atropine overdose

A

physostigmine
it crosses the BBB so it has an effect on the CNS and PNS

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41
Q

can neostigmine, a reversible AChE inhibitor be used to reverse CNS effects, why

A

no, it doesn’t cross the BBB

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42
Q

what AChE inhibitor drug is used to treat myasthenia gravis, paralytic ileus, and urinary retention

A

neostigmine

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43
Q

what drug is used in the Tensilon test

A

edrophonium

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44
Q

what drug is used in the Tensilon test

A

edrophonium

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45
Q

what is the Tensilon test with endrophonium used for

A

to differentiate a cholinergic crisis from a myasthenic crisis

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46
Q

how does a cholinergic crisis differ from a myasthenia crisis

A

cholinergic crisis- overdose of AChE inhibitor
myasthenia- acute exacerbation of the disease

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47
Q

the Tensilon test can either improve or worsen symptoms. which tells of a myasthenia crisis vs a cholinergic crisis

A

myasthenia= improvement of symptoms
cholinergic= worsening of symptoms

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48
Q

what drug class is used for postoperative decurarization

A

AChE inhibitor

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49
Q

are organophosphate compounds:
direct or indirect acting
reversible or irreversible

A

indirect
irreversible

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50
Q

what is the treatment for organophosphate poisoning

A

organophosphates are an AChE inhibitor= increased ACh= increased parasympathetic activity

administration of atropine= blockage of muscarinic receptors= decreased parasympathetic activity= atropinized= pupils dilate (reverse of muscarinic activity)

pralidoxime reverses the nicotinic receptor effects

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51
Q

what is the function of palidoxime

A

oximes bind to free AChE allowing it to act as an AChE inhibitor

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52
Q

what is the effect of atropine

A

blocks muscarinic drugs competitively centrally and peripherally

53
Q

does atropine cross the BBB

54
Q

what are 2 examples of natural alkaloid antimuscarinic drugs

A

atropine
scopolamine (Hyoscine)

55
Q

what are 2 synthetic antimuscarinic drugs which are used for ophthalmic practice to dilate eyes in the short term

A

cyclopentolate
tropicamide

56
Q

what is the main action of atropine on the cardiovascular system

A

tachycardia

57
Q

why does atropine not affect blood pressure

A

sympathetic is dominant in vasculature
histamine caused vasodilation
atropine causes vasodilation

58
Q

what is the cause of atropine flush

A

release of histamine dilates cutaneous blood vessels

59
Q

what are 2 antimuscarinic drugs are used in ophthalmology due to their short acting duration

A

cyclopentolate
tropicamide

60
Q

what is the effect of atropine on body temperature

A

increased body temp leading to atropine fever

61
Q

what medication is used for motion sickness

A

scopolamine

62
Q

what is one of the adverse effects of scopolamine

A

it causes euphoria so it is subject to abuse

63
Q

what is the effect of using phenylephrine for funduscopic exam

A

it produced a short lasting mydriasis without cycloplegia

64
Q

atropine is contradicted for what 2 condition

A

peptic ulcer disease
glaucoma

65
Q

traveler’s diarrhea is treated with what 2 drugs, why combined

A

atropine and diphenoxylate
atropine is added for it’s side effects to prevent addiction to the diphenoxylate opioid

66
Q

what are the 4 classes of skeletal muscle relaxants

A

competitive (non-depolarizing)
non-competitive (depolarizing)
direct acting
centrally acting

67
Q

what are the main class of non-depolarizing skeletal muscle relaxanta

A

curare (-curonium)

68
Q

what is the main class of depolarizing (non-competitive) skeletal muscle relaxants

A

succinylcholine

69
Q

what are the 3 main classes of centrally acting skeletal muscle relaxants

A

benzodiazepines
GABA derivatives
alpha2 agonist

70
Q

what drug acts as an antagonist to non-depolarizing competitive skeletal muscle blockers

A

neostigmine

71
Q

how do curare drugs produce a fall in BP, flushing, and bronchoconstriction

A

they release histamine and ganglionic blocking activity

72
Q

since succinylcholine, a depolarizing (non-competitive) skeletal muscle relaxant, does not dissociate rapidly from the receptor, what is the effect

A

prolonged depolarization
inactivation of Na+ channels
ACh is unable to generate AP

73
Q

what enzyme metabolizes succinylcholine

A

pseudocholinesterase

74
Q

what is an adverse effect of atracurium

A

it’s metabolite (Laudanosine) can cause seizures

75
Q

what are the 3 main side effects of succinylcholine

A

hyperkalemia
malignant hyperthermia
prolonged apnea

76
Q

what patients is scoline apnea seen in

A

those who are genetically deficient in plasma cholinesterase or have an atypical form of plasma cholinesterase

77
Q

succinylcholine is contradicted in patients with what 2 conditions

A

atypical pseudocholinesterase
malignant hyperthermia

78
Q

what drug can be given to overcome competitive non-depolarizing skeletal muscle relaxants

A

cholinesterase inhibitors such as neostigmine

79
Q

what is an example pf a direct acting skeletal muscle relaxant

A

dantrolene

80
Q

how does the direct acting skeletal muscle relaxant dantrolene work

A

it blocks ryanodine receptors which causes a reduction/block in calcium release, leading to skeletal muscle relaxation

81
Q

how does baclofen work as a central skeletal muscle relaxant

A

it activates GABA b receptors leading to skeletal muscle relaxation

82
Q

what is the difference between central and peripheral skeletal muscle relaxants

A

central- inhibit polysynaptic reflexes in the CNS
peripheral- clock neuromuscular transmission

83
Q

what is the difference between central and peripheral skeletal muscle relaxants in terms of uses

A

central- chronic spastic conditions
peripheral- short surgical procedures

84
Q

ganglionic blockers act on what receptor

A

they’re competitive antagonists at Nn, reducing parasympathetics

85
Q

ganglion blockers are similar to the effect of atropine except in what 2 sites

A

sweat glands
blood vessels

86
Q

what drug will block the reflex bradycardia that occurs when phenylephrine or other vasopressors cause vasoconstriction

A

hexamethonium (a ganglion blocker)

87
Q

what drug interferes with the synthesis of catecholamines by inhibiting tyrosine hydroxylase

A

metyrosine

88
Q

what drug blocks the storage of catecholamines in granule or granular uptake by inhibiting vesicular monoamine transporter (VMAT) into vesicles

89
Q

what 2 drugs cause displacement of catecholamines from vesicles, causing their release

A

amphetamine
tyramine

90
Q

what 2 drugs prevent the release of catecholamines from adrenergic terminals

A

bretylium
guanethidine

91
Q

what 2 drugs block the reuptake of catecholamines at the nerve terminal

A

cocaine
imipramine

92
Q

how does the metabolism of norepinephrine differ from serotonin

A

norepinephrine is metabolized by MAO then COMT
serotonin is metabolized by MAO only

93
Q

what is the effect of alpha2 receptor activation in the pancreas

A

decrease insulin secretion

94
Q

what is the affect of alpha2 receptor activation on platelets

A

aggregation

95
Q

what is the effect of beta2 activation on the uteru

A

relaxation

96
Q

what is the effect of beta2 activation on the uterus

A

relaxation

97
Q

what adrenergic receptor is found on adipose tissue to increase lipolysis

98
Q

alpha1 receptors use what G protein, what is the effect

A

Gq
IP3/Ca2+

99
Q

alpha2 receptors use what G protein, what is the effect

A

Gi
decrease cAMP

100
Q

beta and dopamine receptors use what G protein, what is the effect

A

Gs
increase cAMP

101
Q

what are 2 examples of alpha1 receptor selective antagonists

A

phenylephrine
methoxamine

102
Q

what is an example of an alpha1 receptor selective antagonist

103
Q

what is an example of an alpha2 receptor selective agonist

104
Q

what is an example of a beta1 receptor selective agonist

A

dobutamine

105
Q

what are 2 examples of beta1 receptor selective antagonists

A

atenolol
metoprolol

106
Q

what are 2 examples of beta2 receptor selective agonists

A

albuterol
terbutaline

107
Q

are alpha or beta receptors more sensitive to activators at a low dose

108
Q

are alpha or beta receptors more sensitive to activators at a high dose

109
Q

epinephrine uses what receptors

A

all (alpha and beta)

110
Q

norepinephrine uses what receptors

A

all except B2 (uses alpha1, alpha2, and beta1)

111
Q

isoproterenol uses what receptors

A

beta only (beta1 and beta2)

112
Q

dobutamine uses what receptors

A

only beta1

113
Q

pulse pressure increases due to stimulation of what receptor

114
Q

why don’t alpha1 receptors change pulse pressure

A

they increase both systolic and diastolic pressure

115
Q

what receptor stimulation increases systolic pressure

116
Q

what receptor stimulation decreases TPR and diastolic pressure

117
Q

does epinephrine or norepinephrine show a biphasic response in which there are different effects based on dose

A

epinephrine

118
Q

what is the biphasic response seen with norepinephrine

A

epinephrine at low dose acts on beta2 receptors–>vasodilation

epinephrine at high dose acts on alpha1 receptors–>vasoconstriction

119
Q

after an alpha receptor block, there is reflex tachycardia in which heart rate is greater then what it was before the alpha blockade. why?

A

decrease in blood pressure with beta receptor activity increases RVLM activity which causes secretion of norepinephrine

120
Q

does epinephrine cause hypo or hyperglycermia

A

hyperglycemia

(there is an increase in glycogenolysis and gluconeogenesis)

121
Q

what is the effect of epinephrine on aqueous humor production

A

reduces production due to vasoconstriction and enhanced aqueous humor flow

122
Q

what is the drug of choice for anaphylactic shock

A

epinephrine

123
Q

epinephrine use is contradicted in what health condition

A

angina pectoris

124
Q

norepinephrine has no effect on what receptors

125
Q

does norepinephrine increase systolic pressure, diastolic pressure, or both

126
Q

isoproterenol has no effect on what receptors

127
Q

what drug is used to increase GFR, renal blood flow, and Na+ excretion to prevent kidney failure in cases of septic shock

A

low dose dopamine

128
Q

high dose of dopamine stimulates alpha1 receptors leading to vaso__

A

vasoconstriction

Pharmacology (16 decks)

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