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Pharmacology > Pharm 8.3 - Nicotinic blockers > Flashcards

Pharm 8.3 - Nicotinic blockers Flashcards

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1
Q

Nicotinic (muscle) (Nm) receptor blockers are for use as

A

skeletal muscle relaxants (neuromuscular blocking angents)

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2
Q

Nicotinic (nerve) (Nn) receptor blockers are for use as

A

ganglion blockers

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3
Q

Skeletal muscle relaxants act on

A

nicotinic receptors present at the neuromuscular junction and reduce muscle tone

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4
Q

Neuromuscular blockers (skeletal muscle relaxants) are clinically useful during

A

surgery for producing complete muscle relaxation without having to emply higher anesthetic doses to achieve comparable muscular relaxation

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5
Q

skeletal muscle relaxants are classified as

A

competitive/non depolarizing, non competitive/ depolarizing, direct acting, centrally acting

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6
Q

skeletal muslce relaxants - nondeplarizing/competitive drugs

A

curare-derivatives that are long acting, intermediate acting, short acting

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7
Q

long acting competitive nicotinic blockers

A

d-tubocurarine, pancuronium, pipecuronium, doxacurium

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8
Q

intermediate competitive nicotinic blockers

A

vencuronium, rocuronium, atracurium

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9
Q

short acting competitive nicotinic blockers

A

mivacurium

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10
Q

muscle relaxants - depolarizing/noncompetitive nicotinic blockers

A

succinylcholine/suxamethonium

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11
Q

direct acting muscle relaxants

A

dantrolene

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12
Q

centrally acting muscle relaxants

A

mephenesin, benzodiazepines, GABA derivative

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13
Q

mephenesin (mus relax)

A

chlorzoxazone, carisoprodol, methocarbamol

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14
Q

benzodiazepines (mus relax)

A

diazepam

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15
Q

gaba derivative (mus relax)

A

baclofen

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16
Q

mechanism of competitive/nondepolarizing agents

A

nicotinic antagonists at Nm receptors. This binding means Ach released form the nerve endings cannot binds with Nm.

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17
Q

how are non-depolarizing/competitive blockers of Nm surmountable

A

the antagonism is surmoundatlbe by increasing the concentration of Ach (by administration of neostigmine, pyridostigmine or edrophonium

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18
Q

what happens at high doses of non-depolarizing agents (competitive blockers)

A

high doses can also block the ion channels of the end plate leading to further weakenting of neuromuscular transmission

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19
Q

sequence of muscle paralysis

A

first small rapidly contracting muscle of the face and eye, followed by the finger, then the limbs, neck and trunk muscles, then intercostal muscles and lastly, the diaphragm muscles are paralyzed

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20
Q

4 drugs that produce a fall in BP, flushing, and bronchoconstriction and how they do it

A

tubocurarine, mivacurium, atracurium, and metocurine by releasing histamine

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21
Q

depolarizing agent (noncompetitive) nicotinic blocker

A

succinylcholine

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22
Q

mechanism of succinylcholine

A

attaches to the nicotinic receptor and like Ach depolarizes at the NMJ (act as nicotinic agonists) but unlike Ach they remain attached for a long period of time and cause constant stimulation fo the receptor leading to initial twitiching and fasciculations (phase I), followed by facid paralysis. continuous depolarization leads to gradual repolarization (na channel closes) resulting in resistance to depolarization (phase II)

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23
Q

Adverse effects of Nondepolarizing blockers (competitive)

A

hypotension, tachycardia, bronchospasm, seizure, postoperative muscle pain, hyperkalemia, malignant hyperthermia, prolonged apnea, bradycarida, inc IOT and intragrastric pressure

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24
Q

competitive nicotinic blocker hypotension due to

A

histamine release and ganglionic blocking activity (isoquinoline derivatives)

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25
competitive nicotinic blocker tachycardia due to
vasolytic activity (steroid derivatives like pancuronium) leading to potential arrhythmias
26
competitive nicotinic blocker bronchospasm due to
histamine release (isoquinoline derivatives)
27
competitive nicotinic blocker seizure due to
antracurium use due to tis metabolite laudanosine
28
competitive nicotinic blocker postoperative muscle pain due to
increased contractions causing soreness
29
competitive nicotinic blocker hyperkalemia due to
loss of tissue potassium due to depolarization
30
competitive nicotinic blocker malignant hyperthermia due to
rapid increase in muslce metabolism
31
malignant hyperthermia is characterized by
tachycardia, intense muscle spasm (muscle rigidity), hyperthermia (pyrexia)
32
malignant hyperthermia is treated by
rapidly cooling the patient and by administration of dantrolene which block release of Ca2+ from the sarcoplasmic reticulum of muscle cells thus reducing heat production and relaxing muscle tone
33
competitive nicotinic blocker prolonged apnea due to
in a patient who is genetically deficient in plasma cholinesterase or has an atypical form of the enzyme can lead to prolonged apnea due to paralysis of the diaphragm
34
competitive nicotinic blocker: paralysis
flaccid
35
noncompetitive nicotingc blocker: paralysis
fassiculations --> flacid
36
competitive nicotinic blocker: neostigmine (inc Ach)
antagonizes
37
noncompetitive nicotinic blocker: neostigmine (inc Ach)
exaggerate phase I, reverse phase II block
38
competitive nicotinic blocker: ex
pancuronium
39
noncompetitive nicotinic blocker: ex
succinylcholine
40
structure of most peripheral neuromuscular blockers
quarternary compounds, not absorbed orally but administered IV, do not cross BBB or placenta
41
Ach is metabolized by
pseudocholinesterase
42
Atracurium is inactivated in plasma by
spontaneous non-enzymatic degradation (Hoffman elimination) not by liver or kidney, hence safe in hepatic or renal imparment --HOWEVER metabolite of atracurium (Laudanosine) can cause seizures
43
Mivacurium is metabolized by
plasma cholinesterase and has a very short duration
44
uses of neuromuscular blockers
adjuvant drugs in anesthesia during surgery to relax skeletal muscle, to facilitate intubation, laryngoscopies and endoscopies, to shorten the surgical procedure, to control ventilation
45
drug interaction with competitive nicotinic blockers
cholinesterase inhibitors, halothane, aminoglycosides, calciumchannel blockers
46
cholinesterase inhibitors with competitive Nm blockers
overcome block
47
halothane w/ competitive Nm blockers
enhance neuromuscular block
48
aminoglycosides with competitive Nm blockers
enhance the block by interfering with the release of Ach from cholinergic nerves
49
Ca-channel blockers w/ competitive Nm blockers
enhance the neuromuscular block
50
direct acting skeletal muslce relaxants work in many disorders
cerebral plasy, multiple sclerosis, spinal cord injury, stroke
51
Dantroline (direct acting musc relaxant) works by
reduces/blocks the release of calcium from the sarcoplasmic reticulum of the skeletal musle, acting directly on muscle to reduce skeletal muslce contractions
52
dantroline is absorbed by
the stomach
53
dantroline is administered
orally and w/ iv
54
dantroline is the drug of choice in
malignant hyperthermia
55
dantrolene is also used in
neuroleptic malignant syndrome (antiphycotic toxicity)
56
dantrolene reduces spasticity so is effective in
hemiplegia, paraplegia, cerebral palsy
57
Dantrolene adverse effects
muscle weakness, sedation, hepatotoxicity (on long term use so monitor it during therapy)
58
Central skeletal muscle relaxants produce selective action in the
cerebrospinal axis --acts as skeletal muslce relaxants
59
central skeletal muscle relaxants depress
the spinal and supraspinal polysynaptic reflexes involved in the regulation of muscle tone, and in ascending reticular formation (sedative action)
60
adverse effects of central skeletal muslce relaxants
sedation, increased frequency of seizures in epileptic patients (esp with Baclofen)
61
central skeletal muscle relaxant features
inhibit polysynaptic reflexes in CNS, CNS depressin, Orally and IV, chronic spastic conditions
62
peripheral skeletal muslce relaxant features
block NM transmission, no effect on CNS, usually IV, short surgical procedures
63
ganglionic blockers
hexamethonium, mecamylamine, trimethaphan, nicotine
64
ganglionic blockers are not as effective as
neuromuscular blockers - responses are complex and unpredictable so rarely used therapeutically
65
other than nicotine, all other ganglionic blockers are
nondepolarizing competitive antagonists at Nn both in PNS and SNS
66
some ganglionic blockers also block
ion channels of autonomic ganglia
67
net effect of ganglionic blocker is
to reduce the prodominant autonomic tone
68
ganglionic blockers can prevent
baroreceptor reflex changes in heart rate
69
predominantly sympathetic tone
arterioles, veins, sweat glands
70
predominantly parasympathetic tone
heart, iris, ciliary muslce, GI, bladder, salivary glands
71
predominantly both PNS and SNS
genital tract
72
meacamylamine and trimethaphan
used in severe refractory hypertension for emergency lowering of BP (caused by pulmonary edema or dissecting aortic aneurysm when other agents cannot be used)
73
hexamethonium
blocks the reflex bradycardia that occurs when phenylephrine causes vasoconstirction - HOWEVER cannot block bradycarida resulting from direct activation of sucarinic receptors in the heart
74
Nicotine benefit
none - deletrious to health
75
Nicotine dose
depending on the dose nicotine can cepolarize ganglia resulting in stimulation and then paralysis of all ganglia
76
low dose nicotine
inc in BP and HR due to release of NT from adrenergic terminals and from the adrenal medulla, inc in peristalsis and secretins
77
high dose nicotine
fall in BP by ganglionic blocking effect and stop of GIT and bladder muslce activity

Pharmacology (15 decks)

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