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Pharmacology > Pharm 8.3 - Nicotinic blockers > Flashcards

Pharm 8.3 - Nicotinic blockers Flashcards

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
Q

competitive nicotinic blocker tachycardia due to

A

vasolytic activity (steroid derivatives like pancuronium) leading to potential arrhythmias

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26
Q

competitive nicotinic blocker bronchospasm due to

A

histamine release (isoquinoline derivatives)

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27
Q

competitive nicotinic blocker seizure due to

A

antracurium use due to tis metabolite laudanosine

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28
Q

competitive nicotinic blocker postoperative muscle pain due to

A

increased contractions causing soreness

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29
Q

competitive nicotinic blocker hyperkalemia due to

A

loss of tissue potassium due to depolarization

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30
Q

competitive nicotinic blocker malignant hyperthermia due to

A

rapid increase in muslce metabolism

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31
Q

malignant hyperthermia is characterized by

A

tachycardia, intense muscle spasm (muscle rigidity), hyperthermia (pyrexia)

32
Q

malignant hyperthermia is treated by

A

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
Q

competitive nicotinic blocker prolonged apnea due to

A

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
Q

competitive nicotinic blocker: paralysis

35
Q

noncompetitive nicotingc blocker: paralysis

A

fassiculations –> flacid

36
Q

competitive nicotinic blocker: neostigmine (inc Ach)

A

antagonizes

37
Q

noncompetitive nicotinic blocker: neostigmine (inc Ach)

A

exaggerate phase I, reverse phase II block

38
Q

competitive nicotinic blocker: ex

A

pancuronium

39
Q

noncompetitive nicotinic blocker: ex

A

succinylcholine

40
Q

structure of most peripheral neuromuscular blockers

A

quarternary compounds, not absorbed orally but administered IV, do not cross BBB or placenta

41
Q

Ach is metabolized by

A

pseudocholinesterase

42
Q

Atracurium is inactivated in plasma by

A

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
Q

Mivacurium is metabolized by

A

plasma cholinesterase and has a very short duration

44
Q

uses of neuromuscular blockers

A

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
Q

drug interaction with competitive nicotinic blockers

A

cholinesterase inhibitors, halothane, aminoglycosides, calciumchannel blockers

46
Q

cholinesterase inhibitors with competitive Nm blockers

A

overcome block

47
Q

halothane w/ competitive Nm blockers

A

enhance neuromuscular block

48
Q

aminoglycosides with competitive Nm blockers

A

enhance the block by interfering with the release of Ach from cholinergic nerves

49
Q

Ca-channel blockers w/ competitive Nm blockers

A

enhance the neuromuscular block

50
Q

direct acting skeletal muslce relaxants work in many disorders

A

cerebral plasy, multiple sclerosis, spinal cord injury, stroke

51
Q

Dantroline (direct acting musc relaxant) works by

A

reduces/blocks the release of calcium from the sarcoplasmic reticulum of the skeletal musle, acting directly on muscle to reduce skeletal muslce contractions

52
Q

dantroline is absorbed by

A

the stomach

53
Q

dantroline is administered

A

orally and w/ iv

54
Q

dantroline is the drug of choice in

A

malignant hyperthermia

55
Q

dantrolene is also used in

A

neuroleptic malignant syndrome (antiphycotic toxicity)

56
Q

dantrolene reduces spasticity so is effective in

A

hemiplegia, paraplegia, cerebral palsy

57
Q

Dantrolene adverse effects

A

muscle weakness, sedation, hepatotoxicity (on long term use so monitor it during therapy)

58
Q

Central skeletal muscle relaxants produce selective action in the

A

cerebrospinal axis –acts as skeletal muslce relaxants

59
Q

central skeletal muscle relaxants depress

A

the spinal and supraspinal polysynaptic reflexes involved in the regulation of muscle tone, and in ascending reticular formation (sedative action)

60
Q

adverse effects of central skeletal muslce relaxants

A

sedation, increased frequency of seizures in epileptic patients (esp with Baclofen)

61
Q

central skeletal muscle relaxant features

A

inhibit polysynaptic reflexes in CNS, CNS depressin, Orally and IV, chronic spastic conditions

62
Q

peripheral skeletal muslce relaxant features

A

block NM transmission, no effect on CNS, usually IV, short surgical procedures

63
Q

ganglionic blockers

A

hexamethonium, mecamylamine, trimethaphan, nicotine

64
Q

ganglionic blockers are not as effective as

A

neuromuscular blockers - responses are complex and unpredictable so rarely used therapeutically

65
Q

other than nicotine, all other ganglionic blockers are

A

nondepolarizing competitive antagonists at Nn both in PNS and SNS

66
Q

some ganglionic blockers also block

A

ion channels of autonomic ganglia

67
Q

net effect of ganglionic blocker is

A

to reduce the prodominant autonomic tone

68
Q

ganglionic blockers can prevent

A

baroreceptor reflex changes in heart rate

69
Q

predominantly sympathetic tone

A

arterioles, veins, sweat glands

70
Q

predominantly parasympathetic tone

A

heart, iris, ciliary muslce, GI, bladder, salivary glands

71
Q

predominantly both PNS and SNS

A

genital tract

72
Q

meacamylamine and trimethaphan

A

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
Q

hexamethonium

A

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
Q

Nicotine benefit

A

none - deletrious to health

75
Q

Nicotine dose

A

depending on the dose nicotine can cepolarize ganglia resulting in stimulation and then paralysis of all ganglia

76
Q

low dose nicotine

A

inc in BP and HR due to release of NT from adrenergic terminals and from the adrenal medulla, inc in peristalsis and secretins

77
Q

high dose nicotine

A

fall in BP by ganglionic blocking effect and stop of GIT and bladder muslce activity

Pharmacology (15 decks)

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