Pharm 8.3 - Nicotinic blockers Flashcards Preview

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Flashcards in Pharm 8.3 - Nicotinic blockers Deck (77)
1

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

skeletal muscle relaxants (neuromuscular blocking angents)

2

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

ganglion blockers

3

Skeletal muscle relaxants act on

nicotinic receptors present at the neuromuscular junction and reduce muscle tone

4

Neuromuscular blockers (skeletal muscle relaxants) are clinically useful during

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

5

skeletal muscle relaxants are classified as

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

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skeletal muslce relaxants - nondeplarizing/competitive drugs

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

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long acting competitive nicotinic blockers

d-tubocurarine, pancuronium, pipecuronium, doxacurium

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intermediate competitive nicotinic blockers

vencuronium, rocuronium, atracurium

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short acting competitive nicotinic blockers

mivacurium

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muscle relaxants - depolarizing/noncompetitive nicotinic blockers

succinylcholine/suxamethonium

11

direct acting muscle relaxants

dantrolene

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centrally acting muscle relaxants

mephenesin, benzodiazepines, GABA derivative

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mephenesin (mus relax)

chlorzoxazone, carisoprodol, methocarbamol

14

benzodiazepines (mus relax)

diazepam

15

gaba derivative (mus relax)

baclofen

16

mechanism of competitive/nondepolarizing agents

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

17

how are non-depolarizing/competitive blockers of Nm surmountable

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

18

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

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

19

sequence of muscle paralysis

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

20

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

tubocurarine, mivacurium, atracurium, and metocurine by releasing histamine

21

depolarizing agent (noncompetitive) nicotinic blocker

succinylcholine

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mechanism of succinylcholine

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)

23

Adverse effects of Nondepolarizing blockers (competitive)

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

24

competitive nicotinic blocker hypotension due to

histamine release and ganglionic blocking activity (isoquinoline derivatives)

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competitive nicotinic blocker tachycardia due to

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

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competitive nicotinic blocker bronchospasm due to

histamine release (isoquinoline derivatives)

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competitive nicotinic blocker seizure due to

antracurium use due to tis metabolite laudanosine

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competitive nicotinic blocker postoperative muscle pain due to

increased contractions causing soreness

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competitive nicotinic blocker hyperkalemia due to

loss of tissue potassium due to depolarization

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competitive nicotinic blocker malignant hyperthermia due to

rapid increase in muslce metabolism

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malignant hyperthermia is characterized by

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

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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

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competitive nicotinic blocker: paralysis

flaccid

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noncompetitive nicotingc blocker: paralysis

fassiculations --> flacid

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competitive nicotinic blocker: neostigmine (inc Ach)

antagonizes

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noncompetitive nicotinic blocker: neostigmine (inc Ach)

exaggerate phase I, reverse phase II block

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competitive nicotinic blocker: ex

pancuronium

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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

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drug interaction with competitive nicotinic blockers

cholinesterase inhibitors, halothane, aminoglycosides, calciumchannel blockers

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cholinesterase inhibitors with competitive Nm blockers

overcome block

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halothane w/ competitive Nm blockers

enhance neuromuscular block

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aminoglycosides with competitive Nm blockers

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

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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

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dantroline is absorbed by

the stomach

53

dantroline is administered

orally and w/ iv

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dantroline is the drug of choice in

malignant hyperthermia

55

dantrolene is also used in

neuroleptic malignant syndrome (antiphycotic toxicity)

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dantrolene reduces spasticity so is effective in

hemiplegia, paraplegia, cerebral palsy

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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

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peripheral skeletal muslce relaxant features

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

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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

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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

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net effect of ganglionic blocker is

to reduce the prodominant autonomic tone

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ganglionic blockers can prevent

baroreceptor reflex changes in heart rate

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predominantly sympathetic tone

arterioles, veins, sweat glands

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predominantly parasympathetic tone

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

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predominantly both PNS and SNS

genital tract

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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

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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