Nicotinic antagonists Flashcards

(38 cards)

1
Q

nondepolarizing competitive antagonists MOA

A

hold the Nm receptor closed, preventing Na+ flow and depolarization–> no muscle contraction

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2
Q

effect of nondepolarizing blockers can be overcome with

A

ACh, as they are competitive antagonists

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3
Q

the only depolarizing blocker

A

succinylcholine

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4
Q

succinylcholine MOA

A

holds Nm open, continual flow of Na+ causes continual, longer than normal depolarization, which causes Nm to desensitize to subsequent ACh stimulation

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5
Q

neuromuscular blocking agents DO NOT

A

produce unconsciousness or anesthesia because they do not enter the brain

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6
Q

due to their high degree of ionization

A

neuromuscular blocking agents are NOT absorbed orally and do NOT enter CNS. IV ONLY.

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7
Q

nondepolarzing blockers interfere with the mobilization of ACh from the nerve terminal by

A

blocking pre-junctional sodium channels

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8
Q

endplate potential _______ when a nondepolarizing blocker is taken

A

decreases, an action potential can no longer be generated –> lack of muscle contraction (paralysis)

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9
Q

pharmacologic reversal for nondepolarizing blockers

A

cholinesterase inhibitors (increase ACh which can outcompete blockers)

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10
Q

muscles that are affected first by nondepolarizing blockers

A

small muscles followed by larger muscles

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11
Q

muscles that are affected last by nondepolarizing blockers

A

diaphragm, intercostal muscles

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12
Q

onset of action and recovery from succinylcholine are ________, so it’s used for

A

rapid

short procedures

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13
Q

succinylcholine’s action is terminated by

A

plama pseudocholinesterase

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14
Q

dibucaine

A

a local anesthetic that causes inhibition of AChE

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15
Q

abnormal dibucaine number

A

20%: abnormal cholinesterase acitivity, succinylcholine with last way too long

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16
Q

normal dibucaine number

A

80%: cholinesterase functions normally and succinylcholine will be short acting

17
Q

delay recover from succinylcholine

A

cholinesterase inhibitors

18
Q

succinycholine contraindications

A

soft tissue damage, burns, non-traumatic rhabdomyolisis, spinal cord injuries, muscular dystrophy, <8 years old

19
Q

inhaled anesthetic

20
Q

halothane is notorious for

A

malignant hyperthermia (also succ can cause)

21
Q

malignant hyperthermia from succinylcholine/halothane treatment

22
Q

patients who are at higher risk of too much K+ released by succinylcholine

A

burns, nerve degeneration, head trauma, peritoneal infection, kidney disease

23
Q

prolonged release of potassium by succinylcholine + risk factor can cause

A

cardiac arrest, life threatening esp in CHF

24
Q

malignant hyperthermia by succinylcholine/halothan MOA

A

uncontrolled release of Ca++ from sarcoplasmic reticulum –> muscle rigidity and high temperature

25
ventilation use of neuromuscular blocking agents
paralyze diaphragm so a ventilator can be used. intubation, bronchoscopy.
26
surgery use of neuromuscular blocking agents
paralysis, relax muscles for surgery
27
orthopedic use of neuromuscular blocking agents
allow manipulation of bones
28
other random ass use of neuromuscular blocking agents
decrease convulsions/muscle spasms (fine) in ECT (idk).
29
ganglion blockers are considered
nondepolarizing competitivie antagonists
30
2 ganglion blockers
hexamethonium mecamylamine (not used clinically)
31
effects of ganglion blockers
fire PNS and SNS so it depends on the dominant tone of the organ
32
ganglion blocker effects in eye
PNS blocked: cycloplegia, mydriasis
33
ganglion blocker effects on blood vessels
SNS blocked: vasodilation causes drop in BP, orthostatic hypotension
34
ganglion blocker effects on heart
SNS blocked: contractility reduced | PNS blocked: decrease in vagal tone causes tachycardia
35
GU ganglion blocker effects
PNS blocked: urinary retention, esp. BPH
36
sex ganglion blocker effects
PNS blocked: erectile dysfunction | SNS blocked: reduced ejaculation
37
ganglion blocker effects on body temp
SNS blocked: can't sweat | maintain body heat through vasodilation
38
ganglion blocker effects if combined with autonomic drugs
normal/exaggerated effects on target organ receptors which are not blocked Feedback and reflexes are decreased/abolished