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Pharmacology Exam 2 (by Richie) > Neuromuscular Relaxants - 8/24/15 (Scrogin) > Flashcards

Neuromuscular Relaxants - 8/24/15 (Scrogin) Flashcards

1
Q

Binding of nicotinic receptor opens cation channels and increases

A

Na+ and K+ conductance.

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2
Q

Action potential- dependent increase in [Ca2+]i

followed by fall in [Ca2+]i due to sequestration by sarcoplasmic reticulum

A

Muscle Twitch

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3
Q

reduced ability to lower calcium between stimulations due to increased frequency of stimulation leads to incomplete relaxation

A

Clonus

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4
Q

Tetanic contraction =

A

no appreciable reduction in [Ca2+]i between stimuli leads to physiological muscle contraction

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5
Q

Propagation of the action potential depends on

A

availability of voltage-gated Na+ channels in the resting state.

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6
Q

Two classes of NM relaxants

A
  1. Non-depolarizing agents (Curare drugs)

2. Depolarizing agents (Succinylcholine)

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7
Q

D-TUBOCURARINE, PANCURONIUM, VECURONIUM

A

Non-depolarizing agents (Curare drugs). Competitive antagonists at nicotinic acetylcholine receptors

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8
Q

Competitive antagonists at nicotinic acetylcholine receptors. Name 3

A

D-TUBOCURARINE, PANCURONIUM, VECURONIUM

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9
Q

Name 2 strategies to overcome NM competitive antagonists

A

by excess Ach through

1) tetanic stimulation
2) Cholinesterase inhibitors

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10
Q

At higher concentrations of ACh, what happens?

A

blockade of channel pore develops Less sensitive to excess Ach.

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11
Q

The biological half- life of the curare compounds tend to be

A

longer than their therapeutic effect. (duration of action)

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12
Q

The percentage of receptors that must be occupied by an antagonist to inhibit contraction is directly related to

A

the receptor reserve

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13
Q

Different muscle beds have different ________ and so will demonstrate the effects of curare type drugs at different plasma concentrations.

A

receptor reserve

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14
Q

_________ have the highest reserve, followed by larger limb and trunk muscles followed by fine muscles

A

Respiratory muscles

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15
Q

Order of muscle weakness/paralysis, after NAChR antagonist?

A

Extraocular, hands and feet, head and neck,

abdomen and extremities, diaphragm-respiratory muscle

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16
Q

3 clinical uses for NAChR antagonists

A
  1. Muscle relaxation for surgical procedures (many different drugs)
  2. Endotracheal intubation (rocuronium, mivacurium)
  3. Reduced resistance during ventilation (many)
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17
Q

SA of NAChR antagonists

A

Non-analgesic

Apnea

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18
Q

Drug interactions with NAChR antagonists

A

Inhalation anesthetics (enhances effect)

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19
Q

Antidotes to NAChR antagonists?

A
  1. AChE inhibitors (neostigmine)

2. Muscarinic blockers (glycopyrrolate) minimizes muscarinic effects of AChE inhibitor

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20
Q

Example of depolarization blocking drug

A

Succinylcholine

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21
Q

During phase 1 block, occupancy of the receptor by succinylcholine causes

A

opening of the ion channel and thus depolarization of the motor end plate.

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22
Q

Succinylcholine is metabolized by

A

plasma cholinesterase (not acetylcholinesterase).

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23
Q

What augments Phase 1 depolarizing block by succinylcholine?

A

Cholinesterase inhibitors augment blockade

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24
Q

Main features of Phase 1 block

A
  1. Depolarization of muscle with sustained muscle contraction - 4-8 min (opens cation channel to cause end plate depolarization)
  2. Flickering of ion conductance due to blockade of channel
  3. Flaccid paralysis
  4. Cholinesterase inhibitors augment blockade
25
Which is faster onset of action? depolarizing or non-depolarizing
depolarizing
26
Clearance of succinylcholine
Rapidly metabolized in plasma by cholinesterase (not at synapse)
27
Action of succinylcholine terminated by
diffusion of drug away from motor end plate.
28
Genetic variant in cholinesterase
can prolong succinylcholine drug action
29
Clinical uses of depolarizing Nm relaxants
Endotracheal intubation | Control convulsions during ECT
30
SA of depolarizing Nm relaxants
Non-analgesic, apnea, muscle pain (fasciculations), arrhythmia HTN bradycardia (stimulation of Nicotinic receptors in autonomic ganglia and muscarinic in SA node), hyperkalemia (low release of K+ from endplate), malignant hyperthermia
31
Antidote for phase 1
none
32
Antidote for phase 2
cholE inhibitors
33
Contra for depolarizing Nm relaxants
Family Hx of malignant hyperthermia
34
Treatment of spasticity involves what 2 things
Reduce activity of Ia fibers that excite the primary motor neuron Enhance activity of inhibitory internuncial neurons.
35
Baclofen - drug class?
spasmolytic drug
36
Baclofen - mechanism of action?
GABAb agonist Reduces Ca influx - reducing release of excitatory NT's and substance P in spinal cord Inhibits neurotransmitter release from skeletal muscle sensory afferent
37
Baclofen - clinical use?
spinal spasticity, MS
38
Baclofen - SA
drowsiness
39
Benzodiazepine - drug class?
spasmolytics
40
Benzodiazepines - 2 examples
Diazepam | Clonazepam
41
Benzodiazepines - mechanism of actions?
Facilitate GABA mediated pre- synaptic inhibition
42
Benzodiazepines - clinical use?
Spinal spasticity, MS (same as baclofen uses)
43
Benzodiazepine - SA?
Sedation | Drowsiness
44
Tizanidine - mechanism of action?
Centrally acting α2 agonist
45
Tizanidine - clinical uses?
Spinal spasticity, MS (same as baclofen and benzodiazepine uses)
46
Tizanidine - SA
Drowsiness | HYPOtension
47
Dantrolene - mechanism of action?
Blocks calcium release from sarcoplasmic reticulum in muscle Uncouples excitation- contraction of skeletal muscle (blocks ryanodine receptor)
48
Dantrolene - clinical use?
Spasticity (stroke, SCI, MS, cerebral palsy) Malignant hyperthermia
49
Dantrolene - SA?
Muscle weakness | Sedation
50
Mivacurium - duration?
15-20 min
51
Vecuronium - duration
30-45 min
52
Rocuronium - duration
25 min
53
Pan/Roco/Miva/Vecuron - ium + D-tubocurarine.... mechanism of action?
Non-depolarizing blockade of muscle nicotinic receptors
54
Succinylcholine - duration?
55
Pancuronium - elimination?
renal, primarily
56
D-tubocurarine - elimination?
Liver & renal
57
Rocuronium - elimination?
Liver
58
Mivacurium - elimination?
Plasma cholinesterase
59
Vecuronium elimination
Liver metab & clearance + Renal elimination

Pharmacology Exam 2 (by Richie) (8 decks)

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