Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Action potential- dependent increase in [Ca2+]i

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

A

Muscle Twitch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Clonus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Tetanic contraction =

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Propagation of the action potential depends on

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Two classes of NM relaxants

A
  1. Non-depolarizing agents (Curare drugs)

2. Depolarizing agents (Succinylcholine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

D-TUBOCURARINE, PANCURONIUM, VECURONIUM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Competitive antagonists at nicotinic acetylcholine receptors. Name 3

A

D-TUBOCURARINE, PANCURONIUM, VECURONIUM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name 2 strategies to overcome NM competitive antagonists

A

by excess Ach through

1) tetanic stimulation
2) Cholinesterase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

At higher concentrations of ACh, what happens?

A

blockade of channel pore develops Less sensitive to excess Ach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

longer than their therapeutic effect. (duration of action)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

the receptor reserve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

receptor reserve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Respiratory muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Order of muscle weakness/paralysis, after NAChR antagonist?

A

Extraocular, hands and feet, head and neck,

abdomen and extremities, diaphragm-respiratory muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SA of NAChR antagonists

A

Non-analgesic

Apnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Drug interactions with NAChR antagonists

A

Inhalation anesthetics (enhances effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Antidotes to NAChR antagonists?

A
  1. AChE inhibitors (neostigmine)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Example of depolarization blocking drug

A

Succinylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Succinylcholine is metabolized by

A

plasma cholinesterase (not acetylcholinesterase).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What augments Phase 1 depolarizing block by succinylcholine?

A

Cholinesterase inhibitors augment blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Which is faster onset of action? depolarizing or non-depolarizing

A

depolarizing

26
Q

Clearance of succinylcholine

A

Rapidly metabolized in plasma by cholinesterase (not at synapse)

27
Q

Action of succinylcholine terminated by

A

diffusion of drug away from motor end plate.

28
Q

Genetic variant in cholinesterase

A

can prolong succinylcholine drug action

29
Q

Clinical uses of depolarizing Nm relaxants

A

Endotracheal intubation

Control convulsions during ECT

30
Q

SA of depolarizing Nm relaxants

A

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
Q

Antidote for phase 1

A

none

32
Q

Antidote for phase 2

A

cholE inhibitors

33
Q

Contra for depolarizing Nm relaxants

A

Family Hx of malignant hyperthermia

34
Q

Treatment of spasticity involves what 2 things

A

Reduce activity of Ia fibers that excite the primary motor neuron

Enhance activity of inhibitory internuncial neurons.

35
Q

Baclofen - drug class?

A

spasmolytic drug

36
Q

Baclofen - mechanism of action?

A

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
Q

Baclofen - clinical use?

A

spinal spasticity, MS

38
Q

Baclofen - SA

A

drowsiness

39
Q

Benzodiazepine - drug class?

A

spasmolytics

40
Q

Benzodiazepines - 2 examples

A

Diazepam

Clonazepam

41
Q

Benzodiazepines - mechanism of actions?

A

Facilitate GABA mediated pre- synaptic inhibition

42
Q

Benzodiazepines - clinical use?

A

Spinal spasticity, MS (same as baclofen uses)

43
Q

Benzodiazepine - SA?

A

Sedation

Drowsiness

44
Q

Tizanidine - mechanism of action?

A

Centrally acting α2 agonist

45
Q

Tizanidine - clinical uses?

A

Spinal spasticity, MS (same as baclofen and benzodiazepine uses)

46
Q

Tizanidine - SA

A

Drowsiness

HYPOtension

47
Q

Dantrolene - mechanism of action?

A

Blocks calcium release from sarcoplasmic reticulum in muscle

Uncouples excitation- contraction of skeletal muscle (blocks ryanodine receptor)

48
Q

Dantrolene - clinical use?

A

Spasticity (stroke, SCI, MS, cerebral palsy)

Malignant hyperthermia

49
Q

Dantrolene - SA?

A

Muscle weakness

Sedation

50
Q

Mivacurium - duration?

A

15-20 min

51
Q

Vecuronium - duration

A

30-45 min

52
Q

Rocuronium - duration

A

25 min

53
Q

Pan/Roco/Miva/Vecuron - ium +
D-tubocurarine….
mechanism of action?

A

Non-depolarizing blockade of muscle nicotinic receptors

54
Q

Succinylcholine - duration?

A
55
Q

Pancuronium - elimination?

A

renal, primarily

56
Q

D-tubocurarine - elimination?

A

Liver & renal

57
Q

Rocuronium - elimination?

A

Liver

58
Q

Mivacurium - elimination?

A

Plasma cholinesterase

59
Q

Vecuronium elimination

A

Liver metab & clearance + Renal elimination

Pharmacology Exam 2 (by Richie) (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions