Brainscape's Knowledge GenomeTM

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


See full index

Fa: Pharm 3 > 6. Neuromuscular > Flashcards

6. Neuromuscular Flashcards

1
Q

how to tx neuromuscular disorders

A

corticosteroids

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

what can cause upregulation of nicotinic NMJ receptors?

A

-motor neuron lesions (MS), -muscle trauma, -burn injury -immobilization, -sepsis / infection ?

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

how does NDMR dosing change during upregulation of nicotinic NMJ receptors

A

more resistant to NDMR, so need to give more

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

how does DMR dosing change during upregulation of nicotinic NMJ receptors

A

enhanced response to DMR

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

what is the risk of DMR during upregulation of nicotinic NMJ receptors

A

lethal hyperkalemia

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

what is usually contraindicated during upregulation of nicotinic NMJ receptors

A

sux

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

what can cause downregulation of nicotinic NMJ receptors?

A

-MG, -organophosphate poisoning, -chronic AChE inhibitor exposure

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

how does NDMR dosing change during downregulation of nicotinic NMJ receptors

A

more sensitive to NDMR

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

how does DMR dosing change during downregulation of nicotinic NMJ receptors

A

limits the effect of DMR (need higher dosing)

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

how to determine levels of plasma cholinesterases in preop

A

-pre op plasmapheresis, -pre op acetylcholinesterase inhibitors

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

what drugs are metabolized by plasma cholinesterases

A

-sux, -mivacurium, -remifentanil, -esmolol

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

what is pseudohypertrophic muscular dystrophy

A

-progressive deterioration of skeletal muscle strength, -degeneration of cardiac muscle, -chronic weakness of respiratory muscles and accumulation of secretions

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

what does pseudohypertrophic mean

A

fatty infiltration

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

risk of anesthesia for patients with pseudohypertrophic muscular dystrophy

A

pulmonary aspiration

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

how do NDMR affect patients with pseudohypertrophic muscular dystrophy

A

normal response to NDMR (or may be prolonged)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do DMR affect patients with pseudohypertrophic muscular dystrophy

A

sux is contraindicated due to risk for rhabdomyolysis, hyperkalemia, and cardiac arrest

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

how do volatile agents affect patients with pseudohypertrophic muscular dystrophy

A

should be avoided!

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

risk for rhabdomyolysis and arrhythmia cardiac arrest (even w/o sux)

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

pseudohypertrophic muscular dystrophy during anesthesia can look similar to…

A

MH

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

how to tx pseudohypertrophic muscular dystrophy during anesthesia

A

dantrolene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is myotonic dystrophy type 1

A

progressive involvement of skeletal, cardiac, and smooth muscle (cardiac conduction abnormalities are common)

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

use of DMR in myotonic dystrophy type 1

A

sux is contraindicated because causes prolonged skeletal muscle contraction

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

use of NDMR in myotonic dystrophy type 1

A

NMBs have a normal response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

reversal agents of NDMR in myotonic dystrophy type 1

A

-neostigmine could potentially precipitate skeletal muscle contraction, -sugammadex is best

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is guillain-barre syndrome (acute idiopathic polyneuritis)?

A

sudden onset of skeletal muscle weakness or paralysis, usually triggered by an infectious process (usually starts in legs and spreads up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

SE of guillain-barre syndrome

A

-bulbar involvement (bilateral facial paralysis): diff swallowing, pharyngeal muscle weakness, -paresthesia (sensory problems) and pain, -ANS dysfx (cardiovascular probs, arrhythmias)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

management of guillain-barre syndrome

A

-supportive respiratory and cardiovascular, -plasma exchange / pheresis or IVIG infusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is multiple sclerosis

A

chronic demyelinating inflammatory disease of the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

sx of MS

A

-Visual disturbances, -sensory disturbances, -pain, -motor deficits, -spasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

tx of MS

A

-immunomodulating agents, -corticosteroids, -IVIG, -plasmapheresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what can trigger MS

A

stress and hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

use of DMR in MS

A

avoid sux due to upregulation of N receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

use of NMDR in MS

A

variable response, titrate carefully

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

where to perform NM monitoring in MS

A

in the limb that is not affected / least affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how is MG classified

A

based on skeletal muscles involved and symptom severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

type I MG

A

extraocular movement

37
Q

type IIa MG

A

slowly progressive; skeletal muscle weakness spares muscles of respiration

38
Q

type IIb MG

A

faster progression, more severe weakness

39
Q

type III MG

A

acute onset with rapid deterioration

40
Q

type IV MG

A

severe weakness from progression of type I or II

41
Q

MOA of MG

A

-antibodies to alpha 1 subunit of nicotinic R channel complex, -receptors crosslink, -lysis of postsynaptic membrane, -binding to nicotinic R and inhibiting fx, (antibodies block ACh from binding R… loss of action causes loss of receptors)

42
Q

symptomatic tx of MG

A

-acetylcholinesterase enzyme inhibitors (edrophonium, pyridostigmine, neostigmine)

43
Q

chronic immunomodulating tx of MG

A

-glucocorticoid, -immunosuppressant (azathioprine, cyclosporine, methotrexate, mycophenolate, tacrolimus, rituximab)

44
Q

rapid immunomodulating tx of MG

A

-IVIG, -plasmapheresis

45
Q

what drugs can potentiate weakness in MG

A

-magnesium, -NMBs, -aminoglycosides (some other abxs, macrolides), -Na channel blocking drugs (lidocaine, procainamide, quinidine), -CCB

46
Q

how to manage chronic meds of MG before surgery

A

take chronic meds up to and including morning of surgery (pyridostigmine, neostigmine)

47
Q

how will chronic MG meds affect NDMR and DMR agents

A

response to reversal agent may be unpredictable or insufficient

48
Q

what can happen if you withhold chronic MG meds

A

makes bulbar sx more severe

49
Q

onset, DOA, and peak of pyridostigmine

A

-rapid onset 15-30 min, -peak in 2 hours, -lasts 3-4 hours

50
Q

oral dose of pryidostigmine

A

start with 30 mg and titrate as needed

51
Q

IV dose of pyridostigmine

A

ratio of IV to PO is 1 mg to 30 mg

52
Q

if patients take chronic glucocorticoids for MG, what can this cause intraop?

A

HPA suppression and adrenal insufficiency

53
Q

for pts that do not have underlying primary adrenal insufficiency, how should the dose of glucocorticoids be before surgery

A

take usual daily dose of glucocorticoid

54
Q

for pts that do not have underlying primary adrenal insufficiency, when is a stress dose NOT needed

A

-steroid taken less than 3 weeks, -daily dose <prednisone 5 mg (or equivalent) for any duration, -or prednisone <10 mg every other day in past 5 months

55
Q

if patients appear cushingoid, what should they receive before surgery

A

stress dose of glucocorticoids

56
Q

how to manage daily dose of a superficial procedure (dental or biopsy)

A

take usual morning steroid dose

57
Q

stress dose ofa superficial procedure (dental or biopsy)

A

none

58
Q

how to manage daily dose of a minor procedure or surgery under LA (inguinal hernia repair)

A

take usual morning steroid dose

59
Q

stress dose of a minor procedure or surgery under LA (inguinal hernia repair)

A

not needed or 25 mg IV just prior to procedure

60
Q

how to manage daily dose of a moderate surgical stress (LE revascularization, total joint replacement, cholecystectomy, colon resection)

A

take usual morning steroid dose

61
Q

stress dose of a moderate surgical stress (LE revascularization, total joint replacement, cholecystectomy, colon resection)

A

-hydrocortisone 50-75 mg IV just before procedure and 25 mg of hydrocortisone q8h for 24 h, -resume usual dose after

62
Q

how to manage daily dose of a major surgical stress (esophagogastrectomy, total proctocolectomy, open heart surgery)

A

take usual morning steroid dose

63
Q

stress dose of a major surgical stress (esophagogastrectomy, total proctocolectomy, open heart surgery)

A

-hydrocortisone 100-150 mg IV just before procedure and 50 mg of hydrocortisone q8h for 24 h, -taper dose by half per day to maintenance level

64
Q

use of NMB agents in MG intraop

A

avoid if possible! and reverse with sugammadex if possible!

65
Q

premedication for MG pts

A

-avoid if possible, -if needed, 0.5 mg IV versed with continuous monitoring

66
Q

what is the best induction for MG pt

A

regional, neuraxial when possible

67
Q

use of inhalational agents in MG pt

A

if provide adequate VA, may not need NMB

68
Q

what is commonly used for induction for MG pt

A

propofol (2 mg/kg) + remi (4-5 mcg/kg)

69
Q

for MG pt, how to tx bradycardia and hypotension

A

ephedrine 10 mg IV as needed

70
Q

if needed, what are the preferred NMB agents for MG

A

roc and vec

71
Q

how to MG pt respond to DMR

A

somewhat resistant

72
Q

how do MG pt respond to NMDR

A

very sensitive to NMDR

73
Q

ED 95% of sux for pts with MG

A

2.6 x normal

74
Q

dosing range of sux for MG pt

A

higher end (1-2 mg/kg), *if 2 mg/kg, expect prolonged duration

75
Q

how is sux metabolized

A

plasma cholinesterases

76
Q

what can acetylcholinesterase inhibitors (pyridostigmine) do to sux in MG pt

A

prolong effect of sux

77
Q

how to dose NDMR in MG pt

A

small doses, 0.1-0.2 times the ED95 and titrate

78
Q

sugammadex dosing in MG pt

A

2-4 mg/kg IV

79
Q

does pyridostigmine affect sugammadex

A

no

80
Q

does pyridostigmine affect neostigmine

A

yes, effect is unpredictable

81
Q

what can neostigmine cause in MG pt

A

-cholinergic crisis (weakness with other signs of cholinergic excess)

82
Q

what is lambert eaton syndrome (myasthenic syndrome)

A

-autoimmune disorder of neuromuscular junction, -antibodies directed against presynaptic voltage gated calcium channels, -muscle weakness due to reduced ACh release from presynaptic nerve terminals

83
Q

how do NDMR affect lambert eaton syndrome

A

very sensitive to NDMR

84
Q

how do DMR affect lambert eaton syndrome

A

very sensitive to DMR

85
Q

how do sx of lambert eaton syndrome compare to MG

A

-more autonomic dysfx, -less bulbar sx

86
Q

is lambert eaton syndrome responsive to AChE inhibitors

A

no

87
Q

is lambert eaton syndrome or MG more sensitive to NDMR

A

lambert eaton syndrome

88
Q

effects of neostigmine on lambert eaton syndrome

A

ineffective, avoid!

89
Q

what can happen with induction agents for pt with lambert eaton syndrome

A

excessive hypotension

Fa: Pharm 3 (10 decks)

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