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*Pharmacology > Progidy- Neuromusuclar blockers > Flashcards

Progidy- Neuromusuclar blockers Flashcards

1
Q

What is ipratropium?

A

an inhaled anticholinergic to prodice bronchodilation that is often used in combination with albuterol in the treatment of COPD (combivent)

-Ep- a- trop- e- um

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2
Q

Treatment for central anticholinergic syndrome

A

-anticholinesterase physostigmine 1-2mg IV

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3
Q

When ATTTTracurium is stored at room temp, it loses potency at a rate of roughtly ___% per month.

A

5%

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4
Q

T/F- inhalational agents can potentiate the effects of neuromuscular blocking agents.

A

True

Des > sevo > iso> n20

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5
Q

If the patient is on long term phenytoin and/or carbamazepine , the duration of aminosteroids is signficiantly (increased/decreased)

A

decreased

smokers [love] A Cold PBR = enzyme induction

-smokers, alcohol, carbamazepine, phenytoin, b…., rifampin

*increases metabolizing enzymes- will metabolize roc/vec faster

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6
Q

T/F- beta blockers have been noted to delay the onset of roc

A

true

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7
Q

How does ephedrine affect NMBs?

A

it can speed the onset of roc

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8
Q

Which AchE inhibitor has the shortest DOA and why?

A

Edrophonium bc it forms an ionic bond with AchE , compared to covalent bonds with neostigmine, ionic bonds are much weaker making it much less effective

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9
Q

Why is edrophonium administered with Atropine instead of glyco?

A

bc of it’s fast onset

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10
Q

What accounts for the short duration of mivacurium

A

bc it’s rapidly hydrolyzed by plasma cholinesterases

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11
Q

A patient presents with elevated liver enzymes, yellow eyes, and diagnosed liver failure. He is scheduled for an ERCP procedure that requires general anesthesia. The liver is critical in creating what enzyme that could be low in this patient? Which paralytic has a relative contraindication as a result of this deficiency?

A

Pseudocholinesterase

-Sux contraindicated

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12
Q

Where is the primary site of action for neuromuscular blocking agents?

A

The nicotinic cholinergic receptor on the muscle endplate (postsynaptic).

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13
Q

How does hypothermia affect neuromuscular blockade?

A

Hypothermia can augment a block by decreasing metabolism or delaying excretion of the drug.

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14
Q

Which of the steroidal muscle relaxants is most affected by renal disease?

A

Pancuronium is about 85% dependent upon renal elimination and is the most affected.

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15
Q

What method is used clinically to speed the onset of rocuronium?

A

Priming, which is the administration of 10% of the intubating dose about 1-3 minutes prior to anesthetizing the patient and administering the remaining dose.

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16
Q

Half lives of: Roc, Vec, and Panc

A

Roc- 0.7 hrs

Vec- 0.9hrs

Panc- 1.7hrs

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17
Q

DOA of Roc

A

30-90 minutes

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18
Q

*How does the elimination half-life of rocuronium differ between pediatric patients, adults, and the elderly?

A

kids - 30 mins

adults - 60 mins

elderly - 130 mins

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19
Q

Elimination half life of sux

A

47 seconds….

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20
Q

intubating dose of sux and how long before effect

A

1-1.5mg/kg

30-60 seconds

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21
Q

*Metabolites of sux

A

Succinylcholine is rapidly degraded into succinylmonocholine which is then degraded into choline and succinic acid.

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22
Q

intubating dose of vec*

A

0.1mg/kg

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23
Q

Intubating dose of Panc

A

0.06mg/kg

Isn’t this the ED 95?

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24
Q

Intubating dose of atracurium

A

0.5mg/kg

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25
Q

What is the structural difference between atracurium and cisatracurium? What are the clinical effects of this difference?

A

Cisatracurium is a potent isomer of atracurium that, unlike atracurium, is devoid of any histamine release.

Cisatracurium has a higher potency and requires less of the drug to be administered to reach the same clinical endpoint.

As a result, less laudanosine and acrylate byproducts are produced and the toxic effects of these agents is essentially nonexistent.

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26
Q

Intubating dose of cistatracurium

A
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27
Q

What two conditions is sux contraindicated in?

A

Duchenne’s muscular dystrophy and guillain-barre

(upregulation with extrajunctional receptors - massive K release)

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28
Q

IM dose of sux

A

4mg/kg

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29
Q

DOA of sux

A

10-15 mins

30
Q

How does the intubating dose of succinylcholine in children compare with that of adults?

A

Kids require a higher dose of sux: 1.5-2mg/kg

Infants even higher: 2-3mg/kg

31
Q

T/F fasciculations from sux are worse in kids

A

false- uncommon in kids

32
Q

You see a patient in the anesthesia preop clinic and they tell you that they were slow to wake up last time and needed a breathing tube for a period of time after surgery. They cannot provide any additional information. You suspect an of pseudocholinesterase deficiency. Your hospital does not have the ability to test for a dibucaine number. What test could you order?

A

Fluoride-resistant test.

-if the pt has pseudocholinesterase deficiency, the fluoride number of 60 is normal and 36 = atypical

33
Q

Max dose of neostigmine

A

0.07mg/kg

OR 5 mg

34
Q

which nerve supplies the adductor pollicis muscle

A

The ulnar nerve

35
Q

Why is the black lead placed distal compared to the red lead for TOF monitoring of the ulnar nerve

A

bc the ulnar nerve is most superficial at the wrist, so that apparently means the negative feedback electrode should go there

36
Q

Which nerve would be most appropriate to assess muscle relaxation prior to ETT placement?

A

Facial nerve

37
Q

T/F- nitrous oxide has some affect on skeletal muscle relaxation

A

false

38
Q

Someone asks you “what actuallly is MH?”

A

It’s a life threatening condition that results in increased skeletal muscle metabolism, which leads to:

>increased O2 consumption

> heat production

>formation of lactate

>rhabdo

39
Q

Clinical manifestations of MH

A

unexplained sudden increase in HR, RR, ETCO2

+ masseter spasm or total body rigidiety

40
Q

T/F- MH is a autosomal- recessive disorder

A

False- autosomal DOMINANT

(Duchennes is X-LINKED RECESSIVE)

41
Q

The administration of reversal agents should not be attempted until patient has at least how many twitches

A

1-2

-otherwise block may be too dense to have desired effect and you might be SOL if you are close to your max dose of neostigmine

42
Q

T/F- administration of a defasiculant dose of a NDMR prevents an increase in K seen with sux

A

false

43
Q

Sux increases IOP up to _____mmHg for ____minutes

A

15mmhg for 5 minutes

44
Q

What drug shouldn’t be given together with VEC bc it can crystalize

A

thiopental

45
Q

What is an autoimmune disorder in which acetylcholine receptors are destoyed or inactivated by circulating antibodies at the NMJ.

Hallmark sign

A

Myasthenia gravis

-hallmark sign = muscle weakeness

46
Q
A
47
Q

Which two NDMR’s have the same ED95 and what is it

A

Vec & Cist - 0.05mg/kg

48
Q

ED 95 of Panc

A

0.07mg/kg

49
Q

ED95 of Atracurium

A

0.25mg/kg

50
Q

T/F- Local anethestics can potentiate both depolarizing and non-depolarizing MR’s

A

true

51
Q

Which agent can prolong the effect of SUX?

  • Phenytoin
  • Metoclopramide
  • Metronidazole
  • Magnesium
A

Metcoclopramide

-it inihibits plasma cholinesterase

52
Q

Which cholinesterase inhibitor has the shortest DOA

  • Physostigmine
  • Edrophonium
  • Pyridostigimine
  • Neostigmine
A

Edrophonium

53
Q

What serious side effect are you most likley to see following hte administration of sugammadex?

A. Hypersensitivity reaction

B. Paradoxical paralysis

C. Transient Blindness

D. Vomiting

A

A. Hypersensitivity reaction

  • usually seen within 4 minutes of administration
  • CV collapse can be treated with fluid resusitation and high-dose epi
54
Q

5 instances where you would see a decrease in plasama cholinesterase activity and and increase DOA sux

A
  1. pregnancy
  2. newborns
  3. acute infections
  4. muscular dystrophy
  5. MI
55
Q

Atracurium should be refrigerated because

A. it has a high-risk for bacterial growth

B. It loses potency if not regrigerated

C. Can precipitate at room temp

D. produces less pain on injection when cold

A

B. loses potency if not refrigerated

56
Q

The recommended unregrigerated shelf life of atracurium

A

14 days

57
Q

Why is edrophonium a weaker reversal agent than neostigmine?

A. It binds using ionic bonds

B. It binds using covalent bonds

C. It has a lower molecular weight

D. It has a lower ED95

A

A. It binds using ionic bonds

(Neo binds using strong, covalent bonds)

58
Q

Select 2 disorders wehre sux is avoided

A. Myasthenia gavis

B. Myotonia

C. Muscular dystrophy

D. SLE

A

Myotonia and Muscualr distrophy

59
Q

What receptors does sugammadex bind?

  • Postjunctional nicotnic acetylcholine receptors
  • Prejunctional nicotinic acetylcholine receptors
  • Both pre and post
  • None
A

None

-it is biologically inactive and binds directly to steroidal neuromuscular blocking drugs

60
Q

What acetylcholinesterase inhibitor is used both as a NDMR reversal and for the treatment of myasthenia gravis?

A

Pyridostigmine

61
Q

T/F- hypokalemia can lead to prolongation of NMB

A

True

-more K inside the cell makes it harder to depolarize (i think thats the reasoning lol)

62
Q

T/F- acidosis and hypercarbia can prolong the effects of NMB

A

True

63
Q

T/F- with acute administration of phenytoin and carbamazepime, NMB can be signficantly potentiated/prolonged.

A

True

-chronic adminsitration, however, leads to significanlty decreased DOA

64
Q

Which patient is most likely to experience myalgia following the administration of succinylcholine?

A. A healthy, 28 year-old female undergoing knee arthroscopy

B. A 67 year-old male with congestive heart failure

C. A 59 year-old female with COPD undergoing blepharoplasty

D. A healthy, 9 year-old female undergoing middle ear surgery

A

A. A healthy, 28 year-old female undergoing knee arthroscopy

-healthy, young adults underoing minor procedures are most likely to be affected

65
Q

Why would neostigmine prolong the effects of sux?

A

because it produces a signficiant decrease in pseudocholinesterase activity (the enzyme that breaks down sux)

66
Q

Which of the following effects of sux administration will not be prevented by the administration of a defasiculating dose of a nondepolarizing muscle relaxant?

A. Increase in intraocular pressure

B. Myalgia

C. Increase in intragastric pressure

D. Increase in intracranial pressure

A

A

67
Q

What is the appropriate intravenous dose for succinylcholine in a 3 month-old patient?

A. 0.5-0.75 mg/kg

B. 1.0-1.2 mg/kg

C. 1.5-2.0 mg/kg

D. 2.0-3.0 mg/kg

A

D. 2.0-3.0 mg/kg

(Kids are 1.5-2; infants are 2-3mg/kg (big bags of water))

68
Q

What may be responsible for the prolonged duration of action of vecuronium when used in intensive care unit patients?

A. Decreased hepatic blood flow

B. Decreased renal function

C. Decreased plasma cholinesterase activity

D. Down-regulation of nicotinic cholinergic receptors

A

B. decreased renal function

metabolite 3-OH is excreted by the kidneys

69
Q

You administer succinylcholine in a high dose to a patient that has a pseudocholinesterase deficiency. What results would you expect to see?

A. A prolonged phase 1 block

B. A prolonged phase 2 block

C. A normal phase 1 block

D. A normal phase 2 block

A

B. prlonged phase 2 block

Small doses of succinylcholine in a normal patient produce a phase 1 block. High doses of succinylcholine or succinylcholine administered to patients with a pseudocholinesterase deficiency will produce a phase 2 block.

70
Q
A

*Pharmacology (25 decks)

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