Progidy- Neuromusuclar blockers

Question 1

What is ipratropium?

Answer 1

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

Question 2

Treatment for central anticholinergic syndrome

Answer 2

-anticholinesterase physostigmine 1-2mg IV

Question 3

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

Answer 3

5%

Question 4

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

Answer 4

True

Des > sevo > iso> n20

Question 5

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

Answer 5

decreased

smokers [love] A Cold PBR = enzyme induction

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

*increases metabolizing enzymes- will metabolize roc/vec faster

Question 6

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

Answer 6

true

Question 7

How does ephedrine affect NMBs?

Answer 7

it can speed the onset of roc

Question 8

Which AchE inhibitor has the shortest DOA and why?

Answer 8

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

Question 9

Why is edrophonium administered with Atropine instead of glyco?

Answer 9

bc of it’s fast onset

Question 10

What accounts for the short duration of mivacurium

Answer 10

bc it’s rapidly hydrolyzed by plasma cholinesterases

Question 11

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?

Answer 11

Pseudocholinesterase

-Sux contraindicated

Question 12

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

Answer 12

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

Question 13

How does hypothermia affect neuromuscular blockade?

Answer 13

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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.

Question 16

Half lives of: Roc, Vec, and Panc

Answer 16

Roc- 0.7 hrs

Vec- 0.9hrs

Panc- 1.7hrs

Question 17

DOA of Roc

Answer 17

30-90 minutes

Question 18

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

Answer 18

kids - 30 mins

adults - 60 mins

elderly - 130 mins

Question 19

Elimination half life of sux

Answer 19

47 seconds….

Question 20

intubating dose of sux and how long before effect

Answer 20

1-1.5mg/kg

30-60 seconds

Question 21

*Metabolites of sux

Answer 21

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

Question 22

intubating dose of vec*

Answer 22

0.1mg/kg

Question 23

Intubating dose of Panc

Answer 23

0.06mg/kg

Isn’t this the ED 95?

Question 24

Intubating dose of atracurium

Answer 24

0.5mg/kg

Question 25

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

Answer 25

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.

Question 26

Intubating dose of cistatracurium

Question 27

What two conditions is sux contraindicated in?

Answer 27

Duchenne's muscular dystrophy and guillain-barre (upregulation with extrajunctional receptors - massive K release)

Question 28

IM dose of sux

Answer 28

4mg/kg

Question 29

DOA of sux

Answer 29

10-15 mins

Question 30

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

Answer 30

Kids require a higher dose of sux: 1.5-2mg/kg Infants even higher: 2-3mg/kg

Question 31

T/F fasciculations from sux are worse in kids

Answer 31

false- uncommon in kids

Question 32

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?

Answer 32

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

Question 33

Max dose of neostigmine

Answer 33

0.07mg/kg OR 5 mg

Question 34

which nerve supplies the adductor pollicis muscle

Answer 34

The ulnar nerve

Question 35

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

Answer 35

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

Question 36

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

Answer 36

Facial nerve

Question 37

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

Answer 37

false

Question 38

Someone asks you "what actuallly is MH?"

Answer 38

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

Question 39

Clinical manifestations of MH

Answer 39

unexplained sudden increase in HR, RR, ETCO2 + masseter spasm or total body rigidiety

Question 40

T/F- MH is a autosomal- recessive disorder

Answer 40

False- autosomal DOMINANT (Duchennes is X-LINKED RECESSIVE)

Question 41

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

Answer 41

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

Question 42

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

Answer 42

false

Question 43

Sux increases IOP up to \_\_\_\_\_mmHg for \_\_\_\_minutes

Answer 43

15mmhg for 5 minutes

Question 44

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

Answer 44

thiopental

Question 45

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

Answer 45

Myasthenia gravis -hallmark sign = muscle weakeness

Question 47

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

Answer 47

Vec & Cist - 0.05mg/kg

Question 48

ED 95 of Panc

Answer 48

0.07mg/kg

Question 49

ED95 of Atracurium

Answer 49

0.25mg/kg

Question 50

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

Answer 50

true

Question 51

Which agent can prolong the effect of SUX? - Phenytoin - Metoclopramide - Metronidazole - Magnesium

Answer 51

Metcoclopramide -it inihibits plasma cholinesterase

Question 52

Which cholinesterase inhibitor has the shortest DOA - Physostigmine - Edrophonium - Pyridostigimine - Neostigmine

Answer 52

Edrophonium

Question 53

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

Answer 53

A. Hypersensitivity reaction * usually seen within 4 minutes of administration * CV collapse can be treated with fluid resusitation and high-dose epi

Question 54

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

Answer 54

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

Question 55

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

Answer 55

B. loses potency if not refrigerated

Question 56

The recommended unregrigerated shelf life of atracurium

Answer 56

14 days

Question 57

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

Answer 57

A. It binds using ionic bonds (Neo binds using strong, covalent bonds)

Question 58

Select 2 disorders wehre sux is avoided A. Myasthenia gavis B. Myotonia C. Muscular dystrophy D. SLE

Answer 58

Myotonia and Muscualr distrophy

Question 59

What receptors does sugammadex bind? - Postjunctional nicotnic acetylcholine receptors - Prejunctional nicotinic acetylcholine receptors - Both pre and post - None

Answer 59

None -it is biologically inactive and binds directly to steroidal neuromuscular blocking drugs

Question 60

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

Answer 60

Pyridostigmine

Question 61

T/F- hypokalemia can lead to prolongation of NMB

Answer 61

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

Question 62

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

Answer 62

True

Question 63

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

Answer 63

True -chronic adminsitration, however, leads to significanlty decreased DOA

Question 64

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

Answer 64

**A. A healthy, 28 year-old female undergoing knee arthroscopy** -healthy, young adults underoing minor procedures are most likely to be affected

Question 65

Why would neostigmine prolong the effects of sux?

Answer 65

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

Question 66

Which of the following effects of sux administration will not be prevented by the administration of a defasiculating dose of a nondepolarizing muscle relaxant? ## Footnote A. Increase in intraocular pressure B. Myalgia C. Increase in intragastric pressure D. Increase in intracranial pressure

Answer 66

A

Question 67

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

Answer 67

D. 2.0-3.0 mg/kg (Kids are 1.5-2; infants are 2-3mg/kg (big bags of water))

Question 68

What may be responsible for the prolonged duration of action of vecuronium when used in intensive care unit patients? ## Footnote A. Decreased hepatic blood flow B. Decreased renal function C. Decreased plasma cholinesterase activity D. Down-regulation of nicotinic cholinergic receptors

Answer 68

B. decreased renal function metabolite 3-OH is excreted by the kidneys

Question 69

You administer succinylcholine in a high dose to a patient that has a pseudocholinesterase deficiency. What results would you expect to see? ## Footnote A. A prolonged phase 1 block B. A prolonged phase 2 block C. A normal phase 1 block D. A normal phase 2 block

Answer 69

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.