NMBS

Question 1

NMBs block

Answer 1

the binding of ACh on NRs on the motor end plate

Question 2

When are NMBs used

Answer 2

During general anesthesia

Question 3

Where are NMBs administered

Answer 3

parenterally

Question 4

Where do NMBs act

Answer 4

The act peripherally

Question 5

NMBS are similar to ACh how?

Answer 5

are structurally similar to ACh:
they act at the post junction NRs

Question 6

MOA of NMD agonists

Answer 6

They are depolarising NMBs:
1. mimic ACh
2.cause a persisitng state of depolarisation

Question 7

MOA of anatgonist NMDs

Answer 7

They are non-depolarising NMBs
1. are competitve inhibitors of ACh
2. prevent depolarisation

Question 8

Which are the Depolarising NMBs

Answer 8

Succinylcholine (suxamethonium)

Question 9

Which are the non-depolarising NMBs?
Isoquinoline derivatives

Answer 9

d-tubocurarine
Mivacurium
Atracurium

Question 10

Which are the non-depolarising NMBs?
Steroid derivatives

Answer 10

Rocuronium
Pancuronium
Vecuronium

Question 11

MOA of Succinycholine

Answer 11

ACh agonist that causes rapid muscle contractions until the muscle becomes rigid
=flaccid paralysis

Question 12

PK of Succinylcholine

Answer 12

M: liver(CYP450), plasma (pseudocholinesterases)
E: renal, only 10% of excreted drug is unchanged

Question 13

CI of succinylcholine

Answer 13

Hx of Malignant hyperthermia
Hyperkalaemia

Question 14

DI of Succinylcholine

Answer 14

Cholinesterase inhibitors
Digoxin

Question 15

AE of Succinylcholine

Answer 15

Malignant Hyperthermia
Myalgia
Bradycardia
Hypotension
Increased IOP
Inxreased intragastric pressure
Increased salivation

Question 16

How are AEs bradycardia, hypotension and increased salivation treated?

Answer 16

Atropine: used prior to repeated doses or continued infusion

Question 17

MOA of Atropine as reversal drug?

Answer 17

competitively antagonises muscarinic act.

Question 18

MOA of Non-depolarising NMBs

Answer 18

-competitively antagonise ACh
-prevent EPP (end-plate potential)
-prevent Ca release from SR
-causes muscle relaxation

Question 19

Are non-depolarising NMBs reversible?

Answer 19

Yes

Question 20

Non-depolarising NMBs release

Answer 20

Histamine EXCEPT Rocuronium

Question 21

Histamine release causes

Answer 21

Hypotension
Bradycardia

Question 22

Onset of Action of non-depolarising NMBs

Answer 22

R: 1-2 mins
M: 2-3mins
A: 2-3mins
V: 2-3 mins
d-t: 3-5mins
P: 3-5mins

Question 23

DOA of non-depolarising NMBs

Answer 23

M: 10-20 mins
A: 20-30mins
V: 20-30mins
R: 30-40 mins
d-t: 30-50 mins
P: 40-60mins

Question 24

Metabolism of Mivacurium

Answer 24

Plasma Cholinesterases

Question 25

AE of Mivacurium

Answer 25

Prolonged NMJ blockade
Hypotension+ Bronchospasm
Bradycardia

Question 26

Metabolism and Excretion of Atracurium

Answer 26

M: spontaneous degradation at body temp. and pH
E: renal mainly

Question 27

AE of Atracurium

Answer 27

Hypotension
Maybe Bronchospasm

Question 28

Metabolism and Excretion of Vecuronium

Answer 28

M: Liver
E: bile mainly

Question 29

AE of Vecuronium

Answer 29

Bronchospasm
Anaphylaxis

Question 30

Metabolism and Excretion of Rocuronium

Answer 30

M: Liver
E: Bile

Question 31

AE of Rocuronium

Answer 31

Anaphylaxis

Question 32

Metabolism and Excretion of d-tubocurarine

Answer 32

M: Hoffman degradation and hepatic
E: renal mainly

Question 33

AE of d-tubocurarine

Answer 33

Hypotension + Bronchospasm

Question 34

Metabolism and Excretion of Pancuronium

Answer 34

M: Liver (small amount)
E: renally–> mainly unchanged

Question 35

AE of Pancuronium

Answer 35

Tachycardia
Elevation in BP

Question 36

Which is the drug of choice in Liver Failure?
NMBs

Answer 36

Atracuronium

Question 37

Which drug is used for NMJ Blockade reversal?

Answer 37

Neostigmine
Blocks ACh hydrolysis
=accumulation of ACh
=NMJ blocker displacement
=incr. ACh effects