Block 2 Exam

Question 1

What does neuromuscular blocking drugs cause?

Answer 1

temporary paralysis of skeletal muscles and muscle relaxation

Question 2

Neuromuscular blocking drugs prevent interaction between what two receptors?

Answer 2

ACh and Nicotinic receptors

Question 3

Neuromuscular blocking drugs act what type of receptor

Answer 3

nicotinic acetylcholine receptor Nm

Question 4

The neuromuscular blocking drug cycle involves what?

Answer 4

depolarization = contraction
repolarization = relaxation

Question 5

Non-depolarizing blockers are also known as?

Answer 5

Competitive blockers

Question 6

Depolarizing blockers are also known as?

Answer 6

Non-competitive blockers

Question 7

For NDMB, what are the long-acting drugs?

Answer 7

d-tubocurarine, Gallamine, Pancuronium, Doxacurarium, Pipercuronium

Question 8

For NDMB, what are the intermediate-acting drugs?

Answer 8

Vecuronium, Atracurium, Rocuronium

Question 9

For NDMB, what are the short acting drugs?

Answer 9

Mivacurium

Question 10

What drugs is associated with DMB?

Answer 10

Succinylcholine and Decamethonium

Question 11

Centrally acting agents are associated with what drugs?

Answer 11

Dantrolene sodium Quinine

Question 12

NDMB- Mechanism of action (MOA) deal with what two drugs? They are also known as the new generation.

Answer 12

pancuronium and gallamine

Question 13

NDMB prevents the binding of what and thus prevents what?

Answer 13

Prevents the binding of ACh at the nicotinic receptors, this prevents contraction

Question 14

Competitive NDMB causes what?

Answer 14

transient relief of the block can be achieved by increasing ACh levels at the synaptic cleft (i.e. use cholinesterase inhibitors

Question 15

NDMB-Pharmacokinetics has what type of characteristics

Answer 15

poor oral absorption - hence its given i.v.
poor membrane permeability, does not cross the BBB
Generally excreted unchanged (i.e. not metabolized). low metabolism

Question 16

Pancuronium characteristics

Answer 16

not metabolized
excreted through kidney
duration of action 2-3 hours

Question 17

Rocu- and Vecu-ronium

Answer 17

liver metabolism
DOA increases in liver diseases
Duration of action 30-40 min

Question 18

In the general anesthesia, NDMB is used to…

Answer 18

facilitate tracheal intubation
induce muscle relaxation
make orthopedic surgery easy
reduce the dose of anesthetics

Question 19

What is the order of paralysis?

Answer 19

fingers, extraocular, hands, feet, arm, leg, neck, face, trunk, intercostal muscles, diaphragm and respiration stops

Question 20

What are the adverse effects of NDMB?

Answer 20

Hypotension, increased respiratory secretion, bronchospasms.
Hyperkalemia
Increased intraocular pressure (Blocks the schlem canal which increases intraocular pressure)

Question 21

Cholinesterase inhibitors i.e. Neostigmine

Answer 21

decrease the effectiveness of NDMB

Question 22

Aminoglycosides antibiotics i.e. streptomycin

Answer 22

prolong action of NDMB

Question 23

Calcium Channel Blockers i.e. verapamil

Answer 23

prolong action of NDMB

Question 24

Halogenated anesthetics i.e. isoflurane

Answer 24

prolong action of NDMB

Question 25

DMB - MOA; what occurs during phase I?

Answer 25

initially, agents activate Nicotinic ACh receptor, opening the channels. This elicits endplate membrane potential with depolarization to -55 mv.  

Question 26

DMB- MOA, what occurs during phase II

Answer 26

continued infusion or activation - flaccid paralysis (due to depolarization blockade produce initial fasciculations and postoperative pain

Question 27

The use for DMB; Succinylcholine is

Answer 27

used as muscle relaxant for passing endotracheal tube Adjuvant drugs in surgical anesthesia

Question 28

Succinylcholine has effects similar in action to

Answer 28

ACh, but longer acting comparatively. t1/2 (min)

Question 29

Halothane combination with DMB may produce what?

Answer 29

malignant hyperthermia in some genetically susceptible people

Question 30

What is the treatment for Halothane and DMB interaction?

Answer 30

rapid cooling of the body and dantrolene

Question 31

AChE inhibitors augment what type of effects?

Answer 31

DMB

Question 32

What factors prolonging the neuromuscular blockage? Age? Disease?

Answer 32

Age: neonates; old age Disease: Obesity, Hepatic disease (both depolarizer & NDMB), Renal disease ( only NDMB), Neuromuscular disease

Question 33

What factors prolonging the neuromuscular blockage? Drugs?

Answer 33

1) Inhalational agents (Prolong the blockade of both depolarizers & NDMB) 2) Antibiotics (Both depolarizers & NDMB)eg.aminoglycosides, tetracyclines; dantrolene; calcium channel blockers

Question 34

What factors prolonging the neuromuscular blockage? Electrolytes?

Answer 34

hypokalemia, hypocalcemia, hypermagnesia

Question 35

What factors prolonging the neuromuscular blockage? Others?

Answer 35

Hypothermia (decreases), metabolic acidosis.

Question 36

Drugs that antagonise NMB

Answer 36

Cholinesterase inhibitors Calcium Phenytoin Carbamazepine Azathioprine Steroids

Question 37

What are some ideal NMB agents?

Answer 37

Stable in aqueous solution High selectivity and potency Action confined to neuromuscular junction Rapid onset (<30 min) No cardiovascular side-effects Non biological metabolism/elimination Rapid recovery Non depolarising mechanism of action Reversible by cholinesterase inhibitor No significant transfer across placenta Lack of histamine release Compatible with other drugs and solution injected during anesthesia Lack of toxicity

Question 38

What is the DIFFERENCE BETWEEN COMPETITIVE AND NON-COMPETITIVE BLOCKERS? Paralysis in human

Answer 38

Flaccid = competetive blocker Fasiculation results in flaccidity

Answer 39

Flaccid = competetive spastic = non competetive

Answer 40

rat>rabbit>cat cat> rabbit>rat

Answer 41

Antagonism block no effect

Answer 42

Synergistic No effect

Answer 43

Fingers-eyes-limbs-neck-face-trunk-intercostal muscles Neck-limbs-face-jaw-eyes-pharynx-trunk-intercostal muscles

Question 44

True or False Central and Direct Muscle Relaxants are Chemically and pharmacologically different from neuromuscular blockers

Answer 44

True

Question 45

Depolarization of central and direct muscle relaxants trigger the release of what?

Answer 45

release of calcium ions from sarcoplasmic reticulum is reduced.

Question 46

Does not affect neuromuscular transmission or EPP

Answer 46

but uncouples contraction from depolarization of the muscle membrane

Question 47

Clinical uses of centrally acting muscle relaxants are

Answer 47

Acute muscle spasms Torticollis Lumbago - pain in the muscles and joints of the lower back. Backache Neuralgia - stabbing, burning, and often severe pain due to an irritated or damaged nerve Muscle pull Anxiety Tension Spastic neurological ailments Tetanus Electoconvulsive therapy Orthopaedic manipulation

Question 48

Fast contracting twitch muscles are affected more than

Answer 48

slow contracting

Question 49

Reduce skeletal muscle tone by a selective action in the cerebrospinal axis

Answer 49

without altering consciousness

Question 50

Has no effect on neuromuscular transmission and on muscle fibres

Answer 50

Reduces rigidity, spasticity and hyperreflexia.