Block 2 Exam Flashcards

1
Q

What does neuromuscular blocking drugs cause?

A

temporary paralysis of skeletal muscles and muscle relaxation

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2
Q

Neuromuscular blocking drugs prevent interaction between what two receptors?

A

ACh and Nicotinic receptors

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3
Q

Neuromuscular blocking drugs act what type of receptor

A

nicotinic acetylcholine receptor Nm

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4
Q

The neuromuscular blocking drug cycle involves what?

A

depolarization = contraction
repolarization = relaxation

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5
Q

Non-depolarizing blockers are also known as?

A

Competitive blockers

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6
Q

Depolarizing blockers are also known as?

A

Non-competitive blockers

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7
Q

For NDMB, what are the long-acting drugs?

A

d-tubocurarine, Gallamine, Pancuronium, Doxacurarium, Pipercuronium

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8
Q

For NDMB, what are the intermediate-acting drugs?

A

Vecuronium, Atracurium, Rocuronium

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9
Q

For NDMB, what are the short acting drugs?

A

Mivacurium

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10
Q

What drugs is associated with DMB?

A

Succinylcholine and Decamethonium

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11
Q

Centrally acting agents are associated with what drugs?

A

Dantrolene sodium Quinine

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12
Q

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

A

pancuronium and gallamine

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13
Q

NDMB prevents the binding of what and thus prevents what?

A

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

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14
Q

Competitive NDMB causes what?

A

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

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15
Q

NDMB-Pharmacokinetics has what type of characteristics

A

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

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16
Q

Pancuronium characteristics

A

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

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17
Q

Rocu- and Vecu-ronium

A

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

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18
Q

In the general anesthesia, NDMB is used to…

A

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

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19
Q

What is the order of paralysis?

A

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

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20
Q

What are the adverse effects of NDMB?

A

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

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21
Q

Cholinesterase inhibitors i.e. Neostigmine

A

decrease the effectiveness of NDMB

22
Q

Aminoglycosides antibiotics i.e. streptomycin

A

prolong action of NDMB

23
Q

Calcium Channel Blockers i.e. verapamil

A

prolong action of NDMB

24
Q

Halogenated anesthetics i.e. isoflurane

A

prolong action of NDMB

25
Q

DMB - MOA; what occurs during phase I?

A

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

26
Q

DMB- MOA, what occurs during phase II

A

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

27
Q

The use for DMB; Succinylcholine is

A

used as muscle relaxant for passing endotracheal tube

Adjuvant drugs in surgical anesthesia

28
Q

Succinylcholine has effects similar in action to

A

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

29
Q

Halothane combination with DMB may produce what?

A

malignant hyperthermia in some genetically susceptible people

30
Q

What is the treatment for Halothane and DMB interaction?

A

rapid cooling of the body and dantrolene

31
Q

AChE inhibitors augment what type of effects?

A

DMB

32
Q

What factors prolonging the neuromuscular blockage? Age?
Disease?

A

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

33
Q

What factors prolonging the neuromuscular blockage? Drugs?

A

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

34
Q

What factors prolonging the neuromuscular blockage? Electrolytes?

A

hypokalemia, hypocalcemia, hypermagnesia

35
Q

What factors prolonging the neuromuscular blockage? Others?

A

Hypothermia (decreases), metabolic acidosis.

36
Q

Drugs that antagonise NMB

A

Cholinesterase inhibitors
Calcium
Phenytoin
Carbamazepine
Azathioprine
Steroids

37
Q

What are some ideal NMB agents?

A

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

38
Q

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

A

Flaccid = competetive blocker
Fasiculation results in flaccidity

39
Q
A

Flaccid = competetive
spastic = non competetive

40
Q
A

rat>rabbit>cat
cat> rabbit>rat

41
Q
A

Antagonism block
no effect

42
Q
A

Synergistic
No effect

43
Q
A

Fingers-eyes-limbs-neck-face-trunk-intercostal muscles

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

44
Q

True or False

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

A

True

45
Q

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

A

release of calcium ions from sarcoplasmic reticulum is reduced.

46
Q

Does not affect neuromuscular transmission orEPP

A

but uncouples contraction from depolarization of the muscle membrane

47
Q

Clinical uses of centrally acting muscle relaxants are

A

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

48
Q

Fast contracting twitch muscles are affected more than

A

slow contracting

49
Q

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

A

without altering consciousness

50
Q

Has no effect on neuromuscular transmission and on muscle fibres

A

Reduces rigidity, spasticity and hyperreflexia.