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1. Pharmacology > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

What is the purpose of neuromuscular blocking drugs

A

Temporary paralysis of skeletal m. and m. relaxation
Prevent interaction between ACh and Nicotinic receptors
Act as nicotinic acetylcholine receptor Nm

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2
Q

MOA of competitive (non-polarizing) neuromuscular blocking drugs

A

Competitive ACh antagonism –> ACh can’t act –> Repolarized plate –> relaxation
NO DEPOLARIZATION (contraction)

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3
Q

How is the block relieved?

A

By increasing ACh levels at the synaptic cleft (Ach competing with the drugs)
Ex: use cholinesterase inhibitors

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4
Q

MOA of depolarizing neuromuscular blocking drugs

A

Sustained repolarization and later block –> ACh cannot act –> depolarization plate
CONSTANT DEPOLIZATION in 2 phases

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5
Q

Phases of depolarizing neuromuscular blocking

A
  1. Agents activate Nicotinic ACh receptor –> channels open –> endplate membrane potential to -55 mv —> flaccid paralysis due to continued activation
  2. Membrane repolarizes but receptor desensitized to ACh
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6
Q

Centrally acting neuromuscular blockers

A

Dantrolene sodium and Quinine

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7
Q

Peripherally acting neuromuscular blockers

A

Depolarizing blockers (non competitive)
Non-depolarizing blockers (competitive)

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8
Q

Depolarizing blockers

A

Succinylcholine and Decamethonium

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9
Q

Long acting non depolarizing blockers

A

D-tubocurarine, Gallamine, pancuronium, doxacurarium, pipercuronium

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10
Q

Intermediate acting non depolarizing blockers

A

Vecuronium, atracirum, roccuronium

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11
Q

Short acting non depolarizing blocker

A

Mivacirum

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12
Q

Non-depolarizing neuromuscular blockers pharmokinetics

A

Poor oral absorption (IV)
Poor membrane permeability (doesn’t cross BBB)
Generally excreted unchanged (not metabolized)
Low metabolism

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13
Q

Pancuronium

A

Not metabolized (long acting, depolarizing blocker)
Excreted through the kidney
Duration of action is 2-3 hours
Onset of action: 2-6 minutes

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14
Q

Vecuronium and roccuronium pharmokinetics

A

Liver metabolism
DOA increases in the liver
Duration of action is 30-40 minutes
Onset of action: 2-6 minutes

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15
Q

Non depolarizing blockers therapeutic uses

A

In general anesthesia: facilitate tracheal intubation
Induce muscle relaxation
Make orthopedic surgery east
Reduce dose of anesthetics
(descending paralysis)

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16
Q

Non depolarizing blockers adverse affects

A

Hypotension, increased respiratory secretion, bronchospasms
Hyperkalemia
Increased intraocular pressure

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17
Q

Which NDMB drugs prolong the action of NDMB?

A

Aminoglycosides antibiotics (streptomycin)
Calcium channel blockers (Verpamil)
Halogenated anesthetics (Isoflurane)

18
Q

Cholinesterase inhibitors (NDMB)

A

Neostigme- decreases the effectiveness of NDMB

19
Q

Calcium channel blockers

A

Verpamil- prolongs the action of NDMB

20
Q

Halogenated anesthetics

A

Isoflurane will prolong

21
Q

Depolarizing muscle blockers uses

A

Adjuvant drugs in surgical anesthesia
Effects similar in action to ACh, but longer acting

22
Q

Succinylcholine uses

A

Only depolarizing drug in clinical use
Use muscle relaxant for passing endotracheal tube

23
Q

DMB interactions

A

Halothane with DMB produces malignant hyperthermia in some
Tx: rapid cooling of the body and dantrolene

24
Q

____________ augment DMB effects

A

AChE inhibitors

25
Q

How does age prolong the neuromuscular blockade?

A

Neonates or old age

26
Q

How does disease prolong the neuromuscular blockade?

A

Obesity, hepatic disease, renal disease, neuromuscular disease

27
Q

How does drugs prolong the neuromuscular blockade?

A

Inhalational agents will prolong the blockade of depolarizes and NDMB
Antibiotics(dantrolene, tetracyclines)

28
Q

How does electrolytes prolong the neuromuscular blockade?

A

Hypokalemia, hypermagnesia, hypocalcemia, hypothermia and metabolic acidosis

29
Q

Drug that antagonize NMB

A

Cholinesterase inhibitors
Calcium
Phenytoin
Carbamazepine
Azathioprine
Steroids

30
Q

Paralysis in humans

A

Competitive: Flaccid
Depolarizing: Fasciculation resulting in flaccidity

31
Q

Paralysis in chicks

A

Competitive: Flaccid
Depolarizing: Splastic

32
Q

Species sensitivity

A

Competitive: Rat> rabbit > cat
Depolarizing: cat<rabbit < rat

33
Q

Neostigmine

A

Competitive: Antagonism block
Depolarizing: no effect

34
Q

Inhalation anesthetic (ether)

A

Competitive: Synergist
Depolarizing: no effect

35
Q

Order of paralysis

A

Competitive: fingers –> eyes –> limbs –> neck –> face –> trunk –> intercostal muscles
Depolarizing: neck –> limbs –> jaw –> eyes –> pharynx –> trunk –> intercostal muscles

36
Q

Central and direct muscle relaxants

A
  1. Doesn’t affect neuromuscular transmission of EPP
  2. Depolarization triggered release of calcium ion from sarcoplasmic reticulum reduced
  3. Fast contracting twitch muscles
  4. Reduce muscle tone by a selective action in cerebrospinal axis without altering consciousness
  5. No effect on neuromuscular transmission
  6. Reduces rigidity, spasticity and hyperreflexia
37
Q

Centrally acting muscle reactants

A

Muscle tone decreased
No reduction in voluntary movements
Postsynap. relfexes in CNS inhibited
CNS depression
Administered orally/ parentally
Value in the treatment of spastic muscle spasms, tetanus

38
Q

Peripherally acting muscle relaxants

A

Muscle paralysis
Voluntary movements are lost
Neuromuscular transmission is blocked
CNS effect no significant
Administed IV
Used for short procedures

39
Q

Dantrolene (central muscle relaxant)

A

Absorbed orally
Penetrated BBB and produces sedation
Metabolized by liver, excreted by kidney
Malignant Hyperthermia

40
Q

Adverse effects of dantroene

A

Muscle weakness, sedation, malaise, light headedness

41
Q

Other central muscle relaxants

A

Mephenesin group: mephenesin, carisoprodol, chlorzoxazone
Benzodiazepines (diazepam)
GABA derivatives: baclofen

42
Q

Clinical uses to centrally acting muscle relaxants

A

Acute muscle spasms, tension, torticollis, lumbago, neuralgia, anxiety, tetanus

1. Pharmacology (29 decks)

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