Block 2 Exam Flashcards
What does neuromuscular blocking drugs cause?
temporary paralysis of skeletal muscles and muscle relaxation
Neuromuscular blocking drugs prevent interaction between what two receptors?
ACh and Nicotinic receptors
Neuromuscular blocking drugs act what type of receptor
nicotinic acetylcholine receptor Nm
The neuromuscular blocking drug cycle involves what?
depolarization = contraction
repolarization = relaxation
Non-depolarizing blockers are also known as?
Competitive blockers
Depolarizing blockers are also known as?
Non-competitive blockers
For NDMB, what are the long-acting drugs?
d-tubocurarine, Gallamine, Pancuronium, Doxacurarium, Pipercuronium
For NDMB, what are the intermediate-acting drugs?
Vecuronium, Atracurium, Rocuronium
For NDMB, what are the short acting drugs?
Mivacurium
What drugs is associated with DMB?
Succinylcholine and Decamethonium
Centrally acting agents are associated with what drugs?
Dantrolene sodium Quinine
NDMB- Mechanism of action (MOA) deal with what two drugs? They are also known as the new generation.
pancuronium and gallamine
NDMB prevents the binding of what and thus prevents what?
Prevents the binding of ACh at the nicotinic receptors, this prevents contraction
Competitive NDMB causes what?
transient relief of the block can be achieved by increasing ACh levels at the synaptic cleft (i.e. use cholinesterase inhibitors
NDMB-Pharmacokinetics has what type of characteristics
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
Pancuronium characteristics
not metabolized
excreted through kidney
duration of action 2-3 hours
Rocu- and Vecu-ronium
liver metabolism
DOA increases in liver diseases
Duration of action 30-40 min
In the general anesthesia, NDMB is used to…
facilitate tracheal intubation
induce muscle relaxation
make orthopedic surgery easy
reduce the dose of anesthetics
What is the order of paralysis?
fingers, extraocular, hands, feet, arm, leg, neck, face, trunk, intercostal muscles, diaphragm and respiration stops
What are the adverse effects of NDMB?
Hypotension, increased respiratory secretion, bronchospasms.
Hyperkalemia
Increased intraocular pressure (Blocks the schlem canal which increases intraocular pressure)
Cholinesterase inhibitors i.e. Neostigmine
decrease the effectiveness of NDMB
Aminoglycosides antibiotics i.e. streptomycin
prolong action of NDMB
Calcium Channel Blockers i.e. verapamil
prolong action of NDMB
Halogenated anesthetics i.e. isoflurane
prolong action of NDMB
DMB - MOA; what occurs during phase I?
initially, agents activate Nicotinic ACh receptor, opening the channels. This elicits endplate membrane potential with depolarization to -55 mv.
DMB- MOA, what occurs during phase II
continued infusion or activation - flaccid paralysis (due to depolarization blockade produce initial fasciculations and postoperative pain
The use for DMB; Succinylcholine is
used as muscle relaxant for passing endotracheal tube
Adjuvant drugs in surgical anesthesia
Succinylcholine has effects similar in action to
ACh, but longer acting comparatively. t1/2 (min)
Halothane combination with DMB may produce what?
malignant hyperthermia in some genetically susceptible people
What is the treatment for Halothane and DMB interaction?
rapid cooling of the body and dantrolene
AChE inhibitors augment what type of effects?
DMB
What factors prolonging the neuromuscular blockage? Age?
Disease?
Age: neonates; old age
Disease: Obesity, Hepatic disease (both depolarizer & NDMB), Renal disease ( only NDMB), Neuromuscular disease
What factors prolonging the neuromuscular blockage? Drugs?
1) Inhalational agents (Prolong the blockade of both depolarizers & NDMB) 2) Antibiotics (Both depolarizers & NDMB)eg.aminoglycosides, tetracyclines; dantrolene; calcium channel blockers
What factors prolonging the neuromuscular blockage? Electrolytes?
hypokalemia, hypocalcemia, hypermagnesia
What factors prolonging the neuromuscular blockage? Others?
Hypothermia (decreases), metabolic acidosis.
Drugs that antagonise NMB
Cholinesterase inhibitors
Calcium
Phenytoin
Carbamazepine
Azathioprine
Steroids
What are some ideal NMB agents?
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
What is the DIFFERENCE BETWEEN COMPETITIVE AND NON-COMPETITIVE BLOCKERS? Paralysis in human
Flaccid = competetive blocker
Fasiculation results in flaccidity
Flaccid = competetive
spastic = non competetive
rat>rabbit>cat
cat> rabbit>rat
Antagonism block
no effect
Synergistic
No effect
Fingers-eyes-limbs-neck-face-trunk-intercostal muscles
Neck-limbs-face-jaw-eyes-pharynx-trunk-intercostal muscles
True or False
Central and Direct Muscle Relaxants are Chemically and pharmacologically different from neuromuscular blockers
True
Depolarization of central and direct muscle relaxants trigger the release of what?
release of calcium ions from sarcoplasmic reticulum is reduced.
Does not affect neuromuscular transmission orEPP
but uncouples contraction from depolarization of the muscle membrane
Clinical uses of centrally acting muscle relaxants are
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
Fast contracting twitch muscles are affected more than
slow contracting
Reduce skeletal muscle tone by a selective action in the cerebrospinal axis
without altering consciousness
Has no effect on neuromuscular transmission and on muscle fibres
Reduces rigidity, spasticity and hyperreflexia.
