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2/4/2013

Dr. Ahmed ALArwali

Depolarizing neuromuscular blocking agent


Succinylcholine
M.O.A: Agonist at nicotinic acetylcholine (ACh)
receptors, especially at neuromuscular junctions depolarizes may stimulate ganglionic nicotinic ACh and cardiac muscarinic ACh receptors.

Effect: Initial depolarization causes transient contractions, followed by prolonged flaccid paralysis depolarization is then followed by repolarization that is also accompanied by paralysis

Dr. Ahmed ALArwali

2/4/2013

Depolarizing neuromuscular blocking agent


C.U: Placement of tracheal tube at start of anesthetic
procedure rarely, control of muscle contractions in status epilepticus. Pharmacokinetics, Interactions : Rapid metabolism by plasma cholinesterase normal duration, ~5 min Toxicities :
Arrhythmias . hyperkalemia. transient increased intra-abdominal Pressure. transient increased intraocular pressure . postoperative muscle pain.

Nondepolarizing neuromuscular blocking agents


d-Tubocurarine
M.O.A: Competitive antagonist at nACh receptors,

especially at neuromuscular junctions. Effect: Prevents depolarization by ACh, causes flaccid paralysis can cause histamine release with hypotension weak block of cardiac muscarinic ACh receptors

Dr. Ahmed ALArwali

2/4/2013

Nondepolarizing neuromuscular blocking agents


C.U: for surgical procedures superseded by newer
nondepolarizing agents

Pharmacokinetics, Interactions : Renal excretion duration, ~4060 min . Toxicities :


Histamine release. hypotension. prolonged apnea

Nondepolarizing neuromuscular blocking agents


Cisatracurium: Cisatracurium:
M.O.A: Competitive antagonist at nACh receptors,

especially at neuromuscular junctions. Effect: Prevents depolarization by ACh, causes flaccid paralysis.

Dr. Ahmed ALArwali

2/4/2013

Nondepolarizing neuromuscular blocking agents


C.U:
Prolonged relaxation of surgical procedures. relaxation of respiratory muscles to facilitate

mechanical ventilation in intensive care unit

Pharmacokinetics, Interactions : Not dependent on renal or hepatic function duration, ~2545 min Toxicities :
prolonged apnea.(less toxic than previous).

Nondepolarizing neuromuscular blocking agents


Rocuronium: Rocuronium:
M.O.A: Competitive antagonist at nACh receptors,

especially at neuromuscular junctions. Effect: Prevents depolarization by ACh, causes flaccid paralysis. slight antimuscarinic effect.

Dr. Ahmed ALArwali

2/4/2013

Nondepolarizing neuromuscular blocking agents


C.U:
Like cisatracurium useful in patients with renal

impairment.

Pharmacokinetics, Interactions : Hepatic metabolism duration, ~2035 min . Toxicities :


prolonged apnea.(less toxic than previous).

Nondepolarizing neuromuscular blocking agents


Mivacurium: Rapid onset, short duration (1020 Mivacurium: min); metabolized by plasma cholinesterase . Vecuronium: Intermediate duration; metabolized in Vecuronium: liver

Dr. Ahmed ALArwali

2/4/2013

Centrally acting spasmolytic drugs


Baclofen: Baclofen:
M.O.A: GABAB agonist, facilitates spinal

inhibition of motor neurons. Effect: Pre- and postsynaptic inhibition of motor output.

Centrally acting spasmolytic drugs


C.U:
Severe spasticity due to :

cerebral palsy, multiple sclerosis. stroke.

Pharmacokinetics, Interactions : Oral, intrathecal . Toxicities : Sedation. weakness.

Dr. Ahmed ALArwali

2/4/2013

Centrally acting spasmolytic drugs


Cyclobenzaprine: Cyclobenzaprine:
M.O.A: Poorly understood inhibition of muscle

stretch reflex in spinal cord. Effect: Reduction in hyperactive muscle reflexes antimuscarinic effects.

Centrally acting spasmolytic drugs


C.U:
Acute spasm due to

muscle injury. inflammation:

Pharmacokinetics, Interactions : Hepatic metabolism duration, ~46 h .


Toxicities :
Strong antimuscarinic effects .

Dr. Ahmed ALArwali

2/4/2013

Centrally acting spasmolytic drugs


Chlorphenesin. Methocarbamol.

Orphenadrine.
others: Like cyclobenzaprine with varying degrees of antimuscarinic effect

Centrally acting spasmolytic drugs


Diazepam:
M.O.A: Facilitates GABAergic transmission in

central nervous system. Effect: Increases interneuron inhibition of primary motor afferents in spinal cord central sedation.

Dr. Ahmed ALArwali

2/4/2013

Centrally acting spasmolytic drugs


C.U:
Chronic spasm due to:

cerebral palsy. Stroke. spinal cord injury. acute spasm due to:

muscle injury

Pharmacokinetics, Interactions : Hepatic metabolism duration, ~1224 h . Toxicities : ????

Centrally acting spasmolytic drugs


Diazepam:
M.O.A: 2 Adrenoceptor agonist in the spinal

cord. Effect: Presynaptic and postsynaptic inhibition of reflex motor output.

Dr. Ahmed ALArwali

2/4/2013

Centrally acting spasmolytic drugs


C.U:
Spasm due to : multiple sclerosis. Stroke. amyotrophic lateral sclerosis.

hepatic elimination duration, 36 h. Toxicities :


Weakness. Sedation. Hypotension. ????

Pharmacokinetics, Interactions : Renal and

Direct-acting muscle relaxants


Dantrolene: Dantrolene:
M.O.A: Blocks

RyR1 Ca2+-release channels in the sarcoplasmic reticulum of skeletal muscle.


skeletal muscle contraction.

Effect: Reduces actin-myosin interaction weakens

Dr. Ahmed ALArwali

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2/4/2013

Direct-acting muscle relaxants


C.U:
IV: Malignant hyperthermia. Oral: Spasm due to : cerebral palsy. spinal cord injury multiple sclerosis.

Pharmacokinetics, Interactions :
oral duration, 46 h . Toxicities :
Muscle weakness .

IV,

Dr. Ahmed ALArwali

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