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Pharm2 Lect 6

Pharm2 NMJ Blockers

QuestionAnswer
Clinical uses of NMJ blockers 1.Relax skeletal muscle for surgical procedures and tracheal intubation. 2.Prevent fractures/dislocations w/ ECT. 3.control spasms and tetnus. 4.sustain NMJ block in critical patients.
Types of NMJ blockers 1.Tubocurarine. 2.Atracurium. 3.Cisatracurium. 4.Mivacurium. 5.Pancuronium. 6.Rocuronium. 7.Vecuronium. 8.Succinylcholine.
All 8 of the NMJ blockers are _______ except for one, which is _______ 1.NON-Depolarizing (not charged). 2.Depolarizing (charged).
Competetive NMJ Blockers (antagonist): Tubocurarine 1.Mech of action: Non-depolarizing NMJ blocker that causes flaccid paralysis of muscles: eyes, face, limbs, abdomen, intercostals, diaphragm. 2.Bioav: Isoquinoline derivative lasting 80-120min, Eliminated renally.
Competetive NMJ Blockers (antagonist): Atracurium 1.Mech of action: Non-depolarizing NMJ blocker that causes flaccid paralysis of muscles: eyes, face, limbs, abdomen, intercostals, diaphragm. 2.Bioav: 30-60min, elminated by plasma esterase.
Competetive NMJ Blockers (antagonist): Cisatracurium 1.Mech of action: Non-depolarizing NMJ blocker that causes flaccid paralysis of muscles: eyes, face, limbs, abdomen, intercostals, diaphragm. 2.Bioav: 30-60min, eliminated spontaneously.
Competetive NMJ Blockers (antagonist): Mivacurium 1.Mech of action: Non-depolarizing NMJ blocker that causes flaccid paralysis of muscles: eyes, face, limbs, abdomen, intercostals, diaphragm. 2.10-20min eliminated by plasma cholinesterase.
Competetive NMJ Blockers (antagonist): Pancuronium 1.Mech of action: Non-depolarizing NMJ blocker that causes flaccid paralysis of muscles: eyes, face, limbs, abdomen, intercostals, diaphragm. 2.Bioav: steroid derivative 120-180min, eliminated renally.
Competetive NMJ Blockers (antagonist): Rocuronium 1.Mech of action: Non-depolarizing NMJ blocker that causes flaccid paralysis of muscles: eyes, face, limbs, abdomen, intercostals, diaphragm. 2.Bioav: 30-60min, eliminated via liver metabolism.
Competetive NMJ Blockers (antagonist): Veruronium 1.Mech of action: Non-depolarizing NMJ blocker that causes flaccid paralysis of muscles: eyes, face, limbs, abdomen, intercostals, diaphragm. 2.Bioav: 60-90min, eliminated via liver metabolism.
Adverse effects of Non-depolarizing NMJ Blockers 1.Release Histamine (except Rocuronium, cisatracurium, & vercuronium). 2.Bronchospasm. 3.Hypotension (caused by ganglionic block of SNS). 4.Excessive salivary & bronchiolar secretions. 6.Tachycardia. 7.Ganglionic blockade (Rocuronium, tubocurarine)
Competetive Depolarizing NMJ Blockers: Succinylcholine 1.Mech of action: Mimics ACh but much longer effects at NMJ, two-phase block. 2.Bioav: 5min, resistant to hydrolysis by AChE in NMJ, metab in plasma and liver. 3.Adverse effects: Bradycardia, post-op muscle pain, Inc histamine, hyperK+, malig hypertherm
What type of Nm antagonist are NMJ antagonist? Competiive
Order of flaccid paralysis in response to NMJ blocker from 1st to last. 1.Eyes. 2.Face. 3.Limbs. 4.Abdominals. 5.Intercostals. 6.diaphragm. **Recovered in reverse order
How can the effects of a NMJ antagonist be reversed? Treat with an AChE inhibitor. **this will create excess ACh in the NMJ to compete with the NMJ competitive antagonist.
Do NMJ blockers enter the CNS or affect sensory neurons? NO!! NONE of them. **they are not anesthetic or analgesic.
Does AChE hydrolyze Succinylcholine? NO, Butyrylcholinesterase does in plasma and liver.
Phase 1 of succinylcholine NMJ block DEPOLARIZING phase: 1.Opens the Nm channel in the same manner as ACh. 2.brief period of repetitive excitation that may cause muscle fasciculations (twitching). 3.followed by depolarization block of neuromuscular transmission and flaccid paralysis.
What is required for E-C coupling after depolarization? End plate repolarization. **This doesnt occur with succinylcholine.
Phase 2 of succinylcholine NMJ block DESENSITIZING: 1.continued exposure. 2.membrane gradually repolarizes but is also desensitized. 3.cannot easily be depolarized again (cholinesterase may reverse). **can directly stimulate by electrical input
Can Succinylcholine be reversed by neostigmine? NO, AChE inhibitors will not have an effect since Succinylcholine is a DEPOLARIZING NMJ antagonist
Short acting NMJ antagonist 1.Succinylcholine (5min). 2.Mivacurium (10-20min). **both eliminated by plasma cholinesterase.
Intermediate acting NMJ antagonists 1.Atracurium (30-60min). 2.Cisatracurium (30-60min). 3.Rocuronium (30-60min). 4.Vecuronium (60-90min). **3&4 are eliminated via liver metabolism.
Long acting NMJ antagonists 1.Tubocurarine (80-120min). 2.Pancuronium (120-180min). **Both eliminated renally.
What is the only competetive NMJ antagonist that causes cardiac M Block? Pancuronium.
What type of patient would likely become hyperkalemic when taking succinylcholine Patients tha have suffered: 1.Stroke. 2.Muscle trauma. 3.Upper & Lower motor neuron denervation. 4.ICU care. **These conditions cause UPregulation of N receptors: Denervation supersensitivity.
What results from malignant hyperthermia in response to succinylcholine? EXESSIVE SR [Ca] release: 1.Rapid Hyperthermia. 2.Metabolic acidosis. 3.tachycardia. 4.Muscle rigidity. **Treat with RYRs Inhibitor (dentrolene).
Created by: WeeG
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