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40 Cards in this Set
- Front
- Back
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NMBA GENERAL INFO
Non-Depolarizing NMBA |
- Competitively binds with NM receptors on the motor end plate without activation
- Muscle relaxation occurs as long as sufficient NMBA remains unbound |
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NMBA GENERAL INFO
Depolarizing NMBA |
- Bind to the NM receptors on the motor end plate and activate them causing depolarization and contraction
- Prevents repolarization leading to relaxation |
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NMBA GENERAL INFO
NDNMBA |
-Competitive blockade of Ach receptors at neuromuscular endplate.
-Have no effect of their own, but prevent depolarization by Ach. -This creates paralysis (muscle flaccidity). |
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NMBA GENERAL INFO
DNMBA |
-Non-Competitive blockade of Ach receptors at neuromuscular endplate.
-Causes continuous depolarization &prevents muscle cells from repolarizing. -This creates fasciculation's, followed by paralysis |
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Rocuronium
Trade type |
Zemuron©
Intermediate Acting NDNMBA |
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Rocuronium
MOA |
-competes with Ach for Nicotinic M receptors at NMJ
-prevents depolarization of skeletal muscle →paralysis |
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Rocuronium
USES |
-induction of paralysis
-maintenance of paralysis -de-fasciculation -intubation, surgery & mechanical ventilation |
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Rocuronium
Pharmacodynamics |
-Paralysis begins in eyelids & jaw.
-Then limbs, abdomen & throat. -finally the muscles of respiration. |
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Rocuronium
Pharmacokinetics |
-Very quick onset of action (1-3 minutes), 2nd only to Succinlycholine.
-Effects persist for approx 30 mins. -Metabolized in Liver. -Cannot cross BBB. |
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Rocuronium
Adverse Effects |
-Hypotension - Nicotinic N Blockade
-Respiratory Arrest - Self Explanatory |
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Rocuronium
Drug Interactions |
-Inhalation Anesthetics - Potentiate
-Cholinesterase Inhibitors - Inhibit -Gentamicin, Tobramycin, Vancomycin, Corticosteroids, CCB’s - Potentiate |
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Rocuronium
Contraindications |
-Myasthenia Gravis
-Hypersensitivity -Lack of Sedation |
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Rocuronium
Dose |
Prep: 10mg/ml-5mlVial
Dose: Ld: 1mg/kg IVP Maint: .5mg/kbIVPq10mPRN De-Fac: 0.1mg/kg IVP q 1-2 mins prior admin of Succinylcholine |
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Pancuronium
Trade type |
Pavulon©
Intermediate Acting NDNMBA |
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Pancuronium
MOA other |
-Does not block Nicotinic N & therefore no hypotension
-Can cause tachycardia due to Vagolytic effects -3-4 minute onset. 40 minute duration. -Elimination is renal |
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Pancuronium
Dose |
Main: 0.1mg/kg IVP q 10 min PRM
De-Fac: 0.01mg/kg IVP |
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Vecuronium
Trade type |
Norcuron©
Intermediate Acting NDNMBA |
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Vecuronium
MOA other |
-Does not block Nicotinic N & therefore no hypotension
-Does not have Vagolytic effects -3-5 minute onset. 25-30 minute duration. -Elimination is Bile |
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Vecuronium
dose |
Main: 0.1mg/kg IVP q 10 minPRM
De-Fac: 0.01mg/kg IVP |
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Succinylcholine
Trade type |
Anectine©
Quelicin© Ultrashort acting DNMBA |
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Succinylcholine
MOA |
-Non-competitive blockade of Nicotinic M receptors at NMJ.
-Causes continuous depolarization (fasciculations) and prevents repolarization (paralysis). |
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Succinylcholine
Uses |
-Induction of Paralysis
-Intubation |
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Succinylcholine
Pharmacodynamics |
-only difference between Succinylcholine & NDNMBA’s is initial fasciculations.
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Succinylcholine
Drug Interactions |
-Cholinesterase Inhibitors - Potentiate
- Pharmacokinetics -Onset of action is 1 min -Duration of action is 5 mins -Degraded quickly by plasma cholinesterase -Antibiotics (Same as Roc) – Potentiate |
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Succinylcholine
Adverse Effects |
-Prolonged effects in pts with genetically low plasma cholinesterase levels.
-Malignant Hyperthermia -Hyperkalemia |
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Succinylcholine
Contraindications |
-Family Hx of Malignant Hyperthermia
-Family Hx of low plasma cholinesterase -Known Hyperkalemia -Penetrating eye injuries -Hypersensitivity |
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Succinylcholine
Precautions |
-Myopathies
-Burns and multi-system trauma -Fasciculations may ↑ ICP & IOP -Can cause vagal induced bradycardia - Sedation FIRST - fractures, glaucoma |
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Succinylcholine
Dose |
Dose: 1.5mg/kg RIVP
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Neostigmine
Trade type |
Prostigmine©
Reversible Cholinesterase Inhibitors |
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Neostigmine
MOA |
-Acts as substrate for active center of ChE
-ChE has more difficult time breaking down Neostigmine, and during that time Ach is not being broken down. |
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Neostigmine
Uses |
-Myasthenia Gravis
-Reversal of NDNMBA OD |
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Neostigmine
Pharmacodynamics |
-At therapeutic doses effects are only seen at Muscarinic and Nicotinic M receptors.
-Muscarinic - Heart, Exocrine Glands, Smooth Muscle, Eye -Nicotinic M -↑force of contraction |
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Neostigmine
Pharmacokinetics |
-Does not cross membranes well - no PO
-Does not cross BBB -Duration is 2-4 hours -Eventually degraded by ChE |
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Neostigmine
Adverse Effects |
-SLUDGEM and Bradycardia
-Neuromuscular Blockade - Similar to Sux |
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Neostigmine
Contraindications |
-GI/Urinary Obstruction
-Peptic Ulcers -Asthma -CAD -Hyperthyroidism -Succinylcholine |
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Neostigmine
Drug Interactions |
-Muscarinic Antagonists - Inhibit
-Muscarinic Agonists - Potentiate |
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Neostigmine
Muscarinic effects of toxicity… |
D - Diarrhea
U - Urination M - Miosis B - Bradycardia, Bronchorrhea, Bronchospasm E - Emesis L - Lacrimation S - Salivation, Secretions, Sweating |
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Neostigmine
Nicotinic effects of toxicity… |
H - HTN, Hyperglycemia
M - Mydriasis W - Weakness T - Tachycardia F – Fasciculations |
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Neostigmine
Other possible causes of toxicity… |
-Physostigmine - Does not carry a charge. Can cross BBB. Used to treat cholinergic antagonist OD.
-Organophosphates -Mushrooms |
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Neostigmine
Toxicity |
• SLUDGEM
• Bradycardia • Resp depression • CNS depression |
