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55 Cards in this Set
- Front
- Back
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The does Ach metabolism take place?
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Mainly in the NMJ.
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What metabolizes succinylcholine? Where is it made? What other drug can it metabolize?
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plasma ChE. Mivacurium.
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Describe the Phase 1 activity of succinylcholine
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Causes initial depolarization of the end plate region, transient muscle fasciculation, then relaxation.
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Describe the Phase 2 Block activity of succinylcholine
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It desensitizes the receptor to Ach. The end plate repolarizes due to conformational change of the receptor molecule.
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What will happen if ChE inhibitors are added at Phase I block? Phase II?
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I - it will intensify the response of succinylcholine
II - it may reinitiate muscle contraction |
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What would be the consequence of a pt with liver dysfxn that takes succinylcholine?
What would be a tx? |
Long duration of action (>2hrs)
Mechanical respiration |
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Which skeletal muscles respond the greatest NM to blockade?
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respiratory, trunk and limbs, speech and deglutition, and the extrinsic eye muscles
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What is an adverse effect of NM drugs?
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CNS fxnality, pain is not dulled
With depolaring drugs: postoperative stiffness, pain, inc. of intraocular and extraocular muscle pressure/contraction, inc. intragastric pressure, hyperkalemia |
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Which pt's are most susceptible to hyperkalemia?
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Those with burns, nerve damage, closed head injury, and renal failure
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These are used to completely paralyze pt's for surgical procedures
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Neuromuscular blockers
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These agents partially block skeletal muscle activity and reduce muscle spasms
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Spasmolytics
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What ion enters the nerve terminal during an AP? What do the vesicles contain which elicit a postsynaptic response?
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Calcium. Ach.
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What type of receptors bind Ach in skeletal muscle? Describe the stx of the receptor?
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Nicotinic. It contains 2 alpha, and 1 of each a Beta, gamma, and delta subunit.
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Curare is a generic term for this very important alkaloid?
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d-tubocurarine
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What triggers the troponin-actin-myosin interaction in muscles?
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Ca+ release from the sarcoplasmic reticulum.
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What serves in place of the Beta subunit in adults? When Ach binds to any one of the alpha subuntis, what is the result?
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An s subunit.
There is an increase of the fluxes of Na+ in, Ca ++, and K+ out. |
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What causes the Ca+ to be restored to the SR? What occurs before repolarization?
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Relaxation and ATPase. A refractory period.
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What are neuromuscular blocking drugs?
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Peripherally acting bisquartery ammonium compds.
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What is the MOA of the NM blocking drugs?
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They act as competitive agonists at Ach receptors.
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Name some of the "nondepolarizing" blocking agents?
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Tubocurarine, Metacurine, Gallamine, Pancurium, Pipecurium, and Dexacurium
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What are the two areas that the quarternary compds cannot cross? How are they absorbed and excreted?
How are they administered? |
The BBB and placenta. Poorly and rapidly. IV.
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What are some use for NM blocking drugs?
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Surgery (intubation) to reduce muscle tone, electroshock therapy (prevents bone breakage), controls convulsive disorders, and respiration.
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What are the two areas that the quarternary compds cannot cross? How are they absorbed and excreted?
How are they administered? |
The BBB and placenta. Poorly and rapidly. IV.
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Name the 3 intermediate acting NM blocking drugs? (20-35 min)
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Vecuroniun, Atracurium, Recuronium
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Name the lone shorting acting NM drug? What does it have a slight affect on?
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Mivacurium. Histamine release.
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Which 2 drugs cause weak blockade of autonomic ganglia?
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Tubocurarine, and Metacurine
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This NM drug has a moderate effect on histamine release?
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Tubocurarine
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These 2 drugs affect cardiac muscarinic receptors?
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Gallamine, and Pancuronium
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How does one reverse the effect on nondepolaring NM blockers? (2 ways)
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Inc the conc. of endogenous Ach at the NMJ. Use ChE inhibitors such as neostigmine, physostigmine, edrophonium w/ atropine to protect muscarinic receptors against excessive stim. by inc. levels of Ach.
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This drug is a Ach-liek agonist at nicotinic receptors and cuase stimulation of autonomic ganglia, effects histamine release, and cardiac muscarinic receptors.
What is its duration and generic name? |
Succinylcholine (Anectine)
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What are the adverse effects of the nondepolarizing drug, tubocurarine?
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Histamine release, bronchospasm, inc. excretions, vasodilation
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What types of drugs or states may potentiate the effect of tubocurarine?
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Methoxyflurane (gen. anesthetic), aminoglycosides (neomycin & streptomycin), fluid and electrolyte imbalance
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What drug interferes with the release of Ca+ from the sarcolemma?
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Dantroline
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What are the indications for dantroline?
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Chronic disorders chx'd by muscle spasms: SC injury, stroke, cerebral palsy, multiple sclerosis.
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What other genetic disorder may dantroline be used to treat?
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Malignant Hyperthemia
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What drugs are considered centrally acting spasmolytics? What are their common side effects?
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The GABA receptor agonists Baclofen and Diazepam.
Sedation and drowsiness. |
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This drug another central acting spasmolytic that is a derivative of clonidine. What is its MOA? What are its side effects?
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Tizanidine. Inhibits nociceptive xmission in the cord.
Sedation, drowsiness, hypotension, dry mouth and asthenia. |
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Name some drugs that are used for acute local muscle spasm.
What are their side effects? |
Carisoprodol, Chlorzoxazone, Cyclobenzaprine, Orphenadrine
Sedative w/ antimuscarinic activity. |
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What is the action of botulinum toxin?
How many types of toxin are there? |
Inhibits the release of Ach from cholinergic nerve terminals.
7 with light and heavy chains. |
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What drug interferes with the release of Ca+ from the sarcolemma?
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Dantroline
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What other genetic disorder may dantroline be used to treat?
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Malignant Hyperthemia
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Botox is approved to treat what types of things?
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strabismus (cross-eyes), uncontrollable blinking, cervical dystonia, frown lines on the brow, & headache
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How do local anesthetics work?
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They block nerve conductoin along axons that utilize Na+ channels. This reduces pain and sympathetic vasoconstriction.
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What is an electrically excitable membrane?
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One that generates an all-or-none action potential in response to depolarization.
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What causes repolarization?
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The outflow of K+.
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What was the first local anesthetic? What was the first synthetic local anesthetic?
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Cocaine. Procaine.
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Local anesthetics have what 3 main groups?
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Lipophilic, an intermediate chain, and an ester/amide-amine group.
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The weak base pKa b/t 8-9 of local anesthetics give them what chx?
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Charged cationic form at physiological pH.
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How can the action of local anesthetics be enhanced?
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Add a vasoconstrictor like epinephrine.
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Name the 4 (PTCB) local anesthetics that are esters?
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Procaine (Novocaine), Tetracaine (Pontocaine), Cocaine, and Benzocaine
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Which ester has the longest duration of action?
Which one is topical? |
Tetracaine. Benzocaine.
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Which anesthetics are amides? (PRoBLEM)
Which have a long duration of action like BEeR? |
Prilocaine, Ropivacaine, Bupivacaine, Lidocaine, Etidocaine, Mepivacaine
Bupivicaine, Etidocaine, Ropivacaine. |
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What are the side effects of anesthetics?
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CNS - agitation, confusion, tremor, resp. depression
Cardiovascular - myocardial depression & vasodilation Allergic rxn |
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What nerves do local anesthetics have the greatest effects on?
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Dorsal Root & Sympathetic Nerves (Type C), and Type A
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What types of nerves do local anesthetics have the least effect on? Why?
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Alpha (Type). Due to heavy myelination. Type C nerves are not myelinated.
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