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55 Cards in this Set

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