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108 Cards in this Set
- Front
- Back
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Nondepolarizing muscle relaxantts are competitive antagonists of what neurotransmitter at the NMJ? What type of cholinergic receptor is occupied here? How is depolarization prevented?
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Nondepol muscle relaxants are competitive antagonists of ach. These agents work primarily on postsynaptic nicotinic receptors of the motor end-plate of skeletal m. by competing with ach for receptors sites. By keeping channels from opening, the nondepolarizing agents prevent depolarization.
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What chemical group do all muscle relaxants have in common? What is the significance of this chemical group?
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All of the muscle relaxants have at least one quaternary ammonium group. Muscle relaxants are completely ionized which means they are lipid insoluble and water soluble.
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*All nondepolarizing muscle relaxants are classified as either benzylisoquinoliniums or steroid derivatives. Which nondepolarizing muscle relaxants are benzyls and which are steroids?
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curiums are benzyls and -curoiniums are steroids.
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Muscle relaxants distribute primarily in what body compartment?
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Muscle relaxants distribute in the ECF
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What law or principal explains the displacement of nondepolarizing muscle relaxant from postsynaptic receptors as ach accumulates in response to an anticholinesterase drug?
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Law of mass action or Le Chatelier's principle
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What percentage of nicotinic cholinergic receptors must be blocked for clinically significant paralysis? For intubation?
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for abdominal muscle relaxation 90%, 99% for intubation. Ok for >90% and >95%.
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By what mechanism does pancuronium increase HR? Pancuronium increases HR by what percent?
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by competitively inhibiting ach from attaching to muscarinic receptors of the SA node. Can increase 10-15%
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List four non-depolarizing muscle relaxants that release histamine.
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dTC, metocurine, atracurium, mivacurium
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Name two nondepolarizing muscle relaxants that antagonize nicotinic receptors at autonomic ganglia and produce a corresponding decrease in SVR and BP.
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dTC and metocurine
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What is the priming principle for nondepolarizing neuromuscular relaxants?
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10% ED95 followed by in 4 minutes by a larger dose (2-3x ED95). Speculated that primary dose will occupy 50-70% of the receptors at the NMJ and the large subsequent dose of rapidly blocks remaining receptors causing a prompt onset of action.
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What is the termination of action of non-depolarizing muscle relaxants usually d/t?
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redistrubution to nonmuscle tissues.
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How is mivacurium eliminated? How does the rate of metabolism of mivacurium compare to the rate of metabolism of sux? What is the half-time of elimination of mivacurium?
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Metabolism by plasma cholinesterase. A rate similar to sux. Half time is 2 minutes.
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How long does it take to reach 25% recovery after an ED95 dose of mivacurium in adults? In children aged 2-12 years?
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13 minutes in adults and 7 minutes in chirrin.
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How does the recovery time from a mivacurium drip compare to the recovery time from a sux drip?
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similar
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How does the recovery time after d/c of an infusion of mivacurium compare with d/c of atracurium or vecuronium?
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half that for atracurium or vecuronium
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How does the duration of action after a single dose of mivacurium compare with the duration of atracurium, vecuronium, and sux?
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1/3 atra, 1/2 vec, and 2-2.5 times sux.
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How does the time-to-maximum effects of mivacurium compare with time-to-maximum effects of atracurium, vec, and sux?
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similar to atra and vec, but longer than sux.
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Does increasing the dose of miva markedly increase the duration of action? Are repeated doses of miva associated with tachyphylaxis?
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does not markedly increase the duration. Repeated doses are of miva are not associated with tachyphylaxis.
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Is miva contraindicated for use in a burn trauma patient?
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no
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A dose of up to 0.15 mg/kg (2xED95) of miva has what effect on BP and HR in adults?
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minimal effects in adults and pedi'
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What happens to BP an dHR when you give miva to 2-12 year old children?
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no change in HR or BP
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What happens to HR and BP if you give a high dose of miva rapidly?
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possible decrease in BP and increase in HR
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State how dTC is eliminated.
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primarily renal, secondary biliary
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Why may dTC be used in the patient with renal failure?
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d/t secondary elimination through bile
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State how vecuronium is eliminated.
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Biliary (primary) renal (secondary), and metabolism (secondary)
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Compared to the skeletal muscle, what protein is not found in smooth muscle?
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Smooth muscle, like skeletal muscle, contains both actin and myosin filaments. Smooth muscle, unlike skeletal muscle, does not contain the regulatory troponin protein complex. Regulation of skeletal and smooth muscle contraction, therefore, also differs.
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Describe how contraction proceeds in skeletal or cardiac muscle after calcium combines with troponin.
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After calcium combines with troponin, tropomyosin is repositioned so sites on actin are exposed, and myosin cross-bridges attach to these exposed actin sites and swivel (pull). The actin-myosin interaction is the cause of contraction.
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With what protein does calcium combine to initiate contraction in skeletal or cardiac muscle?
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Calcium combines with troponin in skeletal or cardiac muscle to initiate contraction.
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Where does the calcium for skeletal muscle contraction come from? For smooth muscle?
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In skeletal muscle, calcium is released from sarcoplasmic reticulum (located within the skeletal muscle cell) to the contractile proteins. In smooth muscle, the calcium for contraction diffuses into the cell from the extracellular fluid.
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What happens to the choline that is produced by metabolism of acetylcholine at the skeletal neuromuscular junction?
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Choline is re-used. Specifically, it is transported back into the nerve terminal and converted to acetylcholine
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Acetylcholine at the skeletal neuromuscular junction is hydrolyzed by what enzyme to what products?
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Acetylcholine is hydrolyzed by acetylcholinesterase to choline and acetate.
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How many molecules of acetylcholine are required to open each acetylcholine channel in the motor end-plate at the skeletal neuromuscular junction?
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Two
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What is the incidence of malignant hyperthermia in children? Adults? What is the mortality rate for malignant hyperthermia?
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The incidence of malignant hyperthermia is 1 in 15,000 anesthetics in children and 1 in 50,000 in adults. The mortality rate is 10%.
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What are eleven clinical manefestations of malignant hyperthermia?
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1. hypercarbia; 2. tachycardia; 3. tachypnea; 4. hyperthermia; 5. hypertension; 6. cardiac dysrhythmias; 7. acidosis (metabolic); 8. hyperkalemia; 9. skeletal muscle rigidity; 10. myoglobinuria; 11. hypoxemia
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What is the earliest sign of malignant hyperthermia?
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The earliest sign of malignant hyperthermia is increased end-tidal CO2
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Can masseter muscle spasm be an early sign of malignant hyperthermia? Will masseter muscle spasm be the first sign of malignant hyperthermia?
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Masseter muscle spasm is an early sign of malignant hyperthermia, though it generally will not be the first.
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What response is considered evidence of malignant hyperthermia in children?
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Masseter muscle rigidity after administration of succinycholine, especially in children undergoing strabismus surgery.
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What percent of children experience masseter muscle rigidity after halothane and succinylcholine administration?
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One percent (1%)
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How fast may temperature increase during an episode of malignant hyperthermia?
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1-2 degrees celcius every five minutes.
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What is responsible for the increased sympathetic nervous system stimulation during an episode of malignant hyperthermia?
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Hypercarbia
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What is the diagnostic test for malignant hyperthermia, and how is it done? Is the test sensitive?
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The halothane-caffeine contracture test remains the standard. A skeletal muscle biopsy is placed in a solution of halothane. Sustained contraction of the skeletal muscle in response to the halothane is diagnostic. Unfortunately, the test is not very sensitive, as tehre are many false-positives.
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Identify the anesthetic agents that are absolutely contraindicated in the patient with a family history of malignant hyperthermia.
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All volatile agents and succinylcholine are absolutely contraindicated in patients with malignant hyperthermia.
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Make a list of eight actions for initial management of malignant hyperthermia.
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1. discontinue inhaled anesthetics and sux. 2. hyperventilate with 100% O2. 3. administer dantroline. 4. treat acidosis with sodium bicarb (1-2 mmmoles/kg). 5.lower body temp to 38C using a variety of cooling techniques including external ice packs and gastric lavage. 6. replace anesthetic circuit and cannister. 7. monitor with capnography and blood gas determinations. 8. if neccessary, treat hyperkalemia and dysrhythmias.
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You know that sux and volatile agents can trigger MH. What nondepolarizing neuromuscular blocking agent may trigger MH?
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Tubocurarine (dTC) may trigger a MH crisis. In general, though, all other nondepolarizing neuromuscular blocking agents may be safely used in patients prone to MH.
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A patient has just experienced masseter muscle rigidity from suz. What lab value may confirm the diagnosis of MH?
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Elevation in creatine phosphokinase (CPK > 20,000)
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A child has received halothane and sux and the mouth cannot be opened. What action should be taken? Why?
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The possibility of MH should be kept in mind and the anesthetic should proceed with careful monitoring for signs of MH. Consider switching to trigger-free anesthetic agent
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How and where does dantrolene work?
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Dantrolene acts at the ryanodine receptor to decrease the calcium level in the skeletal muscle cell by decreasing the release of calcium from the sarcoplasmic reticulum. Skeletal muscle relaxes when the supply of calcium to th contractile proteins is impaired.
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What is the dose of dantrolene for MH treatment? How long should dantronene be given in the management of MH?
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Dose of dantrolene for treatment in MH is 2.5 mg/kg IV every 5 mintues. Max dose is 10 or 20 mg/kg.
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What is the therapeutic blood level for dantrolene? What is the maximum dose of dantrolene for MH?
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2.5 mcg/ml. Max dose is 10 mg/kg
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How much dantrolene is found in each vial of dantrolene? How must each vial of dantrolene be prepared?
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20 mg to be mixed with 60 mL of sterile water.
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You have successfully treated an acute episode of MH with dantrolene. Dantrolene should be readministered at what intervals for how long?
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Dantrolene should probably be repeated every 10-15 hours for 3 days.
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What is the best method of decreasing temperature during MH? Where would you not monitor the temp of a patient being cooled for MH?
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Gastric lavage is best tx for decreasing body temp. Therefore, esophageal monitoring of temp is inaccurate. Best to measure at other places (rectal, bladder, nasal)
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At what body temp should cooling of the patient with MH be stopped? Why?
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38C to prevent hypothermia.
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Once the initial episode of MH is controlled, the patient will remain at risk for what five complications?
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1. reoccurence 2. DIC 3. myoglobinuric renal failure 4. skeletal muscle weakness 5. electrolyte abnormalities
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A patient in a MH crisis has premature ventricular ventricular contractions. What is the antiarrythmic drug of choice?
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Procainamide, 15 mg/kg IV. Lidocaine is also acceptable.
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A woman in labor is identified as being susceptible to MH. What anesthetic techniques are acceptable?
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Epidural without dantroline pretreatment for routine labor; if general anesthesia is selected, administer dantrolene prophylactically and use non-triggering agents.
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During the preoperative assessment of the patient, you discover a positive family history for MH. What isx steps need to be taken to manage this patient? Are nondepolarizing muscle relaxants safe in this patient?
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1. admin standard preop meds 2. use clean anestheisa machine with disposable circuit, use new soda lime, drain vaporizers, and flush for several hours with oxygen flowing at 3-5 L/min, 3. measure ETCO2; 4. monitor body temp; 5. use nontriggering drugs and techniques; 6. observe patient closely in postop period. Nondepolarizing drugs can be safely reversed.
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Why might 2.5 mg dantrolene be administered to a patient preoperatively?
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To prevent, prophylacticaly, and episode of MH.
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What changes in the gas machine would you make if your patient developed MH?
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Change the circuit and soda lime, if possible, or get a clean anesthesia machine.
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Why is a Bain circuit inappropriate during an episode of MH?
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You do not want the patient to rebreathe Vas that may have triggered the episode of MH, and there is definitely the potential to rebreathe gases with the Bain circuit.
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What syndrome can mimic MH?
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The neuroleptic malignant syndrome has many features in common with MH but the mode of onset and recovery are quite different.
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Patients treated with what drugs are susceptible to NMS? What patient group takes these meds?
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Haldol, Prolixin, or Thorazine. Schizo's take these.
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Who is primarily affected by Duchenne's muscular dystrophy?
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X-linked therefore males. 1-3 cases per 10,000 male births. Presents 3-5 years.
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List five anesthetic concerns for the patient with Duchenne's muscular dystrophy.
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1. cardiac arrest upon induction because of myocardial depression; 2. Sux induced hyperkalemia; 3. Delayed gastric emptying; 4. retention of pulmonary secretions; 5. unpredictable susceptibility to MH
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How does the patient with Duchenne's muscular dystrophy respond to anesthetics? What muscle relaxant should be avoided in the patient with Duchenne's muscular dystrophy? Why?
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Vulnerable to cardiac arrest d/t admin of cardiodepressant drugs. Sux should be avoided. Respond to sux with hyperkalemia.
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*What are the clinical manifestations of myotonic dystrophy (Steinert's disease)?
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facial weakness, wasting and weakness of the sternocleidomastoid muscles, ptosis, dysarthria, dysphagia, and inability to relax the handgrip. Frontal balding, cataracts, and testicular atrophy are the recognizable triad.
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Identify the genetic pattern of inheritance of myotonic dystrophy and describe the pathophysiology of this group of degenerative diseases.
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MD is autosomal dominant presenting in 20s or 30s. MDs have persistent contracture after voluntary contracture of skeletal muscle or following electrical stimulation. EMG findings are diagnostic. Skeletal muscle RMPs are lower. Pumps fail to return Ca++ to SR
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*What four anethetic concerns should you have for the patient with myotonic dystrophy?
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1. cardiomyopathy; 2. respiratory muscle weakness and sensitivity to respiratory depressants; 3. vulnerability to aspiration of gastric contents; 4. potential for abnormal responses to anesthetic drugs.
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*Should sux be used in the anesthetic management of the patient with myotonic dystrophy?
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Sux should NOT be used in the patient with MD b/c sux can produce intense generalized myotonic contracture that makes ventilation or intubation difficult or impossible.
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*What is the medical management of the patient with MD?
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Tx of MD is symptomatic and may include the use of phenytoin, quinine, and procainamide. These agents delay the return of membrane excitation by blocking rapid Na+ influx into muscles. Quinine and procainamide should be used with caution as they maay worsen cardiac conduction abnormalities (longer PR)
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*Myasthenia gravis is characterized by what symptoms? What is the cause of those symptoms?
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MG is characterized by weakness and easy fatigability of skeletal muscles. Weakness can be asymmetric, confined to one group of muscles, or generalized. Easy fatigability of skeletal muscle in MG is caused by autoimmune destruction of nicotinic acetylcholine receptors at the NMJ.
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*Onset of MG is slow and insidious and any skeletal muscle group may be involved. Onset is most common in which muscles?
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Ocular. Ptosis and diplopia result. If stays to eyes for two years then generalization risk is low.
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What drugs are most commonly used in the tx of MG?
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anticholinesterases.
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What s/s appear if the pt with MG takes too much anticholinesterase?
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cholinergic crisis d/t accumulation of acetylcholine. Increased muscle weakness, excessive muscarinic receptor stimulation, causing diarrhea, salivation, miosis, and bradycardia
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What is the major surgical risk for the pt with MG?
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postop respiratory failure
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What five factors predict a need for postop mechanical ventilation in the pt with MG?
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1. disease duration of more than 6 yrs; 2. concomitant pulmonary dx; 3. PIP of < -25 cmH2O; 4. VC < 4 ml/kg; 5. pyridostigmine doses of > 750 mg/day. (all following thymectomy)
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What is the BEST way to maintain ventilation in the patient with MG?
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mechanical ventilation.
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Lambert-Eaton myasthenic syndrome (LEMS) is characterized by what?
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LEMS is characterized by proximal skeletal muscle weakness that typically affects the lower extremities
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LEMS is associated with what problems in addition to muscle weakness?
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LEMS associated with small-cell carcinoma of the lung, or less commonly, other occult malignancies, or autoimmune disorders
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What is thought to cause weakness in the patient with LEMS?
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defect in the motor nerve terminal causes a decreased release of acetylcholine. Thought to be d/t antibodies directed against voltage gated Ca++ channels
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How does muscle weakness of the pt with LEMS differ from the weakness of the pt with MG?
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muscle strength deteriorates rapidly with repeated effort to the pt with MG but improves with repeated effort in the pt with LEMS
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How does anicholinesterase tx alter muscle strength in the pt with LEMS? MG?
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improves with MG but doesn't change with LEMS
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List four additional problems that should be anticipated in the pt with scleroderma.
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1. poor gastric emptying (tx with antacids and H2 antagonists); 2. risk for aspiration pneumonitis during induction is increased d/t a high incidence of GERD; 3. venous access may be difficult; 4. skeletal muscle involvement increases the sensitivity to muscle relaxants
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List 10 anesthetic concerns associated with rheumatoid arthritis pt.
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1. cervical spine involvement; 2. synovitis of the TMJ; 3. cricoarytenoid arthritis manifested by hoarseness; 4. pericarditis; 5. aortic regurg; 6. pulmonary fibrosis; 7. peripheral nerve compression; 8. hepatitis; 9. anemia; 10. drug-induced Ses associated with asa and/or steroid tx.
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There are 8 anesthetic problems, in addition to those related to the airway and pulmonary system, that should be anticipated in the pt with scleroderma. List four of them.
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1. profound hypoTN may occur following induction. 2. regional anesthesia although there may be prolonged effects; 3. BP measurments may be difficult; U/S or doppler may be necessary. ART not recommended; 4. skin temp is reduced; warm the room and use warm compresses for the extremities.
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List pulmonary manifestations of scoliosis:
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1. lung volumes are decreased; 2. chest wall compliance is decreased; 3. arterial hypoxemia and possibly hypercarbia are present secondary to V:Q mismatching. Pulm HTN secondary to hypoxia and elevated PVR may also be present.
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*Identify the anesthetic concerns for the pt with scoliosis d/t muscular dystrophy
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predisposed to MH, cardiac dysrhythmias, and untoward effects of sux (hyperkalemia, myoglobinuria, sustained muscular contraction)
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Are the pharmacodynamic actions of acetylcholine and sux similar?
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Yes, actions are similar. Six is two acetylcholine molecules linked together. Sux mimics the action of acetylcholine.
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Sux produces parasympathomimetic effects by integrating with which type of cholinergic receptor.
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muscarinic receptors found in tissues innervated by the parasympathetic nervous system
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How does sux produce bradycardia?
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stimulates muscarinic receptors at the SA node.
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Sux interacts with what type of cholinergic receptors at the NMJ?
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Sux directly stimulates nicotinic receptors found in the motor-end plate of skeletal muscle.
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What could cause HR and/or BP to increase in response to Sux?
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Sux stimulates nicotinic receptors at the autonomic ganglia. Sux induced increase in HR and/or BP reflects the ability of sux to mimic the normal effects of acetylcholine at the nervous system ganglia.
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How are the actions of Sux and acetylcholine terminated?
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Sux is enzymatically hydrolyzed by plasma cholinesterase. Ach is hydrolyzed by true cholinesterase, which is found at the NMJ as well as at tissues innervated by parasympathetic nerves.
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What are two other names for plasma cholinesterase?
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Pseudocholinesterase or butyrocholinesterase
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Describe the two phases of sux metabolism, and state where the second phase of sux breakdown occurs?
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1. metabolized by pseudocholinesterase to succinylmonocholine plus choline; 2. succinylmonocholine is metabolized by pseudocholinesterase to succinic acid.
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Is succinylmonocholine an active metabolite of succinylcholine?
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yes, has same actions at its parent molecule, sux.
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*Is there an active metabolite of sux?
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Yes, succinylmonocholine is much weaker but is metabolized much slower to succinic acid and choline.
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Compare the potency of succinylmonocholinewith the potency of sux.
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Suxmono is only 1/20th to 1/80th as potent as sux. Suxmono is, therefore, much weaker than sux.
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Would you think that suxmono contributes to phase 1 block? Phase 2 block?
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Yes. Suxmono mimics sux and, therefore, would contribute some to both phase 1 and 2 blocks.
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What are eleven possible complications associated with sux admin?
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1. hyperkalemia; 2. bradycardia; 3. increased HR and/or BP; 4. skeletal muscle myalgia; 5. allergic rxn; 6. MH trigger; 7. sustained contraction of skeletal muscle (masseter); 8. myoglobinuria; 9. increased intraocular pressure; 10. increased intragastric pressure; 11. increased ICP.
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What is sux's effect on ICP and IOP?
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Sux raises both ICP and IOP
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Why is sux contraindicated in pts with nerve damage?
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up regulation of nicotinic receptors. These are exceptionally responsive to sux. K leaves cells in excessive quantities when sux triggers these channels to open.
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List 5 conditions that may accentuate sux-induced hyperkalemia.
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1. unhealed 3rd degree burns; 2. denervation of skeletal m.; 3. severe skeletal m. trauma; 4. upper motor neuron injury; 5. muscular dystrophy
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You administer a non-depolarizing muscle relaxant for induction and maintenance of anesthesia for abdominal surgery. What happens if you administer sux to close the peritoneum near the end of this case?
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If enough sux is given to overcome residual nondepolarixing agent, muscle relaxation will be facilitated. This approach, however, is controversial.
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Sux is contraindicated for pt's taking what eye drop medication? Why?
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Echothiophate b/c depresses plasma cholinesterase activity, which would prolong the duration of sux.
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What IV dose of sux should be administered to treat laryngospasm? If an IV site is not available, how can sux be administered?
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0.1-0.5 mg/kg or IM 4-6 mg/kg or sublingual.
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How should you tx bradycardia caused by sux?
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atropine b/c it competitively inhibits sux at muscarinic receptors.
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After sux admin to a normal pt, how much can the serum K be elevated?
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0.5-1.0 mEq/L
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