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Pharm1Test3NMB
Pharm1 Test3 Neuromuscular Blockers and Neurotransmission
| Question | Answer |
|---|---|
| What are the two processes of cellular communication? | Chemical and electrical. |
| What do cells use to communicate chemically? | Neurotransmitters. |
| What do cells use to communicate electronically? | Passive and active conduction. |
| What is the normal resting potential of most cells? | About -80 mv. |
| What are intra and extra Na+ levels? | Intra: 15, extra: 145. |
| What are intra and extra K+ levels? | Intra: 145, extra: 5. |
| What are intra and extra Cl- levels? | Intra: 10, extra: 150. |
| What are intra and extra Ca++ levels? | Intra: 0.0001, extra: 2. |
| What channel is the primary contributor to resting charge? | K+. |
| What is the only channel open at rest? | K+. |
| Dendritic conduction is active or passive electrical conductance? | Passive electrical conductance. |
| Axonic conduction is active or passive electrical conductance? | Active. |
| Axonic conduction involves what channels? | Voltage-gated Na+ and K+ channels. Some Ca++ also. |
| What is needed to restore chemical equilibrium? | Na+-K+ ATPase to restore chemical equilibrium. |
| Where is axonic conduction initiated? | At axon hillock by internally ligand-gated Na+ channels. |
| What are four factors leading to increased conduction rates? | Myelination, lower resting potential, increasing Na+ channel density, and increasing Axonal diameter. |
| What are the two ways myelination increases conduction rates? | Decreased Capacitance, and Saltatory Conduction. |
| What act begins synaptic transmission? | Ca++ channel stimulation. |
| What happens after Ca++ channel stimulation? | Ca++ released from storage in sarcoplasm. |
| What happens after Ca++ is released from storage in the Sarcoplasm? | Increased Ca++ leads to biochemical change allowing fusion of vesicles with inner cell membrane. |
| What happens after increased Ca++ leads to biochemical change allowing fusion of vesicles with inner cell membrane. | Ca++ rapidly removed back into sarcoplasm. |
| What happens after Ca++ rapidly removed back into sarcoplasm? | Fused vesicles open to synaptic space, releasing contents into synaptic cleft. |
| What happens after fused vesicles open to synaptic space, releasing contents into synaptic cleft? | Vesicles reformed by endocytotic process, and can then be refilled. |
| Some vesicles are... | Transported down axon from cell body. |
| One vesicle contains how much neurotransmitter? | One quanta. |
| How many molecules of neurotransmitter are in one quanta? | Estimated at 5,000 – 10,000 molecules. |
| True or false: neurotransmitters are the only substances in vesicles. | False. There are other substances in vesicles. |
| What are the excitatory neurotransmitters? | Acetylcholine, Norepinephrine, Epinephrine, Dopamine, Serotonin, Glutamic Acid, and Aspartic Acid. |
| What are the inhibitory neurotransmitters? | Gamma Amino Butyric Acid (GABA), and Glycine. |
| The ganglionic blockers were primarily experimental. What were they used for? | BP control. However they were very dangerous. |
| D-tubocurarine chloride is derived from what plant? | Chondodendron Tomentosum. |
| Why did S. American Indians use curare? | To kill animals. |
| Curare was first used in medicine in 1932 to treat... | Tetanus and spasticity. |
| True or false: In the 1960’s it was discovered that curare gave adequate skeletal muscle relaxation during operative anesthesia without using excessive amounts of general anesthetics. | False. It was discovered in the 1940's. |
| In addition to its use to promote skeletal muscle relaxation during surgery, tubocurarine has been used... | As an aid to mechanical respiration, to prevent trauma during electroconvulsive therapy and as an aid to the diagnosis of myasthenia gravis. |
| What is Gallamine? | A D/C'd NMB. |
| How do depolarizing blockers work? | These agents cause an initial stimulation (depolarization) of the receptor, followed by long-term blockade (due to keeping receptor depolarized, and not able to repolarize for re-stimulation). |
| What is the main benefit of Succinylcholine? | Short duration. |
| What is Decamethonium? | An experimental depolarizing blocker. (not clinically used - experimental neuromuscular nicotinic blocker). |
| How is Decamethonium composed? | It is comprised of a 10 carbon chain separating two tri-methyl amines (Quats). |
| How does the structure of Decamethonium compare to Ganglionic Blockers? | Compare this to hexamethonium, a ganglionic blocker with a 6 carbon chain between the two tri-methyl amines (Quats). This demonstrates the difference in physical layout of the two ACh sites on ganglionic and neuromuscular nicotinic receptors. |
| How do non-depolarizing blockers work? | Agents in this class act as competitive antagonists of ACh at the neuromuscular junction. This blocks the ability of ACh to stimulate the muscle at the motor end plate, resulting in muscle weakness (at lower doses) or paralysis (at higher doses). |
| Onset/duration of Atracurium? | 3-5, 60. |
| Onset/duration of Cisatracurium? | 1.5-2, 55-60. |
| Onset/duration of Pancuronium? | 2-4, 65. |
| Onset/duration of Rocuronium? | 1, 20-60. |
| Onset/duration of Succinylcholine? | 0.5-1, 4-6. |
| Onset/duration of Vecuronium? | 2.5-3, 25-30. |
| Unique in its depolarizing mechanism and is also the shortest-acting (both onset and duration) neuromuscular blocker, with effective intubation conditions occurring within 60 seconds, and persisting for 2—3 minutes. | Succinylcholine. |
| What are the CV effects of Succinylcholine, and what causes them? | Can cause transient sinus bradycardia accompanied by hypotension, cardiac arrhythmias, tachycardia, and possible cardiac arrest by increased vagal stimulation. |
| What electrolyte imbalance can be caused by Succinylcholine? | Hyperkalemia. |
| How can we reduce Succinylcholine-induced bradycardia? | Pre-treatment with anticholinergic agents, e.g., atropine, may reduce the occurrence of bradyarrhythmias. |
| Does Succinylcholine release histamine? | Yes, significantly. |
| Classified as a short-acting, nondepolarizing agent and has been shown to be an effective alternative to succinylcholine for rapid sequence endotracheal intubation, due to it’s short onset and fairly short duration of action. | Rocuronium. |
| What are the intermediate-acting NMB? | Atracurium, Cisatracurium, and Vecuronium. |
| What is the duration of action of the intermediate-acting NMB? | 30-60 minutes. |
| What is the long-acting NMB? What is its duration of action? | Pancuronium. 60-120 minutes. |
| Atracurium and Cisatracurium are metabolized by... | Serum esterases and spontaneous Hofmann elimination. |
| Laudnosine is a metabolite of what NMB? | Atracurium and Cisatracurium. |
| What can Laudanosine do? | Excite the CNS. |
| What NMB requires dosage adjustment and careful monitoring in a renal impaired patient? | Pancuronium. |
| Agents which are primarily excreted by hepatic metabolism or biliary excretion and require precautions in patients with hepatic disease. | Rocuronium and Vecuronium. |
| Succinylcholine has <blank> histamine-releasing properties | Moderate. |
| Atracurium and Cisatracurium have <blank> histamine-releasing potential; histamine-release is generally dose-related. | Mild-to-moderate. |
| Agents with histamine-releasing properties have precautions for use in... | Asthma or cardiac disease. |
| What are some adverse CV effects seen with histamine release? | Flushing, hypotension, sinus tachycardia, and bronchospasm. |
| Agents which lack significant histamine-releasing effects and do not block cardiac muscarinic receptors may be preferred in patients with... | Compromised cardiovascular status, cardiac disease, or asthma. |
| What are the NMB that do not significantly release histamine and do not block cardiac muscarinic receptors? | Rocuronium and Vecuronium. |
| What agent is more likely to cause prolonged muscular blockade or paralysis? | Pancuronium. |
| Prolonged blockade can result in... | Muscle paralysis, apnea, dyspnea, or respiratory depression. |
| Patients at risk for prolonged neuromuscular blockade with neuromuscular blockers include those with conditions or receiving medications that... | Impair neuromuscular function (e.g., myasthenia gravis) or potentiate the pharmacological actions of neuromuscular blockers (e.g., electrolyte imbalance). |
| Patients with myasthenia gravis are very sensitive to these agents and... | Small doses should be used. |
| What are some drugs that can potentiate neuromuscular blockade with the non-depolarizing agents? | Lithium, calcium salts, magnesium salts, inhalational anesthetics, local anesthetics, certain antibiotics, quinidine, procainamide, lidocaine, and others. |
| Tachycardia is most common with what NMB? Why? | Pancuronium, because it inhibits muscarinic receptors. |
| What conditions can increase Pancuronium's SE of tachycardia? | Age, electrolyte imbalance, and renal or hepatic failure. |
| What are some effects of histamine release? | flushing, hypotension, sinus tachycardF, urticaria, wheezing, and bronchospasm. |
| asthmatic patients treated with steroids and steroidal neuromuscular blockers (e.g., Vecuronium, Pancuronium) while on mechanical ventilation have experienced... | An acute myopathy lasting days to weeks. |
| <Blank> and <blank> has been reported with peripheral intravenous administration of non-depolarizing neuromuscular blockers. | Phlebitis, pain. |
| MH is initiated by uncontrolled release of <blank> from the <blank> in skeletal muscle. | Ca++, sarcoplasmic reticulum. |
| True or false: MH is more commonly seen with depolarizing blockers given with an anesthetic, even though it has also been reported with Succinylcholine alone or a volatile anesthetic alone. | True. |
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