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Nicotinic Pharma
Nicotinic pharmacology
| Question | Answer |
|---|---|
| What type of response at the membrane potential is caused by M1 receptor activation? | Secondary slow EPSP |
| What type of response at the membrane potential is caused by M2 receptor activation? | Inhibitory postsynaptic potential |
| What type of response at the membrane potential is caused by nicotinic receptor activation? | Action potential spike |
| What type of response at the membrane potential is caused by myriad peptides activation? | Late, slow EPSP |
| What agents can cause inhibitory effects at the ganglia? | dopamine, norepinephrine, acetylcholine (via M2), others; act by causing hyperpolarization |
| Why are agents that activate the ganglionic nicotinic receptor not good? | Actions too diffuse; better to use neuromodulating agents |
| What was trimethaphan used for? | Short acting blocker; rarely used for emergency control of blood pressure in patients with acute dissecting aortic aneurysm; rapidly reduce blood pressure in critically high hypertension |
| What are the effects of nicotine? | stimulates ganglia to cause diffuse responses (depends on underlying tone); desired effect in smoking, desensitization in smoking, toxicities from ingestions due to overstimulation of underlying tone followed by blockade |
| What are the effects of succinylcholine? | short acting depolarizing neuromuscular blocker; rapidly degraded by plasma butylcholinesterase; rarely reaches ganglia in sufficient quantities unless cholinesterase used |
| * Describe the physiolgical steps that lead to muscle action | Nerve action potential, vesicular acetylcholine release, depolarization (increased permeability to Na+ and K+), hydrolysis of acetylcholine by cholinesterase, muscle action potential, spread of excitation in muscles, muscle contraction |
| What is the underlying cause of myastenia gravis? | antibody mediated autoimmune disease targeting alpha-subunit of nAChRs at the neuromuscular junction |
| What are the treatment options for patients with myesthenia gravis? | No specific immunotherapy; symptomatic treatment with cholinesterase inhibitors combined with nonspecific immunsuppression with steroids and other drugs, plasmapheresis, and possible thymectomy |
| What anticholinesterase inhibs. are given to myesthenia gravis patients? | Pyridostigmine and neostigmine; ineffective to non-antibody mediated myesthenia gravis |
| Why can't neuromuscular blocking agents be used as substitutes for anesthesia? | Don't cross CNS and have no anxiolytic, sedative, or pain relieving properties |
| What class of drugs do tubocurarine, benzylisoquinolines, and ammonio steroids belong to? | Nondepolarizing (competitive) neuromuscular agents |
| What class of drugs does succinylcholine belong to? | depolarizing (noncompetitive) blocker |
| Competitive antagonists act by reducing the ___ but not the ____ or the ____ of opening for a single channel | frequency of channel opening; conductance or duration of channel opening |
| What therapy (drugs) can be given to reverse the effects of nondepolarizing neurmuscular blocking agents? | Since they are competitive, increase ACh action by blocking AChE with inhibitors (neostigmine, edrophonium); antimuscarinic can be given to prevent muscarinic actions of increased ACh |
| What is the series of events that occurs when a person is injected with nondepolarizing neuromuscular agents? | motor weakness --> flacid paralysis; small, rapid muscles relax before limbs and trunk; lastly, intercostal and diaphragm paralyzed; respiration ceases; recovery is in reverse order (diaphragm first) |
| How does succinylcholine work? | Depolarizing drug; acts by extending duration of channel opening; not degraded in synapse; it is the only depolarizing blocking drug |
| What occurs when a person is injected with succinylcholine? | Binds to nicotining receptor, opens channel, depolarizes motor end plate, spreads to adjacent membranes (contractions of motor units--> fasciculations), depolarizing (Phase I) block, flaccid paralysis, phase II block (rare) |
| What is the cause of phase II block? | Prolonged exposure to succinylcholine eventually results in membrane that is repolarized bu that is still blocked due to receptor desensitization (rare and not well understood; rare since AChE typically degrade succynilcholine quickly) |
| What things should you be concerned when choosing a neurmuscular blocker? | 1) duration , 2) minimize cardiovascular compromise and side effects, 3) mode of elimination (renal and hepatic failure) |
| Succinylcholine is only approved for procedures that are how long? | Only approved for ultrashort acting neuromuscular blocker |
| When is sugammadex used? | cyclodextrin compound; binds to ammonio steroids and prevents binding of the neuromuscular blocker to the receptor and increases renal elimination (don't use with renal failure); good for patients with liver failure |
| What are the biochemical considerations of succinylcholine (i.e. when is it contraindicated)? | patients with extensive tissue injury due to risk of ion imbalance; epecially excessive potassium loss |
| When should benzylisoquinones be avoided? | carry high risk of histamine release (compromises lung and cardiovascular function) |
| Atracurium might be chosen over rocuronium or vecuronium in what cases? | In patients with hepatic or renal failure ven though it has slight risk of histamine release since it is degraded in the plasma |
| Why shouldn't you mix succinylcholine with halogenated anesthetics? | Might precipitate life threatening malignant hyperthermia |
| How can antibiotics potentiate competitive blockers? | Antibiotics (AMINOGLYCOSIDES, TETRACYCLINES) that reduce Ca++ actions through chelation or interference with signaling can reduce ACh levels and increase potency of competitive blockers |
| What ionic imbalance caused by succinylcholine can be life threating? | Prolonged depolarization may cause K+ release and loss of systemic Na+, Cl-, and Ca++ (absorbed by muscles); efflux of K+ in patients with tissue injury may be deadly |
| Tubocurarine and other quarternary neuromuscular blocking devoid of ___ effects following clinical doses because they can't ___. | Central; cross the BBB |
| What are the effects on autonomic ganglia and muscarinic sites of tubocurarine? | partial blockade-->fall in blood pressure and tachycardia |
Created by:
karkis77
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