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Autonomic pharma
UVa Med pharmacology block 2
| Question | Answer |
|---|---|
| Methacholine | synthetic Muscarinic agonist asthma diagnosis - exacerbates bronchospasm Inhalation |
| Carbachol | Synthetic muscarinic agonist miosis in opthalmic surgery via intraocular injection and WA glaucoma via topical tx causes accomodation of eye |
| Bethanechol | synthetic muscarinic agonist tx urinary retention, paralysis of GI tract phys fx: M3-stims exocrine glands, SMC, relaxes most sphincters,indirect vasodilation(NO, EDRF) M2-neg ino/chronotropic oral admin onset: 30min t1/2 1-6hrs, SC on5-15min t1/2 2hrs |
| Pilocarpine | Natural alkaloid muscarinic agonist WA glaucoma (prod's miosis) Topical admin M3-stims exocrine glands, SMC, relaxes most sphincters,indirect vasodilation(NO, EDRF) M2-neg ino/chronotropic |
| Atropine | Non-specific Muscarinic inhibitor organophosphate poisoning, mild diarrhea, pylorospasm, sinus bradycardia 2ndary to MI IM (for poision)Oral (for diarrhea), excr liver, kidney, feces side fx incr resp, restless, irritable, CI: NA glaucoma |
| Scopolamine | Non-specific Muscarinic inhibitor Sedation, motion sickness, dry secretions skin patch (motion sick), IM/IV/SC (sedation) excr liver,kidney,feces sidefx: drowsiness/sleep hallucinations, delirium CI NA glaucoma |
| Glycopyrrolate | Non-specific Muscarinic inhibitor, Polar, 4° decr salivation before anesthesia IM/IV admin onset 1min/15-30min respectively excr urine side fx: no CNS effects CI renal impairment |
| Tolterodine | Non-specific Muscarinic inhibitor overactive bladder t1/2 1-2hrs by oral admin, met'd liver, exc urine CI: urinary/gastric retention, NA glaucoma |
| Tropicamide/Cyclopentolate | non-specific muscarinic inhibitor produces mydriasis/cycloplegia short acting via local admin CI: primary glaucoma |
| Ipatropium Bromide | Muscarinic inhibitor Asthma, COPD tx phys fx: dilates bronch airways (useful when B2 agonists CI) Side fx: less drying than atropine, leaves ciliary motion intact |
| Nicotine | Nicotinic agonist stimulates ALL autonomic ganglia (both symp/parasymp effects) - tolerance to some effects but not CV t1/2 1-2hrs, met'd liver/kidney/lung sidefx: CNS stim, incr resp, emesis, tremors, addiction |
| Succinylcholine | nicotinic agonist but NM blocking agent muscle relaxant in surgery phase 1 block - motor endplate depol->inactivates NA/Ca channels->blocks trans Phase2 block: desensitization onset:.5-2min duration:5min sidefx: resp arrest in OD, malig hypertherm |
| Curare | Competitive nicotinic antagonist muscle relaxant in surgery physfx paralysis progs from small/rapid muscles first, NM blockade potent'd by ABs Onset:4-5min duration 1.5-2hr IV admin excr kidney66% sidefx NO CNS effects, histamine release, ANS ganglia |
| Cisatracurium | Competitive nicotinic antagonist muscle relaxant in surgery physfx paralysis progs from small/rapid muscles first, NM blockade potent'd by ABs onset 2min duration .5-1hr met'd plasma esterase +hoff degr. NO CNS effects, no histamine release |
| Rocuronium | Competitive nicotinic antagonist muscle relaxant in surgery physfx paralysis progs from small/rapid muscles first, NM blockade potent'd by ABs onset 1min duration .7-1.5hr excr liver sidefx: no cns effects, histmine release or ANS stim |
| Mivacurium | Competitive nicotinic antagonist muscle relaxant in surgery physfx paralysis progs from small/rapid muscles first, NM blockade potent'd by ABs onset 1min duration .5hrs met'd plasma esterase sidefx: no CNS, histmine, ANS effects |
| Physostigmine | AChE inhibitor Atropine poisoning, WA glaucoma, Alzheimer's physfx: forms covalent complex with AChe inhibs ACh hydrolysis T1/2:45min by IV/IM admin - well absorbed(lipid soluble) CI: AchE inhib hypersensitivity, stims @ musc & nic receptors |
| Neostigmine | AChE inhibitor Paralytic ileus, Myasthenia gravis, terminate competitive NM blockade T1/2:52min duration 4-6hrs by oral admin - 4`ammonium->poorly absorbed CI: AChE inhib hypersensitivity, stims @ musc & nic receptors |
| Edrophonium | AChE inhibitor Dx of cholinergic vs myasthenic crises, termination of compet NM blockade Onset 30-60sec duration 10 min by IV/IM admin-4`ammonium->poor abs CI: AChE inhib hypersensitivity, stims @ musc & nic receptors |
| Pyridostigmine | AChE inhibitor Myasthenia gravis Duration>6hrs by IV, oral admin physfx/sidefx: like neostigmine but decr fx |
| Isoflurophate (sim to DFP) | AChE inhibitor-organophosphate Insecticides physfx: very lipid soluble - irreversible inhibitor of AChE extremely toxic CNS, nic, musc fx, death by resp failure & CV collapse |
| Pralidoxime | Oxime - AChE reactivator after alkylphosphorylation Organophosphate poisoning (coadmin w/atropine) T1/2 75min via IV/injection, excr urine sidefx: early tx important or will not work, has weak neostimine-like fx in absence of organophos |
| How do Muscarinic Agonists dilate essentially all vascular beds despite a lack of parasympathetic innervation? | Endothelial cells have muscarinic receptors, and when stimulated, release Nitric Oxide or Endothelium Derived Relaxing Factor (EDRF). |
| What are some drug interactions to look out for with Neuromuscular Blocking Agents? | Neostigmine can stimulate motor end plates - used to reverse neuromuscular blockade by non-depolarizing antagonists can cause muscarinic effects. - ABs can chelate with Ca, potentiate neuromuscular blockade. Succcholine can cause malignant hyperthermia. |
| Which Neuromuscular Competitive Antagonist causes Histamine release? | Curare. This can cause hypotension (due to vasodilating effect of Histamine) |
| What is the effect of Acetylcholine on Sphincters? | Relaxation |
| What is the theraputic use for Scopolamine? | Sedation, and treats Motion Sickness |
| How do Cholinesterase inhibitors affect the GI tract? | Stimulate contractions along entire length |
| What is the effect of Acetylcholine on the Bronchi? | Contraction |
| How might the effects of a cholinesterase inhibitor differ from those of a muscarinic agonist? | A muscarinic agonist is going to enhance the response of muscarinic receptors. A cholinesterase inhibitor will enhance the response of muscarinic AND nicotinic receptors, because acetylcholine's life is prolonged and acts at both types. |
| What is the mechanism of action of Atropine and Scopolamine, and at which receptor types? | Competitive Inhibitors of ALL muscarinic receptors. Very little effect on nicotinic ganglia receptors, and no effect on NM junction. |
| What is the theraputic use for Neostigmine? | Paralytic Ileus Urinary Retention Myasthenia Gravis |
| What is the effect of Acetylcholine on the Intestines? | Contraction |
| What is the effect of Acetylcholine on Exocrine glands? | Secretion |
| Which sites in the body have predominantly parasympathetic tone? | Heart (slowing effect) Iris (constriction) Ciliary Muscle (Accomodation) GI Tract (enhances motility/secretions) Urinary Bladder (smooth muscle relaxation) Salivary Glands (secretion) |
| What is the effect of Acetylcholine on the Atria of the heart? | Decreased Contractility |
| How well are Cholinesterase Inhibitors absorbed? | Poorly, due to quarternary ammonium structure. Need large doses (Physostigmine is exception). |
| How do the effects of Atropine and Scopolamine differ in the CNS? | Atropine: Excitation of respiration, restlessness, irritability Scopolamine: Drowsiness, sleep, hallucinations, delirium. At high doses they both cause hallucinations/delirium. |
| What is the difference between the molecular mechanisms of M1/M3 and M2? | M1/M3 act through Phospholipase C --> IP3 + DAG --> Increased Ca2+ M2 acts through activation of K+ channels and inhibition of Adenylyl Cyclase. |
| What is the effect of Acetylcholine on the SA Node of the heart? | Decreases rate |
| What is the effect of Acetylcholine on the Uterus? | Contraction |
| What is the theraputic use for Pilocarpine? | Standard cholinergic used to treat Open-angle Glaucoma. (topical agent) **The miosis opens trabecular meshwork, increasing rate of aqueous humor flow and decreasing ocular pressure (Wikipedia) |
| What is the theraputic use for Ipratropium Bromide? | Asthma. It dilates bronchial airways, and dries them out less than atropine, and also leaves ciliary motion intact. **Not on drug list at end of chapter for pharm, but the drug was mentioned in the pharm notes, and in POM2 |
| How do the Nicotinic "Muscular", and the Nicotinic "Neuronal" receptors differ? | They have different responses to agonists and antagonists. Agonists: Phenyltrimethylammonium (Nm) as opposed to Dimethylphenylpiperazinium (Nn) Antagonists: Tubocurarine (Nm) as opposed to Trimethaphan (Nn) |
| Acetylcholine binds to what type of receptor in the neuro-muscular junction? | Nicotinic |
| What parts of the body are affected first when using a Neuromuscular Competitive Antagonist? | Small, rapidly moving muscles (eyes, fingers, ears, toes) |
| What is the theraputic use for Physostigmine? | Glaucoma, Atropine Poisoning |
| What are some unwanted effects of Neuromuscular Blocking Agents? | Poisoning/Clinical overdose is main concern. Can cause respiratory arrest. |
| What is the theraputic use for Glycopyrolate? | Pre-anesthetic to inhibit excessive salivation caused by inhalation anesthetics. |
| What are possible complications of using Synthetic Choline Esters? | Can exacerbate the following: Asthma Peptic Ulcer Coronary Insufficiency Intestinal Obstruction |
| What effects might you expect from a Cholinesterase Inhibitor? (Keeps Acetylcholine around longer, thus...) | Eye: Miosis/Accomodation spasm Skeletal Muscle: More excitable Exocrine Glands: Stimulated Bronchi: Contraction GI Tract: Contraction Urinary Tract: Contraction Heart: Bradycardia and decreased output |
| What is a dangerous complication of Atropine's effect on the eye? | Patients with narrow-angle Glaucoma can have a sharp rise in intraocular pressure, which can cause blindness. |
| Which sphincters are contracted by acetylcholine? (most are relaxed by acetylcholine) | Cardiac Pyloric Ileocecal |
| How do Depolarizing Neuromuscular Blocking agents work? | They are nicotinic agonists. They depolarize motor endplates tonically, inactivating voltage-dependent sodium/calcium channels and blocks synaptic transmission. |
| Which Neuromuscular Competitive Antagonist(s) can affect the Autonomic Ganglia? | Curare |
| Which sites in the body have predominantly Sympathetic tone? | Arterioles (constriction) Veins (dilation) Sweat Glands (secretion) Genital Tract (both para and symp tone cause stimulation) |
| What is the effect of Acetylcholine on the AV Node of the heart? | Decreased conduction velocity |
| How do Neuromuscular Competitive Antagonists work? | Interact with postjunctional nicotinic receptor and competitively block ACh action. Paralysis progresses from motor weakness to total paralysis. |
| What is the theraputic use for Atropine? | Treats mild diarrhea, pylorospasm, bradycardia (caused by hyperactive carotid sinus reflex, or in some cases of MI associated bradycardia). |
| What is the effect of Acetylcholine on arteries? | Dilation |
| What is the effect of Acetylcholine on the Lens of the eye? | Accomodation for near vision |
| What is DFP (Diisopropylflurophosphate)? | A Cholinesterase Inhibitor used as an insectiside. It is extremely toxic, and is a lipid soluble irreversible inhibitor of cholinesterase, causing CNS, muscarinic, and nicotinic effects |
| What is the effect of Acetylcholine on the Pupil of the eye? | Constriction |
| Why is Physostigmine used over Neostigmine to treat Atropine poisoning? | Physostigmine can cross the blood-brain barrier, and therefore treat CNS effects of atropine. Neostigmine cannot. |
| Acetylcholine binds to what type of receptor in the postganglionic parasympathetic nervous system? | Muscarinic ** EVERY response to Acetylcholine that is not at the ganglion or neuro-muscular junction is Muscarinic. |
| What is the effect of Acetylcholine on the Ureter? | Contraction |
| What is the theraputic use for Edrophonium? | Diagnostically to differentiate a Cholinergic crisis from a Myasthenic crisis. It is used for this purpose because of its short half-life. |
| How do Neuromuscular Competitive Antagonists affect consciousness and sensorium? CNS? | They do not affect them at all. They have no anesthetic, analgesic or CNS effects whatsoever. |
| How do Pancuronium and Rocuronium affect the ganglia? | They have very little effect (Important) |
| What is the mechanism of action for Cholinesterase Inhibitors? | Inhibit hydrolysis of Acetylcholine via covalent enzyme-substrate complex with Acetylcholinesterase (mimicks structure of acetylcholine and blocks it). They are hydrolyzed much more slowly, thus prolonging life of Acetylcholine. |
| What muscles are the first to recover after using a Neuromuscular Competitive Antagonist? | Recovery occurs in reverse order of paralysis (Ex: Diaphragm, then Limbs, etc. etc., Fingers, Eyes...) |
| How do Muscarinic Agonists decrease heart rate? | Decrease the rate of phase 4 SA Node spontaneous diastolic depolarization, and slow conduction and increase refractory period in AV Node. They also have a negative inotropic action on atrial muscle. |
| What is the effect of Acetylcholine on the Bladder? | Contraction |
| What is the theraputic use for Bethanechol? | Because of its marked effects on GI/Urinary tract, and miniscule effects on CV system, it is used to treat: Urinary Retention (minor use, alpha antagonists normally used) Paralysis of GI Tract (very minor use) |
| What is the effect of Acetylcholine on Sweat glands? | Secretion **Sympathetic Cholingeric |
| What are the five sites of drug action in the Acetylcholine life cycle that can be used pharmacologically? | 1. Blockade of Release 2. Interference with synthesis and uptake 3. Displacement of Transmitter 4. Mimic/Block Action at Receptor 5. Inhibit Destruction of Transmitter |
| How are Ganglionic Blockers used clinically? | They are not used clinically anymore. |
| What is the theraputic use for Carbechol? | Induce Miosis in opthalmic surgery Treat Wide-angle Glaucoma |
| Where are the main sites of action for theraputic Cholinesterase Inhibitors? | Eye Intestine Bladder NM Junction |
| What are the effects of nicotine acting on autonomic ganglia? (Important to know for smokers) | Can elicit both parasympathetic and sympathetic responses. Increases: HR/BP (via Sympathetic ganglia and Adrenal Medulla), GI Motility/Tone & Mouth/Bronchi Secretions (via Parasympathetic ganglia) |
| How does Succinylcholine affect CNS/Ganglia/Histamine release? | No CNS effect Affects both Vagal and Sympathetic. Significant Histamine release. |
Created by:
sam.mrosenfeld
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