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158 Cards in this Set
- Front
- Back
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What neurotransmitters are at work in the parasympathetic nervous system?
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ACh is the only one. Presynaptic and postsynaptic.
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What neurotransmitters are at work in the sympathetic nervous system and what do they enervate?
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Presynaptic transmits ACh to postsynaptic ganglion which then sends:
NE to nicotinic receptors ACh to muscarinic receptors in sweat glands DA to DA receptors in renal system Some preganglionic sympatheric fibers project directly to Adrenal Medulla to trigger Epinephrine release into bloodstream |
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List the Non-selective Alpha-receptor blockers:
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• Phentolamine (Regitine)
• Phenoxybenzamine (Dibenzyline) |
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List the Alpha1 selective blockers
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• Prazosin (Minipress)
• Terazosin (Hytrin) • Doxazosin (Cardura) • Alfuzosin (Uroxatral) • Tamsulosin (Flomax) • Silodosin (Rapaflo) |
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List the Alpha2 selective blockers
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Yohimbine
(you didn't fall for the whole "list" thing, did you?) |
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List the Non-selective Beta-receptor blockers
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• Propranolol (Inderal)
• Timolol (Timoptic) • Nadolol (Corgard) |
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List the Beta1-blockers (cardioselective):
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• Metoprolol (Lopressor)
• Atenolol (Tenormin) • Bisoprolol (Zebeta) • Esmolol (Brevibloc) • Betaxolol (Betoptic) • Nebivolol (Bystolic) |
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List the Beta-Blockers with (ISA) Intrinsic Sympathetic Activity
(aka Partial Agonists) |
• Pindolol (Visken)
• Acebutolol (Sectral) • Carteolol (Cartol) |
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List the Combined alpha & beta-blockers:
(aka antisympathetics) (aka antiadrenergics) |
• Labetalol (Normodyne)
• Carvedilol (Coreg) |
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List the Drugs affecting sympathetic neurotransmitter release
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• Guanethidine (Ismelin)
• Reserpine |
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List the Neurotransmitter Synthesis inhibitors
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Metyrosine (Demser)
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List the Catecholamines
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• Epinephrine (Adrenalin)
• Norepinephrine (Levophed) • Isoproterenol (Isuprel) |
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List the Alpha agonists
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• Phenylephrine (Neo-Synephrine)
• Pseudoephedrine (Sudafed) • Xylometazoline (Otrivin) • Oxymetazoline (Afrin) • Midodrine (ProAmatine) |
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List the Alpha-2 agonists
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• Clonidine (Catapres)
• Methyldopa (Aldomet) • Apraclonidine (Iopidine) |
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List the Beta-1 agonists
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• Dobutamine (Dobutrex)
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List the Beta-2 agonists
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• Albuterol (Ventolin)
• Terbutaline (Brethine) • Ritrodine (Yutopar) • Salmeterol (Serevent) |
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List the Indirect Adrenergic Stimulants
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• Ephedrine
• Amphetamine • Methylphenidate (Ritalin) • Methamphetamine • Cocaine • Tyramine |
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List the Dopamine Agonists
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• Dopamine (Intropin)
• Fenodolpam (Corlopam) |
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List the Non-Depolarizing Neuromuscular Blockers
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• d-Tubocurarine
• Pancuronium (Pavulon) • Vecuronium (Norcuron) • Doxacurium (Nuromax) • Atracurium (Tracurium) • Cisatracurium (Nimbex) • Rocuronium (Zemuron) |
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List the Depolarizing Neuromuscular Blocker
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Succinylcholine (Anectine)
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List the Ganglion Blockers
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• Mecamylamine (Inversine)
• Trimethaphan • Hexamethonium |
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List the Cholinergic (Muscarinic) Antagonists
(aka anticholinergics) |
• Atropine (generic)
• Scopolamine (generic) • Tolterodine (Detrol) • Fesoterodine (Toviaz) • Darifenacin (Enablex) • Oxybutynin (Ditropan) • Trospium (Sanctura) • Glycopyrrolate (Robinul) • Dicyclomine (Bentyl) • Solifenacin (Vesicare) • Ipratropium (Atrovent) • Tiotropium (Spiriva) • Tropicamide (Mydriacil) • Diphenoxylate-atropine (Lomotil) • Benztropine (Cogentin) There's no way you knew this whole list! |
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List the Direct-Acting Cholinergic Agonists
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• Acetylcholine (Miochol)
• Bethanechol (Urecholine) • Pilocarpine (Isopto Carpine; Pilocar) • Cevimeline (Evoxac) • Carbachol (Isopto Carbachol) • Methacholine (Provocholine) • Nicotine • Varenicline (Chantix) |
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List the Cholinesterase Inhibitors
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• Edrophonium (Tensilon)
• Neostigmine (Prostigmin) • Physostigmine (Eserine) • Pyridostigmine (Mestinon) • Echothiophate • Ambenonium (Mytelase) • Demecarium (Humorsol) • Organophosphate pesticides • Donepezil (Aricept) • Rivastigmine (Exelon) • Galantamine (Reminyl) • Pralidoxime (2-PAM) |
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What autonomic transmitters work on the GI track and what are their effects?
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Sympathetics: NE and E inhibit GI activity and descrease ACh release
Parasympatherics: ACh excites GI activity; stimulates smooth muscle; stimulates secretion of mucus and gastric acid. |
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What are the major intrinsic transmitters of the enteric system and what are their effects?
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Serotonin (5HT): excitatory
Nitric Oxide (NO): inhibitory |
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what are the primary locations and actions of the muscarinic receptors?
What mechanisms do they use? |
M1 - CNS and exocrine glands. Primarily Increase Secretions.
- Gq coupled. (PLC->IP3 and DAG->^C++-> depolarization. M2 - heart, some smooth muscle, and presynaptically on neurons; slows heart, and decreases neurotransmitter release - Gi receptors. inhibit adenylyl cyclase -> reducing cAMP -> open K+ channels -> hyperpolarizing cells M3 - exocrine glands, smooth muscle and endothelium; contracts smooth muscle; increases saliva - Gq receptor. Like M1 above. M4 & M5 are found mostly in the brain and will not be tested for this unit. |
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what are the nicotinic receptor subtypes? Where are they located? What do they do? What mechanisms do they use?
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Nn receptors are found in autonomic ganglia and the adrenal medulla
Nm receptors are in skeletal muscle - all nicotinic receptors open Na+ channels and depolarize neurons or muscle cells. |
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What are the types of cholinergic receptors?
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Muscarinic (M1, M2, M3, M4, M5)
Nicotinic (Nn & Nm) |
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What are the adrenergic receptors? Where are they located? What are their mechanisms of action?
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Alpha1 (α1) receptors are found in smooth muscle
- coupled to Gq protein (excitatory) - PLC -> IP3 and DAG -> Ca++ increase -> cell depolarizes Alpha2 (α2) receptors are found on presynaptic terminals, in platelets, lipocytes, and smooth muscle - coupled to Gi protein (inhibitory) - inhibits adenylyl cyclase, decreasing cAMP Beta1 (β1) receptors are found on many pre- and post-synaptic sites and in the heart - coupled to Gs (excitatory) - stimulates adenylyl cyclase => increasing cAMP Beta2 (β2) receptors are found on postsynaptic smooth muscle, bronchioles, heart - coupled to Gs, stimulate adenylyl cyclase - effect in tissue may be stimulation or relaxation, depending on tissue Beta3 is found on lipocytes - coupled to Gs, stimulate adenylyl cyclase |
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What are the dopaminergic receptors? Where are they located? What are their mechanisms of action?
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D1, D5: found in brain and renal vascular bed
- stimulate adenylyl cyclase, increasing cAMP D2, D3, D4: found in brain and various other tissues - inhibit adenylyl cyclase |
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Describe receptor down-regulation?
Describe receptor up-regulation? |
receptors become internalized or destroyed in response to repeated stimulation from agonist. Decreases pharmacological effect
receptors increase in number or affinity in response to missing or diminished neurotransmitters. ay increase pharmacological effect |
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Describe autonomic nervous system effect on blood vessels
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Parasympathetic: No parasympathetic innervation. However, muscarinic receptors on endothelium can trigger release of NO which relaxes blood vessels.
Sympathetic: - B2 receptors dilate coronary arteries and vessels to skeletal muscles. Increases flow to muscles and heart. - A2 receptors constrict small vessels to skin, nose, eyes, etc. Constrict veins. Decreases flow to skin. Increases venous return to heart. |
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Describe ANS effects on heart
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Parasympathetic: M2 receptors in atrium decrease heart rate at the SA node, slightly decrease atrial contractility, and slows AV conduction.
Sympathetic: B1 (and B2) receptors in heart increase heart rate, AV and SA node conduction, automaticity, and atrial contractility |
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Describe ANS effect on lungs
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Parasympathetic
M2 and M3 receptors in the lung cause bronchoconstriction, especially in asthmatics. Sympathetic β2 receptors in the lung respond to circulating epinephrine to relax the bronchioles and increase secretions |
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Describe ANS effect on HEENT
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Parasympathetic
- M3 receptor activation causes profuse secretion from salivary and lacrimal glands - M3 receptors cause miosis and contraction of the ciliary muscle, which decreases intraocular pressure and produces accommodation for near vision in the eye Sympathetic - M1 and M3 receptors increase sweating (ACh from cholinergic fibers of sympathetic chain) - α1-receptors increase secretion from the salivary gland, but to a much smaller degree than does muscarinic stimulation - α1 receptors constrict the radial muscle, causing dilation of pupils - α2 receptors in the eye decrease intraocular pressure - α receptors cause vasoconstriction in nasal passages, and are used as decongestants |
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Describe ANS effect on Genitourinary system
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Parasympathetic
- M3 receptors contract the bladder wall detrusor muscle and relax the sphincters and trigone muscle, making it easier to void - M3 receptors promote erection in men Sympathetic - β2 receptors relax the urinary bladder and uterus - α1 receptors usually contract sphincters, and increase motility and tone in the ureter - α1 receptors promote ejaculation in men - β1 receptors increase release of renin from the kidney |
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Describe metabolic effects of ANS
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Parasympathetic
No direct innervation; however, reduced HR and increased GI activity do effect metabolism Sympathetic: - β2 and α1 receptors increase glycogenolysis and gluconeogenesis in the liver - α2 receptors decrease secretion of insulin from the pancreas - β3 receptors increase lipolysis - β2 receptors increase increase potassium uptake into skeletal muscle |
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What are total effects of Alpha1 receptors?
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- contracts radial iris mm (mydriasis)
- contracts skin, splachnic vessels - contracts GI sphincters - contracts urinary sphincter - promotes ejaculation - promotes apocrine secretion - contracts pilomoter mm (goosebumps) - promotes Gluconeogenesis and Glycogenolysis |
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what are total effects of Alpha2 receptors?
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- contracts skin, splachnic vessels
- relaxes GI walls - promotes ejaculation - promotes apocrine secretion - contracts pilomoter mm (goosebumps) - promotes Gluconeogenesis and Glycogenolysis |
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what are total effects of B1 receptors?
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- relax ciliary muscle
- accelerate SA node - accelerate ectopic pacemakers - increase contractility - promote renin release in kidney |
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what are total effects of B2 receptors?
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- all B1 heart effects but less responsible
- relax skeletal muscle vessels - relaxes bronchiolar smooth muscle (bronchodilates) - relaxes GI walls - relaxes bladder wall - relaxes uterus - promotes Gluconeogenesis and Glycogenolysis |
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What do B3 receptors do?
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promote lipolysis
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What are the total effects of M3 receptors?
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- contract Iris circular muscle (miosis)
- contract ciliary muscle (accomodation) - relaxes endothelium (releasing NO in bloodstream) - contracts bronchiolar smooth muscle (bronchoconstricts asthmatics) - contracts GI walls - relaxes GI sphincters - increases GI secretion - contracts bladder wall - relaxes urinary sphincter - contracts uterus - promotes erection - increase eccrine secretion (sympathetic) |
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What are the total effects of M2 receptors?
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- decelerates SA node
- decreases atrial contractility - promotes erection - increase eccrine secretion (sympathetic) |
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Where are the effects of muscarinic receptor agonists are most pronounced?
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in the eye, GI tract, bladder, and salivary and sweat glands.
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Choline esters
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include methacholine, carbachol (carbamoylcholine) and bethanechol. They are similar to ACh in their effects, but are not hydrolyzed as rapidly by cholinesterase.
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Alkaloids
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include muscarine, pilocarpine and oxotremorine. These are relatively specific for muscarinic receptors. They are tertiary amines, and thus are well absorbed and get into the brain.
- Pilocarpine (Pilocar) is the only one of these drugs used clinically Nicotine, lobeline and dimethylphenylpiperazinium (DMPP) are alkaloids that are fairly selective for nicotinic receptors. Varenicline is a partial agonist at nicotinic receptors. Nicotine and varenicline are the only ones used clinically. |
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What are Effects of Muscarinic Receptor Stimulation on the Eye?
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• miosis
• accommodation for near vision • increases drainage of aqueous humor and decreases intraocular pressure. |
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What are Effects of Muscarinic Receptor Stimulation on the Heart?
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• decrease heart rate.
• decreases contractility • decrease conduction • M2 receptors decrease the release of NE in the heart, causing further slowing. • M3 receptors relax endothelial cells releasing nitric oxide, which produces vasodilation. • In contrast to the effects of vagal stimulation, which can be profound, most muscarinic agonists in normal therapeutic doses have very few cardiovascular effects. |
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What are the Side Effects and Toxicity of Muscarinic Agonists?
What are the contraindications? |
Side Effects
• Nausea, vomiting, diarrhea • Abdominal cramps, belching • Salivation and sweating • Cutaneous vasodilation • Bronchoconstriction, esp in asthma • Bladder tightness • Blurred vision and difficulty with visual distance accommodation Contraindications ● peptic ulcer ● coronary insufficiency ● asthma |
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How are cholinergic agonists used to treat glaucoma?
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muscarinic agonists reduce intraocular pressure by causing contraction of the iris sphincter and ciliary muscle, thus increasing outflow of aqueous humor. They may also decrease production of aqueous humor.
Pilocarpine is sometimes administered into the eye for treatment of glaucoma. |
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How are cholinergic agonists used to treat GI and urinary tract?
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some conditions that involve decreased bowel activity without obstruction, post-operative ileus and congenital megacolon, may be treated with muscarinic agonists. Bethanechol (Urecholine) is most commonly used to stimulate peristalsis in the GI tract. Bethanechol is also used to facilitate voiding in patients with urinary retention.
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How are cholinergic agonists used to treat dry mouth?
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Pilocarpine (Pilocar) and cevimeline (Evoxac) are used to increase salivation in treatment of Sjögren’s sydrome, or for dry mouth following head and neck radiation. The main side effect, especially with pilocarpine, is sweating. Cevimeline is selective for M3 receptors and does not cause as much sweating.
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How is Nicotine poisoning treated?
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1. with atropine to block muscarinic receptors
2. with anticonvulsants to decrease seizures 3. with mechanical respiration until neuromuscular blockade is reversed |
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What are the symptoms of nicotine poisoning?
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• Vomiting, which generally occurs fairly rapidly (central and peripheral actions)
• Convulsions from CNS stimulation, followed by coma and respiratory arrest • Muscle contractions due to NMJ stimulation, followed by desensitization and paralysis • Hypertension and cardiac arrhythmias may also occur, followed by hypotension |
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Varenicline (Chantix)
Group? Receptor: Type and Location Clinical Uses? Side Effects? Contraindications? |
Group: Nicotinic Agonist (partial)
Receptor Type: A4B2 Receptor Location: Brain Clinical Uses: Treats nicotine addiction; substitutes for nicotine to relieve the craving; diminishes the effects of nicotine if a person smokes Side Effects: nausea, vomiting, constipation and flatulence; sleep disturbance, vivid nightmares, psychosis and mania, anxiety, and suicidal ideation. Contraindications: none |
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What are general uses of Cholinesterase Inhibitors?
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• inhibit the breakdown of ACh following its release into the synaptic cleft.
• This increases the amount of time that ACh is available to act on the receptors. • Cholinesterase inhibitors are especially useful in diseases in which cholinergic inputs have been decreased, or where the responsiveness of receptors to ACh is reduced. • They are also used to reverse the effects of neuromuscular blocking agents in surgery |
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What are the general effects of AChE inhibitors?
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The effects of cholinesterase inhibitors will be similar to stimulation of both muscarinic and nicotinic receptors, because the effect of ACh is enhanced at all sites where it is released. However, prolonged stimulation of nicotinic receptors may result in desensitization. As with nicotine, the effect in a particular tissue will reflect the predominant tone in that tissue.
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What are the effects of AChE inhibitors on the brain?
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increased alertness and improved memory via stimulation of M1 and NN receptors in low doses. High concentrations may desensitize nicotinic receptors, cause convulsions, and produce respiratory arrest.
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Neostigmine (Prostigmin)
Group? Receptor/Method of Action? Clinical Uses? Side Effects? Contraindications? |
Group: AChE inhibitor; carbamate
Mechanism of action: Binds to AChE and extends duration of action of ACh Special Features: quaternary amine, does not penetrate the blood brain barrier; poor oral absorption Clinical Uses: nevertheless given orally to increase the duration of action of ACh in myasthenia gravis; may have some direct stimulatory effect on the neuromuscular junction that contributes to its beneficial effect. Side Effects: muscarinic side effects (Nausea, vomiting, diarrhea, Abdominal cramps, belching, Salivation and sweating, Cutaneous vasodilation, Bronchoconstriction, Bladder tightness, Blurred vision) Contraindications: peptic ulcer, coronary insufficiency, asthma |
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Edrophonium (Tensilon)
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is a quaternary ammonium compound that does not cross the blood brain barrier. It must be injected and is very short-acting (5-10 min). It is used for diagnosis of myasthenia gravis.
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Physostigmine (Eserine)
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AChE inhibitor;
instilled directly in the eye to treat glaucoma. Because it can easily get into the CNS and cause side effects, it is rarely if ever used orally |
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Donepezil (Aricept)
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AChE inhibitor; very similar to physostigmine; well absorbed orally and gets into the brain. Used to treat Alzheimer’s disease
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Echothiophate
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irreversible AChE inhibitor;
organophosphate with a very long duration of action. It is applied in the eye when long-term control of intraocular pressure is required, often in glaucoma emergency situations. It is not lipid soluble, so does not get absorbed systemically |
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Pilocarpine (Isopto Carpine; Pilocar)
Group? Receptor? Considerations? Uses? Side Effects? Contraindications? |
Group: Cholinergic Agonist; alkaloid
Receptors: muscarinic Consideration: tertiary amines are well-absorbed and can cross BBB. Uses: glaucoma; dry mouth Side Effects: sweating; blurred vision; muscarinic side effects Contraindications: muscarinic contraindications; peptic ulcer; coronary deficiency; asthma |
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Bethanechol (Urecholine)
Group? Receptor? Considerations? Uses? Side Effects? Contraindications? |
Group? Cholinesterase Inhibitor; choline ester
Receptor? muscarinic Considerations? quaternary structure; will not cross BBB; poor oral absorption Uses? GI increase; urinary retension; Side Effects? muscarinic side effects Contraindications? muscarinic contraindications |
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Neostigmine (Prostigmin)
Group? Receptor/Method of Action? Clinical Uses? Side Effects? Contraindications? |
Group: AChE inhibitor; carbamate
Mechanism of action: Binds to AChE and extends duration of action of ACh Special Features: quaternary amine, does not penetrate the blood brain barrier; poor oral absorption Clinical Uses: nevertheless given orally to increase the duration of action of ACh in myasthenia gravis; may have some direct stimulatory effect on the neuromuscular junction that contributes to its beneficial effect. Side Effects: muscarinic side effects (Nausea, vomiting, diarrhea, Abdominal cramps, belching, Salivation and sweating, Cutaneous vasodilation, Bronchoconstriction, Bladder tightness, Blurred vision) Contraindications: peptic ulcer, coronary insufficiency, asthma |
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Edrophonium (Tensilon)
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- AChE inhibitor
- quaternary ammonium compound that does not cross the blood brain barrier. - must be injected and is very short-acting (5-10 min). - used for diagnosis of myasthenia gravis. |
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Physostigmine (Eserine)
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AChE inhibitor;
instilled directly in the eye to treat glaucoma. Because it can easily get into the CNS and cause side effects, it is rarely if ever used orally |
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Donepezil (Aricept)
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AChE inhibitor; very similar to physostigmine; well absorbed orally and gets into the brain. Used to treat Alzheimer’s disease
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Echothiophate
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irreversible AChE inhibitor;
organophosphate with a very long duration of action. It is applied in the eye when long-term control of intraocular pressure is required, often in glaucoma emergency situations. It is not lipid soluble, so does not get absorbed systemically |
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Cevimeline (Evoxac)
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Cholinergic Agonist
M3 specific Pilocarpine (Pilocar) and cevimeline (Evoxac) are used to increase salivation in treatment of Sjögren’s sydrome, or for dry mouth following head and neck radiation. The main side effect, especially with pilocarpine, is sweating. Cevimeline is selective for M3 receptors and does not cause as much sweating |
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Carbachol (Isopto Carbachol)
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non-specific Cholinergic Agonist
mimics parasympathetic response |
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Nicotine
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selective Cholinergic Agonist
alkaloid nicotinic receptors at Low Doses: increases alertness and attentiveness; analgesic; promotes dopamine release contributing to addictive behavior; increases BP & HR followed by reactive bradycardia at high doses: cause tremor, convulsions, vomiting and increased respiration, followed by respiratory depression Poisonous, especially if eaten |
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Pralidoxime (2-PAM)
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antidote for acute organophosphate poisoning
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Glaucoma:
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may be treated either with direct acting cholinergic agonists or with cholinesterase inhibitors. Pilocarpine is sometimes used to treat open-angle glaucoma, although it may cause blurred vision. Acute closed-angle (AKA narrow angle) glaucoma is treated with a combination of pilocarpine and a cholinesterase inhibitor (physostigmine or echothiophate) until the pressure is controlled and the problem can be corrected with surgery
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Gastrointestinal and Urinary problems
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Neostigmine has been used for paralytic ileus or atony of the urinary bladder, but the dose is very high, due to poor absorption. Bethanechol is a better choice.
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Myasthenia gravis
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Neostigmine, pyridostigmine or ambenonium are the drugs used for chronic therapy of this disease. These are fairly short acting, and need to be administered several times a day.
Edrophonium is used for diagnosis of myasthenia gravis, due to its short action. If the patient has myasthenia gravis, edrophonium will cause an improvement in muscle strength that lasts about 5 minutes and then fade. |
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Reversal of neuromuscular blockade in surgery:
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The effects of the non-depolarizing neuromuscular blocking agents can be reversed by administration of cholinesterase inhibitors. Neostigmine or edrophonium are commonly injected for this purpose.
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SLUDGE
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used to describe the muscarinic manifestations of Salivation, Lacrimation, Urination, Defecation, Gastric distress, and Emesis
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What are the signs of acute organophosphate poisoning?
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• SLUDGE
• Other muscarinic manifestations include miosis, sweating, bronchoconstriction, nausea, vomiting, diarrhea, bradycardia and hypotension. • Stimulation of nicotinic receptors will lead to neuromuscular blockade. Initial muscle twitching is followed by weakness that eventually leads to paralysis. Paralysis of the respiratory muscles is especially serious and may lead to death. • CNS effects include confusion, ataxia, slurred speech, convulsions and coma, similar to nicotine overdose. • If exposure is by inhalation, effects on respiration and the eye (miosis, ocular pain, vision impairment) will be observed first. |
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How do you treat acute organophosphate poisoning?
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1. administration of atropine to decrease muscarinic effects until pupils become dilated
2. injection of pralidoxime (PAM) to prevent enzyme aging- this must be done rapidly 3. maintenance of respiration |
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Understand the mechanism of action of muscarinic receptor blockers
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bind to muscarinic receptors and block the effects of acetylcholine. Their effect will be to antagonize the actions of parasympathetic stimulation (think "semi-sympathetic")
The prototype drug for this class is atropine. |
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which muscarinic receptor blockers enter the CNS
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Scopolamine
Atropine at toxic doses |
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describe the effects and clinical uses of muscarinic receptor blockade in the eye
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Clinical Use: mydriasis - used for eye exams. Tropicamide preferred choice bc short acting
Side Effects - cycloplegia (loss of accomodation), photophobia (light sensitivity), dry eyes Contraindications: Do not use on pts with narrow angle glaucoma |
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Understand the cardiovascular effects of muscarinic receptor blockade
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React on M2 receptors in atria and sinoatrial node.
Effects are dose dependant Very Low Doses: slight bradycardia due to only affecting presynaptic Moderate Doses: remove vagal tonic inhibition -> tachycardia Most noteable in young, healthy adults. Very little effect on infants and elderly Atropine is used in early myocardial infarction to decrease bradycardia or AV block |
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Ipratropium (Atrovent)
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- used in treatment of COPD and in acute asthma attacks.
- quaternary ammonium compounds; not well absorbed; effects limited to the lung - Does NOT decrease bronchial secretions, unlike other M-receptor antagonists - most common side effect will be dry mouth |
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What are the effects of muscarinic receptor blockade on the gastrointestinal and genitourinary tracts and clinical uses related to it.
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• inhibit motility and secretions in the GI tract
• antispasmodics; Dicylomine (Bentyl) • do not provide complete inhibition of gastric acid secretion, and there are better drugs for treatment of peptic ulcer. • Atropine is combined with an opioid (diphenoxylate; Lomotil) to treat diarrhea • Relaxes ureter and bladder wall; reduces voiding • treats overactive bladder and urinary frequency. |
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What are the effects of muscarinic receptor blockade in the CNS, and why it is useful?
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Effect: causes drowsiness and amnesia at low doses. Use: pre-anesthetic to cause sedation and amnesia
Effect: counters vestibular disturbances: Uses: treat motion sickness and nausea Effect: restore balance between ACh and DA in the corpus striatum Uses: treat Parkinson's and Parkinson-like symptoms of antipsychotic drugs |
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What are the symptoms of atropine overdose
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Dry as a bone, blind as a bat, mad as a hatter, red as a beet
1. dry mouth 2. mydriasis, loss of accomodation, visual disturbances 3. agitation, delirium, toxic psychosis 4. tachycardia, hot flushed skin |
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What are the contraindications to muscarinic receptor blockers?
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• Uncontrolled or narrow angle glaucoma,
• Elderly men with benign prostatic hyperplasia (BPH). Muscarinic blockade will cause urinary retention |
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How and when is atropine used to treat poisoning?
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- Treats Cholinesterase Inhibitor poisoning (organophosphates) and Muscarine poisoning (mushrooms).
- Administer until dry mouth and mydriasis appear (tells you M recpetors are being blocked) - continue maintenance dose until other effects of AChEI and Muscarine poisoning wear off |
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Atropine (generic)
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- Prototype Muscarinic Receptor Antagonist
- alkaloid found in Belladonna plant and Jimson weed - Effect is Dose Dependant - Low = dry mouth and reduced sweating - Medium = tachycardia and visual disturbances - High = GI decrease and urinary retention - Very High/Toxic = CNS effects ( ataxia, hallucinations, delirium and coma) - Does not freely cross BBB so little CNS effect at moderate doses Clinical Uses: 1. decrease bradycardia due to excessive vagal tone or to reverse AV block 2. combined with opioid to treat diarrhea (Lomotil) |
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Scopolamine (generic)
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Group: Muscarinic Antagonist
- Alkaloid - derived from Belladonna plant Notable: enters the CNS very easily; Well absorbed through skin Uses: 1. Transderm Scop (patch) is used to prevent motion sickness. Also useful in treating nystagmus 2. can be used as pre-anesthetic to cause sedation and amnesia, and to dry bronchial and salivary secretions Side Effects: 1. euphoria/abuse potential 2. dry mouth, drowsiness, amnesia. Patch reduces these effects. 3. Toxic Dose: excitement, agitation, hallucinations and coma |
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Tolterodine (Detrol)
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Selective M3 receptor antagonist
Treats overactive bladder and bladder spasms. Does not cross BBB and has few CNS side effects Preferred Rx for elderly pts with urinary frequency |
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Oxybutynin (Ditropan)
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Selective M3 receptor antagonist
Similar to Tolterodine. Used to prevent bladder spasm after prostate surgery. |
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Glycopyrrolate (Robinul)
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Muscarinic Receptor Antagonist
used in surgery to prevent vagal responses when visceral organs are to be handled. |
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Dicyclomine (Bentyl)
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Muscarinic receptor antagonist
used as a gastrointestinal antispasmodic |
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Solifenacin (Vesicare)
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Selective M3 receptor antagonist
used for treatment of overactive bladder It has little effect on salivation. |
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Tropicamide (Mydriacil)
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muscarinic receptor antagonist
synthetic derivative of atropine with shorter duration used to dilate pupils not recommended for pediatric use |
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Diphenoxylate-atropine (Lomotil)
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combination of opioid with atropine
used to treat diarrhea unpleasant effect of high doses of atropine limits abuse potential with opioid |
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what effect will M-receptor antagonists have on blood vessels
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very little. No M receptors in blood vessels
Will counter release of NO from endothelial M receptors Toxic doses of atropine will results in vasodilation of face to counter hyperthermia |
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Tropicamide (Mydriacil)
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muscarinic receptor antagonist
synthetic derivative of atropine with shorter duration used to dilate pupils not recommended for pediatric use |
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Diphenoxylate-atropine (Lomotil)
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combination of opioid with atropine
used to treat diarrhea unpleasant effect of high doses of atropine limits abuse potential with opioid |
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what effect will M-receptor antagonists have on blood vessels
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very little. No M receptors in blood vessels
Will counter release of NO from endothelial M receptors Toxic doses of atropine will results in vasodilation of face to counter hyperthermia |
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Understand the mechanisms of neuromuscular blockade by non-depolarizing agents.
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- bind to Nm receptor and do not allow Ca++ channel to open.
- reduces the endplate potential so that an action potential can no longer be generated - results in a decrease in muscle contraction and paralysis of the muscle - Because they are competitive antagonists, their effect can be overcome by increasing ACh - The prototype drug is d-tubocurarine. |
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Understand the difference between non-depolarizing and depolarizing neuromuscular blockade.
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Non-depolarizing Nm blockades prevent channel from opening. Slow onset with extended duration of effect.
Depolarizing Nm blockades result in an initial stimulation and contraction of the muscle followed by desensitization and blockade. Onset of action and recovery are very rapid. Used for procedures that require rapid and short-acting effects such as intubation. |
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Describe the "train of four" with each type of neuromuscular blocker.
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Thumb twitch that measures paralysis effectiveness during anesthesia.
With non-depolarizing block, twitch starts high and then diminishes in amplitude over time. (i.e. Fades) With Phase I polarizing block, twitch is constant but diminished amplitude. Phase II polarizing block is rare and only occurs if succinylcholine is used in excessive doses, for too long or reacts withother anesthetics. In this case, the Phase I diminished twitch wears off and twitch becomes identical to Nondepolarizing twitch. |
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which neuromuscular blocking agents have cardiac side effects?
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- Succinylcholine may stimulate cardiac muscarinic receptors, which may slow the heart and decrease force of contraction
- Pancuronium causes a moderate block of ganglionic N & M receptors, resulting in vagal blockade, tachycardia, NE release which increases tachycardia |
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what are the drug interactions you need to be aware of with Nm blackades?
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• Inhaled anesthetics augment blockade in a dose-related fashion.
- Isoflurane = most effect - nitrous oxide =least. • The combination of halothane and succinylcholine may cause malignant hyperthermia. • Local Anesthetics enhance blockade - low doses depress post-tetanic potentiation - high doses inhibit ACh-induced muscle contraction by blocking ion channels • Aminoglycoside antibiotics (e.g. streptomycin) enhance Nm blockade • Tetracyclines may also enhance neuromuscular blockade, through Ca++ chelation. • Ca++-channel blockers may increase sensitivity to neuromuscular blockade. |
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which neuromuscular blocking agents cause release of histamine?
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• d-Tubocurarine
• Atracurium • mivacurium |
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What are the effects and problems specific to use of succinylcholine
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- only depolarizing Nm blocker
- hydrolyzed by plasma pseudocholinesterase - genetic differences create wide range of ability to metabolize - prolonged depolarization results in K+ exiting cell and entring bloodstream. Too much K+ in blood can cause cardiac arrest - may stimulate M receptors in heart causing bradycardia, decreased CO - may stimulate N receptors in heart causing arrthymias - muscle pain common side effect - may cause increase intragastric pressure resulting in regurgitation and aspiration - may increase ocular pressure for about 5 minutes - may cause Malignant hyperthermia when mixed with halothane Contraindications - Patients with extensive soft tissue damage or burns, with nontraumatic rhabdomyolysis, spinal cord injuries with paraplegia or quadriplegia, or muscular dystrophy - children under 8 yo if avoidable |
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What are the effects of disease states on the actions of neuromuscular blocking agents.
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• Patients with myasthenia gravis will have a much greater response to non-depolarizing Nm blockers
• Older patients have slower recovery from the drugs, due to decreased metabolism • Patients with severe burns or upper motor neuron disease will be more resistant to non-depolarizing blockade, probably because they have developed more receptors. However, succinylcholine is not a good choice in these patients. |
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Understand the effects of ganglion blockade
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- block all Autonomic innervation
- effects depend on dominant tone in specific organs CNS - sedation, tremor, abnormal movements, and mental status changes Eye - cycloplegia, mild dilation of pupil Blood vessels - vasodilation; decreased BP; orthostatic hypotension; Heart - decreased contractility; tachycardia GU - bladder retention; penile dysfunction No Sweating |
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d-Tubocurarine
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Prototype Non-Depolarizing Nm Blocker
Slow onset (4-6 min) with long duration of action (2-3 hrs). Difficult to reverse if needed Eliminated by kidney causes histamine release, which can produce hypotension and bronchospasm no longer used clinically |
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Pancuronium (Pavulon)
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Non-Depolarizing Nm Blocker
Slow onset (4-6 min) with long duration of action (2-3 hrs). Difficult to reverse if needed Eliminated by kidney Causes a moderate block of ganglionic N and M receptors, resulting in vagal blockade and tachycardia. Release of NE may also be increased as a result of blocking pre-synaptic M2 receptors in the heart, again contributing to tachycardia. |
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Vecuronium (Norcuron)
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- Non-depolarizing Nm blocker
- intermediate duration of action (20-40 min), with an onset of 2-4 min. - Metabolized by the liver |
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Cisatracurium (Nimbex)
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- most commonly used non-depolarizing neuromuscular blocking agent.
- It is spontaneously hydrolyzed, and has low toxicity - intermediate duration of action (20-40 min), with an onset of 2-4 min. - unlikely to cause release of histamine, which has contributed to its popularity |
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Rocuronium (Zemuron)
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- Non-depolarizing Nm blocker
- intermediate duration of action (20-35 min), but onset is rapid (1-2 min), - can be used for intubation |
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Mecamylamine (Inversine)
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- Only clinically available ganglion blocker.
- a tertiary ammonium compound, enters the brain where it blocks nicotinic receptors. - causes sedation, tremor, abnormal movements, and mental status changes. - once used for hypertensive emergencies, but is not used now. - being tested in the treatment of Tourette’s syndrome and for nicotine and cocaine addiction, where desensitization of CNS nicotinic receptors may be beneficial. |
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Hexamethonium
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Prototype ganglion blocker.
No clinical uses |
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What is the prototype alpha1 receptor agonist and what are its effects?
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Phenylephrine
• causes vasoconstriction and increases peripheral vascular resistance • blood pressure increases, causing a reflex decrease in heart rate • may be used in hypotensive emergency to raise blood pressure • vasoconstriction in nasal mucosa makes it an effective decongestant; although rebound effect may occur when discontinued • prolonged use may result in ischemic changes in the mucous membranes • now widely used in oral preparations, although effectiveness is uncertain • people with hypertension should use caution with phenylephrine • produces mydriasis and may be used topically to dilate the eye for examination, without affecting accommodation Methoxamine (Vasoxyl) is used intravenously to treat hypotension Midodrine (ProAmantine) is given orally to treat postural hypotension and autonomic insufficiency. Given during the day as it can cause hypertension when the patient lies down. |
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What is the prototype alpha2 receptor agonist and what are effects of the class?
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Clonidine
• located on presynaptic nerve terminals and inhibit transmitter release • cause aggregation of platelets • contract some vascular smooth muscle • decrease insulin secretion (small effect) |
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What is the prototype Beta1 receptor agonist and what are its effects?
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Dobutamine
• increase the force and rate of contraction of the heart (positive inotropic and chronotropic effect) • increase AV conduction velocity and automaticity • increase renin secretion from the kidney |
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What is the prototype Beta2 receptor agonist and what are its effects?
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Albuterol
• cardiac effects similar to β1, but less pronounced • cause relaxation of respiratory, uterine, gastrointestinal smooth muscle • cause relaxation of blood vessels supplying skeletal muscle • promote potassium uptake into skeletal muscle • activate glycogenolysis and gluconeogenesis in the liver |
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Clonidine (Catapres)
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• selective α2 agonist, which acts in the brain
• stimulation of α2 receptors on presynaptic terminals in the CNS decreases release of NE, reducing overall sympathetic output to the periphery • reduced sympathetic tone leads to a decrease in blood pressure • clonidine may also increase parasympathetic outflow, decreasing heart rate • clonidine is administered orally or by transdermal patch • used for treatment of hypertension • reduces craving in recovering addicts and alcoholics and decreases withdrawal symptoms • transdermal patch decreases hot flashes in menopause • clonidine may be used as pre-anesthetic medication, to cause sedation, and dry secretions, and decrease the amount of anesthetic required • side effects include dry mouth, sedation, sexual dysfunction in males, and possible bradycardia • side effects are reduced by use of the transdermal patch, but the patch may cause dermatitis and should be rotated to a new skin area each week • the patient should avoid getting the patch too hot, as a massive release of clonidine may occur, resulting in severe hypotension • hypertension may occur if the drug is withdrawn abruptly |
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Apraclonidine (Iopidine)
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• selective α2 agonist,
• used in the eye to decrease intraocular pressure by reducing the formation of aqueous humor thru α2 receptor mediated vasoconstriction |
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Pseudoephedrine (Sudafed)
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• alpha agonist similar to phenylephrine
• widely used in OTC decongestant preparations • use caution in patients with hypertension, as may increase blood pressure • less tachycardia and CNS effects than ephedrine • because pseudoephedrine is a precursor in the manufacture of methamphetamine, it has recently been removed from over the counter shelves and placed in the pharmacy, where patients must show ID and sign for it. Many companies are now promoting use of phenylephrine as a replacement for pseudoephedrine, although phenylephrine is not as effective. |
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Epinephrine (Adrenalin)
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prototype sympathetic agonist
• stimulates α, β1 and β2 receptors • effect depends upon the dose administered Low Dose • beta1 activation produces a positive inotropic and chronotropic effect in the heart • alpha receptor stimulation causes vasoconstriction, especially in skin, mucosa and kidney • this leads to initial increased systolic and diastolic blood pressure, followed by a decrease in diastolic pressure resulting from β2 mediated dilation of blood vessels to skeletal muscle • overall, the effect of intravenous infusion is an increase in pulse pressure, little change in overall pressure, and increased heart rate • at high doses, the effect of alpha receptors is evident, and a pressor effect is seen - both systolic and diastolic pressure will increase - mean pressure increases, there is less increase in heart rate Uses of Epinephrine • used for treatment of anaphylactic shock to restore blood pressure, decrease bronchospasm, decrease congestion and angioedema, and reverse cardiovascular collapse • used in emergency treatment for cardiac arrest and complete heart block • vasoconstrictor property used to decrease diffusion of injected drugs such as local anesthetics • instilled in the eye to treat glaucoma; increase removal and decrease production of aqueous humor • epinephrine causes bronchodilation (β2); emergency treatment of asthma (rarely) |
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Norepinephrine (Levophed)
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• stimulates α and β1 receptors, but not β2 receptors
o (α = β1>> β2) • must be injected; very short duration of action due to rapid metabolism • vasoconstriction mediated by α receptors increases vascular peripheral resistance • diastolic and systolic blood pressure increase, with little change in pulse pressure • constriction of blood vessels by α receptors decreases blood flow to the kidney, spleen and liver • baroreceptor reflexes compensate for increased blood pressure and decrease heart rate slightly • therefore, cardiac output is either unchanged or decreased • if atropine is given prior to norepinephrine, and the vagal reflex is inhibited, the baroreceptor effect will not occur, and heart rate will increase • NE can cause severe vasoconstriction at the infusion site resulting in necrosis • NE is used very rarely, possibly to treat severe hypotension when nothing else has worked |
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Isoproterenol (Isuprel)
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• very potent selective β1 and β2 agonist
• β stimulation increases rate and force of contraction of the heart • β2 effect causes vasodilation in some blood vessels • systolic pressure may rise initially due to increased cardiac output, but dilation of blood vessels by β2 receptors will lead to a decrease in blood pressure, with a reflex increase in heart rate • used in emergency treatment for cardiac arrest and complete heart block • once used in emergency treatment of asthma, but has been replaced by β2-selective agents • large doses may cause tachycardia, palpitations and arrhythmias |
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Dobutamine (Dobutrex)
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• somewhat selective β1 agonist
• small effect on alpha receptors • prominent postitive inotropic effect in the heart • increases cardiac output and cardiac contractility • little effect on peripheral vascular resistance • frequently used in cardiac stress tests if the patient cannot exercise • half-life is about 2 minutes, so the effect is very short-lived • some patients may develop increased blood pressure and heart rate, especially if they have a history of hypertension, This is prevented by slowing the rate of infusion • may be infused intravenously on a continuous basis to increase cardiac output in cardiogenic shock and in congestive heart failure. |
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Ritrodine (Yutopar)
Terbutaline (Brethine) Albuterol (Ventolin) |
• selective β2 agonists that have little effect on β1 receptors in normal doses
• ritrodine is used to relax the uterus and suppress premature labor; it may be given orally or infused intravenously • albuterol, pirbuterol and salmeterol are used as inhalation agents for treatment of asthma- these drugs will be discussed in detail in section on treatment of asthma • terbutaline is sometimes, although rarely, used orally for treatment of asthma • headache, tachycardia and skeletal muscle tremor are common side effects of β2 agonists, especially when given orally |
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Dopamine (Intropin)
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• low doses of dopamine activate D1 receptors in renal vascular beds, causing vasodilation and increasing renal blood flow
• this increases glomerular filtration rate and sodium excretion • mesenteric and coronary arteries are also dilated • at higher concentrations, dopamine stimulates β1 receptors in the heart, producing a positive inotropic and chronotropic effect • given intravenously to treat cardiac shock, as it will increase cardiac output without causing vasoconstriction, but is not very effective • high doses may cause release of norepinephrine and stimulate α1 receptors, causing vasoconstriction and increasing blood pressure; effect of high doses similar to epinephrine • side effects include nausea and vomiting (stimulation of chemoreceptor trigger zone), tachycardia, angina, arrhythmias, headache and peripheral vasoconstriction |
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Fenoldopam (Corlopam)
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• selective D1 receptor agonist
• causes dilation of vascular beds, decreasing blood pressure • used short-term to produce rapid decrease of blood pressure in severe hypertension |
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Amphetamine
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• indirect-acting sympathomimetic that displaces NE (and DA) from vesicles, increasing their release from neurons, especially in the CNS
• CNS stimulant: increases alertness, decreases need for sleep, decreases appetite, causes euphoria, and increases motor activity • peripheral actions include tremor, tachycardia, and hypertension • psychosis may occur in susceptible individuals, as well as dizziness, restlessness, tremor, irritability, fever and aggression • other effects include: headache, chills, pallor or flushing, arrhythmias, angina, hypertension or hypotension, sweating • cerebral hemorrhage, convulsions and coma may occur at high doses • causes strong contraction of the urinary bladder sphincter; has been used to treat enuresis • methamphetamine has more central actions and fewer peripheral effects; it has become an major drug of abuse • methylphenidate (Ritalin) and similar drugs are used in children with attention deficit hyperactivity disorder, where they cause a paradoxical decrease in hyperactivity • amphetamine-like compounds have been used for weight loss, but the long-term effect is minimal, and the weight is generally re-gained if the drug is stopped |
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Cocaine
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• inhibits re-uptake of DA and NE into nerve terminals
• amphetamine-like effect that is shorter acting and more intense • now smoked (crack) to increase intensity of effect and speed of onset • once thought safe, now considered to be highly addicting • may cause severe hypertension and stroke in otherwise healthy young adults • often causes tachycardia, may cause arrhythmias and myocardial infarction • long-term use may cause cocaine-induced psychosis • cocaine may be used for nasopharyngeal surgery to decrease blood flow and produce local anesthesia |
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Tyramine
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• indirectly acting compound that will increase release of catecholamines from nerve terminals
• taken up into storage vesicles and displaces NE, forming a false transmitter, octopamine • because NE becomes replaced with octopamine, tachyphylaxis will develop to the effects of tyramine • tyramine is a normal component of food and by-product of tyrosine metabolism • normally hydrolyzed by monoamine oxidase (MAO) in the GI tract and the liver; inactive when administered orally • if injected i.v., it may cause massive release of stored catecholamines and have a norephinephrine-like effect • in patients treated for depression with monoamine oxidase inhibitors, ingestion of large amounts of tyramine may cause a severe hypertensive crisis! |
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Ephedrine
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• mixed acting: stimulates both α and β receptors, and enhances NE release
• effects are similar to epinephrine, but usually much less pronounced • since mixed acting, denervation will decrease, but not abolish, its effect • high bioavailability and long duration of action- effect may last hours • excreted in the urine; excretion can be accelerated by acidifying the urine • CNS stimulant, increases heart rate and may increase blood pressure • causes bronchodilation • ephedra, found in many herbal (ma huang) and over the counter weight loss preparations, was taken off the market by the FDA due to many adverse effects, including deaths due to hypertension • a similar compound, phenylpropanolamine, a component of many OTC decongestants and weight-loss drugs, was also taken off the market by the FDA because of hemorrhagic stroke in women |
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What will Alpha agonists do to the eye?
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- mydriasis without affecting accomodation
- increase removal of aqueous humor |
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What will Alpha agonists do to the respiratory tract?
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- constrict vessels in upper airway and mucous membrane
- decreases nasal stuffiness |
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What will Alpha agonists do to the GI tract?
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minor inhibition due to
relaxing smooth muscle (a1) decreasing ACh release (a2) |
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What will Alpha agonists do to the metabolism and endocrine secretions?
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Minor effects
- a1 receptors increase glycogenolysis and gluconeogenesis - a2 receptors inhibit lipolysis, insulin secretion, and inhibit renin secretion |
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What will Beta agonists do to the eye?
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increase aqueous humor (B2 only)
increases occular pressure |
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What will Beta agonists do to the respiratory tract?
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B2 only
relax bronchial smooth muscle |
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What will Beta agonists do to the GU tract?
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B2 only
relax uterus relax bladder wall |
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What type of drugs end in "-osin"
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A1 selective blockers
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My Pt wants something to counter the dry mouth caused by his ADhD medication, but doesn't want to sweat a lot. What can I give him?
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Cevimeline
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My surgical pt still hasn't pooped two days after surgery. He's taking stool softener already. What else can I give him to help move things along?
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bethanecol
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What muscarinic agonist can be used to treat glaucoma?
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Pilocarpine
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What pt should not receive muscarinic agonists?
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Pts with qny of the following:
peptic ulcers coronary deficiency asthma |
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What medication would you prescribe to a pt who wants to quit smoking?
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Varenicline (Chantix)
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How do you treat open angle glaucoma?
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Pilocarpine
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How do you treat acute narrow angle glaucoma?
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Pilocarpine + a cholinesterase inhibitor (physostigmine or echothiophate)
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What drugs are used for chronic therapy of myasthenia gravis?
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Neostigmine, pyridostigmine or ambenonium
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What drug is used to diagnose myasthenia gravis?
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Edrophonium
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Your opthomologist needs to dilate your pupils for an exam. What's she likely to use?
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Tropicamide
Phenylephrine |
