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Pharmacology
Nervous System, Cholinergic and Adrenergic Agonists/Antagonists
| Question | Answer |
|---|---|
| What are the 2 divisions of the peripheral nervous system? | Autonomic and Somatic |
| Which peripheral nervous system division is under more conscious control? | Somatic nervous system |
| Which peripheral nervous system division has both a preganglionic and a postganglionic nerve connected in series by a ganglion? | Autonomic Nervous System |
| Which peripheral nervous system division consists of a single motoneuron? | Somatic nervous system |
| Where do autonomic nervous system pathways originate? | Brain or spinal cord |
| Where is the origin and termination of somatic nervous system pathways? | Originate in the ventral horn of the spinal cord and terminate in muscle |
| What are the two divisions of the autonomic nervous system? | Parasympathetic and Sympathetic |
| What is the neurotransmitter and receptor of all preganglionic fibers? | Acetylcholine, Nicotinic receptors (a cholinergic receptor) |
| What is the length of postganglionic fibers in the parasympathetic nervous system? | Short |
| Which neurotransmitter do the parasympathetic postganglionic fibers release? | Acetylcholine |
| Which neurotransmitter do the parasympathetic preganglionic fibers release? | Acetylcholine |
| Which autonomic nervous system division releases the same neurotransmitter from both preganglionic and postganglionic fibers? And what is that neurotransmitter? | Parasympathetic; acetylcholine |
| Where do the parasympathetic preganglionic fibers exit the spinal cord? | With the cranial nerves and 3/4 sacral spinal roots |
| Where do the sympatheric preganglionic fibers exit the spinal cord? | With the thoracic and lumbar spinal nerves |
| What is the length of postganglionic fibers in the sympathetic nervous system? | Long |
| Which neurotransmitter is released by MOST sympathetic postganglionic fibers? | Norepinephrine |
| Which neurotransmitter is released by sympathetic postganglionic fibers innervating sweat glands? | Acetylcholine |
| Which neurotransmitter is released by sympathetic postganglionic fibers innervating renal blood vessels? | Dopamine |
| Which neurotransmitter is released by the adrenal medulla? | Epinephrine |
| Acetylcholine released by parasympathetic postganglionic nerves utilize which receptor? | Muscarinic |
| Norepinephrine, released by most sympathetic postganglionic nerves, utilize which receptors? | Alpha and Beta |
| Acetylcholine, released by sympathetic postganglionic nerves to sweat glands, utilizes which receptor? | Muscarinic |
| Acetylcholine utilizes what receptor when binding to the adrenal medulla and causing the release of epinephrine? | Nicotinic |
| What neurotransmitter receptor is found in renal vascular smooth muscle? | Dopaminergic |
| Acetylcholine utilizes what receptor on skeletal muscle? | Nicotinic |
| What 5 steps are essential in functioning of a neurotransmitter? | SYNTHESIS of nt, STORAGE of nt in vesicles, RELEASE from vesicles due to action potential, RECEPTOR ACTIVATION by nt binding to postsynaptic neuron, and TERMINATION of nt action by enzyme degradation or reuptake |
| What two reactants are needed for acetylcholine synthesis? | Choline and Acetyl CoA |
| What enzyme is needed for acetylcholine synthesis? | Choline acetyltransferase |
| How is the function of acetylcholine terminated? | It is hydrolyzed by acetylcholinesterase in the synaptic cleft |
| What two receptors does acetylcholine bind to? | Nicotinic and Muscarinic |
| What are the step-wise precursors of epinephrine? | Tyrosine-> l-dopa -> Dopamine -> norepinephrine -> epinephrine |
| Which two drugs cause release of norepinephrine from the presynaptic terminal (only if innervation is intact)? | Tyramine and Amphetamine |
| What two receptors does norepinephrine/epinephrine bind to? | alpha and beta |
| How is the function of norepinephrine terminated? | Reuptake into presynaptic terminal |
| What two drugs clock reuptake of norepinephrine? | Antidepressants and cocaine |
| Where are M1 cholinergic receptors commonly found? | Sweat glands *Sympathetic postganglionic |
| What is the mechanism of action/cascade of events of M1 (and M3) cholinergic receptors once activated? | Gq -> activate PLC -> IP3 and DAG -> Ca release -> activate protein kinases |
| Where are M2 cholinergic receptors commonly found? | Heart, smooth muscle |
| What is the mechanism of action/cascade of events of M2 cholinergic receptors? | Gi -> inhibit adenylyl cyclase -> opens K channels = hyperpolarize neurons (membrane potential becomes more negative = more depolarization required to fire an action potential) |
| Where are nicotinic cholinergic receptors commonly found? | Postganglionic neurons and skeletal muscle |
| What is the mechanism of action of nicotinic receptors? | ACh binding opens Ca channels = depolarizes cell (bring closer to action potential) |
| Where are alpha1 adrenergic receptors commonly found? | In smooth muscle |
| What is the mechanism of action of alpha1 adrenergic receptors? | Gq -> activate PLC -> IP3 and DAG -> Ca release -> activate protein kinases |
| What is the mechanism of action of alpha2 adrenergic receptors? | Gi -> inhibit adenylyl cyclase -> opens K channels = hyperpolarize neurons (membrane potential becomes more negative = more depolarization required to fire an action potential) |
| Explain the purpose and differences between autoreceptors and heteroreceptors. | Both receptors are on presynaptic terminals and regulate neurotransmitter release. Autoreceptors bind the same neurotransmitter that is being regulated. Heteroreceptors regulate a neurotransmitter other than the one it binds. |
| Presynaptic alpha2 receptors serve what purpose? | They are an autoreceptor and decrease norepinephrine release |
| Presynaptic beta receptors serve what purpose? | They are an autoreceptor and increase norepinephrine release |
| Presynaptic M2 receptors serve what purpose? | They are a heteroreceptor and decrease norepinephrine release |
| Explain the process of down-regulation. | Receptors are less responsive to neurotransmitter due to decreased affinity or decreased receptor number (internalization or destruction) |
| What causes down-regulation to occur? | Repeated receptor stimulation with lots of neurotransmitter |
| Explain the process of up-regulation. | Receptors become more sensitive/responsive to neurotransmitter by increasing affinity or increased receptor number |
| When does receptor up-regulation occur? | When minimal amounts of neurotransmitter are present. |
| What is the mechanism of action of antidepressants and cocaine? | They block norepinephrine re-uptake |
| What is the mechanism of action of drugs such as tyramine and amphetamine? | Increase/cause norepinephrine release from presynaptic terminal |
| What type of innervation do blood vessels primarily receive? | Sympathetic |
| Which autonomic nervous system division is more widely distributed in the body? | Sympathetic |
| What physical effects does the parasympathetic nervous system have on the heart, salivary glands, stomach, sphincters, and pupils? | Slow heart rate, increase saliva, increase gastric acid and gastric activity = digestion, relax sphincters = elimination, contract pupils = near vision |
| What is the preganglionic-postganglionic ratio in the parasympathetic nervous system, and what is the purpose of this ratio? | 1:1. Purpose is for discrete responses |
| What is the preganglionic-postganglionic ratio in the sympathetic nervous system, and what is the purpose of this ration? | 1:20. Purpose is for massive activation of the whole system. |
| What does the term "ergotropic" mean, and which autonomic nervous system division is it used to describe? | It means to cause energy expenditure. It is used to describe the sympathetic nervous system. |
| What does the term "trophotrophic" mean, and which autonomic nervous system division is it used to describe? | It means to cause/facilitate growth. It is used to describe the parasympathetic nervous system. |
| What are the physical responses of the sympathetic nervous system on the heart, blood vessels, lungs/bronchioles, stomach, sphincters, pupils, and metabolism? | Increases HR/CO, relax blood vessels to muscle, constrict blood vessels to skin (decrease bleeding of injuries), bronchioles dilate, GI activity decreases, sphincters contract, pupils dilate/ciliary mm contract = distance vision, sugar release/breakdown |
| What receptors on the heart respond to parasympathetic innervation (ACh) and slow heart rate? | M2 |
| What receptors in the lungs respond to parasympathetic innervation (ACh) and cause bronchoconstriction? | M3 |
| What are the effects of M2 receptors in the heart? | Repond to parasympathetic ACh release = slow heart rate/decrease AV conduction |
| What are the effects of M3 receptors in the lungs/bronchioles? | Respond to parasympathetic ACh release = cause bronchoconstriction |
| What receptors in the heart respond to sympathetic innervation (NE) and increase heart rate? | Beta 1 and 2 |
| What receptor in the lungs/bronchioles respond to sympathetic innervation (NE) and cause the bronchioles to relax? | Beta 2 |
| What receptors respond to sympathetic innervation (NE) and cause blood vessels in the skin and skeletal muscle to constrict? | Alpha |
| What receptors respond to sympathetic innervation (NE) and cause blood vessels in skeletal muscle to relax? | Beta 2 |
| What are the effects of Beta 1 and 2 receptors on the heart? | Increase heart rate/AV conduction/contractility |
| What are the effects of Beta 2 receptors on the bronchioles? | Relax bronchioles |
| What are the effects of Alpha receptors on blood vessels of skin and skeletal muscle? | Constrict blood vessels |
| What are the effects of Beta 2 receptors on the blood vessels of skeletal muscle? | Relax blood vessels |
| What receptors respond to parasympathetic innervation (ACh) and cause increased salivation and tears (lacrimal glands)? | M3 |
| What receptors respond to parasympathetic innervation (ACh) and cause miosis (Pupil constriction)/near vision? | M3 |
| What receptor responds to sympathetic innervation to cause increased sweating? (ACh) | M1 |
| What receptors respond to sympathetic innervation (NE) and cause increased sweating and salivation? | Alpha |
| What receptors respond to sympathetic innervation (NE) to cause mydriasis (pupil dilation)/far vision? | Alpha |
| What are the effects of M3 parasympathetic receptors on salivary/lacrimal (tears) glands? | Increased secretion |
| What are the effects of M3 parasympathetic receptors on pupils? | Miosis/constrict pupils/near vision |
| What are the effects of M1 sympathetic receptors on sweating? | Increase sweating |
| What are the effects of alpha sympathetic receptors on apocrine (sweat) and salivary glands? | Increase sweating and salivation |
| What are the effects of alpha sympathetic receptors on the pupils? | Mydriasis/dilation/far vision |
| What receptor responds to parasympathetic innervation (ACh) to stimulate contraction of the GI tract (digestion) and relax sphincters (elimination)? | M3 |
| What receptor respons to parasympathetic innervation (ACh) to cause the bladder wall to contract and sphincters to relax? | M3 |
| What receptors respond to parasympathetic innervation (ACh) and cause an erection in men? | Muscarinic |
| What receptors respond to sympathetic innervation (NE) and cause walls of the GI tract to relax (stop digestion)? | Alpha 2 and Beta 2 |
| What receptors respond to sympathetic innervation and cause the bladder wall to relax? | Beta 2 |
| What receptor responds to sympathetic innervation (NE) and causes sphincters to contract? | Alpha 1 |
| What receptors respond to sympathetic innervation (NE) and promote ejaculation in men? | Alpha 1 |
| What effect does M3 parasympathetic innervation (ACh) have on the GI tract/sphincters? | Contract GI tract wall = digestion, relax sphincters = elimination |
| What effect does M3 parasympathetic innervation (ACh) have on the bladder wall and sphincters? | Contract bladder wall and relax sphincters = urination |
| What effect does muscarinic parasympathetic innervation (ACh) have on sexual activity in men? | Erection |
| What effect does Alpha 2 and Beta 2 sympathetic stimulation (NE) have on the walls of the GI tract and sphincters? | Relax GI tract walls = prevent digestion, contract sphincters = prevent elimination |
| What effect does Beta 2/Alpha 1 (respectively) sympathetic innervation (NE) have on the urinary bladder and sphincters? | Relax urinary bladder and contract sphincters = prevent urination |
| What effect does Alpha 1 sympathetic innervation have on sexual activity in men? | Promote ejaculation |
| What physiological action to baroreceptors in the aortic arch/carotid artery respond to? | Increased blood pressure |
| What is the response of the nervous system to baroreceptor stimulation/increased blood pressure? | Decrease sympathetic output/increase parasympathetic activity via vagus nerve |
| When does reflex bradycardia occur and what is the physiology associated with this response? | Reflex bradycardia occurs when blood pressure increases due to constricted blood vessels. The response to these conditions involves decreasing heart rate and cardiac output |
| When does reflex tachycardia occur and what is the physiology associated with this response? | Reflex tachycardia occurs when blood pressure decreases due to dilated blood vessels. The response to these conditions involves increasing the heart rate. |
| What reflexive response (bradycardia/tachycardia) occurs in response to norepinephrine infusion? | Reflex bradycardia. NE = blood vessel constriction = ^BP = activates baroreceptors. Response: decrease sympathetic innervation of blood vesself and increase parasympathetic innervation via vagus n. = slow heart rate |
| Parasympathetic innervation has what effect on the eye/ciliary muscle/pupil/intraocular pressure? | Parasympathetic innervation contracts ciliary muscle/constricts pupil = widens trabecular meshwork = aqueous humor cleared = DECREASES intraocular pressure |
| Sympathetic stimulation of alpha receptors has what effect on intraocular pressure? | DECREASES intraocular pressure |
| Which autonomic nervous system division(s) cause(s) decreased intraocular pressure? | Parasympathetic stimulation, and sympathetic stimulation of alpha receptors |
| Sympathetic stimulation of beta receptors has what effect on intraocular pressure? | INCREASES intraocular pressure |
| Which autonomic nervous system division causes increased intraocular pressure? | Sympathetic stimulation of beta receptors |
| What is the mechanism of action of cholinergic agonists in treating glaucoma? | Cholinergic agonists. Parasympathetic (ACh) stimulation/ M receptors -> iris sphincter and ciliary muscles contract + miosis = increase aqueous humor drainage through trabecular meshwork = decrease intraocular pressure |
| What is the mechanism of action of alpha receptor agonists in treating glaucoma? | Sympathetic stimulation of alpha receptors -> contracts iris radial muscle = mydriasis = promote intraoclar fluid drainage = decrease intraocular pressure |
| What is the mechanism of action of beta receptor blockers in treating glaucoma? | Blocking sympathetic stimulation of beta receptors would prevent production of aqueous humor = decreases intraocular pressure |
| What three classes of drugs affect the autonomic nervous system to treat glaucoma? | Cholinergic agonists, Alpha receptor agonists, Beta receptor blockers |
| Which autonomic nervous system-targeting class of drugs treats glaucoma without affecting near/far vision accomodation and why? | Alpha receptor agonists because they do not affect the ciliary muscle. |
| Name 6 drugs that act as cholinergic agonists. | Acetylcholine, bethanechol, cevimeline, nicotine, pilocarpine, varenicline |
| Name 7 drugs that act as cholinesterase inhibitors | Donepezil, Echothiophate, Edrophonium, Neostigmine, Organophosphate pesticides, Physostigmine, Pralidoxime |
| Name 13 drugs that act as Cholinergic Antagonists. | Atropine, Darifenacin, Dicyclomine, Diphenoxylate-atropine, Fesoterodine, Glycopyrrolate, Homatropine, Ipratropium, Oxybutynin, Scopolamine, Solifenacin, Tolterodine, Tropicamide |
| Acetylcholine is categorized as what class of drug? | Cholinergic Agonist |
| Bethanechol is categorized as what class of drug? | Cholinergic Agonist |
| Pilocarpine is categorized as what class of drug? | Cholinergic Agonist |
| Cevimeline is categorized as what class of drug? | Cholinergic Agonist |
| Nicotine is categorized as what class of drug? | Cholinergic Agonist |
| Varenicline is categorized as what class of drug? | Cholinergic Agonist |
| Edrophonium is categorized as what class of drug? | Cholinesterase Inhibitor |
| Neostigmine is categorized as what class of drug? | Cholinesterase Inhibitor |
| Physostigmine is categorized as what class of drug? | Cholinesterase Inhibitor |
| Echothiophate is categorized as what class of drug? | Cholinesterase Inhibitor |
| Donepezil is categorized as what class of drug? | Cholinesterase Inhibitor |
| Organophosphate pesticides are categorized as what class of drug? | Cholinesterase Inhibitor |
| Pralidoxime is categorized as what class of drug? | Cholinesterase Inhibitor |
| Atropine is categorized as what class of drug? | Cholinergic Antagonist |
| Scopolamine is categorized as what class of drug? | Cholinergic Antagonist |
| Glycopyrrolate is categorized as what class of drug? | Cholinergic Antagonist |
| Dicylomine is categorized as what class of drug? | Cholinergic Antagonist |
| Tolterodine is categorized as what class of drug? | Cholinergic Antagonist |
| Fesoterodine is categorized as what class of drug? | Cholinergic Antagonist |
| Darifenacin is categorized as what class of drug? | Cholinergic Antagonist |
| Solifenacin is categorized as what class of drug? | Cholinergic Antagonist |
| Oxybutynin is categorized as what class of drug? | Cholinergic Antagonist |
| Ipratropium is categorized as what class of drug? | Cholinergic Antagonist |
| Diphenoxylate-atropine is categorized as what class of drug? | Cholinergic Antagonist |
| Tropicamide is categorized as what class of drug? | Cholinergic Antagonist |
| Homatropine is categorized as what class of drug? | Cholinergic Antagonist |
| What 3 drugs act as non-depolarizing neuromuscular blockers? | d-Tubocurarine, Vecuronium, and Cisatracurium |
| What drug acts as a depolarizing neuromuscular blocker? | Succinylcholine |
| What 2 drugs act as ganglion blockers? | Mecamylamine, and Hexamethonium |
| d-Tubocurarine is categorized as what class of drug? | Non-depolarizing neuromuscular blocker |
| Vecuronium is categorized as what class of drug? | Non-depolarizing neuromuscular blocker |
| Cisatracurium is categorized as what class of drug? | Non-depolarizing neuromuscular blocker |
| Succinylcholine is categorized as what class of drug? | Depolarizing neuromuscular blocker |
| Mecamylamine is categorized as what class of drug? | Ganglion blocker |
| Hexamethonium is categorized as what class of drug? | Ganglion blocker |
| Acetylcholine transport into vesicles for storage is blocked by what compound? | Vesamicol |
| What is the function of Vesamicol? | It blocks transport of acetylcholine into vesicles for storage. |
| Release of Acetylcholine into the synaptic cleft may be blocked by what compound? | Botulinum toxin |
| What is the function of Botulinum toxin? | It blocks the release of Acetylcholine into the synaptic cleft |
| Where are muscarinic receptors located? | On smooth muscle |
| What organs have the greatest muscarinic effects? | Eye, GI Tract, Bladder, and salivary and sweat glands |
| What cellular structure are muscarinic receptors linked to? | G-proteins (Gi or Gq) |
| What organs have nicotinic receptors? | Autonomic ganglia, the brain, skeletal muscle |
| What cellular structure are nicotinic receptors linked to? | Sodium channels = depolarization |
| Fact about cholinergic stimulant (cholinergic agonists/cholinesterase inhibitors) drugs... | Most discriminate between muscarinic and nicotinic receptors |
| Are cholinesterase inhibitors considered direct-acting or indirect-acting drugs? | Indirect acting |
| Which receptor, muscarinic, nicotinic, or both, do cholinesterase inhibitors effect? | Both nicotinic and muscarinic receptors... ACh effects increase |
| What is the difference between direct-acting and indirect-acting drugs? | Direct-acting drugs bind to and activate the receptor. Indirect-acting drugs affect the neurotransmitter/receptor signal without interaction with the receptor... Ex: they interact with the neurotransmitter, preventing it's degradation. |
| In which organs is Bethanechol effective? | Urinary and GI tracts |
| What receptor does Bethanechol bind to? | Muscarinic |
| In which organs is Pilocarpine effective? | Sweat and salivary glands |
| What receptor does Pilocarpine bind to? | Muscarinic |
| What receptor does Cevimeline bind to? | M3 = fewer side effects than Pilocarpine |
| What are Nicotine and Varenicline used for clinically? | Help to quit smoking |
| Muscarinic Agonists have what effects on the eye? | They have similar effects as the parasympathetic nervous system: Miosis, contract ciliary muscle (accomodate to near vision), open trabecular meshwork by pulling iris away from angle of anterior chamber = decreases introcular pressure |
| Muscarinic Agonists have what effects on the cardiovascular system? | They have similar effects as the parasympathetic nervous system: slow heart rate *primarily affect atria = decrease AV node conduction. *DO NOT DIRECTLY AFFECT BLOOD VESSELS = no parasympathetic innervation. ***FEW HEART EFFECTS. |
| Muscarinic Agonists have what effects on the respiratory system? | Cause bronchoconstriction = be careful with asthmatics!!! |
| What muscarinic agonist is used to diagnose asthma? | Methacholine |
| Methacholine, a muscarinic agonist, is used to diagnose what condition? | Asthma |
| Muscarinic Agonists have what effects on the GI system? | They have similar effects as the parasympathetic system: increased secretions, increased peristalsis = digestion, relax sphincters = elimination |
| Which muscarinic agonist has the greatest GI effects? | Bethanechol |
| Muscarinic Agonists have what effects on salivary/gastric glands? | They have similar effects as the parasympathetic nervous system: increased salivary and gastric secretions |
| Which muscarinic agonist has the greatest effects on salivary secretion? | Pilocarpine |
| Muscarinic Agonists have what effects on the Genitourinary system? | They have similar effects as the parasympathetic nervous system: contract detrusor muscle, relax trigone and sphincters = urination |
| Which muscarinic agonist has the greatest bladder/GU effects? | Bethanechol |
| Muscarinic Agonists have what effects on sweat, lacrimal (tears), and nasopharyngeal glands? | They have similar effects as the paresympatheic nervous system: increased secretions |
| Which muscarinic agonist has the greatest effects on the glands (sweat/lacrimal (tears)/ nasopharyngeal)? | Pilocarpine |
| Muscarininc Agonists (M1) have what effects on the brain? | They are involved in memory = clinical trials for Alzheimer's disease |
| Muscarinic agonists are rare in glaucome treatment. If one is chosen, however, which one is most likely? | Pilocarpine |
| Which muscarinic agonist is most commonly used to increase peristalsis in the GI tract and increase voiding in urinary retention? | Bethanechol |
| Which two muscarinic agonists are used to increase salivation, and what is one notable difference between the two drugs? | Pilocarpine and Cevimeline. Pilocarpine also causes profound sweating, where as Cevimeline does not due to it's selectivity of M3 receptors |
| What are the 4 most notable side effects of muscarinic agonists? | Diarrhea, abdominal cramps, salivation, and sweating. |
| In what 3 conditions are muscarinic agonists contraindicated? | Peptic Ulcer, Coronary insufficiency, and Asthma |
| What is the difference between low doses and high doses of nicotinic agonists on the central nervous system? | Low doses increase alertness and attention, while high doses cause tremor, vomiting, and increased respiration |
| Which division of the autonomic nervous system do nicotinic agonists effect in the periphery? | Both sympathetic (cardiac effects) and parasympathetic (GI and urinary effects) |
| What effects do nicotinic agonists have on the heart? | Effects are sympathetic: Hypertension and increased heart rate *may induce reflex bradycardia |
| What effects do nicotinic agonists have on the GI and urinary tracts? | Effects are parasympathetic: vomiting, diarrhea, urination |
| What is the initial response of the neuromuscular junction to nicotinic agonists? | Muscle stimulation ranging from a twitch to a strong contraction, depending on the size of the stimulus |
| What effects do long-lasting stimulation of the neuromuscular junction with nicotinic agonists produce? | Flaccid paralysis due to desensitization of receptors |
| What are 7 important symptoms of nicotine poisoning? | Vomiting, convulsions, coma, respiratory arrest, paralysis (preceded by muscle contractions), hypertension, cardiac arrhythmias |
| What 3 treatments are utilized in nicotine poisoning? | Atropine to block muscarinic receptors, anti-convulsants, and respiratory assistance |
| Which nicotinic (partial) agonist is used as an aid in quitting smoking by relieving cravings? | Varenicline (Chantix) |
| What are the common side effects seen with the nicotinic partial agonist Varenicline/Chantix? | Nausea and vomiting; sleep disturbance, vivid nightmares, psychosis, mania, anxiety, and suicidal ideation (CNS side effects) |
| What 2 Cholinesterase Inhibitors are classified as Carbamates, and what is their mechanism of action? | Neostigmine and Physostigmine; they form covalent bonds |
| What are the structural and functional differences between the cholinesterase inhibitor carbamates Neostigmine and Physostigmine? | Neostigmine is a quaternary amine, is not well absorbed orally, and does not cross the BBB. Physostigmine is a tertiary amine that is well absorbed orally, and can cross the BBB. |
| Which cholinesterase inhibitor must be administered by injection, and binds reversibly with a short duration of action (5-10 min)? | Edrophonium |
| Which cholinesterase inhibitor is used as a pesticide/nerve gas? | Organophosphates |
| What mechanistic step causes organophosphate cholinesterase inhibitor effects to be irreversible, and potentially fatal? | Aging: breaking an Oxygen bond that increases the bonding strength of the rest of the compound = irreversibly bound |
| What compound/nucleophile can be added in the case of organophosphate exposure to prevent aging, which causes irreversible organophosphate binding to a cholinesterase, and may be fatal? | 2-PAM |
| In what situation is 2-PAM not used, and why? | Carbamate pesticide exposure; carbamate pesticides do not undergo the aging process. Therefore, the addition of 2-PAM, which also binds to and inhibits cholinesterase, may make the situation worse. |
| What effects of cholinesterase inhibitors are seen in the brain? | Effects similar to nicotine: low doses may cause memory improvement, while high doses may cause convulsions and respiratory arrest due to desensitization of nicotinic receptors. |
| The effects of cholinesterase inhibitors on the eyes, respiratory tract, GI tract, and genitourinary tract are similar to which division of the autonomic nervous system? | Parasympathetic = effects similar to those of muscarinic agonists |
| What effects of cholinesterase inhibitors are seen in the cardiovascular system? | Effects similar to parasympathetic innervation: bradycardia, decreased atrial contraction, and decreased cardiac output. *No cholinergic innervation on vasculature |
| What effects of cholinesterase inhibitors are seen in the neuromuscular junction? | Effects are similar to those of nicotinic agonists: low concentrations increase contraction strength of skeletal muscles, while higher concentrations may result in muscle fibrillation/neuromuscular blockade due to nicotinic receptor desensitization |
| What class of drugs is useful in treating myasthenia gravis and why? | Cholinesterase inhibitors; low concentrations will increase contraction strength in skeletal muscle |
| Which cholinesterase inhibitor is useful in treating myasthenia gravis? | Neostigmine |
| What is the cholinesterase inhibitor Neostigmine useful in treating? | Myasthenia gravis |
| Which cholinesterase inhibitor may be used locally in the eye to treat glaucoma? | Physostigmine |
| Which 2 cholinesterase inhibitors are used to treat Alzheimer's disease and why? | Donepezil and Rivastigmine: they are well-absorbed orally and cross the BBB |
| Donepezil and Rivastigmine are cholinesterase inhibitors that are useful in treating what disease? | Alzheimer's disease |
| Which cholinesterase inhibitor is useful in diagnosing myasthenia gravis and why? | Edrophonium; it forms a reversible bond and is short acting (5-10 min). A diagnosis is made if patient experiences increased muscle strength after Edrophonium administration |
| The cholinesterase inhibitor Edrophonium forms a reversible bond and is short-acting (5-10 min), which is helpful in diagnosis what condition? | Myasthenia gravis |
| Which organophosphate cholinesterase inhibitor is applied to the eye for long-term control of intraocular pressure/glaucoma emergencies? | Echothiophate |
| The organophosphate cholinesterase inhibitor Echothiophate is useful in treating what condition? | Long-term control of intraocular pressure or glaucoma emergencies |
| Which organophosphate cholinesterase inhibitor is not lipid soluble, and therefore is used locally in the eye for long-term control of intraocular pressure? | Echothiophate |
| What is the name of an organophosphate cholinesterase inhibitor developed as a pesticide, but is highly lipid soluble and easily absorbed by the skin, lungs, gut, or eye? | DFP |
| What is the name of two organophosphate cholinesterase inhibitors used as nerve gases, but are highly lipid soluble and easily absorbed by the skin, lungs, gut, or eye? | Soman and Sarin |
| What is the name of two organophosphate cholinesterase inhibitors developed as insecticides, but are highly lipid soluble and easily absorbed by the skin, lungs, gut, or eye, and inactivated rapidly by mammals and birds? | Parathion and Malathion |
| Which two cholinesterase inhibitors are used to treat open-angle glaucoma? | Physostigmine, Echothiophate; Pilocarpine (muscarinic agonist) is used most often though |
| A combination of what two drugs is used to treat closed-angle glaucoma until surgery can correct the problem? | Pilocarpine (muscarinic agonist) and cholinesterae inhibitor |
| Which cholinesterase inhibitor is used in GI and urinary problems, such as paralytic ileus or bladder atony? | Bethanechol |
| Which two cholinesterase inhibitors are commonly used to reverse the effects of non-depolarizing neuromuscular blockers after surgery? | Neostigmine and Edrophonium |
| Cholinesterase inhibitors Neostigmine and Edrophonium are commonly used for what purpose? | After surgery to reverse the effects of non-depolarizing neuromuscular blockers. |
| Which three cholinesterase inhibitors are used for chronic therapy of myasthenia gravis? | Neostigmine, Pyridostigmine, or Ambenonium |
| What symptoms occur with cholinesterase inhibitor toxicity, and note whether they are muscarinic or nicotinic manifestations. | SLUDGE (M): Salivation, Lacrimation, Urination, Defecation, Gastric distress, and Emesis; miosis (M), sweating (M), bronchoconstriction (M), nausea/vomit/diarrhea (M), neuromuscular blockade (N) -> paralysis/death if respiratory muscle paralysis |
| What is the treatment for cholinesterase inhibitor toxicity? | Rapid injection of PAM, administer atropine until pupils dilate = muscarinic receptors are blocked. *Only use 2-PAM if organophosphate poisoning occurred, not if carbamate poisoning. Respiratory assistance if needed |
| Which two muscarinic antagonists are naturally found in belladonna? | Atropine and scopolamine |
| Which muscarinic antagonist is well-known for penetrating the CNS, causing sedation and amnesia? | Scopolamine |
| Which muscarinic antagonist is well absorbed through the skin, and therefore used as a patch to prevent motion sickness? | Scopolamine |
| Which class of drugs has a dose-related response? | Muscarinic antagonists |
| What organs are affected by low doses of atropine (a muscarinic antagonist), and what are the effects? | Salivary and sweat glands, and bronchial tissues = dry mouth and decreased sweating |
| What CNS effects are seen with high/toxic doses of the muscarinic antagonist, atropine? | Confusion and coma |
| What CNS effects are seen with low doses of the muscarinic antagonist, Scopolamine? | Drowsiness and amnesia |
| What are two common uses of the muscarinic antagonist, scopolamine? | Used as a pre-anesthetic to cause sedation, amnesia, and to dry secretions, and for motion sickness |
| What class of drugs is used to restore the balance between neurotransmitters acetylcholine and dopamine? | Muscarinic antagonists |
| Dopamine receptor blockade or reduced dopamine is commonly seen in what two conditions? | Use of antipsychotic drugs, and Parkinson's disease |
| What two muscarinic antagonist drugs are used to treat dopamine receptor blockade or reduced dopamine in cases such as use of antipsychotic drugs or Parkinson's disease? | Benztropine and trihexyphenidyl |
| Muscarinic antagonists have what effects on the eye? | Mydriasis, Cycloplegia (loss of accommodation for near vision due to decreased ciliary muscle stimulation), photophobia, inhibit ciliary muscle = close trabecular meshwork = obstruct aqueous humor drainage = increase intraocular pressure, dry eyes |
| Which class of drugs should be avoided in narrow/closed angle glaucoma? | Muscarinic antagonists |
| What muscarinic antagonist effects are seen in the heart? | Tachycardia, reverse effects of reflex vagal decreased cardiac output |
| Which part of the heart is not affected by muscarinic antagonists and why? | Ventricles, because they do not receive parasympathetic innervation |
| Which muscarinic antagonist is commonly used in surgery to prevent vagal responses when handling visceral organs? | Glycopyrrolate |
| Which muscarinic antagonist is commonly used to reverse bradycardia produced by muscarinic agonists, cholinesterase inhibitors, MI, or AV block? | Atropine |
| Which part of the cardiovascular system is not affected by muscarinic antagonists and why? | Blood vessels and ventricles; they do not receive parasympathetic innervation |
| Although blood vessels do not receive parasympathetic innervation, they may still vasodilate in the presence on muscarinic agonists. How does this happen? | Endothelial cells may release nitric oxide in response to muscarinic agonists. Nitric oxide will cause vasodilation |
| What effect do muscarinic antagonists have in the lungs/bronchioles? | Bronchodilation |
| Which respiratory disorders may be treated with muscarinic antagonists? | COPD, asthma because muscarinic antagonists cause bronchodilation. *Jimson weed and belladonna cigarettes were smoked to treat asthma |
| Which two muscarinic antagonists are used to treat asthma and COPD by causing bronchodilation? | Ipratropium and Tiatropium |
| Which class of drugs is commonly used before anesthesia to inhibit salivary and respiratory secretions, and decrease laryngospasm? | Muscarinic antagonists |
| What effects do muscarinic antagonists have on the GI and GU tracts? | Inhibit motility and secretions = antispasmodic |
| Which muscarinic antagonist is commonly used as an antispasmodic for the GI/GU tracts? | Dicylomine |
| What muscarinic antagonist + opiod combination is commonly used to treat diarrhea? | Atropine + opiod = Diphenoxylate |
| What is Tolterodine, a muscarinic antagonist, commonly used for? | It targets M3 receptors to decrease bladder overactivity. |
| Which muscarinic antagonist is commonly used after prostrate surgery to prevent bladder spasm? | Oxybutynin |
| Which muscarinic antagonist targets M3 receptors to decrease bladder overactivity? | Tolterodine |
| What is Oxybutynin, a muscarinic antagonist, commonly used for? | To prevent bladder spasm after prostate surgery |
| What effect do muscarinic antagonists have on sweat and salivary glands? | Decrease secretions. Body temperature may rise in atropine poisoning, especially children. Salivary glands are extremely sensitive because they contain M3 receptors |
| Why is dry mouth a common effect of even low doses of muscarinic antagonists? | Salivary glands have M3 receptors = very sensitive |
| Which two muscarinic antagonists are used locally in the eye to produce mydriasis and cycloplegia? | Tropicamide and Homatropine |
| What are 4 side effects commonly seen with muscarinic antagonists? | Dry mouth, mydriasis, decreased GI motility, urinary retention |
| What are 2 contraindications to muscarinic antagonists? | Glaucoma and Benign Prostatic Hyperplasia |
| Why are muscarinic antagonists commonly contraindicated in adults? | Children are more sensitive to hyperthermia |
| Which 3 muscarinic antagonist drugs may result in atropine poisoning? | Tricyclic antidepressants, antihistamines, and phenothiazine antipsychotics |
| What 6 symptoms are seen with atropine (a muscarinic antagonist) poisoning? | Dry mouth, mydriasis, tachycardia, hot flushed skin, agitation, and delirium |
| What are the effects of non-depolarizing competitive antagonists/ganglion blockers in the eye? | Mydriasis, cycloplegia |
| Which division of the autonomic nervous system do non-depolarizing competitive antagonists/ganglion blockers inhibit? | Sympathetic and parasympathetic... effects on organs depend on predominant tone |
| What effect do non-depolarizing competitive antagonists/ganglion blockers have on blood vessels and why? | Vasodilation/orthostatic hypotension because sympathetic innervation predominates |
| What effect do non-depolarizing competitive antagonists/ganglion blockers have on the heart? | Tachycardia, decreased contractility |
| What GU effects are seen with non-depolarizing competitive antagonists/ganglion blockers? | Urinary retention, and erection and ejaculation prevented/reduced. |
| What drug is the only known depolarizing neuromuscular blocker? | Succinylcholine |
| What occurs in the muscle with depolarization? | Contraction |
| In what situation is the depolarizing neuromuscular blocker succinylcholine used? | In procedures that need a rapid, short-acting effect of muscular blockade (neuromuscular blockade occurs because of receptor desensitization) |
| What compound hydrolyzes the depolarizing neuromuscular blocker succinylcholine? | Plasma pseudocholinesterase |
| What is the reason for differences in the ability to metabolize the depolarizing neuromuscular blocker succinylcholine? | Genetic differences |
| In what conditions is the depolarizing neuromuscular blocker succinylcholine contraindicated and why? | Burn patients, nontraumatic rhabdomyolysis, nerve degeneration, spinal cord injuries with paraplegia or quadriplegia, muscular dystrophy, & CHF because prolonged depolarization of muscle cells causes release of K into the blood = potential cardiac arrest |
| Which depolarizing neuromuscular blocker may cause malignant hyperthermia with repeated doses? | Halothane |
| What drug is used to treat malignant hyperthermia due to repeated doses of depolarizing neuromuscular blockers such as halothane? | Dantrolene |
| What 5 situations commonly call for use of depolarizing neuromuscular blockers? | Surgery to relax muscles, Ventilation to paralyze diaphragm, Orthopedics to allow bone manipulation, Intubation/bronchoscopy, and Convulsions to decrease muscle spasms |
| What is the mechanism by which non-depolarizing neuromuscular blocking agents produce an effect? | They are competitive antagonists of nicotinic receptors at the neuromuscular junction |
| How can the effects of non-depolarizing neuromuscular blocking agents be reversed, and what is a specific example? | Increasing the amount of ACh in the synaptic cleft/Cholinesterase inhibitors (since non-depolarizing neuromuscular blocking agents are competitive antagonists); Ex: Neostigmine |
| What route of administration is needed for non-depolarizing neuromuscular blockers and why? | IV injection because they are highly ionized and not orally absorbed |
| What effect is seen with non-depolarizing neuromuscular blockers in the CNS? | None- they do not cross the BBB = they only paralyze muscles/no sedation or consiousness effects |
| Which muscle groups are paralyzed first by non-depolarizing neuromuscular blockers? | Small muscles: eye/jaw/larynx etc. |
| Which muscle groups are paralyzed last/recovered first with non-depolarizing neuromuscular blockers? | Large muscles: *Intercostal muscles and diaphragm |
| What is the pattern of paralysis and recovery with non-depolarizing neuromuscular blockers? | Recovery occurs in the reverse order of paralysis: first paralyzed = last to recover/ last paralyzed = first to recover |
| Which receptors are targeted by organophosphate cholinesterase inhibitors? | Muscarinic and nicotinic receptors are stimulated |
| Cholinesterase inhibitor poisoning is reversed by what drug and by what mechanism? | Atropine (a muscarinic antagonist) blocks the muscarinic-stimulating effects of organophosphate cholinesterase inhibitors. **Muscarinic receptors only. Nicotinic receptors are not effectively blocked |
| What symptoms indicate atropine, a muscarinic antagonist, has been effective in blocking muscarinic receptors in the case of organophosphate cholinesterase inhibitor poisoning? | Dry mouth and mydriasis |
| Which effect of organophosphate cholinesterase inhibitor poisoning can not be reversed? | Stimulation/Increased ACh of nicotinic receptors |
| What are the mechanisms of action seen with the two types of neuromuscular junction blocking agents? | Non-depolarizing competitive antagonists bind directly to the receptor and keep the Na channel closed- overcome by increasing ACh. Depolarizing neuromuscular junction blockers prolong depolarization and desensitization occurs |
| What is an example of a non-depolarizing neuromuscular junction blocker? | d-tubocurarine |
| What 3 drugs are classified as catecholamines? | Epinephrine, Norepinephrine, and Isoproterenol |
| What 5 drugs are classified as Alpha Agonists? | Phenylephrine, Pseudoephedrine, Xylometazoline, Oxymetazoline, and Midodrine |
| What 3 drugs are classified as Alpha-2 Agonists? | Clonidine, Methyldopa, and Apraclonidine |
| What drug is classified as a Beta-1 Agonist? | Dobutamine |
| What 2 drugs are classified as Beta-2 Agonists? | Albuterol and Ritrodine |
| What 2 drugs are classified as dopamine agonists? | Dopamine and Fenodolpam |
| What 6 drugs are adrenergic stimulants, but are not classified as catecholamines, alpha agonists, alpha-2 agonists, beta-1 agonists, beta-2 agonists, or dopamine agonists? | Ephedrine, Amphetamine, Methylphenidate, Methamphetamine, Cocaine, and Tyramine |
| What is the rate-limiting step in the synthesis of norepinephrine or dopamine from tyrosine? | Tyrosine to l-dopa conversion |
| Which two enzymes metabolize norepinephrine, and what are their locations? | Monoamine Oxidase (MAO) found on outer surface of mitochondria = breakdown NE released in synaptic terminal; Catechol-O-methyl transferase (COMT) found in the liver |
| Which two metabolites can be measured in a 24-hour urine sample to determine NE and epinephrine metabolism? | 3-methoxy-4-hydroxy-mandelic acid (VMA) and homovanillic acid (HVA) |
| What effects of sympathomimetic drugs are seen in blood vessels, and what receptors are utilized? | Blood vessels to the skin, kidney, and mucous membranes are constricted via alpha-1 receptors. Blood vessels to skeletal muscle are relaxed via beta-2 receptors |
| What effects of sympathomimetic drugs are seen in sweat and salivary glands, and what receptor is utilized? | Sweat and salivary glands are stimulated via alpha and muscarinic receptors |
| What effects of sympathomimetic drugs are seen in the gut and brinchioles, and what receptor is utilized? | Smooth muscle in gut and bronchioles relaxes via beta-2 receptors |
| What effects of sympathomimetic drugs are seen in the heart, and what receptors are utilized? | Increased HR and contraction force via beta-1 and beta-2 receptors |
| What effects of sympathomimetic drugs are seen on metabolism, and what receptors are utilized? | Increased glycogenolysis in the liver and muscle, and release of free fatty acids from adipose cells via beta-2 and beta-3 receptors |
| Which alpha receptor is excitatory, and which alpha receptor is inhibitory? | Alpha-1 receptors are excitatory; Alpha-2 receptors are inhibitory (Gi protein activation -> inhibit adenylyl cyclase -> decrease intracellular cAMP) |
| Stimulation of alpha-1 receptors has what effect on peripheral vasculature? | Vasoconstriction, especially in the skin |
| Stimulation of alpha-1 receptors has what effect on nasal mucosa? | Vasoconstriction in nasal mucosa = decrease nasal congestion |
| Stimulation of alpha-1 receptors has what effect on pupils? | Mydriasis |
| Stimulation of alpha-1 receptors has what effect on prostate gland? | Contract prostate gland |
| Stimulation of alpha-1 receptors has what effect on pilomotor smooth muscle (hair)? | Stimulate pilomotor smooth muscle = erect hair |
| Stimulation of alpha-2 receptors has what effect on presynaptic nerve terminals? | Inhibit transmitter release |
| Which neurotransmitter has a high affinity for Beta-2 receptors? | Epinephrine... not norepinephrine |
| What is the cellular mechanism activated by all beta receptors? | Gs -> activate adenylyl cyclase -> increase intracellular cAMP |
| Which drug is a selective agonist of alpha-1 receptors? | Phenylephrine |
| Which drug is a selective agonist of alpha-2 receptors? | Clonidine |
| Phenyephrine is a selective agonist of which adrenergic receptor? | Alpha-1 |
| Clonidine is a selective agonist of which adrenergic receptor? | Alpha-2 |
| Which drug is a selective agonist of beta-1 receptors? | Dobutamine |
| Dobutamine is a selective agonist of which adrenergic receptor? | Beta-1 |
| Which drug is a selective agonist of beta-2 receptors? | Albuterol |
| Albuterol is a selective agonist of which adrenergic receptor? | Beta-2 |
| What effect does beta-1 receptor stimulation have on the heart? | Increase contraction force and rate |
| What effect does beta-1 receptor stimulation have on the kidney? | Increase renin secretion |
| What effect does beta-2 receptor stimulation have on respiratory, uterine, and GI smooth muscle? | Relaxes them |
| What effect does beta-2 receptor stimulation have on blood vessels to skeletal muscle? | Relaxes them |
| What effect does beta-2 receptor stimulation have on potassium in skeletal muscle? | Promotes potassium uptake into skeletal muscle |
| What effect does beta-2 receptor stimulation have on metabolism? | Increase glycogenolysis and gluconeogenesis in the liver |
| What effect does beta-3 receptor stimulation have on metabolism? | Increases lipolysis in fat cells |
| Dopamine receptors are of particular importance in what 3 organs/areas of the body? | Brain, and renal and splanchnic vasculature |
| Which dopamine receptors are stimulatory, and stimulate adenylyl cyclase, and which receptors are inhibitory and inhibit adenylyl cyclase? | D1 receptors are stimulatory, D2 receptors are inhibitory |
| What are the effects seen with D1 dopamine receptor stimulation? | Stimulate adenylyl cyclase = dilate renal blood vessels |
| What are the effects seen with D2 dopamine receptor stimulation? | Inhibit adenylyl cyclase = open K channels, and decrease Ca influx = inhibit neurotransmitter release |
| Which size blood vessels have a greater response to alpha receptor stimulation, and why? | Small blood vessels because they have more innervation |
| The body uses what response to the increased blood pressure caused by alpha receptor stimulation? | Baroreceptors recognize increased blood pressure, and slow the heart rate via the vagus nerve |
| What medical condition might cause a magnified response to alpha agonists on blood pressure and why? | Atherosclerosis because the baroreceptor response may be impaired |
| What effect do alpha receptors have on the eye? | Mydriasis, and increased removal of aqueous humor = decreased intraocular pressure = glaucoma treatment |
| What adrenergic stimulating class of drugs may serve as a decongestant and what is the mechanism behind this? | Alpha-1 receptor stimulants; vasoconstrict blood vessels in mucous membranes |
| What adrenergic stimulating class of drugs may serve to promote continence and what is the mechanism behind this? | Alpha receptor stimulants; they constrict the bladder base, urethral sphincter, and prostate |
| What adrenergic-stimulating class of drugs may serve to assist in ejacultion? | Alpha receptor stimulants |
| What effects do beta receptors have on the heart? | Increase contractility and conduction velocity, increased automaticity = increased oxygen demand = increase coronary blood flow |
| What effect does beta receptor stimulation have on blood vessels to skeletal muscle? | Relax smooth muscle of blood vessels = vasodilate = decreased diastolic blood pressure even with increased cardiac output |
| What effect do beta receptor agonists have on the eye? | Increase production of aqueous humor = increase intraocular pressure. **Beta receptor antagonists used for glaucoma |
| What effect do beta-2 receptors have on the bronchioles? | Relax smooth muscle in bronchioles = widely used to treat asthma |
| Which adrenergic-stimulating class of drugs is useful for treating asthma? | Beta-2 agonists |
| Which receptors are most affected by Norepinephrine? | Alpha and Beta-1 receptors |
| How is norepinephrine administered? | Injection. Rapid metabolism = short duration of action |
| What effect does norepinephrine have on blood pressure? | Increases blood pressure |
| Administration of what drug inhibits vagal reflex/baroreceptor effect, and allows heart rate to increase with norepinephrine administration? | Norepinephrine |
| What effect of norepinephrine should be watched for upon injection? | Severe vasoconstriction at the infusion site = necrosis |
| How is epinephrine administered? | Injected. Rapid metabolism = short duration of action |
| Which receptors are stimulated by epinephrine? | Alpha, Beta-1, and Beta-2 |
| What effect does epinephrine have on the heart and by what receptor? | Positive inotropic and chronotropic effects (increased heart contraction strength and contraction rate) via Beta-1 receptors |
| What effect does epinephrine have on blood vessels to skin, mucosa, and kidneys? | Vasoconstriction = increased blood pressure. Increased pulse pressure, and increased heart rate |
| What effect does epinephrine have on metabolism? | Increased blood glucose due to increased glycogenolysis (Beta-2), decreased insulin secretion (Alpha-2) |
| What effect does epinephrine have on the kidneys? | Increased renin secretion (Beta-1) |
| What difference is seen between low dose with slow infusion and high dose with fast infusion of epinephrine? | Low dose/slow infusion: Beta-1 ^ HR, conduction, CO, & O2 consumption. Alpha vasoconstict = ^ BP systolic & diastolic. Beta-2: vasodilate to skeletal m. = decrease diastolic BP, ^ pulse pressure; ^ HR. High dose/fast infusion: ^^BP |
| Which adrenergic-stimulating drug is used in anaphylactic shock? | Epinephrine |
| Which emergency cardiac situations utilize epinephrine? | Cardiac arrest and complete heart block |
| Which emergency respiratory situation may utilize epinephrine? | Asthma attack |
| What medical use may benefit from the vasoconstricting effects of epinephrine? | Decreased diffusion of injected drugs, such as local anesthetics |
| What are 4 side effects seen with epinephrine? | Tremor, Throbbing headache, Increased blood pressure, and Tachycardia |
| What is a potential problem in patients with coronary artery disease who use epinephrine? | Angina, due to increased O2 consumption and increased cardiac work |
| When does vasoconstriction occur and when does vasodilation occur in epinephrine use? | Vasodilation occurs at low doses, vasoconstriction occurs at high doses |
| When is epinephrine use contraindicated and why? | When a patient is taking beta-blockers because effects of alpha receptors will be unopposed and can cause severe hypertension |
| What 3 effects are common with Ephedrine? | CNS stimulant, bronchodilation, and hypertension |
| What effect of ephedrine in weight loss preparations has caused it's removal from the market? | Hypertension |
| What receptor is phenylephrine a selective agonist for? | Alpha-1 |
| What are 3 main effects seen with phenylephrine, an adrenergic alpha agonist? | Vasoconstriction = increased blood pressure, decongestant, mydriasis with no effect on accommodation |
| Patients with what condition should use caution with phenylephrine, an adrenergic alpha agonist? | Hypertension |
| Which two adrenergic-stimulating drugs are used to treat hypotension | Phenylephrine or Methoxamine |
| What is pseudoephedrine, an adrenergic alpha agonist, commonly used for? | Decongestant |
| Patients with what condition should use caution with pseudoephedrine, an adrenergic alpha agonist? | Hypertension |
| Xylometazoline and Oxymetazoline both target what adrenergic receptors? | Alpha receptors = alpha agonists |
| What effects are seen with Xylometazoline and Oxymetazoline? | Vasoconstriction in the eye and nasal mucosa = decongestant |
| How are adrenergic alpha agonists Xylometazoline and Oxymetazoline administered? | Topically as nasal sprays for decongestion |
| Oxymetazoline has the potential to cause what cardiovascular condition if absorbed in large quantities systemically, and why? | Hypotension because it also acts on alpha-2 receptors |
| Adrenergic alpha agonists Xylometazoline and Oxymetazoline are contraindicated in what 2 conditions? | Narrow-angle glaucoma and hypertension |
| What drug are 4 selective alpha-2 agonist? | Clonidine, Methyldopa, Apraclonidine, and Tizanidine |
| What is the primary organ affected by the alpha-2 agonist clonidine, and what effects are seen? | The brain: decreased release of NE in presynaptic CNS terminals = decrease sympathetic output = decreased blood pressure |
| How is the alpha-2 agonist clonidine typically administered? | Transdermal patch, oral |
| Which adrenergic stimulating drug helps to reduce cravings and withdrawal symptoms in addicts and alcoholics? | Clonidine |
| What medical condition is the alpha-2 agonist clonidine commonly used to treat? | Hypertension |
| What adrenergic alpha-agonist is helpful in treating menopause hot flashes? | Clonidine |
| What are 3 side effects of the alpha-2 agonist clonidine? | Dry mouth, sedation, and sexual dysfunction in males |
| What actions should be avoided with the alpha-2 agonist clonidine patch and why? | Getting the patch too hot because it may cause a massive release in clonidine and cause severe hypotenstion |
| Why should the alpha-2 agonist clonidine not be withdrawn abruptly? | Hypertension may occur |
| Which alpha-2 agonist is effective in the eye to decrease aqueous humor production, and therefore decreasing intraocular pressure? | Apraclonidine |
| Which alpha-2 agonist is effective in treating muscle spasticity and has less of an effect on blood pressure than clonidine? | Tizanidine |
| What receptors do Isoproterenol target? | Beta-1 and Beta-2 receptors |
| What cardiovascular effects are seen with the Beta-agonist Isoproterenol? | Beta-2 = vasodilation in skeletal muscle = decreased blood pressure = reflex increased heart rate |
| What emergency conditions is the beta-agonist Isoproterenol used for? | Cardiac arrest and complete heart block. Used to be used for emergency asthma treatment but is now replaced by Beta-2 selective agents |
| What 3 concerning side effects may occur with large doses of the beta-agonist Isoproterenol? | Tachycardia, palpitations, and arrhythmias |
| Dobutamine targets what receptor? | Beta-1 receptors = agonist |
| What effect does the beta-1 agonist Dobutamine have on the heart? | Positive inotropic effect = increase contraction strength |
| What is a common clinical use of the beta-1 agonist Dobutamine? | In a cardiac stress test of the patient cannot exercise |
| Ritrodine and Albuterol target what receptor? | Beta-2 receptors = agonists |
| Ritrodine, a beta-2 agonist, has what clinically relevant effect? | It relaxes the uterus to prevent premature labor |
| Albuterol, a beta-2 agonist, is commonly used to treat what condition? | Asthma |
| What 2 side effects are common with beta-2 agonists? | Tachycardia and skeletal muscle tremor, especially when given orally |
| What effects are seen with low doses of dopamine? | D1 receptor activation causes vasodilation and increases renal blood flow |
| What receptor is activated with low doses of dopamine? | D1 |
| What effects are seen with high doses of dopamine? | Beta-1 receptor stimulation = positive inotropic and chronotropic effects = increased contraction strength and increased rate of contraction |
| What receptor is activated with high doses of dopamine? | Beta-1 |
| What condition is dopamine given to increase cardiac output without causing vasoconstriction? | Cardiac shock |
| What are 2 common side effects of dopamine? | Nausea and vomiting |
| What receptor is activated by Fenoldopam? | D1 |
| What effects are seen with use of the dopamine receptor agonist, Fenoldopam? | Vasodilation and decreased blood pressure |
| Amphetamine, an indirect-acting sympathomimetic causes what CNS effects and by what mechanism? | Increased release of NE and dopamine stimulates the CNS = increased alertness, decreased need for sleep, decreased appetite, euphoria, psychosis in some |
| Amphetamine, an indirect-acting sympathomimetic, causes what peripheral actions? | Tachycardia, and hypertension |
| What is the mechanism of action of the indirect-acting sympathomimetic, cocaine? | It inhibits dopamine and NE reuptake in nerve terminals |
| What effects are seen with use of cocaine, an indirect-acting sympathomimetic? | Hypertension, stroke, addiction, arrhythmias, MI, and psychosis |
| What is the mechanism of action of the indirect-acting sympathomimetic, tyramine? | It increase catecholamine release from nerve terminals, replaces NE in storage vesicles, and forms a false neurotransmitter = tachyphylaxis (acute decrease in response to tyramine) |
| The indirect-acting sympathomimetic tyramine is inactivated by what compound? | Monoamine oxidase (MAO) = in GI tract and liver = tyramine is inactive when given orally |
| Where is the indirect-acting sympathomimetic, tyramine, naturally found? | Food and as a by-product of tyrosine metabolism |
| Ingestion of large amounts of tyramine may cause what condition in depression patients being treated with MAO inhibitors and why? | Severe hypertension because MAO usually inactivates tyramine |
| What are two drugs classified as general alpha-receptor blockers? | Phentolamine and Phenoxybenzamine |
| What 5 drugs are classified as alpha-1 receptor blockers? | Alfuzosin, Doxazosin, Prazosin, Tamulosin, and Terazosin |
| What drug is classified as an alpha-2 receptor blocker? | Yohimbe |
| What 3 drugs are classified as general beta-receptor blockers? | Propranolol, Timolol, and Nadolol |
| What 7 drugs are classified as cardiospecific, or beta-1 receptor blockers? | Acebutolol, Atenolol, Betaxolol, Bisoprolol, Esmolol, Metoprolol, and Nevibolol |
| What 3 drugs are classified as beta-blockers with intrinsic sympathetic activity? | Acebutolol, Carteolol, and Pindolol |
| What 2 drugs are combined alpha and beta blockers? | Carvedilol and Labetalol |
| What 2 drugs are classified as affecting neurotransmitter release (adrenergic inhibitors)? | Guanethidine and Reserpine |
| What drug is classified as inhibiting neurotransmitter synthesis (adrenergic inhibitor)? | Metyrosine |
| What are 5 effects of alpha-1 blockers? | Decrease blood pressure by decreasing peripheral vascular resistance, cause orthostatic hypotension, miosis, vasodilation in nasal mucosa = congestion, easier urination, inhibit ejaculation |
| What 2 effects seen with alpha-2 blockers? | Increase norepinephrine release and increase insulin secretion |
| What effect is seen specifically with beta-1 blockers? | decrease renin secretion |
| What effects are seen specifically with beta-2 blockers? | Bronchoconstriction, decreased glycogenolysis |
| What effect is seen specifically with beta-3 blockers? | Inhibit lipolysis |
| What effects are seen, in general, with beta blockers? | Decrease rate and force of contraction of the heart (negative chronotropic and inotropic effects), decreased intraocular pressure by decreasing aqueous humor production |
| By what mechanism do most alpha blockers function, and how is the maximum effect of norepinephrine on tension affected? | Competitive antagonists; dose-response curve is shifted right, but maximum effect of norepinephrine on tension is unaffected |
| Which alpha blocker does not function as a competitive inhibitor, what is it's mechanism of action, and how does it affect the dose-response curve and maximum response of norepinephrine on tension? | Phenoxybenzamine acts as a non-competitive irreversible antagonist. It shifts the dose-response curve to the right and decreases the maximum response |
| What response occurs in the body when blood pressure decreases as a result of alpha receptor blockade? | Reflex tachycardia due to: recognition of decreased blood pressure by baroreceptors, and increased NE release due to alpha-2 blockade = stimulates beta receptors |
| What category of drugs is commonly used to treat benign prostatic hyperplasia? | Alpha blockers *Alpha-1 |
| On what receptors and by what mechanism does Phentolamine act? | Competitive antagonist of alpha-1 and alpha-2 receptors |
| What effects does the alpha blocker phentolamine have on the cardiovascular system? | Decrease peripheral resistance and blood pressure, indirectly cause cardiac stimulation due to baroreceptors recognizing low bp and increased NE release acting in beta receptors, tachycardia, arrhythmias, myocardial ischemia, hypotension |
| What effects does the alpha blocker phenolamine have on the GI system? | Gastric stimulation, blockade of serotonin receptors = increase gastric acid release, abdominal pain, exacerbate peptic ulcers |
| What is the mechanism of action of phenoxybenzamine and what receptors does it target? | Irreversible alpha blocker that binds covalently. Some blockage of alpha-2 receptors |
| What cardiovascular effects are seen with the irreversible alpha blocker, phenoxybenzamine? | Tachycardia from increased NE = beta stimulation and baroreceptor response to decreased bp,severe hypotension in hypovolemic pt's |
| The irreversible alpha blocker phenoxybenzamine is a major therapeutic treatment for what condition? | Pheochromocytoma (chronically high sympathetic tone) |
| What effects does the irreversible alpha blocker phenoxybenzamine have on the nose and reproductive organs? | Vasoconstriction of nasal mucosa = congestion, inhibit ejaculation by blocking smooth muscle in vas deferens |
| Administration of both the irreversible alpha blocker phenoxybenzamine and epinephrine could cause what 2 conditions and what is the mechanism/explanation of this? | Hypotension and tachycardia due to alpha blockade and beta-1 and beta-2 stimulation |
| What receptor does the adrenergic-antagonizing drug Prazosin target? | Alpha-1 receptors |
| What response is less likely with the alpha-1 selective antagonist Prazosin? | Increased heart rate due to lack of alpha-2 blockade |
| What effect does the alpha-1 selective antagonist Prazosin have on the cardiovascular system? | Vasodilates/decreases peripheral vascular resistance, decreases preload to heart = cardiac output not likely to increase |
| What is a concern with alpha-1 selective antagonist Prazosin dosage in CHF? | The half-life is doubled from ~3 hours to 7-10 hours, so it must be given at least 2X/day |
| What are two conditions in which the alpha-1 selective antagonist Prazosin is used for? | Hypertension and benign prostatic hyperplasia |
| What 3 side effects are commonly seen with the alpha-1 selective antagonist Prazosin? | First dose phenomenon: marked postural hypotension and syncope within 30-90 min after first dose is administered = take first dose at bed time; dizziness, congestion |
| Combined use of the alpha-1 selective antagonist Prazosin and erectile dysfunction drugs may cause what serious condition? | Severe hypotension |
| What is the mechanism of action of the drugs Terazosin and Doxazosin? | Selective alpha-1 blockers, very similar to Prazosin |
| What is an important difference between alpha-1 blockers Prazosin, and Terazosin and Doxazosin? | Terazosin and Doxazosin have longer half-lives of 12 and 20 hours, respectively = given once/day. |
| What is an important precaution/side effect seen with alpha-1 selective blockers Terazosin and Doxazosin? | First-dose phenomenon- marked postural hypotension within 30-90 minutes after first dose = take first dose before bed so lying down |
| Which alpha-blocker has the most direct effect on the prostate, with minimal effect on blood pressure? | Tamsulosin |
| What receptor is the main target of the adrenergic-inhibiting drug Tamsulosin? | Alpha-1a = prominent effect on the prostate |
| What effect does the alpha-1a selective blocker Tamsulosin have on the prostate and bladder? | Relaxes prostate and bladder sphincter = easier urination for men = effective in treating benign prostatic hyperplasia |
| The alpha-1a selective blocker Tamsulosin is effective in treating what condition? | Benign prostatic hyperplasia |
| What effect does the alpha-1a selective blocker Tamsulosin have on ejaculation? | Decreases ability to ejaculate |
| What receptor does the adrenergic-inhibiting drug Yohimbe target, and what is a direct effect of this drug? | Alpha-2 selective antagonist = increases NE |
| What effects result from administration of Yohimbe, an alpha-2 selective antagonist? | Increased NE release = increase blood pressure and heart rate |
| What is a popular-marketed use of Yohimbe? | As a natural alternative to Viagra to treat erectile dysfunction **Has not been proven effective in controlled studies |
| In what condition is it dangerous to use Yohimbe? | Hypertension in men |
| What is the overall effect of partial beta-antagonists with intrinsic sympathetic activity in relation to a beta agonist? | Partial beta antagonists with intrinsic sympathetic activity cause limited receptor activation = maximal effect on receptor is less than that of an agonist |
| What general cardiovascular effects are seen with beta blockers? | Negative inotropic and chronotropic effects (decreased rate and strength of heart contractility), decreased ability to increase heart rate during stress or exercise, slowed AV and atrial conduction, and decreased bp with chronic administration |
| What effect do beta blockers have on the kidney? | Decreased release of renin |
| When should beta-blockers never be given? | When a person has pheochromocytoma and is not also given alpha-blockers |
| What general respiratory effects are seen with beta blockers? | Bronchoconstriction **Beta-2 blockers |
| What respiratory condition should avoid, or use extreme caution with the use of beta-blockers, especially beta-2 blockers? | Asthma... bronchoconstriction could be fatal. |
| What effects do beta blockers have on the eye? | They decrease production of aqueous humor = reduce intraocular pressure |
| What effect do beta blockers have on metabolism? | They decrease glycogenolysis and glucose release from liver |
| Why might use of beta-blockers in diabetics (insulin-dependent type-I diabetics) be dangerous? | Impaired glycogenolysis and glucose release from the liver due to beta-blockade may prevent hypoglycemia recovery because response to glucagon is already impaired in the diabetic |
| What potential effect may be seen with chronic use of beta blockers (Beta-3 blockers)? | Increased VLDL and decreased HDL concentrations |
| Which beta blockers have local anesthetic activity? | Acebutolol, Labetalol, Metoprolol, Pindolol, and Propranolol |
| Where should beta blockers with local anesthetic activity (Acebutolol, Labetalol, Metoprolol, Pindolol, and Propranolol) not be used and why? | In the eye because they will anesthetize the cornea |
| What is the target and mechanism of action of the adrenergic-inhibiting drug, Propranolol? | Non-selective antagonism of Beta-1 and Beta-2 receptors |
| What effect does the non-selective competitive Beta receptor antagonist Propranolol have on the heart, kidney, metabolism, and Na channels? | Slows heart rate, decreases renin release, decreases lipolysis and glycogenolysis, and bloacks Na channels at high doses = local anesthetic |
| What cardiovascular condition is the non-selective competitive beta receptor antagonist propranolol used to treat? | Chronic use to treat hypertension, decrease mortality in pt's who have had a MI, angina, arrhythmias, and improve survival in CHF |
| What effect does the non-selective competitive beta receptor antagonist Propranolol have in treating hyperthyroidism? | Slows heart rate and decreases blood pressure |
| What beta-blocker is useful in preventing migraines? | Propranolol |
| What effect does the non-selective competitive beta receptor antagonist Propranolol have in patients with cirrhosis? | It decreases portal vein pressure and decreases the risk of bleeding |
| What common side effects are seen with use of the non-selective competitive beta receptor antagonist propranolol? | Bronchoconstriction in asthmatics, bradycardia from decreased AV conduction, cardiac arrhytmias is abrupt discontinuance after chronic use, sedation, fatigue, and mask hypoglycemic symptoms and make hypoglycemic recovery more difficult |
| What drug inhibits metabolism of the non-selective competitive beta receptor antagonist propranolol? | Cimetidine = may increase antihypertensive effects |
| What 3 drugs increase metabolism of the non-selective competitive beta receptor antagonist propranolol? | Barbiturates, Phenytoin, and Rifampin. Also: smoking. = decrease effectiveness of propranolol |
| What beta-blocking effects does the non-specific beta antagonist Timolol have? | Helpful for glaucoma treatment when administered in eye, may be absorbed systemically = avoid in asthma patients |
| What is an important CNS property of the non-specific beta antagonist Nadolol? | It doesn't enter the brain = doesn't cause sedation |
| What organ is predominantly targeted by beta-1 selective antagonists Metoprolol, Atenolol, and Bisoprolol? | The heart |
| What cardiovascular effects are seen with beta-1 selective antagonists Metoprolol, Atenolol, and Bisoprolol? | Negative inotropic and chronotropic effects (decreased rate and force of contraction), hypotension, bradycardia, increase life expectancy after MI |
| What effects are seen with beta-1 selective antagonists Metoprolol, Atenolol, and Bisoprolol in exercise? | Increase exercise tolerance due to beta-1 specificity **will not block vasodilation in skeletal muscle like beta-2 receptors |
| Why are beta-1 selective antagonists, such as Metoprolol, Atenolol, and Bisoprolol, safer for use in diabetics than non-specific beta blockers? | They are less likely to inhibit glycogenolysis = reduced risk of hypoglycemia |
| Beta-1 selective antagonist Atenolol may increase the risk of developing what disease? | Type II diabetes |
| What receptor does the adrenergic-inhibiting drug Nebivolol target? | Beta-1 receptors |
| What are 2 significant effects seen with the beta-1 selective antagonist Nebivolol? | Vasodilation due to increased nitric oxide release from endothelial cells, and reduce cholesterol/triglycerides/blood glucose |
| What receptor does the adrenergic-inhibiting drug Esmolol target? | Beta-1 |
| What is a notable characteristic of the beta-1 selective antagonist Esmolol? | It has a short duration of action: half life is ~8 minutes. |
| What receptor does the adrenergic-inhibiting drug Acebutolol target? | Beta-1 *intrinsic activity |
| What two conditions are beta-antagonists with intrinsic sympathetic activity used for, and what is the theory behind their use (what common beta-blocking effects do they avoid)? | Used to treat hypertension and angina; risk of bradycardia may be lower, and smaller effect on plasma lipids |
| Which beta anatagonist with intrinsic sympathetic activity is useful in treating glaucoma, and what is a potential benefit of its use over the non-specific beta antagonist timolol? | Carteolol; it has less systemic effects than timolol |
| What receptors does the adrenergic-inhibiting drug Labetalol target? | Beta-1, Beta-2, and Alpha-1 receptors |
| What effects are seen with the beta and alpha-1 blocker Labetalol? | Vasodilation via alpha-1 receptor blockade, and beta-1 blockade prevents a compensatory increase in heart rate with that alpha-1 induced decrease in blood pressure |
| What condition is the beta and alpha-1 blocker Labetalol used for? | Oral administration for hypertension, IV administration for hypertensive emergencies |
| What receptors does the adrenergic-inhibiting drug Carvedilol target? | Non-selective beta blocker, and alpha-1 receptor blocker |
| What 2 conditions is the non-selective beta blocker/alpha-1 blocker used for? | Treatment of hypertension and CHF |
| What are 7 clinical uses of beta blockers? | Treat hypertension, Ischemic heart disease (improves survival after MI, CHF, improves exercise tolerance in angina), cardiac arrhythmias, improves stroke volume in obstructive cardiomyopathies, dissecting aortic aneurysm, hyperthyroidism, migraines |
| What class of drugs is the treatment of choice for open-angle glaucoma? | Prostaglandin analogues |
| What class of drugs is the second most popular treatment for open-angle glaucoma? | Beta-blockers: decrease aqueous humor production with few visual side effects. *Timolol, carteolol, and Betaxolol (Beta-1 selective = fewer side effects) |
| What is the third line of choice for treating open-angle glaucoma? | Selective alpha-2 agonists: decrease aqueous humor production and increase drainage. *Apraclonidine and Brimonidine |
| What class of drugs work in the epithelium of the ciliary body to decrease formation of bicarbonate ions -> decrease aqueous humor production = decrease intraocular pressure = useful in treating open angle glaucoma? | Carbonic anhydrase inhibitors |
| Which cholinergic agonist may be used for glaucoma, and why is it rarely used? | Pilocarpine; used rarely because it affects vision |
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mccullough87
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