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191 Cards in this Set
- Front
- Back
- 3rd side (hint)
What is the major neurotransmitter of the parasympathetic autonomic nervous system
|
Acetylcholine
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Where are four places where nicotinic receptors are located
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Postsynaptic neurons in ganglia of both the parasympathetic nervous systems and sympathetic nervous systems
Neuromuscular junction Central nervous system Adrenal medulla |
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Where are three places where muscarinic receptors are located
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Organs innervated by the PNS
Thermoregulatory sweat glands innervated by the SNS CNS (cortex, hippocampus) |
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What drug inhibits transport of choline from the extracellular fluid into the cytoplasm of a cholinergic neuron
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Hemicholinium
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What enzyme catalyzes the reaction between choline and acetyl CoA to form Ach
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Choline acetyltransferase (CAT)
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The neuronal release of Ach into the synapse is inhibited by what toxin
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Botulinum toxin
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What organism produces botulinum toxin
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Clostridium botulinum (anaerobic, spore-forming, gram positive rod)
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The venom of what spider results in the release of stored Ach into the synapse
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Black widow
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What enzyme degrades Ach
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Acetylcholinesterase (AchE)
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What are the breakdown products of Ach
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Choline and acetate
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Where is AchE located
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Synaptic cleft
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What is muscarine
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Alkaloid compound found in various poisonous mushrooms
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Where is the M1 muscarinic receptor found in the body
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Neurons
Gastric parietal cells |
None
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Where is the M2 muscarinic receptor found in the body
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Neurons
Cardiac cells Smooth muscle |
None
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Where is the M3 muscarinic receptor found in the body (7)
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Neurons
Smooth muscle Exocrine glands Lungs GI tract Eye Bladder |
None
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Where is the M4 muscarinic receptor found in the body
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Neurons
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Where is the M5 muscarinic receptor found in the body
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Neurons
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Name the type of G protein that M1 is coupled to
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Gq coupled
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Name the type of G protein that M2 is coupled to
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Gi coupled
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Name the type of G protein that M3 is coupled to
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Gq coupled
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Does the PNS innervate the vasculature
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No (however there are muscarinic receptors located on the vasculature)
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How can Ach lower blood pressure
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Ach binds to Ach receptors in the vasculature leading to increased synthesis of NO via second messenger pathways
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NO is also known as what
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Endothelial-derived relaxation factor (EDRF)
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What amino acid is a precursor to NO synthesis
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Arginine
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None
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Does AchE have a high affinity for Ach
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Yes
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Does Ach increase or decrease blood pressure
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Decreases
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Does Ach increase or decrease heart rate
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Decreases
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Does Ach increase or decrease salivation
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Increases
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Dose Ach increase or decrease lacrimation
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Increases
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Does Ach increase or decrease sweating
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Increases
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Does Ach increase or decrease GI secretions
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Increases
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Does Ach increase or decrease GI motility
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Increases
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Does Ach increase or decrease Miosis (constriction of pupil)
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Increases
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Does Ach increase or decrease bladder detrusor muscle tone
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Increase (this lead to increased urination)
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Does Ach increase or decrease Bronchodilation
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Decrease
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What does Ach do to the ciliary muscle of the eye
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Increased contraction which leads to increased accommodation
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How does Ach cause miosis
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Increased contraction of the circular muscle in the iris
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Does bethanechol have muscarinic activity
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Yes (agonist)
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Does AchE have a high affinity for bethanecol
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No (zero affinity)
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Does bethanechol have nicotinic activity
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No
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What is bethanechol used for
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Neurogenic bladder (nonobstructive urinary retention)
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Does carbachol have muscarinic activity
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Yes (agonist)
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Does carbachol have nicotinic activity
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Yes (agonist)
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Does AchE have a high affinity for carbachol
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No (zero affinity)
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What is carbachol used for
|
Miotic agent to reduce intraocular pressure (IOP)
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Does pilocarpine have muscarinic activity
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Yes (agonist)
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Does pilocarpine have nicotinic activity
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No
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Does AchE have a high affinity for pilocarpine
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No (zero affinity)
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What is pilocarpine used for
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Mitotic drug of choice to lower IOP in emergency settings of narrow-angle and open-angle glaucoma
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Can pilocarpine cross the blood-brain barrier (BBB)
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Yes (tertiary amine)
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Give examples of reversible AchE inhibitors
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Neostigmine
Pyridostigmine Physostigmine Edrophonium Rivastigmine, Donepezil, Galantamine, Tacrine |
None
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What are donepezil, galantamine, rivastigmine, and tacrine used for
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Alzheimer’s disease
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What two AchE inhibitors are quaternary ammonium compounds and therefore cannot cross the BBB
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Neostigmine
Pyridostigmine |
None
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What short-acting AchE inhibitor is used to diagnose myasthenia gravis and is also used to differentiate myasthenic from cholinergic crisis
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Edrophonium
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Which reversible AchE inhibitor is used as an antidote in atropine overdose
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Physostigmine (tertiary amine therefore crosses BBB to enter CNS)
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Give examples of irreversible AchE inhibitors
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Sarin
Malathion Parathion Echothiphate Isoflurophate |
None
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Which irreversible AchE inhibitor is used as nerve gas
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Sarin
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Which two AchE inhibitors are used as insecticides
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Malathion
Parathion |
None
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What is another name for the irreversible AchE inhibitors
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Organophosphates
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How do organophosphates irreversibly inhibit AchE
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Phosphate group covalently binds to serine hydroxyl group in the active site of AchE thereby rendering the enzyme permanently inactive
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What is used to counteract the muscarinic and CNS effects during organophosphate poisoning
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Atropine (protects muscarinic receptors, via competitive inhibition, from the increased levels of Ach thereby preventing overstimulation)
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What agent is used to reactivate inhibited AchE during organophosphate poisoning
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Pralidoxime (2-PAM)
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True or False? The effectiveness of 2-PAM in counteracting organophosphate poisoning is not time dependent
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False, 2-PAM must be given before the “aging” process of the organophosphate-AchE complex is complete
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What are the signs and symptoms of organophosphate poisoning
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Miosis
Diarrhea Urination Bradycardia Sweating Lacrimation Salivation Bronchoconstriction Peripheral nerve demyelination |
None
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Does atropine block nicotinic receptors, muscarinic receptors, or both
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Muscarinic receptors
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What are the pharmacologic actions of atropine
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Mydriasis
Cycloplegia Tachycardia Sedation Urinary retention Constipation Dry mouth Dry eyes Decreased sweating Hallucination Sedation Hyperthermia Delirium Blurred vision Coma (high doses) |
None
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What class of drugs can be used to counteract atropine overdose
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AchE inhibitors
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Name three drug classes, other than atropine, that may cause antimuscarinic adverse effects
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Sedating/ first generation antihistamines (diphenhydramine)
Tricyclic antidepressants (TCAs) Phenothizines |
None
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Low dose (<0.5 to 1 mg) atropine does what to heart rate
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Decreases heart rate (unknown paradoxical vagalmimetic effect)
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High dose(>0.5 to 1 mg) atropine does what to heart rate
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Increases heart rate (parasympatholytic effect)
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What is the half life of atropine
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4 hours
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Name four belladonna alkaloids
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Belladonna
Atropine Scopolamine Hyoscyamine |
None
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What is belladonna
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Perennial atropine-based plant; also known as “nightshade”
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How does scopolamine differ from atropine (3)
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Longer duration of action
More potent CNS effects Able to block short-term memory |
None
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What is the main therapeutic indication of scopolamine
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Motion sickness
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Giving drugs with anticholinergic activity can precipitate an emergent situation in what type of patients
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Patients with narrow-angle glaucoma
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What are the signs and symptoms of acute angle closure glaucoma
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General distress
Pain Headache Red eye Photophobia Increased IOP Visual changes Malaise Nausea Vomiting |
None
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What two anticholinergic agents are quaternary ammonium compounds used for the treatment of asthma and COPD
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Ipratropium
Tiotropium |
None
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How often is tiotropium dosed
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Once daily (longer half-life vs. ipratropium)
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Does ipratropium affect airway secretions
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No (unlike atropine)
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None
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Name three ganglionic blocking agents
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Hexamethonium
Mecamylamine Trimethaphan |
None
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What are ganglionic blocking agents primarily used for
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Lowering blood pressure
Blocking autonomic nervous system reflexes |
None
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Will trimethaphan block a reflex bradycardia after a vasoconstricting agent is given
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Yes
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Will trimethaphan block a directly induced bradycardia by a muscarinic agonist
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No
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Neuromuscular blocking agents can be grouped into what two general categories
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Depolarizing and nondepolarizing
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Do neuromuscular blockers (NMBs) work at muscarinic or nicotinic receptors
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Nicotinic (NMJ has nicotinic receptors)
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How many subunits is the nicotinic receptor made of
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Five
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Which subunit of the nicotinic receptor does Ach bind to
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Alpha subunit (nicotinic receptors have two alpha subunits)
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Binding of Ach to the nicotinic receptor at the NMJ is required to open which type of ion channel
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Sodium channel
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What is the most commonly used NMB
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Succinylcholine (depolarizing NMB)
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How does succinylcholine work at the NMJ
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Behaves as a cholinergic agonist that remains bound to the Ach receptor for a prolonged period
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What happens during phase I of succinylcholine activity at the NMJ
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Receptors become depolarized and transient fasciculations are observed
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None
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What happens during phase II of succinylcholine activity at the NMJ
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Receptor becomes resistant to depolarization and a flaccid paralysis ensues
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What are the main uses of succinylcholine
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Endotracheal intubation
Adjunct during electroconvulsive shock therapy |
None
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Is succinylcholine short or long acting
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Short acting (duration 4-8 minutes) because of rapid hydrolysis by cholinesterase
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Where is the enzyme (cholinesterase) that metabolizes succinylcholine found
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Plasma
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What are the adverse effects of succinylcholine
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Malignant hyperthermia
Apnea Hypertension Hyperkalemia |
None
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What are the signs and symptoms of malignant hyperthermia
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Sudden onset of hyperthermia
Tachycardia Tachypnea Sweating Cyanosis Muscle rigidity |
None
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How is malignant hyperthermia treated
|
Rapid cooling of patient
Dantrolene |
None
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What is the mechanism of action of dantrolene
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Inhibits calcium release from the sarcoplasmic reticulum of muscle cells thereby relaxing muscle tone and reducing heat production
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Succinylcholine may have a prolonged half-life in what type of patients
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Patients with a genetic deficiency or altered form of plasma cholinesterase
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What is the mechanism of action of nondepolarizing NMBs
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Competitive antagonists of Ach at the NMJ
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Which drug is the prototype of the nondepolarizing NMBs
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Tubocurarine
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What antidote is used in tubocurarine overdose
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AchE inhibitor (increases Ach concentration which competes with tubocurarine at the NMJ)
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List in order, from first to last, the muscles that are paralyzed by nondepolarizing NMBs
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Small muscles of the face and eye; fingers; limbs, neck, trunk; intercostals; diaphragm
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Which antimicrobial class of drugs may act in synergy with nondepolarizing NMBs by inhibiting release of Ach from nerve endings by competing with calcium ions, thereby increasing neuromuscular blockade
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Aminoglycosides (most likely to occur with high doses; patients with hypocalcemia, hypomagnesemia, or neuromuscular disorders)
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None
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Give examples of nondepolarizing NMBs
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Tubocurarine
Atracurium Rocuronium Mivacurium, Vecuronium, Pancuronium, Pipercuronium |
None
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What is the only nondepolarizing NMB that does not require dosage reduction in patients with renal failure
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Atracurium
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What nondepolarizing NMB has the most rapid onset of action
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Rocuronium
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In what situations are nondepolarizing NMBs used
|
Adjunct to general anesthesia to facilitate endotracheal intubation and to relax skeletal muscles during surgery
Facilitate mechanical ventilation in ICU patients |
None
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What are the two major neurotransmitters of the SNS
|
Epinephrine; norepinephrine
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What amino acid is the precursor to dopamine, norepinephrine, and epinephrine
|
Tyrosine
|
None
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What are the steps, in order, to the synthesis of epinephrine starting from tyrosine
|
Tyrosine converted into DOPA by tyrosine hydroxylase (rate limiting step);
DOPA is converted into dopamine by DOPA decarboxylase; Dopamine is converted into norepinephrine by dopamine β-hydroxylase; Norepinephrine is converted into epinephrine by methylation in the adrenal medulla |
None
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What is the mechanism of action of fuanethidine and bretylium
|
Inhibits the release of norepinephrine into the synapse
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What two enzymes metabolize norepinephrine
|
Monoamine oxidase (MAO); catechol-O-methyltransferase (COMT)
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What is the mechanism of action of reserpine
|
Inhibits the transport of norepinephrine from the neuronal cytoplasm into the synaptic vesicles
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What are the common side effects of reserpine
|
Depression
Sedation |
None
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What breakdown products of norepinephrine are excreted in the urine and can be measured to help diagnose pheochromocytoma
|
Vanillylmandelic acid (VMA)
Metanephrine Normetanephrine |
None
|
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How does cocaine increase norepinephrine levels in the synaptic cleft
|
Inhibits reuptake of neurotransmitter back into the presynaptic neuron
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What are the two major classes of adrenergic receptors
|
α-receptors; β-receptors
|
None
|
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What drug can inhibit tyrosine hydroxylase
|
Methyl-p-tyrosine; feedback inhibition by norepinephrine
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What neurotransmitters are metabolized by MAO type A
|
Norepinephrine
Serotonin Tyramine |
None
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What neurotransmitters does MAO type B metabolize
|
Dopamine
|
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How do amphetamine, ephedrine, and tyramine increase norepinephrine levels
|
Act as indirect sympathomimetic agents by displacing norepinephrine from the mobile storage pool (drug enters presynaptic nerve terminal and displaces stored norepinephrine)
|
None
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Where are α2-receptors found
|
Presynaptic neurons
Pancreatic β cells |
None
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What happens when α2-receptors are activated
|
Inhibits the release of norepinephrine from synaptic vesicles
|
None
|
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Give examples of α2-receptor agonists
|
Clonidine
Dexmedetomidine α-methyldopa; guanabenz; guanfacine; |
None
|
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What are the therapeutic indications (7) of clonidine
|
Hypertension
Severe pain Heroin withdrawal Nicotine withdrawal Ethanol dependence Clozapine-induced sialorrhea Prevention of migraines |
None
|
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What is dexmedetomidine used for
|
Sedation of intubated and mechanically ventilated patients
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With drugs that activate both α and β-receptors, which receptors are generally activated first (which receptors are more sensitive)
|
β-receptors
|
None
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Activation of what receptor type in the eye will lead to contraction of the radial muscle and subsequently lead to mydriasis
|
α1-receptor
|
None
|
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Name the G-protein associated with α1 receptors
|
Gq
|
None
|
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Name the G-protein associated with α2 receptors
|
Gi
|
None
|
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Name the G-protein associated with β1, β2, and D1 receptors
|
Gs
|
None
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Name the major effects mediated by α1 receptors (7)
|
Mydriasis
Vasoconstriction Increased blood pressure Increased glycogenolysis Decreased renin release Decreased urination Ejaculation |
None
|
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Name the major effects mediated by α2 receptors (3)
|
Inhibition of norepinephrine release
Inhibition of insulin release Platelet aggregation |
None
|
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Name the major effects mediated by β1 receptors (4)
|
Increased heart rate
Increased conduction velocity Increased force of heart contraction Increased renin release |
None
|
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Name the major effects mediated by β2 receptors (5)
|
Vasodilation
Bronchodilation Increased insulin secretion Increased glycogenolysis Relaxation of uterine smooth muscle |
None
|
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Name the major effects mediated by peripheral D1 receptors (4)
|
Vasodilation of coronary, renal, and mesenteric vasculature
Increased GFR Increased renal blood flow Increased sodium excretion |
None
|
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α2-receptor activation in the pancreas will cause insulin secretion to increase or decrease
|
Decrease
|
|
|
β2-receptor activation in the pancreas will cause insulin secretion to increase or decrease
|
Increase
|
None
|
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Which receptor type does epinephrine preferentially bind to at low doses
|
β-receptors (vasodilation in vasculature)
|
None
|
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Which receptor type does epinephrine preferentially bind to at high doses
|
α-receptors (vasoconstriction in vasculature)
|
None
|
|
What is the drug of choice in patients with type 1 hypersensitivity reactions
|
Epinephrine
|
|
|
Why is epinephrine often given in combination with local anesthetics
|
Epinephrine causes a vasoconstriction thereby inhibiting the local anesthetics redistribution away from its site of action (increases the duration of local anesthesis)
|
None
|
|
What is the concentration of epinephrine when given in combination with local anesthetics
|
1:100,000
|
|
|
State whether peripheral vascular resistance increases or decreases with low dose epinephrine
|
Decreases
|
|
|
State whether systolic blood pressure increases or decreases with low dose epinephrine
|
Increases
|
|
|
State whether diastolic blood pressure increases or decreases with low dose epinephrine
|
Decreases
|
|
|
State whether pulse pressure increases or decreases with low dose epinephrine
|
Increases
|
|
|
What receptors are activated by isoproterenol
|
β1=β2
|
None
|
|
What receptors are activated by dopamine
|
D>β>α
|
None
|
|
What receptors are activated by dobutamine
|
β1>β2
|
None
|
|
What receptors are activated by phenylephrine
|
α1>α2
|
None
|
|
What receptors are activated by methoxamine
|
α1>α2
|
None
|
|
Does norepinephrine activate β2 receptors
|
No
|
None
|
|
Activation of dopamine receptors will cause what type of response in the mesenteric and renal vasculature
|
Vasodilation
|
|
|
What is dopamine metabolized to
|
Homovanillic acid (HVA)
|
|
|
What is dobutamine used for
|
Increases cardiac output in congestive heart failure without affecting RBF (unlike dopamine)
|
|
|
Tyramine is a breakdown product of which amino acid
|
Tyrosine
|
|
|
Where is tyramine found
|
Cheeses (aged)
Alcoholic beverages Fish Chocolates Red wines Processed meats (fermented, aged, and pickled foods) |
None
|
|
What enzyme is responsible for the breakdown of tyramine
|
MAO type A
|
|
|
What can potentially happen if a patient on a MAOI consumes large amounts of fermented cheese
|
Hypertensive crisis
|
|
|
What are phenylephrine and pseudoephedrine used to treat
|
Nasal congestion
|
None
|
|
What are mixed action adrenergic agonists
|
Substances that release stored norepinephrine from nerve terminals
Directly stimulate α and β receptors |
None
|
|
What are some examples of mixed action adrenergic agonists
|
Ephedrine
Metaraminol |
None
|
|
Which drug is a nonselective, competitive antagonist at both α1 and α2 receptors
|
Phentolamine
|
None
|
|
Which drug is a nonselective, irreversible antagonist at both α1 and α2 receptors
|
Phenoxybenzamine
|
None
|
|
What are phentolamine and phenoxybenzamine mainly used for
|
Pheochromocytoma
|
None
|
|
What is the mechanism of action of prazosin
|
Selective α1 antagonist
|
None
|
|
What are prazosin, terazosin, and doxazosin used to treat
|
Benign prostatic hypertrophy
Hypertension |
None
|
|
What is alfuzosin used to treat
|
BPH
|
|
|
This drug is a selective α1A receptor antagonist, used in the treatment of BPH, and has less cardiovascular side effects vs. traditional α1 antagonists
|
Tamsulosin
|
None
|
|
What advantage do selective α1 antagonists have over nonselective α antagonists
|
Less reflex tachycardia
|
None
|
|
What CNS prejunctional α2 receptor antagonist is used to treat postural hypotension and impotence
|
Yohimbine
|
None
|
|
What CNS prejunctional α2 receptor antagonist is used to treat depression
|
Mirtazapine
|
None
|
|
Give examples (6) of β1 selective antagonists
|
Acebutolol
Atenolol Bisoprolol Betaxolol Exmolol Metoprolol |
None
|
|
Give examples (4) of nonselective β antagonists
|
Propranolol (angina pectoris)
Pindolol (ISA) Sotalol (anti-arrythmic) Timolol Nadolol |
None
|
|
Give two examples of mixed α2/β antagonists
|
Carvedilol
Labetalol |
None
|
|
What is the name of a β antagonist that also blocks potassium channels and is used as an antiarrhythmic
|
Sotalol
|
None
|
|
Which two β antagonists have intrinsic sympathomimetic activity (ISA)
|
Acebutolol
Pindolol |
None
|
|
What is ISA
|
Drugs act as partial agonists and only work when there is increased sympathetic drive such as with exercise
This results in less bradycardia and less effects on lipid metabolism |
None
|
|
What happens to exercise tolerance in patients being treated with β-blockers
|
Decreased exercise tolerance
|
None
|
|
What are the main therapeutic indications (6) of β-blockers
|
Angina
Arrhythmias Hypertension CHF (not all β-blockers) Thyrotoxicosis Glaucoma (ophthalmic formulations) |
None
|
|
What are some noncardiovascular uses of propranolol
|
Migraine prophylaxis
Performance anxiety (stage fright) |
None
|
|
β-blockers can inhibit the majority of effects caused by thyrotoxicosis except for what sign
|
Diaphoresis
|
None
|
|
β-blockers can inhibit the majority of effects caused by hypoglycemia except for what sign
|
Diaphoresis
|
None
|
|
What does propranolol do to serum triglycerides
|
Increases serum triglycerides
|
|
|
What does propranolol do to serum LDL
|
Increases serum LDL
|
|
|
Why does propranolol cause vivid dreams
|
Crosses the BBB
|
|
|
Why should β-blockers be tapered down instead of abruptly discontinued
|
Chronic therapy leads to upregulation of β-receptors; therefore, abrupt discontinuation may lead to life-threatening cardiovascular rebound effects (tachycardia; hypertension; arrhythmias; death)
|
None
|