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108 Cards in this Set

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: A 12yo patient was treated for a reaction to a bee sting, what drug provides the best coverage of sympathomimetic receptors?
Epinephirine(Alpha1,2 and Beta 1,2)
A 57 yo heart failure pt develops cardiac decompensation, what drug will give you adequate perfusion of his kidneys as well as tx for his Hypotension
Dopamine
A fellow passenger on a Carnival cruise ship looks pale and diaphoretic, what antimuscarinic agent would you give them?
scopolamine
A group of pts are rushed into the ER complaining of excessive sweating, tearing, salivation, HA, N and V, muscle twitching, difficulty breathing and diarrhea. What drug would be the most effective immediate tx
Atropine pts are suffering from Cholinestrase inhibitor poisining(Nerve gas/Organophosphate poisining)
As an Anes you want to use a depolarizing neuromuscular blocking drug on your pt, what do you use
Succinylcholine
By what mechanism does this drug help(Succinylcholine)
Prevents the release of Ca from SR of skeletal muscle
Clonidine is the preferred sym pathomimetic tx of HTN in pts with renal disease, why?
Centrally acting alpha agonist, thus causing a decrease in central adrenergic outflow, spairing renal blood flow
Cocaine casues vasoconstriction and local anesthesia by what mechanism?
Indirect agonist, uptake inhibitor
Cocaine shares is mechanism of action with what antidepressant
TCA
Dobutamine used for the tx of shock acts on which receptors?
Beta1 more than B2
Guanethidine enhances the release of Norepi?
No, it inhibits the release of Nor Epi
How does angiotensin II affect NE release?
It acts presynaptically to increase NE release.
How does botulinum toxin result in respiratory arrest?
Prevents the release of ACh, which results in muscle paralysis.
How does dantrolene work?
Prevents the release of calcium from the sarcoplasmic reticulum of skeletal muscle.
How does NE modulate its own release? What other neurotransmitter has this same effect?
A: NE acts presynaptically on alpha-2 receptors to inhibit its own release.
A: ACh also acts presynaptically through M1 receptors to inhibit NE release.
How would hemicholinium treatment affect cholinergic neurons?
Hemicholinium inhibits the transport of choline into the nerve, thus inhibiting formation of ACh.
How would you reverse the effect of a neuromuscular blocking agent?
Give an anti-chloinesterase - neostigmine, edrophonium, etc
If a patient is given hexamethonium, what would happen to his/her heart rate?
It would increase to ~ 100 beats/min. Both sympathetic and vagal stimulation would be knocked out, but the SA node has an intrinsic pace of 100 beats/min, which is normally checked by vagal stimulation.
Q: Isopoterenol was given to a patient with a developing AV block, why?
A: Stimulates beta adrenergic receptors
Q: Norepi feedbacks and inhibits the presynaptic receptor by what mechanism
A: Binding to the presynaptic alpha 2 release modulating receptors
Q: Reserpine will block the syntheis of this drug and but not its precursor.
A: Blocks Norepi, but not Dopamine
Q: These drugs acts indirectly by releasing strored catecholamines in the presynaptic terminal
A: Amphetamine and Ephedrine
What anticholinesterase crosses the blood-brain-barrier?
physostigmine
Q: What antimuscarinic agent is used in asthma and COPD?
A: Ipratropium
What antimuscarinic drug is useful for the tx of asthma
Ipratropium
What are the classic symptoms of cholinesterase inhibitor poisoning (parathion or other organophosphates)?
Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, and Salivation = DUMBBELS; also abdominal cramping
Q: What are the clinical indications for bethanechol?
A: Activates cholinergic receptors on bladder and bowel smooth muscle, alleviating post-op and neurogenic ileus and urinary retention.
What are the clinical indications for neostigmine?
Post-op and neurogenic ileus and urinary retention, myasthenia gravis, and reversal of neuromuscular junction blockade (post-op) through anticholinesterase activity.
Q: What are the indications for using amphetamine?
A: narcolepsy, obesity, and attention deficit disorder (I wouldn't recommend this)
What are the nondepolarizing neuromuscular blocking drugs?
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium
Q: What are the phases of succinylcholine neuromuscular blockade?
A: Phase 1 = prolonged depolarization, no antidote, effect potentiated by anticholinesterase; Phase 2 = repolarized but blocked, an anticholinesterase is the antidote for this phase
Q: What are two indirect acting adrenergic agonists?
A: amphetamine and ephedrine
Q: What beta 2 agonist will help your 21yo Astma pt?
A: Albuterol, tertbutaline
What cholinergic inhibitor acts by directly inhibiting Ach release at the presynaptic terminal
Botulinum
Q: What cholinomimetic is useful in the diagnosis of Myasthenia Gravis
A: Edrophonium
What cholinomimetics might your pt be taking for his glaucoma
Carbachol, pilocarpine, physostigmine, echothiophate
Q: What class of drug is echothiophate? What is its indication?
A: anticholinesterase
A: glaucoma
Q: What conditions would you use dantrolene?
A: In treatment of malignant hyperthermia, due to concomitant use of halothane and succinylcholine. Also in neuroleptic malignant syndrome, a toxicity of antipsychotic drugs.
Q: What drug is used to diagnose myasthenia gravis?
A: edrophonium (extremely short acting anticholinesterase)
Q: What cholinomimetics might your pt be taking for his glaucoma
A: Carbachol, pilocarpine, physostigmine, echothiophate
Q: What class of drug is echothiophate? What is its indication?
A: anticholinesterase
A: glaucoma
Q: What conditions would you use dantrolene?
A: In treatment of malignant hyperthermia, due to concomitant use of halothane and succinylcholine. Also in neuroleptic malignant syndrome, a toxicity of antipsychotic drugs.
Q: What drugs target this enzyme (cholinesterase)
A: Neostigmine, pyridostigmine edrophonium physostigmine echothiophate
Q: What effect would atropine have on a patient with peptic ulcer disease?
A: Theoretically it could be used to block the cephalic phase of acid secretion (vagal stimulation).
Q: What effect would atropine have on the preganglionic sympathetic activation of sweat glands? Would this person sweat?
A: None. No, because atropine would block the postganglionic muscarinic receptors involved in sweat gland stimulation.
Q: What enzyme is responsible for the breakdown of ACh in the synaptic cleft?
A: Acetylcholinesterase; ACh is broken down into choline and acetate.
Q: What enzyme is responsible for the degredation of Ach
A: Acetylcholine esterase
Q: What enzyme is responsible for the production of Ach from Acetyl CoA and Choline
A: Choline acetyltransferase
Q: What is the clinical utility of clonidine?
A: Treatment of hypertension, especially with renal disease (lowers bp centrally, so flow is maintained to kidney).
Q: What is the clinical utility of cocaine?
A: The only local anesthetic with vasoconstrictive properties.
Q: What is the difference between the affinity for beta receptors between albuterol/terbutaline and dantroline?
A: Dobutamine has more of an affintiy for beta-1 than beta-2, and is used for treating heart failure and shock. Albuterol and terbutaline is the reverse, and is used in treatment of acute asthma.
Q: What is the difference in receptor affinity of epinephrine at low doses? High doses?
A: Prefers beta's at low doses, but at higher doses alpha agonist effects are predominantly seen.
Q: What is the effect of epinephrine infusion on bp and pulse pressure?
A: Increased systolic and pulse pressure, decreased diastolic pressure, and little change in mean pressure.
Q: What is the effect of guanethidine on adrenergic NE release?
A: It inhibits release of NE.
Q: What is the effect of norepinephrine on bp and pulse pressure?
A: Increases mean, systolic, and diastolic bp, while there is little change in pulse pressure.
Q: What is the effect of TCA's on the adrenergic nerve?
A: They inhibit reuptake of NE at the nerve terminal (as does cocaine).
Q: What is the only depolarizing neuromuscular blocking agent?
A: Succinylcholine
Q: What is the receptor affinity and clinical use of isoproterenol?
A: It affects beta receptors equally and is used in AV heart block (rare).
Q: What makes this drug effective (isoproterenol)
A: It antagonizes Ach M receptors and decreases parasym (GI) rxn
Q: What nondepolorizing agents could you have used
A: Tubocurarine, atra-, miv-, pan-,ve-, rapacuronium
Q: What other substances regulate the Norepi nerve ending
A: Ach, AngiotensinII
Q: What other syndrome can this drug tx
A: Neuroleptic malignant syndrome
Q: What physiological effects was the Anes using Atropine to tx
A: SLUD (salivation, Lacrimation, urination, Defecation)as well as airway secretion, GI motility, acid secretions
Q: What reversal agent could a Anes give to reverse the effects of Atropine
A: Bethanechol, Neostigmine, physostigmine
Q: What side effect of using atropine to induce pupillary dilation would you expect?
A: Atropine would also block the receptors in the ciliary muscle, causing an impairment in accommodation (cycloplegia).
What sympathomimetic would you not prescribe for hypotension in a pt with renal artery sclerosis.
Norepinephrine (Alpha1,2 and beta 1)
Q: What type of neurological blockade would hexamethonium create?
A: Hexamethonium is a nicotinic antagonist, and thus is a ganglionic blocker.
Q: What would be the effect on blood pressure with infusion of the alpha -2 agonist clonidine?
A: Initially vasoconstriction would increase bp, but then it acts on central alpha-2 receptors to decrease adrenergic outflow resulting in decreased bp.
Q: What would be the next drug that you would give and why
A: Pralidoxime, regenerates active cholinestrase
Q: Which antimuscarinic agents are used in producing mydriasis and cycloplegia?
A: atropine, homatropine, tropicamide
Q: Which drug increases Sys BP w/o affecting Pulse Pressure
A: Epinephrine
Q: Which of epi, norepi, or isoproterenol results in bradycardia?
A: Norepinephrine
Q: Which of the following would atropine admi
nistration cause? Hypothermia, bradycardia, excess salivation, dry flushed skin, or diarrhea
A: Dry flushed skin, due to inhibition of sympathetic post-ganglionic blockade on muscarinic receptors of sweat glands. All others are opposite of what would be expected.
Q: Which of these three drugs will cause a reflex bradycardia in your pt (Norepi, Epi, or Isoporterenol)
A: Norepinephrine
Q: Which receptors does phenylephrine act upon?
A: alpha-1 > alpha-2; used as a pupil dilator, vasoconstrictor, and for nasal decongestion
Q: While at a tail gait party, you bite into a sandwich that a yellow jacket is also enjoying. Knowing your allergy to this creature, what should you do?
A: Epinephrine to treat anaphylaxis. Also useful if you have open angle glaucoma, asthma, or hypotension.
Q: Why are albuterol and terbutaline effective in tx of acute asthmatic attacks?
A: These B-2 agonists cause respiratory smooth muscle to relax.
Q: Why does atropine dilate the pupil?
A: Blocking muscarinic receptors in the circular fibers of the eye, results in unopposed action of radial muscles to dilate.
Q: Why does NE result in bradycardia?
A: NE increases bp, which stimulates baroreceptors in the carotid sinus and the aorta. The CNS signals through vagal stimulation to decrease heart rate.
Q: Why is carbachol and pilocarpine useful in treatment of glaucoma?
A: They activate the ciliary muscle of the eye (open angle) and pupillary sphincter (narrow angle).
Q: Why is pyridostigmine effective in the treatment of myasthenia gravis?
A: As an anticholinesterase it increases endogenous ACh and thus increases strength
Q: Why is reserpine effective in treating HTN?
A: Reserpine inhibits dopamine transport into vesicles, attenuating its conversion to NE by dopamine beta-hydroxylase.
Q: Why is there a drop in systolic, mean, and diastolic bp with infusion of isoproterenol?
A: Stimulating beta receptors stimulates heart rate, but beta receptor induced vasodilation reduces peripheral resistance.
Q: Why would a patient with cog-wheel rigidity and a shuffling gait be given benztropine?
A: Parkinson patients benefit from antimuscarinic agents through its inhibitory action within the indirect pathway.
Q: Why would dopamine be useful in treating shock?
A: Receptors = D1=D2>beta>alpha, thus increasing heart rate (beta) and blood pressure (alpha vasoconstriction) while maintaining kidney perfusion (dopamine receptors)
Q: Why would you give a drug like pancuronium or succinylcholine?
A: Useful in muscle paralysis during surgery or mechanical ventilation.
Q: Why would you use pralidoxime after exposure to an organophosphate?
A: Pralidoxime regenerates active cholinesterase.
Q: Will Hemicholinum affect the release of stored Ach during Cholinergic Stimulation
A: No, hemicholinum block the uptake of Choline and thus Ach synthesis
Q: Would blockade of muscarininc receptors in the bladder be useful in treating urinary retention?
A: No. Atropine is used to reduce urgency in mild cystitis. So it would aggravate the urinary retention
Q: Would Hexamethonium be an effective substitute
A: No, hexamethonium targets Nicotinc receptors and will block Parasym, Sym, as well as Somatic systems
Q: While at a tail gait party, you bite into a sandwich that a yellow jacket is also enjoying. Knowing your allergy to this creature, what should you do?
A: Epinephrine to treat anaphylaxis. Also useful if you have open angle glaucoma, asthma, or hypotension.
Q: Why are albuterol and terbutaline effective in tx of acute asthmatic attacks?
A: These B-2 agonists cause respiratory smooth muscle to relax.
Q: Why does atropine dilate the pupil?
A: Blocking muscarinic receptors in the circular fibers of the eye, results in unopposed action of radial muscles to dilate.
Q: Why does NE result in bradycardia?
A: NE increases bp, which stimulates baroreceptors in the carotid sinus and the aorta. The CNS signals through vagal stimulation to decrease heart rate.
Q: Why is carbachol and pilocarpine useful in treatment of glaucoma?
A: They activate the ciliary muscle of the eye (open angle) and pupillary sphincter (narrow angle).
Q: Why is pyridostigmine effective in the treatment of myasthenia gravis?
A: As an anticholinesterase it increases endogenous ACh and thus increases strength
Q: Why is reserpine effective in treating HTN?
A: Reserpine inhibits dopamine transport into vesicles, attenuating its conversion to NE by dopamine beta-hydroxylase.
Q: Why is there a drop in systolic, mean, and diastolic bp with infusion of isoproterenol?
A: Stimulating beta receptors stimulates heart rate, but beta receptor induced vasodilation reduces peripheral resistance.
Q: Why would a patient with cog-wheel rigidity and a shuffling gait be given benztropine?
A: Parkinson patients benefit from antimuscarinic agents through its inhibitory action within the indirect pathway.
Q: Why would dopamine be useful in treating shock?
A: Receptors = D1=D2>beta>alpha, thus increasing heart rate (beta) and blood pressure (alpha vasoconstriction) while maintaining kidney perfusion (dopamine receptors)
Q: Why would you give a drug like pancuronium or succinylcholine?
A: Useful in muscle paralysis during surgery or mechanical ventilation.
Q: Why would you use pralidoxime after exposure to an organophosphate?
A: Pralidoxime regenerates active cholinesterase.
Q: Will Hemicholinum affect the release of stored Ach during Cholinergic Stimulation
A: No, hemicholinum block the uptake of Choline and thus Ach synthesis
Q: Would blockade of muscarininc receptors in the bladder be useful in treating urinary retention?
A: No. Atropine is used to reduce urgency in mild cystitis. So it would aggravate the urinary retention
Q: Would Hexamethonium be an effective substitute
A: No, hexamethonium targets Nicotinc receptors and will block Parasym, Sym, as well as Somatic systems
Q: You tx your pt with halothane as well and he has also developed malignant hypothermia, what drug can you give
A: Dantrolene
Q: Your patient develops a marked arrythmia due to a prolonged depolarization, can you tx this w/ Neostigmine
A: No cholinesterase inhibitors will potentiate the stimulating action of Succinlycholine
Q: Your patient has acute angle glaucoma, does this affect your tx
A: Yes, Scopolamine would antagonize his glaucoma