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31 Cards in this Set
- Front
- Back
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Mechanism of action for the adrenergic receptors
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a1: increase Ca++
a2: decrease cAMP b1, b2, b3: increase cAMP |
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Nicotinic receptors
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Na+ channels
(ACh binds --> Na+ channel opens --> Na+ influx) - Nm (on skeletal muscle): contraction |
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Cholinergic actions on the cardiovascular system
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- decrease heart rate
- decrease atrial contractility - decrease AV conduction (AV block) |
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Cholinergic actions on the respiratory system
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- bronchoconstriction
- increased bronchial secretion |
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Cholinergic actions on the GI system
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- increase motility
- increase secretion - relax sphincters |
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Cholinergic actions on the urinary bladder
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- contract detrusor muscle
- relax internal sphincter |
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Cholinergic actions on the eye
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- contract sphincter muscle and iris (to constrict the pupil: miosis)
- contract ciliary muscle for accommodation |
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M1 receptor
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- excitatory
- close K+ channels / activate PLC to increase Ca++ |
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M2 receptor
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- inhibitory
- open K+ channels / inhibit adenylyl cyclase - bradycardia (receptors in myocardium) |
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M3 receptor
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- excitatory
- activate PLC to increase Ca++ - increased secretion of exocrine glands - relaxation of sphincters - bronchoconstriction |
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How to treat overdose toxicity of succinylcholine
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Just provide artificial ventilation
(Do not use cholinergic agonists!) |
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How to treat toxicity of curare
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Use AChE inhibitor (to have enough ACh around to outcompete the curare) along with atropine (to counteract the bradycardia caused by the excess ACh)
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Treatment of glaucoma
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Cholinomimetics
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Treatment of urinary bladder atony
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Cholinomimetics
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Treatment of strychnine poisoning
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Curare (symptomatic treatment- for muscle spasms)
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Treatment for nasal congestion
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Phenylephrine (a1 agonist)
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Which pharmacological property of dopamine is uniquely useful in the management of long-standing hypovolemic shock?
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Activation of dopamine receptors in renal vascular beds --> renal vasodilation
(prevents renal ischemia/damage because epi causes constriction of those vessels) |
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Treatment for anaphylactic shock?
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Epinephrine
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How does using a solution saturated with carbon dioxide affect the onset of action of local anesthetics?
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Accelerates onset of action!
(CO2 diffuses into cell, causes intracellular acidosis) |
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Where/how is procaine metabolized?
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- in blood
- by serum pseudocholinesterase (so short half-life) |
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Where/how is lidocaine metabolized?
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- In the liver
- by hepatic amidase |
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Regarding local anesthetics, which occurs first, CNS toxicity or cardiovascular toxicity?
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CNS
(higher blood concentration needed to cause CV toxicity) |
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Species-specific effects of prilocaine or benzocaine
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- cats, rabbits
- metabolite (o-toluidine) --> methemoglobin |
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Can a local anesthetic be used to control premature ventricular contractions?
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Lidocaine
- blocks fast Na channels, which decreases heart rate |
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How does extracellular pH affect the action of local anesthetics?
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the lower the pH, the less action there is (more anesthetic stays ionized outside the cell, doesn't cross in)
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How does intracellular pH affect the action of local anesthetics?
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the lower the pH, the more action there is (more ionized anesthetic to bind to receptor)
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How does the firing rate of neurons affect the action of local anesthetics?
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neurons that fire faster are more affected (so pain fibers > neuromuscular)
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How does extracellular potassium affect the action of local anesthetics?
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decreasing extracellular K causes membrane hyperpolarization, which decreases the ability to produce nerve block
(high extracellular K --> depolarization --> more effect of local anesthetic) |
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How does extracellular calcium affect the action of local anesthetics?
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increasing extracellular Ca causes membrane hyperpolarization (favors low-affinity resting state of the channels, so it is harder for anesthetic molecule to get to receptor), which decreases the ability to produce nerve block
(high extracellular Ca --> less effect of local anesthetic) |
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Treatment for status epilepticus
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- benzodiazepine (e.g. diazepam)
- followed by phenobarbital |
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Primary mechanism of action of local anesthetics
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Block voltage-gated Na+ channels
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