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177 Cards in this Set
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Cholinergic transmission
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Ach formed in cell
Ca++ influx Ach released in junction Achase degrades ach in nmj. Choline is recycled Ach attaches to muscarinic (g protein)--> response takes a few mins Or to nicotinic (ion gated) --> rapid release |
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Botox
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Keeps ach from being released from neuron
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Mydriasis
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Pupil dilation
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Miosis
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Pupil constriction
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Adrenergic transmission
(from NE being released) |
NE binds to alpha 2--> inhibit further NE release
Binds to beta 2--> increases NE release Binds to alpha and beta to cause g protein-->slower response NE is taken up (reuptake), metabolized by catacholamine and monoamine oxidase, or diffuses away. |
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Alpha 1
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Eye, vascular smooth m., urinary sphincter
Causes constriction decreases GI motility |
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Alpha 2
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Decrease insulin by acting on pancrease
decrease secretions |
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Beta 1
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Juxtaglomerula cells, heart
Renin release, increase heart rate and etc |
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Beta 2
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Trachea smooth m., liver (gluconeogensis), skeletal m. Blood vessel smooth m. (dilation), uterus (relaxation) bladder wall relaxation
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Direct acting
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Binds to receptor
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Indirect acting
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Acts by releasing nt-->nt to receptor
Drug itself does not bind receptor |
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Selective
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Acts on a few receptors
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Non-selective
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Acts on several receptors
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Epinephrine
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Alpha & beta
Adrenergic agonist nonselective |
Heart excitation, inhibit GI, decrease secretions, relaxation of GI/gallbladder, inhibit mucus glands,, urine retention, epi release>NE release
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Isoproterenol
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Adrenergic agonist beta selective
Beta |
Increase heart rate and bronchodilation
increase HR/contractility, relax GI smooth muscle, relax urinary fundus, increase renin release, lipolysis vasodilation in smooth m,brain ,kidney, heart; bronchodilation, relax splenic capsule, glycogenolysis, gluconeogenesis, increased NE release |
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Phenylpropanolamine
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Non selective Adrenergic agonist
Alpha and beta |
Heart excitation, inhibit GI, decrease secretions, relaxation of GI/gallbladder, inhibit mucus glands,, urine retention, epi release>NE release
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Dopamine
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Adrenergic agonist
Alpha 1, beta 1, dopamine receptor (dopamine is a precursor to NE) |
vasoconstriction, mydriasis, scant viscous saliva, contraction of uterus
increase HR/contractility, relax GI smooth m., relax urinary fundus, increase renin release, lipolysis decreases renal vascular resistance |
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Dobutamine
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Adrenergic agonist
Alpha 1, beta 1 & 2 but beta 1 is primary |
Used to titrate IV to inc. Heart rate
vasoconstriction, mydriasis, scant viscous saliva, contraction of uterus increase HR/contractility, relax GI smooth m., relax urinary fundus, increase renin release, lipolysis |
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Phenylephrine
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Adrenergic agonist
Alpha 1 selective |
vasoconstriction, mydriasis, scant viscous saliva, contraction of uterus
often used in nasal sprays to vasoconstrict BVs to dec. snot and dec red eye |
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Isoproteronol
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Adrenergic agonist
Beta selective |
increase HR/contractility, relax GI smooth m., relax urinary fundus, increase renin release, lipolysis
vasodilation to sm. mm., brain, kidney, heart; bronchodilation, relax splenic capsule, glycogenolysis, gluconeogenesis, increased NE release |
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Albuterol
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Andrenergic agonist
Beta 2 selective |
vasodilation to sm. mm., brain, kidney, heart; bronchodilation, relax splenic capsule, glycogenolysis, gluconeogenesis, increased NE release
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Clenbuterol
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Andreneric agonist
Beta 2 selective DO NOT use in food animal |
vasodilation to sm. mm., brain, kidney, heart; bronchodilation, relax splenic capsule, glycogenolysis, gluconeogenesis, increased NE release
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Carvedilol
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Adrenergic antagonist
Alpha 1, beta 1 & 2, antioxidant Counteracts dobutamine |
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Phenoxybenzamine
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Adrenergic antagonist
Alpha selective |
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Propanolol
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Adrenergic antagonist
Beta selective |
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Timolol
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Adrenergic antagonist
Beta selective |
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Atenolol
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Adrenergic antagonist
Beta 1 selective |
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-olol
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beta-blockers (propranolol type)
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-terol
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bronchodilators (phenethylamine derivatives)
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-stigmine
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cholinesterase inhibitors (physostigmine type)
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-caine
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local anesthetics
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-curium
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neuromuscular blocking agents
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-curonium
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neuromuscular blocking agents
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cholinergic agonists
direct mechanism |
bind to receptor and illicit an action
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Bethanecol, Pilocarpine, Carbachol
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Cholinergic agonist
indirect mechanism |
interact with acetylcholinesterase/ pseudocholinesterase to increase concentration of Acetylcholine-->less specific so more side effects
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physostigmine, neostigmine, edrophonium, pyridostigmine, organophosphates
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Cholinergic over stimulation results in:
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SLUDD
salivation lacrimation urination, defecation death (relaxation of diaphragm) |
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muscarinic effector organ responses
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Heart: general inhibition, vasodilation
GI: excitation (secretions, motility inc.) bronchoconstriction, miosis urination (contract detrussor, relax sphinter) contract uterus/erection, increase pancreatic secretions |
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nicotinic effector organ responses
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ganglionic transmission
muscle twitching, tremors leading to muscle paralysis |
we do not learn a drug that only effects nicotinic
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bethanecol
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direct acting
cholinergic agonist muscarinic only |
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pilocarpine
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direct acting
cholinergic agonist muscarinic only |
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carbachol
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direct acting
cholinergic agonist muscarinic and nicotinic |
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physostigmine
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Cholinergic Agonist
indirect- all muscarinic and nicotinic |
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neostigmine
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Cholinergic Agonist
indirect- all muscarinic and nicotinic |
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edrophonium
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Cholinergic Agonist
indirect- all muscarinic and nicotinic |
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pyridostigmine
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Cholinergic Agonist
indirect- all muscarinic and nicotinic reversibly binds ACHase and eventually diffuses away |
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organophosphates
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Cholinergic Agonist
indirect- all muscarinic and nicotinic Irreversibly binds AChase! Atropine in antidote |
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Cholinergic antagonist mechanism
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competitively prevents action of ACH at muscarinic receptors
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Atropine
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Cholinergic antagonists
muscarinic |
increase HR
decrease GI secretions/motility bronchodilation decrease bladder contrations often pre-anesthetic |
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Glycopyrrolate
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Cholinergic antagonists
muscarinic |
decrease GI secretions/motility w/o cardiovascular effects
often pre-anesthetic |
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adrenergic agonist mechanism
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acts directly on receptor to induce action of endogenous NT at receptor
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adrenergic antagonist mechanism
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inhibits actions of agonists at adreneric receptors, selective or non-selective= how many receptors they bind
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N-butylscopolammonium bromide
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cholinergic antagonist
also, antispasmotic, antimuscarinic/anticholinergic |
produces parasymp effect by blocking cholinergic receptors
most commonly used in LA to inhibit GI, used for spasmodic colic and to dec. rectal tone during palpation |
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mechanism of local anesthetics
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dec. permeability of Na channels in excitable cell membranes to stop nerve conduction
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metabolism of local anesthetics
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amides: biotransfered from liver
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aminoesters: hydrolysis of ester link by plasma esterase (safer for liver dx)
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toxicity of local anesthetics
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neurotoxicity: mm. twitching, convulsions, CNS depression-->dose related
Cardiotoxicity: hypotension + dysrythmias |
lidocaine can be given as an antiarythemic if given IV
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Lidocaine
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local anesthetic
amide->liver metabolism |
sometimes given w/epinephrine to cause vasoconstriciton to allow drug to stick around longer
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local anesthetic approved by FDA for use in animals
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Mepivacaine (local anesthetic approved in horses)
proparacaine approved for use in animals (as opthalmic?) |
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Mepivicaine
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local anesthetic
amide->liver metabolism |
only parentally (not PO) administered local anesthetic FDA approved in horses
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Bupivacaine
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local anesthetic
amide->liver metabolism |
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Benzocaine
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local anesthetic
aminoester--> safer in pts w/ liver dx |
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Poparacaine
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local anesthetic
aminoester--> safer in pts w/ liver dx |
approved for use in animals
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mechanism of neumuscular blockers
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compettive (non-depolarizing): binds to ACh receptors preventing Ach from binding-->no depolarizing activity, Na+ does not enter the cell
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Depolarizing: binds to receptor and allows influx of Na+ causing depolarization of end plate region but stays bound -->does not allow membrane to completely repolarize-->moter end plate is non-responsive.
mm. contration-->paralysis metabolized by plasma cholinesterase |
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What do neuromuscular blocking agents do?
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paralyze the animal. however, the animal can still feel pain
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elimination of neuromuscular blockers
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liver metabolism (clearance) and then renal elimination->renal and hepatic disease witll inc. duration of drugs
Vercuronium, Pancuronium |
hydrolysis by plasma cholinesterases
Atracurium (+spontaneous degradation), succinylcholine |
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Atracurium
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Neuromuscular blocker
competitive (non-depolarizing) hydrolysis by plasma cholinesterases |
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Vecuronium
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Neuromuscular blocker
competitive (non-depolarizing) liver metabolism and renal elimination |
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Pancuronium
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Neuromuscular blocker
competitive (non-depolarizing) liver metabolism and renal elimination |
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Succinylcholine
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Neuromuscular blocker
Depolarizing hydrolysis by plasma cholinesterases |
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effect of cholinesterase inhibitor on NON-depolarizing neuromuscular blockers
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reverse (becuz competitive and inc Ach)
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effect of cholinesterase inhibitor on depolarizing neuromuscular blockers
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enhanced (blocks metabolism of drug by inhibiting plasma cholinesterase)
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what is the reversal agent of depolarizing neuromuscualr blockers
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there is none
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Are initial fasciculations present or absent in non-depolarizing or depolarizing neuromuscular blockers
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non-depolarizing: absent
depolarizing: present |
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name the opiod receptors
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Mu, Kappa, delta, sigma
however we don't have drugs that affect delta/sigma so we don't talk about them |
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what are opiods used for
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dec. diarhea, antitussive (cough supressent), analgesia, sedation, calming/euphoria, immobilization/chemical restraint(really just highly sedate), inhibit GI motility, increase locomotor activity
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opiods are regulated by
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DEA (drug enforcement administration)
5 schedules: 1 is the most addictive (high abuse potential) |
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common adverse effects of opiods
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respiratory depression, nausea, vomiting, dysphoria (anxiety), CNS excitation, dependence if given long term, decreased urination, constipation, hypotension
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opiod receptors causing analgesia
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all
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opiod receptors that increase appetitie
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all
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opiod receptors that decrease GI motility
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Mu, Kappa
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opiod receptors that cause Sedation
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Mu, Kappa
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opiod receptors that cause miosis/mydriasis
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Mu, Kappa
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opiod receptors that cause immunomodulation
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Mu, delta
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opiod receptors that cause euphoria
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Mu
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opiod receptors that cause antidiuresis
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Mu
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opiod receptors that decrease urine voiding reflex
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Mu
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opiod receptors that decrease uterine contrations
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Mu
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opiod receptors that cause respiratory depression
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Mu
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opiod receptors that cause nausea/vomiting/decrease biliary secreation
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Mu
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opiod receptors that cause diuresis (decrease ADH release)
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Kappa
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Morphine
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Opiod
Mu agonist |
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Hydromorphone
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Opiod
Mu agonist |
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Codeine
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Opiod
Mu agonist |
rarely used in vet med
less potent |
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Fentanyl
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Opiod
Mu agonist |
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Buprenorphine
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Opiod
partial Mu agonist Kappa ANTagonist?? |
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Tramadol
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Opiod
Mu agonist muscarinic ANTagonist alpha-2 agonist 5-HT agonist (seratonin/ dopamine receptor) |
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Butorphanol
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Opiod
Kappa agonist partial Mu agonist |
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Nalbuphine
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Opiod
Kappa agonist partial Mu ANTagoinst |
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Naloxone
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Opiod
ANTagonist at all receptors partial Mu |
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Naltrexone
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Opiod
partial ANTagonist at all receptors |
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mechanism of anticonvulsant drugs
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1 of 3:
*alter electolyte conductance *decrease excitatory neurotransmitters (less common) *increase inhibitory nerutransmitters (GABA) |
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status epilepticus
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appears to be a continuous seizure becaus no post-ictal phase
always a medical emergency |
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Anticonvulsants used for:
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stop/prevent seizures, epilepsy (having multiple seizures over time), and status epilepticus
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Phenobarbital
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anticonvulsants
GABA Agonists (inc. flow of Cl into cell) #1 drug used, barbituate |
use: chronic management, status epilepticus
adverse effects: sedation, polyphagia, PU/PD, behvior changes, elevated hepatic enzymes/hepatotoxicity, dec. T4 levels Other: induces liver enzymes so metabolizes other drugs faster including its own metabolism |
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Diazepam
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anticonvulsants
GABA Agonists (inc. flow of Cl into cell) used to treat status epilepticus |
also used as anxiolytic (dec. anxiety)
binds GABA receptor, inc. GABA binding affinity, inc. Cl- into the cell, increases GABA toxicity: low, sedation, tachyphylaxis, dependence, idiosyncratic hepatic necrosis in cats; tolerance can develop with chronic use |
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Clonazepam
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anticonvulsants
GABA Agonists (inc. flow of Cl into cell) more potent than Diazepam and less toxic benzodiazepine, tolerance quickly |
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Clorazepate
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anticonvulsants
GABA Agonists (inc. flow of Cl into cell) benzodiazepine, tolerance quickly |
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Pentobarbital
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anticonvulsants
GABA Agonists (inc. flow of Cl into cell) treats status epilepticus; euthanasia |
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Primidone
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anticonvulsant
historical drug: rarely used now, never used in cats metabolized into phenobarbital not controlled unlike phenobarbital |
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Phenytoin
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anticonvulsant
historical drug: rarely used now, never used in cats blocks Na channel, never worked that well |
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Felbamate
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NMDA receptor antagonist
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Gabapentin
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anticonvulscent
MOA unclear: might block Ca-dependent channels-->sedation, ataxia |
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Levetiracetam
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anticonvulscent
MOA unclear: believed to work by binding to SUZA receptor to inhibit presyn. Ca++ channels use: chronic management |
adverse effects: none at reccomended doses
not metabolized in liver-->good for pts with liver disease |
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Potassium Bromide
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anticonvulscent
MOA unclear: interfers with Cl- transport used for chronic management of seizures NOT commercially available |
takes months to reach thereaputic levels, long half life, must give loading dose
only eliminated via renal adverse effects: sedation, polyphagia, behavior changes, bromide toxicosis, joint stiffness, ataxia, PU/PD, altered Cl- on chem panel |
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Zonisamide
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anticonvulscent
MOA unclear: blocks Na channels by blocking Ca channels-->sedation, ataxia, vomiting |
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Clorazepate
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Behavior modifying drug
Bensodiazepine (BZD) GABA agonist- binds GABA receptor and inc. GABA binding affinity, increases Cl- into cell Anxiolytic |
increases GABA
Toxicity- low; tolerance can develop with chronic use |
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Buspirone
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Behavior modifying Drug
Azapirone Full agonist at presynaptic and partial at postsynaptic 5HT-1A agonist |
used in cats to reduce urine spraying, may be used with other drugs for complex behavior cases
decreases serotonin syntheis at postsynaptic toxicity-GI signs |
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Amitriptylin
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Behavior modifying drug
Tricyclic antidepressants (SNRIs) Serotonin&NE reuptake inhibitor in CNS used for seperation anxiety in dogs, excessive grooming, spraying, anxiety in cats, reduce feather plucking in birds |
increases serotonin and NE
also an alpha-1 antagonist, antihistaminic, anticholinergic-->side effects result from these effects:decresed secretions, dry mouth, sedation, constipation |
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Clomipramine
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Behavior modifying drug
Tricyclic antidepressants (SNRIs) Serotonin&NE reuptake inhibitor Potential anticholonergic effect used for anxiolytic, urine spraying in cats, |
increases serotonin and NE
also acts on alpha-1 antagonist, antihistaminic, anticholinergic--side effects result from these effects toxicity: can cause testicular hyperplasia, do not use w/drug that lower seizure threshold |
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Fluoxetine
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Behavior modifying drugs
SSRIs: selective seratonin reuptake inhibitor anxiolytic, urine spraying in cats |
increases erotonin
toxicity: sedation, anorexia, irritability, agitation |
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Paroxetine
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Behavior modifying drugs
SSRIs: selective seratonin reuptake inhibitor anxiolytic, canine aggression |
increases serotonin
dry mouth, sedation, GI upset, irritability |
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Selegiline
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Behavior modifying drugs
MAOIs: monoamine oxidase inhibitors cognitive dysfunction syndrome, pituitary dependent HAC |
increases dopamine
toxicity: hyperactivity |
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Benzodiazepines
Mechanism |
Mech: GABA Agonist: bind to/activate benzodiazepine receptor on GABA-a; increses opening of Cl- ion channels which leads to hyperpolarization of post synaptic neuron, decreasing neuronal trnsmission
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GABA Antagonists: competitively antagonizes action of benzodazepines on BZ receptor site on GABa, prevents hyperpolariztion of postsynaptic neuron, increasing transmission
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Benzodiazepines
Uses |
GABA Agonist: MM. relaxant in conjunction with anesthesia (does not give analgesia); decrease seizures; decrease anxiety; sedation/sleep aid
Diazepam least potent, Lorazepam is most Diazepam works much quicker and is a level 4 controlled drug |
Flumazenil: reversal of other benzodiazepines (agonists)
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Benzodiazepines
adverse effects |
Agonists: transient agitation/vocalization/excitation/excitation-->sedation, MM> relaxation, inc. appetite, disinhibition of behavior
Diazepam- hepatic toxicosis (cats), also, propylene glycol will also cause hemolysis of RBCs, pain when injected, cardio depression |
Flumazenil: abstinence syndromes-->tremors, hot foot walking, twitches, tonic-clonic seizures, death
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"-am"
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benzodiazepines
Midazolam Diazepam Lorazepam etc |
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Benzodiazepines
contraindictions |
agonists:
hypersensitivity to benzodiazepines, hepatic dysfunction, narrow angle glaucoma, must taper off drug |
Flumazenil: chronic dosing with benzodiazepines, suspected OD of TCAs-->seizures, arrhythmia, death
or if getting BZs for life-threatening condition |
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Diazepam cont.
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GABA Agonists
Benzodiazepines |
MM. relaxant in conjunction with anesthesia; decrease seizures; decrease anxiety; sedation
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Midazolam
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GABA Agonists
Benzodiazepines undergoes glucoronidation but can still use in cats, alternate pathways don't produce toxic metabolites |
MM. relaxant in conjunction with anesthesia; decrease seizures; decrease anxiety; sedation
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Lorazepam
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GABA Agonists
Benzodiazepines |
MM. relaxant in conjunction with anesthesia; decrease seizures; decrease anxiety; sedation
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Flumazenil
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GABA Antagonist
Compettive on GABAa receptor |
abstinence syndromes-->tremors, hot foot walking, twitches, tonic-clonic seizures, death
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Diuretics
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Mechanism depends on drug type
uses: dec. edema, bp, intraocular pressure, intracranial pressure-->bsically get rid of excess H2O |
types: carbonic anhydrase inhibitors, osmotic diuretics, loop diuretics, thiazide diuretics, inhibitors of renal epith. Na channels, aldosterone antagonists
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Acetozolamide
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Carbonic anhydrase inhibitors (PT)
this causes H (broken off from bicarb) to dec--> less H pumped into lumen-->HCO3 builds up-->inc. Na in lumen and forms NaHCO3-->water follow into lumen |
uses: dec. production of aqueous humor to cntl glaucoma
inc. excretion of Na + K toxicitiy: urine pH inc., metabolic acidosis, K wasting |
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Mannitol
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Osmotic Diuretics (entire loop/neph)
increse osmotic pressure-->pull water into tubular lumen inc. excretion of Na and K |
prevent/treat renal failure, decrease intracranial/intraocular pressure, mobilize edema with other diuretics
toxicity: hyponatremia |
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Furosemide
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Loop diuretic (thick ascending lumen)
Most potent diuretic blocks NaK2Cl symporter--> dec Na in cell--> dec H2O reabsorbed inc excretion of Na, K, Cl, Ca, Mg |
toxicity: K wasting (arrhythmia, changes mem. pot)
use: general diuretic |
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Chlorothiazemide
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Thiazide diuretic: Inhibits apical Na Cl symporter (distal convoluted tubule)
general diuretic |
inc. excretion of Na Cl
toxicity: hyperglycemia, hypercalcemia, K wasting |
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Hydrochlorothiazide
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Thiazide diuretic: Inhibits apical Na Cl symporter (distal convoluted tubule)
general diuretic |
inc. excretion of Na Cl
toxicity: hyperglycemia, hypercalcemia, K wasting |
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Triamterene
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inhibitors of renal epithelium Na channels (late distal tubule and CD)
used in combo w/other diuretics to dec. K excretion |
inc. excretion of Na, dec. excretion of K
toxicity: hyperkalemia, inc. risk of renal stones |
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Amiloride
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inhibitors of renal epithelium Na channels (late distal tubule and CD)
used in combo w/other diuretics to dec. K excretion |
inc. excretion of Na, dec. excretion of K
toxicity: hyperkalemia, inc. risk of renal stones |
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Spironolactone
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aldosterone antagonists (late distal tubule and CD)
blocks effect of aldosterone use: general diuretic *aspirin blocks effects |
inc. excretion of Na, dec. excretion of K
don't use w/ dehydration, hyperkalemic patients |
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K+ sparing diuretics
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Amiloride
Spironolactone |
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Ammonium chloride
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Urinary tract drug: urinary acidifier-->oxidized to urea in liver
prevent/dissolve stones; enhance efficacy of antimicrobials when treat w/ uti |
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Atropine (urinary tract)
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muscarinic antagonist
decrease detrussor mm. contraction; Urinary retention |
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Bethanechol (urinary tract)
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direct muscarinic agonist
increase detrussor mm. contration |
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Dantrolene
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skeletal muscle relaxant
dec. external urethral sphincter tone |
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Diazepam (urinary tract)
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skeletal muscle relaxant
dec. Ca release from SR in sk. mm. dec. external urethral sphincter tone |
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phenoxybenzamine (urinary tract)
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alpha adrenergic antagonist
dec. Ca release from SR in sk. mm. dec. internal urethral sphincter tone |
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Phenylpropanolamine
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adrenergic agonist
inc. internal urethral sphincter tone |
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Potassium citrate
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Urinary alklinizer-->oxidized to bicarbonate in liver
dec. calcium oxlate stone formation not usually given long term |
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estriol
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natural estrogen, used for incontinence in spayed female
inc. the resting mm. tone of the urethra in females |
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receptors related to urinary tract
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detrussor mm.: beta 2 relaxes, musc. contracts
int. urethral sphincter: alpha 2 inc. tone ext. urethral sphincter: nicotinic only |
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inotrophy
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change in contractile strength related to Ca entering cell to bind to troponin
unrelated to mm. length |
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preload
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force that stretches relaxed mm.
L. vent= pressure from blood filling and stretching the wall during diastole (EDV) |
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afterload
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force against whcih contracting mm. must act
L. vent= pressur ein aorta which must be overcome to eject blood |
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Heart rate is most affected by:
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parasymp. nn.
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chronotroph
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+ increases HR
- dec. HR |
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lusiotrope
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inc. relaxation of cardiac mm.
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Digoxin
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Positive Inotrope
MOA: inhibits Na,K, ATPase--> Na cell inc -->inc NaCa exhanger act which pumps more Ca in cell-->inc. contractions |
effects: inc. strength of contractions of cardiac mm., inc. CO, dec HR/BV/BP, cntl arrhythmia, dec. heart size, inc. baroreceptor reflex sensitivity so dec heart failure
toxicity: GI upset, arrhythimas, voimiting, monitor drug conc |
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Pimobendan
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Inodilators: + inotrope, vasodilator
MOA: inhibits Phosphodiesterase III (in vasculaure, heart), inc. cAMP(phosphodiesterase inhibits it), makes troponin C more sensitive to Ca, inc. contractility BETTER than digoxin |
effects: vasodilation at venous and art. blood supply, dec afterload/preload, + lusiotrope
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prodrug
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a drug that is metabolize into an active form after being given
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RAAS
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body's way to inc. bp
stimulated by dec Na in JG cells |
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Enalapril
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Ace Inhibitors
MOA: inhibits bradykinin breakdown (vasodilators) so inc. amount of bradykinin in cell and prevent conversion of Ang I --> ang II-->no ang II leads to vasodilation |
effects: dec. bp/preload/afterload, dec aldosterone release, inc Na excretion, dec K excretion (slight dieresis effect), helps prevent cardiac remodeling
used for hypertension, and CHF toxicity; renal failure, coughing (inc. bradykinin), angioedema (humans), hypokalemia, azotemia drug interaction with NSAIDs, diuretics |
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Benazepril
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Ace Inhibitors
MOA: inhibits bradykinin breakdown (vasodilators) so inc. amount of bradykinin in cell and prevent conversion of Ang I --> ang II-->no ang II leads to vasodilation |
effects: dec. bp/preload/afterload, dec aldosterone release, inc Na excretion, dec K excretion (slight dieresis effect)
used for hypertension, and CHF toxicity; renal failure, coughing, angioedema drug interaction with NSAIDs, diuretics |
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heart failure
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heart failure= inability to provide adequate CO at normal filling pressures
in CHF L. vent under performs --> hemodynamic stress dec CO kicks in symp nn.-->vasoconstrict to inc. bp/preload/afterload |
use vasodilators to combat this catch 22
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diltiazem
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vasodilator
MOA: Ca channel blockers, dec. intracellular Ca, dec contractility effects:vasodilation, dec afterload, - inotopic effect, dec AV impulse conduction adverse: hypotension-->reflex tachycardia |
more heart effects than amlodipine
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amlodipine
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vasodilator
MOA: Ca channel blockers, dec. intracellular Ca, dec contractility effects:vasodilation, dec afterload, - inotopic effect, dec AV impulse conduction adverse: hypotension-->reflex tachycardia |
more vasculature effects than diltiazem
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Hydralazine HCl
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vasodilator
MOA: direct arteriolar dilator effects: dec TPR--> dec afterload, inc SV/CO, dec ESV, dec wall tension/heart size adverse: hypotension-->reflex tachycardia |
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Carvedilol
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vasodilators
MOA: alpha 1, beta 1&2 antagonist effects: vasodilation, dec HR, TPR, myocardial workload adverse: bronchoconstriction contra: asthmatics |
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antiarrhythmics are used to fix what
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disruption in impulse conduction,
abnormality in rate/regularity/site of origin of cardiac impulse |
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types of Antiarrhythmics
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Class I: local anesthetics
Class II: Beta blockers Class III: K+ channel blockers Class IV: Ca++ channel blockers |
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Quinidine
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Class I Antiarrhythmics
slow phase 0 depolarization-->prolongs action potential, slows conduction-->prolongs refractory period |
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Procainamide
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Class I Antiarrhythmics
slow phase 0 depolarization-->prolongs action potential, slows conduction-->prolongs refractory period |
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Lidocaine
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Class I Antiarrhythmics
shortens Phase 3 repolarization -->dec. duration of action potential -->accelerates repolarization |
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Amiodarone
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Class III Antiarrhythmics
K+ channel blockers-->diminish outward K+ current during repolarization effects:prolongs phase III repolarization w/o altering phase 0, prolongs refractory period, prolongs action potential |
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Sotalol
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Class III Antiarrhythmics
K+ channel blockers-->diminish outward K+ current during repolarization effects:prolongs phase III repolariztion w/o altering phse 0, prolongs refractory period, prolongs action potential |
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class II antiarrhythmics
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Beta Blockers: Carvedlol, Propanolol
reduces symp input effects: shortens Phase III repolarization, dec. duration of action potential-->accelerates repolarization |
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Diltiazem
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Class IV antiarrhythmic
Ca++ channel blockers (L type?) effects: Slows phase IV spontaneous depolarization and slows conduction in tissues dependent on Ca++ currents--slow influx of Ca++ s/a AV node-->prolongs refractory period |
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Verapamil
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Class IV antiarrhythmic
Ca++ channel blockers (L type?) effects: Slows phase IV spontaneous depolarization and slows conduction in tissues dependent on Ca++ currents--slow influx of Ca++ s/a AV node-->prolongs refractory period |
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