Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
64 Cards in this Set
- Front
- Back
- 3rd side (hint)
non-selective adrenergic agonist
|
- epinepherine
- phenylpropanolamine |
|
|
some alpha and beta adrenergic agonist
|
- dopamine - alpha 1, beta 1, dopamine receptor
- dobutamine - alpha 1, beta 1, beta 2 (beta 1 is primary effect) |
|
|
alpha-1 selective adrenergic agonist
|
- phenylephrine
|
|
|
beta selective adrenergic agonist
|
- isoproteronol
|
|
|
beta-2 selective adrenergic agonist
|
- albuterol
- clenbuterol (do not use in food animal - ever) |
|
|
general alpha/beta effector organ responses
|
- heart excitation
- inhibit GI - decrease secretions - relaxation of GI/gallbladder - inhibit mucus glands - urine retention - epi release > NE release |
|
|
general alpha effector organ responses
|
- contract GI sphincters
- contract urinary sphincter - contract splenic capsule - contract piloerector muscles - ejaculation - decrease pancreatic acinar secretions |
|
|
alpha 1 effector organ responses
|
- vasoconstriction
- mydriasis - scant viscous saliva - contraction of uterus |
|
|
alpha 2 effector organ responses
|
- vasodilation of blood vessels to endothelium
- decrease kidney renin release - decrease pancreatic islet cell secretions - decrease NE release - platelet aggregation |
|
|
beta 1 effector organ responses
|
- increase HR/contractility
- relax GI smooth muscle - relax urinary fundus - increase renin release - lipolysis |
|
|
beta 2 effector organ responses
|
- vasodilation to smooth muscle, brain, kidney, heart
- bronchodilation - relax splenic capsule - glycogenolysis - gluconeogenesis - increased NE release |
|
|
adrenergic agonists
|
- epinephrine
- phenylpropanolamine - dopamine - dobutamine - phenylephrine - isoproteronol - albuterol - clenbuterol |
|
|
adrenergic antagonists
|
- carvedilol
- phenoxybenzamine - propanolol - timolol - atenolol |
|
|
some alpha and beta adrenergic antagonists
|
- carvedilol - alpha 1, beta 1 and beta 2 (counteracts dobutamine)
|
|
|
alpha selective adrenergic antagonist
|
- phenoxybenzamine
|
|
|
beta selective adrenergic antagonist
|
- propanolol
- timolol |
|
|
beta 1 selective adrenergic antagonist
|
- atenolol
|
|
|
cholinergic agonist mechanism
|
- direct - bind to receptor and illicit an action
- indirect - interact with acetylcholinesterase to increase concentrations of acetylcholine = less specific so result in inceased side effects |
|
|
cholinergic direct acting drugs
|
- muscarinic only
- bethanecol - pilocarpine |
- muscarinic and nicotinic
- carbachol |
|
cholinergic indirect acting drugs
|
- all muscarinic and nicotinic
- physostigmine - neostigmine - edrophonium - pyridostigmine - organophosphates - irreversible! atropine is antidote |
|
|
muscarinic effector organ responses
|
- gereral inhibition of heart
- vasodilation - excitation of GI tract - bronchoconstriction - miosis - urination (contract detrussor mm., relax sphincter) - contract uterus - erection - increase pancreatic secretions - SLUDD |
|
|
nicotinic effector organ response
|
- ganglionic transmission
- muscle fasiculations - tremors leading to muscle paralysis |
|
|
cholinergic antagonist mechanism
|
- competitively prevent action of acetylcholine at muscarinic receptors
|
|
|
cholinergic antagonist drugs
|
- muscarinic antagonists
-atropine (increase HR, decrease secretions/GI motility, bronchodilation, decrease bladder contractions) - glycopyrrolate (decrease secretions/GI motility without cardiovascular effects) |
|
|
local anesthetics mechanism
|
- interact with sodium channels to decrease permeabiliity of excited cell membranes to sodium ions = blocks sodium channles to stop nerve conduction
|
|
|
local anesthetics metabolism
|
- amides = first step is biotransfermation by the liver
- aminoesters = hydolysis of ester link by plasma esterases |
|
|
local anesthetics toxicity
|
- neurotoxicity = dose related
- muscle twitching - convulsions - CNS depression and death |
- cardiotoxicity
- hypotension - dysrhythmias |
|
local anesthetics drugs
|
- amides
- lidocaine - mepivicaine - only parentally admin local anesthetic FDA approved in horses - bupivacaine |
- aminoesters
- benzocaine - proparacaine - approved for use in animals |
|
neuromuscular blockers mechanism
|
- competitive (non-depolarizing) - bind to or interlock with Ach receptors, preventing transmitter fxn of Ach
- no depolarizing activity - no end plate potential = no muscle contraction because sodium doesn't enter cell |
- depolarizing - binds to receptor and allows influx of sodium causing depolarization of end plate
- does not allow subsynaptic membrane to completely repolarize - remains bound to receptor and renders motor end plate non-responsive - length of action depends on amount of plasma cholinersterases because is metabolized by them = muscle contraction then paralysis |
|
neuromuscular blockers elimination
|
- liver metabolism and renal clearance
- vecuronium - pancuronium - kindey and liver disease will increase duration of these drugs |
- hydrolysis by plasma cholinesterases
- atracurium (spontaneous degradation) - succinylcholine |
|
neuromuscular blocker drugs
|
- competitive (non-depolarizing)
- atracurium - vecuronium - pancuronium |
- depolarizing
- succinylcholine |
|
effect of cholinesterase inhibitor
|
- non-depolarizing
- reverse (becasue competitive) - increases Ach |
- depolarizing
- enhanced (blocks metabolism of drug) |
|
reversal agent
|
- non-depolarizing
- cholinesterase inhibitor (neostigmine) |
- depolarizing
- none |
|
initial agent
|
- non-depolarizing
- absent |
- depolarizing
- present |
|
analgesic
|
- non-depolarizing
- no |
- depolarizing
- no |
|
opioids mechanism
|
- mu and kappa receptor agonists and antagonists
|
|
|
opioids actions at receptors
|
- analgesia = all
- increase appetite = all - decrease GI motility = mu/kappa - sedation = mu/kappa - miosis/mydriasis = mu/kappa - immunomodulaiton = mu/kappa - euphoria = mu - antidiuresis = mu - decrease urine voiding reflex = mu - decrease uterine contractions = mu - respiratory depression = mu - nausea/vomiting/decrease biliary secretions = mu - diuresis (decrease ADH release) = kappa |
|
|
opioids uses
|
- decrease diarrhea
- antitussive (cough suppressor) - analgesia - sedation - calming/euphoria - immobilization/chemical restraint - inhibit GI motility - increase locomotor activity |
|
|
opioids common adverse effects
|
- respiratory depression
- nausea - vomiting - dysphoria - CNS excitation - dependence - decreased urination - hypotension |
|
|
opioid agonists
|
- mu agonsits
- morphine - hydromorphine - codeine - rarely used in vet medicine; less potent - fentaanyl - buprenorphine - partial (kappa antagonist) -tramadol (also muscarinic antagonist; alpha-2 agonist; 5-HT agonist) |
- kappa agonist
- butorphanol - also partial mu agonist - nalbuphine - also partial antagonist of mu |
|
opioid antagonists
|
- naloxone - all receptors (partial mu)
- natrexone - partial at all receptors |
|
|
anticonvulsant uses and mechanisms
|
- uses
- stop/prevent seizures, epilepsy and status epilepticus |
- mechanisms
- increase inhibitory NT (GABA) - decrease excitatory NT (less common) - alter electrolyte conductance |
|
anticonvulsant GABA agonist
|
- increase flow of chloride into cell
- phenobarbital - diazepam - clonazepam - more potent and less toxic than diazepam - clorazepate - pentobarbital - treats status epilepticus; euthanasia |
|
|
anticonvulsant historical drugs
|
- primidone
- phenytoin |
|
|
NMDA receptor antagonist
|
- felbamate - old, rarely used
|
|
|
anticonvulsant MOA unclear
|
- gabapentin - sedation, ataxia
- levetiracetem - zonisamide (blocks Na, Ca channels) - sedation, ataxia, vomiting - potassium bromide (interferes with Cl transport) |
|
|
Phenobarbital
|
MOA - GABA agonist
Use - chronic management and STATUS EPILEPTICUS |
Adverse effects - sedation, polyphagia, PU/PD, behavior changes, elevate liver enzymes*, hepatotoxicity, decrease T4 levels
*metabolizes other drugs faster |
|
Diazepam
|
MOA - GABA agonis
Use - STATUS EPILEPTICUS |
Adverse effects - sedation, tachyphylaxis, dependence, hepatic necrosis in cats
|
|
Levitiracetam
|
MOA - unknown
Use - chronic management |
Adverse effects - none at recommended dosing
not metabolized in liver, so good for patients with liver disease |
|
Potassium Bromide
|
MOA - unknown
Use - chronic management |
Adverse effect - sedation, polyphagia, behavior changes, bromide toxicosis, joint stiffness, ataxia, PU/PD, altered chloride on chem profile
must be compounded and given at loading dose renal elimination so can be used in liver disease patients |
|
behavior modifying drugs
|
Benzodiazepines (BZDs)
Asapriones Tricyclic antidepressants (TCA) SSRIs MAOIs |
|
|
Diazepam
|
- benzodiazepine
- MOA - GABA agonist (binds GABA receptor, increasing GABA binding affinity, increases Cl- into cell) - Use - anxiolytic - decrease anxiety; used in storms |
- NT - increases GABA
- adverse effects - low toxicity; idiosyncratic hepatic necrosis in cats; also tolerance can develop with chronic use |
|
clorazepate
|
- benzodiazepine
- MOA - GABA agonist (binds GABA receptor, increasing GABA binding affinity, increases Cl- into cell) - Use - anxiolytic - decrease anxiety; used in storms |
- NT - increases GABA
- adverse effects - low toxicity; idiosyncratic hepatic necrosis in cats; also tolerance can develop with chronic use |
|
buspirone
|
- azapirones
- MOA - full agonist at PRESYNAPTIC and partial at postsynaptic 5HT-1A agonist - uses - used in cats to reduce urine spraying; used with other drugs to treat complex behavior cases |
- NT - decreases serotonin synthesis (increase at postsynaptic)
- adverse effects - GI signs |
|
amitriptyline
|
- TCA
- MOA - SNRI = blocks serotonin and NE uptake - uses - separation anxiety in dogs, excessive grooming, spraying, anxiety in cats, reduce feather plucking in birds |
- NT - increases serotonin and NE
- adverse effects - also alpha-1 antagonist, antihistaminic, anticholinergic - side effects result from these; decreased secretions, dry mouth, sedation, constipation |
|
clomipramine
|
- TCA
- MOA - SNRI = blocks serotonin and NE uptake - uses - anxiolytic, urine spraying in cats |
- NT - increases serotonin and NE
- adverse effects - also alpha-1 antagonist, antihistaminic, anticholinergic - side effects result from these |
|
fluoxetine
|
- SSRIs
- MOA - inhibits serotonin reuptake - uses - anxiolytic, urine spraying in cats |
- NT - increases serotonin
- adverse effects - sedation, anorexia, irritability, agitation |
|
paroxtine
|
- SSRIs
- MOA - inhibits serotonin reuptake - uses - anxiolytic, canine aggression |
- NT - increases serotonin
- adverse effects - sedation, dry mouth, GI signs, irritability |
|
selegiline
|
- MAOIs
- MOA - beta antagonist - decreases dopamine metabolism - uses - cognitive dysfunction syndrome, pituitary dependant HAC |
- NT - increases dopamine
- adverse effects - hyperactivity |
|
benzodiazepines mechanism
|
- GABA-agonist: bind to/activate benzodiazepine receptor on GABA-a; increases opening of chloride ion channels which leads to hyperpolarization of postsynaptic neuron, decreasing neuronal transmission
- GABA-antagonist: competitively antagonize action of benzodiasepines on BZ receptor site on GABA-a, prevents hyperpolarization of postsynaptic neuron, increasing transmission |
|
|
benzodiazepines uses
|
- GABA-agonist used as muscle relaxants in conjunction with anesthesia; decreases seizures; decreases anxiety; sedation
- diazepam is least potent; lorazepam is most potent - diazepam is used to treat status epilepticus because it acts much quicker than lorazepam (even though it is less potent) - diazepam is a level 4 controlled drug - flumazenil - reversal of other benzodiazepines (agonists) |
|
|
benzodiazepines adverse effects
|
- agonists: transient period of agitation, vocalization, excitation, muscle fasiculations, ataxia; then sedation, ataxia, muscle relaxation, increased appetite, disinhibition of behavior
- diazepam - hepatic toxicosis in cats; has additional side effects due to propylene glycol - hemolysis of RBCs, pain when injected, cardio depression - flumazenil: abstinence syndromes-tremors, hot foot walking, twitches, tonic-clonic seizures, death |
|
|
benzodiazepines contraindictions
|
-agonists: hypersensitivity to benzodiazepines, hepatic dysfunction, narrow angle glaucoma, must taper off drug
- flumaenil: chronic dosing with BZs, suspected OD of TCAs - seizures, arrythmia, death; or if getting BZs for life-threatening condition |
|
|
benzodiazepine drugs
|
*GABA-agonists:
- diazepam - midazolam - undergo glucoronidation but can still use in cats - alternate pathways don't produce toxic metabolites - lorazepam *GABA-antagonists: - flumazenil |
|