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Pharm Exam 2

QuestionAnswer
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, likpolysis
beta 2 effector organ responses vasodilation to smooth muscle, brain, kidney, heart; bronchodilation, relax splenic capsule, glycogenolysis, gluconeogenesis, increased NE release
mechanism of action: direct cholinergic agonist bind to receptor & illicit an action
mechanism of action: indirect cholinergic agonist interact w/acetylcholinesterase to increase concentration of ACh -> less specific = result in increased side effects
muscarinic effector organ responses general inhibition of heart, vasodilation, excitation of GIT (increased motility, secretions); bronchoconstriction, miosis, urination (contract detrussor m, relax sphincter), contract uterus, erection, increase pancreatic secretions, SLUDD
SLUDD salivation, lacrimation, urination, defecation, death; muscarinic effector organ responses
nicotinic effector organ responses ganglionic transmission, muscle twitching, tremors leading to muscle paralysis
MoA: cholinergic antagonists competitively prevent action of ACh at muscarinic receptors
Atropine: effects on body increase HR, decrease secretions/GI motility, bronchodilation, decrease bladder contractions
Glycopyrrolate: effects on body decrease secretions/GI motility without cardiovascular effects
MoA: local anesthetics interact with sodium channels to decrease permeability of excited cell membranes to Na+ ions = blocks Na+ channels to stop nerve conduction
metabolism of amides first step is biotransformation by the liver; important if patient has liver disease
metabolism of aminoesters hydrolysis of ester link by plasma esterases (such as cholinesterase); can use without potential side effects in liver disease patients
toxicity of local anesthetics neuro (m twitching, tonic/clonic convulsions, CNS depression/death; dose-related); cardio (hypotension, dysrhythmia)
what local anesthetics are FDA-approved for use in animals? mepivicaine (only parentally admin local anesthetic FDA approved in horses); proparacaine
MoA: competitive (non-depolarizing) neuromuscular blockers bind to/interlock wtih ACh receptors, preventing transmitter function of ACh; no depolarizing activity; no end plate potential -> no muscle contraction because Na+ doesn't enter cell
MoA: depolarizing neuromuscular blockers binds to receptor & allows influx of Na+ causing depolarization of end plate region but does not allow subsynaptic membrane to completely repolarize bcz remains bound to receptor & renders motor end plate non-responsive
depolarizing neuromuscular blockers: how are they metabolized? plasma cholinesterases
elimination of vecuronium neuromuscular blocker; liver metabolism & clearance & then renal elimination (vecuronium, pancuronium); liver/kidney disease increases duration of these drugs
elimination of pancuronium neuromuscular blocker; liver metabolism & clearance & then renal elimination (vecuronium, pancuronium); liver/kidney disease increases duration of these drugs
elimination of atracurium neuromuscular blocker; hydrolysis by plasma cholinesterase + spontaneous degradation
elimination of succinylcholine neuromuscular blocker; hydrolysis by plasma cholinesterase
neuromuscular blockers: analgesic potential none
effect of cholinesterase inhibitor on non-depolarizing vs depolarizing neuromuscular blockers N-Dep: reverse; Dep: enhanced (blocks metabolism of drug)
reversal agents for nondep vs dep neuromuscular blockers non-dep: cholinesterase inhibitor (ie neostigmine); dep: none
initial fasciculations in nondep vs dep neuromuscular blockers non-dep: absent; dep: present
MoA: opiods Mu, kappa receptor agonists/antagonists
receptor for analgesia? mu, kappa, delta
receptor for increased appetite? mu, kappa, delta
receptor for decreased GI motility? mu, kappa
receptor for sedation? mu, kappa
receptor for miosis/mydriasis? mu, kappa
receptor for immunomodulation? mu, delta
receptor for euphoria? mu
receptor for antidiuresis? mu
receptor for decreased urine voiding reflex? mu
receptor for decreased uterine contractions? mu
receptor for respiratory depression? mu
receptor for nausea/vomiting/decreased biliary secretions? mu
receptor for diuresis (decreased ADH release)? kappa
opioid uses decrease diarrhea, antitussive, analgesia, sedation, calming/euphoria, immobilization/chemical restraint, inhibit GI motility, increase locomotor activity
most addictive schedule of opioid? schedule 1
who regulates opioids? DEA
common adverse effects of opioids? respiratory depression, nausea, vomiting, dysphoria, CNS excitation, dependence, decreased urination, hypotension
which opioid(s) is(are) a partial mu agonist? buprenorphine (possibly also a K antagonist); butorphanol (also a full kappa agonist)
which opioid(s) is/are partial mu antagonist? nalbuphine (also full kappa agonist); naloxone; naltrexone
naloxone & natrexone: full or partial antagonists? which receptors? naloxone: all receptors, partial mu; natrexone: partial at all receptors
anticonvulsants: use? stop/prevent seizures, epilepsy, and status epilepticus
define seizure abnormal electrical activity in teh brain that causes altered behavior
define epilepsy disease preocess of having multiple seizures over time - not all animals that have seizures have epilepsy
define status epilepticus series of seizures with no post-ictal phase
MoA: anticonvulsants increase inhibitory neurotransmitters (ie GABA), decrease excitatory neurotransmitters (less common), alter electrolyte conductance
anticonvulsants: goals of treatment treat underlying disease, decrease seizure frequency, minimal side effects, maintain serum drug levels
compare clonazepam to diazepam clonazepam is more potent & less toxic
pentobarbital is used for what? treat status epilepticus, euthanasia
how do GABA agonists work? increase flow of chloride into cell
list 5 GABA agonists phenobarbital, diazepam, clonazepam, clorazepate, pentobarbital
what drug is an NMDA receptor antagonist? felbamate (old, rarely used)
phenobarbital: use anticonvulsant; chronic management; status epilepticus
phenobarital: adverse effects sedation, polyphagia, PU/PD, behavior changes, elevated hepatic enzymes, hepatotoxicity, decrease T4 levels
Phenobarbital: what is notable? induces liver enzymes - metabolizes other drugs faster; induces its own metabolism so over tiem have to increase dose to maintain serum concentration
diazepam: use status epilepticus
diazepam: adverse effects sedation, tachyphylaxis, dependence, hepatic necrosis in cats
levitiracetam: use anticonvulsant; chronic management
levitiracetam: adverse effects none at recommended dosing
levitiracetam: what is notable? not metabolized in liver, so good for patients with liver disease
potassium bromide: use anticonvulsant; chronic management
potassium bromide: adverse effects sedation, polyphagia, behavior changes, bromide toxicosis, joint stiffness, ataxia, PU/PD, altered chloride on chem profile
potassium bromide: what is notable? must be compounded; must give loading dose to increase plasma concentrations until therapeutic range is reached (time to reach steady state remains the same); elimination is renal only so can be used in liver disease patients
MoA: BZDs GABA agonist - binds GABA receptor, icnreases GABA binding affinity, increases Cl- into cell
Diazepam, clorazepate - uses anxiolytic - decrease anxiety; storm anxiety decrease
Diazepam, clorazepate - adverse effects low toxicity; idiosyncratic hepatic necrosis in cats; tolerance can develop with chronic use
MoA: azapirones full agonist at presynaptic & partial at postsynaptic 5HT-1A agonist
uses: azapirones used in cats to reduce urine spraying; used with other drugs to treat complex behavior cases
azapirones: effect on neurotransmitters decreases serotonin synthesis (increase at postsynaptic)
azapirones: adverse effects GI signs
MoA: TCAs SNRI - blocks serotonin & NE uptake
amytriptyline: uses separation anxiety in dogs, excessive grooming, spraying, anxiety in cats; reduce feather plucking in birds
TCAs: effects on neurotransmitters increases serotonin & NE
TCAs: adverse effects also alpha-1 antagonist, antihistaminic, anticholinergic - side effects result from these effects: decreased secretions, dry mouth, sedation, constipation
clomipramine: uses anxiolytic, urine spraying in cats
MoA: SSRIs inhibit serotonin reputake
fluoxetine: uses anxiolytic, urine spraying in cats
paroxetine: uses anxiolytic, canine aggression
SSRIs: effect on neurotransmitters increases serotonin
fluoxetine: adverse effects sedation, anorexia, irritability, agitation
paroxetine: adverse effects dry mouth, sedation, GI upset, irritability
MoA: MAOIs MAO-B antagonist: decreases dopamine metabolism
MAOI: uses cognitive dysfunction syndrome, pituitary dependent HAC
MAOI: effect on neurotransmitters increases dopamine
MAOI: adverse effects hyperactivity
what must be done in conjunction with any behavior modifying drug? behavior modification program
MoA: GABA agonists bind to/activate benzodiazepine receptor on GABA-a; increases opening of chloride ion channels which leads to hyperpolarization of postsynaptic neuron, decreasing neuronal transmission
MoA: GABA antagonists competitively antagoniszes action of benzodiazepines on BZ receptor site on GABA, prevents hyperpolarization of postsynaptic neuron, increasing transmission
GABA agonists: uses muscle relaxants in conjunction with anesthesia; decrease seizures; decrease anxiety; sedation
under what level of control is diazepam? level 4
potency of benzodiazepines diazepam least potent; lorazepam most potent
why use diazepam over lorazepam for status epilepticus treatment? diazepam acts much quicker
GABA agonists: adverse effects transient period of agitation, vocalization, excitation, m fasciculations, ataxia; then sedation, ataxia, m relaxation, increased appetite, disinhibition of behavior
diazepam: adverse effects hepatic toxicosis in cats; has additional side effects due to propylene glycol - hemolysis of RBCs, pain when injected, cardio depression
flumazenil: adverse effects abstinence syndromes - tremors, hot foot walking, twitches, tonic-clonic seizures, death
GABA agonists - contraindications hypersensitivity to BZDs, hepatic dysfunction, narrow angle glaucoma, must taper off drug
flumazenil: contraindications chronic dosing with BZs, suspected overdose of TCAs - seizures, arrhythmia, death; or if getting BZs for life-threatening condition
diuretics: uses decrease edema, BP, intraocular pressure, intracranial pressure
carbonic anhydrase inhibitors: location of actino proximal tubule
MoA: carbonic anhydrase inhibitors inhibit CA, decrease protons pumped into lumen, HCO3- builds up, Na+ in lumen increases -> forms NaHCO3, water follows into lumen
Carbonic anhydrase inhibitors: uses decrease production of aqueous humor - manage glaucoma
carbonic anhydrase inhibitors: effect on electrolytes increase excretion of Na, K
carbonic anhydrase inhibitors: toxicity urine pH increases; metabolic acidosis; K+ wasting
osmotic diuretics: locatino of action entire loop/nephron
MoA: osmotic diuretics increase osmotic pressure -water is retined in tubular lumen
osmotic diuretics: uses prevent/treat renal failure, decrease intracranial/intraocular pressure, mobilize edema with other diuretics
osmotic diuretics: effect on electrolytes increase excretion of Na, K
osmotic diuretics: toxicity hyponatremia
loop diuretics: location of action thick ascending limb
loop diuretics: potency most potent of diuretics
MoA: loop diuretics blocks Na-K-2CL symporter
loop diuretics: uses mobilize edema (NSAIDS decrease effects)
loop diuretics: effects on electrolytes increase excretion of Na, K, Cl, Ca, Mg
loop diuretics: toxicity K+ wasting
thiazide diuretics: place of action distal convoluted tubule
MoA: thiazide diuretics inhibits apical Na-Cl symporter
thiazide diuretics: uses general diuretic
thiazide diuretics: effects on electrolytes increase excretion of Na, Cl
thiazide diuretics: toxicity hyperglycemia, hypercalcemia, K+ wasting
inhibitors of renal epithelium sodium channels: location of action late distal tubule & collecting duct
MoA: inhibitors of renal epithelium sodium channels inhibits Na+ channels
inhibitors of renal epithelium sodium channels: uses used in combo with other diuretics to decrease K+ excretion
inhibitors of renal epithelium sodium channels: effect on electrolytes increase excretion of Na; decrease excretino of K
inhibitors of renal epithelium sodium channels: toxicity hyperkalemia, increase risk of renal stones
aldosterone antagonists: place of action late distal tubule & collecting duct
MoA: aldosterone antagonists blocks effect of aldosterone
aldosterone antagonists: uses general diuretic; aspirin blocks effects
aldosterone antagonists: effect on electrolytes increase excretion of Na; decrease excretion of K
aldosterone antagonists: toxicity don't use with dehydration, hyperkalemic patients
MoA: ammonium chloride urinary acidifier - oxidized to urea in liver
MoA: atropine muscarinic antagonist
MoA: bethanechol direct muscarinic agonist
MoA: dantrolene muscle relaxant
MoA: diazepam muscle relaxant
MoA: phenoxybenzamine alpha adrenergic antagonist
MoA: phenylpropanolamine adrenergic agonist
MoA: potassium citrate urinary alkalinizer: oxidized to bicarbonate in liver
ammonium chloride: result prevent/dissolve stones; enhance efficacy of antimicrobials when treating UTI
atropine: result in urinary tract decrease detrussor mm contraction; urinary retention
bethanechol: result in urinary tract increase detrussor mm contraction
dantrolene: result in urinary tract decrease external urethral sphincter tone
diazepam: result in urinary tract decrease external urethral sphincter tone
phenoxybenzamine: result in urinary tract decrease internal urethral sphincter tone
phenylpropanolamine: result in urinary tract increase internal urethral sphincter tone
potassium citrate: result in urinary tract decreases calcium oxalate stone formation
how do you contract/relax the detrussor m? beta 2 relaxes; muscarinic contracts
how do you increase/decrease tone in internal urethral sphincter? alpha-2 innervations only; stimulate = increase tone, antagonize = decrease tone
how do you increase/decrease tone in external urethral sphincter? nicotinic only
define inotropy change in contractile strength independent of muscle length -> change in contractility; sympathetic system affects inotrpy (contraction occurs when Ca2+ enters cell & binds to troponin)
define preload force that stretches relaxed muscle; in L ventricle, the blood filling & stretching the wall during diastole (EDV)
define afterload force against which contracting muscle must act; in L ventricle, afterload is pressure in teh aorta which must be overcome to eject blood
define chronotroph + = increases HR; - = decreases HR
vasconstrictor increases or decreases BP increases
vasodilator increases or decreases BP decreases
define lusiotrope increases relaxation of cardiac muscle
MoA: digoxin inhibits Na-K-ATPase (Na in cell increase, increase Na-Ca exchanger activity, increase Ca in cell, increase contractions -> Ca in cell goes to sarcoplasmic reticulum & binds to troponin C for muscle contraction)
Digoxin: effects increased strength of contraction of cardiac muscle; increased CO, decreased HR/BV/BP, control arrhythmias, decrease heart size, increase baroreceptor reflex sinsitivity so decrease heart failure
digoxin: toxicity GI upset, arrhythmias, vomiting; measure concentration in blood to check for toxicity
inodilators do what? + inotrope, vasodilation
MoA: inodilators inhibit Phosphodiesterase III (located in vasculature & heart), increase cAMP (bcz PDEIII normally inhibits cAMP); makes troponin C more sensitive to Ca, increase contractility better than digoxin
inodilators: effects vasodilation at venous & arterial blood supply, decrease afterload/preload, + lusiotrope
define prodrug drug that is metabolized to active form after being given
goal of RAAS increase BP; renin release stimulated by decreaseing Na in JG cells
MoA: ACE inhibitors inhibit bradykinin breakdown (vasodilator) so increase amount of bradykinin in cell & prevent conversion of Ang I to Ang II
ACE inhibitors: effect lack of Ang II = major vasodilation effect bcz AngII = vasoconstrictor; decreased BP, decreased preload/afterload, decreased aldosterone release, increased Na+ excretion, decreased K+ excretion (slight diuresis)
ACE inhibitors: uses hypertension, use with other drugs for congestive heart failure
ACE inhibitors: adverse effects renal failure, coughing, angioedema
ACE inhibitors: drug interactions NSAIDs, Diuretics
define heart failure heart fails to provide adequate forward output at normal filling pressures
define congestive heart failure left ventricular performance is impaired leading ot chronic hemodynamic stress
result of decreased cardiac output? sympathetic NS activation (increasing HR, TPR), resulting in increased preload/afterload
Moa: diltiazem/amlodipine Ca2+ channel blockers, decrease intracellular Ca2+, decrease contractility
diltiazem/amlodipine: effects vasodilation, decreased afterload, - inotropic effect, decrease AV impulse conduction
diltiazem/amlodipine: adverse effects hypotension -> tachycardia
MoA: hydralazine HCl direct arteriolar dilator
hydralazine HCl: effects decrease TPR -> decrease afterload, increase SV/CO, decrease ESV, derease wall tension/heart size
hydralazine HCl: adverse effects hypotension -> reflex tachycardia
MoA: carvedilol beta 1&2 and alpha 1 antagonist
carvedilol: effects vasodilation, decreased HR, TPR, myocardial workload
carvedilol: adverse effects bronchoconstriction
carvedilol: contraindications asthmatics
class 1 antiarrhythmics local anesthetics
MoA: Class 1 antiarrhythmics block fast Na+ channels -> slows conduction velocity, delays point at which channels have recovered
class 2 antiarrhythmics beta blockers
MoA: class 2 antiarrhythmics reduce sympathetic input
class 2 antiarrhythmics: effects decreases phase IV slope, decrease HR, decrease inotropy -> increases time between action potentials
class 1 antiarrhythmics: effects slow phase 0 depolarization, prolonging AP, slows conduction -> prolongs refractory pd; OR shortens phase III repolarization, decrease duration of AP -> accelerates repolarization
MoA: class 3 antiarrhythmics K+ channel blockers -> diminish outward K+ current during repolarizatino
class 3 antiarrhythmics: effects prolongs phase III repolarization w/o altering phase 0; prolongs refractory period, prolongs AP
MoA: class 4 antiarrhythmics Ca2+ channel blockers
class 4 antiarrhythmics: effects slows phase IV spontaneous depolarization & slows conduction in tissues dependant on Ca2+ currents - slow influx of Ca2+ s/a AV node -> prolongs refractory period
Created by: shelbell8389