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Pharm Exam 2
| Question | Answer |
|---|---|
| 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 |
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