Tufts Pharmacology NBDE Part II

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Terms in this set (142)
GuanethidineHTN, neuronal blockers, only for severe hypertension, prevents release and causes depletion of catecholamines taken up into storage vesicles and is released like false transmitter, does not cross blood-brain barrierCaptopril, lisinoprilHTN, ACE inhibitorsNitroglycerinangina, increases oxygen supply to heart by direct vasodilatory action on smooth muscle in coronary arteriesPropranololangina, reduces oxygen demand by preventing chronotropic responses to endogenous epinephrineVerapamilangina, Ca2+ channel blocker, decrease oxygen demand by reducing afterload by reducing peripheral resistance via vasodilationLidocaine (Type 1B drugs)arrhythmia, decrease cardiac excitability, for ventricular arrhythmiasPhenytoinarrhythmia, to reverse digitalis induced arrhythmiasQuinidine (Type 1A drugs)arrhythmia, increases refractory period of cardiac muscle, for supraventricular tachyarrhythmias and atrial fibrillationVerapamilarrhythmia, for supraventricular tachyarrhythmias and paroxysmal tachycardia and atrial fibrillationDigitalisarrhythmia, decreases rate of AV conduction, for atrial fibrillation and paroxysmal tachycardiaPropranololarrhythmia, for paroxysmal tachycardiaGlycosidesCHF, ex: digitalis and digoxin, have positive inotropic effect, increasing force of contraction of myocardium by inhibiting Na+/K+ ATPase and thus increasing Ca2+ influx, reduces compensatory changes associated with CHF like heart size, rate, edemaCaptoprilCHF, ACE inhibitorDigitalis toxicitynausea and vomiting, yellow-green vision, extrasystole, AV conduction block related to coadministration with chlorothiazideAspirin mechanisms of actionanalgesic effects: inhibits synthesis of prostaglandins antipyretic effects: inhibits synthesis of prostaglandins in hypothalamus, cutaneous vasodilation bleeding time: inhibits thromboxane A2 synthesis and thus platelet aggregation slowsAspirin therapeutic effectspain relief, antipyretic effects, antirheumatic, anti-inflammatory effectsAspirin adverse/toxic effectsoccult bleeding from GI tract, tinnitus, nausea and vomiting, acid-base disturbance, metabolic acidosis, decreased tubular resorption of uric acid, salicylism, delirium, hyperventilationAcetaminophenno anti-inflammatory activity, is hepatotoxic, does not cause GI upset, liver toxicity esp when combined with alcohol or taking 4g/day, is choice for feverish kid, may induce methemoglobinemia at high dosesCorticosteroids (like Prednisone, Hydrocortisone, Triamcinolone)inhibit phospholipase A2, enzymatic step that precedes prostaglandin synthetaseIbuprofenmuch less GI irritation, is anti-inflammatory, will have gastric irritation and bleeding after prolonged useDiflunisal (Dolobid)salicylate analgesic, longer half-life than acetaminophen and ibuprofenPentazocinemixed agonist-antagonists, has both agonistic and antagonistic activitiesNalbuphinemixed agonist-antagonists, has both agonistic and antagonistic activitesNalozoneantagonist to treat overdose of morphineMethadoneused in detox of morphine addicts, is full agonist with analgesic properties, when taken orally is not euphoric in addicts, just acts to produce tolerance and physical dependence, withdrawal is less severe because of long half-lifeMorphine effectsrespiratory depression, euphoria, sedation, dysphoria, analgesia, constipation, urinary retentionMorphine overdosecoma, respiratory depression, miosisMorphine mechanism of actionbinds mu receptors in CNS causes vomiting by stimulating medullary chemoreceptor trigger zone decrease in ventilation due to loss of sensitivity of medullary resp center to CO2OpioidsMeperidine, morphine, codeineCodeineis the best opioid for suppressing cough reflexCompetitive muscarinic receptor blockersatropine, scopolamine, propantheline, are sometimes used to control salivary secretionsAtropinecompetitive muscarinic receptor blocker blocks vagal reflexive control of heart rate => results in tachycardiaPhysostigminereversible anticholinesterase, acts both centrally and peripherally, sometimes for treating xerostomiaNeostigminereversible anticholinesterase, acts peripherally only, has some direct ACh-like activity at NMJ => prolongs activity of endogenous ACh, sometimes for treating xerostomiaDirect acting cholinergic agonistspilocarpine, methacholine, may be used for xerostomiaIrreversible inhibitors of cholinesteraseorganophosphates and insecticidesPralidoximeenzyme regenerator used in organophosphate toxicitySuccinylcholineagonist at nicotinic receptors, depolarizing NMJ blocker subject to rapid inactivation by plasma pseudocholinesterase, used to prevent laryngospasm paralyzing dose causes muscle stimulationd-tubocurarinenon-depolarizing neuromuscular junction blockerGanglionic blockersmecamylamine and hexamethonium, produce orthostatic hypotensionPrazosinalpha blocker, competitive inhibitor of postjunctional adrenergic receptors, associated with epinephrine reversalPropranololbeta blocker, competitive inhibitor of postjunctional adrenergic receptorsReserpinedepletes norepinephrine by inhibiting reuptake, causes depletiong from storage sitesGuanethidineinhibits release of catecholamines (like norepinephrine)Alpha methyldopaacts centrally as false neurotransmitter which gets taken up into storage vesicles and is released with norepinephrine, decreases sympathetic activity, reduces sympathetic outflow via alpha agonist actionClonidinestimulates alpha2 receptors in CNS with resulting decrease in sympathetic outflowEphedrinecauses release of stored norepinephrine and acts at receptor itselfAmphetaminestimulates release of stored norepinephrine and stimulates alpha receptors in CNSCocainenorepinephrine reuptake inhibition and releaseTCA antidepressantnorepinephrine reuptake inhibitionMAO inhibitorsblocks enzymatic destruction of norepinephrineEpinephrine reversalwhen epinephrine is administered in the presence of an alpha blocker (Prazosin or Chlorpromaxine), will cause decrease in BP rather than increase because beta-mediated vasodilation predominatesVagal reflexinjection of pressor dose of norepinephrine may result in decreased heart rate due to activation of baroreceptors that stimulate vagal reflex to reduce heart rateAlpha1 receptor stimulationvasoconstriction, urinary retention, mydriasisAlpha2 receptor stimulationhypotention, reduces sympathetic outflow from CNSBeta1 receptor stimulationincreased heart rate, increased force of contraction, positive inotropic and chronotropic actionsBeta2 receptor stimulationbronchodilation, vasodilation, dilation of skeletal muscleLevodopa with Carbidopalevodopa: is a dopamine precursor that can cross the blood brain barrier carbidopa: is a dopa decarboxylase converter blocker used to treat Parkinson'sPhentolaminenonselective alpha blocker, will cause vasodilationEpinephrinerise in BP due to myocardial stimulation that increases ventricular contraction, increase in heart rate, vasoconstriction because of alpha receptor stimulationNorepinephrineleads to decreased heart rate because of baroreceptor reflexes, stimulates alpha and beta1 receptorsIsopreterenolbeta2 receptor stimulatorPhenylephrinealpha1 receptor agonistMethoxaminevasoconstrictor that stimulates alpha receptorsAlbuterolbeta2 agonist for bronchodilatory effectsPhysiological antagonismtwo drugs produce opposite effects but don't act on the same receptor ex: epinephrine and histamine, epinephrine and nitroglycerinIdiosyncratic reactionsgenetically determined abnormal responses to a drug, are most unpredictable because may not be shown until drug is taken for the first time by a pt ex: succinylcholine and atypical plasma cholinesteraseBenzodiazepinesmodulates the action of inhibitory neurotransmitter GABA, many form active metabolites, is most common drug group given for oral sedation ex: diazepam, chlordiazepoxideBenzodiazepines > barbituratesless addiction potential, less profound CNS depression, larger therapeutic index, less resp depressionBenzodiazepine adverse effectsIV injection of diazepam can cause irritation like thrombophletbitis due to solvent (propylene glycol)Diazepambenzodiazepine, Valium, is given most commonly for oral sedationTriazolambenzodiazepine, Halcion, is ultrashort acting versionMidazolambenzodiazepine, water soluble (doesn't cause thrombophlebitis), shorter acting than valium because it doesn't have active metabolites, has more rapid and predictable onset of action when given IM than valiumFlumazenilreverses effect of benzodiazepinesBarbituratesCNS depressants, will depress all levels of CNS, are not analgesic, will often induce excessive salivation and bronchial secretion and require use of anticholinergic drug to reduce these, are metabolized by the liver, are classified according to duration of actionThiopentalaction is terminated by redistribution of drug out of the chain, will enter and exit the brain rapidly, thus quick onset and short duration of actionPhenobarbitallong acting barbiturateBarbiturate toxicityoverdose kills you because of respiratory depressionBarbiturate contraindicationsintermittent porphyria: will enhance porphyrin synthesis and will aggravate the disease undiagnosed severe pain: may make the pain worse and result in arousal, rage, delirium emphysemaBarbiturate toxicity treatmentneed to maintain open airway, increase input of afferent stimuli, maintain respiration, administer CNS stimulant1st generation antipsychotic drugsPhenothiazine or Haloperidol, specific D2 (dopamine) receptor blockerSide effects of 1st generation antipsychotic drugsanticholinergic effects and anti-alpha adrenergic side effects, extrapyramidal stimulation resulting in tardive dyskinesia, may have jaundice due to allergic reaction2nd generation antipsychotic drugsClozapine, block dopamine receptors and serotonin 5HT receptors, treat negative and positive symptoms, have fewer extrapyramidal side effectsAntipsychoticsmostly dopaminergic receptor blockers, are often used as antiemetic drugsChlorpromazineprototypic phenothiazine, used in treatment of schizophreniaTricycline antidepressantsImipramine or Amitriptyline, are reuptake inhibitors for amine neurotransmitters, were most commonly used in the past, are strong anticholinergicsMAO inhibitorsTranylcypromine or Phenylene2nd generation antidepressant drugsFluoxetine or Trazadone, much more commonly used now, block amine reuptake or alterations of receptor numberSide effects of 2nd generation antidepressant drugsanticholinergic side effectsLithiumdrug of choice for manic phase of manic depression (bipolar disorder)Corticosteroids or glucocorticoidssuppress immune system in addition to anti-inflammatory activity, so latent infection like TB may go systemic and opportunistic infections like Candidiasis may become more of a problemSide effects of corticosteroids or glucocorticoidsgastric ulcers, immunosuppression, acute adrenal insufficiency, osteoporosis, hyperglycemia, redistribution of body fatGeneral anesthesia onset and rate of inductioninversely proportional to solubility of anesthetic in the blood, also influenced by pulmonary ventilation, blood supply to lungs, concentration of anesthetic in inspired mixtureHalothaneassociated with hepatotoxicity, may use atropine before to reduce salivation and bronchial secretionsStages of anesthesiaI: analgesia II: delirium III: surgical anesthesia IV: medullary paralysis (once you start depressing medullary centers, pt will stop breathing and die)Ester anestheticsprocaine, tetracaine, cocaine, metabolized by esterases in the plasma and some in the liverAmide anestheticslidocaine, mepivacaine, bupivacaine, prilocaine, dibucaine, metabolized in the liverAnesthetics mechanism of actionprevent generation of nerve impulses by interfering with sodium transport into neuron, only non-ionized form can penetrate tissue membranes because inflamed tissue has a lower than normal pH, the amount of non-ionized form available to penetrate is decreasedShort acting anestheticsprocaineModerate acting anestheticsprilocaine, mepivacaine, lidocaineLong acting anestheticsbupivacaine, tetracaine, etidocaineLidocaineinteracts with propranolol by slowing down heart via beta receptor blockade and keeping lidocaine in the circulation longer and causing toxicity and by competing for the same enzyme in the liverPrilocainecan cause methemoglobinemia because of toluidine metabolite called orthotoluidineToxic reactions to anestheticmostly related to excessive blood levels arising from inadvertent intravascular injection CNS stimulation because of inhibition of central inhibitory neurons at higher doses, will inhibit inhibitory and excitatory neurons => generalized state of CNS depression => respiratory depression and deathEpinephrine toxicityelevated pulse rate in pt's with Grave's disease, will have heightened sympathetic activity and could result in hypertensive crisisAnesthetics that are vasodilatorsprocaine, lidocaine, tetracaine, mepivacaineAHA limit of epinephrine that pt with CV disease can have0.04mg normal pt is 0.2mgPenicillin Gmore sensitive to acid degradation, so is usually injected rather than taken orally, not really used that much anymoreAmpicillinbest gram negative spectrumCross-allergenic with penicillincephalosporins and ampicillins are erythromycin is notDicloxacillinpenicillin useful against penicillinase-producing bugs (like staphylococcus)Carbenicillinextended spectrum, specific for Pseudomonas infections and indole-positive Proteus speciesClindamycinhigher concentration in bone than in serum, mostly affects gram positive organismsTetracyclinehigher concentration in gingival fluid than in serum, pretty broad spectrum against gram positive and negative cocci and bacilliCephalosporins 1st geneffective against both gram negative and gram positive organismsCephalosporins 3rd genincreased activity against gram negative, greatly decreased activity against gram positiveProphylaxis no-no'sdon't use tetracycline because endocarditis is streptococcal infection and some are resistant to tetracyclinesProphylaxis for prosthetic jointKeflex 2g, take 1hr before txSulfonamidescompete with PABA in folic acid synthesis so there is folic acid deficiencyAllergic reactions to penicillinsdermatitis, stomatitis, bronchoconstriction, cardiovascular collapseClindamycin side effectsGI upset and pseudomonas colitisChloramphenicolantbiotic, associated with aplastic anemiaTetracycline adverse effectsliver damage or hepatotoxicity, esp in pregnant pts with history of renal disease, superinfection, photosensitivity, discoloration of newly forming teeth, GI symptoms, diarrheaErythromycin estolateassociated with allergic cholestatic hepatitisStreptomycin adverse effects8th nerve damage, will affect balance and healingAmphotericin B adverse effectsnephrotoxicity and hypokalemiaTetracycline and penicillincancel each other out because they ahve opposing mechanisms of actionTetracycline interactionswill chelate with calcium, reduced by concurrent ingestion of antacids or dairy productsProbencidalters rate of renal clearance of penicillin, is a uricosuric agent that tends to enhance excretion of uric acid by reducing renal tubular transport mechanismsAntibiotics interaction with coumarindeplete vitK sources so will enhance coumarin anticoagulantsAntibiotics interaction with oral conctraceptivessuppress normal flora involved in active steroids from bile conjugates => more rapid excretion of steroid from bodyMacrolide interactionsinhibit metabolism of drugs like seldane, digoxin erythromycin blocks the metabolism of seldane to antihistamine metabolity => will stay unmetabolized and cause cardiac arrhythmias