| Term 
 
        | netrotransmitters - chemical signaling between cells |  | Definition 
 
        | each neuron is a distinct anatomical unit - no structural continuity exists between most neuronscommunication between nerve cells & between nerve cells & effector organs - occurs through the release of specific chemical signals (neurotransmitters) from the nerve terminalsrelease of neurotransmitters depends on processes that are triggered by Ca uptake & regulated by phosphorylation of synapitc proteinsneurotransmitters rapidly diffuse across the synaptic cleft or synapse btwn nerve endings & combine w/ specific receptors on the postsynaptic (target) cell 
 |  | 
        |  | 
        
        | Term 
 
        | types of neurotransmitters |  | Definition 
 
        | over 50 chemical signal molecules have been identified in the nervous systemsix signal compounds are most commonly involved in the actions of therapeutic drugsNE and EAChdopamineserotonin (5-HT)glutamategamma-amminobutyric acid (GABA)
each of these binds to a specific family of receptorscholinergic (ACh-transmitter) & adrenergic (NE & E-transmitters) are the primary signals in the autonomic nervous system 
 |  | 
        |  | 
        
        | Term 
 
        | neurotransmitters in the CNS:   basic functioning of neurons in the CNS is similar to that of the autonomic NS   similarities:  |  | Definition 
 
        | in both systems, transmission of info involve the release of neurotransmitters that diffuse across the synaptic space to bind to specific receptors on the postsynaptic neuronin both systems, recognition of the neurotransmitter by the membrane receptor of the postsynaptic neuron triggers intracellular changes
 |  | 
        |  | 
        
        | Term 
 
        | neurotransmitters in the CNS   differences from those in the autonomic NS  |  | Definition 
 
        | circuitry of the CNS-much more complex than the autonomic nervous systemnumber of synapses in the CNS - much greaterCNS communicates through the use of >10 (and perhaps as many as 50) different neurotransmitters; in contrast, the autonomic NS uses only 2 primary neutrotransmitters, ACh & NE 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | chronic brain disorder characterized by recurrent seizures, ranging from brief unconsciousness to violent, life threatening convulsionsseizure: an abnormal discharge of electrical impulses within the brain, resulting in changes in awareness, sensory alterations & involuntary muscle movements; in most pts, intelligence is not affected3 or more seizures = epilepsyepilepsy affects about 2.3 million Americans (1% population), with circa 181,000 new cases/year
 |  | 
        |  | 
        
        | Term 
 
        | etiology:   primary epilepsy  |  | Definition 
 
        | no specific anatomic cause is evident & the pt has no other neurologic abnormalitycalled idiopathic or primary epilepsy ("essential")may be prodcued by an inherited abnormality in the CNSabout 70% of all seizurespts are treated w/ antiepileptic drugs, often for life
 |  | 
        |  | 
        
        | Term 
 
        | etiology:   secondary epilepsy  |  | Definition 
 
        | can be a sympton of an underlying condition or illness & may resolve spontaneously when the problem is treatedetiology of isolated seizures:electrolyte imbalances (esp low sodium)renal & liver failurehypertensive encephalopathy (major issue)hypoglycemiaacute head traumaingestion of toxins (e.g. mercury, lead, CO) - esp heavy metalsCNS infection (meningitis)fever (kids usually grow out of this)
antiepileptic drugs are given untilthe primary cause can be corrected
 |  | 
        |  | 
        
        | Term 
 
        | CLASSIFICATION OF EPILEPSY   Partial (one hemisphere of brain)  |  | Definition 
 
        | Simpleno loss of consciousnessdiverse symptomslimited motor involvementsensory or psychic symptomsresponsive during attackusually less than 1 min
Complex: psychomotor-temporal lobe seizuresusually preceeded  by auraloss of impaired consciousnesssymptoms may be similar to "simple"coordinated involuntary movements (drooling, wandering, laughing)usually 1-2min in duration
 |  | 
        |  | 
        
        | Term 
 
        | CLASSIFICATION OF EPILEPSY   Generalized (both hemispheres of brain)   *partial may spread to this  |  | Definition 
 
        | Absence seizures: non-convulsive; "petit mal"abrupt loss of consciousnessno loss of postural controlfixed stare, blinking, mild jerking, mouth movements or grimacingusually 15-30sec durationabrupt end of seizurefully alert (consciousness almost immed. returns)
 Tonic-Clonic seizures: convulsive; "grand mal"arms & legs flex rigidlyaudible cry heardarms & legs extend rigidlywhole body jerking and spasmsloss of consciousnesstonic-clonic phase usually 1 mindisorientation & slow recovery (post-ictal phase= 15-30min)no recall of event 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | continuous seizure state, lasting for 30min or more without the pt regaining consciousness & usually accompanied by respiratory distress - medical emergencycan occur during all types of seizuresemergency tx usually consists of diazepam, pheytoin, or phenobarbitalif seizures are secondary to hypoglycemia - IV dextrose 50%
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | about 40-80% of pts w/ epilepsy respond to drug therapy, have good quality of life and a normal life spanmost other cases can be cured by neurosurgery that involves destroying or ablating the epileptic focus within the brain or sectioning the corpus callosum between the hemispheres to decrease the transmission of abnormal impulsesnoncompliance with the drug regime-major reason of seizure control failure
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations with epilepsy |  | Definition 
 
        | teach pt to avoid factors that can precipitate a seizure, including stress, excessive heat, ETOH, sleep deprivation & certain drugspregnancy lowers seizure threshold
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | antiepileptic (anticonvulsant) drugs   three basic targets for antiepileptic drugs: neuronal membrane stabilization (Na or Ca channels)potentiate GABA (inhibitory neurotransmitter)decrease actions of glutamate and/or aspartate 
 |  | 
        |  | 
        
        | Term 
 
        | antiepileptic drugs:   Barbiturates  |  | Definition 
 
        | phenobarbital (Luminal)   only limitation to using these in seizure management is their sedative effect which increases as dosage increasescontrols seizures by inhibiting the spread of focal firing of abnormal neurons in the CNS, which suppresses the seizureits mechanism of action is not fully understood; may involve potentiation of the inhibitory effects of GABA-mediated neurons; it also  decreases Na/K conduction at high levelsdoses required for antiepileptic action are lower than those that cause pronounced CNS depression 
 |  | 
        |  | 
        
        | Term 
 
        | pharmacotherapeutics of barbiturates |  | Definition 
 
        | all types of seizures, except absence seizures (may actually worsen these seizures)more effective in simple partial seizures than in complex partial seizuresregarded as the first choice in treating recurrent seizures in children, including febrile seizureseffective in status epilepticus 
 |  | 
        |  | 
        
        | Term 
 
        | pharmacokinetics of barbiturates |  | Definition 
 
        | well absorbed POfreely penetrates the brainabout 75% is metabolized by liver & 25% is excreted unchanged by kidneylong half-life (60-120hrs)potent inducer of the P-450 system & when given chronically, it enhances the metabolism of other agents
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of barbiturates |  | Definition 
 
        | hypersensitivitysevere respiratory disorders h/o ETOH & drug abusesevere liver & kidney impairmentcaution in elderly: increased sedation; measures to ensure safety especially important
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of barbiturates |  | Definition 
 
        | sedation, ataxia, nystagmus, vertigo, hangover effect & drowsiness - most commonGI problems, Stevens-Johnson syndrome - less commonparadoxical rxn (CNS excitation) - restlessness, anxiety, irritability,tachycardia, insomniaacute toxic effect can be potentially lethal; requires serum blood level monitoring; TI: 15-40barbiturates have an addictive nature w/ long term use
 |  | 
        |  | 
        
        | Term 
 
        | drug-food interactions with barbiturates |  | Definition 
 
        | ETOH & CNS depressants: severe CNS depressionanticoagulants: their effects decreasedestrogen-containing oral contraceptives: reduced reliabilitymany other drug interactions b/c potent inducer of P-450 system
 |  | 
        |  | 
        
        | Term 
 
        | antiepileptic drugs:   Hydantoins  |  | Definition 
 
        | phenytoin (Dilantin)   most commonly prescribed antiepileptic agentknown as broad-spectrum; effective in basically all forms of epilepsy except absence seizuresoften drug of choice in adults & older kidsat therapeutic doses, does not cause general CNS depressionbelieved to stabilize membranes (hyperpolarization) & prevent spread of seizures from a hyper-reactive focus 
 |  | 
        |  | 
        
        | Term 
 
        | pharmacotherapeutics of hydantoins |  | Definition 
 
        | effective in treating tonic-clonic seizures & partial seizures but not absence seizuresalso used in tx of status epilepticus after administration of diazepamused in prevention & tx of seizures in pts undergoing neurosurgery (prophylactic)
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | oral absorption is slowhalf-life varies from 12-36hrs, with an average of 24hrspt-pt variation in absorption/metabolismsteady-state blood levels may be reached in 5-7 days at low serum levels & 4-6 weeks at higher blood levelstherapeutic plasma level range: 10-2090% of the drug is protein bound, therefore in hypoalbuminemic states, there will be an increase in free drug & serum levels; protein bidning competition with valproic acid, salicylates, sulfa drugsmetabolize in the liver & excreted in the bile & urine as inactive metabolitebioavailabilities of phenytoin preparations differ significantly (caps vs. tabs) & from one manufacturer to another - preparations should not be switched
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of hydantoins |  | Definition 
 
        | contraindicated in hypersensitivity reactions, bradycardia & severe kidney & liver diseasecaution in elderlycaution in pregnancy pts: congenital defects (if status epilepticus, no other choice)multiple drug/food interactions, check when administering
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of hydantoins |  | Definition 
 
        | common: ataxia, nystagmus & alterations in extraoccular movements, diplopia, slurred speech, stuttering, trembling of hands - occur when serum levels are above 20GI: constipation, n/v/dcosmetic (may affect compliance):gingival hyperplasia, hirsutism, nystagmus, rash, coarsening of facial features
serious: arrhythmias, seizures, leukopenia, thrombocytopenia, abnormalities in vit D metabolism, teratogenic (produces fetal hydantoin syndrome, which is characterized by prenatal growth/mental deficiences; also incrase incidence of congenital malformations such as cleft palate) 
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations for hydantoin |  | Definition 
 
        | elderly tend to metabolize hydantoins slowly, increasing potential for toxic serum levelstolerated well when given IM (if IV, must be hung within 15 min and infused at quick rate)avoid ETOH and other CNS depressantsavoid abrupt discontinuation
 |  | 
        |  | 
        
        | Term 
 
        | antiepileptic agents:   carbamazepine (Tegretol)  |  | Definition 
 
        | has become a mainstay in tx of many forms of epilepsy (safer than the others)therapeutic levels range from 4-12reduces the propagation of abnormal impulses in the brain by blocking Na channels, thereby inhibiting generation of repetitive action potentials in the epileptic focushighly effective for all partial seizures (simple & complex) - often drug of first choicehighly effective for tonic-clonic seizuresused to treat trigeminal neuralgia & chronic pain syndromesused in main-depressive pts to ameliorate symptoms 
 |  | 
        |  | 
        
        | Term 
 
        | pharmacokinetics of carbamazepine: |  | Definition 
 
        | absorbed slowly following PO adminenters brain rapidly b/c of high lipid solubilityinitial half-life: 40hrs; continued use = 15hrsinduces its own metabolism, which is known as time-dependent kinetics; shortly after therapy begins, metabolism of this drug may increase significantly & half-life decreases w/ chronic use, causing fluctuation in serum levels over timeenhanced hepatic P-450 system activity also incrases the metabolism of other antiepileptic drugs
 |  | 
        |  | 
        
        | Term 
 
        | contraindications and drug interactions of carbamazepine |  | Definition 
 
        | h/o bone marrow suppressionhypersensitiity to the tricyclic antidepressentstaking monoamine oxidase (MAO) inhibitorshepatic metabolism of carbamazepine is inhibited by several drugs; toxic symptoms may arise if the dose is not adjustedOC: increased metabolism of estrogen - a decreased effectiveness of OC (all inducers of P-450 do this)anticoagulants: decreased effectiveness (all inducers do this)
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of carbamazepine |  | Definition 
 
        | sedation (common, but usually disappear over time)drowsiness, vertigo, ataxia, blurred visionirritating to the stomach: nausea, emesisaplastic anemia, agranulocytosis, thrombocytopenia - possibilitypotential for inducing serious liver toxicityCBC initially, then weekly x 4mo, then q3moliver enzymes initially @ 2wks, then q3-6mo
in most pts, adverse effects usually disappear within 2-3wks after initiation of therapy
 |  | 
        |  | 
        
        | Term 
 
        | antiepileptic drugs:   valproic acid (Depakene, Depakote)  |  | Definition 
 
        | broadest spectrum form of antiepileptics (all but febrile)second drug of choice for absence seizures (drug of choice for myoclonic)therapeutic levels range from 50-100inhibits enzyme breakdown of GABA to a simpler form, thereby selectively increasing the coc of GABA in the synapses, which reduces seizures activity
 |  | 
        |  | 
        
        | Term 
 
        | pharmacotherapeutics of valproic acid: |  | Definition 
 
        | similar to carbamazepine + absence seizuresmost effective agent available for tx of myoclonic seizuresused for igraine prophylaxisused in tx of refractory bipolar disorders
 |  | 
        |  | 
        
        | Term 
 
        | pharmacokinetics of valproic acid |  | Definition 
 
        | effective PO & rapidly absorbed; bioavailability after PO dosing is > 80%peak levels occur within 2 hrs; food may delay absorption90% is boind to plasma proteinsonly 3% is excreted unchanged; the rest is converted to active metabolites by the livermetabolized by the P-450 system but does not induce the enzymes of the system
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of valproic acid |  | Definition 
 
        | pts w/ hepatic disease b/c of its hepatotoxic effectspts w/ bleeding disorders secondary to decreased clottingcaution in pregnancycaution in clients taking warfarin b/c of potential displacement 
 |  | 
        |  | 
        
        | Term 
 
        | drug/food interactions with valprioc acid |  | Definition 
 
        | carbamazepine, phenobarbital: inhibited metabolism and increased levels of these drugs (use w/ phenobarb. may cause excessive sedation leading to coma)chlorpromazine, cimetidine, salicylates: incrased valproic acid levelsphenytoin: displacement of phenytoin from plasma protein
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of valproic acid |  | Definition 
 
        | low incidence of adverse effectsCNS: tremors (at high doses), sedation, HA, diplopia, dizzinessalopeciafatal heptotoxicity (primary adverse rxn), nausea, GI distress, weight gainthrombocytopenia, alterations in platelet aggregationadmin w/ food may delay absorptionblood levels don't correlate well w/ effectscaution in pts using ASA/NSAIDs (inhibition of platelets aggregation)
 |  | 
        |  | 
        
        | Term 
 
        | antiepileptic drugs:   benzodiazepines  |  | Definition 
 
        | diazepam (Valium) lorazepam (Ativan)   classified as sedative-hypnotic agentsboth antiepileptic & anxiolytic properties that reduce seizures & anxietyproduce all levels of CNS depression ranging from mild sedation to coma, depending on the dose ("minor tranquilizers")used for acute attacks, not maintenance 
 |  | 
        |  | 
        
        | Term 
 
        | pharmacotherapeutics of benzodiazepines |  | Definition 
 
        | suppress seizure activity by producing GABA - inhibitory neurotransmittermanagement of status epilepticus, severe recurrent seizures & ETOH withdrawl seizuresparenteral diazepam & lorazepam - drugs of chice in treating status epilepticus
 |  | 
        |  | 
        
        | Term 
 
        | atypical drugs   ethosuximide (Zarontin)  |  | Definition 
 
        | drug of choice for absence seizures (many pediatric pts)inactive against grand mal & partialmechanism of action unknownwell toleratedgenerally devoid of serious side effects or drug interactions (does not induce P-450 enzyme synth)most common side effect: GI upset (irritating to the stomach): some drowsiness & dizziness possiblerarely can cause bone marrow suppression, renal & hepatic damageTherapeutic levels: 40-100
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | a disturbance in mood or affectcommon, debilitating, life threatening illness that can be successfully treatedcan be MILD, MODERATE, SEVERE; duration of untreated episodes ranges from 6-24mo; episodes continue in up to 80% of untreated pts10-14mil people in the US are depressed in any one year; affects 2-4% of the population; seen in 5-10% of pts in the primary care setting; during their lifetime, 1 in 8 people may require tx for depression 
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | USPSTF recommendations (May 2002)   affirmative response to two questions may be as efective as using longer screening measures or may indicate the need for the use of more in-depth diagnositic tools   "over the past two weeks, have you ever felt down, depressed, or hopeless?"   "over the past 2 weeks, have you felt little interest or pleasure in doing things?"  |  | 
        |  | 
        
        | Term 
 
        | types of depressive disorders:   Major Depressive Disorder (MDD) (Major Depression)  |  | Definition 
 
        | lasts at least 2 weeks, marked by depressed mood, anhedonia (no pleasure in anything); symptoms include loss of appetite, weight loss, psychomotor agitation, insomnia, fatigue, feelings of worthlessness or guilt, diminished ability to think or concentrate recurrent thoughts of death or suicidehigh co-morbidity w/ anxiety disorders (58%), substance abuse disorder (38.6%)
 |  | 
        |  | 
        
        | Term 
 
        | types of depressive disorders:   Dysthymic Disorder  |  | Definition 
 
        | onset of depressive symptoms less discreet and acute, the experience more chronic in naturegreatly underdiagnosed; characterized by chronic mild-to-moderate depression lasting about 2 hrs or longer (1yr in kids)
other depressive disorders: substance-induced depressive disorder, season affective disorder, bipolar disorder, postpartum depression, atypical depression 
 |  | 
        |  | 
        
        | Term 
 
        | pathophysiology of depression |  | Definition 
 
        | genetic factorspersonality and environmental factorsbiochemical abnormalities
 |  | 
        |  | 
        
        | Term 
 
        | monoamine hypothesis (biological basis of depression)     pharmacological targets  |  | Definition 
 
        | stimulation (agonism) of the 5-HT (serotonin) 1A (depression) receptor is currently believed to be the mechanism mediating the antidepressant efficacy of antidepressantsincreased synaptic serotonin levels (major)increased synaptic NE levelsblock of specific serotonin receptors 
 |  | 
        |  | 
        
        | Term 
 
        | treatment for depression   nonpharmacologic treatment  |  | Definition 
 
        | cognitive behavioral therapy & interpersonal psychotherapy (best/first approach)electroconvulsive therapy (ECT) (for those that don't respont to therapy/meds)transcranial magnetic stimulationvagus nerve stimulation (VNS)deep brain stimulation (DBS)complimentary therapieshypericum perforatum - St. John's wortuseful in depression of mild intensityshould not be used by pts taking SSRIs - both agents increase serotonin levels and could cause overdose
 |  | 
        |  | 
        
        | Term 
 
        | pharmacologic treatment of depression     tricyclic antidepressants (TCAs)  |  | Definition 
 
        | amitriptyline   block the reuptake of monoamine neurotransmitters, exerting influence predominately on NE & serotonin: block cholinergic, dopaminergice, histaminergic, and alpha1 and alpha2 adrenergic receptorstherapeutic response may take 3-4wks or longer to occureffective & long clinical experience: main problem side effects:sedation, orthostatic hypotension, constipation, dry mouth, urinary hesitancy, tremor, tachycardia, cardiac a rrhythmias, blurred vision, LETHAL OVERDOSESmost side effects subside after few weeks; persistence of anticholinergic side effects can e minimized by adding cholinergic smooth-muscle stimulantsobtain EKG before therapy initiation & after four weeks of TCA tx
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of TCAs |  | Definition 
 
        | pts during the acute recovery phase following an MI or for those w/ severe CADpts w/ hyperthyroidism & those who are undergoign thyroid hormone therapy (b/c of possible cardiotoxic effects)current use of MAO inhibitorspts w/ benign prostatic hypertrophy, seizure disorders & narrow-angle glaucoma
 |  | 
        |  | 
        
        | Term 
 
        | drug interactions with TCAs |  | Definition 
 
        | use of other CNS depressants (barbiturates, opioids, alcohol) can increase CNS depressionsmoking may lower plasma conc of TCAswhen cimetidine, SSRIs, OCs are given together w/ TCAs, TCA blood levels & the risk of adverse effects are increasedconcurrent use of TCAs and MAO inhibitors may cause extreme excitation, hyperpyrexia & seizures
 |  | 
        |  | 
        
        | Term 
 
        | pharmacologic treatment for depression:   selective serotonin reuptake inhibitors (SSRIs)  |  | Definition 
 
        | sertraline (Zoloft)   mechanism of action complex & includes inhibition of serotonin neurotransmission; block uptake of serotonin by presynaptic neuron, making more available at postsynaptic receptor; initial overstimulationfirst-line agentsalso have other psychiatric application: obsessive compulsive disorde,r panic disorder, bulimiaadvantages: few anticholinergic effects, non-sedating, non-fatal in overdosetakes up to 10-21 days to notice changes in symptoms: full therapeutic effect in up to 6 wksside effects: sexual dysfuction (esp Zoloft), insomnia, anorexia (initially), nausea, diarrhea, weight gain (loss of a sence of satiety & reduction in metabolism)Discontinuation Syndrome:  flulike symptoms (taper doses to avoid this)
 |  | 
        |  | 
        
        | Term 
 
        | drug interactions with SSRIs |  | Definition 
 
        | can be significant enzyme inhibitors of the P450 system of hepatic metabolism (e.g. carbamzepine)serotonin syndrome can develop in pts taking greater than or equal to 2 drugs that affect serotonin system (MAOIs, TCAs, sympathomimetics - ephedrine)Citalopram & sertraline cause less inhibition of the cytochrome P-450 - good for pts taking multiple drugs
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of SSRIs |  | Definition 
 
        | hypersensitivitycaution in lactation/pregnancy (cat C)concurrent use w/ MAOIs due to risk of hypertensive crisis or "serotonin syndrom" (hyperthermia, autonomic instability, rigidity, myoclonus, confusion, delirium, coma)pts w/ hepatic/renal dysfunctionsafety for use in kids is not establishedcaution in elderly
 |  | 
        |  | 
        
        | Term 
 
        | drug interactions with SSRIs |  | Definition 
 
        | when regimen is changed from MAOIs to SSRIs, the pt should be off the MAOI for at least 14 days before initiation of the SSRI: be aware that when the med regimen goes from SSRIs to MAOIs, a longer period (5 wks) off SSRI is needed between the discontinuation of the SSRI and the initiation of the MAOIcimetidine (Tagamet): increased antidepressantMAOIs: possible hypertensive crisis and syndrome of autonomic instabilityTCAs: elevated plasma levels and increased toxicities
 |  | 
        |  | 
        
        | Term 
 
        | overdose of SSRIs is considered ____dangerous than a TCA overdose because: |  | Definition 
 
        | less dangerous     b/c SSRIs are not cardiotoxic  |  | 
        |  | 
        
        | Term 
 
        | pharmacological treatment for depression:   monoamine oxidase (MAO) inhibitors  |  | Definition 
 
        | tranylcypromine (Parnate)   block or diminish the actions of MAO, an enzyme that is widely distributed throughout the body w/ the highest conc in the brain, liver, and kidneysin the neuron, MAO functions as a "safety valve" & inactivates any excess of the monoamine neurotransmitters (NE, E, dopamine, serotonin)when the enzyme is inhibited, the neurotransmitters are available within the synapse, aiding impulse transimission between pre-and post-synaptic neuronsMAO in the liver and intestine inactivates amines that are present in foods and drugs, and when this is inhibited, the biogenic amines become more available to exert their action 
 |  | 
        |  | 
        
        | Term 
 
        | parmacotherapeutics of MAOIs |  | Definition 
 
        | tx of major depression unrelieved by TCAs, SSRIs, or miscellaneous agents; although MAOIs are considered to be as effective as other antidepressants, they are not the drug of first choice for major depression due to their potential adverse and hazardous effects
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of MAOIs |  | Definition 
 
        | known sensitivity to MAOIshyperthyroidismcongestive heart failure or other CV diseaseshypertensionpts over 60 or under 16 yrs oldmay drugs as well as foods containing tyramine are contraindicated w/ concurrent MAOI use due to the possible development of either hypertensive effect, severe anticholinergic effect, or profound CNS depressiontyramine is an amino acid that is a precursor to dopamine, E, and NE; it promotes the release of NE from sympathetic nerve, resulting in hypertensive cdrisis when MAOIs are used; avoid tyramine-containing foods for several d ays before regimen begins, throughout tx, and for 2 wks after discontinuation 
drug interaction:b/c there are so mnay drug interactions, no drugs should be added to the pt's regimen w/o consideration of the MAOI interaction
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations for MAOIs |  | Definition 
 
        | teach pt dietary/medication precaution required during regimenaccess to MAOIs should be limited to prevent self-administered overdose
 |  | 
        |  | 
        
        | Term 
 
        | pharmacological treatment of depression:   buproprion (Wellbutrin)  |  | Definition 
 
        | affects both NE & dopamine neurotransmission, leaving the serotonin system unaffectedadvantages: shown to be effective in tx of ADD & smoking cessation; non-sedating, limited drug interaction problems; rare sexual dysfunctiondisadvantages: significant incidence of seizures as an adverse effect in overdose, about 4x that of other antidepressants; it is of specific concern for pts w/ a h/o seizures, head injury, anorexia, or bulimia (secondary to electrolyte imbalances)insomnia
 |  | 
        |  | 
        
        | Term 
 
        | pharmacological treatment of depression:   mood stabilizing drugs/animanic agents  |  | Definition 
 
        | lithium carbonate (Eskalith, Lithane) lithium cytrate syrup (Cibalith-S)   mania: elevated mood w/ grandiose ideas, expansiveness, pressred speech, flight of ideas, decreased sleep, increased activitylithium = drug of choice for long-term tx of bipolar disorder (manic-depression); the drug of choice for tx of the manic phase, anthough both episodes respondalso used as an adjunct w/ antidepressants to treat major depression and with antipsychotics to tx schizophreniaspecific mechanism of action is unknowngive PO & ion is excreted by the kidney pts w/ impaired kidney functions can develop toxic levels of lithium saltsthere is a direct relationship between Na intake & lithium excretion; low Na intake slows lithium excretion & leads to toxicity; excessive Na intake lowers lithium levelslithium salts: very toxic; TI = very low; therapeutic levels are 1-1.5 in the acute manic pahse; for maintenance, the levels should be 0.6-1.2; 2.0 = max serum levelPO preps are rapidly absorbed, peak serum levels are reached in 1-2hrs; clinical response is noted in 1 week or longer; complete response usually takes 3 weeks; the lithium therapy is continued for yers in bipolar disorderuntil therapeutic levels are achieved,symptoms of mania may be controlled by antipsychotics: chlorpromazineLithium causes no noticeable effect on normal individuals, it is not sedative, a euphoriant, or depressant
 |  | 
        |  | 
        
        | Term 
 
        | contraindications of mood stabilizing drugs (lithium) |  | Definition 
 
        | elderly - lower dose (decreased renal & CV function)severe renal or CV diseaseNa depletion that could occur w/ diuretic admin, dehydration, or low Na diet will cause increased lithium levels & possible toxicityteratogenic 
 |  | 
        |  | 
        
        | Term 
 
        | drug interactions with mood stabilizing agents (lithium) |  | Definition 
 
        | antipsychotics, carbamzepine, diuretics, indomethacin, ibuprofen, methyldopa, pheytoin:  increased toxic effects of lithiumBenzodiazepines: life-threatening hypothermiaHaldol: severe encephalopathic symptoms such as parkinsonism, dyskinesia, and dementianeuromuscular blockers: prolonged effects of thesesympathomimetics: reduced pressor effectsurinary alkalinizers (antacids, caffeine, NaCl, sodium bicarb) - decreased effects of lithium 
 |  | 
        |  | 
        
        | Term 
 
        | adverse effects of mood stabilizing agents (lithium) |  | Definition 
 
        | CNS:mild: hand tremors, fatigue, muscle weakness, lethargymoderate: coarse hand tremors, confusion, incoordination, increased lethargy, muscle hyperirritabilitysevere: ataxia, slurred speech, fasciculation, extrapyramidal symptoms, blurred vision, seizures, coma
CV: ECG changes and hypotensionGI: anorexia, nausea, vomiting, diarrhea, increased thirst, gastritis, increased salivation, indigestion, flatulence, taste distortion, salty taste in mouthGU: polyuriarenal: albuminuria, oliguria, glycosuria, hyperkalemiaderm: pruritus, rash, thinning of hair, acne, cutaneous ulcerationsendo: hypothyroidism, hyperglycemia, hyperparathyroidism, nephrogenic diabetes insipidusEENT: worsening of cataracts, eye irritationmost pts experience some adverse effects from admin of lithium, but toxicity usually depends on dose and length of therapy; development of toxic symptoms is gradual; usually starts from nausea, gastric upset, fine tremors, urinary frequency
 |  | 
        |  | 
        
        | Term 
 
        | nursing considerations for lithium |  | Definition 
 
        | admin PO in both liquid and tablet form (also sustained-released)instruct pt to never double dosage if a dose is missed but contact physician immediately for instructionstake w/ meals/milkwith normal renal function, 10-12 days may be required for lithium to be completely clear of bodyadvice pt to carry medicalert card
 |  | 
        |  | 
        
        | Term 
 
        | antipsychotic agents/ neuroleptic drugs/major tranquilizers/antischizophrenic drugs |  | Definition 
 
        | used primarily to tx psychotic states like schizophrenia, delusional disorder & other hallucinatory statesblock various receptors including cholinergic, adrenergic, serotoninergic, muscarinic & histamine receptorsantipsychotic actions are thought to be due to blocking of dopamine receptors in the CNS, particularly the D2 receptors in the mesocortical and mesolimbal systems of the braindrug's potency parallels its affinity for D2 receptors
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | particular type of psychosis, that is mental disorder caused by some inherent dysfunction of the braincharacterized by delusions, hallucinations (often in form of voices), and thinking/speech disturbancescommon affliction, occuring in 1% of population, or at about the same incidence as DMmost commonly affects young adultsstrong genetic predisposition & reflects some fundamental biochemical abnormality, maybe overactivity of the mesolimbic dopaminergic neurons 
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        | Term 
 
        | neuroleptic drugs are classified as either tranditional or nontraditional (atypical) antipsychotics |  | Definition 
 
        | traditional antipsychotics are categorized according to their potency (high, medium, or low) or their strucutrepotency refers to size of the dose & achievement of therapeutic effect; also has implications re: the inceidence of anticholinergic & extrapyramidal symptoms (EPS)
management of psychotic disorders can typically be achieved by familiarity w/ the effects of one or two drugs in each classtraditional antipsychotics are all considered equivalent in efficacy; there is no "perfect" antipsychotic, b/c all produce severe adverse effects; high potency drugs are more likely to produce extrapyramidal adverse effects, while low potency produce sedation & hypotension; drug of choice is the one that pt can tolerateantipsychotic drugs do not cure psychosis; suppress or minimize symptomsthey are no addictive, even w/ overdose; have high TI & can be taken in high doses w/ little riskoptimum therapeutic effects may take up to 6-7wkshighly pipophilic & protein bound so they accumulate in body tissues; drug efefcts continue for weeks or months after last dose
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        | Term 
 
        | examples of antipsychotic agents |  | Definition 
 
        | low potency: chlorpromazine (Thorazine)high potency: haloperidol (Haldol)atypical: risperidone (Risperdal)
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        | Term 
 
        | extrapyramidal side effects of antipsychotics   (75-80% of pts, both high and low potency)  |  | Definition 
 
        | acute dystonia (onset 1-5 days)spasm of muscles of tongue, face, backtx with benadryl
parkisonism (onset 5-30 days)bradykinesia, tremor, gait, "pill rolling"tx with benadryl
akathisia (onset 5-60 days)resless,compulsive, anxietytx w/ reduced dose ore switch to low-potency drug
tardive dyskinesia (onset month-yrs)oral-facial dyskinesiastx w/ prevention (can be irreversible)
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        | Term 
 
        | neuroleptic malignant syndrome     |  | Definition 
 
        | neuroleptic malignant syndrome (NMS) is a rare, idiosyncratic rxn thought to be caused by extreme dopamine receptor blockade at the basal ganglia secondary to antipsychotic therapy   characterized by series of symptoms including severe muscle rigidity, hyperthermia, and stupor   associated w/ traditional high-potency antipsychotic therapy but can occur w/ any antipsychotic  |  | 
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        | Term 
 
        | low, medium, and high potency agents produce similar adverse effects, however, certain effects may occur more commonly with one potency than another: |  | Definition 
 
        | low potency: EPS, NMS; more commonly anticholinergic effects, sedation, hypotension   medium/high potency: more liekly to produce EPS and have less sedative and hypotensive effects; NMS more common in high and long-term therapy  |  | 
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        | Term 
 
        | nursing considerations with antipsychotics: |  | Definition 
 
        | after IM doses, have pt remain lying in bed for 30 minparenteral sol'n may have lemon yellow colorurine may be pink to red-brownprotect skin from sun exposureavoid ETOH, drugs
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        | Term 
 
        | atypical antipsychotic drugs:   limitations of the traditional antipsychotics:  |  | Definition 
 
        | inadequate response in 20-40% of ptsrelapse reate of about 35%/yrlack of impact upon neg symptoms very highincidence of side effects
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        | Term 
 
        | atypical antipsychotic drugs:   advantages:  |  | Definition 
 
        | clozaril, zyrexa, respirdol, seroquel, geodon   generally better tolerated (better compliance, fewer relapses)much lower observed rate of EPSsefficacy against neg symptomsefficacy against cognitive impairmentefficacy against depression and suicide 
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        | Term 
 
        | traditional (1st generation) antipsychotics may still be appropriate for: |  | Definition 
 
        | pts w/ hx of good response w/o EPSpts who ahve responded better to these drugs than the atypicalspts who have responded better to depot versus oral
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        | Term 
 
        | indications for atypical (2nd generation) antipsychotics: |  | Definition 
 
        | pts experiencing first episode of psychosis or pts w/ no avaiable hx concerning response to antipsychotics
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        | Term 
 | Definition 
 
        | anxiety: unpleasant state of tension, apprehension, or uneasiness; a fear that seems to arise from an unknown sourcesymptoms of severe anxiety: similar to those of fear (tachycardia, sweating, trembling, palpitations); may range from mild to panicdisorders involving anxiety are the most common mental disturbancesanxiety disorder incidence in US = 16%family providers treat 90% of anxiety ptsrefer < 10% of pts to psychiatryelderly have lower incidence, but elderly women more affected than menoften associated w/ depression
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        | Term 
 
        | primary anxiety disorder types: |  | Definition 
 
        | generalized anxiety disorder   panic disorder   OCD   PTSD   social phobia  |  | 
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        | Term 
 
        | pathophysiology of anxiety |  | Definition 
 
        | hyperarousal statebegins in breainstem reticular formationLocus Ceruleus (secretes NE)dorsal and medial raphe nuclei (secrete serotonin)
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        | Term 
 | Definition 
 
        | the most widely used anxiolytic drugslargely replaced barbiturates in tx of anxiety, since they are more effective & saferabout 20 benzodiazepine derivatives are availableessentially, all drugs in the class have the same much of action and clinical effectsdifferences exist in pharmacokinetics & hence, there are different indications; it is the pharmacokinetic differences that determine clinical usecan cause several levels of CNS depression, ranging from sedation to general anesthesia; this effect is dose related
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        | Term 
 
        | examples of benzodiazepines |  | Definition 
 
        | anxiety: alprazolam (Xanax)   seizues: lorazepam   anesthesia: lorazepam  |  | 
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        | Term 
 
        | pharmacodynamics of benzodiazepines |  | Definition 
 
        | bind to GABA receptors & enhance the binding of GABA to its receptorreason for increased safety is due to limited supply of GABA 
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        | Term 
 
        | pharmacotherapeutics of benzodiazepines |  | Definition 
 
        | tx of chronic anxiety, anxiety r/t a crisis event, panic disorderto decrease anxiety accompanyingsurgical & diagnostic procedurestx of ETOH & drug withdrawal, seizure disorders, sleep disordersinduction of anesthesia
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        | Term 
 
        | pharmacokinetics of benzodiazepines |  | Definition 
 
        | all can be admin PO & taken w/ food to decrease GI upsethalf-life, onset, peak & duration of action vary among specific agents; these agents are highly lipid soluble - cross the BBB
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        | Term 
 
        | drug interactions with benzodiazepines |  | Definition 
 
        | other CNS depressants, OTC sleep/cold preps, antihistamines, ETOH: additive effect (these include deepened/prolonged sedative effect, motor impairment, enhanced CNS/respiratory depression, death)cigarettes: decreased sedative effect
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        | Term 
 
        | contraindications of benzodiazapines |  | Definition 
 
        | hypersensitivity, angle-closure glaucoma, severe respiratory distresspregnancy/lactation (unless nothing else avail)
 cross placentabeleived to cause fetal anomalies when taken during early stages of pregnancy; may cause fetal dependence w/ resulting withdrawl symptoms in the neonate when taken at the end of the 3rd trimeste; when taken at labor will cause CNS depression in the neionate 1st trimester deformities
caution in pts w/ h/o ETOH/drug abusecaution in elderly or debilitated pts b/c of altered metabolism that may allow then or their metaboites to accumulate in the plasma & lead to excessive sedation & ataxia; the outcome of these common effects is incrased risk of falls & injury
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        | Term 
 
        | adverse effects of benzodiazepines |  | Definition 
 
        | GI disturbances (dry mouth, n, constipation)most common: drowsiness, sedation, ataxia, dizziness, blurred visionhypotensionincontinencepsychological/physical dependence can develop of high doses are given over a prolonged periodabrupt discontinuation results in withdrawl symptoms: confusion, anxiety, agitation, restlessness, insomia, tension (so, taper off)those w/ a short 1/2-life induce more abrupt & severe withdrawl reactions than those seen w/ drugs that are slowly eliminated 
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        | Term 
 
        | nursing considerations with benzodiazepines |  | Definition 
 
        | respiratory distress, apnea, cardiac arrest have been reported w/ IV use - admin slow IV pushnote that withdrawal symptoms are associated w/ abrupt withdrawal of BZDs; gradual tapering is indicated
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        | Term 
 
        | nonbenzodiazepine anxiety agents:   buspirone (Buspar)  |  | Definition 
 
        | structurally and pharmacologically unrelated to the BZDs, barbiturates, or other CNS depressantsdo not produce CNS depressant activity of any sedative actions; however, they do lower or alleviate many symptoms of generalized anxiety 
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        | Term 
 
        | pharmacotherapeutics of buspirone: |  | Definition 
 
        | axiety disorderstx of ETOH & substance abuse b/c there is no physical or psychological dependencybenefits:less sedatingnot additive w/ CNS depressantspreg cat Blittle abuse potentialno physical dependence
limitations:slow onsetmay take 2 wks for effectmax effect in 3-6wks
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        | Term 
 
        | contraindications/drug interactions with buspirone |  | Definition 
 
        | hypersensitivityconcurrent use w/ MAOIscontraindicated in kids under 18yrs oldEtOH: increased sedative effects of ETOHpsychotropic drugs: increased levels of these drugsMAOIs: increased BPadverse effects: n/dizziness/HAs, restlessnesstake w/ food for increased drug effectivenessopimal effects may not appear for 3-4wks
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