Exam 3 V2: NURS 660 / NURS660 Psychopharmacology and Advanced Mental Health | Complete Questions and Verified Answers (Latest 2026 / 2027)100% Correct - Maryville

Exam 3 V2: NURS 660 / NURS660 Psychopharmacology and Advanced Mental Health | Complete Questions and Verified Answers (Latest 2026 / 2027)100% Correct - Maryville Q: Sertraline (Zoloft) Major Side Effects insomnia, somnolence, HA, dry mouth, sex dysfunction, nausea & diarrhea Q: Fluoxetine (Prozac) Major Side Effect Activating (UPPER); AGITATION, INSOMNIA, nausea, vomiting, sex dysfunction, GI, serotonin syndrome Q: Paraoxetine (Paxil) Major Side Effects Anticholinergic (can't see, can't sleep, can't shit, can't spit), CYP2D6 inhibitor, increases TCA, phenothiazines, Type 1C antiarrhythmics, weight gain, GI, sex dysfunction, insomnia, serotonin syndrome Q: Lithium Major Side Effects increased thirst & urination, impaired concentration/memory, fatigue, tremor, weight gain. Toxicity: cramps, v/d, kidney dysfunction, coarse tremor, confusion, irritability. Severe toxicity: seizures, coma, death. Q: Fluvoxamine (Luvox) Major Side Effects nausea, vomiting, weight gain, sex dysfunction; BIG BBW for SI on this drug Major side effects for sertraline, fluoxetine, paroxetine, and fluvoxamine (generals for all) •Most side effects are immediate and go away with time sexual dysfunction (dose dependent- men: delayed ejaculation, ED; men and women: decreased sexual desire, anorgasmia) GI: decreased appetite, nausea, diarrhea, constipation, dry mouth Mostly CNS: insomnia, sedation, agitation, tremors, headache, dizziness Autonomic: sweating Bruising and rare bleeding Rare hyponatremia (mostly in elderly) Rare hypotension SIADH Weight gain Rare: seizures, induction of mania, activation of suicidal ideation and behavior Q: Major side effects for sertraline, fluoxetine, paroxetine, and fluvoxamine (generals for all) r/t to increased serotonin concentrations at serotonin receptors in parts of brain and body other than those that cause therapeutic actions (e.g. unwanted actions of serotonin in sleep centers causing insomnia or in gut causing diarrhea) can cause diminished dopamine release and might contribute to emotional flattening, cognitive slowing, and apathy in some patients Q: Major side effects for sertraline, fluoxetine, paroxetine, and fluvoxamine (generals for all) Patients with diagnosed or undiagnosed bipolar or psychotic disorders may be more vulnerable to CNS-activating actions of SSRIs Q: Know major side effects for lithium (typically dose related) Ataxia, dysarthria, delirium, tremor, memory problems Polyuria, polydipsia (nephrogenic diabetes insipidus) Diarrhea, nausea Weight gain Euthyroid goiter or hypothyroid goiter, possibly with increased TSH and reduced thyroxine levels Acne, rash, alopecia Leukocytosis Life Threatening: TOXICITY: TREMOR, ATAXIA, N/V/D, SEDATION, DI, INTESTINAL NEPHRITIS, T WAVE FLATTENING, SEIZURES Q: Atomoxetine (Strattera) - SNRI - inhibits NET, increases DA and NE in prefrontal cortex (pg 493 Stahl) *no potential for abuse *ADHD medication in US Trazodone - 5-HT2 -A&C antagonist, increases serotonin release Duloxetine (Cymbalta) - inhibits neuronal serotonin and NE reuptake, weak DA reuptake inhibitor - SNRI Q: Carbamazepine (Tegretol) - VSSG binding, enhances GABA inhibitory actions, depresses thalamus & temporal activity Q: Lithium - promotes neuroprotection and long-term plasticity - enhances 5-HT actions, reduces catecholamine activity - inhibits GSK-3, affects signal transduction through inhibiting inositol monophosphatase and modulating G proteins or interaction with downstream signal transduction cascades, regulates gene expression for growth factors Q: Lamotrigine (Lamictal) Anticonvulsant First line treatment for bipolar depression and is approved for acute and maintenance therapy. A potential life-threatening rash may occur. inhibits VSSG binding, inhibits release of glutamate (an excitatory neurotransmitter). Weak 5HT3 inhibition. Know how to discontinue fluoxetine Fluoxetine (Prozac) - no taper needed, long half life Know how to discontinue lamotrigine Lamotrigine (Lamictal) - decrease dose by 50% per week, over at least 2 weeks (unless there is a safety concern = rash) Why is L-methylfolate prescribed or augmented to current therapy Important regulator of critical cofactor for monoamine neurotransmitter synthesis (mostly tetrahydrobiopterin or BH4) It is needed for serotonin and dopamine synthesis 4. Know why L-methylfolate might be prescribed or augmented to current therapy Two theories: 1. Low amounts of L-methylfolate = low synthesis of monoamines = depression/resistance or unresponsive to antidepressants (because SSRIs/SNRIs need good synthesis of monamines to work - messes with the reuptake blockade) 2. Methylation of genes silences them. So, if there is low L-methylfolate, the gene silencing could also be low = increased enzyme activity (COMT) = decreased dopamine levels = cognitive dysfunction. So adding L-methylfolate to someone who is deficient can increase dopamine and help with cognition. Causes of low L-methylfolate: Dietary deficiency Genetic variations in folate metabolism (you can test for this genetic variation (MTHFR) through tests like Genesight). Theories are that having this genetic problem with folate metabolism can increase or cause depression and resistance to antidepressants What is BDNF is and how it works Protein of the CNS that stimulates cell proliferation, aids in cell survival and synaptic restructuring. It is also implicated in the neurotrophic hypothesis of depression. BDNF (brain-derived neurotrophic factor) BDNF sustains viability of brain neurons- neurotropic factor- most common Growth factor in brain- role in neuroplasticity, differentiation, synaptic formation What blocks: stress, fat and sugar, no sleep, isolation, no exercise What helps: sun, exercise, sleep, antioxidants, meds, therapy, ECT, Stress represses gene for BDNF = lower 5HT levels and changes NE and DA (acute=increase, chronic-deplete) Causes atrophy and apoptosis of neurons in hippocampus, prefrontal cortex Low monoamine = low BDNF Can be reversible with antidepressants Prefrontal cortex Depression: psychomotor fatigue, concentration, interest/pleasure, guilt SI, worthlessness, mood. Striatum Depression: psychomotor fatigue (physical) Nucleus accumbens Depression: pleasure, interests, fatigue, energy Hypothalmus Depression: sleep, appetite Amygdala Depression: guilt, suicidality, worthlessness, mood Spinal cord Depression: fatigue (physical) Cerebellum Depression: psychomotor DA and NE dysfunction decrease + affect 5HT and NE dx increase - affect Prefrontal cortex Mania: racing thoughts, grandiosity, distractibility, talkative/pressured speech. Basal Forebrain Mania: Decreased sleep/arousal Striatum Mania: Motor/agitation. Nucleus accumbens Mania: racing thoughts, goal-directed activity, grandiosity. Thalamus Mania: Decreased sleep/arousal Hypothalmus Mania: Decreased sleep/arousal. Amygdala Mania: Mood. Psychomotor fatigue Prefrontal cortex Striatum Cerebellum Spinal cord Interest/Pleasure Prefrontal cortex Nucleus accumbens Concentration Prefrontal cortex Guilt/worthlessness Amygdala Sleep/arousal Hypothalmus Basal forebrain Thalamus Racing thoughts Prefrontal cortex Nuclean acumbens Suicidality Amygdala Mood Amygdala Pressured speech Prefrontal cortex Distractibility Prefrontal cortex Racing thoughts Prefrontal cortex Nuclean acumbens Grandiosity Prefrontal cortex Nuclean acumbens Symptoms of mania Abnormally elevated, expansive, or irritable mood If just irritable- needs 4 other sx Plus: Inflated self-esteem/grandiosity Increased goal-directed activity or agitation Risk taking Decreased need for sleep Distractible concentration More talkative/pressured speech Flight of ideas/racing thoughts DIG FAST Distractible Insomnia Grandiosity Flight of ideas (racing thoughts) Agitation Speech (pressured) Thoughtlessness (risky behavior) MOA: Lithium promotes neuroprotection and long-term plasticity enhances 5-HT actions reduces catecholamine activity, inhibits GSK-3 affects signal transduction through inhibiting inositol monophosphatase and modulating G proteins or interaction with downstream signal transduction cascades regulates gene expression for growth factors Lithium side effects Common: increased thirst & urination, impaired concentration/memory, fatigue, tremor, weight gain. Toxicity: 1.5 Early: cramps, n/v/d, kidney dysfunction, coarse tremor, confusion, irritability, blurred vision, vertigo, decreased DTRs. 2.5 Intoxication: severe neuro complications, seizures, coma, cardiac dysrhythmia, permanent neuro impairment 3.5 Severe toxicity: death. Lithium Therapeutic level: Maintenance: 0.6-1.2 mEq/L Lithium Advantages Effective for mania & depressive episodes Prevents suicide in patients with mood disorders Can be used to augments antidepressants in unipolar depression Timing of lithium level draws: trough level 8-12 after last dose (before next dose) the advantages of 2nd generation antidepressants Unlike the TCAs, these alternative agents possess almost no anticholinergic effects or potential for cardiac dysrhythmias. Fewer side effects and more rapid onset of action than TCAs. major disadvantages of MAOI's (phenelzine, tranylcypromine, ipronizide, iproclozpide, phenooxypropazine, lazabemide, moclobemide, selegeline, rasogiline) Drug-food interactions "cheese reaction" red wine, pickled foods "tyramine" Hypertensive crisis, liver toxicity, hemorrhage Can't be used with SSRIs or TCAs major disadvantages of TCA's (desipramine, nortriptyline, imipramine, doxepin, amitriptyline) Overdose Lethal Sedating Norepinephrine (NE) Mainly excitatory; involved in arousal and mood Norepinephrine transporter (NET) proteins that remove norepinephrine from the synapse Dopamine - DA regulates motor behavior, motivation, pleasure, and emotional arousal dopamine transporter (DAT) membrane protein that enables the presynaptic neuron to reabsorb dopamine after releasing it Serotonin (5-HT) Excitatory or inhibitory; involved in sleep, mood, anxiety, and appetite Serotonin transporter - SERT proteins that remove serotonin from the synapse Voltage sensitive sodium channel - VSSC allows ion flow in response to membrane depolarization SSRI - generally C Celexa-C Lexapro-C Prozac-C LuvoxC Paxil-D Zoloft-C SNRI - generally C Cymbalta-C Effexor-C Pristiq-C NRI Strattera-C Wellbutrin-B MAOI - generally C Phenelzine-C tranylcypromine-C ipronizide-C iproclozpide-C phenooxypropazine-C lazabemide-C moclobemide-C selegeline-C rasogiline-C TCA- generally C Desipramine-C Nortriptylin-C ImipramineC doxepin-C amitriptyline-C Mood stabilizers (D) & others Depakote-D Lithium-D Tegretol-D Buspar-B Mirtazapine-C Trazodone-C Viibryd-C Category X Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in use of the drug in pregnant women clearly outweigh potential benefits. Category D There is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks. Category C Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks. Category B Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in pregnant women. Category A Adequate and well-controlled studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of risk in later trimesters). the events step-by-step during stress activation of the hypothalamic-pituitary-adrenal (HPA) axis? NE and ACh regulate the release of corticotrophin-releasing factor (CRF) from the hypothalamus. This hormone signals pituitary gland to secretes ACTH ACTH causes the release of cortisol from the adrenal gland. Cortisol mobilizes energy of glucose to cope High levels of Cortisol feeds back to shut down HPA activation (negative feedback mechanism) What is the dexamethasone challenge is and why it would be ordered Tests the function of the negative feedback mechanism regulating the HPA axis. It tests how your cortisol levels are affected by taking dexamethasone. Depressed patients are injected with 1mg dexamethasone and then the cortisol level is drawn. If the level is not decreased, they have failed to respond and their negative feedback mechanism is not working properly. stress-diathesis model of depression, know what it is, what the studies in rats showed, and how it applies to practice (can't find anything about rats) Researchers believe that depressed individuals have either genetically determined HPA reactivity or low monoamine levels in the brain. The depression model is similar to the schizophrenia model except suggests the following: S variant genefor SERT= more vulnerable to depression + stressors I variant for SERT= less vulnerable HIGH RISK GENES= LOWER TOLERANCE TO STRESS Useful antidepressant treatments might focus on the HPA axis. Nature vs nurture GENETIC RISK FACTORS + STRESS = SCHIZOPHRENIA. Too many genetic biases combines with too many stressors results in schizophrenia (this might explain why some people with the propensity to have schizophrenia have it and some don't) Genetically "biased" circuit: Sufficient backup mechanisms are not present to compensation for inefficient information processing Overactivation isn't compensated partially, fully, or at all by circuit Abnormal biological endophenotype + abnormal behavioral phenotype = hallucinations, delusions, and thought disorder (positive symptoms) Learned helplessness (LH) in rats, an experimental model for depression, involves exposing animals to a number of uncontrollable and unpredictable aversive stimuli. Such animals later exhibit an inability to learn, increased turnover and reduced levels of NA in the nucleus coeruleus, as well as resistance to dexamethasone Although there are parallels between LH and depression, there are important differences. LH is transient, lasting only 2 or 3 days, although it may be reinstated by cues associated with the inducing stimuli or context but human depression is not context dependent. While LH in rats requires a certain minimum number and intensity of shocks (e.g., a minimum of 50 foot shocks at 1 mA), a far lower number of shocks at the same intensity induces a long lasting increase in vigilance in the sudden silence test, an effect not seen after the LH induction procedures Hypocortisolemia has been associated with a number of symptoms, including PTSD, atypical seasonal depression, fibromyalgia, autoimmune disorders, and hypothyroidism. A number of studies, both human and animal, suggest that HPA dysfunction may be a risk factor for PTSD or PTSD-like symptoms rather than a consequence Like depression, PTSD is associated with lower hippocampal volume. Studies of Vietnam veterans and their twins suggest that low hippocampal volume represents a familial vulnerability rather than a consequence of trauma A 2013 review of human data suggests that vulnerability to PTSD is associated with lower GC responsiveness at the time of or shortly after the trauma, associated with a preexisting high sensitivity to GCs An alternative is that the hypocortisolemia is a consequence of earlier trauma, excessive secretion of GCs, and a subsequent downregulation of the system or overshoot Stress - diathesis model of depression The diathesis component refers to the genetic predisposition to depression. Researchers believe that depressed individuals have either genetically determined HPA reactivity or low monoamine levels in the brain. Useful antidepressant treatment might focus on the HPA axis. SIG E CAPS Sleep Interest Guilt Energy Concentration Appetite Psychomotor Suicide AD can be added with anhedonia and/or dysphoria monamine neurotransmitters norepinephrine dopamine Serotonin STAR*D trial - Large NIMH study across US 4000 pts in 3 years. Level 1 - SSRI - Celexa; Level 2 - Switch to another SSRI - Zoloft, Effexor, Buspar or switch to CBT or augment with Wellbutrin SR or Buspar; Level 3 - sitch to mirtazapine or nortriptaline or augment with lithium or T3 hormone; Level 4 - switch to MAOI or combo mitrazepine and Wellbutrin XR. ***might be on boards Increase NE neurotransmission by increasing synaptic NE most are effective symptomatic treatments for major depression may cause adrenergic side effects (increased blood pressure, heart rate, dry mouth, tremor) Presynaptic reuptake blockers for NE imipramine, venlafaxine; etc. not cocaine Indirect effects on NE neurotransmission fluoxetine and other SSRIs - neuronal crosstalk; lithium & ECT Enzyme inhibitors (NE) MAOIs; phenelzine etc Decreased NE neurotransmission risk of inducing or worsening depression adrenergic side effects sedation, bradycardia, hypotension (esp postural), bronchoconstriction Categories of mood disorder (2) -depressive disorder -bipolar related disorder Common features of two categories of mood disorders (3) -presence of sad mood -empty and irritable mood accompanied by somatic and cognitive changes -significant affect the individuals capacity to funciton Depressive disorders that arent other specific/unspecpified (6) -major depressive disorder -persisintent depressive disorder (dysthmymia) -premenstrual dysphoric disorder -disruptive moodle dysregulation disorder -substance/medication induced dpressive disorder -depressive disorder due to another medical condition Bipolar and related disorders that arent unspecified (5) -bipolar I disorder -bipolar II disorder -cyclothymic disorder -substance/medication induced bipolar and related disorder -bipolar and related disorders secondary to general medial condition Most common, second most common mood disorders 1) major depressive disorder 2) disruptivem ood disregulation disorder Gender ratios and age on onset for -MDD -bipolar I -bipolar II MDD --- 2:1 ---mean: 40 years, less than after age 65 Bipolar I ---1:1 female:male ---mean:30 years Bipolar II ---femalesmales Pathophysiology of depressive disorders -abnormalities in biogenic amines (both increased and decresaed) ---norepinephrine ---serotonin ---dopamine Causes of dysregulation of biogenic amines in depressive disorders (3) -neuroendocrine disregulation ---adrenal axis (HPA_ ---thyroid axis ---growth hormone axis Depression and hypothyroidism -depression can be first symptom of hypothyroidism ---high TSH Brain regions that emotions -prefrontal cortex -anterior icngulate -hippocampus -amygdala Categories of symptoms of depressive disorder (2) +examples of each -reduced positive effect: depressed mood, loss of happiness, loss of interest/poleasure, loss of energy/enthusiasm, decresaed alertness, decresed self confidence -increased negative effect: depressed mood, guilt/disgust, fear/anxiety, hostility, irritability, loneliness Predispositions to mood disorder (4) -Psychosocial factors -Stressful life events: Loss of loved ones -Psychodynamic factors: Loss -Disturbance in mother-infant relationship Major depressive disorder diagnostic 5 or more of the following, present for at least two weeks Mood depressed most of the day, nearly everyday ---children/adolescents: irritable -sleep disturbance: more waking up earlier than difficulty fallingasleep --insterest/pleasure reduciton -guit (worthlessness) -energy changes/faitgue -concentration and attention impairment (indecisiveness) -appetite and weight changes -psychomotor disturbances (objective) -suicidal thoughts (thoughts, ideation, attempt, plan) Schematic of diagnostic criteria for major depressive disorder Major depressive disorder -what it is (3) -clinically significant distreess or impairment in social, occupational, or other important areas of functioning -the episode is not attributable to the physiologic effects of a stubstance of another medical condition -never has been a manic episode or hypomanic episode What to be careful about when diagnosing MDD -there is a FH of bipolar disorder and theyre actually in a depressive episode instead of MDD, you can put them into mania by giving them an antidepressant Adjustment disorder -hallmark feature -mood improves when significant stress is removed Features that distringuish grief from major depressive episode -MDE has (6) -persistent depressed mood and anhedonia -dysphoryia more persistent and not tied to specific thoughts or preoccupations -pervasive unhappiness and misery -self critical or pessimistic ruminations -feelings of worhtlessness and self loathing MDD with anxious distress (5) Need two: -feeleing keyed up or tense -feeling unusally restless -difficulty concentrating due t oworry -fear that something awful may happen -feeling of loss of control Major depressive disorder: suicide -lifetime death rate -ages -lifetime death by suicide: 15% -ages 16 to 24 and over 65 Major depressive disorder: management -mild depression: psychotherapy -moderate to severe: combined pharmacotherapy/ psychoterapy *combined treatment is most effective for all ages Major depressive disorder teratment: antidepressants -5 categories, drugs in each -SSRI: fluoxetine, paroxetine, sertaline, citalopram, escitalopram, vilazodone, vortioxetine -SNRI: valafaxine, duloxetine, levomilnacipran, nefazodone Antidepressants and suicide risk -children and adolescents at higher risk -there is increase risk of suicide attempts but better to treat because less suicide from medication than not treating Non medication treatment modalities for MDD -electroshock therapy: best in elderly ----treatment refractory, psychotic or severe depressions or when meds contraindicated -trans magnetic stimulation: magnetic pulses to specific areas of the brain ---used for treatment resistant depression MDD adjunctive and augementing strategies -antipsychotics in psychotic depression -anxiolytics in high level of anxiety -lithium -thyroid hormone -psychostimulants -atypical anti psychotics Symptoms of persistent depressive disorder (3) -Neruovegitative: sleep and appetite disturbances, decreased concentration, hopelessness Double depression -dythymia and MDD Treatment for dysthymia -psychotherapy, similar to MDD with longer course Treatment for premenstrual dysphoric disorder -SSRIs: fluoxetine Substance/medication induced mood disorder -what it is -there is evidence of history physical exam or lab findgins that the distrubance is the direct conequence of substance intoxicaiton or withdrawal and does not persist after the cessation of medicaiton Disruptive mood dysregualtion disorder -findings -timing -baseline -when to diagnose -severe temper outbursts (verbal/behavioral), out of proportion in intensity or duration of situation or provocation, inconsistent with development level -three or more times per week -cannot be made before 6 or after 18 Subtypes of disruptive mood disregualtion disorder (4) -melancholic depression: severe form, guilt remorse loss of pleasure and extreme vegetative -postpartum depression: within 4 weeks of delivery -seasonal affective disorder -atypical depression: hypersomnia, increased appetitie or weight gain, mood reactviity, long standing rejection sensitivity, anergia, leaden paralysis Bipolar I -feature -defining features of manic episode (2) -manic episode preceded by and followed by hypomanic or major depressive episodes -manic episode defined by elevated, expansive or irritable mood ----at least one week and present most of the day, nearly every day Bipolar I manic episode picture Bipolar disorder -requirement -symotoms -one episode of mania lasting for at least one week Symptoms -Distractibility -Irresponsibility/erratic behavior -Grandiosity -Flight of ideas -Activity increased -Sleep decrease -Talkativeness Hypomania, dysthemia -hypomania: just a bit manic but still elevated -dysthemia: minor depression Bipolar I mood chart Bipolar I -gender distribution -age of onset -suicide -male:female 1:1 -mean age is 18 years, late onset consider other medical conditions -suicide rate: 10-15% Treatment of bipolar I Treatment of bipolar I -maintenance -atypical antipsychotics ---olanzapine --quetiapine --aripirazole --ziprasidone --lurasidone Bipolar II -genreal -hypomaic + MDD -manic episode all same symptoms as bipolar I manic episode but not as manic and doesnt last as long Bipolar II manic episode core symptoms (7) Hypomania -inflated self esteem or grandiosity Hypomanic episode in bipolar II features -abnormally and persistently increased acitivity or energy; elevated ,expansive or irritable mood -lasts at least 4 consecutive days Bipolar II symptoms chart Course of bipolar II -onset -starts with -mania -depressive episodes quality -psychotic symptoms -develops to -average age of onset is mid 20s -stars with depressive episodes -hypomanic episodes start later -depressive episodes are more enduring and disabiling over time -psychotic symptoms are much less in bipolar II during MDD than bipolar I -5-15% are ultimately develop bipolar I w manic episode Subtypes of bipolar disorder -rapid cycling: 4 mood disturbances per year, a high suicide rate -catatonic: present with mood disorder when there are pronounced movement abnormalities (motoric immobility, purposeless motor activity, echolalia, echopraxia) Rapid cycling bipolar disorder mood chart Cyclothymic disorder -what it is -time course -recurrent, chronic, mild cycles through dysthymia and hypomania -for at least 2 years (at least 1 year in children and adolescents) Cyclothymic disorder -presentation -numerous periods of hypomanic symptoms that do not meet the criteria of a hypomanic episode -numerous depressive symptoms that do not meet the criteria for a major depressive episode -has not been without symptoms for more than 2 months at a time Cyclothymic disorder mood chart Flow chart for mood disorder diagnosis What are the main indications for all antidepressants? -Major depression -Depressive phases of bipolar disorder (usually given with a mood stabilizer) -Depressive sx include: Dysphoria, change in appetite and energy, anhedonia, difficulty concentrating, hopelessness, and suicidality -Sometimes for anxiety disorders What is general pt education for antidepressant therapy? -May not see improvement for 4-8 weeks -Physiological sx improve before psychological sx -SE may occur, but usually, be handled by dosage adjustment or switching to a different med -Discontinuing meds as soon as pt feels better can result in relapse. Stay on med at least 6mo and up to 12-24 -NO ALCOHOL What are common SRIs? -fluoxetine (Prozac) -paroxetine (Paxil) -sertraline (Zoloft) -citalopram (Celexa) -escitalopram (Lexapro) -vortioxetine (Trintellix) -vilazodone (Viibryd) -venlafaxine (Effexor) -duloxetine (Cybalata) What are possible SE of SRIs? -Drowsiness -Nausea (take with food) -Dry mouth -Insomnia -Diarrhea -Nervousness/agitation/restlessness -Dizziness -Sexual problems -HA -Blurred vision What are the implications of SRIs? -Medication effectiveness takes 4-8 weeks What are frequently used TCAs? -imipramine (Tofranil) -desipramine (Norpramin) -doxepin (Sinequan) -amitriptyline (Elavil) What should the you understand about TCAs? -Equally useful as SSRIs in treating depression -Increased danger of death by overdose than SRIs -Increased and potentially fatal CNS depression with ETOH and other CNS depressants -Less expensive than SSRIs What are implications for the administration of TCAs? -Before initiating, check ECG for cardiac disorders and hx of seizures worry/anxiety What are common anticholinergic SE for TCAs and sometimes SRIs? -Can't see can't pee can't spit can't shit -Hot as a hare (increased temp) -Dry as a bone (dry mouth, urinary retention, constipation) -Blind as a bat (mydriasis, dilated pupils, blurred vision) -Red as a beet (flushed face) -Mad as a hatter (confusion, delirium) -Also sedation and weight gain What are nursing interventions for TCAs? -Dry mouth: Sugar-free hard candy/gum -GI upset: Take med with food -Diarrhea: Eat frequent small meals -Constipation: Increase fiber/fluids in diet, exercise -Insomnia: Sleep hygiene/change dosing/time of med admin (in AM) -Orthostasis: Keep hydrated, get up slowly -Sexual SE: Erectile dysfunction meds -Urinary hesitancy: Running water while trying to void, check amount of voiding What are frequently used MAOIs? -phenlyzine (Nardil) -tranylcypromine (Parnate) -selegiline (Emsam): Transdermal patch changed q24hr What are nursing implications for MAOI use? -Avoid tyramine-rich foods to prevent a hypertensive crisis -Avoid using Demerol and OTC cold meds -Rarely used with SSRIs for refractory depression (serotonin syndrome) -Avoid high consumption of caffeine b/c can increase BP What are examples of tyramine rich foods? -Red wines -Aged, smoked, fermented, marinated, and processed meats like sausages, pepperoni, bacon, ham -Aged cheese -Overripe fruits and vegetables -Beans -Condiments -Beer, ales, whiskey, liquors What are the key sx of a hypertensive crisis? -Occipital HA -Palpitations -N/V -Usually hypertension, but HYPOtension possible -Dyspnea/SOA -Mental status changes -Blurred vision -Diaphoresis What is the tx for a hypertensive crisis? -Regitine (phentolamine): Vasodilator -Procardia (SL nifedipine): relaxes cardiac muscle -Sympomatic and supportive -Pt education regarding diet What are potentially harmful serotonin combinations? -SSRIs + supplements/excess dietary tryptophan (turkey, chicken, beef, brown rice, nuts, fish, milk, eggs, cheese, fruit/veg are all precursors to serotonin) -SSRIs + herbal supplements (St. John's Wort, Sam-e) -MAOI + Dextromethorphan -SSRI + SSRI -SSRI + SNRI, etc. What are the sx of serotonin syndrome? -Mental status changes: Agitation, confusion, restlessness, lethargy, delirium, irritability, dizziness, hallucinations -ANS: Diaphoresis, flushing, fever, tachycardia, mydriasis -Neuromuscular: Myoclonus (muscle twitching/jerking), hyperreflexia, tremors -GI: N/V/D What can happen if the serotogenic med is not discontinued? Worsening myoclonus, HTN, rigor, acidosis, respiratory failure, rhabdomyolysis What should you know about serotonin syndrome? -Sx can develop within 6 hours of either first dose of new med, change in dosing, or intentional OD -Can be fatal -Sx can resolve within 24 hours but can take several weeks to go away completely How is serotonin syndrome treated? -Stop or reduce med contributing to SS depending on the severity of sx per HCP -IV fluids: Treat dehydration and fever -Symptomatic and supportive measures What medications are used in treating serotonin syndrome? -Benzos: diazepam (Valium) and lorazepam (Ativan) can help control agitation, seizures, and muscle agitation -HR and BP meds: emolol (Brevibloc), nitroprusside (Nitropruss) -Hypotension: Phenylephrine -Serotonin-production blocking agents What is lithium used for? Mood stabilizer for mania. What should you understand about lithium? -Maintenance dose based on blood levels of 0.6-0.8 -MOA uncertain -Onset between 5-7 days, but can take up to 2 weeks -Thyroid function may decrease between 6-18 months (observe for dry skin, constipation, bradycardia, hair loss, and cold intolerance) lithium; it is a narrow therapeutic index? -Decreased sodium and/or body fluids can cause lithium toxicity -Initial labs 1-2 times/week then CBC, creatinine, and thyroid q6mo What should the nurse teach the patient who is prescribed lithium? -Increased risk of suicidal ideation with abrupt discontinuation -DO NOT RESTRICT SODIUM -Hydrate -Hydrate when anticipating strenuous activity -If illness causes loss of fluids, contact HCP -Intermittent blood tests are required What anticonvulsants are frequently used in mania as mood stabilizers? -valproic acid (Depakote) -carbamazepine (Tegretol) -lamictal (lamotrigine) -topiramate (Topamax) What are nursing considerations for anticonvulsants used as mood stabilizers? -Carbamazepine: Risk of decreased WBCs so check serum levels. Check hepatic and renal function. RASH MAY BE LIFE THREATENING -Lamotrigine: RASH MAY BE LIFE THREATENING What is a lamictal rash? -Allergic reaction. -Flu-like sx, sore throat, fever, chills, blisters, burning eyes -STOP MED IMMEDIATELY -Can advance to Steven Johnson Syndrome and eventually toxic epidermal necrosis What is the role of antipsychotics and benzodiazepines in adult bipolar and related illnesses? -APs and benzos may be given together with an anti-manic/mood stabilizer such as lithium or Depakote -AP: For agitation, psychosis, out of control pt, a low dose of antipsychotics may be started -Benzos: To enhance sleep and relaxation and treat comorbid anxiety What should the nurse understand about the role of SSRIs in children? -BLACK BOX WARNING of increased risk of suicidal ideation -Prozac first line of tx and sometimes venlafaxine -Low SE: Mild nausea, HA, stomach ache -Improvement in 1-2 weeks but up to 12 weeks for full effect (usually 4-8 weeks) -Given 6-24 months Types of antidepressants -TCAs -SSRIs -SNRIs -MAOIs -Atypical Antidepressants Amitriptyline TCAs Clomipramine TCAs Desipramine TCAs Doxepin TCAs Imipramine TCAs Nortriptyline TCAs Protriptyline TCAs Trimipramine TCAs Citalopram SSRIs Fluoxetine SSRIs Fluvoxamine SSRIs Paroxetine SSRIs Sertraline SSRIs Escitalopram SSRIs Desvenlafaxine SSRIs Duloxetine SSRIs Levomilnacipran SSRIs Isocarboxazid MAOIs Phenelzine MAOIs Tranylcypromine MAOIs Bupropion Atypical antidepressants Mirtazapine Atypical antidepressants Nefazodone Atypical Antidepressants Trazodone Atypical antidepressant Vilazodone Atypical antidepressant Mechanism of action for TCA Blocks the reuptake of norepinephrine and serotonin What are the therapeutic uses for TCA They are used for depression, bipolar disorder, chronic pain, and OCD What are the adverse effects of TCA Orthostatic hypotension, weight gain, sedation, anti-cholinergic effects, paradoxical effect, cardio toxic, seizures, hypomania What is the toxic dose of TCA Eight times the average daily dose What drug interactions are with TCA MAOI, anticholernergic, CNS depressants How would we educate the patient on TCAs Keep small supply, keep taking medication after symptoms subside, they take time to work, drink lots of water, no alcohol dangle before standing up Why are SSRIs the first drug of choice They work faster What is the mechanism of action of an SSRI Inhibits re-uptake of serotonin What are the therapeutic uses of SSRIs Mood disorders, eating disorders, anxiety disorders, substance-abuse treatment What are the three most important adverse affects of SSRIs Sexual dysfunction, weight gain, nausea and vomiting What does SSRIs interact with Lithium, MAOI, warfarin What is serotonin syndrome Happens within hours, over activation of serotonin receptors, Minix neuroleptic malignant syndrome but not as severe What are symptoms of serotonin syndrome Fever, agitation, sweating, rigidity, increase blood pressure, increased heart rate, this could lead to death Why are SNRIs good? They have a better side effect profile Therapeutic uses of SNRIs Depression, anxiety, chronic pain Mechanism of action of MAOIs These drugs prevent metabolism of norepinephrine serotonin and open mean which increases the concentration of neurotransmitters What foods do MAO I interact with They interact foods containing tyramine. What can happen from interactions with food while taking MAOI Hypertensive crisis Therapeutic uses of MAO I Major depressive disorder or, bulimia, anxiety disorder What are warning signs of hypertension crisis Set an elevation of blood pressure, explosive headache, flushed face, palpitations, sweating, fever, nausea, vomiting Treatment of hypertensive crisis Hold medication, do not lay down, IV vasodilators, manage fever Nursing implications of taking MAOI Teach patient what to avoid, Monitor intake, educated seek help immediately with a headache, avoid Chinese and pizza, Monitor blood pressure, medical or bracelet Bupropion is used for Increased risk for seizures - smoking cessation and ADHD What is Duloxetine used for Chronic pain, diabetic neuropathy, Fibeymyalgia Mood is defined as what The way the person feels and prolonged emotional tone that influences behavior, personality, perception Defined what affect is Gives her verbal response a person has to their feelings and how an individual presents those feelings What might suggest a mood disorder Extreme intense prolong and interfering with functioning Signs and symptoms of mood disorders Agitation, sadness, elation, blunting, speech maybe monotone during blunting and responses maybe unusually brief What is disturbed vegetative functioning No appetite, lose weight, no sleep or sleep all the time What is the leading cause of disability Major depressive disorder What does SIGECAPS stand for Sleep disturbance, decreased interest in things they're normally interested in, guilt, energy decrease, concentration decrease, appetite change, psycho motor behavior, suicide What are the key assessment findings of major depressive disorder Depressed mood, Anergia, anxiety, psychomotor agitation, psycho motor retardation, vegetative signs of depression, chronic pain When is the acute phase of major depressive disorder and what are the goals 6 to 12 weeks, we want to reduce symptoms, restore psycho social and occupational functioning, patient may need hospitalization meds or other treatments When and how long is the continuation phase of major depressive disorder or and what is the goal of this phase This is from 4 to 9 months and the goal is to prevent relapse with medication education and specific therapy When is the maintenance phase of major depressive disorder or and what are the interventions One year or more and the importance of this phase is to prevent further episodes and just start weaning off medication What is the classification of lithium Mood stabilizer What is the therapeutic use of lithium Control acute mania in patients with bipolar disorder, long-term prophylaxis against reoccurrence of mania or depression, decreases euphoria, hyperactive and other manic symptoms, only approved treatment of bipolar disorder. Does lithium cause sedation No What pre-lithium work up in monitoring do we need to watch for Renal and thyroid function Lithium level below 1.2 toxicity signs Nausea, vomiting, diarrhea, thirst, polyuria, lethargic, slurred speech, muscle weakness, fine hand tremor Lithium level between 1.2-2 toxic signs Persistent G.I. upset, course hand tremors, confusion, hyper irritability of muscles, ECG changes, sedation, and coordination Lithium levels between two and 2.5 signs of toxicity Ataxia, giddiness, High output of dilute urine, tinnitus, blurred vision, clonic movements, seizures, stupor, severe hypotension, coma, death What are adverse affects there occur at therapeutic levels of lithium GI, fatigue, muscle weakness, confusion, memory impairment, polyuria, thirst are early adverse affects. Other adverse effects are tremor, renal toxicity, hypothyroidism. What causes lithium toxicity Lack of hydration, use of diuretics, overdose, fluid electrolyte in balance, poor kidney function, in adequate intake of sodium How do you manage lithium toxicity Adjust or stop dosage of lithium, treat presenting symptoms, Restore fluid electrolyte in balance. What is divalproex used for? Bipolar disorder What is a serious and chronic complication of Divoroex sodium therapy Excessive Weight gain What are signs of toxicity in Depakote therapy Thrombocytopenia, pancreatitis, liver failure What is Carbamazepine (Tegretol) use for? Mixed mania or rapid cycling bipolar disorder What are adverse effects of carbamazepine Neurological side effects like visual disturbance, ataxia, vertigo, unsteadiness, and hematologic effects What medication causes Steven Johnson syndrome Lamotrigine What is Stevens-Johnson syndrome? Severe allergic reaction that is a medical emergency When asking a patient about suicide ideology what should you ask Be direct and ask if they are thinking about committing suicide Describe mania Elevated, expansive, irritable mood Describe bipolar Cyclic disorder Other than bipolar illness what can cause mania SSRIs, steroids, substances, drug interactions What symptoms would diagnose a person with acute mania Euphoric mood, impaired functioning, irritability maybe pre-dominant, impaired judgment, hospitalization Hypomania A manic episode that is not severe enough to cause social problems Mood of a manic Over Joyous, elation, irritability and hostility, argumentative and combative, respond to hurt with laughter, agitation Behaviors of manic Increase goal directed activities, increase in pleasurable activities, high-energy and productability, spending sprees, unable to set boundaries, hyper talkative, pressured speech, overly friendly, increase motor activity, manipulative behavior, increase in sexual activities, poor judgment, poor impulse control, grandiose Physiological assessment of a manic They don't eat, they don't sleep, minimal G.I. activity causing constipation, agitation.