NSG 552/ NSG552 Exam 1 V1 – Psychopharmacology Review | Wilkes (Latest 2026/ 2027 Update) 100% Verified Questions & Answers | Grade A

NSG 552/ NSG552 Exam 1 V1 – Psychopharmacology Review | Wilkes (Latest 2026/ 2027 Update) 100% Verified Questions & Answers | Grade A What are the 6 general principles of psychopharmacological treatment? Safety Tolerability Efficacy Practicality Treatment accessibility Treatment compliance Pharmacokinetics How the drug moves in the body. (ex. Where is it absorbed? How and where is it metabolized? Where is it excreted?) Pharmacodynamics What the drug does to the body. (consider mechanism of action) Define First-generation antipsychotics Referred to as Typical Antipsychotics. Most have strong bond with D2 receptors only, cause EPS symptoms faster due to prolonged receptor dissociation, have more dangerous side effect profiles, have been around longer, more effective at treating positive symptoms, less expensive. (Ex. Haloperidol, Chlorpromazine, Thioridazine, Fluphenazine) Define Second-generation antipsychotics Referred to as Atypical Antipsychotics. Most have a weak bond with D2 receptors and block serotonin receptors leading to anti-depressive and anxiolytic effects. They cause less EPS due to rapid receptor disassociation which leads to rapid dopamine neurotransmission. Have less dangerous side effect profiles but can cause metabolic syndromes, have been around shorter time, more expensive, more effective at treating negative symptoms but can treat positive symptoms as well, long-acting injections available for several of these. (Ex. Risperidone, Clozapine, Quetiapine, Aripiprazole, Ziprasidone) Extra Pyramidal Symptoms (EPS) Side effects caused by certain antipsychotic medications, which include: involuntary or uncontrollable movements. tremors. muscle contractions. Tardive dyskinesia A neurological disorder characterize by involuntary movement of the face and jaw. Upregulation Occurs through chronic use of antagonists which causes an increase in the number of receptors, externalization of receptors, and increased sensitivity of the receptors. Prolonged use of antagonist - Up-regulation of receptors - Sudden withdrawal of antagonist - increased number of receptors and increased sensitivity of receptors *YOU MUST GRADUALLY TAPER A DRUG TO AVOID BINDING TO ALL NEW RECEPTORS FROM UPREGULATION Down regulation Occurs by chronic exposure of agonists which causes decreased number of receptors, internalization of receptors, and decreased sensitivity of the receptors. Prolonged use of agonist down-regulation of receptors - decreased effectiveness of agonist mediated clinical response. You have two options: 1 Increase the drug dose OR 2 Switch to another drug(BEST OPTION) Receptor profile The receptors that each drug binds to (example, risperidone's receptor profile would like... (a) Blockade of 5HT2A and D2 receptors (b) High affinity for a1, a2, and H1 receptors) Binding Refers to a drug metabolite or neurotransmitter attaching to a receptor Affinity refers to the "preference" or likelihood of a drug to bind to a certain receptor. Linked to potency. CYP450 A group of enzymes in the liver that metabolize different drugs. There are six. List the 7 CYP450 Enzymes (1) CYP1A2 (2) CYP2B6 (3) CYP2C9 (4) CYP2C19 (5) CYP2D6 (6) CYP3A4 (7) CYP2EI CYP2B6 Metabolizes arteminsin, bupropion, cyclophosphamide, efavirenz, ketamine, and methadone (2B6, there are two psych drugs (bupropion, methadone (ketamine...?) and six altogether. CYP1A2 metabolizes AcetAminophen (two As) CYP2C9 metabolizes Warfarin/Coumadin (think warfarin factors 2, C, 9) CYP2C19 metabolizes PPIs, antidepressants, antiplatelet, antifungals, and anticancer drugs (2C19, two see one, there is only one class of psych drugs that are metabolized, you ONLY SEE one! antidepressants) CYP2D6 Metabolizes Cardiovascular drugs (2-D echo, echo is a test for heart) CYP3A4 Most common and ambiguous (if not above, then it's this one, a lot of psych drugs are involved with this one) CYP2EI ETOH (You have to be 21 to drink) CYP450 inhibitors Decreases drug metabolism: (1) Valproate (2) Ketoconazole (3) Isoniazid (4) Sulfonamides (5) Chloramphenicol (6) Amiodarone (7) All macrolides (think mycins) except azithromycin (8) Quinidine (9) Grapefruit juice CYP450 inducers Increases drug metabolism: (1) Carbamazepine (2) Rifampin (3) Alcohol (4) Phenytoin (5) Griseofulvin (6) Phenobarbital (7) Sulfonylureas Dopamine Pathways (1) Mesolimbic (2) Tuberoinfundibular (3) Mesocorticial (4) Nigrostriatal Mesolimbic pathway Increase in dopamine in this pathway causes positive symptoms Tuberoinfundibular pathway Increase in dopamine in this pathway causes hypoprolactinemia Mesocortical pathway Decrease in dopamine activity can cause negative, cognitive, and affective symptoms Nigrostriatal pathway Decrease in dopamine activity can cause EPS and TD Metabolic syndrome A cluster of biochemical and physiological abnormalities associated with the development of cardiovascular disease and type 2 diabetes High potency antipsychotics high affinity to a receptor (FGAs are highly potent in terms of D2 blockade), most likely to cause EPS/TD Low potency antipsychotics low affinity to a receptor (SGAs are lowly potent in terms of D2 blockade), most likely to cause metabolic syndrome Neuromalignant syndrome Is a rare, but life-threatening, idiosyncratic reaction that occurs after exposure to a neuroleptic drug (1st and 2nd generation antipsychotics). Caused by excessive dopamine receptor blockage. NMS often occurs shortly after the initiation of neuroleptic treatment, or after dose increases. Usually occurs within the FIRST TWO WEEKS However, NMS can occur years into therapy. Once the syndrome starts, it usually evolves over 24-72 hours. Symptoms include: muscle rigidity, fever, altered mental status, unstable BP, seizure, hyperactive reflexes, increased CPK, Leukocytosis, tachycardia, tachypnea, delirium Treatment: D/C antipsychotic medication! and administer dantrolene/bromocipritine, IV hydration, anti-pyretic treatment (APAP), cooling blanket, benzo QTc interval Measure of time between start of Q wave and end of T wave in cardiac cycle (c = corrected) FGA side effect profile (selected Haldol): EPS, TD, dystonia, hyperpyrexia, heat stroke, NMS, pneumonia, hypotension, HTN, QT prolongation, torsade de pointes, arrythmia, sudden death, hyponatremia, seizures, hepatic impairment, leukopenia, neutropenia, agranulocytosis, cataracts, retinopathy, withdrawal sx if abrupt D/C (long term use) SGA side effect profile (selected Seroquel): suicidality, depression exacerbation, EPS, TD, dystonia, NMS, hyper/hypothermia, anaphylaxis, acute generalized exan. pustulosis, SJS, drug rxn with eosinophilia and systemic sx, severe hypotension, seizures, syncope, TIA, stroke, QT prolongation, diabetes mellitus, hyperglycemia, hypothyroidism, pancreatitis, rhabdomyolysis, agranulocytosis, leukopenia, neutropenia, cataracts, severe dysphagia, priapism, intestinal obstruction What antipsychotic medication is likely to have the least amount of weight gain? Ziprasidone What antipsychotic medication is least likely to result in metabolic syndrome? Haloperidol What antipsychotic medications are least likely to cause increased prolactin? Aripiprazole, Asenapine, Clozapine, Quetiapine, Olanzapine What antipsychotic medications are least likely to cause QT elongation? Haloperidol, Olanzapine, Aripiprazole What antipsychotic medications are least likely to cause EPS? Clozapine, Quetiapine What are the four steps to monitor for metabolic syndrome? 1) Obtain Baseline - weight, BMI, fasting glucose and lipids, BP, EKG 2) Recheck weight+BMI at 4 weeks, 8 weeks, 12 weeks, 6 months, quarterly, and annually 3) Check fasting glucose and lipids at Biannually 4) If metabolic syndrome is suspected then switch agents, lower dose, and/or add metformin T/F ETOH use increases risk for TD? TRUE Akasthesia A state of agitation, distress, and restlessness that is an occasional side-effect of antipsychotic and antidepressant drugs Dystonia Involuntary muscle contraction that cause repetitive or twisting movements. Psuedo-parkinsonism AKA DRUG INDUCED PARKINSONISM is a reversible condition that resembles parkinsonism. Parkinsonism refers to any condition that causes the movement irregularities seen in Parkinson's disease, a brain disorder. How to manage EPS? 1) Add benztropine, Benadryl, amantadine DO NOT USE FOR PROPHLAYXIS DUE TO SIDE EFFECTS 2) Or Consider switching medications. (EPS is less likely to be caused by clozapine or quetiapine) Name 3 options to treat psychotic agitation? 1) PO risperidone + lorazepam 2) IM haloperidol + lorazepam 3) Asenapine can be given sublingual to TOP OFF or provide additive effect to current APS treatment Clozapine Use only in drug-resistant tx of schizophrenia. Do NOT use in teens. Most common side effects: dyslipidemia, hyperglycemia, weight gain, drowsiness, sialorrhea, tachycardia, dizziness, constipation, hypotension, headache, EPS, diaphoresis, xerostomia, tremor, nausea, vomiting, fever, visual/sleep disturbance, dyspepsia, HTN, restlessness, confusion, impaired body temperature regulation Most severe side effects: agranulocytosis, neutropenia, seizures, myocarditis, cardiomyopathy, mitral valve incompetence, cardiovascular collapse, QT prolongation, arrhythmia, torsades de pointes, stroke, syncope, orthostatic hypotension, NMS, TD, dystonia, heat stroke, severe constipation, intestinal infarction/ischemia, GI obstruction, paralytic ileus, hepatotoxicity, hepatic failure, angle closure glaucoma, PE, DM, hypersensitivity, erythema multiforme, SJS, eosinophilia, withdrawal sx if abrupt D/C What receptor is most responsible for EPS? D2 T/F FGAs are more likely to result in EPS TRUE (because they occupy D2 receptors stronger and longer) T/F SGAs are more likely to result in EPS FALSE (because they occupy D2 receptors weaker and for a shorter amount of time RAPID DISSOCIATION). Lamotrigine Treats both bipolar disorder and seizure disorders at once, can be given with other drugs except bupropion (PLAYS WELL WITH OTHERS), less severe side effects, comes in PO route in tablets, chewable tablets, or dissolvable form. 5 things to know when combining Lamotrigrine and Depakote (1) If adding Depakote to lamotrigine, reduce the dose of lamotrigine by 50% (2) If adding lamotrigine to Depakote: start with half a dose, or start with 5mg and add 5mg pill every day until you reach your target dose (3) At 250 mg of Depakote you are half way to a drug reaction. (4) At 500 mg of Depakote you are all the way to a drug reaction (5) DEPAKOTE DOUBLES LAMOTRIGINE LEVELS Drugs that can cause SJS (1) Anticonvulsants (a) Phenytoin (b) Carbamazepine (c) Oxcarbazepine (d) Valproic acid (e) Lamotrigine (f) Barbiturates (2) Antipsychotics (a) Ziprasidone Treatment for episodic patterns of mania With agitation rapid acting oral or non-oral APS or benzo (a) PO olanzapine, risperidone, quetiapine, or lorazepam (i) Secondary options = loxapine inhalation 10 mg or haldol (b) IM aripiprazole, lorazepam, olanzapine (i) Secondary options = IM ziprasidone, IM haloperidol lactate, SL asenapine Treatment for episodic patterns of mania Without agitation Mood stabilizer or antipsychotics Primary options: Lithium, divalproex sodium, risperidone, quetiapine, aripiprazole, cariprazine, asenapine, paliperidone Secondary options: Carbamazepine, olanzapine, ziprasidone, haloperidol Treatment for episodic depression Bipolar I depression 1. Mood stabilizer and/or atypical APS (i) Primary options: quetiapine, lamotrigine, lithium, lurasidone, may add or may not add lithium or divalproex sodium 2. Switch to alternative first-line drug or combination therapy SEE ABOVE 3. Mood stabilizer or atypical APS + antidepressant (i) Primary options: lithium, divalproex sodium, quetiapine PLUS escitalopram or bupropion hydrochloride 4. Olanzapine/fluoxetine or cariprazine Treatment for episodic depression Bipolar 2 depression 1. Quetiapine 2. Mood stabilizer or antidepressant 3. Lithium, lamotrigine, sertraline, or venlafaxine Treatment for episodic patterns of euthymia (after stabilization) Bipolar I 1. Mood stabilizer and/or atypical APS (i) Lithium, quetiapine, divaloprex sodium, lamotrigine, asenapine, aripiprazole AND/OR quetiapine OR aripiprazole 2. Switch to OR ADD ON alternative first line drug SEE ABOVE 3. Alternative mood stabilizer and/or atypical APS (i) Olanzapine, carbamazepine, risperidone, paliperidone, lurasidone, ziprasidone AND/OR lithium OR divalproex sodium Treatment for episodic patterns of euthymia (after stabilization) Bipolar 2 1. Mood stabilizer or APS (i) Quetiapine, lithium, lamotrigine 2. Switch to alternative first-line drug SEE ABOVE 3. Venlafaxine Treatment for rapid-cycling mania 1. Mood stabilizer or atypical APS (a) Lithium, divalproex sodium, olanzapine, quetiapine 2. Combination therapy SEE ABOVE a) Carbamazepine side effects 1) Serious reactions: hypersensitivity, anaphylaxis, angioedema, drug rxn w/ eosinophilia and systemic sx, SJS, TEN, EM, pulmonary hypersensitivity, arrhythmia, syncope, AV block, aplastic anemia, agranulocytosis, thrombocytopenia, leukopenia, pancytopenia, hepatotoxicity, hyponatremia, SIADH, water intoxication, acute intermittent porphyria, pancreatitis, suicidality, withdrawal seizures and symptoms if abrupt D/C 2) Common reaction: dizziness, drowsiness, unsteadiness, nausea, vomiting, ataxia, constipation, pruritus, zerostomia, asthenia, rash, blurred vision, speech disturbance, HTN, tremor, muscle twitching, hyponatremia, photosensitivity, hypogammaglobulinemia 3) Carbamazepine induces its own metabolism (auto-induction) within the first month of treatment and accelerates the metabolism of other hepatically metabolized drugs. The half-life in chronic therapy, after autoinduction is complete, is about 10-20 hours. 4) ATAXIA = impaired balance/coordination, can be due to damage of brain, nerves, or muscles 5) Carbamazepine toxicity can be divided into the following three levels: (1) disorientation and ataxia at levels of 11-15 mg/L (2) aggression and hallucinations with levels of 15-25 mg/L (3) seizures and coma with levels above 25 mg/L. Lithium toxicity Toxicity can occur at levels 1.2 mEq/L 1) Acute Toxicity (1) Acute lithium toxicity occurs when someone not prescribed lithium but ingests it. Acute toxicity may carry less medical risk and less severe symptoms than the other types, depending on the amount taken, because lithium will clear out of your body more quickly when your system is not used to it 2) Chronic Toxicity (1) The chronic form of toxicity occurs when you take lithium daily, but your levels are at a toxic level. Possible causes are a dosage increase, being dehydrated, interactions with other medications, or problems with kidney function. This type of toxicity is less likely to be detected early than the other types, so more severe symptoms may appear before it's identified. Medications that can contribute to dehydration or cause your kidneys not to function as well as normal include diuretics, angiotensin-converting enzyme (ACE) inhibitors, and nonsteroidal anti-inflammatory drugs (NSAIDs). 3) Acute-on-Chronic Toxicity (1) When you regularly take lithium and you accidentally or deliberately take a higher dose than prescribed. Because the levels in your blood to make lithium effective and the levels that make it toxic are so close, the additional amount that causes acute-on-chronic toxicity doesn't have to be terribly high. This type of lithium toxicity is the Most Severe Form, with the highest potential for long-term consequences. Name the mood stabilizers that require therapeutic serum levels. Lithium Divalproex sodium Carbamazepine Nortriptyline ALL OTHERS DO NOT Name the 5 types of antidepressants. i) SSRIs - Selective Serotonin Reuptake Inhibitors ii) SNRIs - Serotonin & Norepinephrine Reuptake Inhibitors iii) TCAs - TriCyclic antidepressants iv) MAOIs - Monoamine Oxidase Inhibitors v) Atypical antidepressants SSRI selectively inhibits serotonin reuptake. although case fatality rates for SSRIs are low, citalopram has a higher mortality rate in overdose than other SSRIs. Citalopram exposures are about four times more likely to be fatal than sertraline or escitalopram SNRI exact mechanism of action is unknown; inhibits norepinephrine and serotonin reuptake TCA exact mechanism of action is unknown; inhibits norepinephrine and serotonin reuptake. TCAs are one of the common causes of a fatal drug overdose. They have a narrow therapeutic window so can be fatal at relatively lower doses and single tablet fatalities have been reported. Its most serious effects are cardiovascular and CNS instability. MAOI non-selectively inhibits monoamine oxidase exhibiting antidepressant effects. They should not be used with other antidepressant medication due to extensive drug-drug interaction. Atypical Antidepressants (1) Bupropion, NDRI - inhibits neuronal uptake or norepinephrine and dopamine (aminoketone) (2) Mirtazapine, TCA/TeCA - antagonizes alpha-2 adrenergic and serotonin 5-HT2 receptors (tetracyclic) (3) Nefazodone, serotonin modulator - antagonizes serotonin 5-HT2 receptors and inhibits norepinephrine and serotonin uptake (4) Trazodone, serotonin modulator - antagonizes serotonin 5-HT2A/C and alpha-1 adrenergic receptors; inhibits serotonin reuptake (5) Vilazodone, serotonin modulator - selectively inhibits serotonin reuptake and partially agonizes serotonin 5-HT1A receptors (6) Vortioxetine, serotonin modulator - selectively inhibits serotonin reuptake, antagonizes serotonin 5-HT3 receptors, and agonizes serotonin 5-HT1a receptors SS of severe depression psychotic, suicidal, severe psychomotor retardation impeding ADLs, catatonia, or severe agitation Severe Depression Treatment (1) Antidepressant + psychiatric referral and/or hospitalization and/or ECT Primary options: citalopram, escitalopram, fluoxetine, paroxetine, sertraline, desvenlafaxine, duloxetine, levominacipran, venlafaxine, buproprion hydrochloride, mirtazapine, vilzodone, vortioxetine (2) Can add immediate sx management with benzo and/or APS Lorazepam, clonazepam, risperidone, olanzapine, quetiapine, fluphenazine, trazodone (3) Switch to alternative antidepressant SS Moderate Depression Severe sx, signification impairment but no psychotic sx, NO Suicidal Ideations, no severe psychomotor retardation or agitation Moderate Depression Treatment (1) Anti-depressant ex. citalopram, escitalopram, fluoxetine, paroxetine, sertraline, desvenlafaxine, duloxetine, levominacipran, venlafaxine, buproprion hydrochloride, mirtazapine, vilzodone, vortioxetine May add immediate sx management with benzo and/or APS ex. Lorazepam, clonazepam, quetiapine, trazodone (2) Switch to alternative antidepressant SS Mild Depression low to moderate severity sx, partial impairment, no psychotic symptoms, no SI, no psychomotor retardation, or agitation Mild Depression Treatment (1) Consider an antidepressant ex. citalopram, escitalopram, fluoxetine, paroxetine, sertraline, desvenlafaxine, duloxetine, levominacipran, venlafaxine, bupropion hydrochloride, mirtazapine, vilazodone, vortioxetine (2) Switch to an alternative antidepressant if needed (3) St John's Wort if safe and pt is willing Treatment resistant/refractory depression (1) Reassess and switch to alternative antidepressant or try combination therapy ex. citalopram, escitalopram, fluoxetine, paroxetine, sertraline, desvenlafaxine, duloxetine, levominacipran, venlafaxine, bupropion hydrochloride, mirtazapine, vilazodone, vortioxetine, amitriptyline, desipramine, doxepin, imipramine, nortriptyline (2) Consider augmentation therapy ex. Lithium, aripriprazole, olanzapine/fluoxetine, brexpiprazole (3) MAOI ex. Isocarboxazid, phenelzine, selegiline transdermal, tranylcypromine (4) ECT SSRI side effects agitation, nausea, diarrhea, sexual problems, dizziness, headaches, insomnia, increased anxiety, exhaustion, diarrhea, dry mouth, tremors SNRI side effects headache, dizziness, nausea, heavy sweating, dry mouth, constipation, insomnia, sexual problems TCA side effects dry mouth, blurred vision, increased fatigue/sleepiness, weight gain, tremors, constipation, bladder problems, dizziness, increased heart rate MAOI side effects drowsiness, dry mouth, dizziness, headache, nausea, insomnia, diarrhea or constipation, weight gain, low blood pressure, tremors, increased sweating, low sex drive, inability to have an organism, difficulty starting urine flow They should not be used with other antidepressant medication due to extensive drug-drug interaction. NDRI side effects headache, insomnia, dry mouth, constipation, nausea, tiredness, tremor, increased sweating Esketamine (NCNMDARAs) dizziness, nausea, sedation, anxiety, increased blood pressure, disassociation, vomiting, feeling drunk, lack of energy Alpha1 adrenergic blockers (ex. Trazodone) common side effect. By reducing alpha-1-adrenergic activity of the blood vessels, these drugs may cause HYPOTENSION and interrupt the baroreflex response. Trazodone Receptor profile reduces levels of neurotransmitters associated with arousal effects, such as serotonin, noradrenaline, dopamine, acetylcholine, and histamine. Low-dose trazodone use exerts a sedative effect for sleep through antagonism of 5-HT2A receptor, H1 receptor, and alpha-1-adrenergic receptors. Trazodone is a mixed agonist and antagonist of various serotonin receptors, antagonist of adrenergic receptors, weak histamine H1 receptor antagonist, and weak serotonin reuptake inhibitor. SSRIs vs TCAs The SSRIs have a more favorable safety profile than the TCAs in both acute and long-term treatment of major depression. SSRIs have a favorable side-effect profile compared to TCAs and are associated with fewer treatment discontinuations. Unlike the TCAs, they do not cause anticholinergic, hypotensive or sedating reactions, and are not associated with impaired cognitive function. Their most common side-effects (nausea, vomiting, nervousness, insomnia, headache, and sexual dysfunction) are usually mild and typically disappear as treatment continues. The SSRIs also exhibit lower toxicity and lower lethality when taken in an overdose situation. Although the safety profiles of the principal SSRIs appear to be comparable, there is some data showing important differences in the severity and frequency of specific adverse events. Antidepressants Classes used for chronic pain TCAs, SNRIs, SSRIs Best Antidepressants for appetite loss TCAs, tetracyclic antidepressants - REMERON Best Antidepressants to avoid sexual dysfunction Bupropion, Nefazodone Antidepressants that lower seizure threshold Amoxapine, Bupropion, Clomipramine and Maprotiline. If pt has epilepsy, consider SSRIs/SNRIs first. Length of antidepressant treatment continue regimen 9 to 12 months after symptom remission