PHAR 191 exam 2 Word Scramble
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Question | Answer |
Categories of symptoms of MDD | Emotional, physical, cognitive, psychotic (in severe), "atypical" |
MOA of TCAs | 5-HT and NE reuptake inhibition. Alpha-1, histamine-1, and muscarinic cholinergic blockade. |
MOA of SNRIs | 5-HT and NE reuptake inhibition. |
MOA of SSRIs | 5-HT reuptake inhibition |
MOA of trazodone | 5-HT reuptake inhibition. 5-HT2a, alpha-1, and histamine-1 blockade |
MOA of bupropion | DA and NE reuptake inhibition |
MOA of mirtazapine | Alpha-2, 5-HT2a, 5-HT2C, 5-HT3, and histamine-1 blockade |
MOA of MAOIs | Inhibit monoamine oxidase |
Antidepressant most likely associated with sedation | Trazodone, mirtazapine |
Antidepressants most likely associated with sexual dysfunction | TCAs, SSRIs |
Antidepressants most likely associated with weight gain | TCAs |
Antidepressant most likely associated with hepatotoxicity | Duloxetine |
Antidepressant most likely associated with increased blood pressure | Venlafaxine, desvenlafaxine |
Antidepressant most likely associated with seizures | Bupropion (CI) |
First-line antidepressant options for depression | SSRIs, bupropion SR/XL, mirtazapine, SNRIs |
Antidepressant augmentation options | Lithium, triiodthyronine, aripiprazole |
Time course to therapeutic effect for antidepressants | 2-4 weeks before improvement in emotional symptoms, as long as 6-8 weeks for full effects |
Potential duration of therapy of antidepressants | additional 4-9 months in continuation phase to prevent relapse |
Symptoms of antidepressant withdrawal | Sleep disturbances, anxiety, fatigue, mood changes, malaise, GI disturbances, return of depressive symptoms |
Lifetime prevalence of depression | 16.2% |
Gender most likely to develop depression | Females (2:1) |
Average age of onset of depression | Mid-twenties |
What psychiatric comorbidities occur most frequently with depression | Anxiety disorders and substance-use disorders |
What causes depression? | Exact cause unkown. Associated with genetics, chornic stresses, and deficiency in monoamines (NE, 5HT, DA) |
Emotional symptoms of depression | Sadness, anhedonia, pessimism, feeling of emptiness, irritability, anxiety, worthlessness, thoughts of death/suicidal ideation (SI) |
Physical symptoms of depression | Disturbed sleep, change in appetite/weight, psychomotor changes, decreased energy, fatigue, bodily aches and pain |
Cognitive symptoms of depression | Impaired concentration, indecisiveness, poor memory |
Psychotic symptoms of depression | Hallucinations, delusions |
"Atypical features" symptoms of depression | Reactive mood, significant increase in appetite/weight gain, hypersomnia, heavy feelings in arms or legs, sensitivity to interpersonal rejection |
Define reactive mood | Mood improves in response to positive events |
What medical conditions might cause/contribute/exacerbate depressive symptoms | Bipolar, hypothyroidism, neoplasms, anemia, infections, electrolyte disturbances, neurological disoders |
What medications might cause/contribute/exacerbate depressive symptoms | CNS depressants, corticosteroids, contraceptives, gonadotropin-releasing hormone agonists, interferon-alpha, interluekin-2, mefloquine, isotretinoin, propranolol, sotalol |
What are the goals of treatment in depression? | Resolution of depressive symptoms, return to euthmia, prevent relapse/recurrence of symptoms, prevent suicidal attempts, improve QOL, normalize functioning areas such as work/relationships, avoid/minimize ADR, reduce health care costs |
Nonpharmacologic therapies available for individuals having depression | Interpersonal therapy, cognitive behavioral therapy, ECT, light therapy, VNS |
What antidepressants have less likelihood of causing sexual side effects? | Bupropion, mirtazapine, nefazodone |
Which antidepressant may cause priapism? | Trazodone |
Which antidepressants have a short half-life? | nefazodone, venlafaxine |
Which antidepressant has a long half-life? | Fluoxetine |
Symptoms of serotonin syndrome | Confusion, restlessness, fever, abnormal muscle movements, hyper-reflexia, sweating, diarrhea, shivering |
Factors to take into account when selecting an antidepressant | Pt hx of response, hx of 1st degree relative response, ADR profile, drug-drug/disease interactions, psychiatric comorbidities, potential for ODing, affordability |
Antidepressants with greatest reproductive safety data | Fluoxetine, citalopram, TCAs |
Antidepressants chosen frequently to treat geriatric depression | SSRIs |
Antidepressants considered intially in pediatric population | SSRIs |
Antidepressants with narrow therapeutic indices | TCAs and MAOIs |
Which drugs are SNRIs? | Duloxetine, venlafaxine, desvenlafaxine |
Which drug is an NDRI? | Bupropion |
Symptoms of GAD | Excessive anxiety or worrying (>6months), restlessness, easily fatigued, poor concentration, irritability, muscle tension, insomnia, unsatisfying sleep |
Role of antidepressants in treating anxiety disorders | Considered first-line agents in management of chronic GAD. |
Antidepressants recommended first line in the management of GAD | SNRI or SSRI |
MOA of benzodiazepines | Enhance transmission of GABA (inhibitor NT) |
MOA of buspirone | 5-HT1a partial agonist-reduce presynaptic 5-HT firing |
Therapeutic uses of benzodiazepines | Acute treatment of GAD when short-term relief is needed, as an adjunct during initiation of antidepressant therapy, or to improve sleep |
Therapeutic uses of buspirone | |
Abuse potential of benzodiazepines | Abuse potential! |
Abuse potential of buspirone | No abuse potential |
Onset of action of benzodiazepines | Fast-acting |
Onset of action of buspirone | Graudal (ie 2 weeks) |
Adverse effects of benzodiazepines | CNS depressive effects, cognitive effects, confusion, irritability, aggression, excitement, withdrawal symptoms, rebound symptoms |
Lifetime prevalence of GAD | 5.7% |
Gender more likely to develop anxiety | Females (2:1) |
Average age of onset for GAD | 24-31 years |
Psychiatric comorbidities that occur most frequently with anxiety disorders | Depression, alcohol or substance use disorders, other co-occuring anxiety disorders |
What causes anxiety? | Anxiety is normal response to stressful or fearful circumstances, allowing to adapt/manage the situation. |
Goals of treatment for GAD | Acutely reduce severity and duration of anxiety symptoms and restore overall functioning. Long-term, achieve and maintain remission |
What medical conditions can cause/contribute/exacerbate anxiety symptoms? | Psychiatric, neurologic, cardiovascular, endocrine and metabolic, respiratory, carcinoid syndrome, anemias, lupus |
What medications can cause/contribute/exacerbate anxiety symptoms? | Anticonvulsants, antidepressants, anti-HTN, antimicrobials, antiparkinson, bronchodilator, corticosteorids, decongestants, herbals, NSAIDs, stimulants, thyroid, toxicity, abrupt withdrawal of CNS depressants |
Nonpharmacologic therapies available for pt with GAD | Psychoeducation, regular exercise, stress management, psychoterapy |
What is recommended if 1st line for GAD fails? | Switch to another SNRI or SSRI |
Which symptoms of anxiety do antidepressants reduce? | Psychic symptoms (worry and apprehension) with modest effect on autonomic or somatic symptoms (tremor, rapid heart rate, and/or sweating) |
Onset of antianxiety effect with antidepressants | 2-4 weeks |
Which antidepressants are used in the management of GAD? | SSRI (citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline) SNRI (venlafaxine XR, duloxetine) TCA (imipramine) |
Which symptoms of anxiety do benzos reduce? | Somatic symptoms (tremor, rapid heart rate, and/or sweating) |
Disadvantages of benzos | lack of effectiveness in treating depression, risk for dependency and abuse, potential interdose rebound anxiety, avoid in pt with chemical dependency |
Which benzos are preferred in patients having hepatic dysfunction or in the elderly? | lorazepam and oxazepam |
Sleep hygiene principles | Regular sleep schedule, exercise frequently but not immediately before bed, avoid alcohol/stimulants in late afternoon/pm, comfortable sleeping environment (dark, quiet, free of intrusions), avoid large quantities food/liquids immediately before bed |
Duration of action of eszopiclone | 8 hours |
Adverse effects of first line agents for insomnia | residual sedation, grogginess, psychomotor impairment, anterograde amnesia, rebound insomnia with D/C |
Antidepressants prescribed for insomnia | Trazodone, amitriptyline, mirtazapine, nefazodone, doxepin |
Gender more likely to develop insomnia | Females (1.5:1) |
Prevalence of chronic insomnia | 10% |
Medical conditions that may cause/contribute/exacerbate insomnia | Pain, thyroid abnormalities, asthma, reflux |
Medications that may cause/contribute/exacerbate insomnia | SSRIs, steroids, stimulants, beta-agonists |
Characterize insomnia | Difficulty falling asleep, frequent nocturnal awakenings, early-morning awakenings, which may result in daytime impairments in concentration or performance |
Transient insomnia | A few days |
Short-term insomnia | Less than 3 weeks |
Chronic insomnia | >1 month |
Treatment goals for insomnia | restoration of normal sleep patterns, elimination of daytime sequelae, improved QOL, prevent complications/ADR from therapy |
Agents recommended 1st line for insomnia? | Benzodiazpine receptor agonists, zolpidem, zaleplon, eszopiclone |
Duration of action of temazepam | 7 hours |
Duration of action of zaleplon | 6 hours |
Duration of action of zolpidem | 7-8 hours |
Advantage of eszopiclone | Can be used for up to 6 months for chronic insomnia |
Advantages of temazepam | Well-tolerated, inexpensive |
Advantages of zaleplon | Short-acting, only for difficulty falling asleep |
Advantage of zolpidem | No effects on sleep architecture |
How does Ramelteon work? | Melatonin receptor agonist- good for insomnia characterized by difficulty with sleep onset |
Reasons why antidepressants are unappealing option for insomnia | at doses for sleep, only mirtazapine exhibits significant antidepressant activity. lack clinical study proving efficacy. frequent and unpleasant SE. |
Symptoms of mania | 1-week period or greater: Abnormal and persistent elevated mood, with 3 of following: grandiosity, FOI, distractible, increase activity/motor activity/agitation, excessive involvement in activities pleasurable but high-risk for serious consequence |
Medications and substances that may cause/contribute/exacerbate symptoms of mania | Corticosteroids, diltiazem, levodopa, oral contraceptives, zidovudine, anabolic steroids, hallucinogens, stimulants |
Potential adverse effects of lithium | GI upset, tremor, polyuria, polydipsia, hypothyroidism, poor concentration, rash, alopecia, worsening of psoriasis, weight gain, metallic taste, benign reversible leukocytosis; cause/worsen arrhythmias |
Drug interactions of lithium | Thiaizde diuretics, NSAIDs, ACEIs |
Potential adverse effects of valproic acid | GI upset, tremor, DW, weight gain, alopecia, change hair color/texture, hair loss, polycystic ovarian syndrome, thrombocytopenia; hepatotoxicity, pancreatitis |
Drug interactions of valproic acid | Anticonvulsants, TCAs, lamotrigine |
Potential adverse effects of carbamazepine | DW, DZ, ataxia, lethargy, confusion, GI upset, antidiuretic, hyponatremia, mild elevation in liver enyzmes; diplopia, dysarthria, leuokopenia; hepatitis, aplastic anemia, agranulocytosis |
Drug interactions of carbamazepine | Induce metabolism of anticonvulsants, antipsychotics, antidepressants, OCs, antiretrovirals. Clozapine. Antidepressants, macrolides, azoles, grapefruit-inhibit metabolism of carbamazepine |
Baseline monitoring parameters for lithium | pregnancy, ECG if >40 or cardiac disease, CBC, glucose, lipids, weight, renal function, thyroid function, electrolytes, dermatologic |
Baseline monitoring parameters for valproic acid | Pregnancy, drug abuse, CBC, glucose, lipids, weight, LFTs, dermatologic |
Baseline monitoring parameters for carbamazepine | Pregnancy, drug abuse, CBC, LFT, renal function, electrolytes, dermatologic |
Routine monitoring parameters for lithium | Every 6-12 months: lithium level, weight, CBC, renal function, thyroid function, electrolytes, dermatologic |
Routine monitoring parameters for valproic acid | CBC, glucose, lipids, weight, LFTs, dermatologic |
Routine monitoring parameters for carbamazepine | CBC, LFT, electrolytes, dermatologic |
Estimated prevalence of schizophrenia | 1% |
Symptoms of schizophrenia | Delusions, hallucinations, disorganized speech, grossly disorganized, catatonic behavior, negative symptoms (flat affect, alogia, avolition) |
Differences between typical and atypical antipsychotics | SGAs have lower risk of motor side effects, may offer greater benefits for affective, negative, and cognitive symptoms, and may prolong the time to psychotic relapse |
Potential EPS | Akathisia (motor and/or subjective restlessness) Dystonia (muscle spasm) Pseudoparkinsonism (akinesia, tremor, rigidity) TD (movement disorder) NMS (severe muscle rigidity, autonomic instability, altered consciousness) |
Medications used to treat EPS | Anticholinergic medications (benztropine, trihexyphenidyl, diphenhydramine) |
Medications sometimes effective for akathisia | Beta-blockers |
Antipsychotics with greatest association for EPS | Haloperidol, risperidone, fluphenazine |
Antipsychotics with greatest association for prolactin elevation | risperidone |
Antipsychotics with greatest association for seizures | Clozapine, thioridazine |
Antipsychotics with greatest association for QTc prolongation | Ziprasidone, thioridazine |
Antipsychotics with greatest association for hyperglycemia | Clozapine, olanzapine |
Antipsychotics with greatest association for hyperlipidemia | Clozapine, olanzapine |
Antipsychotics with greatest association for weight gain | Clozapine, olanzapine |
How often should weight be checked in patients taking SGAs? | Baseline, week 4, week 8, week 12, and quarterly |
How often should blood pressure and glucose be checked in patients taking SGAs? | Baseline, week 12, and annually |
How often should lipids be checked in patients taking SGAs? | Baseline, week 12, and every 5 weeks |
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