Test Bank for PMHNP Boards 2022 Questions and Answers Already Passed

1. Mood Disorders Most common psych illnesses 2. Primary characteristic is per- sistent disturbance in mood 3. Often occurs without precipi- tating event Major Depressive Disorder MDD 4. Object loss theory Fairbairn, Winnicott & guntrip 5. Aggression turned inward the- ory of MDD Freud 6. Cognitive Theory Beck 7. Learned Helplessness-Hope- lessness Theory Seligman 8. Genetic predisposition Strong genetic load for depression for child of depressed parent -having 3 fold in- crease in lifetime risk of MDD & 40% chance of depressive episode before age 18. 9. Endocrine dysfunction Theory Probably related to etiology of MDD 10. Sleep disturbances, appetite disturbances, libido distur- bances, lethargy, anhedonia are neurovegitative symptoms that are related to functions of the 11. Endocrine dysfunction and pregnancy 12. Hypothalamic-pituitary-adren- al axis (HPA) Hypothalamus and pituitary gland secre- tions A high incidence of postpartum mood dis- turbances is suggested with this A theory of MDD, may be a result of an abnormal stress response related to dys- regulation of this system 13. HPA axis Controls the physiological response to stress and is composed of interconnective feedback pathways between the hypothal- amus, pituitary gland, and adrenal gland. 14. Hypothalamus releases corticotropin-releasing hormone (CRH) 15. Adrenocorticotropin hormone (ACTH) Released by pituitary in response to CRH by hypothalamus 16. Cortisol Released by adrenal glands in response to ACTH by pituitary gland 17. Hyperactivity of the HPA axis Demonstrated to be present in individuals with MDD. May also have elevated cortisol levels 18. Elevated cortisol levels Over time damages the CNS by alter- ing neurotransmission and electrical signal conduction. Cortisol over time can cause changes in size and function of brain tissue 19. Dexamethasone suppression test (DST) 20. Hypovolemic hippocampus and hypovolemic prefrontal cortex-limbic striatal regions 21. Brain damage, including that from stroke and trauma 22. What is the Chronobiological theory of MDD 23. Circadian rhythms control these biological processes Not commonly used in clinical practice for screening of depression as it is too non specific. Abnormalities demonstrated by neu- roimaging in individuals with chronic and severe depression Depression is a acommon comorbidity in individuals who have experienced these events Desynchronization of the circadian rhythms produces the symptom constella- tion collectively called MDD Sleep-rest cycle disturbances * Increased cortisol secretions * that are frequent problems with depressed individuals REM abnormalities Increased emotional reactivity Frequent waking More intensified dreaming Diurnal variations to circadian-related be- haviors Decreased arousal and energy levels Decreased activity patterns * 24. Incidence of MDD 5% of U.S. population ages 18 and older each year. About 9.9 million Americans 25. Most common psychiatric ill- ness seen in primary care practices; only 50% of people receive treatment MDD 26. 25% women, 12% men Risk during reproductive years 27. Risk of MDD is for both genders below puberty and after menopause 28. MDD is (greater) or (lesser) source of morbidity for women than other illnesses. equal Greater 29. Fifteen percent (15%) Of people with MDD will commit suicide 30. People with MDD - Four times greater risk of premature death Than normal control population 31. Episodes of MDD do not vary Not true. Disease course is variable and can involve isolated episodes separated by many years, clusters of episodes or a severe episode with some remission of symptoms but with chronic symptoms per- sisting over time. 32. If untreated an episode of MDD Usually lasts 4 months or longer 33. Major Depressive Disorder Tends to be a chronic, recurrent illness 34. One year after initial diagnosis 40% of patients are symptom free 35. Risk of future episodes of MDD: First episode = 60% risk of 2nd Second episode = 70% risk of 3rd Third episode - 90% risk of 4th 36. Name 4 risk factors for MDD Family history (esp first degree relative); prior episode, female gender, postpartum period, medical comorbidity; single marital status; significant environmental stressors, esp multiple losses 37. Four to six weeks: Length of time for therapeutic effect of an- tidpressants 38. Appearance, speech, af- fect, mood, thought process, thought content (including suicidal thoughts/behaviors); cognition, orientation, memo- ry, concentration, abstraction, judgment 39. Endocrine Disorders implicat- ed in MDD 40. Infectious and inflammatory states implicated in MDD 41. Nutritional disorders implicat- ed in MDD 42. Psychiatric disorders com- monly associated with MDD Mental Status Exam Hypothyroidism, DM, hyperaldosteronism, and Cushing's/Addison's Disease Mono, AIDS, viral and bacterial pneumo- nia; systemic lupus erythematosus, tempo- ral arteritis, tuberculosis Pernicious anemia and pellagra Anxiety disorders, eating disorders, Bipo- lar disorder, substance abuse/depen- dence disorders 43. One should continue use of an- tidepressants for a minimum of 44. If patient has prior episodes of depression, than consider us- ing antidepressants 8-12 months For longer than 8-12 months 45. Medication and counseling Research demonstrates that the most ef- fective intervention is a combination of these two treatment modalities 46. Action primarily to increase serotonin levels in CNS by in- hibiting their reuptake: 47. Elevate serotonin and norepi- nephrine levels primarily by in- hibiting their reuptake 48. Elevate serotonin and norepi- nephrine levels primarily by in- hibiting MAO, the enzyme that destroys neurotransmitters 49. Serotonin Norepinephrine Re- uptake Inhibitors (SNRIs) 50. Norepinephrine Dopamine Re- uptake Inhibitors (NDRIs) 51. Serotonin Agonist and Reup- take Inhibitors (SARIs) 52. SSRIs side effects Selective Serotonin Reuptake Inhibitors (SSRIs) Tricyclic Antidepressants (TCAs) Monoamine Oxidase Inhibitors (MAOIs) Inhibit dual reuptake; action very selec- tive on neurotransmitters; elevate sero- tonin and norepinephrine levels by inhibit- ing their reuptake. Inhibit dual reuptake; action very selective on neurotransmitters; elevate dopamine and norepinephrine levels by inhibiting their reuptake. Dual action; agonist of serotonin 5HT-2 receptors; action very selective on neuro- transmitters; elevates serotonin levels by inhibiting serotonin reuptake Most common side effects of this class: gi upset, sexual dysfunction, nervousness, headache and dry mouth 53. Name the six SSRIs Celexa, Lexapro, Prozac, Luvox, Paxil (Pexeva), Zoloft. 54. Which is safer in overdose, Paxil or Nortriptyline? 55. SSRI's are also effective for treatment of panic disorder, OCD, bulimia, GAD social pho- bia and Paxil. SSRIs are safer in overdose than TCAs. PTSD and premenstrual dysphoric disor- der 56. Which SSRI has long half-life? Prozac 57. Two SSRIs have potential for teratogenic effects, name them. 58. This SSRI has a black box warning for liver toxicity. 59. GI upset, sexual dysfunction, nervousness, headache and dry mouth are common side ef- fects associated with... 60. Second line drugs for treat- ment of MDD: Paxil and Zoloft Luvox SSRIs Tricyclic Antidepressants (TCAs) 61. The side effect profile for TCAs Dirty side-effect profile 62. Dirty side effect profile con- tributes to 63. Anticholinergic dirty side ef- fects associated with TCA's: Poor patient compliance Dry mouth, blurred vision, constipation, memory problems. Caused due to mus- carinic receptor blockade. 64. Antiadrenergic dirty side ef- fects associated with TCAs: 65. Antihistaminergic dirty side ef- fects associated with TCAs: 66. Cardiac side effects associat- ed with TCAs: Orthostatic hypotension (from alpha 1 re- ceptor blockade) Sedation and weight gain from histamine receptor blockade EKG changes and cardiac dysrythmias 67. TCAs are inexpensive and.... Available in generic form 68. TCAs tend to "slow down" the gut, so Are good for patients with gi problems 69. Lethal dose of TCA's 1000 mg or more (usually equal to a week's supply of an average dose). 70. Avoid abrupt withdrawal of TCAs due to 71. TCAs should not be prescribed with 72. What can happen if you pre- scribe TCAs with an SSRI due to Significant abstinence syndrome MAOIs due to potential for lethal reaction Risk of elevated TCA concentration in the bloodstream - need to monitor TCA levels 73. Name the eight TCAs: Elavil, Anafranil, Norpramin, Sinequan, Tofranil, Pamelor, Vivactil and Surmontil. 74. A TCA also used for enuresis and ADHD 75. A TCA also used for enuresis and separation anxiety Pamelor Tofranil (imipramine) 76. A TCA also used for insomnia Sinequan (doxepin) 77. Two TCAs are also used for ADHD: Pamelor & Norpramin (desipramine) 78. A TCA approved for OCD: Anafranil (clomipramine) 79. Dose Anafranil no higher than mg. due to increased seizure risk. 80. A TCA with multiple uses that include chronic pain, in- somnia, sciatica, fibromyalgia, trigeminal neuralgia and dia- betic neuropathy. 81. Never first-or second-line agents for MDD 82. Occurs with MAOIs are taken with foods containing tyramine 250 mg/day Elavil. MAOIs Hypertensive crisis 83. Tyramine A dietary precursor to norepinephrine 84. When monoamine oxidase is inhibited 85. What is released when tyra- mine exerts vasopressor ef- fects? Tyramine exerts a strong vasopressor ef- fect Catecholamines, epinephrine, and norep- inephrine which will increase blood pres- sure and heart rate 86. Certain medications can cause Meperidine, SSRIs, decongestants, TCAs, hypertensive crisis and possi- ble death when administered with an MAOIs. Name them: 87. Symptoms of hypertensive cri- sis: 88. What medication is given to treat hypertensive crisis? atypical antipsychotics; St. John's wort, L-trytophan, Ritalin, asthma medications. Sudden, explosive-like headache, usual- ly in occipital region; increased BP, facial flushing, palpitations; pupillary dilation; di- aphoresis and fever. Phentolamine 89. Phentolamine Binds with norepinephrine receptor sites, blocks norepinephrine. 90. MAOI's are in over- dose. 91. Dirty side-effect profile and stringent dietary restrictions promote . 92. In addition to hypertensive cri- sis, clinically significant side effects of MAOIs include: Not safe. Poor patient compliance Insomnia, weight gain, anticholinergic side effects, light-headedness and dizziness, and sexual dysfunction. 93. MAOI, generic selegiline Ensam 94. MAOI, generic isocarboxazid Marplan 95. MAOI, generic phenelzine Nardil 96. MAOI, generic tranylcypromine Parnate 97. No dietary restrictions with 6 mg dosage Ensam transdermal patch (Restrictions needed for 12 mg patch) 98. MAOI also used for panic disor- Marplan, Nardil and Parnate. der, phobic disorders, and se- lective mutism 99. Oral MAOIs should be given in doses. Divided doses, bid and qid. 100. Two SNRIs: Effexor and Cymbalta 101. NDRI: Wellbutrin 102. Wellbutrin and Wellbutrin XL dosing: 150-450 mg daily. 103. Wellbutrin, an NDRI antidepressant Headache, nervousness, tremors, tachycardia, insom- nia, decreased appetite are side effects from: 104. Wellbutrin, bupropion, is also used for ADHD and . 105. Wellbutrin SR requires . Smoking cessation. BID dosing. 106. Wellbutrin can increase: Energy level 107. Wellbutrin in contraindicated in patients with eating disor- ders and . Seizures. 108. Dosing for Wellbutrin SR: 150-400 mg/day 109. Remeron has an rela- tionship between dosage and sedation. 110. Must monitor LFT's with this antidepressant. 111. Most commonly used as hyp- notic; not well tolerated at an- tidepressant dosage due to sedation; may potentially pro- long QTc interval. 112. Can raise BP and is a potent in- hibitor of cyp450 system; safer in overdose than TCAs 113. Effexor should be tapered when stopping the drug due to... Inverse Serzone (nefazodone) Trazodone (Desyrl) (an SARI) Effexor (an SNRI) Significant discontinuation syndrome 114. Could possibly elevate LFTs, can possibly elevate BP, usu- ally given once daily, an SNRI that is helpful in pain control: 115. There is strong potential for discontinuation syndrome with Cymbalta so the drug 116. Non-pharmacological treat- ment for depression involving 6-12 initial treatments 117. Neurotransmitter theory of ECT Cymbalta Should not be stopped abruptly .ECT.. Increases dopamine, serotonin, and nor- epinephrine 118. Neuroendocrine theory of ECT Releases hhormones such as prolactin, thyroid-stimulating hormone, pituitary hor- mones, endophins, and adrenocorticotrop- ic hormone 119. Anticonvulsant theory of ECT Exerts an anticonvulsant effect, which then produces an antidepressant effect. 120. Contraindications for ECT Cardiac disease, compromised pulmonary status, h/o brain injury or brain tumor, anesthesia medical complications 121. Adverse effects of ECT Possible cardiovascular effects, systemic effects (headaches, anorexia, muscle aches, drowsiness) and cognitive effects such as confusion and memory difficulties 122. Therapies used with the de- pressed individual 123. Identify 12 risk factors for sui- cide CBT and Brief (Solution focused) Therapy, Group therapy, Family therapy >45 & male; >55 & female; divorced, sin- gle, separated; white; living alone, psychi- atric disorder; physical illness; substance 124. Symptoms of depression that may be more pronounced in children: 125. Core symptoms of depression that are less common in chil- dren before onset of puberty: abuse; previous attempt; FH of suicide; re- cent loss, male gender. Irritability, somatic complaints and social withdrawal. Psychosis, motor retardation, hypersom- nia and increased appetite. 126. In children, MDD has a strong separation anxiety component 127. Population that responds bet- ter to SSR's than to TCA's: 128. Children taking antidepres- sants should be monitored closely for 129. Individuals admitted to long term care facilities are % more likely to die within the first year than the normal con- trol population 130. It is important to complete a for elder- ly individuals with depression. 131. One reasons to complete a functional assessment on an elderly patient is to 132. Drug combinations that may cause serotonin syndrome: 133. Autonomic instability, restless- ness, agitation, myoclonis, hy- perreflexia, hyperthermia, di- Children Suicide 65 Functional Assessment Identify whether problems are related to dementia or depression. SSRIs & MAOIs; Durg and herbal interac- tions; SSRIs & St. John's wort Symptoms of serotonin syndrome aphoresis; altered sensorium, tremor, cills, diarrhea and cramps, ataxia, headache and insomnia: 134. Flu-like symptoms, fatigue and lethargy, myalgia, de- creased concentration, nau- sea/vomiting, impaired memo- ry, shock-like sensations; irri- tability, anxiety, insomnia, cry- ing without provocation, dizzi- ness and vertigo: 135. Why should TCAs be discon- tinued slowly? 136. Patients who have had two or more episodes of MDD usually require Symptoms of discontinuation syndrome Clients can get cholinergic rebound syn- drome: nausea, gi upset, diaphoresis, myalgias, especially of neck muscles. Lifelong medication. 137. Time criteria for MDD Symptoms present over a two week period 138. Symptom criteria for MDD Either depressed mood OR loss of interest or pleasure AND four other symptoms: Weight loss/gain, insomnia/hy- persomnia, psychomotor agitation/retar- dation, fatigue/loss of energy, feelings of worthlessness/guilt, poor concentra- tion/thinking, recurrent thoughts of death.