PMHNP Final Exam Guide 2026: Psychopharmacology & DSM-5-TR Questions, Exams of Health psychology

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CMN 552

Final Exam

Comprehensive Guide

1. Identify symptoms, characteristics, and potential complications of Bipolar Postpartum. (Page 486- 487??)

“Postpartum psychosis” typically resembles a manic or mixed mood episode with psychotic symptoms and is strongly associated with bipolar I disorder.

With peripartum onset: This specifier is applied to the current manic, hypomanic, or major depressive episode in bipolar I disorder (or the most recent manic, hypomanic, or major depressive episode if bipolar I disorder is currently in partial or full remission) or to the current hypomanic or major depressive episode in bipolar II disorder (or the most recent hypomanic or major depressive episode if bipolar II disorder is currently in partial or full remission) if onset of mood symptoms occurs during pregnancy or in the 4 weeks following delivery.

Note: Mood episodes can have their onset either during pregnancy or postpartum. About 50% of postpartum major depressive episodes begin prior to delivery. Thus, these episodes are referred to collectively as peripartum episodes.

Between conception and birth, about 9% of women will experience a major depressive episode. The best estimate for prevalence of a major depressive episode between birth and 12 months postpartum is just below 7%.

Peripartum-onset mood episodes can present either with or without psychotic features. Infanticide (a rare occurrence) is most often associated with postpartum psychotic episodes that are characterized by command hallucinations to kill the infant or delusions that the infant is possessed, but psychotic symptoms can also occur in severe postpartum mood episodes without such specific delusions or hallucinations.

Postpartum mood (major depressive or manic) episodes with psychotic features appear to occur in from 1 in 500 to 1 in 1,000 deliveries and may be more common in primiparous women. The risk of postpartum episodes with psychotic features is particularly increased for women with prior postpartum psychotic mood episodes but is also elevated for those with a prior history of a depressive or bipolar disorder (especially bipolar I disorder) and those with a family history of bipolar disorders.

Once a woman has had a postpartum episode with psychotic features, the risk of recurrence with each subsequent delivery is between 30% and 50%. Postpartum episodes must be differentiated from delirium occurring in the postpartum period, which is distinguished by a fluctuating level of awareness or attention.

Peripartum-onset depressive disorders must be distinguished from the much more common “maternity blues,” or what is known in lay terms as “baby blues.” Maternity blues is not considered to be a mental disorder and is characterized by sudden changes in mood (e.g., the sudden onset of tearfulness in the absence of depression) that do not cause functional impairment and that are likely caused by physiological changes occurring after delivery. It is temporary and self-limited, typically improving quickly (within a week) without the need for treatment. Other symptoms of maternity blues include sleep disturbance and even confusion that can occur shortly after delivery.

Perinatal women may be at higher risk for depressive disorders due to thyroid abnormalities as well as other medical conditions that can cause depressive symptoms. If the depressive symptoms are judged to be due to another medical condition related to the perinatal period, depressive disorder due to another medical condition should be diagnosed instead of a major depressive episode, with peripartum onset.

episodes

~ 20% of people with BP disorder have rapid cycling.

~ Most rapid cyclers are women (90%).

• Identifying rapid cycling is important.
• Antidepressants may accelerate the cycling.
• Persons with rapid cycling have a poorer prognosis.

5. What are the diagnostic criteria and characteristics of cyclothymia in adolescents. (Pg 468 – 69 combined readings exam 1)

A. For at least 2 years (at least 1 year in children and adolescents) there have been numerous periods with hypomanic symptoms that do not meet criteria for a hypomanic episode and numerous periods with depressive symptoms that do not meet criteria for a major depressive episode.

B. During the above 2-year period (1 year in children and adolescents), Criterion A symptoms have been present for at least half the time and the individual has not been without the symptoms for more than 2 months at a time.

C. Criteria for a major depressive, manic, or hypomanic episode have never been met.

D. The symptoms in Criterion A are not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder.

E. The symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).

F. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Specify if: With anxious distress (see pp. 169–170)

The essential feature of cyclothymic disorder is a chronic, fluctuating mood disturbance involving numerous periods of hypomanic symptoms and periods of depressive symptoms (Criterion A). The hypomanic symptoms are of insufficient number, severity, pervasiveness, and/or duration to meet full criteria for a hypomanic episode, and the depressive symptoms are of insufficient number, severity, pervasiveness, and/or duration to meet full criteria for a major depressive episode. During the initial 2-year period (1 year for children or adolescents), the symptoms must be persistent (present more days than not), and any symptom-free intervals last no longer than 2 months (Criterion B). The diagnosis of cyclothymic disorder is made only if the criteria for a major depressive, manic, or hypomanic episode have never been met (Criterion C).

If an individual with cyclothymic disorder subsequently (i.e., after the initial 2 years in adults or 1 year in children or adolescents) experiences a major depressive, manic, or hypomanic episode, the diagnosis changes to major depressive disorder, bipolar I disorder, or other specified or unspecified bipolar and related disorder (subclassified as hypomanic episode without prior major depressive episode), respectively, and the cyclothymic disorder diagnosis is dropped.

The cyclothymic disorder diagnosis is not made if the pattern of mood swings is better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders (Criterion D), in which case the mood symptoms are considered associated features of the psychotic disorder. The mood disturbance must also not be attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism) (Criterion E). Although some individuals may function particularly well during some of the periods of hypomania, over the prolonged course of the disorder, there must be clinically significant distress or impairment in social, occupational, or other important areas of

changes in appetite or weight, sleep, and psychomotor activity; decreased energy; feelings of worthlessness or guilt; difficulty thinking, concentrating, or making decisions; or thoughts of death, suicidal ideation, a suicide attempt, or a specific plan for suicidal behavior. To count toward a diagnosis of a major depressive episode, a symptom must either be newly present or have clearly worsened compared with the individual’s pre-episode status. Moreover, the symptoms must occur nearly every day, for at least 2 consecutive weeks, with the exception of thoughts of death and suicidal ideation, which must be recurrent, and attempting suicide or making a specific plan, which only needs to occur once. The episode must be accompanied by clinically significant distress or impairment in social, occupational, or other important areas of functioning. For some individuals with milder episodes, functioning may appear to be normal but requires markedly increased effort. The presenting complaint is often insomnia or fatigue rather than depressed mood or loss of interest; thus, the failure to probe for accompanying depressive symptoms can result in under diagnosis. Fatigue and sleep disturbance are present in a high proportion of cases; psychomotor disturbances are much less common but are indicative of greater overall severity, as is the presence of delusional or near-delusional guilt.

The mood in a major depressive episode is often described by the individual as depressed, sad, hopeless, discouraged, or “down in the dumps” (Criterion A1). In some cases, sadness may be denied at first but may subsequently be elicited by interview (e.g., by pointing out that the individual looks as if he or she is about to cry). In some individuals who complain of feeling “blah,” having no feelings, or feeling anxious, the presence of a depressed mood can be inferred from the individual’s facial expression and demeanor. Some individuals emphasize somatic complaints (e.g., bodily aches and pains) rather than reporting feelings of sadness. Many individuals report or exhibit increased irritability (e.g., persistent anger, a tendency to respond to events with angry outbursts or blaming others, an exaggerated sense of frustration over minor matters). In children and adolescents, an irritable or cranky mood may develop rather than a sad or dejected mood. This presentation should be differentiated from a pattern of irritability when frustrated.

Diminished interest or pleasure in usual activities is nearly always present, at least to some degree. Individuals may report feeling less interested in hobbies, “not caring anymore,” or not feeling any enjoyment in activities that were previously considered pleasurable (Criterion A2). Family members often notice social withdrawal or neglect of pleasurable avocations (e.g., a formerly avid golfer no longer plays, a child who used to enjoy soccer finds excuses not to practice). In some individuals, there is a significant reduction from previous levels of sexual interest or desire.

Appetite change may involve either a reduction or an increase. Some depressed individuals report that they have to force themselves to eat. Others may eat more and may crave specific foods (e.g., sweets or other carbohydrates). When appetite changes are severe (in either direction), there may be a significant loss or gain in weight, or, in children, a failure to make expected weight gains may be noted (Criterion A3).

Sleep disturbance may take the form of either difficulty sleeping or sleeping excessively (Criterion A4). When insomnia is present, it typically takes the form of middle insomnia (i.e., waking up during the night and then having difficulty returning to sleep) or terminal insomnia (i.e., waking too early and being unable to return to sleep). Initial insomnia (i.e., difficulty falling asleep) may also occur. Individuals who present with oversleeping (hypersomnia) may experience prolonged sleep episodes at night or increased daytime sleep. Sometimes the reason that the individual seeks treatment is for the disturbed sleep.

Psychomotor changes include agitation (e.g., the inability to sit still, pacing, hand-wringing; or pulling or rubbing of the skin, clothing, or other objects) or retardation (e.g., slowed speech, thinking, and body movements; increased pauses before answering; speech that is decreased in volume, inflection, amount, or variety of content, or muteness) (Criterion A5). The psychomotor agitation or retardation must be severe enough to be observable by others and not represent

merely subjective feelings. Individuals who display either psychomotor disturbance (i.e., psychomotor agitation or retardation) are likely to have histories of the other.

Decreased energy, tiredness, and fatigue are common (Criterion A6). An individual may report sustained fatigue without physical exertion. Even the smallest tasks seem to require substantial effort. The efficiency with which tasks are accomplished may be reduced. For example, an individual may complain that washing and dressing in the morning are exhausting and take twice as long as usual. This symptom accounts for much of the impairment resulting from major depressive disorder, both during acute episodes and when remission is incomplete.

The sense of worthlessness or guilt associated with a major depressive episode may include unrealistic negative evaluations of one’s worth or guilty preoccupations or ruminations over minor past failings (Criterion A7). Such individuals often misinterpret neutral or trivial day-to- day events as evidence of personal defects and have an exaggerated sense of responsibility for untoward events. The sense of worthlessness or guilt may be of delusional proportions (e.g., an individual who is convinced that he or she is personally responsible for world poverty). Blaming oneself for being sick and for failing to meet occupational or interpersonal responsibilities as a result of the depression is very common and, unless delusional, is not considered sufficient to meet this criterion.

Many individuals report impaired ability to think, concentrate, or make even minor decisions (Criterion A8). They may appear easily distracted or complain of memory difficulties. Those engaged in cognitively demanding pursuits are often unable to function. In children, a precipitous drop in grades may reflect poor concentration. In elderly individuals, memory difficulties may be the chief complaint and may be mistaken for early signs of a dementia (“pseudodementia”). When the major depressive episode is successfully treated, the memory problems often fully abate. However, in some individuals, particularly elderly persons, a major depressive episode may sometimes be the initial presentation of an irreversible dementia.

Thoughts of death, suicidal ideation, or suicide attempts (Criterion A9) are common. They may range from a passive wish not to awaken in the morning or a belief that others would be better off if the individual were dead, to transient but recurrent thoughts of dying by suicide, to a specific suicide plan. More severely suicidal individuals may have put their affairs in order (e.g., updated wills, settled debts), acquired needed materials (e.g., a rope or a gun), and chosen a location and time to accomplish the suicide. Motivations for suicide may include a desire to give up in the face of perceived insurmountable obstacles, an intense wish to end what is perceived as an unending and excruciatingly painful emotional state, an inability to foresee any enjoyment in life, or the wish to not be a burden to others. The resolution of such thinking may be a more meaningful measure of diminished suicide risk than denial of further plans for suicide.

The degree of impairment associated with a major depressive episode varies, but even in milder cases, there must be either clinically significant distress or some interference in social, occupational, or other important areas of functioning (Criterion B). If impairment is severe, the individual may lose the ability to function socially or occupationally. In extreme cases, the individual may be unable to perform minimal self-care (e.g., feeding and clothing self) or to maintain minimal personal hygiene.

The individual’s report of symptoms may be compromised by difficulties in concentrating, impaired memory, or a tendency to deny, discount, or explain away symptoms. Information from additional informants can be especially helpful in clarifying the course of current or prior major depressive episodes and in assessing whether there have been any manic or hypomanic episodes. Because major depressive episodes can begin gradually, a review of clinical information that focuses on the worst part of the current episode may be most likely to detect the presence of symptoms.

The evaluation of the symptoms of a major depressive episode is especially difficult when they occur in an individual who also has another medical condition (e.g., cancer, stroke, myocardial infarction, diabetes, pregnancy). Some of the criterion signs and symptoms of a major

Indiscretion (excessive involvement in pleasurable activities that have a high potential for painful consequences) Grandiosity or inflated self-esteem Flight of ideas or racing thoughts Activity increase (increase in goal directed activity or psychomotor agitation) Sleep deficit Talkativeness (pressured speech)

11. Identify diagnostic criteria and characteristics in persistent depressive disorder. Pg 510- 12 module 1 readings :

This disorder represents a consolidation of DSM-IV-defined chronic major depressive disorder and dysthymic disorder. A. Depressed mood for most of the day, for more days than not, as indicated by either subjective account or observation by others, for at least 2 years. Note: In children and adolescents, mood can be irritable and duration must be at least 1 year. B. Presence, while depressed, of two (or more) of the following:

1. Poor appetite or overeating.
2. Insomnia or hypersomnia.
3. Low energy or fatigue.
4. Low self-esteem.
5. Poor concentration or difficulty making decisions.
6. Feelings of hopelessness. C. During the 2-year period (1 year for children or adolescents) of the disturbance, the individual has never been without the symptoms in Criteria A and B for more than 2 months at a time. D. Criteria for a major depressive disorder may be continuously present for 2 years. E. There has never been a manic episode or a hypomanic episode. F. The disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder. G. The symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hypothyroidism). H. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. Note: If criteria are sufficient for a diagnosis of a major depressive episode at any time during the 2-year period of depressed mood, then a separate diagnosis of major depression should be made in addition to the diagnosis of persistent depressive disorder along with the relevant specifier (e.g., with intermittent major depressive episodes, with current episode). The essential feature of persistent depressive disorder is a depressed mood that occurs for most of the day, for more days than not, for at least 2 years, or at least 1 year for children and adolescents (Criterion A). This disorder represents a consolidation of DSM-IV-defined chronic major depressive disorder and dysthymic disorder. Major depression may precede persistent depressive disorder, and major depressive episodes may occur during persistent depressive disorder. Individuals whose symptoms meet major depressive disorder criteria for 2 years should be given a diagnosis of persistent depressive disorder as well as major depressive disorder. Individuals with persistent depressive disorder describe their mood as sad or “down in the dumps.” During periods of depressed mood, at least two of the six symptoms from Criterion B are present. Because these symptoms have become a part of the individual’s day-to-day experience, particularly in the case of early onset (e.g., “I’ve always been this way”), they may not be reported unless the individual is directly prompted. During the 2-year period (1 year for children or adolescents), any symptom-free intervals that have occurred have lasted no longer than 2 months (Criterion C).

Persistent depressive disorder often has an early and insidious onset (i.e., in childhood, adolescence, or early adult life) and, by definition, a chronic course. Borderline personality disorder is a particularly robust risk factor for persistent depressive disorder. When persistent

depressive disorder and borderline personality disorder coexist, the covariance of the corresponding features over time suggests the operation of a common mechanism. Early onset (i.e., before age 21 years) is associated with a higher likelihood of comorbid personality disorders and substance use disorders.

When symptoms rise to the level of a major depressive episode, they are likely to subsequently revert to a lower level. However, depressive symptoms are much less likely to resolve fully in a given period of time in the context of persistent depressive disorder than they are in a nonchronic major depressive episode.

12. Identify the following regarding bright light therapy: contraindications, indications. Pg 625; 627

Indications:

Seasonal affective disorder (SAD)[1]

• Circadian rhythm sleep disorders (e.g.,jet-lag, shift-work)
• Insomnia: A systematic review and meta-analysis reported that light therapy was found effective in the treatment of sleep problems in general and for circadian rhythm sleep disorders, insomnia, and sleep problems related to Alzheimer’s disease/dementia specifically

•Efficacy of light therapy for antepartum or post partum depression reported in a few published studies that have produced mixed results

• Nonseasonal depression: Randomized double-blind placebo-controlled studies showed that BLT, both as monotherapy and as adjunctive therapy, was efficacious and well tolerated in the treatment of adults with nonseasonal unipolar and bipolar depression; combination treatment had the most consistent effects[2]. BLT was more effective than placebo (sham treatment) in drug-resistant depression. Inconsistent results reported in a recent overview of systematic reviews of 18 RCTs[3]
• Bipolar depression – BLT shown to be effective as adjunctive therapy in double-blind studies.[4, 5] Response reported within 48 h in conjunction with sleep deprivation and consecutive sleep phase advance; patients treated with bright white light experienced a significantly higher remission rate. Caution suggested regarding possible risk for mood shift. A meta-analysis of 6 RCTs was unable to demonstrate efficacy of BLT for bipolar depression, however, a sensitivity analysis did show a significant effect[6]
• Parkinson’s disease: Several studies have demonstrated a positive effect of BLT on quality of sleep; total salivary cortisol secretion was decreased; suggested to decrease daytime drowsiness[7]; variable effects seen on mood and motor function
• ADHD: Preliminary data suggest that morning BLT in combination with melatonin in the afternoon/evening effective in sleep-onset insomnia (delayed phase sleep disorder) in adolescents and adults. Pilot study in adults showed that BLT significantly advanced the phase of dim light melatonin onset and mid sleep time, which was correlated with decreased ADHD rating scale scores and hyperactive-impulsive sub scores; total sleep time, sleep efficiency, wake after sleep onset, or percent wake during sleep interval did not improve[8]

•Dementia: Early data suggest possible role of BLT in treating sleep disorders in patients with mild to moderate Alzheimer’s dementia. A systematic review and meta-analysis identified 7 multimodal intervention studies, all incorporating light exposure; 6 of these reported improved objective or subjective sleep[9]

•Fibromyalgia: A pilot study demonstrated that morning light treatment improved function and pain sensitivity in 10 female patients with fibromyalgia

episodes from significant others. Lack of insight also unfortunately means that hospitalization must often be arranged on an involuntary basis.

MOOD-INCONGRUENT PSYCHOSIS. Psychosis in the setting of mania and mixed manic episodes is typically mood congruent. The sense of physical well- being and mental alacrity is so extraordinary that it is understandable why manic patients believe that they possess superior powers or perhaps are great scientists or famous reformers. Moreover, their senses are so vivid that reality appears richer and more exotic and can be easily transformed into a vision.

Likewise, their thoughts are so rapid and vibrant that they feel that they can hear them. Thus, certain first-rank schneiderian-type symptoms that have been traditionally considered mood incongruent can be understood phenomenologically to arise from the powerful mental experiences of mania.

The vignette illustrates the possibility that even some of the most psychotic manifestations of mania represent explanatory delusions, the patient’s attempt to make sense of the experience of mania. Many manic patients abuse alcohol and stimulants to enhance their mental state; mood incongruence can sometimes be explained on that basis

HYPOMANIA VERSUS MANIA. Nonpsychotic and nondisruptive variants of mania are much more common and are recognized by DSM-5 as hypomanic episodes. They are the historical clinical marker for bipolar II. Diagnostically, history of hypomania is preferably obtained from significant others who have observed the patient; the experience is often pleasant, and the subject may be unaware of it or may tend to deny it. Others experience irritable or dysphoric hypomanic episodes, which may be difficult to recognize clinically because of a stereotype that emphasizes the positive aspects of hypomania. Some patients feel that they benefit from the energy and confidence of hypomania. This is true if hypomania is mild and “sunny.” But, many patients, especially those with “darker” irritable activation, experience impairment in occupational and interpersonal functioning over time. DSM-5 stipulates a minimum duration of 4 days for hypomania; however, current evidence indicates that bipolar II disorders with long (4 or more days) and short (2 to 3 days) hypomania are indistinguishable on the basis of bipolar family history. It is, therefore, recommended that the threshold for detecting the duration of hypomania be set at 2 days. Ultimately, the duration of hypomanic experiences might be less important than the fact that they recur. In other words, the occurrence of brief recurrent hypomanias, even if their duration is 1 day, interspaced with major depressive episodes can be taken as presumptive evidence for bipolar II. Finally, although DSM-5 states that treatment- emergent hypomania in a depressed patient does not count toward a diagnosis of bipolarity, prospective observations show that nearly all such episodes are followed eventually by spontaneous hypomania (or mania); moreover, family history for bipolar disorder is comparable in patients with spontaneous and antidepressant-associated hypomania. In brief, antidepressant-associated hypomanias are best considered as a genetically less penetrant variant of bipolarity (which, in the literature, are often referred to as bipolar III disorders).

15. What are potential functional consequences of disruptive mood dysregulation disorder? Pg 495 module 1 readings

Chronic, severe irritability, such as is seen in disruptive mood dysregulation disorder, is associated with marked disruption in a child’s family and peer relationships, as well as in school performance. Because of their extremely low frustration tolerance, such children generally have difficulty succeeding in school; they are often unable to participate in the activities typically enjoyed by healthy children; their family life is severely disrupted by their outbursts and irritability; and they have trouble initiating or sustaining friendships. Levels of dysfunction in children with bipolar disorder and disruptive mood dysregulation disorder are generally comparable. Both conditions cause severe disruption in the lives of the affected individual and his or her family. In both disruptive mood dysregulation disorder and pediatric bipolar disorder, aggression and psychiatric hospitalization are common.

16. What are the types of sleep disturbances that can be associated with major depressive disorder? Pg 501 module 1 readings

Sleep disturbance may take the form of either difficulty sleeping or sleeping excessively (Criterion A4). When insomnia is present, it typically takes the form of middle insomnia (i.e., waking up during the night and then having difficulty returning to sleep) or terminal insomnia (i.e., waking too early and being unable to return to sleep). Initial insomnia (i.e., difficulty falling asleep) may also occur. Individuals who present with oversleeping (hypersomnia) may experience prolonged sleep episodes at night or increased daytime sleep. Sometimes the reason that the individual seeks treatment is for the disturbed sleep.

17. Differentiate between: CBT, mindfulness, interpersonal therapy, and psychodynamic therapy.

CBT (pg 78 SG M1) - Whatever the differences in specific models of CBT, all emphasized the role of the therapist as a teacher of specific skills that are intended to help the depressed person reduce depressive symptoms and/or improve coping. Moreover, virtually all models of CBT emphasize the importance of homework assignments to enhance mastery and generalization of these skills in “real world” environments. this form of therapy focused more on identifying the negatively valenced automatic thoughts associated with depressed moods and using strategies to both test the accuracy of the negative thoughts and consider more rational (and less depressogenic) alternatives. (Pg49) Modify perceptions, decrease negativity, increase sense of internal control, enhance coping skills, modify environmental factors contributing to illness.

Mindfulness (pg 79-80 SGM1) – Mindfulness meditation, developed from Buddhist techniques, emphasizes two skills: observing one’s perceived sensations and accepting and experiencing those sensations non judgmentally. In the application of this technique to depression, sensations include cognition and emotional states, as well as input through the five senses.

Interpersonal therapy (pg 79 SGM1) – IPT incorporated many of the more pragmatic methods used by social workers in case management to develop a time- limited therapy that addresses the common problematic patterns in relationships that plague the lives of people with depression, including unresolved grief, role disputes, role transitions, and interpersonal deficits. Beyond eliciting an interpersonal inventory and identifying the area or areas of interpersonal difficulty of greatest relevance to a particular patient, the interventions used in IPT are relatively eclectic and can include psychoeducation, nondirective questioning and empathic support, and role playing and social problem solving. IPT thus may be particularly well-suited for more traditionally trained psychotherapists or counselors who find it difficult to implement the structure, activity level, and the more directive posture that characterize most models of CBT.

Psychodynamic therapy (pg 78 SGM1) – treatment was long-term, focused on developing awareness of these internal conflicts through identification and interpretation of historical experiences that reflected such conflicts. Intervention emphasized developing insight into these conflicts through the use of free association and the therapist’s interpretations. This treatment also used the patient’s projections onto the therapist (the transference neurosis) as a means of studying early object relationships and conflicts. In contrast to more traditional approaches, behavioral theories of depression treatment emphasized observable factors, such as decreased participation in potentially rewarding or pleasurable activities, and suggested that the negative emotional symptoms of depression could be understood as a consequence of withdrawal of reinforcement. (APA defined) Psychodynamic therapy focuses on the psychological roots of emotional suffering. Its hallmarks are self-reflection and self-examination, and the use of the relationship between therapist and patient as a window into problematic relationship patterns in the patient’s life. Its goal is not only to alleviate the most obvious symptoms but to help people lead healthier lives.

• Increased intracranial pressure •Recent intracerebral hemorrhage/unstable aneurysm, recent ischemic stroke, suggested wait after event is approximately 8 weeks
• Extremely loose teeth which may be aspirated if dislodged
• Threatened retinal detachment •Concurrent administration of an irreversible MAOI, which may interact with anesthetic agents (although most reports have implicated meperidine as the interacting drug). Severe impairment in cardiac output and hypotension during ECT may require resuscitation with a pressor agent; the choice may be limited in the presence of an irreversible MAOI. The literature therefore recommends that MAOIs be discontinued 14 days prior to elective anesthesia; if there are compelling reasons to continue the MAOI, or start ECT prior to this waiting period, obtain anesthesia consultation. The potential for a hypertensive response is much less in the presence of a selective, reversible MAOI (RIMA) such that their concurrent administration is acceptable
• Concurrent drug toxicity

22. What baseline labs are recommended prior to treatment with Celexa (Citalopram)? Pg 730 M1 readings Serum sodium at baseline and after 4 weeks. Baseline EKG.
23. Identify antidepressant that may cause dose-dependent cardiac irregularities. Pg 771 M readings Citalopram (Celexa) at doses of 80mg a day or higher
24. Which SNRI is recommended for use in the treatment of panic and major depression? Pg 109 SG Venlafaxine
25. Which antidepressant has the potential to cause a false amphetamine lab result? Pg 565 Desvenlafaxine (Pristiq) and venlafaxine (Effexor)
26. Which SSRI is considered least sedating? Most likely to cause discontinuation syndrome? Pg 776 Celexa (Citalopram). Paxil (fluoxetine) [this is not accurate according to the literature but was in the professors slides]
27. Which SNRI has the fewest drug interactions? Pg 561 Desvenlafaxine
28. Identify behavioral adverse effects in children taking SSRIs. Pg 546 M1 Reading Agitation, restlessness (32–46%), activation, hypomania (up to 13%), insomnia (up to 21%), irritability, and social disinhibition (up to 25%)
29. Why is slow upward titration recommended when prescribing lamotrigine? Pg 326 M readings Lamotrigine is titrated upward slowly due to concerns about skin rash with rapid titration. Other risk factors for skin rash include younger age, a prior history of rash with another drug, and taking lamotrigine in conjunction with valproate. Rash more commonly occurs within the first few weeks of therapy. A recent review concluded that the incidence of skin rash was about 10 percent in prospective studies. The incidence of serious skin rash (i.e., Steven Johnson syndrome or toxic epidermal necrolysis) is rare (about 1 to 10 per 10,000) with slow dose titration. A recent review reported that about 50 percent of patients with serious skin rash had received lamotrigine in conjunction with valproate.
30. Identify the gold standard for the maintenance of treatment of bipolar disorder. Pg 323 M readings Lithium

31. What is the recommended serum lithium schedule? Pg 732 M1 readings

Serum lithium* at baseline, following dosage changes, and at least every 2 months in those 65 or older, or every 3 months in those under 65 years; BMP at baseline and every 3 months; TSH and T4 at baseline, then every 6 months

32. Identify important education for patients on maintenance treatment with lithium. Pg 324 and 301 M1 readings Patients on maintenance treatment of lithium should be educated about symptoms of lithium toxicity and the preventive measures. Risk factors for lithium toxicity include renal diseases, dehydration, drug interactions, elderly and those with organic brain syndromes. Lithium toxicity is a medical emergency, and if not treated can result in irreversible organ damage and death. Patients should be educated and clinically monitored for signs of lithium toxicity that may include gastrointestinal (vomiting and diarrhea), neurological (coarse tremor, agitation, dysarthria, drowsiness, lethargy, ataxia) renal (polyuria and polydipsia), and cardiovascular (syncope, dizziness, arrhythmias) symptoms.
33. What is the recommended first line adjunct to antidepressant medication in MDD? Pg 775 M1 readings; pg 630 Aripiprazole (ability) and Quetiapine (Seroquel)
    • Aripiprazole: Initial dose 2–5 mg/day; recommended dose 5–10 mg/day; maximum dose 15 mg/day
    • Quetiapine: Initial dose 50mg/day; recommended dose 150 – 300mg/day; maximum dose 300 mg/day
    • Risperidone: 0.25 mg/day for 3 days; 0.5 mg/day on days 4 – 15, 1 mg/day on days 6 – 28. Increase to 2 mg if necessary
34. What are some potential side effects for a patient taking trazodone (Desyrel)? Pg 47 & 570 M1 readings; pg 774 Sedation, nausea, headache, hypotension, weight gain, priapism, spontaneous orgasm with yawning, other sexual s/e
35. Identify a potential side effect for women taking valproate. Pg 325 module 1 reading Some patients experience weight gain and hair loss, women taking valproate should be monitored for polycystic ovary syndrome with questions about menstrual irregularities, fertility issues, hirsutism, and galactorrhea.

Module 2 – Anxiety Disorders (PD = panic disorder)

1. Identify the neurotransmitters associated with anxiety disorder. Pg 49-50 SG 2; pg 65 serotonin, GABA, dopamine, norepinephrine, glutamate, and voltage-gated ion channels greatly overlapping with many of the same neurotransmitters and regulators known to modulate the amygdala.

6. Identify the hallmark symptom of GAD in children. Pg 55 SG Anxiety which if difficult to control (Sadock, pg. 3712)
7. Differentiate glutamate vs GABA (hint: excitability). Pg 74 SG2; pg 6 SG2; pg 8 inhibitory signaling by gamma-amino-butyric acid (GABA) or increased excitatory neurotransmission by glutamate. Glutamate is the primary excitatory neurotransmitter of the CNS, is the precursor compound of GABA, and modulates pathways that mediate panic and defensive responses. Results from human and animal studies suggest that panic might arise from an imbalance between tonic GABAergic inhibition and glutamate-mediated excitation, with predominance of the latter. For example, reduced GABAergic tone has been reported in patients with PD. Further, glutamate is known to regulate other neurotransmitters involved in PD, including serotonin and NE. GABA is the primary inhibitory neurotransmitter in the brain and a metabolic product of glutamate, the excitatory neurotransmitter.
8. What are the diagnostic criteria for panic disorder? Pg 45 SG A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and during which time four (or more) of the following symptoms occur: Note: The abrupt surge can occur from a calm state or an anxious state.
   1. Palpitations, pounding heart, or accelerated heart rate.
   2. Sweating.
   3. Trembling or shaking.
   4. Sensations of shortness of breath or smothering.
   5. Feelings of choking.
   6. Chest pain or discomfort.
   7. Nausea or abdominal distress.
   8. Feeling dizzy, unsteady, light-headed, or faint.
   9. Chills or heat sensations.
   10. Paresthesias (numbness or tingling sensations).
   11. Derealization (feelings of unreality) or depersonalization (being detached from oneself).
   12. Fear of losing control or “going crazy.”
   13. Fear of dying. Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms. B. At least one of the attacks has been followed by 1 month (or more) of one or both of the following:
   14. Persistent concern or worry about additional panic attacks or their consequences (e.g., losing control, having a heart attack, “going crazy”).
   15. A significant maladaptive change in behavior related to the attacks (e.g., behaviors designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar situations). C. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism, cardiopulmonary disorders). D. The disturbance is not better explained by another mental disorder (e.g., the panic attacks do not occur only in response to feared social situations, as in social anxiety disorder; in response to circumscribed phobic objects or situations, as in specific phobia; in response to obsessions, as in obsessive-compulsive disorder; in response to reminders of traumatic events, as in posttraumatic stress disorder; or in response to separation from attachment figures, as in separation anxiety disorder).
9. Identify risk factors for developing social anxiety disorder. Pg 56 SG •Family history •Female gender

•Childhood signs of behavioral inhibition

10. What are the psychotherapeutic and pharmacologic treatments for specific phobia? Pg 15 & pg 123 MD2Readings The treatment of choice for Specific Phobia is a behavioral therapy series that includes exposure- based, systematic desensitization. There are small, placebo-controlled studies involving serotonergic antidepressants or atypical antipsychotics, but the data is very limited. There is ongoing work on augmenting exposure-based psychotherapy with d-cycloserine, though the data requires ongoing interpretation and study replication to avoid harm via administration of this medication in the wrong context. There is very little long-term data on the durability of remission in pharmacologic studies. Psychological interventions, particularly exposure-based therapies are considered to have the most evidence for efficacy. The benefit of pharmacotherapy has not been well studied, but preliminary evidence suggests that SSRIs (escitalopram and paroxetine) may be useful as second-line treatments if patients do not respond to psychotherapy. Thus, in general, there is little evidence to support the benefit of pharmacotherapy in the management of specific phobias.
11. Identify differential diagnoses for agoraphobia. Pg 45-46 SG Differentiating agoraphobia from situational specific phobia can be challenging in some cases, because these conditions share several symptom characteristics and criteria. Specific phobia, situational type, should be diagnosed versus agoraphobia if the fear, anxiety, or avoidance is limited to one of the agoraphobic situations. Requiring fears from two or more of the agoraphobic situations is a robust means for differentiating agoraphobia from specific phobias, particularly the situational subtype. Additional differentiating features include the content of the individual’s cognitions. Thus, if the situation is feared for reasons other than panic-like symptoms or other incapacitating or embarrassing symptoms (e.g., fears of being directly harmed by the situation itself, such as fear of the plane crashing for individuals who fear flying), then a diagnosis of specific phobia may be more appropriate. Separation anxiety disorder can be best differentiated from agoraphobia by examining the individual’s cognitions. In separation anxiety disorder, the thoughts are about detachment from significant others and the home environment (i.e., parents or other attachment figures), whereas in agoraphobia the focus is on panic-like symptoms or other incapacitating or embarrassing symptoms in the feared situations. Agoraphobia should be differentiated from social anxiety disorder based primarily on the situational clusters that trigger fear, anxiety, or avoidance and the individual’s cognitions. In social anxiety disorder, the focus is on fear of being negatively evaluated. When criteria for panic disorder are met, agoraphobia should not be diagnosed if the avoidance behaviors associated with the panic attacks do not extend to avoidance of two or more agoraphobic situations. Acute stress disorder and posttraumatic stress disorder (PTSD) can be differentiated from agoraphobia by examining whether the fear, anxiety, or avoidance is related only to situations that remind the individual of a traumatic event. If the fear, anxiety, or avoidance is restricted to trauma reminders, and if the avoidance behavior does not extend to two or more agoraphobic situations, then a diagnosis of agoraphobia is not Warranted. In major depressive disorder, the individual may avoid leaving home because of apathy, loss of energy, low self-esteem, and anhedonia. If the avoidance is unrelated to fears of panic-like or other incapacitating or embarrassing symptoms, then agoraphobia should not be diagnosed. Individuals with certain medical conditions may avoid situations because of realistic concerns about being incapacitated (e.g., fainting in an individual with transient ischemic attacks) or being embarrassed (e.g., diarrhea in an individual with Crohn’s disease). The diagnosis of agoraphobia should be given only when the fear or avoidance is clearly in excess of that usually associated with these medical conditions
12. What are the levels of anxiety and what occurs during each level? Pg 347 M2Readings