2 Case Studies- Psychopharmacology Paper

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ADULT DEPRESSION

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ADULT DEPRESSION

SAMPLE PAPER

Case Study of Adult Depression

Charles R. Drew University

ADULT DEPRESSION

According to the American Psychiatric Association, depression (major depressive disorder) is define as a common and serious medical illness that negatively affects how you feel, the way you think and how you act (Parekh, 2017). Fortunately, it is also treatable. Depression causes feelings of sadness and/or a loss of interest in activities once enjoyed. It can lead to a variety of emotional and physical problems and can decrease a person’s ability to function at work and at home (Depression Basics, 2016). Everyone feels sad or low sometimes, but these feelings usually pass with a little time. Depression, also called “clinical depression” or a “depressive disorder” is a mood disorder. To be diagnosed with depression, symptoms must be present most of the day, nearly every day for at least 2 weeks (Depression Basics, 2016). 2 Case Studies- Psychopharmacology Paper

Symptoms of depression include feeling sad or having a depressed mood, loss of interest or pleasure in activities once enjoyed, changes in appetite, weight loss or gain unrelated to dieting, trouble sleeping or sleeping too much, loss of energy or increased fatigue, increase in purposeless physical activity (e.g., hand-wringing or pacing) or slowed movements and speech (actions observable by others), feeling worthless or guilty, difficulty thinking, concentrating or making decisions, thoughts of death or suicide (Sadock et al., 2015).

Thyroid problems, a brain tumor or vitamin deficiency can mimic symptoms of depression so it is important to rule out general medical causes.

In any given year, one in fifteen people (16.6%) will experience depression. Depression may first appear during the late teens to mid-20s. Women are more likely to experience depression than men and up to one-third of women may experience a major depressive episode in their lifetime. It is important to differentiate clinical depression from the normal sadness of bereavement. Those experiencing loss often might describe themselves as being “depressed” but being sad is not the same as having depression. The grieving process is natural and unique to each individual and shares some of the same features of depression. Both grief and depression may involve intense sadness and withdrawal from usual activities (NIMH, 2016). Having said all these, it is true to say that depression is a common, but a serious mood disorder. If one is not sure that you are clinically depressed, the following are assessments that a doctor can perform to help make a diagnosis, such as the Hamilton Depression Scale or HAM-D; Beck Depression Inventory or BDI; and the Zung Self-Rating Scale for Depression (SCHWARTZ, 2017).

Several factors can play a role in depression such as biochemistry where differences in certain chemicals in the brain may contribute to symptoms of depression. Genetics can result in depression running in families. For example, if one identical twin has depression, the other has a 70 percent chance of having the illness sometime in life. People who have low self-esteem and are easily overwhelmed by stress are more likely to experience depression. Environmental factors such as continuous exposure to violence, neglect, abuse or poverty may make some people more vulnerable to depression (Parekh, 2017).

Case study: Jane Doe is a 58-year-old Caucasian female patient who came in to the clinic for a follow up visit, recently diagnosed with depression. Patient appeared quiet with sad affect, disheveled in appearance. Complained of having depressed mood, Loss of interest, decreased appetite, weight loss unrelated to dieting, difficulty sleeping, patient stated “I sleep about 3-4 hours a night”, decreased level of energy, and feeling of worthlessness. Patient endorses SI with no plans, denies AH, seeing things, hurting self or others. Patient denies having any medical problems. Denies any pain. No known drug or food allergy. Patient has not been on any medication and wishes to be medically treated now. 2 Case Studies- Psychopharmacology Paper

A diagnostic evaluation (interview and a physical examination) was done to identify specific symptoms (medical and family history, cultural factors and environmental factors) to plan a course of action for the patient. Different treatment course of action was discussed with the patient as follows.

There are a variety of treatments available for major depressive disorder. Medication alone and brief psychotherapy (e.g., cognitive-behavioral therapy, interpersonal therapy) may relieve depressive symptoms. Brief psychotherapy (CBT) may help to prevent relapse (Halverson, 2019).

Pharmacotherapy for the treatment of depression includes the following categories: SSRIs, SNRIs, Atypical antidepressants, SDAMs, TCAs, MAOIs, NMDAs, Herbal remedies and “psychedelic” drugs.

SSRIs (Selective serotonin reuptake inhibitors) includes, Citalopram (Celexa), Escitalopram (Lexapro), Fluoxetine (Prozac), Fluvoxamine (Luvox), Paroxetine (Paxil), Sertraline (Zoloft), Vilazodone (Viibryd), Vortioxetine (Brintellix). These drugs have advantage of ease of dosing and low toxicity in overdose. The adverse effect of SSRIs are less than that of some other antidepressant drug categories, which promotes better compliance. Adverse effects include gastrointestinal upset, sexual dysfunction, and changes in energy level. SSRIs don’t complicate cardiac disease, as these agents do not appear to affect blood pressure, heart rate, cardiac conduction, or cardiac rhythm (Halverson, 2019).

SNRIs (Serotonin/norepinephrine reuptake inhibitors) are venlafaxine (Effexor), desvenlafaxine (Pristiq), duloxetine (Cymbalta), and levomilnacipran (Fetzima). These can be used as first-line agents, particularly in patients with significant fatigue or pain syndromes associated with the episode of depression. SNRIs have an important role as second-line agents in patients who have not responded to SSRIs. The safety, tolerability, and side-effect profiles of SNRIs include those of the SSRIs, as well as noradrenergic side effects, such as hypertension. In July 2013, the FDA approved the newest SNRI levomilnacipram (Fetzima) which is available as a once-daily sustained-release formulation. It has greater potency for norepinephrine reuptake inhibition than for serotonin reuptake inhibition without directly affecting the uptake of dopamine or other neurotransmitters.

Atypical antidepressants include bupropion (Wellbutrin), mirtazapine (Remeron), nefazodone, and trazodone (Desyrel). They have all been found to be effective in monotherapy in major depressive disorder and may be used in combination therapy for more difficult to treat depression. Nevertheless, this group also shows low toxicity in overdose. In addition, bupropion has the advantage over the SSRIs of causing less sexual dysfunction and less GI distress. Mirtazapine is associated with a high risk of weight gain, so patients who are treated with this agent should have careful monitoring of weight.

SDAMs (Serotonin-Dopamine Activity Modulator) are brexpiprazole (Rexulti) and aripiprazole (Abilify). They act as a partial agonist at 5-HT1A and dopamine D2 receptors at similar potency, and as an antagonist at 5-HT2A and noradrenaline alpha1B/2C receptors. Brexpiprazole is used for adjunctive therapy for major depressive disorder (MDD). Aripiprazole is indicated for schizophrenia, acute treatment of manic and mixed episodes associated with bipolar I, as an adjunct to MDD, irritability associated with autistic disorder, and treatment of Tourette disorder. Also, aripiprazole prompt-acting injection is indicated for agitation associated with schizophrenia or bipolar mania. 2 Case Studies- Psychopharmacology Paper

Tricyclic antidepressants (TCAs) include the following: Amitriptyline (Elavil), Clomipramine (Anafranil), Desipramine (Norpramin), Doxepin (Sinequan), Imipramine (Tofranil), Nortriptyline (Pamelor), Protriptyline (Vivactil), Trimipramine (Surmontil). TCAs have a long record of efficacy in the treatment of depression. They are used less commonly because of their side-effect profile and their considerable toxicity in overdose.

Monoamine oxidase inhibitors (MAOIs) include isocarboxazid (Marplan), phenelzine (Nardil), selegiline (Emsam), and tranylcypromine (Parnate). These agents are widely effective in a broad range of affective and anxiety disorders. Because of the risk of hypertensive crisis, patients on these medications must follow a low-tyramine diet. Other adverse effects can include insomnia, anxiety, orthostasis, weight gain, and sexual dysfunction.

N-methyl-D-aspartate (NMDA) receptor antagonists receptor antagonist esketamine intranasal (Spravato) has been shown to improve treatment-resistant depression in conjunction with an oral antidepressant. The precise mechanism by which esketamine elicits its antidepressant effect is not fully understood. NMDA is an ionotropic glutamate receptor.

St. John’s wort (Hypericum perforatum) is an herbal remedy available over the counter. Although St. John’s wort is considered a first-line antidepressant in many European countries, it has only recently gained popularity in the United States. Uses include treatment of mild to moderate depressive symptoms, but of note, it has not been shown to be effective in major depressive episodes and cannot be recommended as a first-line treatment in moderate depression. St. John’s wort may act as an SSRI. The common dosage is 300 mg 3 times a day with meals to prevent GI upset. If no clinical response occurs after 3–6 months, encouraging the use of another medication is recommended. In addressing the issue of alternative therapies for depression, the 2011 APA guideline noted that St. John’s wort might be considered, but evidence for its effectiveness is modest, and more information is needed about its interaction with other drugs.

Psilocybin, a classic “psychedelic” drug, along with psychological support, is showing promise as a treatment for patients with treatment-resistant depression. Research showed decreased depressive symptoms in those treated with this drug Whole-brain analyses revealed post-treatment decreases in CBF in the temporal cortex, including the amygdala (Carhart-Harris et al., 2017). 2 Case Studies- Psychopharmacology Paper

Jane Doe was taught that brain chemistry can contribute to depression and may factor into their treatment. Antidepressants are prescribed to help modify one’s brain chemistry. They are not sedatives, “uppers” or tranquilizers. They are not habit-forming (Halverson, 2019). Jane Doe was prescribed Prozac with starting dose of 20mg/day X4 weeks. Medication treatment as prescribed, risk and benefits discussed. Therapy discussed with Jane Doe and encouraged to start therapy, exercise and sleep hygiene discussed. Follow up appointment in one month.

She was further taught that antidepressants may produce some improvement within the first week or two of use. Full benefits may not be seen for two to three months. If a patient feels little or no improvement after several weeks, his or her psychiatrist can alter the dose of the medication or add or substitute another antidepressant. In some situations, other psychotropic medications may be helpful. It is important to let your doctor know if a medication does not work or if you experience side effects (Halverson, 2019). It is also important to be compliant with medication regimen. Psychiatrists usually recommend that patients continue to take medication for six or more months after symptoms have improved. Longer-term maintenance treatment may be suggested to decrease the risk of future episodes for certain people at high risk (Halverson, 2019).

In a meta-analysis, Fournier et al found that medication superiority over placebo increased with increases in baseline depression severity, crossing the threshold for a clinically significant difference at a baseline Hamilton Depression Rating Scale (HDRS) score of 25. In patients with mild or moderate depression, antidepressant medication had minimal or no benefit compared with placebo, but in patients with very severe depression, antidepressant drugs provided a substantial benefit compared with placebo.

More confirmation that antidepressants work for depression came from a large meta-analysis of 522 randomized controlled trials that compared 21 different antidepressants with placebo in more than 116,000 patients with major depressive disorder. The 21 antidepressants included in the trials were agomelatine, amitriptyline, bupropion, citalopram, clomipramine, desvenlafaxine, duloxetine, escitalopram, fluoxetine, fluvoxamine, levomilnacipran, milnacipran, mirtazapine, nefazodone, paroxetine, reboxetine, sertraline, trazodone, venlafaxine, vilazodone, and vortioxetine. Results showed that each studied antidepressant was significantly more efficacious, defined as yielding a reduction of at least 50% in the total score of a standardized scale for depression, than placebo after 8 weeks. Patients who received agomelatine, escitalopram, and vortioxetine had both high response rates and low dropout rates (Halverson, 2019).

Depression is a real, help is available. The majority of people with depression will overcome it with professional help. The first step is to see a physician or psychiatrist. All antidepressants on the market are potentially effective.  Medication choices are guided by anticipated safety and tolerability. Often, treatment failures are caused not by clinical resistance but by medication noncompliance, inadequate duration of therapy, or inadequate dosing. 2 Case Studies- Psychopharmacology Paper

Antidepressants can have central and peripheral anticholinergic effects, as well as sedative effects, and can block the active reuptake of norepinephrine (NE), serotonin (5-HT), and dopamine. SSRIs are metabolized via the cytochrome P-450 system and may have drug interactions on that basis. The degree of enzyme inhibition varies among SSRIs. Effects on blood levels and bioavailability of coadministered drugs, as well as pharmacodynamics interactions, account for most clinically significant SSRI-drug interactions.

All available antidepressants appear to work via one or more of the following mechanisms.

· Presynaptic inhibition of uptake of 5-HT or NE

· Antagonist activity at presynaptic inhibitory 5-HT or NE receptor sites, thereby enhancing neurotransmitter release

· Antagonism of NE beta or serotonin 5-HT2 receptors

· N-Methyl-D-aspartate (NMDA) receptor antagonism

· Induction of brain-derived neurotrophic factor (BDNF)

· Inhibition of monoamine oxidase, thereby reducing neurotransmitter breakdown.