Short Answer Assessment
In 3 or 4 sentences, explain the appropriate drug therapy for a patient who presents with
MDD and a history of alcohol abuse. Which drugs are contraindicated, if any, and why? Be
specific. What is the timeframe that the patient should see resolution of symptoms?
Before beginning drug therapy for MDD, the provider must first assess for the root cause
of the MDD. If the patient also has a history of alcohol abuse, it will be essential to determine if
the depression results from the alcohol abuse or if the alcohol is a self-medication tool of the
untreated depression (Dongier, 2005). Once established, it is indeed the depression that needs to
be treated as the primary diagnosis; choosing a drug therapy that will be as safe as possible if the
patients drink is imperative. Since alcohol and depression both cause low levels of serotonin, it is
appropriate to prescribe an SSRI. SSRIs have “minimal anticholinergic, antihistaminic, and α1-
adrenergic blocking effects, and potent pre-synaptic inhibition of serotonin reuptake” (Fava et
al., 2015, p. 380). This makes them less likely to interact with the depressing effects of alcohol
and helps increase serotonin levels to combat depression.
MAOIs are contraindicated with alcohol use. There is an increased risk of a
cardiovascular event such as elevated blood pressure or stroke if a patient drinks alcohol while
on an MAOI (Fava et al., 2015). Some other drugs that are contraindicated for MDD and alcohol
abuse are mirtazapine and bupropion. Mirtazapine, because of its sedation effects that will be
increased with alcohol and could lead to serious injury (IBM Corporation, 2021). Bupropion,
because of its increased risk of seizures, is dangerous to mix with alcohol (IBM Corporation,
2021).
It would be expected that an MDD patient with a history of alcohol abuse starting on an
SSRI would see a decrease in symptoms typically in 4-6 weeks, but if they are still drinking, that
may be prolonged. Alcohol can increase depressive symptoms making it harder for the
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medication to do its job. While antidepressants have been shown to help treat alcohol abuse as
well as MDD, the dosages required are higher than usual, and the time to effectiveness is
prolonged (DeVido & Weiss, 2012).
List 4 predictors of late-onset generalized anxiety disorder.
The four predictors of late-onset generalized anxiety disorder are:
1. Being a female
2. Having a mental health disorder such as depression
3. Experiencing a recent adverse life event
4. Having a chronic physical health issue
(Ancelin et al., 2015).
List 4 potential neurobiology causes of psychotic major depression.
1. The first potential neurobiological of psychotic major depression is low levels of plasma brain-
derived neurotrophic factor (BDNF) (Aitchison et al., 2011).
2. Another possibility is the dysfunctional regulation of the hypothalamic-pituitary-adrenal axis
(Domschke. 2013).
3. The third potential cause is DRD4 gene polymorphism (Cieslak et al., 1996).
4. The last potential cause is a decreased functional connectivity (FC) in the right part of the
bilateral frontoparietal network (Barkhof et al., 2019).
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An episode of major depression is defined as a period of time lasting at least 2 weeks. List
at least 5 symptoms required for the episode to occur. Be specific.
1. When a patient displays a depressed mood most of the day, nearly every day. This can be either
self-reported or observed by another. Feelings and actions include feeling sad, empty, or hopeless
and being very tearful.
2. When a patient report and displays insomnia or hypersomnia every day.
3. When a patient report feeling fatigued or having a loss of energy every day.
4. When a patient indicates they have had recurrent thoughts of death, recurrent suicidal ideation
without a plan, or a suicide attempt or a specific plan to commit suicide.
5. When the patient indicates a diminished interest or pleasure in all or almost all activities most of
the day, every day. This has been self-reported or observed by others.
(American Psychiatric Association, 2013).
List 3 classes of drugs, with a corresponding example for each class, that precipitate
insomnia. Be specific.
The first class of drug is SSRIs (select serotonin reuptake inhibitors). An example of an
SSRI is Zoloft. According to IBM Corporation (2021), the most common reported adverse effect
with Zoloft is insomnia. Zoloft can precipitate insomnia by selective inhibition of
serotonin reuptake. The second class of drugs is Corticosteroids. An example of this is
Methylprednisolone. Methylprednisolone can precipitate insomnia by exhausting the adrenal
glands, not allowing patients to relax and sleep. The third class of drugs is Cholinesterase
inhibitors. An example of a Cholinesterase inhibitor is Donepezil. Donepezil precipitates
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insomnia by inhibiting acetylcholine, thus increasing the amount in the brain and elsewhere in
the body, interfering with the body processes related to sleep.
References
Aitchison, K. J., Cattaneo, A., Dazzan, P., Di Forti, M., Handley, R., Hepgul, N., Miorelli, A.,
Mondelli, V., Morgan, C., Murray, R. M., Murri, M. B., Navari, S., Papadopoulos, A. S.,
& Pariante, C. M. (2011). Stress and inflammation reduce brain-derived neurotrophic
factor expression in first-episode psychosis: A pathway to smaller hippocampal volume.
The Journal of Clinical Psychiatry, 72(12), 1677–1684.
https://doi.org/10.4088/JCP.10m06745
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental
disorders (5th ed.). American Psychiatric Association
Ancelin, M. L., Carrière, I., Chaudieu, I., Norton, J., Ritchie, K., & Zhang, X. (2015). Risk
factors for late-onset generalized anxiety disorder: results from a 12-year prospective
cohort (the ESPRIT study). Translational Psychiatry, 5(3), e536.
https://doi.org/10.1038/tp.2015.31
Barkhof, F., Bouckaert, F., De Winter, F., Dols, A., Eikelenboom, P., Emsell, L., Oudega, M. L.,
Rhebergen, D., Sienaert, P., Stek, M. L., Vandenbulcke, M., Van den heuvel, O. A., Van
Exel, E., Van der Werf, Y. D., & Wattjes, M. P. (2019). Exploring resting state
connectivity in patients with psychotic depression. PLOS ONE, 14(1), e0209908.
https://doi.org/10.1371/journal.pone.0209908
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Cieslak, A., Forssmann, W.G., Mägert, H.J., & Weiss, J. (1996). Association between different
psychotic disorders and the DRD4 polymorphism, but no differences in the main ligand
binding region of the DRD4 receptor protein compared to controls. Eur J Med Res,
1(9):439-45. PMID: 9353244
DeVido, J. J., & Weiss, R. D. (2012). Treatment of the depressed alcoholic patient. Current
Psychiatry Reports, 14(6), 610–618. https://doi.org/10.1007/s11920-012-0314-7
Domschke, K. (2013). Clinical and molecular genetics of psychotic depression. Schizophrenia
Bulletin, 39(4), 766-775. https://doi.org/10.1093/schbul/sbt040
Dongier M. (2005). What are the treatment options for comorbid alcohol abuse and depressive
disorders?. Journal of Psychiatry & Neuroscience, 30(3), 224.
Fava, M., Rosenbaum, J. F., Stern, T. A., & Wilens, T. E. (2015). Massachusetts General hospital
comprehensive clinical psychiatry (1st ed.). Elsevier Health Sciences.
IBM Corporation. (2021). IBM Micromedex.
https://www.micromedexsolutions.com/micromedex2/librarian/deeplinkaccess?so
urce=deepLink&institution=SZMC%5ESZMC%5ET43537
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