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the office visit, I will ask the patient whether he was compliant with the
medications that he had been taking over the years. This will help me to
understand why some medications are not working. I will also question the
patient to see if he is noticed any symptoms of another illness such as
dementia. I will ask the patient whether he has trouble falling asleep or has
the urge to sleep more than usual. I will ask the patient whether he has been
diagnosed with any new medical illnesses. I will also ask him whether he has
been prescribed any new medications from other providers. This may give an
answer to some of the patient’s symptoms and why some drugs were not  successful. I will ask him whether he has
been feeling helpless, worthless, or has problems concentrating. I will also
ask whether he has been attending any psychotherapy because psychotherapy is
always good for the patient’s disease. I will ask his wife, caregivers and any
grown children whether they noticed any changes in the patient lately or at any
time during his treatment. I will ask them about his sleeping, eating habits,
memory, behaviors and about any other life changing events or changes that
involved the patient.  The families are
always a good source of information for the history of the patient.


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will order blood tests to check TSH and thyroxine to exclude
hypothyroidism,  basic electrolytes and
serum calcium to rule out a metabolic disturbance; and a full blood count
including erythrocyte sedimentation rate (ESR) to rule out a systemic infection
or chronic disease. According to Hage and 
Azar (2012), patients with hypothyroidism usually manifest features
of depression. Also, patients with hyperthyroidism present a wider spectrum of
neuropsychiatric symptoms including both depression and anxiety. I will also
order vitamin D level.  According to Li,
Mbuagbaw, Samaan, Zhang, Adachi, Papaioannou, and Thabane (2013), vitamin D deficiency is strongly linked to
depression. Genetic testing could be done to target depression. Stahl (2013) concluded
that genetic testing has the potential of assisting both in diagnoses of
psychiatric illnesses and selecting psychotropic drugs.  

Differential Diagnoses

depressive disorder: is a mood
disorder that causes a persistent feeling of sadness and loss of interest. This
is the most likely diagnosis of choice due to the patient having no joy, sad,
feeling helpless, hopeless, worthless, and problems concentrating.

episodes with irritable mood or mixed episodes:
in this situation, the patient may be very irritable or have mood symptoms that
are similar to those seen in bipolar disorder.

disorder due to another medical condition: This is most
likely not the diagnosis. The patient does not have any medical conditions such
as multiple sclerosis, stroke, or heart disease that cause depression.

Pharmacologic Agents

will start with Effexor ER and Latuda as adjunct therapy.  Lenze, 
Mulsant, Blumberger, Karp, Newcomer, Anderson, and Reynolds (2015)  reported that the effectiveness of
second-generation atypical antipsychotics (SGA) can act as a successful
adjunctive medical agent for patients who fail to respond to pharmacological
monotherapy with antidepressants. Since the patient has been taking SSRIs, TCAs,  SNRI, Tetracyclic antidepressants, and
Anxiolytics, I will discontinue all anxiolytics at a tapered rate. Stahl (2013)
concluded that anxiolytics are known to cause worsening of depression and
suicidal ideations. Since the patient tolerated Effexor
XR without any significant side effects, I will start  Effexor XR with an initial dose of 75mg then
increase  the dosage until the patient is
stable. Since the patient has no heart problems , the Effexor XR can be
augmented with Latuda starting at a dose of 20 mg per day with meals then increase
it until the max dose of 120mg is reached. I would not use the combination of  MAOIs and TCAs because this combination is
ineffective. The combination of the MAOI with the second-generation
antipsychotic can also cause symptoms of bipolar disorder (Yingli, Huan,
Shichang, Wei,Ping, Changhong, & Yalin, 2013). The patient takes a Lipitor that
can also cause depression.

were no improvements in depression from the first interim follow-up through the
sixth interim follow-up. When the venlafaxine dose increased to 600 mg in the sixth
interim follow-up, the patient achieved complete remission of depression but
decreased to 450 mg due to irritability, insomnia and elevated blood pressure. According
to Mbaya (2002), high doses of venlafaxine is safe, well tolerated, improves
social functioning, and is effective in a small number of severe treatment
resistant patients with major depression.

Roy (2005) concluded that gene
polymorphisms are DNA variations that affect drug metabolizing enzymes. The
hepatic cytochrome P450s are a multigene family of enzymes that play a critical
role in the metabolism of many drugs and xenobiotics with each cytochrome
isozyme responding differently to exogenous chemicals in terms of its induction
and inhibition. Poolsup and Knight (2000) concluded that people from different
ethnic backgrounds respond differently to certain drugs used to treat mental
disorders. According to  Roy (2005), genetic
differences are more likely to provide the explanation for slower drug
metabolism rather than race.  

Lessons learned

learned from this case study was that depression can be recurrent and can
manifest due to shorter periods of wellness, poor inter-episode recovery and
ultimately treatment resistance. Continuous research and study should be done
to look at what ways depression could be fought. I learned a great deal about
adjunct therapy that will help me  treat
my patients with depression. I also learned about the different classes of
drugs that are used for multiple diagnoses (Buck & Ruskin, 2008).


A., & Ruskin, A. (2008).
Depression: what you need to know. Practice Nurse, 36(10),

Hage, M. P., & Azar, S. T. (2012).
The Link between Thyroid Function and Depression. Journal of Thyroid
Research, 2012, 1-8. doi:10.1155/2012/590648

E. J., Mulsant, B. H., Blumberger, D. M., Karp, J. F., Newcomer, J. W.,
Anderson, S. J., & Reynolds,
C. F. (2015). Efficacy, safety, and tolerability of augmentation
pharmacotherapy with aripiprazole for treatment-resistant depression in late
life: a randomised, double-blind, placebo-controlled trial. The Lancet, 386(10011),
2404-2412. doi:10.1016/s0140-6736(15)00308-6

Li, G., Mbuagbaw, L., Samaan, Z.,
Zhang, S., Adachi, J. D., Papaioannou, A., & Thabane, L. (2013).
Efficacy of vitamin D supplementation in depression in adults: a systematic
review protocol. Systematic Reviews, 2(1).

Mbaya, P. (2002). Safety and efficacy of
high dose of venlafaxine XL in treatment resistant major depression. Human
Psychopharmacology: Clinical and Experimental, 17(7), 335-339.

N., Po, A., & Knight, T. (2000).
Pharmacogenetics and psychopharmacotherapy. Journal of Clinical
Pharmacy & Therapeutics, 25(3), 197-220.

Roy, J. (2005).
Cyp3A5 Genetic Polymorphisms In Different Ethnic Populations. Drug
Metabolism and Disposition, 33(7), 884-887. doi:10.1124/dmd.105.003822

Samantha J., T., Mirae, S., Melvin G., M., &
Jolene R., B. (2015). Combination Therapy with Monoamine
Oxidase Inhibitors and Other Antidepressants or Stimulants: Strategies for the
Management of Treatment-Resistant Depression. Pharmacotherapy: The
Journal Of Human Pharmacology And Drug Therapy, (4), 433.

S. M. (2013). Stahl’s essential
psychopharmacology: Neuroscientific basis and practical applications (4th
ed.). New York, NY: Cambridge University Press

Z., Huan, Y., Shichang, Y., Wei, L., Ping, D., Changhong, W., & Yalin, Z.
(2013). Antidepressants for bipolar disorder: A meta-analysis of randomized,
double-blind, controlled trials**. Neural Regeneration Research,
(31), 2962. doi:10.3969/j.issn.1673-5374.2013.31.009

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