Duringthe office visit, I will ask the patient whether he was compliant with themedications that he had been taking over the years. This will help me tounderstand why some medications are not working. I will also question thepatient to see if he is noticed any symptoms of another illness such asdementia. I will ask the patient whether he has trouble falling asleep or hasthe urge to sleep more than usual.
I will ask the patient whether he has beendiagnosed with any new medical illnesses. I will also ask him whether he hasbeen prescribed any new medications from other providers. This may give ananswer to some of the patient’s symptoms and why some drugs were not successful. I will ask him whether he hasbeen feeling helpless, worthless, or has problems concentrating. I will alsoask whether he has been attending any psychotherapy because psychotherapy isalways good for the patient’s disease. I will ask his wife, caregivers and anygrown children whether they noticed any changes in the patient lately or at anytime during his treatment. I will ask them about his sleeping, eating habits,memory, behaviors and about any other life changing events or changes thatinvolved the patient. The families arealways a good source of information for the history of the patient.
DiagnosticsIwill order blood tests to check TSH and thyroxine to excludehypothyroidism, basic electrolytes andserum calcium to rule out a metabolic disturbance; and a full blood countincluding erythrocyte sedimentation rate (ESR) to rule out a systemic infectionor chronic disease. According to Hage and Azar (2012), patients with hypothyroidism usually manifest featuresof depression. Also, patients with hyperthyroidism present a wider spectrum ofneuropsychiatric symptoms including both depression and anxiety. I will alsoorder vitamin D level. According to Li,Mbuagbaw, Samaan, Zhang, Adachi, Papaioannou, and Thabane (2013), vitamin D deficiency is strongly linked todepression. Genetic testing could be done to target depression.
Stahl (2013) concludedthat genetic testing has the potential of assisting both in diagnoses ofpsychiatric illnesses and selecting psychotropic drugs. Differential DiagnosesMajordepressive disorder: is a mooddisorder that causes a persistent feeling of sadness and loss of interest. Thisis the most likely diagnosis of choice due to the patient having no joy, sad,feeling helpless, hopeless, worthless, and problems concentrating.Manicepisodes with irritable mood or mixed episodes:in this situation, the patient may be very irritable or have mood symptoms thatare similar to those seen in bipolar disorder.Mooddisorder due to another medical condition: This is mostlikely not the diagnosis. The patient does not have any medical conditions suchas multiple sclerosis, stroke, or heart disease that cause depression.
Pharmacologic AgentsIwill start with Effexor ER and Latuda as adjunct therapy. Lenze, Mulsant, Blumberger, Karp, Newcomer, Anderson, and Reynolds (2015) reported that the effectiveness ofsecond-generation atypical antipsychotics (SGA) can act as a successfuladjunctive medical agent for patients who fail to respond to pharmacologicalmonotherapy with antidepressants. Since the patient has been taking SSRIs, TCAs, SNRI, Tetracyclic antidepressants, andAnxiolytics, I will discontinue all anxiolytics at a tapered rate. Stahl (2013)concluded that anxiolytics are known to cause worsening of depression andsuicidal ideations.
Since the patient tolerated EffexorXR without any significant side effects, I will start Effexor XR with an initial dose of 75mg thenincrease the dosage until the patient isstable. Since the patient has no heart problems , the Effexor XR can beaugmented with Latuda starting at a dose of 20 mg per day with meals then increaseit until the max dose of 120mg is reached. I would not use the combination of MAOIs and TCAs because this combination isineffective. The combination of the MAOI with the second-generationantipsychotic can also cause symptoms of bipolar disorder (Yingli, Huan,Shichang, Wei,Ping, Changhong, & Yalin, 2013). The patient takes a Lipitor thatcan also cause depression. Therewere no improvements in depression from the first interim follow-up through thesixth interim follow-up. When the venlafaxine dose increased to 600 mg in the sixthinterim follow-up, the patient achieved complete remission of depression butdecreased to 450 mg due to irritability, insomnia and elevated blood pressure. Accordingto Mbaya (2002), high doses of venlafaxine is safe, well tolerated, improvessocial functioning, and is effective in a small number of severe treatmentresistant patients with major depression.
Roy (2005) concluded that genepolymorphisms are DNA variations that affect drug metabolizing enzymes. Thehepatic cytochrome P450s are a multigene family of enzymes that play a criticalrole in the metabolism of many drugs and xenobiotics with each cytochromeisozyme responding differently to exogenous chemicals in terms of its inductionand inhibition. Poolsup and Knight (2000) concluded that people from differentethnic backgrounds respond differently to certain drugs used to treat mentaldisorders. According to Roy (2005), geneticdifferences are more likely to provide the explanation for slower drugmetabolism rather than race. Lessons learnedLessonslearned from this case study was that depression can be recurrent and canmanifest due to shorter periods of wellness, poor inter-episode recovery andultimately treatment resistance. Continuous research and study should be doneto look at what ways depression could be fought. I learned a great deal aboutadjunct therapy that will help me treatmy patients with depression. I also learned about the different classes ofdrugs that are used for multiple diagnoses (Buck & Ruskin, 2008).
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