Appropriate Drug Therapy for a Patient who Presents with MDD and a History of Alcohol Abuse

The patient can benefit from a combination of antidepressants and drugs used for managing alcohol use disorder. Relevant antidepressant medications include serotonin-norepinephrine reuptake inhibitors such as sertraline (McHugh & Weiss, 2019). On the other hand, examples of medications used to manage alcohol use disorder include naltrexone and disulfiram (McHugh & Weiss, 2019). Notably, a combination of sertraline with naltrexone provides adequate symptomatic relief and minimizes relapse to alcohol use (McHugh & Weiss, 2019). Pharmacotherapy is contraindicated in people with known hypersensitivity. The oral solution of sertraline should not be administered concomitantly with disulfiram because it contains alcohol (McHugh & Weiss, 2019). Patients are likely to experience symptom relief after three weeks of antidepressant therapy (Stern et al., 2016).

Predictors of Late Onset Generalized Anxiety Disorder

Generalized anxiety disorder (GAD) presents with various manifestations. To begin with, patients exhibit considerable worry and anxiety for a minimum of six months (Showraki et al., 2020). Secondly, they demonstrate an inability to control worry. Also, the patient presents with at least three of the following symptoms:  restlessness, fatigue, inability to concentrate, irritability, impaired sleep, and muscle tension (Showraki et al., 2020). Fourthly, social and vocational spheres are impaired by anxiety (Showraki et al., 2020). Fifthly, there is no biological reason/cause for the anxiety. Late-onset GAD has been linked to different risk factors. They include the female population, recent traumatic events, separation or loss of loved ones, and chronic medical conditions such as heart failure, cognitive impairments, phobias, dyslipidemia, and depression (Hellwig & Domschke, 2019).

Potential Neurobiology Causes of Psychotic Major Depression

Various pathways have been implicated in the neurobiology of psychotic major depression. The first cause is neurotransmitter abnormalities. Defective monoamine transmission increases the risk of depression (Rege, 2022). Examples of monoamines include serotonin, dopamine, and noradrenaline (Rege, 2022). The action of these neurotransmitters is interrelated. Depletion of monoamine neurotransmitters increases the risk of psychotic major depression (PMD) (Rege, 2022). Also, elevated glutamatergic neurotransmission increases the risk of PMD. The second cause is abnormalities in the structure and function of the brain. Dysregulation of the ventral and dorsal networks increases the risk of PMD (Rege, 2022). Thirdly, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis increases the likelihood of PMD (Rege, 2022). Notably, hypersecretion of corticotropin-releasing hormone predisposes an individual to PMD (Rege, 2022). Fourthly, neuro-inflammation and decreased neuroplasticity increase the risk of PMD (Rege, 2022).

Symptoms Required for an Episode of Major Depression to Occur

Firstly, an individual should be depressed most of the time, almost daily. Secondly, an individual should demonstrate anhedonia for the majority of the time, almost daily (Truschel & Fazel, 2022). Thirdly, an individual should demonstrate unexplained changes in weight or appetite almost daily (Truschel & Fazel, 2022). Fourthly, there should be an objective diminution in physical movement and thought processes (Truschel & Fazel, 2022). Fifthly, an individual should experience fatigue almost daily. Sixthly, an individual should feel worthless or unwarranted guilt almost daily (Truschel & Fazel, 2022). In addition, the individual should experience decreased mental clarity or indecisiveness almost daily. Lastly, there should be persistent suicidal ideations or attempts (Truschel & Fazel, 2022).

Three Classes of Drugs That Precipitate Insomnia

Dopheide (2020) reports that examples of drugs that cause insomnia are alpha-blockers, beta-blockers, corticosteroids, and selective serotonin-reuptake inhibitors (SSRIs). Alpha-blockers cause insomnia by decreasing rapid eye movement sleep (Neel, 2013). Examples of alpha-blockers include prazosin, tamsulosin, and doxazosin (Neel, 2013). On the other hand, beta-blockers cause insomnia by inhibiting the secretion of melatonin (Neel, 2013). Examples of beta blockers include propranolol, metoprolol, timolol, and carvedilol (Neel, 2013). Further, corticosteroids cause insomnia by activating the HPA axis, decreasing melatonin levels, and decreasing the activation of GABAergic transmission (Neel, 2013). Examples of corticosteroids include prednisone, betamethasone, triamcinolone, fluticasone, and methylprednisolone (Neel, 2013). Finally, SSRIs cause insomnia in about 10 to 20 percent of patients (Neel, 2013). Examples of SSRIs include fluoxe