NURS 6501 Week 9 Assignment Psychological Disorders

Pathophysiology of Primary Diagnosis

Depression pathophysiology is highly polygenic, with thousands of variants influencing serotonin, dopamine, and BDNF signaling, leading to impaired neuroplasticity and stress resilience (Cui et al., 2024). Major Depressive Disorder (MDD) results from multifactorial impairments in brain chemistry, stress regulation, and immune function. Traditional monoamine hypotheses highlight deficits in serotonin, norepinephrine, and dopamine signaling, which underlie low mood and anhedonia. Chronic stress triggers hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, causing prolonged elevations in cortisol that impair hippocampal neurogenesis and encourage neuronal atrophy. In parallel, neuroinflammation—marked by increased cytokines IL-6 and TNF-α—redirects tryptophan metabolism towards neurotoxic kynurenine metabolites, further reducing serotonin and intensifying glutamatergic excitotoxicity (Kouba et al., 2024). Genetic susceptibility (e.g., SLC6A4, BDNF) and early‐life adversity converge epigenetically to increase vulnerability, as decreases in BDNF and EGF impair synaptic plasticity, reinforcing depressive phenotypes.

Causes 

Risk Factors (genetic/ethnic/physical)

Major Depressive Disorder is caused by the interplay of genetic, neurochemical, inflammatory, and neuroplastic changes. Genomic studies have identified thousands of small-effect variants that converge on neurotransmitter systems (serotonin, dopamine), neurotrophic factors (BDNF), and stress‐response pathways (HPA axis) (Cui et al., 2024). Microglial activation and peripheral cytokines induce neuro-inflammation that disrupts tryptophan metabolism, lowering serotonin availability and synaptic plasticity. 

·         Genetic/Ethnic: MDD family history; SLC6A4, BDNF, and FKBP5 gene polymorphisms (de Menezes Galvão et al., 2021).

·         Physical: Chronic diseases (e.g., cardiovascular disease), sleep disorders, and HPA-axis dysregulation due to chronic stress (Kouba et al., 2024).

·         Environmental: Early‐life trauma, social isolation, and socioeconomic adversity epigenetically alter stress-response genes, enhancing vulnerability.

Signs and Symptoms – Common presentation

How does the diagnosis impact each body system? Complications?

·         Persistent depressed mood and anhedonia (lack of pleasure).

·         Sleep disturbances can manifest as hypersomnia or insomnia.

·         Changes in appetite/weight loss or gain.

·         Psychomotor agitation or retardation.

·         Fatigue, low energy.

·         Neuroendocrine: Hypercortisolemia due to HPA-axis overactivity → metabolic syndrome, osteoporosis.

·         Cardiovascular: Inflammatory marker increase and platelet activation → higher risk of myocardial infarction and stroke (Cui et al., 2024).

·         Immune: Chronic inflammation increases vulnerability to infections and autoimmune diseases (Kouba et al., 2024).

·         Cognitive: Impaired concentration/memory raises risk of dementia and functional decline.

·         Psychosocial: Social withdrawal, occupational impairment, and increased suicide risk (Cui et al., 2024).

·         Hypothyroidism (E03.9): May simulate depressive symptoms—fatigue, weight gain, low mood—ruled out by TSH assay.

·         Bipolar II Disorder (F31.81): Has depressive episodes but with history of hypomania—screen with Mood Disorder Questionnaire.

·         Adjustment Disorder with Depressed Mood (F43.21): Depressive symptoms due to identifiable stressor—remission within 6 months of stress resolution.

·         PHQ-9 Questionnaire: Standardized screening instrument for depression severity.

·         Thyroid Stimulating Hormone (TSH): To rule out hypothyroidism.

·         Complete Blood Count and CMP: • To diagnose anemia, electrolyte abnormalities affecting mood.

·         Serum B12 and Folate: Deficiency can manifest with depressive-like behaviour.

·         Urine Drug Screen: To exclude substance-induced mood disorder.

Pharmacologic

·         First-line Antidepressants: SSRIs (e.g., sertraline 50 mg daily)—well tolerated with evidence of efficacy (Tian et al., 2022).

·         Rapid‐acting Agents: Ketamine infusions for treatment-resistant depression.

Non-Pharmacologic

·         Cognitive Behavioral Therapy (CBT): • Meta-analyses demonstrate strong improvement in MDD symptoms compared to control (Cuijpers et al., 2023).

·         Physical Exercise: Aerobic exercise decreases inflammatory markers and enhances mood.

·         Mindfulness‐Based Stress Reduction (MBSR): Enhances HPA-axis regulation and reduces rumination.

Referrals

·         Psychiatry: For refractory or complex cases needing advanced interventions (ECT, TMS).

·         Psychology/Counseling: For group or individual therapy modalities.

·         Social Work/Psychosocial Support: To counteract socioeconomic and environmental stressors.