NR 603 WEEK 2 Mental Health Management Plan and Analysis

Sample Answer

Management plans and analysis of different medical, psychiatric, and surgical diseases are key in integrating learned knowledge into practice. This paper aims to develop a patient management plan that includes pharmacological and non-pharmacological interventions. The paper will also discuss the analysis of a mental health case by describing the pathophysiology, pharmacology, practical clinical guidelines, follow-up and referrals, quality of care, and coding and billing.

Management Plan

Primary Diagnosis

Patient’s SD. primary diagnosis is generalized anxiety disorder (GAD). However, for a diagnosis to be established, several diagnostic tests should be performed to exclude medical, psychiatric, and surgical causes of anxiety (Meuret et al., 2020).

Diagnostic testing

The tests will include complete blood count, urinalysis, thyroid function tests, toxicology screens, electrolyte studies, and blood sugars. In addition, imaging tests should also be performed, including chest or brain computed tomography or magnetic resonant imaging, chest radiograph, electroencephalogram, and electrocardiography.

The tests exclude several differential diagnoses, including drug or alcohol use, depression, insomnia, diabetes mellitus, pheocytochroma, pulmonary diseases, ischemic heart disease, thyroid diseases, and brain lesions. GAD-2 and GAD-7 are the two screening and diagnostic tests commonly used in establishing and grading the severity of GAD after the exclusion of other causes of anxiety.

Medications

The most frequently used medications used in the management of GAD are selective serotonin reuptake inhibitors (SSRIs). The patient will be prescribed fluoxetine 20 mg PO once daily.

Non-pharmacologic interventions

Psychotherapy interventions like cognitive-behavioral therapy, relaxation therapy, and worry exposure will be used as adjuncts to pharmacotherapy (Gray et al., 2024).

Follow-up schedule and referrals

A weekly follow-up will be scheduled for the patient to review any symptomatic relief, new symptoms, and adverse effects of the prescribed medications. However, if there is marked improvement to the prescribed medications and psychotherapy, the follow-up visits will be spaced to once every two weeks and once monthly. The patient will be referred to a psychiatrist, clinical psychologist, and community social groups to offer additional specialist support to the patient.

Analysis

Pathophysiology

GAD pathogenesis occurs due to disruption in neurotransmission between the prefrontal cortex and the amygdala, hippocampus, insula, and thalamus and alteration in serotonin activity. Several genetic and environmental factors cause altered serotonergic neurotransmission. For example, a genetic mutation in genes such as MAOA that encodes for serotonin neurotransmitter channels and receptors causes disruptions in its neurotransmission pathway and predisposes persons to GAD (Mishra et al., 2023).

On the other hand, environmental factors that predispose persons to GAD include constant stress. Stress causes upregulation in the production of cortisol in the body, resulting in an increase in the amount of inflammatory cytokines in the body, which inhibit 5-hydroxytryptophan 1 (5-HT1) neurotransmission between the amygdala and the prefrontal cortex, resulting in anxiety.

Reduction in brain-derived neurotrophic factor (BDNF) causes alterations in hippocampal brain cell connections, thus promoting the release of cortisol and increasing the risk for anxiety(Bamalan et al., 2023).Neuroplasticity in the hippocampus and amygdala causes disruptions in the circuitry of the prefrontal cortex, resulting in disruptions in attention, emotion, learning, and memory.

Additionally, enhanced prefrontal and amygdala activity causes an unregulated response to stress, resulting in anxiety. Neurotransmitter imbalances affecting serotonin, dopamine, GABA, and norepinephrine also predispose persons to GAD, where reduced GABA activity causes a reduction in inhibition of anxiety and fear responses in the amygdala, resulting in GAD. In contrast, decreased serotonin affects neurotransmission between the amygdala and prefrontal cortex.

Pharmacology

SSRIs are commonly used in managing GAD as they have minimal side effects. SSRIs inhibit serotoninreuptake transporter (SERT) located at neuronal axonal terminals in various sites, including the amygdala and thalamus. In addition, the drugs may inhibit dopamine and norepinephrine reuptake weakly at various sites. Inhibition of serotonin uptake increases its concentration at the synapse (Edinoff et al., 2021). This promotes the diffusion of serotonin to the post-synaptic neuron, increasing serotonin neurotransmission.

As a result, serotonin neurotransmission between the prefrontal cortex and the thalamus, hippocampus, and amygdala is restored, and anxiety relief is achieved. In addition, SSRIs’ effect on inhibiting the reuptake of norepinephrine causes an increase in its output, which leads to upregulation in levels of regulatory factors such as BDNF, reducing the number of inflammatory mediators and neuroinflammation. SSRIs also reduce neuronal plasticity in the amygdala and hippocampus, improving memory and attention.

Additional Analysis

Clinical guidelines in GAD provide a plan of management for GAD patients. The guidelines state that a GAD diagnosis is made after medical and psychiatric causes of anxiety are excluded. What follows should be severity grading and approach to treatment. Patient education, pharmacotherapy, and psychotherapy should be initiated for the diagnosed patients (Raju et al., 2023). In addition, the patient is provided with relevant information that can help him while at home and connected to persons who can provide specialized psychotherapy.

Pharmacotherapy with SSRIs is often recommended as the first-line therapy, with benzodiazepines, serotonin-norepinephrine receptor inhibitors (SNRIs), buspirone, and bupropion used as alternatives (Faganet et al., 2023). However, clinical guidelines recommend the use of one form of pharmacotherapy or psychotherapy in the management of GAD. In addition, they recommend the initial use of psychotherapy before introducing pharmacotherapy. However, this decision lies in the physician’s clinical judgment based on the patient’s symptoms and whether the patient is willing to use both forms of treatment.

Guidelines also recommend regular therapy, starting with short intervals at the beginning of therapy and moving to longer intervals with eventual symptom relief.

Follow-Up and Referral

As mentioned earlier, clinical guidelines recommend regular follow-ups for GAD patients after initiation of treatment. During the follow-up session, an inquiry into symptomatic alleviation should be done (Toledo-Chávarri et al., 2020). Modification should begin if there is a poor or inadequate response to the treatment. For example, if the patient was on once-weekly psychotherapy, the number of sessions may be increased to meet the patient’s needs. This also applies to the patient’s medication, where the dosage may be up-titrated to higher doses or an adjunct drug prescribed.

During these sessions, the healthcare provider should also inquire whether the patient is experiencing any adverse effects of the medications prescribed, such as sexual dysfunction. Alternatives to SSRIs should only be considered if the patient is not tolerant (Faganet et al., 2023). Follow-up sessions can also provide positive feedback where there is a significant improvement in the patient’s symptoms, necessitating a reduction in the number of sessions or dosage of medication. However, the medications should continue up to a year after the prescription. Referral sessions to psychiatrists are commonly done for further evaluation to ensure optimal results.

Quality

This week’s discussion has majored in GAD. I have learned about the DSM-V diagnosis of GAD in adults and the recommended steps required to establish the diagnosis. I have also learned that medical and psychiatric diseases such as hyperthyroidism, pheocytochroma, brain tumors, depression, and pulmonary diseases are also associated with anxiety and the need to screen for such diseases through laboratory and imaging tests (Meuret et al., 2020). Furthermore, I have gained knowledge on various screening tests, including the role of GAD-2 and GAD-7 in screening and grading the severity of GAD in patients.

The clinical guidelines have also provided me with procedural step knowledge on managing patients who are either responsive or poorly responding to pharmacotherapy or psychotherapy (Raju et al., 2023). I have also learned about the different pharmaco-therapeutic agents that can be used to manage GAD, with SSRIs being the first-line agents (Faganet et al., 2023). In addition, I have learned the importance of regular follow-up of GAD patients and the role of referring patients to various specialists for optimal results.

Coding and Billing

F41.1 is a billable ICD-10-clinical modification code used to indicate a diagnosis for reimbursement purposes for GAD (ICD-10-CM Diagnosis Code F41.9, n.d.). It is also applicable to anxiety neurosis, reaction, and state or an overanxious disorder. Other billable codes used include F41.8. F41.8 codes for other unspecified anxiety disorders and applies to mild or non-persistent anxiety depression, anxiety hysteria, and mixed anxiety and depressive disorder.

Conclusion

GAD is an anxiety disorder characterized by increased worry present for more days than not for a six-month duration. The diagnosis causes disruptions in memory, attention, and sleep. When establishing a diagnosis, one must screen and exclude medical and psychiatric illnesses associated with heightened anxiety. It is also vital to follow provided clinical guidelines that provide steps crucial in the management of anxiety.

References

• Bamalan, O. A., Alosaimi, N. M., Alfryyan, A. A., Aljubran, H. J., Alanazi, F. H., & Siddiqui, Z. I. (2023). Generalized Anxiety Disorder A Review of Current Literature in Saudi Arabia. Psychology, 14(01), 35–51. https //doi.org/10.4236/psych.2023.141003
• Edinoff, A. N., Akuly, H. A., Hanna, T. A., Ochoa, C. O., Patti, S. J., Ghaffar, Y. A., Kaye, A. D., Viswanath, O., Urits, I., Boyer, A. G., Cornett, E. M., & Kaye, A. M. (2021). Selective Serotonin Reuptake Inhibitors and Adverse Effects A Narrative Review. Neurology International, 13(3), 387–401. https //doi.org/10.3390/neurolint13030038
• Fagan, H. A., & Baldwin, D. S. (2023). Pharmacological treatment of generalised anxiety disorder Current practice and future directions. Expert Review of Neurotherapeutics, 23(6), 535–548. https //doi.org/10.1080/14737175.2023.2211767
• Gray, B., Asrat, B., Brohan, E., Chowdhury, N., & Dua, T. (2024). Management of generalized anxiety disorder and panic disorder in general health care settings New WHO recommendations. World Psychiatry, 23(1), 160-161. https //doi.org/10.1002/wps.21172
• ICD-10-CM Diagnosis Code F41.9 Anxiety disorder, unspecified. (n.d.). Www.icd10data.com. https //www.icd10data.com/ICD10CM/Codes/F01-F99/F40-F48/F41-/F41.9
• Meuret, A. E., Tunnell, N., & Roque, A. (2020). Anxiety Disorders and Medical Comorbidity Treatment Implications. Advances in Experimental Medicine and Biology, 1191, 237–261. https //doi.org/10.1007/978-981-32-9705-0_15
• Mishra, A. K., & Varma, A. R. (2023). A Comprehensive Review of the Generalized Anxiety Disorder. Cureus, 15(9). https //doi.org/10.7759/cureus.46115
• Raju, N. N., Naga Pavan Kumar, K. S. V. R., &Nihal, G. (2023). Clinical Practice Guidelines for Assessment and Management of Anxiety and Panic Disorders in Emergency Setting. Indian Journal of Psychiatry, 65(2), 181–185. https //doi.org/10.4103/indianjpsychiatry.indianjpsychiatry_489_22
• Toledo-Chávarri, A., Ramos-García, V., Torres-Castaño, A., Trujillo-Martín, M. M., Castro, W. P., Cura-Castro, I. D., Serrano-Aguilar, P., & Perestelo-Pérez, L. (2020). Framing the process in the implementation of care for people with generalized anxiety disorder in primary care A qualitative evidence synthesis. BMC Family Practice, 21. https //doi.org/10.1186/s12875-020-01307-6