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Question 1 – 4 A 21-year-old male college student was brought to Student Health Services by his girlfriend who was concerned about changes in her boyfriend’s behaviors. The girlfriend says that recently he began hearing voices and believes everyone is out to get him. The student says he is unable to finish school because the voices told him he was not smart enough. The girlfriend relates episodes of unexpected rage and crying. Past medical history noncontributory but family history positive for a first cousin who “had mental problems”. Denies current drug abuse but states he smoked marijuana every day during his junior and senior years of high school. He admits to drinking heavily on weekends at various fraternity houses. Physical exam reveals thin, anxious disheveled male who, during conversations, stops talking, cocks his head and appears to be listening to something. There is poor eye contact and conversation is rambling. Based on the observed behaviors and information from girlfriend, the APRN believes the student has schizophrenia.

Question 1 of 4: Describe the positive symptoms of schizophrenia and relate those symptoms to the case study patient. Question 2 of 4: Explain the genetics of schizophrenia. Question 3 of 4: The APRN reviews recent literature and reads that neurotransmitters are involved in the development of schizophrenia. What roles do neurotransmitters play in the development of schizophrenia? Question 4 of 4 The APRN reviews recent literature and reads that structural problems in the brain may be involved in the development of schizophrenia. Explain what structural abnormalities are seen in people with schizophrenia.

Question 1 – 6 A 34-year-old female was brought to the Urgent Care Center by her husband who is very concerned about the changes he has seen in his wife for the past 3 months. He states that his wife has had been depressed and irritable, has complaints of extreme fatigue, has lost 10 pounds and has had insomnia. He has come home from work to find his wife sitting in front of the TV and not moving for hours. In the past few days, she suddenly has become very hyperactive, has been talking incessantly, has easily distracted and seems to “flit from one thing to another.” She hasn’t slept in 3 days. The wife went on an excessive shopping spree for new clothes that resulted in their credit card being denied for exceeding the line of credit. The wife is unable to sit in the exam room and is currently pacing the hallway muttering to herself and is reluctant to talk with or be examined the ARNP. Physical observation shows agitated movements, rapid fire speech, and hyperactivity. Based on the history and observable symptoms, the APRN suspects that the patient has bipolar type 2 disorder. The APRN refers the patient and husband to the Psychiatric Mental Health Nurse Practitioner for evaluation and treatment.

Question 1 of 6: Discuss the role genetics plays in the development of bipolar 2 disorders. Question 2 of 6: Explain how the hypothalamic-pituitary-adrenal (HPA) system may be associated with bipolar type 2 disease. Question 3 of 6: Discuss the role inflammatory cytokines play in the development and exacerbation of bipolar type 2 symptoms Question 4 of 6: Discuss the role of the amygdala in bipolar disorder. Question 5 of 6: How does neurochemical dysregulation contribute to bipolar disorders? Question 6 of 6: What is the current status of the use of nutraceuticals in management of depression?

Question 1 – 2 A 27-year-old female presents to the Emergency Room, with a chief complaint of palpitations, rapid heart rate, sweating, tremors, and inability to catch her breath. The symptoms started about 10 hour ago and have gotten worse. She states that she has some chest pain that remains constant no matter what. She also has numbness and tingling around her mouth and lips. She says she knows something “terrible is going to happen.” She denies having any similar episode in the past. Past medical history noncontributory. Social history significant for recent stressor of applying for medical school and taking the Medical College Admission Test (MCAT). She had not received the results prior to the episode but is sure that the failed the test. Says she doesn’t know if anyone else in her family has had similar episodes. Physical exam reveals a thin, anxious appearing female who is profusely sweating despite cool ambient air temperature. BP 176/88, Pulse 136, and respirations 26. Electrocardiogram negative for evidence of myocardial infarction and all lab data within normal limits except for mild respiratory alkalosis. The patient’s symptoms are subsiding and the patient states he is feeling better. The APRN suspects the patient has just experienced a panic attack.

Question 1 of 2: What are panicogens and how do they contribute to the development of panic attack symptoms? Question 2 of 2: How does the GABA-benzodiazepine (BZ) receptor systems contribute to panic attacks/disorders?

Question 1 – 2 A 21-year-old female college junior makes an appointment to see the APRN in the Student Health Clinic. The student tells the APRN that it has gotten harder and harder for her to attend classes, especially her history class where the class is preparing for the semester’s end presentations. She says that she is terrified to speak to the class and is considering dropping the class so she will not have to present. She has a significant impairment in social activities and has resigned from her sorority. She is unable to go to the library to study as she feels everyone is looking at her and mocking her. She admits to having some of these symptoms in high school, but the guidance counselor was able to work with her to decrease some of her symptoms. Past medical history noncontributory except for the milder symptoms exhibited in high school. Family history noncontributory. Social history positive for anxiety related to social situations that has had a negative impact on both her scholarly and social endeavors. The APRN diagnoses the student with social anxiety disorder (SAD).

Question 1 of 2: Describe the areas of the brain that are associated with social anxiety disorder. Question 2 of 2: How is oxytocin associated with SAD?

Question 1 – 2 A 36-year-old female comes to see the APRN in clinic with a chief complaint of “I’m so and I feel all keyed up all the time”. She states that she feels restless, keyed up, and on edge most of the time. She fatigues easily and has difficulty concentrating and says her mind goes blank. She admits to being irritable and snapping at her coworkers which she worries will affect her job. She says the symptoms have been present for about 8 or 9 months. and Increased muscle tension. She has had difficulty falling asleep or stay sleeping. Further questioning revealed that prior to her symptoms, her parents got divorced which has been a great stressor for her. Past medical history noncontributory. Social history positive for a case of “nerves” when she was in high school that seemed to resolve after she graduated from college. No drug or alcohol history. The APRN believes the patient has generalized anxiety disorder (GAD). Question 1 of 2: Discuss the role of neurotransmitters in the expression of GAD. Question 2 of 2: Explain the structural brain changes that occur in people with GAD.

Question 1 – 2 A 27-year-old man comes to the Veteran’s Administration Hospital at the insistence of his fiancée who accompanies him to the appointment. She tells the APRN that her fiancée has not “been the same” since he returned from his second tour in Iraq. He was an infantryman with a local Marine Reserve unit and served 2 tours and was honorably discharged. Since his return, he has had difficulty sleeping, and says that he “sleeps with one eye open” and fears sleep. Deep sleep brings vivid nightmares. He gruffly admits to having experienced several traumatic events during his second tour of duty. He is unwilling to discuss them and will not reveal specific details. He is short tempered and irritable and is afraid to be around people as he doesn’t want to snap at people and alienate them. He startles easily at loud noises, especially the sounds of cars backfiring. He admits to thinking there are threats everywhere and spends an excessive amount of time searching for them but never finding any. He has intrusive memories almost every day and says he really isn’t interested in doing much of anything. He is very worried that these symptoms are irreparably hurting his relationship with his fiancée who he loves very much. The APRN diagnoses him with post-traumatic stress disorder (PTSD).

Question 1 of 2: Describe the changes seen in the brain structure in patients with PTSD. Question 2 of 2: Briefly discuss the role glucocorticoids may have on the development of PTSD.

Question 1 – 2 A 17-year-old male high school junior comes to the clinic to establish care. He recently moved from a relatively urban area to a very rural area and has just started his junior year in a new school. The mother states that she has noticed that her son has been frequently washing his hands and avoids contact with any dirty or soiled object. He uses paper towels or napkins over the knob on a door when opening it. According to the mother, this behavior has just appeared since moving. The patient, upon close questioning, admits that he is “grossed out” by some of the boys in the boys’ room since they use the toilet and do not wash their hand afterwards. He is worried about all the germs the boys are carrying around. Past medical history is noncontributory. Social history -lives with parents and 2 siblings in a house in a new town. Is an honors student. Based on these behaviors, The APRN thinks the patient has obsessive-compulsive disorder (OCD).

Question 1 of 2: What is primary pathophysiology of OCD? Question 2 of 2: Describe the role the dorsal anterior cingulate cortex (dACC) has in reinforcement of obsessive behaviors.

Paper For Above Instructions

Schizophrenia case and questions: The positive symptoms of schizophrenia are overt, experiential phenomena that reflect an excess or distortion of normal functioning. They include delusions (believing others intend to harm you or that you possess special powers), hallucinations (most commonly auditory, such as hearing voices), disorganized speech (loosely connected or incoherent speech), and disorganized or abnormal behavior (agitation, unpredictable actions, or catatonia). In the presented case, the patient reports auditory hallucinations (“voices”) and persecutory delusions (believing others are out to get him), along with rambling and impaired communication, which align with classic positive symptoms. Neurobiologically, positive symptoms have been linked to excess dopaminergic activity in mesolimbic pathways (particularly with the ventral tegmental area projecting to the nucleus accumbens and limbic structures). Antipsychotic medications that block D2 receptors are effective at reducing these symptoms, supporting a dopaminergic contribution (APA, 2022). Genetic factors contribute to schizophrenia risk, with heritability estimates around 80%, indicating strong polygenic risk and gene-environment interactions; however, no single gene explains most cases (APA, 2022; Kahn et al., 2008). Neurotransmitter systems implicated include dopamine, glutamate, GABA, and serotonin, with dysregulation across development leading to symptom emergence (Kapur et al., 2005; Javitt, 2009). Structural abnormalities frequently reported in schizophrenia include ventricular enlargement, reduced gray matter in prefrontal and temporal regions, and disrupted white matter integrity, reflecting neurodevelopmental disturbances (Lawrie & Abukmeil, 1998; Shenton et al., 2001). These findings help explain cognitive deficits and disconnection syndromes observed in schizophrenia (APA, 2022; Lewis & Lieberman, 2000).

The bipolar II case highlights several core themes in mood disorders. Genetics contribute to bipolar disorders with a substantial heritable component, though specific genes remain polygenic and complex (Merikangas et al., 2011). The HPA axis can be dysregulated in mood disorders; chronic stress exposure can influence cortisol levels and stress responsiveness, potentially contributing to mood episode onset and recurrence (Keller et al., 2017). Inflammatory cytokines have been associated with mood symptomatology and may participate in neuroinflammatory processes that accompany mood dysregulation (Miller et al., 2009). The amygdala often shows heightened reactivity in bipolar disorder, particularly during mood shifts or emotional processing, implicating limbic dysregulation in symptom expression (Phillips & Swartz, 2008). Neurochemical dysregulation, including alterations in monoamines (dopamine, norepinephrine, serotonin) and glutamatergic signaling, underpins mood instability and manic/depressive episodes (Benabara et al., 2012). Nutraceuticals continue to be explored for antidepressant effects; however, evidence remains variable and not uniformly recommended in standard practice (Gelenberg et al., 2010).

Panic attack physiology centers on autonomic arousal and limbic-cortical circuitry. Panicogens are substances or stimuli that trigger panic attacks via abrupt activation of fear networks, including the amygdala and interoceptive pathways. GABAergic inhibitory control via GABA-A receptors and modulation by benzodiazepines helps dampen excessive excitability in fear circuits, reducing panic symptoms; dysregulation of this system is linked to susceptibility to panic attacks and panic disorder (Nutt & Ballenger, 2001; Taylor et al., 2012). In the presented vignette, the acute panic-like surge with autonomic symptoms aligns with panicogenic system activation, while treatment targets often include GABAergic modulation to restore inhibitory control (APA, 2023).

The social anxiety case emphasizes neurocircuitry for social threat processing. Brain regions implicated in SAD include the amygdala, prefrontal cortex (particularly medial PFC), anterior cingulate, and hippocampus, which together contribute to heightened vigilance and avoidance in social contexts (Etkin & Wager, 2007). Oxytocin, a neuropeptide involved in social affiliation and trust, has been studied for its potential to modulate social anxiety symptoms by influencing amygdala reactivity and social information processing (Heinrichs & Domes, 2008).

The generalized anxiety disorder vignette highlights neurotransmitter involvement in sustained worry and hyperarousal, with dysregulated GABAergic, glutamatergic, and serotonergic systems implicated in anxious arousal and excessive sympathetic output (Nutt et al., 2010). Structural brain changes in GAD may include altered connectivity in fear and affect regulation networks, such as the prefrontal cortex, amygdala, and anterior cingulate, contributing to sustained anxious symptoms (Etkin & Wager, 2007).

The PTSD case reflects enduring fear conditioning and stress-related neurobiological changes. Brain structure and function alterations in PTSD commonly involve reduced hippocampal volume, amygdala hyperresponsivity, and prefrontal cortex hypoactivity, which contribute to impaired fear extinction and dysregulated fear responses (Yehuda, 2002; Bremner, 2003). Glucocorticoids and the HPA axis are central to the stress response and modulate memory consolidation and fear processing, with dysregulation contributing to PTSD maintenance and symptom severity (Keller et al., 2017).

OCD hinges on dysregulated cortico-striato-thalamo-cortical circuits, with the dorsal anterior cingulate cortex (dACC) playing a crucial role in error monitoring and reinforcement of compulsive behaviors. Pathophysiology involves abnormal glutamatergic and serotonergic signaling within these circuits, contributing to the persistence of obsessions and compulsions (Saxena & Rauch, 2000; Menzies et al., 2008).

In sum, these cases illustrate core psychiatric phenomena underpinned by shared and distinct neurobiological mechanisms: positive symptoms and dopaminergic hypersensitivity in schizophrenia; genetic vulnerability and neurochemical/inflammatory pathways in bipolar disorder; amygdala-centric fear circuitry in panic and SAD; GAD’s diffuse neurotransmitter involvement and structural connectivity alterations; PTSD’s stress biology with hippocampal/prefrontal-amygdala changes and glucocorticoid involvement; and OCD’s CSTC circuit dysfunction with the dACC central to symptom reinforcement. Clinically, understanding these mechanisms informs diagnosis, prognosis, and multimodal treatment approaches, including pharmacotherapy, psychotherapy, and, where appropriate, nutraceuticals and lifestyle interventions (APA, 2022; NIMH, 2023).

References

• American Psychiatric Association. DSM-5-TR. American Psychiatric Publishing; 2022.
• National Institute of Mental Health. Schizophrenia. https://www.nimh.nih.gov/health/topics/schizophrenia. Accessed 2024.
• Kapur S, Kishore KS, et al. The dopamine hypothesis of schizophrenia: making sense of an old idea. Am J Psychiatry. 2009;166(5):547–558.
• Lawrie SM, Abukmeil SS. Brain MRI structural abnormality in schizophrenia: a meta-analysis of systematic reviews. Hum Brain Mapp. 1998;6(6):395–404.
• Lewis DA, Lieberman JA. Catching up to the circuitry of schizophrenia: a focus on the prefrontal cortex. Nat Rev Neurosci. 2000;1(1):13–23.
• Javitt DC. Glutamate and schizophrenia: phasic and tonic signaling. Trends Pharmacol Sci. 2009;30(1):2–4.
• Etkin A, Wager TD. Functional neuroimaging of anxiety: a meta-analysis. Am J Psychiatry. 2007;164(10): 806-–15.
• Yehuda R. PTSD: role of the hippocampus in memory and fear processing. Dialogues Clin Neurosci. 2002;4(3): 287-–90.
• Bremner JD. Structural and functional brain changes in PTSD: insights from neuroimaging. Neuropsychol Rev. 2003;13(3): 147–75.
• Saxena S, Rauch SL. Functional neuroimaging and OCD: a critical review. Psychiatr Clin North Am. 2000;23(2): 257–74.