Mental Health: Mental disorder case analysis

This Knowledge Check reviews the topics in Module 6 and is formative in nature. It is worth 20 points where each question is worth 1 point. You are required to submit a sufficient response of at least 2-4 sentences in length for each question.

Mental disorder case analysis

Schizophrenia

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A girlfriend brought a 21-year-old male college student to Student Health Services because she was concerned about changes in her boyfriend’s behavior. According to his girlfriend, he has recently begun hearing voices and believes that everyone is out to get him. The student claims he is unable to complete his education because the voices told him he was not intelligent enough. The girlfriend describes bouts of unexpected rage and sobbing. Past medical history was noncontributory, but there was a positive family history for a first cousin who “had mental problems.” He denies current drug use but admits to smoking marijuana every day during his junior and senior years of high school. On weekends, he admits to binge drinking at various fraternity houses. Physical examination reveals a thin, anxious, disheveled male who stops talking, cocks his head, and appears to be listening to something during conversations. The conversation is rambling and there is little eye contact.

The APRN believes the student has schizophrenia based on the observed behaviors and information from the girlfriend.

Q1.Describe the symptoms of schizophrenia and relate them to the patient in the case study

Schizophrenia frequently alters how people think, feel, and behave, and this varies from person to person. Symptoms can appear and disappear abruptly. Nobody has all of the symptoms at the same time. Positive symptoms of schizophrenia include highly exaggerated ideologies, perceptions, or actions that demonstrate an individual’s inability to distinguish between what is real and what is not. Positive symptoms include hallucinations, in which the individual sees, hears, smells, or feels things that no one else does; and delusion, which refers to beliefs that appear strange to most people but are easily disproven. However, the affected person may believe that someone else is attempting to control their brain through means such as television or the belief that someone is out to get them; confused thoughts and disorganized speech; difficulty concentrating, movement disorders. In this scenario, for example, the patient believes that someone is out to get him when this is not the case. Furthermore, the patient’s behavior changed and he began to drink heavily on weekends.

Q2. Describe the genetics of schizophrenia

The precise cause of schizophrenia is unknown, but a combination of genetic and environmental, altered brain chemistry and structure may all play a role. Furthermore, the inheritance pattern is unknown. Individuals with a family member who has schizophrenia, on the other hand, have a higher risk of developing schizophrenia than the general population. Most people who have a close relative with schizophrenia will not develop the disorder themselves. Schizophrenia and bipolar disorders share some genetic similarities in that they share risk genes. A proclivity for schizophrenia can run in families. However, only one percent of the general population develops it over their lifetime, but if one of the parents has schizophrenia, the children have a 10% chance of developing it. In this particular case, the patient has a positive family history for a first cousin who “had mental problems,” implying that he is also at high risk for schizophrenia.

Q3. What roles do neurotransmitters play in the development of schizophrenia?

There are approximately 100 neurotransmitters in the brain that are responsible for transporting messages from the end of one nerve branch to the cell body of another. Something goes wrong with this communication system in the brain of a person suffering from schizophrenia. Notably, two neurotransmitters are implicated in the development of schizophrenia. DOPAMINE and SEROTONIN are two of them. An increase in dopamine in certain areas of the brain causes overstimulation and excess sensory information, resulting in difficulty with concentration, thought process, reality orientation, feelings, and behaviors. Furthermore, any abnormalities in serotonin activities result in a sensitive brain, making the nerve cells appear sandpapered, leading to schizophrenia. Dopamine and serotonin action explains why the client in this case scenario experiences unexpected rage and crying.

Q4. According to the APRN’s review of recent literature, structural problems in the brain may play a role in the development of schizophrenia. Describe the structural abnormalities seen in schizophrenia patients.

Structural abnormalities in the brain, like complications from other diseases, can cause structural brain damage, which can lead to schizophrenia later in life. Alterations or abnormalities of both the white and gray mater occur as people get older due to structural changes. These changes cause brain abnormalities and begin before the onset of clinical symptoms of schizophrenia, particularly those involving language processing. Other abnormalities include neuroanatomical abnormalities prior to and following the onset of psychosis, which leads to schizophrenia.

Bipolar Disorder

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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 been 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.

Q1. Discuss the role genetics plays in the development of bipolar 2 disorders

Bipolar 2 disorder is caused by multiple genes, each of which contributes only a small percentage of vulnerability, but which act in concert with other environmental factors such as stress, lifestyle, habits, and sleep to cause bipolar 2 disorder. G72/DAOA, DISC1, NRG1, TPH2, BDNF, 5-HTT, and DAT1 are among the genes implicated in bipolar disorder. As a result, genetics play a significant role in the development of bipolar disorder. Although the exact inheritance pattern is unknown, variations in many genes are likely to combine to increase an individual’s risk of developing bipolar 2 disorders. As seen in this patient, this combination causes mood swings ranging from depressive lows to manic highs. The patient went on a shopping spree until they ran out of credit.

Q2. Explain how the hypothalamic-pituitary-adrenal (HPA) system may be associated with bipolar type 2 disease

The hypothalamic-pituitary-adrenal (HPA) system is linked to bipolar 2 disorders because it is involved in the pathogenesis of depressive symptoms and cognitive deficits, which can lead to neurocytotoxic effects of elevated cortisol levels. Manic episodes in individuals with bipolar 2 disorders are caused by dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, which is preceded by an increase in ACTH and cortisol levels, resulting in cognitive problems and functional impairments. For example, in this scenario, the patient was irritable and depressed, indicating a compromised HPA system.

Q3. Discuss the role inflammatory cytokines play in the development and exacerbation of bipolar type 2 symptoms

Inflammatory cytokines are thought to play a role in the development and exacerbation of bipolar type 2 symptoms. Cytokines are proteins that regulate and orchestrate the immune response. Cytokines have the ability to directly affect neuronal activity, causing neuronal excitability and plastic changes in mood-regulating areas of the brain, as well as neuroprogression of the bipolar diathesis. Furthermore, inflammatory cytokines influence the symptoms and exacerbation of type 2 bipolar by influencing the HPA axis and increasing cortisol levels.

Q4. Discuss the role of the amygdala in bipolar disorder

Amygdale is involved in both physiologic and behavioral arousal in response to environmental stimuli. Amygdale is involved in emotion-related brain function in bipolar disorder. Any amygdale damage causes changes in mood states such as facial expression and social withdrawal, as observed in the patient in this scenario. The patient has suddenly become very hyperactive and has been talking nonstop, indicating behavioral arousal and emotional changes.

Q5. How does neurochemical dysregulation contribute to bipolar disorders?

Bipolar 2 disorders are caused by a chemical imbalance in the brain. As a result, neurochemical dysregulation implies that neurotransmitters, the chemicals responsible for controlling brain functions such as noradrenaline, serotonin, and dopamine, are out of balance. Any disruption in the homoeostasis of noradrenaline, serotonin, and dopamine transporters and receptors results in bipolar disorder’s depressive and manic phases.

Q6. What is the current status of the use of nutraceuticals in management of depression?

Due to a lack of prescription options, nutraceuticals are increasingly being used in the management and treatment of depression. However, studies show that patients with long-term depression are unlikely to benefit from nutraceuticals, which are more effective in patients with milder forms of depression. As a result, physicians are encouraged to constantly monitor side effects and potential drug-drug interactions, and to use their critical judgment in determining whether the agents are making a difference.

Panic Disorders and Attacks

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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 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 she is feeling better. The APRN suspects the patient has just experienced a panic attack.

Q1. What are panicogens and how do they contribute to the development of panic attack symptoms?

Panicogens are substances that cause a state of fear or anxiety. Severe stress, Yohimbine, CCK tetrapeptide (CCK-4), caffeine, m-chlorophenylpiperazine, and the benzodiazepine partial inverse agonist FG 7142 are among them. Anxiety, nervousness, fear, nausea, palpitations, restlessness, and tremors are all exacerbated by these agents. For example, in this scenario, the patient’s main complaint was palpitations, rapid heart rate, sweating, and tremors, all of which were caused by the panicogenic agents.

Q2. How does the GABA-benzodiazepine (BZ) receptor systems contribute to panic attacks/disorders?

The GABA-benzodiazepine (BZ) receptor systems play a role in panic attacks because blocking them with antagonists causes severe anxiety, which eventually leads to a panic attack. Increasing GABA receptor function with antagonists, on the other hand, reduces anxiety and changes in panic disorders.

Social Anxiety Disorder (SAD)

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 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).

Q1. Describe the areas of the brain that are associated with social anxiety disorder

The brain stem, prefrontal cortex, and amygdale, which play a key role in modulating fear and anxiety, are the areas of the brain most commonly associated with social anxiety. The prefrontal cortex is in charge of pathological anxiety responses related to negative emotions caused by the amygdala, whereas the brain stem controls the rate of breathing, and any error can result in social anxiety. In these cases, the patient’s social anxiety may have stemmed from the prefrontal cortex, which is responsible for negative emotions. The patient has significant impairment in social activities, has resigned from her sorority, and is unable to go to the library to study because she believes everyone is staring at her and mocking her, all of which are negative social emotions.

Q2. How is oxytocin associated with SAD?

SAD is associated with the oxytocin hormone, which is known to promote positive social interactions such as feelings of love, social bonding, and well-being. The hormone works by lessening the impact of SAD on an individual and improving emotional health.

Generalized Anxiety Disorder (GAD)

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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 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).

Q1. Discuss the role of neurotransmitters in the expression of GAD

GAD is caused by a number of neurotransmitters, including serotonin, glutamate, gamma-aminobutyric acid, cholecystokinin, adenosine, and others. Some of these neurotransmitters, however, are inhibitory, while others are excitatory. As a result, these neurotransmitters play an important role in the up- or down-regulation of GAD. The neural circuitry involved in anxiety is modulated by neurotransmitters in the brain. For example, dysregulation of GABA, an inhibitory neurotransmitter, particularly the GABAA variant, tends to increase amygdala activity in the brain, resulting in GAD.

Q2. Explain the structural brain changes that occur in people with GAD

Changes in the gray and white matter of the brain cause structural changes in people with GAD. Gray matter structural changes include macrostructural changes like decreased cortical thickness and volume, as well as microstructural changes like increased gray matter mean diffusivity. Structure changes in white matter, on the other hand, include changes in macrostructural lesions as measured by the total white matter hyper-intensity (WMH) burden and microstructural damage in white matter tracts.

Post-Traumatic Stress Disorder (PTSD)

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 he “sleeps with one eye open” and fears sleep. Deep sleep brings vivid nightmares. He grudgingly 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).

Q1. Describe the changes seen in the brain structure in patients with PTSD

Changes in brain structure in PTSD patients result from severe emotional trauma, which causes long-term changes in the ventromedial prefrontal cortex region of the brain. The prefrontal cortex is in charge of regulating amygdale-induced responses. PTSD patients have a significant decrease in the volume and functional ability of the ventromedial prefrontal cortex. For example, in this scenario, the patient reluctantly admits to having experienced several traumatic events during his second tour of duty, indicating changes in the ventromedial prefrontal cortex region of the brain.

Q2. Briefly discuss the role glucocorticoids may have on the development of PTSD

Glucocorticoids are crucial in the development of PTSD. Notably, moderate glucocorticoid secretion improves a patient’s coping mechanism by assisting them in processing information in a way that reduces the retrieval of fear-inducing memories. However, when glucocorticoids, such as cortisol, a stress hormone, are insufficiently produced, individuals may struggle to emotionally adapt following a traumatic event, as seen in the patient in this scenario.

Obsessive-Compulsive Disorder (OCD)

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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).

Q1. What is primary pathophysiology of OCD?

Obsessive-compulsive disorder (OCD) is a mental disorder characterized by bizarre, recurring, and uncontrollable thoughts that cause anxiety, followed by repetitive behaviors designed to alleviate anxiety. The primary pathophysiology of OCD is excessive and uncontrolled neural activity in SMS, which may be caused by a dopamine-serotonin imbalance. In the case scenario, for example, the patient admits that he is “grossed out” by some of the boys in the boys’ room because they use the toilet and do not wash their hands afterwards. He is also concerned about all the germs the boys are carrying around, implying that he is concerned that other boys’ hands may be contaminated with germs.

Q2. Describe the role the dorsal anterior cingulate cortex (dACC) has in reinforcement of obsessive behaviors

The dACC acts as a hub in patients with OCD, processing negative emotional and reinforcing information and then using that information to direct motivated behavior. As a result, dACC modulation is likely to reinforce OCD processes such as anxiety and depression.

history of an individual