Pathophysiology of Mental Disorders Essay

Pathophysiology of Mental Disorders Essay

Psychiatric disorders and other mental health illnesses pose a significant threat to individual and population health. The processes through which most of these diseases have been less understood; thus, hypotheses and theories have been put forward to explain their pathogenesis and pathophysiologic processes. Understanding the pathophysiology of some of these diseases has led to their successful treatments. This paper describes pathophysiologic processes for selected mental health disorders.

Generalized Anxiety Disorder

Generalized anxiety disorder is among the commonest anxiety disorders. According to the American Psychiatric Association (2013), generalized anxiety disorder (GAD) is characterized by excessive worry about a stressor, but this worry is disproportionate to the magnitude of the stressor. Therefore, the symptoms have a significant impact on the social and occupational functioning of the individual. Patients with generalized anxiety disorder mostly manifest physically with sweating and jitteriness. Emotionally and psychologically, these patients have feelings about the catastrophe of the self or the family. Social stressors such as relationship issues, economic stressors such as the inability to meet self and family needs, and physiological stressors such as chronic disease contribute to generalized anxiety disorder pathophysiology.

Struggling to meet your deadline ?

Get assistance on

Pathophysiology of Mental Disorders Essay

done on time by medical experts. Don’t wait – ORDER NOW!

Many psychiatric scholars have argued that GAD is biologically mediated despite earlier documented evidence that GAD is psychogenic. That The notwithstanding, GAD is an anxiety disorder. The cognitive theory for anxiety disorder suggests that there are distortions in an individual’s perception and thinking that lead to GAD. Therefore, this hypothesis can explain the pathophysiology of GAD, leading to psychological and physical symptoms. The role of the limbic system in the brain is fundamental in the stress reaction in GAD because it perceives the emotional environment for threats and initiates an appropriate emotional and physical response. Its ability to terminate this response is important in preventing excessive worry.


Depression is a group psychological illness seen in various mental illnesses. Depression seen in the various depressive states has been explained in literature items through various mechanisms and hypotheses. The neurotransmitter hypothesis suggests that neurotransmitter dysfunction leads to depression. Alterations, especially deficiency or reduction, in the levels of serotonin and dopamine in the brain. Recent research evidence has suggested that patients with depression have low serotonin levels. However, there are various serotonin receptors in the brain whose upregulation and downregulation lead to depression. 5-HT1 downregulation by social isolation leads to depression. Inhibition of 5-HT1 by 5-HT2 upregulation and hypercortisolemia leads to impaired 5-HT1 neurotransmitter dysfunction and, thus, depression.

Dysfunction of neurotrophic factors such as BDNF and neurotrophin-3 have also been hypothesized to cause depression through alterations in serotonin neurotransmission and receptor function (Li et al., 2021).  Dopamine in the brain is a dominant neurotransmitter whose alteration is implicated in depression.  According to Tian et al. (2022), depressed patients have increased dopamine transport. Increased dopamine transport in the presynaptic neurons makes them more effective in the reuptake of dopamine, as seen in depressions. This explains the action of dopamine antagonists used in depression. Genetic susceptibility has also been implicated in depression. Other mechanisms in depression from the literature are neuroinflammation, dysfunction of energy metabolism, and dysfunction of gut microbes in the microbe-gut-brain axis. These mechanisms can explain the heterogeneous etiology of depression in various depressive states.

Bipolar Disorder

Bipolar disorder is a mental illness with a high propensity for recurrence and worsening with time. Suicidality and functional impairment are some of the adverse complications of bipolar disorder. Bipolar disorder (BD) is characterized by periods of depression and mania. Alterations in mood leading to elation and depression are associated with self-destructive behavior, suicidal ideation, homicidal ideation, and poor functioning (American Psychiatric Association, 2013). The pathophysiology of depression is related to dysregulation in dopamine and serotonin levels that regulate emotions and behavior. According to Kato (2019), bipolar disorder is heritable and tends to run in families.

The genetic vulnerability causes mitochondrial dysfunction due to calcium influx dysregulation and hyper-excitability of serotonergic neurons. Disruption of the in-and-out movement of calcium into the neurons in the brain makes these cells susceptible to oxidative stress. This hypothesis explains the efficacy of some anticonvulsant meditations in bipolar disorder treatment (Woo & Robinson, 2019). The intracellular signaling mechanism in particular neurons is the key pathophysiology process for episodic alterations in their excitation and depression. The outcome is an imbalance between emotions and cognition. Overall, monoamines such as dopamine and serotonin play key roles in mood dysregulation.


Schizophrenia is among the common psychotic illnesses. It’s, therefore, one of the most studied mental illnesses. There are various pathophysiology mechanisms put forward to understand this illness. Abnormalities in neurotransmission have been the basic processes used to explain every mechanism. Different mechanisms involve different neurotransmitters. Most theories hypothesize that deficiencies or excess of these neurotransmitters cause schizophrenia (Ľupták et al., 2021). The most common neurotransmitters involved are dopamine, serotonin, and glutamate. However, other neurotransmitters such as gamma-aminobutyric acid, aspartate, and glycine have been recently added as crucial players in schizophrenia pathophysiology. Risk factors that imbalance these neurotransmitter levels include genetic susceptibility, ethnicity, and environmental influences (Zamanpoor, 2020). In other studies, in-utero factors such as asphyxia, gestational diabetes mellitus, and antepartum bleeding have been associated with schizophrenia in later life (American Psychiatric Association, 2013).


Dopamine imbalances are associated with motor symptoms due to Extrapyramidal effects. A serotonin imbalance in certain brain regions is hypothesized to cause mood and affect abnormalities. A new hypothesis suggests that the implication of a gene mutation involves the C4 gene. When dopaminergic transmissions in the frontal lobe cortex reduce functions such as memory, thinking, language, and mood deteriorate. Therefore, negative symptoms such as avolition, affect flattening, alogia, and diminished emotional expression occur. In other brain regions, such as the mesolimbic system, it shows increased dopaminergic transmission and leads to positive symptoms of schizophrenia, such as delusions, hallucinations, and disorganized speech. Overall, schizophrenia pathophysiology mainly involves neuropsychological deficits from genetic and environmental risks.

Delirium and Dementia

Mental health disorders can be broadly divided into psychotic and organic based on etiology. Organic brain syndromes are classified based on the duration of the symptoms. Delirium is an acute type of organic brain disease whose causes are numerous and multi-faceted. Acute disturbances in neurotransmitters in the brain and some endocrine chemicals in the system cause delirium. These disturbances are organic and arise from identifiable physiological processes. Whether physiological or psychological, stress causes the body to respond by releasing neurotransmitters and endocrine substances.

An increase in sympathetic tone and a decrease in parasympathetic tone arise from organic disease leading to cholinergic activation, serotonin deficiency, hypercortisolemia, and sometimes cholinergic inhibition. In the brain, GABA activity can reduce or increase, dopaminergic activity changes, and glutamate pathways are activated. The patient, therefore, presents with disturbances in cognition, alertness and consciousness, psychomotor activity, emotional dysregulation, and disturbance in the circadian rhythm. The symptoms can be hypoactive, such as sluggishness, drowsiness, and inactivity. Hyperactive delirium can present as restlessness, agitation, mood change, and hallucinations. However, these symptoms can occur concurrently in the mixed type.

Dementia is a chronic type of organic brain disease characterized by no loss of consciousness as opposed to delirium. Increasing age, alcoholism, cerebrovascular accidents, amyloidosis, down syndrome, and genetic susceptibility are key risk factors for dementia. Various types of dementia include but are not limited to Alzheimer’s disease, vascular dementia, and Lewy body dementia (Zhu et al., 2021). In Alzheimer’s disease, amyloid deposition, inflammation, and neurotoxicity cause neurodegeneration. This degeneration results from deficits in memory, aphasia, motor dysfunction, and visuospatial abnormalities. Delusions, irritability, and aggression are some of the common reasons for seeking psychiatric help.

Obsessive Compulsive Disorder

Obsessive Compulsive Disorder (OCD) is an anxiety disorder with high comorbidity risks and suicidality.  Obsession and compulsions are key psychological processes in OCD (Varcarolis & Fosbre, 2020). Various hypotheses have been put forward to explain the pathophysiology of OCD. The psychological hypotheses argue that OCD is an anxiety state, and thus dysfunctional beliefs about situations or external stimuli lead to emotional disturbance. Compulsions are thus maladaptive mechanisms to maintain these dysfunctional beliefs. These hypotheses are backed by cognitive behavioral theory for anxiety states.  Biological hypotheses argue that in OCD, the postsynaptic serotonin receptors become hypersensitive, thus leading to anxiety in response to obsessions (Fineberg et al., 2020).

In the other biological model, dysfunctional brain circuits in the orbital, frontal, and sub-cortical regions (Stein et al., 2019). Genetics has also been implicated in some cases. Overall, compulsions are patients’ responses to urges to reduce obsessional anxiety and avert perceived consequences. Repeated episodes of obsessions and complications when the recurrent triggers or stressors are encountered can cause impairments in social and occupational functioning (Nazeer et al., 2020). These beliefs are usually intrusive and incongruent with the patient’s existing belief systems.


The discussed disorders represent both organic and psychotic brain diseases. The role of critical neurotransmitters such as serotonin, dopamine, and GABA has been evident. These pathophysiologic expansions have been based on hypotheses and theoretical concepts because carrying out actual scientific research on live patients’ brains may not be realistic. GAD is believed to be biologically mediated through cognitive distortions in perception and thinking, as well as dysfunction in the limbic system of the brain. Depression is believed to be caused by dysfunction in neurotransmitters such as serotonin and dopamine, as well as by genetic susceptibility, neuroinflammation, dysfunction of energy metabolism, and dysfunction of gut microbes in the microbe-gut-brain axis. Bipolar disorder is characterized by periods of depression and mania and is believed to be caused by heritability, mitochondrial dysfunction, and dysregulation in the in-and-out movement of calcium into neurons in the brain, which leads to an imbalance between emotions and cognition. Schizophrenia is believed to be caused by imbalances in neurotransmitters such as dopamine, serotonin, and glutamate, as well as by genetic susceptibility, ethnicity, and environmental influences, and in utero factors such as asphyxia, gestational diabetes mellitus, and antepartum bleeding.


American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5 (R)) (5th ed.). American Psychiatric Association Publishing.

Fineberg, N. A., Hollander, E., Pallanti, S., Walitza, S., Grünblatt, E., Dell’Osso, B. M., Albert, U., Geller, D. A., Brakoulias, V., Janardhan Reddy, Y. C., Arumugham, S. S., Shavitt, R. G., Drummond, L., Grancini, B., De Carlo, V., Cinosi, E., Chamberlain, S. R., Ioannidis, K., Rodriguez, C. I., … Menchon, J. M. (2020). Clinical advances in obsessive-compulsive disorder: a position statement by the International College of Obsessive-Compulsive Spectrum Disorders. International Clinical Psychopharmacology35(4), 173–193.

Kato, T. (2019). Current understanding of bipolar disorder: Toward an integration of biological basis and treatment strategies. Psychiatry and Clinical Neurosciences73(9).

Li, Z., Ruan, M., Chen, J., & Fang, Y. (2021). Major depressive disorder: Advances in neuroscience research and translational applications. Neuroscience Bulletin37(6), 863–880.

Ľupták, M., Michaličková, D., Fišar, Z., Kitzlerová, E., & Hroudová, J. (2021). Novel approaches in schizophrenia-from risk factors and hypotheses to novel drug targets. World Journal of Psychiatry11(7), 277–296.

Nazeer, A., Latif, F., Mondal, A., Azeem, M. W., & Greydanus, D. E. (2020). Obsessive-compulsive disorder in children and adolescents: epidemiology, diagnosis, and management. Translational Pediatrics9(Suppl 1), S76–S93.

Stein, D. J., Costa, D. L. C., Lochner, C., Miguel, E. C., Reddy, Y. C. J., Shavitt, R. G., van den Heuvel, O. A., & Simpson, H. B. (2019). Obsessive-compulsive disorder. Nature Reviews. Disease Primers5(1), 52.

Tian, H., Hu, Z., Xu, J., & Wang, C. (2022). The molecular pathophysiology of depression and the new therapeutics. MedComm3(3), e156.

Varcarolis, E. M., & Fosbre, C. D. (2020). Essentials of psychiatric mental health nursing: A communication approach to evidence-based care (4th ed.). Elsevier – Health Sciences Division.

Woo, T. M., & Robinson, M. V. (2019). Pharmacotherapeutics for Advanced Practice Nurse Prescribers (5th ed.). F.A. Davis Company.

Zamanpoor, M. (2020). Schizophrenia in a genomic era: a review from the pathogenesis, genetic and environmental etiology to diagnosis and treatment insights: A review from the pathogenesis, genetic and environmental etiology to diagnosis and treatment insights. Psychiatric Genetics30(1), 1–9.

Zhu, H.-Y., Hong, F.-F., & Yang, S.-L. (2021). The roles of nitric oxide synthase/nitric oxide pathway in the pathology of vascular dementia and related therapeutic approaches. International Journal of Molecular Sciences22(9), 4540.



Please discuss the pathophysiology of the following topics, including citations and references:

Generalized anxiety disorder
Bipolar disorders
Delirium and dementia
Obsessive-compulsive disease


Struggling to meet your deadline ?

Get assistance on

Pathophysiology of Mental Disorders Essay

done on time by medical experts. Don’t wait – ORDER NOW!

Open chat
WhatsApp chat +1 908-954-5454
We are online
Our papers are plagiarism-free, and our service is private and confidential. Do you need any writing help?