Anxiety pathophysiology: Difference between revisions
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== Overview== | == Overview== | ||
The pathophysiology of [[anxiety]] is attributed to various theories that have been proposed which constitute: [[Biologic]], [[psychoanalytic]], [[learning]], and [[genetic]] component. There is increased [[sympathetic]] tone, decreased levels of [[ | The [[pathophysiology]] of [[anxiety]] is attributed to various theories that have been proposed which constitute: [[Biologic]], [[psychoanalytic]], [[learning]], and [[genetic]] component. There is increased [[sympathetic]] tone, decreased levels of inhibitory neurotransmitter [[Gamma-aminobutyric acid|GABA]], and alterations in [[neurotransmitters]] such as [[dopamine]] and [[serotonin]]. A [[gene]] coding for [[serotonin]] transport has also been implicated. | ||
==Pathophysiology== | ==Pathophysiology== | ||
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=== Biologic component=== | === Biologic component=== | ||
*There is an increased [[sympathetic | *There is an increased [[Sympathetic nervous system|sympathetic]] tone. | ||
* There is a surge of [[catecholamines]]<nowiki/> | * There is a surge of [[catecholamines]]<nowiki/>. | ||
*Decreased levels of [[Gamma -aminobutyric acid | *Decreased levels of gamma - aminobutyric acid ([[Gamma-aminobutyric acid|GABA]]). | ||
* | *Alterations in [[serotonergic]] and [[dopaminergic]] system. | ||
* In | * In anxiety states like [[panic]] attacks, the [[locus ceruleus]] is [[hyperactive]]. | ||
* [[Hyperactivity]] of [[amygdala]] has been implicated in [[social anxiety]] | * [[Hyperactivity]] of [[amygdala]] has been implicated in [[social anxiety]]. <ref name="pmid26791511">{{cite journal |vauthors=Baslet G, Seshadri A, Bermeo-Ovalle A, Willment K, Myers L |title=Psychogenic Non-epileptic Seizures: An Updated Primer |journal=Psychosomatics |volume=57 |issue=1 |pages=1–17 |year=2016 |pmid=26791511 |doi=10.1016/j.psym.2015.10.004 |url=}}</ref> | ||
=== Psychoanalytic component=== | === Psychoanalytic component=== | ||
* [[Freud]] described that [[anxiety]] is developmentally related to childhood | * [[Freud]] described that [[anxiety]] is developmentally related to childhood fears of disintegration that derived from the fear of actual or imagined loss of a love object or fear of bodily harm. | ||
* He used the term | * He used the term "signal anxiety" to describe anxiety that triggers [[defense mechanisms]] used by the person to cope with the potential threat, but anxiety in fact, is not consciously experienced. | ||
=== Learning theory=== | === Learning theory=== | ||
* [[Anxiety]] is produced due to continued [[stress | * [[Anxiety]] is produced due to continued [[Stress (medicine)|stress]]. | ||
* The anxiety eventually becomes a conditioned response to | * The anxiety eventually becomes a [[Conditioned place preference|conditioned]] response to stressful situations of less severity. | ||
===Genetic studies=== | ===Genetic studies=== | ||
* About 5% individuals with anxiety have [[polymorphic]] variant of the gene associated with [[serotonin]] [[transporter]] [[metabolism]].<ref name="pmid28413930">{{cite journal |vauthors=Ersig AL, Schutte DL, Standley J, Leslie E, Zimmerman B, Kleiber C, Hanrahan K, Murray JC, McCarthy AM |title=Relationship of Genetic Variants With Procedural Pain, Anxiety, and Distress in Children |journal=Biol Res Nurs |volume=19 |issue=3 |pages=339–349 |year=2017 |pmid=28413930 |doi=10.1177/1099800417692878 |url=}}</ref> | * About 5% individuals with [[anxiety]] have [[polymorphic]] variant of the [[gene]] associated with [[serotonin]] [[transporter]] [[metabolism]].<ref name="pmid28413930">{{cite journal |vauthors=Ersig AL, Schutte DL, Standley J, Leslie E, Zimmerman B, Kleiber C, Hanrahan K, Murray JC, McCarthy AM |title=Relationship of Genetic Variants With Procedural Pain, Anxiety, and Distress in Children |journal=Biol Res Nurs |volume=19 |issue=3 |pages=339–349 |year=2017 |pmid=28413930 |doi=10.1177/1099800417692878 |url=}}</ref> | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[Category:Psychiatry]] | [[Category:Psychiatry]] | ||
[[Category:Needs overview]] | [[Category:Needs overview]] | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
Latest revision as of 20:26, 29 July 2020
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Anxiety Microchapters |
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Diagnosis |
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Treatment |
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Anxiety pathophysiology On the Web |
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American Roentgen Ray Society Images of Anxiety pathophysiology |
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Risk calculators and risk factors for Anxiety pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]
Overview
The pathophysiology of anxiety is attributed to various theories that have been proposed which constitute: Biologic, psychoanalytic, learning, and genetic component. There is increased sympathetic tone, decreased levels of inhibitory neurotransmitter GABA, and alterations in neurotransmitters such as dopamine and serotonin. A gene coding for serotonin transport has also been implicated.
Pathophysiology
Various theories have been implicated in the pathogenesis of anxiety which are as follows:
Biologic component
- There is an increased sympathetic tone.
- There is a surge of catecholamines.
- Decreased levels of gamma - aminobutyric acid (GABA).
- Alterations in serotonergic and dopaminergic system.
- In anxiety states like panic attacks, the locus ceruleus is hyperactive.
- Hyperactivity of amygdala has been implicated in social anxiety. [1]
Psychoanalytic component
- Freud described that anxiety is developmentally related to childhood fears of disintegration that derived from the fear of actual or imagined loss of a love object or fear of bodily harm.
- He used the term "signal anxiety" to describe anxiety that triggers defense mechanisms used by the person to cope with the potential threat, but anxiety in fact, is not consciously experienced.
Learning theory
- Anxiety is produced due to continued stress.
- The anxiety eventually becomes a conditioned response to stressful situations of less severity.
Genetic studies
- About 5% individuals with anxiety have polymorphic variant of the gene associated with serotonin transporter metabolism.[2]
References
- ↑ Baslet G, Seshadri A, Bermeo-Ovalle A, Willment K, Myers L (2016). "Psychogenic Non-epileptic Seizures: An Updated Primer". Psychosomatics. 57 (1): 1–17. doi:10.1016/j.psym.2015.10.004. PMID 26791511.
- ↑ Ersig AL, Schutte DL, Standley J, Leslie E, Zimmerman B, Kleiber C, Hanrahan K, Murray JC, McCarthy AM (2017). "Relationship of Genetic Variants With Procedural Pain, Anxiety, and Distress in Children". Biol Res Nurs. 19 (3): 339–349. doi:10.1177/1099800417692878. PMID 28413930.