Describe the ‘Fight or Flight’ System and How That Relates to Anxiety Disorder

This corresponds to the hypothalamus located in the brain when stimulated it moderates a succession of nerve cells emission and chemical release prompting our bodies to either fight or run away at the face of harm (Nolen – Hoeksema, Fredrickson, Loftus, Wagenaar, 2009. ) Several types of neurotransmitters are involved in the system, collectively known as the hypothalamus pituitary – adrenocortical (HPA) axis, has a vital contribution to our moods, such as anxiety, panic disorder and many physical disorders (Nolen – Hoeksema et al. 009. ). Anxiety is the most frequent stressor response in humans; these are the normal reactions to stress (Smith, Nolen – Hoeksma, Fredrickson and Loftus, 2003) daily encounter. Studies have indicated a connection between the HPA axis and psychiatric problems such as anxiety (Kallen, Tulen, Utens, Treffers, De Jong and Ferdiand, 2008) panic disorder (Aberlson, Khan, Liberzon and Young, 2007) and also some HPA dysregulation in PSTD (Van Der Klok, 2001).

There is an increased in the cortisol secretion when in stressful circumstances in adults with anxiety disorder (Kallen et al. 2008) HPA axis fluctuates in patients with panic disorder (Aberlson et al. 2007). Further insight as to how the fight or flight system relates to anxiety is discuss in more details. Fight or flight response mechanism is hard-weird into the brain and is activated by a genetic wisdom contrived to protect the body from potential danger (Cacioppo et al. 2002. When the brain detects danger the pituitary gland is activated releasing ACTH which then stimulates the adrenal gland producing cortisol hormone into the bloodstream (Bernstein et al. 2008) the body metabolism increases as it prepares for using energy, i. e. heart rate, blood pressure, breathing rate increases, muscles tense, shakiness etc. (Nolen – Hoeksema et al. 2009) are all factors of the fight or flight in motion. HPA is convoluted set of explicit authority and feedback communications among the hypothalamus, the pituitary gland and the adrenal gland (Cacioppo et al. 002) this occurs in the first stage (Alarm) of a prolonged sequence of reactions known as GAS (general adaptation syndrome) according to Selye (1956) as cited in Barker, (2002) the hypothalamus stimulates the pituitary gland secreting adrenocorticotropic hormone which then activates the cortex of the adrenal gland to produce corticosteroids releasing supplies of energy and fight inflammation; the pituitary glands initiates the emission of endorphins, a natural painkiller in the body figure two (Barker, 2002) Cells in the hypothalamus produce corticotrophin releasing factor (CRF) in response any given stress (Cacioppo et al. 002)

The CRF in turn adheres to specific receptors on the pituitary gland which is then used to secrete ACTH transporting to the adrenal gland, this is then stimulated to release adrenal hormones preparing the body to β€˜fight or flight’ increasing the emission of cortisol (Smith et al. 2003) this initiates a series of metabolic effects aimed at alleviating the harmful stressors through negative feedback to both the hypothalamus and the pituitary gland decreasing the concentration of the ACTH and cortisol in the blood once the stress has subsides figure one (Smith et al. 003) This is a major part of the neuroendocrine system that governs reactions to stress and moderates many body processes such as moods and emotions and energy storages etc. (Barker, 2002) Anxiety is actually a built in response to perceived threat allowing us to do the necessary in order to protect you from dangerous encounters which in turn activates our fight or flight response (Smith et al. 2003).

People experience a general state of fear and worry before confronting a challenge such as a driving test; this is a normal encounter of anxiety, on the other hand if this were to interfere ith a person’s ability to function normally as expected in a situation then it is seen as abnormal (Nolen – Hoeksema et al. 2009) Panic disorder is a type of anxiety disorder characterised by brief sudden attacks of intense terror and apprehension leading to physical symptoms such as shaking, nausea, confusion, dizziness and breathing difficulties etc. (Smith et al. 2003) Panic disorder is diagnosed when a person/sufferer expects future attacks and makes drastic behavioural changes to avoid these attacks (Nole – Hoeksema et al. 009). According to the APA (2000) as cited in Smith et al, (2003), only 1. 5% to 3. 5% of the population will develop this disorder and only about 2. 1% of European adults (Nolen – Hoeksema et al. 2009) Post – traumatic stress disorder PSTD is another form of anxiety disorder on a more serve level. PSTD results from previous trauma and often leads to flashbacks and behavioural changes in order to avoid certain stimuli (Bernstein et al. 008) There are four sets of symptoms of PSTD; physiological – a deep detachment from daily life, cognitive- reliving the trauma, behavioural – sleep disturbance and the sense of terror or horror – survivor guilt (Smith et al. 2003, and Nolen – Hoeksema et al. 2009)

Research shows that people with PSTD are more to likely to experience physiological changes in situations reminding them of previous trauma exposures causing changes in several neurotransmitters and hormones in connection to the fight or flight response (Nolen – Hoeksema et al. 009) Sufferers of PSTD have an inability to accurately assimilate the memories of previous trauma (Van Der Kolk, 2001) they tend to a have an impediment counteracting stimuli in their environment when dealing with general tasks (Van Der Kolk, 2001) The cortisol levels among people with the disorder are lower than among those without; the cortisol shuts down the sympathetic nervous system after a stressful encounter, as this activity is prolonged dealing with stress/trauma hence the PSTD (Bernstein et al. 008).

Studies have indicated that victims of panic disorder are more likely to experience a panic attack when asked to inhale small amount of carbon dioxide than those without (Nolen – Hoeksema et al. 2009) Those susceptible to panic attacks have an over-reactive fight or flight response and they have lower metabolism in areas that a vital in the moderations of fear (Nolen – Hoeksema et al. 2009) Studies have also pointed out that significant levels f anxiety in children and adolescents are affiliated with higher cortisol concentration in the presence of a stressful situation and findings showed alterations in the basal HPA axis activity (Kallen et al. 2008) Approximately about 40% of young adults experienced some sort of panic attack at point or another especially at stressful times (Smith et al. 2003)

Research has found that there is an increase in overnight cortisol levels in relations to sleep disruption, the HPA axis dsyregulaion in panic is due to hypersensitivity to contextual cues (Abelson et al. 007) however, this is a concrete fact as the results are indecisive i. e. patients with occasional panic have normal resting level of cortisol but on the other hand elevation of resting cortisol as also been reported (Abelson et al. 2007) Anxiety disorder can be seen as an existing on a continuum with fewer emotional difficulties. It is a term used generally for several disorders that cause nervousness, fear, apprehension and worry (Barker, 2002) these disorders affects people’s behaviour and feelings and can manifest real physical syndrome at the face of threat (Smith, 2003).

Research has found that there is an increase in overnight cortisol levels in relations to sleep disruption, the HPA axis dsyregulaion in panic is due to hypersensitivity to contextual cues (Abelson et al. 2007) however, this is a concrete fact as the results are indecisive i. e. patients with occasional panic have normal resting level of cortisol but on the other hand elevation of resting cortisol as also been reported (Abelson et al. 2007) According to the APA (2000) as cited in Smith et al, (2003), only 1. 5% to 3. 5% of the population will develop this disorder and only about 2. 1% of European adults (Nolen – Hoeksema et al. 009) Research shows that people with PSTD are more to likely to experience physiological changes in situations reminding them of previous trauma exposures causing changes in several neurotransmitters and hormones in connection to the fight or flight response (Nolen – Hoeksema et al. 2009) Sufferers of PSTD have an inability to accurately assimilate the memories of previous trauma (Van Der Kolk, 2001) they tend to a have an impediment counteracting stimuli in their environment when dealing with general tasks (Van Der Kolk, 2001) References Barker. , L. 2002. Psychology. New Jersey; Prentice Hall Barnstein. , D. , A. Nash. , P. , W. 2008. Essentials of Psycholgy. U. S. A; Houghton Mifflin Cacioppo. , J. , T. , Bersnston. , G. , G. , Adolphs. , R Carter. , S. , C. , Davidson. , R. , J. , McClintock. , M. , K. , McEwen. , B. , S. , Meaney. , M. , J. , Schater. , D. , L. , Sternberg. , E. , M. , Suomi. , S. , S. ,Taylor. , S. , E. 2002. Foundations in Social Neuroscience. U. S. A; Massechusettes Institue of Technology Nolen-Hoeksma. , S. , Fredrickson. , B. , L. , Loftus. , G. , R. , Wagenaar. , W. , A. 2009. Atkinson and Hilgard’s: Introduction to Psychology. Wandsworth; Cengage Learning Abelson. , J. , L. , Kahn. , S. , Lixerzon. I. , Young. , E. , A. (2007). HPA axis activity in patients with panic disorder: Review and synthesis of four studies. Depression & Anxiety, 24, 66-76. Kallen. , V. , L. , Tulen. , J. H. ,M. , Utens. , E. , M. W. J. , Treffers. , P. , D. , A. , Jong. , F. , H. , Ferdiand. , R. , F. (2008). Associations between HPA axis functioning and levels of anxiety in children and adolescents with an anxiety disorder. Depression & Anxiety, 25, 131-141. Van der Kolk, B. A. (2001). The psychobiology and psychopharmacology of PTSD. Human Psychopharmacology, 16, S49-S64. Appendices Figure one Figure two Figure three

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