The Stress Response

Concept Map for Stress on an Adult Age 40-64
Student Name
Course
Code
Instructor
Submission Date
Stress among women 40-64 YearsBehavioral and Psychological Changes Altered Cellualr Machinery Synaptic Plasticity Neuronal Plasticity Cellular Excitability Epignetic Programming Genomic effects Immune reactivity Non-Genomic effects BrainEx ternal/Physical Stressors Metabolic changes Energy mobilization Digestion suppression Immune system activation Reproduction shutdown Body Affected Body Parts Hypothalamus-Pituitary-Adrenal Axis Symphatetic-Adrenomedullar Axis Internal/Psychological Stressors
Response to Stressor
Processing and dealing with stressful instances need to engage different mechanisms that connect the brain and body during stressful moments. Responses to stressful stimulations are conducted by a wide range of brain structures that together interpret or detect events as either potential threats or real (stressors) (McEwen, & Gianaros, 2010).
The stressors can either be external or internal. External stressors are caused by physical factors, assault, or rape, while internal stressors can be caused by stigmatization and racial discrimination, among other social factors. Stressor identification results in the activation of two main components of the stress system and the release of stress molecules (McEwen, & Gianaros, 2010).
The hypothalamus-pituitary-adrenal HPA0 axis aids the secretion of glucocorticoids. The sympathetic-adreno-modellar (SAM) axis aids in the secretion of norepinephrine and noradrenalin that are activated due to the responses to a stressor. When they are released, they generate coordinated responses that begin within a few seconds and may last for months, weeks, or days and enables homeostasis restoration. To enable this, the responses to stress systematically promote the mobilization of energy, activation of the immune system, metabolic changes, and suppression of reproductive and digestive systems (McEwen, & Gianaros, 2010).
In the brain, stress responses may induce long and short-term effects in the form of epigenetic, genomic, and non-genomic mechanisms. The pro-inflammatory signals, together with the central effects of epigenetics, genomics, and non-genomic mechanisms, result in cellular excitability, neuronal and synaptic plasticity changes. Together, the body and brain effects cause cha...