Lecture

• Allostasis: ability to adapt successfully to challenges
• Stress: non specific response to any challenge the body faces; real or perceived
• Hans Selye made the GAS theory and model
• Stressor cause increase in the fxn of the adrenal cortex, atrophy of the thymus gland and stimulation of the SNS
• GAS consists of Alarm, Resistance and Exhaustion
• Alarm stage: fight or flight response is initiated at the hypothalamus after having info relayed to it from the cerebral cortex, hippocampus, limbic system and amygdala.
• The alarm stage has little resistance and there are no adaptations occurring; its similar to the survival stage of cell injury. It's like redlining a car in which the body is performing to its maximum capacity; not sustainable long term
• Resistance/Adaptation stage: moving back to homeostasis by following allostasis. There is a decrease in alarm reactions.
• Resistance phase causes a decrease in B/T lymphocytes and the body is a hypermetabolic state.
• Depression of B/T lymphocytes in the resistance phase can be beneficial to protect against harmful immune responses
• Exhaustion stage: body cannot compensate or adapt due to these factors: lacking nutrition/resources, due to harmful effects of stress response causing wear and tear/chronic effects.
• Compensation is relatable to negative feedback while decompensation is relatable to positive
• Adaptation to stress requires physiological responses from these 3 systems: neurological, endocrine and immune
• Parts of the brain dealing with stress are the: cerebral cortex, limbic system, Reticular formation and the hypothalamus
• Thalamus: redirects sensory information
• Limbic system: fxns in emotions and behaviours that ensure survival and self-preservations. Communicates with cerebral cortex for emotions; releases endorphins
• Reticular formation: length of the brainstem that extends into the midbrain. Contains the RAS, aids with fight or flight responses and receives input from the PNS and hypothalamus
• Hypothalamus: receives traumatic stimuli via spinothalamic pathways and baroreceptors and emotional stimuli via limbic system. Stimulates the ANS
• These are the hormones that increase during stress: ACTH, ADH, Aldosterone, TSH, Glucagon and EPI/NE
• Angiotensin 2 stimulates release of aldosterone and vasoconstriction
• Increased release of glucocorticoids: decreases # of circulating WBCs, decreases B/T lymphocytes, decreases inflammation and increases gastric secretions
• Chronic stress causes immune cells to release proinflammatory cytokines.
• Prostaglandins and leukotrienes are inflammatory mediators formed from arachidonic acid, which is formed from cell membranes
• Prostaglandins: made from lipids and act as local hormones. Functions are: promoting pain responses, producing fevers, recruiting WBCs, local vasodilation for inflammation and inhibit platelet aggregation
• Acute inflammation is considered the movement of neutrophils into the tissue space
• Chronic inflammation is marked by the movement of T and B lymphocytes into tissues
• Hallmarks signs of inflammation: edema and the prescence of neutrophils
• Inflammation function: remove debris/pathogen, protect other tissues from the damage and assisting to heal the tissue
• PAMP(Pathogen associated molecular pattern) molecules detect pathogens while DAMPs (Damage associated molecular patterns) molecules detect damage
• LAS or local adaption syndrome refers to the inflammatory process
• Clinical manifestations of inflammation are: calor(heat), dolor(pain), tumor(swelling), rubor(redness) and loss of function
• Positive effects of inflammation: dilutes toxins, brings antibodies and drugs to the area, fibrin formation, bring nutrients/O2 to the area and stimulates the immune system
• Negative effects of inflammation: excess swelling, damage to normal tissues and inappropriate activation
• Arachidonic acid: creates inflammatory mediators in response to tissue injuries, bradykinins, angiotensin 2 and EPI. It's derived from the phospholipids from the cell membrane
• Arachidonic acid metabolizes into 2 different pathways: Cyclooxygenase (COX) pathway for prostaglandins and lipoxygenase(LOX) for leukotrienes
• The deciding factors of which arachidonic pathway is pursued are: enzyme activity/presence and fxn
• COX pathway can be blocked by NSAIDs
• Concentration of arachidonic acid in the body is stable and stimulated continuously; considered a non-essential acid
• The COX 1 pathway is in the platelets and it's changed to create thromboxane
• The COX 2 pathway is in the endothelial cells