W3 GAS, LAS, Allergies, Pain

• Allostasis: The ability to adapt to challenges based on context or circumstance dependent set points
• Adrenal cortex: Organ region involved in GAS that releases glucocorticoids like cortisol
• Adrenal medulla: Organ region involved in GAS that releases catecholamines like epinephrine and norepinephrine
• Atrophy of thymus gland: Chronic stress can cause this which leads to immune system suppression
• Alarm: First stage of GAS when person perceives stress and hypothalamus release corticotropin stimulating hormone to stimulate adrenal medulla and anterior pituitary
• Resistance: Second stage of GAS during which there is a reduction in alarm reaction because the body uses allostasis to change bodies homeostasis. This stage also has fewer overt S/S but body is still in hypermetabolic state
• Resistance: Atrophy of thymus gland occurs during this stage and causes immune depression
• Resistance: The stage that includes B and T lymphocyte reduction and increase in neutrophils
• Exhaustion: Stage of GAS when body can no longer compensate for stress and reach new homeostasis
• Adaptation: Combination of neurological, endocrine, immunologic mechanisms to respond to stress
• Epinephrine: Produces positive chronotropy and inotropy as part of SNS stimulation
• Glycogenolysis: Response to stress that is stimulated by epinephrine and increases blood glucose
• RAAS: SNS produces increase in blood pressure using this mechanism
• Norepinephrine: Constricts smooth muscle to create peripheral vasoconstriction in SNS response
• Reticular formation: Brain region that is the connection between brainstem and diencephalon
• Thalamus: Brain region that directs sensory information and is involved in memory
• Limbic system: Brain system that is involved in feeling emotions and releasing endorphins
• Endorphins: Chemical released by laughter and happiness that reduces pain perception
• Hypothalamus: Brain region that receives traumatic stimuli and emotional stimulation, stimulates anterior and posterior pituitary as well as ANS
• ACTH: Stimulates adrenal cortex to release glucocorticoids like cortisol
• Steroids: Best anti-inflammatory, some available OTC
• Aldosterone: Increases sodium retention and potassium excretion
• TSH: Increases conversion of T4 into usable T3
• Cytokines: Proinflammatory peptide factors released in response to stress that enhance pain
• Prostaglandins: Product of lipids on phospholipid cell membrane that act as local hormones and are released by almost all cells
• Inflammation: Sequence of vascular and cellular responses to injury characterized by movement of neutrophils into interstitial fluid
• Calor: Heat of body related to inflammation
• Dolor: Word for pain related to inflammation
• Tumor: Swelling related to inflammation caused by increased capillary permeability
• Rubor: Redness associated with inflammation
• Arachidonic Acid: Inflammatory mediator created from omega 6 acids from phospholipids
• Cyclooxygenase: First pathway that arachidonic acid can follow (COX)
• Lox: Second pathway that arachidonic acid can follow
• COX 1: Arachidonic acid pathway responsible for thromboxane to promote platelet aggregation, mucosal maintenance, and increased renal perfusion
• COX 1: Arachidonic acid pathway responsible for gastric protection and platelet function
• Thromboxane: Pro-coagulation product of COX 1 pathway that is also vasoconstrictive
• ASA: Drug that inhibits thromboxane in low doses
• COX 2: Arachidonic acid pathway induced in infections to produce fever and pain
• COX 2: Pathway that creates prostacyclin and prostaglandins to promote blood cycling
• Prostacyclin: Product of COX 2 pathway that promotes blood flow through endothelium by inhibiting platelet aggregation and promoting vasodilation