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31 Cards in this Set
- Front
- Back
When does stress occur |
When a persons status is altered by reaction to the stressor |
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What is the stress response |
Generic but complex response made by the body to any stressor (systemic response; same every time) |
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What is the physiological response |
Same response but varies in intensity and effects to each situation and every person |
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What happens if a stressor is severe, negative influence, or multiple factors effect change at one time |
Body systems will be disrupted or maladaptive and homeostasis can be effected |
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How can coping lead to more stress |
Maladaptive coping (ignoring stress, overeating, drinking) add additional problems creating more stress |
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What is general adaptation syndrome? |
Fight or flight concept; the body responds to minor changes (activity, food intake) by maintaining homeostasis |
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Nonspecific stress response triad (in rats) |
Adrenal glands enlarge, bleeding gastric ulcers develop, and a decrease in lymphocytes in the blood (thymus atrophies) |
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3 stages of GAS |
Alarm, resistance, exhaustion |
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Process of alarm stage of GAS |
In potentially stressful situations, eyes and ears send stimuli to the amygdala where it is processed. If danger is perceived, stimulus is sent to the hypothalamus (control center) which communicates with the body via the autonomic nervous system (trigger the SNS). Stressors cause an increase in ACTH which causes an increase in cortisol secretions |
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Effects of the alarm stage of GAS |
Increase in blood pressure, heart rate, blood sugar, respirations, bronchioles and pupils dilate, vasoconstriction Peripheral (pale), kidneys (decreased urine output), GI (nausea) Short term stress, mild or moderate, increases cognitive function and short term memory, increased endorphins that block pain |
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Process of the resistance stage of GAS |
Hypothalamus activates anterior pituitary to release ACTH, which stimulates release of cortisol. Also causes release of aldosterone and ADH to increase the reabsorption of sodium and water, as well as increasing blood volume and blood pressure |
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Effects of the resistance stage of GAS |
Increase reabsorption of sodium and water, increase blood volume and blood pressure, increased gastric secretions (leading to ulcers) Long-term cortisol release causes decreased memory, delayed healing, long-term increased blood sugar, lowers inflammatory/immune response Person may be irritable, frustrated, have poor memory |
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Exhaustion stage of GAS |
If stress stays for too long, the body becomes exhausted, which leads to burn out, increased illness, increased risk of disease, and increased risk of death |
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Differences between long-term and short-term cortisol release |
Long term - decreased immune system and inflammatory response, increase blood pressure, increased blood sugar (increased risk of diabetes), increased thirst/urination/weight gain, anxiety/depression, decreased memory Short term - increased blood sugar for energy, increased inflammatory response, increased memory |
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What does prolong vasoconstriction lead to? |
Inflammation/necrosis Stomatitis (ulcers in mouth), necrotizing periodontal disease, more severe complications (impaired function/necrosis in GI tract/kidneys) |
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How does stress and disease affect pre-existing problems? |
May become exacerbated High blood pressure can lead to cardiac dysrhythmias/CHF, seizures, asthma (asthma attacks), MS, rheumatoid arthritis, lupus, eczema, ulcerative colitis |
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What are some potential effects of prolonged and severe stress? |
Acute renal failure, stress ulcers, infection, slow healing, PTSD |
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How does prolonged/ severe stress cause acute renal failure |
Prolonged/severe vasoconstriction leads to ischemia which causes cell damage and can lead to permanent kidney damage (prevent this by giving IV fluids and possible renal drugs to increase dilation) |
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How does prolonged/ severe stress cause stress ulcers |
Intense vasoconstriction and glucocorticoids lead to a decrease in mucosal regeneration and mucus production (prevent by giving medication to decrease acid production) |
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How does prolonged/ severe stress cause infections |
Decreases inflammatory and immune responses |
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How does prolonged/ severe stress cause slowed healing |
Increase secretion of glucocorticoid causes a decrease in protein synthesis and tissue regeneration Increase in catecholamine levels causes vasoconstriction and decrease in nutrients and oxygen to the tissue |
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How does prolonged/ severe stress cause PTSD |
Usually occurs within three months of the event (sometimes years later) increased risk of developing dependence on drugs and/or alcohol |
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Ways to cope with stress |
Adequate rest, healthy diet, minimize stressors, regular moderate exercise, distracting activities, counseling and support services, relaxation techniques, anti-anxiety meds |
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Physiology of inflammation and what is it initiated by |
Protective defense mechanism (same each time though timing and severity may vary) Initiated by tissue injury (intend to localize and remove injurious agent) leads to general S&S as warning signs (redness, warmth, swelling, pain, loss of function) |
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Basic steps of inflammation |
Injury (bradykinin released from injured cells and activates pain receptors) Cells release chemical mediators (pain stimulates, mast cells, prostaglandins, and basophils to release histamine) Vasodilation (bradykinin and histamine increase capillary dilation, which increases blood flow and capillary permeability) Increase capillary permeability (allows fluid and proteins to leak into the interstitial area; called exudate) Exudate (dilutes bacteria and puts pressure on the capillary bed to decrease the amount of fluid leaking out) Leukocytes (brought to the injury with increased blood flow, called by chemotactic factors, find their way by margination/pavementing/diapedesis) Phagocytosis (removal of debris in preparation for healing; neutrophils, arrive first and macrophages arrive later) |
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What do platelets do? |
Bind together when they recognize a damaged blood vessel (forming a clot) Circulate until activated by bradykinin or a vascular injury Stop bleeding (participate in coagulation cascade) Degranulate (release mediators such as serotonin) Make thromboxane (potent vasoconstrictor, induces platelet aggregation) |
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Where are mast cells found and what do they do? |
Found in the loose connective tissues, close to blood vessels, and widely distributed in the body Have cellular bags of chemical and undergo degranulation when stimulated to release histamine, leukotrienes, prostaglandins, chemotactic factors, cytokines |
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What do the chemical mediators histamine, leukotrienes, prostaglandins, chemotactic factors, and cytokines |
Histamine - vasodilation and increased capillary permeability Leukotrienes - later response - vasodilation and increased capillary permeability Prostaglandins - vasodilation in increased capillary permeability, pain, fever Chemotactic factors - guide leukocytes to area of injury Cytokines - allows communication between cells (ex. Proliferation, induce fever) |
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How is the compliment system activated and what does isn’t compliment/how |
Activated by the antibody/antigen reaction or by ischemia Will complement the inflammatory response by causing vasodilation, increased capillary permeability, chemotaxis, and increased histamine release (allows inflammatory response to be prolonged) |
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What are cytokines and what do they do? |
Diverse proteins released from cells that communicate with other cells to improve the immune response Increases proliferation of immune cells, increases plasma proteins, and induce fever |
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What is margination, pavementing, and diapedesis |
Margination - move to margins/sides of the blood vessel Pavementing - rolling along vessel (do this until they find areas of increased permeability to escape) Diapedesis - ameboid movement through retracted endothelial cells of the blood vessel into the injured tissue (going through gap) |