Unit 2 Patho Exam

Front 1

When does stress occur

Back 1

When a persons status is altered by reaction to the stressor

Front 2

What is the stress response

Back 2

Generic but complex response made by the body to any stressor (systemic response; same every time)

Front 3

What is the physiological response

Back 3

Same response but varies in intensity and effects to each situation and every person

Front 4

What happens if a stressor is severe, negative influence, or multiple factors effect change at one time

Back 4

Body systems will be disrupted or maladaptive and homeostasis can be effected

Front 5

How can coping lead to more stress

Back 5

Maladaptive coping (ignoring stress, overeating, drinking) add additional problems creating more stress

Front 6

What is general adaptation syndrome?

Back 6

Fight or flight concept; the body responds to minor changes (activity, food intake) by maintaining homeostasis

Front 7

Nonspecific stress response triad (in rats)

Back 7

Adrenal glands enlarge, bleeding gastric ulcers develop, and a decrease in lymphocytes in the blood (thymus atrophies)

Front 8

3 stages of GAS

Back 8

Alarm, resistance, exhaustion

Front 9

Process of alarm stage of GAS

Back 9

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

Front 10

Effects of the alarm stage of GAS

Back 10

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

Front 11

Process of the resistance stage of GAS

Back 11

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

Front 12

Effects of the resistance stage of GAS

Back 12

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

Front 13

Exhaustion stage of GAS

Back 13

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

Front 14

Differences between long-term and short-term cortisol release

Back 14

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

Front 15

What does prolong vasoconstriction lead to?

Back 15

Inflammation/necrosis

Stomatitis (ulcers in mouth), necrotizing periodontal disease, more severe complications (impaired function/necrosis in GI tract/kidneys)

Front 16

How does stress and disease affect pre-existing problems?

Back 16

May become exacerbated

High blood pressure can lead to cardiac dysrhythmias/CHF, seizures, asthma (asthma attacks), MS, rheumatoid arthritis, lupus, eczema, ulcerative colitis

Front 17

What are some potential effects of prolonged and severe stress?

Back 17

Acute renal failure, stress ulcers, infection, slow healing, PTSD

Front 18

How does prolonged/ severe stress cause acute renal failure

Back 18

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)

Front 19

How does prolonged/ severe stress cause stress ulcers

Back 19

Intense vasoconstriction and glucocorticoids lead to a decrease in mucosal regeneration and mucus production (prevent by giving medication to decrease acid production)

Front 20

How does prolonged/ severe stress cause infections

Back 20

Decreases inflammatory and immune responses

Front 21

How does prolonged/ severe stress cause slowed healing

Back 21

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

Front 22

How does prolonged/ severe stress cause PTSD

Back 22

Usually occurs within three months of the event (sometimes years later) increased risk of developing dependence on drugs and/or alcohol

Front 23

Ways to cope with stress

Back 23

Adequate rest, healthy diet, minimize stressors, regular moderate exercise, distracting activities, counseling and support services, relaxation techniques, anti-anxiety meds

Front 24

Physiology of inflammation and what is it initiated by

Back 24

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)

Front 25

Basic steps of inflammation

Back 25

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)

Front 26

What do platelets do?

Back 26

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)

Front 27

Where are mast cells found and what do they do?

Back 27

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

Front 28

What do the chemical mediators histamine, leukotrienes, prostaglandins, chemotactic factors, and cytokines

Back 28

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)

Front 29

How is the compliment system activated and what does isn’t compliment/how

Back 29

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)

Front 30

What are cytokines and what do they do?

Back 30

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

Front 31

What is margination, pavementing, and diapedesis

Back 31

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)