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170 Cards in this Set
- Front
- Back
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1. How does stress affect health?
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Via a stress-diathesis model.
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2. What is a moderator?
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Interaction between X & Y
A moderator is a variable that affects the direction and/or strength of the relationship between an independent variable and a dependent variable. |
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3. What is an example of a moderator?
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Acute stressors result in an increase in immune function in women, but a decrease in men.
Interaction between gender and dependent variable. |
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4. What is a mediator?
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Mechanism between X & Y
A mediator accounts for the relation between the independent variable and dependent variable |
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5. What is an example of a mediator?
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Drinking alcohol protects against heart disease because it reduces tension and anxiety.
Alcohol is the mechanism by which tension and anxiety are reduced. |
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6. What is endocrine reactivity?
Six things... |
1. Involve increases in peripheral catecholamines and glucocorticoids.
2. Tends to be stable over time. 3. Laboratory measures of reactivity are correlated with reactivity in real life. 4. Can lead to cardiac arrhythmias and contribute to atheroschlerosis. 5. Can impact immune function. 6. May be related to diabetes. |
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7. What is cardiovascular reactivity?
Five things... |
1. Physiological changes that occur in the heart, blood vessels, and blood in response to stressors.
2. Tends to be stable over time as well. 3. Linked to stroke, CHD, and hypertension. 4. Laboratory measures of reactivity are correlated with reactivity in real life. 5. Stress may promote atheroschlerosis via activated platelets and increased cholesterol |
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8. What is immune reactivity?
Four things... |
1. Catecholamines and glucocorticoids can impair immune function.
2. Decreases in lymphocyte activity. 3. Related to development and progression of infectious disease. 4. Development and prognosis of cancer. |
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9. What did Beecher (1956) discover during WWII?
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During WWII, 50% of soldiers that suffered severe wounds claimed that had moderate to severe pain and only 32% requested medication.
Then..years later he examined civilians with less severe wounds and 75% claimed they had moderate or severe pain and 83% requested medication. |
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10. What did Beecher (1956) conclude?
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The battlefield wounds marked the end of disaster for the soldiers so they experienced less pain.
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11. What is the definition of pain?
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An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
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12. Describe the overall gist of feeling pain.
Four things... |
1. Happens in the somatosensory system.
2. It has specialized receptors that convert physical energy to action potentials. 3. Afferent neurons relay sensory info to the brain via somatic nervous system. 4. Interpretation of this info by the brain results in perception. |
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13. What are pain receptors called?
What is the experience of pain called? |
Nociceptors
Nociception |
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14. Why does pain occur?
What substances are released in response to pain? |
Damage to nerve endings
or Action of substances released by damaged tissue that bind to receptors. Substances released in response to pain: -Prostaglandins -Histamine -Substance P |
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15. What are the differences between fast and slow pain?
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FAST PAIN:
Reaches the spinal cord quickly and the pain is localized. SLOW PAIN: Slow burning, lasting pain that influences emotion. |
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16. What is the spinothalamic pathway of pain?
Ascending or descending? |
Crosses the midline and ascends on the opposite side of the spinal cord the thalamus. The thalamus is subdivided for specific areas of the body, and each area projects to its own section of the primary sensory cortex -- a thin band of cortex in the parietal lobe just posterior to the central sulcus.This discriminative pathway transmits to conciousness precise information about the location of pain.
This pathway is ascending. |
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16. What is the spinoreticular pathway of pain?
Ascending or descending? |
Also ascending on both sides of the spinal cord to the intralaminar nuclei of both the right and left thalamus. From there the next neuron in the chain takes the information to many areas of the brain, e.g., the anterior part of the cingulate gyrus ( emotion ), the amygdala ( memory and emotion ), and hypothalamus ( emotion and the vascular response to emotion ).
Unofficially it's called the "suffering" pathway. |
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18. How do we measure the cortical representation of pain?
What does the representation show? |
Via a PET scan
Shows that people reporting pain have activity in two regions of the brain: 1. Somatosensory cortex 2. Limbic system |
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19. Describe the sequence of events that occur when one experiences pain...
Four things... |
1. Injury activates nociceptors
2. Signal is sent through dorsal root into spinal cord 3. Spinothalamic pathway sends info about location and severity of injury 4. Spinoreticular pathway sends info that guides our emotional response |
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20. What is the specificity theory of pain?
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Pain results from neural messages sent along the pain pathways.
Pain is proportional to the amount of tissue damage. |
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21. When you think about the determinants of pain, what is missing?
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There is no one center "in control". Rather we see that pain can be all-pervasive, affecting our thoughts and memories, attitudes and emotions, movements and behavior -- and in turn be affected by each and all of them.
Also, hypnosis/tranquilizers affect pain perception |
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22. What is the Gate-Control theory of pain by Melzack and Wall (1965)?
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They theorized that signals can descend from the brain and activate neural gating circuits in the spinal cord to block incoming pain signals.
The chemical gate in the spinal cords can be open or closed. |
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23. What causes the gates to open/close?
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Activity of the large A-beta fibers causes the gates to close.
Also, the release of endogenous opioids also shuts the gates. Think about rubbing a stubbed toe. |
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24. What are A-beta fibers?
What are A-delta fibers? What are C fibers? |
A-beta: Large sensory fibers involved in rapidly transmitting sensation and possibly in inhibiting the transmission of pain.
A-delta fibers: Small sensory fibers that are involved in the experience of “fast” pain. C fibers: small-diameter nerve fibers that provide information concerning slow, diffuse, lingering pain. |
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25. What evidence is there for descending pain pathways?
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The periaqueductal gray!
It's an area of the midbrain that, when stimulated, decreases pain. Furthermore, lesions to this area increases pain. It was here that endogenous opiates and their receptors were discovered. |
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26. What is pain hypersensitivity?
Why might a hypersensitivity to pain be disadvantageous? |
Can take two forms:
1. Thresholds are lowered 2. Responsiveness is increased Can be adaptive to ensure contact with injured tissue is minimal. When persists after healing or occurs in the absence of injury it is not beneficial and can lead to chronic pain. |
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27. How does pain hypersensitivity occur?
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Two known mechanisms:
1. Peripheral Sensitization 2. Central Sensitization |
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28. What is Peripheral Sensitization?
What does COX-2 have to do with this shit? |
Peripheral Sensitization reduces the threshold or increases response at the level of the nociceptor.
Ex: heat sensitivity after sunburn Inflammatory chemicals released at the site of the damaged tissue. COX-2 enzymes lead to the production of prostaglandin which increases the resposne of nociceptors. |
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29. What is Central Sensitization?
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Central Sensitization is the increased excitability of neurons within the CNS.
Leads to abnormal pain response via alteration in synaptic connections. May contribute to fibromyalgia which is a painful muscular disorder. |
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30. What is neuropathic pain?
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Neuropathic pain is pain in which there are structural and/or functional nervous system adaptations secondary to injury, (i.e. nerves are damaged or dysfunction) that take place either centrally or peripherally.
It is not due to a traumatic head injury! Ex: phantom limb syndrome |
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31. What are the parts of the cardiovascular system?
Three main things Jimmy... |
Involves:
1. Heart and blood vessels -Pumps blood around the body to deliver O2 and nutrients and remove waste products -Also transports hormones and is a temperature control mechanism 2. Arteries 3. Veins |
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32. What are the four chambers of the heart?
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Left and right atrium
-Reservoirs for venous blood, small pumping action helps move blood into ventricles Left and right ventricles - Left ventricle pumps blood to the rest of the body. - Right ventricle is the weaker of the two pumps |
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33. What are the heart valves and what do they do?
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They open/close in response to changes in pressure.
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34. What are the AV (Atrioventricular) valves?
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AV (Atrioventricular) valves
-between atria and ventricles -stops backflow from ventricles to atria -opens when the heart filsl with blood, closes when ventricles contract. |
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35. What are the left and right AV valves called?
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Left: Mitrial valve
Right: Tricuspid valve |
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36. What/where are the semilunar valves?
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Semilunar valves are between the ventricles and the vessels leaving the heart.
They stop blood from leaking back into the heart. |
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37. What are the left and right semilunar valves called?
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Left: Aortic valve
Right: Pulmonary valve |
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38. Describe the flow of blood through the heart and lungs...
Four main steps here... |
1. Blood from the body enters right atrium by blood vessels called the vena cava.
2. When the right atrium fills with blood, it contracts, sending blood to the right ventricle. 3. When the right ventricle fills with blood, it contracts, sending blood to the lungs through the pulmonary arteries. 4. In the lungs, blood picks up oxygen, and then returns to the heart’s left atrium through the pulmonary veins. When the left atrium contracts, it sends blood to the left ventricle. From the left ventricle, blood is pumped out the aorta and through the body. |
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39. How does myocardial contraction occur?
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Results from a change in voltage across cell membrane which leads to an action potential.
Starts with the SA node -causes atrial contraction. Then, the atrioventriclar (AV) node delays impulse following atrial contraction and leads to simulataneous contraction of ventricles. |
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40. What are systole and diastole?
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Systole - blood pumped out of heart and blood pressure in the blood vessels increases (lub)
Diastole - heart muscle relaxes - blood pressure drops and blood enters heart(dub) |
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40. Describe the sequence of events in pulmonary circulation...
Four things again... |
1. O2 depleted and CO2 rich blood enters through right atrium
2. Right ventricle forces blood into lungs 3. O2 and CO2 exchange 4. O2 rich blood returns to heart via pulmonary veins |
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41. Describe the sequence of events in systemic circulation...
Three steps here... |
1. O2 rich blood enters through left atrium
2. Left ventricle pushes blood in to general circulation 3. Involves arteries, arterioles, capillaries, and veins. |
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43. What is stroke volume?
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The volume of blood ejected from the heart.
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44. What is cardiac output?
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The amount of blood pumped by each ventricle in 1 minute
CO = SV x HR Approximately 5 liters/min |
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45. What is peripheral resistance?
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The increase in blood pressure due to friction from atherosclerosis or plaque buildup
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46. High blood pressure results from what...?
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High cardiac output and/or
High peripheral resistance |
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47. How do cardiovascular diseases rank amoung major causes of death?
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Number one cause of death!
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48. What is atherosclerosis?
What can it lead to? |
The formation of plaque within the arteries.
Can lead to a thrombus, which is a blood clot |
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49. What is ateriosclerosis?
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A condition marked by loss of elasticity and hardening of arteries.
Cannot adapt to changes in blood pressure. |
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50. What is Coronary artery disease (CAD)?
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A disorder of the myocardium arising from atherosclerosis and/or arteriosclerosis.
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51. What is Coronary Heart disease (CHD)?
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Any damage to the myocardium due to insufficient blood supply.
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52. What are some symptoms of CHD?
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-Transient chest pain with radiation
-Uncomfortable pressure, tightness around chest -Severe chest pain -Usually accompanied by sweating, shortness of breath, weakness, and indigestion |
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53. What are three consequences of CHD?
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1. Angina pectoris
2. Myocardial infarction 3. Sudden cardiac death |
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54. What causes atherosclerosis?
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Unknown how it begins or what causes it
Risk factors: -elevated cholesterol and TAGs -high BP -smoking -diabetes -obesity -physical inactivity |
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55. What is hypertension?
What are the two types of hypertension? |
Abnormally high blood pressure, with either a systolic reading in excess of 160 or a diastolic reading in excess of 105.
Primary hypertension: no known cause (most common) Secondary hypertension: due to another disease |
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56. What are some consequences of having high BP?
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Common stroke: lack of blood due to blockage of an artery
Hemorrhagic stroke: bleeding due to the rupture of a weakend artery in the brain. |
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57. What are some treatment options for CHD?
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Lifestyle modifications to control risk factors
Angioplasty -balloon tipped catheter passed through blocked arteries -coronary artery stent where a tiny coil is expanded inside blocked artery and left in place -coronary bypass in which a detour is made around blocked artery. |
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58. What are cardiovascular diseases (CVD)?
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Disorders of the circulatory system, including coronary artery disease and stroke
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59. What is responsible for the decline in death rates for CVD?
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Improved medical care and changes in behaviors
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60. What is up with heart disease and women?
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1/3 of all deaths of US women each year from heart disease.
500,000 US women die/year Heart attack kills 244,000 women a year 40% of women with heart diease with eventually die of it. |
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61. What ethnicities are most likely to die of CHD?
Least likely to die of CHD? |
Most likely to die of CHD:
-Blacks, non-hispanic -Whites, non-hispanic Least likely to die of CHD: -American Indians/Alaska natives -Asian/Pacific islanders |
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62. What are some risk factors for cardiovascular disease?
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Age
Gender (Greater risk for men before age 50) Family history Diabetes Race Hypertension High cholesterol Smoking Diet Obesity |
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63. What is a good cholesterol profile?
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Total < 240mg/dL i.e.200mg/dL
LDL < 160mg/dL i.e.40mg/dL HDL > 40mg/dL i.e.160mg/dL |
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64. What are some psychosocial risk factors for CVD?
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Stress
Sleep Low social support Personality Depression |
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65. What about stress and CVD?
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Psychological stress can trigger ischemia in 40-70% of patients with CAD
Acute clinical events are often triggered by physical and mental stress |
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66. What about marital stress and women in the study by Orth-Gomer et al. (2000)?
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Women with a moderate to severe amount of marital stress were 2 to 3 times more likely to suffer from CHD
Work related stress was not significant |
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67. What is cardiovascular reactivity?
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An increase in blood pressure and heart rate as a reaction to frustration or harassment
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68. What about social support and CVD?
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Low social support yields a high risk of dying from CVD.
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69. What is the type A personality?
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Suggested by Friedman and Rosenman (1974)
-Hostile -Competitive -Struggle to achieve more and mroe in less time -Time urgency -Concerned with numbers and acquisition of objects |
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70. What the type A personality supported by any studies?
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Yes, Rosenman et al., (1975)
-Type A's were two times more likely to develop CHD than type B's. However !! Other studies have failed to replicate this effect |
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71. What about anger and heart disease?
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High anger = more likely to die of CHD than low or moderate levels of anger.
Angry individuals can lessen their risk by speaking softly and by remaining calm during angry/stressful situations. |
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72. What is the immune system?
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The immune system is a complex & highly developed system- yet it's mission is simple: to seek and kill invaders.
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73. What are the two types of immunity?
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1. Innate Immunity
2. Acquired Immunity |
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74. What is innate immunity?
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Has no memory
Anatomical barriers Includes: -Phagocytes -Natural killer cells -Histamine -Cytokines |
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75. What are natural killer cells?
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A type of lymphocyte that attacks invading organisms.
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76. What are cytokines?
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Chemical messengers secreted by cells in the immune system, forming a communication link between the nervous and immune systems.
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77. What is acquired immunity?
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Protects against specific microorganisms
Aquire through having disease or immunization |
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78. What is an antigen?
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Anything foreign to the body
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79. What are the organs of the immune system?
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Lymphoid Organs:
Bone marrow Thymus Spleen Lymph nodes and Lymphatic system |
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80. What is bone marrow and what does it do?
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All immune cells originate here and some mature here such as B and NK cless while others leave and mature in other places
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81. What/where is the thymus and what does it do?
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Behind sternum
Matures T cells visa thymic education: Keeps beneficial T cells and destroy detrimental autoimmune T cells |
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82. What/where is the spleen and what does it do?
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In the abdominal cavity
-Immunological filter of the blood -Contains B cells, T cells, phagocytes, NK cells Immunological "conference center" - some cells bring antigens here to trigger response from cells of the aquired immune system |
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83. What about the lymphatic system?
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Filled with lymph which is clear, colorless and has no red blood cells.
Largely responsible for transporting agents of the immune system. |
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84. What are leukocytes?
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Come on BALTHAZAR!
They're WHITE BLOOD CELLS! |
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85. What are phagocytes?
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The attack, adhere to, and engulf and ingest foreign bodies
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86. What are macrophages?
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EATERS!
They are antigen presenting cells -Present parts of antigen on surgace and presents it to B & T cells. |
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87. What are granulocytes?
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A type of lymphocyte that acts rapidly to kill invading organisms.
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88. What are dendritic cells?
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Also an antigen presenting cell
Usually found in lymphatic organs Less is known about function |
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89. Is acquired immunity present in other species?
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ONLY PRESENT in VERTEBRATES
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90. What are the two paths for acquried immunity?
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Antibody mediated (Humoral) immunity
& Cell mediated immunity |
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91. What is humoral immunity?
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Immunity created through the process of exposure to antigens and production of antibodies in the bloodstream.
Involves B cell activation |
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92. How do B Cells produce antibodies?
Three steps... |
1. Antigen is presented on cell surface
2. Helper T cell interacts with bound antigen and helps activate B cell that recognizes that particular protein 3. B cell divides, most of which become plasma cells which produce and release large amounts of antibodies |
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93. What happens to the other B cells?
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The become memory cells with other T cells which are long-lived and important for subsequent responses
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94. What are immunoglobulins?
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ANTIBODIES!
Protein substances produced in response to a specific invader or antigen, marking it for destruction and thus creating immunity to that invader |
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95. How do antibodies work?
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They bind to virus particles, and prevent infection.
They also recruit macrophages which ingest the antigens and displays antigens on its surface Travels to lymph nodes T cells become sensitized to recognize these antigens and they multiply to become helper T cells and cytotoxic T cells |
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96. How was psychoneuroimmulogy discovered?
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Ader & Cohen (1975) found that rats given saccharin had weaker immune responses and fewer antibodies produced after being conditioned to respond to saccharin with cyclophosphamide which decreases immune response
In other words, the rats shouldn't have responsed that way without the cyclophosphamide (saccharin is only sugar!) |
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97. How do our bodies respond to brief, naturalistic stressors?
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During exams, students show a decrease in circulating numbers of T and NK cells, decreased ability of lymphocytes to divide
and decreased NK cell activity. However, humoral immunity is generally unchanged. |
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98. How do our bodies respond to chronic stressors?
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GAS
Reduced innate immunity (e.g. NK cell activity) Reduced acquired immunity (e.g. lymphocyte proliferation |
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99. What is the link between stress and infectious diseases?
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Consistent evidence that stress is associated with increased upper respiratory infection symptoms
Study by Stone, Reed & Neale (1987) found that undesirable life events increased 3-4 before onset of self-reported symptoms of a cold. |
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100. What did the Marsland et al., (2001) study find?
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Lower antibody response, as assessed after the second hepatitis B injection, was predicted independently by (a) high trait negative affect and (b) diminished T-cell proliferation in response to PHA. These data provide evidence that trait negative affect and the magnitude of stress-induced suppression of immune function may have clinical significance.
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101. What did the Cohen et al., (2002) study find?
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Acute HPA and immune responses to laboratory stressors are markers of how vulnerable people are to the increased risk for URI associated with stressors in the natural environment.
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102. What is HIV?
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Attacks helper T cells and macrophages
Destroys defenses against attack Leads to AIDS Takes months to years to get AIDS from HIV |
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103. What did the Frasure-Smith et al., (2003) study find?
This card is outta order... |
Negative affectivity and some unique aspect of depression predict long-term cardiac-related mortality following a myocardial infarction independently of each other and cardiac disease severity. Additional research is needed to characterize the mechanisms involved.
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104. What did the Giltay et al., (2006) study find?
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Dispositional optimism is a relatively stable trait over 15 years and shows a graded and inverse association with the risk of cardiovascular death
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105. What are the symptom progressions like in HIV to AIDS?
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1. Virus multiplies weeks after HIV infection and affects helper T cells and macrophages - flu like symptoms
2. Asymptomatic period but virus levels still rising 3. Immune system no longer functional, fever, night sweats, fatigue 4. AIDS & opportunistic infection, i.e. Kaposi's Sarcoma |
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106. What are some stressors associated with HIV progression?
Why might this be an important factor? |
-Concealment of homosexual identity
-Stressful life events -Less social support -Pressimistic style -Depression All of these factors contribute to a more rapid disease progression. |
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107. What are autoimmune diseases?
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Disorders that occur as a result of the immune system's failure to differentiate between body cells and foreign cells, resulting in the body's attack and destruction of its own cells.
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108. What is rheumatoid arthritis?
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An autoimmune disorder characterized by a dull ache within or around a joint.
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109. What is asthma?
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A chronic disease that causes constriction of the bronchial tubes, preventing air from passing freely and causing wheezing and difficulty breathing during attacks.
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110. What did the Sandberg et al., (2004) study find?
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Children who experienced major stressful life events had an immediate 5 fold increase in risk of asthma attack within 2 days
Then, a delayed 2 fold increase about 5-7 weeks later. |
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111. Why was there a delayed response in asthma attacks?
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Cells in lungs turn over every 5-7 weeks.
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112. What is cancer?
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100 different diseases
All involved uncontrolled cell growth and division (neoplastic tissue) Can be malignant (cancerous & metastasize) or benign(do not metastasize) Second leading cause of death in USA - 1/3 Americans with develop cancer in his or her lifetime |
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113. What about cell division and cancer?
Two parts... |
1. Healthy cell division
-regulated by DNA -freq. and timing is controlled -genes signal start and stop division 2. Cancer cell division -out of control -damage to DNA via mutations to gens that control cell division |
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114. What are oncogenes?
Mutations to them result in what? |
Oncogenes encourage cell divison
Mutations to oncogenes keep cells continously dividing. |
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115. What are Tumor-suppressor genes?
Mutations to them result in what? |
Tumor suppressor gens restrain cell growth
Mutations to them lead to uncontrollable cell growth |
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116. What are DNA repair genes?
Mutations to them result in what? |
DNA repair genes fix damaged DNA
Mutations to them result in the survival & replication of damaged DNA |
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117. How has the death rates for cancer changed since the 1950's?
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They remain approximately the same around 195,000 people/year
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118. What are the estimated top 5 cancer deaths for men in 2007?
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1. Lung and bronchus
2. Prostate 3. Colon and rectum 4. Pancreas 5. Leukemia |
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119. What are the estimated top 5 cancer deaths for women in 2007?
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1. Lung and bronchus
2. Breast 3. Colon and rectum 4. Pancreas 5. Ovary |
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120. How are incidence rates different from survival rates?
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Survival rates are different from the total number of people dying; it is a conditional probability "if you develop cancer, what are the chances you will survive?"
Typically measured as 5 year survival. |
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121. What are some risk factors for cancer?
Four main ones... |
1. Environmental risk factors
-radiation, asbestos, pesticides 2. Ethnic background -African americans 40-50% > incidence and mortality than European Americans > Hispanic Americans, Asian Americans, and Native Americans 3. Age 4. Family History -Only 10% of cancers are inherited, but a genetic predisposition can interact with other risk factors. |
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122. What are some behavioral risk factors for cancer?
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Smoking
Diet EtOH Physical Activity Ultraviolet light Sexual Behavior |
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123. Give some facts about cigarette smoking...
5 Facts.... |
1. It's the #1 preventable cause of death in the US
2. Accounts for about 30% of all cancer deaths 3. Causal relationship between smoking and lung cancer 4. Lung cancer 9 times more likely among smokers than non-smokers 5. Also associated w/increased risk of breast CA, leukemia, oral and throat CA, bladder and kidney CA, cervical CA, and stomach CA |
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124. Give some facts about second hand cigarette smoke...
3 Facts... |
1. Comes from burning tobacco and exhaled smoke
2. Contains more than 50 known carcinogens 3. It's estimated that 3,000 lung CA deaths per year are attributable to second hand smoke |
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125. What percentage of Americans are overweight or obese?
How does this compare to 40 years ago? |
65% of Americans of overweight or obese!
That is more than twice as many compared to 40 years ago |
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126. What percentage of cancers are the result of diet, physical inactivity and obesity?
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ACS estimates that 1/3 of all cancers are the result of diet, physical inactivity and obesity.
It's related to wide range of cancers including breast, stomach, colon, liver, ovary, prostate, and esophagus CA |
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127. What are some important dietary findings from table 10.1 in the book?
Three things... |
1. Antioxidants (eg beta-carotene, Vit C, selenium) clearly have a protective effect in animals, however, clinical data is mixed.
2. Vitamin C does seem to protect against lung cancer in smokers 3. Water protects against bladder CA |
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128. What are some risks of a sedentary lifestyle?
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Recent study found that the risk of dying from CA increased 45% for men and 28% for women due to lack of physical activity
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129. What are some benefits of a physically active lifestyle?
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Individuals who are physically active can reduce their risk of developing colon CA by 40-50%
Physically active women have up to a 40% reduced risk of developing breast CA It probably also reduces men's risk for prostate CA by 10-30% |
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130. What about obesity and mortality?
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Obesity is related to esophageal, colon, uterine, kidney, breast, prostate, and pancreatic CA, as well as non-Hodgkin lymphoma.
Approximately 41,000 new cases of CA in 2002 were estimated to be due to obesity. As many as 14-20% of CA deaths may be attributable to obesity. |
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131. What are some other behavioral risk factors for developing CA?
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Alcohol
-pancreatic, liver, breast, and synergistic effect with throat CA UV Light -melanoma Sexual behavior -HIV, AIDS related cancers, Kaposi's sarcoma -early first intercourse increases risk for cervical, ovarian, and vaginal CA -many sexual partners increases men's risk of prostate cancers |
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132. What is a way that woman can reduce their likelihood of developing breast, ovarian, and endometrial CA's?
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Pregnancy and childbirth offer some protection against these cancers.
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133. What did the meta analysis by Garson (2004) find?
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Found moderate evidence that helplessness/repression is related to poor prognosis and denial/minimizing is related to favorable prognosis.
Little to no evidence for a fighting spirit, active coping style, or a fatalistic view of world. |
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134. What did the study by Schultz (1996) find?
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They found that a pessimistic outlook is an important risk factor for mortality, but only among younger patients (ages 30-59).
They found no link between depression or optimism for either younger or older CA patients. |
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135. What can be said about depression and CA?
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Depression has been associated with chronic activation of HPA axis and SNS which likely has implications for immune function
Early evidence suggest a link but not clear in more recent studies May be related to mortality, but not related to developing cancer |
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136. What can be said about stress and CA?
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In animal studies, exposure to stress leads to decreases in some immune function (e.g. NK cells) and higher malignant tumor rates.
In human studies, there is less conclusive evidence -Retrospective, correlational support for this link, however, definitive studies have not been reported. -Immune systems altered by stress, but the link between those immune effects and cancer have not been clearly demonstrated |
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137. What are some difficulties in demonstrating the links between psychosocial problems and cancer?
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1. Impossible to identify when cancers start.
2. Many different types of cancer. 3. Would need an enormous longitudinal study, given the low prevalence of many cancers. 4. Lack of attention to interactions (stress-diathesis model). |
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138. What are some possible mechanisms linking psychosocial factors and cancer?
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Immune surveillance, e.g. NK cells are suppressed by stress and negative emotions
DNA repair is impaired by stress. |
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139. What are the statistics associated with diabetes?
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Total: 20.8 million children and adults
7.0% of the population have diabetes. Diagnosed: 14.6 million people Undiagnosed: 6.2 million people Pre-diabetes: 54 million people 1.5 million new cases in people aged 20+ in 2005 Each day, approximately 4,110 people are diagnosed with diabetes |
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140. What about the statistics associated with childhood diabetes?
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Under 20 years of age: 176,500, or 0.22% of all people in this age group have diabetes.
About one in every 500 children and adolescents has type 1 diabetes. 2 million kids aged 12-19 have pre-diabetes (above normal fasting blood glucose) Although Type 2 diabetes in children is rare, the incidence has begun to increase |
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141. What are some mortality facts with regards to diabetes?
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6th leading cause of death in the U.S. in 2002.
73,249 deaths were recorded as underlying cause Diabetes contributed (along with other factors) to 3x as many deaths (224,092). 2x the death risk compared to same age group Death rate due to diabetes has increased by 45 percent, while the death rates due to heart disease, stroke, and cancer have declined. |
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142. How much did the US spend on treating diabetes in 2002? How about in 1997?
What % of US health care expenditure is spent on diabetes? |
Estimated at $92 billion in 2002, compared to $44 billion in 1997.
11% of the US health care expenditure. Almost 2.5X greater personal medical expenditure $40.3 billion was spent for inpatient hospital care and $13.8 billion for nursing home care |
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143. What is the most costly complication of diabetes?
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Cardiovascular disease is the most costly complication of diabetes, accounting for more than $17.6 billion
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144. What is the definition of diabetes mellitus?
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Diabetes Mellitus: a chronic, currently incurable, disease in which the body produces either too little or cannot properly utilize insulin.
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145. Physiologically, what occurs with diabetes?
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Glucose cannot move from the bloodstream to the cells
A high level of glucose remains in the blood Cells do not have energy for basic functioning Results: possible coma or death |
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146. Under normal conditions, what is the concentration of blood glucose levels?
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80 mg/dL - very stable
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147. Describe the pancreas...
What are its two major functions? |
It's an endocrine gland that has two major functions:
1. Produces and secretes digestive enzymes 2. Produces and secretes hormones |
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148. What are the Islets of Langerhans?
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Small clusters of cells that secrete insulin and glucagon
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149. Real quick- what do insulin and glucagon do?
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Insulin: allows cell walls to open so glucose can leave the bloodstream and enter the cells. This hormone lowers blood glucose levels.
Glucagon: stimulates the release of glucose from cells. This hormone elevates blood glucose levels These hormones work together to regulate a persons' blood glucose level |
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150. What is Type I diabetes?
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Type I: ‘insulin-dependent’ diabetes mellitus
Marked by decreased or ceased insulin production. Islet cells do not produce adequate insulin. Commonly referred to as ‘juvenile’ diabetes because onset is usually during childhood or adolescence Individuals must give themselves daily injections of insulin to survive |
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151. What is the prevalence of Type I diabetes?
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Affects equal # of men and women.
Not affected by socioeconomic status or ethnicity Accounts for 5-10% of all diabetes mellitus diagnoses |
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152. What are the causes of Type I diabetes?
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Autoimmune disease:
Immune system destroys β-cells of pancreas Non-autoimmunity: Genetic Abnormalities – 10% chance of disease if first degree relative has diabetes (not only factor) Viral infection |
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153. What are some symptoms of Type I diabetes?
Seven... |
Frequent urination
Excessive thirst Extreme hunger Unusual weight loss Increased fatigue Irritability Blurry vision |
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154. What is Type II diabetes?
What % of diabetes diagnoses does it account for? |
Type II: ‘non-insulin dependent diabetes mellitus’
Insulin resistance: glucose does not move into the cells Since the cells are not getting enough glucose the pancreas secretes more and more insulin Does not require the daily injections of insulin More insulin will not help if it is a delivery problem Onset is usually after the age of 30 Accounts for 90 % of diagnoses |
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155. What is insulin resistance?
What about obesity and insulin resistance? |
The body's cells have a diminished ability to respond to the action of the insulin hormone
Obesity: More weight means more insulin is produced More insulin promotes more deposition of fat |
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156. What is the prevalence for Type II diabetes?
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The prevalence of type 2 diabetes is higher in African Americans, Asian Americans, Pacific Islanders, Hispanic Americans, and Native Americans compared with whites.
2.8 million African Americans who have diabetes, which represents 13% of the African-American population in the United States This is 7% of the overall US population! |
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157. What about children and Type II diabetes?
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ADA reports between 8-45 % of new cases are Type 2 for individuals under 20 years of age
Prior to 1994, it had been diagnosed in fewer than 5% of the cases for this age group |
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158. Why was there a rapid increase in Type II diabetes in children?
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Increase in childhood obesity!
16% of kids between 6-19 years are overweight -Compared to 5% in 1980 85% of kids with Type II diabetes are overweight or obese However, increases not uniform across ethnicities. -21% African American and Hispanic children are overweight/obese |
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159. What are some risk factors for Type II diabetes?
Five risk factors... |
1) Ancestry:
minorities at greater risk AA have higher level of insulin compared to white 2) Obesity 3) Relatives with Type II diabetes -45-85% at least have one parent 4) Gender: more girls than boys 5) Acanthosis nigricans |
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160. What is Acanthosis nigricans?
Why is this relevant? |
Characterized by thickening and darkening of upper layers of the skin
It's found on knees, elbows and neck Children with this condition are 1.6- 4.2 times more likely to have hyperinsulinema (which is high levels of insulin) |
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161. How are health psychologists involved in diabetes prevention/management?
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Focus their efforts on improving adherence so diabetics can control blood glucose levels
Want to improve quality of life |
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162. How do adolescents and adults perform with regards to adherence?
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Many adolescents and adults fail to adhere properly to the complex treatment regimen placing themselves at great health risk
Many fail to monitor blood glucose level, relying on “what they feel like.” |
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163. What are the stats associated with this poor adherence?
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80% diabetics administer insulin incorrectly (58% wrong dose)
75% not eating at regular intervals 75% not adhering to prescribed diet Only 50% can recognize high/low blood glucose |
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164. Why is this adherence so low?
Six reasons... |
1.Lifestyle modifications are difficult
2.The consequences are not immediate 3.Have to check blood sugar even when they feel well 4.Adherence can be painful 5.Diabetes is chronic 6.Complexity |
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165. What are some behaviorally oriented interventions for improving adherence?
Five ways... |
1. Injection training
2. Monitor blood sugar levels 3. Stress management 4. Weight management 5. Social skills – e.g., resisting influences to consume the wrong foods |
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166. What are some complications associated with diabetes?
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Atherosclerosis develops much faster…
Heart Disease and Stroke Amputation- poor circulation leads to gangrene Kidney Disease (nephropathy) Retinal damage Hypoglycemia (coma) |
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167. What is a diabetic coma?
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Diabetic Coma
Occurs in Type 2 diabetics when ill or stressed Blood glucose is very high and the body becomes severely dehydrated Usually above 600 mg/dl (normal is 80 mg/dL) Dehydration leads to coma or death |
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168. What is diabetic ketoacidosis?
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Occurs in Type 1 when glucose is not available
Build up of ketones, a by-product of fat metabolism, that increases acidity of blood plasma Difficultly breathing, brain swelling, coma or death |
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169. What is the treatment for Type II diabetes?
Four ways.. |
1. Managing blood glucose levels
2. Insulin injections 3. Diet and exercise 4. Oral hypoglycemic agents Ex: Metformin tells the liver to decrease its production of glucose |
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170. What about stress and diabetes?
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Two Roles:
1. A possible cause of diabetes -Family stress in the development of diabetes (Sepa et al., 2005) 2. A factor in the regulation of blood glucose -Stress management techniques lead to better blood glucose levels (HbA1c ).(Surwit, et al.) |
