Midterm 2 Review

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Published on December 16, 2008

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Health Psychology : Health Psychology Midterm #2 Review Midterm : Midterm Thursday: 5:00-6:15 PM Bring Parscore and pencil 40 multiple choice questions: Approximately 30 from lecture and 10 from readings “Does that mean I don’t have to read?” NO!!! ? You want your top possible score to be 100% not 75%, Right? Office Hours: Tomorrow 3:00-5:00 Email questions to mangel@psych.ucsb.edu (not during office hours) Disclaimer : Disclaimer This review is not meant to be comprehensive. There will be material on the test not covered by this review ? You have to actually study on your own as well!!! I have focused on the readings because Alex did such a great job with the lectures in class. Please stop me at anytime with any questions! Why Zebras Don't Get Ulcers : Why Zebras Don't Get Ulcers Chapter 4: Stress, Metabolism, and Liquidating Your Assets Energy Storage and Mobilization : Energy Storage and Mobilization Enzymes in Gastrointestinal tract break down into usable energy Insulin stimulates the transport and storage of energy Stress hormones* reverse storage process *Stress Hormones include glucocorticoids, glucagon, epinephrine, and norepinephrine Energy Mobilization During a Stressor : Energy Mobilization During a Stressor Stop energy storage ? Sympathetic ? Parasympathetic (? Insulin) Secrete Glucocorticoids Blocks the transport of nutrients into fat cells and muscles Exercising muscles override block to use circulating nutrients Counteracts what’s left of insulin in blood stream Gain access to stored energy Protein ? Amino Acids (poor energy form) ? glucose Glycogen ? Glucose Triglycerides ? Fatty Acids, Glycerol, Ketone Bodies Gluconeogenesis ? Liver generates new glucose When Energy Mobilization Goes Wrong : When Energy Mobilization Goes Wrong Inability to mobilize the body during energetic demands Addison’s Disease: not enough glucocorticoids secreted Shy-Dager Syndrome: not enough epinephrine and norepinephrine Underactive Stress-Response Chronic Fatigue Syndrome: not enough circulating glucocorticoids When Energy Mobilization Goes Wrong : When Energy Mobilization Goes Wrong Turning on Stress-Response too often for too long Inefficiency: lose potential energy each time there is a shift between stored and circulating forms of energy Myopathy (muscle atrophy): Chronic stress ? chronic protein breakdown ? muscles can’t rebuild Atherosclerosis: the constantly circulating fat, glucose, and cholesterol gets stuck to damaged blood vessels “Bad” cholesterol (LDL): gets added to atherosclerotic plaques “Good” cholesterol (HDL): cholesterol removed from plaques (on its way to liver for degradation) Stress causes: ? LDL ? HDL Juvenile Diabetes, Type 1, or Insulin-Dependent Diabetes : Juvenile Diabetes, Type 1, or Insulin-Dependent Diabetes Cause: Immune System misidentifies insulin-producing cells in Pancreas as foreign invaders and kills them ? very little insulin production Problem: Too little insulin ? can’t store energy in target cells ? cells die ? organ function declines Too little insulin ? too much glucose and fatty acids circulating ?atherosclerosis (damaged blood vessels) In kidneys ? kidney failure In eyes ? blindness Treatment: Insulin injections Type 1 Diabetes and Chronic Stress : Type 1 Diabetes and Chronic Stress Chronic stress causes: ? circulating glucose and fatty acids ? atherosclerotic plaques Insulin resistance: Glucocorticoids reduce fat cell insulin sensitivity ? fat cells release hormones that make other tissues (e.g. muscle, liver) less sensitive to insulin ? need more insulin ? cells become more resistant When stressor’s over different parts of body regain insulin sensitivity at different rates ? right insulin dose? Might increase the odds of getting juvenile diabetes Can accelerate the development of juvenile diabetes Adult-Onset, Type 2, Insulin-Resistant or Non-Insulin-Dependent Diabetes : Adult-Onset, Type 2, Insulin-Resistant or Non-Insulin-Dependent Diabetes Cause: Excess Fat in Body Fat cells get full and stop responding to insulin’s attempts to store more fat ? these cells secrete hormones that make other cells (muscle) insulin-resistant Problem: Too much glucose and fatty acids circulating ?atherosclerosis Cells fail to respond to insulin ? Pancreas secretes more and more insulin ? burns out insulin-secreting cells (Juvenile Diabetes) Chronic Stress Worsens atherosclerosis Stress-response tells fat cells not to respond to insulin (worsens this process) Treatment: Lose weight/Exercise Metabolic Syndrome/Syndrome X : Metabolic Syndrome/Syndrome X Characterized by a subset of the following: Elevated blood insulin levels Elevated blood glucose levels Elevated blood pressure Insulin resistance Too much LDL-cholesterol Too little HDL-cholesterol Too much fat or cholesterol in blood Predict major disease outcomes like heart attacks or stroke, and mortality rates If there is enough things still within the normal range, but toward the high end, you’re in trouble! Why Zebras Don't Get Ulcers : Why Zebras Don't Get Ulcers Chapter 5: Ulcers, the Runs, and Hot Fudge Sundaes (Yum!) Stress and Food Consumption : Stress and Food Consumption Stress makes 2/3 of people hyperphagic (eat more) and the rest hypophagic (eat less) CRH and Glucocorticoids released during stress-response CRH ? appetite and Glucocorticoids ? appetite CRH is secreted and begins working on the body within seconds and is cleared from the body within seconds when the stressor is over Glucocorticoids are the slowest stress hormone to be secreted, begin working, and to be cleared from the system Stress and Food Consumption : Stress and Food Consumption CRH/Glucocorticoid Pattern 1st mins of stressor: ? CRH ~0 Glucocorticoids ? appetite ? Sustained stressor: ? CRH ? Glucocorticoids ? depends on which is stronger Stressor recovery: ? CRH ? Glucocorticoids ? appetite ? Therefore: Frequent intermittent stressors ? appetite ? Prolonged stressors (couple days) ? appetite ? Other predictors of hyper/hypophagia: Individual differences in psychological response to a particular stressor or in individual physiology Glucocorticoid hyper-secreters most likely hyperphagic when stressed Psychological need: stress-eaters eat for emotional as opposed to nutritive needs Restrained eaters (dieters) more likely hyperphagic when stressed Stress and Fat Storage : Stress and Fat Storage Glucocorticoids preferentially promote fat storage in abdominal fat cells Apple shape: ? abdominal fat, WHR > 1, secrete higher than average glucocorticoids Pear shape: ? gluteal fat, WHR < 1 When matched for weight, Apple shapes at higher risk for metabolic and cardiovascular disease then Pears Stress and Digestion : Stress and Digestion Gastrointestinal (GI) tract: esophagus ? stomach ? small intestines ? colon Digestion requires lots of energy (muscle contraction) and lots of water to keep things moving Stress stops digestion, extreme stressors cause colon to contract quicker which moves waste products through colon before water can be reabsorbed ? diarrhea (Why? dump dead weight) “Functional” GI disorders (can’t find an organic cause) are very sensitive to stress (most common = IBS) Irritable Bowel Syndrome (IBS) AKA “Spastic Colon”: Symptoms: Abdominal pain relieved by defecation, diarrhea or constipation, passage of mucus, bloating, abdominal distention, ? sensitivity to cutaneous (skin/skeletal muscle) pain, and ? in sensitivity to visceral (organ) pain Chronic stressors ? risk of developing IBS and making IBS worse But, IBS can also mean too much GI sensitivity to stress (over-reactive colon) Physiology: Overactive Sympathetic Nervous Systems (made worse by visceral pain) Ulcers : Ulcers Peptic Ulcers: Hole in the wall of stomach or immediately bordering organ Gastric Ulcer: In stomach Esophageal Ulcer: higher than stomach Duodenal Ulcer: border of stomach and intestine (most common) Ulcers can be created rapidly (sometimes in days) when faced with extremely stressful crises Helicobacter pylori (bacteria) has a lot to do with 85-100% of peptic ulcers in western populations But, need a combination of bacteria, stress, and lifestyle risk factors to develop peptic ulcers Theories on How Stress Helps Form Ulcers : Theories on How Stress Helps Form Ulcers Acid Rebound Prolonged stressor causes ? in stomach acid ? cut backs on stomach protection (e.g. stomach wall thickening, mucus and bicarbonate secretion) When the stressor ends and appetite ? the stomach isn’t well equipped to handle the ? in acid Bacterial infection + repeated acid rebound cycles = ulcer Decreased Blood Flow When a lot of blood is diverted away from the gut, lack of O2 causes small strokes in the stomach wall ? lesions of dead tissue ? ulcers Immune Suppression Chronic stress suppresses immune system, can’t fight off Helicobacter Insufficient Amounts of Prostaglandins Stomach regularly develops micro-ulcers which can normally be repaired with prostaglandins, but during stress, glucocorticoids inhibit prostaglandin synthesis ? full-blown ulcers Stomach Contractions Stress causes the stomach to engage in slow, rhythmic contractions which ? ulcer risk Why Zebras Don't Get Ulcers : Why Zebras Don't Get Ulcers Chapter 8: Immunity, Stress, and Disease Immune System : Immune System Acquired Immunity (Response to Novel Pathogen X): Acquire the ability to target Pathogen X specifically, with antibodies and cell-mediated immunity that specifically recognize that pathogen Figure out which antibody fits Pathogen X best and then make tons of copies of it (takes time!) Now geared up to specifically attack Pathogen X for a long time and repeated exposure strengthens defense Innate Immunity (Nonspecific Immune Response) Antibodies that generically attack any type of microbe are secreted by mucosal surfaces Capillaries in infected areas loosen up allowing cells (i.e. macrophages, neutrophils, & natural killer cells) and fluid containing proteins that fight invasive microbes to flow out Fluid in proteins cause edema (swelling) ? Inflammation Cell-Mediated Immunity (T Cells) : Cell-Mediated Immunity (T Cells) Macrophage encounters a foreign agent Macrophage presents the infectious agent to a T helper cell and releases Interleukin-1 to stimulate it This makes the T helper cell release Interleukin-2 which triggers T cell proliferation Eventually this causes cytotoxic killer cells (type of WBC) to proliferate and destroy the infectious agent Macrophage T helper T T T T T T C C C C C 1 2 3 4 Interleukin-1 Interleukin-2 Antibody-Mediated Immunity (B Cells) : Antibody-Mediated Immunity (B Cells) Macrophage encounters a foreign agent Macrophage presents the infectious agent to a T helper cell and releases Interleukin-1 to stimulate it This makes the T helper cell secrete B-cell growth factor which triggers B cell proliferation The B cells make and release specific antibodies that bind to surface proteins on the infectious agent, targeting it for destruction Macrophage T helper B B B B B B 1 2 3 4 Interleukin-1 B-cell Growth Factor Antibodies How Stress Inhibits Immune Function : How Stress Inhibits Immune Function Glucocorticoids: Shrink the thymus gland ? halts formation of lymphocytes (e.g. T cells) Inhibit the release of messengers (e.g. interleukins) ? circulating lymphocytes become less responsive to infectious alarm Cause lymphocytes to be pulled from circulation and stored back in immune tissues Can kill lymphocytes (“programmed cell death” = cellular suicide) Disrupt cell-mediated immunity (T cells) more than antibody-mediated immunity (B cells) Sympathetic nervous system hormones, beta-endorphin, and CRH also play a role in immunosuppression Why Stress Inhibits Immune Function : Why Stress Inhibits Immune Function Immunosuppression is a costly process, why do we do it when we should be conserving resources? In the 1st 30 mins after stressor onset we actually enhance immune function, particularly innate immunity ~ an hour after stressor onset immunity suppressed If stressor ends around then, immune system is brought back to baseline Slight, short rise in glucocorticoids ? kill old lymphocytes Many circulating lymphocytes are redirected to the site of infection Prolonged major stressors cause immune function to plummet below baseline by 40-70% Why not maintain enhanced immune function? Too costly Overactive immune system ? risk of autoimmune diseases Immune System Overreaction : Immune System Overreaction Autoimmune diseases: Immune system decides a part of own body (e.g. juvenile diabetes) is an infectious agent and attacks it Numerous transient stressors (frequently turning immune system on and off) also ? risk of autoimmune disease Allergy: Immune system decides an innocuous compound (e.g. pollen) is an infectious agent and reacts Chronic Stress and Disease Risk : Chronic Stress and Disease Risk Psychoneuroimmune Route to Disease Risk Individuals have been stressed Causes them to turn on stress-response (glucocorticoids) Duration and magnitude of stress-response is large enough to suppress immune function Makes them more likely to get a disease and impairs ability to defend against it Lifestyle Route to Disease Risk Individuals stressed Effects of treatment compliance, and protective and risk factors Stress-Disease Link : Stress-Disease Link Stressors Shown to Effect the Psychoneuroimmune Route: Lack of social support/social isolation Bereavement without social support Illnesses Effected by Stress at Least Partially Through the Psychoneuroimmune Route: The common cold AIDS Latent Viruses (e.g. Herpes) Jury’s still out on Psychoneuroimmune Route to Cancer: No link yet found between ? stress ? ? cancer risk or ? relapse Mixed results on whether psychosocial stress reduction interventions improve cancer outcomes, and when it does work, the Lifestyle Route is a better explanation (e.g. group therapy ? better compliance) ? Happy thoughts and self-love does NOT cause cancer nor does an ? in happy thoughts cure cancer (Cancer is not the patient’s or their parent’s fault) Why Zebras Don't Get Ulcers : Why Zebras Don't Get Ulcers Chapter 14: Stress and Depression Depression : Depression Symptoms: Anhedonia or dysphoria: an inability to feel pleasure Too few positive emotions and too many negative emotions Incapacitating grief and guilt (not just about contributing events to the Depression, but about Depression itself) Delusional Thinking (sometimes): facts are distorted so it looks like things are terrible and only getting worse Psychomotor retardation: moving and speaking slowly Vegetative Symptoms: Eating ? Sleeping ?: not problem with ability to fall asleep, but with early morning wakening Glucocorticoids ?: linked to problems with memory storage and retrieval Quick Neurobiology Review : Quick Neurobiology Review Wave of electrical excitation moves from dendrites to axon terminals When excitation reaches the synaptic bulb at the end of the axon terminal, chemical messengers called neurotransmitters are released into the synapse. Neurotransmitters bond to the appropriate receptor sites on the dendrite of the next neuron which causes this neuron to now become electrically excited (and on and on….) Neurotransmitters must be cleared from synapse after use (reuptake = recycling; degraded = thrown out) or it will make the 2nd neuron fire too strongly Neurochemistry and Depression : Neurochemistry and Depression Depression involves abnormal levels of the neurotransmitters: Norepinephrine : psychomotor retardation Serotonin: obsessive thoughts (e.g. failure, despair, doom) Dopamine: loss of pleasure Antidepressants: Drugs used to treat depression which leave more of neurotransmitters in synapse by inhibiting reuptake or degradation, so they can hit the appropriate receptors again Tricyclics: Stop the reuptake of these neurotransmitters MAO Inhibitors: Blocks degradation of neurotransmitters by inhibiting MAO’s function, an enzyme crucial for degradation Selective Serotonin Reuptake Inhibitors (SSRIs): Stop serotonin reuptake Neuroanatomy and Depression : Neuroanatomy and Depression The Anterior Cingulate Cortex (ACC): Very concerned with negative emotions Resting activity is elevated in depressed people Disconnected as a last resort treatment of depression Amygdala: Usually involved in fear/anxiety—not in Depressives In Depressives exaggerated response to sad faces Prefrontal Cortex (PFC): Left PFC: associated with positive moods Right PFC: associated with negative moods Depressives show ? Left PFC activity & ? Right PFC activity Additional Factors in the Biology of Depression : Additional Factors in the Biology of Depression Depression has a genetic component Gene that codes for the pump that reuptakes serotonin Immunology and Depression Chronic illness that involves overactivation of immune system more likely to cause depression than non-immune-related diseases matched for severity Cytokines (messengers between immune cells) can cause depression Endocrinology and Depression Too little thyroid hormone ? Depression Speculated that massive changes in levels of progesterone and estrogen can throw off the appropriate ratio and trigger depression Stress and Depression Biology : Stress and Depression Biology Stress and Depression Risk Factors: People with lots of life stressors are more likely to develop depression (stress can trigger depression) ? Glucocorticoids ? Depression risk Genes can ? risk of Depression but must be coupled with stressful environments Depression often characterized by overactive stress-response and ? glucocorticoids ? glucocorticoids in depressed people linked to immunosuppression, osteoporosis, heart disease, hippocampal and frontal cortex atrophy = memory problems Drugs that ? glucocorticoid secretion or block glucocorticoid receptors in brain show promise in ? depressive symptoms (for ? glucocorticoid secreting depressives) Stress, Learned Helplessness and Depression : Stress, Learned Helplessness and Depression Learned Helplessness: Caused by repeated uncontrollable stressors Leads to an inability to cope with many kinds of tasks Similarities between Animals suffering from Learned Helplessness and Depressives: Motivational Problem: won’t even try coping responses Cognitive Problem: distorted world view ? overgeneralizing from 1 bad thing to how world works Animals display behaviors equivalent to dysphoria, psychomotor retardation, and self-mutilation. Also, sleep disorganization and loss, ? glucocorticoids, ? norepinephrine. Recovery speed up by ECT and antidepressants Learned Helplessness can be induced in humans too. Ps with an “externalized locus of control” were more vulnerable to learned helplessness than Ps with an “internalized locus of control” Real life: More internalized locus of control, ? Depression risk Lecture : Lecture Pathogen Avoidance Adaptations : Pathogen Avoidance Adaptations Disgust and transmission: avoid bodily gases and fluids Disgust and Stigma: Avoiding Human vectors Hygiene: itching/scratching Culture-Specific Food Aversion: food taboos may be the product of an adaptation to take cultural input about local food quality “One-Time Learning” (Garcia/Sauce Béarnaise Effect): Can acquire taste aversion after 1 incident Precautionary Reasoning: e.g. If you sleep with a prostitute, then wear a condom (maybe garbage bag too?) OCD: excessive precautionary reasoning Why Do We Get Sick? : Why Do We Get Sick? Environmental Dangers (e.g. drowning) Pathogens (e.g. viruses, parasites) Trading off for the Future (i.e. select early reproductive success over longer life span) Why? Anxiety Adaptation : Anxiety Adaptation Take inputs from environment ? Calculate danger ? Motivate precautions if necessary Social Phobia: Fear of embarrassment (? risk of social exclusion ? value as exchange partner) Panic Attacks: looks like symptoms of drowning or being choked Variation in species typical anxiety ? some anxiety disorders Stress : Stress Acute Stressors (e.g. speeding ticket) vs. Chronic Stressors (e.g. financial problems) Homeostasis: maintaining some internal variable at a level conducive to proper functioning (e.g. pH levels) Allostasis: Maintaining positive outcomes through changing levels of homeostasis (e.g. BP varies around different points when sleeping vs. running) Stressors knock body out of allostatic balance ? stress-response attempts to restore it Stress-Response : Stress-Response Collection of physiological and behavioral responses designed to deal with stressor and restore homeostasis Sympathetic Adrenomedullary (SAM) System: quick, short acting response “fight or flight” Hypothalamic Pituitary Adrenocortical (HPA) Axis: slower and longer response Depression = Functional Design? : Depression = Functional Design? Designed to: Motivate Goal Reassessment: Infant Viability: Birth complications correlated with PPD Resource Availability: financial concerns correlated with PPD ? Motivation in nonessential goals: e.g. successful depressives Attract Social Support: PPD related to low social support Best of Luck on the Midterm!!! : Best of Luck on the Midterm!!!

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