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Bio Week of 2.2.16

by: Shayla Pedigo

Bio Week of 2.2.16 Bio 111 - Fundamentals of Biology II

Shayla Pedigo

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Athena Anderson
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Biology, Bio, Biology 111
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This 18 page Class Notes was uploaded by Shayla Pedigo on Tuesday February 9, 2016. The Class Notes belongs to Bio 111 - Fundamentals of Biology II at Purdue University taught by Athena Anderson in Spring 2016. Since its upload, it has received 14 views. For similar materials see Biology in Biology at Purdue University.

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Date Created: 02/09/16
Bio Notes week of 2.2.16 PHYSIOLOGY AND HOMEOSATASIS Complex multicellular animals have a hierarchical organization of structures:  Cells organized into tissue, organized into organs, organized into organ systems  Emergent properties appear at each new level (characteristics that are seen at the higher level that were not exhibited at the level below). Complex living systems exhibit homeostasis HOMESTASIS The ability to maintain a constant internal environment despite fluctuating external environment; requires internal communication about the state of the organism Concentration of important molecules in body fluids have set points – levels at which a physiological state is regulated  Get above set point, respond by lowering  Get below set point, respond by raising  Like a thermostat in a house connected to heating and cooling systems SIGNALING MOLECULES Recall different ways cells send signals:  Autocrine: same cell type sends and receives signal  Paracrine: one cell type sends signal, other cell type receives signal Recall location of target- close or distant  Local signaling molecules: neurotransmitters, histamines, etc.  Distant signaling molecules: hormones, growth factors ENDOCRINE SYSTEM  Regulates body’s ‘set points’- temperature, heart rate, metabolism, “fight or flight” response  Triggers important physiological events- puberty, reproduction  Facilitates cell to cell communication- glucose uptake, antihistamine release, “fight or flight” HORMONE  A chemical secreted by an endocrine gland/organ into the blood for transport  Effective at low concentrations (10 to 10 -1M)  Affect growth, metabolism, development, and/or homeostasis ENDOCRINE GLAND  A ductless gland or single cell that secretes a hormone, which travels through blood  Targets the cell(s) or organ(s) that have receptors for the hormone Human endocrine glands  Hypothalamus  Pituitary  Thyroid  Thymus  Adrenal  Pancreas  Testes/ Ovaries HYPOTHALAMUS Maintains homeostasis by controlling autonomic nervous system; “link” between endocrine & nervous systems Releases… 1. Neurotransmitters (epinephrine, serotonin) 2. Hormones that regulate anterior pituitary (thyrotropin-releasing hormone) 3. Hormones that are stored in posterior pituitary for later release (oxytocin, vasopressin) PITUITARY GLAND Structure below the hypothalamus, has 2 regions:  Posterior: Also part of CNS. Receives neurohormones from hypothalamus and stores them until needed.  Anterior: Not part of CNS. Receives hormonal signals from hypothalamus. Hypothalamus & Pituitary Glands Hormone Pathways ADH: Anti-diuretic hormone OT: oxytocin GnRH: Gonadotropin- releasing hormone TRH: Thyrotropin- releasing hormone PRH: prolactin- releasing hormone GHRH: Growth hormone-releasing hormone CRH: corticotropin- releasing hormone Classes of Hormones 1. Steroids (derived from cholesterol), example: cortisol, estrogen, testosterone 2. Peptide (< 40 amino acids), example: ACTH 3. Protein (>40 amino acids), example: growth hormone 4. Glycoprotein, example: thyroid stimulating hormone Negative Feedback Loops  Hormone regulation often involves negative feedback loops, where an increase in a hormone leads to the inhibition of that hormone Response to altered set point stops its own production: self-limiting  Exceed set point in one direction, and glands produce hormone, leading to response  Exceed in the opposite direction, and glands stop production, stopping the response >>Example: level of glucose in blood Controlled by 2 hormones, both produced by Islets of Langerhans cells in pancreas Hormones have antagonistic effects  Insulin responds to  blood glucose  Glucagon responds to  blood glucose After eating, blood glucose rises, 1. Stimulating insulin production by pancreas 2. Insulin lowers blood glucose;  Cells take up glucose  Cells convert glucose to glycogen  Slows gluconeogenesis (synthesis of carbohydrates from fat & protein) 3. Insulin production stops 4. Overall result: blood sugar drops Eating very sugary foods causes the “sugar crash” feeling of abrupt decrease in energy because it triggers quick decrease in blood sugar Between meals or after skipping a meal... 1. Blood glucose falls, stimulating glucagon production (from pancreas) 2. Glucagon raises blood glucose  Glucose released by liver cells  Glycogen is converted to glucose  Increases gluconeogenesis 3. Glucagon production stops 4. Overall result: blood glucose rises DIABETES Diabetes is a disease that disrupts insulin/glucose regulation Type I: genetic, pancreas doesn’t produce enough insulin, treated w/ insulin injection, 10% Type II: usually acquired through lifestyle, pancreas can’t make enough insulin to keep blood glucose down, 90% >>1/3 people in US will have diabetes by 2050 (ADA). >>Type II on rise in children, usually attributed to diet & inactivity. >>Children from some racial & ethnic groups at higher risk: African American, Hispanic, Asian, Native American. Associated risks  heart disease  nerve, eye, kidney, foot damage  skin conditions  hearing impairment  Alzheimer’s disease Fight or Flight Response 1. Brain tells hypothalamus a threat is perceived 2. Hypothalamus signals pituitary to release ACTH 3. ACTH signals adrenal gland to release epinephrine (adrenalin) and cortisol 4. Together, they increase blood pressure & sugar, increase gluconeogenesis, & metabolism of protein & fat to glucose 5. Result is burst of energy to muscles, to prepare body to fight or flee o pupils dilate o tunnel vision o hearing loss o digestion slows o shaking o blood flow diverted o from extremities to muscles Effects of Chronic Stress >Some stress is good (eustress); keeps you alert and engaged in activities >Constant high stress (distress) keeps the body in “fight or flight” mode >Chronic pain also causes chronic stress Some side-effects of chronic stress  decreased productivity  difficulty thinking  high blood pressure  stroke  heart disease  insomnia  decreased immunity  depression  anxiety  obesity  fatigue  increased risk of alcohol/drug abuse College students are at high risk of chronic stress • high course load • jobs • pressure to finish quickly because of cost • financial burden • social life THYROID  Controls metabolism, affects temperature, heart rate, growth Produces two hormones: 1. Triiodothyronine (T )3 2. Thyroxine (T )4  Have similar effects, but T m3de from T and more potent 4 Hypothyroidism  Caused when thyroid doesn’t produce enough T or T 3 4  Est. 10 million Americans suffer from this  Can take years for correct diagnosis; often discounted as “all in your head”  Est. 10% of women have some degree of thyroid dysfunction  Can have “normal” levels of TSH, T and3T and s4ill suffer from this! Goiter Enlarged thyroid gland, can be caused by numerous conditions: • iodine deficiency • hyperthyroidism • nodules • cancer • pregnancy • inflammation Most common in developing countries, where iodine deficiency more likely. THYMUS  Only active during youth, starts to atrophy at puberty- turns to fat  Produces T-cells (essential for immune function) & thymosin, which causes maturation of T-cells  Both endocrine and immune Function Sjörgens Syndrome  Pronounced “SHOW-grins”  Autoimmune disease, thought to come from T-cells that aren’t “trained” in thymus long enough  Causes range of symptoms, esp. fatigue & drying of body’s moisture- producing glands  Equally affects all ethnic groups  U.S. tennis player Venus Williams diagnosed in 2011  Had to withdraw from 2011 U.S. Open tournament due to symptoms  Est. 4 million Americans with disease  Avg 6 yrs to diagnosis Adrenal Glands Sit on top of kidneys >>Produce many hormones: • estrogen & progesterone- female sex hormones • cortisol & cortisone- anti-inflammatory, stimulate gluconeogenesis • epinephrine & norepinephrine- increase heart rate, sugar metabolism, threat response • dopamine- neurotransmitter gives happy feeling from award- seeking behavior, counters norepinephrine Addison’s Disease  Adrenal glands produce insufficient cortisol  Causes severe fatigue, weight loss, vomiting, pain, depression... PANCREAS  Produces insulin & glucagon to regulate blood glucose  Also produces enzymes that help with digestion Testes/ Ovaries  Testes: male gonads, produce testosterone & other androgens  Ovaries: female gonads, produce estrogen & progesterone  Up to 6 weeks post-fertilization males and females are indistinguishable gonadally  Wolffian ducts (male) will inhibit Mullerian ducts (female) when Sertoli cells in teste secrete Mullerian inhibiting substance (MIS).  If not inhibited by sex determining substances from Y chromosome, Mullerian system develops. Acromegaly  Caused by overproduction of GH from pituitary.  90% of sufferers have pituitary tumor; grow continuously  Causes elongation of legs, feet, arms, hands, jaw.  Associated risks include type II diabetes, high blood pressure, arthritis, cardiovascular disease. Robert Wadlow - 8’ 11” 439lbs tallest person 1940, died of infection, age 22 Cushing’s Syndrome  Most often caused by overuse of glucocorticosteroid medication, which mimics cortisol  Tumors most common natural cause Hormones and Development  Hormones control normal development in all complex animals.  Molting in insects is caused by hormone ecdysone, a steroid secreted by glands in the thorax.  Metamorphosis in amphibians is stimulated by release of T fro3 the thyroid Endocrine Disruptors (EDs)  Environment al chemicals that interfere with normal endocrine signaling; mimic effects of steroid hormones Examples: 1. Diethylstilbestrol (DES) 2. Bisphenol A (BPA)  Diethylstilbestrol (DES), a non-steroidal estrogen mimic, was synthesized in 1938  FDA approved its use for menopause symptoms in 1941 & to prevent miscarriage in 1947  1953- first study suggesting it wasn’t effective for preventing miscarriage  1971- first study published linking it to vaginal cancer in female offspring of mothers who used it Risks of exposure to DES during fetal development: Males • feminization of reproductive organs • undescended testes • abnormal development of penis and urethra Females • increased risk of uterine and cervical cancer • abnormal development of uterus Normal>> <<DES >>BPA used in production of plastics, exhibits hormone-like properties. Risks of exposure to BPA during fetal development: Males • increased probability of abnormal development of penis, testes and prostate Females • in rats, causes suppression of ‘Hox A’ genes, which regulate uterine development • alters uterine lining and progesterone sensitivity in adults


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