EXSC 224 Week 8 Notes
EXSC 224 Week 8 Notes Exsc 224
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This 5 page Class Notes was uploaded by Jane Warther on Friday March 4, 2016. The Class Notes belongs to Exsc 224 at University of South Carolina taught by Dr. Thompson in Spring 2016. Since its upload, it has received 39 views. For similar materials see Anatomy and Physiology 224 in Education and Teacher Studies at University of South Carolina.
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Date Created: 03/04/16
3/1/2016 Chp. 16 Gonads Females Estrogen steroid o Alone Maturation of female reproductive organs Sex characteristics o Lack of testosterone results in female genitalia o Under control of hypothalamus Progesterone steroid o In combination with estrogen Breast development Menstrual cycle regulation o Not made in same pathway as estrogen Produce cortisol and aldosterone from progesterone o Not responsible for primary formation of secondary sex characteristics o Causes downregulation of estrogen receptors o Promotes development of endometrium furthers so that is prepared for fertilized egg or corpus luteum dies o Under control of hypothalamus Menopause cessation of menstruation o One calendar year without a period o No more ovulation o Can’t become pregnant naturally Gonads Males Testosterone o DHT is the variant, helps to produce male pattern baldness Not normally present in large amounts o Responsible for secondary sex male characteristics o Coming down from high levels of testosterone is when aggression occurs o Andropause age related decline in circulating testosterone o Not like menopause o Age of 25 on , testosterone levels in men decrease Throughout rest of life, levels will decrease Associated with beer gut Women who have had testosterone exposure earlier in life more likely to experience this too Will produce testosterone for rest of life unless castrated or given meds Reninangiotensinaldosterone system (RAAS) Ace inhibitors (treat hypertension)affect this pathway this pathways is unique with how it is activated and regulated more of a longterm regulator than an acute regulator under humoral regulation liver produces angiotensin o produced at constant rate low but constant rate o not regulated o renin , the enzyme that activates the pathway, is regulated 1. Decrease in renal perfusion o Activation of pathway is regulated by kidneys o Kidneys regulate water reabsorption and detect change blood pressure High blood pressure produce urine Low blood pressure save water, no urine Produce enzyme called renin BP falls secrete renin Enters blood stream, converts angiotensin to angiotensin I How we activate reninangiotensin aldosterone system 2. Angiotensin I o Weak weak hormone o Has to be converted to angiotensin II to activate a potent hormone o Converted in lungs Lungs has angiotensin converting enzyme (ACE) o Angiotensin II Very potent hormone Can help stimulate sympathetic activity Stimulate aldosterone secretion Reabsorb water and sodium Will cause blood vessels to constrict Induces secretion of ADH Reabsorb more water in kidneys As a result blood pressure will go up Pathway causes of BP to rise o Helps regulate BP o Altered pharmacologically to reduce BP ACE inhibitors stop ACE from converting 1 to 2 Less expensive Angiotensin II receptor blocker Prevent them binding to their receptor which stops all that angiotensin does Under negative feedback regulation Leptin Produced by adipocytes o Circulates through blood , goes to hypothalamus, causes decreases in appetite(feel full) Regulates eating behavior Inhibits hunger, promotes satiety factor Goes up following a meal , goes back down sometime later and you get hungry Secreted after a meal when nutrients are high Insulin doesn’t cause an increase in leptin Atrial Natriuretic Peptide (ANP) Cardiac distension ANP is an antagonistic to aldosterone Aldosterone causes sodium reabsorption, water follows, produce less urine ANP inhibits secretion and actions of aldosterone, don’t reabsorb sodium, don’t reabsorb water, produce more urine Pathways is talking about ANP Signal is the effects of increase of blood volume on the heart o Increase in blood volume, more blood returns to heart, place stretch on cells of heart, that stretch signals heart to secrete ANP, inhibit aldosterone, produce more urine decreasing blood volume and decreasing stretch of heart cells Under negative feedback control What should I know for the Exam? What is the endocrine system and how does it work? o What are its components? o How does it work? Hormones o Site of secretion o Regulation o Action o Pathology Which hormones have: o Positive or negative feedback regulation o Similar action ADH and aldosterone both cause water conservation Synergistic hormones Aldosterone- Causes sodium reabsorption that leads to water conservation Regulation- potassium, BP, stress Urine output: concentrated urine but not high sodium levels o May have potassium levels ADH- secreted by hypothalamus Operates by aquaporins o Allow for reabsorption of water in nephrons but has nothing to do with sodium Regulated by urine osmality Increased in ADH secretion, decrease urine production o Concentration of urine will go up though o Urine may have elevated sodium concentrations o Urine may have high potassium levels Goiter – not specific to hypo or hyper thyroidism Presence of goiter means you have an overactive thyroid Different causes of it that can lead to different concentrations of thyroid hormone Cushing’s syndrome- vague Elevated cortisol Don’t know reason why Cushing’s disease- Elevated cortisol We know causes o Causes is increase in ACTH that stimulates cortisol Increase in BP, blood sodium , high blood volume, high blood glucose Addison’s disease Hypo-secretion of cortisol or aldosterone Cause could be low ACTH Opposite of Cushing’s Quiz 6 1. Name the stress hormones. Cortisol Epinephrine 2. Males and females secrete androgens from the adrenal medulla. False , secrete from adrenal cortex 3. What stress hormone increases Glycogenolysis(breakdown of glycogen)? -epinephrine Increases gluconeogenesis ?- cortisol 4. Which endocrine disorder causes polydipsia, polyuria, and polyphagia?- diabetes mellitus 5. Three hormones increase blood glucose. What is the antagonistic to insulin?- glucagon
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