Final Exam: Endocrine
Final Exam: Endocrine BSCI 201
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This 3 page Study Guide was uploaded by Brooke Sullivan on Thursday May 12, 2016. The Study Guide belongs to BSCI 201 at University of Maryland taught by Dr. Meredith Bohannon in Spring 2016. Since its upload, it has received 213 views. For similar materials see Human Anatomy and Physiology in Biological Sciences at University of Maryland.
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Date Created: 05/12/16
Basics of Hormones • Proteins: water soluble, regulate gens for other protein manufacture, growth hormone • Amine Hormones: water soluble, products of enzymatic reactions, epinephrine • Steroids: lipid soluble, synthesized from cholesterol, products of enzymatic synthesis, cortisol • They exert their effects through hormone receptors on their effector cells. Water soluble hormones use second messenger systems while lipid soluble hormones use gene activation • They are generally regulated through negative feedback Hypothalamic Control of Pituitary • Posterior: neurons in the hypothalamus synthesize either oxytocin or ADH; they are transported though the hypothalamic-hypophyseal tract; they are stored in the axon terminals in the posterior pituitary, when the neurons from the hypothalamus fire, the action potentials cause the release of ADH and oxytocin into the blood. • Anterior: in response to stimulus, neurons in the hypothalamus secrete releasing or inhibiting hormones into the primary capillary plexus; they travel through portal veins and either stimulate or inhibit the release of the hormones produced in the anterior pituitary gland; if releasing hormones are released, the anterior pituitary will secrete hormones into the secondary capillary plexus, where they then travel to the blood. • Hypothalamic Hormones: Gonadotropin releasing hormone, growth hormone releasing and inhibiting hormone, thyrotropin releasing hormone, corticotropin releasing hormone, and prolactin inhibiting hormone • Anterior Hormones: growth – systemic effects; thyroid-stimulating – causes release of T3 and T4; adrenocorticotropic – causes release of cortisol from adrenal cortex; follicle-stimulating and luteinizing – reproductive effects, cause release of estrogen and testosterone; prolactin – causes milk production • Posterior Hormones: oxytocin – uterine contractions in labor, milk let-down, possibly responsible for postpartum maternal behavior, increases pair- bonding; antidiuretic – controls blood water concentration • HPA Axis: Hypothalamus sends corticotropin releasing hormone to Pituitary, Pituitary sends adrenocorticotropic hormone to Adrenal cortex, Adrenal cortex releases cortisol on a negative feedback loop • HPG Axis: Hypothalamus sends GnRH to Pituitary, Pituitary sends LH and FSH to gonads, testes release testosterone and ovaries release estrogen and progesterone, both on negative feedback loops • HPT Axis: Hypothalamus sends TRH to Pituitary, Pituitary sends TSH to Thyroid, Thyroid releases T3 and T4 on negative feedback loops Growth Hormone • Increased cartilage formation and skeletal growth; increased proteins synthesis, and cell growth and proliferation; increased fat breakdown and release; increased blood glucose and other anti-insulin effects • The anterior pituitary releases growth hormone. One of its indirect effect is the production of insulin0like growth factors. These work on a negative feedback loop by inhibiting GH synthesis and release, inhibiting GHRH release, and stimulating GHIH release. Thyroid System • Both T3 and T4 start with tyrosine from thyroglobulin. The tyrosine then attaches to either 1 or 2 iodine atoms. These molecules then bind together to form T3 (3 iodine) or T4 (4 iodine) • Maintains BMR, stimulates sympathetic effects, body temp, glucose catabolism, fat mobilization, maintains heart beat, nervous system development from fetus to child, development of skeleton, development and function of reproductive system, motility of GI tract • Hyperthyroidism: Grave’s disease; Hyperthyroidism: goiter, Hashimoto’s syndrome, cretinism, congenital hyperthyroidism, “American lifestyle” hyperthyroidism Adrenal System • Adrenal Cortex: corticosteroids - glucocorticoids (cortisol and coticosterone), mineralocorticoids (aldosterone), and gonadocorticoids (androstenedione) • Adrenal Medulla: catecholamines – epinephrine and norepinephrine • Mineralocorticoids regulate mineral salts in extracellular fluid • Glucocorticoids in normal amounts will increase blood glucose and pressure (through vasoconstriction) • Gonadocorticoids contribute to armpit and pubic hair during puberty. They are also the only source of sex hormones for women after they have gone through menopause • Epinephrine and norepinephrine respond to acute stress • All steroids are derived from cholesterol. CYP450scc cleaves the side chain off of cholesterol, producing pregnenolone. The final results are cortisol, corticosterone, aldosterone, and androsterone. • Cushing’s disease is caused by excess cortisol; Addison’s disease is caused by too little cortisol. The Pancreas • Insulin and glucagon • Insulin decreases blood sugar after eating by increasing cell metabolic activity and glycogen conversion and storage. Glucagon increases blood sugar by stimulating the break down of glycogen back into glucose so that it can be sent back to the blood and body cells • Type 1 Diabetes is an autoimmune disorder were the body attacks its own beta cells in the pancreas and leads to lower levels of insulin which allows glucose to remain in the blood for too long. Type 2 Diabetes is a cellular insensitivity to insulin, in part caused by genes, and in part caused by lifestyle. Gestational diabetes is short-lived Type 2 diabetes that occurs during pregnancy. It is caused by pregnancy hormones, and therefore subsides after birth. The Reproductive System • Male hormones are testosterone and dehydrotestosterone and produced in the testes. Female hormones are estradiol and progesterone and are produces in the ovaries • Testosterone leads to spermatogenesis and estradiol leads to the establishment of an ovarian cycle. It also helps with breast development in puberty, systemic vascularization during pregnancy, and masculinization of the male brain. • Cycling of Testosterone: GnRH causes a rise in LH and FSH levels, which in turn increase the levels of testosterone to rise. This is a negative feedback system. • Cycling of Estradiol: GnRH causes a rise in FSH and LH levels, which in turn causes levels of estradiol to rise. The estradiol will increase in the estradiol cells. This increase will cause the production of follicles. An even larger increase in estradiol causes positive feedback on the GnRH, FSH and LH. The surge of LH causes ovulation. • Androgen receptor deficiency results in persons that are genotypically and hormonally male, but are phenotypically male since hormones with no receptors are practically useless in the body. With 5 alpha reductase deficiency, the children are phenotypically and hormonally female until puberty because they do no have receptors for dehydrotestosterone. When puberty hits, however, testosterone takes over and the children become phenotypically male as well.
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