Note for KIN 172 at UMass
Popular in Course
Popular in Department
This 11 page Class Notes was uploaded by an elite notetaker on Friday February 6, 2015. The Class Notes belongs to a course at University of Massachusetts taught by a professor in Fall. Since its upload, it has received 18 views.
Reviews for Note for KIN 172 at UMass
Report this Material
What is Karma?
Karma is the currency of StudySoup.
Date Created: 02/06/15
Chapter 16 Endocrine System L5 I Homeostasis balance inbody systems a Receptor senses monitors environment amp responds to stilnuli chemical neural hormonal b Control center determines set point range at which variable is maintained c Effector provides means to respond to sti1nulus d Negative Feedback output shuts off original stimulus ex Body temp II Autocrine tissue releases substance that acts on itself III Paracrine tissue releases substance that acts locally IV Endocrine System body system including internal organs that secretes hormones Ductless secretion rich capillary network a Hormones chemical messengers released into blood to be transported through out body i Long distance chemical signal blood lymph ii Widespreaddiverse effects metabolism growth water reproduction iii Upregulation target cells form more receptors in response to hormone iv Downregulation target cells lose receptors in response to hormone v Circulate freely or bound steroid thyroid in blood vi Concentration based on release rate amp speed of inactivation and removal from body degrading enszymes kidneys liver enzyme systems Negative feedback systems vii Halflife viii Hormone action variablility ex epinephrine vs growth hormone V Hormone interactions a Permissiveness one hormone can t exert its effects w out another hormone being present b Synergism more than one hormone produces same effects amplification c Antagonism one or more hormones opposes e others actions VI Hormone classification according to derivationstructure a Peptide hormones most abundant water soluble ex insulin i act at target cell surface too big to diffuse amp can t pass through ii 2Dd messenger 1 Hormone 1st messenger binds to receptor 2 G protein activated 3 Enzyme adenylate cyclase activated generates cAMP 2nd 4 cAMP activates protein kinase enzymes a activate or inhibit via phosphorylation b Tyrosine derivatives amines i Water soluble epi NE dopamine ii Lipid soluble T3 T4 c Steroid synthesized from cholesterol long lasting effects gonads estrogen testosterone and adrenocorticol hormones aldosterone cortisol i diffuse into cell amp bind to DNA HRE transcription factor ii prompts DNA transcription mRNA protein iii lipid soluble iv bind to carrier protein in blood then receptor in cell d Eicosanoids lipid based leukotrienes in ammation allergic reactions Prostaglandins BP clotting pain VII Hormone Action Change plasma membrane permeability amp transport Stimulate protein synthesis enzymes lnduce secretion of other substances Stimulate mitosis contraction 9 9 ET Lecture 2 amp 3 I Pituitary two lobed organ that secretes eight major hormones a Posterior amp Anterior lobe inferior to hypothalamus connected by infundibulum b Receives stores amp releases hormones from the hypothalamus c Synthesizes amp secretes some hormones II Anterior pituitary hormone synthesis amp secretion regulated by hypothalamic releasing and inhibiting hormones RHampIH a blood connection w hypothalamus b Hormones FSH LH ACTH TSH Prolactin GH i All use cAMP except CH C Growth Hormone GH stimulates most cells main targets bone amp skeletal muscle i Circadian rhythm high at night low during day overall levels decrease w age ii Growth effect promotes protein synthesis iii Metabolic effect fats 9 fuel promotes fat breakdown amp inhibits glucose uptake by skeletal muscle inc blood glucose iv Major target adipocytes GH effects mostly directed by IGFs insulin like growth factors synthesized in liver cells that respond to GH binding by acting on bone amp muscle v Hypothalamic control 1 GHRH growth hormone releasing hormone 2 GHIH growth hormone inhibiting hormone vi Hyposecretion of GH short stature extreme dwarfism vii Hypersecretion of GH tall 1 Acromegaly too much GH after growth plates close 9 excess cartilage growth can lead to diabetes high blood sugar lvls a Late onset often caused by pituitary tumor b bone shapes change facial features distorted lower jaw protrudes hands and feet enlarged 2 Gigantism early onset of GH hypersecretion d Thyroid Stimulating Hormone TSH stimulates thyroid gland for normal development amp secretory activity i Hypothalamic control triggered by TRH thyrotropin releasing hormone cold temps in infants pregnancy ii Negative feedback inc blood levels of TH act on pituitary amp hypothalamus to block TSH release 1 GHIH also inhibits release e Adrenocorticotropic Hormone ACTH stimulates adrenal cortex to release corticosteroids aid body in resisting stress i Hypothalamic control releases corticotrophin releasing hormone CRH circadian rhythm that peaks just before waking ii lnternal amp external regulation 1 Fever low blood sugar amp stress can trigger CRH release 2 Negative feedback Hypothalamus releases CRH9 triggers ACTH release from pituitary ACTH travels bloodstream amp stimulates adrenal glands to release cortisol helps provide energy 02 amp stimulates brain heart muscles amp organs to support body s stress response f Gonadotropins FSH amp LH follicle stirnulating hormone amp luteinizing hormone regulate ovary amp teste functions i Absent from pre pubertal children s blood regulate egg amp sperm production ii Hypothalamic control releases GnRH gonadotropin releasing hormone during and after puberty iii Negative feedback 1 Females LH FSH cause maturation of ovarian follicle LH triggers ovulation amp promotes estrogen amp progesterone synthesis amp release 2 Males FSH stimulates sperm production LH stimulates teste cells to produce testosterone 3 g Prolactin PRL stimulates milk production in breasts during pregnancy amp nursing i Hypothalamic control releases prolactin releasing hormone transient monthly eleveations in PRL breast swelling amp tenderness blood levels rise end of pregnancy suckling stimulates PRH release amp continued milk production III Posterior pituitary made of axons of hypothalamic neurons a Releases stored neurohormones that are made in hypothalamus Oxytocin ADH i Triggered by neural stimuli b Neurohypophysis Posterior pituitary Hypothalamus C Antidiuretic hormone ADH in uences uid balance i Prevents urine formation release osmoreceptors monitor solute conc of blood high ion conc ADH synthesisamprelease H20 preserved ii Prevents uid overload inhibition low ion conc SDH not released water loss from body iii Alcohol inhibits ADH9 inc urine output iv Also stilnulated by pain nicotine amp low BP d Oxytocin stimulates smooth muscle contraction in breasts and uterus via pos feedback i Strong stiInulant of uterine contraction stimulated by cervical uterine stretch inc intensity of uterine contractions feed forward response ii Triggers milk ejection in lactating women stimulated by child suckling crying iii Sexual satisfaction amp orgasm only this role in males Lecture 4 I Thyroid gland located in anterior neck Parathyroid glands rest on dorsal side a Produces thyroglobulin inactive i Thyroglobulin iodine active form of thyroid hormone TH 1 TH body s major metabolic hormones Triiodothyronine T3 and thyroxine T4 TABLE 163 Amine hormones w iodine from single amino acid ie tyrosine Ex EPI amp NE In uenced by TRH hypothalamus amp TSH ant Pituitary Activation via intracellular receptor binding and DNA transcription ii Effects on body 1 Large calorigenic Effect effects gene transcription of gene for glucose metabolism 2 BP regulation via adrenergic sti1nulation inc adrenergic receptors in blood vessels Receptors regulate BP 919 3 Tissue growth and development skeletal nervous and reproductive systems iii Mechanism of Action of THs on Target Cells 1 2 3 4 Needs protein carrier to travel in blood Need TBG thyroid binding globulins which are produced by liver protect TH in inactive state until it reaches the target cell SO carrier protein ensures only target cell is affected Transposed into T3 which binds to TH receptors on DNA to activate transcription Physiological effects glucose oxidation inc BMR heat production maintaining BP regulating tissue growth developing skeletal amp nervous systems in uences maturation amp reproductive capabilities iv Hypothyroidism inadequate thyroid hormone production 1 2 Usually problem in gland amp not with pituitary production of TSH or hypothalamus production of TH Adult subcutaneous swelling dry skin hair loss low body temp low BMR muscle weakness slow re exes May be accompanied by goiter enlarged thyroid gland 0 Low iodine low TH synthesis Lack of negative feedback High TSH thyroid growth by colloid production goiter Myxedema thyroid gland can t synthesize and release TH o Endemic goiter inadequate iodine o Hashirnoto s thyroiditis in ammation of thyroid v lnfants Late childhood Cretinism genetic deficiency with thyroid or maternal factors lack of iodine 1 Retards growth delays puberty affects mental development short disproportionately sized body thick tongue amp neck vi Hyperthyroidism Grave s Diseas autoimmune disorder antibodies target thyroid follicle cells mimic TSH trigger release 1 vii Symptoms increased metabolic rate ushed amp moist skin inc heart rate and BP restlessness excitable insomnia mood shits limited energy easily fatigued eye bulging Exophthalmos Treatment Removal of thyroid gland radioactive iodine treatment b Location of Parafollicular C cells produce Calcitonin i Targets skeleton lowers blood Ca2 1 2 Inhibits osteoclast activity to dec bone breakdown and dec calcium release from bone matrix Stimulates osteoblast activity inc calcium uptake amp incorporation into bone to inc bone density ii Opposes PTH parathyroid hormone 1 negative feedback mechanism High Ca2 levels triggers calcitonin release II Parathyroid gland 2 8 tiny glands embedded in posterior aspect of thyroid a Parathyroid Hormone stiInulated by drop in blood Ca2 i PTH release inc Ca2 in blood by 1 Stilnulating osteoclasts to break down matrix 2 Enhancing resorption of Ca2in kidney tubules and secretion of phosphates from kidneys 3 Inc vitamin D activation in kidney calcium absorption from food by intestinal mucosal cells digestive system 4 Rising Ca in blood inhibits PRH release Lecture 5 I Adrenal glands paired pyramid shaped organs atop kidneys 2 glands in one medulla amp cortex II Cortex three layers synthesize amp release different corticosteroids a Corticosteroids cholesterol based hormones synthesized as needed i Mineralocorticoids outside regulate electrolyte conc in extracellular uids Na K HC03 Cl 1 Aldosterone secretion stilnulated by inc blood K dec blood Na volume or pressure ii Glucocorticoids middle help body resist stress by regulating blood sugar volume amp pressure 1 EX cortisol hydrocortisone 2 Regulation 3 Fight or Flight gluconeogenesis synthesis of glucose from non carb sources rise in blood sugar FA and AA 4 Excess cortisol inhibits in ammation dec cartilage amp bone formation depresses iInmune system promotes changes in cardiovascular neural amp gastrointestinal function iii Gonadocorticoids inside most are androgens converted to testosterone estrogen 1 Contribute to onset of puberty rises 7 13 y secondary sex characteristics appear sex drives in females converted into estrogens after menopause b Disorders i Hypersecretion ii Hyposecretion iii Chronic administration of large cortisol doses treatment for asthma arthritis prevention of transplanted organ rejection produces symptoms like Cushing s or Addison s disease iv Cushing SyndromeDisease chronic excess of cortisol inc ACTH secretion from antpit adrenal tumors secrete extra cortisol 1 Symptoms acne hyper pigmentation thinning skin inc body facial hair trunk obesity buffalo hump easily bruised muscle wasting suppressed immunity inc BP 2 Treatment tumor removal discontinuing drug use V Addison Disease 1 Causes hyposecretion of cortisol from adrenal insufficiency inadequate stimulation of adrenal cortex by ACTH or autoimmune disease that destroys adrenal cortex 2 Symptoms weakness muscle wasting weight loss hypoglycemia hypotension 3 Treatment cortisol supplementation III Adrenal Medulla secretes epi amp nor causes inc blood sugar blood vessel constriction faster heart beat amp diverts blood to brain heart amp skeletal muscle a Epinephrine 80 more potent heart amp metabolic activity stilnulator i cAMP mediation breaks down fast so effects last less than 15 min ii binds to heart arteriole smooth muscle adipose tissue muscle amp liver b Norepinephrine 20 in uences peripheral vasoconstriction amp BP c Ephedrine syntheticextract from ephedra plant that milnics epi action with more sustained response i Decongestant bronchodilators amp appetite suppressant ii Marketed to inc energy burn fat inc metabolic rate lose weight elevate mood iii Ephedra natural form plants w mix of alkaloid cmpds including ephedrine amp pseudoephedrine 1 Ma Huang powdered extract in a lot of ephedrine products 2 Possibly dangerous Lecture 6 I Gonads femalesovaries malestestes a Gonadotropin stimulation i GnRH hypothalamus ii FSH LH anterior pituitary iii Steroid hormones 1 Females ovaries produce estrogen amp progesterone 2 Males testes produce testosterone b Hypothalamuspituitarygonad Axis Control System Hypothalamus releases GnRH9 Ant Pit releases FSH amp LH9 Gonads release estrogen amp androgens i Neg feedback caused by sex steroid hormones 1 lnhibit GnRH secretion from hypothalamus 2 Inhibit anterior pituitary responsiveness to GnRH c Female paired ovaries in abdominal cavity produce estrogen progesterone amp some testosterone i Maturation of reproductive organs ii Appearance of secondary sex characteristics 1 Boobs body hair vaginal amp uterine growth 2 Wide hips inc oil amp sweat secretion 3 Change in weight amp fat distribution more subcutaneous fat amp fat around butt thighs amp hips iii Breast developent amp monthly menses EP iv Metabolic effects enhance HDL lower LDL Male testes in extra abdominal sac scrotum produce testosterone i Testosterone initiates maturation of male reproductive organs secondary sex characteristics sex drive sperm production Hormonal Regulation i GnRH hypothalamus ii FSH amp LH in uence sperm production via androgen binding protein keeps local testosterone levels high iii LH causes testosterone release iv Inhibin regulates spermatogenesis Birth control pills high estrogen amp progestin levels affect hypothalamus to inhibit GnRH release pregnancy like situation i Effects 1 inc cancer risk cervical amp liver dec cancer risk ovarian endometrial 2 Estrogen inc HDL amp dec LDL 3 Progestin dec HDL amp inc LDL 4 Inc in elevated BP w age amp duration of use Menstrual Dysfunction i Dysmenorrhea menstrual cramps affects 50 75 b w 15 25 yrs doesn t occur when ovulation is inhibited 1 Endometrial cells lining uterus secrete excessive levels of prostaglandins Uterine vasoconstriction Dec 02 supply to endometrium Uterine contractions Diarrhea Headache 7 Vomiting ii Amenorrhea 1 Primary failure to begin menses a Genetic disorders b Congenital CNS defects c Extreme energy deficit 2 Secondary cessation of menses misses 3 consecutive periods a Extreme weight loss energy deficit 9019 b Pregnancy c Lactation h Normal physiology i Cysts follicles in ovaries hold eggs ii Eggs mature iii Cyst ruptures amp releases egg iv Egg travels through fallopian tube to uterus v Egg fertilization menstruation occurs vi Cyst dissolves i Polycystic Ovary Syndrome PCOS multiple follicles develop with no ovulation amp ovaries accumulate numerous cysts causes are unknown i Women bw 11 and 30 yrs ii Progression Positive feedback cycle of abnormal hormone secretion 1 FSH is low and LH is high 2 High LH9 adrenal cortex amp ovary secrete high androgen levels 3 High estrogen inhibits FSH amp stimulates LH 4 Causes more follicles cysts to develop iii Symptoms obesity hypertension high cholesterol excessive facial hair growth acne amenorrhea irregular heavy bleeding from inc estrogen lvls infertility diabetic symptoms iv Treatment anti estrogen anti androgen drugs progesterone birth control pills Metformin ovarian surgery j Endometriosis tissue spreads beyond uterus i Normal endometrial tissue found in uterus undergoes monthly changes and estrogen secreted from ovaries stimulates tissue growth of lining of uterus endometrial lining ii Responsive to reproductive hormones amp undergoes cyclic changes iii Occurs in 3 10 women during reproductive years iv Genetic predisposition but underlying cause is unknown v Symptoms pelvic pain irregular bleeding dysmenorrheal infertility vi Treatment birth control pills to suppress tissue growth 1 GnRH agonists for 3 6 months dec estrogen production a Gives uterus amp endometrial tissue rest b Menopausal symptoms 2 Surgical removal of excessive growth 3 Hysterectomy followed by hormone replacement therapy k Anabolic steroids variations of testosterone manufactured in lab introduced in 1950s as anemia treatment amp treatment for muscle wasting diseases amp muscle atrophy after long term immobilization i Abuse used mostly by athletes in 1960s ii Typical use up to 200mg day several derivatives of testosterone stacking orally injected or in patch inc dose over time pyramid iii Risks acne hair loss facial swelling atrophied testes enlarged breasts infertility liver damage cancer dilated cardiomyopathy inc risk for coronary heart disease amp artherosclerosis inc LDL cholesterol roid rage Lecture 7 I Pancreas acinar cells form an enzyme rich pancreatic juice used for digestion exocrine function a Islet of Langerhans produce hormones two major cell types i Alpha u produce glucagon ii Beta produce insulin b Glucagon smaller 29 AA polypeptide hormone that inc blood glucose i Major target liver ii Glucogenolysis glycogen glucose iii Gluconeogenesis lactic acid noncarb glucose 1 Release stimulated by hypoglycemia sympathetic NS 2 1 glucagon 100 miillion glucose c Insulin lowers blood glucose i Enhances transport into muscle amp fat inhibits glycogenolysis amp gluconeogenesis ii Once in cell prioritized catalyses glucose oxidation for ATP production iii Links glucose units glycogen iv Converts glucose to fat adipose tissue v Released by high glucose high AA high FA acetylcholine by parasympathetic NS C Type 1 Diabetes Diabetes Mellitus DM i Symptoms insulin loss inadequate production loss impairment f cells ability to absorb glucose tissues glucose starved 1 acute effect following meal high in carbs blood glucose is so high that kidneys can t reclaim it all and glucose spills into urine a limits kidney ability to conserve water b frequent urination can lead to dehydration c dehydration neural disturbances blurred vision tingling sensations fatigue muscle weakness 2 inc fat amp protein breakdown 3 inc in ketone bodies which dec pH ketoacidosis a may cause vomiting coma death 4 Three cardinal signs of DM a Polyuria huge urine output b Polydipsia excessive thirst c Polyphagia excessive hunger amp food consumption ii Treatment Long term 1 Diet modification 2 Blood glucose monitoring 3 Insulin administration injection infusion via pump nasal spray patch 4 Treatment complications tissue glucose demands vary w food composition exercise amp emotional state e Type 2 Diabetes 95 of all cases of diabetes i Higher prevalence in minority groups ii No longer adult onset adolescent diabetes on the rise iii General characteristics of at risk 1 Normal elevated insulin lvls 2 Peripheral tissues stop responding normally to insulin down regulation 3 Insulin resistance glucose challenge test iv Lifestyle treatment 1 Improved diet amp inc physical activity can reverse and or prevent TZD 2 Weight loss in obese individuals can reverse and or prevent TZD II Other Hormone producing structures a Pineal Gland produces melatonin amp works w hypothalamus to regulate bio clock b Heart produces atrial naturetic peptide ANP which dec BP blood volume amp blood sodium conc c Gastrointestinal Tract enteroendocrine cells release local acting digestive hormones gastrin d Placenta releases hormones that in uence pregnancy estrogen progesterone e Kidneys secrete Erythropoietin which stimulates bone marrow to make RBC f Adipose tissue releases Leptin satiety sensation amp stimulates increased energy expenditure i Leptin Peptide hormone made by adipocytes 1 Leptin receptors in brain neurons involved with energy intake amp expenditure 2 Obese high blood leptin levels 3