Physiology Exam Study Guide

Physiology Exam 4 Urinary System     Functions o Excretion o Elimination o Homeostatic regulation  Ion composition, pH, blood volume, blood pressure, osmolarity, glucose levels, acid-base Anatomy of Kidney o Retroperitoneal- covered by 11th and 12th rib- fat capsule o Hilum- where ureters, blood vessels, lymph and nerves exit and enter  Renal capsule  Adipose capsule  Renal fascia o Renal pelvis – funnel shaped chamber  Connects to ureter to drain kidney o Nephroptosis i Kidneyprolapse o Cortex-medulla-pyramids o Parenchyma- functional portion of kidney in cortex and medulla o Nephron- function unit found in parenchyma Blood and nervous Supply o Nephron- 1 afferent and 1 efferent arteriole o Renal nerves= Sympathetic stimulation  Physical activity and stress  Adjusts flow and pressure at nephron  Vasoconstriction allowing for more blood to vital organs duringFF  Stimulates release of renin outefferent  RAAS- stimulating of reabsorption Nephron o Vascular and tubular  Renal corpuscle- vessels  Renal tubule- filtered fluid passes  Afferent wider the Efferent  Causes pressure increase for better filtration o Glomerulus- fenestrated capillaries  Moves fast o Glomerular capsule=Bowman’s Capsule  Surrounds glomerular capillaries  Plasma is filtered in capsule then filtered fluid passes into the tubule  PCT- Loop of Henle- DCT o Collecting Duct  Merge to empty in papillary ducts then to calyces o Flow  Bowmen’s capsule-PCT-Descending loop-ascending loop- DCT  Histology o Glomerular  Visceral and parietal  Podocytes extensionswraparoundvesselenhance filtration SSE cells   Capsular space o Renal Tubule  Epithelial shapes vary mostreabsorption Secretion  PCT- simple cuboidal with microvilli  DL- SSE  Thin AL- SSE  Thick AL- simple cuboidal  DCT- simple cuboidal  Collecting Duct- simple cuboidal, principal and intercalated cells o Juxtaglomerular apparatus monitorconcentration offiltrate  Macula densa Chemoreceptors  Juxtaglomerular cells – secrete renin wraparoundafferentarterioles smoothmus  Regulate BP- smooth muscle fibers large  Principal cells- receptors for ADH and aldosteronerole SU BP retainingwater  Intercalated cells- pH regulator bases  Renal Physiology BPHomeostasis w removingacidsor o Glomerular Filtration  Filtration- use of pressure to force fluids and solutes through a membrane  Capillaries and podocytes Spertension has risk  Permits water and small solutes 0 damage capillaries  PREVENTS- plasma proteins, blood cells and plateletsnowhere disease on nephronallows nd cause kidney  Regulators toolargeandnegative forpassage ofproteins  Endothelial cells- leaky fenestrations  Mesangial cells- contractile to regulate filtration o Produce cytokines, maintain basement membrane and hold capillaries together  Basal lamina- collagen prevent protein filtrationhas a e charge  Pedicles-wrap around capillary nephrotic disease  Slits- space between pedicles- permit small molecules Filter more fluid of podocytes  failure  Large surface area in Proteins will belost  Thin and porous membrane urine  High Blood pressure afferentarteriole widediameter pressure oncotic pressure  Net filtration efferentarteriole narrowdiameter inglomerulus  FORCE-GBHP Bloodpressure pushingfluidout o Dependent of on contraction of heart o 55mmHg  COUNTERFORCE – CHP go Keeping fluid in o Against filtration membrane o 15mmHg  COUNTERFORCE-BCOP in Keeping o Presence of proteins in plasma ifBp Netpressuret o 30mmHg  NFP= GBHP-(CHP+BCOP)= 10mmHg if BCOP Netpressure o Changes in systemic BP can alter filtration o Long Standing HTN= increased BP- Increased P at kidney  Damage to glomerulus leading to renal failure  Glomerular filtration Rate (GFR)  Amount filtrate formed by kidneys per minute o 125 in males; 110 in females  Alteration o Too fast- needed substance may not be reabsorbed o Too slow- waste products reabsorbed and not eliminated  Mechanisms of Regulation Protectagainshigh BP  Autoregulation (Local) o Myogenic- stretching causes contraction of smooth muscle in afferent arterioles  Narrowing vessels=decreased flow=normal GFR  Low BP- dilate vessels= increase flow= normal GFR o Tubuloglomerular feedback- chemical changes  Increase salt= constricting vessel= less water loss/less constriction filtrate  Decrease salt= dilate vessel= increase filtrate/ increase water loss  Neural Regulation o Sympathetic Nervous system only  Baroreceptors BP vasoconstriction  Increase BP= dilation of arterioles  NE onafferent  Vasoconstrict via alpha 1 arterioles o Increase blood flow to other tissuesdecrease urine output  Hormonal Regulation systemically released in c o ANG II- vasoconstrictor= increases glomerular pressure response to decreased regulating GFR flow to kidneys o ANP- increase GFR- increase capillary surface for filtration o Reabsorption SV relaxesmesagial cells atrial  Tubule to bloodstream stretch o Secretion  Bloodstream to tubule  Eliminate additional substance that did not get filtrated  Control pH or remove substance for elimination fluid KGentation o o o  Composition of filtrate changes across flow of nephron Reabsorption routes  Paracellular  Transcellular Transport mechanisms  Transport proteins present on apical and basolateral surfaces  Passive and active o Na/K pump only in basolateral membrane  Sodium moves one way concentration  Has a capacity limit regulatedbasedon o Solute reabsorption = water reabsorption  Obligatory water reabsorption- PCT  Facultative water reabsorption- Collecting ducts-ADH Proximal Convoluted Tubule Final 10 ofwater  Edges contain brush border of microvilli for increased reabsorption  Reabsorb  Na, K, glucose, AA, Cl, Ca, Mg, HPO4transporter  Glucose moves via SGLT back into vasculature o Threshold 180-200  Water follows solutes o Aquaporins cf.fraomPitinfothe filtrate Secretion  secreted  H, NH4, urea,  Ammonia o By product of broken down proteins o Conjugates into urea at live and filtered by glomerulus Loop of Henle  Reabsorbs  Water- descending loop  Na, K, Cl- ascending loop o Primary Na/Cl reabsorption  Loop diuretics-prevent Na/Cl reabsorption- hold water in nephron  Filter Ca and Mg Distal Convoluted Tubule  Reabsorbs smallamount ofwater NaCl reabsorbed  Water, Na/Cl= most has already been returned to blood stream o Thiazide diuretics  2 cell types: o Principal cells= reabsorb Na; secrete K o Intercalated cells= acid/base balance  Reabsorb HCO3; secrete H Collecting Duct WhereADHworks  In absence of ADH= impermeable to water  Hypotonic urine (dilute urine) frtmbf o o o waterreabsorbed   µ ADH makes hypertonic (concentrated urine)  V2 receptors Homeostatic Regulation of Tubular Reabsorption and Secretion o RASS- ANGII  Normalize GFR by vasoconstrictionperiphalarterioles BP GBHP  Enhance Na/cl and water reabsorption= ADH and aldosterone  Stimulate aldosterone release= reabsorb Na/Cl and increase thirst o Renin  Regulated baroreceptors  Low BP- stimulated release  Macula densa  Senses low Na or hypotesnion  Renin increase Sympathetic Nervous system   Increase renin  ANG II feedback Negativefeedback  Decrease renin o ADH- Vasopressin  Released by pituitary made in hypothalamus  Primary for fluid balance- regulating water reabsorption at DCT and collecting duct  V2 receptors v1receptors vasoconstriction waterreads p  Stimulated by decreased in blood volume or increase in plasma osmarility (lots of solutes)  Diabetes insipidus o Atrial natriuretic Peptide and brain natriuretic peptide and C-type (ANP, BNP, CNP) cardigated  Stimulated by increase blood volume-stretching of atria  Inhibit reabsorption of water and sodium at PCT and CD- promote diuresis  Inhibit renin whole o PTH ofheart  Released when calcium levels fall  Stimulates reabsorption of calcium reabsorption in DCT Outcomes of Secretion o Control pH  Secreting H3O+PCT CD secrete130intofiltrate  Removal on nitrogen waste  Removal of unwanted drugs o Acid/Base at kidney  pH of blood -7.35-7.45  Buffering system  Kidney secretes hydronium (H3O)  Na-H exchanger  For every H+ secreted one Na+ and one HCO3- enter the interstial fluid o Urine pH- 4.5 In   Renal acid secretion is altered by changes in intracellular fluid o High CO2= acidic urine o Excess K+= acid secretion limited o Low carbonic anhydrase- acid secretion limited becomeacidotic o Aldosterone- secretes h+ and K+ Blood Supply increased risk of alkalosis o Controlled by Sarecta  Sympathetic innervation= constriction surroundsloop of  Dopamine= vasodilation henle  ANG II= vasoconstriction  PG= increase blood flow in cortex and reduce flow in medulla  Dilute and Concentrated Urine ADH CD o Dilute Mainly  Glomerulus has some ratio as blood  Initial high concentration in loop attract water  Absence of ADH keeps water in tubules – solutes get reabsorbed o Concentrated ductsimpermeable towater  Water intake low  Presence of ADH- holding onto water  Countercurrent multiplier makes concentration gradient  Increasing osmotic gradient formed between interstitial fluid of medulla and blood flow o Increases water reabsorption at collecting duct via osmosis  Counter current flow the loop established a concentration gradient o Water reabsorbed at descending loop o Collecting duct absorb urea and water- ADH  Urea constantly moving back and forth causing more concentrated urine  Evaluation of Kidney Function o UA  Protein free normal components waste  Solutes: urea, uric acid, creatinine, urobilin, pigments o Blood Tests  BUN- blood urea nitrogen  Catabolism of amino acids  Increased BUN= high protein diet, decreased GFR, CHF, GI bleed, fever  Plasma Creatinine  Catabolism of creatine phosphate  Completely filtered by glomerulus  NOT GREAT FOR RENAL FUNCTION o o EPO- increase RBC production produced in kidneys  Secreted by kidney when low pressure detected or hypoxic  Deactivated by liver  of ESRDpatientsare anemic due to EPOproduction  Urine Tranpsort o Peristalsis pushes urine toward urinary bladder along with gravity o Micturition Reflex voidingreflex  Contraction of detrusor muscle  Relaxation of internal sphincter involuntary  Relaxation of external sphincter voluntary Acid/ Base Balance      Upper limit of anion gap= 15 o Calculated by: Na – (Cl + bicarbonate) Measuring H+ o Narrow pH range because of enzyme function Potassium follows t.am 9sbiqYtim o Acidosis K+ moves out of cell  o Alkalosis Hypokalemia  K+ moves into the cell o Potassium follows Hydrogen Sodium o Acidosis  Decreased Na reabsorption- inhibits H exchange  Excess hydrogen in blood  Hypernatremia o Alkalosis  Increase Na reabsorption – more H exchange  Less H in blood  Hyponatremia Calcium Calciumbinds better in an acidicenvironment o Acidosis hypocalcemia is bound to proteins  More calciumLessavailableg  Hypocalcemia salicylate o Alkalosis L Lactic  More free calcium Uremia  Hypercalcemia Anion Gap M Methanol DiarrheatRenal failure o Increased Anion gap= anion gap metabolic acidosis Paraldehyde  Causes: SLUMPED It 5  4 seizure Acid P E Ethanol RespiratoryAcidosis D Diabetic Ketoacidosis Acuterespirtorydistress syndrome cantexpellcoz compensationisdelayed Renal toman Registent.it n Ever Yi in acenei metabolic rate have Tumors higher Eiiii iiiiii.fi useglucose mellituscant Diabetes i iiiiiii.it smaamam Endocrine system REVIEW CHART    Functions Utilizeschemical messengers o Regulation long and short term o Growth and development o Reproduction o Electrolyte imbalance o Stress response o Communication Chemical messenger system o Hormones in blood stream for global effects o Based on receptors Hormones o Most negative feedback regulated  Target cells – express receptor or not  Hormone Specificity – only contain receptors for specific hormone  Actions – increase or decrease protein/enzyme synthesis kih.EE for wionictwatersoluble Polar Charged Quick response Short duration Neegatignsporters G-protein mediated (hydrophilic) Amino acid derivatives Non-polar Uncharged Slow response pailifficien Long duration Cross membrane Lipid derivatives Requires constant stimulation for longer action Made in RER- no protein carrier for blood Exception: Thyroid Hormone Made from cholesterol- requires protein carrier Quickonset winces T only given injection Others can be given by mouth Longeronset longerduration wecanpharmacologically manipulatethese All medications are injections    p should we Second messenger System o 1st- hormone interactsw receptor knowabout o 2nd- G-protein activation  Leads to cell activity (apoptosis, proliferation) o Inactivated once hormone is no longer present poicihifmfnnetigtionsildenaphi saut.it Non Polar hormone ide o Diffuse across membrane o Receptor at nucleus o Initiate transcription of new RNA and synthesis of proteins o Slower onset of action duration Longer o Exception: Thyroid hormone crosses membrane and binds at nucleus Distribution Freehormon active Bound hormone transported o Released from capillary beds into bloodstream Goes totargetsite o Bound to protein = inactive but reserves o Free circulating= active, short lived  Hypothalamus o Highest level of control  Secreting regulatory hormones  CRH,TRH,GHRH, GnRH GHH (somatostatin), PH (dopamine) produces  Direct release  Oxytocin, ADH senttopituitaryglandtobestored released  Autonomic Centers- neural control over release  Epi and NE  Pituitary Gland o Connected to hypothalamus via infundibulum o 2 glands  Adenohypophysis – anterior  Travel via hypophyseal portal vein system  Regulatory hormones  Neurohypophysis -posterior Oxytocin_ADH  Axons directly from hypothalamus Waterloss  Antidiuretic hormone o V1- on vasculature= Ca ontrolled Fannstaffeliso diPmlevels sodium o V2- in kindeys= reabsorb water osmolarity asma  Diabetes Insipidus  Decrease of ADH – AVD centralcase pressure studies  Lack V2 receptors- AVR peripheral  Oxytocin o Positive feedback- more contraction lead to more oxytocin release o Let down of the milk milkrelease  Prolactin o Produces the milk inhi mammarygland development milkproduction release  Growth hormone proteinsynthesis activatesgenetranscriptionof o Somatotropin o Released during deep sleep proteinsusedinmilkproduction repair growth o INCREASE GH makesproteins proteindiet  Sleep, exercise, diet high o Somatomedins- released by liver  Increase collagen formation and osteoblast activity o High serum Somatomedins= Turn off GH negativefeedback o Somatostatin also inhibits GH- released when GH levels are high arbintake  Pituitary Dwarfism released frompancreasorLiverwhenGHlevelishigh o GH grows cartilage- Estrogen and Testosterone grow Bone  Puberty- sex hormones are faster then GH ca build cartilage fusing the epiphyseal plate  Melanocyte Stimulating hormone not.ie i i iiiiiiiiiiii.siiiiiii A Chart by 9 13 not DCT sm88h.atInluter in ohreleasedrpffititaylivefke liverreleas.es somatomeans bone muscle Hypothalmus Anteriolititary produced in sun exposure o Relatively inactive in adults TSH  MSH produced locally with sun exposure  Blood level low to zero Thyroid o Released during: T4  Fetal development Tissues  Young children  Pregnant women  Addison’s disease  Thyroid Hormone (smallest hormone) o Controls basal metabolic rate (energy at rest) o Increases target cell responsiveness to catecholamines by increases receptor production aboida follicles T4storageform o ThyroidSynthesis of thyroglobulin (precursor)  Tyrosine and iodine for production of thyroid hormone  active form T3  T4- long acting can be converted Shorthalflife  T3- short but readily available o Activate genes for catabolic metabolism RHR increaseHR Hyperthyroidipps  Cardiac muscle- activate beta1 receptor gene  Increase SV, HR, CO o Fetal development  Developing of nervous system o Cretinism  Lack of hormone- leads to neurologic defects, short stature, facial deformities  Calcitonin o Regulating calcium concentrations calciumlevels inblood o Inhibits osteoclast activity and inhibit calcium reabsorption 949 o High calcium levels  Parathyroid Hormone mttsneinresboipf.in bonebreakdown o Increases secretion of RANKL  Mobilize calcium from bone by increasing osteoclast activity  Enhance Ca reabsorption at kidneys DCT  Stimulate calcitriol formation – increase Ca absorption from small intestine ndstomacrophages o Low calcium levels  Vitamin D c'Ests o Needed for calcium absorption intestine in o Activated by liver and kidneys  PTH stimulates activating enzyme Suprarenal Gland (adrenal)  o Zona Glomerulosa- mineralocorticoids o Zona Fasciculata - glucocorticoids co o Zona Reicularis – androgens, DHEA, androstenedione sexsteroids  Adrenocorticotropic Hormone o Released in response to corticotropin from hypothalamus o Stimulates zona fasciculata- cortisol release Teterf T.fi iorage released stress g  Highest in the morning and cycle Glucocorticoids ensurewehaveenoughglucose inbody o Role in carb, protein and fat metabolism ammunTinflammatoryo Accelerates glucose synthesis  Increased in stress m response arachidonicacid o Anti-inflammatory pinhibitsWBCactivation bloodglucose  Inhibit WBC with synthesis of phospholipase  Decrease healing and immune response o Decrease AA uptake in skeletal muscle- impair repair o facilitate lipolysis  Cushings Disease v Syndrome  AldosteroneYFhdrettfiffainswatertsodiumns.ir works DCT collectingducts o Released: low BP, dehydration, elevated k+ electrolyteimbalance  Sex Steroids excretesK o Zona retiuclaris- pre puberty and post menopausal aromatase fieeststrogencanc  produce precursors then travel to ovaries and testes for conversion one  Aromatase Found in adiposetissue ovaries aromataseinhibitors IEA  Ovaries contain great quantity of aromatase just as fat tissue  Catecholamines Peptidehormones o Directly into blood stream-SNS o Epi and NE o Attach to alpha and beta receptors  SM- trigger glycogen reserves, accelerate breakdown of glucose  Fat- breakdown lipids  Liver- glycogen breakdown  Heart- increase HR and contractility  Lungs- bronchodilate  Melatonin o Pineal gland secretesmelatonin o Made from serotonin glucosein 61Tract  Inhibit reproductive functions attsieie.iosmiiepciniiicis  Influence circadian rhythms  Pancreas imulatestriglyceride islets oflangernan Gift2releasesinsulin o Endocrine- directly into bloodstream rmationinadipose o Islets (tyrosine kinase 2nd messenger) outtureceptors  Alpha- glucagon oncells Beta-insulin, amylin  Glucose  Delta- somatostatin enters glycogen  Insulin Releasedwhenglucoseis high o Glucose uptake into cells expressing GLUT4 sulinindependent o GLIT2 on islet cells- signaling for release  Basal insulin release- constant amount throughout the day  Meal release- stored insulin released immediately Iiestivetrace  T.EE 9 9111 fishiates formgn RBCs niny glut 1 glut 30minsafterstarting a meal mustbestoredasglycogenor fat am c insulin g  Increased glucose level- secrete more insulin (phase 2)  Glucagon glucose up tonormalwhenitslow Brings o Glucose levels fall o Stimulate glycolysis, lipolysis, gluconeogenesis, inhibit hepatic protein synthesis  Amylin released w insulin o Secreted based on food intake slowsabsorption in GItract o Slows gastric emptying and suppresses glucagon secretion o All Type 1 and Type 2 diabetics are amylin deficient sends satietysignal  Diabetes Mellitus o Polyuria, polyphagia, polydipsia IDDM Type1 autoimmuneattack onbetacells receptors insulin g lucose o Complications due to vasculature damage inadequateinsulinproduction  Gonadotropins o LH- induce ovulation ulationtest children  Stimulate androgens by testes Hypogonadism nosexualmaturation in amount o FSH- secretion of estrogen by ovarian cells emeguus infertility in adults  Nurse cells to develop sperm a seta cells I Ie Reproductive System    Not essential to life of the individual Function o Store and produce specialized reproductive cells o Secrete hormones  Females- one gamete per month  Males- large quantities of gametes per day Male System o Testes- secrete androgens  Produce gametes (spermatozoa) o Testes-epididymis-vas deferens- ejaculatory duct-urethra  Male inguinal hernias- protrusion of visceral tissue into canal- spermatic cord is weak spot in abdominal wall o Dartos Muscle- smooth muscle  Wrinkling of scrotal surface o Cremaster muscle- skeletal muscle  Temperature regulation- pulls closer to body  Descent of testes: o Gubernaculum testes- tissue fibers that extends from testes to pockets in peritoneum o 7th month- fetus grows rapidly- stimulating contraction of testis  Each move through abdominal musculature  Cryptorchidism- testes remain in abdomen o Spermatogenesis – Puberty  Seminiferous tubules  Leydig cell- secrete testosterone  Sertoli cell (nurse cells) protect nuvishspermcells Sperm production egg production constant cyclic o o o Stimulated by FSH and T Nourish sperm cells Help maintain blood/teste barrier  Protect from chemicals and immune system o Spermatogonium= stem cell  Undergoes mitosis  1 stay in tubule stemcell  1 becomes primary spermatocyte (meiosis)  Spermatid- acrosome formation and flagella o Hormones for spermatogenesis spermatids  GnRH stimulates pituitary releaseFSH LH  FSH- nurse cells to enhance spermatogenesis  FSH promotes sperm development in testes  Inhibin released to turn off FSH and GnRH  LH- Leydig cells to regulate T producetestosterone  Androgen binding protein- released by nurse cellselevate and stimulate spermiogenesis stimulated FSH Testosterone- regulated by LH  Stimulates spermatogenesis  Affects CNS sex drive  Stimulates metabolism size  Established secondary characteristicsfacialhair musclemassbody  Maintains accessory glands Sperm Maturation  Spermatozoa detach from nurse cells- no locomotion or fertilization  Mature Spermatozoon: loseorganelles lossof size mass  Lack ER, Golgi, peroxisomes  FRUCTOSE Epididymis Maturessperm  Monitors, recycles, and stores spermatozoa  Capacitation spermmix withsecretionsof seminalgland becomemotile  Spermatozoa become motile when mixed with seminal glands  Become fertile- exposed to female tract Vas deferens  Ciliated to move sperm  Peristaltic contraction Ejaculatory Duct Urethra Seminal glands - alkaline  High fructose concentration  Prostaglandins for contraction stimulation  Fibrinogen to clot in vagina  First step of capacitation Prostate Gland Join o o o o o o o o by  Fluid slightly acidic  Seminal plasmin-abx o Bulbo-urethral glands (Cowper Gland)  Alkaline mucus  Lubrication and neutralize acids Female System  o Ovaries- release one oocyte per month  Produce hormones of meiosis o Oogenesis 1nutrientdensehearty  Starts before birth, accelerate and puberty, ends at menopause  Oogonium- mitotic division before birth  Primary oocyte- partially undergo meiosis  Each month one primary oocyte triggered to undergo first meiosis o Results in 2 unequal sized cells  One secondary oocyte and one polar body willundergo o Secondary oocyte will undergo division = fertilization o Ovarian Cycle he zygotepolarbody After puberty  follicle ovulation SH grows pegginfollicleby  Follicular phase (preovulatory phase)  Luteal phase (postovulatory phase) eggreleasesintotubesfolliclebecomescorpusluteu releases  Primordial Follicle- egg nest nourishes egg o Oocyte and follicle= but mature independently o Components of oocyte  Granulosa cell=follicular cell  Zona pellucida= nourish ovum  Thecal cell= produce estrogen  Antrum= chamber of follicle  Corpus Luteum= collapsing follicle post ovulation, small estrogen release, progesterone release in pregnancy maintains uterusenviormentuntilplacentaismac  Corpus Albicans- remnant if not fertilized o Transport movesegginto uterus hypogastricplexus  Ciliary movement and peristaltic contraction o Fertilization  Secondary must reach sperm in first 24 hours – ampulla and isthmus vascular o Endometrium  Uterine glands- secrete estrogen- causes changes in monthly uterine cycle fornutrient support  Two divisions estrogen progesterone o Functional zone- contains most glands controlproduction oflining  Thickness, undergoes dramatic changes during cycle o Basilar zone- attaches myometrium to endometrium  Contains terminal branches of tubular glands o Uterine Cycle (28 day cycle) 21 35  Follicular phase= menses+ proliferative (run by FSH)  ESTROGEN stimulates and sustains end egg egg  o Luteal phase= secretory phase (spike of LH- continued by progesterone being released from corpus luteum)  Peaks 12 days after ovulation- glandular activity declines Hormones of Cycle  GnRH from hypothalamus goestopituitarygland FSH Pulse frequency controlled by estrogen and progestin  o Estrogen increase pulse o Progestin decrease pulse  GnRH acts on pituitary- release FSH  Stimulate follicles  Follicles enlarge thecal cells released androstenedione precursor estrogen  Synthesis of estrogen and androgens (aromatase)  Type of estrogen converts estrogen via o Estradiol- premenopausal aromatase o Estrone- post menopausal o Estriol- pregnancy  LH released by pituitary  Stimulates ovulation- follicle into corpus luteum  Corpus luteum- progesterone (increases temp)  Estrogen- stimulates endometrial growth estrogensecreted oocytes  Progesterone- inhibit contraction and thickening cervical mucus  Implantation- zygote releases hcG  Stimulate luteum to continue to release progesterone until placenta forms  Menstruation- progesterone levels decrease  Relaxin- produced by placenta during pregnancy Bloodvolume  Allows for stretch, found in seme to help maintain motility  Estrogen functions:  Stimulate bone and muscle growth  Sex characteristics  CNS activity hypothalmusestrogens sexdrive  Functionality of accessory glands and organs  Initiate repair and growth of endometrium ty to by hat controlsgrowth of myegg hat controls release ofmyegg hat controls FSH LH growth of endometrial lining hat controls growth of endometrial lining estrogen occurs ifimplantation corpus luteumprogesterone ensturation occurs when progesterone decreases menses West levels of estrogen progesterone during eak levelsof estrogen during ovulation ak levels of progesterone duringsecretoryphase luteum releasesHCG to maintain corpus implanted egg ygote produceprogesterone tomaintain lining roliferative phase vascularized endometriumgrows becomes enlargment of follicles in ovary stimulated estrogenfromfollicles by Secretory Phase endometrial glandsenlarge rate of secretion Menarche irst uterine cycle menopause euminationofuterinecycles Decline in estrogenleves uterussize breast size eduction in bone deposition