Wk8 Ch 24 & 26 PDF

Chapter 24 The Immune System About this Chapter Anatomy and function of immune system Response to different pathogens Innate immunity: nonspecific body defenses Acquired immunity: specific defenses that target one pathogen Combined defenses against bacteria and viruses...

Chapter 24 The Immune System About this Chapter Anatomy and function of immune system Response to different pathogens Innate immunity: nonspecific body defenses Acquired immunity: specific defenses that target one pathogen Combined defenses against bacteria and viruses Neuro-endocrine-immune interactions Immune System: Functions Specificity and memory enables the body to distinguish “self” cells from “non-self” to target a response to specific invaders - we want to recognize nomal cells The immune system has 3 functions: 1. Protects from pathogens and foreign molecules Parasites (hookworms and tapeworms) Bacteria Viruses 2. Removes dead or damaged cells 3. Attempts to recognize and remove abnormal cells Immune System: Pathologies If the immune system fails to function, develop pathologies, including: 1. Incorrect responses cells Sobeta Autoimmune disease (Type 1 diabetes) – fails to recognize self and attacks the body’s normal cells 2. Overactive responses Allergies – creates a response that is out of proportion to the threat 3. Lack of response Immunodeficiency disease (AIDS) – components of the immune system fails to work illness and sickness ~ increased instances of Pathogens: Bacteria and Viruses No cell walls , & > - be live inside nost & , ↳ easier to target not as - many · host toxicity : when dig doesn't work right , Viral Structure and Replication Protein coat nucelic acid core L X Figure 24-1 How does " body protect itself from these pathogens Body Defenses: Two Lines The body has 2 lines of defense: 1. Physical and chemical barriers First line of defense stomach A respiratory tract Skin, epithelial linings, cilia, acids, mucous, and lysozymes 2 ex: open wand compromises us. try to keep pathogens out of the body’s internal environment If this line fails, then … 2. Immune defenses Immune cells Second line of defense Innate, non-specific, immediate response Acquired; attack a specific pathogen (antigen) Immune System The immune system is integrated into other tissues and organs, but it does have 2 anatomical components: 1) The lymphoid tissue 2) The cells responsible for the immune response ↳ WBC  Secondary were talked abt it twice : (B 3raplace is here , Immune s lymphoid Lymphatic System tissue matures here Primary lymphoid Lymphatic tissues = distributed throughout body tissue Primary lymphoid tissues include: any Bone marrow and the thymus gland Where immune cells form Iborn) and mature - Secondary lymphoid tissue include: everythingelse is herel Lymph nodes and spleen Where mature immune cells interact with pathogens and initiate a response Lymph vessels – carry fluid from blood to lymph nodes where immune cells intercept pathogens Diffuse tissues – immune cells that appear in organs of the body (e.g., tonsils and gut-associated lymphoid tissue) associated with the skin, respiratory, urinary, and reproductive tracts Figure 24-2 The primary cells of the immune system are leukocytes (white blood cells), divided into 6 types; Chapter 16 review: Phgocytosis so eats up Leukocytes D , Pathogens 8 pacman · Looks like they have granules. ↓ · are toxic , destroys pathogens antigen-anything our antibody binds to typically binds to foreign p. , takes a piece of 4. [ presents it on c Surface. Figure 24-4 Innate Immunity: Nonspecific The body’s first line of defense is to exclude pathogens by physical and chemical barriers, but if it fails, the innate immune system responds: Consists of leukocytes (WBCs) that attack and destroy Considered nonspecific because the leukocytes will attack any material they identify as foreign Phagocytes (macrophages, neutrophils, natural killer (NK) cells) destroy or suppress invaders via phagocytosis, and they attract additional immune cells by secreting cytokines p , arand So it helps call more to hunt it down 2 why : When youhave one p., there's probably more , Engulf and digest “tagged” cells Inflammatory response Innate Immunity: Phagocytosis and Scorers in Masks surface markers so D - Antibodies “tag” the pathogen so phagocytes recognize it phagocytes recognize it less Acting as opsonins formed met Pic now Figure 24-6 Inflammatory Response: Roles Inflammation is a hallmark reaction of innate immunity GThe inflammatory response is created when macrophages release cytokines to attract other immune cells Roles of the inflammatory response include: 1. Attracting immune cells and chemical mediators to the site of Other o infection 2. Producing a physical barrier to prevent the infection from spreading 3. Promote tissue repair other players inv in. ] Inflammatory Response: Players ↑ also know as membrace attack canDiex Complement proteins are involved in the complement cascade Lipid-soluble proteins that insert themselves into the cell membranes of pathogens and virus- infected cells and form pores Iwater pores) , sowater rushes in & lysis eventually Figure 24-8 Acquired Immunity: Antigen-Specific Acquired immune responses are antigen-specific in which the body recognizes a particular foreign substance and reacts It is mediated primarily by 3 types of lymphocytes: T-cells T lymphocytes, once activated, develop into: Helper T cells – regulate other immune cells essentially > calls for more help. Cytotoxic T cells – attack and destroy virus-infected cells B-cells B lymphocytes, once activated, develop into: Plasma cells – secrete antibodies makes it too. Memory cells – are long lived and continue reproducing themselves Remembers pathogen E specificity. has NK cells – attack and destroy virus-infected cells and tumors (Natural killer B lymphocytes: Humoral Immunity B lymphocytes Insert antibodies, also known as immunoglobulins, into their cell membranes When activated a Differentiate into: Plasma cells – effector cells that do not have antibodies on their membrane but secrete antibodies Memory cells – are long lived and continue reproducing themselves in case of next exposure to the antigen quicker response So we have.  Pathogen has tree reign it not cought it reproduces Macrophage funds its pathogen (phgocytosis. , ex : let's act, immunes eventual antibodies made. say we are exposed to a B lymphocytes: Humoral Immunity We want antibodies be it creates the immune complex, so. cut do bad 4 things anymore Preventing illness.. Memory in the immune system Primary immune response week after Likelyat abt z After initial exposure, is slower Taks A for 2tonapeak sick - vegottenpoint. * next slide X this and lower in magnitude + Then igf most make IgM Secondary immune response After subsequent exposure, is pathogen to same quicker and larger memory bc of cells , so we make antibodies right away land morel We tend to not. get sick bc of this This is what makes vaccinations work!! creating We are ess memory (ells.. Figure 24-11 Plasma Cells: Antibodies l also called Immunoglobulin ↳ hence lg 1) ifferent classes: Antibodies are divided into 5 classes: GAMED 1. IgG – make up 75% in adults. Maternal IgGs cross the most abudandant Wht we make most. placental membrane and give infants immunity in the first few. months of life as very small , 2. IgA – found in external secretions such as saliva, tears, mucus, and breast milk to disable pathogens before they reach the internal environment 3. IgE – associated with allergic reactions 4. IgM – associated with primary immune response Wht we tend to make Ist 5. IgD – on the surface of B lymphocytes, role unclear Antibody shape: Light and heavy chain, Fab and Fc region Functions of Antibodies arms have binding site Imagineeaching out. water pores slysis Surface on B-cells , So when binds to p, activates B cells. Then... d) shaped like yeta S When mast cell falls apart & rel chemicals inv in Imme.. response ex : M binds [deachrates as rel them bed. binds tags So... why ? each arm can bind so. Makes it it can cluster easier to phagocytosis bcwedn't have to look for it , all come together Figure 24-13  20 : 50 Antigen-Presenting Cells TMHC receptors spec. MHC 2 pieces men lysosome destroys - ate it , presents on MHC-11 , So T-cell helper can come , bind to it Calls for more. help via Cytokines a cel or Itinfected destroyed ,Theuesamacha in ↑? Figure 24-16 How Body Responds to Bacterial Infection: defense ist line of L 2nd line (B Defenses binds [tays against Bacteria activates agradors s ve 1 Chemical by attractant to degrading vasodilata wbC of capillaries ↑ immune ent So more blood ~more o tu ae con act kill tem ~/ wbc co Come more to site of infection. So we can tag more Figure 24-17 How Body Responds to Viral Infection: > - on other hand : starts here ↓ tags it. We have immune So now it out complex infect mae cells. ells ec tc inf ot ca nn Defenses normal cel ↓ formsn calls for more help against viruses -o b they come as response If you dut sacrifice. the cell , then you risk virus replicating & infecting more. So reinforces it. Figure 24-18 (2 of 5)  Blood Types: ABO Blood Groups Le determined by antigen on rbc. V join cellular elements opposite of antigen be to you the opp antigen is foreign.. Antigens on RBCs universal donor why ? A, B, AB or none (O) rbc You have no antigen on , Antibodies in plasma So whoever you donate to , wht have anythingto react to. from You can only receive blood Otybe , be you have both antibodies and will bind to other blood. Anti A, anti B, anti AB What happens if you mix wrong blood type : Clumping Universal Recipent Wantibodies When red blood cells with group A antigens on antigens their membranes are mixed with plasma containing antibodies to group A, the antibodies cause the blood cells to clump, or agglutinate. as each arm binds So if you've clumping donating O yare donating rbc antibody , , When not blood cut circulate the way it's intended , ,. Figure 24-20 Autoimmune Diseases examples : Produces 2 19 ( / ↑ destroys / o destroys destroys 5 so muscles ant contract voluntarly destrogs Neuro-Endocrine-Immune Interaction The link between the mind and body Model for interaction There are tales of people who lost the will between nervous, to live and subsequently died without endocrine, and immune obvious illness, or of people given up systems for dead who made remarkable recoveries lot of infl. Not fully understoodbut mind has a body How you think [ emotions infl. ex-therapy dogs Neuroimmunomodulation – study of brain-immune interactions Common signal molecules and receptors Overlapping responses Figure 24-21 Tennessee Couple Dies Just Hours Apart After Nearly 64 Years of Marriage Dolores Winstead, 83, and her husband, 88-year-old Trent Winstead Trent was admitted to the hospital earlier this month, and Dolores unexpectedly suffered an aneurysm while visiting him https://gma.yahoo.com/tennessee-couple-dies-just-hours-apart-nearly-64-045539728--abc- news-topstories.html?soc_src=mediacontentsharebuttons&soc_trk=ma Summary Immune function Immune pathologies Pathogens (bacteria vs. viruses) First and second line of defense Lymphatic system (primary vs. secondary lymph tissue) Innate immunity, inflammation Acquired immunity (T-cells and cell mediated immunity) (B-cells and humoral immunity), MHC I and MHC II Antibodies, classes, function, opsonins Example of defense against bacteria and viruses ABO blood types, antigens/antibodies Autoimmune diseases Neuro-endocrine-immune interaction Chapter 26 Reproduction and Development About this Chapter Sex determination and differentiation Gametogenesis and patterns of reproduction Development in males and females Procreation Pregnancy and the birth process Reproductive and developmental maturation and aging  Sex Determination Humans are sexually dimorphic: Males and females are physically distinct: sex organs consist of 3 sets of structures: 1. Gonads I same function here : differs Produce gametes (eggs and sperm) Male gonads ! testes ! sperm which make o Female gonads ! ovaries ! eggs which make o Undifferentiated gonadal cells destined to produce eggs and sperm are called germ cells 2. Internal genitalia I Glands and ducts that connect the gonads with the outside Struct. differ in environment q but 3. External genitalia have both it Sex Determination Each nucleated cell of the body (except eggs and sperm) contains: 46 Chromosomes 22 matched pairs of autosomes Ea Direct development of the body and of characteristics (hair color, blood type, etc.) 1 pair of sex chromosomes For X and Y Direct development of internal and external sex organs Figure 26-1 Sex Determination Inheritance of X and Y chromosomes determines the genetic sex of the individual when we make gamete The presence of a Y We take sex chr. unpair them , chromosome means the embryo will be male, even if males have both the zygote has multiple X fer only have , X chrom. chromosomes (XXY) whichever chr Fertilizes. it will A zygote that only has a Y determine sex. (OY) will die because the X contains essential genes missing in the Y chromosome Figure 26-2 Sexual Differentiation [o Chara. dev how do In uteru , you have I Bipotential tissues – before differentiation when the embryonic tissue cannot be morphologically identified as male or female dep you have you , on wht o or f , organs will dow. , SRY gene (sex-determining region of the Y chromosome) – in the presence of a functional SRY gene, the bipotential gonad develops into testes The bipotential gonad will develop into testes or ovaries The biopotential internal genitalia consist of 2 pairs of accessory ducts: 1. Wolffian duct – Proceeds along male line 2. Mullerian duct – Proceeds along female line  Development of Internal Organs S · dre to lack of testosterone (b notestes) in their regress [die/disappear ot. ~ , LB structures To become of , or to have things , You have have oare all abt having be they goes & , they have say protein. Y chromosome , They have SRygene : sex-determing ! LB region on y chromosome , UD TO I makes SRy protein. ↓ They start differentiating a+ 6 weeks, They have b for of this bC of testis a bc for not testis ! v 7 into internale of structures I & ! Figure 26-3  Development of External Organs be of have test is , make testosterone , which converts to 6 no DHT or test. DHT Idihydrotestosterone). So they have this too. So... Testosterone & DHT v Figure 26-3 V Internal 0. external 0. Embryonic Development: Males o centric SRY gene produces SRY protein - directs development of the testis, which have: Sertoli cells, secrete: Anti-Müllerian hormone (AMH) which causes the Müllerian ducts to regress Leydig cells, secrete andorgen hormones: I Testosterone and dihydrotestosterone (DHT) Are the dominant steroid hormone in males Bind to same androgen receptor, but elicit different responses (Testosterone – converts Wolffian ducts to male accessory structures, migrates testes into scrotum, DHT – external genitalia and prostate development) Figure 26-4 Embryonic Development: Females Female embryos have no SRY gene, and the cortex of the biopotential gonad develops into ovarian tissue Without anti-Müllerian hormone (because there are no testis to secrete them), the Müllerian ducts develop into: structures Internal female Upper portion of the vagina Uterus Fallopian tubes Without testosterone: The Wolffian ducts degenerate Without DHT: The external genitalia take on female characteristics Now the we've differentiated , process of making gametes' Gametogenesis o eggs - 9-sperms Gametogenesis is gamete production Women are born with all the eggs (oocytes) they will have Men manufacture sperm continuously Gametogenesis begins in utero and resumes during puberty Germ cells of the embryonic gonads first undergo mitotic divisions to increase their numbers Then, the germ cells are ready to undergo meiosis Meiosis is the cell division process through which gametes are formed  O - so while you're in embryo you're only ,. For of going to do mitosis , as reproductive Gametogenesis (this is why adults , they can still do mitosis Oogonia they remain viable I have. babies throughout life) for sperm. They can just make more spermatognia complete. ~ At birth, cells mitotic making a copy of a cell ? have not replication and progressed first stage of beyond meiosis by 5th born mitosis and month of fetal contain only development X you copies will make all the u will ever have. takes chromosomes and divides them Y immature Start the ""phase of At birth, ovary meiosis too Once born ,. you germ cells has ~ half a will have all the Ogonia You will ever have e At puberty,. birth million primary Xonce divides some cells oocytes You've hit puberiy undergo At puberty, divides again mitosis while primary stays paired until fertilization others oocytes divides undergo 3 dies away. into eggs meiosis do Once this occurs , will 2 - for egg. 12 you mom , 12 you dad Figure 26-5 Al of this directed byhormones Synthesis Pathways Hypothalamic and anterior pituitary hormones control gonadal secretions of steroid sex hormones Both sexes produce androgens and estrogens In women: The ovary produce progesterone and estrogen The ovary and adrenal cortex produce small amounts of androgens In men: The testis produce most of the testosterone The adrenal cortex produce 5% of the testosterone Testosterone gets converted to DHT in peripheral tissue The enzyme aromatase converts testosterone to estradiol (main estrogen hormone in men)  Synthesis Pathways for Steroid Hormones Incl this as. reminder the all SexEsteroid Homones come from Entero !! - All steroid sex hormones arise form cholesterol The enzyme aromatase converts testosterone to estradiol (main estrogen hormone in men) Figure 26-6 Whe hormones involved : Regulation of Reproduction Reproductive hormone control follows the hypothalamic-anterior pituitary- peripheral gland pattern Hypothalamus: pulse generator (small pulses every 1-3 hrs) released in ↓ pulses o Lis Gonadotropin releasing hormone (GnRH) & Isamen brain). in - ~ through hypothalmic-hyphoseal portal system Anterior Pituitary Lutenizing hormone (LH) Follicle stimulating hormone (FSH) ~ Gonads Thisis where it differs /00 - ovaries/testes legg - sperm FSH (with sex hormones) initiates/maintains gametogenesis LH stimulates steroid sex hormone production Gonads also secrete inhibins (inhibit FSH secretion) and activins (stimulate FSH secretion)  same thing in figure form. General Pathways Inhibins YActivins In (FSH secretion) Figure 26-7 Consequences of Feedback SO... in ↑ & nomones At least 36 3 then uniqu D n n hours In Hypothalmus Male Reproductive Structures External genitalia = Penis and scrotum (which contains the testes) Passageway = Urethra (common passageway for sperm and urine Accessory glands, ducts = Prostate, seminal vesicle, bulbourethral gland ↓ ex: Secretes extra antibacterial secretions unfair i Which is why they're at less risk of utI Figure 26-8 Male Reproductive Structures Testis' Sperm produced here. b) In the Testis = Seminiferous tubules ! Epididymis ! Ductus deferens/Vas deferens vretur -they person of Figure 26-9 Spermatogenesis in the Testes Seminiferous tubules (constitute 80% of testes mass), contains: Sperm in various stages of development ~ where gameogenesis takes place. Sertoli cells – act as blood-testis barrier, regulates sperm development by providing nourishment, secrete hormones such as inhibin, activin (FSH), and androgen-binding protein (ABP) which makes testosterone less lipophilic and concentrates it in the luminal fluid Interstitial tissue (between seminiferous tubules) Leydig cells – testosterone producing cells Capillaries Spermatogenesis in the Testes Cross section of the seminiferous tubule M Spermatogonium - The germ cells that undergo meiotic division to become sperm are found near the basal lamina, and move toward the tubule lumen as they differentiate Figure 26-9 Spermatozoa Structure Spermatids remain embedded in the apical membrane of Sertoli cells while · has nucleus chromosome the allows they complete the transformation into Sperm to egg. penetrate sperm, losing most of its cytoplasm and developing a flagellated tail Head Acrosome and nucleus Midpiece Centrioles and mitochondria & be we need energy to swim Tail (flagellum) to eg9] Microtubules - llows movement Figure 26-10 Regulation of Spermatogenesis rel. reli GnRH ! LH ! Leydig cells ! testosterone ! sex characteristics rel, rel, GnRH ! FSH ! Sertoli cells ! spermatocyte maturation Feedback Inhibin inhibits FSH release Activins activate FSH release Testosterone inhibits LH and GnRH release Short and long loops GnRH release is pulsatile (peaking every 1.5 hours) and LH release follows the same pattern. However, FSH release does not because it is also influenced by inhibin and activin Same thing but figure form Regulation of Spermatogenesis gametogenists set. Makes testosterone less lipophilic, concentrating it in the luminal fluid Figure 26-11 Female Reproductive Structures Figure 26-12a, b Reproduction Sperm deposited in the vagina passes through the cervix The cervical canal is lined with mucus glands whose secretions create a barrier between the vagina and uterus Sperm that makes it through enter the lumen of the uterus, into fallopian tubes where fertilization of an egg can occur The uterus is where fertilized eggs implant and develop during pregnancy and is composed of 3 tissue layers: 1. A thin out connective tissue covering 2. Myometrium – a thick middle layer of smooth muscle 3. Endometrium – an inner layer made of epithelium. Its thickness varies during the menstrual cycle Structure of the & produces wall that fills up wiblood - Smooth muscles when have cramps This is contracting v. Uterus and Ovary homores L FSH - Stimulates it - eggs C e99 matres once egg matures , ovviates , L wht our egg was in turns into this growing. Impt. be figure e. Impt for menstrual c., reproduction Efetus grath... wall of uterus ovaries help sweep up egg in fallopian tube. Uterus Efallopian Tube Figure 26-12 Phases of the Menstrual Cycle. last a month Stuff going on approx. in ovaries utens. Females produce gametes in monthly cycles (every 24-35 days), commonly called menstrual cycles because of 3-5 day J periods of bloody uterine discharge known as menstruation The ovarian cycle is divided into 3 phases: 1. Follicular phase (lasts 10 days to 3 weeks) egg growing/mathing Follicle growth in ovary (egg matures) 2. Ovulation Ripened follicles release oocyte(s) into fombrie up to fallopian tube , egg 3. Luteal phase i4 days last pregnancy unless longer occurs then. Ruptured follicle becomes the corpus luteum and will secrete hormones that continue the preparation for pregnancy or will regress if pregnancy does not occur While Ovarian cycle is occuring. Endometrial Lining: Uterine Cycle The endometrial lining of the uterus goes through its own cycle, the uterine cycle (regulated by ovarian hormones): 1. Menses (during beginning of ovary’s follicular phase) Occurs when no s No pregnancy Bleeding from uterus as endometrium sheds. 2. Proliferative phase (latter part of ovary’s follicular phase) New layer of endometrium in preparation of pregnancy 3. sostarts to refill wiblood grow Secretory phase (after ovulation, during the luteal phase) Once egg ovulates , utens lining toms into 3 ↳ where endometrium is waiting for sperm to fervine and implant into uterine wall. Hormones from the corpus luteum convert the thickened endometrium to a secretory structure If not pregnant, menstruation begins again with the Menses phase of the uterine cycle  no preg , so you start to grow a matueegy oncemature waits to see if preg occurs , waits 14 days. X If not,dies , The Menstrual and N if not preg. ↑ llook at next slide = makes estrogen Uterine Cycles Wolit , no ovulation * LH surge causes ovulation. , know surge occuring ovulation kits test for LH in crine to. causes bumps in FSH is trom GNRH , which is follicle to growanewe99star i X X this is steady by of estrogen(next slide) ↑ X feedback to brain , which a FSHELH FSH We dut Why : We just made mature egg to ovulate , ↑ -. · & d nt want follicule to after ovul. grow another egg , want to give current & relTo. egg a chance. fallopian we · If corpus luter Kept v B I alive be preg, , placenta X Supports it. & 14 days i know how the thick healthy · keeps endo. phases coincide I ↓ in this phase So when ovulating , you're transitioning from proliferative phase rel. GNRH, LH r and secretory phase. &rel. FSHELH FSH Think abt it-views vises a when sustained has before - rises right to be ready to receive it. (for 36 hus, switches inhibiting ~droese ~ back ovul, feedback ↑ to ·When in follicular phase , uterine FSH in menses & prolif-phase. ~ menses · , uters in when in luteal phase secretary phase. they all drop it corpus dies So-feedback gone EFSH. C We start again. Sned build wait & LH go back up. D build back uc to see if yo Waiting for fertilized egg implant to. will , preg Shed if you didn't get , & in temp show we. ovulated but oblation Kit more accurate. Figure 26-13 shows same but Hormones : Hormonal Control of the Menstrual Cycle: Luteal Phase and Late Luteal Phase on7 i makes Figure 26-14 Procreation: Sexual Response Intercourse The 4 phases of coitus (sexual intercourse or copulation) 1. Excitement – preparation of genitalia for copulation 2. Plateau – changes started during excitement intensify 3. Orgasm – climax, muscular contractions accompanied by intense pleasure and increased BP, HR, and respiratory rate 4. Resolution – physiological parameters return to normal  cephalic Erection and Ibrain Ejaculation in Males autonomic NS : Erection is just penis filled up with blood. - touch Figure 26-15 Pregnancy Prevention Contraceptive practices include: Unintentional is"yr Pregnancy. Abstinence – no sexual intercourse 100 % Barriers – prevents union of eggs and sperm via chemical or physical barriers (diaphragm, sponge, condom) Surgical – sterilization (females = tubal fallopian tobe ligation, males = vasectomy) Ned Pills – hormonal treatments that decrease or stop gamete production ↳. eggs Estrogen and progesterone that inhibit FSH and LH release from pituitary Side effects = increased incidence of so not guaranteed. blood clots and strokes Fertilization Fertilization steps: Capacitation = The final maturation step of the sperm which ↓ enables it to swim rapidly and fertilize the egg (usually takes place in the female reproductive tract) Swimming and attractants, egg contact attracted egg to Penetration Acrosomal reaction – Sperm release enzymes from acrosome to get past egg barriers (corona radiata – outer layer of loosely connected granulosa cells, zona pellucida – protective glycoprotein coat) Nuclear fusion of the sperm and oocyte form a zygote Cortical reaction – a chemical reaction to prevent more than one sperm fertilizing an egg so ist get to in Fertilization Once sper fertres, meiosis occurs in egg. Figure 26-16 Zygote Development: Ovulation, Fertilization, and Implantation Cell division occurs as the embryo migrates through the Fallopian tube By the time the egg reaches the uterus, it consists of a hallow ball of about 100 cells called a blastocyst happens in upper" g be we need time for It to divide into endometrium Figure 26-18 The Placenta Z where fetus s mothers blood mix supplies O2, nutrients , hormones. , Figure 26-19 Further Embryonic Development The placenta: Exchange site between the embryo and mother Secretes hormones S thiskeeps now placent a arre I it Human chorionic gonadotropin (hCG) – keeps corpus luteum active so it secretes progesterone, is similar to LH prevents keeping endo Thick healthy shedding.. I , Human placental lactogen (hPL) – related to growth hormone and prolactin. Contributes to lactation and alters mother’s glucose and fatty acid metabolism to support fetal growth CHEFSH of Estrogen and progesterone – maintains feedback suppression of the pituitary throughout pregnancy, preventing ovulation. (Estrogen) contributes to development of milk-secreting ducts of the breasts. (Progesterone) maintains endometrium and suppresses uterine contractions ↑ throughout C Wht live too since Corpus. placenta rel. 3 months. pregnancy sticks and , Parturition: Birth Process (Labor and Delivery) Parturition occurs between 38th-40th weeks of gestation. Begins with: 1. Labor Rhythmic uterine contractions that pushes the fetus out Initiation could begin with the mother or fetus Oxytocin – triggers contractions because its uterine receptors increase near full term (used to induce labor) Coricotropin releasing hormone (CRH) from placenta Cervical dilation 2. Delivery Baby Placenta Parturition: Birth Process The fetus is At the beginning of labor, the fetus repositions normally oriented itself lower in the abdomen (“the baby drops”) head down and begins to push on the softened cervix Relaxin, secreted by the ovaries and placenta, helps soften (“ripen”) the cervix and loosen ligaments holding the pelvic bones together to help deliver baby. Figure 26-20a, b Parturition: Birth Process As contractions intensify, the The placenta detaches from fetus moves down through the the uterine wall and is expelled vagina and out into the world, still attached to the placenta Figure 26-20c, d Regulators of Parturition The positive feedback loop of parturition Labor onset Cervical stretch triggers uterine contractions Oxytocin – secreted by the posterior pituitary reinforces contractions Prostaglandins – secreted by uterine wall in response to CRH and oxytocin, reinforces contractions (cause of menstrual cramps) Positive feedback – cycle of escalating contractions Figure 26-21 Mammary Development and Glands Breast Feeding Estrogen – directs breast development during puberty Milk ducts grow and branch, fat is deposited behind glandular tissue During pregnancy, estrogen, GH, and cortisol result in further gland development Progesterone – converts duct ↑ secrete so we can act , epithelium into secretory structures Composed of 20 milk-secreting lobules made of branched hollow ducts of secretory epithelium surrounded by myoepithelial contractile cells Figure 26-22a Lactation: Milk Secretion Prolactin-inhibiting hormone (PIH) – hypothalamic hormone that. 2 controls prolactin secretion towards end of preg, it d so prolactin con ↑ , , Prolactin – stimulates milk production, secreted from anterior pituitary + milk PIH levels fall during late stages of pregnancy, increasing prolactin by 10 times After delivery, when estrogen and progesterone levels are low, prolactin stimulates large amounts of milk production Suckling – mechanical stimulus of infant nursing breastfeeding thts why when women stop dries up milk Inhibits PIH. , Oxytocin – required for the “Let-down reflex” which is the ejection of Deceit milk from the glands come out  Stim production , & let down of molk. Lactation: Milk Secretion The hormonal control of milk secretion and release allows us to keep inhibitingPlH Figure 26-23 Reproductive Maturation: Puberty Puberty marks the beginning of the reproductive years Increase production of sex hormones Maturation of reproductive organs and gamete production Characteristics of puberty Females: menarche (1st menstrual period), pubic hair, and breasts Males: pubic and facial hair, growth spurt, and deep voice Aging WOMEN: Menopause – cessation of a women’s reproductive cycle reproduce diminishes (~40 years of age) ability to. canhappen later Causes: ovaries cease responding to GnRH, lower levels of estrogen and progesterone, cessation of egg development Symptoms: hot flashes and increased risk of osteoporosis as beloss of estrogen calcium is lost from bone ↑ risk of fracture as & ↓ one is demineralized Therapies: hormone replacement, debate of Cancer bc can trisk MEN: Andropause – the existence is controversial Causes: lower levels of testosterone production with age Affects about 50% of men over the age of 50 Reproductively active but less testosterone Summary Sex determination and differentiation of male and female structures Mullerian vs. Wolffian ducts, development of internal and external reproductive organs in males and females Gametogenesis (meiosis vs. mitosis in males and females) Reproductive hormones (GnRH, LH, FSH, inhibit, activin) Hormone feedback Sperm, acrosome Menstrual cycle (ovarian and uterine phases, average length, hormones involved) Procreation, erection, ejaculation Fertilization, blastocyst, zygote development Function of the placenta Breastmilk production and secretion and hormones involved Puberty Aging (menopause)