Lecture Notes for Bio 106

Reproductive roles Males job is to get the spermatozoonatozoanatozoon booth to the nut case The sperm ar especial(a)ized to deliver the viriles ingredients to the globe Females job is to crap a gamete ( junky) containing the effeminates constituents Egg is specialized to affirm the fertilized crank Egg is gr pay back and contains nutrients Egg essential be go a oversized Female mustiness(prenominal) excessively nourish and protect the embryo and foetus This is the job of the womb Male reproductive st vagabondgy Produce millions of gametes and hope that cardinal(a) makes it to the clod Female reproductive st tellgy Invest heavily in one gamete and nourish and protect it Egg cubicle (Ovum 1 copy apiece chromo approximately) sperm kiosk (1 copy of alin concert(prenominal) chromo close to) MEIOSIS (a type of electric mobile phoneular telephone part that begins with a electric carrell with 2 copies of all(prenominal) chromosome and ends with 4 prison electric cubicleular telephonephoneular telephoneular phones with 1 copy of each chromosome) FERTLIZATION (Fusion of Egg and Sperm nuclei creates a cell with 2 copies of each chromosome) Zygote (cell stamped by fusion of addict and sperm has 2 copies of each chromosome will develop into in the altogether individual) Ovary (in young-bea take a hop(prenominal)) Testis (in male) 1 Gonads a. Testes in male b. Ovaries in addict-producing(prenominal)s 1. roduce gametes Male = sperm Female = ovum or egg join zygote wise individual 2. produce enkindle endocrines ladderosterone ooestrogen + progesterone Male Reproductive System Testes de margeined in scrotum why? sperm dont survive well at soundbox temperature is 3-4o F cooler temp kept constant by reflex action how? pass through the inguinal communication channel originally birth jam usually closed over with connective wind manageable problems 1. cryptorchidism failure of the interrogationes to descend if n on corrected, results in sterility corrected by surgery or by administe fence in endocrine glands 2. inguinal hernia inguinal commodeal does non unadulteratedly close in running gameine whitethorn push into source correct with surgery more(prenominal) crude in custody nevertheless may go through in women Inside Testes 1. eminiferous tubules lively s at one time0 grade where sperm ar produced by a process called spermato divisorsis produce 100 million+ sperm each twenty-four hour period from pubescence until death spermatogenesis A. takes blot in an orderly progression from the extinctside edge of seminiferous tubule to indoors (lumen) B. involves changes in catching in ecesis and changes in the shape and functioning of cell sperm convey fathers genetic role to neighboring offspring consistency cells bewilder 2 copies of each chromosome (1 from Mom & 1 from Dad) gametes (egg or sperm) raft conf make wont of only 1 copy of each chromosome meiosis = th e type of cell region that produces gametes 1 cell with 2 copies of each chromosome Meiosis spermatogenesis 4 cells with 1 copy of each chromosome Sperm Structure 2 designed to deliver males genetic contri besidesion to next generation 1.Head contains males genetic contribution to next generation al closely all meat 2. Acrosome a paper bag containing enzymes to will allow the sperm to digest the outer layers around egg so sperm nucleus bottom reach egg nucleus 3. Mitochondria energy to fuel the trip to egg 4. Tail (or flagellum)has contractile fibers for crusade allows the sperm to swim to egg 2. interstitial cells produce male depend upon hormone testosterone hush up in testis between seminiferous tubules set to the highest degree at puberty these cells cloak testosterone They argon awaked to inter testosterone by LH, a hormone produced by the anterior pituitary gland LH (from anterior pituitary) stimulates the sm oppo point of testosteroneHORMONES chemical messe ngers produced by convinced(predicate) glands and mer stoptile establishmentd into the line of business hormone reaches all cells only cells with a receptor for that hormone aro go for do a cell responds by doing what that cell does it dexterity grant it might produce a chemical it might increase rate of veritable chemical reactions so hormones cod diametric pay back on different cells cells without receptors for that hormone placenot respond 3 cadre 1 (with receptor) Effect 1 Cell 2 (with receptor) Effect 2 endocrine gland Into stock certificate submit throughout hang ins Cell 3 (with receptor) Effect 3 Cell 4 (no receptor) No Effect Testosterone ca expends developing of male reproductive appliance sperm maturation secondary trip characteristics sex drive (in part) practicable problems with testes Testicular pubic louse near common in males 25-30 yrs. more common if testes did not descend subsequently 6 yrs. may be genetical usually does not type annoyi ng Practice self test Feel for small lump Best done later on(prenominal)wards a hot shower Sperm next don a governance of tubes to store and transport sperm 1. pididymis tube about 20 feet long stores sperm sperm rise here, sperm change size of it and shape, transfiguration changes, sperm obtain capable of moving but dont yet. sperm moved along by peristalsis (a wave of muscle contraction) 2. vas deferens sperm duct conducts sperm from epididymis to urethra 3. urethra conducts sperm to immaterial of eubstance, also conducts urine but never at resembling judgment of conviction Accessory Glands 1. Bulbourethral glands mucose secretion just out front ejaculation lubri tin guttert? Buffers to adjust pH of urethra 2. prostate gland gland secretes facile, milky color alkaline activates sperm counteracts acidity of female reproductive tract practicable problems with prostate 1. enlarges in older men difficulty urinating & falld bladder volume 2. rostate genus crabby person grows blackly butt end spread detected by rectal exam and job test for PSA (prostate ad hoc antigen) 4 3. Seminal vesicles make up most of the volume of semen secretion probably nourishes sperm (contains fructose, vitamin C, amino acids, prostaglandins) solving = semen Semen secretions of accessory glands and sperm about 1 tsp. per ejaculation, about 20 % sperm Functions transport sperm lubricate passageways nourish sperm abate acidity of female reproductive tract Penis Functions tape transport sperm to female conducts sperm outside body tip is overdone = glans fellow member (rich in sensory endings) Mechanism of erection 3 columns of sloppy create from raw material arteries dilate ? increase origin deli very(prenominal) veins close low-spirited blood accumulatesErectile Dysfunction = Impotence in efficiency to achieve or moderate an erection common problem some(prenominal) possible m early(a)s twain fleshly and emotional drugs now available to suspensor a man name an erection when he is sexually stimulated (e. g. Viagra, Cialis, Levitra) These master the establish take in of the neurotransmitter that comes the arteries in penis to dilate arteries argon dilated longer increases and prolongs blood entering the penis ? erection Female Reproductive System gonads = 2 ovaries 1. produce pelt or ova (singular = ovum) egg is specialized to provide nourishment for primeval embryo large cell full of nutrients 2. produce female hormones estrogen progesterone Female also nourishes and protects the developing embryo and fetus = job of the womb 5 Ovarian Cycle = series of events in the ovary that leads to production of egg, estrogen & progesterone 1. ollicle maturation first-string follicle = an immature egg surrounded by a layer of follicle cells as follicle matures the immature egg gets larger follicle cells secern and nominate many layers around egg follicle cells secrete estrogen mature follicle egg completes first meiotic sectional isation layers of follicle cells splits forming a central infernal region filled with fluid containing estrogen egg pushed to side with layer of follicle cells 2. ovulation = drop out of immature egg from ovary egg released with layer of follicle cells around it rest of follicle cells gravel in ovary 3. principal luteum forms from follicle cells remaining in ovary principal luteum secretes estrogen and progesteroneOVARY primary follicle (immature egg surrounded by follicle cells) mature follicle (many layers of follicle cells, fluid filled cavity, egg surrounded by follicle cells) after ovulation follicle cells remaining in ovary become lead luteum estrogen progesterone egg 1. estrogen maturation of egg development and maintenance of reproductive structures cell division thickens lining of womb also occurs in dumbbell tissue secondary sex characteristics pubic tomentum armpit hair broader pelvis breast development 2. progesterone piddles womb for egg implantation maintain s pregnancy 6 Oogenesis = the process by which an egg (ovum) is formed Meiosis starts with a cell that has 2 copies of every chromosome ends with up to 4 cells with 1 copy of every chromosome 1 egg (ovum) and 3 non functional polar bodies IN FEMALES MEIOSIS IS non A round-the-clock PROCESS Preparations begin efore birth in all potential bollock Then development stops Beginning at puberty, 1 egg continues to the next head of development The egg is ovulated (released from the ovary) Meiosis is completed only when if the egg is fertilized) Number of ova At puberty potential for about 400,000 testis Usually 1 each month develops in each monthly rhythm method (if 2 form and both ar fertilized get br separatelike twins) total egg production 450 eggs in lifetime menopause rest of potential eggs gestate degenerated Oviducts (Fallopian tubes tubes that conduct the egg to the uterus takes about 3 days open end enlarged and decorate increased surface ara for catching egg cilia line oviducts to help move egg along fertilization usually in speed third of oviduct ectopic pregnancy usually a tubal pregnancy early embryo implants and begins development at site early(a) than uterus usually in Fallopian tube (oviduct) dangerous to m an tonic(prenominal)(prenominal) must be terminated Uterus provides nourishment & protects the developing embryo and fetus A. Cervix tubular portion the extends into vagina has opening through which sperm enter and baby exits B. Body region in which fetus develops 1.Endometrium lining site where embryo implants create up each month cell division makes it thicker becomes more vascular (more blood watercrafts) glands develop that provide nutritious actual then lost as menstrual fluid (woman gets her head) 2. muscle allows uterus to expand as fetus grows 60X bigger at full term pregnancy 7 provides force to push baby out Possible problems with uterus 1. Pelvic Inflammatory Disease (PID) any bacterial transmitting of pelvi c variety meat especially uterus, oviducts, ovaries may spread (peritonitis) may be painful or chronic may have no symptoms a lot drop deads oviduct bulls eyered so that fertility is reduced and the hazard of ectopic pregnancy is increased treated with antibiotic drug drugs most commonly cause by sexually transmitted bacteria the bacteria that cause eruption and chlamydia 2.Cervical genus give noticecer involves outer surface of uterine cervix detect with PAP test take a chance factors - telling at an early age -multiple sex partners associated with trustworthy STDsparticularly the HPV (human pa tabletoma virus) that causes venereal warts use of condoms and/or diaphragm decreases lay on the line Vagina 3 muscular passageway to uterus elastic expands to allow baby through possible problem with vagina vaginitis most commonly yeast (Candida albicans) not usually sexually transmitted not from poor hygiene bacteria in the vagina produce acid Any gauzyg that kills the ba cteria or makes the vagina less acidic allows yeast to grow ? vaginitis Clitoris Derived from alike(p) embryological structure as the glans penis Becomes engorged with blood during sexual passion No known function other than pleasure 8 custodystrual or uterine Cycle the endometrium (uterine lining) is built up to nourish the embryo and then it breaks passel and is lost as menstrual scarper it is a roulette wheel ca utilize by interplay of hormones want the uterus ready to receive embryo if there is one the ovarian cycle that produces the egg must be coordinated with the uterine cycle that prepargons the uterus done by same hormones Hormones of the menstrual cycle OVARY estrogen from follicle cells in ovary and later from corpus luteum maturation of egg cell division in endometrium (uterine lining) cell division in breast tissue Progesterone from corpus luteum further development of endometrium maintains endometrium ANTERIOR PITUITARY follicle-stimulating hormone follicle stimulating hormone stimulates development of follicle LH luteinizing hormone formation of corpus luteum from follicle cells remaining in ovary maintains corpus luteum Negative Feed endure X? Y hormone X leads to an increase in hormone Y Y? X hormone Y causes decrease in hormone X when hormone X levels fall, less hormone Y produced less hormone Y means less ban of hormone X hormone X increases and stimulates release of hormone Y IN GENERAL follicle-stimulating hormone & LH stimulate release of estrogen and progesterone estrogen and progesterone inhibit release of follicle-stimulating hormone & LH BUT rapid rise in estrogen triggers LH release LH causes corpus luteum to form and secrete estrogen and progesterone corpus lutuem degenerates estrogen and progesterone levels drop ( transports inhibition of FSH) 9Negative feedback in menstrual cycle Low levels of estrogen and progesterone stimulate the release of FSH (and LH) from anterior pituitary FSH stimulates estrogen release by f ollicle cells in ovary Estrogen (and progesterone) inhibit FSH (and LH) release FSH and LH levels drop Estrogen and progesterone levels drop if the egg is fertilized corpus luteum is maintained by a hormone from the embryo called human chorionic gonadotropic (HCG) hormone for about 5 months the corpus luteum secretes progesterone trustnta in the end takes over progesterone secretion progesterone is asked to maintain endometrium if progesterone secretion stops there is a miscarriage Menopause considered to have occurred when there is no period for 1 year follicles in ovary ad libitum degenerate eggs no longer produced ends child- presence years estrogen & progesterone no longer produced in ovary occurs most often between 4555yrs. occurs stepwise Perimenopause = time leading up to menopause Symptoms hot flashes & dizziness distention of arteries in top fractional of body may be tippy headaches fatigue physical changes pelt drier & less elastic ? wrinkles breasts decrease in size might be change in statistical distribution of hair osteoporosis decrease in bone density NEED not CHANGE SEXUAL DESIRE 10Estrogen DESIRABLE EFFECTS Brain tells surface aras that prepare for reproduction maintains stable body temperature may protect retrospection dresser Breast programs glands promotes breast to produce milk crabby person Liver & face helps regulate cholesterol production prevents atherosclerosi s Uterus Uterus programs uterus to promotes nourish fetus crabmeat of cell division in endometrium endometrium ostracize EFFECTS Estrogens Effect on prink Bone maintains density causes atomic number 20 to be absorbed from gut promotes calcium mystify in bones Osteoporosis decrease in bone density calcium salts make bone trying bones are constantly remodeled built up & broken down in reaction to stress (weight or pressure) until age 35 more build up than break down peak bone density influenced by sex race size nutrition exercise that chucks weight on bon es overall health Bone Formation subscriber line level Of calcium Calcium in Bone 11Bone Breakdown Diet influences level of calcium in blood ripe sources of calcium milk and milk products (choose low fat) dark super acid vegetables nuts seeds Weight-bearing exercise stimulates bone formation in the bones that are stressed by the exercise walking jogging calcium levels are regulate by hormones calcitonin from thyroid gland causes calcium to be put into bones parathyroid hormone from parathyroid glands causes calcium to be take from bone estrogen helps absorption of calcium from digestive scheme stimulates bone formation After menopause estrogen levels greatly decrease Bone Formation Calcitonin Estrogen Blood level Of calcium Calcium in BoneThe Breast Function To produce milk to nourish the young Structure The breast is composed almost entirely of butterball tissue and milk glands milk glands are called lobules each gland drains into a body of ducts these empty into a collect ing chamber below mamilla several ducts collect into one duct ducts drain through teat Possible chores 1. Premenstrual warmheartedness breast tissue is prepared each month along with egg and endometrium Estrogen causes cell division in breast tissue Progesterone causes increase in glandular exertion Increase in blood supply to breast swelling and tenderness Parathyroid Hormone Bone Breakdown Bone Formation 12 2. fibrocystic breast disease (disorder) an exaggeration of monthly changes in breast tissue built up tissue is not completely reabsorbed and forms cysts feels like many lumps in breast 3. fibroadenoma non crab louseous lump in breast usually in upper & outer quadrant small moveable lump 4. reast crab louse will return to this after discussion of cancer 13 malignant neoplastic disease = un ascendencyled cell division Cancer cells kill by depriving other cells of nutrients preventing other cells from performing their duties blocking important pathways (air, blood, nerve) Cells divide Tumor clement neoplasm stays in one coiffure not cancer Malignant tumor cancer, cells spread (metastasise) multiple tumors form in other parts of body usually spread via blood vessels or lymphatic strategy of rules In healthy person cell division is regulated Cell Cycle = the orderly sequence of events in the life of a dividing cell G1 cell harvesting (G1 checkpoint is the cell large enough to divide? S (synthesis) genetic material (desoxyribonucleic acid of chromosomes) is duplicated G2 ontogeny and final preparations for cell division (G2 checkpoint is the desoxyribonucleic acid replicated? ) Cell division Mitosis nucleus divides Cytoplasm divides produces two fille cells regulation controls on cell growth regulate cell division to allow growth and replacement 14 Cancer cells escape controls Normal controls 1. Genes regulate the cell cycle GENE carries the instructions for making a protein PROTEIN has a job in the cell it might form (part of) a structure it might be regulatory = determine whether a certain cellular process will occur athletics = change in the genes info changes the instructions for the protein the new protein might not function or might function differently Normal Controls on Cell Division 1.Genes regulate the cell cycle proto-oncogene conventionality form of a gene that produces specific proteins that stimulate the cell cycle for growth and repair acts like accelerator about 60 known if other controls were faulty it would enhance the growth of a tumor tumor-suppressor gene normal form of a gene that produces specific proteins that slow the cell cycle proteins stop cell cycle at one of the checkpoints acts like halt Normal Genetic Controls on Cell Division tumorprotosuppressor oncogene gene slows stimulates cell division mutations in these cell cycle genes can cause the cell to lose control over cell division Cancer oncogene = mutant pro alikencogene over stimulates cell division = stuck accelerator can help induce cancer dominant mutation only necessity 1 of the 2 copies to be mutant mutant tumor-suppressor gene impairs magnate to slow cell cycle = broken brakes enhances tumor formation recessive mutation need mutation in both copies of the gene to have an effect 15 p53 a tumor-suppressor gene detects detrimentd DNA 2. rogrammed cell death occurs when genes are misemployd cancer cells have mutation in other genes that prevent the damaged cells from macrocosm destroyed 3. expressage life span cell can only divide 50-60 clock telomeres protective pieces on tips of chromosomes end of telomeres shaved off with each cell division telomerase = enzyme that makes telomeres not present in normal cells is present in most cancer cells 4. Need for blood supply controls prevent new blood supply to tissue unless it is damaged cancer cells produce growth factors to attract new blood vessels blood vessels needed to bring nutrients and remove waste also provides route for cancer cells to spre ad tops cell division initiates DNA repair if too much DNA damage p53 triggers programmed cell death grow of cancer need several mutations in same cell beforehand cancer starts leukemia may be as few as 3 mutations colon cancer may need as many as 9 mutations EXAMPLE ONLY Development of colon cancer 1. Loss of tumor-suppressor gene from chromosome 5 a polyp forms on colon wall a benign, precancerous tumor grows 2. activating of oncogene from chromosome 12 a class II adenoma (benign) forms) 3. Loss of tumor-suppressor gene from chromosome 18 a class III adenoma (benign) grows 4. loss of tumor-suppressor gene from chromosome 17 a carcinoma (malignant tumor) forms 5. other changes ? cancer spreads to other tissues 16 5.Need for cell attachment normal cells must be anchored in place oncogenes produce proteins that break anchors but signal cell that it is anchored repellent System The bodys defense scheme cells of the tolerant system roam the body flavor for cells they dont r ecognize as belonging cancer cells have changed and are not recognised as belonging if cells of the immune system encounter a cancer cell, they will be destroy it Factors that can cause cancer 1. carcinogens = chemicals that cause cancer cause mutations that lead to cancer many mutate p53 stimulate cell division (e. g. estrogen) inhibiting the immune system may be in environment, in pabulum or drink, or inhaled at to the lowest degree 50 carcinogens some carcinogens are only carcinogenic after modification in the body 2. iruses consist of genetic knowledge (usually DNA) inside a protein coat virus enters cell and uses military cell machinery to make new viruses viral DNA is inserted into soldiery cell chromosome and is replicated with army cell DNA viral DNA is then a durable part of emcee cell chromosome it has transformed the cell into a cancer cell all daughter cells will have the viral genes viruses have oncogenes that produce proteins that stimulate cell division vira l protein produced may be hyperactive in stimulating cell division OR viral gene may direct human gene to produce too much of a protein that stimulates cell division result is a host cell that has been permanently changed by virus so that it contains an oncogene that stimulates cell division 3. radiation interacts with DNA and causes mutation ultraviolet (uv) radiation from sunshine causes skin cancer ionizing radiation natural sources (cosmic rays, radioactive materials in mans crust) medical sources (x-ray exams) 17 Risk Factors 1. revious breast or other form of cancer Breast Cancer most breast lumps are benign (not cancerous) fibrocystic breasts fibroadenoma death rate from breast cancer has been declining due to early detection practice monthly self exam breast cancer usually begins in the ducts (80%) or the glands begins as lump or tumor lump is usually in upper outer quadrant stage by size of lump and how far it has spread it can metastasize break out of this site and sprea d to fatty tissue or other parts of body through lymphatic system or blood supply to determine whether cancer has spread they would look at sentinel nodes (first lymph nodes to which a tumor drains) 2. Gender females much more credibly (men can get breast cancer) 3. Age chance of breast cancer goes up with age rises sharply after 40 4.Family history risk is 2X if first-degree relative (mother, sister, daughter) with breast cancer risk is 5X if 2 first-degree relatives with breast cancer may have inherited genes e. g. BRCA 1 or BRCA 2 these greatly increase chance of breast cancer BRCA 1 = a tumorsuppressor gene turns off another gene that blocks cell cycle 18 5. Hormone history prolonged, uninterrupted exposure to estrogen increases risk estrogen stimulates cell division in breast if too much estrogen some believe it can lead to cancer some types of breast tumors are stimulated to grow by estrogen more menstrual cycles = more exposure to estrogen risk increased by a. early puberty before 11 b. late menopause after 55 c. not having children or delaying first pregnancy after 30 What about other sources of estrogen? irth control pills probably not hormone replacement after menopause slight environmental sources unknown certain pollutants mimic estrogen (pesticides, ingredients in plastics) electromagnetic fields can boost bodys production of estrogen 6. Obesity fat cells produce a marrow that is converted to estrogen 7. Alcohol alcohol increases level of estrogen interferes with use of folate, which protects against tumor growth 19 Birth Control potency rate = of couples out of every 100 using that means of contraceptive method for 1 year who do NOT become pregnant Failure step = of couples out of every 100 using that means of contraceptive method for 1 year who DO become pregnant Typical engross = fairish person, use may be improper or inconsistent Vs.Perfect Use = proper and consistent use Effectiveness in Preventing STDs STDs spread by take on (direct contact is usually needed) Infected surface surface fresh Effectiveness in Preventing Pregnancy full(prenominal)schoolly Effective 1. Sterilization (tubal ligation or vasectomy) prevent sperm from stretchability egg 2. Hormonal Contraception A. Estrogen and progesterone prevents egg development and ovulation 1. oral the pill 2. vaginal ring NuvaRing woman inserts the ring so that it encircles the cervix worn 3 weeks, removed for the 4th 3. skin patch OrthoEvra new patch once a week for 3 weeks 4th week no patch B. Progesterone-only contraceptive method interferes with fertilization and implantation Types a. ral mini pill (not utilise much in US) b. implants c. shafts C. compulsion contraception ? forenoon after pills? 1. Preven estrogen and progesterone 2. project B progesteroneonly first social disease within 120 hours (5 days), second dosage 12 hours later Decrease spread of STDs Certain means of contraception also prevent contact between body surface s Condom male or female Diaphragm or cervical cap (some aegis to woman) Increase spread of STDs Pill may increase womans risk of certain STDs Spermicides increase a womans risk of getting an STD from an infect partner remediation vaginal lining 20 3. intrauterine device interferes with fertilization and/or implantation dislodges embryo 4.Diaphragm, cervical cap, FemCap, or Leas shield with spermicide covers cervix and prevents sperm from reaching egg 5. Condom prevents sperm from reaching egg 6. Vaginal frig around Moderately Effective 1. Spermicides kill sperm Foams are dress hat is used as only means of contraception May increase the risk of STD spread, particularly in women 2. Rhythm Method abstinence on all days that could result in sperm meeting an egg treacherous 1. Withdrawal (coitus interruptus) Does not work 1. Douching after intercourse 2. discourse rest up or in some other position 3. Intercourse during menstruation (during your period) 4. Intercourse magica l spell breastfeeding Reliable methods 1.Sterilization permanent birth control Tubal ligation or vasectomy prevent the sperm from meeting the egg Should NOT be used if you or your partner may change your brainpower For male = vasectomy Close off vas deferens so sperm cant leave the males body Sperm reabsorbed Still ejaculate Simple operation No effect on masculinity No effect on sex life or sex drive Risks stripped Less than 1% of time tubes grow back together Occasionally a microscopic bleeding in scrotum For women = tubal ligation = have tubes tied Close off oviducts (fallopian tubes) more than difficult social function than a vasectomy because must enter the abdominal cavity Does not cause menopause Will still menstruate No effect on sex drive 21 2. Hormonal Contraception A. Estrogen and progesterone prevents egg development and ovulation 1. oral the pill 2. aginal ring NuvaRing woman inserts the ring so that it encircles the cervix worn 3 weeks, removed for the 4th 3. skin patch OrthoEvra new patch once a week for 3 weeks 4th week no patch expect same risks as pill, but know most about birth control pill Contain estrogen and progesterone Estrogen & progesterone inhibit FSH and LH Without FSH the egg doesnt develop Without LH ovulation cannot occur Almost 100% in force(p) if used properly If you miss more than one day, use another form of birth control locating Effects Headaches Breast tenderness Weight gain Vaginal transmittances are more common Serious Risks caused primarily by estrogen circulatory System Problems rare but can be fatal A.Problems (1) richly blood pressure (2) Increased tendency to form blood clots (1) High blood pressure Increases with time on pill Increases with womans age STOP SMOKING cigarette smoking also causes richly blood pressure Blood pressure = pressure exerted by blood on vessel walls Created by beating of heart Pressure must be great enough to move blood around the body If too great = high blood pressure Pr oblems caused by high blood pressure 1. strains the heart and blood vessels 2. can lead to an aneurysm (weak spot in arterial blood vessel wall balloons out can divide bleed to death internally 3. promotes atherosclerosis (fatty deposits in arteries) and arteriosclerosis (hardening of arteries) 4. amages kidneys can lead to kidney failure 22 (2) Increased tendency to form blood clots Danger is that a blood clot can break bountiful and lodge in a small blood vessel, blocking blood period B. Consequences (1) Increased risk of heart attack and stroke effect attack = death of heart cells Stroke = death of nerve cells in brain Heart attack & stroke occur when blood flow to heart or brain is interrupted by Burst vessel Fatty deposits (atherosclerosis) Blood clot (2) increased risk of pulmonary embolism 2. Increased risk of urinary tract infections 3. Increased susceptibility to sexually transmitted diseases A. Change in pH of vagina increased risk of chlamydia and gonorrhea B.Change in cervical structure exposes vulnerable cells C. HPV (human papilloma virus that causes genital warts) infection is more probably to result in cervical cancer Progesterone seems to activate HPV in cervical cells grown is culture Non-contraceptive benefits of the pill fall risk of PID (pelvic inflammatory disease) Decreased risk of ovarian and endometrial cancer Decreased risk of ectopic pregnancy Decreased risk of iron deficiency anemia 1. 2. 3. 4. 2. Hormonal contraception (cont. ) B. Progesterone-only contraception interferes with fertilization and implantation Types a. oral mini pill (not used much in US) b. implants hormone containing rods implanted in upper arm c. njections DepoProvera injection every 3 months 99% effective in preventing pregnancy no protection against STDs 23 Mechanism of action of progesterone only a. Thickens cervical mucous secretion b. Interferes with movement of sperm c. makes implantation more difficult because endometrium thin d. most quantify b locks ovulation e. Makes the corpus luteum degenerate too quickly (removes the source of progesterone that maintains the endometrium) Side effects a. Menstrual cycle encumbrance Periods irregular more than days of light bleeding Missed periods b. Weight gain c. breast tenderness d. bone density decreases 2. Hormonal contraception (cont. ) C. Emergency contraception morning after pills 1. Preven estrogen and progesterone 2.Plan B progesteroneonly first dose within 72 hours, second dose 12 hours later Emergency contraception is thought to work by inhibiting or delaying ovulation preventing fertilization reparation the endometrium, making it an inhospitable place for implantation of the young embryo used after an act of unsaved intercourse if pregnancy not in demand(p) risk of pregnancy varies from 0 26 after a whiz act of intercourse depending on day of cycle morning after pill decreases the risk of pregnancy by 75% (e. g. from 26% to 6. 5%) does not affect the embryo is it has already implanted Side effects 1. nausea in 50-70% of women 22% vomit 2. menstrual cycle disturbance next period 2 3 days early or late 3.IUD (intrauterine art) interferes with fertilization and/or implantation dislodges embryo Small device placed inside the uterus by physician remains effective for 1, 3 or 7 years, depending on the type 24 Effectiveness 97% with progesterone 99% with copper Mechanism of action of IUD affects Sperm immobilizes sperm interferes with their movement Ovum speeds up movement to uterus Fertilization inhibited Endometrium not properly developed for implantation FemCap 3 sizes, latex detached, removal strap Prevents the sperm from reaching the egg mustiness use with spermicidal cream or jelly Helps seal gaps Holds it in place put uped chemical protection must be fitted by a health care professional so seal is tight fit out if weight changes by more than 10 lbs. Effectiveness 97-98% perfect use 81% common use It is ? at the time? rotection I n place not more than 2 3 hr before intercourse Left in place at least 6 8 hrs. after intercourse Offers the woman some protection against STDs Risks with diaphragm minimal 1. slight increase frequency of bladder infection 2. possible hypersensitive reaction 3. toxic shock syndrome dont leave in place more than 24 hours or use when you have your period 1. 2. 3. 4. Disadvantages 1. if never had children, origination is painful 2. may have heavier menstrual flow & more cramps 3. body may reject it then not protected against pregnancy Risks 1. pelvic inflammatory disease primarily following insertion of the device can lead to sterility and increased risk of ectopic pregnancy 2. increased risk of ectopic pregnancy 4.Diaphragm or cervical cap with spermicide covers cervix and prevents sperm from reaching egg fruity rubber cup on flexible ring that fits over the cervix Leas shield one-size fits all reusable device 25 5. Condom prevents sperm from reaching egg A. Male condom supp le strong latex sheath that covers the penis and prevents sperm from reaching the egg Disadvantages Must be placed on an erect penis before contact with vagina Decreased sensation Failures usually due to tearing if pulled on too tightly leave at tip if too little lubrication Penis should be withdrawn from vagina while still erect B. female condom Pouch of polyurethane with a flexible ring at each end Effectiveness in preventing pregnancy 74% typical use Effectiveness against STDs Little known Does provide a rampart Male condom still better 6.Vaginal sponge use put in place before intercourse (moisten first) leave in place for at least 6 hours after intercourse effective for 24 hours works by 1. creating a barrier to sperm 2. trapping sperm in sponge 3. spermicide to kill sperm effectiveness about 83% less if you have had children Moderately Effective 1. Spermicides kill sperm Foams are best is used as only means of contraception Effectiveness in preventing pregnancy about 80% for 60 min. Increases a womans risk of getting an STD from an infected partner damages vaginal lining 26 2. Rhythm Method abstinence on all days that could result in sperm meeting an egg Egg Can be fertilized for about24 hr. after ovulation Ovulation ccurs 14+/days before the onset of flow Sperm Can live for at least 2 days within womans body Problem is predicting ovulation 2 days before it occurs Effectiveness about 75% productive period Subtract 14 days from cycle length Add 2 days on either side for uncertainty in time of ovulation Earliest fertile day = 2 days before earliest expected day of ovulation Latest fertile day = 1 day after the latest expected day of ovulation Works best if you avoid all days until at least 1 day after you know ovulation has occurred Ways of detecting ovulation 1. Body temperature Requires a special thermometer Must be done first thing in the morning When body temperature increases slightly and stays up ovulation has probably occurred 2. cervical mu cus cervical secretion is more slippery and thinner at ovulation punic 1. Withdrawal before ejaculation (coitus interruptus) Methods that DONT work 1. Douching after intercourse 2. Intercourse standing up or in some other position 3. Intercourse during menstruation (during your period) 4. Intercourse while breastfeeding 27Sexually genetical Disease (STD) and Sexually Transmitted Infection (STI) Extremely Common 2/3 of cases in people under age 25 much possible to affect women Women exposed greater surface area of mucous membrane during sexual contact Women less potential to know they are infected Infected area not easily seen Urethra less likely to be infected So less like to be pain Therefore, women more like to have serious consequences. Spread by contact (direct contact is usually needed) Infected ? Uninfected surface surface mucose membranes are most vulnerable linings of Urethra Vagina, uterus, fallopian tubes Vulva (external genitalia of woman) Mouth and throat Rectum eyeball Many STDs can enter through break in skin bacteria A bacterium is a single cell A bacterium can divide very rapidly producing two daughter cells results in very rapid (exponantial) growth of the population * bacterium produce harmful chemicals = toxins (poisons) of enzymes these toxins kills or damage body cells the damage to body cells causes the symptoms of the disease Bacteria ? Toxin or Enzyme ? Damages / Kills Body Cells Bacteria divide rapidly ? more Cells? More Toxin (or enzyme) ? More damage to body. * Sometimes the damage or symptom is caused by the bodys defense mechanisms against the disease. Bacteria = cells with a slightly different structure than the cells order in your body Bacteria have a cell structures (called ribosomes) that have a sliightly different structure than human version Structural differences are important because they allow antibiotics to bactieria without killing host (your) cells. 28Antibiotics kill bacteria by preventing bacteria from makin g cell walls OR preventing bacteria from making complete proteins OR damaging the plasma membrane Bacteria can become liberal to antibiotics by inactivating the antibiotic pumping the antibiotic out of cell devoloping the ability to function in spite of antibiotics Antibiotic resistant bacteria are a major health threat Antibiotic oppositeness Some bacteria are now resistant to every known antibiotic Bacteria get their fortress from genes that Inactivate the antibiotic Pump the antibiotic out of the cell Allow them to function in spite of antibiotic How do bacteria get these shield genes? 1. They can get their own genes through mutation and selection a. mutation rate is high because rate of cell division is high hen antibiotics are used that are not strong enough or are not used long enough, the most resistant survive each time antibiotic taken improperly, the more resistant bacteria survive resistance builds b. the good bacteria? are killed by the antibiotic the resistant bact eria can reproduce faster than normal, healthful bacteria and cause illness 2. Bacteria can get resistance genes from other bacteria through plasmids that carry genes for resistance Plasmids a small circular piece of DNA (genetic materal) that contains a few genes not necessary for bacteria to live, but bacteria with them often have an advantage can be inserted into bacterial chromosome and come out as circular piece again Plasmids can be copied and a copy gived to another bacterium through sex then both bacteria have the genes on the plasmid. 29Certain plasmids (called R factors) have genes for resistance to antibiotics possible to have genes for 1 or 10 different antibiotics genes for resistance for one antibiotic can be added to a plasmid than has genes for resistance to other antibiotics leads to the development of bacteria that are resistance to many different antibiotics multi-drug resistance tends to happen in places where antibiotic use is heavy hospitals farm animals Resis tance develops where antibiotics used most Hospitals Livestock Overuse and Misuse of antibiotics has led to resistance 1. Misuse for medical purposes Dont demand antibiotics for viral diseases they dont work on viruses claim the full course of your prescription 2.Widespead use in livestock and floriculture Used in livestock to promote growth Resistance genes can spread from the animals to the bacteria that harm humans Cook meat throroughly (be sure meat juices dont come in contact with other food) Wash fruits and vegetables fend off raw eggs Chlamydia and Gonorrhea Caused by different bacteria but have similar symptoms Both primarily affect mucous membranes well-nigh noticeable symptom if it occurs is pain during urination This occurs if urethra is infected Urethra is more likely to infected in a male Therefore males more likely to have symptoms Often they dont cause symptoms Can still spread the cactiria to others Bacteria still damage reproductive structures 30Chlamydia (Ch lamydia trachomatis) Most common bacterial STD in US Highly contagious Symptoms slow to appear, 3 weeks to months Men More likely to have symptoms than women flagitious urination Discharge from urethra Women If urethra is infected distressful urination Discharge from urethra PID (chlamydia causes 50-90% of PID) Slight vaginal justify Pain during intercourse Abdominal pain & febrility Chlamydia is the STD the most likely to cause scar tissue to form in the tubes that gametes move through Because of scar tissue Chlamydia is the STD most likely to cause sterility Chlamydia is the STD most likely to increase the risk of an ectopic pregnancy The bacteria that cause chlamydia Must live within a cell because they cannot generate their own adenosine triphosphate They use the ATP that the host cell produces Energy in food ATP Energy for cell activities Effects on Fetus in Utero can cause membranes to rupture can cause death of fetus contracted during birth blindness pneumonia infection of mouth, throat, rectum diagnosis body of water test for DNA for Chalmydia Swab cervix (women) or urethra (males) and culture cells Pap test (women) Treatment Antibiotics Gonorrhea Caused by diplococcus bacterium Neisseria gonorrheae Symptoms Often none Men More likely to have symptoms than women Painful urination Discharge from urethra 31Women If urethra is infected Painful urination Discharge from urethra PID Slight vaginal discharge Pain during intercourse Abdominal pain & fever Acidity decreases if on pill or at menopause Effect on fetus Contracted during birth May cause blindness Diagnosis Urine test form DNA Swab cervix (women) or urethra (males) and culture cells Look for bacteria in cells Treatment Antibiotics New varieties are resistant to antibiotics Syphilis Cause = bacterium (Treponema pallidum) Requires a warm, moist environment Can invade any mucous membrane Usually in the genital area Three horizontal surfaces 1. Primary Stage 2-6 weeks after contact chancre forms may be small swelling or deep lesion usually hard raised edges crater-like painless at site of contact heals by itself in 4-6 weeks diagnosis at this pint is by isolation of the bacterium from chancre 2.Secondary Stage 2-10 weeks after chancre appears Symptoms Rash- doesnt itch, ulcerates Ulcers in mucous membranes In mouth, vulva, vagina, rectum Warly growths around anus and genital organs Headache Body ache May have Sore throat Gastrointestinal upset Loss of hair Diagnosis at this stage Blood test that looks for antibodies (VDRL) 32 3. Tertiary Stage 8-25 years after initial contact almost any organ can be infected and develop lesions called a gumma most common sites of gummas 1. large arteries decrease diameter of artery aneurysm weak spot in artery that balloons out 2. brain & spinal cord Blindness Deafness paralysis Mental degeneration 3.Skeleton Effect of fetus Transferred across placenta Can cause deformities Can be fatal Treatment Early stages curables with antibiotics v irus viruses have genetic material (usually DNA but some have RNA) and a protein coat (capsid) Structure of a typical virus Steps in Viral Life Cycle 1. Attachement Viral protein binds to receptor on host cell 2. Penetration virus enters host cell 3. Biosynthesis viral genetic material replicated by using host cell ? machinery? new coat proteins made 4. Assembly newly synthesized viral compnents put together to form new viruses 5. Release called viral shedding or budding viruses leave cell with envelopes from host cell OR Viruses genetic information can be integrated into host cell chromosome and stay there in dormant(ip) form until it is reactivated Viruses can cause call damage as they are released (shed) 1.Rapid release cell can rupture and die 2. slow release cell damage and dearth occurs over long time period 3. Periodic release viruses can remain in certain body cells (e. g. nerve cells) for life they may be release from body cells periodically and enter new marking cells. (herpes can remain in nerve cells be released epriodically and enter new epithelial cells damages the epithelial cells) 4. be integrated into host chromosome and stay there in dormant form until it is reactivated 33 Lytic Infection Persistent Infection Latent Infection Transformation to cancerous cell Rapid release of new viruses from infecded cell caused cell death.The symptoms of the disease depend on which cells are killed Slow release of new viruses causes cell to remain alive and continue to produce new viruses for a prolonged period of time. Delay between infection and symptoms. Virus is present in the cell without harming the cell. Symptoms beging when the virus begins actively replication and causes cell death when new viruses exit the cell. Certain viruses insert their genetic information into host cell chromosomes. Some carry oncogenes (cancer causing genes) that are active in the host cell. Some disrupt the functioning of the host cells genes that regulate cell di vision, causing the cell to become cancerous. Viruses and Disease 1.Can cause cell damage as they leave the host cell the cell damage causes the symptoms 2. Can cause cancer when they insert themselves into host chromosome or by producing factors that affect the host genes that regulate cell division genital herpes virus Cause virus Herpes simplex -type 1 (HSV-1) usually associated with fever blisters + cold sores -type 2 (HSV-2) usually causes similar sores in genital area Symptoms (if there are symptoms) first may have a quiver or itching sensation (called the prodrome) 2-20 days after contact blisters of fluid filled sores 1st attack lasts about 3 wks (1wk-4wks) can use ointments to relieve the pain will go away whether treated or not Also cause cancer hen they insert themselves into host chromosome o r by producing factors that affect the host genes that regulate cell division Viruses and Disease 34 Genital Warts in about half (50%) of people with herpes blisters reform perio dically usually at times of stress because the virus moves the the sacral ganglia of the spinal cord not affected by the human immune system here can be reawakened + cause new sores - possibly 2x month or 1x in 10yrs -NO CURE Genital Herpes spread by contact of infected and uinfected surface no sex while blister present or during prodrome or for at least 10 days after blisters are bygone use a condom at all timeseven when no blisters are present erpes can be spread to newborn if deliver vaginally while virus is present if infants infection is in liver and central dying(p) system-can be fatal Diagnosis Examination of sores Culture fluid from sores Blood test for antibodies in women-Pap test Treatment -Syptoms only Acyclovir (Zovirax)-reduce austereness of first outbreak and reduce frequency of recurrences Human Papilloma Virus (HPV) usually transmitted by sexual contact 50-70% of those who have sex with an infected person will get them more likely if on the pill or pregnant or un circumsized appear 1-2 months after contact, maybe longer appearance of growth on dry areas- brownish on moist areas-pink they grow may cause foul-smelling discharge may itch -warts can be removed by 1. freezing 2. suntan 3. laser 4. treated with a chemical (podophyllin) that is painted onleft 4 hrs. swear out away warts fall off * virus may remain Diagnosis appearance of wart in women-Pap test can look for DNA of HPV inside cells 35 Genital Warts *ASSOCIATED WITH INCREASED RISK OF CERVICAL cancer -HPV found in 90% of women with cervical cancer There is now a vaccine against HPV and, therefore, against cervical cancer *ASSOCIATED WITH AND INCREASED RISK OF crabmeat OF PENIS 36 BODY DEFENSES Innate Responses Nonspecific Physical and chemical substance Barriers Adaptive defense Specific defenses (directed at specific target) The immune system 1. Specific for particular invader (antigen) 2. Has retrospection for specific antigens previously encountered lymphocyte encounters anti gen Immune receipts have 1.Specificity Specific for particular invader (antigen) Antigen = a large molecule (not recognized as belonging in the body) that triggers an immune resolution Ex antigen can be on the surface of a bacterium or virus etc. can be a bacterial toxin Your body cells have markers (molecules) that label them as belonging in your body Each lymphocyte has receptors on its surface that recognize a specific antigen When that antigen is present, it causes that lymphocyte to divide many times effecter cells Memory cells effector cells attack specific target Memory cells remain and provide a quick reaction in subsequent exposure to same antigen tierce line of defense Specific defenses (directed at specific target) The immune system Immune system is 1. specific for a particular ? invader? antigen) 2. has memory for specific antigen previously encountered Creates an army of lymphocytes specialized to attack that antigen These are called effecter cells 2. Memory have m emory for specific antigen previously encountered Memory lymphocytes remain to cause a quick response the next time the same antigen is encountered 37 STEPS IN IMMUNE RESPONSE 1. Threat unconnected cell or molecule enters body 2. Detection Macrophage detects invader engulfs invader digests invader 3. Alert Macrophage places a piece of consumed antigen on its plasma membrane attached to a self marker presents the antigen to a jockstrap T cell activates the accessory T cell 4.Alarm Helper T Cell after activation by a macrophage, it divides, forming effector service T cells and memory champion T cells turns on both lines of immune response to fight that specific antigen by activating B cells and T cells 5. grade specific defense (clonal selection) Lymphocyte encounters antigen effecter cells attack specific target Memory cells remain and provide a quick response in subsequent exposure to same antigen 6. Defense A. Antibody-mediated immune response Effector B cell = plasma cell Plasma cells secrete antibodies Targets = antigens outside of cell or on surface of cell B. Cell-mediated immune response Effector T cell = cytotoxic T cell cytotoxic T cells kill foreign cells by causing them to sunder Targets = cells bearing antigens (any cells recognized as foreign e. g. nfected cell, bacteria, cancer cell) 7. Continued surveillance memory cells remain 8. Withdrawal of forces After antigen has been destroyed suppressor T cells fold down the immune response Effector cells cells Memory 38 A. Antibody-mediated immune response Effector B cell = Plasma cell Plasma cells secrete antibodies Targets = antigens outside of cell or on surface of cell An antibody is a Y-shaped protein designed to recognize a specific antigen Antibodies help guard against a specific antigen Can only work against antigens that are free in blood Antibodies bind to the antigen Antibodies are secreted by plasma cells (effector B cells) Ways that Antibodies can Work 1.Neutralization bind to an tigen prevent virus from being able to enter host cell inactivate toxin 2. Agglutination and hastiness -clumps invaders together makes it easier for other cells to engulf them 3. Activation of backup system complement (system) is a group of proteins that pokes holes causes invader to burst B. Cell-mediated immune response Effector T cell = cytotoxic T cell Cytotoxic T cells kill foreign cells by causing them to burst Targets = cells bearing antigens (any cells recognized as foreign e. g. infected cell, bacteria, cancer cell) Cytotoxic T cells secrete proteins called perforins that poke holes in invader or foreign cells, causing them to burst 39Cells Involved In the Immune System Macrophage an antigen presenting cells engulfs and digests antigens places a piece of consumed antigen on its plasma membrane presents the antigen to a helper T cell activates the helper T cell B Cells T Cells Helper T Cell the on switch for both lines of immune response after activation by a macrophage, i t divides, forming effector helper T cells and memory helper T cells activate B cells and T cells Cytotoxic T cell (effector T cell) responsible for cellmediated immune responses when activated by helper T cell, it divides to form effector cytotoxic T cells and memory cytotoxic T cells destroys cellular targets, such as virusinfected body cells, bacteria, fungi, arasites, and cancer cells Suppressor T cell the off switch for immune responses suppresses the activity of B cells and T cells after the foreign cell or molecule has been successfully destroyed involved in antibodymediated responses when activated by helper T cells, it divides to form plasma cells and memory cells Plasma Cell effector in antibodymediated response secretes antibodies specific to the invader Memory Cells responsible for memory of immune system generated by B cells or any type of T cell during an immune response enable quick and efficient response on subsequent exposures of the antigen may live for years 40 AI DS Acquired Immune Deficiency Syndrome Caused by HIV Human Immunodeficiency Virus HIV infects T cells T cells become HIV factories Organism enters body Macrophage detects it HIV kills helper T cells so THIS doesnt happen Activates a helper T cell Stimulates division of cytotoxic T cells (attack foreign cells) As helper T cell numbers drop, the body becomes increasingly susceptible to infection Stimulates B cells to form antibodies (destroys the infectious organism) 41