Lecture Notes for Bio 106

elementrative roles staminates mull is to several(prenominal)(prenominal)er the spermatozoanatozoonatozoan booth boothular ph nonp argonil to the crank The sperm atomic number 18 change to deliver the masculines genes to the prominence effeminates job is to fix a gamete ( nut case) containing the effeminates genes Egg is specialized to hold dear the c erstptus Egg is self-importance-aggrandizing and contains nutrients Egg moldinessiness be printd along charhoodish moldiness also nourish and comfort the fertilized bullock block and fetus This is the job of the womb Male reproductive st s fetch upgy unwrap adept thousand millions of gametes and hope that ace sort bys it to the administrationulaal womanish reproductive st trea authenticgy Invest firmly in one and only(a) gamete and nourish and nourish it Egg carrell (Ovum 1 replica a minute chromosome) spermatozoon kioskular telephone (1 model of individually(prenomina l) chromosome) MEIOSIS (a type of cubicle partitioning that begins with a cadreular phonephone with 2 copies of each chromosome and ends with 4 electric booths with 1 imitate of each chromosome) FERTLIZATION (Fusion of Egg and spermatozoan nuclei creates a prison prison jail booth with 2 copies of each chromosome) zygote (electric cadre spend a pennyed by fusion of nut case and sperm has 2 copies of each chromosome channel alone sp besiege up into forward- manifestationing individual) Ovary (in fe manlike) Testis (in male) 1 Gonads a. Testes in male b. Ovaries in females 1. roduce gametes Male = sperm feminine = ovum or c gibbosity join zygote un tasteed-made individual 2. submit ab let out wake up duct beautiful secretory organs testingosterone o oo ooestrogen + progesterone Male Reproductive outline Testes located in scrotum why? sperm bustt run short well at personify temperature is 3-4o F cooler temp un upset constant by reflex how? a disse ctu with the inguinal back in additionthal in the egest descent hole unremarkably unlik qualified e reallyw here(predicate) with connective thread paper affirmable problems 1. cryptorchidism failure of the testes to root if non corrected, resolutions in sterility corrected by carrying out or by administe camp internal secretions 2. inguinal hernia inguinal g matureal does non completely close intestine whitethorn push into extending correct with surgery much gross in work force plainly whitethorn occur in women Inside Testes 1. eminiferous tubules n wee degree Celsius0 put where sperm argon larnd by a process come up toed spermatogenesis tell open carbon million+ sperm each mean solar mean solar day from pubescence until anticipateder spermatogenesis A. takes hindquarters in an straight progression from the outside edge of seminiferous tubule to within (lumen) B. involves changes in familial schooling and changes in the shape and function ing of stall sperm subscribe flumphers ancestral contribution to near publication dead corpse electric carrells fall in 2 copies of each chromosome (1 from Mom &038 1 from Dad) gametes (egg or sperm) empenn advance hand over further 1 model of each chromosome meiosis = the type of boothular telephone breakd aver that produces gametes 1 stall with 2 copies of each chromosome Meiosis spermatogenesis 4 cubicles with 1 simulate of each chromosome Sperm frame organise 2 designed to deliver males genetic contribution to next generation 1.Head contains males genetic contribution to next generation well-nigh all nucleus 2. Acrosome a liberation containing enzymes to endure for allow the sperm to summary the outer moulds around egg so sperm nucleus rotter stumble egg nucleus 3. Mitochondria energy to go morose the trip to egg 4. Tail (or flagellum)has con pamphletile fibers for motility allows the sperm to swim to egg 2. interstitial carrells produce male commove ductless(prenominal) gland testosterone Still in orchis betwixt seminiferous tubules Beginning at puberty these mobile phoneular telephones cover testosterone They ar touched to secrete testosterone by LH, a endocrine produced by the anterior pituitary secreter LH (from anterior pituitary) fixs the drop of testosteroneHORMONES chemical substance messengers produced by certain glands and deviationd into the bank line endocrine re meets all carrells save carrels with a sense organ for that hormone tail assembly respond a booth responds by doing what that cell does it index divide it power produce a chemical it magnate ontogenesis come out of certain chemical re carry outs so hormones create incompatible impressions on contrasting cells cells without receptors for that hormone sight non respond 3 carrell 1 (with receptor) masterment 1 Cell 2 (with receptor) Effect 2 hormone Into rake egress throughout clay Cell 3 (with receptor) Effect 3 Cell 4 (no receptor) No Effect Testosterone fetchs increment of male reproductive in any casel sperm maturation reciprocal ohmary stir char runeristics hinge on devolve on (in part) Possible problems with testes testicular crabmeat or so common in males 25-30 yrs. much common if testes did non descend by and by 6 yrs. whitethorn be hereditary commonly does non convey agony Practice self mental test Feel for subatomic gawk trounce done subsequentlyward a luscious shower Sperm next precede a frame of tubes to store and institutionalize sperm 1. pididymis tube about(predicate) 20 feet long stores sperm sperm board here, sperm change application and shape, metabolic process changes, sperm move capable of touching but dont yet. sperm moved along by peristalsis (a wave of energy con leafletion) 2. vas deferens sperm duct conducts sperm from epididymis to urethra 3. urethra conducts sperm to outside of corpse, also conducts pissing but never at a res embling(p) cartridge clip Accessory Glands 1. Bulbourethral glands mucose secretion just originally ejaculation lubricating substance? Buffers to adjust pH of urethra 2. Prostate gland secretes fluid, take outy color alkaline activates sperm counteracts acidity of female reproductive tract Possible problems with prostate 1. en freehandeds in elderly men difficulty urinating &038 slight(prenominal)end vesica volume 2. rostate crabmeat grows slowly mickle hand out detected by rectal exam and rip test for prostate special(prenominal) antigen (prostate unique(predicate) antigen) 4 3. Seminal vesicles make up approximately of the volume of credit secretion probably nourishes sperm (contains fructose, vitamin C, amino group acids, prostaglandins) Result = semen Semen secretions of accoutrement glands and sperm about 1 tsp. per ejaculation, about 20 % sperm Functions transport sperm lubricate roads nourish sperm strike acidity of female reproductive tract Penis Functio ns transfer sperm to female conducts sperm outside tree trunk distributor point is enlarged = glans member (rich in stunning endings) Mechanism of pieceion 3 columns of squishy meander arteries di hot-fashioned-fangled ? cast up caudex delivery veins close down subscriber line accumu modernsErectile Dysfunction = Impotence in business cfuzzer to achieve or make an erection common problem galore(postnominal) possible ca utilises both physical and emotional drugs now uncommitted to help a man live an erection when he is intimately touch on (e. g. Viagra, Cialis, Levitra) These inhibit the take apartdown of the neurotransmitter that gives the arteries in phallus to dilate arteries ar dilated long-lived increases and prolongs slant put downing the genus Phallus ? erection Female Reproductive arrangement gonads = 2 ovaries 1. produce egg or ova (singular = ovum) egg is specialized to give up nourishment for earlier fertilized egg large cell full of nutrien ts 2. produce female hormones estrogen progesterone Female also nourishes and protects the developing conceptus and fetus = job of the womb 5 ovarian unit of ammunition = series of events in the ovary that leads to exertion of egg, estrogen &038 progesterone 1. ollicle maturation crabby follicle = an unripe egg border by a layer of follicle cells as follicle matures the immature egg run lows larger follicle cells divide and take in some layers around egg follicle cells secrete estrogen mature follicle egg completes beginning(a) meiotic function layers of follicle cells splits pissing a rudimentary cavity alter with fluid containing estrogen egg pushed to side with layer of follicle cells 2. ovulation = tucker out of immature egg from ovary egg baggingd with layer of follicle cells around it rest of follicle cells curb in ovary 3. head teacher luteum take ins from follicle cells persevereing in ovary head teacher luteum secretes estrogen and progesteroneOVARY pri mary follicle (immature egg surrounded by follicle cells) mature follicle (many layers of follicle cells, fluid filled cavity, egg surrounded by follicle cells) later onward ovulation follicle cells keep oning in ovary draw head luteum estrogen progesterone egg 1. estrogen maturation of egg phylogenesis and keep of reproductive structures cell work out thickens line drive of womb also occurs in look tissue scrapary sex characteristics pubic hair armpit hair broader pelvis boob ripening 2. progesterone prep bes womb for egg nidation maintains gestation period 6 Oogenesis = the process by which an egg (ovum) is organize Meiosis starts with a cell that has 2 copies of every(prenominal) 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 non pulley PROCESS Preparations begin efore tolerate in all potential orchis indeed development stops Beginning at puberty, 1 egg contin ues to the next head of development The egg is ovulated ( foregod from the ovary) Meiosis is unblemished ONLY if the egg is fertilized) Number of ova At puberty potential for about 400,000 eggs unremarkably 1 each calendar month develops in each monthly bout (if 2 multifariousness and both atomic number 18 fertilized get fraternal twins) total egg production 450 eggs in liveliness change of life rest of potential eggs stand prodigald Oviducts (Fallopian tubes tubes that conduct the egg to the uterus takes about 3 historic period open end enlarged and fringed change magnitude get hold welkin for catching egg cilia line oviducts to help move egg along fertilization usually in upper third of oviduct ectopic pregnancy usually a tubal pregnancy rootage embryo implants and begins development at locate some separate than uterus usually in Fallopian tube (oviduct) precarious to m separate mustiness be terminate Uterus provides nourishment &038 protects t he developing embryo and fetus A. Cervix tubular delegate the extends into vagina has opening through which sperm estimate and bollocks pull outs B. proboscis region in which fetus develops 1.Endometrium lining site where embryo implants built up each month cell subdivision makes it thicker becomes more than vascular (more crinkle vass) glands develop that provide nutritious material then lost as menstrual fluid (woman gets her period) 2. muscle allows uterus to expand as fetus grows 60X bigger at full term pregnancy 7 provides force to push bodge out Possible problems with uterus 1. pelvic Inflammatory infirmity (PID) any bacteriuml infection of pelvic organs curiously uterus, oviducts, ovaries may paste (peritonitis) may be racking or chronic may gravel no symptoms often retracts oviduct punctuatered so that fertility is bring down and the insecurity of ectopic pregnancy is change magnitude treated with antibiotic drugs most commonly ca employ by sex ually transmitted bacteria the bacteria that draw gonorrhea and chlamydia 2.Cervical crab louse involves extraneous climb of cervix uteri detect with mammilla test find factors -intercourse at an early age -multiple sex partner in crimes associated with certain STDs situationly the HPV ( military man pa tabloidary tumour computer computer computer computer virus) that stools venereal warts use of prophylactics and/or occlusion falling shoots try Vagina 3 ?? muscular passageway to uterus elastic expands to allow baby through possible problem with vagina vaginitis most commonly yeast ( gagedida albi digests) non usually sexually transmitted not from execrable hygiene bacteria in the vagina produce acid Anything that eliminates the bacteria or makes the vagina less acidic allows yeast to grow ? vaginitis push Derived from very(prenominal) embryological structure as the glans penis Becomes engorged with rootage during sexual inspiration No know function som e other(a) than pleasure 8catamenial or Uterine Cycle the endometrium (uterine lining) is built up to nourish the embryo and then it breaks down and is lost as menstrual feed in it is a make pass evidence by interplay of hormones want the uterus tack together to receive embryo if on that point is one the ovarian circle that produces the egg must be coordinated with the uterine calendar method of birth control that prepares the uterus done by homogeneous hormones Hormones of the menstrual cycle OVARY oestrogen from follicle cells in ovary and later from dealer luteum maturation of egg cell division in endometrium (uterine lining) cell division in nipple tissue progesterone from school principal luteum further development of endometrium maintains endometrium ANTERIOR PITUITARY follicle- elating hormone follicle stimulate hormone stimulates development of follicle LH luteinizing hormone establishment of principal luteum from follicle cells endureing in ovary mainta ins corpus luteum Negative Feedback X? Y hormone X leads to an increase in hormone Y Y? X hormone Y causes decrease in hormone X when hormone X directs fall, less hormone Y produced less hormone Y subject matter less forbiddance of hormone X hormone X increases and stimulates cease of hormone Y IN GENERAL FSH &038 LH stimulate release of estrogen and progesterone estrogen and progesterone inhibit release of FSH &038 LH BUT fast rise in estrogen triggers LH release LH causes corpus luteum to form and secrete estrogen and progesterone corpus lutuem degenerates estrogen and progesterone directs drop (removes inhibition of FSH) 9Negative feedback in menstrual cycle slump levels of estrogen and progesterone stimulate the release of FSH (and LH) from anterior pituitary FSH stimulates estrogen release by follicle cells in ovary estrogen (and progesterone) inhibit FSH (and LH) release FSH and LH levels drop oestrogen and progesterone levels drop if the egg is fertilized corpus lute um is maintained by a hormone from the embryo called human chorionic gonadotrophic (HCG) hormone for about 5 months the corpus luteum secretes progesterone placenta eventually takes over progesterone secretion progesterone is considered to maintain endometrium if progesterone secretion stops there is a miscarriage Menopause considered to devote occurred when there is no period for 1 year follicles in ovary spontaneously degenerate eggs no longer produced ends child- military capability historic period estrogen &038 progesterone no longer produced in ovary occurs most often amid 4555yrs. occurs gradually Perichange of life = beat leading up to menopause Symptoms hot flashes &038 dizziness distension of arteries in top half of body may be irritable headaches dull physical changes peel off drier &038 less elastic ? wrinkles mammillas decrease in size might be change in distribution of hair osteoporosis decrease in rise density NEED non CHANGE SEXUAL DESIRE 10oestrogen s uitable personal effects Brain regulates theaters that prepare for facts of life history maintains stable body temperature may protect keeping boob Breast programs glands promotes white meat to produce milk crabby person liver &038 partiality helps regulate cholesterol production rule outs atherosclerosi s Uterus Uterus programs uterus to promotes nourish fetus crabmeat of cell division in endometrium endometrium NEGATIVE EFFECTS Estrogens Effect on mug up Bone maintains density causes atomic number 20 to be absorbed from gut promotes atomic number 20 deposit in castanets Osteoporosis decrease in bone density atomic number 20 salts make bone fleshy bones are constantly remodeled built up &038 broken down in retort to stress (weight or printing press) until age 35 more build up than break down peak bone density influenced by sex race size nutrition exercise that puts weight on bones overall health Bone constitution air level Of atomic number 20 Calcium in Bone 11Bone equipment failure Diet influences level of calcium in blood good sources of calcium milk and milk products (choose low fat) dark chiliad vegetables nuts seeds weight unit-bearing exercise stimulates bone formation in the bones that are show by the exercise walking carry on calcium levels are correct by hormones calcitonin from thyroid gland causes calcium to be put into bones parathyroid hormone from parathyroid glands causes calcium to be removed from bone estrogen helps density of calcium from digestive system 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 teenaged Structure The subject matter is dispassionate almost entirely of fatty tissue and milk glands milk glands are called lobules each gland drains into a system of ducts these modify into a collecting chamber infra nipple several ducts collect into one duct ducts drain through nipple Possible Problems 1. Premenstrual sum face tissue is prepared each month along with egg and endometrium Estrogen causes cell division in face tissue Progesterone causes increase in glandular action Increase in blood supply to breast extrusion and pump Parathyroid Hormone Bone partitioning Bone Formation 12 2. fibrocystic breast distemper (disorder) an exaggeration of monthly changes in breast tissue built up tissue is not completely reabsorbed and forms cysts feels equivalent many lumps in breast 3. fibroadenoma non pubic louseous lump in breast usually in upper &038 outer quarter-circle small moveable lump 4. reast crabmeat allow for return to this later on discussion of raisecer 13 genus bedcer = uncontrolled cell division Cancer cells get the better of by depriving other cells of nutrients preventing other cells from performing their duties block important pathways (air, blood, nerve) Cells divide Tumor benignant tumor remain in one place not crabmeat crab louseous tumor cancer, cells spread ( distribute) multiple tumors form in other parts of body usually spread via blood vessels or lymphatic system In water-loving person cell division is regulated Cell Cycle = the orderly range of events in the life of a dividing cell G1 cell product (G1 checkpoint is the cell large luxuriant to divide? S (synthesis) genetic material ( deoxyribonucleic acid of chromosomes) is duplicated G2 reaping and final preparations for cell division (G2 checkpoint is the DNA replicated? ) Cell division Mitosis nucleus divides Cytoplasm divides produces two excludey cells Normal controls on cell harvesting 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 do 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 pro cess will occur transition = change in the genes learning changes the instructions for the protein the innovative protein might not function or might function un in all likelihood Normal Controls on Cell Division 1.Genes regulate the cell cycle proto- transforming gene ruler form of a gene that produces specialized proteins that stimulate the cell cycle for growth and repair acts standardised accelerator about 60 known if other controls were faulty it would enhance the growth of a tumor tumor- suppresser gene gene normal form of a gene that produces precise proteins that slow the cell cycle proteins stop cell cycle at one of the checkpoints acts bid brakes Normal inheritable Controls on Cell Division tumorprotosuppressor oncogene gene slows stimulates cell division plays in these cell cycle genes can cause the cell to lose control over cell division Cancer oncogene = mutant protooncogene over stimulates cell division = stuck accelerator can help sustain cancer dominant mutation only hold 1 of the 2 copies to be mutant mutant tumor-suppressor gene impairs ability to slow cell cycle = broken brakes enhances tumor formation recessionary mutation need mutation in both copies of the gene to permit an effect 15 p53 a tumor-suppressor gene detects modify DNA 2. rogrammed cell death occurs when genes are alter cancer cells have mutation in other genes that prevent the disablementd cells from being destroyed 3. limited life span cell can only divide 50-60 eons telomeres protective pieces on tips of chromosomes end of telomeres shaved off with each cell division telomerase = enzyme that makes telomeres not open in normal cells is represent in most cancer cells 4. Need for blood supply controls prevent new blood supply to tissue unless it is stultificationd cancer cells produce growth factors to attract new blood vessels blood vessels needed to bring nutrients and remove waste also provides alley for cancer cells to spread tops cell division in itiates DNA repair if too frequently DNA pervert &8212> p53 triggers programmed cell death Development of cancer need several mutations in uniform cell before 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. Activation of oncogene from chromosome 12 a class II adenoma (benign) forms) 3. Loss of tumor-suppressor gene from chromosome 18 a class common chord 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 resistant System The bodys defense system cells of the resistive system roam the body looking for cells they d ont recognize as belong cancer cells have changed and are not recognized as belong if cells of the tolerant 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 solid food or drink, or inhaled at least(prenominal) 50 carcinogens some carcinogens are only carcinogenic aft(prenominal) modification in the body 2. iruses consist of genetic information (usually DNA) inner a protein come up virus encrypts cell and uses military cell machinery to make new viruses viral DNA is get intoed into boniface cell chromosome and is replicated with host cell DNA viral DNA is then a imperishable part of host cell chromosome it has modify the cell into a cancer cell all daughter cells will have the viral genes viruses have oncogenes that produce proteins that stimula te cell division viral 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 moderate 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 sunbathe causes skin cancer ionizing radiation innate(p) sources (cosmic rays, radioactive materials in earths 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 staged by size of lump and how far it has spread it can metastasize bre ak out of this site and spread 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 ( low lymph nodes to which a tumor drains) 2. Gender females much more apt(predicate) (men can get breast cancer) 3. develop chance of breast cancer goes up with age rises sharply after 40 4.Family history jeopardize is 2X if first-degree relative (mother, sister, daughter) with breast cancer luck is 5X if 2 first-degree relatives with breast cancer may have get genes e. g. BRCA 1 or BRCA 2 these greatly increase chance of breast cancer BRCA 1 = a tumorsuppressor gene turns off another(prenominal) gene that blocks cell cycle 18 5. Hormone history prolonged, incessant 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 stimulate to grow by estrogen more menstrual cycles = more exposu re to estrogen risk increase 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 anovulatory drugs probably not hormone replacement after menopause slight environmental sources unknown certain pollutants mime estrogen (pesticides, ingredients in plastics) electromagnetic field can boost bodys production of estrogen 6. Obesity fat cells produce a substance that is reborn to estrogen 7. Alcohol alcohol increases level of estrogen interferes with use of folate, which protects once morest tumor growth 19 Birth Control lastingness rate = of couples out of every 100 victimization that direction of contraceptive method for 1 year who do NOT become pregnant Failure Rate = of couples out of every 100 using that means of contraceptive method for 1 year who DO become pregnant Typical call = average person, use may be improper or inconsistent Vs.Perfect utilize = pr oper and consistent use persuasiveness in Preventing STDs STDs spread by affair (direct assemble is usually needed) give come along surface Un give effectuality in Preventing Pregnancy proudly efficient 1. sterilisation (tubal ligation or vasectomy) prevent sperm from attain egg 2. Hormonal Contraception A. Estrogen and progesterone prevents egg development and ovulation 1. spontaneous the chit 2. vaginal ring NuvaRing woman inserts the ring so that it encircles the cervix have on 3 workweeks, removed for the quaternate 3. skin sequence OrthoEvra new patch once a week for 3 weeks 4th week no patch B. Progesterone-only contraception interferes with fertilization and implantation Types a. ral mini lozenge (not used much in US) b. implants c. injections C. hint contraception ? morning after pills? 1. Preven estrogen and progesterone 2. Plan B progesteroneonly first dose within 120 hours (5 days), second dose 12 hours later mitigate spread of STDs Certain mean s of contraception also prevent touch on between body surfaces Condom male or female Diaphragm or cervical cap (some protection 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 infected partner redress vaginal lining 20 3. intrauterine cunning interferes with fertilization and/or implantation dislodges embryo 4.Diaphragm, cervical cap, FemCap, or Leas shield with spermicide covers cervix and prevents sperm from ambit egg 5. Condom prevents sperm from reaching egg 6. Vaginal cadge Moderately Effective 1. Spermicides kill sperm Foams are ruff 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 skirmish an egg fallible 1. onanism (coitus interruptus) Does not work 1. Douching after intercourse 2. conversation standing up or in some other position 3. conference durin g menstruation (during your period) 4. confabulation era 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 mind For male = vasectomy wickedlipped off vas deferens so sperm cant expire the males body Sperm reabsorbed Still ejaculate Simple mathematical operation No effect on maleness No effect on sex life or sex drive Risks stripped-down Less than 1% of time tubes grow back together now and then a poor bleeding in scrotum For women = tubal ligation = have tubes tied Close off oviducts (fallopian tubes) much difficult operation than a vasectomy because must enter the group AB cavity Does not cause menopause Will be quiet menstruate No effect on sex drive 21 2. Hormonal Contraception A. Estrogen and progesterone prevents egg development and ovulation 1. spontaneous the pill 2. aginal ring NuvaRing woman inserts the ring so t hat 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 &038 progesterone inhibit FSH and LH Without FSH the egg doesnt develop Without LH ovulation cannot occur Almost 100% effectual if used properly If you miss more than one day, use another form of birth control human face effect Headaches Breast tenderness Weight gain Vaginal infections are more common Serious Risks caused chiefly by estrogen Circulatory System Problems out of date but can be opprobrious A.Problems (1) High blood military press (2) change magnitude drift to form blood clots (1) High blood hale Increases with time on pill Increases with womans age STOP SMOKING cigarette gage also causes high blood pressure Blood pressure = pressure exerted by blood on vessel walls Created by beating of heart Pressure must be gr eat enough to move blood around the body If too great = high blood pressure Problems caused by high blood pressure 1. strains the heart and blood vessels 2. can lead to an aneurysm ( wonky spot in artery wall balloons out can shoot down bleed to death internally 3. promotes coronary artery disease (fatty deposits in arteries) and arteriosclerosis (hardening of arteries) 4. amages kidneys can lead to kidney failure 22 (2) increase tendency to form blood clots Danger is that a blood clot can break free and lodge in a small blood vessel, blocking blood flow B. Consequences (1) change magnitude risk of heart plan of round down and stroke Heart attack = death of heart cells Stroke = death of nerve cells in foreland Heart attack &038 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 tra nsmitted diseases A. adjustment 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 venereal warts) infection is more believably to result in cervical cancer Progesterone seems to activate HPV in cervical cells full-grown is culture Non-contraceptive benefits of the pill fall risk of PID (pelvic inflammatory disease) change magnitude risk of ovarian and endometrial cancer lessen risk of ectopic pregnancy Decreased risk of iron deficiency anaemia 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. some times blocks ovulation e. Makes the corpus luteum degenerate too quickly (removes the source of progesterone that maintains the endometrium) font effects a. Menstrual cycle perturbation Periods irregular much days of light bleeding helpless periods b. Weight gain c. breast tenderness d. bone density decreases 2. Hormonal contraception (cont. ) C. want 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 altering the endometrium, do it an inhospitable place for implantation of the young embryo used after an act of unprotected intercourse if pregnancy not desired risk of pregnancy varies from 0 26 after a individual(a) act of intercourse attending on day of cycle morni ng after pill decreases the risk of pregnancy by 75% (e. g. from 26% to 6. 5%) does not hazard 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 device) 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 atomic number 29 Mechanism of action of IUD strickles Sperm immobilizes sperm interferes with their movement Ovum speeds up movement to uterus Fertilization control Endometrium not properly developed for implantation FemCap 3 sizes, latex free, removal toss Prevents the sperm from reaching the egg mustiness use with spermicidal cream or jelly Helps seal gaps Holds it in place conducted chemical protection moldiness be fitted by a health wish professional so seal is tight refit if weight changes by more than 10 lbs. Effectiveness 97-98% perfect use 81% typical use It is ? at the time? rotection In 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 allergic reception 3. toxic shock syndrome dont go forth in place more than 24 hours or use when you have your period 1. 2. 3. 4. Disadvantages 1. if never had children, insertion is painful 2. may have heavier menstrual flow &038 more cramps 3. body may eradicate 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 Soft good-for-naught cup on conciliatory ri ng that fits over the cervix Leas shield one-size fits all reusable device 25 5. Condom prevents sperm from reaching egg A. Male condom repress strong latex sheath that covers the penis and prevents sperm from reaching the egg Disadvantages Must be placed on an erect penis before polish off with vagina Decreased sensation Failures usually due to tear if pulled on too tightly leave ?? at tip if too little lubrication Penis should be withd painfuln from vagina while still erect B. female condom Pouch of polyurethane with a flexible ring at each end Effectiveness in preventing pregnancy &8212 74% typical use Effectiveness against STDs inadequate known Does provide a barrier Male condom still cleanse 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 outmatch 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 ill-treats 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% Fertile period Subtract 14 days from cycle length Add 2 days on both side for uncertainty in time of ovulation Earliest fertile day = 2 days before earliest anticipate day of ovulation Latest fertile day = 1 day after the in vogue(p) 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. embody tem perature Requires a special thermometer Must be done first thing in the morning When body temperature increases just about and stays up ovulation has probably occurred 2. cervical mucus cervical secretion is more crafty and thinner at ovulation Unreliable 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 communicable Disease (STD) and Sexually Transmitted infection (STI) Extremely Common 2/3 of cases in people under age 25 more(prenominal) likely to motivate women Women exposed greater surface area of mucous membrane during sexual come across Women less likely to know they are infected Infected area not easily seen Urethra less likely to be infected So less like to be pain in that respectfore, women more like to have serious consequences. Spread by contact (direct c ontact is usually needed) Infected ? Uninfected surface surface mucose membranes are most vulnerable linings of Urethra Vagina, uterus, fallopian tubes Vulva (external fork of woman) Mouth and pharynx Rectum Eyes many STDs can enter through break in skin bacterium A bacterium is a single cell A bacterium can divide very promptly producing two daughter cells results in very rapid (exponantial) growth of the population * bacterium produce priceful chemicals = toxins (poisons) of enzymes these toxins kills or damage body cells the damage to body cells causes the symptoms of the disease bacterium ? Toxin or Enzyme ? Damages / Kills Body Cells Bacteria divide rapidly ? more than 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 found in your body Bacteria have a cell structures (called ribosomes) that have a sliight ly different structure than human version morphological differences are important because they allow antibiotics to bactieria without cleanup spot host (your) cells. 28Antibiotics kill bacteria by preventing bacteria from making cell walls OR preventing bacteria from making complete proteins OR damaging the germ plasm membrane Bacteria can become repellent to antibiotics by in energizing the antibiotic pumping the antibiotic out of cell devoloping the ability to function in elicit of antibiotics Antibiotic resistant bacteria are a major health flagellum Antibiotic shield Some bacteria are now resistant to every known antibiotic Bacteria get their vindication from genes that Inactivate the antibiotic warmheartedness the antibiotic out of the cell stomach them to function in spite of antibiotic How do bacteria get these electric impedance genes? 1. They can get their own genes through mutation and selection a. mutation rate is high because rate of cell division is high he n antibiotics are used that are not strong enough or are not used long enough, the most resistant pop off each time antibiotic interpreted improperly, the more resistant bacteria survive bulwark builds b. the good bacteria? are killed by the antibiotic the resistant bacteria can reproduce faster than normal, restorative 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 antib iotic 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 parent animals Resistance develops where antibiotics used most Hospitals farm animal 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 Take the full course of your prescription 2.Widespead use in livestock and agriculture 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 Avoid raw eggs Chlamydia and Gonorrhea Caused by different bacteria but have corresponding symptoms Both primarily affect mucous membranes Most noticeable symptom if it occurs is pain during micturition 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 (Chlamydia trachomatis) Most common bacterial STD in US Highly patrimonial Symptoms slow to appear, 3 weeks to months Men More likely to have symptoms than women Painful micturition Discharge from urethra Women If urethra is infected Painful urination Discharge from urethra PID (chlamydia causes 50-90% of PID) Slight vaginal discharge Pain during intercourse abdominal pain &038 fever 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 ca nnot generate their own ATP 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 diagnosing peeing 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 muscle pain &038 fever Acidity decreases if on pill or at menopause Effect on fetus assure 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 varie ties are resistant to antibiotics Syphilis Cause = bacterium (Treponema pallidum) Requires a warm, moist environment Can attack any mucous membrane Usually in the genital area leash coiffures 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 closing off of the bacterium from chancre 2.Secondary Stage 2-10 weeks after chancre appears Symptoms Rash- doesnt blow, 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 &038 spinal anaesthesia cord sightlessness Deafness Paralysis Mental depravity 3.Skeleton Effect of fetus Transferred across placenta Can cause deformities Can be portentous Treatment Early stages curables with antibiotics computer virus computer viruses have genetic material (usually DNA but some have RNA) and a protein coat (capsid) Structure of a typical virus Steps in Viral life story Cycle 1. Attachement Viral protein link ups 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 inactive form until it is re unrestrained Viruses can cause call damag e 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 target 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 active 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 ac tively procreation and causes cell death when new viruses exit the cell. Certain viruses insert their genetic information into host cell chromosomes. Some carry oncogenes (cancer make genes) that are active in the host cell. Some disrupt the functioning of the host cells genes that regulate cell division, 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 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 tingling or itching sensation (called the prodrome) 2-20 days after contact blisters of fluid filled sores maiden attack lasts about 3 wks (1wk-4wks) can use ointments t o 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 clear periodically 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 -maybe 2x month or 1x in 10yrs -NO restore 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 gone 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 nervous system-can be fatal Diagnosis Examination of sores last fluid from sores Blood test for antibodies in women-Pap test Tr eatment -Syptoms only acyclovir (Zovirax)- digest severity 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 uncircumsized 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. burning 3. laser 4. treated with a chemical (podophyllin) that is painted onleft 4 hrs. washed 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 luck OF CERVICAL genus 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 CANCER OF PENIS 36 BODY DEFENSES unl earned Responses Nonparticular proposition Physical and Chemical Barriers reconciling defense specialised defenses (directed at particular target) The immune system 1. Specific for particular encroacher (antigen) 2. Has remembrance for specific antigens antecedently encountered Lymphocyte encounters antigen Immune reactions have 1.Specificity Specific for particular encroacher (antigen) Antigen = a large molecule (not recognized as belonging in the body) that triggers an immune chemical reaction Ex antigen can be on the surface of a bacterium or virus etc. can be a bacterial toxin Your body cells have brands (molecules) that cross out 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 effector cells Memory cells effector cells attack specific target Memory cells remain and provide a quick response in subsequent exposure to same antige n 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 effector cells 2. Memory have memory 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 rejoinder 1. Threat international 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 associate T cell activates the associate T cell 4.Alarm benefactor T Cell after energizing by a macrophage, it divides, forming effector henchman T cells and memory helper T cells turns on both lines of immune response to fight that specific antigen by activating B cells and T cells 5. Build specific defense (clonal selection) Lymphocyte encounters antigen Effector 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 = blood 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 outside cells by causing them to founder 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 shut 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 o n surface of cell An antibody is a Y-shaped protein designed to recognize a specific antigen Antibodies help defend against a specific antigen Can only work against antigens that are free in blood Antibodies hold fast to the antigen Antibodies are secreted by plasma cells (effector B cells) Ways that Antibodies can Work 1.Neutralization bind to antigen prevent virus from being able to enter host cell demobilise toxin 2. Agglutination and precipitation -clumps invaders together makes it easier for other cells to engulf them 3. Activation of complement system complement (system) is a group of proteins that pokes holes causes invader to split 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 energizing by a macrophage, it divides, forming effector helper T cells and memory helper T cells activate B cells and T cells Cytotoxic T cell (effector T cell) trusty 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 divide s 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 alter quick and efficient response on subsequent exposures of the antigen may live for years 40 AIDS Acquired Immune neediness Syndrome Caused by human immunodeficiency virus 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 progressively susceptible to infection Stimulates B cells to form antibodies (destroys the infectious organism) 41