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Human Reproductive System (RIT BRANCH): Physiology, Hormonal Control & Clinical Correlates.pptx
- 1. HUMAN REPRODUCTION (RIT) PREPAREDBY Dr. SOMA BALAJI PT MSK & SPORTS
- 2.
- 3. ANATOMY & HISTOLOGYOF TESTES Basic Structure - 2 in Number Each testis contains: • Seminiferous tubules (site of sperm production) • Interstitial (Leydig) cells • Epididymis sperm maturation →
- 4. Seminiferous Tubules Walls oftubules contain: • Spermatogenic cells (develop into sperm) • Sertoli cells (supporting cells) Outside tubules: • Leydig cells (produce testosterone)
- 5. PRIMARY FUNCTIONS OFTESTES There are two major functions: • Spermatogenesis • Secretion of male sex hormones (testosterone) Both are essential for fertility.
- 6. SPERMATOGENESIS (FORMATION OFSPERM) Definition • Spermatogenesis = process of formation of mature spermatozoa in the seminiferous tubules. • Occurs from puberty lifelong. → • Duration: ~64 days.
- 7. Stages of Spermatogenesis 1.Spermatogonia (mitosis) 2. Primary spermatocyte secondary spermatocyte → (meiosis) 3. Spermatids spermatozoa (spermiogenesis) → 4. Spermiation (release into lumen)
- 8. Requirements for Spermatogenesis •Testosterone • Follicle-stimulating hormone (FSH) • Luteinizing hormone (LH) • Sertoli cells • Optimal temperature (2–4°C below body temp)
- 9. SECRETION OF MALESEX HORMONES Leydig Cell Function • Also called as interstitial cells • Located outside seminiferous tubules • Produce testosterone main male sex hormone → • Stimulated by: LH (Luteinizing Hormone)
- 10. Functions of Testosterone •Development of male genital organs • Secondary sexual characters (hair, voice, muscle mass) • Growth of bones & epiphyseal closure • Libido (sexual drive) • Stimulates spermatogenesis • Anabolic effects (protein synthesis) • Maintains accessory sex glands (prostate, seminal vesicles)
- 11. SUPPORTING CELL FUNCTIONS SertoliCells • Also known as “nurse cells” of testes. Functions: • Provide nutrition to developing sperm • Form blood–testis barrier • Produce inhibin inhibits FSH → • Secrete androgen-binding protein (ABP) → concentrates testosterone • Phagocytosis of degenerating sperm • Convert testosterone estradiol → • Maintain optimum environment for sperm maturation
- 12. Blood–Testis Barrier • Formedby tight junctions between Sertoli cells. Functions: • Protect germ cells from toxins • Prevent autoimmune attack • Maintain special environment for meiosis
- 13. FUNCTIONS OF LEYDIGCELLS Leydig cells produce: • Testosterone • Small amounts of estrogen • Other androgens Role: support spermatogenesis & male secondary sexual characteristics.
- 14. TEMPERATURE REGULATION OFTESTES Importance of Temperature • Optimal sperm production requires temperature 2–4°C below body temperature. • Heat damages sperm infertility. →
- 15. Mechanisms of TemperatureControl • Scrotum – external position lowers temperature • Pampiniform plexus – countercurrent heat exchange • Cremaster muscle – raises or lowers testes • Dartos muscle – tightens or relaxes scrotal skin
- 16. ENDOCRINE CONTROL OFTESTES Hypothalamus GnRH → ↓ Anterior pituitary FSH & LH → ↓ Testes spermatogenesis + testosterone → FSH acts on Sertoli cells (sperm maturation) → LH acts on Leydig cells (testosterone production) → Feedback: Testosterone inhibits LH Inhibin inhibits FSH
- 17. ADDITIONAL FUNCTIONS OFTESTES • Production of small amounts of estrogen • Storage of sperm (in seminiferous tubules before transport to epididymis) • Secretion of growth factors essential for sperm cells
- 18. Disorders Related toTesticular Function • Cryptorchidism (undescended testes) reduced fertility, cancer risk → ↑ • Hypogonadism low testosterone, infertility → • Varicocele increased testicular temperature low sperm count → → • Klinefelter syndrome small testes, low testosterone → • Testicular torsion ischemia emergency → →
- 19.
- 20. Definition • Puberty =the period during which a child develops secondary sexual characteristics and becomes capable of reproduction. • It marks the activation of the hypothalamic–pituitary– gonadal (HPG) axis.
- 21. Age of Puberty Girlsreach puberty earlier than boys Gender Typical Onset Completion Girls 8–13 years 14–16 years Boys 9–14 years 16–18 years
- 22. PHYSIOLOGY OF PUBERTY Activationof HPG Axis • Puberty begins when the hypothalamus increases secretion of GnRH (Gonadotropin-Releasing Hormone). • GnRH stimulates anterior pituitary releases: → → - FSH - LH • These stimulate gonads: • In boys testes produce testosterone → • In girls ovaries produce estrogen →
- 23. Hormonal Cascade • GnRH↑ • FSH & LH ↑ • Gonads activated Testosterone/Estrogen → ↑ • → Development of secondary sexual characteristics
- 24. Adrenarche Before true puberty: •Adrenal cortex increases production of androgens (DHEA, androstenedione) • Leads to: - Pubic hair - Axillary hair - Body odor • Occurs at 6–8 years.
- 25. PHYSICAL CHANGES DURINGPUBERTY PUBERTY IN BOYS Sequence of Pubertal Changes in Boys • Testicular enlargement (first sign) • Growth of scrotum • Pubic hair development • Penile growth • Growth spurt • Appearance of axillary & facial hair • Voice deepening • Increased muscle mass
- 26. Testosterone Effects inBoys • Growth of penis & scrotum • Spermatogenesis begins • Secondary sexual characters: • Beard, mustache • Deep voice (larynx growth) • Increased muscle mass • Increased RBC count • Libido
- 27. PUBERTY IN GIRLS Sequenceof Pubertal Changes in Girls • Thelarche (breast development – first sign) • Pubarche (pubic hair) • Growth spurt • Menarche (onset of menstruation) • Pelvic widening, fat distribution Menarche occurs 2–2.5 years after thelarche.
- 28. Estrogen Effects inGirls • Breast development • Growth of uterus & ovaries • Fat deposition on hips & thighs • Onset of menstrual cycle • Closure of epiphyseal plates (ends height increase)
- 29. GROWTH SPURT DURINGPUBERTY Height & Weight Changes • Caused by growth hormone + sex hormones ↑ Girls: peak growth at 11–12 years Boys: peak growth at 13–14 years Boys grow taller due to: • Later epiphyseal closure • Higher GH & testosterone
- 30. PSYCHOLOGICAL & SOCIALCHANGES Behavioral Changes • Increased self-awareness • Mood swings (hormonal) • Interest in opposite sex • Development of identity & independence
- 31. REGULATION OF PUBERTY BiologicalClock The timing of puberty is regulated by: • Genetics • Nutrition • Body fat (leptin) • Stress • Chronic illness • Adequate body fat is required for puberty onset.
- 32. Role of Leptin Leptin(from fat cells): • Signals hypothalamus about adequate energy stores • Stimulates GnRH release • Early puberty in obese children
- 33. TANNER STAGING (SEXUALMATURITY RATING) Tanner Stages • 5 stages describing pubic hair + genital (boys) or breast (girls) development. Used for: • Tracking puberty progress • Identifying delayed or precocious puberty
- 34. DISORDERS OF PUBERTY PrecociousPuberty Definition: Puberty occurring before 8 years (girls) or before 9 years (boys). Causes: • CNS disorders (tumors, infections) • Early activation of HPG axis • Adrenal tumors • Exogenous hormones Effects: • Early menarche • Advanced bone age • Short adult height
- 35. Delayed Puberty No secondarysexual characteristics by: • 13 years in girls • 14 years in boys Causes: • Malnutrition • Chronic illness • Hypothyroidism • Hypogonadotropic hypogonadism • Gonadal failure
- 36.
- 37. Where Does SpermatogenesisOccur? • Occurs inside seminiferous tubules of testes. Inside tubules: • Outer layer → spermatogonia • Middle → developing germ cells • Luminal side mature spermatozoa → Supportive cells: • Sertoli cells • Leydig cells (outside tubules)
- 38. Duration • Total timefor spermatogenesis = ~64 days • Sperm maturation in epididymis = ~12 days • Total ≈ 76 days for fully functional sperm.
- 39. STAGES OF SPERMATOGENESIS Thereare three major phases: • Spermatocytogenesis (mitosis) • Meiosis (reduction division) • Spermiogenesis (transformation of spermatids into sperm)
- 40. SPERMATOCYTOGENESIS (MITOSIS) Definition -Formation of primary spermatocytes from spermatogonia through mitosis. Steps • Type A spermatogonia • Stem cells • Self-renew and produce Type B • Type B spermatogonia • Differentiate into primary spermatocytes These cells are diploid (46 chromosomes). • Importance - Maintains continuous supply of germ cells throughout male life.
- 41.
- 42. MEIOSIS Purpose - Reduceschromosome number from diploid (46) → haploid (23). Steps Primary spermatocyte (46 chromosomes) Meiosis I ↓ Secondary spermatocytes (23 chromosomes) Meiosis II ↓ Spermatids (23 chromosomes) Form 4 haploid spermatids from each primary spermatocyte.
- 43. Key Features • Geneticrecombination occurs • Diversity in offspring • Essential for fertility
- 44. SPERMIOGENESIS Definition • Transformation ofround spermatids into mature spermatozoa. • No cell division here—only morphological changes.
- 45. Changes During Spermiogenesis •Nucleus elongates & condenses • Formation of acrosome (from Golgi) • Development of flagellum (tail) • Formation of midpiece (packed with mitochondria) • Shedding of excess cytoplasm (residual bodies)
- 46. Structure of MatureSperm • Head nucleus + acrosome → • Neck • Middle piece mitochondria → • Tail motility → Length: 60 μm
- 47. SPERMIATION Definition - Releaseof mature spermatozoa from Sertoli cells into the lumen of seminiferous tubules. These sperm are: • Non-motile • Not yet fertile They gain motility later in the epididymis.
- 48. HORMONAL CONTROL OFSPERMATOGENESIS Hormone Source Function GnRH Hypothalamus Stimulates FSH & LH release FSH Pituitary Acts on Sertoli cells → ABP + support LH Pituitary Acts on Leydig cells → testosterone Testosterone Leydig cells Essential for spermatogenesis Inhibin Sertoli cells Inhibits FSH (negative feedback)
- 49. Role of FSH •Stimulates Sertoli cells • Promotes spermiogenesis • Increases androgen-binding protein (ABP) • Maintains spermatogonia division
- 50. Role of LH •Stimulates Leydig cells testosterone → • Testosterone diffuses into seminiferous tubules to support sperm formation
- 51. Role of Testosterone •Main hormone for spermatogenesis • Maintains meiosis • Required for normal sperm maturation
- 52. Role of SertoliCells • Provide nutrients • Form blood–testis barrier • Phagocytose debris • Secrete ABP • Convert testosterone estrogen → • Produce inhibin
- 53. ENVIRONMENTAL & PHYSICALFACTORS Temperature Regulation • Spermatogenesis requires 2–4°C lower than body temperature. • High temperature decreased sperm count → (oligospermia). Causes: • Tight clothing • Varicocele • Fever • Undescended testes
- 54. Factors That ReduceSperm Count • Smoking • Alcohol • Radiation • Chemotherapy • Hormonal imbalance • Obesity • Environmental toxins
- 55. CLINICAL CORRELATES Male InfertilityCauses • Low sperm count • Poor motility • Abnormal morphology • Testicular failure • Sertoli cell-only syndrome • Klinefelter syndrome
- 56. Abnormal Sperm Forms •Double head • Double tail • Short tail • Round head • Bent tail Can affect fertility even if count is normal.
- 57.
- 58. Where is TestosteroneProduced? 1. Leydig cells of testes PRIMARY source → 2. Small amounts from: • Adrenal cortex • Sertoli cells (converted to estrogen)
- 59. Regulation of Testosterone •Hypothalamus → GnRH Anterior pituitary → LH LH stimulates Leydig cells → → Testosterone secretion Negative feedback: • Testosterone inhibits LH & GnRH • Inhibin (from Sertoli cells) inhibits FSH
- 60. FUNCTIONS OF TESTOSTERONE FUNCTIONSDURING FETAL LIFE (Role of Testosterone in Male Fetus) Secreted by fetal testes (from 7th week of gestation). Functions: Development of male internal genital organs • Epididymis • Vas deferens • Seminal vesicles • Ejaculatory ducts Descent of testes into scrotum (via gubernaculum) Differentiation into male phenotype under influence of DHT
- 61. FUNCTIONS AT PUBERTY Testicular& Genital Development • Growth of testes, scrotum & penis • Enlargement of prostate & seminal vesicles • Initiation of spermatogenesis
- 62. Secondary Sexual Characteristics Testosteroneis responsible for: • Deepening of voice (laryngeal enlargement) • Growth of facial, axillary & pubic hair • Male pattern body hair distribution • Increased sebaceous gland activity acne → • Increased muscle mass & body strength
- 63. Growth & SkeletalEffects • Stimulates bone growth during puberty • Later causes epiphyseal plate closure • Increases bone density • Responsible for greater height in males
- 64. FUNCTIONS IN ADULTLIFE Reproductive Functions • Maintains spermatogenesis • Maintains accessory sex organs • Maintains libido (sex drive) • Stimulates erection & ejaculation pathways
- 65. Metabolic & SystemicEffects Testosterone has anabolic actions: • Protein metabolism • Promotes protein synthesis • Increases muscle mass • Enhances nitrogen retention • Fat metabolism • Decreases fat stores • Increases basal metabolic rate • Carbohydrate metabolism • Increases insulin sensitivity • Electrolyte balance • Enhances reabsorption of Na⁺ & water • Mild mineralocorticoid effect
- 66. Hematopoietic Effects • Increaseserythropoietin production RBC count → ↑ • Explains why males have higher hemoglobin than females
- 67. Psychological & BehavioralEffects Testosterone influences: • Aggressiveness • Assertiveness • Competitive drive • Sexual behavior
- 68. CONVERSION TO DHTAND ESTROGEN DHT (Dihydrotestosterone) • Converted from testosterone by 5-α-reductase. DHT responsible for: • Prostate growth • External genitalia development • Facial beard growth • Male-pattern baldness
- 69. Aromatization to Estrogen Sometestosterone converts to estrogen in: • Sertoli cells • Fat tissues • Brain Estrogen in males: • Required for spermatogenesis • Modulates libido • Maintains bone health
- 70. CLINICAL CORRELATES Effects ofTestosterone Deficiency In children: • Delayed puberty • Eunuchoid body proportions In adults: • Decreased libido • Erectile dysfunction • Infertility • Decreased muscle mass • Osteoporosis • Depression
- 71. Excess Testosterone Causes: • Earlypuberty (precocious puberty) • Aggressive behavior • Acne & oily skin • Infertility (due to feedback suppression) • Prostate hypertrophy • Male-pattern baldness
- 72.
- 73. WHAT IS SEMEN? •Definition - Semen is a thick, whitish fluid containing spermatozoa suspended in seminal plasma. • It is ejaculated during sexual climax. Semen is composed of secretions from: • Seminal vesicles 60% → • Prostate gland 20–30% → • Testes (sperm + fluid) 10% → • Bulbourethral glands (Cowper glands) 5% →
- 74. PROCESS OF SEMENFORMATION Steps of Semen Formation • Spermatogenesis in seminiferous tubules • Sperm storage and maturation in epididymis • Mixing with accessory gland secretions during ejaculation Sequence of ejaculation: • Vas deferens contractions sperm enters urethra → • Seminal vesicle secretion added • Prostate secretions added •
- 75. COMPOSITION OF SEMEN MajorComponents • Spermatozoa • Seminal plasma containing: • Fructose • Citric acid • Fibrinogen-like proteins • Prostaglandins • Alkaline fluid • Enzymes • Zinc, calcium, magnesium • Semenogelin
- 76. Functions of ImportantComponents Component Function Fructose Primary energy source for sperm Prostaglandins Enhance sperm motility; help transport through female tract Alkaline pH Neutralizes vaginal acidity (pH 7.2–8.0) Enzymes (PSA) Liquefy semen after ejaculation Fibrinogen-like proteins Clot formation immediately after ejaculation Zinc & Ca²⁺ Sperm membrane stability & acrosome reaction
- 77. ROLE OF ACCESSORYGLANDS Seminal Vesicles Produce ~60% of semen: • Fructose • Prostaglandins • Fibrinogen • Vitamin C Functions: • Provide energy • Nurture sperm • Help cervical mucus thinning • Induce uterine contractions for sperm transport
- 78. Prostate Gland Produces 20–30%of semen: • Thin, milky, alkaline fluid • Contains citrate, phosphatase, zinc Functions: • Neutralizes vaginal acidity • Enhances sperm motility • Helps liquefaction of semen (PSA enzyme)
- 79. Bulbourethral Glands Secrete: • Mucus-likepre-ejaculate Functions: • Lubricates urethra • Neutralizes residual urine acidity
- 80. PHYSICAL & CHEMICALPROPERTIES OF SEMEN Physical Properties Property Normal Value Color Whitish-gray Odor Musky/Chlorine-like Viscosity Initially thick, then liquefies in 20–30 min Volume 2–5 mL per ejaculation pH 7.2–8.0
- 81. Chemical Properties • Richin fructose • Contains buffers (alkaline) • Enzymes: PSA (prostate-specific antigen), proteases • Mineral ions: Zinc, Ca, Mg • DNA from spermatozoa
- 82. FUNCTIONS OF SEMEN MainFunctions • Transport medium for sperm • Energy source (fructose) • Protection from vaginal acidity • Activation of sperm motility • Facilitates fertilization • Coagulation liquefaction cycle → aids deposition in vagina • Capacitation support (preparation for fertilization)
- 83. Importance of Alkalinity •Neutralizes vaginal pH (normally acidic at 3.5–4.0). • Sperm survive best at pH 7.2–8.0.
- 84. SEMEN ANALYSIS WHO NormalSemen Parameters (2021) Parameter Normal Value Volume ≥ 1.5 mL Sperm concentration ≥ 15 million/mL Total sperm count ≥ 39 million per ejaculate Motility ≥ 40% total OR ≥ 32% progressive Morphology ≥ 4% normal forms Vitality ≥ 58% live sperm Liquefaction time < 60 minutes pH ≥ 7.2
- 85. Abnormal Semen Parameters ConditionMeaning Oligospermia Low sperm count Azoospermia No sperm present Asthenospermia Poor motility Teratospermia Abnormal morphology Aspermia No semen volume Hypospermia Low semen volume
- 86. Causes of AbnormalSemen Quality • Varicocele • Hormonal imbalance • Smoking/alcohol/drugs • Heat exposure • Testicular injury • Infections • Genetic disorders
- 87. CLINICAL CONDITIONS Seminal FluidDisorders • Prostatitis affects pH & liquefaction → • Ejaculatory duct obstruction low volume → • Seminal vesicle damage low fructose → • Androgen deficiency reduced secretion →
- 88. HORMONES SECRETED BYTHE OVARY
- 89. Ovarian Hormones Main hormones: •Estrogen (estradiol, estrone, estriol) • Progesterone • Inhibin • Relaxin Produced by: • Graafian follicle • Corpus luteum • Placenta (during pregnancy)
- 90. ESTROGEN (The primaryfemale sex hormone) Types of Estrogen • Estradiol (E2) – most potent, reproductive age • Estrone (E1) – menopause • Estriol (E3) – pregnancy Major source: • Preovulatory follicle • Corpus luteum • Placenta (later)
- 91. FUNCTIONS OF ESTROGEN Effectson Reproductive Organs • Growth & maturation of ovaries • Growth of fallopian tubes • Thickening of endometrium (proliferative phase) • Growth of vagina & labia • Maintains vaginal epithelium • Increases cervical mucus (thin, watery – fertile mucus)
- 92. Breast Development • Estrogenstimulates: • Growth of breast ducts • Deposition of fat • Enlargement during puberty • (Progesterone develops alveoli – see later)
- 93. Secondary Sexual CharacteristicsResponsible for: • Feminine body shape (wide hips due to fat deposition) • Soft skin • High-pitched voice • Narrow shoulders • Breast development • Female-type fat distribution (breasts, thighs, hips)
- 94. Bone & SkeletonEffects • Stimulates bone growth during puberty • Inhibits osteoclasts prevents bone resorption → • Closes epiphyseal plates (end of height increase) • Deficiency osteoporosis (postmenopausal) →
- 95. Metabolic Actions • ↑Protein synthesis (anabolic) • ↑ HDL (“good” cholesterol) • ↓ LDL • Salt & water retention (mild) • Supports female metabolism and fertility.
- 96. Effects on MenstrualCycle During follicular phase: • Estrogen prepares endometrium for proliferation • High estrogen → LH surge ovulation →
- 97. Effects on Mood& Brain • Enhances serotonin improves mood → • Affects cognition and memory • Deficiency mood swings, irritability →
- 98. PROGESTERONE (“Hormone ofPregnancy”) Source of Progesterone - Produced mainly by: • Corpus luteum (after ovulation) • Placenta (after 3rd month of pregnancy) • Small amount from follicles and adrenal cortex.
- 99. FUNCTIONS OF PROGESTERONE Effectson Uterus Most important function: Converts proliferative endometrium into → secretory endometrium (nutrient-rich) Essential for implantation of fertilized ovum → Also: • ↓ Uterine contractions (prevents miscarriage) • Maintains pregnancy
- 100. Effects on Cervix •Thick, sticky cervical mucus prevents sperm entry → • Opposite action of estrogen Effects on Fallopian Tubes • Promotes secretion to nourish fertilized egg • Slows tubal motility to support early embryo transport
- 101. Effects on Breast •Develops lobules & alveoli • Prepares for milk secretion • Inhibits actual milk production until after delivery • Works with estrogen for complete breast maturation. Effects on Menstrual Cycle • Dominant hormone in luteal phase • Fall in progesterone → menstruation • Helps regulate ovulation feedback on LH/FSH
- 102. Body Temperature Regulation •Progesterone causes: Increase in basal body temperature by 0.5°C post-ovulation • Useful in ovulation testing Effects on Pregnancy • Maintains uterine lining • Suppresses uterine contractions • Supports fetal development • Relaxes smooth muscles ( constipation, reflux in → pregnancy)
- 103. OTHER OVARIAN HORMONES Inhibin •Produced by granulosa cells. • Functions: • Inhibits FSH secretion • Helps regulate follicular development
- 104. Relaxin - Producedby: • Corpus luteum • Placenta Functions: • Relaxes pelvic ligaments during pregnancy • Softens cervix for labor • Inhibits uterine contractions early in pregnancy
- 105. CLINICAL ASPECTS Estrogen Deficiency Seenin: • Menopause • Ovarian failure Effects: • Osteoporosis • Hot flashes • Vaginal dryness • Mood changes
- 106. Progesterone Deficiency Causes: • Repeatedmiscarriages • Luteal phase defects • Irregular cycles
- 107.
- 108. Definition • The menstrualcycle is the cyclic series of physiological changes in the female reproductive system that prepare the body for possible pregnancy. • Average duration: 28 days (normal range 21–35 days) • Day 1 = first day of menstruation.
- 109. COMPONENTS OF THEMENSTRUAL CYCLE Two Major Cycles 1. Ovarian Cycle Follicular phase Ovulation Luteal phase 2. Uterine (Endometrial) Cycle Menstrual phase Proliferative phase Secretory phase Both cycles are regulated by hormones.
- 111. OVARIAN CYCLE FOLLICULAR PHASE(Day 1–14) Events • Hypothalamus secretes GnRH • ↑ FSH stimulates growth of → primary follicles • Dominant follicle selected • Follicle produces estrogen
- 112. Hormonal Changes inFollicular Phase • FSH high initially then decreases → • LH slowly rising • Estrogen gradually increases reaches peak just before → ovulation
- 113. Functions of Estrogenin Follicular Phase • Proliferation of endometrium • Thinning of cervical mucus • Increases LH receptors in the dominant follicle • Prepares for LH surge
- 114. OVULATION (Around Day14) What Happens in Ovulation? • Graafian follicle ruptures • Releases secondary oocyte into fallopian tube • Triggered by LH surge
- 115. Why Does LHSurge Occur? • High estrogen (for ~48 hours) → positive feedback on hypothalamus → massive rise in → LH (= LH surge) • LH surge causes: • Follicle rupture • Resumption of meiosis • Formation of corpus luteum
- 116. Signs of Ovulation •Mittelschmerz (ovulation pain) • Slight rise in basal body temperature (0.5°C) • Thin, stretchy cervical mucus (spinnbarkeit) • LH peak in blood/urine
- 117. LUTEAL PHASE (Day15–28) Events • After ovulation follicle transforms into → corpus luteum • Corpus luteum secretes progesterone (dominant hormone) + estrogen
- 118. Hormonal Pattern • Progesteronehigh • Estrogen moderate • FSH & LH suppressed by negative feedback
- 119. If Fertilization DoesNot Occur • Corpus luteum degenerates corpus albicans → • Progesterone & estrogen levels fall • Endometrium sheds → menstruation
- 120. If Fertilization Occurs •hCG from trophoblast maintains corpus luteum • Progesterone remains high • Pregnancy maintained
- 121. UTERINE (ENDOMETRIAL) CYCLE MENSTRUALPHASE (Day 1–5) - Events • Shedding of superficial endometrial layer • Occurs due to fall in progesterone • Associated with menstrual bleeding (30–80 mL blood loss)
- 122. PROLIFERATIVE PHASE (Day6–14) Events • Under influence of estrogen • Endometrium regenerates and thickens • Glands become straight and narrow • Cervical mucus becomes thin & watery (helps sperm entry)
- 123. SECRETORY PHASE (Day15–28) Events • Under influence of progesterone • Endometrial glands become tortuous & secrete glycogen • Endometrium becomes highly vascular • Ideal environment for implantation • If pregnancy fails hormone levels drop menstruation → → resumes.
- 124. HORMONAL REGULATION OFMENSTRUAL CYCLE Hypothalamic–Pituitary–Ovarian Axis • Hypothalamus → GnRH (pulsatile) • Pituitary → FSH & LH • Ovary Estrogen & progesterone → • Negative & positive feedback mechanisms
- 125. Role of FSH •Stimulates follicle growth • Stimulates estrogen production Role of LH • LH surge ovulation → • Maintains corpus luteum • Stimulates progesterone secretion Role of Estrogen • Follicular phase proliferation • Positive feedback LH surge → • Endometrial thickening
- 126. Role of Progesterone •Secretory transformation • Inhibits uterine contractions • Maintains early pregnancy • Raises basal temperature
- 127. CHANGES DURING MENSTRUALCYCLE Basal Body Temperature • Progesterone raises body temperature by 0.5°C after ovulation • Useful in ovulation tracking Cervical Mucus Changes • Follicular phase thin mucus → • Ovulation egg-white stretchable mucus (maximum → fertility) • Luteal phase thick mucus (prevents sperm entry) →
- 128. Endometrial Changes Phase HormoneChange Menstrual Low E & P Shedding Proliferative Estrogen Thickening Secretory Progesterone Secretory, vascular
- 129. CLINICAL CONDITIONS Amenorrhea • Primary(never menstruated) • Secondary (absence for > 3 months) • Causes: PCOS, pregnancy, ovarian failure, pituitary tumors Dysmenorrhea • Painful menstruation due to prostaglandins. PMS & PMDD • Due to fluctuations in estrogen & progesterone.
- 130. HORMONAL BASIS OFMENSTRUAL CYCLE Hypothalamic–Pituitary–Ovarian (HPO) Axis Hormonal control involves: • Hypothalamus GnRH (pulsatile) → • Anterior Pituitary FSH & LH → • Ovary Estrogen & Progesterone → • Feedback modifies GnRH, FSH & LH secretion →
- 131. Pulsatile GnRH Secretion •GnRH released every 60–90 minutes • Pulsatile pattern is essential • Continuous GnRH suppresses cycle (medical use: GnRH → analog therapy)
- 132. HORMONAL CHANGES INTHE EARLY FOLLICULAR PHASE (DAY 1–5) Hormone Levels At the start of cycle: • Progesterone is low menstruation begins → • Estrogen low FSH rises → due to loss of negative feedback Effects • FSH stimulates primary follicle growth • Follicles begin secreting small amounts of estrogen • Endometrium is shedding (menstrual phase)
- 133. MID–LATE FOLLICULAR PHASE(DAY 6–13) Follicular Recruitment • FSH causes maturation of dominant follicle • Rising estrogen from follicles endometrial → proliferation
- 134. Hormone Interactions • Increasingestrogen = negative feedback lowers FSH → • Low FSH prevents other follicles from maturing (selects dominant follicle) • LH slowly rises due to estrogen sensitization
- 135. Effect on CervicalMucus • Estrogen makes mucus: • Thin • Watery • Stretchy • → helps sperm penetration (fertile window).
- 136. OVULATION (DAY ~14) EstrogenPositive Feedback • When estrogen remains high for 48 hours, it switches from negative to positive feedback. This causes: • The LH surge • Smaller rise in FSH
- 137. LH Surge LH surgetriggers: • Rupture of Graafian follicle • Release of oocyte • Completion of first meiotic division • Formation of corpus luteum • This is the most important hormonal event of the cycle.
- 138. Peri-Ovulatory Physical Changes Risein basal body temperature Peak cervical mucus stretchability Slight pelvic pain (mittelschmerz)
- 139. LUTEAL PHASE (DAY15–28) Corpus Luteum Formation • LH converts ruptured follicle into the corpus luteum which secretes: • Progesterone (dominant) • Moderate estrogen
- 140. Progesterone Actions • Convertsendometrium → secretory • Prepares uterus for implantation • Inhibits uterine contractions • Thickens cervical mucus • Raises basal body temperature
- 141. Negative Feedback • Highprogesterone + estrogen: • Inhibit GnRH • Suppress FSH & LH Prevents new follicle development during luteal phase. →
- 142. IF FERTILIZATION DOESNOT OCCUR Hormonal Withdrawal • Corpus luteum degenerates → Progesterone & estrogen levels fall sharply. Effects: • Spiral arteries constrict • Endometrium sheds → menstruation • Removal of negative feedback FSH rises new cycle → → begins
- 143. IF FERTILIZATION OCCURS Maintenanceof Corpus Luteum • The developing embryo (trophoblast) secretes hCG, which: • Maintains corpus luteum • Keeps progesterone levels high • Prevents menstruation
- 144. Shift to PlacentalHormones • By 10–12 weeks: Placenta takes over progesterone & estrogen production
- 145. HORMONAL BASIS OFUTERINE CHANGES Menstrual Phase Low estrogen & progesterone shedding. → Proliferative Phase Estrogen causes: Endometrial thickening Glandular proliferation Increased blood supply Secretory Phase Progesterone causes: Glands to become tortuous Glycogen secretion Highly vascular endometrium
- 146. Amenorrhea Causes • LowGnRH hypothalamic dysfunction → • Low FSH/LH pituitary disorders → • Ovarian failure low estrogen → PMS (Premenstrual Syndrome) Due to fluctuations in estrogen & progesterone.
- 147.
- 148. Definition Family planning refersto the practices that help individuals or couples: • Avoid unwanted pregnancies • Achieve desired spacing and number of children • Plan the timing of births • Improve maternal and child health
- 149. Importance • Reduces maternal& infant mortality • Controls population growth • Allows spacing between pregnancies • Improves women's education & career opportunities • Prevents adolescent pregnancy • Prevents sexually transmitted infections (STIs) (with barrier methods)
- 150. TYPES OF CONTRACEPTIVEMETHODS Classification Contraception is classified into: • Natural Methods • Barrier Methods • Hormonal Methods • Intrauterine Devices (IUDs) • Emergency Contraception • Permanent Methods (Sterilization)
- 151. NATURAL METHODS • Nodrugs or devices • Based on fertility awareness • Less reliable • Require discipline and regular cycles
- 152. Types of NaturalMethods • Rhythm method (Calendar method) • Basal Body Temperature method • Cervical mucus method (Billings method) • Coitus interruptus (withdrawal) • Lactational Amenorrhea Method (LAM)
- 153. Rhythm Method • Avoidintercourse on fertile days • Fertile window: Day 10–17 (in 28-day cycle) • Failure rate: 15–25%
- 154. Cervical Mucus Method •Observe thin, watery, stretchy mucus fertile period → • Avoid intercourse during fertile mucus • Failure rate: 20–30%
- 155. Basal Body Temperature •Body temperature rises 0.5°C after ovulation • Avoid intercourse until 3 days after temperature rise • Failure rate: 15–20%
- 156. Lactational Amenorrhea Method(LAM) Requirements: • Exclusive breastfeeding • Baby < 6 months • No return of menstruation Failure rate: 2% under strict conditions.
- 157. BARRIER METHODS Male Condom Advantages: •Prevents pregnancy • Protects against STIs & HIV • Easily available • Failure rate: 2% (perfect) / 13% (typical) Female Condom • Lines the vagina • Protection against STIs • Failure rate: 5–21%
- 158. Diaphragm & CervicalCap • Must be used with spermicides. Failure rate: 14–20%
- 159. INTRAUTERINE DEVICES (IUDs) Typesof IUDs • Copper IUDs (Cu-T 380A, Cu-375) • Hormonal IUDs (Levonorgestrel IUS – Mirena)
- 160. Copper IUD (Cu-T) Mechanism: •Copper ions toxic to sperm → • Prevent fertilization • Prevent implantation • Effectiveness: >99% Duration: • Cu-T 380A 10 years → • Cu-375 5 years → Side effects: • Heavier periods • Dysmenorrhea
- 161. Hormonal IUD (LNG-IUS) Mechanism: •Thickens cervical mucus • Thins endometrium • Suppresses ovulation (in some women) Advantages: • Decreases menstrual bleeding • Treats dysmenorrhea Failure rate: <1%
- 162. HORMONAL CONTRACEPTIVES Types • CombinedOral Contraceptive Pills (COCP) • Progestin-Only Pills (POP) • Injectable contraceptives (Depo-Provera) • Implants (Norplant, Nexplanon) • Transdermal patches • Vaginal rings
- 163. Combined Oral ContraceptivePills Contain: Estrogen + Progestin Mechanism: • Inhibit ovulation • Thicken cervical mucus • Thin endometrium Advantages: • Regular cycles • Reduces dysmenorrhea • Treats acne & PCOS Failure rate: 0.3% (perfect) / 7% (typical)
- 164. Progestin-Only Pills Mechanism: • Thickenscervical mucus • Suppresses ovulation variably Used when: • Breastfeeding • Estrogen contraindicated
- 165. Injectable Contraceptives • (DepotMedroxyprogesterone Acetate – DMPA) • Given every 3 months • Highly effective Side effects: • Irregular bleeding • Weight gain
- 166. Implants (Nexplanon) • Active for3 years • Very effective • Releases progestin continuously Failure rate: 0.1%
- 167. EMERGENCY CONTRACEPTION Options • Levonorgestrel(1.5 mg) – within 72 hours • Ulipristal acetate – within 120 hours • Copper-T IUD – within 5 days (most effective) Mechanism: • Delays ovulation • Prevents fertilization • Prevents implantation (Cu-T)
- 168. PERMANENT METHODS (STERILIZATION) FemaleSterilization (Tubal Ligation) • Fallopian tubes cut/blocked Effectiveness: >99% • Permanent prevention of pregnancy. Male Sterilization (Vasectomy) • Vas deferens cut/blocked Advantages: • Simple, safe, OPD procedure Failure rate: 0.15% • Sperm absent in semen after 3 months.
- 169. ADVANTAGES & LIMITATIONSOF FAMILY PLANNING Advantages • Prevents unintended pregnancy • Improves maternal & child health • Reduces unsafe abortions • Empowers women • Reduces population burden
- 170. Limitations / Challenges •Lack of awareness • Cultural & religious barriers • Access issues • Fear of side effects
- 171.