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Human adloscent physiology

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Adloscent Education lecture for School Children

Adloscent Education lecture for School Children

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  • 1. DR. AVINASH BHONDWE
  • 2. Hormones  Hormones are chemicals released by cells that affect cells in other parts of the body  The endocrine system is a system of glands that involve the release of extracellular signaling molecules known as hormones.  The endocrine system is instrumental in regulating metabolism, growth, development and puberty, and tissue function and also plays a part in determining mood.  The field of study that deals with disorders of endocrine glands is endocrinology, a branch of the wider field of internal medicine.
  • 3. Hormones  A number of glands that signal each other in sequence is usually referred to as an axis, for example, the hypothalamic-pituitary-adrenal axis.  Typical endocrine glands are the pituitary, thyroid, and adrenal glands.  Features of endocrine glands are, in general, their ductless nature, their vascularity, and usually the presence of intracellular vacuoles or granules storing their hormones.  In contrast, exocrine glands, such as salivary glands, sweat glands, and glands within the gastrointestinal tract, tend to be much less vascular and have ducts or a hollow lumen. Also controls metabolism in our body system
  • 4. Effects of hormone  stimulation or inhibition of growth  mood swings  induction or suppression of apoptosis (programmed cell death)  activation or inhibition of the immune system  regulation of metabolism  preparation of the body for fighting, sex, fleeing, mating, and other activity  preparation of the body for a new phase of life, such as puberty, parenting, and menopause  control of the reproductive cycle
  • 5. Effects of hormone  A hormone may also regulate the production and release of other hormones. TSH, FSH  Hormone signals control the internal environment of the body through homeostasis
  • 6. HORMONE PRODUCING ORGANS 1. HYPOTHALAMUS 2. PITUTARY 3. THYROID 4. THYMUS 5. ADRENALS 6. PANCREAS 7. OVARIES 8. TESTES
  • 7. MALE ANATOMY
  • 8. THE MALE UROGENITAL TRACT Popad Rep Physiol MRP 8
  • 9. FEMALE ANATOMY
  • 10. VI. Pineal Gland A. Hormones Melatonin & Arginine vasotocin inhibits GnRH from hypoth. B. Trigger Photoperiod: increase secretion in dark C. Target Hypothalamus involved with sleep cycle affects the immune system
  • 11. Physiology of Reproduction I. Male reproductive physiology A. Structures 1. Testes a. Seminiferous tubules Sertoli cells - spermatogenesis secretes inhibin
  • 12. TESTIS: THE MALE GONAD VAS DEFERENS EPIDIDYMIS SEMENIFEROUS TUBULE RETE TESTIS EFFERENT DUCTULES Popad Rep Physiol MRP 13
  • 13. b. Connective tissue leydig cells- testosterone B. Spermatogenesis 1. Spermatogonia at puberty – divide (mitosis) 2. Primary spermatocytes Meiosis I -> secondary spermatocytes Meiosis II -> spermatids 3. Sertoli cells blood-testes barrier
  • 14. TESTES: ONE PAIR  HAS SEMENIFEROUS TUBULES:  SERTOLI CELLS  SPERMATOGONIA  SPERM CELLS IN VARIOUS STAGES  INTERSTITIAL CELLS OF LEYDIG:  SECRETE TESTOSTERONE, THE MALE REPRODUCTIVE HORMONE Popad Rep Physiol MRP 15
  • 15. DUCTULAR SYSTEM  RETE TESTIS  EFFERENT DUCTULES  EPIDIDYMIS  VAS DEFERENS  FUNCTION: TRANSPORT OF MATURE SPERMATOZOA. Popad Rep Physiol MRP 16
  • 16. GLANDS  SEMINAL VESICLES  PROSTATE GLAND:  BOTH SECRETING SEMEN  BULBO-URETHRAL GLANDS:  SECRETE A MUCOID SUBSTANCE Popad Rep Physiol MRP 17
  • 17. PENIS  ERECTILE:  DUE TO SPONGIOUS TISSUES  DUAL STATES:  FLACCID  ERECT  DUAL FUNCTIONS:  EXPULSION OF URINE  EXPULSION OF SEMEN Popad Rep Physiol MRP 18
  • 18. PENIS: DUAL STATES Popad Rep Physiol MRP 19
  • 19. SPERMATOGENESIS: some definitions  The production of spermatozoa which occurs in the sertoli cells of the semeniferous tubules is called as spermatogenesis.  The conversion of the spermatids into spermatozoa is called as spermiogenesis.  The release of the spermatazoon into the lumen of the semeniferous tubule is called as spermiation.  The final maturation of the spermatazoon which occurs in the female genital tract is called as capacitation. Popad Rep Physiol MRP 20
  • 20. FROM SPERMATID TO SPERM: SPERMIOGENESIS… Popad Rep Physiol MRP 21
  • 21. MALE REPRODUCTION: HORMONAL REGULATION HYPOTHALAMUS - ve feedback GONADOTROPIN RELEASING HORMONE ANTERIOR PITUITARY - ve feedback FSH LH TESTES S E LEYDIG CELL R T O TESTOSTERONE L I REP.TRACT CELL SPERMATOGENESIS & OTHER ORGANS INHIBIN Popad Rep Physiol MRP 22
  • 22. TESTOSTERONE - FUNCTIONS 1. INITIATION & MAINTAINANCE OF SPERMATOGENESIS. 2.  GnRH FROM THE HYPOTHALAMUS 3. INHIBITS LH SECRETION VIA ANTERIOR PITUITARY. 4. DIFFERENTIATION & MAINTAINANCE OF MALE SECONDARY SEXUAL CHARACTERISTICS:Facial Hair & Body Habitus. Popad Rep Physiol MRP 23
  • 23. TESTOSTERONE - FUNCTIONS 5. INDUCES DIFFERENTIATION & MAINTAINS ACCESSORY REPRODUCTIVE ORGANS. 6. STIMULATES PROTEIN ANABOLISM, BONE GROWTH & IT’S CESSATION. 7. ENHANCES LIBIDO & AGGRESSIVE BEHAVIOUR BY MASCULINIZING THE BRAIN. 8. STIMULATES SECRETION OF ERYTHROPOIETIN FROM THE KIDNEYS Popad Rep Physiol MRP 24
  • 24. Popad Rep Physiol MRP 25
  • 25. PENILE ERECTION: REFLEX PATHWAYS INPUT FROM THOUGHTS MECHANORECEPTORS EMOTIONS OF PENIS SIGHT, SMELL NEURONS TO PENIS NEURONS RELEASE GASEOUS NEUROTRANSMITTER NITRIC OXIDE INHIBITION ON SYMPATHETIC NEURONS DECREASED PENIS ARTERIAL DILATATION + VENOCOMPRESSION = ERECTION Popad Rep Physiol MRP 26
  • 26. FUNCTION OF PENIS IN COITUS (SEXUAL INTERCOURSE)  ERECTION  EJACULATION Popad Rep Physiol MRP 27
  • 27. ERECTION  VASCULAR:  SMALL ARTERIAL DILATATION  VENOCONSTRICTION  PARASYMPATHETIC FACILITATION (Point)  SYMPATHETIC INHIBITION  SMOOTH MUSCLES RELAX Popad Rep Physiol MRP 28
  • 28. EJACULATION  SYMPATHETIC FACILITATION (“Shoot”)  SKELETAL MUSCLES CONTRACT  HAS TWO EVENTS: 1. EMISSION: SMOOTH MUSCLES CONTRACT & SEMEN SENT INTO URETHRA 2. EXPULSION: RAPID CONTRACTION OF URETHRAL SMOOTH MUSCLES & SEMEN IS SENT OUT OF THE PENIS. Popad Rep Physiol MRP 29
  • 29. MALE REPRODUCTIVE ABNORMALITIES  CRYPTORCHIDISM (UNDESCENDED TESTES)  THE DESCENT OF TESTES IS INCOMPLETE IN 10% OF NEONATES  SPONTANEOUS DESCENT OCCURS LATER  INCIDENCE: 2% AT INFANCY & 0.3% AFTER PUBERTY  COMPLICATIONS: INCREASED INCIDENCE OF TESTICULAR MALIGNANCIES & INFERTILITY. Popad Rep Physiol MRP 30
  • 30. CRYPTORCHIDISM Popad Rep Physiol MRP 31
  • 31. MALE HYPOGONADISM  HYPERGONADOTROPIC:  IN THIS CONDITION THE GONADOTROPINS ARE INCRESED IN CIRCULATION  THE LESION IS AT THE TESTES.  HYPOGONADOTROPIC:  A PITUITARY OR HYPOTHALAMIC DISORDER  KALLMAN’S SYNDROME. Popad Rep Physiol MRP 32
  • 32. EUNUCHOIDISM  DEFICIENCY OF LEYDIG CELLS FROM CHILDHOOD.  TALL, NARROW SHOULDERS  SMALL MUSCLES  FEMININE HABITUS  SMALL GENITALIA  HIGH PITCHED VOICE  FEMALE PATTERN PUBIC HAIR Popad Rep Physiol MRP 33
  • 33. PENILE ABNORMALITIES  HYPOSPADIAS: URETHRAL ORIFICE VENTRAL TO THE SHAFT.  EPISPADIAS: ORIFICE DORSAL TO THE SHAFT.  COMPLICATIONS: INFERTILITY Popad Rep Physiol MRP 34
  • 34. HYPOSPADIAS Popad Rep Physiol MRP 35
  • 35. KLINEFELTERS SYNDROME  ALSO CALLED  TESTOSTERONE SEMENIFEROUS ENOUGH FOR TUBULE DYSGENESIS SEC.SEXUAL  MOST COMMON SEX FEATURES CHROMOSOMAL  SEMENIFEROUS DISORDER TUBULES ARE  EXTERNAL ABNORMAL GENITALIA LIKE  INFERTILITY NORMAL MALES  INCIDENCE OF MENTAL RETARDATION MORE Popad Rep Physiol MRP 36
  • 36. K L I S N Y E N F D E R L T O E M R E S Popad Rep Physiol MRP 37
  • 37. C. Hormonal control 1. GnRH - hypothalamus every 2 hrs 2. FSH & LH from Ant Pit FSH – targets sertoli cells -> stimulate spermatogenesis LH – targets Leydig cells -> testosterone 3. Negative feedback Testosterone inhibits GnRH and LH Inhibin inhibits FSH
  • 38. Female Reproductive Physiology A. Structure 1. Ovaries B. Oogenesis 1. Oogonia under go Mitosis (as fetus) 2. Primary oocytes result of Mitosis infant - all primary oocytes
  • 39. Timing events in the menstrual cycle. 1. Onset of menstruation Day 1 Day 1 0 4 8 12 16 20 24 28 Menstruation
  • 40. Timing events in the menstrual cycle. 2. LH surge LH Days before Days after Day 1 Day 1 Follicular Luteal phase phase 0 4 8 12 16 20 24 28 Menstruation OVULATION
  • 41. Animated ovarian events Key events in the ovarian cycle LH 1. Follicular Day 1 growth 0 4 8 12 16 20 24 28 Menstruation Oestradiol OVULATION
  • 42. Animated ovarian events Key events in the ovarian cycle 2. Ovulation LH 1. Follicular Day 1 growth 0 4 8 12 16 20 24 28 Menstruation Oestradiol OVULATION
  • 43. Animated ovarian events Key events in the ovarian cycle 2. Ovulation LH 1. Follicular 3. Luteal Day 1 growth function 0 4 8 12 16 20 24 28 Menstruation Progesterone Oestradiol (and oestradiol) OVULATION
  • 44. Animated ovarian events Key events in the ovarian cycle 2. Ovulation LH 1. Follicular 3. Luteal Day 1 growth function 4. Luteal regression 0 4 8 12 16 20 24 28 Menstruation Progesterone Oestradiol (and oestradiol) OVULATION
  • 45. What controls Hypothalamus follicular growth? GnRH(gonadotrophin Pituitary releasing hormone) LH (“gonadotrophins” FSH ) Steroid feedback Ovaries + Oestradiol (E2) + Reproductive tract Other targets
  • 46. Polycystic ovaries The classical picture of PCO: a string of follicles, 2-8 mm in diameter Section of ovary showing multiple follicles Ultrasound of ovary showing multiple in PCO follicles
  • 47. 4. The disturbed steroid feedback re-inforces the abnormal LH/FSH secretion 1. Raised LH, lowered FSH 3. The high LH induces high androgen secretion from the theca 2. ….. leads to disturbed follic growth HIRSUTISM ANOVULATION Disturbed cycles
  • 48. Other changes in the cycle a) Outer muscle layer – the myometrium b) Inner glandular mucosa – the endometrium
  • 49. Uterine changes in the menstrual cycle. Endometri al depth More secretion from the glands – hence Oestradiol the term “secretory causes an phase” increase in thickness (the “proliferative phase”) 0 4 8 12 16 20 24 28 Menstruation OVULATION
  • 50. Terminal differentiation of stromal cells – “decidualisation” Characteristic “spiral arteries” 0 4 8 12 16 20 24 28 Optimal time for Menstruation implantation
  • 51. Menstruation - WHY? In preparation for pregnancy, the human uterine stromal cells go through complex changes and the stromal cells terminal differentiate - “Decidualization”. If implantation and pregnancy do not occur, this tissue is lost - and the uterus prepares itself again for another possible pregnancy.
  • 52. 19 Nov. 2008 Fertilization.ppt 55
  • 53. Coitus & Sperm Transfer  2-3 phases  Erection/engorgement: Parasympathetic reflex  Plateau  Orgasm: Sympathetic reflex  Heart rate, contractility increase (pulse & BP)  Intense pleasure  Ejaculation by male 19 Nov. 2008 Fertilization.ppt 56
  • 54. Fertilization  Contact of sperm & secondary oocyte occurs in uterine tube  Sperm penetration  Oocyte completes meiosis II  Nuclear fusion 19 Nov. 2008 Fertilization.ppt 57
  • 55. Fertilization  Sperm penetration  Why so many? 19 Nov. 2008 Fertilization.ppt 58
  • 56. Early Development  Implantation  6-7 days after fertilization  Trophoblast forms placenta  “Inner cell mass” forms embryo  (pp. 1118-1119) 19 Nov. 2008 Fertilization.ppt 59
  • 57. Early Development  Placenta  Provides large area for exchange of O2, CO2, nutrients, metabolic wastes between fetal and maternal blood 19 Nov. 2008 Fertilization.ppt 60
  • 58. Labor & Delivery  Dilation  Cervix dilates to ~ 10 cm diameter  Effacement  Descent of fetus into birth canal (“Station”)  Expulsion  Placental stage  “afterbirth” 19 Nov. 2008 Fertilization.ppt 61
  • 59. Many people also see "sex change" as factually inaccurate. Sex in humans is usually determined by four factors: 1. Chromosomes 2. Gonads (Ovaries and/or testicles) 3. Hormone status 4. Primary sex characteristics, 5. secondary sex characteristics
  • 60. SEX CHANGE  Not all of these  Existing sex characteristics can to some extent be changed; factors can be  existing ones mostly through changed, however: surgery,  Chromosomes cannot  non-existing ones can be induced be changed. to grow through hormones.  Gonads can be  Changing a male genital anatomy removed, but not into a good or even excellent female appearing and functioning replaced one is complicated, but entirely  Hormone status is possible; easily changed  Changing a female genital  Existing sex anatomy into an even reasonably male appearing one however is characteristics can to extremely complicated and not some extent be successful very often; function is changed always limited.