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Female Infertility

Female Infertility. Infertility. In order for a woman to become pregnant: Egg must be released from one of her ovaries (ovulation) Egg must be picked up from the ovary and travel through the fallopian tube toward the uterus

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Female Infertility

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  1. Female Infertility

  2. Infertility • In order for a woman to become pregnant: • Egg must be released from one of her ovaries (ovulation) • Egg must be picked up from the ovary and travel through the fallopian tube toward the uterus • Sperm must fertilise the egg in the fallopian tube (fertilization) • Fertilized egg must attach to the uterine wall (implantation) • Infertility can result from problems that interfere with any of these steps.

  3. DEFINITION • Failure to conceive within one year of regular unprotected intercourse. • Interval shortened to 6 months - after the age of 35 yrs in woman and 40 yrs in man..

  4. CLASSIFICATION • Primary Infertility :- Patients who have never conceived. • Secondary Infertility :- Indicates previous pregnancy but failure to conceive subsequently.

  5. FECUNDABILITY Probability of achieving a pregnancy within one menstrual cycle. In a normal couple it is 20 % On this basis about 90% of couples should conceive within 12 months of unprotected intercourse. FECUNDITY Probability of achieving a live birth within single cycle.

  6. INCIDENCE 10 - 15 % of the couples • Male Factor 25 – 40 % • Both Male and Female Factor 10 % • Female Factor 40 –55 % • Unexplained Infertility 10 %

  7. Prevalence Of Causes Of Infertility • Tubal / Peritoneal factor - 25 – 35 % • Ovarian Factor - 15 – 25 % • Uterine Factor - 10 % • Cervical Factor - 5 % • Miscellaneous - 10 – 15 % • Unexplained Infertility - 10 – 15 %

  8. ETIOLOGY • Age • Life Style and Environmental Factors • Endocrinopathies • Ovarian Factor - Anovulation. -Luteal Phase Defect. - LuteinisedUnruptured Follicle.

  9. 5. Tubal Factors and Peritoneal Factors a)Tubal Occlusion PID b)Adnexal Adhesions Endometriosis Previous Surgery

  10. 6. Uterine Factors -Congenital Malformations -Leiomyoma -Intra Uterine Adhesions/ Asherman’s syndrome -Endometrial polyp -Chronic Endometritis

  11. 7. CERVICAL FACTORS ANATOMIC -Congenital Elongation of Cervix -Second Degree Uterine prolapse -Acute Retroverted Uterus - Cervical Canal Occluded by Polyp -Cervical stenosis

  12. b)PHYSIOLOGIC : Fault in composition of cervical mucus Mucus Scanty * Amputation * Conisation * Deep Cauterisation of cervix Excessive Mucus ( Viscous / Purulent ) Chronic Cervicitis Immunologic Factors Antisperm Antibodies

  13. 8. Vaginal Factors -Atresia of Vagina (Partial / complete) -Transverse Vaginal Septum -Septate Vagina -Narrow Rigid Introitus -Vaginismus

  14. AGE Infertility Incidence 25 – 29 yrs = 4 –8 % 30 – 34 yrs = 15 – 19 % 35 – 39 yrs = 26 – 46 % 40 – 45 yrs = 95 %

  15. During reproductive life, the rate of follicular depletion is relatively constant and gradual until 37 – 38 yrs( approximately 25000 oocytes remain ) then accelerate over 10 – 15 yrs preceding menopause Menopause occur when the number of remaining follicles fall below a critical threshold(approximately 1000) regardless of age.

  16. LIFE STYLE & ENVIRONMENTAL FACT. SMOKING: ACCELERATES FOLLICULAR DEPLETION GAMETE OR EMBRYO MUTAGENESIS MENSTRUAL IRREGULARITIES MARIJUANA: INHIBIT GnRH SECRETION ALCOHOL : DECREASES FERTILITY

  17. OBESITY: INCREASE IN ESTROGENS & ANDROGENS : 1. ADIPOSE TISSUE:ANDROSTENEDIONEESTRONE TESTOSTERONEESTRADIOL(E2) 2. HEPATIC: INCREASE FREE TESTOSTERONE , CAUSES DECREASE IN SHBG. 3. OVARY: STROMAL TISSUE ANDROGENS STIMULATING FACTORS: HIGH INSULIN & DHEAS LEVELS. 4. ADRENALS: INCREASE ANDROGENS.

  18. WEIGHT LOSS & STRESS: HYPOTHALAMIC AMENORRHOEA. • WEIGHT LOSS: *MINIMUM % OF FAT FOR MAINTENANCE OF NORMAL CYCLES: 22% *FOR INITIATING MENARCHE: 17% • SUDDEN WEIGHT LOSS: LACK OF PULSE OF GnRH FROM HYPOTHALAMUS • LH & FSH LOW • LOW LEVELS OF ESTRADIOL.

  19. STRESS : - INCREASE IN “STRESS HORMONES” CORTISOL, CATECHOLAMINES, BETA-ENDORPHINS & PROLACTINS  GnRH DECREASE.

  20. ENDOCRINOPATHIES • HYPERPROLACTINEMIA: 1.INHIBIT GnRH PULSE SECRETION 2. INHIBIT OVARIAN STEROIDOGENESIS Inhibits aromatisation of Testosterone to oestrodiol within the follicle – ANDROGENIC ENVIRONMENT 3. INHIBIT PROGESTERONE SYNTHESIS in corpus luteum

  21. HYPOTHYROIDISM Decreased SHBG & Increased free Oestradiol and Testosterone which leads to • Inhibit ovarian follicular development • Pituitary/ Hypothalamic dysfunction from excess androgens and oestrogen

  22. HYPERTHYROIDISM Causes increased SHBG and decreased free oestradiol and androgen,therefore metabolic clearance rate is decreased therefore infertility due to hormone level alteration

  23. OVARIAN FACTORS • ANOVULATION • LUTEAL PHASE DEFECT (LPD) • LUTEINISED UNRUPTURED FOLLICLE (LUF)

  24. PCOD IT’S A STATE OF ANDROGEN EXCESS AND CHRONIC ANOVULATION

  25. LUTEAL PHASE DEFECT Defined as abnormality of corpus luteum function with insufficient progesterone production Life span of corpus luteum is shortened to less than 10 days..

  26. ETIOLOGY 1.WEIGHT LOSS AND STRESS 2.ENDOCRINOPATHIES -Hypothyroidism -Hyperthyroidism -Hyperprolactenemia 3.DRUGS USED FOR OVULATION -Clomiphene Citrate -Gonandotrophins

  27. PATHOPHYSIOLOGY - Delayed endometrial maturation - Failed or late implantation

  28. LUTENISED UNRUPTURED FOLLICLE OVUM IS TRAPPED INSIDE THE FOLLICLE WHICH GET LUTEINISED. CAUSE: NOT KNOWN. MAY BE ASSOCIATED WITH ENDROMETRIOSIS, HYPERPROLACTINEMIA, NSAID’S

  29. TUBAL FACTORS: PELVIC ENDOMETRIOSIS CAUSE OF INFERTILITY: 1.TUBAL OCCLUSION DUE TO ADHESIONS 2. ADHESIONS PREVENT OVUM MIGRATION.

  30. 3.EXTENSIVE DESTRUCTION OF OVARIAN TISSUE OR REPLACEMENT BY ENDOMETRIOSIS CYST- INTERFERE WITH OVULATION

  31. 4. DYSPAREUNIA 5. ROLE OF PROSTAGLANDINS: ENDOMETRIAL TISSUE PRODUCES THROMBOXANE A2 & PROSTACYCLIN(PGI 2)  INHIBIT OVULATION. 6. IMMUNOLOGICAL FACTOR:PERITONEAL MACROPHAGES NORAMLLY REMOVE MENSTRUAL DEBRIS BY PHAGOCYTOSIS. IN ENDOMETRIOSIS ACTIVATED MACROPHAGES SECRETES CYTOKINES, IL-4, INTEGRINS - REDUCES SPERM MOTILITY INCREASE SPERM PHAGOCYTOSIS.

  32. UTERINE FACTORS • FIBROID: -DISTORTION & OR ELONGATION OF CAVITY  DIFFICULT SPERM ASCENT. • ELONGATION & DILATATION OF ENDOMETRIAL VENOUS PLEXUSES  DIFFICULT NIDATION. • ATROPHY & ULCERATION OF ENDOMETRIUM OVER FIBROID.

  33. History and evaluation • Age • Occupation • Infertility duration • Frequency of intercourse/sexual dysfunction • Detailed menstrual history • Prior pregnancies IUD’s, OCP’s, • Fertility in other relationships

  34. Gynecologic history (PID, endometriosis, fibroids, ) • Medical and surgical history • Medications • General physical examination: development of secondary sexual characters breast and thyroid examination body mass index • Systemic examination: CVS ,RS PER ABDOMEN LOCAL EXAMINATION PER SPECULUM PER VAGINAL

  35. INVESTIGATIONS. • OBJECTIVE OF INVESTIGATIONS: • TO DISCOVER ANY AETIOLOGICAL FACTORS • TO RECTIFY ABNORMALITY IN AN ATTEMPT TO IMPROVE INFERTILITY. • TO GIVE ASSURANCE WITH EXPLANATION TO THE COUPLE IF NO ABNORMALITY DETECTED.

  36. WHEN TO INVESTIGATE? -ONE YEAR AFTER REGULAR UNPROTECTED INTERCOURSE. - INTERVAL SHORTENED TO 6 MINTHS AFTER AGE OF 35 YRS WOMEN & 40 YRS OF MEN.

  37. INVESTIGATIONS REQUIRED 1. OVARIAN FACTORS 2. TUBAL FACTORS 3. UTERINE FACTORS 4. CERVICAL FACTORS. 5. ENDOCRINOPATHY 6. IMMUNOLOGICAL FACTORS

  38. OVARIAN FACTORS. • THREE IMPORTANT FACTORS ARE • ANOVULATION • LUTEAL PHASE DEFECT (LPD) • LUTEINISED UNRUPTURED FOLLICLE(LUP)

  39. DIAGNOSIS OF OVULATION • INDIRECT • DIRECT.

  40. INDIRECT .MENSTRUAL HISTORY .EVALUATION OF PERIPHERAL OR ENDORGAN CHANGE - BASAL BODY TEMPERATURE - CERVICAL MUCUS STUDY - VAGINAL CYTOLOGY -HORMONE ESTIMATION SERUM PROGESTERONE SERUM LH SERUM OESTRADIOL. -ENDOMETRIAL BIOPSY -SONOGRAPHY

  41. DIRECT - LAPROSCOPY.

  42. INDIRECT • MENSTRUAL HISTORY: -REGULAR NORMAL MENSTRUAL LOSS -MIDMENSTRUAL BLEEDING(SPOTTING) OR PAIN OR EXCESSIVE MUCOID VAGINAL DISCHARGE (MITTELSCHMERZ SYNDROME). -SPASMODIC DYSMENORRHOEA.

  43. EVALUATION OF PERIPHERAL OR ENDORGAN CHANGES. • BASAL BODY TEMPERATURE: OBSERVATION– “BIPHASIC PATTERN” OF TEMP IN OVULATORY CYCLE; IF PREGNANCY OCCURS- SUSTAIN RISE OF TEMPERATURE. IF ANOVULATION – NO TEMP RISE

  44. INTERPRETATION • IN FOLLICULAR PHASE: TEMP FLUCTUATE BETWEEN 97.0 & 98.0 F • AFTER OVULATION RAISED TO 0.5 TO 1.0 F • RISE SUSTAIN THROUGH OUT THE SECOND HALF & FALLS ABOUT 2 DAYS PRIOR TO NEXT PERIOD CALLED “ BIPHASIC PATTERN” • BBT FALLS TO ITS LOWEST ON THE DAY BEFORE OR DAY OF OVULATION. • DEMONSTRABLE RISE ABOUT 2 DAYS AFTER LH PEAK WITH PERIPHERAL LEVEL OF PROGESTERONE >4 ng/ml

  45. CLINICAL IMPORTANCE • 1..DETERMINESOVULATION • 2.DETERMINES TIME FOR POST COITAL TEST • 3.TIME FOR ENDOMETRIAL BIOPSY FOR OVULATION • 4. CERVICAL MUCUS STUDY • 5. VAGINAL CYTOLOGY STUDY/

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