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Dysfunctional Uterine Bleeding (DUB)
- 1. DYSFUNCTIONAL UTERINE BLEEDING ‘PATHO –PHYSIOLOGY’ Dr Sonali Ingole Asst Professor OBGY
- 2. DUB : Definition •Abnormal uterine bleeding, in the absence of any demonstrable organic disease of the genital tract – Neoplasm – Infection – Pregnancy related complication • Abnormal uterine bleeding in the absence of genital tract pathology or medical illness • Abnormal uterine bleeding for which no specific cause has been found
- 3. DUB : Classification •Primary • Secondary – Thyroid dysfunction – Haematologic disorders • Thrombocytopenia • Von Willebrands disease • Leukemias – Hepatic dysfunction • Iatrogenic – IUCD – Progesterone only contraception – Low dose Combined OC pills
- 4. DUB • DUB occursmost often shortly after menarche and at the end of the reproductive years. –20% of cases are adolescents –50% of cases in 40-50 year olds • Diagnosis of EXCLUSION
- 5. DUB • Patients presentwith “Abnormal uterine bleeding”
- 6. NORMAL MENSTRUATION • Durationof flow : 2 – 7 days – Average duration : 4 – 6 days • Volume of flow : 20 – 70 ml – Average flow : 30 ml • Cycle length : 24 – 35 days* – Average cycle length : 28 – 30 days *Speroff L, Glass RH, Kase NG (Eds). Clinical Gynaecologic Endocrinology & Infertility. 7th Edn. Baltimore, 2005; 549 - 554
- 7. MENORRHAGIA • Volume offlow ≥ 80 ml • Duration of flow > 7 days • Bleeding occurs at regular intervals • Common causes – Fibroids – DUB – IUCD – Adenomyosis – Thyroid dysfunction – Pregnancy related bleeding
- 8. HYPOMENORRHOEA • Volume offlow < 10 ml • Duration of flow < 2 days • Common causes – Endometrial tuberculosis – Combined OC pill use – Ashermann’s syndrome – PCOD – Hyperprolactinemia
- 9. POLYMENORRHOEA • Frequent menses •Bleeding intervals < 24 days* • Common causes – PID – Endometriosis – DUB * Speroff L, Glass RH, Kase NG (Eds). Clinical Gynaecologic Endocrinology & Infertility. 7th Edn. Baltimore, 2005; 549 - 554
- 10. POLYMENORRHAGIA • Frequent &heavy / prolonged menses • Common causes – Fibroids uterus – PID – DUB – Endometriosis – Ovarian cysts
- 11. OLIGOMENORRHOEA • Infrequent menses •Bleeding intervals > 35 days, upto 6 months • Common causes – PCOD – DUB – Hyperprolactinemia – Ovarian cysts – Thyroid dysfunction – Stress & Exercise related ( Hypothalamic)
- 12. METRORRHAGIA / MENO- METRORRHAGIA •Irregular, acyclical bleeding / Heavy or prolonged irregular, acyclical bleeding • Common causes – Improper hormonal contraceptive use – DUB – Pregnancy related bleeding – Submucous fibroids & Fibroid polyps – Carcinoma cervix – Carcinoma endometrium – Progesterone only contraception
- 13. Genesis of normalmenstruation
- 14. Alternatives for estrogen– progesterone primed endometrium
- 15. Genesis of normalmenstrual flow • Estrogen – progesterone withdrawal due to luteolysis results in enzymatic auto-digestion of non-gestational hormonally primed endometrium which is then discharged as menstrual flow
- 16. Genesis of normalmenstrual flow : Role of vascular endothelium • Synthetic activity – Paracrine factors – Angiogenic factors – Vasoactive factors – Haemostatic factors • Modulation of – Vasoactivity – Haemostasis – Thrombolysis – Angiogenesis
- 17. Autocrine / paracrineregulation of gene transcription affecting vascular function
- 18. Effects of progesteronewithdrawal
- 19. Genesis of normalmenstrual flow • Cyclic vasomotor response of spiral arterioles (end arteries) in the endometrium
- 20. Genesis of normalmenstrual flow • Increasing duration and intensity of vasospasm results in ischaemic damage to endometrium and breakdown of tissue
- 21. Genesis of normalmenstrual flow • During periods of relaxation of vasospasm, blood extravasates though damaged vessel walls, cleaving the endometrium between stratum basalis and stratum spongiosum
- 22. Genesis of normalmenstrual flow • Progesterone withdrawal induces release of matrix metalloproteinases from the endometrial cells resulting in breakdown of cell membranes and extracellular matrix
- 23. Genesis of normalmenstrual flow • Endometrial tissue and extravasated blood are shed as menstrual flow
- 24. Haemostaisis within uterus •Vasospasm • Platelet plug • Thrombin generation in the basal endometrium • Re-epithelialization • Myometrial contractions do not play a part in controlling menstrual blood loss ( in contrast to control of post – partum hge)
- 25. Why is Estrogen– Progesterone withdrawal menstrual bleeding not heavy ? • It is a universal event occurring simultaneously throughout the entire endometrium
- 26. Why is Estrogen– Progesterone withdrawal menstrual bleeding not heavy ? • The endometrium primed with estrogen and progesterone is structurally stable and random breakdown due to fragility is avoided
- 27. Why is Estrogen– Progesterone withdrawal menstrual bleeding not heavy ? • Inherent in the events (vasospasm) that start the menstrual flow are the factors involved in stopping the menstrual flow
- 28. Why is Estrogen– Progesterone withdrawal menstrual bleeding not heavy ? • Denudation of the functional layers of the endometrium allows the reparative process of re-epithelializtion to begin from the stratum basalis
- 29. Dysfunctional Uterine Bleeding •Hormonally imbalanced conditions can give rise to abnormal uterine bleeding –Hyper-estrogenic state / Unopposed estrogen action –Hyper-progestogenic state / Abnormal progestogen – estrogen ratio
- 30. Dysfunctional Uterine Bleeding •Anovulatory – Estrogen withdrawal – Estrogen breakthrough • Threshold bleeding • Supra-threshold bleeding – Progesterone breakthrough • Ovulatory – Irregular ripening – Irregular shedding – Abnormal local haemostatic mechanisms
- 31. Estrogen withdrawal • Oneof the mechanisms of anovulatory uterine bleeding • Occurs on withdrawal of estrogen support to the endometrium • Common following menarche. Midcycle spotting can occur due to pre-ovulatory fall in E2 levels
- 32. Estrogen breakthrough bleeding •Threshold bleeding – The levels of E2 waver around the threshold below which endometrium cannot be supported – Results in intermittent / prolonged spotting – May occur at extremes of reproductive age
- 33. Estrogen breakthrough bleeding •Supra-threshold bleeding –Continuous E2 production unopposed by progesterone due to anovulation –Delayed periods followed by prolonged moderate to profuse bleeding –Endometrium thick without concomitant stromal structural support –Random breakdown common
- 34. Progesterone breakthrough bleeding • Seenin the presence of an unfavourably high ratio of progesterone to estrogen (use of progesterone only contraception) • Results in intermittent spotting of variable duration • Prolonged progestogenic exposure results in atrophic changes and altered gland –stromal ratio within the endometrium • Bleeding occurs from unsupported endometrial vessels
- 35. Progesterone withdrawal bleeding •Medical curettage • Poor compliance with progestogen therapy
- 36. Ovulatory DUB • Lutealphase insufficiency – Irregular ripening – Mixed proliferative - secretory patterns • Prolonged luteal function / Corpus luteum cysts – Irregular shedding / Delayed prolonged menses • Primary pathology of haemostatic processes
- 37. Mechanisms of DUB •Hyper-estrogenic / Hyper-progestogenic state • Abnormal angiogenesis and vascular fragility • Increased / Asynchronous tissue breakdown • Impaired haemostatic mechanisms • Impaired re-epithelialization
- 38.