A brief note on WHAT causes AUB and WHY it does so.

1. AETIOPATHOGENESIS
OF
ABNORMAL UTERINE BLEEDING
K. MANIEVELRAAMAN
FINAL YEAR MBBS
MADRAS MEDICAL COLLEGE

2. AUB IS A SYMPTOM; NOT A DISEASE

3. AETIOLOGY
CLASSIFIED AS
• ORGANIC CAUSES
• Systemic
• Local ( pelvic )
• Iatrogenic
• DYSFUNCTIONAL ( DUB )
• Anovulatory
• Ovulatory

4. SYSTEMIC CAUSES
• BLOOD DYSCRASIA
• LEUKEMIA
• THROMOCYTOPENIC PURPURA
• SEVERE ANEMIA
• COAGULATION DISORDERS
• VON WILLEBRAND’S DISEASE
• THYROID DYSFUNCTION
• HYPOTHYROIDISM
• HYPERTHYROIDISM ( INITIAL STAGE)
• TUBERCULOSIS OF GENITAL TRACT
• LIVER AND KIDNEY DISORDERS

5.  VWD is the most common inherited
bleeding disorder with a prevalence of
approximately 1 in 100; and 1 in 1000 is
symptomatic.

6. LOCAL ( PELVIC ) CAUSES
• OBSTETRIC CAUSES
• ABORTION
• ECTOPIC PREGNANCY
• HYDATIDIFORM MOLE
• ENDOMETRIAL CAUSES
• FIBROID
• POLYP
• ADENOMYOSIS
• ENDOMETRIAL HYPERPLASIA
• CA ENDOMETRIUM

7. • CERVICAL CAUSES
• POLYP
• ENDOMETRIOSIS
• CERVICITIS
• CA CERVIX
• OVARY
• OVARIAN TUMOUR
• PCOD
• CHOCOLATE CYST ( ENDOMETRIOSIS)

8. • VASCULAR ( trauma following D&C)
• UTERINE AV FISTULA
• VARICOSITY OF VASCULATURE
• INFLAMMATION
• SALPINGO-OOPHORITIS
• PID
• GENITAL TB

9. IATROGENIC CAUSES
• INTRAUTERINE DEVICES
• OCP – MINI PILLS
• PSYCHOTROPIC DRUGS

12. Increased VASCULARITY
Increased endometrial
SURFACE AREA
Impeded uterine
CONTRACTIONS with
menstruation
 CLOTTING less efficient
locally

15. FIGO CLASSIFICATION OF CAUSES

18. PATHOPHYSIOLOGY
 Endometrium normally produces Prostaglandins (PGs)
from the arachidonic acid.
 Such PGs include : PGE2, PGI2, PGF2α, Thromboxane A2
PGE2 & PGI2  Vasodilation & Platelet aggregation
PGF2α, Thromboxane A2  Vasoconstriction
Platelet aggregation
Progesterone is responsible for the production of PGF2α

19. • In PRE-OVULATORY phase, endometrial proliferation
occurs under the effect of estrogen. (PGF2α /PGE2 : 1)
• In POST-OVULATORY phase, progesterone causes
endometrial differentiation and stabilisation.
(PGF2α/PGE2=2:1)
• As long as progesterone (in optimum levels) is provided by corpus
luteum, this phase maintains.
• Once corpus luteum ceases to function  MENSES

20.  Absence of progesterone
Absence of PGF2α
Relative in PGE2
 Tissue Plasminogen
Activator ( TPA)
 Endothelin
PATHOGENESIS

21. DYSFUNCTIONAL UTERINE BLEEDING
 Abnormal heavy menstrual bleeding in the
absence of organic lesions of the genital tract
 Absence of pregnancy
 It’s due to changes in HORMONE levels

22. DYSFUNCTIONAL UTERINE BLEEDING
ANOVULATORY
80%
OVULATORY
20%

23. ANOVULATORY - DUB
CAUSE FOR ANOVULATION CAN BE
• Hyper androgenic anovulation ( PCOS, CAH, Androgen producing tumours)
• Hypothalamic dysfunction ( stress, anorexia, exercise)
• Hyperprolactinemia
• Hypothyroid
• Primary pituitary disease
• Premature ovarian failure
• Secondary to radiation and chemotherapy

24. ANOVULATORY - DUB
PATHOGENESIS
• ESTROGEN WITHDRAWAL (sudden decrease in estrogen levels- following bilateral
oophorectomy, cessation of exogenous estrogen therapy, or just before ovulation in the normal menstrual cycle)
• ESTROGEN BREAKTHROUGH (Estrogen breakthrough bleeding occurs when excess
estrogen causes the endometrium to grow in an undifferentiated manner; thick without stromal support)
• PROGESTERONE BREAKTHROUGH (when the progesterone/estrogen ratio is
high, leading to an atrophic and ulcerated endometrium; progestogen only pills)

25. METROPATHIA HAEMORRHAGICA
• ANOVULATORY AUB
• PAINLESS bleeding preceded by AMENORRHOEA
• 40 – 45 yrs of age
• UNIFORMLY ENLARGED UTERUS
• SWISS CHEESE PATTERN endometrium (CYSTIC GLANDULAR HYPERPLASIA)

26. OVULATORY - DUB
PATHOGENESIS
• LUTEAL PHASE INSUFFICIENCY
• Irregular ripening ( deficient progesterone support- resulting in breakthrough bleeding
before actual menstruation)
• PROLONGED LUTEAL FUNCTION
• Irregular shedding ( lag in shedding of secretory endometrium; prolonged 7+ days)
Primary pathology of HEMOSTATIC processes