NORMAL AND ABNORMAL

MENSTRUATION
 MENSTRUAL CYCLE

Menstruation is the cyclical uterine

bleeding occurring during the reproductive
age between menarche to menopause with
cyclical changes in the endometrium which
may be regarded as a periodic preparation for
fertilization and pregnancy.

Normal Duration : 28 days

 HYPOTHALAMO-PITUITARY
OVARIAN AXIS
+
FSH ESTROGEN
-
GnRH
+
LH PROGESTRONE
-
(Hypothalamus) (pituitary) (ovary)
 PHASES OF MENSTRUATION

PHASES :

1. MENSTRUATION 1–4 DAYS

2. PROLIFERATIVE PHASE 5–13 DAYS
3. PHASE OF OVULATION 14th
DAY
4. SECRETORY PHASE 15–28 DAYS
 PROLIFERATIVE PHASE

• This phase is due to estrogen

• Corresponds to proliferative phase or
estrogenic phase of ovarian cycle
• Starts when regeneration of endometrium is
complete lasts until the 14th day of 28 days
cycle
• At the end of menstruation the endometrium is
represented by basal layer and its thickness is
about 1mm
• The uterine glands are short,straight,simple tubular
glands.

• Uterine glands grow in length and about the 10 th day

the glands become slightly sinous and their columnar
epithelium becomes taller than before.

• Epithelial cells also increase in number by mitosis and

stromal blood vessels of the endometrium also grow
with increase in number of coils.

Before ovulation the endometrial thickness becomes

5-6mm.
 OVULATION
 Occurs at the 14th day.
 Due to action of LH,the graffian follicle
ruptures and ovulates forming CORPUS
LUTEUM.
 LUTEAL PHASE
• Due to the action of progesterone
• Begins on the 15th day until the onset of
menstruation
CHANGES :
1. Development of subnuclear vacuolation - Day 17
2. Uterine glands become tortuous (cock screw) and
glycogen appears in the glandular lumen
Endometrial thickness : 8-10mm Day 19
3. Stromal edema-Day 21.
 Perivascular cuffing – Day 23
 Coiled arteries becoming more closely
wound,lymphocyte infilteration occur –Day 25

MENSTRUAL PHASE

 Lasts for 3-5 days

 Superficial endometrium becomes ischemic due
to vasoconstriction and blood stasis
 Tissue sloughs off and blood vessels open up
 HEMOSTASIS

Achieved in a normal menstruation by 2

mechanisms:

 Formation of platelet plug

 Constriction of spiral arterioles

Vasoconstriction is brought about by means of

prostaglandins
 DEFICIENT HEMOSTASIS

DUE TO:
 Disturbance in prostanoid metabolism
 Increased fibrinolysis in endometrium

NORMAL:
• In proliferative phase the endometrium
synthesizes equal amount of PGE2 & PGF2α
• In luteal phase PGF2α increases due to estradiol
& progesterone
PGF2α : PGE2 =2:1
Endometrium – PGF2α, PGE2 & PGD2
Myometrium – PGE2 from arachidonic acid &
endoperoxidases.

Phospholipid

Free Arachidonic Acid

Endoperoxides

PGE2 PGF2 α

PGI2
1. First, PGF2 α produces vasoconstriction

2. Endoperoxides from endometrium are deviated

to the myometrium which produces PGI2

3. This then diffuses back into endometrium

which causes vasodilation followed by
vasoconstriction of spiral arterioles preceding
menstruation
 WITHDRAWAL OF PROGESTERONE

BREAKDOWN OF LYSOSOMES

RELEASE OF PHOSPHOLIPASE A2

PROSTANOID CASCADE

PREDOMINATION OF VASOCONSTRICTOR PROSTANOIDS

ORDERLY BLEEDING
 ABNORMAL HEMOSTASIS IN
DUB
 Failure in vasoconstriction due to excessive
secretion of PGE2 & increase in PGE2 :PGF2α.

 Failure in formation of adequate thrombotic

plugs due to PGI2 excess.

 Increased fibrinolysis due to increase in the

tissue plasminogen activator.
 Increased endometrial lysosomal enzymes with
excessive prostanoid formation.

 Failure in vascular endothelial proliferation due

to relaxin.

 Delay in endometrial regeneration.

 O U
K Y
A N
TH