Physiology Of Menstruation
By: Nur Afiqah Binti Jasmi (11-2013-031) & Luqman Hakim Bin Mohd Jais (11-2013-170)
Dokter Pembimbing: Dr. Harianto Wijaya Sp.OG
This PPT covers Anatomy and Physiology of Female reproductive system. Anatomy of female reproductive organs, oogenesis, hormonal regulation of ovaries and Female reproductive cycle (Mentrual cycle) are explained.
PHYSIOLOGY OF MENSTRUATION
Introduction :
Typically, a woman of childbearing age should menstruate every 28 days or so unless she's pregnant or moving into menopause. But numerous things can wrong with the normal menstrual cycle.
Definition:
Menstruation means cyclic uterine bleeding caused by shedding of progestational endometrium it occurs between menarche and menopause
Menstruation (also called menstrual bleeding, menses, or a period)
Characteristics of normal menstruation
1-Menarche: 10-16 years. average 13 years.
2-Duration: 2-7 days (<2days>7 days is menorrhagia
3-Amount: 30-80 ml., uses 3 napkins per day, >80 ml. is menorrhagia and < 30 ml. is hypomenorrhea.
4-Normally menstrual blood doesn’t coagulate as a result of secretion of fibrinolysin enzyme (plasmin) secreted by the endometrium.
5-Menstrual molimina refers to mild symptoms of 7-10 days before menstruation relieved once menstruation occurs exaggerated condition called (premenstrual syndrome).
The hypothalamic-pituitary-ovarian axis:
There are two main components of the menstrual cycle,
1. the changes that happen in the ovaries in response to pituitary hormones (the ovarian cycle)
2. and the variations that take place in the uterus,
but it is important to remember that both cycles work together simultaneously to produce the menstrual cycle.
Changes in cervical mucus also take place during the course of the menstrual cycle.
Physiology Of Menstruation
By: Nur Afiqah Binti Jasmi (11-2013-031) & Luqman Hakim Bin Mohd Jais (11-2013-170)
Dokter Pembimbing: Dr. Harianto Wijaya Sp.OG
This PPT covers Anatomy and Physiology of Female reproductive system. Anatomy of female reproductive organs, oogenesis, hormonal regulation of ovaries and Female reproductive cycle (Mentrual cycle) are explained.
PHYSIOLOGY OF MENSTRUATION
Introduction :
Typically, a woman of childbearing age should menstruate every 28 days or so unless she's pregnant or moving into menopause. But numerous things can wrong with the normal menstrual cycle.
Definition:
Menstruation means cyclic uterine bleeding caused by shedding of progestational endometrium it occurs between menarche and menopause
Menstruation (also called menstrual bleeding, menses, or a period)
Characteristics of normal menstruation
1-Menarche: 10-16 years. average 13 years.
2-Duration: 2-7 days (<2days>7 days is menorrhagia
3-Amount: 30-80 ml., uses 3 napkins per day, >80 ml. is menorrhagia and < 30 ml. is hypomenorrhea.
4-Normally menstrual blood doesn’t coagulate as a result of secretion of fibrinolysin enzyme (plasmin) secreted by the endometrium.
5-Menstrual molimina refers to mild symptoms of 7-10 days before menstruation relieved once menstruation occurs exaggerated condition called (premenstrual syndrome).
The hypothalamic-pituitary-ovarian axis:
There are two main components of the menstrual cycle,
1. the changes that happen in the ovaries in response to pituitary hormones (the ovarian cycle)
2. and the variations that take place in the uterus,
but it is important to remember that both cycles work together simultaneously to produce the menstrual cycle.
Changes in cervical mucus also take place during the course of the menstrual cycle.
Although the events that regulate the ovarian and endometrial cycles are complex, a clear understanding of the basic physiology of the cycle will improve the management of menstrual disorders.
Ovarian cycle (the guyton and hall physiology)Maryam Fida
Ovarian cycle
The germ cells that migrate into the ovaries during early embryonic development multiply, so that by about 5 months of gestation (prenatal life) the ovaries contain approximately 6 million to 7 million oogonia.
Most of these oogonia die prenatally through a process of apoptosis.
The production of new oogonia stops at this point and never resumes again.
The oogonia begin meiosis toward the end of gestation, at which time they are called primary oocytes.
Like spermatogenesis in the prenatal male, oogenesis is arrested at prophase I of the first meiotic division.
The primary oocytes are thus still diploidPrimary oocytes decrease in number throughout a woman’s life.
The ovaries of a newborn girl contain about 2 million Primary oocytes—all she will ever have.
Each Primary oocyte is contained within its own hollow ball of single layer of granulosa cells, the Primordial follicle.
By the time a girl reaches puberty, the number of Primary oocytes and follicles has been reduced to 400,000.
Only about 400 of these Primary oocytes will ovulate during the woman’s reproductive years, and the rest will die by apoptosis.
Oogenesis ceases entirely at menopause
Definition:
“Monthly rhythmical changes in the secretion of the female hormones and corresponding physical changes in the ovaries and other sexual organs”.
Duration: The duration of the cycle averages 28 days. It may be as short as 20 days ar as long as 45 days.
PHASES
Follicular Phase (Proliferative Phase) (1-14 Day)
Menstrual Phase (Day 1-5)
Preovulatory Phase. (Day 6-14)
Ovulation (Day 14)
Post Ovulatory Phase (Secretory Phase). (15-28 Day)
Leuteal Phase (Day 15-26)
Premenstrual phase. (Last 2 Day)
Concept of Hypothalamic-Pituitary-ovarian Axis
Overall, the most advanced follicle reduces the FSH supply to other follicles while at the same time it makes itself more sensitive to the FSH that remains.
The less developed, less sensitive follicles undergo atresia, while the most developed follicle attains a diameter of up to 2.5 cm. This follicle, called a mature (graafian) follicle, protrudes from the surface of the ovary like a blister.
As the follicle matures, the primary oocyte completes meiosis I and becomes a secondary oocyte.
This cell begins meiosis II but stops at metaphase II. It is now ready for ovulation.
FSH and estrogen also stimulate the maturing follicle to produce LH receptors, which are important to the next phase of the cycle
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3. At the end of the class you are expected to:
Define normal menstrual cycle
Understand physiology of menstrual cycle
Know the clinical importance of normal menstrual
cycle
4. tightly coordinated cycle of stimulatory and
inhibitory effects that results in release of single
matured oocyte from a pool of hundreds of thousands
of primordial oocytes.
5. Menstrual length is 28+/- 7
days(<1% women have length <21 or
>35days)
Duration of flow is 1-8 days( average
3-5 days)
Amount of flow is 10-80 ml( average
30-50 ml)
20. BIRTH
Age from conception
No. of
germ cells
(millions)
Conception
3 6 9
months
1 10 20 40
years
Puberty
99.9% by
“Atresia”
Ovulation
(post-puberty)
Continuous loss
(Fig adapted from Johnson
& Everitt, 2000)
~7 m
~ 300,000
21. Growth and atresia of follicles are not interrupted
by pregnancy, ovulation, or periods of anovulation
This dynamic process continues at all ages,
including infancy and around the menopause
From this large reservoir, about 400 to 500 follicles
will ovulate during a woman's reproductive years
23. Menstruation
How many follicles
reach this point?
Ovulation
Lets look at follicular growth first…
There are a number of questions to ask…
Normally 1
34. 0 4 8 12 16 20 24 28
Insufficient FSH to
keep smaller follicles
going – they become
atretic.
Oestradiol
FSH
FSH
secretion
suppressed
Dominant follicle(s) can
survive.
The total duration of time to
achieve preovulatory status is
approximately 85 days
35. Granulosa cells
Theca
Androgens
LH
(Note: the production of
androgens is a normal
part of ovarian
physiology)
Androgens are
converted
(aromatized) to
oestradiol by the
granulosa cells
OESTRADIOL
(steroid)
FSH
The Two-Cell, Two-
Gonadotropin System
44. How does the LH surge
affect the follicle?
About 36 h between LH
surge and oocyte release…..
45. Oocyte:
• Completion of the 1st meiotic
division (unequal division;
extrusion of 1st polar body)
• 2nd meiotic division starts
but becomes arrested before
completion.
Loosening of cumulus cells
Microvilli across the
zona pellucida are
withdrawn.
47. • Ruptured follicle
becomes solid corpus
luteum
•has one of the highest
blood flows per unit mass
in the body
• Thecal cells and blood
vessels invade
• Granulosa cells
hypertrophy and
terminally differentiate
(“luteinisation”). Progesterone
+
Oestradiol
Steroid secretion changes –
Transformation of ruptured follicle into corpus luteum (CL)
48. 0 4 8 12 16 20 24 28
OVULATION
Oestradiol
Progesterone
What maintains
the CL?
Why does the
CL degenerate
at the end of the
cycle?
Follicular phase:
Oestradiol domination
Luteal phase:
Progesterone domination
49. Hypothalamus
Pituitary
LH
(low levels in
luteal phase)
GnRHSteroid negative
feedback keeps
LH and FSH
levels relatively
low
CL very
sensitive
CL
Progesterone
+ E2
-
-
+
Reproductive tract etc
What maintains
the CL?
52. 0 4 8 12 16 20 24 28
Menstruation
OVULATION
Oestradiol causes
an increase in
thickness (the
“proliferative
phase”)
More secretion from
the glands – hence the
term “secretory
phase”
Endometrial
depth
53. 0 4 8 12 16 20 24 28
Menstruation
Characteristic “spiral arteries”
Terminal differentiation of
stromal cells – “decidualisation”
Optimal time for
implantation
55. 1. At end of the luteal phase, steroid production declines.
2. Loss of oedema and gradual shrinking of endometrial tissue. The
spiral arteries become more highly coiled
3. Gradual reduction in blood flow to superficial layers – leading to
ischaemic hypoxia and damage to the epithelial and stroma cells.
4. 4 24 hours prior to menstrual bleeding, an intense constriction of‑
spiral arteries occurs.
5. Individual arteries re-open at different times, tearing and
rupturing the ischaemic tissues.
6. Bleeding into the cavity occurs via:
1. red cells diapedese between surface epithelial cells;
2. tears develop in the surface epithelium
3. pieces of weakened superficial endometrium crumble away
7. About 50% of degenerating tissues is resorbed and 50% is lost as
'menstrual bleeding'.
56. Probably 95% of women have
a total blood loss of less than
60 mls.
This blood loss can represent a
significant loss of iron (leading
to anaemia) – especially in
women on marginal diets
57. 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.
58. Probability of clinical pregnancy following intercourse on a given day
relative to ovulation (estimated from basal body temperature).
Day of intercourse Ovulation?
Nearly all
pregnancies
in a 6-day
fertile window
59. 0 4 8 12 16 20 24 28
Menstruation
OVULATION
Cervical
mucus
Variable
number of
“dry” days
Production
of low
viscosity
mucus
increases
Abundant mucus
- like “raw egg
white”
Thick, rubbery, high
viscosity -
impenetrable to
sperm.
60. With increasing oestradiol:
1. The mucus becomes more
abundant - up to 30x more and
its water content increases.
2. Its pH becomes alkaline.
3. Increased elasticity –
("spinnbarkeit test")
5. “Ferning pattern” caused by the
interaction of high concentrations
of salt and water with the
glycoproteins in the mucus.
Characteristic fernlike pattern as
the mucus dries on a glass slide.
61. 0 4 8 12 16 20 24 28
Menstruation
OVULATION
LH
36
36.2
36.4
36.6
36.8
37
37.2
37.4
37.6
37.8
38
A small (0.5 o
C) rise
in BBT typically
follows ovulation.
Basal body temperature
63. Basal body temperature
Plasma oestradiol
Plasma progesterone
Volume of cervical mucus
– and sperm penetration
Uterine endometrium
64. a) Calendar Method - which is essentially
based on the previous menstrual history.
b) Temperature method - using a midcycle
rise in body temperature as a sign when
ovulation has occurred.
c) Cervical changes - which can be detected
by feeling the cervix and cervical mucus.
d) Hormonal methods - using over-the-
counter "kits" to assess urinary hormone
levels.
There are a number of potential ways of trying
to identify the “fertile” period..:
65. Follicular phase estrogen production is explained by the
two-cell, two-gonadotropin mechanism, allowing the critical
creation of an estrogen-dominated microenvironment.
Selection of the dominant follicle is established during days
5 to 7, and consequently, peripheral levels of estradiol begin
to rise significantly by cycle day 7.
66. Estradiol levels, derived from the dominant follicle,
increase steadily and, through negative feedback
effects, exert a progressively greater suppressive
influence on FSH release.
While directing a decline in FSH levels, the
midfollicular rise in estradiol exerts a positive
feedback influence on LH secretion
67. A unique responsiveness to FSH allows the
dominant follicle to utilize the androgen as
substrate and further accelerate estrogen
production.
FSH induces the appearance of LH receptors on
granulosa cells
The LH surge initiates the continuation of meiosis
in the oocyte, luteinization of the granulosa, and
synthesis of progesterone and prostaglandins
within the follicle
68. 1. Williams obstetrics, 24th
edition
2. Williams Gynecology, 2nd
edition
3. Gabbe, Normal and problem pregnancies, 6th
edition
4. Uptodate, 21.6
OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based.
This synchronisation is between many parts of the body…..
Ovary, uterus, oviduct, brain, vagina….
And is achieved by hormones! - very dynamic
Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally
Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things:
a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization)
b) time for response - eg. E2 induces mitoses… cornification in vagina at oestrus AFTER peak of e2
c) profile that matters - interactions between P and e (e.g. implantation window)
In rats, pattern of T and androstenedione mirror e2
Dominant progestin is 20 alpha OH-P - from newly formed CL
OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based.
This synchronisation is between many parts of the body…..
Ovary, uterus, oviduct, brain, vagina….
And is achieved by hormones! - very dynamic
Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally
Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things:
a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization)
b) time for response - eg. E2 induces mitoses… cornification in vagina at oestrus AFTER peak of e2
c) profile that matters - interactions between P and e (e.g. implantation window)
In rats, pattern of T and androstenedione mirror e2
Dominant progestin is 20 alpha OH-P - from newly formed CL
OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based.
This synchronisation is between many parts of the body…..
Ovary, uterus, oviduct, brain, vagina….
And is achieved by hormones! - very dynamic
Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally
Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things:
a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization)
b) time for response - eg. E2 induces mitoses… cornification in vagina at oestrus AFTER peak of e2
c) profile that matters - interactions between P and e (e.g. implantation window)
In rats, pattern of T and androstenedione mirror e2
Dominant progestin is 20 alpha OH-P - from newly formed CL
OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based.
This synchronisation is between many parts of the body…..
Ovary, uterus, oviduct, brain, vagina….
And is achieved by hormones! - very dynamic
Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally
Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things:
a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization)
b) time for response - eg. E2 induces mitoses… cornification in vagina at oestrus AFTER peak of e2
c) profile that matters - interactions between P and e (e.g. implantation window)
In rats, pattern of T and androstenedione mirror e2
Dominant progestin is 20 alpha OH-P - from newly formed CL
OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based.
This synchronisation is between many parts of the body…..
Ovary, uterus, oviduct, brain, vagina….
And is achieved by hormones! - very dynamic
Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally
Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things:
a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization)
b) time for response - eg. E2 induces mitoses… cornification in vagina at oestrus AFTER peak of e2
c) profile that matters - interactions between P and e (e.g. implantation window)
In rats, pattern of T and androstenedione mirror e2
Dominant progestin is 20 alpha OH-P - from newly formed CL
OK, so the control of the oestrous cycles has to be seen from a very broad perspective - but lets focus in a bit and see what we can say about the general principles on which the variability is based.
This synchronisation is between many parts of the body…..
Ovary, uterus, oviduct, brain, vagina….
And is achieved by hormones! - very dynamic
Note the delay between the high steroid levels and oestrus! Remember while we use criteria to follow cycles, these are just convenient reflections of what is happening internally
Also, in terms of hormones, you have to remember that these are the circulating signals - not an end in themselves. The important thing is how the tissues respond - and in terms of the response we have to consider three things:
a) level of hormone may affect different tissues differently(in sheep, with low levels of e2 the LH surge and mating are not particularly closely synchronized, while high levels produces high level of synchronization)
b) time for response - eg. E2 induces mitoses… cornification in vagina at oestrus AFTER peak of e2
c) profile that matters - interactions between P and e (e.g. implantation window)
In rats, pattern of T and androstenedione mirror e2
Dominant progestin is 20 alpha OH-P - from newly formed CL