hello and welcome to this aapko basic
00:02
science objective video about the
00:04
physiology of the menstrual cycle the
00:07
objectives of this video are to
00:09
summarize how the hypothalamic pituitary
00:11
ovarian axis regulates ovarian function
00:13
and the menstrual cycle to explain how
00:16
the HPA axis defines the phases of the
00:19
menstrual cycle and to differentiate
00:21
between how the hpo axis interacts to
00:23
define the stages of the reproductive
00:25
cycle puberty menstruation and menopause
00:29
hey mama dad I found these in the
00:31
bathroom what are they for
00:33
well that might take a while but let’s
00:36
start from the beginning the menstrual
00:38
cycle is divided into menses follicular
00:41
phase and the luteal phase the average
00:44
cycle is between 22 to 35 days only
00:47
about 15% of women have a 28-day cycle
00:50
the follicular phase is variable between
00:53
14 to 21 days while the luteal phase is
00:56
fixed at 14 days by convention the first
01:00
day of the cycle is the first day of
01:02
menstruation remember the goal of the
01:05
menstrual cycle is to release a mature
01:06
oocyte through a tight coordination of
01:08
stimulatory and inhibitory factors
01:11
that’s right and to understand this
01:14
tightly woven story we must understand
01:16
the players and how they interact from
01:18
fetal development through puberty kanata
01:22
trip and releasing hormone or GnRH
01:24
is secreted by neuro endocrine cells in
01:26
the hypothalamus it is secreted in a
01:29
pulsatile fashion and is regulated by
01:31
neurotransmitters follicle stimulating
01:33
hormone or FSH and luteinizing hormone
01:36
LH are both protein hormones from the
01:40
anterior pituitary gland they are
01:42
composed of two subunits the alpha
01:44
subunit resembles the thyroid
01:46
stimulating hormone and human chorionic
01:48
gonadotropin LH is critical in
01:51
triggering ovulation estrogen plays an
01:54
important regulatory role in the
01:56
menstrual cycle and stimulates blood
01:58
flow to the uterus progesterone is
02:00
critical for endometrial receptivity as
02:03
well as functioning as a uterine
02:05
relaxant inhibin a is from the corpus
02:08
luteum while inhibin b is from the
02:11
developing follicles and
02:12
have a role in keeping FSH levels low in
02:15
the follicular phase now let’s pause
02:18
think and apply disruption of the
02:21
hypothalamic pituitary ovarian access
02:23
may alter hormone levels that support
02:26
and control what three functions of the
02:28
reproductive cycle ovulation
02:31
reproduction and menstruation is the
02:33
answer okay but when are you going to
02:37
tell me what this is for we’re getting
02:40
there this is a complex physiology and
02:42
you must understand the scene first so
02:44
as we were saying in the early
02:47
follicular phase FSH has three effects
02:49
on the ovaries it recruits follicles
02:52
it increases LH receptors and it
02:54
increases aroma taste enzymes in the
02:56
ovary LH increases androgens in the
02:59
theca cells androgens then diffuse into
03:02
the granulosa cells where it is
03:03
converted to estrogen through aroma
03:05
taste estrogen acts synergistically with
03:08
FSH to increase the number of FSH
03:10
receptors on the cells and increase
03:12
mitotic activity of the granulosa cells
03:15
it is important to remember early in the
03:18
follicular phase there are low levels of
03:20
estrogen and progesterone the negative
03:22
feedback on the anterior pituitary and
03:24
hypothalamus lead to an increase in GnRH
03:27
pulsatilla T which leads to an increase
03:30
in FSH during the mid follicular phase
03:33
FSH stimulates
03:34
folliculogenesis and ultimately
03:36
recruitment of the dominant follicle
03:39
recall that the oocyte has been halted
03:41
in meiosis 1 prophase prior to the
03:44
initiation of the menstrual cycle with
03:47
the initiation of the menstrual cycle
03:48
and the stimulation of the OS 8 by FSH
03:51
the primary oocyte becomes a secondary
03:54
oocyte and is again halted this time in
03:57
meiosis 2 metaphase until fertilization
04:01
granulosa so hypertrophy leads to an
04:04
increase in estrogen through FSH
04:06
stimulation of aromatase estrogen goes
04:09
on to stimulate proliferation of the
04:11
endometrium and eventually negative
04:13
feedback on the hypothalamus and
04:15
pituitary to suppress FSH and LH during
04:19
the late follicular phase the dominant
04:21
follicle is selected and estrogen levels
04:24
increase
04:25
before ovulation FSH induces LH
04:28
receptors in the ovary and lead to an
04:31
increase in ovary intrauterine growth
04:33
factor 1 or igf-1 estrogen causes the
04:37
endometrium to thicken as well as change
04:39
cervical mucus consistency
04:41
during this phase estrogen goes from
04:44
being a positive feedback on FSH to
04:46
ultimately being a negative feedback as
04:48
estrogen begins to have a negative
04:50
feedback on FSH non-dominant follicles
04:53
undergo atresia and disappear this
04:56
usually occurs between days 5 to 7
04:59
ovulation occurs 34 to 36 hours after
05:02
the start of the LH surge estrogen
05:05
levels must be above 200 pika grams per
05:08
milliliter for 50 hours to stimulate
05:11
adequate LH surge low levels of
05:14
progesterone promote the positive
05:16
feedback on LH LH is responsible for the
05:20
resumption of meiosis 1 prophase lutein
05:23
ization of granulosa cells and synthesis
05:25
of prostaglandin and progesterone both
05:29
of these mechanisms along with lysosomal
05:31
enzymes are essential for follicular
05:33
rupture with ovulation we move to the
05:37
luteal phase the corpus luteum which
05:39
forms from the luminous ation of the
05:41
brain illusive cells produces
05:43
progesterone and prostaglandin the
05:45
levels of progesterone peak at day 21
05:48
progesterone leads to further negative
05:50
feedback and decreased estrogen
05:52
production gluteal phase can be broken
05:55
into the early and late luteal phase in
05:58
the early luteal phase estrogen Peaks
06:01
one day prior to ovulation during this
06:03
phase the dominant follicle completes
06:06
the first meiotic division just before
06:09
ovulation granulosa cells produced
06:11
progesterone which leads to the
06:13
cessation of endometrial mitosis and
06:16
organization of glands in the late
06:19
luteal phase progesterone comes mainly
06:21
from the corpus luteum progesterone has
06:24
a negative feedback on LH and eventually
06:26
decreased LH levels decrease the
06:28
progesterone and estrogen made by the
06:30
corpus luteum
06:32
the oocyte is fertilized the early
06:34
embryo makes chorionic gonadotropin
06:36
which maintains the corpus luteum and
06:38
progesterone production
06:40
if there is no fertilization the drop in
06:44
estrogen and progesterone levels
06:45
decrease the blood supply to the
06:47
endometrium and leads to slaughtering of
06:49
the endometrial lining usually 14 days
06:53
after LH surge only the functional layer
06:56
of the endometrium is lost as it is
06:58
responsive to hormonal stimulation in
07:01
contrast the basal layer is not hormonal
07:04
irresponsive with atresia of the corpus
07:07
luteum there is a decrease in steroid
07:09
production and the hypothalamic
07:11
pituitary axis is released from negative
07:14
feedback leading to the eventual rise of
07:16
FSH and resumption of the next cycle now
07:20
let’s pause think and apply in primary
07:24
hyperkinetic trophic hypogonadism where
07:27
there is impaired response of gonadal
07:29
tissue to LH and FSH how is ovulation
07:31
and menstruation affected you would see
07:35
an ovulation primary infertility in
07:38
primary amenorrhea recall that LH
07:41
stimulates theca cells to produce
07:43
androgens which diffuse to nearby
07:45
granulosa cells granulosa cells
07:48
stimulated by FSH convert androgens into
07:51
estrogen therefore in these patients
07:54
there would be an overall lack of
07:56
estrogen up until now we have only
07:58
described the hpo axis at maturity
08:01
however many factors are in play to keep
08:04
the HPA axis quiet prior to puberty and
08:07
then begin the hormonal cascade which
08:09
continues until menopause yes in the
08:12
fetus kanata trip and release is
08:14
suppressed by circulating estradiol from
08:16
the mother and placenta the acute
08:19
decrease in estradiol at birth removes
08:22
the negative feedback on the pituitary
08:23
gland Peak gunatit riffin production
08:26
occurs by 3 months but by age 4 gunatit
08:29
driven levels are undetectable it is
08:33
important to remember that the highest
08:34
number of oocytes 5 to 7 million exists
08:38
at 20 to 24 weeks in utero the numbers
08:41
decrease until birth with only 300,000
08:44
remaining
08:45
and arrested in meiosis 1 prophase the
08:49
HPA axis remains suppressed from age 4
08:51
to 10 by an unknown mechanism in
08:54
adolescence the hypothalamus begins to
08:57
secrete gnrh initially during sleep
08:59
eventually there is an evening postal
09:02
release and finally a 24 hour pulse Atal
09:05
release this begins the Cascade of
09:07
puberty which occurs about two and a
09:09
half years prior to menarchy
09:11
perimenopause is defined by menstrual
09:14
irregularities as well as menopausal
09:17
symptoms such as hot flashes and night
09:18
sweats menopause is defined by the
09:21
absence of menses for 12 months hormonal
09:24
irregularities occur three to ten years
09:26
before menopause the average age of
09:29
menopause is 51.4 in the United States
09:32
there is an elevated level of FSH and LH
09:35
during this time there is no laboratory
09:38
testing that can confirm menopause
09:39
status during the transition as FSH
09:42
levels do not stabilize for one to two
09:44
years of note if amenorrhea comes before
09:48
the age of 40 it is considered a
09:50
premature ovarian failure and may
09:52
warrant further workup menopause is
09:55
experienced differently by different
09:57
women it is often accompanied by hot
09:59
flashes mood lability vaginal dryness
10:02
dyspareunia and urinary symptoms so you
10:06
see Sun this is just a normal part of a
10:08
woman’s reproductive lifespan and really
10:10
only a small portion
10:11
oh and the tampon you asked about it’s
10:14
just a small roll of cotton used to soak
10:17
up the menstrual flow at the beginning
10:18
of the cycle you have any questions and
10:21
thanks I think that was plenty
10:27
this concludes this aapko basic science
10:30
objective video on the physiology of the
10:32
menstrual cycle you should be able to
10:34
summarize how the HPA axis regulates
10:36
ovarian function and the menstrual cycle
10:38
explain how the HPA axis defines the
10:41
phases of the menstrual cycle and the
10:44
stages of the reproductive cycle thanks
10:47
for watching
11:10
you

There once was an OBGYN who had an ultrasound scanner in his office, some extra time, and an inventive curiosity. He wanted to know what uteri did all day long. He thought that being a smooth muscle organ, it probably would contract from time to time, but he wasn’t sure.

So he persuaded some of his patients to lie very still while he scanned them continuously, while he watched the monitor screen carefully for any signs of contractions. He didn’t see anything.

So he called on his friend, another OBGYN, to watch the videotapes of his scanning to confirm that nothing was happening on them. His friend agreed, but found that watching these tapes was very tedious, so he hit the fast forward button.  To his surprise, the uterus that appeared to be at rest at normal speed, was visibly contracting when he sped up the tape.

Not only was the uterus contracting constantly, it was contracting in a very consistent pattern. The contractions mostly started at the fundus and squeezed down and out the cervix, just like it would do if it were trying to deliver a baby.

With further study, several additional things were discovered that I think provide insight into several of the many unanswered questions in OBGYN.

First, this down and out contraction pattern was quite evident during menses and also leading up to ovulation. But with ovulation, the contraction pattern reversed, with most contractions starting near the cervix and squeezing up and out the fallopian tube.

Well, this is very important in terms of sperm transport. You see, sperm are microscopic creatures who couldn’t swim one centimeter in an entire sperm lifetime. So how is it that sperm deposited around the cervix will appear at the fimbriated end of the fallopian tube 10 minutes later? It’s because they’re not swimming that far…they’re being propelled by the uterine muscular squeeze that picks them up at the cervix and delivers them deep into the fallopian tube, where the villous membrane further propels them to their target, the ovum.

This may also be important in some cases of infertility. You see, not everyone followed this pattern of up and out squeezes during ovulation. For some women, the contractions were not coordinated, or the uterine squeezes were from right to left or left to right, not a pattern that would be expected to contribute to sperm transport.

This may also be important in the pathogenesis of endometriosis. If, during menses, instead of most of the contractions being in a down and out pattern, many are starting near the cervix and squeezing up and out, I would expect more than an average amount of menstrual products to be propelled through the fallopian tubes and into the abdomen, where some may successfully implant. It takes no great imagination to connect these dots and say that if uterine contraction patterns are abnormal, that may increase the likelihood both of endometriosis and of infertility.

Following ovulation, the uterine contractions largely stop, and the uterus remains relatively relaxed until shortly before menstruation. This period of quiescence coincides with the ovaries production of progesterone. Progesterone is known to have smooth muscle relaxing properties. It’s absence immediately after conception is an established cause of infertility, and abnormally low levels are known as a “luteal phase defect” and are believed by many to lead to loss of an early pregnancy. The mechanism by which lack of progesterone leads to these early losses is not known, but one contributing factor may be lack of progesterone-inspired uterine contractile quiescence that is normally seen during the luteal phase.

The progesterone effect on uterine contractions may also play a role in hormone-based contraceptives. These contraceptives are thought to exert their effects in a number of overlapping ways, among them ovulation suppression, and a change in cervical mucous making it less permeable to sperm. An additional factor may be the impact of progestins on uterine contractility, interfering with the ovulatory surge in cervix to fallopian tube uterine contractions, thus interfering with sperm transport to the fallopian tube.

So what does a uterus do all day long? It contracts in ways that are beneficial to preserving health and our species.

Dr. Hughey

I think the hardest thing about being on
00:09
streets is probably being a female if
00:21
you’re a woman you like your face clean
00:23
you know you like feeling good selling
00:25
good
00:26
yeah period times are not good times for
00:29
us hi how are you and very uncomfortable
00:37
[Music]
00:41
and every day I wake up and I do my
00:44
daily routine because nobody wants to
00:46
smell you know and that’s that’s kind of
00:49
a big deal out here I’ve been doing this
00:55
for so long I’m 27 years old
00:58
this will be my eighth winter out here
01:00
straight we had a pretty rough childhood
01:03
growing up my mom was a victim of
01:05
domestic violence and so she put us
01:08
through a lot I went into the system she
01:11
got custody of me again and basically
01:14
she was like you know what I don’t want
01:16
you in the system anymore but you can’t
01:18
be here I hadn’t lived on him since I
01:21
was you know 10 years old you know and I
01:24
took care of myself it was no keeping me
01:26
home anyway you know whether she if she
01:29
wanted to or not there’s so many kids
01:31
that it’s like they fall through the
01:33
cracks I guess and that’s kind of what
01:36
happened with me
01:39
[Music]
01:44
if you got cramps good luck hunchback
01:47
for now they get a water bottle and some
01:50
hot water from Starbucks or something
01:51
you know you can do that maybe some
01:55
steal some motrin it’s a little
01:57
stressful you know it’s hot stuff and
01:59
you’re running around trying to get what
02:01
you need
02:02
every month they are placed in a crisis
02:05
situation you shouldn’t have to decide
02:07
between a pad and having lunch a big box
02:10
of tampons probably runs around $10 so
02:13
that could be half of what we made
02:15
during the day
02:17
tampons that I need that’ll leave me
02:20
with nothing then they have then I can’t
02:22
eat
02:23
tampons and pots are so expensive here I
02:26
mean like the cheapest box of tampons in
02:30
this Walgreens right here it’s like a
02:32
little over seven dollars it’s more
02:34
money than me and my boyfriend spent on
02:36
a meal together I would rather be
02:42
be full this is not a poor issue this is
02:46
not just about getting products to those
02:48
who need them which is obviously a
02:50
priority this is really about bringing
02:53
dignity to women
03:02
my tend to flock to places like this
03:04
which is like public parks where they
03:07
have public bathrooms
03:09
I come here to Thompson Square Park and
03:12
I do my mind cleaning up in the in the
03:15
sink and get a big cat like with like
03:17
the big McDonald cup and I fill it up
03:20
with water actually like I’ll straddle
03:23
it this way you’re able to you know pour
03:26
water and use the soap and and basically
03:30
watch over the toilet and get a really
03:33
good cleansing that’s the best way to
03:36
actually get you know your feminine
03:38
hygiene I’m accomplished there’s a like
03:43
little tricks that I’ve picked up along
03:45
the way and it’s only a few minutes like
03:48
a couple of minutes I’ve always just
03:50
used like paper towels or toilet paper
03:53
them like that it was like a napkin from
03:56
some you know there’s like big white
03:59
napkins I be taught a paper and plastic
04:02
bags
04:03
I’m mind Bosworth makeup head dude
04:09
socks I had to ball up the socket when I
04:12
had an old tank top that was bleach
04:15
I had to go and rinse it out squeeze it
04:18
out dry it put it back like four times
04:20
that dish sometimes if we didn’t get
04:22
things right away we just sit still
04:24
but you know just as still until we came
04:27
up with something and I’ve learned how
04:34
to make my own tampons out of pads so
04:37
you take the pad I try to use tampons as
04:40
much as I can but tampons are expensive
04:43
and of course ladies you want to wash
04:44
your hands first
04:46
people tend to when they do give care
04:49
packages it’s usually pads and then you
04:52
tie them like this and but usually
04:54
they’re a little longer and then you can
04:56
tie a knot here and then you can still
04:58
have like the string basically that’s it
05:01
it produces infections especially in
05:04
some cases when women are wearing
05:06
tampons for longer than they should
05:07
toxic shock syndrome it is a health
05:11
issue
05:12
[Music]
05:18
unfortunately there really wasn’t a
05:20
clear policy on where women can access
05:22
the products there’s different levels of
05:25
homelessness there’s women in shelters
05:27
there’s women in Subway’s there’s women
05:30
you know sleeping in parks I used to be
05:32
in a shelter but I haven’t been in one a
05:35
lot because I don’t drink and that was a
05:37
choice and that’s where most of the
05:39
clinic crowd is in shelter I feel safer
05:42
out on the streets and I went in a
05:44
shelter won’t do it I can do it I choose
05:46
to be out on the streets
05:48
so why we needed to legislate this as
05:51
opposed to just changing a policy here
05:53
or there is that it is now the law of
05:55
the land
05:57
you want to feel clean like everybody
05:59
else you know what I mean I like being
06:02
out here but everybody has a story
06:05
see you never you don’t really know
06:07
people and everybody has a reason for
06:09
the things that they do they do you know
06:12
so that’s kind of my story

00:00
aapko basic science topic dysmenorrhea
00:02
and endometriosis dysmenorrhea is pain
00:05
associated with menstruation is the most
00:08
commonly reported menstrual disorder
00:10
with more than half of menstruating
00:11
women experiencing some pain each month
00:14
the objectives of this video are
00:16
understand the histology of normal
00:19
endometrium and myometrium to understand
00:22
the pathophysiology behind dysmenorrhea
00:24
and endometriosis and to understand the
00:26
pharmacological treatment of
00:28
dysmenorrhea to review the clinical
00:30
management of dysmenorrhea and
00:32
endometriosis please view the Affco
00:34
clinical educational videos topic number
00:36
46 and 38 let’s meet our patient –
00:40
amenorrhea is a 19 year old female who
00:42
presents to your clinic for dysmenorrhea
00:44
mitakuye was age 12 and menstruation has
00:47
been painful for as long as she
00:48
remembers she is regular monthly cycles
00:51
that lasts five days pain begins on day
00:54
one gradually decreases and is gone by
00:56
day three she asks you why are my period
01:00
so painful to answer her question let’s
01:04
take a closer look at the uterus and
01:05
endometrium the uterus is a muscular and
01:08
glandular organ the myometrium is a
01:10
highly vascular muscular layer composed
01:13
of bundles of smooth muscle and
01:14
interwoven layers responsible for
01:16
uterine contractions it surrounds the
01:19
endometrium the inner glandular layer
01:21
Vanda metrium is composed of simple
01:24
columnar epithelium with some both
01:26
tubular glands as we zoom out it has two
01:29
layers the stratum function nail in the
01:31
stratum basale also known as the stratum
01:33
function Ellis and basalis
01:35
the stratum function nail is the luminal
01:38
layer and contains the tubular glands
01:40
surrounded by endometrial stroma as well
01:42
as the distal portions of the spiral
01:44
arteries and it’s arterioles the stratum
01:46
function nail is hormonal irresponsive
01:48
in proliferates and degenerates with the
01:50
menstrual cycle is the temporary layer
01:53
of the endometrium as lost during menses
01:55
the stratum basale is deep to the
01:58
stratum functional and contains the
02:00
basal portion of the endometrial glands
02:02
and the proximal portion of the spiral
02:04
arteries
02:04
unlike the stratum function nail the
02:06
stratum basale
02:07
is retained during menses and does not
02:09
change with the menstrual cycle
02:11
now that we’ve reviewed the tissues
02:13
let’s answer our patients question what
02:15
is going on to cause the pain primary
02:18
dysmenorrhea is painful menstruation
02:20
without a clinically identifiable
02:22
ideology while secondary dysmenorrhea is
02:25
painful menstruation caused by an
02:27
identifiable underlying condition such
02:29
as endometriosis primary dysmenorrhea is
02:33
mediated by prostaglandins let’s discuss
02:36
prostaglandins in more detail
02:38
prostaglandins contribute to painful
02:40
menses in two ways prostaglandins
02:43
resulting contractions in ischemia as
02:45
well as overall increased pain
02:46
sensitivity by increasing the resting
02:48
membrane potential of pain neurons
02:50
resulting in painful menses
02:52
prostaglandins e 2 and F 2 alpha are
02:55
produced by the endometrium in response
02:57
to progesterone levels which increased
02:59
during the menstrual cycle and peak at
03:00
the mid luteal phase
03:02
most of the prostaglandins present
03:04
during the endometrial Slough are
03:06
created at that moment secondary to a
03:08
short half-life the prostaglandins are
03:10
liberated by cell wall break down from
03:12
the shedding endometrium prostaglandins
03:14
mediate smooth muscle contraction and
03:16
act on the myometrium to cause
03:18
contractions which lead to high entry
03:20
and pressures the increased intrauterine
03:22
pressure exceeds arterial pressure the
03:25
arteries serving the uterine tissues are
03:27
compressed and caused mudra ischemia in
03:30
ischemia anaerobic metabolites
03:33
accumulate and stimulate type C pain
03:35
neurons other causes of dysmenorrhea are
03:38
mediated by stretch receptors and other
03:40
mechanisms
03:41
let’s pause read and apply when does
03:45
pain with primary despond area typically
03:47
occur with each menstrual cycle pain
03:50
typically begins right before
03:52
menstruation as the level of
03:53
prostaglandins are high with endometrial
03:55
sloughing as menstruation continues and
03:59
the endometrium is shed prostaglandins
04:01
and pain levels decrease the onset of
04:04
primary dysmenorrhea in a woman’s life
04:06
often coincides with the onset of
04:08
menarche consistent with their patient’s
04:10
history
04:11
conversely secondary dysmenorrhea is
04:13
painful menstruation caused by an
04:15
identifiable underlying condition of the
04:17
reproductive system pain onset maybe
04:20
later in life with the onset of the
04:22
underlying condition
04:23
also pain is often not historically
04:26
associated timing with menses as in
04:28
primary dysmenorrhea pay may begin a few
04:31
days before menses may worsen is menses
04:33
continues and may not cease after it
04:35
ends common causes of secondary
04:38
dysmenorrhea include endometriosis and
04:41
no meiosis public inflammatory disease
04:43
and uterine fibroids let’s go back to
04:47
our patient dish’ has heard of
04:49
endometriosis before and wants to know
04:51
more about it she asks you what is
04:53
endometriosis you discussed with her
04:56
that endometriosis is the presence of
04:58
endometrial tissue outside of the uterus
05:01
common areas for these endometrial
05:03
deposits include the ovaries fallopian
05:05
tubes called the sac Brad ligaments
05:08
uterus sacral ligaments and peritoneum
05:10
deposits can be superficial or deeply
05:13
infiltrating and are responsive to
05:15
hormonal stimulation like normal
05:17
endometrial tissue these extra uterine
05:20
lesions trigger inflammation leading to
05:22
dysmenorrhea the etiology of
05:25
endometriosis is thought to be
05:27
multifactorial and there are multiple
05:29
hypotheses about its pathophysiology
05:31
including the retrograde menstruation
05:34
theory aberrant lymphatic or vascular
05:36
spread of endometrial tissue and the
05:39
salome achmed aphasia theory in
05:42
retrograde menstruation endometrial
05:44
debris travels backwards through the
05:46
fallopian tube during menses into the
05:47
peritoneal cavity tissue implants on
05:50
various structures women without flow
05:53
tract anomalies have been shown to have
05:55
high incidence of endometriosis which
05:57
supports this theory however most women
06:00
have retrograde menstruation but only a
06:02
few have endometriosis other factors
06:05
must play a role and a material tissue
06:08
may also spread through the lymphatic
06:09
and Vascular systems for instance
06:12
endometriosis has been found in public
06:14
lymph nodes of women with endometriosis
06:16
in addition endometriosis can be found
06:20
in unusual and distant locations like
06:22
the lungs one way to remember the celiac
06:25
metaplasia theory is to remember that
06:26
silom means body cavity this theory
06:29
suggests that cells in the peritoneum
06:31
are pluripotent and can undergo
06:33
transformation to tissue identical to
06:35
metrium this may explain endometrium
06:38
less of the ovary since both the ovary
06:39
and mullerian ducts which give rise to
06:41
the endometrium are derived from the
06:43
same epithelium this also helps explain
06:45
how some girls have endometriosis prior
06:48
to menarche our patient wonders could I
06:51
have endometriosis how would we know you
06:54
explain how an ohmmeter iosys is often
06:56
suspected clinically based on history
06:58
and physical exam and treated
06:59
empirically however the gold standard of
07:02
diagnosis is laparoscopy in these
07:05
laparoscopic images the top image is the
07:08
typical lesion while the bottom is a
07:10
endometrium oh where there is
07:11
endometriosis within an ovary
07:14
endometrium us are also called chocolate
07:16
cysts
07:16
since their contents can have a brown
07:18
tar-like appearance inflammatory cells
07:21
break down the red blood cells in the
07:22
tissue deposits resulting in pigmented
07:24
lesions as shown here lesions may be red
07:27
white or black
07:28
also known as powder burn lesions and
07:30
the older the lesion is the more likely
07:33
it is to be pigmented lesions can be
07:36
biopsied and sent to pathology zooming
07:39
in this is a typical on Demetri attak
07:41
lesion with endometrial glands and blood
07:43
in the background of endometrial stroma
07:46
imaging and biomarkers can also be used
07:48
to aid diagnosis transvaginal ultrasound
07:51
AG Rafik an detect endometrium as if
07:53
they are present and helps exclude other
07:55
potential causes of pelvic pain with
07:58
ultra sonography and the metrio m’as can
08:00
range in appearance from a hemorrhagic
08:02
functional assist to similar to
08:04
malignancy on the left is a hemorrhagic
08:06
cyst basis have a reticular pattern with
08:10
a fishnet or lacy appearance on the
08:12
right is a classic appearance of a
08:14
endometrium ah with a diffuse
08:15
ground-glass
08:16
appearance ca-125 can be a biomarker
08:20
but it’s not often clinically used in
08:22
general levels correlate with disease
08:24
severity though ca-125 has poor
08:26
sensitivity to detect mild disease as
08:30
dysmenorrhea is mediated by
08:32
prostaglandins release from endometrial
08:34
tissue
08:34
first-line treatment is targeted at
08:36
decreasing prostaglandins as well as by
08:38
reducing a new material tissue for our
08:42
patient you recommend taking a
08:44
non-steroidal anti-inflammatory drug
08:45
such as ibuprofen
08:47
in addition you recommend hormonal
08:49
suppression such as with an oral
08:51
contraceptive pill which will help
08:53
decrease pain and service birth control
08:55
of needed
08:56
let’s pause read and apply wire NSAIDs
09:00
commonly used in the treatment of
09:01
dysmenorrhea NSAIDs inhibit cox-1 and
09:05
cox-2 in the Cascade leading to
09:07
prostaglandin production cox-1 and cox-2
09:10
are involved in the production of
09:12
prostaglandins from arachidonic acid
09:14
inhibiting cox-1 and cox-2 with NSAIDs
09:17
thus decreased prostaglandin / formation
09:20
hormone suppression another 1st line for
09:22
dysmenorrhea also decreases
09:24
prostaglandin production at the level of
09:26
arachidonic acid hormonal suppression
09:29
such as with oral contraceptive pills
09:31
inhibits gonadotropin release which
09:33
suppresses hormonal stimulation and
09:35
proliferation of the endometrium
09:36
resulting in endometrial atrophy but
09:40
then and the metrium contains relatively
09:42
small amounts of arachidonic acid
09:44
decreasing the amount of prostaglandins
09:46
this concludes the Affco basic science
09:48
video and dysmenorrhea we’ve discussed
09:50
the histology of normal and metrium in
09:52
myometrium the pathophysiology behind
09:55
dysmenorrhea and endometriosis and the
09:57
pharmacological treatment of
09:59
dysmenorrhea
10:00
[Music]
10:11
you