PCOD || Gynecology
Summary
TLDRThis lecture covers polycystic ovarian syndrome (PCOS), detailing its pathology rooted in increased androgen production leading to hirsutism and hormonal imbalances. It explains how elevated estrogen negatively impacts follicle-stimulating hormone, disrupts ovulation, and causes endometrial issues. The talk also addresses PCOS's link to insulin resistance, cardiovascular risks, and potential cancers. The Rotterdam criteria for diagnosis and treatment options, including lifestyle changes, medications, and surgery, are also discussed.
Takeaways
- π Polycystic Ovarian Syndrome (PCOS) is also known as Stein-Leventhal Syndrome and is characterized by increased androgen production.
- π¬ The excess androgens lead to hirsutism (excessive hair growth) and are converted to estrogens by the aromatase enzyme, causing a cascade of hormonal imbalances.
- π High estrogen levels decrease follicle-stimulating hormone (FSH) and increase luteinizing hormone (LH), resulting in an altered LH to FSH ratio, typically more than 2:1 in PCOS.
- π« The lack of a LH surge, which is necessary for ovulation, leads to oligomenorrhea or amenorrhea, and eventually, multiple cysts in the ovaries.
- β οΈ Increased LH stimulates theca cells to produce more androgens, perpetuating the cycle and contributing to the thickening of ovarian tissue.
- π‘ Unopposed estrogen can lead to endometrial hyperplasia, which may progress to cancer, and PCOS patients are at higher risk for endometrial and breast cancers.
- πββοΈ Lifestyle modifications and weight reduction are the first-line treatments for PCOS, aiming to reduce obesity and improve insulin resistance.
- π Oral contraceptive pills (OCPs) are often prescribed to regulate menstrual cycles and manage hirsutism in PCOS patients.
- π©Ί Metformin is used to address insulin resistance, a common comorbidity in PCOS that can lead to type 2 diabetes.
- π₯ Infertility in PCOS may be treated with selective estrogen receptor modulators like clomiphene citrate, with gonadotropins or LH/FSH injections as second-line options.
Q & A
What is Polycystic Ovarian Disease (PCOS) also known as?
-Polycystic Ovarian Disease (PCOS) is also known as Polycystic Ovarian Syndrome and Stein-Leventhal Syndrome.
What is the basic pathology behind Stein-Leventhal Syndrome?
-The basic pathology in Stein-Leventhal Syndrome is increased androgen production, which leads to various symptoms such as hirsutism.
How does increased androgen production lead to hirsutism?
-Increased androgen production stimulates the growth of sexual terminal hair, resulting in hirsutism.
What is the role of the aromatase enzyme in the context of PCOS?
-The aromatase enzyme converts androgen to estrogen, which has several effects including decreasing follicle stimulating hormone (FSH).
Why does increased estrogen lead to a decrease in FSH?
-Increased estrogen exerts a negative feedback mechanism on FSH, as estrogen is produced by the ovaries in response to FSH stimulation from the pituitary gland.
What is the significance of the LH to FSH ratio in patients with PCOS?
-In patients with PCOS, the LH to FSH ratio is more than 2:1, indicating an imbalance in these hormones.
How does the absence of an LH surge affect ovulation in PCOS?
-The absence of an LH surge, which is necessary for ovulation, leads to a lack of ovulation in PCOS.
What are the long-term consequences of PCOS on a woman's health?
-Long-term consequences of PCOS include increased cardiovascular risk factors, risk of diabetes mellitus due to insulin resistance, and increased risk of endometrial and breast carcinomas.
What is acanthosis nigricans and how is it related to PCOS?
-Acanthosis nigricans is a condition characterized by pigmented, velvety skin, often in the neck and axilla areas, and it is related to insulin resistance, which is common in PCOS.
What are the Rotterdam criteria for diagnosing PCOS?
-The Rotterdam criteria for diagnosing PCOS include the presence of oligomenorrhea or amenorrhea, clinical and biochemical symptoms such as hirsutism and increased serum testosterone, and the presence of 12 or more cysts in the ovaries on ultrasonography.
What is the first line of treatment for PCOS?
-The first line of treatment for PCOS is weight reduction and lifestyle modifications. If necessary, treatment may also include oral contraceptive pills (OCPs) for irregular periods and metformin for insulin resistance.
What are the treatment options for infertility in PCOS?
-For infertility associated with PCOS, the first line of treatment includes selective estrogen receptor modulators such as clomiphene citrate. Second line treatments may include gonadotropins or LH/FSH injections, and third line treatments may involve the use of GnRH analogs.
Outlines
π Understanding Polycystic Ovarian Disease (PCOS)
This paragraph introduces Polycystic Ovarian Disease (PCOS), also known as Stein-Leventhal Syndrome, highlighting the key pathology of increased androgen production. It explains how this leads to hirsutism due to androgen stimulation of sexual terminal hair growth. The androgen is then converted to estrogen by the aromatase enzyme, which has three main effects: decreasing follicle-stimulating hormone (FSH), altering the ratio of luteinizing hormone (LH) to FSH, and causing continuous LH increase without an LH surge, preventing ovulation. This results in decreased progesterone levels, leading to oligomenorrhea and potentially secondary amenorrhea. The paragraph also discusses the impact of LH on the theca cells, causing them to produce more androgens.
π± Complications and Clinical Features of PCOS
The second paragraph delves into the complications of PCOS, including the formation of multiple cysts in the ovaries due to the lack of a dominant follicle and ovulation. It explains how increased androgens lead to higher estrogen levels, which can cause endometrial hyperplasia and potentially endometrial cancer and breast carcinoma. The paragraph also addresses the impact of PCOS on lipid profiles, leading to increased LDL and decreased HDL, which raises cardiovascular risks. It mentions insulin resistance caused by increased androgens inhibiting sex hormone-binding globulin, predisposing patients to diabetes mellitus. Additionally, it covers the psychological effects of PCOS, such as obesity leading to mood changes, depression, and sleep apnea. Clinical features include menstrual irregularity, obesity, hirsutism, acne, alopecia, altered lipid profiles, and insulin resistance.
π Hormonal Changes and Diagnostic Criteria for PCOS
This paragraph discusses the hormonal changes in PCOS, including increased androgens like testosterone, androstenedione, and DHEA, as well as increased LH and estrogen. It also points out the presence of insulin resistance, high insulin levels, and increased LDL cholesterol. The diagnostic criteria for PCOS, known as the Rotterdam Criteria, are outlined, which include the presence of oligomenorrhea or amenorrhea, clinical symptoms like hirsutism, and biochemical symptoms such as elevated serum testosterone levels. The criteria also involve the ultrasound detection of 12 or more cysts in the ovaries, each 2-9 mm in size, with enlarged ovaries over 10 ml in volume.
π Treatment Approaches for PCOS
The fourth paragraph focuses on the treatment of PCOS, starting with weight reduction and lifestyle modifications as the first line of treatment. It mentions the use of oral contraceptive pills (OCPs) for managing irregular periods and metformin for insulin resistance. For hirsutism, a combination of OCPs with ciproteron acetate is suggested. The paragraph also outlines the treatment for infertility associated with PCOS, which involves selective estrogen receptor modulators like clomiphene citrate, tamoxifen, and reloxifen. It discusses the use of second-line treatments such as gonadotropins or LH/FSH injections and third-line treatments like leuprolide or ganirelix, which are GnRH analogs. In cases where medical treatments fail, laparoscopic ovarian drilling is considered as a surgical option.
π Surgical Intervention and Conclusion
The final paragraph briefly touches on the surgical intervention for PCOS, specifically laparoscopic ovarian drilling, which involves the destruction of ovarian theca cells using a monopolar cautery to reduce the number of cysts. The paragraph concludes the lecture by summarizing the key points about PCOS and thanking the audience for their attention.
Mindmap
Keywords
π‘Polycystic Ovarian Syndrome (PCOS)
π‘Androgens
π‘Hirsutism
π‘Aromatase Enzyme
π‘Follicle Stimulating Hormone (FSH)
π‘Luteinizing Hormone (LH)
π‘Ovulation
π‘Endometrial Hyperplasia
π‘Insulin Resistance
π‘Rotterdam Criteria
Highlights
Polycystic ovarian disease (PCOD) is also known as polycystic ovarian syndrome or Stein-Leventhal syndrome.
Increased androgen production is the basic pathology in PCOD.
Androgen increase leads to hirsutism, the growth of sexual terminal hair.
Androgen is converted to estrogen by the aromatase enzyme, impacting follicle stimulating hormone (FSH) levels.
Elevated estrogen decreases FSH and increases the ratio of luteinizing hormone (LH) to FSH, which is typically greater than 2:1 in PCOD.
The absence of an LH surge due to constant LH increase prevents ovulation.
No ovulation results in decreased progesterone levels, leading to oligomenorrhea and potentially secondary amenorrhea.
Increased LH stimulates theca cells, causing hypertrophy and further androgen production.
In PCOD, multiple follicles form but do not mature into a corpus luteum, leading to cysts in the ovary.
Increased estrogen can cause endometrial hyperplasia, which may progress to cancer.
PCOD alters lipid profiles, increasing LDL and decreasing HDL, contributing to cardiovascular risks.
Increased androgens inhibit the production of sex hormone-binding globulin, leading to insulin resistance and diabetes risk.
PCOD can cause obesity, mood changes, depression, and an increased risk of obstructive sleep apnea.
Acanthosis nigricans, pigmented linear marks, are a sign of insulin resistance seen in PCOD.
Hormonal changes in PCOD include increased androgens, LH, estrogen, insulin, and LDL, with decreased FSH, sex hormone-binding globulin, progesterone, and HDL.
Long-term consequences of PCOD include increased cardiovascular risks, diabetes, endometrial and breast cancers, sleep apnea, and mood disorders.
The Rotterdam criteria (2003) are used for diagnosing PCOD, focusing on symptoms, clinical and biochemical signs, and ultrasound findings.
First-line treatment for PCOD includes weight reduction, lifestyle modifications, and oral contraceptive pills (OCPs) for irregular periods.
For insulin resistance, metformin is prescribed, and for hirsutism, OCPs with ciproteron acetate are used.
In cases of infertility with PCOD, selective estrogen receptor modulators like clomiphene citrate are the first line of treatment.
If medical treatments fail, laparoscopic ovarian drilling may be performed as a surgical option for PCOD.
Transcripts
hello friends let us now learn some
important points about
polycystic ovarian disease or polycystic
ovarian syndrome also called has steen
lavental syndrome
so in this steel levinthal syndrome the
basic pathology in this is increased
androgen production
whatever the reason is here
most commonly there will be increased
androgen production
this increased androgen reduction will
first leads to historism this increased
androgen stimulates the growth of sexual
terminal hair resulting in hirsutism
then
this increased androgen
undergoes peripherally we have aromatase
enzyme
in the presence of this aromatase enzyme
this androgen
gets converted to estrogen
when this androgen gets converted to
estrogen this is trojan has three
effects
one estrogen can decrease follicle
stimulating hormone
once it decreases follicle why does it
decrease follicle stimulating hormone
so increased estrogen is estrogen is
actually produced from ovary ovary
produces estrogen
this production of east ocean by ovary
is activated by follicle stimulating
hormone which is produced by pituitary
so if estrogen is increased in any
regression due to any reason if estrogen
is increased then it exerts negative
feedback mechanism on follicle
stimulating hormone thus there is
decreased follicle stimulating hormone
once there is decreased follicle
stimulating hormone
if you do
a ratio of luteinizing hormone to
follicle stimulating hormone normally it
is one is to do but in patients with
pcod this utilizing heart moon
to follicle stimulating hormone ratio
will be more than two is to one
fine this increased east trojan
will have negative feedback on follicle
stimulating hormone whereas this
estrogen has positive feedback on
luteinizing heart mole and thus
increasing the action of utilizing
hormone
now this luteinizing hormone is
increased
then this luteinizing hormone is
increased first thing is there is no lh
search
normally whenever there is increased lh
surge
that causes an ovulation you can ask me
there is increased neutrinizing hormone
that means there is increased utilizing
that means there is a lh
but this increased
luteinizing hormone is constant
there is constant continuous increase in
luteinizing hormone
but in lh search there will be increase
in
luteinizing hormone
it is strike like suddenly and then it
falls this is a leth search
but here there is continuous increase in
utilizing hormone
this
absence of lh surge
will cause an ovulation ovulation mainly
occurs due to a lh search once there is
no lh search there is no ovulation now
when there is no ovulation this will
decrease the progesterone levels
ovulation will lead to increased
progesterones but because there is no
ovulation there is decreased
progesterone levels overall this will
lead to
in the beginning there will be
oligomenorrhea
but slowly as the days progresses this
disease progresses to secondary
amenorrhoea
right
then
this lh hormone will cause one more
cause we'll have one more issue see
because of this lh increased lh this
increased lh also stimulates
the causes
because lh stimulates the castles this
thicker cells will undergo
hypertrophy and they will produce
androgens again
and this leads to increased androgens
overall
because of thick cell hypertrophy
then
right there is an ovulation very good
if there is an ovulation then what about
the eggs which are to be released
normally every month there will be one
egg which is released one follicle which
is released but if there is an ovulation
there will be formation of multiple
follicles in the ovary and among these
one will grow to a bigger size and it
will form graphene follicle and that is
released outside but in pcod there is no
formation of graphene follicle so there
will be multiple cysts will remain in
the ovary due to this an ovulation
so in pcod you see
the follicles are converted to multiple
cysts in the ovary
right next
then if there is increased androgens now
there is increase so increased estrogens
increased east ocean will act on the
endometrium and it causes endometrial
hyperplasia
as days progresses this endometrial
hyperplasia
will convert into endometrial
hyperplasia with atypia and finally it
can cause
endometrial cancer
and this will also predispose to
breast carcinoma
also
right then
this pcod there is one more important
thing
this pcod also causes alters the lipid
profile
it alters the lipid profile
and it increases the ldl and decreases
hdl and thus it will
lead to cardiovascular risk factors that
is future in future it can cause or it
can lead to heart disease
right now
one important thing is
when there is increased androgens there
is one more important thing
even whenever there is increased
androgens
this increased androgens will inhibit a
hormone
a protein actually this increased
androgens will inhibit a protein called
as serum
sex hormone binding globulin
okay when it inhibits the protein serum
sex hormone binding globulin production
this will result in
increased insulin
this will result in insulin resistance
because of this insulin resistance this
will predispose a patient with
polycystic ovarian disease to diabetes
mellitus
so
so in so this is the main thing that
happens in pcod
right there is one more thing
right because of this increased or
altered lipid profile
this will cause
obesity in the patient
okay because of this excess obesity this
can lead to
mood changes
and depression
and this can also lead to this opacity
can also
cause
sleep apnea especially obstructive sleep
apnea
the increased risk of obstructive sleep
apnea is also seen in these patients
fine
so
if you see the clinical features it's
nothing but whatever is here so the
uh a woman of middle aged women comes to
us with history of menstrual
irregularity that is
primarily irregular cycles and
amenorrhea
and on you can observe that the patient
is obese and there is history of
hirsutism that is acne
alopecia is seen
and you will see that on lipid profile
examination you see there is altered
lipid profile and there is insulin
resistance
so
that is the clinical picture there is
one important thing that occurs in pcod
which is called as a kantosis nigricans
a kantosis nigricans is pigmented linear
marks
which you see in the neck and axilla are
seen in acanthosis nigricans these
acanthosis nigricans occur due to
insulin resistance
insulin resistance leads to this
acanthosis nigricles
right
then
what are the hormonal changes that you
see in pcod
see
in pcod there will be
in pcod there will be increased
androgens number one
that is there will be increased
testosterone increased androstene ion
and increased dihydroxy ep androsterone
then there will be increased luteinizing
hormone
there is increased estrogen
and because of this insulin resistance
the insulin will not dixie because of
this insulin resistance insulin will not
act on peripheral tissues
so there will be increased insulin which
is present in our body because it is not
going to act on the peripheral tissues
so there will be increased insulin and
there will be increased
ldl
low density lipoproteins so water
increased in pcod there will be
increased androgens increased estrogens
increased luteinizing hormone and
increased
insulin and increased
low density lipoprotein is seen in
utilizing hormone that water decreased
in
polycystic ovarian disease in polycystic
ovarian disease there will be decreased
follicle stimulating hormone
there will be androgens will inhibit
sex hormone binding globulin so sex
hormone binding globulin is decreased
and there will be
decreased progesterone
okay
and there will be decreased hdl
so in polycystic ovarian disease you see
there is decreased sex hormone binding
globulin decreased follicle stimulating
hormone decreased hdl and decreased
progesterone
then
if you are asked about the long term
consequences of this newtonizing
of this follicle sorry polycystic
ovarian disease what are the long term
consequences
due to this polycystic ovarian disease
in the long term because of this altered
lipid profile this will cause increased
cvs risk factors especially coronary
artery disease increases in the patient
on long term because of insulin
resistance there is increased risk of
diabetes mellitus in the future due to
increased estrogen there is increased
risk of endometrial carcinoma and also
breast carcinoma is noted in the future
then
because the patient becomes obese there
is increased risk of sleep apnea
and also there will be more changes and
depression these more changes and
depression are also attributed to
estrogen
estrogen and project decreased
progesterone
also causes more changes and depression
and there is one important long-term
consequence which is not there in this
chat that is non-alcoholic
steatohepatitis
non-alcoholics tiato hepatitis
is also long-term risk factor of
polycystic ovarian disease
right
now what about the diagnostic criteria
so the diagnostic criteria we have a
name for this diagnostic criteria that
is rotterdam criteria this is rather
damn criteria according to this
rotterdam criteria 2003
first there will be symptoms of
oligomenorrhea
or amnoria are seen
then clinically
there the patient will have increased
serum testosterone will be diagnosed or
that is first clinical efficacy the
first we have first
criteria is symptoms that is presence of
oligomenorrhea
or amenorrhea second symptom is clinical
plus biochemical symptom
okay in clinical symptom we have the
patient will have hypsotism
comes under clinical symptom
whereas in biochemical symptom
we have increased serum testosterone
actually this serum testosterone levels
should be between 70 to 150 nanogram per
deciliter
these should not be more than 200
nanogram per deciliter
if the serum testosterone levels are
more than 200 nanogram per deciliter
then we do not consider polycystic
ovarian disease
then what do we consider if there is
serum testosterone levels are more than
200 nanograms per deciliter then we will
consider presence of ovarian tumor
rather than polycystic ovarian disease
so in polycystic ovarian disease serum
testosterone should be between
70 to 150 nanogram per deciliter
then third criteria is radiology that is
in usg you will see presence of two or
more cysts
which are of size 2 to 9
mm so 12 or more cysts which are of size
2 to 9 mm which is present in one or
both ovaries
with ovaries more than 10 ml that is
enlarged ovaries so this numbers are
important in usg you will see 12 or
presents of 12 or more cysts which are
of 2 to 9 mm in diameter present in one
or both the ovaries
and each ovary is enlarged that is more
than 10 ml
volume
so this is the rotterdam criteria which
includes
clinical symptoms then clinical and
biochemical symptoms then
ultrasonography
then
how are you going to treat these
patients with pcod
so if a patient comes to you with
pcod
so if a patient comes to you with pcod
first line treatment is giving selective
estrogen receptor modulator
so in this selective estrogen receptor
modulator
the
we can give
clomiphene citrate
and tamoxifen
and reloxified
fine this is fine but do you give them
for first line no they are actually the
first line for infertility
so this is if the patient suffers from
infertility with pcod then the first
line is
selective estrogen receptor modulators
if the patient suffers from pcod always
ask her for weight reduction
and lifestyle modifications are the
first line
first step you give the patient is
to decrease obesity through weight
reduction lifestyle modifications and
exercises
even after that if there is no
uh you know it does not resolve and if
there are irregular periods
then you should give
ocps
oral contraceptive pills
and if there is insulin resistance or
hyperinsulinism
then you should give
metformin
so treatment mainly depends upon the
symptoms
if there is hyposodism if there is
similar if there is hirasutism then you
should give ocps with clomiphene citrate
so the treatment mainly depends with the
sorry
i'm really sorry you should give oc
piece with
c protein acetate
i'm really sorry ocp is with ciproterron
acetate
bro
i'll write it properly
cipro tear on
acetate
okay for his hisotism you should give
ocps with ciproteuron acetate
okay so pcod first line you will do
weight reduction and lifestyle
modifications followed by you should
give symptomatic treatment for irregular
periods you should give ocps
okay for insulin
should be given
sorry metformin should be given for
insulin resistance so you will treat it
according to the symptoms but if there
is infertility with pcod
in such cases the first line is giving
selective estrogen receptor modulators
then following these selective estrogen
receptor modulators in these the drug of
choice is chlamyfin citrate
okay among these selective estrogen
receptor modulators drug of choice is
chromophil citrate if the person cannot
tolerate chlamyfin citrate then you give
them oxyphen
even if the person
okay this reloxifen is not normally used
it is not generally used then if you see
the second lines second line will be you
can use either gonadotropins
or you can use lh and fsh injections can
also be used
and if you see the third line
in third line we can use leukolyte or
gaucher aline can also be used third
line is mainly gnrh analogs
so for pcod with infertility you can use
selective estrogen receptor modulator
and second line drugs like gonadotropins
and lhfsh injections can be given and
you can also use chronotropine releasing
hormone analogs
but
then
if even after doing everything if still
this does not dissolve then you should
do surgery
and in the surgery for pcos we have
laparoscopic ovarian drilling
where you will pass a monopolar cautery
into the ovary this is the ovary with
polycysts many cysts then you will pass
a monopolar cautery into the
ovary and destroy the ovarian thicker
all the thicker you will destroy it
so this is about the polycystic ovarian
disease thank you guys for watching my
lecture
thank you
you
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