NAME – SOHON SEN

CLASS – XI

SECTION – B

SUBJECT - BIOLOGY
Sl.No. TOPIC PAGE NUMBER DATE

1. ACKNOWLEDGEMENT 1 27 / 5 / 2019

2. POLYCYSTIC 2 - 27 27 / 5 / 2019
OVARIAN SYNDROME

CERTIFICATE OF 28 27 / 5 / 2019
3. APPROVAL
I am very much thankful to our
”BIOLOGY TEACHER ” ,for giving us
such a nice assignment to write upon. I
am very happy to say that i really
enjoyed writing this project because i
could know very interesting facts
about this topic and i have gained
some knowledge from it.
POLYCYSTIC OVARIAN SYNDROME
Polycystic ovary syndrome (PCOS) is a set of symptoms due to
elevated androgens (male hormones) in females. Signs and symptoms
of PCOS include irregular or no menstrual periods, heavy
periods, excess body and facial hair, acne, pelvic pain, difficulty getting
pregnant, and patches of thick, darker, velvety skin. Associated
conditions include type 2 diabetes, obesity, obstructive sleep
apnea, heart disease, mood disorders, and endometrial cancer.

PCOS is due to a combination of genetic and environmental factors.

Risk factors include obesity, a lack of physical exercise, and a family
history of someone with the condition. Diagnosis is based on two of the
following three findings: no ovulation, high androgen levels, and ovarian
cysts. Cysts may be detectable by ultrasound. Other conditions that
produce similar symptoms include adrenal hyperplasia, hypothyroidism,
and high blood levels of prolactin.

PCOS has no cure. Treatment may involve lifestyle changes such as

weight loss and exercise. Birth control pills may help with improving the
regularity of periods, excess hair growth, and acne. Metformin and anti-
androgens may also help. Other typical acne treatments and hair
removal techniques may be used. Efforts to improve fertility include
weight loss, clomiphene, or metformin. In vitro fertilization is used by
some in whom other measures are not effective.

PCOS is the most common endocrine disorder among women between

the ages of 18 and 44. It affects approximately 2% to 20% of this age
group depending on how it is defined. When someone is infertile due to
lack of ovulation, PCOS is the most common cause. The earliest known
description of what is now recognized as PCOS dates from 1721 in Italy.
Common signs and symptoms of PCOS include the following:

 Menstrual disorders: PCOS mostly produces oligomenorrhea (fewer

than nine menstrual periods in a year) or amenorrhea(no menstrual
periods for three or more consecutive months), but other types of
menstrual disorders may also occur.
 Infertility: This generally results directly from chronic anovulation (lack
of ovulation).
 High levels of masculinizing hormones: Known as hyperandrogenism,
the most common signs are acne and hirsutism(male pattern of hair
growth, such as on the chin or chest), but it may
produce hypermenorrhea (heavy and prolonged menstrual
periods), androgenic alopecia (increased hair thinning or diffuse hair
loss), or other symptoms. Approximately three-quarters of women
with PCOS (by the diagnostic criteria of NIH/NICHD 1990) have
evidence of hyperandrogenemia. Metabolic syndrome: This appears
as a tendency towards central obesity and other symptoms
associated with insulin resistance. Serum insulin, insulin resistance,
and homocysteine levels are higher in women with PCOS.

Asians affected by PCOS are less likely to develop hirsutism than those
of other ethnic backgrounds.

Women with PCOS tend to have central obesity, but studies are
conflicting as to whether visceral and subcutaneous abdominal fat is
increased, unchanged, or decreased in women with PCOS relative to
reproductively normal women with the same body mass index. In any
case, androgens, such
as testosterone, androstanolone (dihydrotestosterone), and nandrolone
decanoate, have been found to increase visceral fat deposition in both
female animals and women.
PCOS is a heterogeneous disorder of uncertain cause. There is some
evidence that it is a genetic disease. Such evidence includes the familial
clustering of cases, greater concordance in monozygotic compared
with dizygotic twins and heritability of endocrine and metabolic features
of PCOS. There is some evidence that exposure to higher than typical
levels of androgens and the anti-Müllerian hormone (AMH) in
utero increases the risk of developing PCOS in later life.

Genetics
The genetic component appears to be inherited in an autosomal
dominant fashion with high genetic penetrance but
variable expressivity in females; this means that each child has a 50%
chance of inheriting the predisposing genetic variant(s) from a parent,
and, if a daughter receives the variant(s), the daughter will have the
disease to some extent. The genetic variant(s) can be inherited from
either the father or the mother, and can be passed along to both sons
(who may be asymptomatic carriers or may have symptoms such as
early baldness and/or excessive hair) and daughters, who will show
signs of PCOS. The phenotype appears to manifest itself at least
partially via heightened androgen levels secreted byovarian follicle
theca cells from women with the allele. The exact gene affected has not
yet been identified. In rare instances, single-gene mutations can give
rise to the phenotype of the syndrome. Current understanding of the
pathogenesis of the syndrome suggests, however, that it is a complex
multigenic disorder.

The severity of PCOS symptoms appears to be largely determined by

factors such as obesity.

PCOS has some aspects of a metabolic disorder, since its symptoms

are partly reversible. Even though considered as a gynecological
problem, PCOS consists of 28 clinical symptoms.
Even though the name suggests that the ovaries are central to disease
pathology, cysts are a symptom instead of the cause of the disease.
Some symptoms of PCOS will persist even if both ovaries are removed;
the disease can appear even if cysts are absent. Since its first
description by Stein and Leventhal in 1935, the criteria of diagnosis,
symptoms, and causative factors are subject to debate. Gynecologists
often see it as a gynecological problem, with the ovaries being the
primary organ affected. However, recent insights show a multisystem
disorder, with the primary problem lying in hormonal regulation in the
hypothalamus, with the involvement of many organs. The name PCOD
is used when there is ultrasonographic evidence. The term PCOS is
used since there is a wide spectrum of symptoms possible, and cysts in
the ovaries are seen only in 15% of people.

Environment
PCOS may be related to or worsened by exposures during the prenatal
period, epigenetic factors, environmental impacts (especially industrial
endocrine disruptors such as bisphenol A and certain drugs) and the
increasing rates of obesity.
Not everyone with PCOS has polycystic ovaries (PCO), nor does
everyone with ovarian cysts have PCOS; although a pelvic ultrasound is
a major diagnostic tool, it is not the only one. The diagnosis is
straightforward using the Rotterdam criteria, even when the syndrome is
associated with a wide range of symptoms.

 Transvaginal ultrasound scan of polycystic ovary

 Polycystic ovary as seen on sonography

Definition
Two definitions are commonly used:

NIH
In 1990 a consensus workshop sponsored by
the NIH/NICHD suggested that a person has PCOS if they have all
of the following:

1. oligoovulation
2. signs of androgen excess (clinical or biochemical)
3. exclusion of other disorders that can result in menstrual
irregularity and hyperandrogenism

Rotterdam
In 2003 a consensus workshop sponsored
by ESHRE/ASRM in Rotterdam indicated PCOS to be present if
any 2 out of 3 criteria are met, in the absence of other entities that
might cause these findings
 1. oligoovulation and/or anovulation
2. excess androgen activity
3. polycystic ovaries (by gynecologic ultrasound)

The Rotterdam definition is wider, including many more women,

the most notable ones being women without androgen excess.
Critics say that findings obtained from the study of women with
androgen excess cannot necessarily be extrapolated to women
without androgen excess.

Androgen Excess PCOS Society

In 2006, the Androgen Excess PCOS Society suggested a
tightening of the diagnostic criteria to all of the following:

1. excess androgen activity

2. oligoovulation/anovulation and/or polycystic ovaries
3. exclusion of other entities that would cause excess
androgen activity

Standard assessment

 History-taking, specifically for menstrual pattern, obesity,

hirsutism and acne. A clinical prediction rule found that
these four questions can diagnose PCOS with
a sensitivity of 77.1% (95% confidence interval [CI] 62.7%–
88.0%) and a specificity of 93.8% (95% CI 82.8%–98.7%).
 Gynecologic ultrasonography, specifically looking for
small ovarian follicles. These are believed to be the result of
disturbed ovarian function with failed ovulation, reflected by
the infrequent or absent menstruation that is typical of the
condition. In a normal menstrual cycle, one egg is released
from a dominant follicle – in essence, a cyst that bursts to
release the egg. After ovulation, the follicle remnant is
transformed into a progesterone-producing corpus luteum,
which shrinks and disappears after approximately 12–14
days. In PCOS, there is a so-called follicular arrest; i.e.,
several follicles develop to a size of 5–7 mm, but not further.
No single follicle reaches the preovulatory size (16 mm or
more). According to the Rotterdam criteria, which are widely
 used for diagnosis, 12 or more small follicles should be seen
in an ovary on ultrasound examination. More recent
research suggests that there should be at least 25 follicles
in an ovary to designate it as having polycystic ovarian
morphology (PCOM) in women aged 18–35 years. The
follicles may be oriented in the periphery, giving the
appearance of a 'string of pearls'. If a high resolution
transvaginal ultrasonography machine is not available, an
ovarian volume of at least 10 ml is regarded as an
acceptable definition of having polycystic ovarian
morphology instead of follicle count.
 Laparoscopic examination may reveal a thickened, smooth,
pearl-white outer surface of the ovary. (This would usually
be an incidental finding if laparoscopy were performed for
some other reason, as it would not be routine to examine
the ovaries in this way to confirm a diagnosis of PCOS.)
 Serum (blood) levels of androgens (hormones associated
with male development),
including androstenedione and testosterone may be
elevated.] Dehydroepiandrosterone sulfate levels above
700–800 µg/dL are highly suggestive of adrenal dysfunction
because DHEA-S is made exclusively by the adrenal
glands. The free testosterone level is thought to be the best
measure, with ~60% of PCOS patients demonstrating
supranormal levels. The Free androgen index (FAI) of the
ratio of testosterone to sex hormone-binding
globulin (SHBG) is high and is meant to be a predictor of
free testosterone, but is a poor parameter for this and is no
better than testosterone alone as a marker for
PCOS,] possibly because FAI is correlated with the degree
of obesity.

Some other blood tests are suggestive but not diagnostic. The
ratio of LH (Luteinizing hormone) to FSH (Follicle-stimulating
hormone), when measured in international units, is elevated in
women with PCOS. Common cut-offs to designate abnormally
high LH/FSH ratios are 2:1 or 3:1 as tested on Day 3 of the
menstrual cycle. The pattern is not very sensitive; a ratio of 2:1
or higher was present in less than 50% of women with PCOS in
one study. There are often low levels of sex hormone-binding
globulin, in particular among obese or overweight women.
 Anti-Müllerian hormone (AMH) is increased in PCOS, and may
become part of its diagnostic criteria.

Associated conditions

 Fasting biochemical screen and lipid profile

 2-Hour oral glucose tolerance test (GTT) in women with risk
factors (obesity, family history, history of gestational
diabetes) may indicate impaired glucose tolerance (insulin
resistance) in 15–33% of women with PCOS. Frank
diabetes can be seen in 65–68% of women with this
condition. Insulin resistance can be observed in both normal
weight and overweight people, although it is more common
in the latter (and in those matching the stricter NIH criteria
for diagnosis); 50–80% of people with PCOS may have
insulin resistance at some level.
 Fasting insulin level or GTT with insulin levels (also called
IGTT). Elevated insulin levels have been helpful to predict
response to medication and may indicate women needing
higher dosages of metformin or the use of a second
medication to significantly lower insulin levels.
Elevated blood sugar and insulin values do not predict who
responds to an insulin-lowering medication, low-glycemic
diet, and exercise. Many women with normal levels may
benefit from combination therapy. A hypoglycemic response
in which the two-hour insulin level is higher and the blood
sugar lower than fasting is consistent with insulin resistance.
A mathematical derivation known as the HOMAI, calculated
from the fasting values in glucose and insulin
concentrations, allows a direct and moderately accurate
measure of insulin sensitivity (glucose-level x insulin-
level/22.5).
 Glucose tolerance testing (GTT) instead of fasting glucose
can increase diagnosis of impaired glucose tolerance and
frank diabetes among people with PCOS according to a
prospective controlled trial. While fasting glucose levels may
remain within normal limits, oral glucose tests revealed that
up to 38% of asymptomatic women with PCOS (versus
8.5% in the general population) actually had impaired
glucose tolerance, 7.5% of those with frank diabetes
according to ADA guidelines.
Differential diagnosis
Other causes of irregular or absent menstruation and hirsutism,
such as hypothyroidism, congenital adrenal hyperplasia (21-
hydroxylase deficiency), Cushing's
syndrome, hyperprolactinemia, androgen secreting neoplasms,
and other pituitary or adrenal disorders, should be investigated.
The primary treatments for PCOS include: lifestyle changes and
medications.
Goals of treatment may be considered under four categories:

 Lowering of insulin resistance levels

 Restoration of fertility
 Treatment of hirsutism or acne
 Restoration of regular menstruation, and prevention of endometrial
hyperplasia and endometrial cancer

In each of these areas, there is considerable debate as to the optimal

treatment. One of the major reasons for this is the lack of large-scale
clinical trials comparing different treatments. Smaller trials tend to
be less reliable and hence may produce conflicting results.

General interventions that help to reduce weight or insulin resistance

can be beneficial for all these aims, because they address what is
believed to be the underlying cause.

As PCOS appears to cause significant emotional distress, appropriate

support may be useful.

Diet
Where PCOS is associated with overweight or obesity, successful
weight loss is the most effective method of restoring normal
ovulation/menstruation, but many women find it very difficult to achieve
and sustain significant weight loss. A scientific reviewin 2013 found
similar decreases in weight and body composition and improvements
in pregnancy rate, menstrual regularity, ovulation, hyperandrogenism,
insulin resistance, lipids, and quality of life to occur with weight loss
independent of diet composition. Still, a low GI diet, in which a significant
part of total carbohydrates are obtained from fruit, vegetables, and
whole-grain sources, has resulted in greater menstrual regularity than
a macronutrient-matched healthy diet.

Vitamin D deficiency may play some role in the development of

the metabolic syndrome, so treatment of any such deficiency is
indicated. However, a systematic review of 2015 found no evidence that
vitamin D supplementation reduced or mitigated metabolic and hormonal
dysregulations in PCOS. As of 2012, interventions using dietary
supplements to correct metabolic deficiencies in people with PCOS had
been tested in small, uncontrolled and nonrandomized clinical trials; the
resulting data is insufficient to recommend their use.

Medications
Medications for PCOS include oral contraceptives and metformin. The
oral contraceptives increase sex hormone binding globulin production,
which increases binding of free testosterone. This reduces the
symptoms of hirsutism caused by high testosterone and regulates return
to normal menstrual periods. Metformin is a medication commonly used
in type 2 diabetes mellitus to reduce insulin resistance, and is used off
label (in the UK, US, AU and EU) to treat insulin resistance seen in
PCOS. In many cases, metformin also supports ovarian function and
return to normal ovulation. Spironolactone can be used for its
antiandrogenic effects, and the topical cream eflornithine can be used to
reduce facial hair. A newer insulin resistance medication class,
the thiazolidinediones (glitazones), have shown equivalent efficacy to
metformin, but metformin has a more favorable side effect profile. The
United Kingdom's National Institute for Health and Clinical
Excellencerecommended in 2004 that women with PCOS and a body
mass index above 25 be given metformin when other therapy has failed
to produce results. Metformin may not be effective in every type of
PCOS, and therefore there is some disagreement about whether it
should be used as a general first line therapy. In addition to this,
metformin is associated with several unpleasant side effects: including
abdominal pain, metallic taste in the mouth, diarrhoea and vomiting. The
use of statins in the management of underlying metabolic syndrome
remains unclear.
It can be difficult to become pregnant with PCOS because it causes
irregular ovulation. Medications to induce fertility when trying to conceive
include the ovulation inducer clomiphene or pulsatile leuprorelin.
Metformin improves the efficacy of fertility treatment when used in
combination with clomiphene. Metformin is thought to be safe to use
during pregnancy (pregnancy category B in the US). A review in 2014
concluded that the use of metformin does not increase the risk of
major birth defects in women treated with metformin during the first
trimester. Liraglutide may reduce weight and waist circumference more
than other medications.

Infertility
Main article: Infertility in polycystic ovary syndrome

Not all women with PCOS have difficulty becoming pregnant. For those
that do, anovulation or infrequent ovulation is a common cause. Other
factors include changed
levelsof gonadotropins, hyperandrogenemia and hyperinsulinemia. Like
women without PCOS, women with PCOS that are ovulating may be
infertile due to other causes, such as tubal blockages due to a history of
sexually transmitted diseases.

For overweight anovulatory women with PCOS, weight loss and diet
adjustments, especially to reduce the intake of simple carbohydrates,
are associated with resumption of natural ovulation.

For those women that after weight loss still are anovulatory or for
anovulatory lean women, then the medications letrozole and clomiphene
citrate are the principal treatments used to promote
ovulation. Previously, the anti-diabetes medication metformin was
recommended treatment for anovulation, but it appears less effective
than letrozole or clomiphene.

For women not responsive to letrozole or clomiphene and diet and

lifestyle modification, there are options available including assisted
reproductive technology procedures such as controlled ovarian
hyperstimulation with follicle-stimulating hormone(FSH) injections
followed by in vitro fertilisation (IVF).

Though surgery is not commonly performed, the polycystic ovaries can

be treated with a laparoscopic procedure called "ovarian drilling"
(puncture of 4–10 small follicles with electrocautery, laser, or biopsy
needles), which often results in either resumption of spontaneous
ovulations or ovulations after adjuvant treatment with clomiphene or
FSH. (Ovarian wedge resection is no longer used as much due to
complications such as adhesions and the presence of frequently
effective medications.) There are, however, concerns about the long-
term effects of ovarian drilling on ovarian function.

Hirsutism and acne

When appropriate (e.g., in women of child-bearing age who require
contraception), a standard contraceptive pill is frequently effective in
reducing hirsutism. Progestogens such as norgestrel and levonorgestrel
should be avoided due to their androgenic effects.

Other medications with anti-androgen effects

include flutamide, and spironoacitone, which can give some
improvement in hirsutism. Metformin can reduce hirsutism, perhaps by
reducing insulin resistance, and is often used if there are other features
such as insulin resistance, diabetes, or obesity that should also benefit
from metformin. Eflornithine (Vaniqa) is a medication that is applied to
the skin in cream form, and acts directly on the hair follicles to inhibit hair
growth. It is usually applied to the face. 5-alpha reductase
inhibitors (such as finasteride and dutasteride) may also be used; they
work by blocking the conversion
of testosterone to dihydrotestosterone (the latter of which responsible for
most hair growth alterations and androgenic acne).

Although these agents have shown significant efficacy in clinical trials

(for oral contraceptives, in 60–100% of individuals), the reduction in hair
growth may not be enough to eliminate the social embarrassment of
hirsutism, or the inconvenience of plucking or shaving. Individuals vary
in their response to different therapies. It is usually worth trying other
medications if one does not work, but medications do not work well for
all individuals.

Menstrual irregularity
If fertility is not the primary aim, then menstruation can usually be
regulated with a contraceptive pill. The purpose of regulating
menstruation, in essence, is for the woman's convenience, and perhaps
her sense of well-being; there is no medical requirement for regular
periods, as long as they occur sufficiently often.

If a regular menstrual cycle is not desired, then therapy for an irregular

cycle is not necessarily required. Most experts say that, if a menstrual
bleed occurs at least every three months, then the endometrium (womb
lining) is being shed sufficiently often to prevent an increased risk of
endometrial abnormalities or cancer. If menstruation occurs less often or
not at all, some form of progestogen replacement is recommended. An
alternative is oral progestogen taken at intervals (e.g., every three
months) to induce a predictable menstrual bleeding.

Alternative medicine
A 2017 review concluded that while both myo-inositol and D-chiro-
inositols may regulate menstrual cycles and improve ovulation, there is a
lack of evidence regarding effects on the probability of pregnancy. A
2012 and 2017 review have found myo-inositol supplementation appears
to be effective in improving several of the hormonal disturbances of
PCOS. Myo-inositol reduces the amount of gonadotropins and the length
of controlled ovarian hyperstimulation in women undergoing in vitro
fertilization. A 2011 review found not enough evidence to conclude any
beneficial effect from D-chiro-inositol. There is insufficient evidence to
support the use of acupuncture.
A diagnosis of PCOS suggests an increased risk of the following:

 Endometrial hyperplasia and endometrial cancer (cancer of the

uterine lining) are possible, due to overaccumulation of uterine lining,
and also lack of progesterone resulting in prolonged stimulation of
uterine cells by estrogen. It is not clear whether this risk is directly
due to the syndrome or from the associated
obesity, hyperinsulinemia, and hyperandrogenism.
 Insulin resistance/Type II diabetes. A review published in 2010
concluded that women with PCOS have an elevated prevalence of
insulin resistance and type II diabetes, even when controlling for body
mass index (BMI). PCOS also makes a woman, particularly if obese,
prone to gestational diabetes.
 High blood pressure, in particular if obese or during pregnancy
 Depression and anxiety
 Dyslipidemia – disorders of lipid metabolism — cholesterol and
triglycerides. Women with PCOS show a decreased removal
of atherosclerosis-inducing remnants, seemingly independent of
insulin resistance/Type II diabetes.
 Cardiovascular disease, with a meta-analysis estimating a 2-fold risk
of arterial disease for women with PCOS relative to women without
PCOS, independent of BMI.
 Strokes
 Weight gain
 Miscarriage
 Sleep apnea, particularly if obesity is present
 Non-alcoholic fatty liver disease, again particularly if obesity is
present
 Acanthosis nigricans (patches of darkened skin under the arms, in
the groin area, on the back of the neck)
 Autoimmune thyroiditis
The risk of ovarian cancer and breast cancer is not significantly
increased overall.
The prevalence of PCOS depends on the choice of diagnostic criteria.
The World Health Organization estimates that it affects 116 million
women worldwide as of 2010 (3.4% of women). One community-based
prevalence study using the Rotterdam criteria found that about 18% of
women had PCOS, and that 70% of them were previously undiagnosed.
Ultrasonographic findings of polycystic ovaries are found in 8–25% of
women non-affected by the syndrome. 14% women on oral
contraceptives are found to have polycystic ovaries. Ovarian cysts are
also a common side effect of levonorgestrel-releasing intrauterine
devices (IUDs).
The condition was first described in 1935 by American gynecologists
Irving F. Stein, Sr. and Michael L. Leventhal, from whom its original
name of Stein–Leventhal syndrome is taken.
The earliest published description of a person with what is now
recognized as PCOS was in 1721 in Italy. Cyst-related changes to the
ovaries were described in 1844.
In 2005, 4 million cases of PCOS were reported in the USA, costing
$4.36 billion in healthcare costs. In 2016 out of the National Institute
Health’s research budget of $32.3 billion for that year, 0.1% was spent
on PCOS research.
Other names for this syndrome include polycystic ovarian syndrome,
polycystic ovary disease, functional ovarian hyperandrogenism,
ovarian hyperthecosis, sclerocystic ovary syndrome, and Stein–
Leventhal syndrome. The eponymous last option is the original name; it
is now used, if at all, only for the subset of women with all the symptoms
of amenorrhea with infertility, hirsutism, and enlarged polycystic ovaries.
Most common names for this disease derive from a typical finding on
medical images, called a polycystic ovary. A polycystic ovary has an
abnormally large number of developing eggs visible near its surface,
looking like many small cysts.
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 Polycystic ovary syndrome

Other names Hyperandrogenic anovulation

(HA),Stein–Leventhal syndrome
 A polycystic ovary shown on an ultrasound image.

Specialty Gynecology

Symptoms Irregular menstrual periods, heavy

periods, excess hair, acne, pelvic
pain, difficulty getting
pregnant, patches of thick, darker,
velvety skin

Complications Type 2 diabetes, obesity, obstructive

sleep apnea, heart disease, mood
disorders, endometrial cancer

Duration Long term

Causes Genetic and environmental factors

Risk factors Obesity, not enough exercise, family

history

Diagnostic Based on no ovulation,

method high androgen levels, ovarian cysts]

Differential Adrenal
diagnosis hyperplasia, hypothyroidism, high
blood levels of prolactin[

Treatment Weight loss, exercise

Medication Birth control pills, metformin, anti-

androgens

Frequency 2% to 20% of women of childbearing

age