Polycystic Ovarian syndrome-PCOD-PCOS
This
disease is very common disorder now days, very frequently spelled as PCOD.
Although
this is not correct, because PCOS is characterized as a syndrome, rather than a
disease. It is the most common cause of Anovulation and secondary Amenorrhoea
in the adolescents. This syndrome is characterized by Oligomenorrhoea,
hirsuitism and obesity; it is associated with insulin resistance and the
development of Diabetes. 1% of female population suffers from PCOS, and the
patients are mostly 15 to 25 years of age group.
This
disease was earlier known as Stein-Leventhal Syndrome. Irving Feiler Stein
graduated from Rush Medical College in 1912. He was trained in obstetrics and
gynaecology at the Michael Reese Hospital, and from 1916 he remained associated
with this hospital for the rest of his life. He also held senior academic
appointment in obstetrics and Gynaecology at the Northwestern University
Medical School and was a senior member of the staff of the Highland Park
Hospital. Stein’s main field of investigation was female infertility. Michael
Leo Leventhal, with whom he shares eponymic fame, was his colleague.
In
polycystic ovary disease, enlarged ovaries with thickened sclerotic capsules
and an abnormally high number of follicles are present. The follicles may
concurrently exist in varying states of growth, maturation, or atresia.
Although
a multiplicity of clinical presentations exists, Stein and Leventhal reported
the classic symptomatology in 1935. They described a group of women with
amenorrhea, infertility, hirsutism, and enlarged polycystic ovaries. The
authors found that, after ovarian biopsy, the women began to menstruate
regularly. As was discovered over time, women may have polycystic ovaries, yet
their cases may not conform to all of the original criteria. Therefore,
Stein-Leventhal syndrome became a subgroup of a more encompassing disease
called polycystic ovary disease.
As
more information regarding the nature of the condition has come to light, other
terms have been applied, including polycystic ovaries syndrome and
polyfollicular ovarian disease. In actuality, polycystic ovaries are not the
primary cause of amenorrhea or hirsutism in this condition. They are simply one
sign of an underlying endocrinologic disorder that ultimately results in
anovulation.
PCOS…Pathophysiology
The
normal adult ovary measures approximately 3-5 cm in length, 1.5-3 cm in width,
and 0.5-1.5 cm in thickness. A thin, fibrous layer called the tunica albuginea
encapsulates the ovary. Within the capsule lies the ovarian stroma, a
combination of fibroblasts, smooth muscle cells, arteries, veins, lymphatics,
nerves, and follicles. The stroma is typically divided into a cortex and
medulla. The medulla is a highly vascular region supplied by the ovarian artery
and branches of the uterine artery, which enter the ovary via the broad
ligament. From here, smaller arteries and arterioles penetrate the cortex. The
peripheral zone, or cortex, is predominantly composed of follicles and
spindle-shaped fibroblasts and smooth muscle cells.
By
the seventh month of gestation, primordial follicles have begun to develop in
the fetal ovary. They consist of primary oocytes encapsulated by single layers
of follicular cells. At birth, each ovary contains approximately 400,000
primordial follicles. After puberty and during each ovarian cycle, a number of
follicles are hormonally stimulated to begin maturing. Usually, only a single
follicle completes the process. Follicular cells proliferate and differentiate
into the granulosa cell layer. The surrounding ovarian stroma differentiates
into thecal cells (internal and external layers). Cell layers play a complex
role in the development of the follicle; in hormonal variations during the
menstrual cycle; and, ultimately, in ovulation.
In
the normal state, the hypothalamus secretes gonadotropin-releasing hormone
(GnRH) in a pulsatile manner. The pituitary gland responds to GnRH by releasing
Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in a similar
cycle. In the follicular phase of the menstrual cycle, LH acts primarily on the
theca cells of the ovary to increase the production of androgenic precursors.
Concurrently, FSH acts on the granulosa cells to promote conversion of the
androgens into estrogens, particularly estradiol, which assists in follicular
development. During the follicular phase, increasing levels of estradiol lead
to an LH surge. In a complex interaction, the LH surge, the elevated levels of
estradiol, and an increase in the circulating progesterone level trigger the
mid cycle surge of FSH.
In
polycystic ovaries syndrome, the cycle is disturbed. Any of several possible
precipitating factors may contribute to the imbalance. Evaluation of blood
serum levels typically reveals elevated LH levels and normal or low FSH levels.
Patients also have increased levels of free oestrogen, primarily estrone and estradiol.
Estrogens exert a complex feedback effect on the pituitary gland that results
in the suppression of FSH secretion and the increased release of LH. Thus, the
production and release of androgen precursors by ovarian theca cells is
increased. The peripheral conversion of androgens to estrogens, primarily
estrone, strengthens the feedback effect on the pituitary gland.
The
same androgens also inhibit the production of sex hormone-binding globulin in
the liver, indirectly increasing levels of free oestrogen in the bloodstream as
well. Locally, elevated androgen levels in the ovary exert a direct inhibitory
effect on follicular maturation. In conjunction with the diminished but steady
presence of FSH, the follicles continue to develop without ever maturing. Thus,
numerous follicles are present in the polycystic ovary and show varying phases
of development and atresia.
PCOS and Insulin Resistance
PCOS
is a hormonal imbalance linked to the way the body processes insulin after it
has been produced by the pancreas to regulate blood sugar. The underlying cause
of PCOS, Insulin Resistance, has many factors that contribute to its presence
in the body. In essence, our environment and lifestyles have evolved too
rapidly for our bodies to keep pace. We are still genetically “wired” to thrive
on the entrenched habits of our ancestors, who consumed different,
nutrient-rich foods, a diet low in carbohydrates and who sustained greater
levels of movement and exercise. Some people may also have a genetic
predisposition to Insulin Resistance, while others develop the condition
through high stress and unhealthy lifestyles.
Over
time, the above factors have damaged the complex ability of the body’s cells to
properly utilize insulin to convert glucose to energy.
This
process creates Insulin Resistance, which causes PCOS in two distinct ways. '
First,
Insulin
Resistance vastly reduces the number of insulin receptor sites or doorways on
the walls of your cells. The average healthy person has some 20,000 receptor
sites per cell, while the average overweight individual with PCOS can have as
few as 5,000. If you have too few receptor sites, glucose bounces off the cell
wall, instead of passing through the insulin door to be burned as energy. With
the cell door almost closed to it, glucose remains in the blood stream, causing
elevated levels of blood sugar, which are sent to the liver. Once there, the
sugar is converted into fat and stored via the blood stream throughout the
body. This process can lead to weight gain and obesity, key factors in creating
PCOS, which is also referred to as Polycystic Ovarian Disease or PCOD.
The second
way
that Insulin Resistance causes PCOS is by raising insulin levels in the blood
stream. Unhealthy lifestyles and genetic conditions cause the pancreas to
overproduce insulin. The cell is, in turn, overwhelmed by this excess insulin
and protects itself by reducing the number of its insulin receptor sites. This
process leaves too few sites for insulin to carry out its normal function,
which is to attach itself to the cell wall and act as a key in a lock allowing
glucose to pass through the cell wall and be converted into energy. The
vastly-reduced number of receptor sites in Insulin Resistant people causes an
excess of insulin “rejected” by the cell to free-float in the blood stream,
creating unbalanced hormone levels in PCOS sufferers. Excess insulin stimulates
the ovaries to produce large amounts of the male hormone testosterone, which
may prevent the ovaries from releasing an egg each month, thus causing
infertility. High levels of insulin also increase the conversion of androgens
(male hormones) to estrogens (female hormones), upsetting a delicate balance
between the two and having a direct effect on weight gain and the formation of
cystic follicles or ovarian cysts.PCOS….
Clinical features
ü Period irregularities and infertility
ü Most patients in whom polycystic ovaries syndrome is ultimately
diagnosed initially present with amenorrhoea, irregular menses or infertility.
ü Although most patients present in their 20s or 30s, polycystic
ovarian disease can affect females of any age, from menarche to menopause.
Findings in almost 75% of patients meet the imaging studies like USG,CT,MRI
criteria for polycystic ovary syndrome. Primary amenorrhoea is a well known but
uncommon presentation.
ü Although infertility is the most common presentation, polycystic
ovaries syndrome may be associated with obesity and insulin resistance, among
other symptoms. A number of patients are identified only when they present with
unrelated complaints. These patients may believe that the symptoms associated
with the syndrome are not of sufficient clinical significance to warrant
medical attention.
ü A second population of patients presents with systemic signs of
androgen excess, namely, hirsuitism, acne, or male-pattern baldness. In
approximately one half of the patients, sonograms show polycystic ovaries.
Additionally,
a significant number of patients with unrelated complaints are incidentally
found to have polycystic ovaries. Further detailed clinical evaluation reveals
that approximately one half of the patients in this group have typical signs
and symptoms of the syndrome (i.e., hirsutism, acne, infertility) and that
one-quarter have related symptoms such as obesity, irregular menses, or insulin
resistance. The remaining one-quarter of the patients may not have any
clinically evident abnormality
Homeo Treatment for PCOD, PCOS,
Symptomatic Homeopathy works well for PCOD, PCOS, It helps to prevent further recurrence
also. So its good to consult a experienced Homeopathy physician without any
hesitation.
Whom to contact for PCOD, PCOS, Treatment
Dr.Senthil
Kumar Treats many cases of PCOD, PCOS, In his medical professional experience
with successful results. Many patients get relief after taking treatment from
Dr.Senthil Kumar. Dr.Senthil Kumar visits Chennai at Vivekanantha
Homeopathy Clinic, Velachery, Chennai 42. To get appointment please call
9786901830, +91 94430 54168 or mail to consult.ur.dr@gmail.com,
For
more details & Consultation Feel free to contact us.
Vivekanantha Clinic Consultation Champers
at
Chennai:- 9786901830
Panruti:- 9443054168
Pondicherry:- 9865212055 (Camp)
For appointment please Call us or Mail Us
For appointment: SMS your Name -Age – Mobile Number - Problem in Single word -
date and day - Place of appointment (Eg: Rajini – 30 - 99xxxxxxx0 – PCOD, PCOS,
Irregular Menses, Obesity – 21st Oct, Sunday - Chennai ), You will receive
Appointment details through SMS
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