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.
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. '
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.
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….
-Period irregularities and infertility
-Most patients in whom polycystic ovaries syndrome is ultimately diagnosed initially present with amenorrhoea, irregular menses or infertility.
-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.
-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.
-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
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