PCOD || Gynecology

Creative Medicine
9 Oct 202123:03

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

  • 🌟 Polycystic Ovarian Syndrome (PCOS) is also known as Stein-Leventhal Syndrome and is characterized by increased androgen production.
  • 🔬 The excess androgens lead to hirsutism (excessive hair growth) and are converted to estrogens by the aromatase enzyme, causing a cascade of hormonal imbalances.
  • 📉 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.
  • 🚫 The lack of a LH surge, which is necessary for ovulation, leads to oligomenorrhea or amenorrhea, and eventually, multiple cysts in the ovaries.
  • ⚠️ Increased LH stimulates theca cells to produce more androgens, perpetuating the cycle and contributing to the thickening of ovarian tissue.
  • 🌡 Unopposed estrogen can lead to endometrial hyperplasia, which may progress to cancer, and PCOS patients are at higher risk for endometrial and breast cancers.
  • 🏃‍♀️ Lifestyle modifications and weight reduction are the first-line treatments for PCOS, aiming to reduce obesity and improve insulin resistance.
  • 💊 Oral contraceptive pills (OCPs) are often prescribed to regulate menstrual cycles and manage hirsutism in PCOS patients.
  • 🩺 Metformin is used to address insulin resistance, a common comorbidity in PCOS that can lead to type 2 diabetes.
  • 🏥 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

00:00

🌟 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.

05:01

🌱 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.

10:02

🔍 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.

15:03

💊 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.

20:04

🛠 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

💡Polycystic Ovarian Syndrome (PCOS)

Polycystic Ovarian Syndrome (PCOS) is a hormonal disorder common among women of reproductive age. It is characterized by the presence of multiple cysts in the ovaries, which can lead to irregular menstrual periods, infertility, and increased androgen levels. In the video, PCOS is discussed as the main theme, with an emphasis on its effects on hormone levels, menstrual cycle, and long-term health implications.

💡Androgens

Androgens are a group of hormones that include testosterone and are responsible for the development of male characteristics. In the context of the video, increased androgen production is a key feature of PCOS, leading to symptoms such as hirsutism (excessive hair growth). The video explains how increased androgens can stimulate the growth of sexual terminal hair, resulting in hirsutism.

💡Hirsutism

Hirsutism refers to the excessive growth of hair in areas of the body where hair growth is typically associated with males, such as the face, chest, and back. The video discusses how increased androgen levels in PCOS patients can lead to hirsutism, which is a common symptom that affects the quality of life for many women with the condition.

💡Aromatase Enzyme

The aromatase enzyme is involved in the conversion of androgens to estrogens in the body. The video explains that in PCOS, increased androgens are converted to estrogens by the aromatase enzyme, which can lead to a series of hormonal imbalances and contribute to the development of PCOS symptoms.

💡Follicle Stimulating Hormone (FSH)

Follicle Stimulating Hormone is a gonadotropin that stimulates the growth of ovarian follicles in women. The video describes how increased estrogen levels in PCOS can lead to a decrease in FSH, which in turn affects the normal development and ovulation of ovarian follicles.

💡Luteinizing Hormone (LH)

Luteinizing Hormone is another gonadotropin that triggers ovulation and the production of testosterone in women. The video highlights that in PCOS, there is often an imbalance in the ratio of LH to FSH, with higher levels of LH contributing to the condition's symptoms.

💡Ovulation

Ovulation is the release of an egg from the ovary, which is a necessary process for fertility. The video explains that one of the key issues in PCOS is the absence of a normal LH surge, leading to a lack of ovulation and resulting in infertility or irregular menstrual cycles.

💡Endometrial Hyperplasia

Endometrial hyperplasia is a condition where the lining of the uterus (endometrium) becomes excessively thick. The video discusses how the increased estrogen levels in PCOS can lead to endometrial hyperplasia, which over time can progress to more severe conditions, including endometrial cancer.

💡Insulin Resistance

Insulin resistance is a condition in which the body's cells do not respond properly to the hormone insulin, leading to high blood sugar levels. The video explains that increased androgens in PCOS can inhibit the production of sex hormone-binding globulin, resulting in increased insulin levels and insulin resistance, which can predispose patients to type 2 diabetes.

💡Rotterdam Criteria

The Rotterdam Criteria are a set of guidelines used to diagnose PCOS. The video mentions these criteria, which include the presence of oligomenorrhea or amenorrhea, clinical and biochemical signs of hyperandrogenism, and polycystic ovaries observed through ultrasound. These criteria help healthcare providers to accurately diagnose and treat PCOS.

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

play00:10

hello friends let us now learn some

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important points about

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polycystic ovarian disease or polycystic

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ovarian syndrome also called has steen

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lavental syndrome

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so in this steel levinthal syndrome the

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basic pathology in this is increased

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androgen production

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whatever the reason is here

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most commonly there will be increased

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androgen production

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this increased androgen reduction will

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first leads to historism this increased

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androgen stimulates the growth of sexual

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terminal hair resulting in hirsutism

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then

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this increased androgen

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undergoes peripherally we have aromatase

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enzyme

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in the presence of this aromatase enzyme

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this androgen

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gets converted to estrogen

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when this androgen gets converted to

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estrogen this is trojan has three

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effects

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one estrogen can decrease follicle

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stimulating hormone

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once it decreases follicle why does it

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decrease follicle stimulating hormone

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so increased estrogen is estrogen is

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actually produced from ovary ovary

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produces estrogen

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this production of east ocean by ovary

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is activated by follicle stimulating

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hormone which is produced by pituitary

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so if estrogen is increased in any

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regression due to any reason if estrogen

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is increased then it exerts negative

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feedback mechanism on follicle

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stimulating hormone thus there is

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decreased follicle stimulating hormone

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once there is decreased follicle

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stimulating hormone

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if you do

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a ratio of luteinizing hormone to

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follicle stimulating hormone normally it

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is one is to do but in patients with

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pcod this utilizing heart moon

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to follicle stimulating hormone ratio

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will be more than two is to one

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fine this increased east trojan

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will have negative feedback on follicle

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stimulating hormone whereas this

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estrogen has positive feedback on

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luteinizing heart mole and thus

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increasing the action of utilizing

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hormone

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now this luteinizing hormone is

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increased

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then this luteinizing hormone is

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increased first thing is there is no lh

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search

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normally whenever there is increased lh

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surge

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that causes an ovulation you can ask me

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there is increased neutrinizing hormone

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that means there is increased utilizing

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that means there is a lh

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but this increased

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luteinizing hormone is constant

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there is constant continuous increase in

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luteinizing hormone

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but in lh search there will be increase

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in

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luteinizing hormone

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it is strike like suddenly and then it

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falls this is a leth search

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but here there is continuous increase in

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utilizing hormone

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this

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absence of lh surge

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will cause an ovulation ovulation mainly

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occurs due to a lh search once there is

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no lh search there is no ovulation now

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when there is no ovulation this will

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decrease the progesterone levels

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ovulation will lead to increased

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progesterones but because there is no

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ovulation there is decreased

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progesterone levels overall this will

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lead to

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in the beginning there will be

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oligomenorrhea

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but slowly as the days progresses this

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disease progresses to secondary

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amenorrhoea

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right

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then

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this lh hormone will cause one more

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cause we'll have one more issue see

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because of this lh increased lh this

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increased lh also stimulates

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the causes

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because lh stimulates the castles this

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thicker cells will undergo

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hypertrophy and they will produce

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androgens again

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and this leads to increased androgens

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overall

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because of thick cell hypertrophy

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then

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right there is an ovulation very good

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if there is an ovulation then what about

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the eggs which are to be released

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normally every month there will be one

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egg which is released one follicle which

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is released but if there is an ovulation

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there will be formation of multiple

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follicles in the ovary and among these

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one will grow to a bigger size and it

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will form graphene follicle and that is

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released outside but in pcod there is no

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formation of graphene follicle so there

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will be multiple cysts will remain in

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the ovary due to this an ovulation

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so in pcod you see

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the follicles are converted to multiple

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cysts in the ovary

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right next

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then if there is increased androgens now

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there is increase so increased estrogens

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increased east ocean will act on the

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endometrium and it causes endometrial

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hyperplasia

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as days progresses this endometrial

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hyperplasia

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will convert into endometrial

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hyperplasia with atypia and finally it

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can cause

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endometrial cancer

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and this will also predispose to

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breast carcinoma

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also

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right then

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this pcod there is one more important

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thing

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this pcod also causes alters the lipid

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profile

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it alters the lipid profile

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and it increases the ldl and decreases

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hdl and thus it will

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lead to cardiovascular risk factors that

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is future in future it can cause or it

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can lead to heart disease

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right now

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one important thing is

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when there is increased androgens there

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is one more important thing

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even whenever there is increased

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androgens

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this increased androgens will inhibit a

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hormone

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a protein actually this increased

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androgens will inhibit a protein called

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as serum

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sex hormone binding globulin

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okay when it inhibits the protein serum

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sex hormone binding globulin production

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this will result in

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increased insulin

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this will result in insulin resistance

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because of this insulin resistance this

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will predispose a patient with

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polycystic ovarian disease to diabetes

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mellitus

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so

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so in so this is the main thing that

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happens in pcod

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right there is one more thing

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right because of this increased or

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altered lipid profile

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this will cause

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obesity in the patient

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okay because of this excess obesity this

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can lead to

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mood changes

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and depression

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and this can also lead to this opacity

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can also

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cause

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sleep apnea especially obstructive sleep

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apnea

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the increased risk of obstructive sleep

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apnea is also seen in these patients

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fine

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so

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if you see the clinical features it's

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nothing but whatever is here so the

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uh a woman of middle aged women comes to

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us with history of menstrual

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irregularity that is

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primarily irregular cycles and

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amenorrhea

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and on you can observe that the patient

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is obese and there is history of

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hirsutism that is acne

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alopecia is seen

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and you will see that on lipid profile

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examination you see there is altered

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lipid profile and there is insulin

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resistance

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so

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that is the clinical picture there is

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one important thing that occurs in pcod

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which is called as a kantosis nigricans

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a kantosis nigricans is pigmented linear

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marks

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which you see in the neck and axilla are

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seen in acanthosis nigricans these

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acanthosis nigricans occur due to

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insulin resistance

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insulin resistance leads to this

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acanthosis nigricles

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right

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then

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what are the hormonal changes that you

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see in pcod

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see

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in pcod there will be

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in pcod there will be increased

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androgens number one

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that is there will be increased

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testosterone increased androstene ion

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and increased dihydroxy ep androsterone

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then there will be increased luteinizing

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hormone

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there is increased estrogen

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and because of this insulin resistance

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the insulin will not dixie because of

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this insulin resistance insulin will not

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act on peripheral tissues

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so there will be increased insulin which

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is present in our body because it is not

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going to act on the peripheral tissues

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so there will be increased insulin and

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there will be increased

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ldl

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low density lipoproteins so water

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increased in pcod there will be

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increased androgens increased estrogens

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increased luteinizing hormone and

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increased

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insulin and increased

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low density lipoprotein is seen in

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utilizing hormone that water decreased

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in

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polycystic ovarian disease in polycystic

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ovarian disease there will be decreased

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follicle stimulating hormone

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there will be androgens will inhibit

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sex hormone binding globulin so sex

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hormone binding globulin is decreased

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and there will be

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decreased progesterone

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okay

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and there will be decreased hdl

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so in polycystic ovarian disease you see

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there is decreased sex hormone binding

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globulin decreased follicle stimulating

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hormone decreased hdl and decreased

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progesterone

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then

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if you are asked about the long term

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consequences of this newtonizing

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of this follicle sorry polycystic

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ovarian disease what are the long term

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consequences

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due to this polycystic ovarian disease

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in the long term because of this altered

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lipid profile this will cause increased

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cvs risk factors especially coronary

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artery disease increases in the patient

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on long term because of insulin

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resistance there is increased risk of

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diabetes mellitus in the future due to

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increased estrogen there is increased

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risk of endometrial carcinoma and also

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breast carcinoma is noted in the future

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then

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because the patient becomes obese there

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is increased risk of sleep apnea

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and also there will be more changes and

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depression these more changes and

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depression are also attributed to

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estrogen

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estrogen and project decreased

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progesterone

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also causes more changes and depression

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and there is one important long-term

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consequence which is not there in this

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chat that is non-alcoholic

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steatohepatitis

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non-alcoholics tiato hepatitis

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is also long-term risk factor of

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polycystic ovarian disease

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right

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now what about the diagnostic criteria

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so the diagnostic criteria we have a

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name for this diagnostic criteria that

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is rotterdam criteria this is rather

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damn criteria according to this

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rotterdam criteria 2003

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first there will be symptoms of

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oligomenorrhea

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or amnoria are seen

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then clinically

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there the patient will have increased

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serum testosterone will be diagnosed or

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that is first clinical efficacy the

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first we have first

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criteria is symptoms that is presence of

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oligomenorrhea

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or amenorrhea second symptom is clinical

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plus biochemical symptom

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okay in clinical symptom we have the

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patient will have hypsotism

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comes under clinical symptom

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whereas in biochemical symptom

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we have increased serum testosterone

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actually this serum testosterone levels

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should be between 70 to 150 nanogram per

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deciliter

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these should not be more than 200

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nanogram per deciliter

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if the serum testosterone levels are

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more than 200 nanogram per deciliter

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then we do not consider polycystic

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ovarian disease

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then what do we consider if there is

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serum testosterone levels are more than

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200 nanograms per deciliter then we will

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consider presence of ovarian tumor

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rather than polycystic ovarian disease

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so in polycystic ovarian disease serum

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testosterone should be between

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70 to 150 nanogram per deciliter

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then third criteria is radiology that is

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in usg you will see presence of two or

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more cysts

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which are of size 2 to 9

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mm so 12 or more cysts which are of size

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2 to 9 mm which is present in one or

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both ovaries

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with ovaries more than 10 ml that is

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enlarged ovaries so this numbers are

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important in usg you will see 12 or

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presents of 12 or more cysts which are

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of 2 to 9 mm in diameter present in one

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or both the ovaries

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and each ovary is enlarged that is more

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than 10 ml

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volume

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so this is the rotterdam criteria which

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includes

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clinical symptoms then clinical and

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biochemical symptoms then

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ultrasonography

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then

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how are you going to treat these

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patients with pcod

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so if a patient comes to you with

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pcod

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so if a patient comes to you with pcod

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first line treatment is giving selective

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estrogen receptor modulator

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so in this selective estrogen receptor

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modulator

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the

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we can give

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clomiphene citrate

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and tamoxifen

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and reloxified

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fine this is fine but do you give them

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for first line no they are actually the

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first line for infertility

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so this is if the patient suffers from

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infertility with pcod then the first

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line is

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selective estrogen receptor modulators

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if the patient suffers from pcod always

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ask her for weight reduction

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and lifestyle modifications are the

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first line

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first step you give the patient is

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to decrease obesity through weight

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reduction lifestyle modifications and

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exercises

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even after that if there is no

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uh you know it does not resolve and if

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there are irregular periods

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then you should give

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ocps

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oral contraceptive pills

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and if there is insulin resistance or

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hyperinsulinism

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then you should give

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metformin

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so treatment mainly depends upon the

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symptoms

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if there is hyposodism if there is

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similar if there is hirasutism then you

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should give ocps with clomiphene citrate

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so the treatment mainly depends with the

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sorry

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i'm really sorry you should give oc

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piece with

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c protein acetate

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i'm really sorry ocp is with ciproterron

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acetate

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bro

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i'll write it properly

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cipro tear on

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acetate

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okay for his hisotism you should give

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ocps with ciproteuron acetate

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okay so pcod first line you will do

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weight reduction and lifestyle

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modifications followed by you should

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give symptomatic treatment for irregular

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periods you should give ocps

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okay for insulin

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should be given

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sorry metformin should be given for

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insulin resistance so you will treat it

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according to the symptoms but if there

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is infertility with pcod

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in such cases the first line is giving

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selective estrogen receptor modulators

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then following these selective estrogen

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receptor modulators in these the drug of

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choice is chlamyfin citrate

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okay among these selective estrogen

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receptor modulators drug of choice is

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chromophil citrate if the person cannot

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tolerate chlamyfin citrate then you give

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them oxyphen

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even if the person

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okay this reloxifen is not normally used

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it is not generally used then if you see

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the second lines second line will be you

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can use either gonadotropins

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or you can use lh and fsh injections can

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also be used

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and if you see the third line

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in third line we can use leukolyte or

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gaucher aline can also be used third

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line is mainly gnrh analogs

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so for pcod with infertility you can use

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selective estrogen receptor modulator

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and second line drugs like gonadotropins

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and lhfsh injections can be given and

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you can also use chronotropine releasing

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hormone analogs

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but

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then

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if even after doing everything if still

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this does not dissolve then you should

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do surgery

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and in the surgery for pcos we have

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laparoscopic ovarian drilling

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where you will pass a monopolar cautery

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into the ovary this is the ovary with

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polycysts many cysts then you will pass

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a monopolar cautery into the

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ovary and destroy the ovarian thicker

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all the thicker you will destroy it

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so this is about the polycystic ovarian

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disease thank you guys for watching my

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lecture

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thank you

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you

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相关标签
Polycystic OvaryHealth LectureWomen's HealthHormonal ImbalanceInfertilityEndocrinologyMedical EducationHealth AwarenessTreatment OptionsDisease Management
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