Polycystic Ovarian Disease (PCOD)

Polycystic Ovarian Disease (PCOD) was originally described in 1935 by Stein and Leventhal as a syndrome manifested by obesity, amenorrhoea and hirsutism associated with enlarged polycystic ovaries. This is one of the most common endocrine disorders in female. PCOD is more common in young women. It is the leading cause of infertility in females.Its incidence is increased as 1 in 15 women are affected with it. PCOD causes irregularities in menstruation  leading difficulties in conceiving.Untreated cases can leads to complications like diabetes ,heart disease etc. Proper treatment on time helps to relieve symptom and long term complications.

PCOD

  • Definition of  polycystic ovarian disease.

  •  Incidence of polycystic ovarian disease.

  • Hormonal changes in polycystic  ovarian disease.

  • Etiology of polycystic ovarian disease.

  • Pathology of polycystic ovarian disease

  • Signs and symptoms of polycystic ovarian disease.

  •  Diagnosis of  polycystic ovarian disease.

  • Differential diagnosis of polycystic ovarian disease.

  • Pathophysiology of polycystic ovarian disease.

  • Management of polycystic ovarian disease.

  • Complications of polycystic ovarian disease.

  • Life style modification of polycystic ovarian disease

  • Conclusion.

                                

Definition of  polycystic ovarian disease.

Polycystic ovarian disease is a complex disorder characterised by excessive production of androgen by the ovaries and adrenal which interferes with ovarian follicular growth. So PCOD is a state of androgen excess and chronic unovulation.

 Incidence of polycystic ovarian disease.

The incidence varies between 0.5-4 percent. Polycystic ovarian disease is more common amongst infertile women. It is more prevalent in young women of reproductive age group.

Hormonal changes in polycystic  ovarian disease.

Hormones plays an important role in maintaining the vital functions of the body. In PCOD sex hormones are affected. In normal state ovaries produces only tiny amount of androgen but in case of  PCOD the ovaries produce more androgen which inhibit ovulation and enhances the acne,hair growth of the body and face.

The bodies capacity to use insulin is  affected  called insulin resistance which in turns leads to high glucose level and diabetes.

 Aetiology of polycystic ovarian disease.

Exact etiology of  PCOD is unknown. But it is believed to be a genetic diseases   as many cases occurs within the family, greater concordance in monozygotic compared with dizygotic twins  and heritability of endocrine and metabolic features of PCOD. The genetic component is inherited in autosomal dominant fashion with high genetic penetrance but varying with individuals. This means the child has 50 % chance of inheriting the predisposing genetic variants from the parent. If the daughter is receiving the variants then she is having more chances of getting disease than the son who may be asymptomatic carriers or may have symptoms such as early baldness or excessive hair. The genetic variant(s) can be inherited from either the father or the mother. The exact gene that causes the disease is not yet identified. The clinical severity of PCOD symptoms appears to be largely determined by factors such as obesity.

Increased amount of insulin can leads to PCOD. In PCOD the ability to utilise the insulin is affected so the pancreas produces more insulin to make glucose available to the cells. Excess insulin again increases the androgen production.It alters the ovulation.

 Pathology of polycystic ovarian disease.

Typically, there is an enlargement in the size of ovaries up to 2 to 5 times from normal; as a result of these stroma is increased. The capsule become pearly white in color and thickened. On bisection, multiple follicular cysts measuring about 8-10 mm in diameter are crowded around the cortex.

Histologically, there is thickening of tunica albuginea. The cysts are follicles at varying stages of maturation and atresia. There is theca cell hypertrophy. The patient may present the feature of diabetes mellitus.

 Signs and symptoms of polycystic ovarian disease.

  • The menstrual abnormalities in the form of oligomenorrhoea, amenorrhoea or dysfunctional uterine bleeding.

  • Acne.
  • Thin brittle hairs.
  • Infertility.
  • Obesity.
  • Hirsutism( abnormal hair growth).It occur more in the face ,chest,belly and back.
  • Infertility -Many women with PCOD have difficulty in getting pregnant.
  • Depression.
  • Virilism is rare.
  • Acanthosis nigricans is characterised by specific skin changes due to insulin resistance. The skin is thickened and pigmented. Commonly affected sites are nape of the neck, inner thighs and axilla.
  • HAIR-AN Syndrome in patient with PCOD is characterised by hyperandrogenism, insulin resistance and acanthosis nigricans.
  • Internal examination reveals bilateral enlargement cystic ovaries which however, may not be revealed due to obesity.

 

Diagnosis of   polycystic ovarian disease.

  • Detailed medical history reveals any history of illness,familial predisposition,signs and symptoms etc.
  • Thorough physical examination helps to identify signs of the client.
  • Pelvic examination helps to identify the pelvic masses.
  • Sonography – Transvaginal sonography is especially useful in obese patient. Ovaries are enlarged in volume. Increased numbers of peripherally arranged cysts are seen.
  • Serum value
  1.  LH(Luteinizing hormone) level is elevated and the ratio LH:FSH is greater than 3:1
  2.  The  oestrone level is markedly elevated:-Reversible oestradiol: oestrone ratio
  3. SHBG level is reduced.
  4.  Androstenedione is elevated.
  5.  Marginally   elevated Serum testosterone and DHEA-S.
  6.  Raised serum insulin level or the ratio fasting glucose:fasting insulin is less than 4.5.
  • Laproscopy – Bilateral polycytitis ovaries are characteristics of PCOD.

 

 Differential diagnosis of polycystic ovarian disease.

Other condition that causes of irregular or absent menstruation and excessive hair growth (hirsutism) are congenital  adrenal hyperplasia (21-hydroxylase deficiency), hypothyroidism , hyperprolactinemia, androgen secreting neoplasm’s, Cushing’s syndrome and other pituitary or adrenal disorders, should be investigated. Occurrence of PCOD in other insulin-resistant situations such as acromegaly has also been reported.

 Pathophysiology of polycystic ovarian disease.

Exact pathology of PCOD is not clearly understood. It can be discussed under the following headings.

a)      Hypothalamic –pituitary compartment abnormality.

b)      Androgen excess.

c)      Anovulation.

d)      Obesity and insulin resistance.

e)      Long term consequences.

a)      Hypothalamic –pituitary compartment abnormality.

  • Increased pulse frequency of GnRH leads to increased pulse frequency of LH. Leptin, a peptide, secreted by fat cells and by the ovarian follicle, in presence of hyperinsulinaemia may be responsible for this.
  • Elevated  level of LH due to increased pulse frequency and amplitude of LH.
  • FSH level is not increased. This is mainly due to the negative feedback effect of chronically elevated oestrogen and follicular inhibin.
  • Increased free oestradiol due to reduced sex hormone binding globulin (SHBG) bears positive feedback relationship to LH.
  • The LH : FSH ratio is increased.

b)      Androgen excess.

Abnormal regulation of the androgen forming enzyme is thought to be the main cause for excess production of androgens from the ovaries and adrenals. The principal sources of androgens are

(A) Ovary

(B)Adrenal

(C) Systemic metabolic alteration.

 

 (A). Ovary produces excess androgens due to

  • High  LH causes stimulation of theca cells.
  • P450 C17 enzyme hyperfunction.
  • Defective aromatisation of androgens to oestrogen.
  • Stimulation of theca cells by IGF-1( Insulin growth factor-1)

 (B). Adrenals are stimulated to produce excess androgens by

  • Stress.
  • P450 C17 enzyme hyper function.
  • Associated high prolactin level (20%).

(C). Systemic metabolic alteration.

  I.    Hyperinsulinaemia causes

  1.  Stimulation of theca cells to produce more androgens.
  2. Insulin results in more free IGF-1 by autocrine action, IGF-1 stimulates theca cells to produce more androgens.
  3. Insulin inhibits hepatic synthesis of SHBG, resulting in more free level of androgens.

  II.   Hyperprolactinaemia

In about 20 per cent cases, there may be mild elevation of prolactin level due to increased pulsitivity of GnRH or due to dopamine deficiency or to both. The prolactin further stimulates adrenal androgen production.

  III.   Anovulation : follicular growth is arrested at different phases of maturation (5-10mm diameter) due to  low FSH level. The net effect is diminished oestadiol and increased inhibin production. Due to elevated LH, there is hypertrophy of theca cells and more androgens are produced either from theca cells or stroma. There is defective FSH induced aromatisation of androgens to oestrogens. Follicular microenvironment is therefore more androgenic rather than oestrogenic. Unless there is oestrogenic follicular microenvironment, follicular growth, maturation and ovulation cannot occur. There is huge number of atretic follicles that contribute to increased ovarian stroma. LH level is tonically elevated without any surge. LH surge is essential for ovulation to occur.

c) Obesity and insulin resistance.

One of the most important contributory factors for the development of PCOD is obesity. Obesity is also associated with reduced SHBG apart from excess production of androgens. It also induces insulin resistance and hyperinsulinaemia which in turn increases the gonadal androgen production.

d) Long term consequences in a patient suffering from PCOD includes.

The excess androgens (mainly androstenedione) either from the ovaries or adrenals are peripherally aromatised to oestrone (E1 ).There is concomitant diminished SHBG. Cumulative excess unbound E2 and oestrone results in a tonic hyper oestrogenic state. There is endometrial hyplasia.

  • Risk of developing (DM) diabetes mellitus due to insulin resistance.
  • Risk of developing endometrial carcinoma due to persistently elevated level of oestrogens. Oestrogen effects are not opposed by progesterone because of chronic anovulatory state.
  • Abnormal lipid profile increases the risk of cardiovascular disease and hypertension.

 Management of polycystic ovarian disease.

Management of PCOD needs individualisation of the patient. It depends on her presenting symptoms, like menstrual disorder, infertility, obesity, hirsutism or combined symptoms. Patient counselling is important. Treatment is primarly targeted to correct the biochemical abnormality.

Weight reduction in obese patients is the first line of treatment. Problems associated with menstrual irregularities, infertility and hirsutism improves in the client with Body mass index (BMI) <25.

Do regular activity to reduce the weight.Walking daily for 30 minutes is a common and good exercise that every one can practice.

Diet should include lot of green leafy vegetables, whole grains, nuts,beans and fruits. The client with PCOD should avoid food containing high saturated fatty acid like meat,dried fruit and cheese.

Fertility not concerned

  • Androgen excess- combined oral contraceptive pills are effective. progestin suppresses LH and oestrogen improves SHBG, reducing free testerone level. Norgestrel  containing pill is avoided because of its high androgenicity. Newer progestins (desogestrel) are best suited.
  • GnRH agonists- Leuprolide acetate 3.75 mg IM or goserelin3.6 mg SC every four weeks can be used to suppress ovarian steroid production.
  • Cyproterone acetate, Ketoconazole , spironolactone Flutamide, Finasteride are the other androgens that can be used for the management of hirsutism.
  • Addition of dexamethasone 0.25 mg-0.5mg at bed time is effective to minimise excess adrenal androgen. However it should not be used in obese patient.

Patient wanting pregnancy

  • Ovulation induction is achieved by ovulation induction drug called clomiphine citrate with or without dexamethone or bromocriptine. In unresponse cases, pure FSH or HMG along with hcg may be administered backed up with monitoring facilities.
  • Anovulatory women with PCOD and obesity, ovulate satisfactorly when clomiphine is combined with metformin. Metformin 500 mg thrice daily is found to correct the biochemical abnormalities observed in PCOD.

Surgery

Surgery is the alternative procedure for PCOD who are resistant to medical therapy. Endoscopic cauterisation or CO2 laser vaporization of multiple cysts is the better substitute of conventional wedge resection of the ovaries.

  Complications of polycystic ovarian disease.

  •  Diabetes due to insulin resistance that is type 2 diabetes.
  •  Elevated blood pressure.
  • Abnormal Cholesterol and lipid level , that is  elevated triglycerides or low high-density lipoprotein (HDL) cholesterol which is considered to be good for the body.
  • High levels of C-reactive protein, a protein released by heart .
  • Cardiovascular diseases.
  • Nonalcoholic steatohepatitis- It is a severe liver inflammation mainly due to the  accumulation of fat  in the liver.
  • Difficulty in breathing while sleeping(Sleep apnea).
  • Abnormal uterine bleeding.
  • Due the continous elevated level of eostrogen leads to endometrial cancer(Cancer of the uterine lining).
  • In pregnancy it can causes Gestational diabetes or pregnancy-induced high blood pressure.

 Life style modification of polycystic ovarian disease.

Life style modification of polycystic ovarian disease include weight reduction ,regular exercise and dietary modification.

Weight reduction helps to reduce the insulin level as well as androgen level.It can be done after consulting with dietitian.For weight reduction the client has to take diet containing low calorie.

Dietary modification is recommended for polycystic ovarian disease.Always prefer the diet containing low fat,low carbohydrates and high fiber diet.High fiber diet will be slowly digested so the glucose will be slowly raised with creating much complications.The diet containing high fiber are whole grains ,fruits,vegetable,cereals, barley,brown rice and beans.

Exercise or regular activity helps to keep your body active. It always help in lower the insulin level and to reduce the weight of the client.

Conclusion

PCOD is a common endocrine disorder found in the woman of reproductive age group but most of them are unaware about it. This is one of the leading causes of infertility in woman. But the proper management on time will help to correct the condition.

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The Team Manager Web Diseases

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