PCOS -What go wrong in a teen aged girl with polycystic ovarian syndrome ?? Which organ initiates fire??

 

Basically two tropic hormone axis are involved in the pathophysiology of PCOS namely somatotropic axis and gonadotropic axis(possibly less important for initiation!!!). Will members believe that?? .

Q. 6A. How somatotropic Axis is affected?? Involvement of somatotropic axis leads to abnormal pattern of synthesis release and target organ sensitivity of (a) Growth hormone (b) IGF-1 (c)  Insulin itself (d) IGFBP-1 (e) SHBG and (f) leptin released from  adipose tissue  & g)Adrenal defects .Any one may be primary and can initiate the ignition of PCO starting mechanism !!!

Q.7: How gonadotropic Axis is affected??  Many are of opinion that Involvement of gonadotropic  axis which we commonly see (rise of LH , AMH) are perhaps may occur secondary  to dysfunction of somatotropic axis. Excess insulin leads to excess androgen production -à alters FSH :LH ratio and also results in excess production of estrogen.

Q. 8: If we accept that there is primary Somatotropic Axis  defect and altered IGF-1 is the main culprit in initiation and continuation of PCO then how many members will believe my statement ?? : _ Possible 1^st  kind of defect What is the relevance of  IGF-1 in the etiogenesis of PCO??    IGF1 are chemically and structurally similar to insulin and as most of us know that there are plenty of IGF-1 receptors on theca cells of ovary --. More IGF 1 will exert action as insulin.

 

Hyperinsulinaemia itself :- another believable primary somatotropic Axis defect which may initiate and propagate PCO!!! Possible 2^nd  kind of defect::  How does excess insulin leads to PCO & hyperandrogenaemia?? 1) Excess insulin through IGF-1 receptors leads to LH  mediated excess  thecal androgen production . 2) Secondly,   excess insulin suppress hepatic  synthesis  of SHBG. This leads to liberation of free testosterone. 3) Excess insulin also  suppresses synthesis  of IGFBP-1  . As such   there is  availability of more free IGF-1  . This  excess free   IGF-1 in synergy with insulin leads to more  thecal  androgen  production.

Q. Primary somatotropic Axis  defect . Possible 3^rd kind of defect ? How adrenals are play a role in the causation of PCO in some cases??  Some cases of PCO are due to hyperactivity of enzyme in adrenalsà  cytochrome P450C17. Not only changes in adrenal enzymatic activity ->it cause more synthesis of adrenal androgens  ,

 

Q 5: primary Somatotropic Axis No 6 defect :How thyroid may  play a subtle  role in the causation of PCO in some cases??  it is possible  there is another disorder of thyroid function may be a source of hyperhyperandrgenism . Because we know that in hypothyroidism there is lowering of synthesis of SHBGà raised Free Testosterone.

 

ABC of intrinsic cytochrome P450C17 Theory . This is a bifunctional enzyme which when deranged leads to a) derangement of serine tyrosine phosphorylation leading to increased release of both insulin  and androgen . Net effect is hyperinsulinemia and hyperandrogenemia . –

What are the primary gonadotrophic  Axis No 2 defect In addition to adrenal  intrinsic enzyme  dysregulation there may be of ovarian intrinsic cytochrome P450C17 a may also  result in hyperandrogenicity 

 

 

 Listen to me: No irrational drug selection for ovulation induction. Classification of PCO according to initial drug selection for ovulation induction!!! This grouping  does work. Believe  me .All PCOS  patients  do not present with equal  degree o