Module 7 Knowledge Check-Pathophysiology of PCOS Paper
Pathophysiology of PCOS
PCOS develops in early puberty. It involves neuroendocrine, metabolic and ovarian dysfunction in females. It is indicated by menstrual abnormalities and increased amounts of androgens. Hirsutism and hyperandrogenism are manifestations of overproduction of androgens. Hyperandrogenism is demonstrated by elevated levels of unbound testosterone in circulation. Hyperandrogenism plays a key role in the pathophysiology of PCOS. The high androgen levels suppress sex hormone-binding globulin (SHBG) concentrations. This contributes to higher free testosterone levels. The common denominator in PCOS is therefore ovarian hyperandrogenism (Witchel et al., 2019).
Insulin resistant hyperinsulinism is an aggravating factor in the pathophysiology. Hyperandrogenism and hyperinsulinism leads to obesity and LH excess. Ovarian hyperandrogenism accounts for oligo-anovulation, hirsutism and polycystic ovaries. Hyperinsulinemia affects the ovaries where it synergizes with LH to upregulate androgen production. these actions aggravate hyperandrogenism and anovulation.
Insulin resistant hyperinsulinemia also promotes the deposition of adipose tissue which further exacerbates insulin resistance. Excessive androgens can cause secondary LH elevation by interfering with the negative feedback of progesterone at the hypothalamus. LH alone however cannot cause ovarian hyperandrogenism due to the homologous desensitization of the ovary when exposed to high to excessive LH.
PCOS and Fertility
PCOS affects fertility by affecting ovulation. PCOS causes oligo-anovulation which causes women with PCOS to ovulate intermittently, which, according to Cooney and Dokras (2018), makes it harder to conceive.
Pathophysiology of Pelvic Inflammatory Disease (PID)
PID is an inflammation of the female upper genital tract. The upper genital tract is usually sterile compared to the lower genital tract which includes the vagina. Most women have a variety of potentially pathogenic bacteria as part of their vaginal flora. These pathogenic bacteria are prevented from entering into the upper genital tract by the endocervical canal which acts as a barrier. PID cases are usually due to sexually transmitted infections (STIs).
The most common pathogens are Neisseria gonorrhoeae and Chlamydia trachomatis (Low & Broutet, 2017). Infection with STIs can interfere with the endocervical barrier. Disruption of the barrier provides bacteria with access to the upper genital tract which leads to ascending infection from the cervix.
Infection of the genital tract leads to inflammatory damage. Infection can either be subclinical i.e., due to Chlamydia trachomatis or can present as severe pelvic inflammatory disease as in the case of Neisseria gonorrhoeae infection. As Jennings and Krywko (2021) note, subclinical PID can still have long-term consequences even if no symptoms are present. Inflammation of the uterus and fallopian tubes leads to scarring and formation of adhesions.
Scarring and adhesion leads to loss of cilia in the fallopian tubes lining thereby affecting the motility of ova. Ovum transport is impaired as a result. Repeated infections can lead to total obstruction of the fallopian tubes. Infertility and an increased risk for ectopic pregnancy are the possible consequences of impaired motility. Adhesions can lead to chronic pelvic pain.
Stages of Syphilis
Syphilis is a bacterial infection that is caused by the spirochete Treponema pallidum. The progression of syphilis occurs through four stages. Many organs can be affected by syphilis. These are primary syphilis, secondary syphilis, latent syphilis, and tertiary syphilis (Peeling et al., 2017). The classic presentation of primary syphilis is a solitary genital chancre on the genitals. The chancre is usually non-tender. The chancre is usually a response to T. pallidum invasion. The chancres are lesions that occur with direct contact with infected lesions.
They are accompanied by lymphadenopathy. Primary syphilis can progress to secondary syphilis if left untreated. Secondary syphilis is due to hematological dissemination and presents as macular rash, headache, diffuse lymphadenopathy hepatosplenomegaly, myalgia etc. both primary and secondary syphilis can resolve without treatment. The patient then goes into the latent phase where no clinical manifestations are present. Some patient may progress into the tertiary phase which is characterized multiple organ system involvement
References
- Cooney, L. G., & Dokras, A. (2018). Beyond fertility: polycystic ovary syndrome and long-term health. Fertility and Sterility, 110(5), 794–809. https://doi.org/10.1016/j.fertnstert.2018.08.021
- Jennings, L. K., & Krywko, D. M. (2021). Pelvic Inflammatory Disease. In StatPearls. StatPearls Publishing.
- Low, N. & Broutet N. J. (2017). Sexually transmitted infections – Research priorities for new challenges. PLoS Medicine, 14(12), e1002481. https://dx.doi.org/10.1371%2Fjournal.pmed.1002481
- Peeling, R. W., Mabey, D., Kamb, M. L., Chen, X. S., Radolf, J. D., & Benzaken, A. S. (2017). Syphilis. Nature Reviews Disease Primers, 3, 17073. https://doi.org/10.1038/nrdp.2017.73
- Witchel, S. F., Oberfield, S. E., & Peña, A. S. (2019). Polycystic Ovary Syndrome: Pathophysiology, Presentation, and Treatment With Emphasis on Adolescent Girls. Journal of the Endocrine Society, 3(8), 1545–1573. https://doi.org/10.1210/js.2019-00078