Menopause pathophysiology
Menopause Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Menopause pathophysiology On the Web |
American Roentgen Ray Society Images of Menopause pathophysiology |
Risk calculators and risk factors for Menopause pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Rahmah Al-Edresi, M.D.[2]
Overview
Menopause is natural amenorrhea that is happened without any pathological causes, but premature menopause/early menopause is caused by pathological diseases in ovaries and other organs such as premature ovarian failure (Primary ovarian insufficiency, POI), Adrenal insufficiency, type1 diabetes mellitus, autoimmune thyroid disease, Fanconi’s anemia, Congenital adrenal hyperplasia, and Turner’s syndrome. Cardiovascular disease and osteoporosis are most important conditions associated with menopause. Women who had genetic disorders ( Fragile X syndrome, Turner’s syndrome) more pronable to early menopause. The histopathological analysis include ovaries's cortex becomes thinner and it has fewer follicles and the medulla develops fibrosis and scars. Decrease of ciliated cells of Fallopian tubes and Uterus and atrophy of vaginal mucosal layer .
Pathophysiology
Physiological menopause
- Menopause happens normally as women age and the main cause of the menopause is the natural shortage of the primordial follicles (oocytes) that stored in the ovaries and the decrease of the response of ovaries to anterior pituitary gonads hormones that include Follicle Stimulating Hormone (FSH) and Luteinizing Hormone(LH).
- These hormones stimulate the ovaries to produce estrogen and progesterone hormones in a cyclic method under the control of the hypothalamus that produces the gonadotropin-releasing hormones which stimulate anterior pituitary gonads hormone secretion and inhibin-B that plays role in the feedback mechanism.
- The anterior pituitary gonads hormones is decreased during the menopause transition result from decreased ovarian feedback of inhibin and are manifested primarily as elevations in follicle-stimulating hormone (FSH).[1]
Pathological menopause
Premature menopause/early menopause is caused by several pathological diseases include:
- Pathological disease in ovaries include premature ovarian failure termed as primary ovarian insufficiency (POI). It is the loss of ovarian function lead to amenorrhea because of ovarian failure to respond for gonads hormone ( FSH, LH) and deficiency production of estrogen and progesterone hormone.[2]
- Pathological disease in other organs such as Adrenal insufficiency, type1 Diabetes mellitus, Autoimmune thyroid disease, Fanconi’s anemia, Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency.[3]
Genetic
There are genetic disorders involved in the premature menopause/early menopause include:
- Fragile X syndrome is a genetic disorder characterized by reduction of ovarian function, women that have Fragile X Syndrome go through early menopause an average 5 years early than other women.[4]
- Turner’s syndrome: women born with missing X chromosome can go through menopause early, due to their ovaries do not form normally at birth.[5]
Associated Conditions
The most important Conditions associated with Menopause include:
- Cardiovascular disease: during menopause, estrogen deficiency causes vasoconstriction of the vessel wall. menopause is linked to the increased risk of cardiovascular disease.
- Osteoporosis is a disease of the bones that causes bones to become weak and break easily. During menopause, estrogen deficiency increases osteoclastic activity.[6]
Microscopic Pathology
On microscopic histopathological analysis of menopause include:
- Ovaries: the ovaries’s structure are change, the difference between the cortex and medulla is less evident. The cortex becomes thinner, it has fewer follicles. And there are invaginations of the surface epithelium of the cortex.The medulla develops fibrosis and scars, also undergoes the hyalinization of vessel walls.
- Fallopian tubes and Uterus: both endometrial and tubal mucosa demonstrated a gradual decrease in the number of ciliated cells and the non ciliated cells of the uterus.
- Vagina: the mucosa layer begins to atrophy due to decreased estrogen that causes this layer to become drier and thinner.[7][8]
References
- ↑ Mason AS (1976). "The menopause: the events of the menopause". R Soc Health J. 96 (2): 70–1. doi:10.1177/146642407609600208. PMID 951489.
- ↑ Hernández-Angeles C, Castelo-Branco C (2016). "Early menopause: A hazard to a woman's health". Indian J Med Res. 143 (4): 420–7. doi:10.4103/0971-5916.184283. PMC 4928547. PMID 27377497.
- ↑ Okeke T, Anyaehie U, Ezenyeaku C (2013). "Premature menopause". Ann Med Health Sci Res. 3 (1): 90–5. doi:10.4103/2141-9248.109458. PMC 3634232. PMID 23634337.
- ↑ Laml T, Preyer O, Umek W, Hengstschlager M, Hanzal H (2002). "Genetic disorders in premature ovarian failure". Hum Reprod Update. 8 (5): 483–91. doi:10.1093/humupd/8.5.483. PMID 12398227.
- ↑ Santoro N (2003). "Mechanisms of premature ovarian failure". Ann Endocrinol (Paris). 64 (2): 87–92. PMID 12773939.
- ↑ Lobo RA, Davis SR, De Villiers TJ, Gompel A, Henderson VW, Hodis HN; et al. (2014). "Prevention of diseases after menopause". Climacteric. 17 (5): 540–56. doi:10.3109/13697137.2014.933411. PMID 24969415.
- ↑ Zerbinati N, Serati M, Origoni M, Candiani M, Iannitti T, Salvatore S; et al. (2015). "Microscopic and ultrastructural modifications of postmenopausal atrophic vaginal mucosa after fractional carbon dioxide laser treatment". Lasers Med Sci. 30 (1): 429–36. doi:10.1007/s10103-014-1677-2. PMID 25410301.
- ↑ Makabe S, Motta PM, Naguro T, Vizza E, Perrone G, Zichella L (1998). "Microanatomy of the female reproductive organs in postmenopause by scanning electron microscopy". Climacteric. 1 (1): 63–71. doi:10.3109/13697139809080683. PMID 11907929.