Menopause pathophysiology

Jump to navigation Jump to search

Menopause Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differential Diagnosis

Epidemiology and Demographics

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Imaging Findings

Treatment

Medical Therapy

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Menopause pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Menopause pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Menopause pathophysiology

CDC on Menopause pathophysiology

Menopause pathophysiology in the news

Blogs on Menopause pathophysiology

Directions to Hospitals Treating Menopause

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 caused by pathological diseases, that are lead to early cessation of menses.

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. "Characteristic changes in the hypothalamic-pituitary-ovarian (HPO) axis during the menopause transition result from decreased ovarian feedback of inhibin and estradiol and are manifested primarily as elevations in follicle-stimulating hormone (FSH). Adrenal changes concurrent with the menopause transition include elevations in serum cortisol and transient elevations in dehydroepiandrosterone sulfate, androstenediol, and other adrenal androgens"[1]

pathological menopause:

Premature menopause/early menopause caused by pathological disease in ovaries, premature menopause or premature ovarian failure termed as Primary ovarian insufficiency (POI).(POI) 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. Premature menopause is a result of several medical condition such as Autoimmune disease(Adrenal insufficiency, Type1 diabetes mellitus, Autoimmune thyroid disease), Fragile X Syndrome, Fanconi’s anemia, Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency.[2][3]


Genetic

Menopause Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differential Diagnosis

Epidemiology and Demographics

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Imaging Findings

Treatment

Medical Therapy

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Menopause pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Menopause pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Menopause pathophysiology

CDC on Menopause pathophysiology

Menopause pathophysiology in the news

Blogs on Menopause pathophysiology

Directions to Hospitals Treating Menopause

Risk calculators and risk factors for Menopause pathophysiology

Associated Conditions[edit | edit source]

  1. Cardiovascular disease: " Estrogen has a positive effect on the tunica intima of the artery wall, helping to keep blood vessels flexible. During menopause, estrogen deficiency causes vasoconstriction of the vessel wall and an accelerated increase of low-density lipoprotein (LDL). Thus, menopause is linked to the increased risk of cardiovascular disease".
  2. Osteoporosis is a disease of the bones that causes bones to become weak and break easily." During menopause, estrogen deficiency increases osteoclastic activity, such that there is an imbalance of osteoclastic and osteoblastic activity. This results in more bone being reabsorbed and overall bone loss.  Estrogen deficiency leads to the release of cytokines among them RANKK ligand (RANKL), which plays a critical role in the osteoclastogenesis cascade. During menopause, women experience an increased rate of bone loss of 3% to 5% per year for 5 to 7 years".[5]


Microscopic Pathology

On microscopic histopathological of menopause," Structures of the ovaries ( cortex and medulla) are change, the distinction between the cortex and medulla is less evident. The cortex becomes thinner, it has fewer follicles that is the tendency towards the fragmentation of the corpora arenacea. Additionally, there are invaginations of the surface epithelium of the cortex, and epithelial inclusion cysts are present. The medulla develops stromal fibrosis and scars. The medulla also undergoes the hyalinization of vessel walls, with architectural changes of vessels. There is also a significant change in the vagina during menopause, the mucosa layer of the vagina begins to atrophy due to decreased estrogen that causes this cell layer to become drier and thinner. As a result, the vaginal mucosa loses its elasticity and becomes fragile".[6]






References


Template:WikiDoc Sources