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Dr. Kavita Priya M.D.

(Obst & Gynae)

The term postmenopause is applied to women who have not experienced a menstrual bleed for a minimum of 12 months, assuming that they do still have a uterus and are not pregnant or lactating. In women without a uterus, menopause or postmenopause is identified by a high FSH level. Thus postmenopause is all of the time in a woman's life that take place after her last period, or more accurately, all of the time that follows the point when her ovaries become inactive.

OSTEOPOROSIS
. Osteoporosis is now defined as a skeletal disorder characterized by compromised bone strength, which predisposes the patient to an increased risk of fracture.[

AGE OF MENOPAUSE
AVERAGE
INDIA
WEST
47 YEARS

RANGE
40.32-48.84 YRS

51 YEARS

48 52 YEARS

SURGICAL MENOPAUSE
Every year thousands of women between the ages of 15 and 44 experience an "Estrogen Crash", a sudden drop in estrogen levels that leaves women in the clutches of early menopause. Although menopause is traditionally seen as a problem in older women, the many younger women who experience early menopause find themselves unprepared for the unexpected changes that occur. Estrogen Crash occurs when both of a woman's ovaries are removed or suddenly stop functioning. When this happens the body stops producing estrogen.

MENOPAUSE
Menopause is a time of upheaval in a womans life.

THE FEMALE HORMONES

ESTROGEN WHY IS IT A BIG YES!!!


Estrogens have an important role on skin tension, Estrogens stabilize and make the bones stronger Estrogens protect against arteriosclerosis and have an important effect on blood vessels. When the estrogen levels decrease and the menopause starts, then the main risks becomeosteoporosis and arteriosclerosis. This is the reason why doctors tend to prescribe hormone based products as therapy.

Estrogen & Bone

HOW DOES ESTROGEN ACT ON BONE?


effects on T cell cytokine production effects on stromal or osteoblastic cells to alter their production of RANKL or OPG direct inhibition of differentiated osteoclasts effects on bone formation mediated by osteoblasts or osteocytes to enhance the response to mechanical forces initiated by these cells

1. Women experiencing natural menopause, where the ovaries have stopped producing desired amounts of estrogen. 2. Women who have undergone surgery to remove ovaries (oophorectomy), and are thus, medically termed as having surgical menopause. 3. Women experiencing early menopause (women below 40 years) are recommended ERT primarily to prevent osteoporosis and bone loss at a young age.

ESTROGEN REPLACEMENT THERAPY

SIDE EFFECTS OF ERT


Headache Nausea Weight gain Bloating Pain in the stomach Weakness (feeling of faintness) Vaginal discharge or bleeding Mood swings Depression Memory loss Enhanced risk of dementia Skin irritation caused by estrogen patches Increase risk of stroke and formation of blood clots Greater risk of breast and ovarian cancer for women on long-term ERT (over 10 years)

SERMS THE VIABLE ALTERNATIVE

SELECTIVE ESTROGEN RECEPTOR MODULATORS

SERMS THE VIABLE ALTERNATIVE


Selective estrogen receptor modulators (SERMs) are a class of compounds that act on the estrogen receptor.[1] A characteristic that distinguishes these substances from pure receptor agonistsand antagonists is that their action is different in various tissues, thereby granting the possibility to selectively inhibit or stimulate estrogen-like action in various tissues. Phytoserms are SERMs from a botanical source

SERMS
clomifene femarelle ormeloxifene raloxifene tamoxifen toremifene lasofoxifene

RALOXIFENE
SERM EFFECTS ON BONE Raloxifene has been extensively studied and data support an estrogen agonist profile in the skeletal system. In the ovariectomized rat model, raloxifene acts as an antiresorptive, with preservation of both bone mineral density and bone strength identical in magnitude to that seen with ethinyl estradiolresults from the Multiple Outcomes of Raloxifene Evaluation (MORE) trial conducted in postmenopausal women with osteoporosis. In this trial, raloxifene increased bone mineral density by 2%-3% and reduced the incidence of new vertebral fractures by 30% and 50% (in women with and without prevalent vertebral fractures, respectively) compared to placebo [7]. While tamoxifen also increases bone density in postmenopausal women [1], its effects on osteoporotic fracture are limited to secondary endpoint data from the large U.S. Breast Cancer Prevention Trial (BCPT), which showed trends toward reduction in vertebral fracture rates in the treated versus control subjects [4]. Toremifene did not increase bone density in a very small study of postmenopausal breast cancer patients [8], but this result may reflect lack of statistical power rather than underlying pharmacology