MENOPAUSE
By
Dr. Eman El Sayed El Fekey
Introduction
• The terms climacteric and menopause are often used
interchangeably, but they have different meanings.
• The climacteric is defined as the period of waning ovarian function
which signals the end of the reproductive life span,
• The menopause meaning is the stoppage of menses. It indicates
the final menstrual period, and it occurs during the climacteric.
Climacteric
Climacteric is the period of life starting from the decline in ovarian activity
until after the end of ovarian function.
Is characterized by endocrinal, somatic, and transitory psychologic
changes.
The climacteric in the female may be classified into three phases: pre-
menopause, menopause, and post menopause.
Climacteric
Pre-menopause:
• Is defined as the period of beginning physiological failure of ovarian function.
• It lasts for a period ranging from two to six years
• It is characterized by increased frequency of anovulatory cycles.
Post-menopausal:
• Phase is defined as the remainder of life after menopause.
• The age of menopause ranges from 45 to 55 years of age.
Climacteric
Menopause:
• It is the permanent cessation of menstruation due to an intrinsic ovarian
failure resulting in follicular inactivity.
• It usually occurs between 45-55 years.
• Menopause is retrospectively defined when cessation of menses
continues for one year after the final menstrual period (FMP), which is
the last menstrual period to occur.
Types of menopause
A. Physiologic menopause.
B. Pathologic menopause.
Types of menopause
A. Physiologic menopause:
Is the spontaneous progressive decline of ovarian function.
Starts at the age of 45 to 55 years.
Types of menopause
B. Pathologic menopause:
1. Premature menopause: It is defined as premature ovarian failure before the
age of 45.
2. Artificial menopause: It is defined as permanent cessation of ovarian function
which brought about by surgical removal of the ovaries or by irradiation using
either intra uterine radium or deep X-ray.
3. Delayed menopause: It is defined as cessation of menstruation above the age
of 55.
Etiology of menopause
Menopause occurs due to physiologic exhaustion and depletion of the ovarian
primordial follicles, being consumed throughout the menstrual cycles till the
time of the menopause. (The adult ovary contains around 400 primordial
follicles at the onset of puberty).
Premature menopause may occur due to premature ovarian failure as in
some cases of gonadal dysgenesis (mosaic turner syndrome), or may be
induced.
Menopausal changes
1. Breast changes
2. Female genital organs
3. Cardiovascular system
4. Psychological changes
5. Obesity
6. Osteoporosis
Menopausal changes
• In addition to the amenorrhea the following changes are related to the
reduction in circulating estrogen and increased production of gonadotrophin.
• Since the secretion of estrogen varies from woman to woman, the changed
which occur are variable in severity.
Menopausal changes
1) Breast changes:
During pre menopausal phase, it shows an increasing the subcutaneous fat,
Later, with the reduction of the circulating estrogen,
The subcutaneous fat is resorbed.
The gland tissue atrophied.
The breasts become flattened and pendulous.
Menopausal changes:
2) Female genital organs:
A. Ovaries:
1. Decrease in size.
2. Become nonfunctional.
3. Unable to respond to the circulating gonadotrophins.
B. Uterus and tubes:
Become progressively atrophic.
Menopausal changes:
C. Vagina and vulva:
Their mucosa is thinned and can be easily irritated.
The vaginal secretion diminishes (acidity), so that pathogenic organisms can be
developed.
Later on, the atrophy of the vaginal epithelium may cause dyspareunia.
Menopausal changes:
D. Urethra:
Their mucosa may become atrophic leading to the development of urethritis.
E. Pelvic floor muscles:
They lose their tone and the connective tissue lose its elasticity,
So that prolapse of the organs and stress incontinence may develop.
Menopausal changes:
3) Cardiovascular system:
A. Vasomotor disturbances:
1. The most frequent are hot flushes.
2. Sweating.
3. Headaches.
4. Fainting.
5. palpitations.
Menopausal changes:
Hot flush:
Lasts between 1.5 and 3 minutes and is often accompanied by perspiration.
They are associated with peripheral vasodilatation and an increase in the heart
rate.
The etiology of hot flushes may be related to the withdrawal of estrogen and
the pulsatile release of gonadotrophin releasing hormone.
Menopausal changes:
B. Atherosclerosis:
Its incidence increased after menopause specially in persons with limited
exercise and excessive eating.
Menopausal changes:
4) Psychological changes:
Irritation, depression and insomnia.
5) Obesity:
Due to increased appetite.
Also the alteration in the carbohydrate metabolism as a result of hyper function
of the anterior lobe of the pituitary gland.
Menopausal changes:
6) Osteoporosis:
Common in post menopausal women and occurs as a result of decrease level of
circulating estrogen.
Early, it affects the vertebrae (trabecular bone) than axial skeleton (cortical
bone).
Menopausal changes:
Osteoporosis presents with one or more of the following features:
A. Bone pain: back pain is the most common complaint in post menopausal
women as vertebral bone mineral content declines much more rapidly with
aging.
B. Fractures: the most common associated fractures include thoracic spinal
wedge fracture, lumbar spinal crush fractures, hip fractures and colles fractures
of the wrist.
Menopausal changes:
C. Loss of height:
compression fractures of the
vertebrae and kyphosis
inevitably lead to loss of
stature.
Menopausal changes:
D. Deformities of the vertebral column: the back may reveal thoracic kyphosis
that may take one of two forms:
Round kyphosis: it develops when several vertebrae are affected. It is
characterized by smooth thoracic curvature.
Angular kyphosis: it develops when only one or few vertebrae are affected and is
known as "Dowager hump".
a. Angular kyphosis b. Round kyphosis
Management of the
menopausal changes
Management of the menopausal changes
1. General treatment:
Reassurance (through proper explanation about this changes).
Improve general health.
Diet control (to avoid obesity).
2. Hormonal treatment:
Through administration of hormones as estrogen, estrogen with progestrogens.
3. Medical treatment:
Sedative drugs, Calcium intake, Vit D.
Physiotherapy management of the
menopausal changes
Preventive treatment:
a . Exercise and cardiovascular disease in post-menopausal women.
b. Exercise and obesity in post-menopausal women .
c . Exercise and depression in post-menopausal women.
d . Exercise and bone loss in post-menopausal women.
a . Exercise and cardiovascular disease in post-
menopausal women
The risk of cardiovascular disease increases in women after menopause, so regular
aerobic exercise may improve cardiorespiratory endurance and reduce the risk of
cardiovascular disease.
The recommended exercise to improve cardiovascular fitness without incurring a
significant risk of injury was 30 minutes at a time, three times/week at 60% of
maximum oxygen consumption or target heart rate.
b. Exercise and obesity in post-menopausal
women
The effectiveness of exercise in promoting loss of fat results from several
mechanisms including:
1. Energy expenditure.
2. Metabolic rate.
3. Altered body composition.
The recommended exercise form:
Walking or jogging and light resistance exercise in post-menopausal women
For 60 minutes / day, three times/week.
At 50% of VO2max or target heart rate.
b. Exercise and obesity in post-menopausal
women
Excessive body fat is a problem for many pre and post-menopausal women especially
preponderance of abdominal fat which has been shown to be a risk factor for
cardiovascular disease and diabetes.
Aerobic exercise promotes loss of abdominal fat more readily than fat at other sites
and obese post-menopausal women are lost fat much more effectively by exercising
than by dieting.
c . Exercise and depression in post-menopausal
women
Some changes in mood and behavior occur in pre and post-menopausal women
who are chronically sleep deprived because of hot flushes that awaken them at
night.
The aging process is also associated with decreased serotonin synthesis and
increased serotonin catabolism.
Aerobic exercise (walking or jogging) leads to high brain concentrations of both
nor epinephrine and serotonin and prevents or relieves depression.
d . Exercise and bone loss in post-menopausal
women
Nowadays one of the most conservative least costly measures generally advocated for
slowing bone loss in post-menopausal women is regular exercise in form of:
1. Weight bearing exercise (walking, jogging and climbing stairs)
2. Non-weight bearing exercise (bicycle, specific exercise for spine and swimming).
The recommended exercise training in post-menopausal women to provide a
protection against bone loss is:
30 minutes/day, three times/week.
At 60% VO2max.
d . Exercise and bone loss in post-menopausal
women
Biological effect of exercise on the bone:
The possible mechanism of exercise for keeping the skeletal integrity are:
1) Changes the biochemical structure of the blood by altering the level of its
component:
Skeletal remodeling is modulated by the availability of:
Calcium.
Phosphorus.
Calcitropic hormones.
d . Exercise and bone loss in post-menopausal
women
Increase in serum calcium associated with
A decreased parathyroid hormone levels.
A small increase in calcitonin levels during and after exercise.
This explained how could exercise increase bone mineral density after exercise.
The estrogen causing
Increased osteoblastic activity and affect bone metabolism
Exercise at 60% VO2max
produced significant increase in the plasma concentration of sex hormone
bonding globulin and B-estradiol.
d . Exercise and bone loss in post-menopausal
women
2) Mechanical load of exercise which can modify and increase bone mass.
Muscular contraction and gravity create piezo electric forces which affect
bone remodeling.
Continual physical stress stimulates osteoblastic deposition of bone.
The deposition of bone at points of compressional stress has been suggested to
be caused by piezo electric effect,
Biological effect of exercise on the bone:
Compression of bone causes a negative potential at
the compressed site
A positive potential elsewhere in the bone.
It has been shown that minute quantities of current
flowing in bone cause osteoblastic activity at the
negative end of the current flow; which could
explain the increased bone deposition at
compression sites.
Piezo electric forces
Prevention of osteoporosis in post-menopausal
women
1. Electromagnetic fields (EMFs).
2. Pulsed ultrasonic (US).
3. Electrical stimulation.
4. Ultraviolet (UV).
1. Electromagnetic fields (EMFs)
Pulsating electromagnetic fields (PEMFs).
Capable of slowing down the loss of bone
mass.
With 10 micro volt/cm.
Frequency between 50-150 Hz.
One hour/day.
1. Electromagnetic fields (EMFs)
Mechanism of action:
A. Piezo electric potentials in loaded bone which influence the tissues cellular
environment and thus affect skeletal mass.
B. It induces a maximum potential gradient which is capable of increasing net
calcium flux in human osteoblast like cells.
C. It maintain a constant high osteogenetic activity and osteogenesis and reduce
the resorption on the bone surface.
2. Pulsed ultrasonic (US)
Using pulsed ultrasound
Is beneficial to reduce pain and to enhance bone regeneration.
An intensity from 0.5 - 2 w/cm2
For 10 -15 minutes/day
Aplication: Para spinally.
Mechanism of action:
1. Enhance bone regeneration
2. Reduce pain by improving circulation and gate control theory.
3. Electrical stimulation:
Functional electrical stimulation or neuro muscular electrical stimulation.
Produces muscle contractions that in turn apply stress to the bone which
stimulate bone regeneration resulting in increases bone mineral density.
4. Ultraviolet (UV)
Wavelength of 280 nm
Suspended from the ceiling of the room at a height of approximately 3 meters.
The patient was irradiated for 3 hours each day.
UV ray must be perpendicular over the patient.
The patients' head, neck, forearms and hands were covered.
While, thighs and legs were exposed to UV.
4. Ultraviolet (UV)
Mechanism of action:
1. UV converted 7 dehydrocholesterol into cholecalciferol (Vit. D3) which converted in
the liver into 25 hydrocholecalciferol (the active form of vit. D)
2. Then in the kidney to the active form of vit. D (25 dihydrocholecalciferol)
3. Active form of vit. D increases the formation of calcium binding protein in the
epithelial cells that aids calcium absorption and also helps to control calcium
deposition in the bone.