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1.

Cardiovascular Changes
After menopause, there is an increased risk of cardiovascular events on
woman compared to men with the same age. It is thought that the reason for
CVD in woman was due to a lower level of high-density lipoprotein, which is
an effect of a lowering level of estrogen. 1
Classification of CVD Risk in Women2
Risk Status
High risk (>1)

At risk (>1)

Criteria
Clinically manifest coronary heart disease
Clinically manifest cerebrovascular disease
Clinically manifest peripheral arterial disease
Abdominal aortic aneurysm
End-stage or chronic kidney disease
Diabetes mellitus
10 year predicted CVD risk > 10%
Cigarette smoking
SBP > 120 mmHg, DBP > 80 mmHg, or treated hypertension
Total cholesterol > 200 mg/dL, HDL-C < 50 mg/dL, or
treated for dyslipidemia
Obesity, particularly central adiposity
Poor diet
Physical inactivity
Family history of premature CVD occurong in first-degree
relatives in men < 55 years of age or in women < 65 years of
age
Metabolic syndrome
Evidence of advanced subclinical atheroscleroris (e.g,
coronary calcification, carotid plaque, or thickened intima
media thickness)
Poor exercise capacity on treadmill test and/or abnormal heart
rate recovery after stopping exercise
Systemic autoimmune collagen-vascular disease (e.g lupus or
rheumatoid arthritis)
History of preeclampsia, gestational diabtes, or pregnancy

Ideal
cardiovascula
r health

induced hypertension
Total cholesterol < 200 mg/dL (untreated)
BP < 120/80 mmHg (untreated)
Fasting blood glucose < 100 mg/dL (untreated)
Body mass index < 25kg/m2Physical activity at goal for adults > 20 years of age: > 150
min/week moderate intensity, > 75 min/week vigorous
intensity or combination
Healthy (DASH like) diet

Several ways can be done to prevent CVD risk in women who are menopausal, such
as lifestyle changes; cessation of smoking, increase in physical exercise, eating
healthy. Pharmacological measure can also be used, to lower blood pressure, to
control lipid profile, or any other comorbidity such as diabetes.
Table 4. Guidelines for the Prevention of CVD in Women
Lifestyle Interventions
Cigarette smoking
Women should be advised not to smoke and to avoid environmental tobacco smoke.
Provide counseling at each encounter, nicotine replacement, and other
pharmacotherapy as indicated in conjunction with a behavioral program or formal
smoking cessation program (Class I; Level of Evidence B).
Physical activity
Women should be advised to accumulate at least 150 min/wk of moderate exercise, 75
min/wk of vigorous exercise, or an equivalent combination of moderate- and
vigorous-intensity aerobic physical activity. Aerobic activity should be performed in
episodes of at least 10 min, preferably spread throughout the week (Class I; Level of
Evidence B).
Women should also be advised that additional cardiovascular benefits are provided by
increasing moderate-intensity aerobic physical activity to 5 h (300 min)/wk, 2 1/2
h/wk of vigorous-intensity physical activity, or an equivalent combination of both
(Class I; Level of Evidence B).
Women should be advised to engage in muscle-strengthening activities that involve
all major muscle groups performed on 2 d/wk (Class I; Level of Evidence B).
Women who need to lose weight or sustain weight loss should be advised to
accumulate a minimum of 60 to 90 min of at least moderate-intensity physical activity
(eg, brisk walking) on most, and preferably all, days of the week (Class I; Level of
Evidence B).
Cardiac rehabilitation
A comprehensive CVD risk-reduction regimen such as cardiovascular or stroke
rehabilitation or a physician-guided home- or community-based exercise training
program should be recommended to women with a recent acute coronary syndrome or
coronary revascularization, new-onset or chronic angina, recent cerebrovascular
event, peripheral arterial disease (Class I; Level of Evidence A) or current/prior
symptoms of heart failure and an LVEF 35% (Class I; Level of Evidence B).
Dietary intake
Women should be advised to consume a diet rich in fruits and vegetables; to choose

whole-grain, high-fiber foods; to consume fish, especially oily fish, at least twice a
week; to limit intake of saturated fat, cholesterol, alcohol, sodium, and sugar; and
avoid trans-fatty acids. See Appendix (Class I; Level of Evidence B).
Note: Pregnant women should be counseled to avoid eating fish with the potential for
the highest level of mercury contamination (eg, shark, swordfish, king mackerel, or
tile fish).
Weight maintenance/reduction
Women should maintain or lose weight through an appropriate balance of physical
activity, caloric intake, and formal behavioral programs when indicated to maintain or
achieve an appropriate body weight (eg, BMI 25 kg/m2 in US women), waist size
(eg, 35 in), or other target metric of obesity. (Class I; Level of Evidence B).
Omega-3 fatty acids
Consumption of omega-3 fatty acids in the form of fish or in capsule form (eg, EPA
1800 mg/d) may be considered in women with hypercholesterolemia and/or
hypertriglyceridemia for primary and secondary prevention (Class IIb; Level of
Evidence B).
Note: Fish oil dietary supplements may have widely variable amounts of EPA and
DHA (likely the only active ingredients).
Major risk factor interventionsBlood pressure: optimal level and lifestyle
An optimal blood pressure of 120/80 mm Hg should be encouraged
through lifestyle approaches such as weight control, increased physical activity,
alcohol moderation, sodium restriction, and increased consumption of fruits,
vegetables, and low-fat dairy products (Class I; Level of Evidence B).
Blood pressure: pharmacotherapy
Pharmacotherapy is indicated when blood pressure is 140/90 mm Hg
((130/80 mm Hg in the setting of chronic kidney disease and diabetes
mellitus). Thiazide diuretics should be part of the drug regimen for most patients
unless contraindicated or if there are compelling indications for other agents in
specific vascular diseases. Initial treatment of high-risk women with acute coronary
syndrome or MI should be with -blockers and/or ACE inhibitors/ARBs, with
addition of other drugs such as thiazides as needed to achieve goal blood pressure
(Class I; Level of Evidence A).
Note: ACE inhibitors are contraindicated in pregnancy and ought to be used with
caution in women who may become pregnant.
Lipid and lipoprotein levels: optimal levels and lifestyle
The following levels of lipids and lipoproteins in women should be encouraged
through lifestyle approaches: LDL-C 100 mg/dL, HDL-C 50 mg/dL, triglycerides
150 mg/dL, and nonHDL-C (total cholesterol minus HDL) 130 mg/dL (Class I;

Level of Evidence B).


Lipids: pharmacotherapy for LDL-C lowering, high-risk women
LDL-Clowering drug therapy is recommended simultaneously with lifestyle therapy
in women with CHD to achieve an LDL-C 100 mg/dL (Class I; Level of Evidence
A) and is also indicated in women with other atherosclerotic CVD or diabetes mellitus
or 10-year absolute risk 20% (Class I; Level of Evidence B).
A reduction to 70 mg/dL is reasonable in very-high-risk women (eg, those
with recent ACS or multiple poorly controlled cardiovascular risk factors) with CHD
and may require an LDL-lowering drug combination (Class IIa; Level of Evidence B).
(Continued)

Table 4. Continued
Mosca et al Guidelines for the Prevention of CVD in Women2011 Update 1253
Lipids: pharmacotherapy for LDL-C lowering, other at-risk women
LDL-Clowering with lifestyle therapy is useful if LDL-C level is 130
mg/dL, there are multiple risk factors, and the 10-y absolute CHD risk is 10% to 20%
(Class I; Level of Evidence B).
LDL-C lowering is useful with lifestyle therapy if LDL-C level is 160
mg/dL and multiple risk factors even if 10-y absolute CHD risk is 10% (Class I;
Level of Evidence B).
LDL-C lowering with lifestyle therapy is useful if LDL 190 mg/dL
regardless of the presence or absence of other risk factors or CVD (Class I; Level of
Evidence B).
In women 60 y of age and with an estimated CHD risk 10%,
statins could be considered if hsCRP is 2 mg/dL after lifestyle modification
and no acute inflammatory process is present (Class IIb; Level of Evidence B).
Lipids: pharmacotherapy for low HDL-C or elevated nonHDL-C
(Niacin or fibrate therapy can be useful when HDL-C is low (50 mg/dL)
(or nonHDL-C is elevated (130 mg/dL) in high-risk women after LDL-C
goal is reached (Class IIb; Level of Evidence B).
Diabetes mellitus
Lifestyle and pharmacotherapy can be useful in women with diabetes mellitus to
achieve an HbA1C 7% if this can be accomplished without significant

hypoglycemia (Class IIa; Level of Evidence B).


Preventive drug interventionsAspirin: high-risk womenAspirin therapy (75325
mg/d) should be used in women with CHD unless contraindicated (Class I; Level of
Evidence A).Aspirin therapy (75325 mg/d) is reasonable in women with diabetes
mellitus unless contraindicated (Class IIa; Level of Evidence B).If a high-risk woman
has an indication but is intolerant of aspirin therapy, clopidogrel should be substituted
(Class I; Level of Evidence B). Aspirin: other at-risk or healthy women
Aspirin therapy can be useful in women 65 y of age (81 mg daily or 100
mg every other day) if blood pressure is controlled and benefit for ischemic stroke
and MI prevention is likely to outweigh risk of gastrointestinal bleeding and
hemorrhagic stroke (Class IIa; Level of Evidence B) and may be reasonable for
women 65 y of age for ischemic stroke prevention (Class IIb; Level of Evidence B).
Aspirin: atrial fibrillation
Aspirin 75325 mg should be used in women with chronic or paroxysmal atrial
fibrillation with a contraindication to warfarin or at low risk of stroke
((1%/y or CHADS2 score of 2) (Class I; Level of Evidence A).
Warfarin: atrial fibrillation
For women with chronic or paroxysmal atrial fibrillation, warfarin should be used to
maintain the INR at 2.0 to 3.0 unless they are considered to be at low risk for stroke
((1%/y or high risk of bleeding) (Class I; Level of Evidence A).
Dabigatran: atrial fibrillation
Dabigatran is useful as an alternative to warfarin for the prevention of stroke and
systemic thromboembolism in patients with paroxysmal to permanent AF and risk
factors for stroke or systemic embolization who do not have a prosthetic heart valve
or hemodynamically significant valve disease, severe renal failure (creatinine
clearance 15 mL/min), or advanced liver disease (impaired baseline
clotting function) (Class I; Level of Evidence B).
-Blockers-Blockers should be used for up to 12 mo (Class I; Level of Evidence A)
or up to 3 y (Class I; Level of Evidence B) in all women after MI or ACS with
normal left ventricular function unless contraindicated.Long-term -blocker
therapy should be used indefinitely for women with left ventricular failure unless
contraindications are present (Class I; Level of Evidence A).
Long-term -blocker therapy may be considered in other women with
coronary or vascular disease and normal left ventricular function (Class IIb; Level of
Evidence C).
ACE inhibitors/ARBs
ACE inhibitors should be used (unless contraindicated) in women after MI and in
those with clinical evidence of heart failure, LVEF 40%, or diabetes

mellitus (Class I; Level of Evidence A).


In women after MI and in those with clinical evidence of heart failure, an LVEF
40%, or diabetes mellitus who are intolerant of ACE inhibitors, ARBs should be
used instead (Class I; Level of Evidence B).
Note: ACE inhibitors are contraindicated in pregnancy and ought to be used with
caution in women who may become pregnant.
Aldosterone blockade
Use of aldosterone blockade (eg, spirololactone) after MI is indicated in women who
do not have significant hypotension, renal dysfunction, or hyperkalemia who are
already receiving therapeutic doses of an ACE inhibitor and -blocker and
have LVEF 40% with symptomatic heart failure (Class I; Level of Evidence B).
LVEF indicates left ventricular ejection fraction; BMI, body mass index; EPA,
eicosapentaenoic acid; DHA, docosahexaenoic acid; ACE, angiotensin-converting
enzyme; ARB, angiotensin receptor blocker; LDL-C, low-density lipoprotein
cholesterol; HDL-C, high-density lipoprotein cholesterol; CHD, coronary heart
disease; CVD, cardiovascular disease; ACS, acute coronary syndrome; hsCRP, highsensitivity C-reactive protein; HbA1C, hemoglobin A1C; MI, myocardial infarction;
CHADS2, Congestive Heart Failure, Hypertension, Age, Diabetes, Prior Stroke; and
INR, international normalized ratio.

2. Weight Gain and Fat Distribution


Weight gain is a common complain among woman in the menopausal
transition. It is caused by slower metabolism due to increasing age, if the
eating and exercise is not adjusted; it may result in weight gain.
Weight gain during this period is associated with fat deposition, which can
increase the risk of developing diabetes mellitus and heart disease.
3. Dermatologic, Dental, and Breast Changes
Possible skin changes during menopausal transition:
Hyperrpigmentation (age spots)
Wrinkles
Itching

4. Central Nervous System Changes


a. Sleep dysfunction

Difficulties in sleep onset and sleep maintenance are common in


menopausal women. As they aged, it is more common to experience
lighter sleep, to be awakened more easily by pain, sound, etc.
Effect of hormonal changes on sleep
Progesterone
Progesterone given intravenously has direct sedative qualities;
stimulation benzodiazepine receptors that in turn stimulate the
production of the NREM associated gamma-aminobutyric acid
(GABA) receptors.
Progesterone has an effect on breathing. It is a respiratory stimulant,
which has been used to treat mild obstructive sleep apnea.
Estrogen
Increases REM cycles. Estrogen is involved in norepinephrine (NE),
serotonin (5-HT) and acetylcholine metabolism.
Estrogen has been shown to decrease sleep latency, decrease the
number of awakenings after sleep occurs, increase total sleep time and
decrease the number of cyclic spontaneous arousals. It is also related to
temperature regulation, which causes hot flashes; higher estrogen level
prevents hot flashes because it has a significant effect on core body
temperature, especially during sleep. Estrogen can also affect sleep due
to its effect to cortisol. Estrogen helps regulate normal cortisol peak in
the morning and therefore helps stabilize nighttime sleep.
Melatonin and estrogen has a very complicated interaction. Melatonin
has a well-known circadian effect on sleep onset, and may also be
involved in sleep maintenance by blocking arousal mechanisms,
thereby tending to keep humans asleep in the dark at night. Prior to
menopause, there is an age related drop in melatonin but immediately
afterward melatonin increases for several years, which can explain the
sleep difficulties experienced by the perimenopausal women.
The National Sleep Foundation recommends several ways to cope with
sleep disturbances during the perimenopausal transition:

Eat healthy. Avoid large meals, especially before bedtime.


Maintain a regular, normal weight. Some foods that are spicy or
acidic may trigger hot flashes. Try foods rich in soy as they
might minimize hot flashes.

Avoid nicotine, caffeine and alcohol, especially before bedtime.

Dress in lightweight clothes to improve sleep efficiency. Avoid


heavy, insulating blankets and consider using a fan or air
conditioning to cool the air and increase circulation.

Reduce stress and worry as much as possible. Try relaxation


techniques, massage and exercise.
(http://sleepfoundation.org/sleep-topics/menopause-andsleep/page/0/2)

b. Cognitive dysfunction
Memory decreases with advancing age. Although no direct effect of
lowered estrogen levels on memory and cognition has been
determined, many investigators suspect a relationship to, or an
acceleration of, cognitive decline during menopause.

The Study of

Womens Health Across the Nation (SWAN) also reported a crosssectional association between self-reported forgetfulness and being
perimenopausal2. (Gold EB, Sternfeld B, Kelsey JL, Brown C, Mouton
C, Reame N, Salamone L, Stellato R. Relation of demographic and
lifestyle factors to symptoms in a multi-racial/ethnic population of
women 40 55 years of age. Am J Epidemiol. 2000 Sep; 152(5):463
73. [PubMed: 10981461]
Consistent with transitioning womens perceived memory difficulties,
perimenopause was associated with a decrement in cognitive
performance, characterized by women not being able to learn as well
as they had during premenopause. Improvement rebounded to premenopausal levels in postmenopause, suggesting that menopause
transitionrelated cognitive difficulties may be time-limited.
.
McEwen BS. Invited review: estrogens effects on the brain: Multiple sites and
molecular mechanisms. J Appl Physiol. 2001; 91:27852801. [PubMed: 11717247]

Prevention of cognitive impairment can be done with lifestyle


change. Maintaining a healthy lifestyle with adequate exercise,
avoidance of obesity, mental and physical stimulation, control
of stress, treatment of medical illness and depression, and
control of vascular risk factor such as diabetes, hypertension,
hyperlipidemia is suggested to prevent cognitive decline.
(Kim SA, Jung H. Prevention of Cognitive Impairment in the
Midlife Women. J Menopausal Med. 2015 Apr; 21(1): 19
23.Published online 2015 Apr 27. doi: 10.6118/jmm.2015.21.1.19)

5. Psychosocial Changes
6. Urogenital Changes (genitourinary syndrome of menopause: new terminology
for vulvovaginal atrophy from International Society for the Study of Womens
Sexual Health and The North American Menopause Society)
Anatomic and physiologic changes in the vagina associated with menopause
are directly related to reduced circulation estrogen levels and aging. The high
concentration of estrogen receptors in the vagina, vestibule, and trigone of the
bladder modulated cellular proliferation and maturation.
Low levels of circulation estrogen after menopause result in physiologic,
biologic, and clinical changes in the urogenital tissues. Anatomic changes
include reduced collagen content and hyalinization, decreased elastin, thinning
of the epithelium, altered appearance and function of smooth muscle cells,
increased density of connective tissue, and fewer blood vessels.
The labia minora thin and regress, the introitus retracts, and the hymenal
carunculae involute and lose elasticity, often leading to significant entry
dyspareunia. The uretral meatus appears prominent relative to the introitus and
becomes vulnerable to physical irritataion and trauma.
Physiologic changes results in reduce vaginal blood flow, dminishe
lubrication, decreased flexibility and elasticity of vaginal vault, and increased
vaginal pH. Furthermore, decreases in vaginal tissue strength and increased
friability may predispose to epithelial damage with vaginal penetrative sexual
activity, leading to vaginal pain, burning, fissuring, irritation, and bleeding
after sex.

Epithelial thinning with decreased glycogenated superficial cells leads to


changes in vaginal flora and loss of lactobacilli, increased pH, and a change in
the microbiome.
Table.2 Genitourinary Syndrome of Menopause (GSM) symptoms and signs
Symptoms
Genital Dryness
Decreased lubrication

Signs
Decreased moisture
with sexual Decreased elasticity
Labia minora resorption
activity
Pallor/Erythema
Discomfort or pain with sexual activity
Loss of vaginal rugae
Post-coital bleeding
Tissue fragility/fissures/pthechiae
Decreased arousal, orgasm, desire
Urethral eversion or prolapse
Irritation/Burning/Itching of vulva or
Loss of hymenal remnants
vagina
Prominence of urethral meatus
Dysuria
Introital retraction
Urinary frequency/urgency
Recurrent urinary tract infections
7. Patient Evaluation
a. Diagnosis
Differential Diagnosis of Menopausal Symptoms 1
Hot flashes, vasomotor symptoms
Hyperthyroidism
Pheochromocytoma
Febrile illness
Anxiety and psychosocial symptoms
Vaginal dryness, dyspareunia
Bacterial vaginosis
Yeast infection
Pelvic pathology
Poor vaginal lubrication
Marital discord
Primary Osteoporosis
Osteomalacia
Primary and secondary hyperparathyroidism
Excess corticoid therapy
Increased calcium excretion
Abnormal uterine bleeding
Anovulation
Endometrial cancer
Cervical cancer
Endometrial hyperplasia
Endometrial polyps
Uterine leiomyoma
Urogenital atrophy
Hormone treatment
b. Physical Examination
Constitutional

Height, weight, BMI needs to be recorded to counsel women about physical


exercise and weight loss or gain. Waist circumference may also be measured
to identify truncal obesity which is associated with other comorbidity such as
CVD or diabetes. Height loss may be associated with osteoporosis. Blood
pressure also needs to be checked, to know whether there is hypertension or
not.
Cognition
To screen for cognition there is a test that can be used
Psychosocial
Can be assessed using questionnaire
Dermatological

Skin changes associated with estrogen deficiency include skin thinning and
wrinkling. In addition, various skin lesions are com- monly associated with
aging and photoaging. Careful inspection for abnormal nevi or excessive sun
exposure may prompt referral to a dermatologist for further skin cancer
evaluation.

Breast
During menopausal transition, estrogen levels fall and glan- dular breast tissue
is gradually replaced by fatty tissue. Breast tissue and axillae are carefully
inspected and palpated. Nipple discharge, skin changes, nipple inversion, and
masses should be documented and evaluated as described in Chapter 12 (p.
334).

Pelvic Examination
Examination of the vulva may demonstrate loss of the connec- tive tissue that
results in shrinkage of the labia majora. The labia minora may disappear
completely, and there is often a narrow- ing of the introitus. The vulva should
be examined for redness, atrophy, or scarring. In those with pain, scar tissue
from a past tear or episiotomy or from surgery should be noted. Specific areas
of tenderness can often be localized with a methodical evaluation of the vulva.

Touch with a cotton swab may locate and reproduce a patients pain (Fig. 4-1,
p. 112).
Vaginal examination will typically reveal a narrow vaginal canal and thin, flat
vaginal epithelium. The classic appearance of vaginal atrophy includes loss of
rugae and a pale, dry vagi- nal mucosa. Epithelial tissues are often friable, and
submucosal petechial hemorrhages may be seen. Markers of vaginal atrophy
include a vaginal pH greater than 5.0 and a change in the vagi- nal walls
maturation index toward basal cell predominance. Culture of the vagina may
reveal pathogenic bacteria not nor- mally found in the vagina.
In addition to a standard gynecologic evaluationthat is, bimanual and
speculum examinationexternal and internal assessment should focus on
pelvic muscle and vaginal muscular tone and strength, as well as mobility and
integrity of the fascia and connective tissues. The degree of introital flexibility,
muco- sal dryness, or atrophy is determined. Integrity of the pelvic organs and
possible prolapse of the bladder, uterus, or rectum is evaluated by having the
patient perform a Valsalva maneuver and observing for bulging of a cystocele,
rectocele, or cervical or vaginal prolapse.

8. Laboratory Testing