Education

2. 2
MENOPAUSE
“The anchor point that is defined after 12
months of amenorrhea following the final
menstrual period (FMP), which reflects a
near complete but natural diminution of
ovarian hormone secretion.” Soules et al.
Menopause 2001

3. 3
NATURAL (SPONTANEOUS)
MENOPAUSE
“Occurs after 12 consecutive months of amenorrhea,
for which there is no other obvious pathologic or
physiologic cause.”
(Average age in Western world is 51 years) Utian.
Climacteric 1999.

4. 4
PREMATURE MENOPAUSE
“Menopause that occurs in women at or
under 40 years old.”
Utian. Climacteric 1999.

5. • PERIMENOPAUSE
– A period of 3years before menopause &
followed by 1 year of amenorrhoea
– Assosiated with mild ovarian hormonal
deficiency
– Leads to anovulation, menorrhagia
5

6. 6

7. 7
 MENOPAUSE
The time of cessation of ovarian function
resulting in permenant amenorrhoea
For confirmation: 12 months
 CLIMACTERIC:
Phase of waning ovarian activity
2-3yrs before and 2-5 yrs after menopause

8. Demography; Indian perspective
8
 60 million women in India are above 55yrs
 Majority of women spend 1/3rd of their life
in postmenopausal period

9. Age
9
 Usual age 45 to 50yrs average being 47yrs.
 Premature menopause - before 40 yrs
 Late menopause – menstruation beyond 52 yrs

10. 10
 DELAYED MENOPAUSE
Due to good health and better nutrition.
Also seen in women with uterine fibroids .
Also in women with high risk of
endometrial cancer

11. 11
Menopausal age is directly associated
with smoking and genetic disposition.
Smoking induces premature menopause.

12. PATHOPHYSIOLOGY
12
 During climacteric, ovarian activity declines.
 Initially, ovulation fails, no corpus luteum forms and
no progesterone is secreted by the ovary.
 Later, graffian follicle fails to develop, estrogenic
activity decreases and endometrial atrophy leading to
amenorrhea.
 Increased secretion of FSH and LH by anterior
pituitary.

13. 13
 FSH 50 times increase, LH 3-4 times increase.
Menopausal urine has become and important
commercial source of gonadotropins.
Later gonadotropin activity of anterior
pituitary ceases and fall in FSH level
eventually occurs.

14. 14

15. HORMONE LEVELS
15
 50% reduction in androgen production and 66%
reduction in oestrogen production..
 Some estrogen produced by ovary (oestrone, E1)
 FSH appears in large concentrations.
 Low oestrogen levels(below 20pg/ml) predisposes to
osteoporosis and ischemic heart disease.

16. Risk factors for menopausal related
problems are as follows:
16
 Early menopause
 Surgical menopause or radiation.
 Chemotherapy esp alkylating agents.
 smoking., caffeine, alcohol.
 Family history of menopausal diseases.
 Drugs related such as GnRH, heparin, corticosteroids and
clomiphene(anti- oestrogen) when given over prolonged
peiod can cause oestrogen deficiency.

17. • ANATOMICAL CHANGES
17
SITE CHANGES
Genital organs Atrophy and regression
Ovary Shrink,surfaces:grooved ,
furrowed
Tunica albuginea Thickens
Size of ovary <2*1.5*1cm in US
Plain muscle in fallopian
tube:
Atrophy
Cilia Disappear
Uterus Smaller
Endometrium As basal layer: deeply stained
stroma and a few glands

18. 18
SITE CHANGES
Cervix Smaller
Vaginal fornices Disappears
Vagina Narrow
Epithelium Pale, thin,and dry: senile vaginitis
Vulva Atrophy (+narrow
vagina:dyspareunia)
Skin of labia minora and vestibule Pale,thin,dry
Labia majora Reduction in fat
Pubic hair Reduced and grey
Breast More pendulous(fat dep)
Glandular tissue <5%
Pelvic cellular tissue Becomes lax
Ligaments supporting the uterus and
vagina
Lose their tone:prolapse of genital
organs, stress incontinence of urine,
and fecal incontinence

19. Menopausal symptoms
19
 Mensural symptoms
 Other symptoms
 Neurological
 Libido
 Urinary tract
 Genital

20. MENOPAUSAL SYMPTOMS
20
 Menstrual
3 classic ways in which the menstrual period
ceases are as follows:
Sudden cessation.
Gradual diminution in the amount of blood loss
with each regular period until menstruation
stops.
Gradual increase in spacing of periods until
they cease for at least a period of one year.

21. Other symptoms
21
 60-70% women go
through menopausal
period without
problems
 Rest needs guidance
and treatment

22. HOT FLUSHES
• Early and acute symptom of estrogen deficiency.
• These are waves of vasodilatation affecting the
face and neck and last for 2-5 mins each.
• Followed by severe sweating.
• Occurring at night may disturb sleep.
22

23. 23
• Sometimes preceded by headache.
• Palpitation and anginal pain maybe felt.
• Mental depression due to lack of sleep,
irritability and lack of concentration.
• With passage of time severity of hot flushes
decreases.

24. Cause of hot flushes
•Caused by noradrenalin, which disturbs the
thermoregulatory system.
•Oestrogen deficiency reduces hypothalamic
endorphins, which release more norepinephrine and
serotonin.
•This leads to inappropriate heat loss mechanism.
24

25. Neurological
25
 Vasomotor symptoms and paraesthesia
take the form of sensations of pins and
needles in the extremities.

26. Libido
26
 E and androgen deficiency causes urogenital
atrophy, which affect sexual function.
 Leads to a decline in sexual interest.

27. 27
 The symptoms which develop a little
later are :
 Urinary
 Dysuria
 Stress incontinence and urge
 Recurrent infection
Genital
Dry vagina
Dyspareunia
Loss of libido
Faecal incontinence

28. URINARY TRACT
28
 Oestrogen deficiency causes
 Urethral caruncle
 Dysuria with or without infection
 Urge
•Stress incontinence( due to poor vascularity and
loss of tone of internal urethral sphincter).
These symptoms are clubbed together under the
term urethral syndrome.

29. 29
 Atrophic vagina reduces the vaginal
secretion, and dry vagina cause dyspareunia.
 Loss of libido adds to sexual dysfunction.

30. 30
COMPLICATIONS

31. 31
Vasomotor symptoms.
HTN
Osteoporosis.
Arthritis
Osteoporosis of vertebral bones, upper
end of hip joint,wrist
frature

32. 32
 Cardiovascular disease.
ischaemic heart disease, MI, HTN
Stroke
Cardiac irregularities
Tachycardia

33. 33
 Urogenital atrophy.
Prolape genital tract
Stress incontinence of urine & feces
Ano-colonic cancer
Cognitive decline and Alzheimer's disease.
Cataract, glaucoma, macular degeneration
Skin changes and Tooth decay

34. 34
Family history of osteoporosis
Low Ca intake in diet
Smoking and excess of caffeine and alcohol intake
Early menopause
Low weight
Surgical menopause
Radiation menopause
Thyrotoxicity
Sedentery life syle
Women on GnRH, heparin, cortico steroids , danazol,
clomiphene

35. CARDIOVASCULAR DISEASE
35
 Estrogen is cardioprotective(antioxidant property also)
 After menopause HDL,LDL, total cholesterol
,
 Estrogen deficiencyatherosclerosis, ischemic heart
disease, MI
 Risk factors: obese women with hypertension ,
previous thromboembolicepisodes

36. Stroke
36
 Incidence of stroke also increase in
menopausal women

37. Skin changes
37
 Collagen content is reduced, causing skin to
wrinkle
 The loss of collagen is more rapid in the first
few years after menopause
 30% of skin collagen is lost within the first 5
years.
 The rate is 2% per year for the first 10 years
after menopause.

38. CNS
38
 ER are abundant in the brain. E have a role in
many brain processes, and it’s absence result in
physiologic and symptomatic changes.
 E is important for
cerebral blood flow
cerebral glucose administration

39. 39
synaptic activity, neuronal growth
survival of cholinergic neurons
complex functions as cognition.
 The role of E deficiency in postmenopausal
depression, declining cognitive function,
dementia, and Alzheimer's disease is not
clear.

40. Pyometra
40
 Years after menopause, women may develop
senile pyometra cervical stenosis
 Rx : drainage by cervical dialatation under
GA

41. Diagnosis
41
1) History
menstrual abnormality

42. 42
2) Symptoms:
• vasomotor symptoms
• vaginal dryness
• urinary frequency
• Insomnia
• Irritability, anxiety
• skin change
• breast changes
• urinary tract problem
• pelvic floor change
• skeletal change(backache, ).

43. 3)Physical examination:
43
The clinical findings vary greatly depending on the time elapsed
since menopause and the severity of the estrogen deficiency
Skin: thin ,dry
Breast loss turgor
The labia are small
The uterus becomes much smaller
The muscles of the pelvic floor are looser in tone and are thin
Prolapse may be present

44. 44
4) Laboratory diagnosis
 General examination: BP, Palpation of breasts, weight,
hirsuitism
 Pap smear
 Mammography, pelvic US
 E2, FSH, LH determination
 Bone density study:
Dual energy X-ray absorptiometry(DEXA)
Single or dual photon absorptiometry

45. Treatment
45
1) Counselling
2) Mild tranquillizers
3) Hormone replacement therapy(HRT)

46. Counselling
 The women often develops pregnancy &
cancer phobia.
 Duty of gynaecologist- exm. &investigation.
 Pelvic ultrasound-ovarian size, endometrial
thickness, mammography & as well as E2
&FSH levels, when HRT is considered.

47.  The advice on contraceptives is necessary.
Until the menopause is well established &
amenorrhea has lasted for 12 month, couple is
advice to use barrier method.
 Diet: least 1.2g of Ca, Vit A,C,E &400mg of Vit
.D & Soya beans are good.
 Weight bearing exercise delay onset of
osteoporosis.

48. Mild tranquillizers
 Anti depressants like sulpiride
 Releives anxiety, depression, sleeplessness

49. Hormone replacement therapy
 Not all women require HRT
 70-85% of women remain
healthy need only good
nutrition and healthy life
style.

50. Indications of HRT
1) Women having climacteric symptoms
 Vasomotor symptoms
 Urinary symptoms
 Sexual dysharmony
 Established osteoporosis on x-ray /B.M.D.
Measurements

51. 2) All asymptomatic high-risk women having
Premature menopause (surgical / spontaneous)
Family history of osteoporosis
Thin, small sedentary women
Poor diet, excess alcohol
CVD, Alzhemeir’s disease, colonic cancer
Corticosteroid & other medications
High urinary calcium / creatinine
Low plasma estradiol
51

52. Contraindications of HRT
 Breast cancer, uterine cancer or family history
of cancer.
 Previous history of thromboembolic episode.
 Liver & gall bladder disease.

53. DRUGS USED IN HRT
 Oestrogen
 Progesterone
 Other drugs:
 Tibolone
 Raloxifene
 Soya
 Bisphosphonates

54. Estrogen therapy
 Short term estrogen therapy
 1) To releive symptoms like; hot flush, night sweats,
palpitations, disturbed sleep
 In smallest effective dose for 3-6 months
 Natural estrogens
 Oral premarin(Conjugated equine estrogen (CEE):
0.625 mg daily)
 Ethinyl estradiol(0.01mg),Evalon(1-2mg),
micronized oestrogen are effective.

55.  Medroxyprogestrone(10mg) or primolut-N
(2.5mg) daily for 10-12d each month.
 Combined hormone therapy(femet). 2mg 17-β-
oestrodiol & 1mg of norethisterone acetate.

56.  2) for dyspareunia, urethral syndrome and senile
vaginitis
Local estrogen cream(oestriol: 1/2g-
everyday-10-12 days each month for- 3-6
months)
Short acting
 Cyclic progesterone administration is
not required.
Postmenopausal withdrawal bleeding do
not occur.
Estring(vaginal ringreleases 5-
10microgram - 3months)

57.  Long term therapy:
 For delaying osteoporosis
 Reduce the risk of CV disease
 Beyond 8-10yr

58. Oral Preparations of estrogen
 Oral: -
 Conjugated equine estrogen (CEE): 0.625 mg daily
 Ethinyl estradiol : 0.01mg
 Micronised estrogen : 1-2g

59. ESTROGEN: ORAL
 Advantages.
*Easy to take & cheap.
*Good control due to short ½ life.
 Disadvantages.
*High dose required.
*first pass effect in liver.
*daily intake
*tablet contain lactose& not suit to women
who are allergic to lactose.

60. Transdermal Preparations of
estrogen
 Transdermal (estradiol): -
 Patches: contains: 3-4mg; releases 50 micro gm / 24 hour twice
weekly.
 Gel :for improving collagen in skin 75 micro gm / 24 hours daily.

61. ESTROGEN: TRANSDERMAL
 Advantages.
 Low dose, pure estradiol.
 Avoids intestine & liver metabolism.
 Reduces serum triglyceride & insulin resistance.
 No thromboembolic risk or hypertension
 Disadvantages.
 More expensive
 Not well tolerated in warm climates
 Variable absorption.

62. ESTROGEN: IMPLANTS
 Sub cutaneous implant (estradiol): -
 25 / 50 / 100 mg. 6 monthly.
 Advantages.
 Pure estradiol, 6 monthly insertion, high level of estradiol in blood.
 Avoids first pass effects
 Better response in severe osteoporosis.
 Disadvantages.
 Needs surgical procedure
 Unable to control absorption
 Difficult to remove pellet

63. THE RISKS OF HRT
 Vaginal bleeding
 Thromboembolism
 Endometrial cancer if E2 is taken alone
 Brest cancer due to progestogen if HRT is
taken over 5yrs.
 CHD in a women with CVD.

64. Progesterone
 Role in HRT
 Prevents endometrial hyperplasia and cancer in non-
hysterectomised women
 Implant may replace oestrogen, where estrogen is c/I
or sensitive
 Prevents breast cancer
 Improves bone mineral density
 primolut-N 2.5mg ,
 medroxyprogestrone & duphaston
 Mirena IUCD- levonorgestrel

65. Tibolone
 Synthetic derivative of 19-nor-testosterone.
 Weak oestrogenic, progestogenic, &
androgenic action.
 Endometrial hyperplasia
 Elevates the mood, relieves the VM symptom,
improves sex drive & reduces bone resoption.
 Cardioprotection(red. TG)
 SE: wt gain, oedema, tenderness in breast, GI
symptom& vaginal bleed.

66. raloxifene
 Non steroidal comp., SERM, reduses the risk
of fracture by 50%, esp. vertebra by BMD by
2-3%.
 It causes 10% reduction in total cholesterol &
LDL & HDL level.
 It does not raise the level of triglycerides.so
cardio protective for long term.
 Reduces osteoporosis.

67. raloxifene
 Side effects
*hot flushes, cramps, venous thrombosis,
retinopathy.
• Cotraindications
*venous thrombosis
*should be given with oestrogen
*hepatic dysfunction
*stop the drug 72 hr before surgery
*indomethacin,naproxen,ibuprofen,diazepam.

68. soya
 Isoflavone.
 Abt 11g soya- 2-4mg phytoestrogen-
oetrogenic- non steroid plant product.
 45-60mg soya daily –protective- breast cancer,
liver disease &other side effect.
 cholesterol ,LDL,TG & marginal HDL.
 Antiviral, antifungal & anticarcinogenic.

69. Bisphosphonates
 etidronate, tiludronate reduce bone resorption
through the inhibition of osteoclastic activity.
 Elidronate(10mg/Kg f body wt-2W followed by
a gap of 2-3M & this course is repeated for 10
such cycles.
 Not given with Ca.(absorption )
 Overdose- hypocalcemia.
 Milk &antacid - gastric irritation.

70.  alendronate (5mg daily or 35mg weakly)
overdose-hypocalcemia.
 Risedronate (5mg/D or35mg/M)- gastric side
effect.
 Zolendronic acid(once yr i.v 5mg over 15min)
SE: osteonecrosis of the jaw & visual dis.
 Calcitonin-inh. Osteoclast activity
*nasal spray(single dose of 200IU daily for
3M)

71. *NS can cause flushes, rhinitis, allergic reaction
&nasal bleeding.
* fracture by 30%
 Subcutaneous inj. Of Calcitonin-GI symptoms
,aneamia &inflammation of joint cause poor
compliants so also the high cost.
 Teriparatide-rec. formation of PIH
*abt 20μg once daily SC inj. Ver. Fracture-
65% others-50% ,if used <2yr

72. *nausea, headache are the complication.
 Strontium ranelate(1-2g daily orally)
BMD-50%, very expensive, not easily
available.
 Clonidine- imidazole der.
*treat hot flushes
*effective in HT
*dose 0.2-0.4mg daily.

73. PREMATURE MENOPAUSE
 Def: ovarian failure occurring 2 SD in year
before the mean menopausal age in the
population.
 Clinically: sec. amenorrhea for at least 3
months with raised FSH/LH & low E2 level in a
women under 40 year of age.
 Inc. 1% -be. 30yr-1:1000
 -at 35yr-1:250
 -be.40yr-1%

74. AETIOLOGY
1.Genetic disorder
 chr. abnormalities (10-20%) –X sex chr.
 AD sex linked inheritance.
 Ovarian dysgenesis-30%
2.Autoimmune disease(30-60%)
 Mumps, thyroid dys.,hypo parathyroidism, &
Addison’s dis.
 Ovarian biopsy –infiltration of follicle with plasma
cells& lymphocytes.
 CD8 & CD4 autoimmune d.
 Antiovarian Ab are present.

75. 3.Tuberculosis
4.Smoking
5.Radiaton & chemotherapy
 Reversible
 Radiation up to 400 to 500 rads. restores normal
ovarian fun. in 50% cases.
 Alkalytic agents.
6.Hystrectomy
 Kinking & blockage of ovarian vessels
 Tubectomy

76. 7.Prolonged GnRH therapy.
8.enz.defect-17α-hydroxylase & galactosemia
have adverse effect on oocytes – pri.
Amenorrhea.
9.Resistant ovary
 Terminology is used less frequently these
days.
 Follicles fail to respond to gonadotropin
stimulation.
10.Induction of multiple ovulation in infertility.

77. PATHOPHYSIOLOGY
 Lack of receptors is explained as the cause of
non response of follicle.

78. C/F
 Hot flushes
 Sweating
 Insomnia
 Headache
 Psychological
 Cancer phobia
 Pseudocyesis
 Irritability
 Depression
 Lack of conc.

79. INVESTIGATION
 FSH level: 40mIU/ml or more.
 E2 level: 20pg/ml or less
 Thyroid fun., Ca level, chr. study,& thyroid Ab.
 Blood sugar.
 X-ray pituitary fossa for the tumour.
 BMD study is not always necessary, it is an
invasive procedure.
 Ovarian biopsy.
 Ultrasound.
 Prolactin level.

80. COMPLICATIONS
 The risks of osteoporosis & cardiovascular
diseases increase in premature menopause.

81. MANAGEMENT
1.Cause of premature menopause should be
ascertained & the cause treated.
2.Ovulation induction or oocyte donation in IVF
programme has caused pregnancies to occur
in some cases.
3.Progestogen challenge test will indicate if
menstruation can be induced, provided
endometrium is primed with oestrogen.

82. 4.Corticosteroid therapy is effective in
autoimmune disease if Ab to sex hormone are
present in the blood. Plasmapheresis has also
been attempted.
5.A women with hypo-oestrogenism may require
HRT or other drugs to prevent osteoporosis .
oestrogen implant with progestogen or Mirena
IUCD offers long-term HRT.

83. LATE MENOPAUSE
 Def: cond. in which menstruation cond.
beyond 52 year.
 Late menopause occurs in women with
fibroids and is seen in women who develop
endometrial cancer. Often it is constitutional.
Beyond 52 yr , endometrial biopsy is required
to rule out endometrial pathology.

84. POSTMENOPAUSAL
BLEEDING
 Normally-1 yr POA –after 40 yr.
 however, VB –anytime after 6 MOA in
menopausal age postmenopausal
bleeding & investigated.
 without amenorrhea / irre. Bleeding , if the
women over the age of 52 yr cont. to
menstruate, she needs investigation to rule out
endometrial hyperplasia & mali. Of genital
tract.

85. AETIOLOGY
1.vulva-trauma , vulvitis ,benign & malignant
lesions.
2.vagina-foreign body such as ring pessary for
prolapse, senile vaginitis , vaginal tumour
(benign as well as malignant) postradition
vaginitis.
3.cervix-cervical erosion, cervicitis, polyp,
decubitus ulcer in prolapse &cervical
malignancy.

86. 4.uterus-senile endometritis, tubercular
endometritis, endometrial hyperplasia(10%) ,
polyp, endometrial carcinoma& sarcoma , &
mixed mesodermal tumour.
5.Dysfunctional uterine bleeding, metropathia
haemorrhagica, uterine polypi & endometrial
hyperplasia.
6.Fallopian tube malignancy .

87.  7. ovary- benign ovarian tumour such as
benner tumour, granulosa & theca cell tumour,
& malignant ovarian tumour.
 8. Hypertension & blood dyscrasia.
 9. Urinary tract- urethral caruncle, papilloma
&CA of bladder. May be mistaken for genital
tract bleeding.
 10.bowel- bleeding from haemorrhoid , anal
fissures, & rectal cancer may be misleading.

88. 11.imp. Reason –indiscriminate. Prolonged use
of oestrogen unopposed by progestogens, &
HRT when applied clinically. Tamoxifen causes
endometrial hyperplasia & cancer.
 30-50% -PMB –malignancy of genital tract
-most common –endometrial cancer ,
cervical cancer& ovarian tumour.
 Common benign conditions are endometrial
hyperplasia and polypi.

89. Clinical Features
 HISTORY
*age –menarche & menopause
*taking oestrogen & tamoxifen
*prolapse details
*abdominal pain &foul smelling discharge-
malignant tumours
*urinary& rectal symptoms .

90.  EXAMINATION
*BP
*GE- obesity& diabetes
*abdominal pain
*speculum & bimanual examination

91. INVESTIGATION
 Aim: Excluding malignancy
1.Blood count & smear- blood dyscrasia.
2.Blood sugar level.
3.Cervical cytology-cervical lesion.
4.Endometrial study.
5.Sonosalpingography –endometrial polyp.
6.ultrasound- endometrial thickness >4mm
indicates the need of endometrial biopsy.

92.  Several methods
 Dilatation & curettage (D&C) – fractional
curettage comprising separate scrap of
endometrium &endocervix not only allows the
exact site of malignancy if present, but also
detect the extent of the tumour & staging.
 Uterine cavity aspiration & endometrial
sampling.

93.  Vibra aspirator, Gravlee’s jet washer , Isaac’s
aspirator & Pipelle aspiration –end. Sample.
7.Hystroscopy inspection& selective biopsy.
8.CT & MRI .
9.Diagnostic laparoscopy .
10.Cytoscopy & proctoscopy.

94. MANAGEMENT
1. Treat the cause.
2. When no cause is found, & if there has been
only one bout of bleeding, the pt should be
kept under observation.
 Abt 80% of cases do not bleed again.
 If cond. to bleed- laparotomy.
 An undiagnosed small tumour may be
discovered & dealt appropriately. – AH with
bilateral oophorectomy histopathological
study.

95. 95