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SANDHYA KUMARI
M.SC. NURSING
AMITY UNIVERSITY
MENSTRUAL IRREGULARITIES
INTRODUCTION
Menstruation is the visible
manifestation of cyclic physiologic
uterine bleeding due to shedding of
the endometrium following invisible
interplay of hormones mainly through
hypothalamo- pituitary- ovarian axis.
MENSTRUATION
The development and maturation of a follicle,
ovulation and formation of corpus luteum and its
degeneration constitute an ovarian cycle. All these
events occur within 4 weeks.
The ovarian cycle consists of:
 Recruitment of groups of follicles.
 Selection of dominant follicle and its menstruation.
 Ovulation
 Corpus luteum formation
 Demise of corpus luteum.
MENSTRUAL IRREGULARITIES
 Menstrual irregularities are common
abnormalities of a woman’s
menstrual cycle. Menstrual
irregularities include a variety of
conditions in which menstruation is
irregular, heavy, painful, or does not
occur at all.
Common types of menstrual irregularities include:
 Amenorrhea
 Dysmenorrhea
 Menorrhagia
 Oligomenorrhea
 Polymenorrhea
 Spotting
 Pre menstrual syndrome
 Menopause
 Metorrhagia
 Dysfunctional uterine bleeding.
AMENORRHOEA
Amenorrhoea means absence of
menstruation. It is not a symptom and
not a disease.
 5 basic factors involved in the onset and
continuation of normal menstruation.
These are:
1. Normal female chromosomal
pattern(46XX).
2. Co- ordinate hypothalamo-pituitary
ovarian axis.
3. Anatomical presence and patency of the
outflow tract.
4. Responsive endometrium.
5. Active support of thyroid and adrenal
CLINICAL TYPES
Physiological
 Primary
(before puberty)
 Secondary
 -during pregnancy
 -during lactation
 -following menopause.
 Pathological
 Concealed
(cryptomenorrhoea)
 Congenital
 acquired
 real (true)
 primary
 secondary
PRIMARY AMENORRHOEA
 A young girl who has not yet
menstruated by her 16 years of age
is giving primary amenorrhoea
rather than delayed menarche. The
normal upper age limit for
menarche is 15 years.
CAUSES:
1. Hypogonadotrophic hypogonadism
 Delayed puberty – delayed Gn RH pulse reactivation.
 Hypothalamic & pituitary dysfunction
 Kallmann’s syndrome – inadequate Gn RH pulse
secreation- reduced FSH & LH.
 CNS tumors- craniopharyngioma- reduce Gn RH- Reduce
FSH & LH.
2. Hypergonadotrophic hypogonadism
 Primary ovarian failure
 Resistant ovarian syndrome
 Galactosemia
 Enzyme edficiency (17 alpha hydroxylase deficiency)
 Others- gonadotrophin receptors mutations
3. Abnormal chromosomal pattern
 Turner’s syndrome(45X)
 Pure gonadel dysgenesis (46XX or 46 XY)
 Androgen insensitivity syndrome ( testicular
feminization syndrome)
 Partial deletion of X chromosome (46XX)
4. Developmental defect of genital tract
 Imperforate hymen
 Transverse vaginal septum
 Atresia upper third of vagina and cervix
 Complete absence of vagina
5. Dysfuction of thyroid and adrenal cortex
 Adrenogenital syndrome
 cretinism
6. Metabolic disorders
 Juvenile diabetes
7. Systemic illness
 Malnutrition, anemia
 Weight loss
 Tuberculosis
8. Unresponsive endometrium
 Congenital (uterine synechiae- tubercular.
SPECIAL INVESTIGATIONS OF PRIMARY
AMENORRHOEA
Mullerian agenesis
 USG
 Laproscopy
 Karyotype
Unresponsive endometrium
 Progesterone challenge test
 HSG/ Hysteroscopy
 Hormonal studies
Uterine synchiae
 Progesterone challenge test
 HSG
 hysteroscopy
tubercular
 blood- ESR
 X ray- chest
 Mantaoux test
 Endometrial biopsy
Hypogonadotrophic gonadism
 Progesterone challenge test
 Serum gonadotrophins
 Serum oestradiol
 Primary ovarian failure
 Karyotype
 Serum oestradiol
 Serum gonadotrophin
 Ovarian biopsy
 Tumer
 Laproscopy
 Serum gonadotrophins
 Karyotype
Androgen insensitivity syndrome
 Laproscopy
 Serum testosterone
 Karyotype
 Gonadal biopsy
Adrenogenital syndrome
 Karyotype
 Serum 17 hydroxy-progesterone
 Urinary pregnanetriol
Thyroid dysfunction (hypo)
 Serum TSH
 T3, T4
Diabetes:
 RBS
 This test is performed by administering inj.
Progesterone in oil 75 mg IM or tab
Medroxyprogesterone 10 mg daily or
micronized progesterone 200mg daily for 10
days. Withdrawl bleeding usually occurs
within 10 days, if the test is positive.
MANAGEMENT OF PRIMARY
AMENORRHOA
In primary amenorrhea:
 correct the underlying cause
 estrogen replacement therapy
 if pituitary tumor: treatment with surgical
resection, radiation and drug therapy
 surgery to correct abnormalities of genital
tract
SECONDRY AMENORRHOEA
 Secondary amenorrhea: is the absence of menses for 3 cycles
or 6 months in women who have previously menstruated
regularly.
Causes:
 Breast feeding
 Emotional stress
 Mal nutrition, tuberculosis
 Pregnancy
 PCOS Premature ovarian failure
 Pituitary, ovarian, or adrenal tumour
 Depression
 Hyper thyroid or hypothyroid
 Diabetes
 Hyper prolactinemia
 Rapid wt gain or loss related to amenorrhoea
 Kallmann syndrome
 post pill amenorrhoea
 Chemotherapy or radiotherapy
 Aneroxia nervosa
 Hypothalamic dysfunction- stress, exercise, rapid wt.
gain or loss.
 Vigorous excrete
 Kidney failure
 Tranquilizers or antidepressant , anti hypertensives
 Post partum pituitary necrosis
 Early menopause
Detailed history:
 Mode of onset- whether sudden or gradual preceded by
hypomenorrhoea or oligomenorrhoea.
 Sudden changes in envt., emotional, stress,
psychogenic shock, eating disorders etc
 Sudden loss or gain weight
 Intake of psychotrophic or anti hypertensive drugs .
 Intake of oral pills or its recent withdrawl. h/o recent
chemo or radiotherapy
 Appearance of abnormal manifestations either by coinciding
or preceeding the amenorrhoea.
 Acne, hirsutism or change in voice.
 Inappropriate lactation galactorrhoea.( abnormal secretion
of milk unrelated to pregnancy and lactation.
 Headache and visual disturbances.
 Hot flushes and vaginal dryness
 Obstetric history- overzealous curettage leading to
synechiae.
 Cessarrian section may be extended to hysterectomy of
which the patient may be unaware.
 Severe PPH, shock, infection.
 Postpartum or postabortal uterine curettage
 Prolonged lactation
 Medical history of TB., Diabetes, chronic nephritis,
hypothyroid.
General examination:
 Nutritional status
 Extreme emaciation or marked obesity
 Presence of acne, hirsutism
 Discharge of milk from breasts
Abdominal examination
 Presence of striae associated with obesity may be
related to Cushing syndrome.
 A mass in lower abdomen.
Pelvic examination
 Enlargement of clitoris.
 Adnexal mass suggestive of tubercular tuboovarian
mass or ovarian tumour.
 Tests that can be done are:
 Progesterone challenging test
 Oestrogen- progesterone challenge test
 Serum gonadotrophins
 Gn RH dynamic test.
 CT
 MRI
 X-RAY
MANAGEMENT FOR SECONDARY AMMENORRHOEA
 1. NO ABNORMALITY DETECTED
 If patient is not anxious, no treatment is required.
Provide assurance.
 If she is anxious provide oral contraceptive pills to be
continued for atleast 3 cycles.
 With low endogenous oestrogen : ethinyl oestradiol 0.02
mg or conjugated equine oestragen 1.25 mg daily is to
be taken for 25 days. Medroxyprogesterone acetate 10
mg daily is added from day 16-25.
The patient is anxious for fertility.
 Husbands semen analysis in primary infertility and the
tubal factor of the women are to be evaluated prior to
2. CASES WITH DETECTABLE CAUSE
 Anxiety and stress- may be corrected by reassurance,
psychotherapy.
 Improve health status
3. POLYCYSTIC OVARIAN SYNDROME (PCOS)
 First correct the biochemical parameters such
as :
 Hyperandrogenemia
 Hyperprolactenemia
 Hyperinsulinemia
 Insulin resistance
 High serum oestradiol
 Low FSH
 Low serum progesterone androgenic follicular
microenvironment
 Weight reduction
If fertility not desired
 Management of hyperandrogenemia
 Combined oral contraceptive pills
 Antiandrogens such as cyproterone acetate, flutamide
may be given.
 Metformin may be given as an oral insulin sensitizing
agent.
 Endometrial biopsy can be done in case of
endometrial hyperplasia.
 Cabergolin, bromocriptine in case of
hyperprolactenemia (if failed surgery can be done as –
transnasal-transsphenoidal adenectomy is done.
 If premature ovarian failure- HRT can be given )
 Thyroxine ---- of hypothyroid state.
SURGERY
 Laproscopic ovarian drilling (LOD)
 Bariatric surgery in case of PCOS
who are morbidly obese
PREMENSTRUAL SYNDROME (PMS)
(Premenstrual tension)
 Premenstrual syndrome is a psychoneuroendocrine
disorder of unknown etiology that occurs just prior to
menstruation.
 There is a cyclic appearance of several symptoms
during the last 7-10 days of the onset of menstrual cycle
which subside the onset of menstrual flow. At least 5 of
the symptoms must have been present in most of the
cycles over the past one year.
 When these symptoms disrupt daily functioning
they are grouped under premenstrual dysmorphic
Clinical manifestation of PMS
 Depressed mood, hopelessness,
and self depreciation.
 Anxiety, tension, fearfulness.
 Affective liability- mood swings
 Anger, irritability, interpersonal
conflict.
 Decreased energy.
 Appetite changes or cravings.
 Changes in sleep.
 Feeling overwhelmed or out of
control.
 Physical symptoms such as breast
tenderness, headache.
 Dyspareunia, bloating.
 Weight gain.
PATHOPHYSIOLOGY
 The exact cause is not known but the following
hypothesis is considered.
 Alteration in the level or ratio of oestrogen and
progesterone from the mid luteal phase.
 Neuroendocrine factors:
 Decreased synthesis in the luteal phase.
 Withdrawl of endorphins from CNS during luteal
phase.
 Psychological and psychogenic factors affecting
behavior.
TREATMENT
General
 Elimination of caffeine from the diet.
 Avoidance of smoking, alcohol.
 Regular exercise.
 Regular meals and nutritious diet.
 Adequate sleep.
 Relaxation techniques like yoga, stress management
and assurance.
 Alternative & complementary therapy.
 Non hormonal
 Tranquilizers or antidepressant drugs
 Pyridoxine
 Diuretics in the second half of the cycle.
 Serotonin reuptake inhibitors such as fluoxetine.
 Hormones
 Oral contraceptives pills to maintain a uniform
hormonal melieu.
 Progestogen.
 Bromocriptine to relieve breast symptoms.
 Gn RH agonists to suppress gonadal steroids.
NURSING MANAGEMENT
 Encourage patient to set
goals for the reduction of
symptoms such as mood
swings, crying, binge eating,
and day to day stressors.
 Teach positive coping
measures, involve and
encourage family members
such as spouse or children
for assistance and care.
 Encourage use of exercise,
meditation and creative
activities to reduce stress.
 Provide instructions about
the desired effects of
DYSMENORRHOEA
 Dysmenorrhoea : painful
menses or cramping during
menstruation of sufficient
magnitude so as to
incapacitate day to day
activities.
 Typically dysmenorrhoea
begins upto 48 hours before
the onset of menses and
resolves within 2 to 4 days of
onset or by the end of
TYPES OF DYSMENORRHOEA
 Primary dysmenorrhoea (spasmodic)
 Secondary dysmenorrhoea (congestive)
 PRIMARY DYSMENORRHOEA (
spasmodic)
 It is painful menses with a uterine cause,
but without pelvic pathology and usually
occurs within 1-3 years of menarche.
Cause:
 Painful uterine contractions stimulated by
prostaglandin produced by the
endometrium during menses are most often
identified as the cause for primary
Others may be like-
 Mostly confined to adolescents.
 Almost always confined to ovulatory cycles.
 The pain is usually cured following pregnancy and
vaginal delivery.
 The pain is related to dysrhythemic uterine
contractions and uterine hypoxia.
 Psychogenic factors- of tension, anxiety lowers the
pain threshold.
 Abnormal anatomical and functional aspect of
myometrium like Uterine myometrial hyperactivity.
 Imbalance in the autonomic nervous control of uterine
muscle.
 Role of prostaglandins.
 Role of vasopressin
Symptoms:
 Sharp, intermittent suprapubic pain radiating
to the back or thigh.
 Headache, fatigue, backache, flushing,
dizziness and syncope.
 Adolescents typically experience the
problem only after menstrual cycles become
ovulatory.
 Women often experience reduction in
dysmenorrhoea after pregnancy.
THERAPEUTIC INTERVENTIONS
 Nonsteriodal anti inflammatory drugs (NSAID) started
1-3 days prior to the onset of menstrual flow (to
decrease prostaglandin production).
 Oral contraceptives, to decrease endometrial
proliferation and therefore production of prostaglandin.
Surgery:
 Transcutaneous electrical nerve stimulation (TENS)
 Laproscopic uterine nerve ablation(LUNA).
 Dilatation of cervical canal.
 Presacral neurotomy (LPSN).
SECONDARY DYSMENORRHOA (congestive)
Secondary dysmenorrhoea is painful menses resulting from a
pathologic process.
Cause:
 pressure from outside the uterus
 tissue ischemia
 cervical stenosis
 congenital abnormality (imperfotate hymen)
 endometriosis
 ovarian cysts
 pelvic inflammatory disease (PID)
 uterine fibroid tumous.
 IUCD in utero and pelvic congestion.
 Obstruction due to mullerian malformation.
clinical features:
 The pain is dull, situated in the back and in front
without any radiation.
 It usually appears 3-5 days prior to the period and
relieves with the start of bleeding.
 The onset and duration depends on the pathology
producing the pain.
 There is no systemic discomfort unlike primary
dysmenorrhoea.
 Other symptoms may be breast tenderness and
change in bowel habits.
diagnostic evaluation:
 Laproscopy
 Hysteroscopy/laparotomy
TREATMENT
 The treatment aims at the cause rather than the
symptom. The type of treatment depends on the
severity, age and parity of the patient.
OVARIAN DYSMENORRHOEA
(RIGHT OVARIAN VEIN SYNDROME)
Right ovarian vein crosses the ureter at
right angle. During premenstrual period,
due to pelvic congestion or increased
blood flow, there may be marked
engorgement in the vein –pressure on
ureter- stasis- infection- pyelonephritis-
pain.
MITTELSCHMERZ’S SYNDROME
(ovular pain)
 Ovular pain is not an infrequent complaint. It appears in
the midmenstrual period. The pain usually situated in the
hypogastruism or in either iliac fossa.
 The pain is usually located at one side and does not
change from from side to side according to which ovary
is ovulating.
 Nausea or vomiting is conspicuously absent.
 It rarely last for 12 hours.
 It may be associated with slight vaginal bleeding or
excessive mucoid vaginal discharge.
Cause:
 The exact cause is
unknown. Other
factors may include:
 Increased tension of
graffian follicle just
prior to rupture
 Peritoneal irritation by
the follicular fluid
following ovulation
 Contraction of the
tubes and uterus.
Treatment:
 Provide assurance
 analgesics
 in obstetrics cases,
the cure is absolute
by making the cycle
anovular with
contraceptive pills.
PELVIC CONGESTION SYNDROME
There is disturbance in the autonomic nervous
system which may lead to gross vascular
congestion with pelvic varicosities. The patient
may be congestive type of dysmenorrhoea
without any demonstrable pelvic pathology.
Symptoms:
 Backache
 Pelvic pain on long standing, dyspareunia
 Menorrhagia or epimenorrhoea
 Uterus may be bulky and boggy.
Diagnosis:
 Pelvic venography
 Doppler scan
 CT/ MRI
 Angiography
Treatment:
 The treatment is unsatisfactory.
 Medroxy progesterone acetate (MPA) 50 mg daily for 4
months was found effective. In parous women with
advancing age, hysterectomy may relieve the symptoms.
ABNORMAL UTERINE BLEEDING
 Menorrhagia
 Polymenorrhoea
 Metrorrhagia
 Oligomenorrhoea
 Hypomenorrhoea
 Dysfunctional uterine bleeding
MENORRHAGIA
 Menorrhagia is defined as the
cyclic bleeding at normal intervals;
the bleeding is either excessive in
amount (> 80ml) or duration (>7
days) or both. The term menotaxis
is often used to denote prolonged
bleeding.
CAUSES:
 Menorrhagia is a symptom of
some underlying pathology-
Cause:
Organic:
 Pelvic:
 Fibroid uterus
 Adenomosis
 Pelvic endometriosis
 IUCD in utero
 Chronic tubo- ovarian mass
 Tubercular endometriotis (early cases)
 Retroverted uterus – due to congestion
 Granulose cell tumour of the ovary.
Systemic:
 Congestive cardiac failure
 Severe hypertension
Endocrinal:
 Hypothyroidism
 Hyperthyroidism
hematological:
 idiopathic thrombocytopenia purpura
 leukemia
 von willebrands disease
 platelet deficiency
emotional upset:
functional
 Due to disturbed hypothalamo- pituitary-
ovarian- endometrial axis.
C. Common causes:
 Dysfunctional uterine bleeding
 Fibroid uterus
 Adenomycosis
 Chronic tubo- ovarian mass
DIAGNOSIS:
 Long duration of
flow.
 Passage of big
clots
 Use of increased
number of thick
sanitary pads
 Pallor and low
level of
hemoglobin
TREATMENT:
 The definitive
treatment is
appropriate to the
cause for
menorrhagia.
POLYMENORRHOEA
(epimenorrhoea)
 Polymenorrhoea is defined as cyclic
bleeding where the cycle is reduced to
an arbitrary limit of less than 21 days
and remains constant at that frequency.
 If the frequent cycle is associated with
excessive and or prolonged bleeding, it
is called epimenorrhoea.
Causes:
 Dysfunctional uterine.
 It is seen predominantly during adolescence,
preceding menopause and following delivery
and abortion. Hyperstimulation of the ovary by
the pituitary hormones may be a responsible
factor.
 Ovarian hyperemia- as in PID or ovarian
endometritis.
Treatment:
 Persistent dysfunctional type is treated by
hormone as in dysfunctional uterine bleeding.
METRORRHAGIA
 Metorrhagia is defined as irregular acyclic bleeding
from the uterus.
 Amount of bleeding is variable. While metorrhagia
strictly concerns uterine bleeding but in clinical
practice, the bleeding from any part of the genital tract
is included under the healing.
 The irregular bleeding in the form of contact bleeding
or intermittent bleeding is an otherwise normal cycle is
also indicated in metorrhagia.
 Menometorrgia:
 Is the term applied when the bleeding is so irregular
and excessive that the menses cannot be identified at
all.
Causes of acyclic bleeding:
 DUB- usually during adolescence following childbirth
and abortion and preceding menopause.
 Submucosal fibroid
 Uterine polyp
 Carcinoma cervix and endometrial carcinoma.
Causes of contact bleeding:
 Ca cervix
 Mucous polyp of cervix
 Vascular ectopy of the cervix specially during
pregnancy, pill use cervix.
 Infections- chlamydial or tubercular cervicitis.
 Cervical endometritis.
Causes of intermenstrual bleeding
 contact bleeding
 Urethral carnucle
 Ovular bleeding
 Breakthrough bleeding in pill use
 IUCD in utero
 Decubitis ulcer
Treatment:
 Treatment is directed to the underlying pathology.
Malignancy is to be excluded prior to any
definitive treatment.
OLIGOMENORRHOEA
 Menstrual bleeding occurring more than 35 days apart
and which remains constant at that frequency is called
oligomenorrhoea.
Causes:
 Age related- during adolescence and preceding
menopause.
 Weight related- obesity
 Stress and exercise related
 Endocrine disorders- PCOS
 Androgen producing tumours- ovarion, adrenal
 Tubercular endometritis
HYPOMENORRHOEA
When the menstrual bleeding is unduly
scanty and lasts for less than 2 days, it is
called hypomenorrhoea.
Causes:
 Local ( uterine synchiae or endometrial
tuberculosis)
 Endocrinal ( use of oral contraceptives,
thyroid dysfunction and premenopausal
periods)
DYSFUNCTIONAL UTERINE BLEEDING (DUB)
 DUB is defined as a state of abnormal uterine bleeding
without any clinically detectable organic, systemic and
iatrogenic cause. (pelvic pathology eg- tumour,
inflammation or pregnancy is excluded.)
 Currently DUB is defined as a state of abnormal uterine
bleeding following anovulation due to dysfunction of
hypothalamo- pituitary- ovarian axis.(endocrine origin).
 Heavy menstrual bleeding (HMB) is defined as a
bleeding that interferes with woman’s physical, emotional,
social and maternal quality of life.
PATHOPHYSIOLOGY
 The physiological mechanism of haemostasis in normal
menstruation are:
 Platelet adhesion formation
 Formation of platelet plug with fibrin to seal the bleeding vessels.
 Locasied vaso constriction.
 Regeneration of vaso constriction.
 Regeneration of endometrium.
 Biochemical mechanisms involved are: inc. endometrial ratio of
PGF2 alpha/ PGE2.
 PGF2alpha causes vasoconstriction and reduces bleeding.
 Progesterone increases the level of PGF2 alpha from
arachidonic acid.
 Levels of endothelin which is a powerful vasoconstrictor is also
increased.
 In anovulatory DUB there is decreased synthesis of PGF2 alpha
and the ratio of PGF2 alpha/ PGE2 is low.
The abnormal bleeding may be associated with
or without ovulation and accordingly gouped
into:
 . Ovular bleeding
 Anovular bleeding
Ovular bleeding includes:
 Polymenorrhoea/ polymenorrhagia
 Oligomenorrhoea
 Functional menorrhagia
Anoovular bleeding includes:
 Menorrhagia
 Cystic glandular hyperplasia.
INVESTIGATION
 Blood investigations including T3, T4, TSH
 USG & color Doppler
 TVS
 Saline infusion sonography (SIS)
 Hysteroscopy
 Endometrial sampling
 Laproscopy
 Diagnostic uterine curettage (D & C)
COMMON CAUSE OF ABNORMAL VAGINAL
BLEEDING
Organic:
 Uterine fibroid
 Endometriosis
 Adenomyosis
 Endometrial polyps
 IUCD
 Adnexal pathology
 Hematological and endocrine:
 Platelet deficiency
 Leukemia
 ITP
 Von willebrand disease
 Thyroid dysfunction
 Non menstrual bleeding:
 Foreign body
 Urethral carnucles
 Genital malignancy
 Postcoital
 Intermenstrual
 Abortion
 Breakthrough bleeding
MEDICAL MANAGEMENT
 HORMONES:
 With the introduction of hormones , potent oral active
progestins, they became the mainstay in the
management of DUB in all age groups and practically
replaced the isolated use of oestrogens and
androgens. Eg medroxyprogesterone acetate,
norethisterone acetate etc.
 Progestins : involves prostaglandin synthetase
inhibitors (PSI) eg; fenamates ( mefenamic acid)
 The preparation are used:
 Cyclic therapy
 Continuous therapy.
 To stop bleeding and regulate the cycle:
 Norethisterone preparations (5mg tab ) are used thrice
daily till bleeding stops which it usually does by 3-7 days.
a. cyclic therapy:
 5th- 25th day course:
 In ovular bleeding----- any low dose combined oral pills
are effective when given from 5-25th day of cycle for 3
consecutive cycles. It causes endometrial atrophy.normal
menstruation is expected to resume with restoration of
normally functioning pituitary ovarian endometrial axis.
 In anovular bleeding--- cyclic progesterone preparation
medroxyprogesterone acetate (MPA)10 MG r
norethisterone 5mg is used from 5th- 25th day of cycle for
3 cycles.
 15-25th day course:
 In ovular bleeding where patient wants pregnancy or
in cases of irregular shedding or irregular ripening of
the endometrium.dydrogesterone 1 tab (10 mg) daily
bd from 15-25th day may cure the state. It does not
suppress the ovulation.
 Anovulatory women have immaturity of H-P-O axis.
They are ideal for the use of short term cyclic therapy
until the maturity of the positive feedback system is
established.
b. Continuous progestins:
 Medroxyprogesterone acetate 10 mg tds daily is
given and treatment is usually continued for
atleast 90 days. Inj DMPA i/m can be given
 Oestrogen
 Intrauterine progestogen
 Danazol
 Mifepristone (RU 486)
 GnRH agonists
NON HORMONAL MANAGEMENT
 Anti fibrinolytic agents (tranexamic acid)
 Prostaglandin synthetase inhibitors
 NSAIDS
 Desmopressin
SURGICAL MANAGEMENT
 Uterine curettage
 Endometrial ablation/ resection
 Laser
 Roller ball
 Thermal balloon
 Microwave
 novasure
 resection
 transcervical resection (TCRE)
 uterine artery embolisation
 hysterectomy
 COMPLICATIONS
 Infections
 Uterine perforations (<1%)
 Fluid absorption may occur during hysteroscopic
procedures.
CONCLUSION
Some menstrual irregularities can be caused by
serious, even life-threatening conditions, such as
uterine cancer. Seek prompt medical care if you
have menstrual irregularities, such as heavy
menstrual periods or a lack of menstrual periods.
Early diagnosis and treatment of menstrual
irregularities reduces the risk of serious
complications, such as infertility and metastatic
uterine cancer.
Menstrual irregularities

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Menstrual irregularities

  • 1. SANDHYA KUMARI M.SC. NURSING AMITY UNIVERSITY MENSTRUAL IRREGULARITIES
  • 2. INTRODUCTION Menstruation is the visible manifestation of cyclic physiologic uterine bleeding due to shedding of the endometrium following invisible interplay of hormones mainly through hypothalamo- pituitary- ovarian axis.
  • 3. MENSTRUATION The development and maturation of a follicle, ovulation and formation of corpus luteum and its degeneration constitute an ovarian cycle. All these events occur within 4 weeks. The ovarian cycle consists of:  Recruitment of groups of follicles.  Selection of dominant follicle and its menstruation.  Ovulation  Corpus luteum formation  Demise of corpus luteum.
  • 4. MENSTRUAL IRREGULARITIES  Menstrual irregularities are common abnormalities of a woman’s menstrual cycle. Menstrual irregularities include a variety of conditions in which menstruation is irregular, heavy, painful, or does not occur at all.
  • 5. Common types of menstrual irregularities include:  Amenorrhea  Dysmenorrhea  Menorrhagia  Oligomenorrhea  Polymenorrhea  Spotting  Pre menstrual syndrome  Menopause  Metorrhagia  Dysfunctional uterine bleeding.
  • 6. AMENORRHOEA Amenorrhoea means absence of menstruation. It is not a symptom and not a disease.  5 basic factors involved in the onset and continuation of normal menstruation. These are: 1. Normal female chromosomal pattern(46XX). 2. Co- ordinate hypothalamo-pituitary ovarian axis. 3. Anatomical presence and patency of the outflow tract. 4. Responsive endometrium. 5. Active support of thyroid and adrenal
  • 7. CLINICAL TYPES Physiological  Primary (before puberty)  Secondary  -during pregnancy  -during lactation  -following menopause.  Pathological  Concealed (cryptomenorrhoea)  Congenital  acquired  real (true)  primary  secondary
  • 8. PRIMARY AMENORRHOEA  A young girl who has not yet menstruated by her 16 years of age is giving primary amenorrhoea rather than delayed menarche. The normal upper age limit for menarche is 15 years.
  • 9. CAUSES: 1. Hypogonadotrophic hypogonadism  Delayed puberty – delayed Gn RH pulse reactivation.  Hypothalamic & pituitary dysfunction  Kallmann’s syndrome – inadequate Gn RH pulse secreation- reduced FSH & LH.  CNS tumors- craniopharyngioma- reduce Gn RH- Reduce FSH & LH. 2. Hypergonadotrophic hypogonadism  Primary ovarian failure  Resistant ovarian syndrome  Galactosemia  Enzyme edficiency (17 alpha hydroxylase deficiency)  Others- gonadotrophin receptors mutations
  • 10. 3. Abnormal chromosomal pattern  Turner’s syndrome(45X)  Pure gonadel dysgenesis (46XX or 46 XY)  Androgen insensitivity syndrome ( testicular feminization syndrome)  Partial deletion of X chromosome (46XX) 4. Developmental defect of genital tract  Imperforate hymen  Transverse vaginal septum  Atresia upper third of vagina and cervix  Complete absence of vagina
  • 11. 5. Dysfuction of thyroid and adrenal cortex  Adrenogenital syndrome  cretinism 6. Metabolic disorders  Juvenile diabetes 7. Systemic illness  Malnutrition, anemia  Weight loss  Tuberculosis 8. Unresponsive endometrium  Congenital (uterine synechiae- tubercular.
  • 12. SPECIAL INVESTIGATIONS OF PRIMARY AMENORRHOEA Mullerian agenesis  USG  Laproscopy  Karyotype Unresponsive endometrium  Progesterone challenge test  HSG/ Hysteroscopy  Hormonal studies
  • 13. Uterine synchiae  Progesterone challenge test  HSG  hysteroscopy tubercular  blood- ESR  X ray- chest  Mantaoux test  Endometrial biopsy Hypogonadotrophic gonadism  Progesterone challenge test  Serum gonadotrophins  Serum oestradiol
  • 14.  Primary ovarian failure  Karyotype  Serum oestradiol  Serum gonadotrophin  Ovarian biopsy  Tumer  Laproscopy  Serum gonadotrophins  Karyotype
  • 15. Androgen insensitivity syndrome  Laproscopy  Serum testosterone  Karyotype  Gonadal biopsy Adrenogenital syndrome  Karyotype  Serum 17 hydroxy-progesterone  Urinary pregnanetriol Thyroid dysfunction (hypo)  Serum TSH  T3, T4 Diabetes:  RBS
  • 16.  This test is performed by administering inj. Progesterone in oil 75 mg IM or tab Medroxyprogesterone 10 mg daily or micronized progesterone 200mg daily for 10 days. Withdrawl bleeding usually occurs within 10 days, if the test is positive.
  • 17. MANAGEMENT OF PRIMARY AMENORRHOA In primary amenorrhea:  correct the underlying cause  estrogen replacement therapy  if pituitary tumor: treatment with surgical resection, radiation and drug therapy  surgery to correct abnormalities of genital tract
  • 18. SECONDRY AMENORRHOEA  Secondary amenorrhea: is the absence of menses for 3 cycles or 6 months in women who have previously menstruated regularly. Causes:  Breast feeding  Emotional stress  Mal nutrition, tuberculosis  Pregnancy  PCOS Premature ovarian failure  Pituitary, ovarian, or adrenal tumour  Depression  Hyper thyroid or hypothyroid  Diabetes  Hyper prolactinemia  Rapid wt gain or loss related to amenorrhoea
  • 19.  Kallmann syndrome  post pill amenorrhoea  Chemotherapy or radiotherapy  Aneroxia nervosa  Hypothalamic dysfunction- stress, exercise, rapid wt. gain or loss.  Vigorous excrete  Kidney failure  Tranquilizers or antidepressant , anti hypertensives  Post partum pituitary necrosis  Early menopause
  • 20. Detailed history:  Mode of onset- whether sudden or gradual preceded by hypomenorrhoea or oligomenorrhoea.  Sudden changes in envt., emotional, stress, psychogenic shock, eating disorders etc  Sudden loss or gain weight  Intake of psychotrophic or anti hypertensive drugs .  Intake of oral pills or its recent withdrawl. h/o recent chemo or radiotherapy
  • 21.  Appearance of abnormal manifestations either by coinciding or preceeding the amenorrhoea.  Acne, hirsutism or change in voice.  Inappropriate lactation galactorrhoea.( abnormal secretion of milk unrelated to pregnancy and lactation.  Headache and visual disturbances.  Hot flushes and vaginal dryness  Obstetric history- overzealous curettage leading to synechiae.  Cessarrian section may be extended to hysterectomy of which the patient may be unaware.  Severe PPH, shock, infection.  Postpartum or postabortal uterine curettage  Prolonged lactation  Medical history of TB., Diabetes, chronic nephritis, hypothyroid.
  • 22. General examination:  Nutritional status  Extreme emaciation or marked obesity  Presence of acne, hirsutism  Discharge of milk from breasts Abdominal examination  Presence of striae associated with obesity may be related to Cushing syndrome.  A mass in lower abdomen. Pelvic examination  Enlargement of clitoris.  Adnexal mass suggestive of tubercular tuboovarian mass or ovarian tumour.
  • 23.  Tests that can be done are:  Progesterone challenging test  Oestrogen- progesterone challenge test  Serum gonadotrophins  Gn RH dynamic test.  CT  MRI  X-RAY
  • 24. MANAGEMENT FOR SECONDARY AMMENORRHOEA  1. NO ABNORMALITY DETECTED  If patient is not anxious, no treatment is required. Provide assurance.  If she is anxious provide oral contraceptive pills to be continued for atleast 3 cycles.  With low endogenous oestrogen : ethinyl oestradiol 0.02 mg or conjugated equine oestragen 1.25 mg daily is to be taken for 25 days. Medroxyprogesterone acetate 10 mg daily is added from day 16-25. The patient is anxious for fertility.  Husbands semen analysis in primary infertility and the tubal factor of the women are to be evaluated prior to
  • 25. 2. CASES WITH DETECTABLE CAUSE  Anxiety and stress- may be corrected by reassurance, psychotherapy.  Improve health status
  • 26. 3. POLYCYSTIC OVARIAN SYNDROME (PCOS)  First correct the biochemical parameters such as :  Hyperandrogenemia  Hyperprolactenemia  Hyperinsulinemia  Insulin resistance  High serum oestradiol  Low FSH  Low serum progesterone androgenic follicular microenvironment  Weight reduction
  • 27. If fertility not desired  Management of hyperandrogenemia  Combined oral contraceptive pills  Antiandrogens such as cyproterone acetate, flutamide may be given.  Metformin may be given as an oral insulin sensitizing agent.  Endometrial biopsy can be done in case of endometrial hyperplasia.  Cabergolin, bromocriptine in case of hyperprolactenemia (if failed surgery can be done as – transnasal-transsphenoidal adenectomy is done.  If premature ovarian failure- HRT can be given )  Thyroxine ---- of hypothyroid state.
  • 28. SURGERY  Laproscopic ovarian drilling (LOD)  Bariatric surgery in case of PCOS who are morbidly obese
  • 29. PREMENSTRUAL SYNDROME (PMS) (Premenstrual tension)  Premenstrual syndrome is a psychoneuroendocrine disorder of unknown etiology that occurs just prior to menstruation.  There is a cyclic appearance of several symptoms during the last 7-10 days of the onset of menstrual cycle which subside the onset of menstrual flow. At least 5 of the symptoms must have been present in most of the cycles over the past one year.  When these symptoms disrupt daily functioning they are grouped under premenstrual dysmorphic
  • 30. Clinical manifestation of PMS  Depressed mood, hopelessness, and self depreciation.  Anxiety, tension, fearfulness.  Affective liability- mood swings  Anger, irritability, interpersonal conflict.  Decreased energy.  Appetite changes or cravings.  Changes in sleep.  Feeling overwhelmed or out of control.  Physical symptoms such as breast tenderness, headache.  Dyspareunia, bloating.  Weight gain.
  • 31. PATHOPHYSIOLOGY  The exact cause is not known but the following hypothesis is considered.  Alteration in the level or ratio of oestrogen and progesterone from the mid luteal phase.  Neuroendocrine factors:  Decreased synthesis in the luteal phase.  Withdrawl of endorphins from CNS during luteal phase.  Psychological and psychogenic factors affecting behavior.
  • 32. TREATMENT General  Elimination of caffeine from the diet.  Avoidance of smoking, alcohol.  Regular exercise.  Regular meals and nutritious diet.  Adequate sleep.  Relaxation techniques like yoga, stress management and assurance.  Alternative & complementary therapy.
  • 33.  Non hormonal  Tranquilizers or antidepressant drugs  Pyridoxine  Diuretics in the second half of the cycle.  Serotonin reuptake inhibitors such as fluoxetine.  Hormones  Oral contraceptives pills to maintain a uniform hormonal melieu.  Progestogen.  Bromocriptine to relieve breast symptoms.  Gn RH agonists to suppress gonadal steroids.
  • 34. NURSING MANAGEMENT  Encourage patient to set goals for the reduction of symptoms such as mood swings, crying, binge eating, and day to day stressors.  Teach positive coping measures, involve and encourage family members such as spouse or children for assistance and care.  Encourage use of exercise, meditation and creative activities to reduce stress.  Provide instructions about the desired effects of
  • 35. DYSMENORRHOEA  Dysmenorrhoea : painful menses or cramping during menstruation of sufficient magnitude so as to incapacitate day to day activities.  Typically dysmenorrhoea begins upto 48 hours before the onset of menses and resolves within 2 to 4 days of onset or by the end of
  • 36. TYPES OF DYSMENORRHOEA  Primary dysmenorrhoea (spasmodic)  Secondary dysmenorrhoea (congestive)
  • 37.  PRIMARY DYSMENORRHOEA ( spasmodic)  It is painful menses with a uterine cause, but without pelvic pathology and usually occurs within 1-3 years of menarche. Cause:  Painful uterine contractions stimulated by prostaglandin produced by the endometrium during menses are most often identified as the cause for primary
  • 38. Others may be like-  Mostly confined to adolescents.  Almost always confined to ovulatory cycles.  The pain is usually cured following pregnancy and vaginal delivery.  The pain is related to dysrhythemic uterine contractions and uterine hypoxia.  Psychogenic factors- of tension, anxiety lowers the pain threshold.  Abnormal anatomical and functional aspect of myometrium like Uterine myometrial hyperactivity.  Imbalance in the autonomic nervous control of uterine muscle.  Role of prostaglandins.  Role of vasopressin
  • 39. Symptoms:  Sharp, intermittent suprapubic pain radiating to the back or thigh.  Headache, fatigue, backache, flushing, dizziness and syncope.  Adolescents typically experience the problem only after menstrual cycles become ovulatory.  Women often experience reduction in dysmenorrhoea after pregnancy.
  • 40. THERAPEUTIC INTERVENTIONS  Nonsteriodal anti inflammatory drugs (NSAID) started 1-3 days prior to the onset of menstrual flow (to decrease prostaglandin production).  Oral contraceptives, to decrease endometrial proliferation and therefore production of prostaglandin. Surgery:  Transcutaneous electrical nerve stimulation (TENS)  Laproscopic uterine nerve ablation(LUNA).  Dilatation of cervical canal.  Presacral neurotomy (LPSN).
  • 41. SECONDARY DYSMENORRHOA (congestive) Secondary dysmenorrhoea is painful menses resulting from a pathologic process. Cause:  pressure from outside the uterus  tissue ischemia  cervical stenosis  congenital abnormality (imperfotate hymen)  endometriosis  ovarian cysts  pelvic inflammatory disease (PID)  uterine fibroid tumous.  IUCD in utero and pelvic congestion.  Obstruction due to mullerian malformation.
  • 42. clinical features:  The pain is dull, situated in the back and in front without any radiation.  It usually appears 3-5 days prior to the period and relieves with the start of bleeding.  The onset and duration depends on the pathology producing the pain.  There is no systemic discomfort unlike primary dysmenorrhoea.  Other symptoms may be breast tenderness and change in bowel habits.
  • 43. diagnostic evaluation:  Laproscopy  Hysteroscopy/laparotomy TREATMENT  The treatment aims at the cause rather than the symptom. The type of treatment depends on the severity, age and parity of the patient.
  • 44. OVARIAN DYSMENORRHOEA (RIGHT OVARIAN VEIN SYNDROME) Right ovarian vein crosses the ureter at right angle. During premenstrual period, due to pelvic congestion or increased blood flow, there may be marked engorgement in the vein –pressure on ureter- stasis- infection- pyelonephritis- pain.
  • 45. MITTELSCHMERZ’S SYNDROME (ovular pain)  Ovular pain is not an infrequent complaint. It appears in the midmenstrual period. The pain usually situated in the hypogastruism or in either iliac fossa.  The pain is usually located at one side and does not change from from side to side according to which ovary is ovulating.  Nausea or vomiting is conspicuously absent.  It rarely last for 12 hours.  It may be associated with slight vaginal bleeding or excessive mucoid vaginal discharge.
  • 46. Cause:  The exact cause is unknown. Other factors may include:  Increased tension of graffian follicle just prior to rupture  Peritoneal irritation by the follicular fluid following ovulation  Contraction of the tubes and uterus. Treatment:  Provide assurance  analgesics  in obstetrics cases, the cure is absolute by making the cycle anovular with contraceptive pills.
  • 47. PELVIC CONGESTION SYNDROME There is disturbance in the autonomic nervous system which may lead to gross vascular congestion with pelvic varicosities. The patient may be congestive type of dysmenorrhoea without any demonstrable pelvic pathology. Symptoms:  Backache  Pelvic pain on long standing, dyspareunia  Menorrhagia or epimenorrhoea  Uterus may be bulky and boggy.
  • 48. Diagnosis:  Pelvic venography  Doppler scan  CT/ MRI  Angiography Treatment:  The treatment is unsatisfactory.  Medroxy progesterone acetate (MPA) 50 mg daily for 4 months was found effective. In parous women with advancing age, hysterectomy may relieve the symptoms.
  • 49. ABNORMAL UTERINE BLEEDING  Menorrhagia  Polymenorrhoea  Metrorrhagia  Oligomenorrhoea  Hypomenorrhoea  Dysfunctional uterine bleeding
  • 50. MENORRHAGIA  Menorrhagia is defined as the cyclic bleeding at normal intervals; the bleeding is either excessive in amount (> 80ml) or duration (>7 days) or both. The term menotaxis is often used to denote prolonged bleeding. CAUSES:  Menorrhagia is a symptom of some underlying pathology-
  • 51. Cause: Organic:  Pelvic:  Fibroid uterus  Adenomosis  Pelvic endometriosis  IUCD in utero  Chronic tubo- ovarian mass  Tubercular endometriotis (early cases)  Retroverted uterus – due to congestion  Granulose cell tumour of the ovary.
  • 52. Systemic:  Congestive cardiac failure  Severe hypertension Endocrinal:  Hypothyroidism  Hyperthyroidism hematological:  idiopathic thrombocytopenia purpura  leukemia  von willebrands disease  platelet deficiency emotional upset:
  • 53. functional  Due to disturbed hypothalamo- pituitary- ovarian- endometrial axis. C. Common causes:  Dysfunctional uterine bleeding  Fibroid uterus  Adenomycosis  Chronic tubo- ovarian mass
  • 54. DIAGNOSIS:  Long duration of flow.  Passage of big clots  Use of increased number of thick sanitary pads  Pallor and low level of hemoglobin TREATMENT:  The definitive treatment is appropriate to the cause for menorrhagia.
  • 55. POLYMENORRHOEA (epimenorrhoea)  Polymenorrhoea is defined as cyclic bleeding where the cycle is reduced to an arbitrary limit of less than 21 days and remains constant at that frequency.  If the frequent cycle is associated with excessive and or prolonged bleeding, it is called epimenorrhoea.
  • 56. Causes:  Dysfunctional uterine.  It is seen predominantly during adolescence, preceding menopause and following delivery and abortion. Hyperstimulation of the ovary by the pituitary hormones may be a responsible factor.  Ovarian hyperemia- as in PID or ovarian endometritis. Treatment:  Persistent dysfunctional type is treated by hormone as in dysfunctional uterine bleeding.
  • 57. METRORRHAGIA  Metorrhagia is defined as irregular acyclic bleeding from the uterus.  Amount of bleeding is variable. While metorrhagia strictly concerns uterine bleeding but in clinical practice, the bleeding from any part of the genital tract is included under the healing.  The irregular bleeding in the form of contact bleeding or intermittent bleeding is an otherwise normal cycle is also indicated in metorrhagia.  Menometorrgia:  Is the term applied when the bleeding is so irregular and excessive that the menses cannot be identified at all.
  • 58. Causes of acyclic bleeding:  DUB- usually during adolescence following childbirth and abortion and preceding menopause.  Submucosal fibroid  Uterine polyp  Carcinoma cervix and endometrial carcinoma. Causes of contact bleeding:  Ca cervix  Mucous polyp of cervix  Vascular ectopy of the cervix specially during pregnancy, pill use cervix.  Infections- chlamydial or tubercular cervicitis.  Cervical endometritis.
  • 59. Causes of intermenstrual bleeding  contact bleeding  Urethral carnucle  Ovular bleeding  Breakthrough bleeding in pill use  IUCD in utero  Decubitis ulcer Treatment:  Treatment is directed to the underlying pathology. Malignancy is to be excluded prior to any definitive treatment.
  • 60. OLIGOMENORRHOEA  Menstrual bleeding occurring more than 35 days apart and which remains constant at that frequency is called oligomenorrhoea. Causes:  Age related- during adolescence and preceding menopause.  Weight related- obesity  Stress and exercise related  Endocrine disorders- PCOS  Androgen producing tumours- ovarion, adrenal  Tubercular endometritis
  • 61. HYPOMENORRHOEA When the menstrual bleeding is unduly scanty and lasts for less than 2 days, it is called hypomenorrhoea. Causes:  Local ( uterine synchiae or endometrial tuberculosis)  Endocrinal ( use of oral contraceptives, thyroid dysfunction and premenopausal periods)
  • 62. DYSFUNCTIONAL UTERINE BLEEDING (DUB)  DUB is defined as a state of abnormal uterine bleeding without any clinically detectable organic, systemic and iatrogenic cause. (pelvic pathology eg- tumour, inflammation or pregnancy is excluded.)  Currently DUB is defined as a state of abnormal uterine bleeding following anovulation due to dysfunction of hypothalamo- pituitary- ovarian axis.(endocrine origin).  Heavy menstrual bleeding (HMB) is defined as a bleeding that interferes with woman’s physical, emotional, social and maternal quality of life.
  • 63. PATHOPHYSIOLOGY  The physiological mechanism of haemostasis in normal menstruation are:  Platelet adhesion formation  Formation of platelet plug with fibrin to seal the bleeding vessels.  Locasied vaso constriction.  Regeneration of vaso constriction.  Regeneration of endometrium.  Biochemical mechanisms involved are: inc. endometrial ratio of PGF2 alpha/ PGE2.  PGF2alpha causes vasoconstriction and reduces bleeding.  Progesterone increases the level of PGF2 alpha from arachidonic acid.  Levels of endothelin which is a powerful vasoconstrictor is also increased.  In anovulatory DUB there is decreased synthesis of PGF2 alpha and the ratio of PGF2 alpha/ PGE2 is low.
  • 64. The abnormal bleeding may be associated with or without ovulation and accordingly gouped into:  . Ovular bleeding  Anovular bleeding Ovular bleeding includes:  Polymenorrhoea/ polymenorrhagia  Oligomenorrhoea  Functional menorrhagia Anoovular bleeding includes:  Menorrhagia  Cystic glandular hyperplasia.
  • 65. INVESTIGATION  Blood investigations including T3, T4, TSH  USG & color Doppler  TVS  Saline infusion sonography (SIS)  Hysteroscopy  Endometrial sampling  Laproscopy  Diagnostic uterine curettage (D & C)
  • 66. COMMON CAUSE OF ABNORMAL VAGINAL BLEEDING Organic:  Uterine fibroid  Endometriosis  Adenomyosis  Endometrial polyps  IUCD  Adnexal pathology
  • 67.  Hematological and endocrine:  Platelet deficiency  Leukemia  ITP  Von willebrand disease  Thyroid dysfunction  Non menstrual bleeding:  Foreign body  Urethral carnucles  Genital malignancy  Postcoital  Intermenstrual  Abortion  Breakthrough bleeding
  • 68. MEDICAL MANAGEMENT  HORMONES:  With the introduction of hormones , potent oral active progestins, they became the mainstay in the management of DUB in all age groups and practically replaced the isolated use of oestrogens and androgens. Eg medroxyprogesterone acetate, norethisterone acetate etc.  Progestins : involves prostaglandin synthetase inhibitors (PSI) eg; fenamates ( mefenamic acid)  The preparation are used:  Cyclic therapy  Continuous therapy.
  • 69.  To stop bleeding and regulate the cycle:  Norethisterone preparations (5mg tab ) are used thrice daily till bleeding stops which it usually does by 3-7 days. a. cyclic therapy:  5th- 25th day course:  In ovular bleeding----- any low dose combined oral pills are effective when given from 5-25th day of cycle for 3 consecutive cycles. It causes endometrial atrophy.normal menstruation is expected to resume with restoration of normally functioning pituitary ovarian endometrial axis.  In anovular bleeding--- cyclic progesterone preparation medroxyprogesterone acetate (MPA)10 MG r norethisterone 5mg is used from 5th- 25th day of cycle for 3 cycles.
  • 70.  15-25th day course:  In ovular bleeding where patient wants pregnancy or in cases of irregular shedding or irregular ripening of the endometrium.dydrogesterone 1 tab (10 mg) daily bd from 15-25th day may cure the state. It does not suppress the ovulation.  Anovulatory women have immaturity of H-P-O axis. They are ideal for the use of short term cyclic therapy until the maturity of the positive feedback system is established.
  • 71. b. Continuous progestins:  Medroxyprogesterone acetate 10 mg tds daily is given and treatment is usually continued for atleast 90 days. Inj DMPA i/m can be given  Oestrogen  Intrauterine progestogen  Danazol  Mifepristone (RU 486)  GnRH agonists
  • 72. NON HORMONAL MANAGEMENT  Anti fibrinolytic agents (tranexamic acid)  Prostaglandin synthetase inhibitors  NSAIDS  Desmopressin SURGICAL MANAGEMENT  Uterine curettage  Endometrial ablation/ resection  Laser  Roller ball  Thermal balloon  Microwave  novasure  resection  transcervical resection (TCRE)  uterine artery embolisation  hysterectomy
  • 73.  COMPLICATIONS  Infections  Uterine perforations (<1%)  Fluid absorption may occur during hysteroscopic procedures.
  • 74. CONCLUSION Some menstrual irregularities can be caused by serious, even life-threatening conditions, such as uterine cancer. Seek prompt medical care if you have menstrual irregularities, such as heavy menstrual periods or a lack of menstrual periods. Early diagnosis and treatment of menstrual irregularities reduces the risk of serious complications, such as infertility and metastatic uterine cancer.