Menses converted - copy

MENSTRUATION AND ITS
CLINICAL ASPECTS
MODERATOR- Dr NEHA KULKARNI MAAM

Menstrual cycle irregularities
• Menstruation is the end point in a series of events which begin in the cerebral cortex and
hypothalamus and ends at the uterus in the Hypothalamus-pituitary-ovarian-uterine axis
• A normal menstruation requires integration of HPO axis with a functional uterus, a patent
lower genital outflow tract and a normal genetic karyotype of 46XX.
• In normal healthy women, menarche occurs between the ages 10 and 16 years, (mean
12.5),menstruation persists throughout the reproductive era of life with an average rhythm
of 28 +/- 7 days, inclusive of 4-6 days of bleeding

Definitions of menstrua irregularities
1. Amenorrhoea- absence of menstruation
2. Oligomenorrhoea- infrequent ,irregularly timed episodes of bleeding usually
occurring at intervals of >35 days
3. Polymenorrhoea – frequent episodes of menstruation, usually occurring at
intervals of 21 days
4. Menorrhagia – regularly timed episodes of bleeding that are excessive in amount
(>80ml) &/or duration in flow (>7days)
5. Metrorrhagia – irregularly timed episodes of bleeding superimposed on normal
cycle bleeding
6. Menometrorrhagia – excessive, prolonged bleeding that occurs at irregularly timed
and frequent interval
7. Hypomenorrhea – regularly timed but scanty episodes of bleeding
8. Intermenstrual bleeding refers to bleeding that occurs between otherwise normal
menstrual cycles.
9. Precocious menstruation denote the occurrence of menstruation before the age of
10 years

history
1. Age of patient –ascertaining age of menarche , (also in mothers & sisters)
2. Marital status- desire for treatment of infertility ,h/o dyspareunia
3. Abnormal pubertal symptoms- hoarsening of voice, hirsutism
4. H/o taking of hormones
5. Medical disorder – Tb
6. h/o Endocrine disorders – hypothyroidism, juvenile diabetes, addisons syndrome
7. h/o raised ICT – headache,vomiting,convulsions,visual disturbances
8. H/o surgeries- laparotomy
9. Intellectual/psychological development
10. h/o endocrine disorders in family – testicular feminizing syndrome, POI
11. h/o radiotherapy/chemotherapy
12. h/o psychiatry d/o- OCD, Schizophrenia
13. Drug history- antiepileptics
14. Obstetric history= H/o PPH with subsequent failure of regular menses to return

Clinical approach :take history , examination
1. h/o DM,TB,mumps
2. Family h/o pcod,delayed puberty,testicualar feminizing syndrome
3. Thyroid enlargement
4. Abdominal mass
5. ultrasound

Examination
1. Height and span –in panhypopituitarism syndrome & Turner’s syndrome, the patient
,may be very short .
2. Weight and Nutrition – high BP in CAH,
3. General examination- Pallor, Edema,secondary sexual characters, hirsuitism,thyroid
enlargement. Anosmia indicates – Kallaman syndrome
4. Systemic disease –TB, Heart disease
5. Local examination –
6. P/a –ascites,lump,mass in iliac fossa with hirsutism (masculinizing ovarian tumour)
7. P.s – look for development of external genitalia,clitoris,hymen, urethral opening,
gonads herniating in inguinal canal. Bulging hymen/transverse vaginal septum
8. Pv- present/absent of uterus (normal/infantile/rudimentary)
9. Presence of mass in fornix- s/o pcos / ovarian tumor

Investigation
1. Pregnancy test
2. Routine investigation- CBC,URE,TSH,BSL R etc
3. Cxr – r/o PUL TB
4. X ray skull – for pituitary fossa: enlargement, erosion of anterior/post. Clinoid
process
5. Tests for Estrogen staus –
 Endocrine evaluation- FSH,LH levels, sr PRL,,
 Progesterone challenge test
 Chromosomal analysis- Turners syndrome(45 XO) , 46 XY (CAH,Swyer
syndrome)

AMENORRHEA: DEFINITION
Amenorrhea: is the absence of menstruation. May be primary or
Ssecondary
Physiological amenorrhoea naturally prevails prior to the onset of puberty, during
pregnancy and lactation and after menopause.
Pathological amenorrhoea- results from genetic factors, systemic disease,
endocrinopathies, disturbance of HPO axis, nutritional factors, drug usage,
psychological factor etc.
*Primary amenorrhea is the absence of menstrual bleeding and secondary
sexual characteristics in a girl by age 14 years or the absence of menstrual
bleeding with normal development of secondary sexual characteristics in a
girl by age 16 years.
*Secondary amenorrhea is the absence of menstrual bleeding in a woman who had
been menstruating but later stops menstruating for three or more months (3
cycles or more).

Primary amenorrhoea
• Primary amenorrhoea at age of 14yrs ,needs the clinicians to undertake investigations for the cause of
failure of occurrence,& institute timely therapy. However with the development of secondary sexual
character, the investigation must be delayed till 16 yrs.(delayed puberty)
• Detailed evaluation of growth charts, height & weight records, chronology of development of
secondary sexual characters, body habitus, history of pain in abdomen, drug intake,Tb,endocrine
disease etc
• Physical examination includes documentation of height-weight ratio,stature,tanner staging
• Ultrasound for uterus, estimation of hormones
• genetics

Classification
 Classified as per serum FSh into->
primary
amenorrhoea
Hypergonadotropic
1.Gonadal dysgenesis:45XO,abnormal X
2.46 XX Pure Gonadal dysgenesis
3.46 XY gonadal dysgenesis: swyer syndrome,
testicular feminizing syndrome
Eugoandotropic
1. Absence of Mullerian duct:
a) Androgen insensitivity sy
b)Mullerian agenesis:-Rokitansky-kustner-hauser syn
2.Normal Mullerian development
2)Female/true intersex
b)Pcos
c)adrenal/thyroid disease
3 Cryptomenorrhoea
4. Tubercular endometriosis
5. Constitutional delay
Hypogonadotropic
1. Hypothalmic cause
a)Delayed menarche
b)Kallaman synd,GnRh deficiency sun
c)Psychogenic cause, weight loss,
anorexia nervosa, malnutrition
2.Pituitary cause
a)Pitutarism
b)Neoplasms- prolactinomas,
craniopharyngiomas
3. Severe systemic disease- TB,
Syphilis
4)Other Endocrine disease
=Thyroid/adrenal glans

Aetiology
 According to cause of location of amenorrhoea
 Delayed puberty
 Pregnancy
 Cerebral cortex –stress, emotional disturbance, infection, trauma, tumor
 Hypothalamus- Kallamann syndrome, vigorous exercise, weight loss
 Pituitary gland- empty Sella turcica ,Frohlich syndrome, pineal tumour, lawerence –moon-
biedl syndrome,cushings disease,prolactinemia
 Ovary- Turners syndrome,PCOS,17 alpha deficiency syndrome
 Genital tract- Mayer-Rokitansky-kustner-hauser syndrome,
 Chromosomal- intersex,Turners , testicular feminizing synd, swyer synd
 Other endocrine glands- Juvinile diabetes, thyroid adrenal glands
 Durgs- tranquillizers, antihypertensive, antidwepressants
 Nutrition- overweight, weight loss, TB, malnutrition

 Anorexia nervosa-
 it is a psychological somatic self-imposed eating disorder mainly affecting adolescents and young
women more than men
 It is the failure to maintain body weight for age and height. For menstruation to occur ,minimal fat
should constitute 22% of body weight
 Loss of weight .15% causes amenorrhea. Leptin in the fat initiates gonadotropin-releasing hormone
(GnRH) secretion. When weight reduction falls below required body fat, GnRH and gonadotropin
secretions fail. Clinically, fasting, excessive exercise with or without purging and self-induced
vomiting cause atrophy or nondevelopment of breasts and amenorrhea
 Hypoestrogenism thus induced causes:
 Mortality through cardiac failure, arrhythmia (15%).
 Amenorrhoea, infertility, decreased libido.
 Osteoporosis.
 Hypercortisolism, decreased muscle mass, low IGF-1, hypothyroidism, anaemia granulocytopenia,
neutropenia.
 Psychiatric problems.
management.
Psychological
Psychotherapy
Nutritional

Kallmann disease
• Occurs in 1:50,000 girls
• Low/absent GnRH is due to either AD or XLR gene.
• It is characterized by anosmia & maldevelopment of neurons in arcuate nucleus
• Management:
• GnRH & pituitary hormones to induce menstruation ,ovulation
• Estrogen & progesterone clinically to induce menstruation.

Hyperprolactinaemia
 Hyperprolactinaemia is defined as persistent high level of prolactin in a nonpregnant
and nonlactating woman.
 causes.
 Apart from the physiological condition of pregnancy and lactation, it occurs in the
following cases:
 During sleep, stress, nipple stimulation and chest wall injury such as herpes zoster.
Empty sella turcica.
 Hypothalamic tumour, pituitary tumour and head injury (acromegaly, Cushing’s
disease, Addison disease).
 Twenty per cent cases of PCOD and in some cases of endometriosis.
 Hypothyroidism because of the stimulating effect of raised thyroid-stimulating
hormone (TSH).
 Liver and chronic renal disease because of altered metabolism and delay in
excretion.
 Drugs like neuroleptics, narcotics, antidepressants, phenothiazine, antihypertensives,
calcium channel blockers, OCs, oestrogen (in high doses), cocaine, amphetamine,

 galactorrhoea.
 Infertility and abortion through corpus luteal phase defect are other features. Headache and
visual disturbances occur when the tumour presses upon the optic nerve.
 In males, it causes loss of libido, impotency and infertility.
 The normal level of prolactin is 25 ng/mL. Levels up to 100 ng/mL suggests
hyperprolactinaemia and more than 100 ng/mL occurs in the presence of a tumour.
 CT, MRI and visual check-up are necessary in the diagnosis and follow-up. Thyroid functions
need to be checked.
 treatment. Treat the cause.
 drug-induced hyperprolactinaemia requires stoppage of drug or alternative therapy.
 Bromocriptine and long-acting derivatives are effective in most cases.
 Menstrual cycles are restored in 3 months time. Ninety per cent ovulate and 70–80%
conceive. Quinagolide 25–150 mg daily in divided doses with a maintenance dose of 75 mg
daily.n Macroadenoma (more than 10 mm) and microadenoma not responding to drugs
require transsphenoidal adenectomy or radiotherapy 4500 cGY for 25 days. However, 30%
recurrence rate is reported within 6 years, and prolonged follow-up is necessary.

Management
 Hypergonadotropic primary amenorrhoea- patients have gonadal failure
 Various types of gonadal dysgenesis account for the cases- streak ovaries with absence of ovarian
follicles,no estrogen production with elevated FSh (>40mIU/ml) & low estradiol level (<25mIU/ml).The
sexual development is prepubertal with no endometrial proliferation, hence PCT is negative.Chromosomal
studies reveal 45 XO chromosomes
• Some patients have mosaicism/minor structural abnormalities have a few functional follicles capable of
inducing menstruation, stray ovulation & pregnancy. Chromosome study is relevant.
• Gonadectomy is indicated with patients with TIF, as these are gonads are prone to malignancy.
• Woman with streak ovaries are infertile ,but they can bear children with oocyte donation.They should be
treated about with cyclic oestrogen & progesterone to promote femizing & secondary sexual character and
prevent osteoporosis.
• Women with resistant ovarian syndrome have normal ovaries on histology & primordial follicles,but there is
probably deficiency of FSh receptors.They are not amenable to treatment
• Savage syndrome- it is due to receptor defect of gonadotropic hormones & resembles autoimmune
disease & resistant ovary syndrome.Their height is normal,ovaries contain follicle & but FSH is raised.

 Eugonadotropic Primary amenorrhoea- The FSH levels are within the normal level ,the woman
have normal breast development, but due to abnormal Mullerian development ,the uterus may be
rudimentary or absent because of androgen insensitivity (called TIF) or due to Mullerian agenesis.
• In woman with Testicular femizing syndrome,- the phenotype is female & karyotype is 46 XY.The
gonads are testes often present in inguinal canal.The gonads produce androgen but d/t androgen
insensitivity at target (deficient androgen receptors/lack of enzymes converting testosterone to
dihydrotestosterone),these patients present with lack of axillary & pubic hair, with absent uterus and
upper vagina.they have bling pouch vagina, normal breast development (peripheral conversion of
androgen to estrogen
).The gonads are prone to mailignancy->gonadectomy after full,sexual development (18-20)yrs ,f/b
estrogen therapy to maintain feminization.Vaginoplasty can be done.

• Woman with simple Mullerian agenesis with karyotype of 46 XX present with normal secondary
sexual character & functional ovaries (Rokitansky syndrome).They reveal a normal hormone
profile.This syndrome is associated with skeletal & renal abnormality in 30% cases.these woman do
ovulate, & appropriate management requires creation of a functional vagina .Surrogacy if they want
to have children
• In woman with cryptomenorrhoea presenting as primary amenorrhoea,the common cause is an
intact hymen / vaginal septum-> h/o cyclic abdominal colicky pain,retention of urine,presence of
palpable abdominal lump, tense blue bulging membrane on ps-> A simple cruciate incision on
hymen cause drainage of collected blood.
• Septate vagina & atresia vagina –vaginoplasty
• The vaginal septum is recognized from imperforate hymen by a pinkish concave covering in
contrast to the bluish bulge in the latter.The vaginal septum i.e. atresia ,requires more extensive
dissection & vaginoplasty.

• pcos
• 17 alpha hydroxylase deficiency causes cortisol secretion & raised levels of
adrenocorticotropic hormone-(hypertension,hypernatraemia,hypokalemia,amenorrhoea)
• Endometrial nonresponsiveness & amenorrhoea is due to absent hormonal
receptors.Hormone profile is normal.
• Tubercular endometritis requires anti-TB treatment.

 Hypogonadotropic primary amenorrhoea-
 FSH <40mIU/ml.
• It is d/t hypothalamic dysfunction , pituitary failure or systemic illness.administration of
GnRH helps to differentiate hypothalamic from pituitary failure.In the latter ,GnRH
stimulation will not raise LH level
• Empty sella turcica is characterized by herniation of subarachnoid membrane into
pituitary sella turcica & may exist with pineal gland tumor as prolactin adenoma.Absence
of Pitutary gland causes absence of FSH & LH .Gonadotropin hormone therapy is
rquired.

• Other hormonal dysfunction
• Both hypothyroidism and hyperthyroidism can cause amenorrhoea
• CAH & tumor –primary amenorrhora & juvenile diabetes
• Premature ovarian failure- seen in 1% cases. It is due to poor germ cell migration from yolk sac during
fetal development or d/t accelerated rate of depletion. (FSH >40mIU/ml, E2 <20pg/ml)
• NUTRITION’
• Excessive weight ,anorexia nervosa & malnutrition with loss of weight are also responsible for
amenorrhoea in young girls.
• Kallmann syndrome- lack of GnRH synthesis & olfactory dysfunction & anosmia
• Pitutary failure generally follows hypopituitarism, neoplasms or empty sella turcica.MRI , estimation of
Prolactin level, ophthalmic evaluation of visual fields.
• Frohlich syndrome- short stature,lethargy,obesity, genital dystrophy ,amenorrhoea
• Laurence-Moon-Biedl syndrome- polydactyly, retinitis pigmentosa & mental deficiency
• In such woman ,cyclic administration of oestrogen & progesterone to maintain femininity and prevent
osteoporosis is essential.
• If woman desires pregnancy – ovulation induction
• In women with neoplasms , appropriate neurological consultation followed by treatment with
bromocriptine for prolactinomas/surgery

Secondary amenorrhoea
• Amenorrhoea for ≥ 6 months with previous normal menstrual patterns in absence of
pregnancy and lactation
• Aetiology:
1. Physiological- pregnancy & lactation
2. Pathological-
A. Genital tract –
• Acquired obstruction (gynatresia) of cervical canal causing sever stenosis/atresia follows
electrocauterization, chemical burns, cervical amputation, conization
• Vaginal atresia d/t scarring following a traumatic delivery
• Asherman syndrome
• Vesicovaginal fistula
B. Ovarian causes:
• Surgical extirpation
• Radiotherapy

• Autoimmune disease (thyroid, diabetes)
• Pcod
• Resistant ovarian syndrome – d/t absent FSH receptors
• Infections- mumps,TB, pyogenic infections,Masculinizing ovarian tumors
• Premature menopause – premature ovarian failure
3. Nutritional cases:
• Anorexia nervosa, bulimia
• Extreme obesity, Excessive weight loss in athletes
4. Pituitary causes
• Insufficiency as in Simmonds's ,Sheehan’s syndrome
• Hyperprolactinaemia
• Tumours like-prolactinomas, chromophobe adenomas,cushings syndrome
• Drugs- ocp, tranquilizers
5. Hypothalamus
• GnRH deficiency, Vigorous exercise- stress, obesity’
• Pseudocyesis
• Brain tumor,Anorexia nervosa
6. Suprarenal causes
• Addison disease
• Adrenogenital syndrome. Suprarenal tumour
7. Thyroid
• Hypothyroidism,
• Graves disease
8. Other causes
• Diabetes,
• Renal disease- d/t decreased excretion of LH & Prolactin
• Severe anaemia

• Resistant ovarian syndrome- ovaries fail to respond to gonadotropin hormones & cause
amenorrhoea. The ovaries show plasma cells and lymphocyte infiltration. Biopsy isn’t
necessary for diagnosis.FSH is high.
• Simmond’s Disease- it is related to pregnancy and sheehan’s syndrome following severe
PPH causes pituitary necrosis by thrombosis of its vessels & panhypopituitarism. The
woman fails to lactate following delivery ,remains lethargic & shows signs of
hypothyroidism & cortisol deficiency.

Question to ask in case of investigation
• Is the patient pregnant?
• Is her serum prolactin level elevated?
• Is there clinical evidence of estrogen deficiency?
• Does she have a positive response to the progesterone challenge test?
• Is it premature menopause?
• What are the levels of her serum FSH and LH?
• The importance of each of the above questions is analyzed in detail below.
• Detailed history is important.

Investigation
• Pregnancy. This is the most common cause of secondary amenorrhea. Hence, its
exclusion must precede all further investigations.
• Elevated Levels of Serum Prolactin. Prolactin secreted by the anterior pituitary gland is
normally under the inhibitory effect of hypothalamus by the prolactin-inhibitory factor
dopamine. It is stimulated by estrogen and suckling. It is also present in the decidua and
amniotic fluid. Prolactin levels fluctuate episodically; therefore, several measurements
may be necessary to confirm hyperprolactinemia.
 Hyperprolactinemia is defined as persistent high level of prolactin in a nonpregnant and
nonlactating woman.
 causes. Apart from the physiological condition of pregnancy and lactation, it occurs in the
following cases:


• During sleep, stress, nipple stimulation and chest wall injury such as herpes zoster.
• Empty Sella turcica.
• Hypothalamic tumor, pituitary tumor and head injury (acromegaly, Cushing’s disease,
Addison disease)
• Twenty per cent cases of PCOD and in some cases of endometriosis.
• Hypothyroidism because of the stimulating effect of raised thyroid-stimulating hormone
(TSH).
• Liver and chronic renal disease because of altered metabolism and delay in excretion.
• Drugs like neuroleptics, narcotics, antidepressants, phenothiazine, antihypertensives,
calcium channel blockers, OCs, estrogen (in high doses), cocaine, amphetamine,
cimetidine, haloperidol, metoclopramide. Serotonin and opiates reduce the level of
dopamine and cause hyperprolactinemia.

• The woman presents with oligomenorrhoea culminating in amenorrhea due to suppression of FSH and LH.
Fifty percent of the cases develop galactorrhea. Infertility and abortion through corpus luteal phase
defect are other features. Headache and visual disturbances occur when the tumor presses upon the
optic nerve.
• In males, it causes loss of libido, impotency and infertility. The normal level of prolactin is 25 ng/mL.
Levels up to 100 ng/mL suggests hyperprolactinaemia and more than 100 ng/mL occurs in the presence of
a tumour.
• CT, MRI and visual check-up are necessary in the diagnosis and follow-up. Thyroid functions need to be
checked. treatment. n Treat the cause.
• Treatment.
• Treat the cause.
• Drug-induced hyperprolactinaemia requires stoppage of drug or alternative therapy. Bromocriptine and
long-acting derivatives are effective in most cases. Menstrual cycles are restored in 3 months time.
Ninety per cent ovulate and 70–80% conceive.
• Quinagolide 25–150 mg daily in divided doses with a maintenance dose of 75 mg daily.
• The drugs are discussed in detail in the chapter on hormonal therapy.
• Macroadenoma (more than 10 mm) and microadenoma not responding to drugs require transsphenoidal
adenectomy or radiotherapy 4500 cGY for 25 days. However, 30% recurrence rate is reported within 6
years, and prolonged follow-up is necessary.
• Evidence of Oestrogen Deficiency. Hot flushes, loss of breast mass, dyspareunia and dryness of vagina are
suggestive of lack of oestrogen and premature menopause. It requires oestrogen replacement therapy.

 Positive Progesterone Challenge Test. This test depends on the presence of oestrogen-primed
endometrium in the uterine cavity. The test is considered positive if the patient responds to the
administration of oral tablet medroxyprogesterone (Provera/Modus/Deviry) 10 mg daily for 5 days
or injection progesterone in oil 100 mg intramuscularly or primolut-N 5 mg three times a day for 3
days. Withdrawal bleeding occurs within 2–7 days.
• A positive test indicates amenorrhoea secondary to anovulation. The common underlying causes
are hypothalamic dysfunction and polycystic ovary syndrome.
• Negative test requires giving oestradiol 0.02 mg or conjugated oestrogen 1.25 mg for 25 days and
progestogen from 16th to 25th day. Negative test suggests endometrial unresponsiveness in the
presence of normal FSH. Pituitary.

• Specific treatment will depend on the cause and the patient’s desire for fertility at the time
of consultation. If she desires fertility, the treatment of choice is induction of ovulation
with clomiphene citrate or gonadotropins.
• On the other hand, if the patient does not desire fertility, she may be advised a
progestational agent (medroxyprogesterone or dydrogesterone) for 7–10 days every 2
months or so to induce periods. This treatment protects the patient against the ill-effects of
endometrial hyperplasia, adenomatous hyperplasia and endometrial carcinoma due to
prolonged unopposed oestrogen action on the endometrium.
• These patients should be advised to use some form of contraception (condoms/diaphragm)
to safeguard them against any unwanted pregnancy resulting from a stray ovulation or
spontaneous recovery of menstrual function.
• Premature menopause requires HRT to protect against osteoporosis and avoid menopausal
symptoms.

AMENORRHEA: ETIOLOGY
• Functional causes
- Anorexia/bulimia
- Chronic diseases (for example, tuberculosis)
- Excessive weight gain or weight loss
-Depression , Psychotropic drug use (drugs prescribed to stabilize or
improve mood, mental status, or behavior)
- Excessive stress, Excessive exercise
- Cycle suppression with systemic hormonal contraceptive pills

Structural causes:
• Hypergonadotropic hypogonadism
Premature ovarian failure
Hypogonadotropic hypogonadism
Hypothalamic hypogonadism
Pituitary disease
Thyroid disease
Absence of the uterus, cervix, or vagina
Pregnancy
Hyperprolactinemia
Elevated levels of androgens (male hormones)
Polycystic ovary syndrome PCOS

AMENORRHEA: SIGNS AND SYMPTOMS
•Milky nipple discharge.
•Unwanted hair growth.
•Headache.
•Vision changes.
•Excess facial hair.
•Pelvic pain.
•Acne
•stops having menstrual periods for three cycles in a row.

AMENORRHEA: TREATMENT
Non-pharmacological treatment:
- women should eat a properly balanced diet.
- women should restrict the amount of fat in their diet
- A moderate exercise program may restore normal menstruation.
- restore and maintain a healthy body weight.
- finding ways to deal with stress and conflicts may help.
-Maintaining a healthy lifestyle by avoiding alcohol consumption and
cigarette smoking is also helpful.

For primary amenorrhea, depending on age and the results of the
ovary function test, health care providers may recommend watchful
waiting. If an ovary function test shows low follicle-stimulating
hormone (FSH) or luteinizing hormone (LH) levels, menstruation may
just be delayed. In females with a family history of delayed
menstruation, this kind of delay is common.
Treatment for secondary amenorrhea, depending on the cause, may
include:

Pharmacological treatment:
Drugs used in polycystic ovary syndrome to induce ovulation:
Metformin (Metformin, TEVA) and
Clomiphene citrate (Ikaclomin, TEVA), (Ovaclomin, BZ)
• Dopamine receptor agonists; for treating hyperprolactinemia:
Bromocriptine (Lactopar, BZ)
Cabergoline (Dostinex, Pfizer), (Goline, BZ)
Hormone replacement therapy HRT consisting of an estrogen and/or
a progestrone can be used in estrogen deficiency:
Dydrogesterone (Duphaston, Abbott)
Progesterone micronized (Utrogestan, CTS)

HYPOMENORRHOEA
• UTERINE BLEEDING MAY BE SLIGHT IN AMOUNT ,SHORT IN DURATION OR BOTH,
• BLEEDING WHICH LASTS 2 DAY OE LESS IS UNUSUAL,IF NOT PATHOLOGICAL & IS
TERMED AS HYPOMENORRHOEA.
 CAUSES->
• CONSTITUTIONAL
• UTERINE( SMALL ENDOMETRIAL SUFACE)- GENITAL TB,ETC,SURGERIES
• HORM0NAL-LONG TERM USE OF OCP
• NERVOUS /EMOTIONAL
• TREATMENT- REASSURANCE

OLIGOMENORRHOEA
• CYCLE LASTS LONGER THAN 35 DAYS
• MENSTRUATION MAY BE BOTH INREQUENT & IRREGULAR , OR MAY BE
REGULARLY INFREQUENT.
• CAUSES:
1. CONSTITUTIONAL % PHYSIOLOGICAL
2. HORMONAL-PCOS
3. PITUITARY DISEASE’
4. UTERINE DISEASE
5. CHROMOSOMAL-XXX
 TREATMENT
 REASSURANCE

PREMENSTURAL
SYNDROME
 Mood and behavior symptoms
 Sad or depressed mood
 Anger, irritability, aggression
 Anxiety
 Mood swings
 Decreased alertness, trouble
concentrating
 Withdrawal from family and
friends
Premenstrual symptoms occur between ovulation
and the start of menstrual bleeding(one to two
weeks before a woman's period)
Common physical symptoms
- Bloating , weight gain
- Fatigue , lack of energy
- Cramps ,aching muscles and
joints, low back Paine
- Sleeping too much or too little
- Constipation and diarrhea
- Acne

PREMENSTRUAL DYSPHORIC DISORDER (PMDD)
- PMDD is characterized by depressed or labile mood, anxiety,
irritability, anger, and other symptoms occurring exclusively during
the 2 weeks preceding menses. Other symptoms may include the
following:
•Decreased interest in usual activities (eg, work, school, friends, and
hobbies)
•Other physical symptoms, such as breast tenderness or swelling,
headaches, joint or muscle pain, a sensation of bloating, or weight
gain
- It have more sever symptoms when compered with PMS

DYSMENORRHEA: DEFINITION
Dysmenorrhea :painful cramps that may occur immediately
before or during the menstrual period.
There are two types of dysmenorrhea: primary and secondary
dysmenorrhea:
•Primary dysmenorrhea is cramping pain in the lower abdomen
occurring just before or during menstruation, in the absence of
other diseases such as endometriosis.
•Secondary dysmenorrhea is pain caused by a disorder in the
woman's reproductive organs, such as endometriosis,
adenomyosis, uterine fibroids, or infection. Pain from secondary
dysmenorrhea usually begins earlier in the menstrual cycle and
lasts longer than common menstrual cramps.

DYSMENORRHEA:
ETIOLOGYRisk factors for primary
dysmenorrhea include the
following:
- Early age at menarche (< 12
years)
-Nulliparity
- Heavy or prolonged menstrual
flow
- Smoking
- Positive family history
- Obesity
Risk factors for secondary
dysmenorrhea include the
following :
- Leiomyomata (fibroids)
- Pelvic inflammatory disease
- Tubo-ovarian abscess
- Ovarian torsion
- Endometriosis

DYSMENORRHEA:
SIGNS & SYMPTOMES
 Primary dysmenorrhea
Onset shortly after the first
occurrence of menstruation (≤6
months)
Usual duration of 48-72 hours
(often starting several hours
before or just after the menstrual
flow)
Cramping or laborlike pain
lower abdominal pain, radiating
to the back or thigh .
Secondary dysmenorrhea
• Dysmenorrhea beginning in the 20s or 30s,
after previous relatively painless cycles .
• Heavy menstrual flow or irregular bleeding
examination
• Dysmenorrhea occurring during the first or
second cycles after menarche (menarch is
the first occurrence of menstruation)
• Pelvic abnormality with physical
• Poor response to nonsteroidal anti-
inflammatory drugs (NSAIDs) or oral
contraceptives (OCs)
• Infertility
• Dyspareunia

DYSMENORRHEA: PHARMACOLOGICAL TREATMENT
NSAIDs are common treatment for both primary and secondary
Dysmenorrhea
NSAIDs are highly effective in treating dysmenorrhea
They decrease menstrual pain by decreasing PGF2α
1-Diclofenac Immediate-release (Cataflam): 100 mg POonce, then 50 po 8th hrly
2 - Ibuprofen OTC: 200-400 mg POq4-6hr;
5-Mefenamic acid -Primary Dysmenorrhea ,Initial 500 mg PO
once, Then250 mg POq6hr PRNusually not to exceed 3 days

Other NSAIDs and analgesics that have been used include the following:
Aspirin may not be as effective as these NSAIDs, and acetaminophen may be a
useful adjunct for alleviating only mild menstrual cramping pain, and both
aspirin and acetaminophen are used when other NASID are not tolerated .
COX-2 inhibitors have also been used in relieving menstrual pain. They
selectively inhabit COX-2 receptor and reduse GI symptoms. But NASID remain
better .

OC may be an appropriate choice for patients who are not
planning to be pregnant . Combination OCs suppress the
hypothalamic-pituitary-ovarian axis, thereby inhibiting ovulation and
preventing prostaglandin production.
Although not approved by the FDA for treating dysmenorrhea, the
following OCs are also used:
1Combination OCs (eg, ethinyl estradiol with progestin or
drospirenone) .
2 Levonorgestrel intrauterine device .
3 Depot medroxyprogesterone acetate .

Analgesics In an emergency setting, patients who do not
respond to NSAIDs may require treatment with narcotics for
pain control.
Moderate to Severe Pain
1-2 tablets (2.5-10 mg hydrocodone; 300-325 mg
acetaminophen) PO q4-6hr PRN
Acetaminophen: Not to exceed 1 g/dose or 4 g/24 hr
Hydrocodone: Maximum daily dose should not exceed 60
mg/24 hr

Non pharmacological treatment :
1. Exercise
2. Heat. Using a hot bath or a heating pad, hot water bottle or heat
patch on your lower abdomen may ease menstrual cramps.
3. Dietary supplements. A number of studies have indicated that
vitamin E, omega-3 fatty acids, vitamin B-1 (thiamine), vitamin B-6
and magnesium supplements may effectively reduce menstrual
cramps.
4. Avoiding alcohol and tobacco. These substances can make
menstrual cramps worse.
5. Reducing stress. Psychological stress may increase your risk of
menstrual cramps and their severity.
DYSMENORRHEA: NON- PHARMACOLOGICAL
TREATMENT

primary dysmenorrhea is treataed by relief cramping pelvic pain
and associated symptoms that accompany menstrual flow.
(NSAIDs) and (OCs) are the most commonly used as treatment
for the management of primary dysmenorrhea.
secondary dysmenorrhea is treated by correction of the
underlying organic cause(treat pelvic pathology like
endometriosis) . use of analgesic agents and narcotics as
adjunctive therapy may be beneficial.

MENORRHAGIA:
DEFINITION
is a menstrual period with abnormally heavy flow and falls under
the larger category of abnormal uterine bleeding (AUB).

MENORRHAGIA: SIGNS & SYMPTOMES
 Heavy menstrual flow
 Passage of blood clots
- Signs and symptoms of anemia which include tiredness,
fatigue and shortness of breath Constant lower abdominal
and pelvic pain.

MENORRHAGIA: ETIOLOGY
•Hormonal disturbances
•Ovarian dysfunction
• Uterine fibroids
• Intrauterine Device (IUD)
•Pregnancy-related complications such as a miscarriage
ovarian cancers Inherited bleeding disorders such
cervical or
•Platelet function disorder Medications, such as anti-inflammatory
and anticoagulants
•thyroid disorders,
•endometriosis,
•and liver or kidney disease.

MENORRHAGIA: PHARMACOLOGICAL THERAPY
• iron supplementation to treat anemia
• NSAIDs: Ibuprofen, Naproxen...
• Oral contraceptives
• Oral progesterone: levonorgestrel (Microlut, BAYER)
Medroxyprogestrone acetate (Provera, Pfizer) (Oralut,
BZ)
• Anti-fibrinolytic drug: tranexamic acid (Hexakapron, TEVA), used in
the treatment of hemorrhages.

Menstrual migraine
 It is defined by International headache society, has 2 subtypes:
• Attacks of menstrually related migraine without aura must have an onset during peri-
menstrual time period and this pattern must be confirmed in 2/3 of menstrual cycles, but
other attacks may occur at other times of the menstrual cycle.
• Attacks of pure menstrual migraine without aura are similar to the above criteria except
migraine headaches are strictly limited to the peri-menstrual time period and do not occur
at other times of the month.

• The condition is familial
• The headaches are localized to one are and are severe enough to be incapacitating,
often accompanied by nausea and vomiting but not preceded by aura.
• Aeitology – multifactorial
• The cause can be attributed to an allergic reaction to gonadotropin,swelling of pituitary
gland,cerebral congestion or edema,increases intracranial pressure,a local release of
serotonin,cerebral iscahemia,psychological factors.
• In all probability, menstrual migraine is associated with changes in the cranial & cerebral
vascular apparatus.
• Oestrogen and progesterone must be concerned with these changes because similar
migraine sometimes results after taking the ocp.
• A fall in estrogen levels may lead to cerebral vascular spasm

Treatment
 General-
 Attention to general health and lifestyle changes
 Hormone therapy
 COCs and Medroxyprogesterone acetate
 Symptomatic-
 An attack may be prevented by giving drugs such as phenobatbitone
,belladonna,chlorpromazine singly or in combination on the day before or at onset of a
period.
 With the patient at rest in a darkened room- the drugs of choice to relieve pain are aspirin,
paracetamol or NSAIDs

 A specifc remedy is ergotamine tartrate (a serotonin agonist) with or without caffeine,
which can be given orally.
• 2mg dose followed by 1mg every 30 min,if required,upto a maximum of 4-6mg,The
weekly dose shouldn't exceed 10mg
• Antiemetics- metoclopramide, phenothiazines
• SSRI- sumatriptan 25-100mg per attack
• Artificial menopause- induction of menopause

CATEMENIAL SEIZURE
 THEY ARE DEFINED AS SEIZURES THAT CLUSTER AROUND MENSTRUAL CYCLE.
 TREATMENT:
 SALT & FLUID INTAKE RESTRICTION
 MDPA-150MG IM EVERY 1-2 MONTHS(PROGESTERONE HAS SEDATIVE EFFECT
ON CNS)

PREMENSTRUAL MASTALGIA
 BREAST BECOMES TENSE ,KNOTTY & TENDER
 CAUSE->DUE TO EDEMA AND CONGESTION OF INTERGLANDULAR CONNECTIVE
TISSUE AS WELL AS TO GLANDULAR ACTIVITY PROMOTED BY HORMONE
STIMULI.
 TREATMENT-
 SUPPORT THE BREAST
 PREMENSTRUAL FLUID AND SALT RESTRICTION
 BROMOCRIPTINE AND PROGESTOGENS SUCH AS DYDROGESTERONE X 7-10
DAYS PREMENSTRUALLY

RECURRENT BUCCAL AND VULVAL ULCERATION
 THE ULCERS DEVELOP DURING THE MIDDLE OF CYCLE OR DURING
PREMENSTRUAL PHASE,AND HEALING DURING AND AFTER MENSTRUATION.
 AEITOLOGY-
1. GENETIC FACTORS- GENES ENCODING TNF
2. ALLERGY-FAMILY H/O ASTHMA,HAY FEVER,ETC
3. VIRUS-HERPETIC APPEARANCE OF ULCERATION’
4. HORMONAL INFLUENCES
5. PSYCHOLOGICAL FACTORS
 TREATMENT-

• ATTENTION TO GEENRAL HEALTH
• TRANQUILLISERS GIVEN REGULARY AT NIGHT
• DENTAL & ORAL HYGEINE
• LOCAL ANTICEPTIC & ASTRINGENTS- H202 MOUTH WASH
• HORMONES- OCPS HELP
• CORTICOSTERIODS- REDUCE PAIN
• GENITAL ULCER- HYDROCORTISONE OINTMENT
• COLCHICINE & AZATHIOPRINE

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