Group Work on Amenorrhoea (Classification, Causes, Diagnosis):

• Primary amenorrhoea - absence of menarche by 16 yrs.

• Secondary “ - Absence of menses for 6 months in a women in whom
normal menstruation has been established or for 3 normal intervals in a women
with oligomenorrhea(menses occurring at an interval exceeding 35 days).
• Amenorrhea can be of eugonadotropic, hypergonadotropic or hypogonadotropic
in type.

Eugonadotropic amenorrhea:
Causes: A. Congenital abnormalities of genital tract.
• Rokitanski Kuster Hauster syndrome – Problems with muller duct. No uterus but
ovaries are normal. So steroid hormones are normal. Combined urinary system
malformations produced.
• Hymen occlusivum – No hole in the hymen. It will results in hematocolpus and
hematometria. Blood goes via fallopian tubes to the abdomen and cause acute
abdomen.
• Septa vaginae – Transverse vaginal septa, usually in upper 1/3 of the vagina
where fusion of parts of mullerign and urogenital sinus.
• Absent vagina.

B. Acquired abnormalities.
• Asherman’s syndrome – Damage of deep basal layer of the endometrium
following D and C will results in formation of adhesions in the cavity. It’ll cause
sterility too.
• The development is similar as in Asherman’s syndrome, but the damage is of
infectious origin.
• Stenosis of cervical canal.

C. Hyperandrogenaemia – of adrenal aetiology. Ovarian origin or of mixed

aetiology.

Diagnosis:
• Pelvic examination – Presence of absence of vagina, uterus, vaginal
abnormalities.
• Hormonal evaluation.
• History of currentage, TBC.
• Clinical presentation.
• US.
• X-ray.
• Laparoscopy.
• Asherman’s syndrome can be diagnosed by administration of conjugated estrogen
2.5 mg orally for 25 days + Medraxyprogesterone acetate 10 mg orally from 16
till 25th day. Patients with Asherman’s syndrome do not bleed following this
 regimen.

Hypergonadotropic forms of amenorrhea:

A. Chromosomal pathology:
• Turners Syndrome – 45 XO or Mosaic 46 XX/45 X, 46 XY/45 XX, 47
XXX/45 X. They have only one functioning X chromosome. Gonads are
imperfectly formed, usually being represented by white streaks of connective
tissue containing no germ cells or granulosa cells. The external body form is
immaturely female, with an infantile vulva, vagina and uterus. As now
hormones are producing by the gonads, 2ndry sexual characteristics are
absent. No breast development. Axillary and pubic hair is absent.

B. Embryonic cell migration problems without chromosomal pathology.

• Pure gonadal dysgenesis(Swyer’s sundrome) – Primitive oogonia hasn’t
migrated to the genital ridges and ovaries failed to develop, streak gonads,
which can’t secrete hormones.

C. Ovarian Resistance Syndrome(Savages Syndrome)

A defect in the cell receptor mechanisms. Patient has Incr. FSH and LH and
ovaries contain primodial germ cells.

D. Testicular feminization:
46 XY karyotype. A testis with defective enzymes will produce mullerian
inhibiting factors but not testerone. Affected individuals have female ext. genitaliaand no
mullerian structures. Breasts are well formed. Vulva is normal. “Testes” may be localized
in abdomen or in groin with excessive development of interstitial cells. After
development of 2dry sexual characteristics, abnormal testes should be removed to prevent
malignant changes.

E. Acquired factors:
Radiation. Chemotherapy. Ovarectomy. Mumps oopheritis.

F. Ovarian dysfunction in polycystic ovary syndrome.

LH:FSH ratio is high.

Diagnosis:
• Clinics, Family history, Pelvic examination.
• Hormonal evaluation.
• Karyotyping.
• Us, CT, X-ray, Laparoscopy.

Hypogonadotropic forms of amenorrhea:

1. Kallmann’s syndrome – Migration of GnRh neurons to the hypothalamus
prevented by congenital abnormalities in the olfactory pathways. So, no LH of
 FSH will be released from the pituitary, No ovulation. Anosmia is associated with
this.
2. Pitiutary pathologies:
* Tumors – Craniopharyngioma, Chromophobe cell adenoma. Prolactin producing
tumors(Prolactin has an inhibitory effect on LH (Partial) via increasing
dopamine).
* Sheehan’s syndrome / Post Partal Pitiutary necrosis. – This occur postpartally
after severe hemorrhage, hypotension. Ischemic necrosis of pituitary gland occurs.
* Thalassemia major – Iron deposition in the pituitary may result in destruction of
the cells that produce LH and FSH. This happens in hemosiderosis which is seen
in thalassemia.
3. Stress – Phychological and Physical.
4. Alimentary problems, Anorrexia nervosa.
5. Medicine.
* Contraceptives.
* Reserpin
* Ganglion blockers.
* GnRh agonists.
* Antigonadotropins(Danazol).
6. Suprarenal gland pathology:
* Steroid hormone defects – 17 hdcroxylase, 17 desmolase.
* Thyroid gland pathology.

Diagnosis: * Medical history. * Clinical presentation. * Brain CT. * US. * Hormonal

evaluation. * X-ray.

Secondary physiological amenorrhea: * Pregnancy. * Lactation. * Menapause.

Group Work on Amenorrhoea (Classification, Causes, Diagnosis)

Report prepared by
1. Dr. Sajid Mahmood, MD (EU), Accident & Emergency Department, NHS Royal infirmary Liverpool United
Kingdom.
2. Dr. Adnan Akram, MD (EU), Department of Infectious Diseases. University Hospital Riga Latvia.
3. Dr. Aftab Ahmed, MD (EU), Infection Control Department, Kaunas Medical University Clinic. Lithuania.

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