amenorrhea Flashcards
Primary Amenorrhea def
is defined either as absence of menses by age 14 years with no development of secondary sexual characteristics
OR as absence of menses by age 16 years with normal development of secondary sexual characteristics.
Secondary amenorrhea def
No menses for 3 months if previous menses were regular.
No menses for 6 months if previous menses were irregular
Oligomenorrhea
Interval of more than 35 days between periods
Events of Puberty
Thelarche (breast development)
Requires estrogen
Pubarche/adrenarche (pubic hair development)
Requires androgens
Menarche Requires: GnRH from the hypothalamus FSH and LH from the pituitary Estrogen and progesterone from the ovaries Normal outflow tract
ETIOLOGY OF PRIMARY AMENORRHEA
Secondary sexual characteristics present
Constitutional delay
Genito-urinary malformation, e.g. imperforate hymen, transverse vaginal septum, absent vagina with or without a functioning uterus
Androgen insensitivity
Resistant ovary syndrome
Pregnancy
Secondary sexual characteristics absent
Hypothalamic dysfunction, e.g. chronic illness, anorexia nervosa, weight loss, ‘stress’
Gonadotrophin deficiency, e.g. Kallman’s syndrome
Hypopituitarism
Hyperprolactinemia
Hypothyroidism
Gonadal failure, e.g. ovarian dysgenesis/agenesis, premature ovarian failure
Ambiguous external genitalia
Congenital adrenal hyperplasia
Androgen-secreting tumor
5-Alpha-reductase deficiency
Turner’s syndrome
Turner’s syndrome is caused by either a complete absence or a partial abnormality of one of the two X chromosomes.
Features : short stature, web neck, lymphedema, shield chest with widely spaced nipples, short metacarpal bones and renal anomalies.
wide carrying angle, coarctation of the aorta.
• High FSH and LH levels.
• Bilateral streaked gonads.
• Karyotype - 80 % 45, X0
Treatment: HRT
20% mosaic forms (46XX/45X0) or 45X/46XY)
Uterovaginal agenesis
15% of primary amenorrhea
Normal secondary development & external female genitalia
Normal female range testosterone level
Absent uterus and upper vagina & normal ovaries
Karyotype 46-XX
15-30% associated renal, skeletal and middle ear anomalies
ex Mayer-Rokitansky-Kuster-Hauser syndrome
Androgen insensitivity syndrome
Normal breasts but no sexual hair
Normal looking female external genitalia
Absent uterus and upper vagina
Karyotype 46, XY
Male range testosterone level
Treatment : gonadectomy after puberty + HRT
The testis present in the inguinal canal and liable to trauma, torsion and malignancy
The receptors in the external genitalia are not sensitive to testosterone and sometimes deficiency of 5alpha reductase which converst T to T2
Imperforate hymen
Imperforate hymen represents the most common and most distal form of vaginal outflow obstruction
Clinical presentations range from an incidental finding on physical examination of an asymptomatic patient to discovery on an evaluation for primary amenorrhea or abdominal or back pain
The differential diagnosis of uterovaginal obstruction includes disorders of vaginal development, such as transverse vaginal septum or complete vaginal agenesis.
Incise the Hymen, drain the blood,
Needs IVP as there is up to 30% association with renal tract abnormalities.
Hypogonadotrophic Hypogonadism
Normal hight Normal external and internal genital organs (infantile) Low FSH and LH 30-40% anosmia (kallmann’s syndrome) Treat with HRT
Constitutional delay
There is no anatomical abnormality or endocrine investigations show normal results
It is caused by immature pulsatile release of gonadotrophin-releasing hormone; maturation eventually occurs spontaneously
delayed bone age
( X-ray Wrist joint)
• Positive family history
• Diagnosis by exclusion and follow up
Weight-related amenorrhoeaAnorexia Nervosa
1o or 2o Amenorrhea is often first sign
A body mass index (BMI) <17 kg/m² menstrual irregularity and amenorrhea
Hypothalamic suppression
Low estradiol risk of osteoporosis
Treatment : body wt. (Psychiatrist referral)
ASSESSMENT OF PRIMARY AMENORRHEA
slides
Etiology of secondary amenorrhea
No features of androgen excess present
Physiologic, e.g. pregnancy, lactation, menopause
Iatrogenic, e.g. depot medroxyprogesterone acetate contraceptive injection, radiotherapy, chemotherapy
Systemic disease, e.g. chronic illness, hypo- or hyperthyroidism
Uterine causes, e.g. cervical stenosis, Asherman’s syndrome (intra-uterine adhesions)
Ovarian causes, e.g. premature ovarian failure, resistant ovary syndrome
Hypothalamic causes, e.g. weight loss, exercise, psychological distress, chronic illness, idiopathic
Pituitary causes, e.g. hyperprolactinaemia, hypopituitarism, Sheehan’s syndrome
Features of androgen excess present
Polycystic ovary syndrome
Cushing’s syndrome
Late-onset congenital adrenal hyperplasia
Adrenal or ovarian androgen-producing tumor
Polycystic ovary syndrome
This condition is characterized by hirsutism, acne, alopecia, infertility, obesity, and menstrual abnormalities (amenorrhea in 19% of cases)
Ultrasound examination of the ovaries typically shows multiple, small peripheral cysts. up to a third of women in the general population have polycystic ovaries on ultrasound examination .
Endocrine abnormalities include increased serum concentrations of testosterone, prolactin, luteinizing hormone (LH) (with normal follicle-stimulating hormone [FSH] levels), and insulin resistance with compensatory hyperinsulinemia
Asherman’s Syndrome
Secondary amenorrhoea following destruction of the endometrium by overzealous curettage multiple intrauterine Synechiae show up on “Hysterography or hysterescopy”.
MANAGEMENT: Under G.A. breakdown Adhesions through hysteroscopeinsert an IUCD to prevent reformation hormone therapy (E2 + P)
Premature ovarian failure
Menopause/ovarian failure occurring before the age of 40 years is considered premature
Auto-immune disease is the most common cause; auto-antibodies to ovarian cells, gonadotrophin receptors, and oocytes have been reported in 80% of cases
Before puberty or in adolescents, ovarian failure is usually due to a chromosomal abnormality, e.g. Turner mosaic, or previous radiotherapy, or chemotherapy
Autoimmune related dysfunction
The most common association is with thyroid disease, but the parathyroids and adrenals can also be affected
Hyperprolactinemia
A prolactinoma is the commonest cause of hyperprolactinemia (60% of cases)
Other causes include non-functioning pituitary adenoma (disrupting the inhibitory influence of dopamine on prolactin secretion)
dopaminergic antagonist drugs (e.g. phenothiazines, haloperidol, clozapine, methyldopa, cimetidine); primary hypothyroidism (thyrotrophin-releasing hormone stimulates the secretion of prolactin), or it may be idiopathic
Prolactin acts directly on the hypothalamus to reduce the amplitude and frequency of pulses of gonadotrophin-releasing hormone
Progestogen-associated amenorrhea
Depot medroxyprogesterone acetate inhibits the secretion of gonadotrophins and thus suppresses ovulation
After 1 year of use, 80% of women have amenorrhoea or very scanty, infrequent vaginal bleeding
There is partial estrogen deficiency in women who use depot medroxyprogesterone acetate
The progestogen-only pill leads to reversible long-term amenorrhoea in a minority of women, due to complete suppression of ovulation
The levonorgestrel-releasing intra-uterine device commonly results in amenorrhoea after a few months. This is thought to be mainly a local effect, but suppression of ovulation can occur in some women (in some cycles)
history taking
symptoms of pregnancy
Associated symptoms, e.g. galactorrhoea, hirsutism, hot flushes, dry vagina, symptoms of thyroid disease
Recent change in body weight
Recent emotional upsets
Previous menstrual and obstetric history
Previous surgery, e.g. endometrial curettage, oophorectomy
Previous abdominal, pelvic, or cranial radiotherapy
Family history, e.g. of early menopause
Drug history, e.g. progestogens, combined oral contraceptive, chemotherapy
Acanthosis nigricans:
\Acanthosis nigricans: this hyperpigmented thickening of the skin folds of the axilla and neck is a sign of profound insulin resistance. It is associated with polycystic ovary syndrome
(PCOS) and obesity.
Breast examination for galactorrhoea
Pelvic examination
Complications and prognosis
Osteoporosis: women with amenorrhoea associated with estrogen deficiency are at significant risk of developing osteoporosis. This increased risk persists even if normal menses are resumed. Estrogen deficiency is of particular concern in younger women as a desirable peak bone mass may not be attained
Cardiovascular disease
Young women with amenorrhoea associated with estrogen deficiency may be at increased risk of cardiovascular disease
Women with polycystic ovary syndrome have an increased risk of developing cardiovascular disease, hypertension, and type 2 diabetes [Hopkinson et al, 1998]
Endometrial hyperplasia: women with amenorrhoea but no associated oestrogen deficiency are at increased risk of endometrial hyperplasia and endometrial carcinoma
Infertility: women with amenorrhoea generally do not ovulate
Psychological distress: amenorrhea often causes considerable anxiety, many women have concerns about loss of fertility, loss of femininity, or worry about an unwanted pregnancy. The diagnosis of Turner’s syndrome, testicular feminization, or developmental anomaly can be traumatic for both girls and their parents