AMENORRHOEA FOR UNDERGRADUATE PCOD

1. DR SALINI MANDAL B.G.
ASST PROFESSOR
DEPT OF OBG
FMHMC

11. HYPOGONADOTROPIC HYPOGONADISM
HYPERGONADOTROPIC HYPOGONADISM
ABNORMAL CHROMOSOMAL PATTERN
DEVELOPMENTAL DEFECT OF GENITAL TRACT
DYSFUNCTION OF THYROID AND ADRENAL CORTEX

14.  DELAYED PUBERTY : DELAYED GnRH pulse reactivation

15.  HYPOTHALAMIC AND PITUITARY DYSFUNCTION: Gonadotropin
deficiency due to stress, weight
loss, excessive exercise, c/c d’se.

16.  KALLMANN’S SYNDROME: Inadequate GnRH pulse secretion
 Kallmann syndrome is a condition characterized by delayed or
absent puberty and an impaired sense of smell.
 This disorder is a condition affecting the production of
hormones that direct sexual development.
 (GnRh neurons are absent due to partial or complete agenesis
of olfactory bulb)

17.  CNS TUMOURS: Craniopharyngioma  reduced GnRH
secretion

18. HYPERGONADOTROPIC
HYPOGONADISM

19.  Primary ovarian faliure (sex chromatin nil)
 Resistant ovarian syndrome (functional disturbance of the
gonadotrophin receptors in the ovarian follicles)

22.  Turner’s syndrome
 Pure gonadal dysgenesis
 Androgen insensitivity syndrome (Testicular
feminization syndrome)
 Partial deletions of the X chromosome.

26.  Absence of uterus
 Atresia of upper third of vagina
and cervix.

30.  Complete agenesis of vagina – vaginal reconstruction.
 Chromosomal abnormalities: hormonal therapy atleast for
development of breast
 Androgen insensitivity syndrome: extra gonad removed.
 Hypothalomopituitary ovarian axis defect:

31.  Metabolic and Nutritional: DM, Tb treated. Correction of
anemia. Correction of malabsorption, weight loss stress.
 Unresponsive endometrium: no known treatment.

37.  There is formation of adhesions following post- abortal and
puerperal curettage and also following diagnostic curettage
in dysfunctional uterine bleeding.
 Menstrual abnormalities include hypomenorrhea,
oligomenorrhea or amenorrhea.
 Hysterosalpingography shows honeycomb appearance.

44. Clinical features:
 The patient complains of increasing obesity
(abdominal – 50%), menstrual abnormalities (70%) in
the form of oligomenorrhea, amenorrhea or DUB
and infertility.
 Presence of hirsutism and acne are the important
features
 Virilism is rare.

46.  HAIR-AN syndrome in patients with PCOS is characterized by
hyperandrogenism, insulin resistance and acanthosis
nigricans.
 Internal examination reveals bilateral enlarged cystic ovaries
which may not be revealed due to obesity.

48.  Sonography — Transvaginal sonography is specially useful in
obese patient.
 Ovaries are enlarged in volume (> 10 cm3).
 Increased number (> 12) of peripherally arranged cysts (2–9
mm) are seen

54. A. Ovary produces excess androgens due to —
(i) stimulation of theca cells by high LH
(ii) P450 C17 enzyme hyperfunction
(iii) stimulation of theca cells by IGF-1 (insulin growth factor-1)

55. B. Adrenals are stimulated to produce excess androgens by
(i) stress
(ii) P450 C17 enzyme hyperfunction

56. C. Systemic metabolic alteration
(i) Hyperinsulinemia causes:
(i) Stimulation of theca cells to produce more androgens.
(ii) Insulin results in more free IGF-1. By autocrine action,
IGF-1 stimulates theca cells to produce more
androgens.
(iii)Insulin inhibits hepatic synthesis of SHBG, resulting in
more free level of androgens.

57. (ii) Hyperprolactinemia:
In about 20% cases, there may be mild elevation of
prolactin level due to increased pulsitivity of GnRH or due to
dopamine deficiency or both.
The prolactin further stimulates adrenal androgen
production.

58.  Anovulation: Because of low FSH level, follicular growth is
arrested at different phases of maturation (2–10 mm
diameter). The net effect is diminished estradiol and increased
inhibin production.

59.  Due to elevated LH, there is hypertrophy of theca cells and
more androgens are produced either from theca cells or
stroma. There is defective FSH induced aromatization of
androgens to estrogens. Follicular microenvironment is
therefore more androgenic rather than estrogenic.

61.  Obesity is also associated with reduced SHBG.
 It also induces insulin resistance and hyper-
insulinemia which in turn increases the gonadal
androgen production.

62.  Etiology of insulin resistance is unknown.
 Mutations of the insulin receptor gene in the peripheral
target tissues and reduced tyrosine autophosphorylation of
the insulin receptor, is currently thought to be an important
cause. Increased central body fat leads to android obesity.

64.  Premature ovarian insufficiency (failure) is defined
when ovarian failure occurs before the age of forty.
 It occurs in about 1% of the female population.

65.  During intrauterine life either there is failure of germ cell
migration or there may be normal germ cell migration but
an accelerated rate of germ cell depletion (apoptosis) due
to various reasons.
 This results in either no follicle or only few follicles left
behind in the ovary by the time they reach puberty

68.  History of amenorrhea in less than 35 years of age.
 Karyotype abnormality
 Ovarian biopsy (afollicular, follicular and autoimmune variety) In
autoimmune variety, there is perifollicular lymphocyte infiltration. In
resistant ovarian syndrome, follicles are present. FSH receptor is either
absent or defective.

69.  Patient presents with amenorrhea — primary (25%) or
secondary (75%). Features of hypoestrogenic state like hot
flushes, vaginal dryness, dyspareunia and psychological
symptoms are there.
 The possibility of autoimmune disorders should be considered
below the age of 35. For this, antithyroid antibodies,
rheumatoid factor and antinuclear antibodies should be
measured.
 In younger patients (age below 30) karyotype is to be done to
rule out chromosomal abnormality.

71.  A. Physiological
◦ stress and exercise
◦ Pregnancy
◦ Stimulation of nipples

74.  Prolactin level is more than 100 ng/mL is often associated
with prolactinoma. (normal: 1-20ng/ml)

76.  There is history of severe postpartum hemorrhage,
shock or severe infection. Depending upon the
degree of anterior pituitary necrosis, the features
vary.

77.  The common manifestations are
◦ failing lactation,
◦ loss of pubic and axillary hair,
◦ lethargy,
◦ hypotension,
◦ secondary amenorrhea and
◦ atrophy of the breasts and genitalia.

78.  Gonadotropin level is low, so also T3, T4 and
cortisol.
 The hormones affected in order of frequency are,
growth hormone (GH), prolactin, gonadotropins (FSH
and LH), TSH and ACTH.
 Hyponatremia may be present (30%).
 The syndrome may develop slowly over 8–10 years
time.