My Clinical Notes

• Oestrogen is responsible for the development of secondary sexual characteristics
• Thelarche – beginning of breast development (9-11)
• Adrenarche – growth of pubic hair (11-12)
• Menarche – onset of menstruations

 

Days 1-4: Menstruation

• Endometrium is shed as hormonal support is withdrawn.

 

Days 5-13: Follicular/Proliferative phase

• Pulses of GnRH stimulate release of LH and FSH from the pituitary. This induces follicular growth and the subsequent release of oestradiol. This normally suppresses FSH such that only one ovum matures. Very high levels of oestradiol have a positive feedback effect on LH causing LH levels to rise sharply, this then results in ovulation.
• Oestradiol also effects the endometrium causing it to proliferate. Stromal cells proliferate and the glands elongate

 

Days 14-28: Secretory/Luteal Phase

• The follicle becomes the corpus luteum which as well as producing some oestradiol produces more progesterone, the levels of which peak around day 21. this has a secretory effect on the endometrium, causing the stromal cells to enlarge, the glands to swell and an increase in blood supply. If the egg has not been fertilised the corpus luteum starts to fail, resulting in a withdrawal of progesterone and oestradiol. This causes the endometrium to break down and be shed. Menstruation occurs and the cycle restarts

 

• Continuous administration of progesterone maintains the secretory phase thus preventing menstruation

 

 

Normal menstruation

 

• Cycle of 21-35 days.
• Any irregularity not being more than 7 days
• 2-7 days of bleeding.
• Not more than 80ml of blood loss per cycle

 

 

Menorrhagia

 

• Occurs when menstrual loss if greater that 80ml
• Affects 5% of women between the ages of 30-49
• Dysfunctional uterine bleeding describes excessive menstrual loss in the absence of any other pathology
• Dysfunctional uterine bleeding can be classified as either ovulatory or anovulatory
• In ovulatory dysfunctional uterine bleeding there are cyclical symptoms. Alterations in production of prostaglandins and fibrinolytic activity  are thought to play a role
• Anovulatory bleeding accounts for 10% of cases. In the case unopposed oestrogen causes a hyperplastic endometrium followed by oestrogen withdrawal bleeds. This type of bleeding is often more prolonged and heavy

 

Causes

• Unexplained – no systemic or anatomical cause can be found, accounts for 60% of cases. May be due to abnormalities in the endometrial fibrinolytic system of uterine prostaglandin levels
• Systemic problems – thyroid disease, haemostatic disorders (von Willebrand’s disease) and anti-coagulant therapy. These are rare causes
• Local anatomical disorders – fibroids, uterine and cervical polyps, adenomyosis and endometriosis

 

 

 

Clinical features

• Anaemia is common
• Irregular enlargement of the uterus suggests fibroids
• Tenderness suggests adenomyosis
• Tenderness and immobile pelvic organs suggests endometriosis or infection

 

Investigations

• Hb to check anaemia
• Coagulation and thyroid function (to exclude systemic causes)
• Transvaginal ultrasound
• Endometrial biopsy
• Hysteroscopy

 

Treatment

Medical

• Antifibrinolytics – tranexamic acid, taken during menstruation only. Can reduce blood loss by 50%
• NSAIDs – eg mefanamic acid, inhibit prostaglandin synthesis and reduce blood loss by 50%
• Combined oral contraceptive
• Progestogen (levonorgestrel) impregnated intrauterine device –releases 20 mg/day. Reduces menstrual flow by >90%. Replacement is required every 5 years
• GnRH – agonists produce amenorrhoea
• Progestogens – high doses cause amenorrhea, bleeding follows withdrawal. Given over 21 days with 7 day break

 

Surgical

• Polyp removal – done hysteroscopically
• Endometrial resection, ablation, diathermy – involve removal or destruction of the endometrium. This is also done hysteroscopically.
• Myomectomy – removal of fibroids from the myometrium either laproscopically or open. GnRH agonists are often used first to shrink the fibroids
• Hysterectomy – may be done vaginally, abdominally or laproscopically

 

 

Polymenorrhoea/intermenstrual bleeding

 

• Coexists with menorrhagia and is more common at the extremes of reproductive age

 

Causes

• Anovulatory cycles
• Local anatomical disorders – fibroids, uterine and cervical polyps, adenomyosis, endometriosis, chronic pelvic infection, endometrial malignancy

 

Investigations

• Hb
• Cervical smear
• Untrasound examination to detect fibroids or ovarian mass
• Endometrial biopsy, generally at hysteroscopy
• Diagnostic laparoscopy

 

Treatment

Medical

• Combined oral contraceptive
• Progestogens
• Hormone replacement therapy in climacteric women
• Intrauterine Uterine device

 

Surgical

• As for menorrhagia but ablative techniques are less used

 

 

Amenorrhoea and Oligomenorrhoea

 

• Amenorrhoea is the absence of menstruation (may be primary or secondary)
• Oligomenorrhoea is when menstruation occurs less frequently than every 35 days

 

Causes

• Physiological – pregnancy, menopause and lactation
• Pathological – may be due to dysfunction of the hypothalamus, pituitary, thyroid, adrenals, ovary, uterus or outflow tract.
• The most common causes of amenorrhoea and oligomenorrhoea are, the premature menopause, polycystic ovary syndrome and hyperprolactinaemia

·        Hypothalamic hypogonadism – common, usually due to psychological factors, anorexia nervosa or athleticism. GnRH is reduced therefore resulting in low levels of FSH, LH and oestradiol

·        Hyperprolactinaemia – usually caused by pituitary hyperplasia or benign adenomas. Treatment is via bromocriptine, carbergoline or surgery. Rare causes include Sheehan’s syndrome.

·        Adrenal or thyroid gland - due to hypo and hyperthyroidism. Rarely congenital adrenal hyperplasia

·        Ovary

• • Acquired disorders – polycytic ovary syndrome, premature menopause (1% or women). Rarely virilizing tumours can arise from the ovary
  • Congenital disorders – Turner’s syndrome

·        Outflow tract problems

• • Congenital – inperforate hymen and transverse vaginal septum can result in obstruction of menstrual flow
  • Acquired – cervical stenosis. Asherman’s syndrome, a rare consequence of excessive curettage.

 

Management

• Premature menopause – HRT
• Polycystic Ovary Syndrome – advice regarding diet and exercise. Oral contraceptive pill to regulate menstruation and prevent endometrial hyperplasia. Cyproterone acetate may be useful for acne management. Finasteride with reduce hirsutism
• Hyperprolactaemia – treatment with dopamine agonist bromocriptine or carbergoline.

 

 

Postcoital Bleeding

 

• Vaginal bleeding following intercourse that is not associated with menstruation.
• Always abnormal (except for first intercourse).
• Malignancy must be excluded

 

Causes

• Cervical ectropions
• Benign polyps
• Invasive cervical cancer
• Atropic vaginal wall

 

Management

• Cervical smear
• Avulsion of polyp
• Cryotherapy for ectropion
• Colposcopy to exclude malignancy

 

 

 

 

 

 

Postmenopausal bleeding

 

• Vaginal bleeding occurring at least 12 months after cessation of menstruation

 

Causes

• Endometrial carcinoma
• Cervical carcinoma
• Ovarian carcinoma
• Atrophic vaginitis
• Endometrial polyps
• Cervical polyps
• HRT
• Forgotten IUD
• Fibroids

 

Management

• Clinical examination to look for lesions of the cervix vagina and vulva
• Cervical smear
• Transvaginal ultrasound to assess endometrial thickness – should be less than 5mm
• Hysteroscopy and endometrial sampling using a Pipelle

 

Treatment

• Oestrogen replacement or HRT if atropic vaginitis

 

 

Dysmenorrhoea

 

• Painful menstruation
• Associated with high prostaglandin levels in the endometrium
• Due to contraction and ischaemia of the uterine muscle

 

Causes/ Management

• Primary dysmenorrhoea – usually no organic cause found. Common. Treated with NSAIDs (diclofenac, ibuprofen, mefenamic acid), progestogens (norehisterone) or suppression of ovulation by the combined contraceptive pill or GnRH analogues (short term)
• Secondary dysmenorrhoea – due to pelvic pathology. Pain often precedes menstruation and is relieved by menstruation. Most common causes are fibroids, adenomyosis, endometriosis, PID and ovarian tumours

 

Hirtsutism

 

• Excessive production of hair with a tendency to male distribution
• Excessive is defined as being beyond socially acceptable and the cause of embarrassment
• Caused by a rise in secretion of free androgens or a decrease in sex hormone binding globulin
• Ferrimen Galwey chart provides an objective scoring system for hirtsutism

 

Causes

• Idiopathic
• Polycystic ovary disease
• Androgen producing tumours – should be considered if testosterone levels are greater than 5nmol/L or if history is of sudden onset
• Congenital adrenal hyperplasia – adrenal disease caused by enzyme defect
• Drugs;
  • Phenytoin
  • Diazoxide
  • minoxidil

 

Investigations

• Serum testosterone
• Gonadotrophins
• Prolactin
• TSH
• Adrenal gland enzymes
  • Dihydroepiandrosterone sulphate
  • 17-hydroxyprogesterone

 

Treatment

• Cosmetic – shaving, electrolysis, depilatory creams
• Drug treatment
• Oral contraceptives – suppress LH and therefore inhibit ovarian androgen function also oestrogen stimulates SHBG production by the liver
• Medroxyprogesterone acetate – progesterone which inhibits LH
• Cyproterone acetate – inhibits LH and acts as an anti-androgen
• GnRH with addback HRT
• Flutamide – non-steriodal antiandrogen
• Finasteride – 5alpha reductase inhibitor

 

• Treatment may take 3-6 months

 

This entry was posted on Saturday, September 29th, 2007 at 4:33 pm and is filed under Gynaecology/Obstetrics. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.