Overview of gynaecological conditions as covered for medical school finals. Contains information about clinical features of each condition, as well as relevant diagnostic tests and investigations, risk factors, causes and management guidelines.
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- Amenorrhoea
o Primary
o Secondary
,ADENOMYOSIS
PRESENTATION SUMMARY
- Dysmenorrhoea Endometrial tissue inside the myometrium
- Menorrhagia More common in later reproductive years and those
- Dyspareunia who are multiparous
May also present with infertility or pregnancy-related Occurs in 10% of women overall – can occur alone or
complications alongside endometriosis and fibroids
About 1/3 are asymptomatic Cause is not fully understood – multifactorial including
O/E sex hormones, trauma, and inflammation
- Enlarged and tender uterus Condition is hormone-dependent and symptoms tend
- Will feel more soft than uterus containing to resolve after menopause, similar to endometriosis
fibroids and fibroids
- ‘boggy’
DIAGNOSIS MANAGEMENT
ST
Transvaginal USS = 1 line Same as for menorrhagia
MRI + transabdominal USS if transvaginal USS No contraception
unsuitable - Tranexamic acid
Gold standard = histological exam of uterus after - Mefenamic acid (associated pain)
hysterectomy (although rarely suitable) Contraception
- Mirena coil
COMPLICATIONS - COCP
- Cyclical oral progestogens
- Infertility
- Miscarriage Other options
- Preterm birth - GnRH analogues
- Small for gestational age - Endometrial ablation
- PPROM - Uterine artery embolization
- Malpresentation - Hysterectomy
- Requirement for C-section
- PPH
, PRIMARY AMENORRHOEA
HYPOGONADOTROPIC HYPOGONADISM
SUMMARY
LH/FSH deficiency oestrogen deficiency
Not starting menstruation by 13 when no other signs of
LH/FSH produced in the anterior pituitary in response pubertal development
to gonadotropic releasing hormone from the
Not starting menstruation by 15 when there are other
hypothalamus
signs of pubertal development
Causes
- Hypopituitarism
- Damage to hypothalamus/pituitary e.g. HYPERGONADOTROPIC HYPOGONADISM
radiotherapy, surgery
Gonads fail to respond to LH/FSH – no negative
- Significant chronic conditions – CF, IBD
feedback so pituitary produces increasing amounts of
- Excessive dieting or exercise
LH/FSH
- Constitutional delay in growth/development
- Endocrine disorders – GH deficiency, - Previous damage to gonads (torsion, cancer,
hypothyroidism, Cushing’s, infection)
hyperprolactinaemia - Congenital absence of ovaries
- Kallmann syndrome - Turner syndrome
OTHER STRUCTURAL PATHOLOGY
Congenital adrenal hyperplasia – autosomal Typical secondary sexual characteristics but no
recessive condition causing reduced cortisol and menstrual periods
overproduction of androgens. In milder cases females May be cyclical abdominal pain as menses build up
can present with:
- Imperforate hymen
Tall for age, facial hair, primary amenorrhoea, deep - Transverse vaginal septae
voice, early puberty - Vaginal agenesis
Androgen insensitivity syndrome – tissues unable to - Absent uterus
respond to androgen hormones female phenotype - FGM
with absent uterus, upper vagina, fallopian tubes and
ovaries
MANAGEMENT
Establish and treat underlying cause
ASSESSMENT
Hypogonadotropic hypogonadism
- Hx and exam
- Underlying medical conditions - Treat with pulsatile GnRH which can be used to
o FBC, ferritin induce ovulation and menstruation
o U+Es, (CKD) o Has the potential to induce fertility
o Anti-TTG - Replacement sex hormones in the form of
- Hormone profile COCP can be used to induce regular
o FSH/LH menstruation and prevent symptoms of
o TFTs oestrogen deficiency if pregnancy not wanted
o IGF-1 (GH deficiency)
o PRL
o Testosterone
Raised in PCOS, androgen
insensitivity syndrome and CAP
- Genetic testing with microarray (Turner
syndrome)
- Imaging
o XR of wrist (asses bone age,
constitutional delay)
o Pelvic USS – assess ovaries and pelvic
organs
o MRI brain (pituitary pathology)
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