Gynaecology And GUM Flashcards
Give five differential diagnoses for intermenstrual vaginal bleeding
Infection Malignancy Fibroids Pregnancy Hormones
Give four diagnoses to consider for post-coital bleeding
Cervical ectropion
Infection
Malignancy
Atrophic vaginitis
Give four causes of post menopausal vaginal bleeding
Infection
Malignancy
Atrophy
HRT
Four things to ask about when considering vaginal discharge indicating infection.
Colour
Consistency
Amount
Smell
Things to consider when taking a menstrual history.
Age of menarche and/or menopause Duration of bleeding Cyclicity (establish accuracy) Any recent changes? Any dysmenorrhea? Date of last menstrual period Use of contraception (what method currently, past methods used, future plans).
A luteal cyst is a physiological ovarian cyst related to ovulation. How do they form?
When the corpus luteum has released its egg, it may become filled with blood or fluid and continue to grow. This does not disappear even if the egg is fertilised.
How does a follicular cyst (Graaffian cyst) (physiological ovarian cyst) develop?
These develop during the run up to ovulation. They occur when the follicle doesn’t rupture or release it’s egg, or when a mature follicle collapses in on itself.
How would Polycystic Ovarian Syndrome (PCOS) present on USS?
Greater than or equal to 12 visible cysts
Ovarian volume greater than 10ml
Ring of pearls
Chocolate cysts are indicative of what?
Endometriosis/Endometrioma. Chocolate cysts are ovarian cysts that present as a result of bleeding into the cyst from ectopic endometrial tissue.
Fibromas (sex cord stromal tumours) are the most common stromal tumour. They often present with Meig’s syndrome. What is Meig’s syndrome?
A triad of:
Benign ovarian tumour
Pleural effusion
Ascites
Ovarian Cysts (teratomas) comprised of mature tissues of different lineages e.g. skin, hair follicles and sweat glands are types of what tumour group?
Dermoid cysts (Benign Germ Cell Tumours).
Cystadenomas (benign epithelial tumours) can be serous, mutinous or papillary. Which of the three are most likely to be bilateral?
Serous cystadenoma.
How do ovarian cysts typically present?
Usually - completely asymptomatic.
Bloating - early satiety and often confused with IBS
Lower abdominal pain
Back pain
Dyspareunia (mass effect)
Urinary frequency
Constipation
Rupture and torsion (Acute severe pain, fever, nausea and vomiting).
Give the structural causes of Heavy Menstrual Bleeding.
PALM COINE - PALM is structural, COINE is non-structural
Polyps
Adenomyosis
Leiomyoma (fibroid)
Malignancy and hyperplasia
Coagulopathy Ovulatory dysfunction Iatrogenic Not yet classified Endometrial
What is the most common coagulopathy to cause heavy menstrual bleeding?
Von Willebrand’s disease.
Suggestions of the history include HMB since menarche, history of post-partum haemorrhage, surgical related bleeding or dental related bleeding, easy bruising, epistaxis, bleeding gums, family history of bleeding disorder.
Also consider an anticoagulant use such as warfarin.
What are the three categories for investigating an ovarian cyst when using the a Risk of Malignancy Index? (RMI)
USS findings (multilocular cyst, solid areas, metastasis, ascites, bilateral lesions - 1 feature = 1pt, 2+ features = 3 points). Ca125 (measured from a blood test giving a value in units/ml). Menopausal status (premenopausal = 1pt, postmenopausal = 3pts).
E.g. a postmenopausal (3pts) patient with a Ca125 of 100 (100 units) and bilateral lesions with solid areas (3pts) identified on USS would score 3x100x3 = 900.
Patients with an RMI greater than 250 should be referred to a specialist gynaecologist.
1st line Investigations for ovarian cyst:
USS (looking for multilocular cysts, solid areas, metastases, ascites and bilateral lesions).
CT
MRI
How would you manage an ovarian cyst in a premenopausal woman?
USS - if nonspecific suspicious - rescan in six weeks, if persistent then recalculate RMI and follow up with booods and biopsy.
If under 40 years, check for markers of germ cell tumours (AFP, Beta HCG, LDH).
If persistent cyst and greater than 5cm, opt for laparoscopic removal.
How would you manage a postmenopausal woman with an ovarian cyst (depends on RMI staging)?
Low RMI - follow up for one year with USS and Ca125
Moderate RMI - bilateral oophorectomy - histology on specimen - if neoplastic, staving scan and surgical removal of uterus and lymphatics.
High RMI - staging laparotomy.
Polycystic ovarian syndrome is characterised by androgen excess and multiple cystic immature follicles in the ovaries, it affects 5-10% of premenopausal women. What are the two key hormonal features of PCOS?
Androgen excess - this is due to excess LH which results from an increase in GnRH pulse frequency. LH stimulates the ovaries (theca cells) to produce androgens which are responsible for the presentation. The high androgens suppress the LH surge and are responsible for anovulation in PCOS
Insulin resistance - this causes hyper insulinaemia. This in turn suppresses the production of sex hormone binding globulin (SHBG) which in turn leads to more unbound androgens.
How does PCOS typically present?
Oligmoenorrhoea/amenorrhoea (primary) Infertility Hirsutism Acne Obesity Depression Acanthosis nigricans Chronic pelvic pain Male pattern baldness Hypertension
What are the three main differential diagnoses for Polycystic ovarian syndrome?
Hypothyroidism - oligomenorrhoea, obesity, insulin resistance and hair loss
Hyperprolactinaemia - oligo/amenorrhoea, acne, hirsutism
Cushing’s - obesity and insulin resistance, acne, depression.
The Rotterdam criteria are used to diagnose PCOS if two of the three criteria are met. What are the three criteria?
Oligo/anovulation
Clinical signs of hyper-androgenism
Cystic changes on ultrasound scan (greater than or equal to 12 cysts or greater than 10ml ovarian volume).
Consider how the following would be affected in PCOS.
(1) testosterone
(2) sex hormone binding globulin
(3) LH
(4) FSH
(5) progesterone
(6) oestrogen
(7) glucose
(8) prolactin
(1) Testerone raised - hyperandrogenism (hair, acne, deeper voice, male pattern baldness etc).
(2) SHBG low - hence more free androgens
(3) LH raised
(4) FSH normal
(5) progesterone usually low
(6) oestrogen usually high
(7) glucose high (insulin resistance)
(8) prolactin - can be slightly high but usually normal
How would you go about managing PCOS?
Consider the following:
(1) Obesity
(2) Hyperglycaemia and insulin resistance
(3) Anovulation
(4) Hirsutism
(5) Menses
(1) Obesity - Seek to achieve a BMI or less than 30 (ideally 17-25).
Consider orlistat.
(2) Insulin resistance - Metformin
(3) Anovulation - Clomiphene citrate induces regular ovulation but can overstimulate the ovaries (OHSS) and increase risk of multiple pregnancies. OHSS presents with enlarged ovaries on USS, abdominal pain, nausea and vomiting, ascites, oliguria, pleural effusion, respiratory distress.
Metformin also helps. It is recommended for women trying to conceive who have a BMI > 25. It improves insulin sensitivity as well as helping with menstrual disturbance and ovulatory function.
Prevention of endometrial hyperplasia - anovulation leaves the endometrium with unopposed oestrogen exposure. There is a need to overcome this by inducing a minimum of three periods a year. This can be done with low dose COCP, or progesterone analogue (dydrogesterone).
(4) Hirsutism - Anti-androgens (cyproterone) as used in CaProstate hormonal therapy. Teratogenic in pregnancy.
(5) Menses - COCP - can be used to provide menstruation and decrease the risk of endometrial cancer, aim for three or more periods a year.
Define primary and secondary dysmenorrhoea.
Dysmenorrhoea (painful periods) is the most common of all gynaecological symptoms. It is generally described as a crappy lower abdominal pain, which starts at the onset of menstruation.
Primary - menstrual pain with no underlying pelvic pathology.
Secondary - menstrual pain that occurs with an associated pelvic pathology.
Explain the pathophysiology behind dysmenorrhoea.
In the absence of fertilisation of the egg, the corpus luteum regresses and there is a subsequent decline in oestrogen and progesterone production. The endometrial cells are sensitive to this decline in progesterone and respond with prostaglandin release. These prostaglandins have two main actions within the uterus.
(1) Spiral artery vasospasm - this leads to ischaemic necrosis and shedding of the superficial layer of the endometrium.
(2) Increased myometrial contractions.
Primary dysmenorrhoea is thought to occur secondary to the excessive release of prostaglandins (PGF2 and PGE2) by endometrial cells.
