Obs and gynae Flashcards
How does endometriosis present?
Infertility
Depends on location:
Pain (often chronic pelvic pain 6 months) - cyclical or constant due to adhesions, severe dysmenorrhoea (can be due to adenomyosis), deep dyspareunia (indicates involvement of uterosacral ligaments), dysuria, dyschezia and cyclic pararectal bleeding, fatigue
-oxford handbook
What causes endometriosis?
The most popular theory is retrograde menstruation with adherence, invasion and growth of the tissue. Metaplasia of endometrial cells, systemic and lymphatic spread, and impaired immunity also contribute.
Most common sites are pelvis.
-oxford handbook
How is endometriosis diagnosed?
Bimanual pelvic exam for adnexal masses (endometriomas) or tenderness
Transvaginal USS - endometriomas, urinary bladder/rectal involvement
Laparoscopy with biopsy - positive is confirmative, negative does not exclude.
How is endometriosis treated?
Pain: COCP, NSAIDs
Fertility: surgical removal or endometriotic lesions.
Give 5 causes of pelvic pain.
Obstetric: Ectopic pregnancy, fibroid red degeneration
Gynae: ovarian cyst accident eg torsion, PID, endometriosis, mittelschmerz, adhesions
GI - appendicitis, hernia strangulation, IBD, IBS
Urological - UTI, renal/bladder calculi
Give 3 risk factors for ectopic pregnancy.
History of PID Prev ectopic IVF Gynae surgery tubal ligation IUD in situ Smoking Age >35 Black race Age <18 at first sexual intercourse
Why is ectopic pregnancy a medical emergency?
Internal bleeding, severe pain and damage to the fallopian tube. The pregnancy pushes against the fallopian tube walls and can rupture. The blood irritates the peritoneum, which can cause referred pain to the shoulder.
What investigations are done when ectopic pregnancy is suspected?
hCG - this doubles every 2 days in uterine pregnancy. Suboptimal rise is suspicious (not diagnostic) of EP. The rate of change is important.
Serum progesterone
Group and save
Rhesus
transvaginal ultrasound to look for uterine pregnancy, adnexal masses or free fluid.
How is ectopic pregnancy managed?
If they are stable, asymptomatic, understand the symptoms and complications, can use expectant and medical management.
Expectant: body sorts it out. Repeat serum hCG 48hourly - should be falling.
Medical: methotrexate 50mg/m2 IM single dose.
Surgical: Laparotomy in haem unstable patients, salpingectomy (remove entire fallopian tube) if contralateral tube normal, salpingotomy if contalateral tube disease.
Anti-D in rhesus negative patients.
Admit if lives far away from hosp.
What are the risk factors for pelvic inflammatory disease?
Young, poor, sexually active, multiple partners unprotected sex, nulliparous. Almost never occurs during viable pregnancy.
What causes pelvic inflammatory disease?
Infection with chlamydia or gonococcus, 40% polymicrobial.
How does PID present?
Chlamydia - asymptomatic, symptoms may be due to secondary infection, or present with subfertility or menstrual problems.
Gonococcus - acute.
Bilat lower abdo pain with deep dyspareunia, vaginal bleeding and discharge.
Peritonism –> bilateral adnexal tenderness, cervical excitation (pain on moving cervix during the exam).
If spread to the liver via the peritoneum, you get Fitz-Hugh-Curtis syndrome, cuases RUQ pain due to adhesions.
How is PID diagnosed?
Clinical diagnosis supported by swabs and blood cultures if fever, raised WCC and CRP.
Pelvic USS excludes abscess or ovarian cyst
Laparoscopy with fimbrial biopsy and culture ‘gold standard’ but not typically performed.
How would you manage PID? What about if the lady has a recently inserted IUS?
Analgesia
Broad spec: IM ceftriaxone (covers gonorrhea), oral doxycycline (covers chlamydia) and metronidazole (covers trichomonas). Dont delay for swabs.
Febrile –> IV therapy.
Review in 24 hours - if not improved, there may be pelvic abscess. Rupture can be life-threatening.
Admit if fever >38 degrees.
Coils:
Leave in a recently inserted coil. If there is no response within 48-72hrs to the antibiotics, remove the coil and prescribe any other necessary emergency contraceptives
What are the non-pathological causes of amenorrhoea?
Primary (never had periods) - alway pathological
Secondary (periods stopped) pregnancy. lactation, menopause, contraceptives (COCP etc)
What are the pathological causes of amenorrhea?
Primary - hypogonadism (either due to hypothalamus/pituitary (hypogonadotropic) or gonads (hypergonadotropic)
Secondary:
- PCOS
- Anorexia nervosa
- Hyperprolactinaemia (usually a pituitary adenoma, 30% have galactorrhea)
- Hypo/hyperthyroidism. Hypo = raised prolactin, amenorrhea
- Cushing’s syndrome
- Premature ovarian insufficiency
- Meds - antidepressants, antipsychotics
How does PCOS present?
Galactorrhea, androgenic sx (eg facial hirsutism, weight gain, acne)
What is Asherman’s syndrome?
Aka iatrogenic intrauterine adhesions, due to excessive curettage at evacuation of retained products of conception (ERPC) procedure following miscarriage or delivery.
What is Turner’s syndrome? Give 3 features.
Absent X chromosome (45XO). short stature, poor secondary sexual characteristics, webbed neck, bicuspid aortic valve.
Normal intelligence.
What are the clinical features of prolactinoma?
Amenorrhoea Galactorrhoea Headache Bitemporal hemianopia Diabetes insipidus --> polydipsia, polyuria.
How is prolactinoma diagnosed?
Imaging using CT/MRI, raised serum prolactin levels.
What can cause hyperprolactinaemia?
Pituitary tumour Hypothalamus or pituitary stalk lesion Normal breastfeeding/pregnancy Hypothyroidism Chronic renal failure Drugs: phenothiazines, metoclopramide, methyldopa.
What is the management of hyperprolactinaemia?
Dopamine receptor agonists (bromocriptine, cabergoline) which reduce prolactin levels. Occasionally, surgery. These need to be stopped in pregnancy. Avoid pregnancy until tumour shrunk, due to risk of enlargement in pregnancy.
What is the most common endocrine disorder in women?
PCOS
What are the diagnostic criteria for PCOS?
Rotterdam criteria:
- exclude other disorders and two out of:
- Cycle >42 days
- Hyperandrogenism - acne, hirsutism, alopecia
- Polycystic ovaries on pelvic USS - >12 antral follicles on one ovary.
- Ovarian volume >10 ml
What causes PCOS?
Hypersecretion of LH in 60%. LH stimulates androgen secretion from thecal cells. Elevated LH:FSH.
Genetics - familial clustering
Insulin resistance with compensatory hyperinsulinaemia - defect on insulin receptor.
Hyperandrogenism - elevated ovarian androgen secretion
Obesity - BMI >30 in 35-60%, central obesity, worsens insulin resistance
How is PCOS managed?
- Lifestyle - even 5% wt loss can improve sx, restore ovulation and improve fertility
- COCP - reduces serum androgen levels by increasing SHBG.
Metformin
depilatory cream for hirsutism, antiandrogens such as finasteride
Need withdrawal bleed every 3-4 months to reduce risk of endometrial hyperplasia and cancer. This is stimulated by regular COCP or medroxyprogesterone.
What is the most common type of malpresentation?
Breech - 3-4% of births. (ox handbook)
How would you diagnose breech presentation?
On examination: Lie is longitudinal Head can be palpated at the fundus Presenting part is not hard Fetal heart is best heard high up in the uterus.
USS confirms diagnosis and should also assess growth and anatomy because of the association with fetal abnormalities.
How would you manage breech presentation?
- Wait - 8% of primiparous breech presentations will revert by 36 weeks.
- After 36 weeks for primiparous/37 for multiparous, use external cephalic version (ECV). Success rate 50%. Absolute Contraindications: C-section indicated, APH, pre-eclampsia, rhesus isoimmunization, oligohydramnios, fetal compromise (so basically ECV is everything is otherwise fine)
- Anti-D if Rh -ve.
- Vaginal birth indicated if no fetal compromise, EFW <4kg, spontaneous onset of labour, extended breech, non-extended neck.
- Elective CS if any of the above.
What is the most favourable position for vaginal delivery?
Occipito-anterior: cephalic, longitudinal, limbs and head flexed. 95% of births.
Occiput means the BACK of the baby’s head so occipito-anterior is face-down.
What causes malpresentations? Give 3 risk factors.
Maternal: Multiparous (lax uterus), uterine abnormalities eg fibroids, tumour/mass
Fetal: Fetal abnormality, multiple pregnancy, preterm labour (not enough time to turn)
Placental: placenta praevia, polyhydramnios
What are the risk factors for endometrial cancer?
Postmenopausal
high estrogen to progesterone ratio - pregnancy and COCP are protective.
Unopposed estrogen (ie, no protective effect of progesterone). This can be endogenous (eg obesity causes peripheral conversion in adipose tissue of androgens to estrogens, nulliparity) or exogenous (eg tamoxifen)
Ox handbook
Which is the most common cancer of the genital tract?
Endometrial carcinoma. Prevalence is highest around 60 years of age. (Impey)
What is the most common histological type of endometrial carcinoma and what is the prognosis like?
> 90% are adenocarcinomas of columnar endometrial gland cells. Prognosis same as ovarian cancer but usually presents early so often wrongly thought as benign. Prognosis is poorer for the rarer histology type, adenosquamous carcinoma (<10% of cases) (Impey)
What are the stages of endometrial carcinoma?
- Myometrial invasion in uterus (1A= <1/2, 1B= >1/2 myometrium invaded)
- Cervical stromal invasion
- Uterus invasion (3A=adnexae, 3B=vaginal, 3Ci=pelvic nodes, 3Cb = para-aortic)
- Spread outside uterus (4A= bowel/bladder, 4B = distant mets)
(Impey and child)
How is endometrial carcinoma treated?
Chemotherapy: Carboplatin +/- paclitaxel or Doxorubicin + cisplatin (Ox handbook)
What is the prognosis like for breast cancer? Does pregnancy have an effect?
Poorer in young women. Pregnancy itself has no effect on prognosis.
How is breast cancer in a pregnant woman managed?
Chemotherapy safe after 1st trimester (12 weeks)
Tamoxifen and trastuzumab are contraindicated in pregnancy
Radiotherapy contraindicated unless life-saving.
Which genes are associated with breast cancer?
BRCA1 and 2 (also in ovarian cancer), TP53, ERBB2 aka HER2.
How is breast cancer treated?
It depends on the type.
ER+ve, HER2-ve =most common.
Selective ER modulator eg tamoxifen/fulvestrant.. If postmenopausal, use aromatase inhibitor eg anastrozole.
What are the signs of malignant breast lumps?
Hard, painless lump, commonly upper outer quadrant., may have axillary lymph node involvement, dimpling
What is Paget’s disease of the breast?
An infiltrating carcinoma of the nipple epithelium which represents about 1% of breast cancers. (Patient.info)
How does Paget’s disease of the breast most commonly present?
Chronic eczematous change of one nipple: Itching, erythema, scales, erosions, nipple discharge including bleeding. Underlying lump usually indicates invasive nature.
What is the pathophysiology of Paget’s disease?
Malignant cells infiltrate into the epidermis via the mammary duct epithelium. The cells proliferate leading to thickening of the affected skin.
[patient.info]
How is Paget’s disease managed?
Usually mastectomy, although recent reports suggest excision may be just as good.
Which forms of breast cancer are associated with Paget’s disease?
Higher histo grade, estrogen receptor -ve, progesterone receptor negative breast cancers.
What is the most common type of breast lump?
Fibroadenoma (benign). [patient.info]
What is a fibroadenoma?
Benign tumour common in women age 20-24. They arise in breast lobules and are composed of fibrous and epithelial tissue. HRT increases incidence.
How does a fibroadenoma present?
Firm, non-tender, highly mobile palpable lump.
How would you manage fibroadenoma?
It is an unexplained lump so refer to breast clinic for triple assessment.
Surgical excision may be done if the lump is large or cancer is not excluded. Complex and multiple fibroadenomas are asso with increased risk of breast cancer.
What is ‘triple assessment’ in breast clinic?
Examination
Imaging (USS <40, mammography >40)
Core needle biopsy
What is an abscess?
A collection of pus. Pus is a thick, yellow/green, smelly fluid that contains WBCs, dead tissue and bacteria. .
What can cause a breast abscess?
Mastitis (infection of the breast) can develop into an abscess. It is usually associated with lactation (puerperal mastitis). Breast ducts become blocked with milk, and bacteria (usually staph aureus) enter from cracks in the nipple.
How can you differentiate an abscess from other breast lumps?
There is inflammation, so the area is red, tender, and warm, and the cyst will be soft and filled with fluid.
How is puerperal mastitis managed?
First-line is reassurance, increase milk removal, and analgesia.
If no improvement after 24 hours, use penicillinase-resistant abx - flucloxacillin/erythromycin.
What is placental abruption?
Separation of part or all of the placenta from the uterine wall before delivery. This causes bleeding, further distress and separation.
Why does placental abruption occur?
The arteries of the decidua basalis degenerate which attach the placenta to the uterine wall. Risk factors: previous abruption, IUGR, pre-eclampsia, smoking, autoimmune disease, multiple pregnancy, high parity and age. Cocaine/amphetamines –> vasoconstriction –> high blood pressure, arterial rupture.
What are the complications of placental abruption?
Acute fetal distress, causing fetal death in 30%.
Maternal death rarely occurs, due to transfusion, DIC and renal failure
How does placental abruption usually present?
Acute onset severe abdo pain, constant with exacerbations. Often dark blood (revealed) but in 20% there is no bleeding (concealed)
Bleeding amount does not correlate to abruption severity.
Shock: tachycardia, hypotension in late stage.
Uterine contractions, may be in labour, tender, late stage: woody and hard.
Fetal heart tones abnormal/absent
How is placental abruption managed?
Admit (all women with unexplained bleed/pain), CTG, USS, IV access, bloods (FBC, u+e, crossmatch, coag screen).
Then if no fetal distress, bleeding and pain stop, can consider delivery by term
If fetal distress/maternal compromise, resuscitate and deliver.
What are the 4 conditions needed for pregnancy to occur?
Ovulation Sperm release Sperm reach egg Blastocyst implantation (impey+child)
Give 3 causes of subfertility in a woman.
Ovarian - PCOS, POF
Hypothalamic - hypothalamic hypogonadism, Kallmann’s syndrome - no GnRH-secreting neurones
Pituitary - hyperprolactinaemia.
Endometriosis (implantation problem)
Tubal damage causing fertilisation problem
Chlamydia - 12% will be infertile after having it once
Low/high BMI, smoking
How is ovulation best detected?
Regular cycles, discharge, pelvic pain are suggestive of ovulation. This is confirmed by high serum progesterone, ultrasound. Over-the-counter urine LH kits can also be used.
What are the causes of male factor subfertility?
Drugs Varicocoele Antisperm antibodies Infection eg epididymitis Klinefelter's syndrome - 47XXY karyotype Smoking Insufficient local cooling Cystic fibrosis
What is clomifene used for and how does it work?
Induce ovulation in someone with PCOS as a fertility treatment. Anti-estrogen, works by blocking estrogen receptors in the hypothalamus and pituitary. Given AFTER lifestyle advice eg losing wt.
(Impey)
What is azoospermia?
No sperm in ejaculate. Usually managed with surgical IVF and intra cytoplasmic sperm injection (ICSI).
What hormone is elevated in testicular failure?
FSH
What initial investigations would you do for oligo/azoospermia?
CF screen: Check for congenital bilateral absence of the vas deference (CBAVD), due to CFTR mutation.
47XXY karyotype
hormone profile: FSH is elevated in testicular failure
How would you manage oligo/azoospermia?
Treat underlying conditions
Address lifestyle issues - alcohol, smoking
Review meds - antispermatogenic eg anabolic steroids, antiandrogenic (cimetidine, spironolactone), erectile/ejaculatory (a/b-blockers, antidepressants)
Give an example of an antispermatogenic substance.
Alcohol
Anabolic steroids
Sulfasalazine
Why might a man with heart failure have subfertility?
They may be on spironolactone which is anti-androgenic.
Give 3 drugs which can cause ejaculatory/erectile dysfunction.
Antidepressants eg sertraline
alpha or beta blockers
diuretics
metoclopramide (antiemetic)
How would you manage subfertility in a man with a varicocoele?
Surgery is not indicated as it does not improve pregnancy rates. Use other management.
What is Kallmann’s syndrome?
Failure of the GnRH-secreting neurones to develop, causing hypogonadism.
What is IVF and what are the indications?
External (in vitro) fertilisation of the sperm and oocyte. Tubal disease, male factor subfertility, endometriosis, anovulation, unexplained
What is IUI and when is it done?
Intrauterine insemination. Mild male factor subfertility, same-sex, unexplained, coital difficulties.
What is ICSI and when is it done?
Intracytoplasmic sperm injection. Men with severely abnormal semen parameters.
What are the side-effects of induction of ovulation?
Risk of multiple pregnancy with gonadotrophins (FSH/LH) and clomifene, but not with metformin.
What causes functional cysts?
Follicular cysts are persistently enlarged follicles, lutein cysts are enlarged corpora lutea. In pregnancy, the CL continues to secrete progesterone, which inhibits LH. If there is no fertilisation, the CL should dissolve to become the corpus albicans. If the follicle fails to rupture (follicular) or ruptures but closes again (lutein) the CL does not dissolve so continues to make LH.
How do ovarian masses generally present?
They usually don’t cause symptoms until there is an ‘ovarian accident’ like haemorrhage, rupture or torsion or they are detected on a scan.
What could cause intense acute pain in someone with an ovarian cyst?
Ovarian torsion - this could cause infarction to the ovary +/- tube, needs urgent surgery and ‘detorsion’ (untwisting).
Rupture - particularly with endometrioma or dermoid cyst
Haemorrhage - if into peritoneal cavity could cause hypovolaemic shock
How are primary ovarian tumours classified?
Not strictly split into benign vs malignancy because benign primary cysts can become malignant
a) epithelial:
- serous or mucinous cystadenoma (benign)
- serous or mucinous adenocarcinoma (malignant)
- Endometrioid carcinoma (malignant)
- Clear cell carcinoma (malignant)
b) Germ cell:
- Teratoma/dermoid cyst (benign, common)
- Dysgerminoma (malignant, rare/young women)
c) sex cord tumours:
- granulosa cell tumours (malignant but slow-growing)
- thecoma (benign)
- fibroma (benign)
What is meant by ‘borderline malignancy’?
Unique to ovarian epithelial tumours, malignant histological features are evident but invasion is not. Surgery is advised but controversial.
[Impey]
Which type of ovarian tumour is most common in postmenopausal women?
Epithelial.
What is the most common malignant ovarian neoplasm?
Serous adenocarcinoma (50% of malignancies). Mucinous are less likely to be malignant (10%) but can become very large.
What is a clear cell carcinoma?
Malignant ovarian epithelial tumour, accounts for <10% of ovarian malignancies, poor prognosis.
Which kind of ovarian tumour secretes oestrogen and inhibin?
Granulosa cell tumours, a type of sex cord tumour. Post-menopausal women. Serum inhibin is used as a marker for recurrence. Usually malignant but slow-growing.
What is Meig’s syndrome?
Rare syndrome associated with fibroma, where you get ascites and (usually) right pleural effusion with small ovarian mass (fibroma). The effusion is benign and cured by removal of the mass.
[Impey]
Which two cancers have a particularly high risk of mets to the ovary?
breast
GI tract
What is a chocolate cyst?
Accumulation of old blood in endometrioma.
Which type of cysts are more likely in pre-menopausal women?
Functional cysts (follicular/lutein) only in pre-menopausal because they are enlarged follicles/corpora lutea. Also dermoid cysts and endometriomas are more likely in pre-menopausal women.
How are functional cysts treated?
OCP inhibits ovulation so reduces risk
lutein cysts tend to cause more symptoms
If no symptoms, no treatment. However, malignancy is excluded by doing Ca125 if tumour persists beyond 2 months and is >5cm. Laparoscopy may be done to remove or drain the cyst.
Who is screened by the NHS breast screening programme?
High risk women eg those with BRCA
All women over 50.
What is ductal carcinoma in situ?
A pre-malignant change.
‘DCIS means that some cells in the lining of the ducts of the breast tissue have started to turn [cancerous] These cells are all contained inside the ducts.’
Cancer research UK.
What causes urinary incontinence?
- URGE incontinence: overactivity of detrusor muscle
- Stress incontinence: Weakness of pelvic floor and sphincter muscles causing LEAKS when coughing, laughing etc. Women
- Mixed - address whichever is having the more significant impact first.
- Overflow incontinence: have they been in retention? Males, anticholinergics, tumours, MS, DM, spinal cord injuries.
[Z2F]
What investigations would you do for urinary incontinence?
Bladder diary over at least 3 days
Urine dipstick
Post void residual bladder volume bladder scan - to assess for incomplete emptying
Urodynamic testing if not responding to treatment.
How is stress incontinence managed?
- Avoid caffeine, diuretics, overhydration and dehydration, wt loss if appropriate
- Supervised pelvic floor exercises 3 months
- Surgery or Duloxetine (SNRI).
How is urge incontinence managed?
- Bladder retraining
- Anticholinergic - oxybutynin, solifenacin, tolterodine
- Mirabegron (b-3 agonist - increases BP)
- Invasive procedures eg botox, nerve stimulation, urinary diversion, bladder enlargement.
What is uterine prolapse?
A type of prolapse where the uterus descends into the vagina. Prolapse is due to weakness of pelvic ligaments and muscles.
What is vault prolapse?
Top of the vagina is called the vault. this descends into the vagina in women with no uterus (hysterectomy).
What is a rectocele?
Defect in POSTERIOR vaginal wall allowing RECTUM to prolapse forwards into vagina. Constipation, urinary retention, palpable lump in vagina that some women have to push back in order to open their bowels.
What is a cystocele?
Defect in the ANTERIOR vaginal wall allowing BLADDER to prolapse backwards into the vagina. Urethra prolapse = urethrocele. Both = cystourethrocele.
How would you investigate a pelvic organ prolapse?
Empty bladder and bowels.
Dorsal and left lateral position
Sims speculum (the U shaped one) - anterior wall, posterior wall.
Uterine prolapse: POP-Q grading 0-4
How is pelvic organ prolapse managed?
- Conservative - physio (pelvic floor exercises), wt loss, lifestyle changes for stress incontinence, vaginal oestrogen cream
- Vaginal pessary - ring, shelf, gellhorn. with estrogen cream to protect vaginal walls from irritation. change every 4 months.
- Surgery
What is a fistula?
Abnormal connection between the urinary tract and other organs.
Urethro-vaginal,
Vesico(Bladder)-vaginal,
Vesico-uterine,
Uretero-vaginal.
Occur due to obstructed labour, surgery, radiotherapy or malignancy.
What investigation would you do in a woman presenting with urinary incontinence, labial swelling and urine coming form the vagina?
This could be urethral injury eg urethrovaginal fistula. CT urogram or cystoscopy.
[OH]
What are fibroids and how are they classified?
Common, benign tumours of the smooth muscle of the uterus, aka uterine leiomyomas. Estrogen-sensitive so they grow in response to estrogen.
- Intramural: within the myometrium –> distort shape
- Subserosal - outer layer of uterus, fill abdo cavity
- Submucosal - inner lining of uterus
- Pedunculated - on a little stalk so could be intra- or extra-uterine.
How would fibroids present and what are 3 risk factors to look for in the history?
Asymptomatic, HMB, long heavy painful periods, bloating, reduced fertility. Abdo/bimanual exam - mass or enlarged firm non-tender uterus.
Black women
Later reproductive years
What imaging is used to diagnose fibroids?
- Hysteroscopy for submucosal fibroids presenting with HMB.
- Pelvic USS for larger fibroids
(MRI before surgery to determine size, shape and blood supply)
How are fibroids managed?
- < 3 cm - medical management as for HMB. IUS (Mirena). symptomatic - NSAIDs, tranexamic acid, COC, cyclical oral progesterones
- Surgery - endometrial ablation, resection of submucosal fibroids during hysteroscopy, hysterectomy.
>3cm: as above (1) and refer to gynae.
GnRH agonists to reduce size before surgery.
Rx for HMB is different to rx for infertility. If treating for infertility, myomectomy is the only effective rx.
What are the important complications of fibroids?
Red degeneration Torsion, especially with pedunculated fibroids. Malignant change (rare) HMB - iron def anaemia reduced fertility pregnancy complications, prem labour, miscarriage Constipation urinary outflow obstruction, UTIs
A woman is 24 weeks pregnant presenting with severe abdominal pain and low grade fever, tachycardia and vomiting. She was treated for fibroids in the past. What could be the diagnosis?
Red degeneration of the fibroid: ischemia, infarction and necrosis due to disrupted blood supply. In larger fibroids, 2nd and 3rd trimester of pregnancy. It enlarged during pregnancy, outgrowing its blood supply and becoming ischemic.
Rx: rest, fluids, analgesia.
Exclude torsion.
[Z to F]
What can cause vulval itching and shiny white patches on the labia, perinium and perianal area in a 50 year old woman?
Lichen sclerosis. This is due to chronic autoimmune inflammation. Associated with other autoimmune disease - T1DM, alopecia, hypothyroid and vitiligo.
Dx clinical but can do vulval biopsy to confirm.
What is the difference between lichen sclerosis, lichen simplex and lichen planus?
Lichen sclerosis = autoiummune disease causing white shiny skin patches especially on the genitals.
Lichen simplex = inflammation and irritation caused by scratching and rubbing the skin, causing plaques, scaling and thickened skin.
Lichen planus = autoimmune condition causing shiny, purplish flat-topped raised areas with white lines across the surface.
How is lichen sclerosis managed?
Potent topical steroids eg clobetasol propionate 0.05% (dermovate). Reduce risk of malignancy and symptoms.
Start daily then gradually reduce to twice weekly, titrate up again in flares.
+ Emollients.
What are the important complications of lichen sclerosis?
5% risk of developing squamous cell carcinoma of the vulva.
Pain, discomfort, sexual dysfunction, bleeding, narrowing of the vaginal or urethral openings.
How is cervical cancer prevented?
Screening - majority diagnosed at stage 1, 90% survival.
Vaccination against HPV high risk strains.
How is cervical cancer staged and treated?
FIGO I-IV.
Ia: LLETx/loop diathermy.
Ib: hysterectomy. consider age, fertility wishes, woman’s choice.
II+ - radio, chemo, palliative.
Why is it important to examine older women with UTI not responding to treatment?
Examine the vulva/vagina for lichen sclerosis which may have progressed to vulval cancer. Ladies may not examine self esp if older.
How is vulval cancer treated?
Surgery
Radiotherapy +/- chemo
What is the pathology of vulval cancer?
90% squamous cell carcinoma.
<10% malignant melanoma.
Rare. RFs: older age, immunosuppression, HPV, lichen sclerosus.
What investigations would you do in a 55 year old woman presenting with bloating, abdominal pain, and change in bowel habit?
Could be IBS but also could be ovarian cancer. Do Ca125, pelvic USS, ask about menopause. Risk of malignancy index (RMI): Menopausal status USS findings Ca125.
Give 3 risk factors for ovarian cancer.
More ovulation = higher risk. OLD NUNS would be at high risk.
Age, early menarche, late menopause, nulliparous, non breastfeeding, no contraception used, hysterectomy, clomifene excessive use, smoking.
How is ovarian cancer treated?
Surgery - if fit, may lead to permanent stoma. Late presentation - poor prognosis.
What is the aetiopathology of cervical cancer?
80% squamous cell carcinoma
<20% Adenocarcinoma
HPV 16 and 18.
Tumour suppressor genes: P53, pRb. HPV produces E6 and E7 which INHIBIT P52 and pRb respectively.
Ask about smears, number of sexual partners, FHx, smoking.
How is cervical cancer diagnosed?
Screening
but if someone presents with symptoms that you suspect could be cancer, do urgent colposcopy referral, NOT unscheduled smear/using the last smear.
What in cervical intraepithelial neoplasia (CIN)? What do each of the grades mean?
Grading system for dsyplasia (premalignant change) in cells of the cervix, diagnosed at colposcopy (not smear).
CIN I: mild dysplasia
CIN II: moderate dysplasia
CIN III: cervical carcinoma in situ. May still spontaneously return to normal, can recur after treatment, and can be associated with areas of CIN I in the same patient.
