Gynae fifth yr Flashcards
1
Q
What is adenomyosis?
A
refers to endometrial tissue inside the myometrium (muscle layer of the uterus)
more common in later reproductive years and with multiparity
can occur alone, or alongside endometriosis and fibroids
cause not fully understood - multiple factors involved - sex hormones, trauma, inflammation
Sx tend to resolve after menopause
2
Q
Features of adenomyosis?
A
Painful periods (dysmenorrhoea)
Heavy periods (menorrhagia)
Pain during intercourse (dyspareunia)
Enlarged, boggy uterus
Can also present with infertility or pregnancy-related complications. Also asymptomatic
O/E - enlarged, tender uterus - softer than uterus with fibroids
3
Q
Dx of adenomyosis?
A
TVUS
MRI and TAUS are alternatives
Histological examination after hysterectomy is gold standard
4
Q
Tx of adenomyosis?
A
Depends on Sx, age and plans for pregnancy
NICE recommend the same treatment for adenomyosis as for heavy menstrual bleeding.
No contraception - symptomatic relief during menstruation - tranexamic acid if no pain, or mefanamic acid if associated pain
If contraception wanted: IUS, COCP, cyclical oral progestogens
Other options - GnRH analogues, endometrial ablation, uterine artery embolisation, hysterectomy
Pregnancy and adenomyosis - associated w/ infertility, miscarriage, preterm birth, SGA, PPROM, malpresentation, need for C-section, PPH
5
Q
What is pelvic organ prolapse?
A
refers to the descent of pelvic organs into the vagina.
Prolapse is the result of weakness and lengthening of the ligaments and muscles surrounding the uterus, rectum and bladder.
6
Q
Types of prolapse?
A
Uterine prolapse is where the uterus itself descends into the vagina.
Vault prolapse occurs in women that have had a hysterectomy, and no longer have a uterus. The top of the vagina (the vault) descends into the vagina.
Rectoceles are caused by a defect in the posterior vaginal wall, allowing the rectum to prolapse forwards into the vagina. Associated w/ constipation, and can develop faecal loading, urinary retention and palpable lump in vagina.
Cystocele - caused by a defect in the anterior vaginal wall, allowing the bladder to prolapse backwards into the vagina
7
Q
Risk factors for prolapse?
A
the result of weak and stretched muscles and ligaments
Multiple vaginal deliveries
Instrumental, prolonged or traumatic delivery
Advanced age and postmenopause status
Obesity
Chronic respiratory disease causing coughing
Chronic constipation causing straining
8
Q
Features of uterine prolapse?
A
Sx:
A feeling of “something coming down” in the vagina
A dragging or heavy sensation in the pelvis
Urinary symptoms, such as incontinence, urgency, frequency, weak stream and retention
Bowel symptoms, such as constipation, incontinence and urgency
Sexual dysfunction, such as pain, altered sensation and reduced enjoyment
Lump or mass in vagina
O/E:
Ideally empty bladder and bowel before examination of a prolapse
Left lateral position w/ Sims speculum
9
Q
What are grades of uterine prolapse?
A
pelvic organ prolapse quantification (POP-Q) system:
Grade 0: Normal
Grade 1: The lowest part is more than 1cm above the introitus
Grade 2: The lowest part is within 1cm of the introitus (above or below)
Grade 3: The lowest part is more than 1cm below the introitus, but not fully descended
Grade 4: Full descent with eversion of the vagina
A prolapse extending beyond the introitus can be referred to as uterine procidentia.
10
Q
Management of uterine prolapse?
A
Conservative management - pelvic floor exercises, WL, lifestyle changes (for associated stress incontinence - reduce caffeine and incontinence pads), Tx of related Sx (anticholinergic meds), vaginal oestrogen cream
Vaginal pessary - provide extra support to pelvic organs - ring, shelf, donut, hodge - changed periodically - can cause vaginal irritation and erosion over time - can use oestrogen cream to protect vaginal walls
Surgery - definitive option - many methods including hysterectomy, complications include pain, bleeding, infection, DVT, risk of anaesthetic, damage to bladder or bowel, recurrence of prolapse, altered experience of sex
mesh repairs should be avoided due to chronic pain, altered sensation, dyspareunia, abnormal bleeding, urinary/bowel problems
11
Q
What is ovarian torsion?
A
defined as the partial or complete torsion of the ovary on it’s supporting ligaments that may in turn compromise the blood supply. Hence necrosis can occur and function of ovary lost - therefore emergency
If the fallopian tube is also involved then it is referred to as adnexal torsion.
If necrotic - infected - abscess - sepsis, or rupture - peritonitis - adhesions
12
Q
RFs for ovarian torsion?
A
ovarian mass: present in around 90% of cases of torsion
being of a reproductive age
pregnancy
ovarian hyperstimulation syndrome
younger girls before menarche and have longer infundibulopelvic ligaments that twist more easily
13
Q
Features of ovarian torsion?
A
Usually the sudden onset of deep-seated colicky abdominal pain.
Associated with vomiting and distress
Fever may be seen in a minority (possibly secondary to adnexal necrosis)
Can twist and untwist intermittently - pain that comes and goes
Vaginal examination may reveal adnexial tenderness and palpable mass
14
Q
Ix and Tx for ovarian torsion?
A
Ultrasound may show free fluid or a whirlpool sign. Doppler show lack of blood flow
Laparoscopy is usually both diagnostic and therapeutic. Detorsion and potentially oophorectomy depending on visual inspection.
15
Q
What is cervical ectropion?
A
Cervical ectropion occurs when the columnar epithelium of the endocervix (the canal of the cervix) has extended out to the ectocervix (the outer area of the cervix).
Cells of endocervix are more fragile and prone to trauma - post coital bleeding
Associated with higher oestrogen levels - common in young women, COCP, pregnancy
16
Q
Features of cervical ectropion?
A
asymptomatic - found incidentally during speculum examination
increased vaginal discharge, vaginal bleeding or dyspareunia
postcoital bleeding
O/E
well-demarcated border between the redder, velvety columnar epithelium extending from the os (opening), and the pale pink squamous epithelium of the ectocervix. This border is the transformation zone.
17
Q
Management of cervical ectropion?
A
Asymptomatic ectropion require no treatment - typically resolve as patient gets older
Not a contraindication to COCP
If problematic bleeding - Cauterisation using silver nitrate or cold coagulation during colposcopy
18
Q
What is an ectopic pregnancy?
A
Implantation of a fertilized ovum outside the uterus results in an ectopic pregnancy
most in ampulla but more dangerous if in isthmus
19
Q
Features of ectopic pregnancy?
A
history of 6-8 weeks amenorrhoea who presents with lower abdominal pain and later develops vaginal bleeding
lower abdo pain - due to tubal spasm, constant, unilateral
vaginal bleeding - less than normal period, dark brown in colour
history of recent amenorrhoea - if longer than 10wks could suggest inevitable abortion
peritoneal bleeding - shoulder tip pain, pain on defeactation/urination
dizziness, fainting, syncope
Sx of pregnancy report
O/E - abdominal tenderness, CMT, adnexal mass (not recommended as can rupture)
serum bHCG >1500 points towards diagnosis
20
Q
Epidemiology and RFs for ectopic pregnancy?
A
Incidence = 0.5% of all pregnancies
RF’s - anything slowing the ovum’s passage to the uterus:
damage to tubes (PID, surgery)
previous ectopic
endometriosis
IUCD
POP
IVF
21
Q
Investigation and management of ectopic pregnancy?
A
Stable - EPAU, unstable - ED
Positive pregnancy test
Investigation of choice - TVUS - may see gestational sac containing yolk sac or fetal pole - empty gestational sac (blob, bagel, tubal ring sign), mass looks similar to corpus luteum but won’t move with the ovary
Beta hCG - A rise of more than 63% after 48 hours is likely to indicate an intrauterine pregnancy. A rise of less than 63% after 48 hours may indicate an ectopic pregnancy. A fall of more than 50% indicates miscarriage
Expectant - size <35mm, unruptured, asymptomatic, no fetal heartbeat, hCG <1000, compatible if another intrauterine pregnancy - involves expectant management over 48 hours, if bHCG rises or symptoms manifest then intervention if performed
Medical - size <35mm, unruptured, no significant pain, no fetal heartbeat, hCG <1500, not suitable if intrauterine pregnancy - involves methotrexate, pt need to be willing to attend follow up, can’t get pregnant for 3 months following treatment
Surgical - size >35mm, can be ruptured, pain, visible fetal heartbeat, hCG >5000, compatible with another intrauterine pregnancy - involves salpingectomy or salpingostomy
Anti-rhesus D prophylaxis is given to rhesus negative women having surgical management of ectopic pregnancy.
22
Q
What is a hydatidiform mole?
A
type of tumour that grows like a pregnancy inside the uterus. This is called a molar pregnancy. There are two types of molar pregnancy: a complete mole and a partial mole.
Complete - two sperm cells fertilise ovum that contains no genetic material. sperm then combine genetic material, and the cells start to divide and grow into a tumour called a complete mole. No fetal material will form.
Partial - two sperm cells fertilise a normal ovum (containing genetic material) at the same time. The new cell now has three sets of chromosomes (it is a haploid cell). The cell divides and multiplies into a tumour called a partial mole. In a partial mole, some fetal material may form.
23
Q
Features of molar pregnancy?
A
Behaves like normal pregnancy
More severe morning sickness
Vaginal bleeding
Increased enlargement of the uterus
Abnormally high hCG
Thyrotoxicosis (hCG can mimic TSH and stimulate the thyroid to produce excess T3 and T4)
USS - snowstorm appearance
Confirmed Dx with histology of mole after evacuation
24
Q
Tx of molar pregnancy?
A
evacuation of the uterus to remove the mole
Then send for histological examination
Patients should be referred to the gestational trophoblastic disease centre for management and follow up
hCG monitored until returns to normal
Can metastasise and pt may require systemic chemotherapy
25
Causes of delayed puberty?
With short stature:
Turners, Prader-Willi, Noonans
Normal stature:
PCOS, androgen insensitivity, Kallmans, Klinefelters
26
Summary of androgen insensitivity syndrome?
X-linked recessive condition. End-organ resistance to testosterone, causing genotypically male children (46XY) to have a female phenotype
Patients have testes in the abdomen or inguinal canal, and absence of a uterus, upper vagina, cervix, fallopian tubes and ovaries. The female internal organs do not develop because the testes produce anti-Müllerian hormone, which prevents males from developing an upper vagina, uterus, cervix and Fallopian tubes
Features of complete - primary amenorrhoea, little or no axillary and pubic hair, undescended testes causing groin swellings, breast development may occur as a result of the conversion of testosterone to estradiol
Partial - partial response to androgens. This presents with more ambiguous signs and symptoms, such as a micropenis or clitoromegaly, bifid scrotum, hypospadias and diminished male characteristics.
Dx - buccal smear or chromosomal analysis to reveal 46XY genotype, after puberty, testosterone concentrations are in the high-normal to slightly elevated reference range for postpubertal boys. High LH, normal/raised FSH, normal or raised testosterone (for male), raised oestrogen (for male)
Tx - counselling, raise child as female, bilateral orchidectomy (increased risk of testicular cancer due to undescended testes), oestrogen therapy, vaginal dilators
27
Grading system for colposcopy results?
grading system for the level of dysplasia (premalignant change) in the cells of the cervix. CIN is diagnosed at colposcopy (not with cervical screening). The grades are:
CIN I: mild dysplasia, affecting 1/3 the thickness of the epithelial layer, likely to return to normal without treatment
CIN II: moderate dysplasia, affecting 2/3 the thickness of the epithelial layer, likely to progress to cancer if untreated
CIN III: severe dysplasia, very likely to progress to cancer if untreated
CIN III is sometimes called cervical carcinoma in situ.
28
Summary of cervical cancer?
3rd most common tumour of lower female genital tract
Most arise in transformation zone
Commonly associated with HPV - high risk 16, 18, 33
2 types - squamous, adenocarcinoma
Cervical intraepithelial neoplasia - premalignant condition of cervix
29
Features of cervical cancer?
Asymptomatic – may be detected on smear
Blood-stained offensive discharge
Abnormal bleeding (intermenstrual, postmenopausal)
Post-coital bleeding
Pelvic pain/dyspareunia
Mucoid, or purulent vaginal discharge
Rarely, if advanced cancer, may present with pelvic discomfort/pain, renal failure, leakage of urine or faeces from a fistula, lymphoedema, or severe haemorrhage
O/E - cervix inflamed or friable, bleed on contact, visible ulcerating or fungating lesion, foul-smelling serosanguineous vaginal discharge.
30
Ix of cervical cancer?
Colposcopy
Large loop excision of the transformation zone
Needle excision of the transformation zone (NETZ)
Cone biopsy
Staging scans
31
Staging of gynaecological cancer?
FIGO Staging
E.g.,
Stage 1: Confined to the cervix
Stage 2: Invades the uterus or upper 2/3 of the vagina
Stage 3: Invades the pelvic wall or lower 1/3 of the vagina
Stage 4: Invades the bladder, rectum or beyond the pelvis
32
Management of cervical cancer?
Cervical intraepithelial neoplasia and early-stage 1A: LLETZ or cone biopsy (The surgeon removes a cone-shaped piece of the cervix using a scalpel)
Stage 1B – 2A: Radical hysterectomy and removal of local lymph nodes with chemotherapy and radiotherapy
Stage 2B – 4A: Chemotherapy and radiotherapy
Stage 4B: Management may involve a combination of surgery, radiotherapy, chemotherapy and palliative care
The 5-year survival drops significantly with more advanced cervical cancer, from around 98% with stage 1A to around 15% with stage 4.
Pelvic exenteration - removing most or all of the pelvic organs, including the vagina, cervix, uterus, fallopian tubes, ovaries, bladder and rectum.
Bevacizumab - Monoclonal antibody that may be used in combination with other chemotherapies in the treatment of metastatic or recurrent cervical cancer.
33
Summary of endometrial cancer?
Usually, good prognosis due to early detection
The 5-year survival is close to 80%.
Cancer of endometrium of the uterus
80% are adenocarcinoma
Oestrogen-dependent
34
Summary of endometrial hyperplasia?
Precancerous condition involving thickening of the endometrium.
Risk factors, presentation and investigations of endometrial hyperplasia are similar to endometrial cancer.
Most cases of endometrial hyperplasia will return to normal over time. Less than 5% go on to become endometrial cancer. There are two types of endometrial hyperplasia to be aware of:
Hyperplasia without atypia
Atypical hyperplasia
Endometrial hyperplasia may be treated by a specialist using progestogens, with either:
Intrauterine system (e.g. Mirena coil)
Continuous oral progestogens (e.g. medroxyprogesterone or levonorgestrel)
35
Features of endometrial cancer?
Post menopausal bleeding (slight and intermittent initially, then heavier) - Also seen in cervical and ovarian cancer
Premenopausal women may have intermenstrual bleeding
Pain is an indicator of extensive disease
Vaginal discharge unusual
Haematuria
Anaemia
Raised platelet count
36
RF's for endometrial cancer?
Unopposed Oestrogen:
^ age
Obesity - adipose tissue (fat) is a source of oestrogen. contains aromatase. unopposed in women that are not ovulating (e.g. PCOS or postmenopause), because there is no corpus luteum to produce progesterone.
Nulliparity
Early menarche
Late menopause
Tamoxifen - anti-oestrogenic effect on breast tissue, but an oestrogenic effect on the endometrium
Polycystic ovarian syndrome - lack of ovulation, no corpus luteum that produces progesterone, and no providing endometrial protection during the luteal phase of the menstrual cycle. Plus insulin resistance
The addition of a progestogen to oestrogen reduces EC risk (e.g. In HRT + PCOS Tx) > IUS, cyclical progestogens
Diabetes mellitus - increased production of insulin stimulate the endometrial cells
Hereditary non-polyposis colorectal carcinoma (Lynch syndrome)
37
Protective factors for endometrial cancer?
Smoking
Due to anti-oestrogenic effect
Oestrogen may be metabolised differently in smokers
Smokers tend to be leaner, meaning they have less adipose tissue and aromatase enzyme
Smoking destroys oocytes (eggs), resulting in an earlier menopause
Increased pregnancies
Less time with unopposed oestrogen
Additional progestogens
COCP
Mirena coil
38
Ix for endometrial cancer?
The referral criteria for a 2-week-wait urgent cancer referral for endometrial cancer is:
Postmenopausal bleeding (more than 12 months after the last menstrual period)
NICE also recommends referral for a transvaginal ultrasound in women over 55 years with:
Unexplained vaginal discharge
Visible haematuria plus raised platelets, anaemia or elevated glucose levels
First-line - TVUS (<4mm has high negative predictive value), pipette biopsy, hysteroscopy with endometrial biopsy
39
Management of endometrial cancer?
Localised disease (stage 1 and 2) is treated with total abdominal hysterectomy with bilateral salpingo-oophorectomy. (TAH and BSO)
Other Tx options depend on individual presentation:
Patients with high-risk disease may have postoperative radiotherapy
Chemotherapy
Radical hysterectomy (also removing the pelvic lymph nodes, surrounding tissues and top of the vagina)
Progestogen therapy is sometimes used in frail elderly women not considered suitable for surgery, slows progression of cancer
40
Summary of ovarian cancer?
Peak at age 60 years
distal end of the fallopian tube is often the site of origin of many 'ovarian' cancers
90% of ovarian cancers are epithelial in origin, with 70-80% of cases being due to serous carcinomas
Presents late due to non-specific Sx
41
Types of ovarian cancer?
Epithelial cell - serous, endometrioid, clear cell, mutinous, undifferentiated
Dermoid/germ cell - benign ovarian tumours - teratomas, associated with ovarian torsion, AFP, hCG
Sex cord/stromal - rare, benign/malignant, Sertoli-Leydig, Granulosa
Metastasis - Krukenberg tumour (typically from GI tumours), signet cells on histology
42
Features of ovarian cancer?
Abdominal distension and bloating
Abdominal and pelvic pain
Abnormal vaginal bleeding
Urinary symptoms e.g. Urgency
Early satiety
Diarrhoea
WL, fatigue, loss of appetite
Hip/groin pain (due to ovarian mass pressing on obturator nerve)
43
RF's for ovarian cancer?
Age – peak 60
Family history: mutations of the BRCA1 or the BRCA2 gene
Many ovulations*: early menarche, late menopause, nulliparity
Obesity
Smoking
Recurrent use of clomifene
44
Protective factors for ovarian cancer?
Factors that stop or reduce ovulations:
COCP
Breastfeeding
Pregnancy
45
Ix for ovarian cancer?
Refer directly on a 2-week-wait referral if a physical examination reveals:
Ascites
Pelvic mass (unless clearly due to fibroids)
Abdominal mass
Carry out further investigations before referral in women presenting with symptoms of possible ovarian cancer, starting with a CA125 blood test. This is particularly important in women over 50 years presenting with:
New symptoms of IBS / change in bowel habit
Abdominal bloating
Early satiety
Pelvic pain
Urinary frequency or urgency
Weight loss
CA125
TVUS
CT scan
Histology
Paracentesis
Germ cell tumour - AFP, hCG
46
What is Risk of Malignancy Index (RMI
Estimates ovarian mass being malignant
Considers:
Menopausal status
US findings
CA-125 level**
RMI score greater than 200: high risk, with referral to specialist gynaecological cancer service, and staging CT advised
47
Management of ovarian cancer?
Managed by specialist gynaecology oncology MDT
Usually, a combination of surgery and platinum-based chemotherapy
Exploratory laparotomy for tumour debulking – major procedure!! Generally comprises total abdominal hysterectomy (TAH) and bilateral salpingo-oophorectomy (BSO), infracolic omentectomy, pelvic and para-aortic lymph node sampling, peritoneal biopsies, multiple pelvic washings, sampling of ascites, inspection and sampling of the underside of the diaphragm, and removal of pretty much anything else that looks suspicious
Can have second debulking after chemotherapy in some cases
Medical therapies adjunct to surgery
Adjuvant chemo – given to all patients > stage 1c, or stage 1a/b with high-grade malignancy. First line – carboplatin + paclitaxel
Radiotherapy – tumours tend to be radioresistant
48
Summary of vaginal cancer?
Mass or ulceration within the vagina
Need biopsy for diagnosis
Very rare
Most common subtype is squamous carcinoma - relation to HPV, adenocarcinoma related to diethylstilbestrol
Ix - colposcopy, biopsy, EUA, staging scans
Tx - radiotherapy main Tx
49
Summary of vulval cancers?
90% of vulval cancers are squamous cell carcinomas. Can also be malignant melanomas
Sx - lump/ulcer on labia majora, inguinal lymphadenopathy, itching, bleeding, irritation, redness
50
RFs for vulval cancer?
Advanced age (particularly over 75 years)
Human papilloma virus (HPV) infection
Vulval intraepithelial neoplasia (VIN)
Immunosuppression
Lichen sclerosus
51
Summary of chlamydia infection?
Organism: Chlamydia trachomatis (intracellular organism)
Features = asymptomatic, cervicitis, dysuria, urethral discharge, pelvic/abdo tenderness, CMT
Screening - all men and women 15-24
Ix - NAATs
Tx - 1 - doxycycline, 2 - azithromycin, pregnancy - azithromycin, erythromycin or amoxicillin
Complications - Epididymitis, pelvic inflammatory disease, endometritis, increased incidence of ectopic pregnancies, infertility, reactive arthritis, perihepatitis (Fitz-Hugh-Curtis syndrome)
52
Management of vulval cancer?
Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for vulval cancer in women with an unexplained vulval lump, ulceration, or bleeding.
Staging:
Biopsy of lesion (incisional)
Sentinel node biopsy (for LN spread)
Further imaging (CT abdo and pelvis)
Uses FIGO system
Management depends on stage:
Wide local excision to remove
Groin LN dissection
Chemotherapy
Radiotherapy
53
Summary of gonorrhoea?
Organism - Neisseria gonorrhoea - gram -ve diplococci
Features - odourless purulent discharge, dysuria, pelvic pain, prostatitis, conjunctivitis
Ix - NAAT, charcoal endocervical swab
Tx - IM ceftriazone 1g, oral ciprofloxacin
Complications - PID, infertility, gonococcal conjunctivitis, disseminated gonococcal infection
54
Summary of bacterial vaginosis?
Not STI
Gardnerella vaginalis
RFs - multiple sexual partners, excesive cleaning, recent ABx, smoking, copper coil
Sx - fishy, offensive, watery grey discharge - Amsels criteria
Ix - vaginal pH, charcoal swab, assess for co-infections - clue cells on microscopy
Tx - oral metronidazole 5-7 days, alternative = topical metronidazole or clindamycin
55
Summary of trichomoniasis vaginalis?
A protozoan
Sx - asymptomatic, vaginal discharge (frothy, yellow green, fishy), itchy, dysuria, dyspareunia, balantitis, strawberry cervix, raised pH
Ix - charcoal swab w/ microscopy - shows motile trophozoites
Tx - oral metronidazole
Complications - increased risk of contracting HIV, BV, cervical cancer, PID, pregnancy complications
56
Summary of herpes?
herpes simplex virus (HSV) (both HSV-1 and HSV-2). HSV-2 typically
Sx - painful genital ulceration (dysuria, pruritus), primary episode also has systemic Sx, tender inguinal lymphadenopathy
Ix - clinically, NAAT, HSV serology
Tx - Sx relief (saline bathing, analgesia, topical anaesthetic), oral Aciclovir
Pregnancy - risk of contracting to neonate during labour - elective C-section if primary infection. Primary infection before 28 wks treated with aciclovir, then prophylactic aciclovir from 36 wks. Asymptomatic then vaginal delivery.
Primary after 28wk, treated for initial infection then prophylactic immediately after. C-section after.
Recurrent genital herpes - low risk of neonatal infection, prophylactic aciclovir
57
Summary of syphilis?
Treponema pallidum
Primary - chancre - painless ulcer, local non-tender lymphadenopathy, often not seen in women
Secondary - 6-10wks, systemic symptoms - fevers, lymphadenopathy, rash on trunk, palms and soles, buccal 'snail trail', condylomata lata
Tertiary - gummas, ascending aortic aneurysms, general paralysis of the insane, tabes dorsals, Argyll-Robertson pupil
Ix - serology, antibody testing, dark field testing, PCR
Tx - IM benzathine penicillin, alternative - doxycycline, non-treponema and treponemal titres
Jarish-Herxheimer reaction after Tx - fever, rash, tachycardia NO wheeze or hypotension
58
Summary of candidiasis?
Candida albicans
RF - DM, drugs (ABx, steroids, pregnancy, immunosuppression), HIV
Features - cottage cheese, non-offensive discharge, vulvitis, itch, vulval erythema, fissuring
Ix - clinical features, can do high vaginal swab
Tx - oral fluconazole 150mg or clotrimazole pessary, pregnancy - only cream or pessary
Recurrent - 4 or more episodes, check BM, exclude DDx, consider induction-maintenance regime
59
Summary of genital warts?
HPV 6&11
Features - small (2-5mm) fleshy protuberances which are slightly pigmented, may bleed or itch
Tx - topical podophyllum or cryotherapy are commonly used as first-line treatments depending on the location and type of lesion
multiple, non-keratinised warts are generally best treated with topical agents
solitary, keratinised warts respond better to cryotherapy
genital warts are often resistant to treatment and recurrence is common although the majority of anogenital infections with HPV clear without intervention within 1-2 years
60
Pathophysiology of ovarian hyper stimulation syndrome?
Complication of ovarian stimulation during IVF infertility treatment.
It is associated with the use of human chorionic gonadotropin (hCG) to mature the follicles during the final steps of ovarian stimulation.
There is an increase in vascular endothelial growth factor (VEGF) released by the granulosa cells of the follicles. VEGF increases vascular permeability, causing fluid to leak from capillaries. Fluid moves from the intravascular space to the extravascular space. This results in oedema, ascites and hypovolaemia.
The use of gonadotrophins (LH and FSH) during ovarian stimulation results in the development of multiple follicles. OHSS is provoked by the “trigger injection” of hCG 36 hours before oocyte collection. HCG stimulates the release of VEGF from the follicles. The features of the condition begin to develop after the hCG injection.
There is also activation of the renin-angiotensin system. A notable finding in patients with OHSS is a raised renin level. The renin level correlates with the severity of the condition.
61
RFs for OHSS?
Younger age
Lower BMI
Raised anti-Müllerian hormone
Higher antral follicle count
Polycystic ovarian syndrome
Raised oestrogen levels during ovarian stimulation
62
Preventing OHSS?
Women individually assessed for risk
During stimulation with gonadotrgophins they are monitored - serum oestrogen levels and USS monitor of follicles
If at high risk, several strategies used to reduce risk:
Use of the GnRH antagonist protocol (rather than the GnRH agonist protocol)
Lower doses of gonadotrophins
Lower dose of the hCG injection
Alternatives to the hCG injection (i.e. a GnRH agonist or LH)
63
Features of OHSS?
Early OHSS presents within 7 days of the hCG injection. Late OHSS presents from 10 days onwards.
Abdominal pain and bloating
N+V
Diarrhoea
Hypotension
Hypovolaemia
Ascites
Pleural effusions
Renal failure
Peritonitis from rupturing follicles releasing blood
Prothrombotic state (risk of DVT and PE)
Mild: Abdominal pain and bloating
Moderate: Nausea and vomiting with ascites seen on ultrasound
Severe: Ascites, low urine output (oliguria), low serum albumin, high potassium and raised haematocrit (>45%)
Critical: Tense ascites, no urine output (anuria), thromboembolism and acute respiratory distress syndrome (ARDS)
64
Management of OHSS?
Supportive:
oral fluids
monitoring fluid output
LMWH - to prevent VTE
paracentesis if required
IV colloids (e.g, HAS)
Patients with mild to moderate OHSS are often managed as an outpatient. Severe cases require admission, and critical cases may require admission to the intensive care unit (ICU).
Haematocrit may be monitored to assess the volume of fluid in the intravascular space. Haematocrit is the concentration of red blood cells in the blood. When the haematocrit goes up, this indicates less fluid in the intravascular space, as the blood is becoming more concentrated. Raised haematocrit can indicate dehydration.
65
Causes of post menopausal bleeding?
defined as vaginal bleeding occurring after 12 months of amenorrhoea
vaginal atrophy - most common cause of PMB - thinning, drying and inflammation of vaginal walls due to reduction in oestrogen following menopause
HRT - can occur with no pathological cause, or endometrial hyperplasia due to long-term oestrogen therapy may occur
Endometrial hyperplasia - abnormal thickening of endometrium and precursor for endometrial carcinoma, RF - obesity, unopposed oestrogen use, tamoxifen use, PCOS, DM
Endometrial cancer - 10% of pt's with PMB
Cervical cancer - obtain full record of prior cervical screening
Ovarian cancer - can present with PMB if oestrogen secreting (theca cell) tumours
Vaginal cancer
Trauma
Vulval cancer
Bleeding disorders
66
Ix for post menopausal bleeding?
women over the age of 55 with postmenopausal bleeding should be investigated within two weeks by ultrasound for endometrial cancer
TVUS - acceptable depth is <5mm
67
Tx of vaginal atrophy?
Topical oestrogens and lifestyle changes such as lubrication can help reduce the symptoms of vaginal atrophy, HRT can also be used
68
Summary of medical abortion?
Two treatments:
Mifepristone - anti-progestogen - halts pregnancy and relaxes cervix
Misoprostol - prostaglandin analogue - 1-2 day later - softens cervix and stimulates uterine contractions
Rhesus negative women with a gestational age of 10 weeks or above having a medical TOP should have anti-D prophylaxis.
69
Summary of surgical abortion?
Can be performed under LA, LA plus sedation, GA
Prior, cervical priming occurs - with misoprostol, mifepristone, osmotic dilators
2 options:
cervical dilatation and suction of the contents of the uterus (up to 14 weeks)
cervical dilatation and evacuation using forceps (between 14 and 24 weeks)
Rhesus negative women having surgical TOP should have anti-D prophylaxis
70
Summary of female genital mutilation?
involves surgically changing the genitals of a female for non-medical reasons
Cultural practice in girls before puberty - form of child abuse and safeguarding
FGM Act 2003
Common cultural practice in African countries - Somalias highest levels. Also Ethopia, Sudan, Eritrea
71
Types of FGM?
Type 1: Removal of part or all of the clitoris.
Type 2: Removal of part or all of the clitoris and labia minora. The labia majora may also be removed.
Type 3: Narrowing or closing the vaginal orifice (infibulation).
Type 4: All other unnecessary procedures to the female genitalia.
72
Complications of FGM?
Short term
Pain
Bleeding
Infection
Swelling
Urinary retention
Urethral damage and incontinence
Long term
Vaginal infections
Pelvic infections
UTIs
Dysmenorrhoea
Sexual dysfunction + dyspareunia
Infertility and pregnancy-related complications
Psychological issues and depression
Reduced engagement with healthcare screening
73
Management of FGM?
Patient education
Report - Mandatory to report all cases of FGM under 18 to police
If over 18, careful consideration about whether to report cases to the police or social services. The RCOG recommends using a risk assessment tool to tackle this issue. I.e. other female relatives at risk?
SS + safeguarding
De-infibulation -Surgical procedure may be performed by a specialist in FGM in cases of type 3 FGM. This aims to correct the narrowing or closure of the vaginal orifice, improve symptoms and try to restore normal function
Re-infibulation is illegal
74
What is PCOS?
condition causing metabolic and reproductive problems in women. There are characteristic features of multiple ovarian cysts, infertility, oligomenorrhea, hyperandrogenism and insulin resistance.
75
What is the Rotterdam Criteria for PCOS?
used for diagnosis
A diagnosis requires at least two of the three key features:
Oligoovulation or anovulation, presenting with irregular or absent menstrual periods
Hyperandrogenism, characterised by hirsutism and acne
Polycystic ovaries on ultrasound (or ovarian volume of more than 10cm3)
76
Features of PCOS?
Oligomenorrhoea or amenorrhoea
Infertility
Obesity (in about 70% of patients with PCOS)
Hirsutism
Acne
Hair loss in a male pattern
77
Complications of PCOS?
Insulin resistance and diabetes
Acanthosis nigricans
Cardiovascular disease
Hypercholesterolaemia
Endometrial hyperplasia and cancer
Obstructive sleep apnoea
Depression and anxiety
Sexual problems
78
Ix for PCOS?
Testosterone (raised)
Sex hormone-binding globulin
Luteinizing hormone (raised LH to FSH ratio)
Follicle-stimulating hormone
Prolactin (may be mildly elevated in PCOS)
Thyroid-stimulating hormone
insulin - raised
oestrogen - normal or raised
pelvic USS
TVUS - for visualising ovaries - follicles around periphery of ovary "string of pearls" - 12 or more developing follicles in one ovary, ovarian volume of more than 10cm3
screening for DM - 2 hour OGTT
79
Management of PCOS?
Reduce risks of obesity, T2DM, hypercholesterolaemia and CVD:
WL, low glycemic index, exercise, smoking cessation, antihypertensive medications where required, statins when indicated
assess for complications - endometrial hyperplasia and cancer, infertility, hirsutism, acne, OSA, depression and anxiety
managing endometrial cancer risk -mirena coil, inducing withdrawal bleed every 3-4 months - cyclical progestogens (medroxyprogesterone), COCP
managing infertility - WL, clomifene, laparoscopic ovarian drilling, IVF, metformin,
managing hirsutism - WL, co-cyprindiol (has anti-androgenic effect - risk of VTE, only 3m use), topical eflornithine, electrolysis, laser hair, spironolactone, finasteride
managing acne - COCP, topical adapalene, topical ABx, topical azelaic acid, oral tetracycline
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Why do women with PCOS have increased endometrial cancer risk?
Don't ovulate so no corpus luteum to release progesterone, and so continuously produce oestrogen which causes uterine lining to proliferate, but no menstruation for regular shedding - similar to giving unopposed oestrogen in women on HRT - endometrial hyperplasia and risk of endometrial cancer
need TVUS to assess endometrial thickness. cyclical progestogens given prior to induce period. if thickness >10mm then refer for biopsy
mirena coil
inducing withdrawal bleed every 3-4 months - cyclical progestogens (medroxyprogesterone), COCP
81
Why do women with PCOS have increased endometrial cancer risk?
Don't ovulate so no corpus luteum to release progesterone, and so continuously produce oestrogen which causes uterine lining to proliferate, but no menstruation for regular shedding - similar to giving unopposed oestrogen in women on HRT - endometrial hyperplasia and risk of endometrial cancer
need TVUS to assess endometrial thickness. cyclical progestogens given prior to induce period. if thickness >10mm then refer for biopsy
82
Features of ovarian cysts?
Most asymptomatic - found incidentally on pelvic USS
Vague Sx - pelvic pain, bloating, fullness in abdomen, palpable pelvic mass
83
Types of ovarian cysts?
Follicular cysts - functional cyst - represents developing follicle, when fail to rupture and release egg, then cyst can persist. Most common, harmless and tend to disappear after a few cycles. Reassuring appearance on USS.
Corpus luteum cysts - functional cyst - when corpus luteum fails to break down and fills with fluid - pelvic discomfort, pain, delayed menstruation - seen in early pregnancy
Serous cystadenoma - benign tumours of epithelial cells - bears resemblance to serous carcinoma
Mucinous cystadenoma - also benign tumours of epithelial cells - can become huge, taking up space in pelvic and abdomen, if ruptures may cause pseudomyxoma peritonei
Endometrioma - lumps of endometrial tissue within ovary, occurring in pt's with endometriosis. Pain and interrupt ovulation
Dermoid cysts/germ cell tumours - benign. Most common benign ovarian tumour in women under age 30. Teratomas - come from germ cells, various tissue types. Ass w/ ovarian torsion.
Sex cord-stomal tumours - benign or malignant. From stroma or sex cords, examples = Sertoli-Leydig, granulosa cell
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Assessing patient with ovarian cyst?
Benign or malignant?
Hx for red flags - bloating, reduced appetite, early satiety, WL, urinary symptoms, pain, ascites, lymphadenopathy
Ix:
premenopausal - simple ovarian cyst on USS - no further Ix
Ca-125 - forms part of RMI
women under 40 years with complex ovarian mass = LDH, AFP, HCG
85
RFs for ovarian malignancy?
Increased number of ovulations
Age
Postmenopause
Obesity
HRT
Smoking
FHx
BRCA1 and BRCA2
86
Factors against ovarian malignancy?
Breastfeeding - protective
reduce number of ovulations - late menarche, early menopause, pregnancy, use of COCP
87
Causes of raised Ca-125?
Epithelial cell ovarian cancer - but not specific!
Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy
88
Summary of Risk of Malignancy Index?
Estimates the risk of an ovarian mass being malignant?
89
Management of ovarian cyst?
Possible ovarian ca? (complex cyst or raised Ca-125) - 2ww referral to gynae
Dermoid - gynae referral for further investigations
Simple ovarian cyst in premenopausal? Based on size:
less than 5cm - resolves within 3 cycles
5-7cm - routine referral to gynae, yearly US monitoring
>7cm - MRI scan or surgical evaluation - difficult to characterise on US
Cysts in post-menopausal women - correlation with Ca-125 result and referral to gynae. Raised Ca-125 = 2ww. Under 5cm and normal Ca-125 = monitor with US every 4-6m
Persistent or enlarging cysts may require surgical intervention - ovarian cystectomy, oophorectomy
90
Complications of ovarian cysts?
Torsion
Haemorrhage into cyst
Rupture - bleeding into peritoneum
91
What is Meigs syndrome?
Ovarian fibroma
Pleural effusion
Ascites
91
What is Meigs syndrome?
Ovarian fibroma
Pleural effusion
Ascites
92
Summary of pelvic inflammatory disease?
used to describe infection and inflammation of the female pelvic organs including the uterus, fallopian tubes, ovaries and the surrounding peritoneum.
Usually due to ascending infection from endocervix
Causative organisms - Chlamydia, Gonorrhoea, mycoplasma genitalium, mycoplasma hominis
Features - chronic lower abdo pain, fever, deep dyspareunia, dysuria, menstrual irregularities, vaginal/cervical discharge, cervical excitation
Ix - pregnancy to exclude ectopic, high vaginal swab, screen for C+G
Tx - low threshold - oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole - remove IUD
Complications - peri hepatitis (Fitz-Hugh Curtis syndrome - RUQ pain), infertility, chronic pelvic pain, ectopic
93
RFs for PID?
Not using barrier contraception
Multiple sexual partners
Younger age
Existing sexually transmitted infections
Previous pelvic inflammatory disease
Intrauterine device (e.g. copper coil)
94
What is menopause?
retrospective diagnosis - woman has had no periods for 12 months
~51 years
postmenopause - 12 months from final menstrual period
95
What is perimenopause?
refers to the time around the menopause, where the woman may be experiencing vasomotor symptoms and irregular periods.
includes the time leading up to the last menstrual period, and the 12 months afterwards. This is typically in women older than 45 years.
96
When is premature menopause?
menopause before the age of 40 years. It is the result of premature ovarian insufficiency.
97
Physiology of menopause?
Lack of ovarian follicular function - oestrogen and progesterone are low, LH and FSH are high due to lack of negative feedback on pituitary
failing follicular development = anovulation
without oestrogen = endometrium doesn't develop = amenorrhoea
98
Perimenopausal Sx?
Hot flushes
Emotional lability or low mood
Premenstrual syndrome
Irregular periods
Joint pains
Heavier or lighter periods
Vaginal dryness and atrophy
Reduced libido
99
Complications of menopause?
Cardiovascular disease and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence
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How to diagnose perimenopause/menopause?
Can be made in women over 45 years with typical Sx, w/o Ix
FSH if:
under 40 with suspected premature menopause
40-45 years with menopausal Sx or change in cycle
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Management of perimenopausal Sx?
Lifestyle - regular exercise, WL and reduce stress (help hot flushes, mood and cognitive Sx), maintain good sleep hygiene,
Vasomotor Sx resolve after 2-5 years w/o Tx
Management of symptoms depend on severity, preference and response to Tx.
HRT - gradually reduce to limit recurrence in short term. Refer to secondary care, if Tx ineffective, ongoing SE, unexplained bleeding
Tibolone - synthetic steroid hormone that acts as continuous combined HRT (only after 12 months of amenorrhoea)
Clonidine - act as agonists of alpha-adrenergic and imidazoline receptors
CBT
SSRI - fluoxetine, citalopram
Testosterone - used to treat reduced libido
Vaginal oestrogen - cream/tablets - help with vaginal dryness and atrophy - alongside systemic HRT
Vaginal moisturisers - Sylk, Replens and YES
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Contraceptive use in perimenopause?
Two years after the last menstrual period in women under 50
One year after the last menstrual period in women over 50
Hormonal contraceptives do not affect the menopause, when it occurs or how long it lasts, although they may suppress and mask the symptoms. This can make diagnosing menopause in women on hormonal contraception more difficult.
UKMEC1 - barrier, mirena/copper coil. POP, implant, depot (under 45), sterilisation
UKMEC 2 - COCP - can be used up to 50 if no CI's - Consider combined oral contraceptive pills containing norethisterone or levonorgestrel in women over 40, due to the relatively lower risk of venous thromboembolism compared with other options.
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Contraindications to management with HRT?
Current or past breast cancer
Any oestrogen-sensitive cancer
Undiagnosed vaginal bleeding
Untreated endometrial hyperplasia
104
Adverse effects of HRT?
VTE
Stroke
CHD
Breast ca
Ovarian ca
105
RFs for urinary incontinence?
Increased age
Postmenopausal
Increased BMI
Previous pregnancies and vaginal deliveries
Pelvic organ prolapse
Pelvic floor surgery
Neurological conditions - such as MS
Cognitive impairment and dementia
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Grading system for pelvic muscle contractions?
modified Oxford grading system:
0: No contraction
1: Faint contraction
2: Weak contraction
3: Moderate contraction with some resistance
4: Good contraction with resistance
5: Strong contraction, a firm squeeze and drawing inwards
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What is urge incontinence?
Caused by overactivity of the detrusor muscle of the bladder
108
What is stress incontinence?
When pelvic floor muscles are weak, canals of female pelvis become lax. This means organs of pelvis are poorly supported. Sphincter muscles are also weak.
Canals - urethral, vaginal, rectal
Urine leaks at times of increased pressure on the bladder.
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What is overflow incontinence?
When there is chronic urinary retention due to obstruction of the outflow of urine - overflow of urine. No urge to pass urine
Can occur with anticholinergic medications, fibroids, pelvic tumours, neurological conditions (MS, DM, spinal cord injuries)
M>F
Women referred for urodynamic testing
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Assessing urinary incontinence?
Hx to distinguish which type
Modifiable lifestyle factors - caffeine consumption, alcohol consumption, medications, BMI
Assess severity - frequency of urination, frequency of incontinence, nighttime urination, use of pads/changing clothing
Examination - assess pelvic tone and examine for - prolapse, atrophic vaginitis, urethral diverticulum, pelvic assess
Ask pt to cough!
Assess strength of pelvic muscle contractions
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Ix for urinary incontinence?
Bladder diary - fluid intake, urination, incontinence over 3 days
Urine dipstick - infection, haematuria
Post-void residual bladder volume - bladder scan
Urodynamic testing - patients with urge incontinence not responding to first-line medical treatments, difficulties urinating, urinary retention, previous surgery or an unclear diagnosis
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What are urodynamic tests?
assessing the presence and severity of urinary symptoms.
Patients need to stop taking any anticholinergic and bladder related medications around five days before the tests.
Catheter in bladder and another in rectum. Measures pressures in both. Bladder filled with liquid - outcome measures = cystometry, uroflowmetry, leak point pressure, post-void residual bladder volume, video urodynamic testing
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Management of stress incontinence?
Lifestyle - avoid caffeine, diuretics and overfilling bladder, avoid excessive or restricted fluid intake, WL if appropriate
Conservative - supervised pelvic floor exercises for at least 3 months
Surgery - tension free vaginal tape, autologous sling procedures, colposuspension, intramural urethral bulking
Medical - duloxetine - SNRI
If neurological disorder - artificial urinary sphincter
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Management of urge incontinence?
Bladder retraining - increasing time between voiding
Anticholinergic medication - oxybutynin, tolterodine, solifenacin. SE = dry mouth, dry eyes, urinary retention, constipation and postural hypotension. Can also lead to a cognitive decline, memory problems and worsening of dementia, which can be very problematic in older, more frail patients.
Mirabegron - alternative to anticholinergic. contraindicated in uncontrolled hypertension. beta-3 agonist, stimulating the sympathetic nervous system, leading to raised blood pressure. This can lead to a hypertensive crisis and an increased risk of TIA and stroke.
Invasive procedures - botulinum toxin type A, percutaneous sacral nerve stimulation, augmentation cystoplasty, urinary diversion
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What is HIV?
species of Lentivirus - subgroup of retroviruses that preferentially infects CD4+ T helper lymphocytes, resulting in the progressive destruction of the immune system and the onset of acquired immunodeficiency syndrome (AIDS).
116
Epidemiology of HIV?
HIV-1 and HIV-2. HIV-1 is the predominant type found in the UK, whereas HIV-2 is mainly found in West Africa
Decline in diagnoses and deaths
‘90-90-90‘ target in UK - diagnosing 90% of HIV positive people, providing antiretroviral therapy for 90% of those diagnosed, and achieving viral suppression in 90% of those on treatment.
in the UK, HIV is most prevalent among men who have sex with men (MSM) and black-African heterosexual men and women.2
117
Pathophysiology of HIV?
1 - Binding: viral protein gp120 on the surface of HIV binds host glycoprotein CD4+ and host co-receptor CCR5 or CXCR4. This is blocked by CCR5 antagonists.
2 - Fusion: viral protein gp41 penetrates the cell membrane, allowing the fusion of the virus and cell. This is blocked by cell fusion inhibitors.
3 - Reverse transcription: viral reverse transcriptase converts HIV single-stranded RNA to double-stranded DNA. This is blocked by non-nucleoside reverse transcriptase inhibitors (NNRTIs) and nucleoside reverse transcriptase inhibitors (NRTIs).
4 - Integration: viral integrase enzymes allows HIV DNA to insert into the host DNA. This is blocked by integrase inhibitors.
5 - Replication: host machinery transcribes and translates new HIV RNA and polyproteins.
6 - Assembly: the new HIV proteins and HIV RNA move to the cell membrane and assemble the immature, non-infectious virion.
7 - Budding: the new HIV virion exits the cell and viral protease cleaves the long HIV protein chains to form the mature, infectious virion. This is blocked by protease inhibitors.
3 stages:
1 - primary HIV infection (seroconversion)
2 - chronic HIV (asymptomatic/clinical latency) - low level of viral replication as immune response controls the virus, pt infectious
3 - AIDS - when HIV compromises ability of immune system to replenish CD4+ cells - CD4+ cell count drops below 200 cells/µL. individual will become susceptible to opportunistic infection and malignancy. If untreated AIDS causes death within around 20 months
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Transmission of HIV?
infected bodily fluids, most commonly through anal or vaginal intercourse.
Other mechanisms include vertical transmission (from an infected mother to child during pregnancy, childbirth or breastfeeding), and inoculation (via contaminated needles, blood/blood products and occupational exposure)
119
RFs for HIV?
Men who have sex with men (MSM)
Female sexual contacts of MSM
Those originating from areas with a high prevalence of HIV
Those in current or former serodiscordant relationships (in which a HIV-negative individual is partnered with a HIV-positive individual)
Intravenous drug use
Occupational exposure (such as accidental needlestick injury)
Sexual risk factors such as unprotected anal or vaginal sex with one or multiple partners, and having another sexually transmitted infection such as hepatitis B or hepatitis C.
120
Features of HIV?
Primary - seroconversion - non-specific Sx - glandular fever-like symptoms, fever of unknown origin, lymphadenopathy and unexplained weight loss, unexplained neutropenia, anaemia and thrombocytopenia.
Longstanding HIV infection - fever/sweats, WL, lymphadenopathy, unexplained neutropenia, anaemia or thrombocytopenia, respectively Sx, neuro Sx, oral conditions (candidiasis, pathos users, hairy leukoplakia, gingivitis, dental abscess), GI Sx (cryptosporidium most common cause of diarrhoea), Kaposi's sarcoma, fungal skin/nil, pityriasis versicolor, GU Sx (candidiasis, herpes, warts)
AIDs - AIDS-defining illnesses
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Examples of AIDS-defining illnesses?
Pneumocystis pneumonia (pneumocystis jirovecii)
Kaposi’s sarcoma
Cryptococcal meningitis
Cerebral toxoplasmosis
Cerebral lymphoma
Cytomegalovirus retinitis
Non-Hodgkin’s lymphoma
Oesophageal candidiasis
Tuberculosis
Primary central nervous system lymphoma
122
Ix for HIV?
NICE recommends testing patients who belong to at-risk groups, those presenting with another sexually transmitted infection, new patients at a GP practice in an area of high prevalence, as part of routine antenatal care, and for those who request it.
If serious HIV complication - admit for urgent specialist assessment
There are two main methods for HIV testing:
Laboratory-based tests on patient venipuncture samples (largely 4th generation tests) - detects the presence of HIV IgM and IgG antibodies as well as the viral p24 antigen - +ve, need second sample for confirmation and need repeat at 12 weeks post-exposure
Point of care tests (largely 3rd generation tests) - finger prick, detect HIV IgM and IgG antibodies with increased sensitivity during early seroconversion and results can be ready in under an hour, has false positives
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Tx of HIV?
No cure
U=U
Early initiation of antiretroviral therapy
Opportunistic infections treated appropriately
HIV highly mutagenic, quickly develop drug resistance so minimum of 3 different drugs to target different parts of HIV life cycle
regimen - two NRTIs with either an integrase inhibitor, a non-nucleoside reverse transcriptase inhibitor or a boosted protease inhibitor
NRTI - emtricitabine, tenofovir, abacavir, lamivudine
NNRTI - efavirenz, nevirapine, rilpivirine,
Protease inhibitor - atazanavir, darunavir, ritonacir
Integrase inhibitor - dolutegravir, elvitegravir, raltegravir
CCR5 antagonist - maraviroc
Fusion - enfuvirtide
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What is pre-exposure prophylaxis and post-exposure prophylaxis?
PrEP
combination of emtricitabine with tenofovir disoproxil
PEP
emtricitabine, tenofovir disoproxil and raltegravir which should be initiated as soon as possible (no later than 72 hours following exposure) and continued for 28 days.10
125
Additional management of HIV?
Prophylactic co-trimoxazole (Septrin) is given to patients with a CD4 under 200/mm3 to protect against pneumocystis jirovecii pneumonia (PCP).
^ risk of CVD - monitoring CVD RFs and lipids
Yearly cervical smears
Vaccinations up to date - influenza, pneumococcal, hep A and B, tetanus, diphtheria, polio
Avoid live vaccines
Advise condoms for vaginal and anal sex and dams for oral sex, even when both partners are HIV positive.
126
HIV and pregnancy?
The mother’s viral load will determine the mode of delivery:
Normal vaginal delivery is recommended for women with a viral load < 50 copies / ml
Caesarean section is considered in patients with > 50 copies copies / ml and in all women with > 400 copies / ml
IV zidovudine should be given during the caesarean if the viral load is unknown or there are > 10000 copies / ml
Prophylaxis treatment may be given to the baby, depending on the mothers viral load:
Low-risk babies, where the mother’s viral load is < 50 copies per ml, are given zidovudine for four weeks
High-risk babies, where the mother’s viral load is > 50 copies / ml, are given zidovudine, lamivudine and nevirapine for four weeks
HIV can be transmitted during breastfeeding, even if the mother’s viral load is undetectable. Breastfeeding is not recommended for mothers with HIV.
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Summary of Kaposi's sarcoma?
caused by HHV-8 (human herpes virus 8)
purple papules or plaques on the skin or mucosa (e.g. gastrointestinal and respiratory tract)
espiratory involvement may cause massive haemoptysis and pleural effusion
radiotherapy + resection
128
Neurocomplications of HIV?
Toxoplasmosis - headache, confusion, drowsiness, CT = single/multiple ring enhancing lesions, mass effect may be seen. Tx = sulfadiazine and pyrimethamine. SPECT negative
Primary CNS lymphoma - ass w/ EBV. CT - single or multiple homogenous (solid) enhancing lesions, Tx - steroids, chemo, brain irradiation. SPECT positive
TB - CT- single enhancing lesion
Encephalitis - CMV or HIV itself. CT - oedematous brain
Cryptococcus - most common fungal infection of CNS. CT: meningeal enhancement, cerebral oedema. Meningitis or can cause SOL
Progressive multifocal leukoencephalopathy - widespread demyelination. CT: single or multiple lesions, no mass effect, don't usually enhance. MRI is better - high-signal demyelinating white matter lesions are seen
AIDS dementia complex - symptoms: behavioural changes, motor impairment, CT: cortical and subcortical atrophy
129
What are fibroids?
Benign tumours of smooth muscle of uterus - uterine leiomyomas
Common.
affecting 40-60% of women in later reproductive years, and are more common in black women compared with other ethnic groups.
Oestrogen sensitive
130
Types of fibroids?
Intramural - within myometrium. As grow can distort uterus.
Subserosal - just below outer layer of uterus - grow outwards, become large, fill abdominal cavity
Submucosal - just below lining of uterus (endometrium)
Pedunculated - on a stalk
131
Features of fibroids?
Often asymptomatic
Heavy menstrual bleeding (menorrhagia) is the most frequent presenting symptom
Prolonged menstruation, lasting more than 7 days
Abdominal pain, worse during menstruation
Bloating or feeling full in the abdomen
Urinary or bowel symptoms due to pelvic pressure or fullness
Deep dyspareunia (pain during intercourse)
Reduced fertility
Polycythaemia secondary to autonomous production of erythropoietin
Abdominal and bimanual examination - a palpable pelvic mass or an enlarged firm non-tender uterus
132
Ix for fibroids?
Hysteroscopy - initial Ix, for submucosal fibroids, presenting with heavy menstural bleeding
Pelvic US - choice for larger fibroids
MRI scanning - before surgery, info about size, shape and blood supply
133
Management of fibroids?
Heavy menstrual bleeding Tx
Fibroids less than 3cm -
mirena coil - and no distortion of uterus
Symptomatic management - NSAIDs and tranexamic acid
COCP
Cyclical oral progestogens
Surgical options for smaller fibroids - endometrial ablation, resection of submucosal fibroids during hysteroscopy, hysterectomy
Fibroids >3cm - referral to gynae for Ix and Tx:
Symptomatic management with NSAIDs and tranexamic acid
Mirena coil - depending on size and shape of fibroids and uterus
Combined oral contraceptive
Cyclical oral progestogens
Surgical options for larger fibroids:
Uterine artery embolisation
Myomectomy
Hysterectomy
GnRH agonists (goesrelin and leuprorelin) - reduce size of fibroids before surgery - induce a menopause like state
134
Complications of fibroids?
Heavy menstrual bleeding, often with iron deficiency anaemia
Reduced fertility
Pregnancy complications, such as miscarriages, premature labour and obstructive delivery
Constipation
Urinary outflow obstruction and urinary tract infections
Red degeneration of the fibroid
Torsion of the fibroid, usually affecting pedunculated fibroids
Malignant change to a leiomyosarcoma is very rare (<1%)
135
What is red degeneration of fibroids?
refers to ischaemia, infarction and necrosis of the fibroid due to disrupted blood supply
Occur in larger fibroids (above 5cm) during second and third trimester of pregnancy
may occur as the fibroid rapidly enlarges during pregnancy, outgrowing its blood supply and becoming ischaemic.
It may also occur due to kinking in the blood vessels as the uterus changes shape and expands during pregnancy.
Sx - severe abdominal pain, low-grade fever, tachycardia, vomiting
Tx - supportive, rest, fluids, analgesia
136
Summary of primary amenorrhoea?
By 13 if no other evidence of pubertal development
By 15 if other signs of puberty - eg. breast bud development
Hypogonadotrophic hypogonadism - deficiency of LH and FSH - hypopituitarism, damage to hypothalamus/pituitary, CF, IBD, excessive exercise/dieting, constitutional delay in growth and development, GH deficiency, hypothyroidism, Cushing's, hyperprolactinaemia, Kallman
Hypergonadotrophic hypogonadism - lack of response to LH and FSH - damage to Gonads, congenital absence, Turners
Congenital adrenal hyperplasia - excess androgens due to deficiency of 21-hydroxylase
Androgen insensitivity syndrome - male genotype, female phenotype
Structural pathology - may be cyclical pain - imperforate hymen, transverse vaginal septa, vaginal agenesis, absent uterus, FGM
137
Normal puberty order in girls and boys?
Girls - breasts, pubic hair, menstrual periods - boobs, pubes, grow, flow
Boys - Grapes (testicles), drapes (hair), grow, blow (ejaculation)
138
Ix for primary amenorrhoea?
Hx - health, development, FHx, diet, lifestyle
Examination
Bloods - FBC, ferritin, U&E (for CKD), anti-TTG or anti-EMA
FSH, LH, TFTs, IGF-1, prolactin, testosterone
Genetic - microarray - Turners
Imaging -
X-ray wrist - bone age, constitutional delay
Pelvic US - ovaries and pelvic organs
MRI brain - pituitary pathology, olfactory bulbs
139
Tx of primary amenorrhoea?
Establishing and treating underlying cause
Replacement hormones if needed
Reassurance and observation for constitutional delay
Stress or LBW - reduce in stress, CBT, healthy weight gain
Hypogonadotrophic hypogonadism - pulsatile GnRH - to induce ovulation and menstruation and can induce fertility. Alternatively, COCP to induce menstruation if pregnancy not wanted
Ovarian causes - COCP
140
What is secondary amenorrhoea?
no menstruation for more than three months after previous regular menstrual periods
Consider investigation after 3-6 months if previously regular
If previously irregular - investigation after 6-12 months
141
Causes of secondary amenorrhoea?
Pregnancy
Menopause and premature ovarian failure
Hormonal contraception (IUS, POP)
Hypothalamic or pituitary pathology
- Physiological/psychological stress - hypothalamus reduces GnRH - excessive exercise, LBW and ED, chronic disease, psychological stress
- pituitary - tumours (prolactinoma), failure (trauma, radiotherapy, surgery, Sheehans)
Ovarian causes - PCOS
Uterine pathology - Asherman's
Thyroid pathology
Hyperprolactinaemia - high prolactin acts on hypothalamus to prevent release of GnRH, and no release of LH or FSH - e.g., pituitary adenoma - Tx = dopamine agonists (bromocriptine)
142
Ix for secondary amenorrhoea?
Hx and examination
Hormone tests:
b-hCG - rule out pregnancy
LH and FSH - high FSH suggests primary ovarian failure, high LH:FSH - PCOS
prolactin - if high, MRI
TFTs
Testosterone - PCOS, androgen insensitivity, CAH
US of pelvis - PCOS
143
Tx of secondary amenorrhoea?
Establishing and treating the underlying cause
Replacement hormones if needed
144
Complications or amenorrhoea?
Risk of osteoporosis due to low oestrogen levels
if amenorrhoea lasts more than 12 months - ensure adequate vitamin D and calcium intake
HRT or COCP
145
What is dysmenorrhoea?
excessive pain during the menstrual period
146
Summary of primary dysmenorrhoea?
No underlying pelvic pathology
thought to be due to excessive endometrial prostaglandin production
Sx - pain typically starts just before or within few hrs of period starting, suprapubic cramping pain
Tx - NSAIDs (mefenamic acid, ibuprofen) - inhibit prostaglandin production. COCP
147
Causes of secondary dysmenorrhoea?
Many years after menarche - due to underlying pathology
Pain starts 3-4 days before period
Endometriosis
Adenomyosis
PID
IUD
Fibroids
Cervical/ovarian cancer
148
Management of secondary dysmenorrhoea?
referring all patients with secondary dysmenorrhoea to gynaecology for investigation.
149
Causes of menorrhagia? (heavy menstrual bleeding)
Dysfunctional uterine bleeding
Extremes of reproductive age
Fibroids
Endometriosis and adenomyosis
PID
Contraceptives - copper coil
Anticoagulant
Bleeding disorders - Von Willebran disease
Endocrine disorders - DM, hypothyroidism
Connective tissue disorders
Endometrial hyperplasia or cancer
Polycystic ovarian syndrome
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Causes of postcoital bleeding?
Red flag = cervical cancer
No cause
Ectropion, infection
Trauma
Atrophic vaginitis
Polyps
Endometrial cancer
Vaginal cancer
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Causes of pelvic pain?
Urinary tract infection
Dysmenorrhoea (painful periods)
Irritable bowel syndrome (IBS)
Ovarian cysts
Endometriosis
Pelvic inflammatory disease (infection)
Ectopic pregnancy
Appendicitis
Mittelschmerz (cyclical pain during ovulation)
Pelvic adhesions
Ovarian torsion
Inflammatory bowel disease (IBD)
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Causes of vaginal discharge?
Bacterial vaginosis
Candidiasis (thrush)
Chlamydia
Gonorrhoea
Trichomonas vaginalis
Foreign body
Cervical ectropion
Polyps
Malignancy
Pregnancy
Ovulation (cyclical)
Hormonal contraception
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Causes of pruritus vulvae?
Irritants such as soaps, detergents and barrier contraception
Atrophic vaginitis
Infections such as candidiasis (thrush) and pubic lice
Skin conditions such as eczema
Vulval malignancy
Pregnancy-related vaginal discharge
Urinary or faecal incontinence
Stress
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What is endometriosis?
condition where there is ectopic endometrial tissue outside the uterus.
A lump of endometrial tissue outside the uterus is described as an endometrioma.
Endometriomas in the ovaries are often called “chocolate cysts”.
Adenomyosis refers to endometrial tissue within the myometrium (muscle layer) of the uterus.
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Aetiology of endometriosis?
Retrograde menstruation
Embryonic cells destined to become endometrial tissue remain in areas outside uterus = later develop into ectopic endometrial tissue
Through lymphatic system
Cells outside uterus change - metaplasia
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Pathophysiology of endometriosis symptoms?
Pelvic pain - during menstruation endometrial tissue sheds, causes irritation and inflammation - dull cyclical pain
Deposits of endometriosis in bladder or bowl can lead to blood in urine or stools
Localised bleeding and inflammation can lead to adhesions. Inflammation causes damage and develop - chronic, non-cyclical pain
Reduced fertility - due to adhesions around ovaries and Fallopian tubes, and obstructing route to uterus
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Presentation of endometriosis?
Can be asymptomatic
Cyclical abdominal/pelvic pain
Deep dyspareunia
Dysmenorrhoea
Infertility
Cyclical bleeding from other sites, such as haematuria
Urinary Sx
Bowel Sx
O/E
Endometrial tissue visible in vagina on speculum examination, particularly in posterior fornix
A fixed cervix on bimanual examination
Tenderness in the vagina, cervix and adnexa
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Ix for endometriosis?
Pelvic ultrasound - may reveal large endometriomas, but often unremarkable
Referral to gynae for laparoscopy
Laparoscopic surgery - gold standard - biopsy of lesions
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Staging of endometriosis?
American Society of Reproductive Medicine
Stage 1: Small superficial lesions
Stage 2: Mild, but deeper lesions than stage 1
Stage 3: Deeper lesions, with lesions on the ovaries and mild adhesions
Stage 4: Deep and large lesions affecting the ovaries with extensive adhesions
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Management of endometriosis?
Initial - establishing diagnosis, clear explanation, listen to patients ICE, analgesia (NSAIDs, paracetamol)
Hormonal - COCP, POP, Depo, Nexplanon, Mirena, GnRH agonist - stop ovulation and reduce endometrial thickening or inducing menopause like state
Surgical - excise or ablate endometrial tissue, remove adhesions, hysterectomy
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Ix for heavy menstrual bleeding?
Pelvic exam - fibroids, ascites, cancers
FBC - iron deficiency anaemia
Outpatient hysteroscopy - suspected submucosal fibroid, suspected endometrial pathology, persistent intermenstrual bleeding
Swabs - if infection
Coagulation screen - if FHx of clotting disorders
Ferritin - clinically anaemic
TFTs - if Sx of hypothyroidism
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Tx of heavy menstrual bleeding?
Start by excluding pathology
No contraception required/wanted:
Tranexamic acid - if no pain
Mefanamic acid - when associated pain
When contraception is wanted:
Mirena coil
COCP
Cyclical oral progestogens - e.g. norethisterone
Also progesterone only contraception
Referral to secondary care for Ix and Tx if Tx unsuccessful, Sx severe or large fibroids (>3cm)
Final options - endometrial ablation and hysterectomy
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Causes of infertility?
Sperm problems (30%)
Ovulation problems (25%)
Tubal problems (15%)
Uterine problems (10%)
Unexplained (20%)
40% of infertile couples have a mix of male and female causes.
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Advice for couples trying to get pregnant?
The woman should be taking 400mcg folic acid daily
Aim for a healthy BMI
Avoid smoking and drinking excessive alcohol
Reduce stress as this may negatively affect libido and the relationship
Aim for intercourse every 2 – 3 days
Avoid timing intercourse
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Ix for infertility?
BMI
Chlamydia screening
Semen analysis
Female hormone testing - LH and FSH on day 2 to 5, progesterone on day 21 of cycle (7 days before end of cycle), AMH, TFTs, prolactin
Rubella immunity
High FSH = poor ovarian reserve
High LH = PCOS
High progesterone = ovulation occurring
AMH = marker of ovarian reserve, released by granuloma cells
Secondary care Ix:
US pelvic - PCOS, structural abnormalities
Hysterosalpingogram - patency
Laparoscopy and dye - potency, adhesions, endometriosis
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Management of an ovulation?
Weight loss for overweight patients with PCOS can restore ovulation
Clomifene may be used to stimulate ovulation - anti-oestrogen, stops -ve feedback of oestrogen, so more GnRH and hence more FH and LSH
Letrozole may be used instead of clomifene to stimulate ovulation (aromatase inhibitor with anti-oestrogen effects)
Gonadotropins may be used to stimulate ovulation in women resistant to clomifene
Ovarian drilling may be used in polycystic ovarian syndrome
Metformin may be used when there is insulin insensitivity and obesity (usually associated with PCOS)
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Summary of premature ovarian insufficiency?
Menopause before age of 40. Hypergonadotrophic hypogonadism.
Causes - idiopathic, iatrogenic, AI, genetic, infections
Sx - menopausal Sx, irregular menstrual periods, secondary amenorrhoea, low oestrogen levels
Dx - <40, menopausal Sx, elevated FSH (on 2 samples)
Risks - CVD, stroke, osteoporosis, cognitive impairment, dementia, Parkinsonism
Tx - HRT until 50. Reduce CVD, osteoporosis, cognitive and psychological risks. Use transdermal to reduce VTE risk. Can also use COCP
