Gynaecological core conditions 2 Flashcards
Molar pregnancy
Abnormal proliferation of trophoblastic tissue (1-2.5/1000)
Types of molar pregnancy
- Complete hydatiform mole: no normal fetal tissue forms
- Partial hydatidiform mole: incomplete fetal tissue develops alongside molar tissue
- Invasive mole: contain many villi, but these may grow into or through the muscle layer of the uterus wall, persistently high HCG
- Choriocarcinoma: have cytotrophoblasts and syncytiotrophoblasrs but no villi form
Complete mole
- Most common type of hydatidiform mole. Diffuse thropoblastic hyperplasia, hydropic swelling of chorionic villi, no fetal tissue or membrane present
- Hydropic villi and focal trophoblastic hyperplasia are associated with 46XX or 46XY
- 10% INVADE AND 3% CHORIOCARCINOMA
Clinical features of a complete mole
- Vaginal bleeding -97%
- Uterus larger than date -51%
- Hyperemesis gravidarum – 26%
- B-hcg > 100,000
- No fetal heart beat
- Presentation similar to threatened/ spontaneous/ missed miscarriage
Incomplete molev
- Often triploid (69(XXY,XYY,XXX) with chromosome complement from both parents 2 sperm fertilize 1 egg or 1 sperms with reduplication.
- 1% RISK OF INVASION, does not become choriocarcinoma
Investigations for molar pregnancy
- UPT (urine pregnancy test): B-hcg level
- U/S Complete – no fetus, classic snow storm
- U/S Incomplete – molar degeneration of placenta +/- fetal anomalies, multiple echogenic regions corresponding to hydropic villi and focal intrauterine haemorrhage
- CXR – may show metastatic lesions
Molar pregnancy: features of high risk neoplasm
- Local uterine invasion
- Beta hG >100,000
- Excessive uterine size
- Prominent theca- lutein cyst
Molar pregnancy- treatment
- Suction and curettage
- Anti-D in rhesus -ve
- If bleeding hysterectomy may ne needed
- Chemotherapy for chorio-carcinoma
Molar pregnancy- follow up
- Register with the national centres
- B-hcg 2/52 till normal
- Follow up monthly for 1 year
- Follow up 3 monthly in 2nd year
Hyperemesis Gravidarum- complications
- Inability to keep down fluids or solids leading to dehydration, electrolytes and nutrients deficiency.
- Leading to weight loss (2-5 kg)
- Dehydration
- Electrolyte imbalance
- Vitamin B deficiency(B6-polyneuropathy, Thiamine deficiency-Wernicke’s encephalopathy)
- Rarely liver failure, renal failure , fetal and maternal mortaliy.
- Mallory-Weiss tears of oesophagus and haematemesis
- Wernicke’s encephalopathy , osmotic demylination syndrome-(pyramidal tract sighs, spastic quadriparasis, pseudobulbar palsy and impaired consciousness).
Hyperemesis gravidarum- risk factors
- Higher levels of HCG
- Multiple pregnancies
- Molar pregnancies
Hyperemesis gravidarum- differential diagnosis
- Maternal medical conditions leading to excessive vomiting
- Anorexia nervosa and Bulimia
- Thyrotoxicosis
- Diabetic ketoacidosis
- Infections- UTI, GI problems, cholecystitis
Hyperemesis gravidarum- Investigations
- FBC and clotting
- U&E, Haematocrit, LFTs, Thyroid Function Tests if prolonged
- Urine for ketones, culture and sensitivity
- USS ? Multiple pregnancies, molar pregnancy
- Social aspects
Hyperemesis gravidarum
Most severe form of nausea and vomiting during pregnancy. This can lead to dehydration and weight loss. Different from morning sickness
Hyperemesis gravidarum- Wernickes encephalopathy
Diplopia, abnormal ocular movement, ataxia and confusion. Typical ocular signs are 6th nerve palsy, gaze palsy or nystagmus
Occurs in the pregnant women secondary to thiamine deficiency
Wernicke’s encephalopathy can be precipitated by I/V dextrose solutions. Severe hyponatremia as well as rapid correction-osmotic demylation syndrome-central pontine mylinolysis
Hyperemesis gravidarum- treatment
- Mild cases can be dealt in Pregnancy assessment unit. Refractory cases will need admission.
- I/V fluids -normal saline, hartman solution and electrolyte replacements.
- Anti-emetics (avoid ondanstron)
- Small frequent meals
- Vitamin B supplements specially thiamine.
- Social and mental health Support.
- Rarely parenteral feeding and steroids.
- Usually Termination of pregnancy is not required and multi-disciplinary care with involvement of Psychiatry, Gasroenterology ,dietetician and obstetric team will resolve the problem.
Ovarian hyperstimulation syndrome
Seen in some forms of infertility treatment. It is postulated that the presence of multiple luteinized cysts within the ovaries results in high levels of not only oestrogens and progesterone but also vasoactive substances such as vascular endothelial growth factor (VEGF). This results in increased membrane permeability and loss of fluid from the intravascular compartment. Most likely seen following gonadotropin or hCG treatment
Up to 1/3 of patients undergoing IVF may have a mild form of OHSS
Mild and moderate OHSS
Mild= abdominal pain, abdominal bloating
Moderate= as for mild, nausea and vomiting, ultrasound evidence of ascites
Severe and critical OHSS
Severe= as for moderate, clinical evidence of ascites. Oliguria, Haematocrit >45%, hypoproteinaemia
Critical= as for severe, thromboembolism, acute respiratory distress syndrome, anuria, tense ascites
Endometriosis
Presence of endometrial like tissue outside the uterus, which induces a chronic inflammatory reaction
About 2-10% of the population and 50% of infertile women.
Common sites: pelvic organs, peritoneum, occasionally other parts of the body like lungs
Clinical features of endometriosis
- Chronic pelvic pain
- Secondary dysmenorrhoea: pain often starts days before bleeding
- Deep dyspareunia
- Subfertility
- Non-gynaecological: urinary symptoms e.g. dysuria, urgency, haematuria. Dyschezia (painful bowel movements)
- On pelvic examination reduced organ mobility, tender nodularity in the posterior vaginal fornix and visible vaginal endometriotic lesions may be seen
- Chronic fatigue
- Can be asymptomatic. Little correlation between stage and type/severity of pain symptoms
Endometriosis- risk factors
- Age
- Increased peripheral body fat
- Greater exposure to menstruation
- Genetic predisposition 6-10 times more common in the first degree relatives of affected women
- Protective factors-smoking ,cocp pills, exercise
Endometriosis- investigations
- Laparoscopy is the gold-standard investigation
- There is little role for investigation in primary care (e.g. ultrasound)- if the symptoms are significant the patient should be referred for a definitive diagnosis
- Examination: possible lass (endometiomas), fixed retroverted uterus with nodules in the uterosacral ligaments in severe disease
- Transvaginal sonography endometrioma
- MRI, trans rectal USS, Ba enema (for bowel symptoms)
Endometriosis management- mild
- NSAIDs and/or paracetamol for symptomatic relief
- If analgesia doesn’t help then hormonal treatment like the COCP or progesterone i.e. medroxyprogesterone acetate should be tried
- Refer to secondary care if symptoms don’t improve or if fertility is a priority
Endometriosis management- secondary care
- GnRH analodues- said to induce a ‘psuedomenopause’ due to low oestrogen levels.
- Dual therapy does not significantly affect fertility
- Surgery: if not responding to medicine. When trying to conceive use laparoscopic excision or ablation of endometriosis plus adhesiolysis. Ovarian cystectomy is also an option
Endometriosis- treatment overview
- ENDOMETRIOSIS ASSOCIATED PAIN
- Presumed endometriosis symptoms-counsel WOMEN
- Treat with - adequate analgesia(NSAID,S)
- Hormonal treatment- COC PILLS
- Progestogens
- Anti progestogens
- GnRH agonists
Endometriosis- surgical treatment (in order of severity)
- At laparoscopy identified-surgically treat (see and treat).
- Consider both ablation and excision of peritoneal endometriosis.
- SURGICAL INTERRUPTION OF PELVIC NERVEPATHWAY-(LUNA,PSN-)should not be performed.
- OVARIAN ENDOMETRIOMA-perform cystectomy instead of drainage and coagulation
- DEEP Endometriosis-perform surgical removal –refer to centre of expertise
- Failure to respond to conservative treatment +family complete-consider HYSTERECTOMY+BSO and removal of all visible lesions
- ADHESION PREVENTION AFTER SURGERY-use oxidised regenerated cellulose
For pain from rectovaginal endometriosis refractory to other medical or surgical treatment
Consider Aromatase inhibitors in combination with oral COCP, progestogens, or GnRH analogues
Pathothsiology of endometriosis
Metaplasia of coelomic epithelium and implantation of viable endometrial cells. Retrograde menstruation.
Endometriosis= Pre-operative and post-operative hormonal treatment
- Do not prescribe pre or post operative hormonal treatment except for pain
- After surgery prescribe a LNG-IUS or a combined hormonal contraception for 18-24 months for secondary prevention of endometriosis associated dysmenorrhoea but not for pain.
Bacterial vaginosis in pregnancy
- BV is treated in pregnancy because it can be associated with miscarriages and preterm labour
- During pregnancy treatment options include Clindamycin cream ; some units use Metronidazole
- In gynaecology, BV is treated by Metronidazole 400 MG BD for 7 days.
Overview of bacterial vaginosis
- pH of vaginal fluid is elevated above 4.5 and up to 6.0
- When levels of lactobacillus drop and other bacteria like Gardnerella vaginalis and Prevotella spp rise
Bacterial vaginosis- risk factors
- Vaginal douching
- Receptive cunnilingus
- Black race
- Recent change of sex partner
- Smoking
- Presence of an STI e.g. chlamydia or herpes
Bacterial vaginosis- clinical presentation
- Offensive, fishy smelling vaginal discharge.
- Not associated with soreness, itching or irritation
- Many women (50%) are asymptomatic
- Signs: thin, white, homogenous discharge coating the walls of the vagina and the vestibule
Diagnosis of bacterial vaginosis
Based on Amsel’s criteria or the Hay/Ison criteria
Amsel’s criteria: At least three of the four criteria are present for the diagnosis to be confirmed.
* Thin, white, homogeneous discharge
* Clue cells on microscopy of wet mount
* pH of vaginal fluid >4.5
* Release of a fishy odour on adding alkali (10% KOH)
Treatment of bacterial vaginosis
- Who to treat: Symptomatic women, Women undergoing some type of surgical procedure
- Metronidazole 400mg twice daily for 5-7 days. OR
- Metronidazole 2g single dose. OR
- Intravaginal metronidazole gel (0.75%) once daily for 5 days. OR
- Intravaginal clindamycin cream (2%) once daily for 7 days
Risk factors for chlamydia and gonorrhoes
- Age <25
- Non-barrier contraception
- Co-infection with another sexually transmitted infection
Symptoms of chlamydia- female
- Usually asymptomatic
- Dysuria – most common symptom
- Fever
- Offensive vaginal discharge
- Lower abdominal pain
Symptoms of chlamydia male
- Usually either presents with unilateral epidydimal-orchitis or dysuria with urethral discharge
- Reiter’s syndrome – more common in males
o Reactive arthritis – urethritis, conjunctivitis and arthritis
o Remember with the mnemonic of can’t see, can’t wee and can’t even climb a tree
Causative agent of chlamydia
Causative agent is Chylamydia trachomatis. An obligate intracellular parasite. 70% of infected women and 50% of infected men no obvious symptoms
Presentation of gonorrhoea
- Gonorrhoea presents quite similarly to chlamydia with mucopurulent discharge, dysuria, lower abdominal pelvic pain and anogenital symptoms in both men and women
- Gonorrhoea is more likely to cause pharyngeal infection
- In pregnant women with gonorrhoea in their reproductive tract, children can develop conjunctivitis <48 hours after delivery and need to be treated effectively and urgently to reduce risk of lasting optical complications
- Thick yellow/green discharge, pain when urinating
- In women: bleeding between periods, pelvic inflammatory disease
- In men: urethritis, dysuria
Investigations for chlamydia and gonorrhoea
- Urine test or endocervical swab/ vulvovaginal swab (recently shown to be more sensitive)
- NAAT is the most sensitive method for testing for gonorrhoea and Chlamydia
Management of chlamydia and gonorrhoea
- Chlamydia= Doxycycline 100mg BD 7 days or azithromycin 1g single dose
- Gonorrhoea= Azithromycin 1g oral with 500mg IM ceftriaxone single dose
- NAAT should be repeated 2 weeks later or cultures >72 hours after antibiotics given to test for adequate treatment of infection
Genital herpes
- Transmission occurs via contact with mucosal secretions from anogenital or oral mucosa or from contact with ulcerative lesions
- HSV-1 is more likely to cause oral infections where as HSV-2 is more likely to cause genitourinary infections however both serotypes can cause infections in either area
Genital herpes- risk factors
- Multiple sexual partners
- History of sexually acquired infections
- Female gender
- HIV
- Men who have sex with men (MSM)
Genital herpes- presentation
- Prodromal features tend to last 5-7 days and mimic features of flu
- Primary infection usually presents with crops of painful blisters in a symmetrical distribution over the anogenital mucosa
- Tender lymphadenopathy and local oedema are a feature of primary infection
- Dysuria
- Vaginal or urethral discharge
- In secondary infection, presentation is more likely to be unilateral and usually less severe with each successive infection
- Primary infections can last several weeks whereas recurrent infections don’t tend to last more than a few days and symptoms of pain and itch aren’t usually as profound
Genital herpes- Investigations
- Viral culture and PCR amplification can be used to identify most cases of infection. Serological tests can take up to 12 weeks to become positive so a negative test before 3 months does not rule out infection (NAAT)
- Urine dipstick/ MSU
- Pelvic USS
Genital herpes- complications
Chronic pelvic pain, Damage to fallopian tubes, risk of infertility, ectopic pregnancy.
Genital herpes- management
- Management is usually supportive however antiretroviral therapy can be given
o Aciclovir 400 mg three times daily; OR
o Valaciclovir, 500 mg twice daily for five days. - Antiretroviral therapy does not alter the course of the infection, the person is likely to still have relapsing recurrence and future flares of anogenital ulceration but it does reduce the severity and duration of the flares
Congenital syphilis
Agent- Treponema pallidum
- Bacterial infection with mother to child vertical transmission still a major cause of still birth and neonatal mortality in the developing world
Congenital syphilis:
o Early: Occurs within the first two years of life
o Late: Disease manifestation is after two years of life
Syphilis- acquires
o Important co-infection with HIV so important to test all patients for HIV with confirmed diagnosis of syphilis
o Primary: Incubation period of 2-3 weeks= Presents with primary Chancre: Single ulcerative lesion to the genitalia
o Secondary: Generalised infection with systemic features
o Tertiary: Widespread multisystem disease, neuro and cardiovascular manifestations are most common= Gummata: A common manifestation of tertiary syphilis with inflammatory fibrous nodules and plaques causing local destruction which can affect any organ but present commonly in bones and skin
Syphilis- investigations
Investigations into syphilis are dependant on the extent and stage of disease. Any patient with a new diagnosis of syphilis should be reviewed for a full sexual health screen and if presenting with tertiary disease, neurological and cardiovascular investigations such as lumbar punctures and ECGs should be considered
Specific screening for syphilis
T. Pallidum immunoassay testing
o IgM for acute infection
o IgG becomes positive after 5 weeks
Management of syhphilis
- Intramuscular benzathine benzylpenicillin
- If pen allergic, doxycycline or azithromycin should be considered
- Screening is offered to all women who become pregnant
- Procaine penicillin if neurological syphilis is confirmed
Jarisch-Herxheimer reaction
- Acute febrile illness that occurs in response to syphilis treatment
- Presents with myalgia, fatigue and headache and rigors, normally resolves with in 24 hours
- May be life threatening if occurs with tertiary syphilis but range of severity
- Management is supportive and patients are advised to use antipyrexials
