Obs and Gynae Flashcards
A 75 year old IDDM has recently been on a course of antibiotics for a chest infection. She has been to her GP complaining of a thick white smelly vaginal discharge
a. Candida Albicans
b. Retained Tampon
c. Granulation Tissue
d. Cervical Carcinoma
e. Vesicovaginal Fistula
f. Bacterial Vaginosis
g. Uterine Carcinoma
h. Ring Pessary
i. Chlamydia Trachomatis
j. Post-menopausal Atrophic Changes
Candida Albicans - yeast like fungus, most common cause of vaginal infection
Candidiasis is more common in diabetics, the obese, pregnancy, when antibiotics have been given or when immunity has been compromised. It tends to present with irritation and soreness of the vulva and anus (inflamed and red), and a ‘cottage cheese’ discharge. Superficial dyspareunia and dysuria may occur.
Diagnosis is established by culture and topical imidazole (e.g. clomtrimazole - Canesten) or vaginal pessaries (imidazole) or oral fluconazole may be required.
A 45 year old has been referred to the hospital with a history of intermittent offensive brown vaginal discharge and post-coital bleeding. She has not attended for cervical smear test for the past 10 years
a. Candida Albicans
b. Retained Tampon
c. Granulation Tissue
d. Cervical Carcinoma
e. Vesicovaginal Fistula
f. Bacterial Vaginosis
g. Uterine Carcinoma
h. Ring Pessary
i. Chlamydia Trachomatis
j. Post-menopausal Atrophic Changes
Cervical Carcinoma - CIN is the pervasive stage therefore the risk factors are the same: smoking, COCP, immunosuppression, HPV is found in all cervical cancers. Most common when screening has been inadequate, and immunosuppression (HIV, steroids) accelerates the process of invasion from CIN.
90% are squamous, also adenocarcinoma.
May present with PCB or IMB, offensive discharge
Screening: 3 yearly 25-49; 5 yearly 50-64, colposcopy if abnormal - LBC
A 55 year old has had an abdominal hysterectomy 2 months ago. She has started noticing clear watery vaginal discharge
a. Candida Albicans
b. Retained Tampon
c. Granulation Tissue
d. Cervical Carcinoma
e. Vesicovaginal Fistula
f. Bacterial Vaginosis
g. Uterine Carcinoma
h. Ring Pessary
i. Chlamydia Trachomatis
j. Post-menopausal Atrophic Changes
Vesicovaginal Fistula: an abnormal connection between the urinary tract and vagina. The most common are vesicovaginal and urethrovaginal fistulae. In the developing world they are common as a result of obstructed labour. In the West they are rare and usually due to surgery, radiotherapy or malignancy. Investigation is with a CT urogram or cystoscopy.
A 22 year old gives a history of grey coloured vaginal discharge, which smells unpleasantly strong but does not itch. It seemed to be associated with the use of barrier contraception
a. Candida Albicans
b. Retained Tampon
c. Granulation Tissue
d. Cervical Carcinoma
e. Vesicovaginal Fistula
f. Bacterial Vaginosis
g. Uterine Carcinoma
h. Ring Pessary
i. Chlamydia Trachomatis
j. Post-menopausal Atrophic Changes
Bacterial Vaginosis (Gardnerella or anaerobic vaginosis) - where normal lactobacilli are overgrown by a mixed flora including anaerobes, Gardnerella and Mycoplasma hominis. A grey, white discharge is present, but the vagina is not red or itchy. There is a characteristic fishy odour from amines released by bacterial proteolysis. Diagnosis is established by a raised vaginal pH, the typical discharge, a positive 'whiff' test (KOH added to secretions) and the presence of 'Clue cells' (epithelial cells studded with Gram variable coccobacilli) on microscopy. Treatment involves metronidazole or clindamycin cream. These bacteria can cause secondary infection in PID and there is also an association with pre-term labour and miscarriage - screening and treatment reduces the risk of preterm birth if used before 20 weeks in woman with a history of preterm birth. The normal vagina is lined by squamous epithelium, richly colonised by bacterial flora, predominantly Lactobacillus, and has an acidic pH (
A 26 year old who has been IDDM since the age of 10 is failing to progress in labour
a. Cervical fibroid
b. Persistant OP position
c. Previous Pelvic fracture
d. Fetal Macrosomia
e. Irregular Contractions
f. Breech Position
g. OT position
h. Rickets
i. Transverse Lie
j. Face Presentation
Fetal Macrosomia
Raised metal blood glucose levels induce metal hyperinsulinaemia, causing metal fat deposition and excessive growth (macrosomia)
Fetal Complications of DM:
- Congenital abnormalities: particularly neural tube and cardiac defects are 3-4X more common in established diabetics and are related to peri-conceptual glucose control.
- Preterm Labour: natural or induced occurs in 10% of established diabetics, and metal lung maturity at any given gestation is less than non-diabetic pregnancies.
- Birthweight: increased - fetal pancreatic islet cell hyperplasia leads to hyperinsulinaemia and fat deposition. This leads to increased urine output and polyhydramnios is common
- Dystocia and birth trauma are more common
- Fetal compromise, fetal distress in labour and sudden fetal death are more common (particularly in 3rd Trimester poor glucose control)
Delivery should be at 39 weeks, during labour glucose levels are maintained with a sliding scale of insulin and dextrose infusion
The neonate commonly develops hypoglycaemia because it has become accustomed to hyperglycaemia and so has high insulin levels
Risk factors for GDM: previous GDM, previous foetus >4.5kg, previous unexplained still birth, first degree relative with diabetes, BMI>30, racial origin, polyhydramnios, persistent glycosuria.
Shoulder dystocia: when additional manoeuvres are required after normal downward traction has failed to deliver the shoulders after the head has delivered. Excessive traction on the neck damages the brachial plexus causing Erb’s Palsy (waiter’s tip) which is permanent in about 50% of cases. Mean time from delivery of the head to delivery of the shoulders should be less than 5 minutes.
Risk Factors: large baby (>4kg), previous shoulder dystocia, increased maternal BMI, labour induction, low height, maternal diabetes, instrumental delivery
HELPERR: Call for help, evaluate for episiotomy, legs in McRoberts position, Suprapubic pressure, enter for manoeuvres (Woodscrew, reverse woodscrew and Rubin 2), Remove the posterior arm, Repeat/Roll onto all fours
Last resorts include symphisiotomy (after lateral replacement of the urethra with a metal catheter, and the Zavanelli manoeuvre
A primiparous patient with a term pregnancy and cephalic presentation. Over the past 4 hours she has remained at 4cm dilatation on vaginal examination. She is not yet requiring analgesia
a. Cervical fibroid
b. Persistant OP position
c. Previous Pelvic fracture
d. Fetal Macrosomia
e. Irregular Contractions
f. Breech Position
g. OT position
h. Rickets
i. Transverse Lie
j. Face Presentation
Irregular Contractions - she is a primp, and not requiring analgesia yet so is not yet experiencing proper contractions.
Once labour is established, the uterus contracts for 45-60 seconds about every 2-3 minutes. This pulls the cervix up (effacement - normally a tubular structure, the cervix is drawn up into the lower segment and becomes flat) and causes dilatation, aided by the pressure of the head as the uterus pushes the head down into the pelvis, this is commonly accompanied by a ‘show’ or pink/white mucus plug from the cervix, and/or rupture of the membranes, causing release of liquor. Poor uterine activity is a common feature of the nulliparous woman and in induced labours.
Involuntary contractions of uterine smooth muscle occur throughout the third trimester and are often felt as Braxton Hicks contractions. Labour is diagnosed when painful, regular contractions lead to effacement and dilatation of the cervix
Movements of the fetal head:
- Engagement in OT
- Descent and Flexion
- Rotation 90 degrees to OA
- Descent
- Extension to deliver
- Restitution and delivery of shoulders
1st Stage: Diagnosis of labour until cervix is fully dilated (10cm) - the descent, flexion and internal rotation occur to a varying degree. Membranes normally rupture prior to or during this stage. Latent phase is where the cervix dilates slowly (3cm) and may take several hours. The active phase follows, averaging 1cm/hour in nulliparous women, 2cm/hour in multiparous women. The active first stage should not normally last longer than 12 hours.
2nd Stage: From full dilation to delivery - descent, flexion and rotation are all complete and followed by extension as the head delivers. Passive stage is from full dilatation to when head reaches the pelvic floor and the women experiences a desire to push. The active stage is when the mother is pushing with contractions, the speed of delivery should be
A 35 year old Nigerian woman who is in spontaneous labour. She has a history of having a myomectomy for previous menorrhagia and is progressing slowly in labour
a. Cervical fibroid
b. Persistant OP position
c. Previous Pelvic fracture
d. Fetal Macrosomia
e. Irregular Contractions
f. Breech Position
g. OT position
h. Rickets
i. Transverse Lie
j. Face Presentation
Cervical Fibroid - Leiomyomata, benign tumours of the myometrium, common near menopause, in Afro-Caribean women and those with a FH. Less common in parous women, those who have taken COCP or injectable contraceptives.
In pregnancy fibroids can cause premature labour, malpresentation, transverse lie, obstructed labour and postpartum haemorrhage.
Red degeneration is common in pregnancy and can cause severe pain. Fibroids should not be removed at C-section as bleeding can be heavy. Pedunculate fibroids may tort postpartum
A 40 year old grand multiparous woman who has attended labour ward at term with a 3 hour history of regular contractions and no PV loss. On abdominal palpation there is nothing in the maternal pelvis
a. Cervical fibroid
b. Persistant OP position
c. Previous Pelvic fracture
d. Fetal Macrosomia
e. Irregular Contractions
f. Breech Position
g. OT position
h. Rickets
i. Transverse Lie
j. Face Presentation
Transverse Lie: lie refers to the relationship between the foetus and the long axis of the uterus. if longitudinal the head and buttocks are palpable at each end (therefore presentation is cephalic or breech). If transverse lie, the foetus is lying across the uterus and the pelvis will be empty. If oblique the head or buttocks are palpable in one of the iliac fossa. Abnormal lie occurs in 1 in 200 births and is more common in early pregnancy (normal if before term).
Therefore preterm labour is more commonly complicated by an abnormal lie than labour at full term.
Polyhydramnios (more room to turn) or high parity (more lax uterus) are the most common causes, frequently resulting in an unstable lie.
Conditions that prevent turning e.g. fetal and uterine abnormalities and twin pregnancies may cause persistent transverse lie, as well as many conditions that prevent engagement, such as placenta praevia and pelvic tumours or uterine deformities. Unstable lie in nulliparous women is rare.
No management is required in transverse or unstable lie before 37 weeks unless the woman is in labour. After 37 weeks the woman is usually admitted to hospital in case the membranes rupture and USS to rule out possible causes (placenta praevia, polyhydramnios)
A 28 year old multiparous patient has had a long latent phase of labour and is not progressing at more than 1cm per hour
a. Cervical fibroid
b. Persistant OP position
c. Previous Pelvic fracture
d. Fetal Macrosomia
e. Irregular Contractions
f. Breech Position
g. OT position
h. Rickets
i. Transverse Lie
j. Face Presentation
Persistant OP position - can be associated with labour abnormalities and maternal and neonatal complications (eg, birth trauma, neonatal acidosis). Commonly prolongs 1st and 2nd stage of labour leading to an increase rate of interventions, such as artificial rupture of membranes, oxytocin augmentation, and operative delivery (vaginal, abdominal), and the mothers experience more delivery-related complications, such as anal sphincter injury
Risk factors: Nulliparity, Maternal age greater than 35 years, Obesity, African-American race, Previous OP delivery, Decreased pelvic outlet capacity, Gestational age ≥41 weeks, Birthweight ≥4000g, Prolonged first and/or second stage of labor
Fifteen to 20 percent of term cephalic fetuses are in occiput posterior (OP) position before labor and approximately 5 percent are OP at delivery. Most fetuses rotate to occiput anterior (OA) position, some maintain a persistent OP position, and others rotate from OA to OP position.
There is no effective method to facilitate rotation from occiput posterior to occiput anterior before labour.
Foetus with Down’s Syndrome
a. Maternal ALT 60iu/L
b. Maternal HbA1c = 15%
c. Fetal Hb 3g/dl, positive Coombs Test
d. Parvovirus IgM positive, IgG negative
e. Maternal Rubella IgG positive
f. 24 hour urinary protein 5.1g/L
g. Fetal Karyotype 47XY
h. Fetal Karyotype 45XO
i. 24 hour urinary protein 0.2g/L
Fetal karyotype 47XY - trisomy 21
((Trisomy 18 - Edwards, Trisomy 13 - Patau’s, 47XXY - Klinefelters, 45XO - Turner’s)
Down syndrome is the most common chromosome abnormality among live births and the most frequent form of intellectual disability caused by a demonstrable chromosomal abnormality. The syndrome is characterized by moderate to severe learning disability (average IQ approximately 40) in combination with short stature, characteristic facial features, heart defects (40 to 50 percent of cases), intestinal malformations (10 percent of cases), problems with vision and hearing (50 percent of cases), an increased frequency of infection, and other health problems.
The first trimester combined test: nuchal translucency (NT), maternal age, gestational age (by crown-rump length) combined with the serum markers pregnancy-associated plasma protein-A (PAPP-A) and free or total beta human chorionic gonadotropin (beta-hCG). Screening can be performed at 9 to 13 weeks of gestation with free beta-hCG or at 11 to 13 weeks with total beta-hCG.
The full integrated test consists of ultrasound measurement of nuchal translucency at 10 to 13 weeks, PAPP-A obtained at 10 to 13 weeks, and alpha fetoprotein (AFP), unconjugated estriol (uE3), hCG, and inhibin A obtained at 15 to 18 weeks. At detection rates of 85 or 95 percent, the full integrated test has the lowest false positive rate among Down syndrome screening tests, leading to the lowest rate of procedure-related losses per woman screened.
The quadruple test is the best available screening test for women who present for prenatal care in the second trimester. At 15 to 18 weeks of gestation (but as late as 22 weeks), the serum markers AFP, uE3, hCG, and inhibin A are measured in maternal serum.
Patients who screen positive are offered fetal karyotype determination for definitive diagnosis.
In the first trimester, karyotype is obtained by CVS - biopsy of the trophoblast by passing a fine gauge needle through the abdominal wall or cervix into the placenta (after 11weeks) - i.e. before amniocentesis and allows earlier identification of an abnormal foetus, at a time when abortion could be performed under GA. Miscarriage rate is higher than amniocentesis (because it is performed earlier, when spontaneous miscarriage is more likely to happen)
In the second trimester, amniocentesis is performed to obtain fetal cells for chromosomal analysis. Amniocentesis involves removing amniotic fluid using a fine gauge needle under USS guidance, it is safest performed from 15 weeks and can also be used to diagnose other chromosomal abnormalities and infections (CMV, toxoplasmosis) and inherited disorders (sickle cell, thalassaemia and cystic fibrosis). 1% miscarry after amniocentesis.
FISH and PCR are used to diagnose common abnormalities within 48 hours
Pre-eclampsia
a. Maternal ALT 60iu/L
b. Maternal HbA1c = 15%
c. Fetal Hb 3g/dl, positive Coombs Test
d. Parvovirus IgM positive, IgG negative
e. Maternal Rubella IgG positive
f. 24 hour urinary protein 5.1g/L
g. Fetal Karyotype 47XY
h. Fetal Karyotype 45XO
i. 24 hour urinary protein 0.2g/L
24 hour urinary protein 5.1g/L
Pre-eclampsia is a multi-system disease that usually manifests as hypertension (BP >140/90) and proteinuria (>0.3g/24hours, 3+ on dipstick, PCR>30mg/nmol). Increased vascular resistance accounts for the hypertension, increased vascular permeability for proteinuria, reduced placental blood flow of IUGR and reduced cerebral perfusion for eclampsia.
Pre-eclampsia affects 6% of nulliparous women, and there is a 15% recurrence rate.
In normal pregnancy, trophoblastic invasion of the spiral arteries leads to vasodilatation of vessel walls. In pre-eclampsia this invasion is incomplete, and the impaired maternofetal trophoblast interaction may be caused by altered immune responses - the result is decreased utero-placental blood flow. The ischaemic placenta induces wide spread endothelial cell damage, causing vasoconstriction, increased vascular permeability and clotting dysfunction.
Predisposing factors: nulliparity, previous/FH pre-eclampsia, lon inter-pregnancy interval, obesity, extremes of maternal age (particularly >40years), disorders characterised by microvascular disease (chronic hypertension, chronic renal disease, sickle cell disease, diabetes, AI disease, APL syndrome), pregnancies with a larger placenta (twins, fetal hydrops, molar pregnancy)
Intra-uterine Fetal Infection
a. Maternal ALT 60iu/L
b. Maternal HbA1c = 15%
c. Fetal Hb 3g/dl, positive Coombs Test
d. Parvovirus IgM positive, IgG negative
e. Maternal Rubella IgG positive
f. 24 hour urinary protein 5.1g/L
g. Fetal Karyotype 47XY
h. Fetal Karyotype 45XO
i. 24 hour urinary protein 0.2g/L
Parvovirus IgM positive, IgG negative
B19 virus infects 0.25% of pregnant women. A ‘slapped cheek’ appearance is typical (erythema infectiosum) but may have arthralgia or be asymptomatic.
Neonatal/fetal effects: virus suppresses fetal erythropoesis causing anaemia, varying degrees of thrombocytopenia also occur. Fetal death occurs in 10% of pregnancies, usually with infection before 20 weeks gestation
Fetal anaemia is detectable on USS, initially as increased blood flow velocity in the fetal MCA and subsequently as oedema (fetal hydrops) from cardiac failure. Spontaneous resolution of anaemia and hydrops occurs in about 50%
Management: infected mother’s are regularly scanned to look for anaemia, where hydrops is detected in utero transfusion is given if severe.
Obstetric Cholestasis
a. Maternal ALT 60iu/L
b. Maternal HbA1c = 15%
c. Fetal Hb 3g/dl, positive Coombs Test
d. Parvovirus IgM positive, IgG negative
e. Maternal Rubella IgG positive
f. 24 hour urinary protein 5.1g/L
g. Fetal Karyotype 47XY
h. Fetal Karyotype 45XO
i. 24 hour urinary protein 0.2g/L
Maternal ALT 60iu/L Characterised by itching of palms of hands and soles of feet, without a skin rash, but with abnormal LFTs, due to abnormal sensitivity to the cholestatic effects of oestrogens. It is familial and tends to re-occur (50%). It is associated with a increased risk of sudden stillbirth (around 1% - likely due to toxic effects of bile salts, possibly precipitating fetal arrhythmia) and preterm delivery. Serum bile acids are raised. There is an increased tendency to haemorrhage so vitamin K 10mg/day is given from 36 weeks. Ursodeoxycholic acid (UDCA) relieves itching and may reduce obstetric risks. USS and CTG are poor at predicting adverse outcomes.
Rhesus Isoimmunisation
a. Maternal ALT 60iu/L
b. Maternal HbA1c = 15%
c. Fetal Hb 3g/dl, positive Coombs Test
d. Parvovirus IgM positive, IgG negative
e. Maternal Rubella IgG positive
f. 24 hour urinary protein 5.1g/L
g. Fetal Karyotype 47XY
h. Fetal Karyotype 45XO
i. 24 hour urinary protein 0.2g/L
Fetal Hb 3g/dl, positive Coombs Test
Occurs when the mother mounts an immune response against fetal red cells that enter her circulation, the resulting antibodies then cross the placenta and cause fetal red blood cell destruction.
The most significant is Rhesus D gene, D is dominant to d. Rhesus negative = dd, and their immune system will recognise the D antigen as foreign if they are exposed to it. Small amounts of blood cross the placenta and enter the maternal circulation in normal pregnancy, and particularly at sensitising events (delivery, TOP, miscarriage or threatened miscarriage after 12 weeks, ERPOC, Ectopic pregnancy, ECV, Invasive uterine procedure - CVS, amniocentesis, vaginal bleeding). If the foetus is D rhesus positive and the mother is D rhesus negative, the mother will mount an immune response (sensitization) creating anti-D antibodies. Immunity is permanent and if the mother’s immune system is again exposed the the antigen (e.g. subsequent pregnancy), a large number of anti-bodies are rapidly created, these can cross the placenta and bind to the fetal rbcs which are then destroyed in the fetal reticuloendothelial system. This can cause haemolytic anaemia and ultimately death (rhesus haemolytic disease). A similar immune response can be mounted against other red blood cell antigens - the most important antibodies are anti-c and anti-kell (a non-rhesus antibody), particularly after blood transfusion
Anti-D is given to all Rhesus negative mothers to ‘mop up’ fetal red cells that cross the placenta by binding to their antigens, preventing recognition by the mothers immune system - 1500IU at 28 weeks or within 72 hours of a sensitising event, although benefit can still be gained within 10 days. Postnatally the neonate’s blood group is checked and if rhesus positive, anti-D is given to the mother within 72 hours of delivery. A Kleihauer test, to assess the number of fetal cells in the maternal circulation is also performed within 2 hours of birth to detect occasional larger fetomaternal haemorrhages that may require larger doses of anti-D to mop up (unnecessary if neonate is rhesus negative). Also check FBC and bilirubin of neonate.
Manifestations of rhesus disease: Haemolysis! If mild will cause neonatal jaundice, or there may be sufficient to cause neonatal anaemia (haemolytic disease of the newborn). More severe disease causes in utero anaemia and, as this worsens cardiac failure, ascites and oedema (hydrous) and fetal death follows. Rhesus disease usually worsens with successive pregnancies as maternal antibody production increases.
Treatment of fetal anaemia: in utero transfusion
15% of caucasian women are rhesus negative
Maternal Diabetes
a. Maternal ALT 60iu/L
b. Maternal HbA1c = 15%
c. Fetal Hb 3g/dl, positive Coombs Test
d. Parvovirus IgM positive, IgG negative
e. Maternal Rubella IgG positive
f. 24 hour urinary protein 5.1g/L
g. Fetal Karyotype 47XY
h. Fetal Karyotype 45XO
i. 24 hour urinary protein 0.2g/L
Maternal HbA1c = 15%
Glucose tolerance decreases in pregnancy due to altered carbohydrate metabolism and antagonistic effects of human placental lactogen, progesterone and cortisol.
NICE: fasting glucose level >7.0mmol/L or >7.8mmol/L 2 hours after a 75g glucose load (GTT) - screening at 28 weeks or at 18 weeks if history of GDM. Aim for HbA1c
55 year old woman with a history of loss of urine on coughing and bending. Urodynamic studies show no evidence of detrusor instability
a. Multiple Sclerosis
b. Urinary Tract Infection
c. Genuine Stress Incontinence
d. Idiopathic Detrusor Overactivity
e. Sensory Urgency
f. Fibroids
g. Fistula
h. Bladder Tumour
i. Prolapsed Disc
j. Detrusor Overactivity secondary to menopause
Genuine stress Incontinence (a symptom 50% incontinence) - Involuntarily leaking urine on effort of exertion, or sneezing or coughing (COPD), and when confirmed on urodynamic studies it is called urodynamic stress incontinence (USI). It commonly arises as a result of urethral sphincter weakness.
On Cystometry (urodynamic studies):
- No increase in detrusor press with filling
- No detrusor contraction with coughing
- Urine flow with cough
Aetiology: pregnancy and vaginal delivery, particularly prolonged labour and forceps delivery, obesity and age (post menopausal). Prolapse commonly co-exists but is not always related. Previous hysterectomy may predispose to USI.
When there an increase in intra-abdominal pressure (“stress”) the bladder is compressed and its pressure rises. Normally the bladder neck is as equally compressed so that the pressure difference is unchanged - urethral pressure = bladder pressure. However if the bladder neck has slipped below the pelvic floor (due to weak supports), and the pelvic floor is unable to compensate, the bladder pressure is greater than the urethral pressure and incontinence results.
Faecal incontinence may also co-exist (also due to childbirth). Examination with a Sims speculum often reveals a cystocoele or urethrocoele.
Management:
- Lifestyle (obesity, COPD, asthma, fluid intake)
- Conservative: strengthen pelvic floor 3 months supervised physiotherapy (PFMT), at least 8 contractions, 3 times per day. Vaginal cones.
- Medical: Duloxetine (moderate to severe USI) serotonin and NA reuptake inhibitor (SNRI) that enhances urethral striated sphincter activity via a centrally mediated pathway. Causes a dose-dependent decrease in frequency of incontinence episodes. Nausea is a common side effect (25%), as well as dyspepsia, dry mouth, dizziness, insomnia and drowsiness
- Surgical: When conservative measures have failed and QoL is compromised. TVT is first line, with cure rates up to 90% - polyprolene tape in a U shape under the mid urethra via a small vaginal anterior wall incision - minimally invasive. Colposuspension if fails.
A 26 year old presents with a 5 day history of worsening urinary frequency, nocturia and dysuria. Urinary testing indicates proteinuria
a. Multiple Sclerosis
b. Urinary Tract Infection
c. Genuine Stress Incontinence
d. Idiopathic Detrusor Overactivity
e. Sensory Urgency
f. Fibroids
g. Fistula
h. Bladder Tumour
i. Prolapsed Disc
j. Detrusor Overactivity secondary to menopause
Urinary Tract Infection - asymptomatic bacteriuria affects 5% of women, but increases to 20% in pregnancy.
Pyelonephritis affects 1-2% of women and is more likely to occur in pregnancy, causing loin pain, rigors, vomiting and a fever - requires IV antibiotics. E.coli accounts for 75% and is often resistant to amoxicillin.
A 60 year old presents with a 6 week history of urgency and nocturia and urge incontinence
a. Multiple Sclerosis
b. Urinary Tract Infection
c. Genuine Stress Incontinence
d. Idiopathic Detrusor Overactivity
e. Sensory Urgency
f. Fibroids
g. Fistula
h. Bladder Tumour
i. Prolapsed Disc
j. Detrusor Overactivity secondary to menopause
Idiopathic Detrusor Overactivity - a urodynamic diagnosis characterized by involuntary detrusor contractions during the filling phase, which may be spontaneous or provoked.
Overactive Bladder = urgency, with/without urge incontinence, usually with frequency or nocturia, in the absence of proven infection. 35% female incontinence.
Most commonly idiopathic, may occur following operations for USI as a result of neck of bladder obstruction, or as a result of underlying neuropathy (MS, spinal cord injury).
Detrusor contraction is normally felt as urgency, and leaking occurs if bladder pressure overcomes the urethral pressure (may be exacerbated by increased intra-abdominal pressure - and so can be confused with stress incontinence)
History of childhood enuresis is common, examination often normal.
Small frequent volumes of urine, high caffeine intake, cystometry demonstrates contractions on filling or provocation.
Conservative: decreased fluid intake, caffeine reduction, review diuretic/antipsychotic use. Bladder training
Medical: anti-cholinergics (anti-muscarinics) suppress detrusor activity - they block the muscarinic receptors that mediate detrusor smooth muscle contractions, relaxing the detrusor muscles
Botulinum toxin: blocks neuromuscular transmission, causing affected muscle to become weak. It is injected cytoscopically under local or general anaesthetic into the detrusor muscle into 10-30 different locations, sparing the trigonum. The most common complication is voiding dysfunction and urinary retention, which usually resolves as the effects of the treatment decline
A 30 year old woman from Somalia, 6 weeks post part, arrived in the UK 2 weeks ago, gives a history of feeling continually damp down below
a. Multiple Sclerosis
b. Urinary Tract Infection
c. Genuine Stress Incontinence
d. Idiopathic Detrusor Overactivity
e. Sensory Urgency
f. Fibroids
g. Fistula
h. Bladder Tumour
i. Prolapsed Disc
j. Detrusor Overactivity secondary to menopause
Fistula - abnormal connections between the urinary tract and other organs. The most common are vesicovaginal and urethrovaginal fistulae. In the developing world they are common as a result of obstructed labour; whereas in the West they are rare and due to surgery, radiotherapy or malignancy. Investigation is with CT urogram or cystoscopy. Whilst small fistulae may resolve spontaneously, surgery is usually required.
A 53 year old woman presents with a 6 week history of hot flushes, sweats and vaginal dryness and urinary frequency
a. Multiple Sclerosis
b. Urinary Tract Infection
c. Genuine Stress Incontinence
d. Idiopathic Detrusor Overactivity
e. Sensory Urgency
f. Fibroids
g. Fistula
h. Bladder Tumour
i. Prolapsed Disc
j. Detrusor Overactivity secondary to menopause
Detrusor Overactivity secondary to menopause
Many women develop bladder filling symptoms after the menopause. Oestrogen treatment in postmenopausal women improves symptoms of vaginal atrophy, such as vaginal dryness and irritation. Vaginal oestrogen administration reduces symptoms of urgency, urge incontinence, frequency and nocturia
A 29 year old needle-phobic who is 8 weeks post partum and breast feeding would like reliable contraception
a. COCP
b. POP
c. Mirena
d. Laparoscopic Sterilisation
e. Diaphragm
f. Condoms
g. Copper IUD
h. COCP + condoms
i. Depot
j. Hysteroscopic Sterilisation
Mirena - Levonorgestrel-releasing IUD: LNg20 IUD initially releases 20 mcg of levonorgestrel daily, declining to 10 to 14 mcg per day after five years. Like the copper IUD, the stem contains barium sulfate so it can be detected by x-ray, and it does not contain latex.
The progestin effect is primarily local. The plasma concentration of levonorgestrel is far lower than the endometrial concentration and varies among patients. It is 100 to 200 pg/mL within the first few weeks of use, with a gradual decline over time and wide individual variation. This level is much less than that associated with progestogen-only pills (1500 to 2000 pg/mL), but high enough to cause systemic side effects in some users, and to suppress ovulation. Serum estradiol levels are not affected.
With perfect use, the probability of pregnancy in the first year is 0.1 percent; comparable to that with sterilization procedures. he LNg20 IUD is approved for up to five years of use.
Advantages: highly effective, dramatic reduction in menstrual blood loss, protective against PID
Disadvantages: persistent spotting/bleeding in first month of use, progestogenic side effects (acne, breast tenderness), no protection against STIs.
Mode of action: all IUDs cause an inflammatory response in the endometrium which prevent implantation. Whereas copper bearing IUDs work primarily by a toxic effect on sperm which prevents fertilisation, the Mirena prevents pregnancy primarily by a local hormonal effect on the cervical mucus and endometrium.
Contraindications: previous PID or ectopic pregnancy, known malformations of the uterus.
Although IUDs increase the risk of PID in the first few weeks after insertion, the long term risk is similar to that of women not using any form of contraception
A 40 year old smoker who has completed her family and wants definitive contraception. She has a history of COPD and PID
a. COCP
b. POP
c. Mirena
d. Laparoscopic Sterilisation
e. Diaphragm
f. Condoms
g. Copper IUD
h. COCP + condoms
i. Depot
j. Hysteroscopic Sterilisation
Hysteroscopic Sterilisation
For an older woman wanting definitive contraception with a complete family sterilisation is the answer. COPD means intubation will be difficult in this patient and previous PID means there may be adhesions and scar tissue, so a hysteroscopic procedure is preferral.
Sterilisation involves the mechanical blockage of both Fallopian tubes to prevent sperm reaching and fertilising the oocyte.
A thorough discussion of the risks, benefits, and alternatives to permanent sterilization should take place and informed consent obtained.
Surgical sterilization is safe (complication rate less than 1 percent) and effective (overall 10-year probability of pregnancy 18.5 per 1000 procedures). Pregnancies occurring after tubal ligation are more likely to be ectopic.
The procedure should be considered permanent. Reversal may be successful, but requires major surgery, is costly, and may not be covered by medical insurance. Regret after sterilization may be related to young age, conflicted feelings at the time of surgery, or a subsequent change in marital status.
Laparoscopic sterilization techniques and sterilization by minilaparotomy have comparable safety and efficacy. The choice of method should be based upon the clinical situation and patient and physician preference.
Women who have undergone tubal ligation are less likely to develop ovarian cancer and pelvic inflammatory disease, but may have a slightly higher rate of future hysterectomy.
A 19 year old student who had Chlamydia in the past is attending for her second termination and wants to discuss contraception. She does not have a regular partner
a. COCP
b. POP
c. Mirena
d. Laparoscopic Sterilisation
e. Diaphragm
f. Condoms
g. Copper IUD
h. COCP + condoms
i. Depot
j. Hysteroscopic Sterilisation
COCP and condoms - at risk of STIs Oral contraceptives (OCs) have several mechanisms of action, including suppression of hypothalamic gonadotropin-releasing hormone (GnRH) and pituitary gonadotropin secretion - FSH and LH. The most important mechanism for providing contraception is inhibition of the midcycle LH surge, so that ovulation does not occur. Combination OCs are potent in this regard, but progestin-only pills are not. Peripheral effects include making the endometrium atrophic and hostile to an implanting embryo and altering cervial mucus to prevent sperm ascending into the uterine cavity. Absolute Contraindications: Circulatory disease (IHD, CVA, significant HTN, thrombosis, any acquired or inherited pro-thrombotic tendency, any significant RF for CVD), acute or severe liver disease, oestrogen dependent neoplasms (particularly breast cancer), focal migraine Relative Contraindications: generalized migraine, long term immobilization, irregular vaginal bleeding (until a diagnosis has been made), less severe CVD RFs (DM, obesity, smoking) Oestrogens induce a pro-thrombotic tendency. The higher the dose of oestrogen, the greater the risk VTE - normal population 5 per 100,000; 30 per 100,000 COC, 60 per 100,000 for pregnant women. Drug interactions: enzyme inducing drugs (e.g. anti-epileptic medications) may decrease the efficacy, and some broad spectrum anti-biotics can alter intestinal absorption of COC and reduce its efficacy. COC can also be used to treat heavy, painful periods, will improve PMS and reduce the risk of PID. COC offers longterm protection against both endometrial and ovarian cancers and can be used as a treatment for acne
A 30 year old who is 4 weeks post partum having previously fallen pregnant whilst on the COCP and is currently breast feeding. She does not intend to fall pregnant for the next 2 years. She has a history of submucosal fibroids distorting the uterine cavity
a. COCP
b. POP
c. Mirena
d. Laparoscopic Sterilisation
e. Diaphragm
f. Condoms
g. Copper IUD
h. COCP + condoms
i. Depot
j. Hysteroscopic Sterilisation
Depot - obviously patient is unreliable at taking medication if she has fallen pregnant whilst on the COCP! If she has a distorted uterine cavity then she isn’t a candidate for an IUD. There is no indication that she has finished her family and so sterilisation isn’t appropriate.
Depot medroxyprogesterone acetate (DMPA) is an injectable, progestin-only contraceptive that provides highly effective, relatively long-acting (three months), reversible contraception.
DMPA is a good contraceptive option for the following groups of women:
- Women who do not want to take a contraceptive pill daily
- Women who have a contraindication to, or wish to avoid, an estrogen-containing contraceptive
- Women who would like to eliminate regular menses
- Adolescents who may not consistently remember to use types of contraception that require frequent administration
- Institutionalized adolescents and women who have difficulty using other forms of contraception
- Wheelchair-bound adolescents and women
DMPA primarily acts by inhibition of gonadotropin secretion, thereby inhibiting follicular maturation and ovulation. The inhibition of ovarian function results in a hypoestrogenic state, which inhibits endometrial proliferation and renders the endometrium less receptive to implantation. Progestins also cause changes in cervical mucus (thicker and less permeable to sperm) and tubal motility (reduced ciliary action) that are unfavorable to sperm migration, thus inhibiting fertilization.
The ideal time to initiate DMPA is within seven days of the onset of menses. This approach increases the certainty that the patient is not pregnant at the time of injection and prevents ovulation during the first month of use, so that back-up contraception is unnecessary. Most women have pharmacologically active drug levels and relatively impermeable cervical mucus within 24 hours after injection.
Fertility is not fully re-established until 18 months after the last injection.
Side effects: Irregular bleeding/spotting, amenorrhoea, weight changes, headache, mood changes.