Women's Health Flashcards

1
Q

Define Pelvic Organ Prolapse?

A

Descent of the pelvic organs into the vagina.

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2
Q

What is the pathology of a Prolapse?

A

The result of weakness and lengthening of the ligaments and muscles surrounding the uterus, rectum and bladder.

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3
Q

What types of prolapse can result from a weakness in the Apical Vaginal Wall?

A
  • Uterine prolapse
  • Vaginal Vault Prolapse
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4
Q

what is a Uterine Prolapse?

A

Where the uterus itself descends into the vagina

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5
Q

What is a Vaginal Vault Prolapse?

A

Occurs in women that have had a hysterectomy and no longer have a uterus.

The top of the vagina (the vault) descends into the vaginal canal

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6
Q

What types of Prolapse can result from a weakness in the Posterior Vaginal Wall?

A
  • Enterocele
  • Rectocele
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7
Q

What is an Enterocele?

A

Defect in the posterior vaginal wall allowing the small intestine to prolapse forwards into the vagina

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8
Q

What is a Rectocele?

A

Defect in the posterior vaginal wall allowing the rectum to prolapse forwards into the vagina

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9
Q

What type of prolapse can result from a weakness in the Anterior Vaginal Wall?

A
  • Cystocele
  • Urethrocele
  • Cystourethrocele
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10
Q

What is a Cysteocele?

A

Prolapse of the bladder backwards into the vagina due to a defect in the anterior vaginal wall

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11
Q

What is a Urethrocele?

A

Prolapse of the Urethra backwards into the vagina due to a defect in the anterior vaginal wall

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12
Q

What is a Cystourethrocele?

A

Prolapse of both the bladder and the urethra into the vagina through the anterior vaginal wall.

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13
Q

What is the Epidemiology of Pelvic Organ Prolapse?

A
  • Common condition
  • More common in Postmenopausal women
  • More common in those who have undergone childbirth
  • Prevalence increases with age
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14
Q

What are some risk factors for developing pelvic organ prolapse?

A
  • Multiple vaginal deliveries
  • Increasing age
  • Instrumental, prolonged or traumatic delivery
  • Hysterectomy
  • Advanced age and postmenopausal status
  • Obesity
  • Chronic respiratory disease causing coughing
  • Chronic constipation causing straining
  • Heavy lifting
  • Connective tissue disorders
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15
Q

What are the clinical features of a pelvic organ prolapse?

A

Depend on the type and severity

  • Pelvic discomfort or Sensation of Heaviness or Sensation of something coming down
  • Visible protrusion of tissue from the vagina
  • Urinary Symptoms such as Incontinence, recurrent UTIs or voiding difficulties
  • Defecatory symptoms such as Constipation or incomplete bowel emptying
  • Sexual Dysfunction
  • Women may notice a lump or mass that they will often push back up themselves.
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16
Q

What clinical features are Rectoceles particularly associated with?

A

Constipation

  • Women can develop Faecal loading in the part of the rectum that ha prolapsed.
  • This may lead to significant constipation and urinary retention
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17
Q

What are some differential diagnoses for pelvic organ prolapse?

A
  • Gynaecologic malignancy: associated with abnormal vaginal bleeding, weight loss, and pelvic pain
  • Cervicitis: characterized by vaginal discharge, bleeding, and pelvic pain
  • Urethral diverticulum: presents with dysuria, recurrent UTIs, and a palpable anterior vaginal mass
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18
Q

What are the investigations for a Pelvic Wall Prolapse?

A
  • Detailed Pelvic Examination
  • Imaging studies: MRI or Ultrasound may be used in complex cases
  • Urodynamic studies if co-existing urinary symptoms.
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19
Q

What is used to examine the pelvis when investigating for Pelvic organ prolapse?

A

Sim’s Speculum

  • U shaped speculum that is used to support the anterior or posterior vaginal wall whilst the other walls are examined.
  • Women are asked to cough or bear down to assess the full decent of the prolapse.
  • Dorsal and Left Lateral position are used.
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20
Q

How is a uterine prolapse graded?

A

Pelvic organ prolapse quantification system (POP-Q):

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.

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21
Q

What is the management for Pelvic Organ Prolapse?

A
  1. Conservative management: appropriate for women able to cope with mild symptoms, who do not tolerate pessaries or are not suitable for surgery
  • Pelvic floor Exercise
  • Avoidance of triggers: Straining, heavy lifting, weight loss (if overweight)
  • Topical Oestrogen
  1. Vaginal Pessaries: Inserted into the vagina to provide extra support to the pelvic organs.
  2. Surgery: Definitive option for treating Pelvic organ prolapse but must consider the risk and benefits of each individual.
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22
Q

What conservative management options are there for Pelvic Organ Prolapse?

A
  • Physiotherapy (pelvic floor exercises)
  • Weight loss
  • Lifestyle changes for associated stress incontinence, such as reduced caffeine intake and incontinence pads
  • Treatment of related symptoms, such as treating stress incontinence with anticholinergic mediations
  • Vaginal oestrogen cream
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23
Q

What are some options for Vaginal Pessaries?

A
  • Ring pessaries are a ring shape, and sit around the cervix holding the uterus up
  • Shelf and Gellhorn pessaries consist of a flat disc with a stem, that sits below the uterus with the stem pointing downwards
  • Cube pessaries are a cube shape
  • Donut pessaries consist of a thick ring, similar to a doughnut
  • Hodge pessaries are almost rectangular. One side is hooked around the posterior aspect of the cervix and the other extends into the vagina.
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24
Q

What is some key information about Vaginal Pessaries?

A
  • Should be removed and cleaned or changed periodically (every 4 months)
  • Can cause vaginal irritation and erosion over time
  • Oestrogen cream helps protect the vaginal walls from irritation
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25
Q

What are some possible complications of Pelvic Organ Prolapse Surgery?

A
  • Pain, bleeding, infection, DVT and risk of anaesthetic
  • Damage to the bladder or bowel
  • Recurrence of the prolapse
  • Altered experience of sex
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26
Q

Define Urinary Incontinence?

A

Involuntary passage of urine

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27
Q

Define Overactive Bladder Syndrome?

A

A chronic condition that results rom hyperactivity of the detrusor muscle. This is primarily characterised by urinary urgency and urge incontinence

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28
Q

What are the clinical features of Overactive Bladder Syndrome?

A
  • Urinary Urgency
  • Urge Incontinence
  • Frequency
  • Nocturia
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29
Q

What is a typical presentation of Overactive Bladder syndrome and Urge incontinence?

A
  • Typical description is of suddenly feeling the urge to pass urine, having to rush to the bathroom and not arriving before urination occurs.
  • Women with urge incontinence are very conscious about always having access to a toilet, and may avoid activities or places where they may not have easy access.
  • This can have a significant impact on their quality of life, and stop them doing work and leisure activities.
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30
Q

What are some differential diagnoses for Overactive Bladder Syndrome?

A
  • Urinary tract infections: Characterised by dysuria, urgency, frequency, suprapubic pain and haematuria.
  • Bladder stones: Symptoms include lower abdominal pain, dysuria, intermittent stream, and blood in the urine.
  • Interstitial cystitis: Presents with symptoms such as chronic pelvic pain, a persistent, urgent need to urinate, and frequent urination.
  • Diabetic neuropathy: Can cause bladder dysfunction, resulting in symptoms like frequent urination and incontinence.
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31
Q

What are the investigations for Overactive Bladder Syndrome?

A
  • Urinalysis and culture: To rule out infection
  • Frequency/volume chart: To assess the severity of the condition
  • Urodynamics: To evaluate bladder muscle function
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32
Q

What is the management for Overactive Bladder Syndrome?

A

First Line: For at least 6 weeks:

  • Bladder retraining: Which aims to increase the interval between voids, and suppress the urinary urge
  • Behavioural modifications: Such as reducing oral fluid intake, and avoiding caffeine and alcohol

Second Line:

  • Anticholinergic drugs: Like oxybutynin, Tolterodine and solifenacin
  • Mirabegron: An alternative to anticholinergics
  • Vaginal oestrogens: Used if urogenital atrophy is a likely contributory factor

Invasive options when medical treatments fail

  • Botulism toxin: Used specifically for refractory cases
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33
Q

Give some anticholinergic drugs used to treat an Overactive Bladder?

A
  • Oxybutynin
  • Tolterodine
  • Solifenacin
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34
Q

What are some side effects of Anticholinergic Mediations?

A
  • Dry mouth and eyes
  • Urinary Retention
  • Constipation
  • Postural Hypotension
  • Cognitive decline and memory problems
  • Worsening of Dementia
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35
Q

What is Mirabegron?

A

A beta 3 agonist that stimulates the sympathetic nervous system causing relaxation of the bladder.

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36
Q

What is a contraindication of Mirabegron?

A

Uncontrolled Hypertension.

  • Since it stimulates the sympathetic nervous system it can lead to a raised blood pressure and can result in a hypertensive crisis!
  • Can also increase the risk of stroke and TIA
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37
Q

What are some examples of Invasive options to treat Overactive Bladder Syndrome when the bladder has failed to respond to medication?

A
  • Botulinum toxin type A injection into the bladder wall
  • Percutaneous sacral nerve stimulation involves implanting a device in the back that stimulates the sacral nerves
  • Augmentation cystoplasty involves using bowel tissue to enlarge the bladder
  • Urinary diversion involves redirecting urinary flow to a urostomy on the abdomen
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38
Q

Define Urinary Incontinence

A

The loss of control of urination leading to involuntary passage of urine

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39
Q

What is the Physiology of the Storage phase of Continence?

A
  • Impulses from the cerebral cortex are transmitted to the pontine continence centre.
  • The pontine continence centre sends signals to sympathetic nuclei within T10-L2 sympathetic ganglia, which then sends further signals to the detrusor and internal urethral sphincter muscles via the sympathetic hypogastric nerve, stimulating:
    • Relaxation of the detrusor muscle.
    • Contraction of the internal urethral sphincter.
  • Somatic innervation of the external urethral sphincter also contributes to continence during bladder filling
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40
Q

What is the Physiology of the Voiding phase of Continence?

A
  • Afferent signals from the distended bladder ascend via the spinal cord to the pontine micturition centre and the cerebral cortex (conscious urge to pass urine).
  • Efferent parasympathetic signals to the detrusor cause it to contract, transmitted via S2-4 pelvic splanchnic nerve.
  • Inhibition of Onuf’s nucleus (due to pontine micturition centre activity) reduces sympathetic storage-promoting activity.
  • Conscious relaxation of external urethral sphincter via somatic pudendal nerve fibres allows passage of urine.
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41
Q

Give a summary of the neurology involved in continence?

A

Sympathetic - T10-L2 hypogastric - detrusor relaxation, IUS closing

  • Parasympathetic - S2-4 pelvic splanchnic - detrusor contraction, IUS opening
  • Somatic afferent - S2-4 pudendal - sensation of bladder fullness
  • Somatic efferent - S2-3 pudendal - closes / opens EUS.
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42
Q

What are the continence mechanisms in response to a raised intra-abdominal pressure?

A
  1. Reflexive contraction of the pelvic floor muscles elevates the IUS.
  2. Augmentation of pelvic floor muscle closure by suspensory ligaments.
  3. Urethrovaginal sphincter and compressor urethrae muscle contraction assists with urethral closure
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43
Q

What are the different types of Urinary Incontinence?

A
  • Stress incontinence
  • Urge incontinence
  • Overflow incontinence
  • Functional incontinence
  • Mixed incontinence
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44
Q

What is Urge incontinence?

A

Caused by Overactivity of the detrusor muscle.

This is also known as overactive bladder syndrome

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45
Q

What is Stress incontinence?

A

Leaking of urine when intra-abdominal pressure is raised that puts pressure on the bladder. The pressure overcomes the mechanisms to maintain continence.

This occurs due to weakness of the pelvic floor and sphincter muscles

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46
Q

What are some risk factors for Stress incontinence?

A
  • Childbirth (Especially vaginal)
  • Hysterectomy
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47
Q

What are some triggers for Stress incontinence?

A

Anything that can increase abdominal pressure sufficiently

  • Coughing
  • Laughing
  • Sneezing
  • Exercising
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48
Q

What is the management for Stress incontinence?

A

Lifestyle Advice:

  • Avoid caffeine, fizzy and sugary drinks
  • Avoid excessive fluid intake
  • Pelvic floor exercises (8x contractions x3 per day)

Medical Management:

  • Duloxetine (only recommended if conservative management fails and the patient is not a surgical candidate)

Surgical Management:

  • Pessaries
  • Bulking agents placed at the bladder neck
  • Colposuspension and fascial slings
  • Mid urethral slings
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49
Q

What is the gold standard treatment for Stress incontinence?

A

Mid-urethral slings is the gold standard surgical treatment of stress incontinence.

It compresses the urethra against a supportive layer and assists in closing the urethra.

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50
Q

What is Functional incontinence?

A

Individual has the urge to pass urine but for whatever reason they are unable to access the necessary facilities and are aw a result incontinent.

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51
Q

What are some potential causes of Functional Incontinence?

A
  • Sedating Medications
  • Alcohol
  • Dementias
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52
Q

What is Overflow incontinence?

A

Occurs when small amounts of urine leak without warning.

This may happen when the pressure within the bladder overcomes the pressures of the outlet structure and thus urine leaks

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53
Q

What are some causes of Overflow incontinence?

A
  • Underactivity of the detrusor muscle such as from neurological damage
  • Urinary outlet pressures are too high Such as in constipation or prostatism
  • Chronic urinary retention due to an obstruction.
  • Anti-cholinergic medications.
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54
Q

What is Mixed incontinence?

A

A combination of urge incontinence and stress incontinence.

It is crucial to identify which of the 2 is having the more significant impact and address this first.

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55
Q

What are the investigations of Incontinence?

A

First Line:

  • Medical history and Assessment
  • Physical Examination
  • Bladder Diary: tracking fluid intake, episodes of urination and incontinence over at least 3 days
  • Urinalysis and Urine-Dip stick: To look for infection or other pathology

Second Line:

  • Urinary Stress Tests: Cough stress test, empty supine stress test
  • Cystometry and Cystogram: Bladder scan to assess for bladder pressures when voiding or fistulas
  • Urodynamics
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56
Q

What information should be obtained from a Medical history assessment for Incontinence?

A

Differentiate between Stress or Urge:

  • Urinary leakage with coughing, laughing or sneezing (Stress)
  • Urinary leakage due to sudden urge to pass with loss of control (Urge)

Assess for Modifiable lifestyle factors:

  • Caffeine consumption
  • Alcohol consumption
  • Medications (anticholinergics)
  • BMI

Assess the Severity:

  • Frequency of urination
  • Frequency of incontinence
  • night-time urination
  • Use of pads and changes of clothing.
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57
Q

What should be done during a Physical examination to look for incontinence?

A

Assessment of Pelvic Tone:

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

Also examine for

  • Pelvic organ prolapse
  • Atrophic vaginitis
  • Urethral diverticulum
  • Pelvic masses
  • urinary incontinence (asking the patient to cough)
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58
Q

What are the indications for Urodynamic testing?

A
  • Patients with Urge incontinence not responding to first line medical treatments
  • Difficulties urinating
  • Urinary retention
  • Previous surgery in and around the pelvis
  • Unclear diagnosis
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59
Q

What is done in Urodynamic testing for incontinence?

A
  • Patients should stop taking anticholinergic and bladder related medications for 5 days before testing.
  • A catheter is inserted into the bladder and the rectum and they measure the pressures for comparison. The bladder is filled with liquid and different measurements are taken.
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60
Q

What are each of these measurements for?

  • Cystometry
  • Uroflowmetry
  • Leak Point Pressure
  • Poist-void residual bladder volume
  • Video urodynamic testing
A
  • Cystometry measures the detrusor muscle contraction and pressure
  • Uroflowmetry measures the flow rate
  • Leak Point Pressure is the point at which the bladder pressure results in leakage of urine. The patient is asked to cough, move or jump when the bladder is filled to various capacities. This assesses for stress incontinence.
  • Poist-void residual bladder volume tests for incomplete emptying of the bladder
  • Video urodynamic testing involves filling the bladder with contrast and taking xray images as the bladder is emptied. Theses are only performed where necessary and not a routine part of urodynamic testing.
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61
Q

Define Urolithiasis?

A

Urinary tract stones or Urolithiasis refer to solid concretions or crystal aggregations formed in the urinary system from substances present in the urine

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62
Q

Define Renal Colic?

A

A condition characterised by severe pain caused by the presence of a stone in the urinary tract

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63
Q

What is the epidemiology of Urinary tract stones?

A
  • Common condition affecting 2-3% of western population
  • More common in males
  • More common in people younger than 65
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64
Q

What is the aetiology of renal stones?

A

Calcium oxalate stones:

  • Represent 85% of stones. They are radiopaque, formed in variable urine pH, and majorly linked to hypercalciuria.

Calcium phosphate stones:

  • Account for 10% of stones. They are radiopaque and linked to renal tubular acidosis type 1 & 3, leading to increased urine pH and supersaturation of calcium and phosphate in the urine.

Cystine stones:

  • Make up 1% of stones. Characterised by a semi-opaque “ground glass” appearance, they result from inherited recessive inborn errors of metabolism causing disruption in cystine transport and decreased absorption from the renal tubule.

Uric acid stones:

  • Comprise 5-10 of stones. They are radiolucent, formed due to acid produced from purine metabolism and precipitate when urinary pH is low. They can be linked to diseases causing extensive tissue breakdown.

Struvite stones:

  • Account for 2-20% of stones. They are radiopaque and formed from magnesium, ammonium, and phosphate, often associated with chronic UTIs from urease producing bacteria like ureaplasma, proteus.

Indinavir stones:

  • Associated with the antiretroviral protease inhibitor Indinavir used in HIV treatment. It can crystallize in renal tubules and result in renal stones. These stones are radiolucent on CTKUB.
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65
Q

What is the most common cause of Renal stones?

A

Hypercalcaemia/Hypercalciuria

Patients may present with symptoms of hypercalcaemia (renal stones, painful bones, abdominal groans and psychiatric moans)

3 Main causes of Hypercalcaemia:

  • Calcium supplementation
  • Hyperparathyroidism
  • Cancer (Myeloma, Breast, Lung)
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66
Q

What are the risk factors for Nephrolithiasis?

A

Modifiable risk factors include:

  • Obesity
  • Dehydration
  • Diet rich in oxalate-rich foods like fruits, nuts, and cocoa

Non-modifiable risk factors include:

  • Previous stone disease
  • Anatomical abnormalities of the collecting system
  • Family history

Underlying medical conditions, such as:

  • Hyperparathyroidism
  • Renal tubular acidosis
  • Myeloproliferative disorders
  • All chronic diarrhoeal conditions
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67
Q

What is Staghorn Calculus?

A

Where the stone forms in the shape of the renal pelvis giving it a similar appearance to the antlers of a deer stag.

Often associated with Struvite stones

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68
Q

What are the clinical features of Renal Colic?

A
  • Unilateral Colicky loin to groin pain that can be excruciating (“worse than childbirth”)
  • Haematuria
  • Nausea or vomiting
  • Reduced urine output
  • Symptoms of sepsis (Fever), if infection is present
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69
Q

cancerWhat are some differential diagnoses for Renal Colic?

A
  • Pyelonephritis: Presents with fever, flank pain, and urinary symptoms such as frequency, urgency, and dysuria.
  • Appendicitis: Presents with right lower quadrant pain, nausea, vomiting, and possibly fever.
  • Diverticulitis: Presents with left lower quadrant pain, fever, nausea, vomiting, and changes in bowel habits.
  • Ovarian torsion: Presents with acute lower abdominal pain, nausea, vomiting, and sometimes fever.
  • Ectopic pregnancy: Presents with lower abdominal pain, vaginal bleeding, and a positive pregnancy test.
  • Abdominal aortic aneurysm: Presents with central abdominal pain, pulsatile/expansile abdominal aorta and if ruptured, haemodynamic instability.
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70
Q

What are the investigations for Renal Colic?

A

Bedside investigations:

  • Urinalysis to detect haematuria
  • Urine MC+S as there may be a co-existing infection/precipitant.
  • Observations to look for any signs of sepsis

Blood tests:

  • Full Blood Count to detect any inflammatory response
  • Urea and Electrolytes to assess any impairment in renal function.
  • Calcium & Uric acid to identify underlying metabolic conditions predisposing to stone formation.

Radiological investigations:

  • A non-contrast helical CT KUB, the gold standard for identifying renal calculi.
  • An x-ray for managing renal colic if there’s a confirmed stone on CT KUB, necessary for the use of extracorporeal shockwave lithotripsy.
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71
Q

What is the initial and gold standard investigation for Renal Colic?

A

Non-contrast CT Kidney, Ureter and Bladder (CTKUB) is both the initial and Gold standard investigation

  • NICE recommend a CT within 24 hours of presentation
  • BAUS recommend a CT within 14 hours of admission
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72
Q

What is the management for Renal Colic?

A
  • Analgesia: NSAIDs such as IM Diclofenac
  • Anti-emetics: Metoclopramide, Cyclizine
  • Antibiotics: If infection is present
  • Medical Expulsive Therapy: Uses Tamsulosin to help passage of distal ureter stones < 5mm
  • Watchful Waiting: If stones are less than 5mm
  • Surgical Intervention: required in larger stones 10mm or more or ones that do not pass spontaneously. Also required if there is complete obstruction or infection.
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73
Q

What are some surgical options for Renal Colic?

A

Stones < 2cm

  • Extracorporeal shockwave lithotripsy (ESWL): shock waves fragment the stone to then be passed
  • Ureteroscopy: Treatment of choice for middle or distal ureteric stones and for Pregnant women

Stones > 2cm

  • Percutaneous nephrolithotomy: for large stones or complex calculi like staghorn or cysteine.
  • Open Stone surgery: when other options have failed.
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74
Q

What is a complication of renal stones?

A
  • Significant risk of recurrent episodes
  • Obstructive infection
  • Sepsis
  • Renal Failure
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75
Q

What advice can be given to reduce the risk of recurrent stones?

A
  • Increase oral fluid intake (2.5 – 3 litres per day)
  • Add fresh lemon juice to water (citric acid binds to urinary calcium reducing the formation of stones)
  • Avoid carbonated drinks (cola drinks contain phosphoric acid, which promotes calcium oxalate formation)
  • Reduce dietary salt intake (less than 6g per day)
  • Maintain a normal calcium intake (low dietary calcium might increase the risk of kidney stones)
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76
Q

Define Oligomenorrhea?

A

Infrequent/irregular menstrual periods (fewer than 6-8 per year)

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77
Q

Define Amenorrhoea?

A

Absence of a menstrual period

Primary: absence of a period at age 15 in the presence of normal secondary sexual characteristics or at age 13 with no secondary sexual characteristics

Secondary: Absence of a period for 3 consecutive cycles in a women with a previously established menstrual cycle

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78
Q

What are some causes of Primary Amenorrhoea?

A
  • Constitutional delay (Familial)
  • Imperforate hymen
  • Endocrinological: Hypo-hyperthyroidism, Hyperprolactinaemia, Cushing’s Syndrome
  • Androgen Insensitivity Syndrome
  • Turners syndrome
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79
Q

What are some causes of Secondary Amenorrhoea?

A
  • Pregnancy (most common cause)
  • Breastfeeding
  • Menopause
  • Intrauterine adhesions leading to outflow tract obstruction (Asherman’s syndrome)
  • Polycystic ovary syndrome (PCOS)
  • Drug-induced amenorrhoea (e.g. contraceptive use)
  • Functional Hypothalamic Amenorrhoea: Physical stress, excess exercise, and weight loss
  • Pituitary gland pathology: such as Sheehan syndrome or hyperprolactinaemia
  • Hypothyroidism or hyperthyroidism
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80
Q

Define Androgen Insensitivity Syndrome?

A

An X-linked Recessive genetic condition where cells are unable to respond to androgen hormones due to a lack of androgen receptors This results in Genetic Males with a Female Phenotype

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81
Q

What is the pathophysiology of Androgen Insensitivity Syndrome?

A
  • Mutation in Androgen receptor gene on the X chromosome results in cells becoming unable to respond to androgens.
  • Excess androgens are converted to Oestrogen resulting in female secondary sexual characteristics
    (Previously known as Testicular feminisation syndrome)
  • Males are genetically XY with a female phenotype
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82
Q

What is the anatomy of a patient with Androgen Insensitivity Syndrome?

A
  • Female External Genitalia and Breast Development
  • Testes located within the abdomen or inguinal canal.
  • Absence of Female internal organs (Uterus, upper vagina, cervix, fallopian tubes and ovaries) due to the testes producing anti-Mullerian hormone.
  • Patients are taller than female average, with a lack of pubic hair, facial hair and male type muscle bulk.
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83
Q

What is a risk of patients with Androgen Insensitivity Syndrome?

A

High risk of Testicular cancer unless the testes are removed

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84
Q

What is the Presentation of Androgen Insensitivity Syndrome?

A
  • Often presents in infancy with Inguinal hernias containing testes
  • May present at puberty with Primary Amenorrhoea
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85
Q

What are the investigations for Primary Amenorrhoea?

A

Exclude pregnancy with urinary or serum bHCG
Full blood count - anaemia
Urea & electrolytes
Coeliac screen
Thyroid function tests
Gonadotrophins (LH/FSH):

  • Low levels indicate a hypothalamic cause where as
  • Raised levels suggest an ovarian problem (e.g. Premature ovarian failure)
  • Raised if gonadal dysgenesis (e.g. Turner’s syndrome)

Prolactin for Hyperprolactinaemia

Androgen levels

  • Raised levels may be seen in PCOS

Oestradiol

Second Line:

  • Genetic Testing: Identify chromosomal or genetic abnormalities
  • Imaging: To identify structural abnormalities
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86
Q

What are the results of hormonal tests in Androgen Insensitivity Syndrome?

A
  • Raised LH
  • Normal or raised FSH
  • Normal or Raised Testosterone levels (For a male)
  • Raised Oestrogen levels (For a male)
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87
Q

What is the management of Primary Amenorrhoea?

A

Depends on the underlying cause

  • Hormone replacement therapy: For hormonal imbalances
  • Surgery: For structural abnormalities
  • Psychological support: For conditions related to stress or eating disorders
  • Lifestyle modifications: For issues related to excessive exercise or low body weight
  • Monitoring and regular follow-ups: To assess effectiveness of treatment and adjust as necessary
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88
Q

What is the management of Androgen Insensitivity Syndrome?

A

MDT Specialist Coordination: Paediatrics, Gynaecology, Urology, Endocrinology, Clinical Psychology

  • Bilateral Orchiectomy: To avoid testicular tumours
  • Oestrogen Therapy
  • Vaginal Dilators or Vaginal Surgery: To create and adequate length vagina

Generally patients are raised as female but this is tailored to the individual

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89
Q

What is responsible for the embryological development of the upper vagina, cervix, uterus and fallopian tubes?

A

They develop from the paramesonephric ducts (Mullerian ducts)

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90
Q

Why do males not develop female gentalia?

A

The testes in a male foetus produce Anti-Mullerian hormone which suppresses the growth of the paramesonephric ducts and so they do not form.

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91
Q

What ae some Congenital structural Abnormalities for the Female Reproductive Tract?

A
  • Bicornuate Uterus
  • Uterus Agenesis
  • Imperforate Hymen
  • Transverse vaginal Septae
  • Vaginal Hypoplasia and Agenesis
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92
Q

What is a Bicornuate Uterus?

A
  • Uterus has 2 horns giving it a heart shaped appearance.
  • This can be associated with adverse pregnancy outcomes however successful pregnancies are generally expected.
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93
Q

What are some complications of a Bicornuate Uterus?

A
  • Miscarriage
  • Premature Birth
  • Malpresentation
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94
Q

What is an Imperforate Hymen?

A

Where the hymen at the entrance of the vagina is fully formed without an opening.

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95
Q

How does an Imperforate Hymen Present?

A
  • May be discovered when the girl starts to menstruate, and the menses are sealed in the vagina.
  • This causes cyclical pelvic pain and cramping that would ordinarily be associated with menstruation, but without any vaginal bleeding.
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96
Q

What is the management of an Imperforate Hymen?

A
  • Diagnosed during a clinical examination
  • Treatment is a Surgical incision to create an opening in the hymen.
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97
Q

What is a complication of an Imperforate Hymen?

A
  • If not treated then retrograde menstruation could occur leading to endometriosis
  • Amenorrhoea
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98
Q

What is a Transverse Vaginal Septae?

A

Caused by an error in development, where a septum (wall) forms transversely across the vagina.

This septum can either be perforate (with a hole) or imperforate (completely sealed).

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99
Q

What is the Presentation of a Transverse Vaginal Septae?

A
  • Perforate Septae: Girls will menstruate but can have difficulty with intercourse or tampon use
  • Imperforate Septae: Presents similarly to an Imperforate Hymen
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100
Q

What are some complications of a Transverse Vaginal Septae?

A
  • Infertility
  • Pregnancy related complications
  • Vaginal Stenosis
  • Recurrence of the Septae
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101
Q

What is the management of a Transverse Vaginal Septae?

A
  • Diagnosis is by Examination, Ultrasound or MRI
  • Treatment with with Surgical Correction
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102
Q

What is Vaginal Hypoplasia and Agenesis?

A

Hypoplasia: An Abnormally small vagina

Agenesis: An absent vagina

These occur due to failure of the Mullerian ducts to properly develop and are often associated with an absent uterus and cervix

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103
Q

What is the difference between Vaginal Hypoplasia and Agenesis and Androgen Insensitivity Syndrome?

A

The Mullerian Ducts fail to develop but not due to Anti-Mullerian Hormone.

Therefore patients do not have Testes (like in AIS) but do have Ovaries

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104
Q

What is the management of Vaginal Hypoplasia and Agenesis?

A
  • Vaginal Dilator over a prolonged period of time to create and adequate vaginal size
  • Vaginal Surgery may be necessary
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105
Q

Define Menarche?

A

The first occurrence of Menstruation

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106
Q

At what age does Menarche normally occur?

A

Mean age 13

11-15 usually.

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107
Q

Define Menopause?

A

This term describes the permanent cessation of menstruation, characterised by at least 12 months of amenorrhoea in otherwise healthy women over the age of 45 who are not using hormonal contraception.

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108
Q

When does Menopause typically occur?

A

Between the ages of 45-55 with the average age being around 51-52 years old.

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109
Q

Define Perimenopause?

A
  • The time around the menopause, where the woman may be experiencing vasomotor symptoms and irregular periods.
  • Perimenopause includes the time leading up to the last menstrual period, and the 12 months afterwards.
  • This is typically in women older than 45 years.
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110
Q

Define Postmenopause?

A

The period from 12 months after the final menstrual period

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111
Q

Define Early Menopause?

A

Menopause between the ages of 40-45 years old.

Premature Menopause is the menopause occuring prior to the age of 40 and is due to ovarian insufficiency

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112
Q

What is the Aetiology of Menopause?

A

Caused by ovarian failure which leads to oestrogen deficiency

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113
Q

What is the physiology of Menopause?

A
  • Decline in the development of Ovarian follicles
  • Without the follicles there is reduced production of oestrogen
  • Oestrogen has a negative feedback effect on the pituitary
  • As oestrogen levels fall in the perimenopause period, this negative feedback is lost
  • Increasing levels of LH and FSH
  • Failing follicular development means ovulation does not occur
  • This results in irregular menstrual cycles.
  • Without Oestrogen the endometrium does not develop eventually leading to a lack of menstruation (amenorrhoea)
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114
Q

What is the cause of the perimenopausal symptoms?

A

Lower levels of Oestrogen

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115
Q

What are some perimenopausal symptoms?

A

Vasomotor Symptoms:

  • Hot flushes
  • Night sweats
  • Irregular periods, Heavy or lighter periods
  • Joint Pains

Sexual Dysfunction:

  • Vaginal dryness and atrophy
  • Reduced libido
  • Problems with Orgasm
  • Dyspareunia

Psychological Symptoms:

  • Depression
  • Anxiety
  • Mood Swings, Low mood and emotional lability
  • Lethargy
  • Reduced Concentration
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116
Q

What are some risks of menoupause?

A

Reduced oestrogen increases the risk of certain conditions:

  • Cardiovascular disease and stroke
  • Osteoporosis due to increased bone turn over since normal oestrogen levels inhibit osteoclast activity
  • Pelvic Organ Prolapse
  • Urinary Incontinence
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117
Q

What are some differential diagnoses for Menopause?

A
  • Thyroid disease: symptoms can include hot flushes, sweating, palpitations, and changes in menstrual cycle
  • Depression: exhibits mood swings, lethargy, reduced concentration
  • Premature ovarian insufficiency: can cause hot flushes, night sweats, vaginal dryness, and reduced libido
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118
Q

What are the investigations for Menopause?

A

Diagnosis of perimenopause and menopause can be made in women over 45 years with typical symptoms without performing any investigations

NICE Guidelines (2015) recommend FSH Blood test to help with Diagnosis:

  • Women under 40 years with suspected premature menopause
  • Women aged 40-45 with menopausal symptoms or a change in menstrual cycle
  • Elevated FSH level (>30 IU/L) may predict impending menopause after several months of amenorrhoea
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119
Q

How long after the last menstrual period before the menopause should women continue to use contraception?

A

Two years after the last menstrual period in women under 50

One year after the last menstrual period in women over 50

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120
Q

What is the relationship between hormonal contraceptives and menopause?

A

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.

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121
Q

What are some good contraceptive options for women approaching menopause?

A

Barrier methods
Mirena or copper coil
Progesterone only pill
Progesterone implant
Progesterone depot injection (under 45 years)
Sterilisation

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122
Q

What are 2 main side effects of the progesterone depot injection?

A

Weight Gain and Reduce bone mineral density (osteoporosis)

This is why this form of contraception is unsuitable for women Over 45 years old

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123
Q

What is the management of Perimenopausal Symptoms?

A

Vasomotor symptoms likely resolve after 2-5 years without treatment

Management of Symptoms depends on severity, personal circumstances and response to treatment

First Line: Lifestyle Measures

  • Regular Exercise
  • Weight Loss (as necessary)
  • Avoidance of triggers (Smoking, alcohol, spicy food)

Second line: Hormone replacement therapy (HRT)

  • Tibolone, a synthetic steroid hormone that acts as continuous combined HRT (only after 12 months of amenorrhoea)
  • Clonidine, which act as agonists of alpha-adrenergic and imidazoline receptors for flushing
  • Cognitive behavioural therapy (CBT)
  • SSRI antidepressants, such as fluoxetine or citalopram
  • Testosterone can be used to treat reduced libido (usually as a gel or cream)
  • Vaginal oestrogen cream or tablets, to help with vaginal dryness and atrophy (can be used alongside systemic HRT)
  • Vaginal moisturisers, such as Sylk, Replens and YES
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124
Q

What is the purpose of HRT?

A

Oestrogens: Overcome oestrogen deficiency

Progesterone’s: Required for endometrial protection from unopposed systemic oestrogens

  • HRT can be given cyclically (for perimenopause) or continuously (for post menopause)
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125
Q

What are some benefits and risks of HRT?

A

Benefits

  • Relief of Vasomotor symptoms
  • Relief of urogenital symptoms
  • Reduced risk of Osteoporosis

Risks

  • Increased risk of Breast Cancer
  • Increased risk of Endometrial Cancer (if given oestrogen alone)
  • Increased risk of VTE
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126
Q

What are some Absolute Contraindications to HRT?

A
  • History of breast cancer, any oestrogen-dependent cancer, current undiagnosed PV
    bleeding, current endometrial hyperplasia.
  • History of idiopathic VTE (if not anticoagulated).
  • Thromboembolic disease e.g. MI, angina
  • Liver disease.
  • Inherited thrombophilia.
  • Pregnancy.
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127
Q

Define Adenomyosis?

A

Refers to a condition where endometrial tissue is inside the myometrium (muscle layer of the uterus)

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128
Q

What is the Epidemiology of Adenomyosis?

A
  • More common in later reproductive years
  • More common in those who have had several pregnancies (Multiparous)
  • Occurs in around 10% of women
  • May occur alone or alongside endometriosis or fibroids
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129
Q

What is the Aetiology of Adenomyosis?

A

Not fully Understood

  • Multiple factors involved including Sex hormones, trauma and inflammation
  • Condition is hormone dependent
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130
Q

What are the clinical features of Adenomyosis?

A
  • Painful periods (dysmenorrhoea)
  • Heavy periods (menorrhagia)
  • Pain during intercourse (dyspareunia)
  • Infertility or pregnancy related complications
  • 1/3 of patients are asymptomatic
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131
Q

What are the investigations for Adenyomyosis?

A

First Line:

  • Transvaginal Ultrasound of the pelvis
  • MRI and Transabdominal ultrasound are alternatives if transvaginal is unsuitable

Gold Standard:

  • Histological examination of the uterus after a hysterectomy
  • Not usually a suitable way of establishing the diagnosis for obvious reasons
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132
Q

What is the management of Adenomyosis?

A

Depends on symptoms, age and plans for pregnancy

Women does NOT want contraception

  • Tranexamic Acid when there is no pain associated (antifibrinolytic)
  • Mefenamic Acid when there is pain associated (NSAID)

Women DOES want Contraception:

  • Mirena coil - First Line
  • Combined Oral Contraceptive Pill (COCP)
  • Cyclical oral progestogens

Other options considered by specialist

  • GnRH analogues to induce menopause like state
  • Endometrial ablation
  • Uterine artery embolisation
  • Hysterectomy
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133
Q

What are some pregnancy complications associated with Adenomyosis?

A
  • Infertility
  • Miscarriage
  • Preterm birth
  • Small for gestational age
  • Preterm premature rupture of membranes
  • Malpresentation
  • Need for caesarean section
  • Postpartum haemorrhage
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134
Q

Define Asherman’s Syndrome?

A

Where adhesions form within the uterus (intrauterine adhesions) following damage to the uterus that lead to outflow tract obstruction.

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135
Q

What is the Aetiology of Asherman’s syndrome?

A

Anything that creates scar tissue within the uterus causing adhesions that are normally not connected

  • Pregnancy related dilation and Curettage procedure
  • Treatment of retained productions of conception (removing placental tissue left behind after birth)
  • Uterine surgery (myomectomy)
  • Pelvic infection (endometritis)
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136
Q

What is the pathophysiology of Asherman’s Syndrome?

A
  • Damage to the uterus causing scar tissue formation and subsequent adhesions.
  • Adhesions form Physical Obstructions and distort the pelvic organs
  • Leads to menstruation abnormalities, infertility, recurrent miscarriages
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137
Q

What are the clinical features of Asherman’s Syndrome?

A

Presents following recent dilatation and curettage, uterine surgery or endometritis with:

  • Secondary amenorrhoea
  • Significantly lighter periods
  • Dysmenorrhoea
  • Infertility

Incidentally found adhesions that are asymptomatic are not classed as Asherman’s Syndrome

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138
Q

What are the investigations for Asherman’s Syndrome?

A

History of uterine surgery

Hysteroscopy is Gold Standard investigation and can involve dissection and treatment of adhesions.

Others:

  • Hysterosalpingography when contrast is injected into the uterus and imaged with X-rays
  • Sonohysterography uterus is filled with fluid and pelvic USS is performed
  • MRI Scan
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139
Q

What is the management of Asherman’s Syndrome?

A
  • Dissecting the adhesions during hysteroscopy.
  • Reoccurrence of the adhesions after treatment is common
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140
Q

What are the clinical features of Secondary Amenorrhea?

A

The primary symptom of secondary amenorrhoea is the absence of menstrual periods for six months or longer.

Additional symptoms, depending on the underlying cause, may include:

  • Pregnancy symptoms: nausea, breast tenderness, increased urination, food cravings or aversions
  • Menopause symptoms: hot flashes, night sweats, sleep problems, mood changes
  • Symptoms of PCOS: acne, weight gain, hirsutism (excessive body hair), thinning hair
  • Symptoms of pituitary gland issues: headaches, vision problems, unexplained weight gain or loss
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141
Q

What are the investigations for Secondary Amenorrhoea?

A
  • Pregnancy test
  • Hormone level checks: including FSH, LH, TSH, prolactin, and testosterone
  • Ultrasound or other imaging studies, to identify potential structural abnormalities
  • Hysteroscopy, in cases where intrauterine adhesions are suspected
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142
Q

What is the management of Secondary Amenorrhoea?

A

Management of secondary amenorrhoea is determined by the underlying cause:

  • Pregnancy: regular prenatal care
  • Menopause: hormone replacement therapy (HRT) if symptoms are troublesome
  • PCOS: lifestyle changes, hormonal contraceptives, and potentially metformin
  • Asherman’s syndrome: surgical removal of adhesions and hormone therapy
  • Drug-induced amenorrhoea: discontinuing the offending drug if possible and safe to do so
  • Conditions related to physical stress, weight loss, or excessive exercise: lifestyle modifications and nutritional counselling.
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143
Q

Define Lichen Sclerosus?

A

A chronic inflammatory skin condition that presents with patches of Porcelain-white skin.

It typically affects the genital and anal regions of the body: labia, perineum, perianal skin, foreskin and glans penis

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144
Q

What is the epidemiology of Lichen Sclerosus?

A
  • Typically affects women
  • Can affect men
  • Considered to be an autoimmune condition and therefore is associated with T1DM, Alopecia, hypothyroid and vitiligo
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145
Q

What is the Aetiology of Lichen Sclerosus?

A

The cause of lichen sclerosus is currently unknown, but it is likely multifactorial.

Potential contributing factors could include autoimmune condition, genetic predisposition, and hormonal factors.

Some studies suggest a possible link with previous skin damage or trauma.

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146
Q

What is Lichen in medicine?

A

Lichen refers to a flat eruption that spreads.

*It is important not to get lichen sclerosus confused with lichen simplex or lichen planus.

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147
Q

Define Lichen simplex

A

Chronic inflammation and irritation caused by repeated scratching and rubbing of an area of skin. This presents with excoriations, plaques, scaling and thickened skin.

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148
Q

Define Lichen planus

A

An autoimmune condition that causes localised chronic inflammation with shiny, purplish, flat-topped raised areas with white lines across the surface called Wickham’s striae.

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149
Q

What is a typical presentation of Lichen Sclerosus?

A

Woman aged 45 – 60 years complaining of vulval itching and skin changes in the vulva

The condition may be asymptomatic, or present with several symptoms:

  • Itching
  • Soreness and pain possibly worse at night
  • Skin tightness
  • Painful sex (superficial dyspareunia)
  • Erosions
  • Fissures
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150
Q

What is the Koebner phenomenon?

A

The appearance of new skin lesions on areas of pre-existing dermatosis and cutaneous injury (skin trauma)

This occurs with Lichen Sclerosus

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151
Q

What is the appearance of Lichen Sclerosus?

A

Changes affect the labia, perianal and perineal skin. There can be associated fissures, cracks, erosions or haemorrhages under the skin.

The affected skin appears:

  • “Porcelain-white” in colour
  • Shiny
  • Tight
  • Thin
  • Slightly raised
  • There may be papules or plaques
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152
Q

What are some differential diagnoses for Lichen Sclerosus?

A
  • Lichen planus: Characterized by purplish, itchy, flat-topped bumps, and white lacy patches in the mouth or on the skin.
  • Psoriasis: Manifests as red patches with silver scales, typically on the scalp, elbows, knees, and lower back.
  • Vitiligo: Presents as patchy loss of skin color, usually first on sun-exposed areas of the skin.
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153
Q

What are the investigations for Lichen Sclerosus?

A

Primarily Clinical Diagnosis based on characteristic appearance of skin lesions

  • Skin biopsy may be performed to confirm diagnosis
  • Blood tests may rule out other potential autoimmune conditions
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154
Q

What is the Management of Lichen Sclerosus?

A

Lichen Sclerosus cannot be cured but symptoms are controlled and should be followed up every 3-6 months

First Line

  • Potent Topical Steroids: Clobetasol propionate 0.05% (dermovate)
    • Steroids used long term to control symptoms
    • Once daily for 4 weeks. Then gradually reduce frequency every 4 weeks to alternate days then twice weekly.
    • Daily steroids when condition flares
  • Emollients should be used regularly both with steroids and as part of maintenance
  • Avoidance of soaps in affected areas to prevent further irritation.
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155
Q

What are some complications of Lichen Sclerosus?

A
  • 5% risk of developing squamous cell carcinoma of the vulva
  • Pain and discomfort
  • Sexual dysfunction
  • Bleeding
  • Narrowing of the vaginal or urethral openings
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156
Q

Define Atrophic Vaginitis?

A

vulvovaginal atrophy is inflammation and thinning of the genital tissues, dryness and atrophy of the vaginal mucosa due to reduced oestrogen levels

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157
Q

What is the Aetiology of Atrophic Vaginitis?

A

Decrease in oestrogen levels most commonly due to menopause

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158
Q

What are the clinical features of Atrophic Vaginitis?

A

Presents in post-menopausal women with:

  • Itching and dryness
  • Loss of pubic hair
  • Dyspareunia (discomfort or pain during sex)
  • Post coital Bleeding due to localised inflammation
  • recurrent UTIs or Stress incontinence
  • Pelvic organ prolapse may also occur.
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159
Q

What are some differential diagnoses for Atrophic Vaginitis?

A
  • Postmenopausal bleeding: malignancy, endometrial hyperplasia
  • For genital itching/discharge: sexually transmitted infection, vulvovaginal candidiasis, skin conditions such as lichen sclerosis, lichen planus, diabetes
  • For narrowed introitus: female genital mutilation
  • For urinary symptoms: urinary tract infection, bladder dysfunction, pelvic floor disfunction, cystitis
  • For dyspareunia: malignancy, vaginismus
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160
Q

What are the investigations for Atrophic Vaginitis?

A

Clinical Diagnosis

  • Clinical examination, including speculum examination if tolerated, to look for vaginal signs of atrophy

Other tests:

  • Transvaginal ultrasound and endometrial biopsy, if necessary, to exclude endometrial cancer
  • An infection screen if itching or discharge is present
  • A biopsy of any abnormal skin lesions, if needed
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161
Q

What would be seen on examination in Atrophic Vaginitis?

A
  • Pale mucosa
  • Thin skin
  • Reduced skin folds
  • Erythema and inflammation
  • Dryness
  • Sparse pubic hair
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162
Q

What is the management of Atrophic Vaginitis?

A

Hormonal treatment:

  • Topical oestrogen preparations:
    • Estriol cream
    • Estriol pessaries
    • Estradiol Tablets
    • Estradiol ring

Non-hormonal treatments:

  • Lubricants such as Sylk, Replens, YES:, which provide short-term improvement to vaginal dryness, alleviating symptoms such as dyspareunia
  • Moisturisers, which should be used regularly
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163
Q

What are some contraindications to Topical Oestrogens?

A
  • Breast Cancer
  • Angina
  • Venous Thromboembolism
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164
Q

Define Vulval Cancer?

A

Malignant growth that primarily affects the skin of the vulva (the external part of the female genitalia).

It can be host to various types of Skin cancers however Squamous Cell Carcinoma is the most prevalent.

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165
Q

What is the Epidemiology of Vulval cancer?

A
  • Rare gynaecological cancer accounting for 4%
  • Most commonly found in older women >60 (but can occur at any age)
  • 90% are Squamous Cell Carcinomas
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166
Q

What are some risk factors for Vulval Cancer?

A
  • Advanced age (particularly over 75 years)
  • Immunosuppression
  • Human papillomavirus (HPV) infection
  • Lichen sclerosus

Around 5% of women with lichen sclerosus get vulval cancer.

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167
Q

What are the different types of Vulval Cancer?

A
  • Squamous Cell Carcinoma (90%)
  • Malignant Melanomas
  • Basal Cell Carcinoma
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168
Q

What are the clinical features of Vulval Cancer?

A
  • A lump, which may be associated with lymphadenopathy of the groin
  • Itching or discomfort in the vulval area
  • A non-healing ulcer
  • Vulval pain
  • Changes in the skin of the vulva, such as thickening or changes in color
  • Bleeding or discharge not related to the menstrual cycle
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169
Q

What region of the Vulva is most common affected in Vulval Cancer?

A

Labia Majora

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170
Q

What are some differential diagnoses for Vulval Cancer?

A
  • Vulval intraepithelial neoplasia: This precancerous condition can cause itching, burning, skin changes, and discomfort.
  • Lichen sclerosus: This condition can cause itching, pain, and white patches on the vulva.
  • Bartholin’s cyst: This may present as a lump or swelling on the vulva, and can cause discomfort or pain.
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171
Q

What are the investigations for Vulval Cancer?

A

Physical Examination

Suspected vulval cancer should be referred on a 2-week-wait urgent cancer referral.

Establishing the diagnosis and staging involves:

  • Biopsy of the lesion
  • Sentinel node biopsy to demonstrate lymph node spread
  • Further imaging for staging (e.g. CT abdomen and pelvis)
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172
Q

What is system is used to stage Vulval Cancer?

A

International Federation of Gynaecology and Obstetrics (FIGO)

Management of Vulval Cancer depends on the stage

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173
Q

What is the Management of Vulval Cancer?

A

Depends on the Stage

  • Wide local excision to remove the cancer
  • Groin lymph node dissection
  • Chemotherapy
  • Radiotherapy
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174
Q

What is Vulval Intraepithelial Neoplasia?

A
  • VIN is a premalignant condition affecting the squamous epithelium of the skin.
  • VIN is similar to the premalignant condition that comes before cervical cancer (cervical intraepithelial neoplasia)
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175
Q

What are the different types of Vulval Intraepithelial Neoplasia?

A
  • High grade squamous intraepithelial lesion: A type of VIN associated with HPV infection that occurs in younger women aged 35-50 years.
  • Differentiated VIN: Type of VIN associated with lichen Sclerosus and typically occurs in older women aged 50-60 years.
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176
Q

How is Vulval intraepithelial neoplasia diagnosed?

A

A biopsy

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177
Q

What are the management options for Vulval Intraepithelial Neoplasia?

A
  • Watch and wait with close follow-up
  • Wide local excision (surgery) to remove the lesion
  • Imiquimod cream
  • Laser ablation
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178
Q

Define Cervical Cancer?

A

Malignant proliferation of the cells of the Cervix (the lower part of the uterus that connects to the vagina)

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179
Q

What is the Epidemiology of Cervical Cancer?

A
  • 3rd most common cancer worldwide and 4th biggest cause of cancer death
  • Strongly associated with Human papilloma virus (HPV)
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180
Q

What are the different types of Cervical Cancer?

A
  • Squamous Cell Carcinoma (80%)
  • Adenocarcinoma (10-20%)
  • Very rarely, Small cell Cancer
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181
Q

What are some risk factors for Cervical Cancer?

A

HPV 16 and 18 infection (accounts for 70% of cases)

Non Engagement with Cervical Screening

Activities that increase risk of catching HPV

  • Early sexual activity
  • Increased number of sexual partners
  • Sexual partners who have had more partners
  • Not using condoms

Other risk factors:

  • Smoking
  • Immunosuppression (e.g. HIV or organ transplants)
  • Combined Contraceptive pill use for >5 years
  • Family History
  • Increased number of full term pregnancies
  • Exposure to Diethylstilboestrol previously used to prevent miscarriages
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182
Q

What is the Human Papilloma Virus?

A
  • HPV is a Sexually Transmitted Infection of the virus that is associated with anal, vulval, vaginal, penile, mouth and throat cancers
  • There are over 100 strains but theHPV 16 and 18 are responsible for 70% of cervical cancers
  • HPV Infection spontaneously resolves within 2 years in 90% of women. At this point the risk returns to baseline.
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183
Q

Which strains of HPV are targeted in the HPV vaccine and when is the vaccine given?

A

Current NHS vaccine is Gardasil protecting against HPV 6, 11, 16, 18, 31, 33, 45, 52, 58

  • HPV 6 and 11 cause Genital Warts
  • HPV 16 and 18 cause Cervical Cancer (plus others)
  • Girls and boys are given the HPV vaccine around age 12-13 years old
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184
Q

How does HPV promote cancer development?

A
  • HPV produces two proteins (E6 and E7) that inhibit tumour suppressor genes.
  • E6 inhibits p53
  • E7 inhibits pRb
  • These cause dysregulated cell cycle regulation leading to the formation of a pre-malignant monoclonal cell population
  • This cell population is cervical intraepithelial neoplasia (CIN) which subsequently mutates further to become an invasive carcinoma
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185
Q

What is Cervical Intraepithelial Neoplasia?

A

What is Cervical Intraepithelial Neoplasia (CIN) is a grading system for the level of dysplasia and premalignant change in the cells of the cervix

CIN is diagnosed at Colposcopy (not with cervical screening)

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186
Q

What are the grades of Cervical Intraepithelial Neoplasia?

A
  • 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.

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187
Q

What is the typical presentation of Cervical cancer?

A

Most cases are picked up asymptomatically during cervical screening or smears.

  • When symptoms are present these are often non-specific and so an examination of the cervix is required to exclude cancer
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188
Q

What are some clinical features of Cervical Cancer?

A
  • Vaginal discharge
  • Abnormal Vaginal Bleeding (e.g. postcoital or with micturition or defaecation)
  • Dyspareunia
  • Vaginal discomfort
  • Urinary or bowel habit change
  • Suprapubic pain
  • Abnormal white/red patches on the cervix.
  • Pelvic bulkiness on PV examination
  • Mass felt on PR examination
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189
Q

What are some differential diagnoses for Cervical Cancer?

A
  • Vaginitis: itching, burning, pain, and abnormal discharge
  • Cervical Ectropion
  • Cervicitis: abnormal discharge, pelvic pain, and postcoital bleeding
  • Endometrial cancer: abnormal vaginal bleeding, pelvic pain, and unintentional weight loss
  • Cervical polyps: abnormal vaginal bleeding, discharge, and pain during intercourse
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190
Q

What are the investigations for Cervical Cancer?

A
  • Clinical History prompting Cervix examination with Speculum +/- Swabs to exclude infection

If there is an abnormal appearance of the cervix suggestive of cancer:

  • First line investigation is an Urgent cancer referral for Colposcopy for visualisation and biopsy of the cervix.
  • HPV testing
  • CT Chest, Abdomen and Pelvis is used for Cancer Staging
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191
Q

What is Colposcopy?

A
  • Involves inserting a speculum and using equipment (a colposcope) to magnify the cervix. This allows the epithelial lining of the cervix to be examined in detail.
  • Stains such as Acetic acid and Iodine solution are used to identify abnormal areas
  • A Punch biopsy or LLETZ Biopsy can be performed to get a tissue sample
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192
Q

What is seen on staining during Colposcopy?

A

Acetic Acid Stain:

  • Abnormal cells appear white (Acetowhite)

Schiller’s Iodine Test:

  • Stains healthy cells of the cervix a brown colour.
  • Abnormal areas/cells will not stain
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193
Q

What may be seen on examination of the cervix that may suggest cervical cancer?

A
  • Ulceration
  • Bleeding
  • Inflammation
  • Visible tumour
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194
Q

What may be seen on Colposcopy that is suspicious of Cervical Cancer?

A
  • Abnormal vascularity
  • White change with Acetic Acid
  • Exophytic Lesions
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195
Q

What are the Stages of Cervical Cancer?

A

FIGO system

Stage 1: Confined to cervix

Stage 2: Extending into the uterus or upper 2/3 of the vagina

Stage 3: Extending into lower third of the vagina or pelvic wall

Stage 4: Spread beyond true pelvis or bladder / rectum involvement

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196
Q

What is the management of Cervical Cancer?

A

Depends on the Stage

CIN and Early Stage 1A:

  • Cone Biopsy
  • Large Loop Excision of the Transformation Zone (LLETZ)

Stage 1B - 2A

  • Fertility Preserved: Radical Trachelectomy which is removal of the cervix, upper vagina and pelvic lymph nodes
  • Fertility not Preserved: Hysterectomy and Lymphadenectomy +/- Chemo/radiotherapy

Stage 2B-4A:

  • Chemotherapy and Radiotherapy + Bevacizumab (Avastin)
  • Werthelm’s Hysterectomy (radical): Is removal of the uterus, primary tumour, pelvic lymph nodes and upper 1/3 of the vagina used in invasive, infiltrating early metastatic cancer

Stage 4b:

  • Management is a combination of Surgery, Radiotherapy, Chemotherapy and Palliative Care
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197
Q

What is the Prognosis for Cervical Cancer?

A

5 year survival drops significantly with an advanced stage.

  • Stage 1a: 98% 5 year survival
  • Stage 4: 15% 5 year survival
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198
Q

What is Bevacizumab (Avastin)?

A
  • Monoclonal antibody used in combination with other chemotherapies in the treatment of Metastatic or Recurrent Cancers.
  • It is a Vascular Endothelial Growth Factor A Inhibitor (VEGF-A) to reduce the development of new blood vessels from the cancer.
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199
Q

What is a Cone Biopsy?

A
  • A cone biopsy is a treatment for cervical intraepithelial neoplasia (CIN) and very early-stage cervical cancer.
  • It involves a general anaesthetic.
  • The surgeon removes a cone-shaped piece of the cervix using a scalpel.
  • This sample is sent for histology to assess for malignancy
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200
Q

What are the main risks of a Cone Biopsy?

A
  • Pain
  • Bleeding
  • Infection
  • Scar formation with stenosis of the cervix
  • Increased risk of miscarriage and premature labour
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201
Q

What is a Large Loop Excision of the Transformation Zone (LLETZ)?

A

Also called a Loop Biopsy

  • Involves a Local Anaesthetic
  • Often performed during a Colposcopy procedure
  • Involves a wire loop with electrical current (diathermy) to remove the abnormal epithelial tissue on the cervix.
  • Electrical current cauterises the tissue and stops bleeding
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202
Q

What are the main risks of Large Loop Excision of the Transformation Zone (LLETZ)?

A
  • Bleeding and Abnormal discharge can occur for several weeks following a LLETZ procedure
  • Intercourse and tampon use after the procedure should be avoided to reduce infection
  • May increase the risk of Preterm labour
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203
Q

Who is Eligible for the Cervical Screening Program?

A
  • For all Women and People (Transmen) with a cervix between the age of 25-64 years
  • Cervical sample is taken and tested for High -risk HPV viruses (hrHPV)
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204
Q

What are the normal intervals for Cervical Screening?

A
  • 3 yearly for women aged 25-49
  • 5 yearly for women aged 50-64
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205
Q

What is involved in the Cervical Screening tests?

A

Aims to pick up precancerous changes in epithelial cells of the cervix.

  • Involves a smear test performed by a qualified practice nurse
  • Test consists of a Speculum examination and collection of cells from the cervix using a small brush.
  • The samples are initially tested for high-risk HPV before examination.
  • The cells are then examined under a microscopy using liquid based cytology (LCB) for precancerous changes (dyskaryosis)

If the HPV is negative then the cells are not examined

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206
Q

What do the results of the Cervical Smear Test indicate?

A

Smear Test for hrHPV:

  • Positive: further testing is indicated with LBC
  • Negative: Return to normal recall (age based intervals)

1st Positive hrHPV:

  • Use LBC to detect cellular atypia
  • Cytology Positive: Colposcopy is indicated
  • Cytology Inadequate: Cytology is repeated in 3 months
    • Repeat cytology inadequate - refer for colposcopy
    • If Colposcopy is normal - test hrHPV in 12 months
  • Cytology Negative: Perform 2nd hrHPV test in 12 months

2nd hrHPV:

  • Negative: return to normal recall
  • Positive: Offer 3rd hrHPV test in a further 12 months (24 months after first positive test)

3rd hr HPV:

  • Negative: Return to normal Recall
  • Positive: Refer to Colposcopy
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207
Q

What are some different Cytology results that may be seen following a smear test and liquid based cytology for cervical screening?

A
  • Inadequate
  • Normal
  • Borderline changes
  • Low-grade dyskaryosis
  • High-grade dyskaryosis (moderate)
  • High-grade dyskaryosis (severe)
  • Possible invasive squamous cell carcinoma
  • Possible glandular neoplasia
  • Infections such as bacterial vaginosis, candidiasis, trichomoniasis
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208
Q

Which groups of people may have exceptions to the normal Cervical Screening Program?

A
  • Women with HIV are screened annually
  • Women over 65 may request a smear if they have not had one since aged 50
  • Women with previous CIN may require additional tests (e.g. test of cure after treatment)
  • Certain groups of immunocompromised women may have additional screening (e.g. women on dialysis, cytotoxic drugs or undergoing an organ transplant)
  • Pregnant women due a routine smear should wait until 12 weeks post-partum
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209
Q

Define Menorrhagia?

A

Clinical condition defined as Heavy menstrual bleeding (excessive blood loss) during a menstrual period to the extent that it is affecting a woman’s quality of life

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210
Q

What level of blood loss is considered menorrhage?

A

It used to be 80ml.

Now it is based on the subjective opinion of the woman

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211
Q

What is the epidemiology of Menorrhagia?

A
  • Common gynaecological complaint
  • 50% of cases no underlying pathology is found and the condition is called Dysfunctional Uterine/endometrial bleeding
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212
Q

Define Dysfunctional Endometrial Bleeding?

A

Menorrhagia (heavy menstrual periods) where there is no underlying pathology identified

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213
Q

What is the Aetiology of Menorrhagia?

A

Local:

  • Dysfunctional Uterine Bleeding
  • Fibroids
  • Adenomyosis
  • Endometrial polyps
  • Endometriosis
  • Pelvic inflammatory disease
  • PCOS
  • Contraceptives such as copper coil
  • Endometrial cancer (be highly suspicious of this if there is postmenopausal bleeding)

Systemic:

  • Bleeding disorders
  • Hypothyroidism
  • Liver and kidney disease
  • Obesity
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214
Q

What is the Clinical Presentation of Menorrhagia?

A

Heavy or prolonged menstrual bleeding

Other features: (Due to Iron deficiency Anaemia)

  • Fatigue
  • Weakness
  • Shortness of Breath
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215
Q

What are some differential diagnoses for Menorrhagia?

A

Differentials that include abnormal uterine bleeding:

  • Fibroids: Often asymptomatic, but can cause heavy or prolonged periods, pelvic pain or pressure, and frequent urination.
  • Adenomyosis: Symptoms can include prolonged, heavy menstrual bleeding, severe menstrual cramps, and pain during intercourse.
  • Endometrial polyps: Can cause irregular menstrual bleeding, bleeding between periods, excessively heavy periods, or postmenopausal bleeding.
  • Endometrial cancer: Symptoms include abnormal vaginal bleeding, pelvic pain, and pain during intercourse.
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216
Q

What are the key things to ask in any presentation with a gynaecological problem?

A
  • Age at menarche
  • Cycle length, days menstruating and variation
  • Intermenstrual bleeding and post coital bleeding
  • Contraceptive history
  • Sexual history
  • Possibility of pregnancy
  • Plans for future pregnancies
  • Cervical screening history
  • Migraines with or without aura (for the pill)
  • Past medical history and past drug history
  • Smoking and alcohol history
  • Family history
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217
Q

What investigations should be performed in Menorrhagia?

A
  • FBC + Iron studies: to look for iron deficiency anaemia
  • Pelvic examination with a speculum: Should be performed unless there is a straightforward history without other risk factors or symptoms or they are young and not sexually active

Imaging Studies if Indicated:

  • Hysteroscopy (outpatient)
  • Pelvic and Transvaginal Ultrasound

Additional Tests based on features:

  • Swabs if there is evidence of infection (e.g. abnormal discharge or suggestive sexual history)
  • Coagulation screen if there is a family history of clotting disorders (e.g. Von Willebrand disease) or periods have been heavy since menarche
  • Ferritin if they are clinically anaemic
  • Thyroid function tests if there are additional features of hypothyroidism
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218
Q

What may indicate the need for an Outpatient Hysteroscopy in Menorrhagia?

A
  • Suspected submucosal fibroids
  • Suspected endometrial pathology, such as endometrial hyperplasia or cancer
  • Persistent intermenstrual bleeding
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219
Q

What may indicate the need for Pelvic and Transvaginal Ultrasound in Menorrhagia?

A
  • Possible large fibroids (palpable pelvic mass)
  • Possible adenomyosis (associated pelvic pain or tenderness on examination)
  • Examination is difficult to interpret (e.g. obesity)
  • Hysteroscopy is declined
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220
Q

What is the Management of Menorrhagia?

A

Exclude underlying pathology/Treat pathology first

Women does NOT want Contraception:

  • Tranexamic acid when no associated pain (antifibrinolytic – reduces bleeding)
  • Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)

Women DOES want Contraception:

  • Mirena coil (first line)
  • Combined oral contraceptive pill
  • Progesterone only contraception can be tried

Medical management Failed:

  • Hysterectomy
  • Endometrial Ablation

Referral to Secondary Care:

  • If treatment is unsuccessful
  • Symptoms are Severe
  • Large fibroids (>3cm)
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221
Q

Define Endometrial Cancer?

A

Malignant proliferation that originals from the endometrium (the inner lining of the uterus)

It is an Oestrogen Depending cancer meaning that oestrogen stimulates the growth of Endometrial cancer cells

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222
Q

What is the epidemiology of Endometrial Cancer?

A
  • 6th Most commonly diagnosed cancer in women
  • 15th most common cancer
  • 80% of cases are adenocarcinoma
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223
Q

What is Endometrial Hyperplasia?

A

a precancerous condition that involves thickening of the endometrium

  • The risk factors, presentation, investigations are similar to Endometrial cancer
  • Most cases of Endometrial Hyperplasia will return to normal over time and <5% become endometrial cancer.
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224
Q

What are the types of Endometrial Hyperplasia?

A
  • Hyperplasia without atypia
  • Atypical Hyperplasia
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225
Q

How can Endometrial Hyperplasia be treated?

A

Without Atypical Cells:

  • Reversal of risk factors: Weight loss, stopping HRT
  • Intrauterine System (IUS/Mirena coil)
  • Continuous Oral Progestogens (Medroxyprogesterone)

With Atypical Cells:

  • Total Hysterectomy with Bilateral Salpingo-oophorectomy (TAH and BSO)
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226
Q

What are the risk factors for Endometrial Cancer?

A

Anything that causes increased Exposure to Unopposed Oestrogen (Oestrogen without progesterone):

  • Increased Age
  • Nulliparity (never given birth or carried child)
  • Obesity
  • Diabetes
  • Early menarche
  • Late menopause
  • Polycystic ovary syndrome
  • Oestrogen-only hormone replacement therapy
  • Tamoxifen
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227
Q

How does PCOS increase your risk of Endometrial Cancer?

A

Polycystic ovarian syndrome leads to increased exposure to unopposed oestrogen due to a lack of ovulation.

Anovulation/oligoovulation means follicles don’t develop

No corpous luteum so no progesterone

Unopposed oestrogen acting on endometrium

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228
Q

What should be given to women with PCOS for Endometrial Protection?

A

Progestrogens
One of:

  • Combined Contraceptive Pill
  • Intrauterine System (Mirena coil)
  • Cyclical Progestogens
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229
Q

How does Obesity increase the risk of Endometrial Cancer?

A

Obesity is a crucial risk factor because adipose tissue (fat) is a source of oestrogen.

Adipose tissue is the primary source of oestrogen in postmenopausal women.

Adipose tissue contains aromatase, which is an enzyme that converts androgens such as testosterone into oestrogen

This extra Oestrogen is unopposed in women that are not ovulating (PCOS/post-menopause)

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230
Q

How does Tamoxifen increase the risk of Endometrial Cancer?

A

Tamoxifen has an anti-oestrogenic effect on breast tissue however it has an oestrogenic effect on the endometrium increasing the risk of endometrial cancer.

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231
Q

What are some protective factors for Endometrial Cancer?

A
  • Combined Contraceptive Pill
  • Mirena Coil
  • Increased Pregnancies
  • Cigarette Smoking
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232
Q

What are the clinical features of Endometrial Cancer?

A

Features vary but commonly include:

  • Postmenopausal Bleeding
  • Postcoital bleeding
  • Intermenstrual bleeding
  • Unusually heavy menstrual bleeding
  • Abnormal vaginal discharge
  • Dyspareunia
  • Abdominal discomfort or bloating
  • Weight Loss
  • Haematuria
  • Anaemia
  • Raised platelet count
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233
Q

What must you think about in women with postmenopausal bleeding?

A

This is endometrial cancer until proven otherwise

Other key risk factors include obesity and diabetes

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234
Q

What are some differential diagnoses for Endometrial Cancer?

A
  • Uterine fibroids: Characterised by heavy menstrual bleeding, pelvic pressure or pain, frequent urination, and constipation.
  • Endometrial polyps: Symptoms may include irregular menstrual bleeding, bleeding between menstrual periods, excessively heavy menstrual periods, and vaginal bleeding after menopause.
  • Cervical cancer: Signs can include abnormal vaginal bleeding, postmenopausal bleeding, and pelvic pain.
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235
Q

What is the Referral Criteria for Endometrial Cancer?

A

Guidelines for a 2 week wait urgent Endometrial cancer referral:

  • Postmenopausal Bleeding more than 12 months after the last menstrual period.

NICE also recommends referral for Transvaginal Ultrasound in women Over 55 years with:

  • Unexplained vaginal discharge
  • Visible haematuria Plus raised platelets, anaemia, or elevated glucose levels
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236
Q

What are the investigations for Endometrial Cancer?

A
  • First Line: Transvaginal Ultrasound: for endometrial thickness (normal is less than 4mm post menopause)
  • Second Line: Endometrial Biopsy
    • Pipelle Biopsy: highly sensitive for endometrial cancer
    • Hysteroscopy with endometrial biopsy
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237
Q

What are the stages of Endometrial Cancer?

A

FIGO System:

Stage 1: Confined to the uterus

Stage 2: Invades the cervix

Stage 3: Invades the ovaries, fallopian tubes, vagina or lymph nodes

Stage 4: Invades bladder, rectum or beyond the pelvis

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238
Q

What is the Management for Endometrial Cancer?

A
  • Progesterone: May be used as a hormonal treatment to slow the progression of the cancer

Stage 1 and 2 Endometrial Cancer:

  • Total Abdominal Hysterectomy with Bilateral Salpingo-oophorectomy (TAH and BSO): Removal of uterus, cervix and adnexa

Later stages spread outside of the uterus:

  • Combination of Hysterectomy, Radiotherapy, Chemotherapy
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239
Q

Define Endometriosis?

A

A gynaecological condition where ectopic endometrium-like tissue (Glands and stroma) , which typically lines the uterus, proliferates outside the uterine cavity.

Endometrioma: A lump of endometrial tissue outside the uterus

Chocolate Cysts: Endometriomas in ovaries

Adenomyosis: Endometrial tissue within the myometrium of the uterus

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240
Q

What is the Epidemiology of Endometriosis?

A

*Approximately estimated to affect 10% of women in their reproductive years

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241
Q

What is the Aetiology of Endometriosis?

A

No clear cause but several theories:

  • Genetic component: Though no specific genes are identified
  • Retrograde menstruation
  • Coelomic metaplasia: Cells outside of the uterus somehow change via metaplasia into endometrial cells
  • Lymphatic or vascular dissemination of endometrial cells: Cells spread similarly to cancer
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242
Q

What are the clinical features of Endometriosis?

A
  • Cyclical abdominal or pelvic pain
  • Dysmenorrhoea
  • Dyspareunia
  • Sub/infertility
  • Cyclical bleeding from other sites (eg. rectal bleeding o haematuria)
  • Urinary and bowel symptoms
  • Palpable mass on examination (endometriomas)
  • Fixed retroverted uterus
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243
Q

What is the pathophysiology of the symptoms of endometriosis?

A

Chronic and cyclical pelvic/abdominal pain occurs due to the ectopic endometrial tissue responding to hormones in the same way normal endometrial tissue does.

Therefore during menstruation, the ectopic endometrial tissue spreads and bleeds in new cavities in the body.

This causes both a cyclical burning, dull pain but also can lead to inflammation and cause further discomfort.

The inflammation may lead to adhesions developing due to damage and scar tissue. This can also lead to chronic non-cyclical pain that is sharp or stabbing.

Adhesions may also contribute to reduced fertilities due to blocking the release of eggs or kinking fallopian tubes and obstructing the route to the uterus.

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244
Q

What are some differential diagnoses for endometriosis?

A
  • Primary dysmenorrhoea: characterised by crampy pelvic pain at the onset of menses with no identifiable pelvic pathology.
  • Uterine conditions (e.g. fibroids, adenomyosis): these can cause heavy menstrual bleeding and pelvic discomfort.
  • Adhesions: pelvic pain and possible bowel obstruction.
  • Pelvic inflammatory disease (PID): presents with lower abdominal pain, fever, abnormal vaginal discharge, and possible dyspareunia.
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245
Q

What are the investigations for Endometriosis?

A

Clinical Examination: May identify endometriomas or deep nodules.

Transvaginal/Pelvic Ultrasound scan: Often unremarkable however they may reveal large endometriomas or chocolate cysts

Referral to gynaecology for ultrasound or Laparoscopy: Patients with severe persistent or recurrent symptoms of endometriosis should be referred.

Laparoscopic Surgery (Gold Standard): Definitive diagnosis is established with a biopsy of lesion during Laparoscopy. Surgeons may also remove deposits of endometriosis to potentially improve symptoms.

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246
Q

What is the Gold Standard investigation for Endometriosis?

A

Laparoscopic Surgery

This however comes with risks of complications such as bowel perforation and therefore is not the first line initial investigation

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247
Q

What is the management of Endometriosis?

A

Initial management involves:

  • Establishing a diagnosis
  • Providing a clear explanation
  • Listening to the patient, establishing their ideas, concerns and expectations and building a partnership
  • First Line: Analgesia as required for pain (NSAIDs and paracetamol)

Hormonal management options can be tried before establishing a definitive diagnosis with laparoscopy:

  • First line: Combined oral contractive pill, which can be used back to back without a pill-free period if helpful
  • Progesterone only pill
  • Medroxyprogesterone acetate injection (e.g. Depo-Provera)
  • Nexplanon implant
  • Mirena coil
  • Second Line: GnRH agonists (Goserelin (Zoladex) or Leuprorelin (prostap))

Surgical management options:

  • Laparoscopic surgery to excise or ablate the endometrial tissue and remove adhesions (adhesiolysis)
  • Bilateral oophorectomy +/-Hysterectomy

Laparoscopic treatment may improve fertility. Hormonal therapies may improve symptoms but not fertility.

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248
Q

Define Fibroids?

A

Benign smooth muscle tumours (uterine leiomyomas) originating from the myometrium of the uterus.

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249
Q

What is the Epidemiology of Fibroids?

A
  • Most prevalent benign uterine tumour in women
  • Leading cause for Hysterectomy
  • Very common affecting 40-60% of women in later reproductive years
  • More common in black women
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250
Q

What is the Aetiology of Fibroids?

A

Unknown but thought to be related to hormonal and environmental factors

Oestrogen sensitive meaning they grow in response to oestrogen

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251
Q

What are the different types of Fibroid?

A
  • Intramural means within the myometrium (the muscle of the uterus). As they grow, they change the shape and distort the uterus.
  • Subserosal means just below the outer layer of the uterus. These fibroids grow outwards and can become very large, filling the abdominal cavity.
  • Submucosal means just below the lining of the uterus (the endometrium).
  • Pedunculated means on a stalk.
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252
Q

What are the clinical features of Fibroids?

A

Often Asymptomatic

Symptoms:

  • 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
  • Palpable mass on abdominal or pelvic exam
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253
Q

What are some differential diagnoses for Fibroids?

A

Other causes of Menorrhagia and Dysmenorrhoea:

  • Endometrial polyps: Present with irregular menstrual bleeding and spotting
  • Endometriosis: Characterized by dysmenorrhoea, deep dyspareunia, chronic pelvic pain, and infertility
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254
Q

What are the investigations for Fibroids?

A

First Line:

  • Transvaginal/Pelvic/Abdominal Ultrasound scan
  • Hysteroscopy is initial investigation for submucosal fibroids presenting with menorrhagia

Second Line:

  • MRI scan if ultrasound does not provide enough detail before considering surgical options
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255
Q

What is the management of Fibroids?

A

Asymptomatic fibroids
no treatment is needed other than periodic review to monitor size and growth

Management of menorrhagia secondary to fibroids

  • IUS
  • useful if the woman also requires contraception
  • cannot be used if there is distortion of the uterine cavity
  • NSAIDs e.g. mefenamic acid
  • tranexamic acid
  • combined oral contraceptive pill
  • oral progestogen
  • injectable progestogen

Treatment to shrink/remove fibroids
medical

  • GnRH agonists may reduce the size of the fibroid but are typically used more for short-term treatment

Surgical management

  • myomectomy: this may be performed abdominally, laparoscopically or hysteroscopically
  • hysteroscopic endometrial ablation
  • hysterectomy
  • uterine artery embolization
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256
Q

What are some complications for Fibroids?

A
  • 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%)
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257
Q

What is Red Degeneration of Fibroids?

A

Red degeneration refers to ischaemia, infarction and necrosis of the fibroid due to disrupted blood supply.

in pregnancy the fibroid outgrows blood supply causing Ischaemia and Infarction.

Red degeneration is more likely to occur in larger fibroids (above 5 cm) during the second and third trimester of pregnancy.

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258
Q

How does Red Degeneration of Fibroids Present?

A

Look out for the pregnant woman (2nd/3rd trimester) with a history of fibroids presenting with severe abdominal pain and a low-grade fever in your exams. The diagnosis is likely to be red degeneration.

  • Severe abdominal pain
  • Low grade fever
  • Tachycardia
  • Vomiting
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259
Q

What is the Management of Red Degeneration of Fibroids?

A

Supportive management

  • Rest
  • Fluids
  • Analgesia
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260
Q

What is a Typical exam patient for Red Degeneration of Fibroids?

A

Look out for the pregnant woman with a history of fibroids presenting with severe abdominal pain and a low-grade fever in your exams. The diagnosis is likely to be red degeneration.

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261
Q

Define Hydatidiform Mole?

A

A type of tumour that grows like a pregnancy inside the uterus. This is known as a Molar Pregnancy

It forms part of a spectrum of disorders known as gestational trophoblastic disease

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262
Q

What are the different Types of Hydatidiform Mole?

A

Complete Mole:

  • Occurs when two sperm cells (or 1 which duplicates DNA) fertilise an ovum that contains no genetic material (an “empty ovum”).
  • These sperm then combine genetic material, and the cells start to divide and grow into a tumour called a complete mole (46YY)
  • No foetal material will form.

Partial Mole:

  • Occurs when two sperm cells fertilise a normal ovum (containing genetic material) at the same time.
  • The new cell now has three sets of chromosomes (triploidy (69 XXX or 69 XXY)
  • The cell divides and multiplies into a tumour called a partial mole.
  • In a partial mole, some foetal material may form.
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263
Q

What is the Epidemiology of a Molar Pregnancy?

A

Women at highest risk of developing a molar pregnancy are at the extreme ends of the fertility age range, specifically those under 16 years of age and over 45 years of age.

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264
Q

What are the clinical features of a Hydatidiform Mole?

A

Molar pregnancy behaves like a normal pregnancy. Periods will stop and the hormonal changes of pregnancy will occur. There are a few things that can indicate a molar pregnancy versus a 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)
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265
Q

What are some differential diagnoses for a Hydatidiform Mole?

A
  • Ectopic pregnancy: Symptoms include lower abdominal pain, vaginal bleeding, and amenorrhea.
  • Miscarriage: Symptoms include vaginal bleeding, abdominal pain, and passage of tissue.
  • Normal pregnancy: Typically characterized by a positive pregnancy test, absence of menstruation, and possible morning sickness.
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266
Q

What are the investigations for a Molar Pregnancy?

A

Molar pregnancy behaves like a normal pregnancy However some indications include:

  • B-hCG Levels are often significantly higher than normally expected
  • Transvaginal Ultrasound: May show a snowstorm appearance of pregnancy, low resistance of blood vessel flow and absence of a foetus
  • Histology may be used to confirm after mole evacuation
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267
Q

What is the management of a Molar Pregnancy?

A

Immediate referral to a specialist centre for treatment

  • Evacuation of the uterus to remove the mole (using suction curettage) which is sent for histological examination
  • Hysterectomy is a possibility if fertility preservation is not a concern
  • Systemic Chemotherapy: may be required if the mole has metastasised
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268
Q

What surveillance should be done in a Molar Pregancy?

A
  • Bimonthly serum and urine hCG testing until levels are normal.
  • In the case of a partial mole, a repeat hCG test is done 4 weeks later - if normal, the patient is discharged from surveillance.
  • In the case of a complete mole, monthly repeat hCG samples are sent for at least 6 months.
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269
Q

Define a Prolactinoma?

A

Pituitary tumours characterized by excessive production of prolactin (leading to hyperprolactinaemia), a hormone that plays a crucial role in lactation.

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270
Q

What is the epidemiology of prolactinomas?

A
  • The most common hormone-secreting tumours originating in the pituitary gland.
  • Can affect people of any age but more commonly diagnosed in adults
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271
Q

What genetic condition is associated with Prolactinomas?

A

Multiple Endocrine Neoplasia (MEN) Type I

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272
Q

What are the different types of Prolactinoma?

A

Microprolactinomas – smaller than 10 mm

Macroprolactinomas – larger than 10 mm

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273
Q

What are the clinical features of Prolactinomas?

A

Both Genders:

  • Reduced Libido
  • Headaches
  • Visual Field Defects (bitemporal hemianopia)

Women:

  • Oligomenorrhoea/Amenorrhoea
  • Galactorrhoea (breast milk production outside of pregnancy or breastfeeding)
  • Infertility
  • Vaginal dryness

Men:

  • Erectile dysfunction
  • Reduced facial hair growth
  • Gynaecomastia
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274
Q

What are the investigations for a Prolactinoma?

A
  • Pregnancy Test: Essential in women with childbearing potential presenting with breast milk production
  • Blood Tests: Serum Prolactin, U&Es, LFTs, TFTs
  • MRI scan is investigation of choice for diagnosing pituitary tumours
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275
Q

What is the management of Prolactinomas?

A

Pharmacological:

  • Dopamine Agonists (e.g. Cabergoline or Bromocriptine): These drugs reduce serum prolactin levels, alleviate galactorrhea, and restore gonadal function.
  • Trans-sphenoidal Surgical Resection is indicated when medical treatment fails to manage the tumour effectively. Definitive treatment
  • Radiotherapy: Reserved for cases where other treatments are unsuccessful.
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276
Q

What are some complications of Prolactinomas?

A
  • Hormonal imbalances
  • Recurrence of the tumour
  • Risks associated with surgical and radiation interventions
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277
Q

Define Ovarian Cancer?

A

Malignant proliferation originating from various cell types within the ovary

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278
Q

What are the different types of Ovarian Tumour?

A
  • Epithelial Cell Tumours
  • Germ Cell Tumours
  • Sex Cord-Stromal tumour
  • Malignant (Krukenberg Tumour)
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279
Q

What are Epithelial Cell Ovarian Tumours?

A
  • Originate from the epithelium which lines the fimbria of the fallopian tubes or the ovaries
  • Epithelial tumours are partially cystic, and the cysts can contain fluid
  • The initial metastatic spread typically involves the peritoneal cavity, with seeding particularly affecting the bladder, paracolic gutters and the diaphragm
  • Around 90% of ovarian cancers are epithelial ovarian tumours.
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280
Q

What are the subtypes of Epithelial Cell Ovarian Tumours?

A
  • Serous tumours (the most common)
  • Endometrioid carcinomas
  • Clear cell tumours
  • Mucinous tumours
  • Undifferentiated tumours
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281
Q

What are Germ Cell Ovarian Tumours?

A
  • Originate from the germ cells in the embryonic gonad (Teratomas)
  • May contain various tissue types such as Skin, teeth, bone and hair
  • Spread predominantly via the lymphatic route
  • Common in young women
  • Tumour markers include alpha-fetoprotein and sometimes beta human chorionic gonadotrophin (B-HCG).
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282
Q

What are Sex Cord-Stromal Tumours?

A
  • Originate Granulosa/Theca (in women) or Leydig/Sertoli cells (In males) or are Fibromas
  • Make up less than 5% of tumours

Often produce Hormones:

  • Granulosa: Oestrogen leading to precocious puberty
  • Leydig: Androgens leading to masculinising features and associated with Peutz Jegher Syndrome
  • Fibroma: Associated with Meigs Syndrome
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283
Q

What is a Krukenberg Tumour?

A

Ovarian Tumours may be due to metastasis from a cancer elsewhere in the body

  • A Krukenberg tumour refers to a metastasis in the ovary, usually from a gastrointestinal tract cancer, particularly the stomach.
  • Krukenberg tumours have characteristic “signet-ring” cells on histology, which look like signet rings on under a microscopy.
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284
Q

Where do Ovarian Cancers typically metastasise to?

A

Occurs via Trans coelomic routes (Across a body cavity) and thus can spread to the liver, bowel and associated mesentery

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285
Q

What are some risk factors for Ovarian Cancer?

A
  • Advanced age (peak age 60 years)
  • Smoking
  • Increased number of ovulations (early menarche, late menopause, no pregnancies)
  • Genetic predisposition (BRCA 1 and 2 genes and family history)
  • Obesity
  • Hormone replacement therapy (HRT)
  • Recurrent use of clomiphene (fertility drug)
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286
Q

What are some protective factors for Ovarian Cancer?

A

Factors that reduce lifetime ovulations

  • Childbearing (parity)
  • Breastfeeding
  • Early Menopause
  • Combined oral contraceptive pill
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287
Q

What are the clinical features of Ovarian Cancer?

A

Often present late in disease progression with Non-specific symptoms

  • Abnormal Vaginal bleeding (post coital, intermenstrual, post menopausal)
  • Vaginal discharge
  • Abdominal bloating/discomfort
  • Early satiety (feeling full after eating) and Loss of appetite
  • Pelvic, back or abdominal pain
  • Urinary symptoms (frequency / urgency)
  • Weight loss
  • Abdominal or pelvic mass
  • Ascites (due to VEGF increasing vessel permeability)
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288
Q

Why may a patient with Ovarian Cancer present with Hip or Groin Pain?

A

An Ovarian mass may press on the obturator nerve causing referred hip or groin pain.

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289
Q

What are some differential diagnoses for Ovarian Cancer?

A
  • Gastrointestinal conditions (e.g., irritable bowel syndrome): Characterised by abdominal pain, bloating, and changes in bowel habits
  • Fibroids: May cause heavy menstrual bleeding, pelvic pressure or pain, frequent urination, and constipation
  • Ovarian cysts: Can cause pelvic pain, fullness or heaviness in the abdomen, and bloating
  • Other cancers (e.g., bladder, endometrial): May present with symptoms such as abnormal bleeding, pelvic pain, and urinary symptoms
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290
Q

When should Suspected Ovarian Cancer prompt an Urgent 2 Week Wait Referral or Carry out further investigations before Referral

A

Direct Urgent 2-Week-Wait Referral

  • Ascites
  • Pelvic Mass
  • Abdominal Mass

Carry out further Investigations before referral Starting with CA125 blood test

  • New symptoms of IBS/change in bowel habit
  • Abdominal Bloating
  • Early Satiety
  • Pelvic Pain
  • Urinary frequency or urgency
  • Weight loss
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291
Q

What are the investigations for Ovarian Cancer?

A

Initial Investigations:

  • CA125 Blood Test: (> 35IU/ml is significant)

Then

  • Urgent Pelvic and Abdominal Ultrasound Scan

Diagnosis is difficult and often done with diagnostic Laparoscopy

Risk of Malignancy Index

Women Under 40 years with complex ovarian mass:

  • AFP and hCG tumour markers for possible Germ cell tumour
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292
Q

What are some causes of a Raised CA125?

A

CA125 is a tumour marker for epithelial cell ovarian cancer.
It is not very specific, and there are many non-malignant causes of a raised CA125:

  • Endometriosis
  • Fibroids
  • Adenomyosis
  • Pelvic infection
  • Liver disease
  • Pregnancy
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293
Q

How is Ovarian Cancer Staged?

A

FIGO System:

Stage 1: Confined to Ovary:

  • IA: Limited to one ovary, Capsule intact
  • IB: Limited to both ovaries, Capsule intact
  • IC: Limited to one or both ovaries, Capsule intact

Stage 2: Spread past the ovary but inside the pelvis:

  • IIA: Extension to uterus or fallopian tubes, No malignant cells in ascites/washings
  • IIB: Extension to other pelvic tissues, No malignant cells in ascites/washings
  • IIC: Pelvic Extension (IIA/IIB) with malignant cells in ascites/washings

Stage 3: Spread past the pelvis but inside abdomen:

  • IIIA: Microscopic peritoneal mets beyond pelvis
  • IIIB: Macroscopic peritoneal mets beyond pelvis < 2cm
  • IIIC: Peritoneal mets beyond pelvis > 2cm and/or regional lymph node mets

Stage 4: Spread outside the abdomen (distant metastasis):

  • Tumour is involving one or both ovaries with distant metastasis
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294
Q

What is the management of Ovarian Cancer?

A

Managed by specialist gynaecology oncology MDT

Surgery: Radical Hysterectomy, BSO, Infracolic omentectomy are options if early stage

Chemotherapy: Used an adjuvant to surgery.

**Bevacizumab (anti-VEGF) may also be used

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295
Q

Define Ovarian Cysts

A

Fluid filled sac that develops within or on the surface of an ovary

They can range in size and occur as a normal part of the menstrual cycle or as a result of an underlying condition.

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296
Q

What is the Epidemiology of Ovarian Cysts?

A
  • Very common in premenopausal women with most women experiencing at least one
  • Cysts in postmenopausal women are more concerning for malignancy and need further investigation
  • Majority of cysts in premenopausal women are benign
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297
Q

What is the Aetiology of Ovarian Cysts?

A

Can be caused by a variety of factors, including:

  • Hormonal imbalances
  • Endometriosis,
  • Pregnancy
  • Pelvic infection
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298
Q

What is a String of pearls appearance?

A

Patients with multiple ovarian cysts may have a String of pearls appearance to the ovaries

This is not PCOS unless they have other features of the condition

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299
Q

What are the clinical features of Ovarian Cysts?

A

Most ovarian cysts are Asymptomatic

May Cause:

  • Pelvic pain (often acute unilateral pain)
  • Bloating
  • Fullness in the abdomen
  • Palpable pelvic mass
  • Intra-peritoneal haemorrhage with haemodynamic compromise
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300
Q

What are the different types of Ovarian Cyst?

A

Functional Cysts:

  • Follicular Cysts: Most common and harmless. they form due to failure to the follicle failing to rupture and release an egg.
  • Corpus Luteum Cysts: Occur when the corpus luteum fails to break down and fills with fluid. Often seen in early pregnancy

Non-Functional Cysts:

  • Serous Cystadenoma: Benign tumours of the epithelial cells
  • Mucinous Cystadenoma: Can become huge and cause psuedomyoxma peritoni
  • Endometrioma: occurs with endometriosis
  • Malignant cysts: Dermoid/ Sex cord/Stromal
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301
Q

What are some differential diagnoses for Ovarian Cysts?

A
  • Ovarian torsion: Characterised by sudden, severe pain, often accompanied by nausea and vomiting.
  • Ectopic pregnancy: Symptoms include abdominal pain, amenorrhea, and vaginal bleeding.
  • Appendicitis: Presents with abdominal pain that begins near the navel and then moves lower and to the right, loss of appetite, nausea, and vomiting.
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302
Q

What are the investigations for Ovarian Cysts?

A

Detailed History and Examination: to establish for features that may suggest malignancy

Pregnancy test: Exclude ectopic pregnancy

Ultrasound Scan if less than 5cm in premenopausal women then no further investigation needed.

Tumour Markers: CA125, AFP, LDH, B-hCG

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303
Q

What are features from the history that may suggest malignancy?

A
  • Abdominal bloating
  • Reduce appetite
  • Early satiety
  • Weight loss
  • Urinary symptoms
  • Pain
  • Ascites
  • Lymphadenopathy
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304
Q

What is the Risk of Malignancy Index?

A

Estimates the risk of an ovarian mass being malignant, taking account of three things:

  • Menopausal status
  • Ultrasound findings
  • CA125 level
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305
Q

What is the management of Ovarian Cysts?

A

Conservative:

  • Monitoring and Pain management (analgesia)
  • Surgical intervention may be required
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306
Q

What are some complications of Ovarian Cysts?

A
  • Torsion
  • Haemorrhage into the cyst
  • Rupture, with bleeding into the peritoneum
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307
Q

What is Meig’s Syndrome?

A

Triad of:

  • Ovarian fibroma (benign ovarian tumour)
  • Pleura effusion
  • Ascites

Treatment is removal of the tumour

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308
Q

Define Ovarian Torsion?

A

A condition where the ovary twists in relation to the surrounding connective tissue, the fallopian tube (Adnexa) and blood supply.

Adnexal torsion: when the fallopian tube is involved

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309
Q

What is the aetiology of Ovarian torsion?

A
  • Usually due to an ovarian mass (often > 5cm) such as a cyst or tumour.
  • Can occur with normal ovaries in girls before menarche when girls have a longer infundibulopelvic ligaments
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310
Q

What are some risk factors for Ovarian Torsion?

A
  • Ovarian mass: present in around 90% of cases of torsion
  • Being of a reproductive age
  • Pregnancy
  • Ovarian hyperstimulation syndrome
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311
Q

What is the pathophysiology of Ovarian Torsion?

A
  • Ovary twists around the adnexa and blood supply
  • Leads to ischaemia of the Ovary
  • If torsion persists then necrosis will occur and the function of the ovary will be lost
  • Ovarian torsion is an emergency where treatment delay can have significant consequences
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312
Q

What are the clinical features of Ovarian Torsion?

A
  • Sudden onset severe unilateral pelvic pain
    • Constant getting progressively worse
    • Associated with Nausea and Vomiting
  • Localised tenderness
  • May have a palpable mass
  • Vaginal examination may show adnexial tightness
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313
Q

What are the investigations for Ovarian Torsion?

A

Pelvic Ultrasound initial investigation of choice

  • Transvaginal is Ideal but Transabdominal can be used if transvaginal is not possible.
  • May show “Whirlpool sign of free fluid” in the pelvis and Oedema of the ovary

Laparoscopic Surgery is definitive diagnostic investigation

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314
Q

What is the management of Ovarian Torsion?

A
  • Patients need emergency admission under gynaecology for urgent investigation and management.
  • Depending on the duration and severity of the illness they require laparoscopic surgery to either:
    • Un-twist the ovary and fix it in place (detorsion)
    • Remove the affected ovary (oophorectomy)
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315
Q

What are some complications of Ovarian Torsion?

A
  • Delayed treatment can lead to loss of function of that ovary
  • If necrotic ovary is not removed it may lead to infection, abscess formation and sepsis
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316
Q

Define Polycystic Ovarian Syndrome (PCOS)?

A

PCOS is the most common endocrine condition in women of reproductive age.

The disorder is characterised by failure of follicles to release eggs leading to anovulation, hyperandrognism features and enlarged/multicystic ovaries

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317
Q

Define these words:
Anovulation
Oligoovulation
Amenorrhoea
Oligomenorrhoea
Androgens
Hyperandrogenism
Hirsutism
Insulin Resistance

A
  • Anovulation: refers to the absence of ovulation
  • Oligoovulation: refers to irregular, infrequent ovulation
  • Amenorrhoea: refers to the absence of menstrual periods
  • Oligomenorrhoea: refers to irregular, infrequent menstrual periods
  • Androgens: are male sex hormones, such as testosterone
  • Hyperandrogenism: refers to the effects of high levels of androgens
  • Hirsutism: refers to the growth of thick dark hair, often in a male pattern, for example, male pattern facial hair
  • Insulin Resistance: refers to a lack of response to the hormone insulin, resulting in high blood sugar levels
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318
Q

What is the Epidemiology of PCOS?

A
  • Prevalent condition affecting up to 1/3 of women during their reproductive years
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319
Q

What is the Aetiology of PCOS?

A

Complex and Multifactorial (still unclear)

  • Hormone imbalances, low oestrogen, high androgens and high insulin (with insulin resistance) leads to increased circulating androgens
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320
Q

What criteria is used to make a diagnosis of PCOS?

A

Rotterdam Criteria: requires at least 2 out of 3 key features:

  • Oligoovulation or Anovulation
  • Biohemical evidence of Hyperandrogenism (hirsutism and acne)
  • Polycystic Ovaries on Ultrasound (> 12 cysts on imaging or ovarian volume > 10 cm3)

Having only one feature such as multiple ovarian cysts does not qualify for diagnosis of PCOS

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321
Q

What are some key clinical features in PCOS?

A
  • Oligomenorrhoea or amenorrhoea
  • Sub/Infertility
  • Obesity (in about 70% of patients with PCOS)
  • Hirsutism
  • Acne
  • Acanthosis Nigricans
  • Mood changes including Anxiety and depression
  • Hair loss in a male pattern
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322
Q

What other features may women with PCOS experience?

A
  • Insulin resistance and diabetes
  • Acanthosis nigricans
  • Cardiovascular disease
  • Hypercholesterolaemia
  • Endometrial hyperplasia and cancer
  • Obstructive sleep apnoea
  • Depression and anxiety
  • Sexual problems
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323
Q

What are some differential diagnoses for PCOS?

A
  • Menopause: characterised by cessation of menstruation, hot flashes, vaginal dryness, mood changes, and sleep problems.
  • Congenital adrenal hyperplasia (CAH): presenting with signs of androgen excess like hirsutism, acne, and irregular periods.
  • Hyperprolactinaemia: symptoms include irregular periods, galactorrhoea, and infertility.
  • Androgen-secreting tumours: may cause virilisation, amenorrhoea, and hirsutism.
  • Cushing’s syndrome: characterised by weight gain, purple stretch marks, and easy bruising.
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324
Q

What are some differential diagnoses for Hirsutism?

A
  • Medications, such as phenytoin, ciclosporin, corticosteroids, testosterone and anabolic steroids
  • Ovarian or adrenal tumours that secrete androgens
  • Cushing’s syndrome
  • Congenital adrenal hyperplasia
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325
Q

What is the relationship between Insulin Resistance and PCOS?

A

When someone is resistant to insulin, their pancreas has to produce more insulin to get a response from the cells of the body.

Insulin promotes the release of androgens from the ovaries and adrenal glands.

Therefore, higher levels of insulin result in higher levels of androgens (such as testosterone).

Insulin also suppresses sex hormone-binding globulin (SHBG) production by the liver.

SHBG normally binds to androgens and suppresses their function. Reduced SHBG further promotes hyperandrogenism in women with PCOS.

The high insulin levels contribute to halting the development of the follicles in the ovaries

This leads to anovulation and multiple partially developed follicles (seen as polycystic ovaries on the scan).

Diet, exercise and weight loss help reduce insulin resistance.

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326
Q

What are the investigations for PCOS?

A

Blood Tests:

  • LH: Raised
  • LH:FSH Ratio increased >2 aids in differentiating from menopause (ratio is normal)
  • Total and Free Testosterone: Raised

Other Blood Tests for Exclusion of conditions

  • Insulin resistance (Fasting and OGTT)
  • Oestrogen Levels: Normal or Raised
  • TFTs: Exclude thyroid dysfunction
  • 17 Hydroxyprogesterone: Exclude CAH
  • Prolactin levels: Exclude hyperprolactinaemia
  • 24 Hour urinary cortisol: Exclude Cushing’s

Imaging: Pelvic Ultrasound

  • Transvaginal Ultrasound is Gold Standard
  • String of Pearls Appearance
  • 12 or more developing follicles in one ovary
  • Ovarian Volume > 10 cm3
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327
Q

What is PCOS a significant risk factor for?

A

Endometrial Cancer

Within the syndrome of PCOS it has multiple risk factors for Endometrial cancer including:

  • Obesity
  • Diabetes
  • Insulin Resistance
  • Amenorrhoea
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328
Q

What is the General Management of PCOS?

A

General Advice:

  • Education and reduction of increased risks of CVD, DM, Endometrial cancer, Obesity
    • Weight Loss,
    • Calorie controlled diet,
    • Exercise,
    • Smoking cessation,
    • Antihypertensives (if required),
    • Statins (if QRISK >10%)

Management if Fertility is NOT Desired:

  • First Line: COCP + Weight Loss
  • Second Line: (if prolonged amenorrhea):
    • Cyclical Progesterone (taken for 14 days every 3 months)
    • Transvaginal USS to assess endometrial thickness

Management if Fertility IS Desired:

  • First Line: Weight Loss Plus:
    • Clomiphene OR Letrozole (aromatase inhibitor)
  • Second Line: Metformin
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329
Q

How is the Risk of Endometrial Cancer reduced in PCOS?

A
  • Weight loss
  • Mirena coil
  • Inducing a withdrawal bleed at least every 3-4 months using:
    • Cyclical Progestogens (medroxyprogesterone acetate 10mg OD for 14 days)
    • COCP
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330
Q

How can Infertility be managed in PCOS?

A

1st Line: Weight loss is the initial step for improving fertility

2nd Line:

  • Letrozole
  • Clomiphene - induces ovulation by inhibiting oestrogen feedback on hypothalamus so increase FSH

3rd Line:

  • Laparoscopic Ovarian Drilling
  • IVF
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331
Q

How can Hirsutism be managed in PCOS?

A

Weight loss may improve the symptoms of Hirsutism

  • Co-cyprindiol (Dianette) is a COCP liscenced for hirsutism and acne with anti-androgenic effects

Others:

  • Topical Eflornithine
  • Electrolysis
  • Laser hair removal
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332
Q

How can Acne be managed in PCOS?

A

Combined Oral Contraceptive Pill (COCP) is First line (Co-cprindiol).

Other treatments:

  • Topical Adapalene (retinoid)
  • Topical Antibiotics (clindamycin + Benzoyl peroxide)
  • Topical Azelaic acid 20%
  • Oral Tetracycline antibiotics (lymecycline)
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333
Q

What is a major side effect of Co-cyprindiol (Dianette)?

A

Significantly increased risk of Venous Thromboembolism

  • This contraindicated in increased risk of clots
  • Medication usually stopped after 3 months of use.
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334
Q

Define Pelvic Inflammatory Disease (PID)

A

Inflammation and infection of the organs of the pelvis, caused by infection spreading up the vagina through the cervix and into the upper genital tract.

It is a significant cause of tubular infertility and chronic pelvic pain

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335
Q

Define these words:

Endometritis
Salpingitis
Oophoritis
Parametritis
Peritonitis

A
  • Endometritis: is inflammation of the endometrium
  • Salpingitis: is inflammation of the fallopian tubes
  • Oophoritis: is inflammation of the ovaries
  • Parametritis: is inflammation of the parametrium, which is the connective tissue around the uterus
  • Peritonitis: is inflammation of the peritoneal membrane
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336
Q

What is the Aetiology of PID?

A

Most commonly via Sexually Transmitted Pelvic Infections:

  • Neisseria gonorrhoeae (produces more severe PID)
  • Chlamydia trachomatis
  • Mycoplasma genitalium

Less commonly via non-sexually transmitted infections:

  • Gardnerella vaginalis (associated with bacterial vaginosis)
  • Haemophilus influenzae
  • Escherichia coli
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337
Q

What are the risk factors for PID?

A
  • Not using barrier contraception
  • Multiple sexual partners
  • Younger age
  • Existing sexually transmitted infections
  • Previous pelvic inflammatory disease
  • Intrauterine device (e.g. copper coil)
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338
Q

What are the clinical features of PID?

A

Women may present with symptoms of:

  • Pelvic or lower abdominal pain
  • Abnormal vaginal discharge
  • Abnormal bleeding (intermenstrual or postcoital)
  • Pain during sex (dyspareunia)
  • Fever
  • Dysuria

Examination findings may reveal:

  • Pelvic tenderness
  • Cervical motion tenderness (cervical excitation)
  • Inflamed cervix (cervicitis)
  • Purulent discharge
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339
Q

What are some differential diagnoses for PID?

A
  • Appendicitis: Presents with right lower quadrant abdominal pain, fever, nausea, and vomiting.
  • Ectopic Pregnancy: Symptoms may include unilateral lower abdominal pain and vaginal bleeding. A positive pregnancy test is a key distinguishing factor.
  • Endometriosis: Chronic pelvic pain, dysmenorrhea, and dyspareunia are common. Pain typically worsens during menstruation.
  • Ovarian Cyst: Symptoms can include unilateral lower abdominal pain, bloating, and a palpable mass on examination.
  • Urinary Tract Infection: Symptoms usually include dysuria, frequency, urgency, suprapubic pain, and possible fever.
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340
Q

What are the investigations for PID?

A

Pelvic Examination

High vaginal Swabs for causative organisms:

  • NAAT swabs for gonorrhoea and chlamydia
  • NAAT swabs for Mycoplasma genitalium (if available)
  • HIV Test
  • Syphilis test

Blood Tests: Inflammatory markers (CRP/ESR) can help support diagnosis

Pregnancy test: To exclude ectopic pregnancy

Transvaginal Ultrasound May be used

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341
Q

What is the management of PID?

A

Combination Antibiotics

  • Ceftriaxone IM 1g Single dose (Cover for gonorrhoea)
  • Doxycycline 100mg BD for 2/52 (cover for chlamydia and Mycoplasma)
  • Metronidazole 400mg BD for 2/52 ( Cover for Gardnerella)

Alternative regime is Ofloxacin + Metronidazole

Analgesia may be required

Contact Tracing

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342
Q

What are the complications of PID?

A
  • Chronic pelvic pain (in around 40% of cases)
  • Infertility (approximately 15%)
  • Ectopic pregnancy (about 1%)
  • Sepsis
  • Abscess
  • Fitz-Hugh-Curtis Syndrome (about 10%)
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343
Q

What is Fitz-Hugh-Curtis Syndrome?

A

Complication of PID, chlamydia and gonorrhoea where adhesions form between the liver capsule and the peritoneum causing inflammation and infection of the liver capsule (Glisson’s capsule)

This results in right upper quadrant pain in about 10% of patients

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344
Q

What is the management of Fitz-Hugh-Curtis Syndrome?

A

Investigations include abdominal ultrasound to exclude stones.

laparoscopy to diagnose, visualise and treat adhesions by Adhesiolysis

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345
Q

Define Baby Blues (Postpartum Blues)?

A

A transient mood disorder that typically manifests around three days after childbirth.

It is characterized by irritability, anxiety about parenting skills, and tearfulness.

The condition typically resolves within two weeks without medical intervention.

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346
Q

What is the Epidemiology of Baby Blues?

A
  • Very common affecting up to 80% of women after childbirth
  • More commonly affects first time mothers
  • 10% of these women may develop a more severe form: Postnatal Depression
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347
Q

What is the Aetiology of Baby Blues?

A

not fully understood

  • Likely due to hormonal changes that occur after childbirth including a rapid drop in oestrogen and progesterone.
  • Fatigue/sleep deprivation, physical discomfort after delivery and stress/challenges of caring for a new baby likely also contribute
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348
Q

what are the clinical features of Baby Blues?

A

Presents within the first week after childbirth

  • Mood swings
  • Low mood
  • Anxiety (about parenting)
  • Irritability
  • Tearfulness
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349
Q

What are some differential diagnoses for Baby Blues?

A

Postpartum blues should be differentiated from other postnatal mood disorders such as postnatal depression and postpartum psychosis. The primary distinguishing symptoms are:

  • Postnatal depression: Persistent feelings of sadness, anxiety, or emptiness; difficulty bonding with the baby; severe mood swings; trouble eating, sleeping, or concentrating; and thoughts of harming oneself or the baby.
  • Postpartum psychosis: Severe confusion and disorientation, hallucinations and delusions, paranoia, and attempts to harm oneself or the baby.
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350
Q

What are the investigations for Baby Blues?

A

Clinical Diagnosis

  • Routine screening at medical appointments is recommended by NICE to identify the approximately 10% of women who may develop postnatal depression following postpartum blues.
  • Use of tools such as the Edinburgh Postnatal Depression Scale
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351
Q

What is the management of Baby Blues?

A

Supportive measures and reassurance (that the condition is common)

  • Symptoms are usually mild and only last a few days.
  • Baby blues tend to resolve within two weeks of delivery without any treatment being required
  • Mothers should be encouraged to seek help if they have symptoms persisting beyond 2 weeks
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352
Q

What is the definition of Postpartum depression?

A

It’s a significant mood disorder that can develop at any time up to one year after the birth of a baby.

This condition represents a considerable aspect of maternal mental health and extends beyond the common “baby blues”.

Typically presenting with persistent depressive symptoms that may interfere with daily functioning and parenting.

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353
Q

What is the Epidemiology of Postpartum Depression?

A
  • Affects approximated 10-20% of mothers within 1 year of childbirth
  • Rates vary depending on population, geographic location, socioeconomic status (low), History of mental health and lack of social support
  • Typically women are affected around 3 months after birth
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354
Q

What causes Postpartum depression?

A

Development of postpartum depression is multifactorial with a combination of Biological, Psychological, and Social factors all contributing.

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355
Q

What biological factors contribute to the development of postpartum Depression?

A
  • Hormonal fluctuations post-delivery, including sudden drops in progesterone, estrogen, and thyroid hormones.
  • Alterations in melatonin and cortisol rhythms and immune-inflammatory processes
  • Genetic predispositions
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356
Q

What Psychological factors contribute to the development of postpartum Depression?

A
  • A history of mood or anxiety disorders
  • Previous episodes of postpartum depression
  • Certain personality traits such as neuroticism
  • Psychological stress from the transition to parenthood
  • Unrealistic expectations of motherhood
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357
Q

What Social Factors contribute to the development of postpartum depression?

A
  • Lack of social support
  • Relationship issues,
  • Life stressors
  • Low socioeconomic status
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358
Q

What are the signs and symptoms of postpartum depression?

A

Classic triad of:

  • Low Mood
  • Anhedonia: reduced enjoyment or interest in activities.
  • Lowering of energy levels.

Others:

  • Biological symptoms of depression like poor appetite and disturbed sleep patterns (not associated with normal disturbed sleep patterns with a baby)
  • Concerns related to bonding with the baby, caring for the baby, and in extreme circumstances, thoughts about harming oneself or the baby.
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359
Q

What are some differentials for postpartum depression?

A

Baby blues
Characterised by mild mood swings, irritability, anxiety, and tearfulness. However, these symptoms usually present within the first two weeks after birth and resolve spontaneously.

Postpartum Psychosis

Adjustment disorders
These disorders may develop in response to a major life change or stressor, such as having a baby, but the emotional or behavioural symptoms are less severe than in depression.

Generalized Anxiety Disorder (GAD)

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360
Q

What is the main screening tool for Postpartum depression?

A

Edinburgh Postnatal Depression Scale (EPDS) assess how the mother has felt over the past week with 30 questions.

A cut-off score of over 10 is used as a positive result.

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361
Q

What is the management of postpartum depression?

A

First-line treatments:

  • Self-help strategies and psychological therapies e.g. Cognitive Behavioural Therapy (CBT) or Interpersonal Therapy (IPT).

Pharmacological treatments

  • Antidepressants (SSRIs) considered in high risk cases

In severe cases admission to a mother and baby inpatient mental health unit might also be necessary.

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362
Q

What antidepressants are preferred to be used in Postpartum Depression?

A

SSRIs such as:

  • Paroxetine
  • Sertraline

Due to their safety profile in breastfeeding

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363
Q

What is the definition of Postpartum Psychosis?

A

Also known as Puerperal Psychosis

It’s a serious psychiatric disorder that typically develops within the first two weeks following childbirth.

It is characterised by a range of psychological symptoms, including paranoia, delusions, hallucinations, mania, depression, and confusion.

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364
Q

What is the Aetiology of Postpartum Psychosis?

A

unknown but thought to be a combination of:

  • Genetic susceptibility
  • Hormonal Changes
  • Psychosocial stressors
  • Prior history of severe mental illness significantly increases the risk
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365
Q

What are the risk factors for Postpartum Psychosis?

A
  • Prior history of severe mental illnesses such as schizophrenia or bipolar affective disorder
  • Family history of postpartum psychosis
  • Previous episode of postpartum psychosis
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366
Q

What is the clinical presentation of Postpartum Psychosis?

A

Often between 2-3 weeks post partum

  • Paranoia
  • Delusions (including Capgras Delusions)
  • Hallucinations
  • Manic episodes
  • Depressive episodes
  • Confusion
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367
Q

What is the main differential for Postpartum Psychosis?

A

Postpartum depression with psychotic features

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368
Q

How is Postpartum depression diagnosed?

A

Diagnosis is predominantly clinical, based on the presenting signs and symptoms.

It requires a thorough psychiatric evaluation.

Consideration should be given to other medical conditions that may cause similar symptoms, such as thyroid disorders or sepsis.

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369
Q

How is Postpartum psychosis managed?

A

Women with Postpartum Psychosis need urgent assessment and input from specialist mental health services

  • Admission to mother and baby unit
  • Cognitive behavioural Therapy
  • May require pharmacotherapy with:
    • Antidepressant medications
    • Antipsychotic medications
    • Mood stabilisers in some instances

Potential referral to a specialist mother and baby inpatient mental health unit in very severe cases (when the mother experiences command hallucinations, thoughts of self-harm or suicide, or delusional beliefs regarding the baby’s role or identity).

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370
Q

What needs to be considered when prescribing medications for Postpartum Psychosis?

A

The mother’s breastfeeding status and the potential for the transfer of drugs to the nursing infant.

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371
Q

What is the Mother and Baby Unit?

A

The mother and baby unit is a specialist unit for pregnant women and women that have given birth in the past 12 months.

They are designed so that the mother and baby can remain together and continue to bond. Mothers are supported to continue caring for their baby while they get specialist treatment.

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372
Q

How can mothers prepare for Postnatal Depression/Psychosis?

A

Women with existing mental health concerns before or during pregnancy are referred to perinatal mental health services.

Advice and input from specialists can help manage decisions around ongoing medications such as SSRIs, antipsychotics and lithium during pregnancy.

They also ensure that mothers are closely followed up after giving birth so management can be put in place early should these conditions occur.

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373
Q

What is a risk of taking SSRIs during pregnancy?

A

Neonatal abstinence syndrome/neonatal adaptation syndrome

  • Presents in first few days after birth
  • Symptoms include irritability and poor feeding
  • Neonates are monitored for this after delivery
  • Treatment is supportive management
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374
Q

Define Ectopic Pregnancy?

A

Gynaecological Emergency
Where a fertilised egg or embryo implants and begins to grow Outside of the uterine cavity.

Most common site is the fallopian tube

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375
Q

What are the regions where an Ectopic Pregnancy may occur?

A
  • Fallopian tube (most common (97%))
  • Ovary
  • Cervix
  • Abdomen
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376
Q

What are some risk factors for an Ectopic Pregnancy?

A
  • Previous ectopic pregnancy
  • Previous pelvic inflammatory disease, STIs or Salpingitis (tubal inflammation)
  • Previous surgery to the pelvis (Especially the fallopian tubes)
  • Intrauterine devices in situ (coils)
  • Endometriosis
  • Older age
  • Smoking
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377
Q

What is the pathophysiology of an Ectopic Pregnancy?

A
  • Fertilisation of the oocyte typically takes place in the ampulla of the fallopian tube; the conceptus must then travel into the endometrial cavity.
    • This occurs due to tubal peristalsis alongside ciliary motion and tubal fluid flow.
    • Any dysfunction in the tubal peristalsis above due to e.g. tubal surgery, salpingitis, PID can prevent the conceptus from implanting in the correct place.
  • A pregnancy that implants in the fallopian tube will grow and eventually lead to rupture and catastrophic bleeding.
  • Most tubal ectopics implant in the ampulla (widest point).
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378
Q

When do Ectopic pregnancies typically present?

A

Around 6-8 weeks gestation

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379
Q

What are the clinical features of an Ectopic Pregnancy?

A
  • Pelvic or abdominal pain Often unilateral to the side of the ectopic (RIF/LIF)
  • Abnormal vaginal bleeding: missed period or intermenstrual bleeding
  • Cervical motion tenderness (Chandeller sign) where pain occurs when moving the cervix during a bimanual examination
  • Haemodynamic instability caused by blood loss if the ectopic ruptures
  • Dizziness or Syncope (due to blood loss)
  • Shoulder tip pain (blood irritating the diaphragm causing referred pain)
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380
Q

What are some differential diagnoses for Ectopic Pregnancies?

A
  • Miscarriage
  • Appendicitis
  • Ovarian Torsion
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381
Q

What are the investigations for an Ectopic Pregnancy?

A

Any female of childbearing age presenting with abdominal pain should be offered a UPT (urine pregnancy test) to exclude ectopic pregnancy

  • Urine Pregnancy Test (First Line)
  • Transvaginal Ultrasound Scan is investigation of choice to locate the pregnancy
  • Serial serum B-hCG if no pregnancy found of USS.
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382
Q

What are the ultrasound findings in an ectopic pregnancy?

A
  • A mass representing a tubal ectopic pregnancy moves separately to the ovary.
  • It may appear similar to the corpus luteum however this will move with the ovary

Other features indicative:

  • An empty uterus
  • Fluid in the uterus (may be mistaken as a gestational sac)
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383
Q

What is the Management of an Ectopic Pregnancy?

A

women with pelvic pain/tenderness and a positive pregnancy test need to be referred to an Early Pregnancy Assessment Unit (EPAU)

All ectopic pregnancies need to be terminated (they are not viable)

Options for terminating an Ectopic Pregnancy:

  • Expectant management (awaiting natural termination)
  • Medical Management (methotrexate)
  • Surgical management (Salpingectomy or Salpingotomy)
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384
Q

What is the Expectant Management for an Ectopic Pregnancy?

A

Criteria:

  • Follow up needs to be possible to ensure successful termination
  • The ectopic needs to be unruptured
  • Adnexal mass < 35mm
  • No visible heartbeat
  • No significant pain
  • HCG level < 1500 IU / l

Women with Expectant management need careful follow up with close monitoring of hCG levels and quick/easy access to services if their condition changes

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385
Q

What is the Medical Management for an Ectopic Pregnancy?

A

Criteria: Injection of Methotrexate

  • Follow up needs to be possible to ensure successful termination
  • The ectopic needs to be unruptured
  • Adnexal mass < 35mm
  • No visible heartbeat
  • No significant pain
  • HCG level < 5000 IU / l
  • Confirmed absence of intrauterine pregnancy on ultrasound

Methotrexate is highly teratogenic and is given as an IM Injection to halt the progress of pregnancy and results in spontaneous termination

Women treated with Methotrexate are advised to not get pregnant for 3 months following treatment as the harmful effects of methotrexate may last this long

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386
Q

What are the monitoring criteria for Expectant or Medical management of Ectopic Pregnancies?

A
  • Measure beta-hCG on days 0, 2, 4, and 7
  • If drop of more than 15% from previous measurement, repeat weekly until beta-hCG is less than 20IU/L.
  • If not, refer for further management.
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387
Q

What are some common side effects of using Methotrexate as medical management for an ectopic pregnancy?

A
  • Vaginal Bleeding
  • Nausea and Vomiting
  • Abdominal Pain
  • Stomatitis (inflammation of the mouth)
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388
Q

What is the Surgical Management for an Ectopic Pregnancy?

A

Anyone that does not meet the criteria for expectant or medical management requires surgical

Criteria for Surgical:

  • Patient is haemodynamically unstable
  • Pain
  • Adnexal mass > 35mm
  • Visible heartbeat
  • HCG Levels > 5000 IU/l

Surgical Options:

  • Laparoscopic salpingectomy (first line treatment for ectopic pregnancy)
  • Laparoscopic salpingotomy (used in women at increased risk of infertility due to damage to other fallopian tube)

Anti-rhesus D prophylaxis is given to rhesus negative women having surgical management of ectopic pregnancy

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389
Q

What is the problem with Laparoscopic salpingotomy as a treatment for ectopic pregnancies?

A

Increased risk of failure to remove the ectopic pregnancy with salpingotomy compared to salpingectomy.

  • 1 in 5 women having salpingotomy may need further treatment with methotrexate or salpingectomy
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390
Q

Define Pregnancy of Unknown Origin/location?

A

Diagnosed when a woman has a positive pregnancy test, but there are no signs of an intrauterine or extrauterine pregnancy on transvaginal ultrasound.

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391
Q

What is the Aetiology of Pregnancy of Unknown Origin/Location?

A
  • An early viable or failing intrauterine pregnancy
  • A complete miscarriage
  • An ectopic pregnancy
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392
Q

What are the differentials for a Pregnancy of Unknown Origin/Location?

A

Early viable or failing intrauterine pregnancy

  • Signs and symptoms: Mild cramping, spotting or delayed menstruation.

Complete miscarriage

  • Signs and symptoms: Severe abdominal pain, heavy bleeding, passage of tissue or clot-like material.

Ectopic pregnancy

  • Signs and symptoms: Sharp or stabbing pain in the abdomen, light vaginal bleeding, dizziness or fainting.
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393
Q

What are the Investigations for Pregnancy of Unknown Origin/Location?

A

Serum hCG is tracked over time to monitor Pregnancy of Unknown Origin/Location

Serum hCG level is repeated after 48 hours to measure change from baseline

Monitoring the clinical signs and symptoms is more important than tracking the hCG level, and any change in symptoms needs careful assessment.

The developing syncytiotrophoblast of the pregnancy produces hCG. In an intrauterine pregnancy, the hCG will roughly double every 48 hours. This will not be the case in a miscarriage or ectopic pregnancy.

Rise of more than 63%:

  • After 48 hours likely indicates an Intrauterine pregnancy.
  • Repeat Ultrasound scan after 1-2 weeks to confirm intrauterine pregnancy
  • Pregnancy should be visible on USS once hCG > 1500 IU/ L

Rise of Less than 63%

  • May indicate an Ectopic pregnancy. This patient needs close monitoring and review

Fall of More than 50%

  • Likely to indicate a miscarriage
  • Urine pregnancy test should be performed after 2 weeks (confirms miscarriage is complete)
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394
Q

Define Miscarriage?

A

Miscarriage is defined as the spontaneous loss/termination of a pregnancy prior to 24 weeks gestation.

Early Miscarriage: Before 12 weeks gestation

Later Miscarriage: Between 12 and 24 weeks gestation

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395
Q

What is the Epidemiology of Miscarriage?

A
  • 10% of recognised pregnancies end in miscarriage.
  • Number is likely higher as many occur without the women realising she in pregnant
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396
Q

What is a missed miscarriage?

A

the foetus is no longer alive, but no symptoms have occurred and thus the miscarriage is often missed as the mother did not know that something was wrong.

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397
Q

What is a threatened miscarriage?

A

vaginal bleeding with a closed cervix and a foetus that is alive

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398
Q

What is an Inevitable miscarriage?

A

vaginal bleeding with an open cervix. Due to the cervix being open the miscarriage is inevitable.

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399
Q

What is an Incomplete miscarriage?

A

retained products of conception remain in the uterus after the miscarriage

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400
Q

What is a complete miscarriage?

A

A full miscarriage has occurred, and there are no products of conception left in the uterus

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401
Q

What is an Anembryonic pregnancy?

A

a gestational sac is present but contains no embryo

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402
Q

What are the various causes of Miscarriage?

A

Often Idiopathic

Foetal Pathology:

  • Genetic disorder
  • Abnormal development
  • Placental failure

Maternal Pathology:

  • Uterine abnormality (Bicornuate uterus, Cervical insufficiency)
  • Cervical incompetence
  • Polycystic ovary syndrome
  • Poorly controlled diabetes
  • Poorly controlled thyroid disease
  • Anti-phospholipid syndrome, Factor V Leiden
  • Infections: Toxoplasmosis, Syphilis
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403
Q

What are some risk factors for a miscarriage?

A
  • Increased Maternal Age
  • Previous Miscarriage
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404
Q

What are the clinical features of a miscarriage?

A

May be Asymptomatic

  • Vaginal Bleeding
  • Pelvic Pain - Often reported to be worse than the pain of a usual period
  • Vaginal tissue loss
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405
Q

What is the main differential for a miscarriage?

A

Main other differential for vaginal bleeding before 24 weeks gestation is an Ectopic Pregnancy

  • Both can present with pain and vaginal bleeding
  • Pain is often the first symptom in an ectopic
  • Vaginal bleeding is usually larger in miscarriage
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406
Q

What are the investigations for a Miscarriage?

A

Transvaginal Ultrasound Scan: Investigation of choice

Viability of Pregnancy features:

  • Mean Gestational Sac Diameter
  • Foetal pole and crown-rump length
  • Foetal Heart Beat
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407
Q

When does a foetal pole develop?

A
  • A foetal pole is expected once the mean gestational sac diameter is 25mm or more.
  • When there is a mean gestational sac diameter of 25mm or more, without a foetal pole, the scan is repeated after one week before confirming an anembryonic pregnancy.
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408
Q

When does the foetal heart beat become visible?

A
  • A foetal heartbeat is expected once the crown-rump length is 7mm or more.
  • When the crown-rump length is less than 7mm, without a foetal heartbeat, the scan is repeated after at least one week to ensure a heartbeat develops
  • When there is a crown-rump length of 7mm or more, without a foetal heartbeat, the scan is repeated after one week before confirming a non-viable pregnancy.

Pregnancy is considered viable when there is a foetal heart beat

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409
Q

What is the Management of a possible miscarriage at less than 6 weeks gestation

A

Women with a pregnancy less than 6 weeks’ gestation presenting with bleeding can be managed expectantly

  • Provided they have no pain and no other complications or risk factors (e.g. previous ectopic).
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410
Q

What is the Expectant Management option in a miscarriage in women less than 6 weeks gestation?

A

Expectant management before 6 weeks gestation involves:

  • Awaiting the miscarriage without investigations or treatment.
    • An ultrasound is unlikely to be helpful this early as the pregnancy will be too small to be seen.
  • A repeat urine pregnancy test is performed after 7 – 10 days, and if negative, a miscarriage can be confirmed.
  • When bleeding continues, or pain occurs, referral and further investigation is indicated.
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411
Q

What is the Management of a Miscarriage at More than 6 weeks gestation?

A

NICE 2019 suggests referral to an early pregnancy assessment service (EPAU) for women with a positive pregnancy test (more than 6 weeks’ gestation) and bleeding.

Expectant Management: Watch and Wait

  • First line for women without risk factors for heavy bleeding or infection
  • 1-2 weeks are given to allow the miscarriage to occur spontaneously
  • repeat UPT preformed 3 weeks after bleeding and pain settle to confirm miscarriage is complete
  • Persistent or worsening bleeding require further assessment

Medical Management: Mifepristone followed by Misoprostol 48 hours later

  • Mifepristone is an anti-progesterone that sensitises the myometrium to prostaglandins and induces breakdown of decidua basalis
  • Misoprostol is a prostaglandin analogue that soften the cervix and stimulates uterine contractions.
  • Can be a vaginal suppository or Oral dose

Surgical Management: Third line:

  • Surgical Options Include:
    • Manual Vacuum aspiration: under local anaesthetic as outpatient
    • Electric vacuum aspiration: under general anaesthetic
  • Prostaglandins (misoprostol) are given before surgical management to soften the cervix.
  • Anti-rhesus D prophylaxis is given to rhesus negative women having surgical management of miscarriage
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412
Q

What are some side effects for Misoprostol?

A
  • Heavier bleeding
  • Pain
  • Vomiting
  • Diarrhoea
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413
Q

What is the management for an Incomplete miscarriage?

A

An incomplete miscarriage occurs when retained products of conception (foetal or placental tissue) remain in the uterus after the miscarriage. Retained products create a risk of infection.

Options for an Incomplete Miscarriage:

  • Medical management (misoprostol)
  • Surgical management (evacuation of retained products of conception)
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414
Q

Define Recurrent Miscarriage?

A

Defined as the loss of 3 or more consecutive pregnancies.

415
Q

What are the investigations for Recurrent Miscarriage?

A
  • Blood tests: antiphospholipid antibodies, thrombophilia screen
  • Cytogenetic analysis of products of conception: if abnormal then the parents should be karyotyped
  • Pelvic ultrasound: to identify uterine abnormalities.
416
Q

What is the Management of Recurrent Miscarriage?

A

The management is tailored to the contributing pathology:

Genetic disorder - refer to a clinical geneticist for genetic counselling. Options include continuing pregnancy attempts with prenatal diagnosis or use of a donor egg/sperm

Uterine structural abnormality - may be treated surgically. For some congenital uterine malformations there is insufficient evidence to recommend surgical treatment

Cervical incompetence - regular ultrasound monitoring of the cervix. May use cervical cerclage

Polycystic ovary syndrome - difficult to manage as pathophysiology is not fully understood. There is no consensus on the most appropriate management. Suppression of the high LH has not been found to be effective

Antiphospholipid syndrome - heparin or low-dose aspirin

Thrombophilia - heparin may increase the live birth rate

Diabetes - improve glycaemic control

417
Q

Define Abortion?

A

A termination of pregnancy (TOP) that is an elective procedure to end a pregnancy governed by the 1967 Abortion Act

418
Q

What are the criteria for an Abortion to be performed prior to 24 weeks gestation?

A
  • Pregnancy has not exceeded 24 weeks gestation
  • Continuing the pregnancy involves greater risk to the physical or mental health of:
    • The woman
    • Existing children of the family

The threshold for when the risk of continuing the pregnancy outweighs the risk of terminating the pregnancy is a matter of clinical judgement and opinion of the medical practitioners.

419
Q

What are the criteria for an Abortion to be performed at anytime during the pregnancy?

A
  • Continuing the pregnancy is likely to risk the life of the woman
  • Terminating the pregnancy will prevent “grave permanent injury” to the physical or mental health of the woman
  • There is “substantial risk” that the child would suffer physical or mental abnormalities making it seriously handicapped
420
Q

What are the legal requirements for an Abortion?

A
  • Two registered medical practitioners must sign to agree abortion is indicated
  • It must be carried out by a registered medical practitioner in an NHS hospital or approved premise
421
Q

What is some Pre-Abortion Care that should be provided?

A
  • Abortion services can be accessed by self-referral or by GP, GUM or family planning clinic referral.
  • Doctors who object to abortions should pass on to another doctor able to make a referral
  • Marie Stopes UK is a charity that provides abortion services
  • Women should be offered counselling and information to help decision making from a trained practitioner
  • Informed consent is essential
422
Q

What are the Medical Options for Abortion?

A

A medical abortion is most appropriate earlier in pregnancy, but can be used at any gestation. It involves two treatments:

  • Mifepristone (anti-progestogen)
  • Misoprostol (prostaglandin analogue) 1 – 2 day later

Rhesus negative women with a gestational age of 10 weeks or above having a medical TOP should have anti-D prophylaxis.

423
Q

What are the Surgical Options for Abortion?

A

Surgical abortion can be performed, depending on preference and gestational age, under: Local anaesthetic (+/-plus sedation) or General anaesthetic

  • Prior to surgical abortion, medications are used for cervical priming. This involves softening and dilating the cervix with misoprostol, mifepristone or osmotic dilators.

Surgical Options:

  • Cervical dilatation and suction of the contents of the uterus (usually up to 14 weeks)
  • Cervical dilatation and evacuation using forceps (between 14 and 24 weeks)

Rhesus negative women having a surgical TOP should have anti-D prophylaxis.

424
Q

What is some Post-Abortion Care?

A
  • Inform women they may experience vaginal bleeding and abdominal cramps intermittently for up to 2 weeks post procedure
  • UPT is performed 3 weeks after abortion to confirm completion
  • Support and counselling is offered
425
Q

What are some complications of an Abortion?

A
  • Bleeding
  • Pain
  • Infection
  • Failure of the abortion (pregnancy continues)
  • Damage to the cervix, uterus or other structures
  • Psychological stress
426
Q

Define Gestational Diabetes?

A

Diabetes that is triggered by pregnancy due to reduced insulin sensitivity during pregnancy and resolves after birth.

427
Q

What is the Epidemiology of Gestational Diabetes?

A
  • Approximately 5% of pregnancies are affected by GDM.
  • Women diagnosed with GDM have an increased risk of developing T2DM
  • Up to a 50% chance of developing T2DM within 5-10 years postpartum
428
Q

What are some risk factors for Gestational Diabetes?

A
  • BMI of > 30 kg/m²
  • previous macrosomic baby weighing 4.5 kg or above
  • previous gestational diabetes
  • first-degree relative with diabetes
  • family origin with a high prevalence of diabetes (South Asian, black Caribbean and Middle Eastern)
429
Q

What is the pathophysiology of Gestational Diabetes?

A
  • In normal pregnancy, local and placental hormones stimulate peripheral insulin
    resistance - the purpose of this is to spare glucose for delivery to the developing foetus.
  • This is accompanied by lipolysis and gluconeogenesis, further increasing free fatty acid and glucose levels.
  • Hypertrophy and hyperplasia of pancreatic beta-cells occurs to protect maternal glucose homeostasis.
  • Failure of this protective mechanism due to beta-cell dysfunction, in combination with insulin resistance, leads to GDM.
430
Q

What are the clinical features of Gestational Diabetes?

A

Often no noticeable symptoms

  • Thirst
  • Polyuria
  • Fatigue
431
Q

What are the differential diagnoses for Gestational Diabetes?

A
  • Type 1 or Type 2 Diabetes Mellitus: Generally presents with symptoms outside of pregnancy, including potential weight loss
  • Other forms of gestational hyperglycaemia: These can be identified through early pregnancy HbA1c testing
432
Q

When should Investigations for Gestational Diabetes take place?

A
  • Women with PMHx of GDM should have OGTT performed ASAP after booking and at 24-28 weeks if first test is normal
  • Women with any other risk factors should be screened for GDM at 24-28 weeks gestation
  • Women with glycosuria detected at a routine antenatal scan should be screened at any time during their pregnancy
433
Q

What are the investigations for Gestational Diabetes?

A

Oral Glucose Tolerance Test (OGTT):
Used in patients with risk factors for gestational diabetes or when there are features suggestive of GDM.

OGTT performed in the morning after fasting. Patient drinks 75g glucose drink and then blood sugar level is measured before and at 2 hours after.

Gestational Diabetes:

  • Fasting: > 5.6 mmol/l
  • At 2 hours: > 7.8 mmol/l

(remember for GDM cut off is 5-6-7-8)

434
Q

What is the Management for Gestaional Diabetes?

A

Patients with GDM need careful explanation about the condition and learn how to monitor and tract blood sugar

First Line:

  • Fasting glucose less than 7 mmol/l: trial of diet and exercise for 1-2 weeks, followed by metformin, then insulin if targets are not met.

Second Line:

  • Fasting glucose above 7 mmol/l: start insulin ± metformin
  • Fasting glucose above 6 mmol/l plus macrosomia (or other complications): start insulin ± metformin
  • Glibenclamide (a Sulfonylurea) Can be used if Insulin or Metformin are not tolerated

Postpartum management includes glucose testing to ensure resolution of GDM

Women with GDM must also have 4 weekly USS to tract foetal growth at 28, 32 and 36 weeks

435
Q

When are the extra scans required if a patient has gestational diabetes?

A

4-weekly scans at: 28, 32 and 36 weeks to monitor foetal growth

436
Q

What are the target blood sugar levels for women with Gestational Diabetes?

A

NICE 2015 Targets:

  • Fasting: 5.3 mmol/l
  • 1 hour post-meal: 7.8 mmol/l
  • 2 hours post-meal: 6.4 mmol/l
  • Avoiding levels of 4 mmol/l or below
437
Q

What are some Maternal Complications of Gestational Diabetes?

A
  • Pre-eclampsia
  • Developing T2DM (50% increased risk)
  • Increased risk of cardiovascular disease
438
Q

What are some Foetal complications of Gestational Diabetes?

A

Key Complications:

  • Macrosomia leading to shoulder dystocia
  • Neonatal hypoglycaemia

Others:

  • Childhood Obesity (2x background risk)
  • Increased risk of Metabolic syndrome + associated complications
  • Polycythaemia (raised haemoglobin)
  • Jaundice (raised bilirubin)
  • Congenital heart disease
  • Cardiomyopathy
439
Q

What is the management for Neonatal hypoglycaemia?

A

Babies born to mothers with GDM need close monitoring for neonatal hypoglycaemia with regular blood glucose checks and frequent feeds.

  • Maintain blood glucose > 2mmol/l
  • If it falls below this they may need IV Dextrose of nasogastric feeding
440
Q

How should you manage women with pre-existing diabetes who are considering getting pregnant?

A
  • Weight loss for women with BMI of > 27
  • Stop oral hypoglycaemic agents, apart from metformin, and commence insulin
  • Folic acid 5 mg/day from pre-conception to 12 weeks gestation
  • Detailed anomaly scan at 20 weeks including four-chamber view of the heart and outflow tracts
  • Tight glycaemic control reduces complication rates
  • Treat retinopathy as can worsen during pregnancy
441
Q

What are the target levels for glucose during pregnancy for women with Pre-existing Diabetes?

A

Both type I and type II diabetes should aim for the same target insulin levels as with gestational diabetes

NICE 2015 Targets:

  • Fasting: 5.3 mmol/l
  • 1 hour post-meal: 7.8 mmol/l
  • 2 hours post-meal: 6.4 mmol/l
  • Avoiding levels of 4 mmol/l or below
442
Q

What medication should women with Pre-existing type 2 diabetes be on during pregnancy?

A

Metformin and Insulin.

Other oral diabetic medications should be stopped

443
Q

What is an important complication to consider in women with Pre-existing diabetes who are pregnant?

A

Diabetic Retinopathy: referral to ophthalmologist for diabetic retinopathy screening

  • Retinopathy Screening should be performed shortly after Dating/Booking scan (11 and 14 weeks) and at 28 weeks gestation
  • Pre-existing diabetes and pregnancy carries a risk of rapid progression of retinopathy
444
Q

What should the planned delivery times be for women with Pre-existing and Gestational diabetes?

A

Pre-existing Diabetes:

  • Planned delivery between 37 and 38+6 weeks

Gestational Diabetes:

  • Women can give birth up to 40+6 weeks
445
Q

What insulin treatment should be used during labour for women with Type I diabetes?

A

Sliding-scale insulin regime considered during labour for women with T1DM.

May also be considered for women with poorly controlled blood sugars with GDM or T2DM.

446
Q

Define Multiple Pregnancy?

A

Refers to a pregnancy with more than one foetus

447
Q

Define monozygotic?

A

identical twins (from a single zygote)

448
Q

Define Dizygotic?

A

non-identical (from two different zygotes)

449
Q

Define Monoamniotic?

A

Single amniotic sac

450
Q

Define Diamniotic?

A

Two separate amniotic sacs

451
Q

Define Monochorionic?

A

Share a single placenta

452
Q

Define Dichorionic?

A

Two separate placentas

453
Q

What type of Multiple pregnancy has the best outcomes?

A

Diamniotic, Dichorionic

Twin pregnancies as each foetus has their own nutrient supply.

454
Q

How is Multiple Pregnancy usually diagnosed?

A

Usually diagnosed on the “booking/dating” ultrasound scan

455
Q

How can the type of twins be identified from an Ultrasound Scan?

A
  • Dichorionic diamniotic twins have a membrane between the twins, with a lambda sign or twin peak sign
  • Monochorionic diamniotic twins have a membrane between the twins, with a T sign
  • Monochorionic monoamniotic twins have no membrane separating the twins
456
Q

What are the risks to the mother in the case of Multiple Pregnancies?

A
  • Anaemia
  • Polyhydramnios
  • Hypertension
  • Malpresentation
  • Spontaneous preterm birth
  • Instrumental delivery or caesarean
  • Postpartum haemorrhage
457
Q

What are the risks to the Foetuses/neonates in the case of Multiple Pregnancies?

A
  • Miscarriage
  • Stillbirth
  • Foetal growth restriction
  • Prematurity
  • Twin-twin transfusion syndrome
  • Twin anaemia polycythaemia sequence
  • Congenital abnormalities
458
Q

What is Twin-Twin Transfusion Syndrome?

A

Twin-twin transfusion syndrome occurs when the foetuses share a placenta. It is called foeto-foetal transfusion syndrome in pregnancies with more than two foetuses.

When there is a connection between the blood supplies of the two foetuses, one foetus (the recipient) may receive the majority of the blood from the placenta, while the other foetus (the donor) is starved of blood.

  • The recipient gets the majority of the blood, and can become fluid overloaded, with heart failure and polyhydramnios.
  • The donor has growth restriction, anaemia and oligohydramnios. There will be a discrepancy between the size of the foetuses.

Women with Twin-Twin transfusion syndrome need to be referred to a tertiary specialist foetal medicine centre

459
Q

What is Twin Anaemia Polycythaemia Sequence?

A

Twin anaemia polycythaemia sequence is similar to twin-twin transfusion syndrome, but less acute.

One twin becomes anaemic whilst the other develops polycythaemia (raised haemoglobin).

460
Q

What additional monitoring is required for Women in the case of Multiple Pregnancy?

A

Women with multiple pregnancies require additional monitoring for anaemia, with a full blood count at:

  • Booking clinic
  • 20 weeks gestation
  • 28 weeks gestation

Additional ultrasound scans are required in multiple pregnancy to monitor for foetal growth restriction, unequal growth and twin-twin transfusion syndrome:

  • 2 weekly scans from 16 weeks for monochorionic twins
  • 4 weekly scans from 20 weeks for dichorionic twins
461
Q

When should Planned birth be offered for Uncomplicated monochorionic monoamniotic twins?

A

32 and 33+6 weeks

462
Q

When should Planned birth be offered for Uncomplicated monochorionic diamniotic twins?

A

36 and 36+6 weeks

463
Q

When should Planned birth be offered for Uncomplicated dichorionic diamniotic twins?

A

37 and 37 +6 weeks

464
Q

When should Planned birth be offered for Triplets?

A

Before 35 +6 weeks

465
Q

What is the mode of delivery for monoamniotic twins?

A

Require elective caesarean section between 32 and 33 +6 weeks

466
Q

What are the options for Delivery in Diamniotic twins?

A

Aim to deliver between 37 and 37 +6 weeks

  • Vaginal delivery is possible when the first baby has a cephalic presentation (head first)
  • Caesarean section may be required for the second baby after successful birth of the first baby
  • Elective caesarean is advised when the presenting twin is not cephalic presentation
467
Q

Why is Anaemia in Pregnancy a common issue?

A

Anaemia is defined as a low concentration of haemoglobin.

In pregnancy, the plasma volume increases and thus there is a reduction in the concentration of haemoglobin leading to anaemia.

It is important to optimise the treatment of anaemia in pregnancy so that the woman has reasonable reserves in cases there is significant blood loss during delivery

468
Q

What is the presentation of Anaemia in pregnancy?

A

Often asymptomatic

May present as:

  • Shortness of breath
  • Fatigue
  • Dizziness
  • Pallor
469
Q

When is anaemia routinely screened for during pregnancy and what are the normal ranges?

A

Booking/dating Bloods: > 110 g/l

28 Weeks Gestation: > 105 g/l

Post-partum: > 100 g/l

Women are also offered Haemoglobinopathy screening at the booking clinic for Thalassaemia and Sickle Cell Disease

470
Q

What are some potential causes of Anaemia in pregnancy?

A

Low MCV Indicates Iron Deficiency Anaemia

Normal MCV: Indicates a physiological anaemia due to increased plasma volume of pregnancy

Raised MCV: Indicates B12 or Folate Deficiency

471
Q

What is the Management of Anaemia in Pregnancy?

A

Depends on the cause:

Iron:

  • Women with anaemia in pregnancy are started on iron replacement: Ferrous sulphate 200mg 3x daily
  • Women who are not anaemic but have low ferritin may also be started on supplementary iron.
  • Treatment should be continued for 3 months after iron deficiency is corrected to allow iron stores to be replenished

B12:

  • The increased plasma volume and B12 requirements often result in a low B12 in pregnancy. Women with low B12 should be tested for pernicious anaemia (checking for intrinsic factor antibodies).
  • IM Hydroxocobalamin injections or Oral Cyanocobalamin Tables

Folate:

  • All women should already be taking folic acid 400mcg OD
  • Women with folate deficiency are started on folic acid 5mg daily
472
Q

Define Spina Bifida?

A

Spina bifida is a neural tube defect characterised by incomplete development of the spinal column, resulting in herniation of the spinal cord.

473
Q

What is Spina Bifida Occulta?

A
  • Incomplete fusion of the vertebrae, but with no herniation of the spinal cord
  • May be visible only as a small tuft of hair overlying the site
474
Q

What is Meningocele?

A
  • Incomplete fusion of the vertebrae, with herniation of a meningeal sac containing CSF
  • Visible prominence at the site, but usually covered by skin
475
Q

What is Myelomeningocele?

A
  • Incomplete fusion of the vertebrae with herniation of herniation of a meningeal sac containing CSF and spinal cord.
  • Usually accompanied by other defects such as hydrocephaly or Chiari malformation
  • Visible prominence at the site, with exposed meninges
476
Q

How can Spina Bifida be prevented?

A

All pregnant women, and those trying to conceive are recommended to take folic acid as this has been shown to decrease the risk of neural tube defects

  • 400 micrograms/day from 3 months prior to conception, until 12 weeks gestation
  • In women at higher risk (e.g. those with a child affected by a neural tube defect, or those on certain medications) are recommended a higher dose of 5mg/day
477
Q

How is Spina Bifida Diagnosed?

A

Usually diagnosed on prenatal scans

478
Q

What are the clinical features of Spina Bifida?

A

Neurological:

  • Motor deficits
  • Sensory deficits
  • Neurogenic bladder or bowel
  • Hydrocephalus
  • Seizures

Musculoskeletal:

  • Increased risk of hip subluxation
  • Scoliosis
  • Contractures
479
Q

What is the Management of Spina Bifida?

A
  • Primary neurosurgical repair
  • Orthopaedic surgery
480
Q

Define Chronic Hypertension/Pre-existing in terms of pregnancy?

A

High blood pressure that exists before pregnancy or is diagnosed before 20 weeks gestation and is longstanding. This is not caused by dysfunction in the placenta and is not classed as pre-eclampsia.

481
Q

Define Pregnancy Induced Hypertension (Gestational Hypertension)?

A

When there is an onset of high blood pressure that occurs after 20 weeks gestation without the presence of proteinuria

482
Q

What is the Aetiology of Gestational Hypertension?

A

Multifactorial, often involving genetic predisposition, lifestyle factors, and physiological changes during pregnancy.

483
Q

What is the Presentation of Gestational Hypertension?

A

Asymptomatic

  • May have headaches and blurred vision
484
Q

What are some differential diagnoses for Gestational Hypertesion?

A
  • Preeclampsia: Characterized by high blood pressure and damage to another organ system, most often the liver and kidneys, after 20 weeks of gestation.
  • Chronic Kidney Disease: Typically presents with proteinuria, haematuria, and a rise in serum creatinine.
485
Q

How is Gestational Hypertension diagnosed?

A

Gestational Hypertension must be new onset after 20 weeks gestation WITHOUT proteinuria

  • Blood pressure Monitoring
  • Urinalysis: To exclude proteinuria and subsequently Pre-eclampsia
486
Q

How is Gestational Hypertension Managed?

A
  • Discontinuation of some anti-hypertensive medications (ACEis and ARBs) to switch to pregnancy safe options.
  • Regular Blood Pressure Monitoring
  • Regular Urinalysis at least weekly
  • Monitoring Foetal growth by serial growth scans
  • PlGF testing on one occasion

Blood pressure control:

  • Gestational Hypertension > 150/100mmHg: Oral Labetalol
  • Treating to aim for BP < 135/85mmHg
  • Admission for women with a BP above 160/110 mmHg
  • Gestational Hypertension (mild) of: 140/90 to 149/99mmHg: No treatment other than regular monitoring

Alternatives if Labetalol is not tolerated:

  • 2nd Line: Nifedipine.
  • 3rd Line: Methyldopa
487
Q

Define Pre-eclampsia

A

Pre-eclampsia refers to new high blood pressure (hypertension) in pregnancy with end-organ dysfunction, notably with proteinuria (protein in the urine).

It occurs after 20 weeks gestation

488
Q

Define Eclampsia?

A

When seizures occur as a result of Pre-eclampsia due to cerebral vasospasm

489
Q

What is the Epidemiology of Pre-eclampsia?

A
  • Significant cause of maternal and foetal morbidity and mortality
  • Occurs after 20 weeks gestation
490
Q

What are some risk factors for Pre-eclampsia?

A

High-risk factors are:

  • Pre-existing hypertension
  • Previous hypertension in pregnancy
  • Existing autoimmune conditions (e.g. systemic lupus erythematosus)
  • Diabetes
  • Chronic kidney disease

Moderate-risk factors are:

  • Older than 40
  • BMI > 35
  • More than 10 years since previous pregnancy
  • Multiple pregnancy
  • First pregnancy
  • Family history of pre-eclampsia
491
Q

What is the Pathophysiology of Pre-eclampsia?

A
  • Blastocyst implants on the endometrium and the outer layer (Syncitiotrophoblast) grows into the endometrium to form chorionic villi.
  • Trophoblast invasion into the endometrium sends signals to the spiral arteries to reduce their vascular resistance making them more fragile and enabling lacunae to form. (Lacunae typically form around 20 weeks gestation)
  • If this process becomes defective, the formation of the lacunae is inadequate and the women can develop Pre-eclampsia.
  • High vascular resistance in the spiral arteries leads to poor perfusion of the placenta
  • This causes oxidative stress in the placenta leading to the release of inflammatory chemicals into systemic circulation.
  • This leads to systemic inflammation and impaired endothelial cell function resulting in the symptoms and complications of Pre-eclampsia
492
Q

What are the clinical features of Pre-eclampsia?

A

Classical Triad:

  • Hypertension
  • Proteinuria
  • Peripheral Oedema

Symptoms:

  • Severe Headaches (potentially due to cerebral oedema)
  • Visual Disturbance (due to retinal artery vasospasm)
  • Epigastric pain (due to reduced blood flow to the liver causing injury and swelling of liver and capsule)
  • Drowsiness
  • Nausea and vomiting
  • Hyperreflexia
493
Q

Why do you get Hypertension, Proteinuria and Peripheral Oedema in Pre-eclampsia?

A

Hypertension

  • Oxidative stress on the placenta causes the release of pro inflammatory cytokines
  • These entre the mothers circulation and cause endothelial cell dysfunction
  • This results in vasoconstriction and salt retention (at the kidneys) leading to hypertension

Proteinuria

  • Local vasospasm and hypertension will result in reduced blood flow to the kidneys.
  • The systemic inflammatory response may also lead to glomerular changes and disruption of the basement membrane and podocytes
  • This results in the leakage of proteins out the kidneys causing proteinuria

Peripheral Oedema

  • Endothelial injury increases vascular permeability enabling water to leak out of blood vessels and into the surrounding tissues
  • Furthermore, the proteinuria leads to low protein concentrations within blood vessels reducing the oncotic pressure and hence leads to further water loss into tissues
  • This results in generalised oedema that is commonly seen in the Legs, face and hands.
  • Pulmonary oedema (causing cough and SOB) as well as cerebral oedema (causing headaches, confusion and seizures)
494
Q

What are some maternal complications of Pre-eclampsia?

A
  • Eclampsia (seizures due to cerebrovascular vasospasm)
  • Organ failure
  • Disseminated intravascular coagulation (DIC)
  • HELLP syndrome (the presence of haemolysis (H), elevated liver enzymes (EL) and low platelets (LP))
495
Q

What are some foetal complications of Pre-eclampsia?

A
  • Intrauterine growth restriction (IUGR)
  • Pre-term delivery
  • Placental abruption
  • Neonatal hypoxia
496
Q

What are the investigations for Pre-eclampsia?

A

Blood Pressure Monitoring

  • Systolic BP > 140mmHg
  • Diastolic BP > 90mmHg
  • Severe Pre-eclampsia: Systolic >160mmHg and Diastolic >110mmHg

Urinalysis:

  • Proteinuria 1+ or more on urine dipstick
  • Urine protein:creatinine ratio > 30mg/mmol is significant
  • Urine albumin:creatinine ratio > 8mg/mmol is significant

Blood Tests:

  • U&E, FBC, LFTs (To assess kidney function, liver function and clotting status)
497
Q

How is Pre-eclampsia diagnosed?

A

NICE guidelines 2019 state diagnosis can be made with:

  • Hypertension (systolic >140mmHg/Diastolic >90mmHg)

PLUS any of:

  • Proteinuria (1+ or more on urine dipstick)
  • Organ dysfunction (e.g. raised creatinine, elevated liver enzymes, seizures, thrombocytopenia or haemolytic anaemia)
  • Placental dysfunction (e.g. foetal growth restriction or abnormal Doppler studies)

NICE Guidelines 2019 and Placental Growth Factor (PlGF):

  • Recommend testing on one occasion during pregnancy in women suspected to have Pre-eclampsia between 20 and 35 weeks gestation to rule out pre-eclampsia
  • sFLT:PlGF ratio >85 is diagnostic
498
Q

When is Aspirin given in pregnancy?

A

Women are offered aspirin from 12 weeks gestation until birth if they have:

  • One high-risk factor
  • More than one moderate-risk factors.
499
Q

What is the Management of Pre-eclampsia?

A
  • Women with 1 High risk or 2 Moderate Risk factors for Pre-eclampsia to take 75mg Aspirin from 12 weeks to delivery
  • Blood pressure is monitored closely (at least every 48 hours)
  • Ultrasound monitoring of the foetus, amniotic fluid and dopplers is performed two weekly

Urine dipstick testing is not routinely necessary (the diagnosis is already made)

Medical Management:

  • Labetolol is first-line as an antihypertensive
  • Nifedipine (modified-release) is commonly used second-line
  • Methyldopa is used third-line (needs to be stopped within two days of birth)
  • Intravenous hydralazine may be used as an antihypertensive in critical care in severe pre-eclampsia or eclampsia
  • IV magnesium sulphate is given during labour and in the 24 hours afterwards to prevent seizures
  • Fluid restriction is used during labour in severe pre-eclampsia or eclampsia, to avoid fluid overload
500
Q

How does Pre-eclampsia or Eclampsia affect the planning of Delivery?

A

Consider early delivery at 37 weeks if blood pressure cannot be controlled or complications occur.

Corticosteroids should be given to the women having a premature birth to help the foetal lungs mature

501
Q

What is the definitive cure for pre-eclampsia and Eclampsia?

A

Delivery of the foetus and placenta

502
Q

What is the Management for Eclampsia?

A

Similar to Pre-eclampsia with additional IV Magnesium Sulphate to manage the seizures

Also treat the cause (HTN) too so Labetalol/nifedipine.

503
Q

What is HELLP Syndrome?

A

Combination of features that occur as a complication of Pre-eclampsia and Eclampsia:

Haemolysis
Elevated Liver enzymes
Low Platelets

504
Q

What is the Epidemiology of HELLP syndrome?

A
  • HELLP syndrome is relatively rare, affecting approximately 0.5-0.9% of all pregnancies.
  • Occurs in 10-20% of women with severe pre-eclampsia or eclampsia
  • However, it is a significant cause of maternal and perinatal morbidity and mortality.
505
Q

What is the Pathophysiology of HELLP Syndrome?

A
  • Reduced perfusion of the placenta and thus oxidative stress releasing inflammatory cytokines.
  • Hypertension and endothelial damage reduces blood flow to the liver causing injury and swelling. This results in elevation of liver enzymes and stretches the liver capsule causing RUQ and epigastric pain
  • Endothelial cell injury leads to formation of thrombi in vasculature using up platelets making their numbers low
  • Thrombi can act as blocks for RBCs which crash into them causing them to become damaged and haemolyse
506
Q

What are the clinical features of HELLP Syndrome?

A

Headache
Nausea and/or vomiting
Epigastric pain
Right upper quadrant abdominal pain due to liver distension
Blurred vision
Peripheral Oedema

507
Q

What are the investigations for HELLP Syndrome?

A
  • Full blood count to assess for low platelet count and evidence of haemolysis
  • Liver function tests to assess for elevated liver enzymes
  • Coagulation studies to evaluate for disseminated intravascular coagulation
  • Ultrasound scans to assess for liver abnormalities and placental abruption
508
Q

What is the Management of HELLP Syndrome?

A

Delivery of the baby and placenta

  • Mothers may also require blood transfusions to manage anaemia and thrombocytopenia
509
Q

Define Obstetric Cholestasis?

A

Obstetric cholestasis, also known as intra-hepatic cholestasis of pregnancy, is a pregnancy-related hepatobiliary disorder that typically manifests after the 24th week of gestation.

The condition is characterised by impaired bile flow leading to the accumulation of bile acids.

510
Q

What is the Epidemiology of Obstetric Cholestasis?

A
  • Relatively common complication of pregnancy occuring in 1%
  • Develops later in pregnancy (Typically after 24-28 weeks)
  • More common in South Asian Ethnicity
511
Q

What is the Aetiology of Obstetric Cholestasis?

A

Multifactorial:

  • Hormonal Factors such as Increased oestrogen and Progesterone
  • Genetic factors
  • Environmental triggers
512
Q

What is the Pathophysiology of Obstetric Cholestasis?

A
  • In obstetric cholestasis, the outflow of bile acids is reduced, causing them to build up in the blood
  • Bile salts are deposited into various tissues such as the skin and placenta
  • Skin deposition leads to pruritus (itching)
  • Placental deposition causes raised foetal bile acid levels causing deterioration potentially due to arrhythmia, cardiomyopathy or placental vasoconstriction

Obstetric cholestasis is associated with an increased risk of stillbirth.

513
Q

What are the clinical features of Obstetric Cholestasis?

A
  • Pruritus: This is often severe and typically more intense on the hands and feet. It is not associated with a rash, although excoriation marks from scratching may be present.
  • General discomfort: Patients may experience fatigue or malaise.
  • Jaundice: Mild maternal jaundice characterised by dark urine and pale stools may occasionally occur.
  • Gastrointestinal symptoms: Nausea and loss of appetite are common.
  • Abdominal pain: Pain is typically localised in the right upper quadrant.
514
Q

What alternative diagnoses should be considered if someone presents similarly to Obstetric Cholestasis however a rash is present?

A
  • Polymorphic eruption of pregnancy
  • Pemphigoid gestationis.
515
Q

What are some differential diagnoses for Obstetric Cholestasis?

A
  • Gallstones
  • Acute fatty liver
  • Autoimmune hepatitis
  • Viral hepatitis
516
Q

What are the investigations for Obstetric Cholestasis?

A
  • Serum Bile Acids: Raised above 19 micromol/l
  • LFTs: Mainly ALT, AST and GGT

ALP typically rises in pregnancy due to it being produced by the placenta.

517
Q

What is the Management of Obstetric Cholestasis?

A

First Line:

  • Emollients: soothe the skin
  • Antihistamines: Chlorphenamine to aid in sleeping (Not improve itching)

Second Line:

  • Ursodeoxycholic acid: Improves LFTs, bile acids and symptoms and helps prevent premature birth

Induction of Labour at 37 weeks

518
Q

Where is Bartholin’s Glands?

A

The Bartholin’s glands are a pair glands located either side of the posterior part of the vaginal introitus (the vaginal opening). They are usually pea-sized and not palpable. They produce mucus to help with vaginal lubrication.

519
Q

What is a Bartholoin’s Gland Cyst

A

This occurs when the duct from the gland becomes blocked, resulting in palpable swelling and pain at the site of the Bartholin’s gland.

520
Q

What is a Bartholin’s Gland Abscess?

A

This occurs when a cyst becomes infected, resulting in extreme pain, lymphadenopathy, erythema, and in rare cases, systemic upset.

521
Q

What is the Aetiology of Bartholin’s Cysts and Abscesses?

A

The primary cause of Bartholin’s gland cysts and abscesses is the blockage of the gland’s duct.

This blockage can be due to thick mucus, inflammation, trauma, or in rare cases, malignancy.

Abscesses are typically caused by infection of a cyst, often with normal vaginal flora or sexually transmitted bacteria.

522
Q

What are the clinical features of Bartholin’s Glands Cysts and Abscesses?

A

Bartholin’s gland cyst:

  • Palpable swelling and without much pain at the site of the Bartholin’s gland.

Bartholin’s gland abscess:

  • Extreme pain
  • lymphadenopathy
  • erythema,
  • rare cases, systemic upset such as fever and malaise.
523
Q

What are some differential diagnoses for Bartholin’s Cysts and Abscesses?

A
  • Vaginal cysts: Typically asymptomatic but can cause discomfort during sex or when sitting.
  • Skene’s duct cysts: Located on either side of the urethra, can cause discomfort during sex or urination.
  • Vulvar cancer: Can present with a vulvar lump, itching, pain, or abnormal bleeding.
524
Q

What are the investigations for a Bartholin’s Cyst or Abscess?

A

Clinical diagnosis with a physical examination

  • Cyst is often painless
  • Absess is often painful + lymphadenopathy

If postmenopausal then may require biopsy to exclude malignancy

525
Q

What is the Management of Bartholin’s Cysts or Abscesses?

A

Cysts:

  • Good hygiene and warm compresses
  • Incision and Drainage is typically avoided due to likelihood of reoccurrence

Abscess:

  • Antibiotics
  • Surgical intervention may be required:
  • Word Catheter: requires local anaesthetic
  • Marsupialisation: requires general anaesthetic
526
Q

What is Sudden Infant Death Syndrome (SIDS)?

A

Also known as Cot death is the sudden unexplained death of an infant.

It usually occurs within the first six months of life

527
Q

What are some risk factors for SIDS?

A
  • Putting the baby to sleep prone
  • Parental smoking
  • Co-sleeping in same bed
  • Prematurity
  • Hyperthermia (e.g. over-wrapping) or head covering (e.g. blanket accidentally moves)
528
Q

What measures can be taken to minimise the risk of SIDS?

A
  • Put the baby on their back when not directly supervised
  • Breastfeeding
  • Keep their head uncovered
  • Place their feet at the foot of the bed to prevent them sliding down and under the blanket
  • Keep the cot clear of lots of toys and blankets
  • Maintain a comfortable room temperature (16 – 20 ºC)
  • Avoid smoking. Avoid handling the baby after smoking (smoke stays on clothes).
  • Room sharing NOT BED SHARING
529
Q

What support is available for families who have experienced SIDS?

A
  • Lullaby Trust is a charity to help support families affected.
  • Bereavement services and counselling should also be available.
  • Care of Next Infant (CONI) Team supports parents with their next infant after SIDS including extra support and home visits and resuscitation training
530
Q

What are the 2 stages of the Menstrual Cycle?

A

Follicular/Proliferative Phase Days 1-14

Luteal/Secretory Phase Days 15-28

531
Q

What happens during the Follicular/Proliferative phase of the Menstrual Cycle?

A
  • Increased frequency of pulsatile GnRH secretion leads to an increase in LH, and an initial increase in FSH.
  • Oestrogen rises gradually as granulosa cells convert thecal androgens under the
    influence of FSH. Progesterone levels remain low after loss of corpus luteum. Moderate levels of oestrogen exert negative feedback on FSH secretion.
  • Days 1-5: Progesterone withdrawal due to degeneration of corpus luteum leads to sloughing of the stratum functionalis (a menstrual bleed).
  • Days 6-14: The endometrium undergoes its proliferative phase due to rising oestrogen levels.
  • Meanwhile, 15-20 early antral (tertiary) follicles undergo development. At approximately day 7, a single dominant follicle is selected.
    • It is thought that this occurs because rising oestrogen levels lower FSH levels through negative feedback - the dominant follicle is the one that can cope with lower FSH.
  • Day 13 - Rising oestrogen levels reach a ‘tipping point’, at which their negative feedback on LH secretion is reversed - the LH surge occurs, stimulating the oocyte to complete meiosis I and form a single Graafian follicle.
  • Day 14 - Ovulation - The secondary oocyte erupts from its follicle, carried by antral fluid.
532
Q

What happens during the Luteal/Secretory phase of the Menstrual Cycle?

A
  • Day 15 - the granulosa cells of the ruptured follicle become luteinised, forming the progesterone-secreting corpus luteum.
  • The corpus luteum’s progesterone acts upon the endometrium to cause it to enter its secretory phase - amongst other things, it secretes glycogen and mucous.
  • Progesterone levels peak 7 days before the next menstrual bleed - 7 days before CL completely degenerates.
  • High levels of progesterone increase the volume and viscosity of cervical secretions; this begins the formation of the protective operculum.
  • After 10 days, if no conceptus has implanted, the corpus luteum spontaneously
    regresses. This leads to diminishing progesterone levels:
    • Without progesterone’s negative feedback on the hypothalamus, GnRH release frequency increases and facilitates a rise in gonadotrophins.
    • Progesterone withdrawal also stimulates the stratum functionalis of the secretory endometrium to be shed.
  • As FSH and LH levels rise, and the menstrual bleed begins, the cycle restarts on Day 1.
533
Q

What are some examples of Non-Hormonal Contraception?

A
  • Copper intrauterine device (Cu-IUD)
  • Barrier methods e.g. male condom, female condom, diaphragm/cervical cap
  • Surgical methods e.g. tubal ligation, vasectomy
  • Lactational amenorrhoea
  • Fertility awareness methods (FAM)
534
Q

What are some examples of Hormonal Contraception?

A
  • Combined Hormonal Contraception (CHC)
  • Combined Oral Contraceptive Pill (COCP)
  • Progesterone Only Pill (POP/Mini-pill)
  • Levonorgestrel Intrauterine System (LNG-IUS commonly known as Mirena)
  • Contraceptive Injection (Depo-Provera)
  • Contraceptive Implant
535
Q

What are some examples of Emergency Contraception?

A
  • Levonorgestrel Pill
  • Ulipristal Acetate Pill (EllaOne)
  • Copper Intrauterine Device (Cu-IUD)
536
Q

What are the features of the Copper Intrauterine Device (Cu-IUD):

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Decreases sperm motility and Survival

Efficacy: 0.8% experience unintended pregnancy after 1 year

Advantages:

  • Effective immediately on insertion (can be used in emergency).
  • No hormonal side effects.
  • High Efficacy

Absolute Contraindications:

  • PID
  • Gonorrhoea/Chlamydia
  • Unexplained vaginal bleeding/endometrial cancer
  • postpartum/postabortion septicaemia
  • Gestational trophoblastic disease
  • Purulent cervicitis, Pelvic TB

Side Effects:

  • Breakthrough bleeding.
  • Increased duration or heaviness of periods

Other:

  • Classified as Long-acting reversible contraceptive (LARC)
  • Left in situ for 5 years
  • Most effective form of emergency contraception.
  • The Cu-IUD is licensed for insertion 5 days post-ovulation.
537
Q

What are the features of the Combined Oral Contraceptive Pill (COCP):

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Inhibits ovulation

Efficacy: 0.03% failure rate if used perfectly but human error is important taking average unwanted pregnancy to 9%

Advantages:

  • Rapidly reversible if unintended side effects
  • Regulars and tends to lighten periods

Absolute Contraindications:

  • <6 weeks postpartum in breastfeeding women
  • Aged 35, smoking >15 cigarettes per day
  • Stage 2 hypertension (160/100)
  • History of VTE
  • Disease: Breast cancer, inherited thrombophilia e.g. Factor V Leiden,
    cardiomyopathy, cirrhosis, vascular disease, SLE, positive antiphospholipid
    antibodies.
  • Migraine with aura

Side Effects:

  • Headache
  • Mood disturbance
  • Breakthrough bleeding
538
Q

What are the features of the Progesterone Only Pill (POP):
Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Thickens cervical Mucus

Efficacy: 9% experience unintended pregnancy after 1 year.

Advantages:

  • Rapidly reversible
  • Far fewer absolute contraindications than the combined pill

Absolute Contraindications:

  • Breast Cancer

Side Effects:

  • Breakthrough Bleeding

Other:

  • Effective after 2 days of administration
539
Q

What are the features of the Levonorgestrel Intrauterine System (LNG-IUS/Mirena)

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Prevents endometrial proliferation and also thickens cervical mucus

Efficacy: 0.2% unintended pregnancy after 1 year

Advantages:

  • Extremely high efficacy
  • Can be left in situ for 3-5 years
  • Lightens periods
  • Systemic absorption is minimal, reducing systemic hormonal side effects

Absolute Contraindications:

  • PID
  • Gonorrhoea or chlamydia
  • Unexplained vaginal bleeding / endometrial cancer
  • Postpartum / post-abortion septicaemia
  • Gestational trophoblastic disease
  • Purulent cervicitis, pelvic TB

Side Effects:

  • Irregular Menstrual Bleeding
540
Q

What are the features of the Contraceptive Injection (Depo-Provera)

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Inhibits Ovulation and also thickens cervical mucus (Medroxyprogesterone acetate)

Efficacy: 6% experience unintended pregnancy after 1 year.

Advantages:

  • Long acting - Requires injection every 12 weeks

Absolute Contraindications:

  • Breast Cancer

Side Effects:

  • Amenorrhoea
  • Weight gain
  • Reduces BMD so cant be given to people beyond age 50
541
Q

What are the features of the Contraceptive Implant:

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Inhibit Ovulation and also thickens cervical mucus

Efficacy: 0.05% experience unintended pregnancy after 1 year

Advantages:

  • Most effective contraception available.
  • Active for 3 years before replacement is required.

Absolute Contraindications:

  • Breast Cancer

Side Effects:

  • Irregular Menstrual Bleeding
542
Q

What are the features of the Levonorgestrel Pill (LNG)?

Mechanism:

Efficacy:

A

Mechanism:

  • Inhibits ovulation
  • Can delay ovulation by 5 days (the viable lifespan of ejaculated sperm).
  • Not effective in the late luteal phase, in which case ulipristal acetate is required.

Efficacy:

  • Effective up to 72 hours post UPSI
  • Not effective if taken after ovulation has occurred
543
Q

What are the features of the Ulipristal Acetate Pill (UPA EllaOne)

Mechanism:

Efficacy:

A

Mechanism: Inhibits ovulation

Efficacy:

  • Effective up to 120 hours post UPSI
  • Can delay ovulation even if LH surge has started
  • Remains effective in late follicular phase
  • Not effective if taken after ovulation
  • Contraception with pill, patch or ring should be restarded after 5 days due to reduced effectiveness
544
Q

What are the guidelines when offering emergency contraception?

A
  • Offer most effective method (Cu-IUD) first line;
    • Can be taken either within 120 hours of first UPSI or within 120 hours of
      calculated date of ovulation; whichever is later.
  • If Cu-IUD not acceptable / appropriate, offer oral emergency contraception;
    • If within 72 hours of UPSI - offer LNG or UPA.
    • If 72-120 hours post-UPSI - offer UPA.
545
Q

Define Fertilisation

A

Fusion of haploid sperm and oocyte, typically occurring in the ampulla of the
fallopian tube.

546
Q

What are the stages of Fertilisation?

A

1. Capacitation - final stage of sperm maturation - involves exposure of receptor sites involved in zona pellucida penetration.

2. Acrosome reaction - loss of the acrosome cap on the head of the sperm cell leads to release of lytic enzymes, which allows the sperm to penetrate the zona pellucida.

3. Adhesion and entry - cell membranes of sperm and egg fuse, and the head of the sperm if phagocytosed - it then breaks down to release the sperm nucleus.

4. Cortical reaction - modification of the zona pellucida to prevent polyspermy, induced by membrane fusion and mediated by cortical granules

5. Meiosis II - the oocyte completes meiosis II (which until this point is arrested in
metaphase II) to give the second polar body.

6. Syngamy - the male and female pronuclei replicate DNA and shed their nuclear
membranes as they move toward one another, before aligning at a common metaphase plate and undergoing mitosis

547
Q

What are the key events in Embryonic Development?

A
  • Day 6-7: implantation of blastocyst into endometrium
  • Week 3: gastrulation - formation of trilaminar disc (endoderm, mesoderm, ectoderm) from the primitive streak
  • Week 3-8: beginning of development of organ systems
  • Week 4: neurulation - development of neural tube from the ectoderm
  • Week 23: generally considered to be the threshold of viability.
548
Q

What are the functions of the Placenta?

A

Exchange:

  • gaseous: Oxygen moves readily from maternal to foetal haemoglobin (HbF) due to HbF’s higher affinity. CO2 diffuses from foetal to maternal blood down the concentration gradient
  • Nutritional: Glucose moves from maternal to foetal circulation via facilitated diffusion; both amino acids and free fatty acids also cross from mother to foetus, the former through active transport.

Endocrine:

  • Human Chorionic Gonadotrophin (hCG) Produced by trophoblast cells -
    maintains the corpus luteum to allow for sufficient progesterone production until
    the placenta takes over
  • Human Placental Lactogen (hPL): Increases maternal free fatty acid and insulin
    levels, as well as inducing maternal insulin resistance.
  • Progesterone: Inhibits uterine contractility and thickens endometrium
  • Oestrogen: Stimulates myometrial growth, oxytocin receptor synthesis and pregnancy related breast changes
549
Q

Explain the phsyiological changes in pregnancy for these systems:

  • Cardiovascular
  • Respiratory
  • Renal
  • Gastrointestinal
  • Haematological
  • Breasts
  • Skin
A

Cardiovascular:

  • Increase oestrogen leads to renal fluid reabsorption, increase preload, increased SV and subsequent increase CO
  • HR increases
  • Progesterone causes vasodilation which reduces TPR and subsequently reduced BP.
  • BP is lower in 1st trimester but due to CO and HR increases it returns to normal by second/third
  • At 20 weeks, uterus can compress IVC in R. lateral position causing varicose veins and peripheral oedema.

Respiratory:

  • Increase in TV by end of first trimester due to increase O2 use and CO2 production
  • Growing uterus compresses diaphragm and lungs leading to decreased FRC

Renal:

  • Progesterone induced Vasodilation on afferent arteriole increasing GFR
  • Increase urine production due to increased GFR

Gastrointestinal:

  • Progesterone increases gastric pressure and reduces smooth muscle motility causing increased gastric reflux and constipation
  • Progesterone reduces gallbladder motility causing bile stagnation and cholestasis of pregnancy

Haematological:

  • Increase plasma volume without as large an increase in RBC leading to reduced haematocrit and subsequent anaemia
  • Hypercoagulability due to increase clotting factors and platelet aggregation

Breasts:

  • Ductal proliferation
  • Prolactin stimulates milk production from alveolar cells
  • Areola grow

Skin:

  • Increased pigmentation of face and areola
  • Linea nigra
  • Stria gravidarum
550
Q

What Vaccines are offered to all pregnant women?

A
  • Influenza (Flu) at any time during pregnancy
  • Pertussis from 16 weeks gestation

Live vaccines such as MMR are avoided

551
Q

How many routine appointments during Pregnancy?

A

8 routine for parous women and 11 for nulliparous women (Women who haven’t given birth to a live baby.) Also possibility of a 41 week appointment if women has not yet delivered

Nulliparous women have an additional 3 at: 25 weeks, 31 weeks and 40 weeks

552
Q

What are the routine appointments during Pregnancy?

A

Before 10+0 weeks: Booking Visit

  • Heigh and weight measurement
  • Screening offered
  • BP and urinalysis
  • Assess for risk of GDM, Pre-eclampsia, FGR, VTE, FGM
  • Offer vaccines (influenza (any time) and pertussis (16-30 weeks)

11+2 to 14+1 weeks: Dating Scan

  • Estimate gestational age
  • Assess for Multiple Pregnancy
  • Foetal anomaly screening

16 Weeks: Blood pressure and urinalysis

18+0 to 20+6 weeks: Anomaly scan

  • Detailed scan to assess for anatomical anomalies (anencephaly, meningocele, exomphalos)
  • Assess position of the Placenta (low lying, Praevia)
  • Foetal movements typically felt at this point

25 weeks: BP and urinalysis + Symphyseal-fundal height (SFH)

28 weeks:

  • Height, Weight, BP, Urinalysis and SFH
  • Anti-D prophylaxis (first dose) for Rhesus negative women

31 Weeks: BP, Urinalysis and SFH

34 Weeks:

  • BP, Urinalysis and SFH
  • Anti-D prophylaxis (second dose) for Rhesus negative women

36 Weeks:

  • BP, urinalysis and SFH
  • Palpate abdomen to assess for breech presentation

38 Weeks:

  • BP, Urinalysis and SFH
  • Discuss possibility of prolonged pregnancy and its management

40 Weeks: BP, urinalysis and SFH

41 Weeks:

  • BP, urinalysis and SFH
  • Sweep offered to induce labour
553
Q

What are the Elements of Pregnancy screening in the UK?

A

All offered at the Booking visit

  • Infectious Disease
  • Sickle Cell and Thalassaemia
  • Foetal Anomaly
554
Q

What Infectious diseases are screened for in pregnancy?

A
  • HIV: 25% risk of MTC transmission if untreated
  • Syphilis: Risk of miscarriage, stillbirth, congenital syphilis
  • Hepatitis B: 70-90% risk of MTC transmission if HBeAg positive
555
Q

What Foetal Anomalies are screened for at the booking visit?

A

Trisomy’s 21 (Down’s), 18 (Edwards’) and 13 (Patau’s)

All Screened for at the booking visit with the combined Test:

  • Maternal age
  • b-hCG, PAPP-A (pregnancy associated Plasma Protein)
  • USS (11+2-14+1) - Nuchal translucency (NT) and Crown-rump Length (CRL)
    • CRL must be 45-84mm to be eligible for combined test
    • Too low then wait and Too high offer Quadruple test

If the mother is late-booking (>14+0) then the quadruple test is used for T21:

  • Maternal age, b-hCG, AFP, inhibin A and Unconjugated Oestriol

If high Chance of Anomaly (> 1/150) there are 3 options:

  • No further testing
  • Non-invasive prenatal testing (NIPT) - Placental cell free DNA
  • Prenatal diagnosis (PND) - Chorionic villus sampling (11-14 weeks), Amniocentesis (15+ weeks)
556
Q

What are the results of the Combined test that are suggestive of Trisomy Anomaly?

A

Tests for Trisomy:

Trisomy 21 (Down’s): high b-hCG, Low PAPP-A, High NT

Edwards and Pataus are similar to Downs but HCG is lower

Trisomy 18 (Edwards’): Low b-hCG, Low PAPP-A, High NT

Trisomy 13 (Patau’s): Low b-hCG, Low PAPP-A, High NT

557
Q

What timeline defines 1st, 2nd and 3rd Trimester?

A

First Trimester Start - 12 weeks
Second Trimester 13 weeks - 26 weeks
Third Trimester 27 weeks - birth

558
Q

When are Fetal movements typically felt?

A

From around 20 weeks gestation until birth

559
Q

When does Labour and Delivery normally occur?

A

Normally occur between 37 and 42 weeks gestation

560
Q

What are the 3 stages of labour?

A
  • First stage – from the onset of labour (true contractions) until 10cm cervical dilatation
  • Second stage – from 10cm cervical dilatation until delivery of the baby
  • Third stage – from delivery of the baby until delivery of the placenta
561
Q

What is classed as the first stage of labour?

A

The first stage of labour is defined as the period that starts with regular uterine contractions and ends when the cervix is fully dilated to 10cm. This stage can be further divided into:

Latent Phase: from 0 to 3cm dilation of the cervix. This progresses at around 0.5cm per hour. There are irregular contractions.

Active Phase: from 3cm to 7cm dilation of the cervix. This progresses at around 1cm per hour, and there are regular contractions

Transition Phase: from 7cm to 10cm dilation of the cervix. This progresses at around 1cm per hour, and there are strong and regular contractions.

562
Q

What is the Physiology of the first stage of labour?

A

The first stage of labour is initiated by a complex interplay of hormonal signals, primarily involving prostaglandins and oxytocin, which stimulate regular uterine contractions. These contractions, in combination with the pressure exerted by the presenting part of the foetus, lead to progressive dilation of the cervix.

563
Q

What are Braxton-Hicks Contractions?

A
  • Occasional irregular contractions of the uterus.
  • They are usually felt during the second and third trimester.
  • Women can experience temporary and irregular tightening or mild cramping in the abdomen.
  • These are not true contractions, and they do not indicate the onset of labour.
  • They do not progress or become regular.
  • Staying hydrated and relaxing can help reduce Braxton-Hicks contractions.
564
Q

What are the Signs of the Onset of Labour?

A
  • Show (mucus plug from the cervix)
  • Rupture of membranes
  • Regular, painful contractions
  • Dilating cervix on examination

Latent First stage: is when there are both

  • Painful contractions
  • Changes to the cervix with effacement and dilation up to 4cm

Established first stage of labour: is when there are both

  • Regular painful contractions
  • Dilation of the cervix from 4cm onwards
565
Q

What is classed as the Second stage of labour?

A

The second stage of labour is defined as the period beginning with complete cervical dilation and ending with the delivery of the foetus. There are 7 Stages:

  1. Descent: the baby’s head (providing it is in cephalic presentation) descends deeper into the pelvis until it is no longer palpable on abdominal examination.
  2. Flexion: the baby’s head flexes (chin to chest) to give the narrowest
    (suboccipitobregmatic) diameter.
  3. Internal rotation: baby’s occiput rotates anteriorly from the lateral position to give the normal occipito-anterior position.
  4. Extension: baby’s occiput contacts the maternal pubic rami - it then extends and crowns
  5. Restitution: baby’s occiput re-aligns with its shoulders, which lie in between the
    anterior-posterior and lateral positions
  6. External rotation: baby’s shoulders rotate into anterior-posterior position (i.e.
    perpendicular to mother’s). At this point, the baby’s head is delivered - it is aligned with its shoulders, so the face looks laterally at the mother’s thigh.
  7. Delivery of shoulders: the anterior shoulder is delivered first from beneath the pubic ramus; the head is then gently lifted anteriorly to deliver the posterior shoulder. The rest of the baby’s body rapidly follows.
566
Q

What is classed as the third stage of labour?

A

The period beginning at the delivery of the foetus and ending with the delivery of the placenta and foetal membranes.

  • This stage generally occurs within 30 minutes of delivery of the baby.
  • Physiological Management: * This stage generally lasts within 30 minutes to an hour when allowed to occur naturally
  • Active Management: It may take as long as 5-10 minutes with administration of IM oxytocin
567
Q

When is Active management of the third stage of labour used?

A

Routinely offered to all women to reduce the risk of postpartum haemorrhage

Initiated if:

  • Haemorrhage
  • More than a 60 minute delay in the delivery of the placenta (Prolonged third stage)
568
Q

What is Induction of Labour?

A

The medically initiated process of starting labour artificially.
It is performed under specific circumstances to ensure the safety of the mother and the child.

569
Q

What are some indications for an Induction of Labour?

A
  • Post-dates/Prolonged pregnancy (>41 weeks gestation)
  • Preterm prelabour rupture of membranes (offered at 37+0)
  • Intrauterine foetal death (IUFD)
  • Abnormal CTG
  • Maternal request
  • Maternal conditions such as pre-eclampsia, diabetes, cholestasis
570
Q

What are some contraindications for an Induction of Labour?

A
  • Previous classical/vertical incision during caesarean section
  • Multiple lower uterine segment caesarean sections
  • Transmissible infections e.g. herpes simplex
  • Placenta praevia
  • Malpresentations
  • Severe foetal compromise
  • Cord prolapse
  • Vasa previa
571
Q

What system is used to determine whether to induce labour?

A

Bishop Scoring System: Score from 0-13

  • Foetal station (scored 0 – 3)
  • Cervical position (scored 0 – 2)
  • Cervical dilatation (scored 0 – 3)
  • Cervical effacement (scored 0 – 3)
  • Cervical consistency (scored 0 – 2)

A score of 8 or more the cervix is ripe and there is a high chance of spontaneous labour or response to induction of labour

A score below 5 suggests that labour is unlikely to start without induction

572
Q

What are some management options to induce labour?

A

Membrane Sweep

  • Inserting a finger into the cervix to stimulate the cervix and begin the labour process
  • Labour should follow within 48 hours if successful
  • Is used from 40 weeks gestation to attempt to initiate labour in women over their EDD (estimated delivery date)

Vaginal Prostaglandin E2 (Dinoprostone)

  • Insert a Gel, Tablet or Pessary into the vagina to slowly release local prostaglandins over 24 hours. to stimulate labour onset.
  • Usually performed when there is a Bishop Score < 6

Amniotomy (Artificial Rupture of Membranes)

  • May be done with/without oxytocin infusion
  • Only used where Vaginal Prostaglandins are not tolerated/successful
  • Used when the Bishop Score > 6
573
Q

What are some options to manage induced labour when there is slow or no progress?

A
  • Further vaginal prostaglandins
  • Artificial rupture of membranes and oxytocin infusion
  • Cervical ripening balloon (CRB)
  • Elective caesarean section
574
Q

What is a key complication of Induced labour?

A

Uterine Hyperstimulation: This is where the contraction of the uterus is prolonged and frequent, causing foetal distress and compromise.

2 Criteria for Uterine Hyperstimulation:

  • Individual uterine contractions lasting more than 2 minutes in duration
  • More than five uterine contractions every 10 minutes
575
Q

What can uterine Hyperstimulation lead to?

A
  • Foetal compromise, with hypoxia and acidosis
  • Emergency caesarean section
  • Uterine rupture
576
Q

What is the Management of Uterine Hyperstimulation?

A
  • Removing the vaginal prostaglandins, or stopping the oxytocin infusion
  • Tocolysis with terbutaline
577
Q

What makes up the initial assessment of Labour?

A
  • Take a history, Assess for risk factors and assess for pain
  • Pules, BP, Resp Rate, Urinalysis
  • Abdominal palpation to determine Lie, presentation, engagement and contraction strength
  • Vaginal examination to determine station, position, cervical effacement and dilation, presence or absence of membranes and caput or cranial moulding.
578
Q

How is the progression of Labour monitored?

A

Partogram

  • Progress: Cervical dilation, descent, contractions (frequency and duration)
  • Foetal wellbeing: Heart rate, Amniotic fluid (liquor)
  • Maternal wellbeing: Pulse, BP, Temp, Urinalysis
579
Q

How can Foetal Heart rate be measured?

A

Low risk deliveries: Intermittent Auscultation with a Doppler Probe

High risk Deliveries: Cardiotocograph (CTG)

580
Q

What is Cardiotocography (CTG)?

A

Used to measure the foetal heart rate and the contractions of the uterus.

CTG Readouts are interpreted as:

Normal: No non-reassuring features

Suspicious: One non-reassuring feature

Pathological: Two non-reassuring features OR one abnormal feature

Need for urgent Intervention: Acute bradycardia or prolonged deceleration of more than 3 minutes

581
Q

What is measured on a CTG?

A
  • Contractions – the number of uterine contractions per 10 minutes
  • Baseline rate – the baseline foetal heart rate
  • Variability – how the foetal heart rate varies up and down around the baseline
  • Accelerations – periods where the foetal heart rate spikes
  • Decelerations – periods where the foetal heart rate drops
582
Q

What are the Reassuring features of the CTG?

A

Baseline Heart Rate: 110-160bpm

Decelerations (Drops of 15 bpm for 15s): Absent

Accelerations (increases of 15 bpm for 15s): Present

Baseline variability: 5-25bpm

583
Q

What are some Non-reassuring features of the CTG?

A

Baseline Rate: 100-109 / +20 from start of labour

Decelerations:

  • Repetitive Variable for < 30 mins
  • Variable for < 30 mins
  • Repetitive late for 30 mins

Accelerations: Absent

Baseline Variability: <5 for 30-50 mins / >25 for <10mins

584
Q

What are some Abnormal features of the CTG?

A

Baseline Rate: <100/ >160

Decelerations:

  • Repetitive variable with concerning characteristics >30 mins
  • Repetitive late > 30mins
  • 3 minutes of Bradycardia

Accelerations: Absent

Baseline Variability: <5 for 50 mins / >25for >10mins / sinusoidal pattern

585
Q

What does a Sinusoidal CTG suggest?

A

Severe Foetal Compromise

Usually associated with severe foetal anaemia caused by vasa praevia with foetal haemorrhage

586
Q

What must be done in the case of Foetal Bradycardia?

A

Rule of 3s:

  • 3 Minutes: Call for help
  • 6 Minutes: Move to theatre
  • 9 Minutes: Prepare for delivery
  • 12 Minutes: Deliver the baby (by 15 Minutes)
587
Q

DR C BRaVADO

What is the approach to assessing CTGs?

A

DRDefine Risk (define the risk based on the individual woman and pregnancy before assessing the CTG)
CContractions
BRaBaseline Rate
VVariability
AAccelerations
DDecelerations
OOverall impression (given an overall impression of the CTG and clinical picture)

588
Q

What are some methods to improve symptoms such as pain in labour without medications?

A
  • Understanding what to expect
  • Having good support
  • Being in a relaxed environment
  • Changing position to stay comfortable
  • Controlled breathing and relaxation techniques
  • Water births may help some women
  • TENS machines may be useful in the early stages of labour
589
Q

What are some Non-regional analgesia that may be used in Labour?

A

Simple Analgesia: Paracetamol or Codeine (NSAIDS are avoided)

Gas and Air (Entonox): 50% nitrous oxide and 50% oxygen used during contractions for short term pain relief

IM Opiates (Pethidine, Diamorphine): Opioid medications given by IM injection

Patient Controlled Analgesia: PCA using IV remifentanil

590
Q

What are some Regional Analgesia that may be used in Labour?

A

Epidural Local anaesthetic medications ((Levobupivacaine or bupivacaine combined with fentanyl injected into the epidural space at L3-4.

591
Q

What are some adverse effects of an Epidural?

A
  • Headache after insertion
  • Hypotension
  • Motor weakness in the legs
  • Nerve damage
  • Prolonged second stage
  • Increased probability of instrumental delivery
592
Q

Why do women need urgent anaesthetic review if they develop significant motor weakness following an Epidural?

A

Women unable to straight leg raise is concerning.

Suggests that the catheter for an epidural is incorrectly sited in the subarachnoid space (within the spinal cord)

593
Q

What is the definition of a Venous Thromboembolism (VTE) in Pregnancy?

A
  • A VTE involves blood clots (thrombosis) developing within the circulation.
  • When they form within the venous system this is known as a Deep Vein Thrombosis (DVT).
  • The thrombosis can mobilise (embolisation) from the deep veins and travel to the lungs, where it becomes lodged in the pulmonary arteries, resulting in a pulmonary embolism (PE).
  • Thrombosis occurs as a result of stagnation of blood as well as in hyper-coagulable states, such as in pregnancy, making it much more likely.
594
Q

What is the epidemiology of VTEs in pregnancy?

A
  • Pulmonary embolism is a significant cause of death in obstetrics.
  • The risk is significantly reduced with VTE prophylaxis.
  • The risk is highest in the postpartum period.
595
Q

What are the risk factors for VTEs in Pregnancy?

A

Women with a previous VTE Hx are automatically considered high risk

  • Smoking
  • Parity ≥ 3
  • Age > 35 years
  • BMI > 30
  • Reduced mobility
  • Multiple pregnancy
  • Pre-eclampsia
  • Gross varicose veins
  • Immobility
  • Family history of VTE
  • Thrombophilia
  • IVF pregnancy
596
Q

When does the RCOG advise starting VTE prophylaxis in pregnant women?

A

Immediately if women have prev Hx of VTE

  • 28 weeks if there are three risk factors
  • immediately if there are four or more of these risk factors
  • It is stopped when the woman goes into labour but can be started again immediately after delivery (except with postpartum haemorrhage, spinal anaesthesia and epidurals)
  • It is continued for 6 weeks postnatally.

VTE prophylaxis should also be given in the following situations regardless of risk factors:

  • Hospital admission
  • Surgical procedures
  • Previous VTE
  • Medical conditions such as cancer or arthritis
  • High-risk thrombophilias
  • Ovarian hyperstimulation syndrome
597
Q

What medications are used for VTE prophylaxis?

A

Low Molecular Weight Heparin (LMWH):

  • Enoxaparin
  • Dalteparin
  • Tinzaparin.

If Heparin is contraindicated, Mechanical prophylaxis may be used:

  • Intermittent pneumatic compression (with equipment that inflates and deflates to massage the legs)
  • Anti-embolic compression stockings
598
Q

What is the clinical presentation of a Deep Vein Thrombosis (DVT)?

A
  • Calf or leg swelling
  • Dilated superficial veins
  • Tenderness to the calf (particularly over the deep veins)
  • Oedema
  • Colour changes to the leg

Deep vein thrombosis is almost always unilateral

599
Q

What is the clinical presentation of Pulmonary Embolism (PE)?

A
  • Shortness of breath
  • Cough with or without blood (haemoptysis)
  • Pleuritic chest pain
  • Hypoxia
  • Tachycardia (this can be difficult to distinguish from the normal physiological changes in pregnancy)
  • Raised respiratory rate
  • Low-grade fever
  • Haemodynamic instability causing hypotension
600
Q

How are VTEs investigated?

A

DVTs:

  • Wells score 1 or less: D-dimer
  • Wells Score 2 or more: Duplex Ultrasound

PEs:

  • Wells score 4 or less: D-Dimer
  • Wells Score >4: Immediate CT pulmonary angiogram (CTPA) or Ventilation-perfusion (VQ) scan.
601
Q

Describe what CT pulmonary angiogram is

A

CT pulmonary angiogram involves a chest CT scan with an intravenous contrast that highlights the pulmonary arteries to demonstrate any blood clots.

This is usually the first choice for diagnostic of a PE (as opposed to a VQ Scan). This is the case because:
* It tends to be more readily available
* It provides a more definitive assessment
* It gives information about alternative diagnoses such as pneumonia or malignancy.

602
Q

Describe what a Ventilation perfusion (VQ) scan is

A
  • Ventilation-perfusion (VQ) scan involves using radioactive isotopes and a gamma camera, to compare the ventilation with the perfusion of the lungs.
  • First, the isotopes are inhaled to fill the lungs, and a picture is taken to demonstrate ventilation. Next, a contrast containing isotopes is injected, and a picture is taken to demonstrate perfusion. The two images are compared.
  • With a pulmonary embolism, there will be a deficit in perfusion, as the thrombus blocks blood flow to the lung tissue. This area of lung tissue will be ventilated but not perfused.
603
Q

What are the possible complications of CTPAs and VQ Scans?

A
  • CTPA carries a higher risk of breast cancer for the mother
  • VQ scan carriers a higher risk of childhood cancer for the fetus
604
Q

Why are D-Dimers not useful in pregnant women?

A

As pregnancy is a cause of a raised D-dimer. So it cannot be used to screen for DVTs and PEs.

605
Q

What is the management of VTE in pregnancy?

A

Low molecular weight heparin (LMWH) (e.g. enoxaparin, dalteparin and tinzaparin).

  • The dose is based on the woman’s weight at the booking clinic, or from early pregnancy.
  • It should be started immediately, before confirming the diagnosis in patients where DVT or PE is suspected; as treatment can be stopped when the investigations exclude the diagnosis.
  • LMWH is continued for the remainder of pregnancy, plus six weeks postnatally, or three months in total (whichever is longer).
  • After giving birth, the mother can swap to oral anticoagulation (e.g. warfarin or a DOAC).

Massive PEs are a medical emergency, and treatment can involve:
* Unfractionated heparin
* Thrombolysis
* Surgical embolectomy

606
Q

What is the definition of Gonorrhoea?

A

Gonorrhoea is a sexually transmitted infection (STI) caused by the gram-negative diplococcus, Neisseria gonorrhoeae.

607
Q

What is the epidemiology of Gonorrhoea?

A
  • It’s most prevalent among young adults, specifically those aged 15–24 years.
  • Increased prevalence in men who have sex with men
608
Q

What is the clinical presentation of Gonorrhoea?

A

Women

  • Vaginal discharge
  • Dysuria
  • Abnormal vaginal bleeding
  • Discharge from the cervical os, Skene’s gland or Bartholin’s gland may be observed.

Extragenital complications can also be observed:

  • Pharyngitis
  • Rectal pain an discharge
  • Disseminated infection.

Men

  • Often asymptomatic
  • Discharge
  • Dysuria
  • Tender inguinal nodes
609
Q

What are some differentials for Gonorrhoea?

A
  • Chlamydia trachomatis infection
    Presents with similar symptoms such as discharge and dysuria, often co-infected with gonorrhoea.
  • Trichomonas vaginalis infection
    May present with pruritus, dysuria, and malodorous discharge.
  • Bacterial vaginosis
    Characterised by a fishy-smelling discharge, increased vaginal pH and positive ‘whiff’ test.
  • Candidiasis
    Symptoms include pruritus, burning sensation and thick, white, ‘cottage cheese’ like discharge.
610
Q

How is Gonorrhoea diagnosed?

A
  • NAAT test from Endocervical, vulvovaginal or ureathral swaps
  • NAAT test from first catch urine sample
  • Endocervical Charcoal Swab taken for MC&S is also vital
611
Q

What is the management of Gonorrhoea?

A

If sensitivities are NOT known: Single dose 1g IM Ceftriaxone

If sensitivities ARE known: Single dose PO 500mg Ciprofloxacin

All patients should have a test of cure

612
Q

What complications can Gonnorhoea cause during pregnancy?

A
  • Increased risk of miscarriage and premature birth; due to pelvic inflammatory disease (PID).
  • There can also be vertical transmission of gonorrhea between the mother and newborn baby during vaginal delivery.
  • neonatal conjunctivitis (gonnorhoea ophthalmia neonatorum)
  • It can also cause future infertility
613
Q

What is the definition of Chlamydia?

A

A genital chlamydia infection sexually transmitted infection caused by the obligate intracellular bacterium Chlamydia trachomatis.

614
Q

What is the epidemiology of Chlamydia?

A
  • It is the most common bacterial STI in the UK.
  • Highest prevalence among young sexually active adults, specifically those aged 15 to 24 years
  • Having multiple partners also increases the risk of catching the infection.
615
Q

What is the clinical presentation of Chlamydia?

A

Chlamydia is very often asymptomatic (especially in women (75% of cases)). But it can cause:

  • Abnormal (prurulent) vaginal discharge
  • Pelvic pain
  • Abnormal vaginal bleeding (intermenstrual or postcoital)
  • Painful sex (dyspareunia)
  • Painful urination (dysuria)
  • Cervical motion tenderness (cervical excitation)
  • Inflamed cervix (cervicitis)

Rectal chlamydia should be considered in patients with anorectal symptoms, such as:

  • Discomfort
  • Discharge
  • Bleeding
  • Change in bowel habits.
616
Q

What are the possible complications of Chlamydia during pregnancy?

A
  • Preterm delivery
  • Premature rupture of membranes
  • Low birth weight
  • Postpartum endometritis
  • Ectopic pregnancy
  • Neonatal infection (conjunctivitis and pneumonia)
617
Q

What are some differentials for Chlamydia?

A

The differentials mainly incude other STIs such as:

  • Gonorrhoea
    Often asymptomatic but may cause urethral discharge, dysuria, intermenstrual or postcoital bleeding, and lower abdominal pain.
  • Trichomoniasis
    May cause pruritus, dysuria, and discharge in both men and women.
  • Genital herpes
    Characterised by painful vesicular lesions, dysuria, and flu-like symptoms.
618
Q

How is chlamydia diagnosed?

A

Nucleic acid amplification tests (NAAT). Which can involve a:

  • Vulvovaginal swab
  • Endocervical swab
  • First-catch urine sample (in women or men)
  • Rectal swab (after anal sex)
  • Pharyngeal swab (after oral sex)
619
Q

What is the management of uncomplicated Chlamydia (not in pregnancy)?

A

First Line - doxycycline 100mg twice a day for 7 days

620
Q

What is the management of Chlamydia during pregancy?

A

Doxycycline is contraindicated in pregnancy and breastfeeding. Alternatives include:

  • Azithromycin 1g stat then 500mg once a day for 2 days
  • Erythromycin 500mg four times daily for 7 days
  • Erythromycin 500mg twice daily for 14 days
  • Amoxicillin 500mg three times daily for 7 days
621
Q

Should a test of cure be done after Chlamydia treatment?

A

No

Apart from in cases of:

  • Rectal Chlamydia
  • Pregnancy
  • when Symptoms persist
622
Q

What are the possible non-pregnancy related complications of Chlamydia?

A
  • Pelvic inflammatory disease
  • Chronic pelvic pain
  • Infertility
  • Epididymo-orchitis
  • Conjunctivitis - is usually as a result of sexual activity, when genital fluid comes in contact with the eye.
  • Lymphogranuloma venereum
  • Reactive arthritis
623
Q

What is the presentation of chlamydial conjunctivitis?

A

Symptoms last for longer than 2 weeks:

  • Chronic erythema
  • Irritation
  • Discharge

Most cases are unilateral

It occurs more frequently in young adults. It can also affect neonates with mothers infected with chlamydia.

624
Q

What is Lymphogranuloma venereum?
What are the stages?

A

It is a condition affecting the lymphoid tissue around the site of infection with chlamydia. It most commonly occurs in men who have sex with men.

  • Primary stage - Painless ulcer (primary lesion) that typically occurs on the penis in men, vaginal wall in women or rectum after anal sex.
  • Secondary stage - lymphadenitis (swelling, inflammation and pain in the lymph nodes infected with the bacteria). The inguinal or femoral lymph nodes may be affected.
  • Tertiary stage - inflammation of the rectum (proctitis) and anus. This leads to anal pain, change in bowel habit, tenesmus and discharge.
625
Q

What is the management of Lymphogranuloma venereum?

A

1st Line - Doxycycline 100mg twice daily for 21 days

626
Q

What is the definition of Syphilis?

A

Syphilis is a sexually transmitted infection caused by the spirochete bacterium Treponema pallidum.

627
Q

What causes a Syphilis infection?

A

As stated, its caused by the bacterium Treponema pallidum. It can be transmitted by:

  • Through direct contact with syphilis sores during sexual activity.
  • Vertical transmission from an infected mother to her unborn child, resulting in congenital syphilis
  • Intravenous drug use
  • Blood transfusions and other transplants
628
Q

What is the clinical presentation of Syphilis?

A

There are three stages of Syphilis:

Primary Syphilis

  • A painless genital ulcer (chancre). That spontaneously recovers within 3 – 8 weeks. The lesion is round, with an indurated base.
  • Local lymphadenopathy

Secondary Syphilis - Typically starts after the chancre has healed. (Or 4-10 weeks post-primary infection). Presents with:

  • Symmetrical maculopapular rash, often involving the palms, soles, and face.
  • Condylomata lata (grey wart-like lesions around the genitals and anus)
  • Low-grade fever
  • Lymphadenopathy
  • Alopecia (localised hair loss)
  • Oral lesions

Tertiary Syphilis - Can occur 20-40 years after the primary infection (in untreated patients). Presents with:

  • Gummatous lesions (gummas are granulomatous lesions that can affect the skin, organs and bones)
  • Aortic aneurysms
  • Neurosyphilis

Neurosyphilis - can occur at any stage if the infection reaches the central nervous system. Presents with:
* Headache
* Altered behaviour
* Dementia
* Tabes dorsalis (demyelination affecting the spinal cord posterior columns)
* Ocular syphilis (affecting the eyes)
* Paralysis
* Argyll-Robertson pupil

629
Q

What is the presentation of Syphilis in Neonates?

A

It can present shortly after birth or later in infancy with:

  • blunted upper incisor teeth (Hutchinson’s teeth), ‘mulberry’ molars
  • rhagades (linear scars at the angle of the mouth)
  • keratitis
  • saber shins
  • saddle nose
  • deafness
630
Q

What is an Argyll-Robertson pupil?

A
  • It is a specific finding in neurosyphilis.
  • It is a constricted pupil that accommodates when focusing on a near object but does not react to light.
  • They are often irregularly shaped.
  • It is commonly called a “prostitutes pupil” due to the relation to neurosyphilis and because “it accommodates but does not react“.
631
Q

What are the investigations for Syphilis?

A

Different types of Serological testing is used for screening and monitoring, and then for confirmation of the diagnosis:

  • Screening and Monitorring - Non-treponemal tests (e.g., VDRL, RPR)
  • Diagnostic - treponemal tests (e.g., EIA, TPPA, FTA-ABS)
  • Dark-field microscopy: Can be used to directly observe T. pallidum in samples from primary lesions or secondary rash.
  • CSF examination: Should be considered in tertiary syphilis to evaluate for CNS involvement.
632
Q

What is the management of Syphilis?

A

Primary, secondary, and early latent syphilis:
* A single dose of intramuscular penicillin G (benzathine benzylpenicillin) is the first-line therapy.

Tertiary and late latent syphilis or syphilis of unknown duration:
* Requires a longer course of intramuscular penicillin G for 2-3 weeks.

Neurosyphilis:
* Treated with intravenous penicillin G for 10-14 days
* Patients allergic to penicillin may be given doxycycline or tetracycline.

633
Q

What is the definition of Bacterial Vaginosis?

A

Bacterial vaginosis is a bacterial imbalance of the vagina caused by an overgrowth of anaerobic bacteria and a loss of lactobacilli (the dominant bacterial species responsible for maintaining an acidic vaginal pH).

It is not a sexually transmitted infection but it increases the risk of developing an STI

634
Q

What is the pathophysiology of Bacterial Vaginosis?

A
  • Lactobacilli are the main component of the healthy vaginal bacterial flora. These bacteria produce lactic acid that keeps the vaginal pH low (under 4.5).
  • The acidic environment prevents other bacteria from overgrowing.
  • When there are reduced numbers of lactobacilli in the vagina, the pH rises. This more alkaline environment enables anaerobic bacteria to multiply.
635
Q

What are the most common anaerobic bacteria associated with bacterial vaginosis?

A
  • Gardnerella vaginalis (most common)
  • Mycoplasma hominis
  • Prevotella species

Bacterial vaginosis can occur alongside STIs like candidiasis, chlamydia and gonorrhoea.

636
Q

What is the epidemiology of Bacterial Vaginosis?

A

It is the most common cause of abnormal vaginal discharge in women of childbearing age.

637
Q

What are the risk factors of Bacterial Vaginosis?

A
  • Multiple sexual partners (although it is not sexually transmitted)
  • Excessive vaginal cleaning (douching, use of cleaning products and vaginal washes)
  • Recent antibiotics
  • Smoking
  • Copper coil
  • Pregnant women are at increased risk of bacterial vaginosis due to hormonal changes.

Bacterial vaginosis occurs less frequently in women taking the combined pill or using condoms effectively.

638
Q

What is the presentation of Bacterial Vaginosis?

A
  • fishy-smelling watery grey or white vaginal discharge (fishy smelling particularly after intercourse)
  • Increased vaginal discharge
  • Vaginal itching or irritation may be present but is less common

Half of women are asymptomatic

639
Q

What are some differentials for Bacterial Vaginosis?

A
  • Vulvovaginal Candidiasis
    Characterised by itching, burning, dyspareunia, and white, curd-like discharge.
  • Trichomonas Vaginalis Infection
    Presents with purulent, frothy, greenish discharge, pruritus, dyspareunia, and dysuria.
  • Chlamydia or Gonorrhoea infection
    May present with increased vaginal discharge and possibly lower abdominal pain, but are often asymptomatic.
  • Atrophic Vaginitis
    Most commonly seen in postmenopausal women, presenting with dryness, burning, dyspareunia, and thin, watery discharge.
640
Q

How is Bacterial Vaginosis diagnosed?

A

The Amsel Criteria - Three out of the following 4 features need to be present:

  • Vaginal pH >4.5 (Vaginal swab with pH paper)
  • Homogenous grey or milky discharge
  • Positive whiff test (addition of 10% potassium hydroxide produces a fishy odour)
  • Clue cells present on wet mount (Microsopy)
641
Q

What is the management of Bacterial Vaginosis?

A
  • First line treatement - Metronidazole is given either orally(5-7/7) or intravaginally.
  • Second line management - Clindamycin
  • Asymptomatic BV does not usually require treatment

You should also assess for the risk of STIs, as well as providing education about how to reduce the risk of recurrence.

642
Q

What do patients on Metronidazole need to avoid?

A

Alcohol

This is because alcohol and metronidazole can cause a “disulfiram-like reaction”, with nausea and vomiting, flushing and sometimes severe symptoms of shock and angioedema.

643
Q

What are the possible complications of Bacterial Vaginosis?

A

Increase the risk of catching sexually transmitted infections, including chlamydia, gonorrhoea and HIV.

During Pregnancy:

  • Miscarriage
  • Preterm delivery
  • Premature rupture of membranes
  • Chorioamnionitis
  • Low birth weight
  • Postpartum endometritis
644
Q

What is the definition of Trichomoniasis?

A

Trichomoniasis is a sexually transmitted infection (STI) caused by the flagellated protozoan parasite, Trichomonas vaginalis.

It primarily infects the urogenital tract, and has an incubation period of around 7 days.

645
Q

What is the epidemiology of Trichomoniasis?

A

It is the most common non-viral STI globally.

646
Q

What is the clinical presentation of Trichomoniasis?

A

Women:

  • Profuse, frothy, yellow-green vaginal discharge
  • Vulval irritation
  • Dyspareunia (painful sex)
  • Asymptomatic presentation is also common (up to 50%)
  • Strawberry Cervix sign may be seen on examination
  • The vaginal pH will be raised (above 4.5) similar to bacterial vaginosis

Men

  • Non-gonococcal urethritis
  • Balanitis (inflammation to the glans penis)
  • Also commonly asymptomatic
647
Q

What can Trichomonas increase the risk of?

A
  • Contracting HIV by damaging the vaginal mucosa
  • Bacterial vaginosis
  • Cervical cancer
  • Pelvic inflammatory disease
  • Pregnancy-related complications such as preterm delivery or low birth weight baby.
648
Q

What investigations are done for Trichomonas?

A
  • Diagnostic - Charcoal swab with microscopy
    This should be taken from the posterior fornix of the vagina (behind the cervix)
  • Urethral swab or first catch urine is used in men
649
Q

What are some differentials for Trichomonas?

A
  • Bacterial vaginosis
    Characterized by a fishy-smelling, grayish-white vaginal discharge and vaginal pH > 4.5
  • Candidiasis
    Presenting with a thick, white, “cottage cheese” like vaginal discharge and vulval itching
  • Gonorrhea or Chlamydia
    These STIs may present with mucopurulent cervical discharge, cervical motion tenderness, and may also be asymptomatic.
650
Q

What is the management of Trichomonas?

A

Oral metronidazole
Either 400–500mg twice a day for 5–7 days, or a single dose of 2g orally.

Its advised to abstain from sexual activity for at least one week, or until the patient and all partners have completed treatment.

651
Q

What is the definition of a Urinary Tract Infection?

A

Lower Urinary Tract Infection - Involves infection of the bladder, causing cystitis.
Upper Urinary Tract Infection - Involves infection up to the kidneys, called pyelonephritis.

652
Q

What is the relationship between Pregancy and UTIs?

A

Pregnant women are at higher risk of developing both lower and upper UTIs

UTIs during pregnancy increase the risk of:

  • Preterm delivery
  • As well as other adverse pregnancy outcomes, like low birth weight and pre-eclampsia.
653
Q

What is Asymptomatic Bacteriuria?

A
  • Asymptomatic bacteriuria refers to bacteria present in the urine, without symptoms of infection.
  • Pregnant women with asymptomatic bacteriuria are at a higher risk of developing UTIs, and subsequently at risk of preterm birth.
  • As a result, pregnant women are tested at booking and routinely throughout pregnancy (urine sample testing for microscopy, culture & sensitivity).
  • Urine testing of asymptomatic patients is not usually done (as it can lead to unescesary antibiotic use) but pregnant women are the exception due to the adverse outcomes associated with infection.
654
Q

What is the presentation of a lower UTI?

A
  • Dysuria (pain, stinging or burning when passing urine)
  • Suprapubic pain or discomfort
  • Increased frequency of urination
  • Urgency
  • Incontinence
  • Haematuria
655
Q

What is the presentation of an upper UTI (Pylonephritis)?

A
  • Fever (more prominent than in lower urinary tract infections)
  • Loin, suprapubic or back pain (this may be bilateral or unilateral)
  • Looking and feeling generally unwell
  • Vomiting
  • Loss of appetite
  • Haematuria
  • Renal angle tenderness on examination
656
Q

What investigation is routinely done in pregnant women to diagnose UTIs?

A
  • Mid-stream urine samples are sent off for cultures and sensitivity testing.
657
Q

What other investigations can be useful for investigating a UTI?

A
  • Mid-stream urine (as stated above) - In children, men and pregnant women
  • Urine Dipstick will be positive for nitrates and leukocytes (although this is unreliable in women older than 65 and those who are catheterised)
  • Blood tests if there are signs of systemic upset (FBC, U+E, and CRP, etc…)
  • Ultrasound scan of bladder/kidney (if there is concern about antecedents/complications (e.g.urinary retention/obstruction)
658
Q

What are the most common causative organisms of UTIs?

A
  • Escherichia coli (E. coli) (Most common)
  • Klebsiella pneumoniae (gram-negative anaerobic rod)
  • Enterococcus
  • Pseudomonas aeruginosa
  • Staphylococcus saprophyticus
  • Candida albicans (fungal)
659
Q

What is the management of UTIs in pregnancy?

A

Urinary tract infection in pregnancy requires 7 days of antibiotics

  • First Line - Nitrofuratoin for 7 days (although this needs to be avoided in the 3rd trimester)
  • Second Line - If nitrofuratoin is unsuitable then use Amoxicillin or Cefelexin for 7 days
660
Q

Why does Nitrofuratoin need to be avoided during the 3rd trimester of pregnancy?

A

As it is associated with an increased a risk of neonatal haemolysis (destruction of the neonatal red blood cells).

661
Q

Trimethoprim is a common alternative first line antibiotic for treatment of UTIs. Why can it not be given in pregnant women (especially in the first trimester)?

A

This is because it works as a folate antagonist. Folate is important in early pregnancy for the normal development of the fetus.

Trimethoprim in early pregnancy can cause congenital malformations, particularly neural tube defects (i.e. spina bifida). It is not known to be harmful later in pregnancy, but is generally avoided unless necessary.

662
Q

What can occur if a pregnant woman becomes infected with the Varicella zoster virus (VZV)?

A

If a non-immune woman contracts the varicella zoster virus (VZV) during the first trimester of her pregnancy, it can cause Congenital varicella syndrome in the foetus (as the virus can have teratogenic effects).

663
Q

What is the management of VZV during pregancy?

A
  • If a non-immune pregnant woman comes into contact with a person infected with the VZV; immunoglobulin can be given as a preventive measure.
  • If maternal infection by VZV occurs, Acyclovir is the treatment of choice and should be administered within 24 hours of the onset of the rash.
  • Pregnant women who lack immunity to the VZV should be counseled to avoid exposure to the virus.
664
Q

What is the definition of Premature ovarian insufficiency (POI)?

A

Premature ovarian insufficiency (POI) is a medical condition characterized by the onset of menopause in a woman aged below 40 years.

665
Q

What can cause premature ovarian insufficiency?

A

The causes can either be idiopathic or iatrogenic e.g.:

  • ovarian surgery
  • radiotherapy or chemotherapy that directly impact the ovaries.
666
Q

What is the clinical presentation of Premature ovarian insufficiency?

A

Women with POI typically develop the same symptoms as those undergoing natural menopause, including:

  • Vasomotor symptoms:
    Hot flushes, night sweats
  • Sexual dysfunction:
    Vaginal dryness, reduced libido, problems with orgasm, dyspareunia
  • Psychological symptoms:
    Depression, anxiety, mood swings, lethargy, reduced concentration
667
Q

What are some differentials for Premature ovarian insufficiency?

A
  • Hypothyroidism:
    Fatigue, weight gain, cold intolerance, depression, hair loss
  • Hyperprolactinemia:
    Irregular menstrual cycles, infertility, breast milk production not related to childbirth or nursing
  • Polycystic Ovary Syndrome (PCOS):
    Irregular periods, hirsutism, obesity, infertility
668
Q

How is premature ovarian insufficiency diagnosed?

A
  • Blood test for raised FSH levels; indicative of the menopause (repeated on at least 2 separate occasions)
669
Q

What is the management of Premature ovarian insufficiency?

A

Hormone Replacement Therapy or COCP (HRT) until at least the age of normal menopause.

  • HRT is done, unless the risks of HRT outweigh the benefits
  • Psychological support should also be provided due to the potential mental health impacts of early menopause.
670
Q

What is the definition of Oligohydramnios?

A

Oligohydramnios is defined as the presence of a lower than normal volume of amniotic fluid within the uterus.

671
Q

What can cause Oligohydramnios?

A
  • premature rupture of membranes
  • Potter sequence (bilateral renal agenesis + pulmonary hypoplasia)
  • intrauterine growth restriction
  • post-term gestation
  • pre-eclampsia
672
Q

Was is the presentation of Oligohydramnios in the neonate?

A

Potter Syndrome which includes:

  • Bilateral Renal Agenesis
  • Clubbed feet, facial deformity, congenital hip dysplasia (Due to foetal compression)
  • Pulmonary hypoplasia (Due to lack of amniotic fluid)

Potter syndrome is largely the result of reduced ““space”” surrounding the fetus as well as the lack of amniotic fluid for fetal lung growth and development.

673
Q

What is the main differential for Oligohydramnios?

A

Polyhydramnios - which is an overabundance of amniotic fluid.

674
Q

How is Olighohydramnios diagnosed?

A

Diagnosis is made via ultrasound:

  • This will show a reduced amniotic fluid index (AFI) or single deepest pocket (SDP)
  • <500ml at 32-36 weeks
  • AFI <5th percentile
675
Q

What is the management of Oligohydramnios?

A

Management depends on the underlying aetiology; but options include:

  • Maternal rehydration
    This may help to increase the amniotic fluid volume in mild cases of oligohydramnios.
  • Amnioinfusion
    This is the infusion of saline into the amniotic cavity to increase the volume of amniotic fluid.
  • Delivery
    In severe cases, or if the fetus is in distress, delivery may be the best option. This may be via induction of labour or caesarean section, depending on the clinical scenario.
676
Q

What is the definition of Polyhydramnios?

A

Polyhydramnios is the presence of too much amniotic fluid within the uterus.

677
Q

What is the aetiology of polyhydramnios?

A

The causes of polyhydramnios can be split into causes due to excessive production of amniotic fluid or insufficient removal of amniotic fluid:

Execessive production is caused by increased foetal urination which can be due to:

  • Maternal diabetes mellitus
  • Foetal renal disorders
  • Foetal anaemia
  • Twin-to-twin transfusion syndrome

Insufficient removal is caused by reduced foetal swallowing which can be due to:

  • Oesophageal or duodenal atresia
  • Diaphragmatic hernia
  • Anencephaly
  • Chromosomal disorders
678
Q

What is the clinical presentation of polyhydramnios?

A
  • A uterus that feels tense or is large for the date of gestation
  • Difficulty of feeling foetal parts upon palpation of the abdomen.
679
Q

What possible maternal complications can polyhydramnios cause?

A

Maternal complications:

  • Maternal respiratory compromise due to increased pressure on the diaphragm
  • Increased risk of urinary tract infections due to increased pressure on the urinary system
  • Worsening of other symptoms associated with pregnancy such as gastro-oesophageal reflux, constipation, peripheral oedema and stretch marks
  • Increased incidence of caesarean section delivery
  • Increased risk of amniotic fluid embolism (although this is rare)
680
Q

What possible foetal complications can polyhydramnios cause?

A

Foetal complications:

  • Pre-term labour and delivery
  • Premature rupture of membranes
  • Placental abruption
  • Malpresentation of the foetus (the foetus has more space to “move” within the uterus)
  • Umbilical cord prolapse (polyhydramnios can prevent the foetus from engaging with the pelvis, thus leaving room for the cord to prolapse out of the uterus before the presenting part)
681
Q

What is the management of polyhydramnios?

A
  • Management of the underlying cause (e.g. maternal diabetes)
  • Amnio-reduction in severe cases of polyhydramnios
682
Q

What is the definition of Malpresentation?

A

This is when the foetus is in a different orientation other than facing head-first down the pelvic inlet as birth approaches.

683
Q

What is the definition of foetal presentation?

A

Fetal presentation is the orientation of the fetus in the womb that determines which part of the fetus presents first at the pelvic inlet during childbirth.

684
Q

What is the most common (and safest) foetal presentation?

A

Cephalic Vertex presentation

Makes up 95% of pregnancies

685
Q

What is the most common type of malpresentation?

A

Breech Presentation - Refers to the positioning of the fetus in a longitudinal lie with the buttocks or feet proximal to the cervix and the head near the fundus.

686
Q

What is the epidemiology of malpresentations?

A

Around 20% of babies are in breech presentation at 28 weeks gestation. But the vast majority of these revert to a cephalic presentation spontaneously, and only 3% are breech at term.

Other types of malpresentation (e.g. shoulder) are much rarer than breech presentations.

687
Q

What are the 3 different types of Breech presentation?

A
  • Complete (flexed) breech – both legs are flexed at the hips and knees (fetus appears to be sitting ‘crossed-legged’).
  • Frank (extended) breech – both legs are flexed at the hip and extended at the knee. This is the most common type of breech presentation.
  • Footling breech – one or both legs extended at the hip, so that the foot is the presenting part.
688
Q

What are the risk factors for a Breech presentation?

A

Uterine:

  • Multiparity
  • Uterine malformations (e.g. septate uterus)
  • Fibroids
  • Placenta praevia

Foetal:

  • Prematurity
  • Macrosomia
  • Polyhydramnios (raised amniotic fluid index)
  • Twin pregnancy (or higher order)
  • Abnormality (e.g. anencephaly)
689
Q

What is the clinical presentation of a Breech presentation?

A

It is usually identified upon clinical examination:

  • Upon palpation of the abdomen the round fetal head will be felt in the upper part of the uterus, and an irregular mass (fetal buttocks and legs) in the pelvis.
  • The foetal heart may be auscultated higher on the maternal abdomen than usual
  • Sometimes it’s not diagnosed until labour, where it can present with signs of foetal distress such as meconium-stained liquor.

Diagnosis of Breech presentation is of limited clinical significance before 32-35 weeks gestation; as most likely the foetus will revert to cephalic presentation by birth.

690
Q

How is Breech presentation diagnosed?

A

Ultrasound Scan

691
Q

What are some differentials for a breech presentation?

A
  • Oblique lie
    The fetus is positioned diagonally in the uterus, with the head or buttocks in one iliac fossa.
  • Transverse lie
    The fetus is positioned across the uterus, with the head on one side of the pelvis and the buttocks on the other. The shoulder is usually the presenting part.
  • Unstable lie
    This is where the presentation of the fetus changes from day-to-day.
692
Q

What is the management of a breech presentation?

A
  • External Cephalic Version (ECV)
    This is the is the manipulation of the fetus to a cephalic presentation through the maternal abdomen. It is offered to primiparous women at 36 weeks, and to multiparous women at 37 weeks. There is a 50% success rate (40% in primiparous, 60% in multiparous); and if successful, it can enable an attempt at vaginal delivery.
  • Caesarean Section
    If ECV is unsuccessful, contraindicated, or declined by the woman, current UK guidelines advise an elective Caesarean delivery.
  • Vaginal Breech Birth
    Some women may still choose to aim for a vaginal breech delivery. A footling breech is contraindicated however as the feet and legs can slip through a non-fully dilated cervix, and the shoulders or head can then become trapped.
693
Q

What are the possible complications for an ECV?

A
  • Transient fetal heart abnormalities (which revert to normal),
  • Persistent heart rate abnormalities (e.g fetal bradycardia)
  • Placental abruption.
694
Q

What are the complications of a breech presentation?

A
  • Cord prolapse - where the umbilical cord drops down below the presenting part of the baby, and becomes compressed. This occurs in 1% of breech presentations (Compared to 0.5% in cephalic presentations)

Less common:

  • Fetal head entrapment
  • Premature rupture of membranes
  • Birth asphyxia – usually secondary to a delay in delivery.
  • Intracranial haemorrhage – as a result of rapid compression of the head during delivery.
695
Q

What is the definition of Cephalopelvic disproportion?

A

Cephalopelvic disproportion occurs when there is mismatch between the size of the fetal head and size of the maternal pelvis, resulting in “failure to progress” in labor for mechanical reasons.

This is a significant risk factor for post term pregnancies

696
Q

What is the definition of a Uterine Rupture?

A
  • Uterine rupture is a complication of labour, where the muscle layer of the uterus (myometrium) ruptures.
  • Uterine rupture leads to significant bleeding. The baby may be released from the uterus into the peritoneal cavity. It has a high morbidity and mortality for both the baby and mother.
697
Q

What are the types of Uterine Rupture?

A

There are two types:

  • Incomplete (or uterine dehiscence) rupture - The uterine serosa (perimetrium) surrounding the uterus remains intact.
  • Complete rupture - The serosa ruptures along with the myometrium, and the contents of the uterus are released into the peritoneal cavity.
698
Q

What are the risk factors for uterine rupture?

A
  • Previous Caesarean section (The most significant)
  • Vaginal birth after caesarean (VBAC)
  • Previous uterine surgery
  • Increased BMI
  • High parity
  • Increased age
  • Induction of labour
  • Use of oxytocin to stimulate contractions
699
Q

Why does a previous caesarian section increase the risk of a uterine rupture?

A
  • The scar on the uterus becomes a point of weakness, and may rupture with excessive pressure (e.g. excessive stimulation by oxytocin).
  • It is extremely rare for uterine rupture to occur in a patient that is giving birth for the first time.
700
Q

What is the clinical presentation of uterine rupture?

A

It presents with an acutely unwell mother. It may occur with induction or augmentation of labour with:

  • Abdominal pain
  • Vaginal bleeding
  • Ceasing of uterine contractions
  • Hypotension
  • Tachycardia
  • Collapse
701
Q

What are some differentials of uterine rupture?

A
  • Placental abruption
    Presents with abdominal pain +/- vaginal bleeding. The uterus is often described ‘woody’ and tense on palpation.
  • Placenta praevia
    Typically causes a painless vaginal bleeding.
  • Vasa praevia
    Characterised by a triad of ruptured membranes, painless vaginal bleeding, and fetal bradycardia.
702
Q

What investigations are done to diagnose a uterine rupture?

A
  • Intrapartum Cardiotocography (first line) - It is continuous recording of the fetal heart rate obtained via an ultrasound transducer placed on the mother’s abdomen. Changes in fetal heart rate pattern and prolonged fetal bradycardia are early indicators for uterine rupture.
  • Ultrasound - Is diagnostic; features include abnormal fetal lie or presentation, haemoperitoneum and absent uterine wall.
703
Q

What is the management of a uterine rupture?

A
  • Uterine rupture is an obstetric emergency.
  • Resuscitation and transfusion may be required.
  • Emergency caesarean section is necessary to remove the baby, stop any bleeding and repair or remove the uterus (hysterectomy).
704
Q

What is the definition of Preterm (or Premature) Labour?

A
  • Preterm Labour - The onset of regular uterine contractions accompanied by cervical changes occurring before 37 weeks gestation.
  • Preterm Birth - The delivery of a baby after 20 weeks gestation but before 37 weeks gestation.

Prematurity is classed as:

  • Under 28 weeks: extreme preterm
  • 28 – 32 weeks: very preterm
  • 32 – 37 weeks: moderate to late preterm
705
Q

What is the clinical presentation of Preterm labour?

A

Regular uterine contractions, changes in cervical effacement or dilation (before 37 weeks gestation)

706
Q

What are some conditions associated with Preterm labour and delivery?

A
  • Overstretching of the uterus
    Multiple pregnancy (commonly due to assisted conception) and polyhydramnios.
  • Foetal risk conditions
    Pre-eclampsia, intrauterine growth restriction, placental abruption.
  • Uterus or cervical problems
    Fibroids, congenital uterine malformation, short or weak cervix, previous uterine or cervical surgery.
  • Infections
    Chorioamnionitis, maternal or neonatal sepsis, bacterial vaginosis, trichomoniasis, Group B Streptococcus, sexually transmitted infections (e.g., Chlamydia), and recurrent urinary tract infections.
  • Maternal co-morbidity
    Hypertension, diabetes, renal failure, thyroid disease, etc.
707
Q

What are some differentials for Preterm Labour?

A
  • Braxton Hicks contractions
    Characterized by irregular, non-painful contractions that do not cause cervical dilation or effacement.
  • Urinary tract infection
    Presents with dysuria, frequency, suprapubic pain, and possibly preterm labour symptoms.
  • Placental abruption
    Presents with vaginal bleeding, abdominal pain, and hypertonic uterus.
  • Uterine rupture
    Signs include severe abdominal pain, vaginal bleeding, abnormal fetal heart rate, and cessation of contractions.
708
Q

What investigations can be done when Preterm labour starts?

A

Foetal fibronectin test (fFN test) - is a screening test used to assess the risk of preterm delivery after the onset of pre-term labour.

A negative fFN test indicates a low risk of delivery occurring within the next 7-14 days.

709
Q

What does the management of a Preterm labour involve?

A
  • Corticosteroids - (2 doses IM betamethasone or dexamethasone) should be administered to accelerate foetal lung maturation.
  • Intravenous antibiotics - if there is an increased risk of infection (evidence of Group B Streptococcus (GBS) in current or previous pregnancy, presence of maternal fever). (Penicillin is the antibiotic of choice if there is no allergy).
  • Tocolytic agents may be considered to delay labour, .
    (Nifedipine is the first-line tocolytic agent).
  • Magnesium Sulphate IV to protect fetal brain given within 24 hours of delivery in preterm babies <34 weeks gestation
710
Q

What is the definition of Premature Rupture of the membranes (PROM)?

A
  • PROM is a condition characterized by the rupture of the amniotic membranes (or sac) before the onset of labour.
  • If this occurs after 37 weeks gestation, it is know as premature rupture of the membranes at term.
  • If this occurs before 37 weeks however, it’s known as Preterm prelabour rupture of membranes (P‑PROM).
  • Most women with PROM at term will spontaneously start labour within 24 hours.
711
Q

What causes Premature Rupture of the membranes?

A

Exact cause isn’t well understood; but can be due to a combination of:

  • Infection: Chorioamnionitis
  • Inflammation
  • Stress
  • Mechanical forces.
712
Q

What is the clinical presentation of Premature rupture of the membranes?

A
  • Foul-smelling or greenish amniotic fluid
  • Maternal fever
  • Reduced foetal movements

A digital vaginal examination should be avoided in the absence of labour. But the foetal heart should be monitored.

713
Q

What are some differentials for premature rupture of the membranes?

A
  • Urinary incontinence
    This can be distinguished by the absence of amniotic fluid and the presence of urinary symptoms.
  • Vaginal discharge or infection
    This can be ruled out by the absence of foul-smelling or greenish discharge and the absence of other infection symptoms.
714
Q

What investigations are done for premature rupture of the membranes?

A

Investigations for PROM should focus on assessing signs of infection and foetal distress, including:

  • Monitoring maternal temperature
  • Assessing foetal movements
  • Monitoring foetal heart rate
  • Observing vaginal discharge
715
Q

What is the management of premature rupture of the membranes?

A
  • If labour does not commence within 24 hours, induction of labour should be offered.
  • If there are any signs of infection, immediate induction of labour should be commenced under consultant guidance and a broad spectrum antibiotic should be given.
  • If there are any signs of foetal compromise, senior review is required to make a decision about whether immediate caesarean section is required.
  • Following delivery, even if both baby and mother are asymptomatic, they should be closely observed in hospital for 12 hours post-birth.
716
Q

What are some complications of premature rupture of the membranes?

A
  • Chorioamnionitis - due to ascending infection
  • Preterm birth - (and the associated complications) e.g. respiratory distress syndrome, necrotising enterocolitis, and foetal death
  • Developmental problems - E.g. pulmonary hypoplasia, facial and limb deformities due to compression in the uterus, and cord prolapse due to low levels of amniotic fluid.
717
Q

What are the investigations to confirm Preterm Prelabour Rupture of Membranes (PPROM)?

A

Sterile Speculum Examination: look for pooling of amniotic fluid in posterior vaginal vault.

Digital examination Should be avoided due to risk of infection

Second Line: Fluid testing for:

  • Insulin Like Growth Factor Binding Protein (IGFBP-1)
  • Placental alpha microglobulin-1 protein (PAMG-1)

Ultrasound scan may show oligohydramnios

718
Q

What is the management for PPROM?

A

Prophylactic Antibiotics: TDS 250mg Erythromycin for 10 days or until labour established

Induction of labour may be offered from 34 weeks but try to get to 37 weeks.

719
Q

What is the definition of Umbilical cord prolapse?

A
  • Cord prolapse is when the umbilical cord descends below the presenting part of the foetus and through the cervix into the vagina, after rupture of the fetal membranes.
  • There is a significant danger of the presenting part compressing the umbilical cord, resulting in fetal hypoxia.
720
Q

What are the risk factors of Cord Prolapse?

A
  • Abnormal presentations e.g. Breech, transverse lie
  • Prematurity
  • Multiparity
  • Polyhydramnios
  • Twin pregnancy
  • Cephalopelvic disproportion
  • Low birth weight (SGA)
721
Q

What is the clinical presentation of Cord Prolapse?

A
  • Sudden change in the fetal heart rate pattern, particularly variable or prolonged decelerations.
  • Feeling of the cord in the vagina or visible cord after rupture of membranes
  • Abnormal fetal heart rate detected on cardiotocography
722
Q

How is a Cord prolapse diagnosed?

A
  • Cardiotocography - Umbilical cord prolapse should be suspected when there are signs of foetal distress on CTG.
  • Vaginal examination - Can then be used to diagnose a prolapsed cord (by confirming the presence of the umbilical cord in the birth canal)
723
Q

What is the management of a Cord prolapse?

A

When cord prolapse is diagnosed, swift action is vital to prevent fetal hypoxia and death:

  • Emergency C-section
  • Presenting part of the fetus may be pushed back into the uterus to avoid compression
  • If the cord is past the level of the introitus, there should be minimal handling and it should be kept warm and moist to avoid vasospasm
  • Patient goes onto all fours until C-section. Left lateral position may also be used.
  • Tocolytics (Terbutaline) may be used to reduce uterine contractions
  • Retrofilling the bladder with 500-700ml of saline may be helpful as it gently elevates the presenting part
724
Q

What is the definition of an Instrumental Delivery?

A

Instrumental delivery refers to a vaginal delivery assisted by either a ventouse suction cup or forceps.

These tools are used to help in the delivery of the baby’s head.

725
Q

What percentage of births are done by Instrumental Delivery?

A

10% of UK Births

726
Q

What are the indications to perform an instrumental delivery?

A
  • Failure to progress
  • Foetal distress
  • Maternal exhaustion
  • Control of the head in various fetal positions
  • The use of an epidural for analgaesia, increases the risk that an instrumental delivery may be nescesary.
727
Q

What are the maternal risks of an instrumental delivery?

A
  • Postpartum haemorrhage
  • Episiotomy
  • Perineal tears
  • Injury to the anal sphincter
  • Incontinence of the bladder or bowel
  • Nerve injury (obturator or femoral nerve)
728
Q

What are the foetal risks of an instrumental delivery?

A
  • Cephalohaematoma with ventouse
  • Facial nerve palsy with forceps

Rarer (more serious complications):

  • Subgaleal haemorrhage (most dangerous)
  • Cerebral Palsy
  • Intracranial haemorrhage
  • Skull fracture
  • Spinal cord injury
729
Q

What is a Ventouse?

A
  • It is essentially a suction cup on a cord.
  • It goes on the baby’s head, and the doctor or midwife applies careful traction to the cord to help pull the baby out of the vagina.
  • Its main complication is a cephalohaematoma - Which involves a collection of blood between the skull and the periosteum.
730
Q

How are forceps used in an instrumental delivery?

A
  • The forceps come as two pieces of curved metal that attach together, go either side of the baby’s head and grip the head in a way that allows the doctor or midwife to apply careful traction and pull the head from the vagina.
  • Main complication is facial nerve palsy, with facial paralysis on one side.
  • The forceps can also cause bruises on the baby’s face
731
Q

What are the 2 nerves in the mother most commonly injured in an instrumental delivery?

A
  • Femoral nerve
  • Obturator nerve

The nerve injury tends to recover over 6 – 8 weeks.

732
Q

How can the femoral nerve be injured during instrumental delivery?

A

The Femoral nerve can be compressed against the inguinal canal during a forceps delivery resulting in nerve injury.

733
Q

What is the clinical presentation of a Femoral Nerve injury?

A
  • Weakness of knee extension
  • Loss of the patella reflex
  • Numbness of the anterior thigh and medial lower leg.
734
Q

How can the Obturator nerve be injured during instrumental delivery?

A

The obturator nerve may be compressed by forceps during instrumental delivery or by the fetal head during normal delivery.

735
Q

What is the clinical presentation of a Obturator Nerve injury?

A
  • Weakness of hip adduction and rotation
  • Numbness of the medial thigh
736
Q

What is the definition of Shoulder Dystocia?

A
  • Shoulder dystocia is a specific type of obstructed labour where the anterior shoulder of the baby becomes stuck behind the pubic symphysis of the pelvis, after the head has been delivered.
  • This is an obstectric emergency
737
Q

What are the risk factors for Shoulder Dystocia?

A
  • Maternal gestational diabetes
  • Macrosomia
  • Birthweight >4kg
  • Advanced maternal age
  • Maternal short stature or small pelvis
  • Maternal obesity
  • Post-dates pregnancy
738
Q

What is the clinical presentation of Shoulder Dystocia?

A
  • Difficult delivery of the foetal face or chin
  • Retraction of the foetal head back into the vagina, after its been delivered (turtle-neck sign)
  • Failure of restitution - where the head remains face downwards (occipito-anterior) and does not turn sideways as expected after delivery of the head.
  • Failure of descent of the foetal shoulders following delivery of the head.
739
Q

What is the management of Shoulder Dystocia?

A

Its an Obstetric emergency that needs prompt intervention to deliver the baby. There are various manouvres to help with this:

  • Call for Senior Help
  • McRoberts manoeuvre
  • Pubic Symphysis Pressure

An episiotomy can be used to enlarge the vaginal opening and reduce the risk of perineal tears. But this isn’t always nescesary.

Other Manouvres

  • Rubins manoeuvre
  • Wood’s screw manoeuvre
  • Zavanelli manoeuver
740
Q

What’s involved in a McRoberts manoeuvre?

A

It involves hyperflexion of the mother at the hip (bringing her knees to her abdomen). This provides a posterior pelvic tilt, lifting the pubic symphysis up and out of the way.

741
Q

What’s involved in a Rubins manoeuvre?

A

It involves reaching into the vagina to put pressure on the posterior aspect of the baby’s anterior shoulder to help it move under the pubic symphysis.

742
Q

What’s involved in a Wood’s Screw Manouvre?

A

It is performed during a Rubins manoeuvre. The other hand is used to reach in the vagina and put pressure on the anterior aspect of the posterior shoulder. The top shoulder is pushed forwards, and the bottom shoulder is pushed backwards, rotating the baby and helping delivery.

743
Q

What’s involved in a Zavanelli Manouvre?

A

It involves pushing the baby’s head back into the vagina so that the baby can be delivered by emergency caesarean section.

744
Q

What are the main complications of Shoulder Dystocia?

A

Maternal

  • Postpartum haemorrhage
  • Perineal tears

Fetal

  • Brachial plexus injury
  • Neonatal death
745
Q

What is the definition of Placenta accreta?

A
  • Placenta accreta refers to when the placenta implants deeper than usual onto the myometrium.
  • It is referred to as placenta accreta spectrum, as there is a spectrum of severity in how deep and broad the abnormal implantation extends.
  • it is due to defective decidua basalis
746
Q

What are the 3 severities of the Placenta Accreta Spectrum?

A
  • Superficial placenta accreta - is where the placenta implants in the surface of the myometrium, but not beyond
  • Placenta increta - is where the placenta attaches deeply into the myometrium
  • Placenta percreta - is where the placenta invades past the myometrium and perimetrium, potentially reaching other organs such as the bladder.
747
Q

What are the risk factors for the placenta accreta spectrum?

A
  • Previous C-Section
  • Previous placenta previa
  • Previous termination of pregnancy
  • Dilatation and curettage
  • Advanced maternal age
  • Low lying placenta or placenta praevia
  • Uterine structural defects
748
Q

What is the pathophysiology of placenta accreta?

A

Defective Decidua Basalis

This deep implantation makes it very difficult for the placenta to separate during delivery, leading to extensive bleeding (postpartum haemorrhage).

749
Q

What is the presentation of placenta accreta?

A
  • It typically doesn’t cause any symptoms during pregnancy.
  • It can present with bleeding (antepartum haemorrhage) in the third trimester.
  • It may be diagnosed at birth, when it becomes difficult to deliver the placenta. It can cause significant postpartum haemorrhage.
750
Q

How is placenta accreta diagnosed?

A

Ideally it is diagnosed before birth with an Antenatal Ultrasound

751
Q

What are the possible complications of placenta accreta?

A
  • Severe Postpartum Haemorrhage
  • Preterm delivery
  • Uterine rupture.
752
Q

What is the management of placenta accreta?

A
  • Elective Ceesarian Section with hysterectomy is the safest management option.

If preserving the patient’s fertility is important to them, then the following can be attempted alongside the C-Section:

  • Uterus preserving surgery, with resection of part of the myometrium along with the placenta
  • Expectant management, leaving the placenta in place to be reabsorbed over time. But this comes with a significant risk of bleeding and infection.
753
Q

What is the definition of Placenta Praevia?

A
  • It’s defined as the placenta overlying the cervical os.
  • This means that the placenta is attached in the lower portion of the uterus; lower than the presenting part of the fetus.
754
Q

What is the difference between a Low lying placenta and Placenta Praevia?

A
  • Low-lying placenta - Is used when the placenta is within 20mm of the internal cervical os
  • Placenta praevia - Is used only when the placenta is over the internal cervical os

NOTE
A 4 stage grading system used to be used, but it’s now considered outdated.

755
Q

What are the complications of Placenta Praevia?

A

It’s associated with increased morbidity and mortality for both the mother and fetus. Risks include:

  • Antepartum haemorrhage
  • Emergency caesarean section
  • Emergency hysterectomy
  • Maternal anaemia and transfusions
  • Preterm birth and low birth weight
  • Stillbirth
756
Q

What are the 3 causes of Antepartum Haemorrhage?

A
  • Placenta praevia
  • Placental abruption
  • Vasa praevia
757
Q

What are the risk factors for Placenta Praevia?

A
  • Previous caesarean sections
  • Previous placenta praevia
  • Older maternal age
  • Multiparity
  • Maternal smoking
  • Structural uterine abnormalities (e.g. fibroids)
  • Assisted reproduction (e.g. IVF)
758
Q

What is the clinical presentation of Placenta Praevia?

A
  • Bright red painless vaginal bleeding.
  • shock in proportion to visible loss
  • no pain
  • uterus not tender
  • lie and presentation may be abnormal
  • fetal heart usually normal
  • coagulation problems rare
  • small bleeds before large
759
Q

How is Placenta Praevia diagnosed?

A

1st Line: Transvaginal Ultrasound scan

  • placenta praevia is often picked up on the routine 20 week abdominal ultrasound

Digital vaginal examination should not be performed before an ultrasound as it may provoke a severe haemorrhage

760
Q

What is the management of Placenta Praevia?

A
  • Repeat TVUS at 32 weeks and 36 weeks to guide delivery decisions
  • Give Corticosteroids between 34-36 weeks of gestation (to mature the foetal lungs, given the increased risk of preterm labour)
  • Planned cesarean section is adviced between 36 and 37 weeks gestation. (Its planned early to reduce the risk of spontaneous labour and bleeding).
  • In cases were premature labour or where antenatal bleeding occurs; an emergency Cesarean section will be required.
761
Q

What would the management of bleeding as a result of Placenta Praevia involve?

A
  • Emergency caesarean section
  • Blood transfusions
  • Intrauterine balloon tamponade
  • Uterine artery occlusion
  • Emergency hysterectomy
762
Q

What is the definition of Placental Abruption?

A
  • Placental abruption is the premature separation of the placenta from the uterine wall during pregnancy.
  • The site of attachment can bleed extensively after the placenta separates. Resulting in significant Maternal Antepartum Haemorrhage.
763
Q

What are the risk factors for Placental Abruption?

A

ABRUPTION:
A for Abruption previously;
B for Blood pressure (i.e. hypertension or pre-eclampsia);
R for Ruptured membranes, either premature or prolonged;
U for Uterine injury (i.e. trauma to the abdomen);
P for Polyhydramnios;
T for Twins or multiple gestation;
I for Infection in the uterus, especially chorioamnionitis;
O for Older age (i.e. aged over 35 years old);
N for Narcotic use (i.e. cocaine and amphetamines, as well as smoking)

764
Q

What is the clinical presentation of Placental Abruption?

A
  • Sudden onset severe abdominal pain that is continuous
  • Vaginal bleeding (However in concealed abruptions; the cervical os remains closed, and any bleeding that occurs remains within the uterine cavity. So the severity of the bleeding would be largely underestimated.)
  • Characteristic ‘Woody’ hard abdomen (Uterus) - suggests a large haemorrhage
  • Hypovolaemic shock which is often disproportionate to the amount of vaginal bleeding visible
  • Abnormalities on the CTG indicating foetal distress
765
Q

How is the severity of Antepartum Haemorrhage graded?

A
  • Spotting - spots of blood noticed on underwear
  • Minor haemorrhage - less than 50ml blood loss
  • Major haemorrhage - 50 – 1000ml blood loss
  • Massive haemorrhage - more than 1000 ml blood loss, or signs of shock
766
Q

What is the initial management of a major or massive haemorrhage?

A
  • Urgent involvement of a senior obstetrician, midwife and anaesthetist
  • 2 x grey cannula
  • Bloods include FBC, UE, LFT and coagulation studies
  • Crossmatch 4 units of blood
  • Fluid and blood resuscitation as required
  • CTG monitoring of the fetus
  • Close monitoring of the mother
767
Q

How is a Placental Abruption diagnosed?

A
  • There are no reliable tests for diagnosing placental abruption.
  • It is a clinical diagnosis based on the presentation
  • Ultrasound can be useful in excluding placenta praevia as a cause for antepartum haemorrhage, but is not very good at diagnosing or assessing abruption.
768
Q

What is the management of a Placental Abruption?

A

Fetus alive and < 36 weeks

  • fetal distress: Emergency caesarean Section
  • no fetal distress: observe closely, steroids, no tocolysis, threshold to deliver depends on gestation

Fetus alive and > 36 weeks

  • fetal distress: Emergency caesarean Section
  • no fetal distress: deliver vaginally

Fetus dead Induce vaginal delivery

Antenatal Steroids: Offered between 24-34+6 weeks

Rhesus D Negative: Women require Anti-D prophylaxis using Kleihauer test to quantify dose required

Active management of third stage

769
Q

What are the complications of Placental Abruption?

A

Maternal

  • Shock
  • DIC
  • Renal failure
  • PPH

Fetal

  • IUGR
  • Hypoxia
  • Death
770
Q

What is the definition of Vasa Praevia?

A
  • Vasa praevia is a condition seen in obstetrics where the foetal vessels, (unprotected by the umbilical cord or placental tissue), run dangerously close to or across the internal cervical os.
  • These vessels are prone to rupture during the rupture of membranes, which can result in foetal haemorrhage and potentially foetal death.
771
Q

What are the types of Vasa Praevia?

A
  • Velamentous umbilical cord (Type 1 Vasa Praevia)
    Is where the umbilical cord inserts into the chorioamniotic membranes, and the fetal vessels travel unprotected through the membranes before joining the placenta.
  • An accessory lobe of the placenta (Type 2 Vasa Praevia)
    (Also known as a succenturiate lobe) is connected by fetal vessels that travel through the chorioamniotic membranes between the placental lobes.
772
Q

What are the risk factors for Vasa Praevia?

A
  • Low lying placenta
  • IVF pregnancy
  • Multiple pregnancy
773
Q

What is the clinical presentation of Vasa Praevia?

A

Often presents as antepartum haemorrhage in 2nd/3rd trimester or during labour

Classic Triad of:

  • Rupture of membranes often followed by:
  • Painless vaginal bleeding
  • Foetal bradycardia (or resulting foetal death)
774
Q

What are some differentials for Vasa Praevia?

A
  • Placenta praevia
    Characterized by painless vaginal bleeding, but without the accompanying foetal bradycardia or death seen in vasa praevia.
  • Abruptio placentae
    Typically presents with painful vaginal bleeding, abdominal pain, and uterine tenderness and rigidity. Foetal distress is common.
775
Q

How is Vasa Praevia diagnosed?

A
  • Transabdominal or Transvaginal Ultrasound
  • The majority of cases are diagnosed antenataly.
  • Although, it may only be diagnosed during labour, when pulsating fetal vessels are seen in the membranes through the dilated cervix.
  • The later this is diagnosed, the greater the risk of foetal mortality.
776
Q

What is the management of Vasa Praevia?

A
  • Corticosteroids, given from 32 weeks gestation to mature the fetal lungs
  • Elective caesarean section, planned for 34 – 36 weeks gestation

When antepartum haemorrhage occurs:

  • Emergency caesarean section is required to deliver the fetus before death occurs.
777
Q

What is the definition of Postpartum Haemorrhage?

A

Postpartum haemorrhage (PPH) refers to bleeding after delivery of the baby and placenta (within 24 hours).

To be classed as a PPH, there need to be a loss of:

  • 500ml after a vaginal delivery
  • 1000ml after a caesarean section
778
Q

What is the epidemiology of Postpartum Haemorrhage?

A

It is the most common cause of significant obstetric haemorrhage.

779
Q

How can Postpartum Haemorrhage be Classified?

A

Minor Vs Major:

  • Minor PPH – under 1000ml blood loss
  • Major PPH – over 1000ml blood loss

Major PPH further classification:

  • Moderate PPH – 1000 – 2000ml blood loss
  • Severe PPH – over 2000ml blood loss

Primary Vs Secondary:

  • Primary PPH - bleeding within 24 hours of birth
  • Secondary PPH - from 24 hours to 12 weeks after birth
    (Infection and RPOC)
780
Q

What are the causes of Postpartum Haemorrhage?

A

The 4 Ts:

Tone (Uterine Atony):

  • Over-distension of the uterus: Multiple pregnancy, twin pregnancy, Polyhydramnios
  • Prolonged delivery causing muscle fatigue
  • Full bladder
  • Medications: Nifedipine, terbutaline, MgSO4

Trauma

  • C-Section
  • Instrumental Delivery
  • Episiotomy/perineal tears
  • Haematoma

Tissue:

  • Retained products of conception
  • Placenta Accreta, increta, percreta

Thrombin:

  • Coagulation disorders, Von willibrand, Placental abruption, Eclampsia/HELLP
781
Q

What are the risk factors for Postpartum Haemorrhage?

A
  • PPH in previous pregnancy
  • BMI >35
  • Multiple pregnancy
  • Parity >4
  • Conditions such as placenta praevia or accreta, placental abruption, pre-eclampsia, gestational hypertension or anaemia
  • Delivery via Caesarean section
  • Induction of labour
  • Instrumented delivery (forceps or ventouse) and episiotomy
  • Prolonged labour (greater than 12 hours)
  • Macrosomia (>4kg baby)
  • Advanced maternal age
782
Q

What investigations need to be done for a Postpartum Haemorrhage?

A

In Primary PPH:

  • Blood tests for Group/Save and Crossmatch

In Secondary PPH:

  • Ultrasound looking for retained products
  • Endocervical/high vaginal swabs looking for infection
783
Q

What is the initial management to stabilise a Postpartum Haemorrage?

A
  • Resuscitation with an ABCDE approach
  • Lie the woman flat, keep her warm and communicate with her and the partner
  • Insert two 14-gauge cannulas
  • Bloods for G&S, FBC, U&E and clotting screen
  • Group and cross match 4 units
  • Warmed IV fluid and blood resuscitation as required
  • Oxygen (regardless of saturations)
  • Fresh frozen plasma is used where there are clotting abnormalities or after 4 units of blood transfusion.
784
Q

How can the bleeding be stopped in a Postpartum Haemorrhage?

A

Mechanical:

  • Fundal Massage through the abdomen to stimulates a uterine contraction (referred to as “rubbing up the fundus”)
  • Catheterisation (bladder distention prevents uterus contractions)

Medical:

  • Oxytocin (slow injection followed by continuous infusion) - 40mg in 500mls
  • Ergometrine (intravenous or intramuscular) stimulates smooth muscle contraction (contraindicated in hypertension)
  • Carboprost(intramuscular) is a prostaglandin analogue and stimulates uterine contraction (caution in asthma)
  • Misoprostol (sublingual) is also a prostaglandin analogue and stimulates uterine contraction
  • Tranexamic acid (intravenous) is an antifibrinolytic that reduces bleeding

Surgical:

  • Intrauterine balloon tamponade – inserting an inflatable balloon into the uterus to press against the bleeding
  • B-Lynch suture – putting a suture around the uterus to compress it
  • Uterine artery ligation – ligation of one or more of the arteries supplying the uterus to reduce the blood flow
  • Hysterectomy is the “last resort” but will stop the bleeding and may save the woman’s life
785
Q

What is the management of a Secondary Postpartum Haemorrhage?

A

It depends on the cause:

  • Surgical evaluation of retained products of conception
  • Antibiotics for infection (endometritis)
786
Q

How can a Rhesus Negative woman become sensitised to Rhesus-D antigens?

A

This can occur when a rhesus-D negative woman has a Rhesus-D positive baby. (Rhesus incompatability)

It is likely at some point in the pregnancy (i.e. childbirth) that the blood from the baby will find a way into the mother’s bloodstream. When this happens, the baby’s red blood cells display the rhesus-D antigen. The mother’s immune system will recognise this rhesus-D antigen as foreign, and produce antibodies to the rhesus-D antigen. The mother has then become sensitised to rhesus-D antigens.

787
Q

What are some examples of sensitisation events where foetal and maternal blood may mix?

A

Examples of these sensitisation events include:

  • Antepartum haemorrhage
  • Placental abruption
  • Abdominal trauma
  • External cephalic version
  • Invasive uterine procedures such as amniocentesis and chorionic villus sampling
  • Rhesus positive blood transfusion to a rhesus negative woman
  • Intrauterine death, miscarriage or termination
  • Ectopic pregnancy
  • Delivery (normal, instrumental or caesarean section)
788
Q

What issues can maternal sensitisation to rhesus-D antigens cause in the foetus?

A
  • Usually, the sensitisation process does not cause problems during the first pregnancy.
  • During subsequent pregnancies, the mother’s anti-rhesus-D antibodies can cross the placenta into the fetus. If that fetus is rhesus-D positive, these antibodies attach themselves to the red blood cells of the fetus and causes the immune system of the fetus to attack them, causing the destruction of the red blood cells (haemolysis).
  • The red blood cell destruction caused by antibodies from the mother is called haemolytic disease of the newborn.
789
Q

What is the management of Rhesus Incompatibility between the mother and foetus?

A

All mothers should be tested for rhesus status and anti-D antibodies at booking

Prevention of sensitisation - is the mainstay of management. This involves giving intramuscular anti-D injections to rhesus-D negative women.

Anti-D injections are given routinely on two occasions:

  • 28 weeks gestation
  • 34 weeks gestation
  • Birth (if the baby’s blood group is found to be rhesus-positive)

Anti-D injections should also be given at any time where sensitisation may occur, such as:

  • Antepartum haemorrhage
  • Termination of pregnancy (ectopic, miscarriage, TOP)
  • Amniocentesis procedures
  • Abdominal trauma
  • ECV

Anti-D is given within 72 hours of a sensitisation event..

790
Q

What is the Kleihauer Test and when is it done?

A
  • The Kleihauer test checks how much fetal blood has passed into the mother’s blood during a sensitisation event.
  • This test is used after any sensitising event past 20 weeks gestation, to assess whether further doses of anti-D is required.
791
Q

What is the definition of a Puerperal Infection?

A

A Puerperal infection is defined as an infection of the genital tract occurring at labour or within 42 days of the postpartum period.

792
Q

What is the definition of Puerperal Pyrexia?

A

Puerperal pyrexia may be defined as a temperature of > 38ºC in the first 14 days following delivery.

Causes:

  • Endometritis: most common
  • UTI
  • Wound infections (perineal tears/c-section
  • Mastitis
  • VTE
793
Q

What can increase the risk of postpartum endometritis?

A
  • More common after caesarean sections compared with vaginal deliveries.
  • Prophylactic antibiotics are given during a caesarean to reduce the risk
794
Q

What bacteria can cause Postpartum Endometritis?

A
  • It can be caused by a large variety of gram-negative, gram-positive and anaerobic bacteria.
  • It can also be caused by sexually transmitted infections such as chlamydia and gonorrhoea.
795
Q

What is the presentation of Puerperal Pyrexia?

A

It can present from shortly after birth to several weeks postpartum, with:

  • >38 degree fever in first 14 days
  • Foul-smelling discharge or lochia
  • Bleeding that gets heavier or does not improve with time
  • Lower abdominal or pelvic pain
  • Fever
  • Sepsis
796
Q

What investigations are done for Puerperal Pyrexia?

A
  • Vaginal swabs (including chlamydia and gonorrhoea if there are risk factors)
  • Urine culture and sensitivities
  • Ultrasound may be considered to rule out retained products of conception (although it is not used to diagnose endometritis).
797
Q

What is the management of Puerperal Pyrexia?

A

Septic patients:

  • SEPSIS SIX

Milder Infections:

  • Referred to hospital for IV antibiotics
  • Clindamycin and Gentamicin until afebrile for 24 hours.
798
Q

What are some differentials of Breast Lumps?

A
  • Breast Cancer
  • Fibroadenoma
  • Breast Cysts/Abscess
  • Fibrocystic Breast Changes
  • Fat necrosis
  • Intraductal Papilloma
  • Lipoma
  • Duct Ectasia
  • Implants
799
Q

What is Fat Necrosis?

What are the common triggers for Fat necrosis?

A

Benign breast lump caused by localised degeneration and scarring of the Fat tissue in the breast

Triggers:

  • Localised trauma
  • Radiotherapy/surgery
  • Inflammatory reaction
800
Q

What is the presentation of Fat Necrosis?

A
  • Painless
  • Firm
  • Irregular
  • Fixed in local structures
  • There may be skin dimpling or nipple inversion
801
Q

What is the Management for Fat Necrosis?

A

Exclude Breast Cancer as it is a close mimic

  • Conservative management
  • May require surgery to remove if troublesome
802
Q

What investigations are performed for Breast Lumps?

A

Triple Assessment to rule out Breast CA

  • Physical Examination
  • Imaging: Mammography/Ultrasound
  • Biopsy and Histology: Fine needle or core
803
Q

What is the definition of Mastitis?

A
  • Mastitis is the inflammation of the breast tissue, which can be with or without an infection.
  • When associated with lactation in postpartum women, the condition is specified as puerperal mastitis.
804
Q

What is the epidemiology of Mastitis?

A
  • Mastitis, (particularly puerperal mastitis), is a common condition among postpartum women
  • It typically occurs within the first six weeks postpartum, particularly in the second and third weeks.
  • It usually affects first-time mothers and those with a history of mastitis in previous pregnancies.
805
Q

What causes Mastitis?

A
  • Milk stasis from poor feeding or inadequate feeding
  • Staph aureus is most common organism
806
Q

What are the risk factors for developing Mastitis?

A
  • Poor breastfeeding technique
  • Nipple damage
  • Maternal stress
  • Previous history of mastitis
  • First time pregnancy
  • Smoking
807
Q

What is the clinical presentation of Mastitis?

A
  • Localised symptoms:
    Painful, tender, red, and hot breast.
  • Systemic symptoms:
    Fever, rigors, myalgia, fatigue, nausea, and headache.
  • The condition is usually unilateral and tends to present within the first week postpartum.
  • In some cases, mastitis may develop into a breast abscess, manifesting as a fluctuant, tender mass with overlying erythema.
808
Q

What are some differentials for Mastitis?

A
  • Breast abscess
    Fluctuant mass, tenderness, overlying erythema, systemic signs of infection.
  • Inflammatory breast cancer
    Swelling, skin changes resembling orange peel, nipple inversion, axillary lymphadenopathy.
  • Breast engorgement
    Typically bilateral and associated with milk stasis, painful, and tense breasts.
809
Q

How is Mastitis investigated?

A
  • Diagnosis of mastitis is primarily clinical
  • An ultrasound may be useful in identifying an abcess if that is suspected
810
Q

What is the management of Mastitis?

A

First Line:

  • Continue breastfeeding.
  • Analgesia
  • A warm compresses

Second Line: if systemically unwell, if nipple fissure present, if symptoms do not improve after 12-24 hours of effective milk removal of if culture indicates infection’

  • Antibiotics 1st Line is oral flucloxacillin
    for 10-14 day
811
Q

What complications can arise as a result of Mastitis?

A
  • Candida infection of the nipple (often after a course of antibiotics). This can lead to Recurrent mastitis
  • Breast Abcess
812
Q

What is Fibrocystic Breast changes?

A

generalised lumpiness to the breast (Not a disease).

The anatomy of the breast may become fibrous and cystic with changes in hormones and this can fluctuate with the menstrual cycle.

813
Q

What are the features of fibrocystic breast changes?

A

will fluctuate with menstrual cycle

  • Lumpiness
  • Breast pain or tenderness (mastalgia)
  • Fluctuation of breast size
814
Q

What is the management of fibrocystic breast changes?

A
  • Wearing a supportive bra
  • Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen
  • Avoiding caffeine is commonly recommended
  • Applying heat to the area
  • Hormonal treatments (e.g., danazol and tamoxifen) under specialist guidance
815
Q

What is the presentation of Candida of the nipple?

A
  • Sore nipples bilaterally, particularly after feeding
  • Nipple tenderness and itching
  • Cracked, flaky or shiny areola

Its associated with oral thrush and candidal nappy rash in the infant.

816
Q

What is the management of Candida of the nipple?

A

Both the mother and baby need treatment, or it will reoccur. Treatment is with:

  • Topical miconazole 2% after each breastfeed
  • Treatment for the baby (e.g. miconazole gel or nystatin)
817
Q

What is the definition of a breast abscess?

A

A breast abscess is a collection of pus within an area of the breast, usually caused by a bacterial infection. This may be a:

  • Lactational abscess (associated with breastfeeding)
  • Non-lactational abscess (unrelated to breastfeeding)

It often occurs as a result of infectious mastitis.

818
Q

What are the most common causative organisms of Mastitis / Breast Abscesses?

A
  • Staphylococcus aureus (the most common)
  • Streptococcal species
  • Enterococcal species
  • Anaerobic bacteria (such as Bacteroides species and anaerobic streptococci)
819
Q

What is the presentation of a Breast Abscess?

A
  • Alongside the features of Mastitis
  • The key feature that suggests a breast abscess is a swollen, fluctuant, tender lump within the breast.
  • As well as more generalised symptoms of infection like; Muscle aches, Fatigue, Fever, Signs of sepsis (e.g., tachycardia, raised respiratory rate and confusion).
820
Q

What is the management of a Breast Abscess?

A
  • Referral to the on-call surgical team in the hospital for management
  • Drainage with need aspiration or surgical incision and Adjuvant Antibiotics
  • Microscopy, culture and sensitivities of the drained fluid

Women are advised to continue breastfeeding. They should regularly express breast milk if feeding is too painful, then resume feeding when possible.

821
Q

How is a Breast Abscess diagnosed?

A

Breast Ultrasound

822
Q

What is the definition of a Fibroadenoma?

A
  • Fibroadenomas are common benign tumours of stromal and epithelial breast duct tissue.
  • They originate from the lobules (the milk-producing glands of the breast)
823
Q

What is the epidemiology of Fibroadenomas?

A
  • More common in younger women (aged between 20 and 40)
  • They’re particularly common in periods of reproductive hormonal change such as puberty, pregnancy, and perimenopause.
824
Q

What causes a fibroadenoma?

A
  • Exact cause is unclear
  • They respond to the increased levels of female reproductive hormones (oestrogen and progesterone). As they often grow in size during pregnancy, and shrink during menopause.
825
Q

What is the clinical presentation of a Fibroadenoma?

A
  • A firm, non-tender breast mass
  • The mass is rounded and has smooth edges
  • The mass is highly mobile upon palpation, sometimes called a “breast mouse”, as they move around within the breast tissue.
  • Often referred to as having a “rubbery” consistency
  • The mass typically does not grow beyond 3cm in diameter
826
Q

What are some differentials for a Fibroadenoma?

A
  • Breast cysts
    These can be soft to firm, mobile, and round with distinct edges, similar to fibroadenomas. However, they may be tender and can fluctuate in size with the menstrual cycle.
  • Invasive breast cancer
    Typically presents with a hard, irregularly shaped, immobile mass. There may be associated nipple discharge, retraction or skin changes.
  • Intraductal papilloma
    Generally presents with nipple discharge, occasionally blood-stained, but may also have an associated palpable mass.
  • Lipoma
    Presents as a soft, mobile mass. Unlike fibroadenomas, lipomas can grow beyond 3cm and are typically painless.
827
Q

What investigations are done for a fibroadenoma?

A

While fibroadenomas are benign, patients usually undergo a triple assessment to exclude more serious pathology. This includes:

  • Clinical examination
  • Imaging (usually ultrasound and/or mammogram)
  • Needle biopsy (fine needle aspiration or core biopsy)
828
Q

What is the management of a fibroadenoma?

A
  • Conservative management
    Many fibroadenomas do not require treatment and will regress naturally after menopause.
  • Surgical excision
    This may be required if the fibroadenoma is large, growing, causing significant symptoms, or if there is diagnostic uncertainty after triple assessment.
829
Q

Are fibroadenomas associated with an increased risk of breast cancer?

A

No
* They are not usually associated with an increased risk of developing breast cancer.

  • Complex fibroadenomas and a positive family history of breast cancer may indicate a higher risk.
830
Q

What is the definition of a Breast Cyst?

A

Breast cysts are benign, individual, fluid-filled lumps of the breast.

831
Q

What is the epidemiology of breast cysts?

A
  • They are the most common cause of breast lumps
  • Occur most often between ages 30 and 50, more so in the perimenopausal period.
832
Q

What is the clinical presentation of breast cysts?

A

The Lumps can be:

  • Possibly painful
  • Smooth
  • Well-circumscribed
  • Mobile
  • Possibly fluctuant

They can also fluctuate in size over the menstrual cycle

833
Q

How are breast cysts investigated?

A

All breast lumps should be investigated with Triple Assessment to exclude cancer):

  • Clinical examination
  • Imaging (usually ultrasound and/or mammogram)
  • Needle biopsy (fine needle aspiration or core biopsy)
834
Q

What is the management of breast cysts?

A
  • Aspiration of the breast cyst is the recommended treatment in symptomatic cases.
  • Repeat aspiration or excision may be required in cases of recurrent cysts
  • Non-symptomatic (non-painful) breast cysts do not need to be drained unless they bother the patient or cause concerns.
835
Q

Do breast cysts increase the risk of cancer?

A

Yes
Having a breast cyst may slightly increase someone’s cancer risk

836
Q

What is the definition of Ductal Ectasia?

A

Mammary duct ectasia is a benign condition where there is dilation of the large ducts in the breasts. Ectasia means dilation. There is inflammation in the ducts, leading to intermittent discharge from the nipple. The discharge may be white, grey or green.

837
Q

What is the Management for Mammary Ductal Ectasia?

A
  • Reassurance after excluding cancer may be all that is required
  • Symptomatic management of mastalgia (supportive bra and warm compresses)
  • Antibiotics if infection is suspected or present
  • Surgical excision of the affected duct (microdochectomy) may be required in problematic cases
838
Q

Who does Mammary Ductal Ectasia affect?

A

SMOKERS and perimenopausal women

839
Q

What is the presentation of Mammary Ductal Ectasia?

A
  • Nipple discharge - white, grey, green
  • Tenderness or pain
  • Nipple retraction or inversion
  • A breast lump (pressure on the lump may produce nipple discharge)
840
Q

What are the investigations for Ductal Ectasia?

A

Triple Assessment first

  • Ductography - contrast injected into abnormal duct and mammograms used to visualise
841
Q

What is the definition of an Intraductal Papilloma?

A
  • An intraductal papilloma is a warty lesion that grows within one of the ducts in the breast.
  • It is the result of the proliferation of epithelial cells.
  • They are benign tumours; however, they can be associated with atypical hyperplasia or breast cancer.
842
Q

What is the epidemiology of an Intraductal Papilloma?

A

Most common between 35-55 years

843
Q

What is the clinical presentation of an Intraductal Papilloma?

A

They may present with:

  • Nipple discharge (clear or blood-stained)
  • Breast tenderness or pain
  • A palpable lump

They are often asymptomatic and can be picked up incidentally on mammograms or ultrasound.

844
Q

How is an Intraductal Papilloma diagnosed?

A

Patients require triple assessment with:
* Clinical assessment (history and examination)
* Imaging (ultrasound, mammography and MRI)
* Histology (usually by core biopsy or vacuum-assisted biopsy)

Ductography may also be used. This involves injecting contrast into the abnormal duct and performing mammograms to visualise that duct. The papilloma will be seen as an area that does not fill with contrast (a “filling defect”).

845
Q

What is the management of an Intraductal Papilloma?

A
  • Intraductal papillomas require complete surgical excision.
  • After removal, the tissue is examined for atypical hyperplasia or cancer that may not have been picked up on the biopsy.
846
Q

What is the definition of Breast Cancer?

A
  • Breast cancer or carcinoma refers to a malignant tumor originating from the cells of the breast tissue.
  • The carcinomas can be invasive, indicating they have broken through the basement membrane of the tissue of origin and have the potential to metastasize, or non-invasive (in situ), suggesting they are confined to the initial location.
847
Q

What is the epidemiology of Breast Cancer?

A
  • Breast cancer is the most common form of cancer in the UK.
  • It mostly affects women and is rare in men (about 1% of UK cases).
  • Around 1 in 8 women will develop breast cancer in their lifetime.
848
Q

What are the risk factors for Breast Cancer?

A
  • Female (99% of breast cancers)
  • BRCA1, BRCA2 genes
  • 1st degree relative premenopausal relative with breast cancer (e.g. mother)
  • nulliparity, 1st pregnancy > 30 yrs (twice risk of women having 1st child < 25 yrs)
  • early menarche, late menopause
  • combined hormone replacement therapy and COCP
  • past breast cancer
  • not breastfeeding
  • ionising radiation
  • p53 gene mutations
  • obesity
  • previous surgery for benign disease
  • Smoking
849
Q

How are BRCA genes?

A
  • BRCA refers to the BReast CAncer gene. The BRCA genes are tumour suppressor genes.
  • Mutations in these genes lead to an increased risk of breast cancer (as well as ovarian and other cancers).
850
Q

What chromosomes are the genes BRCA 1 and 2 on?

A

BRCA1 gene is on chromosome 17

  • 70% will develop breast cancer by aged 80
  • 50% will develop ovarian cancer
  • Also increased risk of bowel and prostate cancer

BRCA2 gene is on chromosome 13

  • 60% will develop breast cancer by aged 80
  • 20% will develop ovarian cancer
851
Q

What are the some types of Breast Cancer?

A

Ductal/Lobular Carcinoma In Situ (DCIS/LCIS)

  • Pre-cancerous or cancerous epithelial cells of the breast ducts
  • Potential to become an invasive breast cancer (around 30%)
  • Good prognosis if full excised and adjuvant treatment is used

Invasive Breast Cancers:

  • Invasive Ductal Carcinoma (Most common at 70%)
  • Invasive Lobular Carcinomas (ILC) - about 10%

Paget’s Disease of the Nipple

  • Eczematous change of the nipple due to underlying malignancy (invasive or in-situ)
852
Q

What is the presentation of Breast Cancer?

A
  • Lumps that are hard, irregular, painless or fixed in place
  • Lumps may be tethered to the skin or the chest wall
  • Nipple retraction
  • Skin dimpling or oedema (peau d’orange)
  • Lymphadenopathy, particularly in the axilla
853
Q

Describe the NHS Breast Cancer Screening program

A

Mammogram is offered every 3 years to women aged 50-70 years

The screening aims to detect breast cancer early, which improves outcomes.

854
Q

What are some potential downsides to Breast Cancer Screening?

A
  • Anxiety and stress
  • Exposure to radiation during mammograms, with a very small risk of causing breast cancer
  • Missing cancer, leading to false reassurance
  • Unnecessary further tests or treatment where findings would not have otherwise caused harm
855
Q

Who is classed as a high risk patient for Breast Cancer?

A

People who have:

  • A first-degree relative with breast cancer under 40 years
  • A first-degree male relative with breast cancer
  • A first-degree relative with bilateral breast cancer, first diagnosed under 50 years
  • Two first-degree relatives with breast cancer

Annual mammogram screening is offered to women with increased risk. Potentially starting from aged 30, if high risk.

856
Q

How can high risk patients decrease their risk of developing Breast Cancer?

A

Chemoprevention may be offered:

  • Tamoxifen if premenopausal
  • Anastrozole if postmenopausal (except with severe osteoporosis)

Risk-reducing bilateral mastectomy or bilateral oophorectomy (removing the ovaries) is also an option for women at high risk; but this is only suitable for a small subset of women.

857
Q

What is the NICE Referral criteria for Breast Cancer?

A

Two week wait referral for:

  • An unexplained breast lump in patients aged 30 or above
  • Unilateral nipple changes in patients aged 50 or above (discharge, retraction or other changes)
  • An unexplained lump in the axilla in patients aged 30 or above
  • Skin changes suggestive of breast cancer
858
Q

What are the differentials for Breast Cancer?

A
  • Fibroadenoma
    Typically presents as a solitary, painless, and well-circumscribed breast lump in young women
  • Cyst
    Characterized by a round or oval, well-defined, and movable mass. It may be painful and size may vary with the menstrual cycle.
  • Mastitis
    Typically presents in breastfeeding women, characterized by a painful, warm, red breast often accompanied by systemic symptoms like fever.
  • Lipoma
    Presents as a soft, mobile, and painless lump.
859
Q

What investigations are used when diagnosing suspected Breast Cancer?

A

Initial Investigations are with a Triple Diagnostic Assesment:

  • Clinical assessment (history and examination)
  • Imaging (ultrasound or mammography)
  • Biopsy (fine needle aspiration or core biopsy)

Then once the woman has been diagnosed with breast cancer, then an assesment of the Lymph nodes is required:

  • Ultrasound of the axilla (armpit)
  • Ultrasound-guided biopsy of any abnormal nodes
  • A sentinel lymph node biopsy may be used during breast cancer surgery where the initial ultrasound does not show any abnormal nodes.
860
Q

What are the advantages of different imaging modalities when investigating Breast Cancer?

A

Ultrasound scans:

  • Are used to assess lumps in younger women (e.g., under 30 years).
  • They are helpful in distinguishing solid lumps (e.g., fibroadenoma or cancer) from cystic (fluid-filled) lumps.

Mammograms:

  • Are generally more effective in older women due to less density in breast tissue
  • They can pick up calcifications missed by ultrasound.

MRI Scans may be used:

  • For screening in women at higher risk of developing breast cancer (e.g., strong family history)
  • To further assess the size and features of a tumour
861
Q

How is Breast Cancer Staged?

A

Nottingham Prognostic Index (NPI) using TNM staging.
Higher the grade the worse the prognosis

  • NPI <2.4 = Excellent prognosis (Normal Population survival)
  • NPI <3.4 = Good prognosis (80% 10 year survival)
  • NPI <5.4 = Intermediate prognosis (50% 10 year survival)
  • NPI >5.4 = Poor prognosis (<20% 10 year survival)
862
Q

Where does Breast Cancer tend to metastasis to?

A

Breast cancer can spread to anywhere in the body, whoever the most common locations are:
2Ls and 2Bs

  • L – Lungs
  • L – Liver
  • B – Bones
  • B – Brain
863
Q

What are the features of Locally Advanced breast cancer?

A
  • Ulceration
  • Peau d’orange
  • Inflammatory Breast Cancer
  • Fixed to chest wall
  • Fixed and matted to axillary lymph nodes

This type of breast cancer is surgically incurable

864
Q

What are the 3 types of receptor that may be present on breast cancer?

A
  • Oestrogen receptors (ER)
  • Progesterone receptors (PR)
  • Human epidermal growth factor (HER2)

These receptors can be targeted with breast cancer treatments

865
Q

What is a triple negative breast cancer?

A

Triple-negative breast cancer is where the breast cancer cells do not express any of the three typical receptors. (ER, PR or HER2)

This carries a worse prognosis, as it limits the treatment options for targeting the cancer.

866
Q

What is Gene Expression Profiling and when is it done?

A
  • Gene expression profiling involves assessing which genes are present within the breast cancer on a histology sample.
  • This helps predict the probability that the breast cancer will reoccur as a distal metastasis (away from the original cancer site) within 10 years.
  • The NICE guidelines recommend this for women with early breast cancers that are ER positive but HER2 and lymph node negative.
  • It helps guide whether to give additional chemotherapy.
867
Q

What does the management of Breast Cancer Involve?

A

Surgical (The aim is removal of the tumour). There are 2 main types:

  • Breast-conserving surgery (e.g. wide local excision), usually coupled with radiotherapy.
  • Mastectomy (removal of the whole breast), potentially with immediate or delayed breast reconstruction.
  • Axillary Clearance - Removal of the axillary lymph nodes is offered to patients where cancer cells are found in the nodes. (although this increases the risk of lymphoedema)

Radiotherapy

  • Adjuvant Radiotherapy is given to patients following breast-conserving surgery to reduce the risk of recurrence.

Chemotherapy

  • Suggested in patients with hormone receptor-negative and HER2 over-expressing patients. Its used in 1 of 3 scenarios:
  • Neoadjuvant therapy – intended to shrink the tumour before surgery
  • Adjuvant chemotherapy – given after surgery to reduce recurrence
  • Treatment of metastatic or recurrent breast cancer

Hormone Treatment:

  • Is used in patients with oestrogen-receptor positive breast cancer. There are 2 main first line options:
  • Tamoxifen for premenopausal women
  • Aromatase inhibitors for postmenopausal women (e.g., letrozole, anastrozole or exemestane)
  • Tamoxifen or an aromatase inhibitor are given for 5 – 10 years to women with oestrogen-receptor positive breast cancer.

Biological Therapy

  • Trastuzumab (Herceptin) is a monoclonal antibody that targets the HER2 receptor. So is used in HER2 positive cancers.
868
Q

When is Axillary Node clearance indicated in breast cancer?
What are some side effects of lymph node clearance?

A

Women with no palpable axillary lymphadenopathy pre-operatively should have an Ultrasound. If negative then a Sentinel node biopsy should be done

Women With palpable lymphadenopathy should have axillary node clearance at primary surgery.

Side effects include: Lymphoedema, functional arm impairment

869
Q

What are the indications for Mastectomy vs Wide local Excision?

A

Wide Local Excision:

  • Solitary Lesion
  • Small lesion in large breast
  • Peripheral Tumour
  • DCIS < 4cm

Mastectomy:

  • Multifocal Tumour
  • Central Tumour
  • Large lesion in small breast
  • DCIS > 4cm
870
Q

What are the side effects of Radiotherapy?

A
  • General fatigue from the radiation
  • Local skin and tissue irritation and swelling
  • Fibrosis of breast tissue
  • Shrinking of breast tissue
  • Long term skin colour changes (usually darker)
871
Q

What are the side effects of Chemotherapy?

A
  • Fatigue
  • Hair loss
  • Easy bruising and bleeding
  • Infection
  • Anaemia
  • Nausea and vomiting
  • Appetite changes
  • Problems with concentration or memory.
872
Q

What are the side effects of Hormone therapy drugs?

A
  • Hot flashes
  • Vaginal dryness or discharge
  • Menstrual changes
  • Fatigue
  • Mood changes
  • Osteoporosis.

In rare cases, tamoxifen can increase the risk of serious conditions like endometrial cancer and blood clots.

873
Q

What is the mechanism of action of Tamoxifen?

A
  • Tamoxifen is a selective oestrogen receptor modulator (SERM).
  • It either blocks or stimulates oestrogen receptors, depending on the site of action.
  • It blocks oestrogen receptors in breast tissue, and stimulates oestrogen receptors in the uterus and bones.
  • This means it helps prevent osteoporosis, but it does increase the risk of endometrial cancer.
874
Q

What is the mechanism of Aromatase Inhibitors?

A
  • Aromatase is an enzyme found in fat (adipose) tissue that converts androgens to oestrogen.
  • After menopause, the action of aromatase in fat tissue is the primary source of oestrogen.
  • Aromatase inhibitors work by blocking the creation of oestrogen in fat tissue.
  • Examples include: letrozole, anastrozole or exemestane
875
Q

When is Breast Reconstruction done?

A

Breast reconstructive surgery is offered to all patients having a mastectomy. There are two options:

  • Immediate reconstruction - done at the time of the mastectomy
  • Delayed reconstruction - which can be delayed for months or years after the initial mastectomy
876
Q

What are the 2 options of Breast Reconstruction after Breast conserving surgery?

A

After breast-conserving surgery, reconstruction may not be required. The standard options, if needed, are:

  • Partial reconstruction (using a flap or fat tissue to fill the gap)
  • Reduction and reshaping (removing tissue and reshaping both breasts to match.
877
Q

What are the 2 options of Breast Reconstruction after a Mastectomy?

A
  • Breast implants (inserting a synthetic implant)
  • Flap reconstruction (using tissue from another part of the body to reconstruct the breast)
878
Q

What are the advantages/disadvantages of implants instead of Flap Reconstruction?

A

Advantages

  • Inserting an implant is a relatively simple procedure (compared with a flap) with minimal scarring.
  • It gives an acceptable appearance

Disadvantages

  • Implants can feel less natural (e.g., cold, less mobile and static size and shape).
  • There can also be long-term problems, such as hardening, leakage and shape change.
879
Q

What are the different types of Breast Implants?

A

Silicon:

  • Advantages: Less likely to fold or rupture. Feel more natural
  • Disadvantages: May cause lumps

Saline:

  • Advantages: if they rupture, can be absorbed into the body safely
  • Disadvantage: More likely to go down/rupture

Both types of implants last about 10 years

880
Q

What are the short term complications of Breast Implants?

A
  • Bleeding
  • Blood clots
  • Infection
  • Allergic reaction
881
Q

What are the long term complications of Breast implants?

A
  • Obvious Scarring
  • Capsular contracture
  • Ruptured implant
  • Produce less breast milk when feeding
  • BIA-ALCL (Breast implant associated, anaplastic large cell lymphoma)
  • Breast Implant Illness
882
Q

What are the 3 different types of Flap reconstruction?

A
  • Latissimus Dorsi Flap
  • Transverse Rectus Abdominis Flap (TRAM Flap)
  • Deep Inferior Epigastric Perforator Flap (DIEP Flap)
883
Q

What is Chronic Lymphoedema?

A
  • Lymphoedema is a chronic condition caused by impaired lymphatic drainage of an area.
  • Lymphoedema can occur in an entire arm after breast cancer surgery on that side, with removal of the axillary lymph nodes in the armpit.
  • lymphatic system is responsible for draining excess fluid from the tissues. The tissues in areas affected by an impaired lymphatic system become swollen with excess, protein-rich fluid (lymphoedema).
  • Areas of lymphoedema are prone to infection
884
Q

What are the treatment options for Chronic Lymphoedema?

A
  • Massage techniques to manually drain the lymphatic system (manual lymphatic drainage)
  • Compression bandages
  • Specific lymphoedema exercises to improve lymph drainage
  • Weight loss if overweight
  • Good skin care
885
Q

What are the possible surgical complications of Breast surgery?

A
  • Pain: Persistent or worsening pain at the surgical site.
  • Bleeding: Increased wound drainage, decreased blood pressure, increased heart rate.
  • Infection: Wound redness, swelling, pain, pus discharge, and fever.
  • Seroma: Swelling at the surgical site, fluid-filled lump.
  • Displeasure with cosmetic outcome: Patient dissatisfaction with the appearance of the breast after surgery.
886
Q

What are the possible anaesthetic complications of Breast Surgery?

A
  • Stroke: Sudden onset of neurological deficits such as weakness, speech impairment, visual changes.
  • Venous thromboembolism: Swelling, pain, and redness in the leg (deep vein thrombosis); shortness of breath, chest pain, and rapid heart rate (pulmonary embolism).
  • Myocardial infarction: Chest pain, shortness of breath, sweating, nausea, and lightheadedness.
  • Aspiration: Sudden onset of coughing, wheezing, and difficulty breathing.
887
Q

What are the possible Axillary node clearance related complications of Breast Surgery?

A
  • Lymphoedema: Swelling of the arm, feeling of heaviness or tightness, restricted range of motion.
  • Damage to brachial plexus: Numbness, tingling, or weakness in the arm.
  • Axillary artery/vein injury: Swelling, pain, pallor, and decreased pulse in the arm.
888
Q

What is the definition of Paget’s disease of the nipple?

A
  • Paget’s disease of the nipple, also known as Paget’s disease of the breast, is a rare condition characterised by the presence of cancer cells in the skin of the nipple.
  • This disease often suggests an underlying ductal carcinoma in situ (DCIS) or invasive breast cancer.
889
Q

What is the epidemiology of Paget’s Disease of the nipple?

A
  • Most common in Postmenopausal women
  • Only accounts for around 5% of breast cancers
890
Q

What are the 2 theories for how Paget’s disease of the nipple occurs?

A
  • Epidermotropic theory - suggests that cancer cells from an underlying breast tumour migrate to the nipple.
  • Intraepidermal origin theory - which proposes the disease originates in the nipple itself.
891
Q

What is the clinical presentation of Paget’s disease of the nipple?

A
  • Eczema-like rash on the skin of the nipple and areola that is often itchy, red, crusty, and inflamed
  • Bloody nipple discharge
  • Burning sensation, increased sensitivity, or pain in the nipple
  • Changes to the nipple, such as retraction or inversion
  • Palpable breast lump (in some cases)
  • Non-healing skin ulcer (in some cases)
892
Q

What are the differentials for Paget’s disease of the Nipple?

A
  • Atopic dermatitis (eczema)
    Characterised by itchy, red, and inflamed skin, usually occurring in patches
  • Contact dermatitis
    Caused by irritants or allergens, presents with a red rash, itching, and possibly blisters
  • Intraductal papilloma
    Produces bloody nipple discharge but typically does not involve skin changes
  • Mastitis or breast abscess
    Presents with breast redness, swelling, pain, and possible fever; often related to breastfeeding
  • Psoriasis
    Presents with silvery scales on red, raised patches, often with itching or burning
893
Q

How is Paget’s disease of the nipple diagnosed?

A
  • Physical examination of the breasts and lymph nodes
  • Mammography or breast ultrasound
  • Punch Biopsy of the affected skin and nipple discharge cytology
  • MRI may be used in certain circumstances to better assess the extent of disease
894
Q

What does management of Paget’s disease of the nipple involve?

A

Management of Paget’s disease of the nipple primarily involves surgical intervention. Approaches can include:

  • Simple mastectomy: Removal of the entire breast, including the nipple and areola
  • Modified radical mastectomy: Removal of the entire breast along with some of the axillary (underarm) lymph nodes
  • Breast-conserving surgery (lumpectomy): If the underlying cancer is small and limited

Additionally, adjunctive treatments such as radiation therapy, chemotherapy, or hormonal therapy may be used depending on the characteristics of the underlying breast cancer.

895
Q

What is the definition of Vulvovaginal Candidiasis?

A
  • Vulvovaginal candidiasis, often referred to as a yeast infection, is an inflammation of the vagina and the vulva due to an overgrowth of the yeast fungus, primarily Candida Albicans.
  • Recurrent vulvovaginal candidiasis is defined as four or more symptomatic episodes in one year, with at least two episodes confirmed by microscopy or culture when symptomatic.
896
Q

What causes Vulvovaginal Candidiasis?

A
  • Candida Albicans is the main causative organism (causing 85-90% of cases)
  • Transmission is usually non-sexual
897
Q

What are the risk factors for developing vulvovaginal candidiasis?

A
  • diabetes mellitus
  • drugs: antibiotics, steroids
  • pregnancy
  • immunosuppression: HIV
898
Q

What is the clinical presentation of Vulvovaginal Candidiasis?

A
  • cottage cheese’, non-offensive discharge
  • vulvitis: superficial dyspareunia, dysuria
  • itch
  • vulval erythema, fissuring, satellite lesions may be seen
899
Q

What are some differentials for Vulvovaginal Candidiasis?

A
  • Bacterial vaginosis
    Characterised by greyish-white discharge, fishy odour, and absence of significant inflammation.
  • Trichomoniasis
    Presents with yellow-green, frothy discharge, dysuria, and itching.
  • Chlamydia or Gonorrhoea
    These sexually transmitted infections can cause similar symptoms such as discharge, but often also present with pelvic pain or bleeding.
  • Genital herpes
    Characterised by painful blisters or open sores in the genital area.
900
Q

What investigations are done for vulvovaginal candidiasis?

A

Routine investigations are not typically required for acute, uncomplicated vulvovaginal candidiasis cases.

However, in instances where the clinical presentation is unclear or recurrent episodes occur, the following investigations may be necessary:

  • Microscopy - Detection of blastospores, pseudohyphae and neutrophils suggests Candida infection.
  • Culture - Recommended for recurrent vulvovaginal candidiasis cases to identify the Candida species.
901
Q

What is the management of Vulvovaginal Candidiasis?

A

First Line:

  • Oral fluconazole 150 mg as a single dose

Second line:

  • clotrimazole 500 mg intravaginal pessary as a single dose if oral therapy is contraindicated
  • If there are vulval symptoms, consider adding a topical imidazole in addition to an oral or intravaginal antifungal

if pregnant then only local treatments (e.g. cream or pessaries) may be used - oral treatments are contraindicated

902
Q

What is the management of Recurrent vulvovaginal candidiasis?

A

4 episodes per year

compliance with previous treatment should be checked

Confirm the diagnosis of candidiasis

  • high vaginal swab for microscopy and culture
  • consider a blood glucose test to exclude diabetes
  • exclude differential diagnoses such as lichen sclerosus

An induction-maintenance regime

  • Induction: oral fluconazole every 3 days for 3 doses
  • Maintenance: oral fluconazole weekly for 6 months
903
Q

What is the definition of Balanitis?

A
  • Balanitis is inflammation of the glans penis.
  • If the foreskin is also inflamed, the correct term is balanoposthitis, although balanitis is commonly used to refer to both.
904
Q

What is the epidemiology of Balanitis?

A
  • More common in Men than boys
  • It’s uncommon in circumcised boys and men (circumcision reduces the risk of inflammatory skin conditions which may cause balanitis).
905
Q

What are the risk factors for Balanitis?

A
  • Diabetes mellitus.
  • Use of oral antibiotics.
  • Poor hygiene in uncircumcised males.
  • Immunosuppression.
  • Chemical or physical irritation of glans.
906
Q

What are the possible causes of Balanitis?

A

Infectious Causes:
* Candida infection
* Staph Aureus
* Anaerobic Bacteria

Dermatological Causes
* Circinate balanitis (Associated with reactive arthritis)
* Psoriasis
* Fixed drug eruption (especially with sulfonamides and tetracycline)

Other causes
* Intertrigo (alot of cases)
* Irritation or contact dermatitis: wet nappies, poor hygiene, smegma, soap, condoms.
* Trauma
* Severe oedema due to right heart failure.
* Morbid obesity

907
Q

What is the clinical presentation of Balanitis?

A
  • Sore, inflamed and swollen glans/foreskin
  • Non-retractile foreskin (phimosis).
  • itchy
  • Penile ulceration.
  • Penile plaques.
  • Satellite lesions.
  • May be purulent and/or foul-smelling discharge (most common with streptococcal/anaerobic infection).
  • Dysuria.
  • Interference with urinary flow in severe cases.
  • Obscuration of glans/external urethral meatus.
  • Impotence or pain during coitus.
  • Regional lymphadenopathy.
908
Q

ts

What is Intertrigo?

A

Intertrigo is a common inflammatory skin condition that is caused by skin-to-skin friction (rubbing) that is intensified by heat and moisture.

909
Q

What investigations are done for Balanitis?

A
  • Blood/urine testing for glucose if diabetes mellitus is possible.
  • Swab of discharge for microscopy, Gram staining, culture and sensitivity.
910
Q

What is the management of Balanitis?

A

Caused by contact dermatitis:
* Avoid Triggers
* Topical hydrocortisone 1% once daily (consider adding an imidazole cream), for up to 14 days.

Caused by Candidal infection
* Clotrimazole cream 1% or miconazole cream 2%; apply twice daily until symptoms have settled.
* Alternative regimens: fluconazole 150 mg stat orally
* Topical imidazole with 1% hydrocortisone if there is marked inflammation

Caused by Bacterial infection
* Common bacterial infection - flucloxacillin (or erythromycin in penicillin-allergic patients).
* Anaerobic infection - metronidazole 400 mg twice-daily for one week

Surgery
* Is not often done, but surgical referral for consideration of circumcision if balanitis is recurrent or pathological phimosis is present.

911
Q

What is the definition of Chancroid?

A
  • Chancroid is a sexually transmitted infection (STI) of the genital skin.
  • It is primarily caused by the gram-negative bacillus Haemophilus ducreyi.
912
Q

What is the epidemiology of Chancroid?

A
  • Most common in tropical and subtropical regions as well as Greenland
  • Sexual behaviour, poor living conditions, and a lack of public health infrastructure contribute to the increased incidence in these areas
913
Q

What causes Chancroid?

A
  • Chancroid is caused by an infection with the gram-negative bacillus Haemophilus ducreyi.
  • The bacterium is sexually transmitted and can cause a genital ulcer and inflammation of the inguinal lymph nodes.
  • Given its higher prevalence in other parts of the world, its important to ask patients about recent travel.
914
Q

What is the clinical presentation of Chancroid?

A
  • Presents as a painful, potentially necrotic genital lesion; that may bleed on contact.
  • Painful lymphadenopathy, commonly known as “bubo,” which may rupture and discharge pus.

Symptoms often develop within 4-10 days after exposure to the bacterium.

915
Q

What are some differentials for Chancroid?

A
  • Herpes Simplex Virus (HSV)
    Presents with multiple, small, vesicular lesions that become ulcers, accompanied by systemic symptoms such as fever and malaise.
  • Syphilis
    Presents with a painless ulcer (chancre) and generalized non-tender lymphadenopathy.
  • Lymphogranuloma Venereum (LGV)
    Presents with a small painless ulcer or papule that often goes unnoticed, followed by painful inguinal lymphadenopathy (“bubo”) similar to chancroid.
916
Q

What investigations are done for Chancroid?

A

Diagnosis is usually based upon the clinical picture. But the following can confirm the diagnosis:

  • Culture - H. ducreyi is a fastidious organism and culture is often difficult and time-consuming.
  • PCR (Polymerase Chain Reaction) - PCR for H. ducreyi can be performed on genital ulcer specimens, providing a more rapid diagnosis.
917
Q

What is the management of Chancroid?

A
  • Single dose 500mg Ciprofloxacin or Single dose 250mg IM Ceftriaxone

Adjunctive therapy can include:

  • Analgesics for pain control
  • Incision and drainage of buboes
918
Q

What is the definition of Lymphogranuloma venereum (LGV)?

A
  • Lymphogranuloma venereum (LGV) is a sexually transmitted infection.
  • Predominantly caused by the L1, L2, or L3 serovars of Chlamydia trachomatis.
919
Q

What is the epidemiology of LGV?

A

More common in Men who have sex with Men

920
Q

What causes LGV?

A

Its caused by infection with the L1, L2, or L3 serovars of Chlamydia trachomatis, typically through sexual contact.

921
Q

What is the clinical presentation LGV?

A
  • Painless genital ulcer - Typically appears 3-12 days after infection. It might go unnoticed, particularly if it occurs inside the vagina
  • Inguinal lymphadenopathy, often noticeable
  • Proctitis, associated with rectal pain and discharge (in case of rectal infections)
  • Systemic symptoms can include fever and malaise
922
Q

What are the differentials of LGV?

A
  • Primary syphilis
    Presents with a solitary, painless genital ulcer (chancre) and regional lymphadenopathy
  • Herpes simplex virus infection
    Characterised by multiple painful vesicles or ulcers, systemic symptoms, and occasional inguinal lymphadenopathy
  • Chancroid
    Caused by Haemophilus ducreyi, it presents with painful genital ulcers and painful inguinal lymphadenopathy
923
Q

How is LGV diagnosed?

A

Polymerase chain reaction (PCR), are employed to detect C. trachomatis from a swab of the genital ulcer.

924
Q

What is the management of LGV?

A

Its managed by anitibiotics. Common regimes include:

  • Oral doxycycline - 100 mg administered twice daily for 21 days
  • Oral tetracycline - 2 g administered daily for 21 days
  • Oral erythromycin - 500 mg given four times daily for 21 days
925
Q

What is the definition of Genital Herpes?

A
  • Genital herpes is an infectious disease characterized by the appearance of painful sores or ulcers on the genitals.
  • It is caused by infection with the herpes simplex viruses, either HSV-1 or HSV-2.
926
Q

What is the epidemiology Genital Herpes?

A

More common in 15 - 24 year olds

927
Q

What is the cause of Genital Herpes?

A
  • HSV-1 - Is traditionally associated with oral herpes, but it is now the most common cause of genital herpes in the UK.
  • HSV-2 - Was reviously the most common cause of genital herpes in the UK, it is more likely to cause recurrent anogenital symptoms.
928
Q

What is the clinical presentation of Genital Herpes?

A
  • Asymptomatic presentation in some individuals
  • Multiple painful genital ulcers
  • Dysuria
  • Vaginal or urethral discharge
  • Crusting and healing of lesions, marking the end of viral shedding
  • Fever, malaise, headache, and urinary retention in some cases

Recurrent episodes are usually less severe and may not have an identifiable trigger. They may be preceded by a prodromal phase characterized by tingling.

929
Q

How is Genital Herpes Diagnosed?

A
  • Clinical history and examination
  • Swab from the base of the ulcer analysed using nucleic acid amplification tests (NAATs), the most effective method
930
Q

What is the management of Genital Herpes?

A

Oral antivirals are the mainstay of treatment. Ideally initiated within 5 days of symptom onset or while new lesions are forming:
* Aciclovir 400 mg three times daily for 5 days
* Valaciclovir 500 mg twice daily for 5 days
* Aciclovir 200 mg five times daily for 5 days
* Famciclovir 250 mg three times daily for 5 days

For symptomatic relief, analgesia such as topical lidocaine may be beneficial.

931
Q

What is the management of Genital Herpes?

What additional aspects are considered in pregnancy?

A

General measures include:

  • Saline bathing
  • Analgesia
  • Topical anaesthetic agents e.g. lidocaine

Medication:

  • Oral Aciclovir (400mg for 5 days)
    some patients with frequent exacerbations may benefit from longer-term aciclovir

Pregnancy:

  • Elective caesarean section at 37 weeks if infected post 28 weeks.
  • Women with recurrent herpes who are pregnant should be treated with suppressive therapy and be advised that the risk of transmission to their baby is low
932
Q

What is the definition of Genital Warts?

A
  • Genital warts, or anogenital warts, are a type of sexually transmitted infection characterised by small, skin-colored or grey growths in the genital area.
  • They are typically painless and present in regions traumatised during sexual intercourse.
933
Q

What are some risk factors for Genital Warts?

A
  • Unprotected sex
  • Multiple sexual partners
  • Immunosuppression
  • Starting sexual activity at a young age.
934
Q

What causes Genital Warts?

A
  • They are caused by the human papillomavirus (HPV)
  • 90% of cases are attributed to attributed to serotypes 6 and 11
  • Transmission primarily occurs through direct skin-to-skin contact during sexual activity.
935
Q

What is the clinical presentation of Genital Warts?

A
  • Painless lumps on the genitals or anal area
  • The lumps are either skin coloured or grey
  • Lumps that are either keratinised (hard) or non-keratinised (soft)
  • Areas of the body that are traumatised during sexual intercourse are commonly affected
936
Q

What are some differentials of Genital Warts?

A
  • Molluscum contagiosum
    Characterised by small, firm, round bumps with a central indentation.
  • Condyloma lata (secondary syphilis)
    Presents as large, flat, grey-white lesions, often with a moist surface.
  • Genital herpes
    Presents with painful blisters or open sores in the genital area.
  • Skin tags
    Small, soft, skin-colored growths that hang off the skin and can appear anywhere.
937
Q

How is Genital Warts Diagnosed?

A
  • Diagnosis is primarily clinical made through a detailed history and visual inspection of the warts.
  • But in uncertain cases the diagnosis can be confirmed through biopsy and histopathological investigation.
938
Q

What does the management of Genital Warts involve?

A

Self Administered
Reassurance partner may not have cheated due to long latency of virus

  • Podophyllotoxin - a plant-based antiviral that can destroy wart tissue
  • Imiquimod -may weaken condoms

Specialist Treatments

  • Cryotherapy (a process that freezes the wart using liquid nitrogen) or ablative therapy can be used to treat keratinised warts
  • Trichloroacetic acid - a chemical treatment that burns off warts.

There is a high chance of reccurrence regardless of treatment.

939
Q

What is the definition of a Primary HIV Infection?

A
  • Primary HIV infection, or acute retroviral syndrome, is the phase that commences immediately after the initial exposure to the Human Immunodeficiency Virus (HIV).
  • This phase is characterised by a surge in viral replication and often coincides with the onset of clinical symptoms.
940
Q

What causes a HIV infection?

A
  • HIV, specifically HIV-1 and HIV-2, are RNA retroviruses that cause primary HIV infection.
  • The virus enters and destroys the CD4 T-helper cells of the immune system.

They are transmitted through:

  • Unprotected anal, vaginal or oral sexual activity
  • Mother to child at any stage of pregnancy, birth or breastfeeding (called vertical transmission)
  • Mucous membrane, blood or open wound exposure to infected blood or bodily fluids (e.g., sharing needles, needle-stick injuries or blood splashed in an eye)
941
Q

What is the clinical presentation of a primary HIV infection?

A

Typically presents experience as a mild flu-like illness 2-6 weeks post-exposure. But it can widely range in the serverity of symptoms. Classic presentation includes:

  • Fever
  • Lymphadenopathy
  • Maculopapular rash (commonly found on the upper chest)
  • Mucosal ulcers
  • Myalgia
  • Arthralgia
  • Fatigue
  • Some people can remain asymptomatic

After this initial flu-like illness within the first few weeks of infection. The infection is then asymptomatic until the condition progresses to immunodeficiency. Disease progression may occur years after the initial infection.

942
Q

What are the indications in a primary HIV infection, that the patient may rapidly progress to AIDS?

A
  • Symptom onset within 3 weeks of infection
  • Symptoms lasting longer than 2 weeks
  • Symptoms involving the central nervous system (CNS)
943
Q

What are some differentials for Primary HIV?

A
  • Influenza
    Characterised by sudden onset fever, cough, headache, muscle and joint pain, severe malaise, sore throat, and a runny nose.
  • Mononucleosis (Epstein-Barr virus or cytomegalovirus)
    Typically presents with fever, pharyngitis, lymphadenopathy, and fatigue.
  • Acute streptococcal pharyngitis
    Symptoms include sore throat, fever, headache, abdominal pain, nausea, and vomiting.
  • Viral hepatitis
    May present with jaundice, fatigue, nausea, fever, and muscle aches.
944
Q

How is a primary HIV infection diagnosed?

A

Serum HIV enzyme-linked immunosorbent assay (ELISA)

A positive result must be confirmed using a second test.

945
Q

What additional tests can be done when investigating a primary HIV infection?

A
  • HIV viral load
  • Full blood count
  • Lymphocyte subset panel (including CD4 count)
  • Screening for other sexually transmitted infections such as chlamydia, gonorrhoea, and syphilis
  • Screening for viral hepatitis
  • Kidney function tests
  • Liver function tests
  • Glucose
  • Lipids
946
Q

What is the management of a HIV infection?

A

Every patient is offered Combination Antiretroviral Therapy regardless of their viral load or CD4 count.

There are several classes of ART drugs:

  • Protease inhibitors (PI)
  • Integrase inhibitors (II)
  • Nucleoside reverse transcriptase inhibitors (NRTI)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTI)
  • Entry inhibitors (EI)

The usual starting regime is:

  • Two NRTIs (e.g. tenofovir plus emtricitabine)
  • Plus a third agent (e.g. bictegravir).

The aim of treatement achieve a normal CD4 count and undetectable viral load.

947
Q

What are the 2 types of HIV Screening test?

A

Fourth-generation laboratory test for HIV

  • Checks antibodies to HIV and the p24 antigen
  • It has a window period of 45 days, meaning it can take up to 45 days after exposure to the virus for the test to turn positive.
  • A negative result within 45 days of exposure is therefore unreliable

Point of care tests for HIV

  • Only checks for HIV antibodies
  • Has a window period of 90 days
948
Q

How is a HIV infection monitored?

A

CD4 Count - gives the number of CD4 cells in the blood. These are the cells destroyed by the virus. The lower the count, the higher the risk of opportunistic infection (and the development of an AIDs defining illness).
* 500-1200 cells/mm3 is the normal range
* Under 200 cells/mm3 puts the patient at high risk of opportunistic infections

HIV RNA per ml of blood indicates the viral load. And is another way to monitor how well controlled a HIV infection is. An undetectable viral load means the level is below the recordable range (usually 20 copies/ml)

949
Q

What treatment should be given to all HIV patients with a CD4 count below 200/mm3?

A

Prophylactic co-trimoxazole is given to protect against pneumocystis jirovecii pneumonia (PCP)

950
Q

What is the definition of AIDS (Acquired immunodeficiency syndrome)?

A
  • AIDS is the terminal stage of HIV infection where combination antiretroviral therapy (cART) has not halted the spread of the virus.
  • It is defined by the presence of an AIDS-defining illness alongside a CD4 count of less than 200 cells/mm³.
951
Q

What is the epidemiology of AIDs?

A

Most common in Sub-Saharan Africa

952
Q

What are some examples of AIDS defining illnesses?

A
  • Kaposi’s sarcoma
  • Pneumocystis jirovecii pneumonia (PCP)
  • Cytomegalovirus infection
  • Candidiasis (oesophageal or bronchial)
  • Lymphomas
  • Tuberculosis
953
Q

What is the clinical presentation of AIDS?

A

It depends on the specific AIDS defining illness that is present, which can include:
* Gastrointestinal symptoms
Such as dysphagia or odynophagia in oesophageal candidiasis
* Respiratory symptoms
In cases of Pneumocystis pneumonia or recurrent pneumonia
* Neurological symptoms
In cases of HIV encephalopathy, toxoplasmosis, or progressive multifocal leukoencephalopathy
* Skin lesions
In cases of Kaposi’s sarcoma or lymphoma
* Visual symptoms
In cases of cytomegalovirus (CMV) retinitis.

954
Q

What investigations are done for AIDS?

A
  • HIV testing: Primary diagnosis of HIV infection
  • CD4 cell count: To determine the progression of the disease
  • Tests specific to AIDS-defining illnesses: For example, bronchoscopy for suspected Pneumocystis pneumonia or biopsy for Kaposi’s sarcoma
955
Q

What does the management of AIDS involve?

A
  • Combination antiretroviral therapy (cART)
    To suppress HIV replication and slow disease progression
  • Prophylaxis against opportunistic infections
    Including Pneumocystis pneumonia and toxoplasmosis
  • Treatment of AIDS-defining illnesses
    Specific to the illness, for example, antifungal therapy for candidiasis or chemotherapy for lymphoma
956
Q

How can the spread of HIV be prevented (or the risk reduced)?

A
  • Correct use of condoms
  • Effective treatment combined with an undetectable viral load appears to prevent the spread of HIV, even during unprotected sex.
  • Post-Exposure Prophylaxis (PEP) - Can be used after exposure to reduce the risk of transmission. Its not 100% effective however and must be commenced within a short window of opportunity (less than 72 hours).
  • Pre-exposure prophylaxis (PrEP) is also available to take before exposure to reduce the risk of transmission.
957
Q

What is the most common form of PrEP?

A

Emtricitabine or tenofovir (Truvada).

958
Q

What is the recommended regime for PEP?

A
  • It involves a combination of Anti-retroviral therapy
  • emtricitabine/tenofovir (Truvada) and raltegravir for 28 days.
  • The sooner PEP is started after exposure, the greater the chance it will work.
959
Q

How can a HIV infection affect a pregnancy?

A

The HIV virus can transfer from mother to child at any stage of the pregnancy; however the greatest risk is during delivery (particularly a vaginal delivery)

The mother’s viral load affects what delivery type is reccomended:
* Under 50 copies/ml - Normal vaginal delivery
* Over 50 copies/ml - Pre-labour Cesaerean section is recommended

IV zidovudine is given as an infusion during labour and delivery if the viral load is unknown or above 1000 copies/ml.

960
Q

After birth, what prophlaxis can be given to the baby with a HIV positive mother?

A

Post Exposure Prophylaxis

  • Low-risk babies (mother’s viral load is under 50 copies per ml) are given zidovudine for 2-4 weeks
  • High-risk babies are given zidovudine, lamivudine and nevirapine for four weeks
961
Q

Can HIV positive mothers breastfeed?

A
  • HIV can be transmitted during breastfeeding.
  • Therefore the safest option is to avoid breastfeeding alltogether and to use formula milk (even if the mother’s viral load is undetectable).
962
Q

What is the definition of Erectile Dysfunction?

A

Erectile dysfunction (ED) is defined as the consistent or recurrent inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance.

963
Q

What is the epidemiology of Erectile Dysfunction?

A
  • It is more common in older men
  • It affects more than 50% of men aged over 60
964
Q

What causes erectile dysfunction?

A
  • Vascular disease
    Atherosclerosis can lead to impaired blood flow to the penis, leading to ED.
  • Autonomic neuropathy
    This can cause penile denervation, most commonly seen in conditions like diabetes or with excessive alcohol intake.
  • Medications
    Certain drugs, such as antihypertensive agents, can cause ED.
  • Psychogenic
    Anxiety, depression, and other psychological factors can contribute to ED.
  • Endocrine causes
    Conditions like prolactinoma and hypogonadism can cause hormonal imbalances leading to ED.
  • Pelvic surgery
    Procedures involving the bladder, prostate, or other pelvic structures can damage nerves and blood vessels, leading to ED.
  • Anatomical abnormalities
    Conditions like Peyronie’s disease, characterized by fibrous scar tissue inside the penis, can cause ED.
965
Q

What is the clinical presentation of Erectile Dysfunction?

A

Primary symptom of erectile dysfunction is the inability to achieve or maintain an erection sufficient for sexual intercourse. This can also lead to:

  • Reduced sexual desire
  • Difficulty in ejaculation
  • Anxiety or depression related to sexual performance

Signs which suggest an organic cause:
* lack tumescence
* slow-onset
* normal libido.

Signs which suggest a psychogenic cause
* If situational
* Acute onset
* High levels of stress
* Still having early morning erections.

966
Q

What are some differentials for Erectile Dysfunction?

A
  • Premature ejaculation
    Characterized by uncontrolled ejaculation either before or shortly after sexual penetration.
  • Hypogonadism
    Characterized by low testosterone levels, resulting in low sex drive, fatigue, and mood changes.
  • Peyronie’s disease
    Presents with a significant bend in the penis during erection, which can interfere with sexual function.
967
Q

How is Erectile Dysfunction investigated?

A
  • Detailed sexual and psychological history to identify potential contributing factors.
  • Blood tests - Full blood count, urea and electrolytes, thyroid function tests, lipid profile, testosterone, and prolactin to evaluate overall health and hormonal status.
  • It can sometimes be the first presentation of sequalae of cardiovascular disease and so presentation should prompt investigation of cardiovascular health.
968
Q

What is the management of Erectile Dysfunction?

A
  • Psychosexual therapy
    To address any underlying psychological factors.
  • Oral phosphodiesterase inhibitors (e.g. Sildenafil)
    To enhance the effect of nitric oxide, increasing blood flow to the penis.
  • Vacuum erection devices
    To draw blood into the penis by applying negative pressure.
  • Intra-cavernosal injections
    To directly increase blood flow.
  • Penile prostheses
    For cases resistant to other treatments.
969
Q

What are the side effects of Phosphodiesterase inhibitors (Sildenafil)?

A
  • Headache
  • Flushing
  • Hypotension
  • Blue tinge to vision (little blue pill).
970
Q

In what patients is Sildenafil contraindicated in?

A
  • Individuals taking nitrates
  • Hypertension/hypotension
  • Arrhythmias
  • Unstable angina
  • Stroke
  • Recent myocardial infarction.
971
Q

What is Nausea and Vomiting in Pregnancy and Hyperemesis Gravidarum?

A

The term ‘nausea and vomiting of pregnancy’ (NVP) to describe troublesome symptoms, with hyperemesis gravidarum being the extreme form of this condition.

972
Q

When is Hyperemesis Gravidarum typically experienced?

A

Most common between 8-12 weeks but may persist up until 20 weeks

973
Q

What are the risk factors for Hyperemesis Gravidarum?

A

Increased levels of beta-hCG

  • Multiple pregnancies
  • Trophoblastic disease

Other:

  • Nulliparity
  • Obesity
  • Thyrotoxicosis (mimic of TSH as bHCG)
  • Family or personal history of NVP

Smoking is associated with a decreased incidence of hyperemesis.

974
Q

What is the criteria for Hyperemesis Gravidarum?

A

Triad of:

  • 5% pre-pregnancy weight loss
  • Dehydration
  • Electrolyte imbalance
975
Q

What scoring system is used to classify the severity of nausea and vomiting in pregnancy?

A

pregnancy-Unique Quantification of Emesis (PUQE) Score

976
Q

When should admission be considered for patients with nausea and vomiting in pregnancy?

A
  • Unable to keep down liquids or oral antiemetics
  • Nausea and Vomiting with ketonuria and/or weight-loss despite treatment with oral antiemetics
  • Confirmed or suspected co-morbidity
977
Q

What is the Management for Hyperemesis Gravidarum?

A

Simple Measures:

  • Rest and avoid triggers
  • Ginger
  • Bland plain food

First Line Medications:

  • Antihistamines: Cyclizine or Promethazine
  • Phenothiazines: Prochlorperazine or chlorpromazine

Second Line Medications:

  • Oral Ondansetron
  • Oral Metoclopramide or Domperidone (only used for no more than 5 days)

Admission:

  • Maybe required for IV anti-emetics
  • Normal saline with added potassium is used to rehydrate.
978
Q

What is the concern with using Ondansetron in pregnancy?

A

Use in first trimester is associated with a small increased risk of Cleft lip/palate

979
Q

What is the concern with using Metoclopramide?

A

May cause extrapyramidal effects so shouldnt be used for more than 5 days.

980
Q

What are the Most common complications of Hyperemesis Gravidarum?
What are some other potential complications?

A

Most Common:

  • Dehydration
  • Weight loss
  • Electrolyte imbalances - notably hypokalaemia

Other Complications:

  • AKI
  • Wernicke’s encephalopathy
  • Mallory-weiss tear
  • VTE
981
Q

Define Premenstrual Syndrome?

A

Emotional and physical symptoms that women may experience in the luteal phase or a normal menstrual cycle

982
Q

What are the symptoms of Premenstrual Syndrome?

A

Emotional symptoms include:

  • Anxiety
  • Stress
  • Fatigue
  • Mood swings

Physical symptoms

  • Bloating
  • Breast pain
983
Q

What is the Management for Premenstrual Syndrome?

A

Lifestyle advice

  • Sleep
  • Exercise
  • Smoking and alcohol cessation
  • Small balanced meals with rich complex carbs

Moderate Symptoms

  • 3rd Generation COCP

Severe Symptoms

  • SSRIs such as fluoxetine taken during the luteal phase
984
Q

What is defined as small for gestational age?

A

Fetus measuring < 10th centile for gestational age based on:

Estimated fetal weight (EFW)
Fetal abdominal circumference

985
Q

What is severe SGA?

A

Fetus is below the 3rd centile for gestational age

986
Q

What defines Low birth weight?

A

Birth weight less than 2500g

987
Q

What are the cause of SGA?

A
  • Constitutionally small
  • Fetal growth restriction/Intrauterine Growth Restriction (IUGR)
988
Q

Define IUGR?

A

When the fetus is small or not growing as expected dur to pathology reducing the amount of nutrients and oxygen delivered to the fetus through the placenta

989
Q

What are the two categories of causes for IGUR?

A

Placental mediated growth Restriction
Non-placental mediated growth restriction

990
Q

What are some placenta mediated growth restriction causes?

A

Conditions that affect the transfer of nutrients across the placenta

  • Idiopathic
  • Pre-eclampsia
  • Maternal smoking
  • Maternal alcohol
  • Anaemia
  • Malnutrition
  • Infection
  • Maternal health conditions
991
Q

What are some Non-placenta mediated growth restriction causes?

A

Pathology of the fetus

  • Genetic abnormalities
  • Structural abnormalities
  • Fetal infection
  • Errors of metabolism
992
Q

What are some short term complications of IUGR?

A
  • Fetal death or still birth
  • Birth asphyxia
  • Neonatal hypothermia
  • Neonatal hypoglycaemia
993
Q

What are some long term complications of IUGR?

A
  • CVD particularly Hypertension
  • T2DM
  • Obesity
  • Mood and behavioural problems
994
Q

What are some risk factors for SGA?

A

Previous SGA baby
Obesity
Smoking
Diabetes
Existing hypertension
Pre-eclampsia
Older mother (over 35 years)
Multiple pregnancy
Low pregnancy‑associated plasma protein‑A (PAPPA)
Antepartum haemorrhage
Antiphospholipid syndrome

995
Q

What monitoring should be done in women with a fetus that is SGA?

A

low risk women have SFH measured at every antenatal appointment from 24 weeks onwards.

Women with 1 major or 3 minor risk factors will have serial growth scans and umbilical artery dopplers every 4 weeks from 28 weeks/

996
Q

What is measured during a serial growth scan for fetuses of SGA?

A
  • Estimated fetal weight (EFW) and abdominal circumference (AC) to determine the growth velocity
  • Umbilical arterial pulsatility index (UA-PI) to measure flow through the umbilical artery
  • Amniotic fluid volume
997
Q

What management steps should be taken if a child is at risk of SGA?

A
  • Identifying those at risk of SGA
  • Aspirin is given to those at risk of pre-eclampsia
  • Treating modifiable risk factors (e.g. stop smoking)
  • Serial growth scans to monitor growth (eg. 4 weekly at 28 weeks)
  • Early delivery where growth is static, or there are other concerns
998
Q

What investigations may be done to identify the underlying cause of SGA?

A
  • Blood pressure and urine dipstick for pre-eclampsia
  • Uterine artery doppler scanning
  • Detailed fetal anatomy scan by fetal medicine
  • Karyotyping for chromosomal abnormalities
  • Testing for infections (e.g. toxoplasmosis, cytomegalovirus, syphilis and malaria)
999
Q

What is the management for a child with IUGR or where growth is static?

A

Planned early delivery

  • Corticosteroids are given to help fetal lungs mature
  • Magnesium sulphate may be given for neuroprotection
1000
Q

Define Large for Gestational Age (LGA)?

A

Macrosomia where the weight of the newborn is >4.5kg at birth.
EFW above the 90th centile is considered LGA

1001
Q

What are some causes for Macrosomia?

A
  • Constitutional
  • Maternal diabetes
  • Previous macrosomia
  • Maternal obesity or rapid weight gain
  • Overdue
  • Male baby
1002
Q

What are the risks to the mother if a fetus is macrosomic?

A
  • Shoulder dystocia
  • Failure to progress
  • Perineal tears
  • Instrumental delivery or caesarean
  • Postpartum haemorrhage
  • Uterine rupture (rare)
1003
Q

What are the risks to the baby if the fetus is Macrosomic?

A
  • Birth injury (Erbs palsy, clavicular fracture, fetal distress and hypoxia)
  • Neonatal hypoglycaemia
  • Obesity in childhood and later life
  • Type 2 diabetes in adulthood
1004
Q

What are the investigations if a baby is found to be LGA?

A
  • Ultrasound to exclude polyhydramnios and estimate the fetal weight
  • Oral glucose tolerance test for gestational diabetes
1005
Q

What are some pregnancy related rashes?

A
  • polymorphic eruption of pregnancy
  • Melasma
  • Pemphigoid Gestations
1006
Q

What is Polymorphic Eruption of Pregnancy?

A

An itchy rash that tends to start in the Third trimester that usually begins on the abdomen

1007
Q

What are the characteristic features of Polymorphic Eruption of Pregnancy

A
  • Urticarial papules
  • Wheals (Raised itchy areas of skin)
  • Plaques
1008
Q

What is the management of Polymorphic Eruption of Pregnancy?

A

Topical emollients, oral antihistamines and topical steroids

Condition gets better towards the end of pregnancy and after delivery

1009
Q

What is Melasma?

A

Increased pigmentation to patches of the skin on the face.

Typically doesn’t require treatment

1010
Q

What are pemphigoid gestations?

A

Autoimmune skin condition occurring in pregnancy.

Auto Abs damage connections between epidermis and dermis produced in response to placental tissue.

1011
Q

What is the cause of Congenital Rubella Syndrome?

A

Maternal infection with the rubella virus during the first 20 weeks of pregnancy. The risk is highest before ten weeks gestation.

1012
Q

What vaccine should women planning to become pregnant ensure they have had?

A

MMR vaccine to prevent congenital rubella syndrome

When in doubt rubella immunity should be tested.
If they do not have antibodies then they can be vaccinated with 2 doses of MMR 3 months apart.

1013
Q

What are the clinical features of congenital rubella syndrome?

A

A Blind deaf neurotic duck

  • Blind - congenital cateracts
  • Deaf - congenital deafness
  • Neurotic - learning disability
  • Duck - PDA and pulmonary stenosis
1014
Q

Why is chicken pox dangerous in pregnancy/what can it cause in the mother and the infant?

A

Mother: Varicella pneumonitis, Hepatitis or encephalitis

Fetal Varicella syndrome

Severe neonatal varicella infection if infected around delivery

1015
Q

What should the mother do if they come into contact with someone with chickenpox whilst pregnant?

A
  • When the pregnant woman has previously had chickenpox, they are safe
  • When they are not sure about their immunity, test the VZV IgG levels. If positive, they are safe.
  • When they are not immune, they can be treated with IV varicella immunoglobulins as prophylaxis against developing chickenpox. This should be given within ten days of exposure.
1016
Q

When may congenital varicella syndrome occur?

A

occurs in around 1% of cases of chickenpox in pregnancy.
It occurs when infection occurs in the first 28 weeks of gestation.

1017
Q

What are the clinical features of Congenital Varicella Syndrome?

A
  • Fetal growth restriction
  • Microcephaly, hydrocephalus and learning disability
  • Scars and significant skin changes located in specific dermatomes
  • Limb hypoplasia (underdeveloped limbs)
  • Cataracts and inflammation in the eye (chorioretinitis)
1018
Q

What is Listeria and Listeriosis?

A

Listeria is a gram positive bacteria that can easily lead to listeriosis in pregnant women

1019
Q

What are the complications of Listeriosis in pregnancy?

A

High rate of Miscarriage or fetal death
Can cause severe neonatal infection

1020
Q

How is Listeria typically transmitted?

A

unpasteurised dairy products
Processed meats

Women are advised to avoid high risk foods such as blue cheese, camembert and brie

1021
Q

What is the management for Listeriosis?

A

Primary treatment involves a combination of the antibiotics ampicillin and an aminoglycoside

1022
Q

What are the features of congenital cytomegalovirus infection (CMV)

A
  • Fetal growth restriction
  • Microcephaly
  • Hearing loss
  • Vision loss
  • Learning disability
  • Seizures
1023
Q

How is Toxoplasmosis spread?

A

Toxoplasma gondii parasite is usually asymptomatic
Spread via contamination with faeces from a cat

1024
Q

What is the classical triad of congenital Toxoplasmosis?

A
  • Intracranial Calcification
  • Hydrocephalus
  • Chorioretinitis
1025
Q

What are the features of Congenital Toxoplasmosis?

A

Cory with the big head likes stiff calcium jerky

Cory (chorioretinitis)
Big head (hydrocephalus)
Stiff (spasticity)
Calcium (cerebral calcifications)
Jerky (seizures)

1026
Q

What are the complications of Parovirus B19 infection during pregnancy?
Which trimesters are most important?

A

Affects first and second trimesters

  • Miscarriage or fetal death
  • Severe fetal anaemia
  • Hydrops Fetalis (fetal heart failure)
  • Mirror Syndrome
1027
Q

What is Mirror Syndrome?

A

Maternal pre-eclampsia like syndrome: A rare complication of hydrops fetalis characterised by the triad:

  • Hydrops Fetalis
  • Placental Oedema
  • Oedema in the mother

PLUS features of hypertension and proteinuria mirroring Pre-eclampsia

1028
Q

What should be done for women suspected for Parvovirus B19 infection during pregnancy?

A
  • IgM to parvovirus, which tests for acute infection within the past four weeks
  • IgG to parvovirus, which tests for long term immunity to the virus after a previous infection
  • Rubella antibodies (as a differential diagnosis)
1029
Q

How is the Zika Virus spread?

A

Host Aedes Mosquitos.
It can be spread by sex with someone infected with the virus

1030
Q

What are the features of Congenital Zika Syndrome?

A
  • Microcephaly
  • Fetal Growth Restriction
  • Intracranial abnormalities: Ventriculomegaly and cerebellar atrophy
1031
Q

What are the classifications of Caesarean Section?

A

Category 1:

  • Within30 mins of decision
  • Immediate threat to life of women or fetus

Category 2:

  • Within 75 mins of decision
  • Maternal/fetal compromise but not immediately life threatening

Category 3:

  • No compromise but early birth is indicated
  • *Category 4:**
  • Elective - maternal choice
1032
Q

What are the indications for Caesarean Section?

A
  • Previous caesarean
  • Symptomatic after a previous significant perineal tear
  • Placenta praevia
  • Placenta accreta spectrum
  • Vasa praevia
  • Breech presentation
  • Multiple pregnancy
  • Uncontrolled HIV infection
  • Cervical cancer
1033
Q

What are the indications for Emergency C-Section?

A
  • Fetal Bradycardia
  • Abruption
  • Uterine rupture
  • Cord Prolapse
  • Fetal pH < 7.2
  • Failure of instrumental delivery
1034
Q

What are some complications of Caesarean Section?

A

Maternal Complications

  • General surgical risks (bleeding, infection, pain ,VTE)
  • Post partum Complications (haemorrhage, infeection, endometritis)
  • Damage to local Structures (Ureter, bladder, bowel, Blood vessels)
  • Effects on abdo organs (Ileus, adhesions, hernias)
  • Effects on future pregnancies ( Repeat c-section, uterine rupture, placenta praevia, still birth)

Effects on Baby:

  • Risk of lacerations
  • Increased risk of Transient Tachypnoea of the Newborn