Womens Health (Joe) 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 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 vagina

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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 sine 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

What 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
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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

Hormonal Tests: To assess levels of FSH, LH and Oestradiol

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 before the age of 40 years old.

It is the result of premature 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 symtpoms?

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 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
  • 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 dilateion 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

When signs and symptoms are made worse by friction to the skin.

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 examination, including speculum examination if tolerated, to look for vaginal signs of atrophy
  • 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 E6) 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
  • 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 volume of blood is considered menorrhagia?

A
  • Average menstruation women lose 40ml of blood
  • Excessive menstrual blood loss involves more than 80ml loss

Volume of blood loss is rarely measured in practice

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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.

Usually, when ovulation occurs, a corpus luteum is formed in the ovaries from the ruptured follicle that released the egg.

It is this corpus luteum that produces progesterone, providing endometrial protection during the luteal phase of the menstrual cycle (the second half of the menstrual cycle).

Women with polycystic ovarian syndrome are less likely to ovulate and form a corpus luteum.

Without developing a corpus luteum during the menstrual cycle, progesterone is not produced, and the endometrial lining has more exposure to unopposed oestrogen

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228
Q

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

A

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
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

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
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

240
Q

What is the Epidemiology of Endometriosis?

A

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

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
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
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.

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.
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.

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

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.

248
Q

Define Fibroids?

A

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

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
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

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.
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
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
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
255
Q

What is the management of Fibroids?

A

For fibroids less than 3 cm, the medical management is the same as with heavy menstrual bleeding:

  • Mirena coil (1st line) – fibroids must be less than 3cm with no distortion of the uterus
  • Symptomatic management with NSAIDs and tranexamic acid
  • Combined oral contraceptive
  • Cyclical oral progestogens

Surgical options for managing smaller fibroids with heavy menstrual bleeding are:

  • Endometrial ablation
  • Resection of submucosal fibroids during hysteroscopy
  • Hysterectomy

For fibroids more than 3 cm, women need referral to gynaecology for investigation and management. Medical management options are:

  • Symptomatic management with NSAIDs and tranexamic acid
  • Combined oral contraceptive
  • Cyclical oral progestogens
  • GnRH Agonists (Goserelin) may be used to shrink fibroids before surgery

Surgical options for larger fibroids are:

  • Uterine artery embolisation
  • Myomectomy
  • Hysterectomy
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%)
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. Red degeneration is more likely to occur in larger fibroids (above 5 cm) during the second and third trimester of pregnancy.

258
Q

How does Red Degeneration of Fibroids Present?

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

What is the Management of Red Degeneration of Fibroids?

A

Supportive management

  • Rest
  • Fluids
  • Analgesia
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.

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

262
Q

What are the different Types of Hydatidiform Mole?

A

Complete Mole:

  • Occurs when two sperm cells 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 (it is a haploid cell).
  • The cell divides and multiplies into a tumour called a partial mole.
  • In a partial mole, some foetal material may form.
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.

264
Q

What are the clinical features of a Hydatidiform Mole?

A
  • Vaginal bleeding
  • More severe morning sickness
  • Hyperemesis gravidarum
  • Thyrotoxicosis (due to hCG being closely related to TSH and therefore able to activate its receptors)
  • Enlargement of the uterus beyond the expected size for gestational age, due to excessive growth of trophoblasts and retained blood.
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.
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
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
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.
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.

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
271
Q

What genetic condition is associated with Prolactinomas?

A

Multiple Endocrine Neoplasia (MEN) Type I

272
Q

What are the different types of Prolactinoma?

A

Microprolactinomas – smaller than 10 mm

Macroprolactinomas – larger than 10 mm

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
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
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.
276
Q

What are some complications of Prolactinomas?

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

Define Ovarian Cancer?

A

Malignant proliferation originating from various cell types within the ovary

278
Q

What are the different types of Ovarian Tumour?

A
  • Epithelial Cell Tumours
  • Dermoid Cysts/ Germ Cell Tumours
  • Sex Cord-Stromal tumours
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.
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
281
Q

What are Dermoid Cysts/ 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
  • These tumours typically grow rapidly and spread predominantly via the lymphatic route
  • Germ cell tumours most commonly arise in young women, which is atypical for most cases of ovarian cancer
  • Tumour markers include alpha-fetoprotein and sometimes beta human chorionic gonadotrophin (B-HCG).
282
Q

What are Sex Cord-Stromal Tumours?

A
  • Originate from connective tissue (stroma) or Sex Cords (Embryonic structures associated with the follicles)
  • They are rare, making up less than 5% of all ovarian tumours. They can be benign or malignant tumours, but are much less aggressive than epithelial tumours
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.
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

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)
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
287
Q

What are the clinical features of Ovarian Cancer?

A

** Often present late in disease progression with Non-specific symptoms**

  • 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)
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.

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
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
291
Q

What are the investigations for Ovarian Cancer?

A

Initial Investigations:

  • CA125 Blood Test: (> 35IU/ml is significant)
  • Pelvic and Abdominal Ultrasound Scan

Risk of Malignancy Index (RMI): Estimates risk of ovarian mass being malignant

  • Menopausal Status
  • Ultrasound findings
  • CA125 Level

Further Investigations in Secondary Care:

  • CT Scan: for Staging
  • Histology: via CT guided biopsy, laparoscopy or laparotomy
  • Paracentesis: Ascitic tap used to look for cancer cells

Women Under 40 years with complex ovarian mass:

  • AFP and hCG tumour markers for possible Germ cell tumour
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
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
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

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.

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
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
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

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
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
  • Endometrioma: occurs with endometriosis
  • Malignant cysts: Dermoid/ Sex cord/Stromal
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.
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

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
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
305
Q

What is the management of Ovarian Cysts?

A

Conservative:

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

What are some complications of Ovarian Cysts?

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

What is Meig’s Syndrome?

A

Triad of:

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

Treatment is removal of the tumour

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

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
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
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
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
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

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)
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
316
Q

Define Polycystic Ovarian Syndrome (PCOS)?

A

PCOS is a heterogeneous condition within the endocrine system, with its onset commonly observed at puberty.

The disorder is characterised by hyperandrogenism (manifesting as oligomenorrhoea, hirsutism, and acne), ovulation disorders, and polycystic ovarian morphology.

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
318
Q

What is the Epidemiology of PCOS?

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

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
  • Mood changes including Anxiety and depression
  • Hair loss in a male pattern
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
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.
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
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.

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)
  • Testosterone: Raised
  • 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
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
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
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
330
Q

How can Infertility be managed in PCOS?

A

Weight loss is the initial step for improving fertility

Other options:

  • Clomiphene - induces ovulation
  • Laparoscopic Ovarian Drilling
  • IVF
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
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)
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.
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

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
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
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)
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
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.
340
Q

What are the investigations for PID?

A

Pelvic Examination

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

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

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%)
343
Q

What is Fitz-Hugh-Curtis Syndrome?

A

Complication of PID 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

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

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.

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
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
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
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.
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
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
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.

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
354
Q

What causes Postpartum depression?

A

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

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
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
357
Q

What Social Factors contribute to the development of postpartum depression?

A
  • Lack of social support
  • Relationship issues,
  • Life stressors
  • Low socioeconomic status
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.
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)

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.

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.

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

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.

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
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
366
Q

What is the clinical presentation of Postpartum Psychosis?

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

What is the main differential for Postpartum Psychosis?

A

Postpartum depression with psychotic features

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.

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).

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.

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.

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.

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
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

375
Q

What are the regions where an Ectopic Pregnancy may occur?

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

What are some risk factors for an Ectopic Pregnancy?

A
  • Previous ectopic pregnancy
  • Previous pelvic inflammatory disease or Salpingitis (tubal inflammation)
  • Previous surgery to the pelvis (Especially the fallopian tubes)
  • Intrauterine devices in situ (coils)
  • Endometriosis
  • Older age
  • Smoking
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).
378
Q

When do Ectopic pregnancies typically present?

A

Around 6-8 weeks gestation

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)
380
Q

What are some differential diagnoses for Ectopic Pregnancies?

A
  • Miscarriage
  • Appendicitis
  • Ovarian Torsion
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.
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)
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)
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

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

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.
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)
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

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
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.

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
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.
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)
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

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
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.

397
Q

What is a threatened miscarriage?

A

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

398
Q

What is an Inevitable miscarriage?

A

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

399
Q

What is an Incomplete miscarriage?

A

retained products of conception remain in the uterus after the miscarriage

400
Q

What is a complete miscarriage?

A

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

401
Q

What is an Anembryonic pregnancy?

A

a gestational sac is present but contains no embryo

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
403
Q

What are some risk factors for a miscarriage?

A
  • Increased Maternal Age
  • Previous Miscarriage
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
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
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
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.
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

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).
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.
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
412
Q

What are some side effects for Misoprostol?

A
  • Heavier bleeding
  • Pain
  • Vomiting
  • Diarrhoea
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)
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
  • Ethnic backgrounds with a high prevalence of type 2 diabetes (e.g., Middle Eastern, South Asian, and Afro-Caribbean)
  • Prior history of GDM
  • Prior delivery of macrosomic babies (>4.5kg)
  • History of stillbirth or perinatal death
  • Maternal obesity (BMI>30)
  • Diabetes in first-degree relatives
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 any risk factor 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

What should women with pre-existing diabetes who are thinking of being pregnancy do?

A

Prior to conception

  • Aim for good glucose control
  • Take 5mg folic acid from preconception until 12 weeks gestation
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.

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 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

What is the Management of Pre-eclampsia?

A
  • Scoring systems are used to determine whether to admit the woman (fullPIERS or PREP‑S)
  • 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
499
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

500
Q

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

A

Delivery of the foetus and placenta

501
Q

What is the Management for Eclampsia?

A

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

502
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

503
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.
504
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
505
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

506
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
507
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
508
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.

509
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
510
Q

What is the Aetiology of Obstetric Cholestasis?

A

Multifactorial:

  • Hormonal Factors such as Increased oestrogen and Progesterone
  • Genetic factors
  • Environmental triggers
511
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.

512
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.
513
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.
514
Q

What are some differential diagnoses for Obstetric Cholestasis?

A
  • Gallstones
  • Acute fatty liver
  • Autoimmune hepatitis
  • Viral hepatitis
515
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.

516
Q

What is the Management of Obstetric Cholestasis?

A

First Line:

  • Emollients: soothe the skin
  • Antihistamines: Chlorphenamine to alleviate itching and aid in sleeping

Second Line:

  • Ursodeoxycholic acid: Improves LFTs, bile acids and symptoms
517
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.

518
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.

519
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.

520
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.

521
Q

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

A

Bartholin’s gland cyst:

  • Palpable swelling and 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.
522
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.
523
Q

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

A

Physical examination: To assess the size, location, and nature (cystic or solid) of the swelling.

Ultrasound: To confirm the diagnosis and rule out other potential causes of vulvar swelling.

Biopsy: In postmenopausal women or in cases where malignancy is suspected.

Culture: In cases of abscess to identify the causative organism.

524
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
525
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

526
Q

What are some risk factors for SIDS?

A
  • Prematurity
  • Low birth weight
  • Smoking during pregnancy
  • Male baby (slightly increased risk)
527
Q

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

A
  • Put the baby on their back when not directly supervised
  • 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).
  • Avoid co-sleeping, particularly on a sofa or chair
  • If co-sleeping avoid alcohol, drugs, smoking, sleeping tablets or deep sleepers
528
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
529
Q

What are the 2 stages of the Menstrual Cycle?

A

Follicular/Proliferative Phase Days 1-14

Luteal/Secretory Phase Days 15-28

530
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.
531
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.
532
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)
533
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
534
Q

What are some examples of Emergency Contraception?

A
  • Levonorgestrel Pill
  • Ulipristal Acetate Pill (EllaOne)
  • Copper Intrauterine Device (Cu-IUD)
535
Q

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

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Copper ions prevent fertilisation by immobilising sperm and inactivating lytic enzymes required for the acrosome reaction

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.
536
Q

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

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Progestogen and Oestradiol components exert negative feedback on hypothalamus and pituitary respectively reducing LH and FSH release and thus ovulation is suppressed

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
537
Q

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

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Progestogen exerts negative feedback on hypothalamus, reducing GnRH release frequency and therefore suppressing secretion of LH and FSH. This suppresses follicle development, the LH surge, and ovulation

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
538
Q

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

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Thinning of endometrium by downregulation of endometrial oestrogen receptors; this prevents implantation. Does not inhibit ovulation.

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
539
Q

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

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Progestogen exerts negative feedback on hypothalamus, reducing GnRH release frequency and therefore suppressing secretion of LH and FSH. This suppresses follicle development, the LH surge, and ovulation

Efficacy: 6% experience unintended pregnancy after 1 year.

Advantages:

  • Long acting - Requires injection every 13 weeks

Absolute Contraindications:

  • Breast Cancer

Side Effects:

  • Amenorrhoea
540
Q

What are the features of the Contraceptive Implant:

Mechanism:

Efficacy:

Advantages:

Absolute Contraindications:

Side Effects:

Other:

A

Mechanism: Progestogen exerts negative feedback on hypothalamus, reducing GnRH release frequency and therefore suppressing secretion of LH and FSH. This suppresses follicle development, the LH surge, and ovulation

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
541
Q

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

Mechanism:

Efficacy:

A

Mechanism:

  • Exogenous progestogen, exerts negative feedback on hypothalamus to
    prevent the LH surge and delay ovulation in event of unprotected sexual intercourse
    (UPSI)
  • 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
542
Q

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

Mechanism:

Efficacy:

A

Mechanism: Selective progesterone receptor modulator, inhibits ovulation (possibly by blocking hypothalamic progesterone receptors, which studies suggest play a role in producing the LH surge)

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
543
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.
544
Q

Define Fertilisation

A

Fusion of haploid sperm and oocyte, typically occurring in the ampulla of the
fallopian tube.

545
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

546
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.
547
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
548
Q

What are the Maternal Physiological Changes that occur in pregnancy?

A

Cardiovascular:

  • TPR decreases
  • Cardiac output increases by 45%

Haematological:

  • Red cell mass increases
  • Physiological anaemia due to an increase in plasma volume diluting the conc of Hb
  • Decreased platelet count
  • Clotting factors VII, VIII, IX, X increase leading to a hypercoagulable state

Renal:

  • Increased renal blood flow and GFR
  • Low serum urea and creatinine due to raised GFR

Respiratory:

  • Lung volume increases
  • Minute ventilation and oxygen consumption in crease by 50% and 30% respectively

Breasts:

  • Ductal proliferation
  • Prolactin stimulates milk production from alveolar cells
  • Alveoli grow

Gastrointestinal:

  • Gastric emptying is slowed and bowel motility is decreased (Gastric reflux and constipation)

Skin:

  • Increased pigmentation of face and areola
  • Linea nigra
  • Stria gravidarum

Endocrine:

  • Oestrogen and progesterone rise throughout pregnancy
549
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

550
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
551
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
552
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
553
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)
554
Q

What are the results of the Combined test that are suggestive of Trisomy Anomaly?

A

Trisomy 21 (Down’s): high b-hCG, Low PAPP-A, High NT (>3.5mm) (Quadruple test: Low AFP, high Inhibin-A, Low Unc Oestriol)

Trisomy 18 (Edwards’): Low b-hCG, Low PAPP-A, High NT

Trisomy 13 (Patau’s): Low b-hCG, Low PAPP-A, High NT

555
Q

When does Labour and Delivery normally occur?

A

Normally occur between 37 and 42 weeks gestation

556
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
557
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.

558
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.

559
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.
560
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
561
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.
562
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
563
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)
564
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.

565
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
566
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
567
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 predicts a successful induction of labour

A score below this suggests cervical ripening may be required to prepare the cervix

568
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
569
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
570
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
571
Q

What can uterine Hyperstimulation lead to?

A
  • Foetal compromise, with hypoxia and acidosis
  • Emergency caesarean section
  • Uterine rupture
572
Q

What is the Management of Uterine Hyperstimulation?

A
  • Removing the vaginal prostaglandins, or stopping the oxytocin infusion
  • Tocolysis with terbutaline
573
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.
574
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
575
Q

How can Foetal Heart rate be measured?

A

Low risk deliveries: Intermittent Auscultation with a Doppler Probe

High risk Deliveries: Cardiotocograph (CTG)

576
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

577
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
578
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

579
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

580
Q

What are some Abnormal features of the CTG?

A

Baseline Rate: <100/ >60

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

581
Q

What does a Sinusoidal CTG suggest?

A

Severe Foetal Compromise

Usually associated with severe foetal anaemia caused by vasa praevia with foetal haemorrhage

582
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)
583
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)

584
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
585
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

586
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.

587
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
588
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)