Week 5 Flashcards

1
Q

Describe the Pathophysiology of Polycystic Ovarian Syndrome.

A

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women. It is characterized by hyperandrogenism (which primarily manifests as hirsutism, acne, and, occasionally, virilization), oligoovulation/anovulation, and/or the presence of polycystic ovaries.

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2
Q

Polycystic Ovarian Syndrome
- Clinical Features?

A
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3
Q

PCOS - Pathology
- Macroscopic appearance?
- Microscopic appearance?

4 Complications of PCOS?

A

Macroscopic appearance
- Multiple, brown cysts arranged in a circular pattern in the subcapsular region of the ovary.
- Cysts are relatively small and of approximately the same size.

Microscopic appearance
- Ovarian hypertrophy with thick capsule
- Stromal hyperplasia and fibrosis
- Multiple enlarged cystic follicles
- Hyperluteinized theca cells
- Decreased granulosa cell layer

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4
Q

Diagnosis of PCOS
- Rotterdam criteria?
- Lab studies?
- Evaluate for comorbidities? (5)

A

Evaluate for comorbidities
Metabolic screening and monitoring
1. Measure weight, height, and waist circumference; calculate BMI. For patients with elevated BMI:
2. Obtain a fasting lipid profile and screen for symptoms of obstructive sleep apnea.
3. Check blood pressure
4. Assess glycemic status
5. Mental health and quality of life: Screen for anxiety, depression, and psychosexual dysfunction.

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5
Q

Describe in detail the biochemical and cellular changes that occur in PCOS.
- 1) Hormonal Imbalances? (3)
- 2) Ovarian Changes? (2)
- 3) Metabolic Disturbances? (4)
- 4) Inflammation? (1)
- 5) Hypothalamic-Pituitary Dysfunction? (1)
- 6) Endometrial Changes? (1)
- 7) Fertility and Reproductive Issues? (3)

A
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6
Q

Outline the treatment of PCOS.
- Recommendations for all patients?
- Patients not planning to conceive?
- Patients planning to conceive?

A

Approach to treating PCOS
Recommendations for all patients
1. Encourage exercise and healthy eating (e.g. caloric restriction), and consider behavioral strategies and modifications (e.g., setting goals, eating more slowly).
2. Target BMI < 25 kg/m2 (can reduce estrone production in the adipose tissue)
3. Screen for comorbidities and provide specific treatment.

Tailor additional therapeutic interventions based on:
1. Reproductive goals
2. Comorbidities
3. Individual risk factors

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7
Q

Describe the changes in vaginal discharge as influenced by hormones through the menstrual cycles.
- Menstrual phase?
- Follicular phase?
- Ovulation phase?
- Luteal phase?
- Pre-menstrual phase?

A

Vaginal discharge is a normal physiological process influenced by hormonal fluctuations throughout the menstrual cycle. The consistency, color, and amount of vaginal discharge can change in response to changes in hormonal levels. It’s important to note that the characteristics of vaginal discharge can vary from person to person, and factors such as hydration, sexual arousal, and infections can also influence its appearance and consistency. Healthy vaginal discharge should generally be odorless, white or clear, and not accompanied by itching, burning, or discomfort. Any significant changes in vaginal discharge, especially if accompanied by other symptoms, should be discussed with a healthcare provider to rule out infections or other underlying issues.

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8
Q

**List the common causes of female pelvic pain and describe the investigations and management thereof. **
- 6 Gynaecological Causes?
- 2 Gastrointestinal Causes?
- 2 Urinary Causes?
- 1 Musculoskeletal Cause?
- 1 Reproductive Cause?
- 1 Other Cause?

A
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9
Q

Explain 12 roles of ultrasound in the diagnosis of gynaecological problems.

A
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10
Q

Uterine Fibroids (Leiomyoma)
- Pathogenesis & Clinical features?
- What are they?
- 3 types?
- 6 Predisposing factors?

A
  • A benign, hormone-sensitive smooth muscle tumor of the uterus.
  • The most common tumor of the female genital tract.
  • Can be submucosal, intramural, or subserosal.
  • Arises from a single myometrial cell (monoclonal growth) and causes:
    1. Upregulation of hormone receptors, particularly estrogen and progesterone
    2. Excessive production of extracellular matrix (hence “fibroids”)
    3. Results in an overgrowth of smooth muscle cells and connective tissue (often multiple tumors)
    4. The myometrium also develops vascular changes (e.g., increased arterioles and venules, dilated veins).
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11
Q

Uterine Fibroids (Leiomyoma)
- Classification? (5)
- Complications? (5)

A

Complications
1. Infertility
2. Iron deficiency anemia (due to heavy menstrual bleeding)
3. Fibroid torsion
4. Thromboembolism
5. Very rare: malignant transformation to uterine leiomyosarcoma

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12
Q

Uterine Fibroids (Leiomyoma)
- Pathology: Macroscopic & Microscopic?
- Clinical features?

A
  • Submucosal leiomyomas are most frequently associated with significantly prolonged or heavy menstrual bleeding. The mechanism may be related to the increased total surface area as a result of the bulging uterine wall, impaired uterine wall contractility, or micro/macrovascular abnormalities. Intramural leiomyomas are also a risk factor for heavy or prolonged menstrual bleeding.
  • E.g., extrinsic compression of the bladder or sigmoid colon. Compression of the ureters results in hydronephrosis.
  • Related to an obstructed uterine cavity and/or impaired contractility of the uterus.
  • Anterior or fundal fibroids are often associated with severe pain during intercourse.
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13
Q

Uterine Fibroids (Leiomyoma) - Diagnostics
- 6 Lab studies?
- Pelvic ultrasound?
- Further imaging? (2)

A

Routine initial studies
1. FBC: to assess for anemia
2. U&Es: to assess renal function
3. Urine pregnancy test/Serum Beta HCG: if patient is of childbearing age
4. Studies to evaluate abnormal uterine bleeding: PT, PTT, fibrinogen
5. Diagnostic studies for von Willebrand disease
6. Consider TSH and liver enzymes if clinically indicated.

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14
Q

What are the clinical manifestations of fibroids based on:
- Site?
- Size?

A
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15
Q

Describe the impact of body weight on disturbances of the menstrual cycle.
- Underweight?
- Overweight?
- Effects on Fertility?

A

Effects on Fertility:
- Both underweight and overweight conditions can impact fertility. Underweight women may experience anovulation and difficulties conceiving due to hormonal imbalances.
- Overweight individuals, particularly those with PCOS, may face challenges in achieving and maintaining pregnancy due to irregular cycles and hormonal disruptions.

Other Factors:
- Nutritional Deficiencies: Underweight individuals may lack essential nutrients needed for proper hormonal function and reproductive health.
- Psychological Stress: Extreme body weight changes, whether due to underweight or overweight conditions, can lead to stress on the body, affecting hormonal regulation.

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16
Q

Identify the various cellular changes at the level of the endometrium in prolonged anovulation and how this relates to an increased risk of carcinoma of the endometrium.
- 2 Cellular changes?
- Relation to Increased Risk of Endometrial Carcinoma? (4)
- Management and Risk Reduction?

A

Prolonged anovulation can lead to an excess of unopposed estrogen = endometrial hyperplasia (the lining of the uterus) = increased risk of endometrial carcinoma.

Cellular Changes in Prolonged Anovulation:
1. Endometrial Hyperplasia: Prolonged exposure to estrogen without the balancing effects of progesterone can lead to endometrial hyperplasia. The corpus luteum (empty egg follicle, temporary gland that helps support the beginning of a pregnancy) produces progesterone. This is a condition where the endometrial lining becomes abnormally thickened due to an increased number of glandular and stromal cells.

  1. Atypical Hyperplasia: In some cases, endometrial hyperplasia can progress to atypical hyperplasia, where the cells show abnormal growth patterns and increased cellular atypia. Atypical hyperplasia is considered a precancerous condition.
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17
Q

Discuss the 4 types of Barrier contraception available and the pros and cons of each.
- Failure rates?

A
  1. Male condoms – typically made of latex, male condoms are rolled down from the tip of the penis to the base. Semen collects in a reservoir at the tip end of the condom. They are proven to reduce transmission of many STIs such as chlamydia and gonorrhoea.
  2. Female condoms – made of polyurethane, these are tubular shaped, where an inner ring sits deep in the vagina, with an open outer ring sitting just outside the vulva. The male inserts their penis into the female condom, preventing contact with the vagina. They are proven to reduce transmission of many STIs, such as chlamydia and gonorrhoea.
  3. Diaphragms – these are typically rubber structures with a metal inner frame that spans the posterior fornix to the anteroinferior wall of the vagina, covering the cervix and therefore preventing entry of semen. They are held in place by a combination of vaginal tone, the rigid metal inner frame and the pubic symphysis. Often combined with spermicide to increase their efficiency.
  4. Cervical caps – these sit directly over the cervix and are held in place by suction and vaginal tone. They are often combined with spermicide to increase their efficiency.
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18
Q

Differentials for an Adenexal mass.
- 7 Cystic ovarian lesions?
- 6 Common non-ovarian lesions?
- 5 Less common non-ovarian lesions?
- 7 Common mimics of cystic lesions?

A
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19
Q

Why is it important to detect and diagnose adenexal masses?

A
  • Approx 5-10% lifetime risk for women undergoing surgery for a suspected neoplasm
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20
Q

What history would you obtain from a patient presenting with an adenexal mass?

A

Weight loss – malignancy
Changes in hair growth/distribution – ovarian tumour secreting hormonal androgens

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20
Q

What examination would you perform for a women presenting with an adenexal mass?

A
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21
Q

Which investigations would you perform for a women presenting with an adenexal mass?
- Bloods?
- Tumour markers?
- Imaging?

A
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21
Q

4 Factors that influence the risk of malignancy with an adenexal mass?

A
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21
Q

What are 6 findings of an adenexal mass on ultrasound that are suggestive of malignancy?
What are the IOTA rules?
- 5 Benign vs. Malignant features

A

Pelvic USS - Findings Suggestive of Malignancy
1. Solid component, not hyperechoic, & often nodular or papillary
2. Septations that are irregularly thick (>2-3mm)
3. Colour or power Doppler demonstration of flow in the solid component
4. Ascites
5. Peritoneal masses, enlarged nodes, matted bowel

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21
Q

Which 9 tumour markers would you measure for investigation of an adenexal mass?

A

Summary for Tumour Markers
- Post menopausal women with an adenexal mass: Ca 125, CEA, CA19-9
- If premenopausal or suspect germ cell tumour or hormone secreting tumour: Ca125, CEA, CA19-9, AFP, LDH, hCG, Inhibin, AMH, testosterone, androgen

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22
Q

Which conditions are associated with an elevated serum Ca 125 concentration?
- Gynaecological malignancies?
- Benign Gynaecological conditions?
- Non-Gynaecological conditions?

A

Anything that stimulates the peritoneum can give you a raised CA125

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23
Q

List 5 Multimodal tests for risk of malignancy of an adenexal mass?

A

Risk of Malignacy Algorithm (ROMA)
- Ca 125 + HE4
- Early stage EOC sens 81% and spec 76%
- Premenopausal sens 82% and spec 82%
- Postmenopausal sens 93% and spec 79%

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24
Q

Differential Diagnosis of an Adenexal Mass – 5 Benign conditions?

A
  1. Physiological Cysts - Corpus luteum or Follicular cyst
  2. Dermoid
  3. Benign Epithelial Ovarian cysts
  4. Fibroids
  5. Endometrioma
    - Pain, dymenorrhoea, dyspareunia, Chocolate cyst, Common cause of Ca 125 increase
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25
Q

Differential Diagnosis of an Adenexal Mass – 6 Acute complications?

A

Acute Complications - Adenexal Mass
1. Ectopic
2. Torsion
3. Intracystic haemorrhage
4. Rupture
5. Infection
6. Malignancy - bowel obstruction/perforation

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26
Q

8 Risk factors for Ovarian Cancer?
5 Protective Factors for Ovarian Cancer?

A

Protective Factors
1. BSO
2. Tubal ligation
3. Previous pregnancy
4. Previous breastfeeding >12 months
5. Previous use of OCP

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27
Q

Outline 4 types of Ovarian Cancer?

A
28
Q

When should you refer a women with an adenexal mass to a gynaecological oncologist?
- Post-menopausal vs. Pre?

A
29
Q

Cervical Cancer
- Epidemiology: Incidence, Peak, Mortality?
- Aetiology?

A

Human papillomavirus virus (HPV) infection
- Infection with high-risk HPV types is the main cause of cervical cancer (DNA of HPV 16 and/or 18 is found in 70% of all patients with cervical carcinoma).
- The major high-risk HPV types are HPV 16 (most common in squamous cell carcinoma) and HPV 18 (most common in adenocarcinoma).

30
Q

Cervical Cancer Risk Factors
- Associated with HPV infection?
- 3 Environmental risk factors?

Clinical Features of Cervical Cancer
- Early?
- Late?
- Exam findings?

A

Risk factors Associated with HPV infection
1. Multiple sexual partners (strongest risk factor)
2. Early-onset of sexual activity
3. Multiparity
4. Immunosuppression (e.g., HIV infection, post-transplantation)
5. History of sexually transmitted infections (e.g., herpes simplex, chlamydia)

Environmental risk factors
1. Cigarette smoking and/or exposure to second-hand smoke (for squamous cell cancer types only)
2. In-utero exposure to diethylstilbestrol (DES)
3. Low socioeconomic status

31
Q

Cervical Cancer Classification?

A
32
Q

Incidence and Peak age occurrence of Cervical Cancer in Australia?

A
33
Q

6 Symptoms of Cervical Cancer?
- 9 Risk factors/aetiology?

A

Symptoms
1. Early disease is often asymptomatic, thus emphasising the importance of regular pap smears.
2. Abnormal vaginal bleeding.
3. Postcoital bleeding.
4. Dyspareunia
5. Purulent or mucoid discharge.
6. Pain or other symptom of advanced pelvic disease such as bladder or bowel obstruction.

34
Q

Outline the pathology of cervical cancer? What can be done to prevent it?

A
35
Q

Diagnosis of Cervical Cancer? (4)
- FIGO staging?

A

Diagnosis of Cervical Cancer
1. History.
2. Visualisation via speculum exam and colposcopy.
3. Directed biopsy of suspicious areas.
4. PET CT to evaluate disease extent.

36
Q

Cervical cancer treatment?
- Prognosis?

A

Prognosis (5 year survival)
- Stage 1a: 95%
- Stage 1b: 80-90%.
- Stage 2: 75%
- Stage 3 and above: less than 50%

37
Q

Endometrial Cancer
- What is it?
- Incidence in Australia?
- Peak age occurrence?
- Symptoms?

A
38
Q

Endometrial Cancer
- 6 Pathophysiological factors possibly associated with endometrial cancer?

A
39
Q

Endometrial Cancer
- 8 Risk factors/aetiologies?

A
40
Q

Endometrial Cancer
- Diagnosis?
- 5 1st Dx tests to order?
- 5 DDxs?

A

DDx of Endometrial cancer
1. Endometrial hyperplasia
2. Endometrial polyp
3. Endometriosis
4. Cervical cancer
5. Pyometria

41
Q

Endometrial Cancer
- Staging?

A
42
Q

Endometrial Cancer
- Treatment? (4)
- Prognosis?

A

Rx approach: goal maximising chance of cure with minimal morbidity
1. Surgery: for staging and removing malignant disease
2. Radiotherapy: reduces local recurrence, no impact on survival, used on patients who are HIR or high risk
3. Chemotherapy: adjuvant for high risk, palliative role for metastatic or recurrent disease
4. Hormonal therapy: considered in inoperable disease with oestogen receptor/progesterone receptor positive tumours

43
Q

Ovarian Cancer
- Incidence?
- Peak age occurrence?
- Symptoms?

A

Ovarian Cancer
Incidence
- ~1,300 women are diagnosed w/ epithelial ovarian Ca each year in Australia
- Ovarian Ca is the 9th most common Ca diagnosed in Australian women; 2nd most common GYN Ca

Peak age occurrence
- >50 y/o – 82% of all new cases diagnosed; risk increases w/ age
- Average age = 63 years

44
Q

Ovarian Cancer
- Pathology?
- 4 Histological types?

A

Pathology of Ovarian Cancer
Current theory of pathogenesis – research suggests that epithelial ovarian tumours arise from a precursor lesion in the fallopian tube. During ovulation, as the fimbria come into close contact with the ovary, Serous Tubal Intraepithelial Carcinoma (STIC) cells exfoliate and implant on the disrupted ovarian surface to form a cortical inclusion cyst, eventually progressing to a serous tumour secondarily involving the ovary. It is also believed that endometriosis is the precursor for endometrioid & clear cell carcinoma, where endometrial tissue implants on the ovary. Based on this theory, only stromal and germ cell tumours are true ovarian cancers.

45
Q

Ovarian Cancer
- 7 Risk Factors?
- 3 Protective factors?
- Diagnosis?

A

Risk Factors/ Aetiology for Ovarian Cancer
1. Age
2. Genetics – mutations of BRCA 1 & BRCA 2
3. FHx of ovarian, breast or colorectal Ca – however 90-95% of ovarian Ca occurs in women w/ no FHx
4. Medical conditions such as endometriosis
5. Long term use of HRT
6. Cigarette smoking
7. Obesity

46
Q

Ovarian Cancer
- Treatment? (3)
- Staging? (4)
- Prognosis (5 year survival)?

A

Treatment
1. Surgical – cytoreduction; can involve oophorectomy, hysterectomy, bi-lateral salpingo- oophorectomy & omentectomy
2. Chemotherapy – carboplatin & cisplatin post surgery in advanced disease
3. Radiotherapy – used initially to reduce size (Whole Abdominal Radiotherapy (WART))

47
Q

Vulvular Cancer
- Incidence in Australia?
- Peak age occurrence?
- 3 Symptoms?
- 6 Pathological types?

A

Incidence
- Uncommon. Accounts for approx. 5% of gynaecologic cancers

Peak age occurrence
- Postmenopausal women. Peaks at ages 60 to 70yrs.
- 75% of patients over 50yrs.

Symptoms
1. Pruritis vulvae or vulvar mass most common.
2. Also bleeding or vulva pain.
3. 20% asymptomatic and found on routine Ex.

48
Q

Vulvular Cancer
- 8 Risk Factors?
- Diagnosis?

A

Diagnosis = Biopsy

49
Q

Vulvular Cancer
- Staging? (4)
- Treatment?
- Prognosis (5 year survival)?

A
50
Q

A 30 year old married woman with 2 children attends your surgery for a check up. Pelvic examination is normal but the HPV testing shows that she is positive for oncogenic HPV types 16 and 18 with Liquid Based Cytology showing pHSIL/HSIL. What would you do?

A

If a CST shows HPV 16/18 and LBC shows pHSIL/HSIL this patient needs a colposcopy.

51
Q

Is management different if HPV testing shows that she is positive for HPV (not 16/18) and the Liquid Based Cytology is negative for pHSIL/HSIL? How does the underlying disease process effect the clinical situation?

A

Regardless of whether LBC showes pHSIL/HSIL or not, a person with HPV 16 or 18 needs a colposcopy.

52
Q

How would you manage a 25-year-old woman who has recurrent episodes of post coital bleeding from the cervix, but HPV testing is negative? What are the causes of cervical bleeding?

A
  • **Postcoital bleeding in pre-menopausal women **: Pre-menopausal women who have a single episode of postcoital bleeding and a clinically normal cervix do not need to be referred for colposcopy if oncogenic HPV is not detected and LBC is negative.
  • Persistent or recurrent post coital bleeding in pre-menopausal women: Pre-menopausal women with recurrent or persistent postcoital bleeding, even in the presence of a negative co-test, should be referred to a gynaecologist for appropriate assessment, including colposcopy, to exclude genital tract malignancy.
  • Postcoital bleeding and sexually transmitted: Sexually transmitted infections, including chlamydia infection, should be considered in all women presenting with postcoital bleeding. It is necessary to obtain a sexual health history and perform appropriate tests and investigations.
53
Q

Discuss the management of an episode of vaginal bleeding in a 62-year-old woman.

A

Endometrial or vaginal atrophy is the most common cause of PMB but more sinister causes of the bleeding such
as carcinoma must first be ruled out. Patients at risk for endometrial cancer are those who are obese, diabetic and/
or hypertensive, nulliparous, on exogenous oestrogens (including tamoxifen) or those who experience late menopause.

54
Q

Describe the pathology and treatment of precancerous lesions of the cervix including the role of colposcopy in the diagnosis of cervical lesions.

A

Precancerous lesions of the cervix, also known as cervical intraepithelial neoplasia (CIN), are abnormal changes in the cells of the cervix that have the potential to develop into cervical cancer if left untreated. These lesions are often categorized into different grades (CIN 1, CIN 2, and CIN 3) based on the extent of cell changes. The main cause of these lesions is persistent infection with high-risk strains of the human papillomavirus (HPV).
- CIN 1: Mild dysplasia or low-grade lesion involving the lower third of the cervical epithelium. It often resolves on its own but might progress.
- CIN 2: Moderate dysplasia or high-grade lesion involving the lower two-thirds of the cervical epithelium.
- CIN 3: Severe dysplasia or carcinoma in situ, where abnormal cells cover the full thickness of the cervical epithelium but have not invaded deeper tissues.

55
Q

List the current Australian guidelines regarding HPV vaccination.
- Who should get the HPV vaccine?
- Who shouldn’t get the HPV vaccine?
- When & How can you get the HPV Vaccine?

A

HPV vaccines should not be given to:
- people who have had anaphylaxis after a previous dose of any HPV vaccine or anaphylaxis after any component of an HPV vaccine.
- people who have had anaphylaxis to yeast (for 9vHPV).
- HPV vaccines are not recommended for pregnant women. Breastfeeding woman can receive HPV vaccines.

56
Q

What is Umbilical Cord Prolapse?
- Classification?
- Pathophysiology?
- Algorithm for management?

A

Pathophysiology - Umbilical cord prolapse is where the umbilical cord descends through the cervix, with (or before) the presenting part of the fetus. Subsequently, fetal hypoxia occurs via two main mechanisms:
- Occlusion – the presenting part of the fetus presses onto the umbilical cord, occluding blood flow to the fetus.
- Arterial vasospasm – the exposure of the umbilical cord to the cold atmosphere results in umbilical arterial vasospasm, reducing blood flow to the fetus.

57
Q

CORD Acronym for the management of Umbilical Cord Prolapse?

A

C - Call for Help
O - Organise delivery/paeds team etc.
R - Reduce pressure on the cord
1. Physically push it back up into the vagina.
2. Changing positions
3. Fill the bladder (catheter) ~750mL
4. Tocolytics

D - Deliver

58
Q

5 Main Risk Factors for Umbilical Cord Prolapse?

A
59
Q

Shoulder Dystocia
- What is it?
- Pathophysiology?

A
  • Shoulder dystocia refers to a situation where, after delivery of the head, the anterior shoulder of the fetus becomes impacted on the maternal pubic symphysis, or (less commonly) the posterior shoulder becomes impacted on the sacral promontory.
  • It is an obstetric emergency, with an incidence of approximately 0.6-0.7% in all deliveries.
60
Q

Management of Shoulder Dystocia?

A
61
Q

HELPERR Acronym for the Management of Shoulder Dystocia?

A

H - call for Help
E - Evaluate for Episiotomy
L - Legs: McRoberts = hips to nips to reduce pressure on the pelvis
P - External Pressure = suprpubic
E - Enter = Internal Rotational Maneouvres
R - Repeat

62
Q

NICE Guidelines 2017
- What precautions should be taken to avoid likelihood of cord prolapse during amniotomy?
- When would you consider cord prolapse as a diagnosis? Recognition?

A

Recognition of Cord Prolapse
- Early diagnosis is important.
- A cord prolapse might be easily visible or it may only be found on VE.
- Cord prolapse should be excluded at every VE.
- Suspect cord prolapse when there is a sudden change in fetal heart rate -eg. bradycardia or abnormal fetal heart rate pattern.

63
Q

NICE Guidelines 2017
- Definition of Cord Prolapse?
- Incidence/Background?

A
64
Q

9 Antenatal Risk Factors for Cord Prolapse?
10 Intrapartum Risk Factors for Cord Prolapse?

A
65
Q

Twin Pregnancy
- Incidence in Australia?
- Factors that increase rates of Dizygotic twins?

A
66
Q

Twin Pregnancy
- What is Zygosity?
- What is Chorionicity?

A
67
Q

Twin Pregnancy
- Ultrasound Diagnosis?

A
68
Q

Twin Pregnancy
- Prenatal Diagnosis - Which tests?

A
69
Q

Twin Pregnancy
- Timing and Mode of Delivery?

A
70
Q

Monochorionic Twins
- 5 Complications?

A

Complications
1. Twin to Twin Transfusion Syndrome (TTTS)
2. Twin Anaemia-Polycythaemia Sequence (TAPS)
3. Twin Reversed Arterial Perfusion Sequence (TRAP)
4. Selective fetal growth restriction
5. Single fetal demise

71
Q

What is Twin to Twin Transfusion Syndrome TTTS?

A
72
Q

What is the Quintero Classification of TTTS?
- Stages I-V?

A
73
Q

What is TAPS- Twin Anaemia Polycythaemia Sequence?
What is TRAP-Twin Reversed Arterial Perfusion?

A

TAPS- Twin Anaemia Polycythaemia Sequence
- Atypical form of TTTS that presents as large inter twin haemoglobin difference without oligohydramnios-polyhydramnios sequence.
- Spontaneous rate is 3-6% of previously uncomplicated third trimester MCDA twins.
- Can occur after laser therapy (2-13%) and secondary to residual anastomoses (usually small and uni directional)