Women’s health - Gynae Flashcards

1
Q

What is an ectopic pregnancy

A

Ectopic pregnancy occurs when a fertilised egg implants outsideof the uterus, most commonly within the fallopian tube.​

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2
Q

Sx of an ectopic pregnancy

A

PV bleeding​

Abdominal pain (usually unilateral, iliac fossa)

Shoulder tip pain​

Dizziness​

SOMETIMES ASYMPTOMATIC

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3
Q

Ix for ectopic pregnancy

A

Usually diagnosed by transvaginal USS +/-bHCG​

Scan signs of tubal ectopic:​
Adnexal mass moving separately to the ovary (sliding sign)comprising
a gestational sac containing a yolk sac or fetal pole
OR a non-specific mass (empty gestational sac)

In 20% of cases apseudosac(fluid) may be seen within the uterine cavity​ - must check all over and not just uterus

HCG- A rise of less than 63% after 48 hours may indicate an ectopic pregnancy. When this happens the patient needs close monitoring and review

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4
Q

Management of ectopic pregnancy

A

There are three options for terminating an ectopic pregnancy:

  • Expectant management(awaiting natural termination)
  • Medical management(methotrexate)
  • Surgical management(salpingectomyorsalpingotomy)

CRITERIA FOR WHICH MANAGEMENT OPTION IS BELOW:

Expectant management 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

Medical management criteria:

Criteria formethotrexateare the same as expectant management, except:

  • HCG level must be < 5000 IU / l
  • Confirmed absence of intrauterine pregnancy on ultrasound

Anyone that does not meet the criteria for expectant or medical management requires surgical management. Most patients with an ectopic pregnancy will require surgical management. This include those with:

  • Pain
  • Adnexal mass > 35mm
  • Visible heartbeat
  • HCG levels > 5000 IU / l
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5
Q

KEY - Ectopic pregnancy and
miscarriage: diagnosis and initial management.

A women presents with PV bleeding and pain at 10 weeks gestation. You perform an USS, what are the 3 possible things you might see on the scan and what would they mean for diagnosis.

A

Quering ectopic vs misscarriage vs viable pregnancy

  • immediate management
    • baseline HcG
    • TV USS - to identify the location of the pregnancy and whether there is a fetal pole and heartbeat.
    3 Findings on ultrasound scan
    - Tubal ectopic - adnexal mass moving separately to the ovary, or a gestational sac contianing a yolk sac and fetal pole in one of the tubes
    - Positive pregnancy test but no sign of pregnancy on ultrasound scan → pregnancy of unknown location. Track the Serum HcG (viable should double every 48, a rise of less than 63% indicates an ectopic, a fall indicates miscarriage)
    - USS shows a possible pregnancy in the uterus - either viable or misscarriage. When afetal heartbeatis visible, the pregnancy is consideredviable. Afetal heartbeatis expected once thecrown-rump lengthis7mmor more.Afetal poleis expected once themean gestational sac diameteris25mmor more.
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6
Q

Sholder tip pain is a sign of what gynaecological pathology

A

Ruptured ectopic pregnancy -> blood causing diaphragmatic nerve irritation (referred pain to the C3) dermatome

Me - techcially also a cyst rupture - blood on diaphragm is all it means really.

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7
Q

What are the three types of miscarriage? How are they each diagnosed?

A

Miscarriage is the spontaneous termination of a pregnancy. In the UK, it is estimated that 1 in 5 pregnancies end in miscarriage.

Complete miscarriage – a full miscarriage has occurred, and there are no products of conception left in the uterus
Usually present following an episode of PV bleeding.
Diagnosed on USS showing an empty uterus. If not previous IUP confirmed then usually require followup of with bHCG monitoring (>50% decrease 48 hours apart is indicative of early pregnancy loss)

Incomplete miscarriage – retained products of conception remain in the uterus after the miscarriage.
Diagnosed on USS – usually see mixed echoes within the uterine cavity
If no previous IUP (intrauterine pregnancy) seen on USS, will require serial bHCG monitoring to ensure failing IUP.

Missed miscarriage – the fetus is no longer alive, but no symptoms have occurred. Diagnosed on transvaginal USS - CRL (crown rump length) >7mm with no foetal heart activity

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8
Q

How is incomplete miscarriage managed?

A

There are two options for treating an incomplete miscarriage:

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

Retained products create a risk of infection. Consider patients condition – are there signs of infection? Does our patient need antibiotics?

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9
Q

Management of missed/delayed miscarriage

A

There are three options for managing a miscarriage:

  • Expectant management (do nothing and await a spontaneous miscarriage for 1/2 weeks) - first line
  • Medical management (misoprostol - prostaglandin analogue -> uterine contraction), only option if CRL is above 54mm
  • Surgical management (manual or electrical vacuum aspiration) can only be used if CRL<54mm BELOW!
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10
Q

What is a Molar Pregnancy?

A

A hydatidiform mole is a type of tumour that grows like a pregnancy inside the uterus. This is called a molar pregnancy. There are two types of molar pregnancy: a complete mole and a partial 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. No fetal material will form.

A 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 fetal material may form.

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11
Q

Medical vs surgical termination of pregnancy

A

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

Mifepristone (anti-progestogen) - halts the pregnancy and relaxes the cervix
Misoprostol (prostaglandin analogue) 1 – 2 day later - softens the cervix and stimulates uterine contraction
From 10 weeks gestation, additional misoprostol doses (e.g. every 3 hours) are required until expulsion.

mnemonic
mifepristONE - anti-progesterONE
misoPROSTol - PROSTaglandin analog

Surgical TOP:
- can be performed at any gestational age
- can be performed under local anaesthetic (+/- sedation) or general anaesthetic
- cervical priming is performed prior with misoprostol, mifepristone, osmotic dilatation
- up to 14 weeks - cervical dilatation + suction of the context
- 14-24 weeks - cervical dilatation + evacuation using forceps

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

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12
Q

Utrasound shows bunch of grapes sign/snowstorm appearance - what is the diagnosis and management?

A

Molar pregnancy

Management involves evacuation of the uterus to remove the mole. The products of conception need to be sent for histological examination to confirm a molar pregnancy (definitive diagnosis) . Patients should be referred to the gestational trophoblastic disease centre for management and follow up. The hCG levels are monitored until they return to normal. Occasionally the mole can metastasise, and the patient may require systemic chemotherapy.

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13
Q

What is an ovarian torsion

A

Occurs when the ovary, and sometimes the fallopian tube twists on its vascular and ligamentous supports

This blocks adequate blood flow to the ovary

Surgical emergency – much like testicular torsion, but much harder to spot

Most commonly seen in women of reproductive age, Ovarian torsion is usually due to an ovarian mass larger than 5cm, such as a cyst or a tumour (usually benign). It is also more likely to occur during pregnancy.

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14
Q

Sx of ovarian torsion

A

The main presenting feature is sudden onset severe unilateral pelvic pain. The pain is constant, gets progressively worse and is associated with nausea and vomiting.

nonspecific - basically very similar to ectopic, but no bleeding

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15
Q

Diagnosis and management of ovarian torsion

A

Pelvic ultrasound is the initial investigation. It may show “whirlpool sign”, free fluid in pelvis and oedema of the ovary (enlarged ovary). Doppler studies may show a lack of blood flow.

The definitive diagnosis is made with laparoscopic surgery.

Management: surgical
Detorsion is preferred -> oophorectomy is required if ovary is necrotic

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16
Q

Cyst accident - three reasons what ovarian cysts can cause acute pelvic pain

A

Functional ovarian cysts related to the fluctuating hormones of the menstrual cycle, and are very common in premenopausal women.

Ovarian cysts may present with acute pelvic pain if there is ovarian torsion, haemorrhage or rupture of the cyst.

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17
Q

Key! What are GnRH angonists? What is the mechanism of action?

A

GnRH agonists, such as goserelin (Zoladex) or leuprorelin (Prostap), are used to shut down production of male and female sex hormones. Usually, GnRH agonists are only used short term, for example, to shrink a fibroid before myomectomy. They are also used for endometriosis and prostate cancer. They work by inducing a menopause-like state and reducing the amount of oestrogen maintaining the fibroid.

Basic mechanism:

GnRH analogues are act just like GnRH and are agonists of GnRH receptors in the anterior pituitary gland. This triggers the release of the gonadotrophins (LH and FSH).
GnRH analogues a very powerful stimulation of these receptors leading to a very large (more than normal) release of gonadotrophins (FSH and LH). However, overtime the anterioir pituitary becomes desensitised to the GnRH hormone leading to a reduction in the production in gonadotrophins and thus sex hormones - A HYPOGONATROPHIC HYPOGONADISM

Background :
The Hypothalamic-pituitary-gonadal axis
Hypothalamus produces GnRH.

In females:

GnRH stimulates the pituitary gland to produces LH/FSH

LH/FSH stimulate the development of ovarian follicles which secrete oestrogen. Oestrogen has a negative feedback effect on the hypothalamus and pituitary gland.

In Males:

LH released from the pitary gland stimulates the testicles to produce testosterone, which also has a negative feedback effect on the hypothalamus and pituitary gland.

GnRH analogues:

GnRH analogues are act just like GnRH and are agonists of GnRH receptors in the anterior pituitary gland. This triggers the release of the gonadotrophins (LH and FSH).

GnRH analogues a very powerful stimulation of these receptors leading to a very large (more than normal) release of gonadotrophins. This causes an initial flare of sex hormones oestrogen and testosterone lasting days-weeks, with worsened symptoms of prostate cancer or endometriosis.

SC or IM injections give a slow release of the medication, and give a continuous stimulation of the GnRH receptors. Overtime the anterioir pituitary becomes desensitised to the GnRH hormone leading to a reduction in the production in gonadotrophins and thus sex hormones - A HYPOGONATROPHIC HYPOGONADISM (Low gonadrophins leading to low production of sex hormones by the gonads). Overtime the effects of overstimulation wear off so the dose needs to be repeated.

GnRH

GnRH antagonists are more complex than agonists, and act through a completely different mechanism but overall both inhibit gonadotropin secretion. GnRH antagonists bind competitively to GnRH receptors, preventing the action of endogenous GnRH pulses on the pituitary. The secretion of gonadotropins is decreased within hours of antagonist administration and no flare-up effect occurs.

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18
Q

KEY Define Pelvic inflammatory disease? what are the symptoms? Management?

A

Infection of the female reproductive system:
Uterus (endometritis)
Fallopian tubes (salpingitis)
ovaries (oophoritis)

Causes
Bacterial infection, usually sexually transmitted e.g. chlamydia, gonorrhoea or mycoplasma

Often asymptomatic, but symptoms can include:
- pelvic pain
- Dyspareunia
- Dysuria
- IMB/PCB
- Change to vaginal discharge

Treatment
14 day course of antibiotics – IM ceftriaxone single dose plus PO metronidazole (to cover gardnerella) and doxycycline (to cover chlamydia and mycoplasma)
Avoid SI until patient and partner completed treatment

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19
Q

What is the cervical cancer screening program frequency (SMEAR TEST)

A

25-49 - every 3 years
50-64 - every 5 years

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20
Q

Red flag symptoms of uterine bleeding

A

ME: you made this from memory so could be wrong
- intermenstrual bleeding - cervical and other cancers
- post-coital bleeding - cervical and other cancers
- post-menopausal bleeding - particularly if there is a large gap between last menstrual period
- post-menopausal - anemia, haematuria, discharge
- weight loss
- note- intermenstrual and postcoital bleeding are also caused by STIs

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21
Q

differential diagnosis for menorrhagia - 4 KEY ONES

A

Menorrhagia refers to heavy menstrual bleeding (more than 80mls). The volume is rarely measured in practice and diagnosis is based on symptoms, such as changing pads every 1 – 2 hours, bleeding lasting more than seven days and passing large clots. A diagnosis can be made based on a self-report of “very heavy periods”. This can be caused by:

  • 50% - Dysfunctional uterine bleeding(no identifiable cause)
  • Fibroids - typically present 40-50s, pressure symptoms (pain/bladder issues)
  • Uterine cancer - high BMI is a risk
  • Endometriosis and adenomyosis (endometrial cells within the myometrium)
  • Contraceptives, particularly the copper coil
  • medications - (Anticoagulants)
  • Systemic disorders (coagulation disorders and hypothyroidism)
  • perimenauapse - ususally less regular
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22
Q

KEY Ix for menorrhagia in primary care? secondary care?

A

GP:

  • FBC (exclude anemia)
  • Pelvic examinationwith aspeculumandbimanual- This is mainly to assess for fibroids, ascites and cancers.

Maybe:

  • thyroid - only if other thyroid symptoms
  • swabs if evidence of infection
  • coagulation screen if periods have been heavy since menarche

Session Secondary care:

  • transvaginal scan - endometrial thickness, fibroids, masses
  • hysteroscopy and endometrial biopsy - gold standard
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23
Q

KEY Management of menorrhagia? Conservative, medical and surgical

A
  • Start by excluding underlying pathology such as anaemia, fibroids, bleeding disorders and cancer → these should be managed initially

Conservative

  • once anything coerncing is exlcuded the patient might be happy with simple reassurance

Medical:

  • Mirena coil(first line) - give it to everybody!!!! thin the endometrium, helps with pain in endometriosis…
  • hormonal treatment options: IUS (above), Combined oral contraceptive pill (not if older or high BMI) or Cyclical oral progestogens, such as norethisterone
  • non-hormonal treatment: Tranexamic acid(when no associated pain antifibrinolytic – reduces bleeding), Mefenamic acid(when there is associated pain - NSAID – reduces bleeding and pain)

Surgical - large fibroids, severe symptoms

  • fibroids - submucous (resection hysteroscopically), myomectomy (muscle wall - laparoscopically for younger)
  • endometrial ablation - hysteroscopically
  • hysterectomy.
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24
Q

ILA - Differentials for post-menaupausal bleeding

A
  • endometrial cancer- top differential
  • vulval masses or other signs of gynaecancers

benign

  • endometrial polyps
  • atrophic vaginitis - irritated on wiping
  • bleeding because of coagulants
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25
Q

KEY - How is PCOS diagnosed

A

Rotterdam Criteria

The Rotterdam criteria are used for making a diagnosis of polycystic ovarian syndrome. A diagnosis requires at least two of the three key features:

Oligoovulation or anovulation, presenting with irregular or absent menstrual periods

Hyperandrogenism (high male sex hormones), characterised by hirsutism and acne

Polycystic ovaries on ultrasound (or ovarian volume of more than 10cm3)

TOM TIP: If you are going to remember one thing about polycystic ovarian syndrome, remember the triad of anovulation, hyperandrogenism and polycystic ovaries on ultrasound. The Rotterdam criteria are commonly tested in MCQs and asked by examiners in OSCEs. It is important to remember that only having one of these three features does not meet the criteria for a diagnosis. As many as 20% of reproductive age women have multiple small cysts on their ovaries. Unless they also have anovulation or hyperandrogenism, they do not have polycystic ovarian syndrome.

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26
Q

What is PCOS- 4 key features

A

Polycystic ovary syndrome (PCOS) is a common endocrine disorder, characterised by excess androgen production (male sex hormones) and the presence of multiple immature follicles (“cysts”) within the ovaries.

Polycystic ovarian syndrome (PCOS) is a common condition causing metabolic and reproductive problems in women. There are characteristic features of multiple ovarian cysts, infertility, oligomenorrhea, hyperandrogenism and insulin resistance.

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27
Q

7 key symptoms of PCOS

A

Women with polycystic ovarian syndrome present with some key features:
- Oligomenorrhoea or amenorrhoea
- Infertility
- Obesity (in about 70% of patients with PCOS)
- Hirsutism - only a few other things cause this!
- Acne
- Hair loss in a male pattern
- chronic pelvic pain

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28
Q

Low yield but good for understanding

Pathophysiology of PCOS - what two key hormonal abnormalities seen in PCOS

A

Think this is low yield but good for understanding

The aetiology of polycystic ovary syndrome is poorly understood, and is thought to be multifactorial in origin.

The two most common hormonal abnormalities present in PCOS are:

  1. Excess luteinising hormone (LH) – produced by the anterior pituitary gland in response to an increased GnRH pulse frequency.
    This stimulates ovarian production of androgens.
  2. Insulin resistance – resulting in high levels of insulin secretion.
    This suppresses hepatic production of sex hormone binding globulin (SHBG), resulting in higher levels of free circulating androgens.

Despite the high levels of LH, the increased circulating androgens suppress the LH surge (which is required for ovulation to occur). Follicles develop within the ovary, but are arrested at an early stage (due to the disturbed ovarian function) – and they remain visible as “cysts” within the ovary.

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29
Q

Early vs late miscarriage

A

Early miscarriage is before 12 weeks gestation.

Late miscarriage is between 12 and 24 weeks gestation.

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30
Q

Differential diagnosis for PCOS

A

Differential Diagnoses
There are a number of differential diagnoses to consider in cases of suspected polycystic ovary syndrome.
The alternative endocrine diagnoses include:

Hypothyroidism – obesity, hair loss and insulin resistance.
Hyperprolactinaemia – oligomenorhoea/amenorrhoea, acne and hirsutism.
Cushing’s disease – obesity, acne, hypertension, insulin resistance and depression.

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31
Q

KEY - Ix for PCOS

A

Hormonal blood tests typically show:

  • LH- Raised luteinising hormone
  • FSH -Raised LH to FSH ratio (high LH compared with FSH)
  • testerone - raised
  • also check prolactin, SHBG and TSH
    TOM TIP: The key thing to remember for your exams is the raised LH, and the raised LH:FSH ratio.

Pelvic ultrasound is required when suspecting PCOS. A transvaginal ultrasound is the gold standard for visualising the ovaries. The follicles may be arranged around the periphery of the ovary, giving a “string of pearls” appearance. The diagnostic criteria are either:

  • 12 or more developing follicles in one ovary
  • Ovarian volume of more than 10cm3 (even without visualisation of follicles)

OGTT for diagnosis of diabetes- the results are:

Impaired fasting glucose – fasting glucose of 6.1 – 6.9 mmol/l (before the glucose drink)
Impaired glucose tolerance – plasma glucose at 2 hours of 7.8 – 11.1 mmol/l
Diabetes – plasma glucose at 2 hours above 11.1 mmol/l

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32
Q

Management of PCOS - BIG BOI

A

Weight loss is a significant part of the management of PCOS. Weight loss alone can result in ovulation and restore fertility and regular menstruation, improve insulin resistance, reduce hirsutism and reduce the risks of associated conditions.

This is usually achieved through lifestyle modification, Orlistat may be used to help weight loss in women with a BMI above 30. Orlistat is a lipase inhibitor that stops the absorption of fat in the intestines.
- antihypertensives and statins where required to help manage cardiovascular risk

Options for reducing the risk of endometrial hyperplasia and endometrial cancer are:
- Mirena coil for continuous endometrial protection
- Inducing a withdrawal bleed at least every 3 – 4 months with either:
- Cyclical progestogens (e.g. medroxyprogesterone acetate 10mg once a day for 14 days)
- Combined oral contraceptive pill

Management of infertility:
- weightless -1st line - can store ovulation
- other options- IVF, clomifene, ovarian drilling

Management of acne:
- COCP - 1st line in PCOS,
- normal acne management - topical retinoids….

Management of Hirsutism:
- weightloss
- Dianette COCP (co-cyprindiol)- has antiandrogen effects
- Topical eflornithine

Background:
Under normal circumstances, the corpus luteum releases progesterone after ovulation. Women with PCOS do not ovulate (or ovulate infrequently), and therefore do not produce sufficient progesterone. They continue to produce oestrogen and do not experience regular menstruation. Consequently, the endometrial lining continues to proliferate under the influence of oestrogen, without regular shedding during menstruation. This is similar to giving unopposed oestrogen in women on hormone replacement therapy. It results in endometrial hyperplasia and a significant risk of endometrial cancer.

Women with extended gaps between periods (more than three months) or abnormal bleeding need to be investigated with a pelvic ultrasound to assess the endometrial thickness. Cyclical progestogens should be used to induce a period prior to the ultrasound scan. If the endometrial thickness is more than 10mm, they need to be referred for a biopsy to exclude endometrial hyperplasia or cancer.

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33
Q

intentional double - a patient with string of pearls appearance on ultrasound, what is the diagnosis?

A

Patients with multiple ovarian cysts or a “string of pearls” appearance to the ovaries cannot be diagnosed with polycystic ovarian syndrome unless they also have other features of the condition. A diagnosis of PCOS requires at least two of:

Anovulation
Hyperandrogenism
Polycystic ovaries on ultrasound

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34
Q

What is an ovarian cyst

A

A cyst is a fluid-filled sac.

Functional ovarian cysts related to the fluctuating hormones of the menstrual cycle, and are very common in premenopausal women.

The vast majority of ovarian cysts in premenopausal women are benign.

Cysts in postmenopausal women are more concerning for malignancy and need further investigation.

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35
Q

Symptoms of ovarian cysts

A

Most ovarian cysts are asymptomatic. Cysts are often found incidentally on pelvic ultrasound scans.

Occasionally, ovarian cysts can cause vague symptoms of:

Pelvic pain
Bloating
Fullness in the abdomen
A palpable pelvic mass (particularly with very large cysts such as mucinous cystadenomas)
Ovarian cysts may present with acute pelvic pain if there is ovarian torsion, haemorrhage or rupture of the cyst.

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36
Q

pathophysiology - Types of ovarian cyst- just name some common ones.

A

Functional Cysts

Follicular cysts represent the developing follicle. When these fail to rupture and release the egg, the cyst can persist. Follicular cysts are the most common ovarian cyst, they are harmless and tend to disappear after a few menstrual cycles. Typically they have thin walls and no internal structures, giving a reassuring appearance on the ultrasound. (I think this is because multiple follicles develop each cycle)

Corpus luteum cysts occur when the corpus luteum fails to break down and instead fills with fluid. They may cause pelvic discomfort, pain or delayed menstruation. They are often seen in early pregnancy.

Other Types of Ovarian Cysts:

Serous Cystadenoma

These are benign tumours of the epithelial cells.

Mucinous Cystadenoma

These are also benign tumour of the epithelial cells. They can become huge, taking up lots of space in the pelvis and abdomen.

Endometrioma

These are lumps of endometrial tissue within the ovary, occurring in patients with endometriosis. They can cause pain and disrupt ovulation.

Dermoid Cysts / Germ Cell Tumours

These are benign ovarian tumours. They are teratomas, meaning they come from the germ cells and may contain various tissue types, such as skin, teeth, hair and bone. They are particularly associated with ovarian torsion.

Sex Cord-Stromal Tumours

These are rare tumours, that can be benign or malignant. They arise from the stroma (connective tissue) or sex cords (embryonic structures associated with the follicles). There are several types, including Sertoli–Leydig cell tumours and granulosa cell tumours.

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37
Q

Ix for ovarian cysts

A

USS is the Ix of choice

Premenopausal women with a simple ovarian cyst less than 5cm on ultrasound do not need further investigations.

ONLY DONE IF POST MENAUPAUSAL, CYST APPEARS ABNORMAL OR IS ABOVE 5CM:
CA125 is the tumour marker to remember for ovarian cancer. It contributes to the overall impression of whether an ovarian cyst is related to cancer and forms part of the risk of malignancy index (remember it is non specific and rises in endometriosis, adenomyosis, fibroids….)

Women under 40 years with a complex ovarian mass require tumour markers for a possible germ cell tumour:

Lactate dehydrogenase (LDH)
Alpha-fetoprotein (α-FP)
Human chorionic gonadotropin (HCG)

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38
Q

KEY - Management of ovarian cysts

A

Simple ovarian cysts in premenopausal women can be managed based on their size:
- Less than 5cm cysts will almost always resolve within three cycles. They do not require a follow-up scan.
- cysts above 5cm require follow up scan to see if they resolve. Peristant or large cysts (above 10cm) may require surgical intervention (usually with laparoscopy). Surgery may involve removing the cyst (ovarian cystectomy), possibly along with the affected ovary (oophorectomy).

Possible ovarian cancer (complex cysts or raised CA125) requires a two-week wait referral to a gynaecological oncology specialist.

Cysts in postmenopausal women generally require correlation with the CA125 result and referral to a gynaecologist. When there is a raised CA125, this should be a two-week wait suspected cancer referral.

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39
Q

What are fibroids? What promotes their growth?

A

Fibroids are benign tumours of the smooth muscle of the uterus. They are also called uterine leiomyomas. They are very common, affecting 40-60% of women in later reproductive years.

They are oestrogen sensitive, meaning they grow in response to oestrogen.

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40
Q

4 types of fibroid

A

Intramural means within the myometrium (the muscle of the uterus). As they grow, they change the shape and distort the uterus.

Subserosal means just below the outer layer of the uterus. These fibroids grow outwards and can become very large, filling the abdominal cavity.

Submucosal means just below the lining of the uterus (the endometrium).

Pedunculated means on a stalk.

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41
Q

Presentation of fibroids

A

Fibroids are often asymptomatic. They can present in several ways, Heavy menstrual bleeding (menorrhagia) is the most frequent presenting symptom

Other Sx:
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

Abdominal and bimanual examination may reveal a palpable pelvic mass or an enlarged firm non-tender uterus.

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42
Q

Ix for fibroids

A

Hysteroscopy is the initial investigation for submucosal fibroids presenting with heavy menstrual bleeding. (basically I think the submucosal ones are the main ones that cause menorrhagia)

Pelvic ultrasound is the investigation of choice for larger fibroids.

MRI scanning may be considered before surgical options, where more information is needed about the size, shape and blood supply of the fibroids.

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43
Q

Management of fibroids - small and large

A

Management can be medical or surgical

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

Medical management for larger fibroids - the same as for smaller basically.

Surgical options for Larger fibroids
- Uterine artery embolisation (interventional radiologists, blocks arterial supply to the fibroid)
- myomectomy
- hysterectomy

44
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. Red degeneration may occur as the fibroid rapidly enlarges during pregnancy, outgrowing its blood supply and becoming ischaemic. It may also occur due to kinking in the blood vessels as the uterus changes shape and expands during pregnancy.

Red degeneration presents with severe abdominal pain, low-grade fever, tachycardia and often vomiting. Management is supportive, with rest, fluids and analgesia.

TOM TIP: 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.

45
Q

When is menopause diagnosed

A

Menopause is a retrospective diagnosis, made after a woman has had no periods for 12 months. It is defined as a permanent end to menstruation. On average, women experience the menopause around the age of 51 years, although this can vary significantly. Menopause is a normal process affecting all women reaching a suitable age.

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 considering an FSH blood test to help with the diagnosis in:

Women under 40 years with suspected premature menopause
Women aged 40 – 45 years with menopausal symptoms or a change in the menstrual cycle

  • in GP you saw FSH used in women who were on hormonal contraception to help diagnose menopause
46
Q

What is perimenopause

A

Perimenopause refers to 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.

47
Q

pathophysiology - What process causes menopause? What causes the symptoms of menopause?

A

Menopause is caused by a lack of ovarian follicular function, resulting in changes in the sex hormones associated with the menstrual cycle:
- Oestrogen and progesterone levels are low
- LH and FSH levels are high, in response to an absence of negative feedback from oestrogen

Background
The process of the menopause begins with a decline in the development of the ovarian follicles. Without the growth of follicles, there is reduced production of oestrogen. Oestrogen has a negative feedback effect on the pituitary gland, suppressing the quantity of LH and FSH produced. As the level of oestrogen falls in the perimenopausal period, there is an absence of negative feedback on the pituitary gland, and increasing levels of LH and FSH.

The symptoms:
The failing follicular development means ovulation does not occur (anovulation), resulting in irregular menstrual cycles. Without oestrogen, the endometrium does not develop, leading to a lack of menstruation (amenorrhoea). Lower levels of oestrogen also cause the perimenopausal symptoms.

48
Q

Sx of menopause (5+)

A

A lack of oestrogen in the perimenopausal period leads to symptoms of:

  • Hot flushes
  • Emotional lability or low mood
  • Premenstrual syndrome
  • Irregular periods
  • Joint pains
  • Heavier or lighter periods
  • Vaginal dryness and atrophy
  • Reduced libido
49
Q

Counselling on contraception for perimenopausal women

A

Women need to use effective contraception for:

  • Two years after the last menstrual period in women under 50
  • One year after the last menstrual period in women over 50

Good contraceptive options (UKMEC 1, meaning no restrictions) for women approaching the menopause are:

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

COCP is UKMEC 2 so still an option.

50
Q

Management of Perimenopausal Symptoms - many have a good few options

A

DONT HAVE TO LEARN WROTE, BUT HAVE AN IDEA

Management of symptoms depends on the severity, personal circumstances and response to treatment. Options include:

  • No treatment
  • 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
51
Q

What is endometriosis and adenomyosis

A

A condition where there is ectopic (abnormal position) endometrial tissue outside of the uterus - endometriomas.

Adenomyosisrefers to endometrial tissue within themyometrium(muscle layer) of the uterus.

Background - not known what causes endometriosis but retrograde menstruation (through fallopian tubes into pelvis) is one notable theory

52
Q

Sx of endometriosis (3+)

A

Endometriosis can be asymptomatic in some cases, or present with a number of symptoms:

  • Cyclical abdominal or pelvic pain
  • Deep dyspareunia (pain on deep sexual intercourse)
  • Dysmenorrhoea (painful periods)
  • Infertility
  • Cyclical bleeding from other sites, such as haematuria

BACKGROUND PATHOPHYSIOLOGY

Dont have to learn this for answering exams but good to have an this for understanding this presentation.

The main symptom of endometriosis ispelvic pain.

Cyclical pain:

The cells of the endometrial tissue outside the uterus respond to hormones in the same way as endometrial tissue in the uterus. During menstruation, as the endometrial tissue in the uterus sheds its lining and bleeds, the same thing happens in the endometrial tissue elsewhere in the body. This causes irritation and inflammation of the tissues around the sites of endometriosis. This results in the cyclical, dull, heavy or burning pain that occurs during menstruation in patients with endometriosis.

Deposits of endometriosis in the bladder or bowel can lead to blood in the urine or stools.

Non-cyclical pain: (non relating to the menstrual cycle)

Localised bleeding and inflammation can lead toadhesions. Inflammation causes damage and development of scar tissue that binds the organs together. For example, the ovaries may be fixed to the peritoneum, or the uterus may be fixed to the bowel. Adhesions can also occur after abdominal surgery. Adhesions lead to achronic,non-cyclicalpainthat can be sharp, stabbing or pulling and associated with nausea.

Endometriosis can lead toreducedfertility. Often it is not clear why women with endometriosis struggle to get pregnant. It may be due to adhesions around the ovaries and fallopian tubes, blocking the release of eggs or kinking the fallopian tubes and obstructing the route to the uterus. Endometriomas in the ovaries may also damage eggs or prevent effective ovulation.

53
Q

Gold standard Investigation for endometriosis

A

Laparoscopic surgeryis thegold standardway to diagnose abdominal and pelvic endometriosis. A definitive diagnosis can be established with abiopsyof the lesions during laparoscopy. Laparoscopy has the added benefit of allowing the surgeon to remove deposits of endometriosis and potentially improve symptoms.

54
Q

Management of endometriosis

A
    • analgesia - NSAIDs and paracetamol first line
    Hormonal managementoptions can be tried before establishing a definitive diagnosis with laparoscopy:
    • COCP
    • Progesterone only pill
    • Depot progesterone injection
    • progesterone inplant implant
    • Mirena coil
    • GnRH agonists - goserilin shut down the ovaries temporary and induce a menopause like state
    Surgical managementoptions:
    • Laparoscopic surgery toexciseorablatethe endometrial tissue and remove adhesions (adhesiolysis)
    • Hysterectomy - final option, induce menopause but still isnt a definitive cure.
    Laparoscopic treatment may improve fertility. Hormonal therapies may improve symptoms but not fertility.
55
Q

3 Sx of adenomyosis

A

Adenomyosis typically presents with:

Painful periods (dysmenorrhoea)
Heavy periods (menorrhagia)
Pain during intercourse (dyspareunia)

56
Q

What is adenomyosis

A

Adenomyosis refers to endometrial tissue inside the myometrium (muscle layer of the uterus).

Extra:
It is more common in later reproductive years and those that have had several pregnancies (multiparous). It occurs in around 10% of women overall. It may occur alone, or alongside endometriosis or fibroids. The cause is not fully understood, and multiple factors are involved, including sex hormones, trauma and inflammation. The condition is hormone-dependent, and symptoms tend to resolve after menopause, similarly to endometriosis and fibroids.

57
Q

Ix for adenomyosis

A

**TV USS - first line
**Can also use TA USS or MRI

Gold Standard- histological examination of uterus following hysterectomy - not approapriate usually.

58
Q

adenomyosis treatement

A

NICE recommend the same treatment for adenomyosis as for heavy menstrual bleeding.

When the woman does not want contraception; treatment can be used during menstruation for symptomatic relief, with:

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

Management when contraception is wanted or acceptable:

Mirena coil (first line)
Combined oral contraceptive pill
Cyclical oral progestogens
Progesterone only medications such as the pill, implant or depot injection may also be helpful.

Other options are that may be considered by a specialist include:

GnRH analogues to induce a menopause-like state
Endometrial ablation
Uterine artery embolisation
Hysterectomy

59
Q

What is atrophic vaginitis and how does it present

A

Atrophic vaginitis refers to dryness and atrophy of the vaginal mucosa related to a lack of oestrogen/perimenaupause (think it resolves)

Oestrogen maintains thickness, estalasticity and secretions in the epithelial lining of the genitourinary tract. It also maintians the connective tissue around pelvic organs hence why menopause causes pelvicu organ prolapse and stress incontinence

Atrophic vaginitis presents in postmenopausal women with symptoms of:

Itching
Dryness
Dyspareunia (discomfort or pain during sex)
Bleeding due to localised inflammation

You should also consider atrophic vaginitis in older women presenting with recurrent urinary tract infections, stress incontinence or pelvic organ prolapse.

60
Q

management of atropic vaginitis?

A

Vaginal lubricants can help with dryness

Topical oestrogen (cream + applictor, pessaries, ring) or estradiol tablets

Topic eosterogen can make a big difference in symptom but like HRT carries tisk of breast cancer, anginga and VTE so should be stopped where possible

61
Q

What is lichen sclerosus? Presentation? How is it diagnosed?

A

Lichen sclerosus is a chronic inflammatory skin condition that presents with patches of shiny, “porcelain-white” skin. It commonly affects the labia, perineum and perianal skin in women. It can affect other areas, such as the axilla and thighs. It can also affect men, typically on the foreskin and glans of the penis.

Presentation -The typical presentation in your exams is a woman aged 45 – 60 years complaining of vulval itching and skin changes in the vulva.

Cause - Lichen sclerosus is thought to be an autoimmune condition. It is associated with other autoimmune diseases, such as type 1 diabetes, alopecia, hypothyroid and vitiligo.

Diagnosis - The diagnosis of lichen sclerosus is usually made clinically, based on the history and examination findings. Where there is doubt, a vulval biopsy can confirm the diagnosis.

Don’t confuse with lichen simplex (caused by stratching) or lichen planus (purplish with white lines, not ususally on vulva)

62
Q

Managment of lichen sclerosis

A

Potent topical steroids are the mainstay of treatment. The typical choice is clobetasol propionate 0.05% (dermovate).

Emollients should be used regularly, both with steroids initially and then as part of maintenance.

Lichen sclerosis cannot be cured, but the symptoms can be effectively controlled.

63
Q

What is pelvic organ prolapse - one phrase

What causes it?
5 risk factors for pelvic organ prolapse?

A

The decent of pelvic organs (uterus, rectum or bladder) into the vagina

Just think about that for one second - the vaginal canal/space, interally is filled by these tissues (only grade 3 and 4 are when it decends passed the introitus)

Prolapse is the result of weakness and lengthening of the ligaments and muscles surrounding the uterus, rectum and bladder. The factors that can contribute to this include:

Multiple vaginal deliveries
Instrumental, prolonged or traumatic delivery
Advanced age and postmenopause status
Obesity
Chronic respiratory disease causing coughing
Chronic constipation causing straining

64
Q

Types of pelvic prolapse (4)

A

Uterine prolapse is where the uterus itself descends into the vagina.

Vault prolapse 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 (where the cervix was).

Rectoceles are caused by a defect in the posterior vaginal wall, allowing the rectum to prolapse forwards into the vagina. Rectoceles are particularly associated with constipation. Women can develop faecal loading in the part of the rectum that has prolapsed into the vagina. Loading of faeces results in significant constipation, urinary retention (due to compression on the urethra) and a palpable lump in the vagina. Women may use their fingers to press the lump backwards, correcting the anatomical position of the rectum, and allowing them to open their bowels.

Cystoceles are caused by a defect in the anterior vaginal wall, allowing the bladder to prolapse backwards into the vagina. Prolapse of the urethra is also possible (urethrocele). Prolapse of both the bladder and the urethra is called a cystourethrocele.

65
Q

Sx of prolapse

A

Typical presenting symptoms are:

A feeling of “something coming down” in the vagina
A dragging or heavy sensation in the pelvis
cystocele - Urinary symptoms, such as incontinence, urgency, frequency, weak stream and retention
rectocele- Bowel symptoms, such as constipation, incontinence and urgency
Sexual dysfunction, such as pain, altered sensation and reduced enjoyment

66
Q

Management of prolapse

A

There are three options for management:

**1. conservative management:
**- supervised (physio) pelvic floor exercises
- weightloss
- caffeine reduction
- smoking cessation
- medical treatment for stress incontinence
- vaginal oestrogen if susepected atrophic vaginitis

**2.Vaginal pessary (ring, shelf/gellhorn)
**

**3.Surgery (definative management, highly effective):
**
- Anterioir (cystocele) or posterioir (rectocele) vaginal wall repair
- hysterectomy, sacrohysteropexy (attach uterus to sacrum)

67
Q

What is androgen insensitivity syndrome

A

Androgen insensitivity syndrome is a condition where cells are unable to respond to androgen hormones due to a lack of androgen receptors. It is an X-linked recessive genetic condition, caused by a mutation in the androgen receptor gene on the X chromosome. Extra androgens are converted into oestrogen, resulting in female secondary sexual characteristics.

Patients with androgen insensitivity syndrome are genetically male, with XY sex chromosome. However, the absent response to testosterone and the conversion of additional androgens to oestrogen result in a female phenotype externally. Typical male sexual characteristics do not develop, and patients have normal female external genitalia and breast tissue.

Patients have testes in the abdomen or inguinal canal, and absence of a uterus, upper vagina, cervix, fallopian tubes and ovaries. The female internal organs do not develop because the testes produce anti-Müllerian hormone, which prevents males from developing an upper vagina, uterus, cervix and fallopian tubes.

68
Q

How does androgen insensitivty syndrome present

A

The insensitivity to androgens also results in a lack of pubic hair, facial hair and male type muscle development. Patients tend to be slightly taller than the female average. Patients are infertile, and there is an increased risk of testicular cancer unless the testes are removed.

Androgen insensitivity syndrome often presents in infancy with inguinal hernias containing testes. Alternatively, it presents at puberty with primary amenorrhoea.

The results of hormone tests are:

Raised LH
Normal or raised FSH
Normal or raised testosterone levels (for a male)
Raised oestrogen levels (for a male)

69
Q

Magement of androgen insensitivity syndrome - 3 things

A

Medical input involves:

  • Bilateral orchidectomy (removal of the testes) to avoid testicular tumours
  • Oestrogen therapy
  • Vaginal dilators or vaginal surgery can be used to create an adequate vaginal length

Generally, patients are raised as female, but this is sensitive and tailored to the individual. They are offered support and counselling to help them understand the condition and promote their psychological, social and sexual wellbeing.

70
Q

What is asheman’s syndrome and how does it present?

Diagnosis and management?

A

Asherman’s syndrome is where adhesions (sometimes called synechiae) form within the uterus, following damage to the uterus.

Damage usually occours due to endometrial curretage (for RPOC), myomectomy or endometritis.

These adhesions form physical obstructions and distort the pelvic organs. Asherman’s syndrome typically presents following recent dilatation and curettage, uterine surgery or endometritis with:

Secondary amenorrhoea (absent periods)
Significantly lighter periods
Dysmenorrhoea (painful periods)
It may also present with infertility.

Hysteroscopy is the gold standard investigation, and can involve dissection and treatment of the adhesions. Although recurrence is common

it can also be diagnosed with imaging technique (wont bother learning).

71
Q

Cheat sheet on cervical cancer:
- who gets it?
- how common is it?
- cell type
- key cause?
- screening programme?

A
  • tends to affect younger women - peaking in the reproductive years
  • second most common type of gynaecological cancer after endometrial
  • 80% of cervical cancers are squamous cell carcinoma. Adenocarcinoma (glandular epithelium) is the next most common type.
  • Cervical cancer is strongly associated with human papillomavirus. Children aged 12 – 13 years are vaccinated against certain strains of HPV to reduce the risk of cervical cancer.
  • Cervical screening with smear tests is used to screen for precancerous and cancerous changes to the cells of the cervix. Early detection of precancerous changes enables prompt treatment to prevent the development of cervical cancer.
72
Q

Cervical cancer - what viral strains are targetted in the HPV vaccine? How does HPV cause cancer?

A

The current NHS vaccine is Gardasil, which protects against strains 6, 11, 16 and 18:

Strains 6 and 11 cause genital warts
Strains 16 and 18 cause cervical cancer

HPV is primarily a sexually transmitted infection.

There are over 100 strains of HPV. The important ones to remember are type 16 and 18, as they are responsible for around 70% of cervical cancers.

There is no treatment for infection with HPV. Most cases resolve spontaneously within two years, while some will persist.

HPV produces two proteins that inhibit tumour supressor genes - E6 inhibits p53 and E7 inhibits pRb

73
Q

How does cervical cancer present?

A

Cervical cancer may be detected during cervical smears in otherwise asymptomatic women.

The presenting symptoms that should make you consider cervical cancer as a differential are:

Abnormal vaginal bleeding (intermenstrual, postcoital or post-menopausal bleeding)
Vaginal discharge
Pelvic pain
Dyspareunia (pain or discomfort with sex)

Speculum examination
- take swabs to rule out infection
- visualise if abnormal appearence (ulceration, inflammation, bleeding, tumour) then urgent cancer referall for colposcy
- NICE CKS - Don’t use normal smear results to exclude cervical cancer if suspected for another reason

74
Q

Colposcopy scores the dysplasia of cells in the cervix using what grading system?

A

CIN- cervical intraeptithelial neoplasia

1- doesnt need treatment
2- likely to progress to cancer without treatment
3- carcinonopma in situ - very likely to progress to caner if unteated

TOM TIP: Try not to get mixed up between dysplasia found during colposcopy and dyskaryosis on smear results.

75
Q

Cervical cancer screening - What are the cells collected in a smear test tested for?

A

Dyskaryosis - pre-cancerous changes (not the same as displasia from colposcopy)

initially cells are tested for high-risk HPV:
- If negative, the cells are not examined.
- If positive -> cytology for dyskaryosis

HPV positive with normal cytology – repeat the HPV test after 12 months

HPV positive with abnormal cytology – refer for colposcopy

Background:
- dyskaryosis - looks at the nucleus of the cells
- dysplacia looks at the tissue architecture of biopsied tissue

76
Q

What happens during colposcpy

A

Colposcopy 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. During colposcopy, stains such as acetic acid and iodine solution can be used to differentiate abnormal areas.

acetic acid - acetowhite - cells with increased nuclear to cytoplasmic ratio (CI neoplasia) appear white

Schiller’s iodine test involves using an iodine solution to stain the cells of the cervix. Iodine will stain healthy cells a brown colour. Abnormal areas will not stain.

A punch biopsy or large loop excision of the transformational zone can be performed during the colposcopy procedure under local anastetic to get a tissue sample/remove abnormal tissue

This is different to a cone bopsy - using a scalpel under general anastetic - very early stage cervical cancer treatment

77
Q

management of cervical cancer

A

Management of cervical cancer depends on the stage and the individual situation. The usual treatments are:

Cervical intraepithelial neoplasia and early-stage 1A: LLETZ or cone biopsy
Stage 1B – 2A: Radical hysterectomy and removal of local lymph nodes with chemotherapy and radiotherapy
Stage 2B – 4A: Chemotherapy and radiotherapy
Stage 4B: Management may involve a combination of surgery, radiotherapy, chemotherapy and palliative care

The 5-year survival drops significantly with more advanced cervical cancer, from around 98% with stage 1A to around 15% with stage 4. Early detection makes a significant difference, which is one reason the screening program is so valuable and important.

Bevacizumab (Avastin) is a monoclonal antibody that may be used in combination with other chemotherapies in the treatment of metastatic or recurrent cervical cancer.

78
Q

Cheat sheet on endometrial cancer

  • cell type
  • what promotes endometrial cancer cell growth
  • the number one presenting symptom
  • typically presents in
  • 2 key risk factors
A

Endometrial cancer is cancer of the endometrium, the lining of the uterus. Around 80% of cases are adenocarcinoma. It is an oestrogen-dependent cancer, meaning that oestrogen stimulates the growth of endometrial cancer cells.

The number one presenting symptom of endometrial cancer to remember for your exams is postmenopausal bleeding - any woman presenting with postmenopausal bleeding has endometrial cancer until proven otherwise.

The key risk factors to remember are obesity and diabetes.

79
Q

What is endometrial hyperplasia?

How is it treated?

A

Endometrial hyperplasia is a precancerous condition involving thickening of the endometrium. The risk factors, presentation and investigations of endometrial hyperplasia are similar to endometrial cancer. Most cases of endometrial hyperplasia will return to normal over time. Less than 5% go on to become endometrial cancer. There are two types of endometrial hyperplasia to be aware of:

Hyperplasia without atypia
Atypical hyperplasia

Endometrial hyperplasia may be treated by a specialist using progestogens, with either:

Intrauterine system (e.g. Mirena coil)
Continuous oral progestogens (e.g. medroxyprogesterone or levonorgestrel)

80
Q

Pathphysiology - what do the risk factors for endometrial cancer all have in common

A

You can think of the risk factors for endometrial cancer in relation to the patient’s exposure to unopposed oestrogen. Unopposed oestrogen refers to oestrogen without progesterone. Unopposed oestrogen stimulates the endometrial cells and increases the risk of endometrial hyperplasia and cancer.

Increased age
Earlier onset of menstruation
Late menopause
Oestrogen only hormone replacement therapy
No or fewer pregnancies

Polycystic ovarian syndrome - lack of ovulation (LH surge lost) so no corpus luterum to produce progesterne in the luteal phase of the menstral cycle -> need COCP, Mirena, or cyclical progesterone for endometrial protection

Obesity - adipose tissue contains aromtase which converts testosterone from the adrenal glands into oestrogen. If a woman is post-menopausal then there is no corpus leuteum to produce progesterone

Tamoxifen - has an anti-oestrogenic effect on breast tissue, but an oestrogenic effect on the endometrium. This increase the risk of endometrial cancer.

T2D - increased production on insulin stimualtes endetrial hyperplasia

81
Q

What are the referal criteria for endometrial cancer

A

The referral criteria for a 2-week-wait urgent cancer referral for endometrial cancer is:

Postmenopausal bleeding (more than 12 months after the last menstrual period)

82
Q

Ix - Endometrial cancer

A

There are three investigations to remember for diagnosing and excluding endometrial cancer:

  • Transvaginal ultrasound for endometrial thickness (normal is less than 4mm post-menopause)
  • Pipelle biopsy, which is highly sensitive for endometrial cancer making it useful for excluding cancer
  • Hysteroscopy with endometrial biopsy
83
Q

Management of endometrial cancer

A

The usual treatment for stage 1 and 2 endometrial cancer is a total abdominal hysterectomy with bilateral salpingo-oophorectomy, also known as a TAH and BSO (removal of uterus, cervix and adnexa (ovaries and tubes)).

Other treatment options depending on the individual presentation include:

A radical hysterectomy involves also removing the pelvic lymph nodes, surrounding tissues and top of the vagina
Radiotherapy
Chemotherapy
Progesterone may be used as a hormonal treatment to slow the progression of the cancer

84
Q

Key - basic physiology of menstrual cycle. 3 sections talk about the hormone levels throughout the menstrual cycle.

A

Follicular phase - At the start of the menstrual cycle, FSH stimulates further development of the secondary follicles. As the follicles grow, the granulosa cells that surround them secrete increasing amounts of oestradiol (oestrogen). The oestradiol has a negative feedback effect on the pituitary gland, reducing the quantity of LH and FSH produced.

LH spike just before ovulation causing the dominant follicle to release the ovum. After ovulation, the follicle that released the ovum collapses and becomes the corpus luteum. The corpus luteum secretes high levels of progesterone, which maintains the endometrial lining.

When no fertilisation of the ovum occours there is no production of hCG and the corpus luterum degenerates - fall in oestrogen and progesterone and the endometrial breaks down.

85
Q

Presentation of ovarian cancer

A

Ovarian cancer often presents late due to the non-specific symptoms, resulting in a worse prognosis. More than 70% of patients with ovarian cancer present after it has spread beyond the pelvis.

Symptoms that may indicate ovarian cancer include:

Abdominal bloating
Early satiety (feeling full after eating)
Loss of appetite
Pelvic pain - due to obturator nerve compression
Urinary symptoms (frequency / urgency)
Weight loss
Abdominal or pelvic mass
Ascites

86
Q

What are the 4 different types of ovarian cancer

A

Epithelial Cell Tumours
- tumours arising from the epithelial cells of the ovary are the most common type.

Subtypes of epithelial cell tumours include:
Serous tumours (the most common)
Endometrioid carcinomas
Clear cell tumours
Mucinous tumours
Undifferentiated tumours

Dermoid Cysts / Germ Cell Tumours
- These are benign ovarian tumours.
- They are teratomas, meaning they come from the germ cells. They may contain various tissue types, such as skin, teeth, hair and bone.
- They are particularly associated with ovarian torsion.
- Germ cell tumours may cause raised alpha-fetoprotein (α-FP) and human chorionic gonadotrophin (hCG).

Sex Cord-Stromal Tumours

These are rare tumours, that can be benign or malignant. They arise from the stroma (connective tissue) or sex cords (embryonic structures associated with the follicles). There are several types, including Sertoli–Leydig cell tumours and granulosa cell tumours.

Metastasis

Ovarian tumours may be due to metastasis from a cancer elsewhere. 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.

87
Q

Ix in ovarian cancer - primary vs secondary care? Women under 40 with complex ovarian mass?

A

The initial investigations in primary or secondary care are:

  • CA125 blood test (>35 IU/mL is significant) - NON SPECIFIC
  • Pelvic ultrasound

These two findings combined with menopausal status feed in a romance Risk of malginancy index (RMI).

Further investigations in secondary care:
- CT scan - establish diagnosis and staging
- Histology
- Paracentesis - test ascitic fluid for cancer cells

Women under 40 years with a complex ovarian mass require tumour markers for a possible germ cell tumour:

Alpha-fetoprotein (α-FP)
Human chorionic gonadotropin (HCG)

88
Q

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

89
Q

Management of ovarian cancer - 2

A

Usually invovlves a combination of surgery and chemotherapy.

90
Q

What is the most common type of vulval cancer? How does it present?

A

Around 90% are squamous cell carcinomas. Less commonly, they can be malignant melanomas.

Vulval cancer most frequently affects the labia majora, it may present with symptoms of:

Vulval lump
Ulceration
Bleeding
Pain
Itching
Lymphadenopathy in the groin

91
Q

What is involved in Antenatal screening for Down’s Syndrome? What happens if the results are high risk?

A

First line - the combined test:
- performed between 11 and 14 weeks gestation
- screens for trisomy’s - down’s syndrome, Edward’s and Patau’s syndrome (down’s- lifelong learning disabilities and cardiac abnormalities, the other two are incompatible with life)
- combines results from ultrasound and maternal blood tests
- ultrasound - nuchal translucency (neck thickness) >6mm
- Maternal blood tests for two hormones - Beta‑human chorionic gonadotrophin (beta-HCG) – a higher result indicates a greater risk; Pregnancy‑associated plasma protein‑A (PAPPA) – a lower result indicates a greater risk

  • other screening tests include the triple and quadruple test (wont bother learning)

The screening test provide a risk score for the fetus having down’s syndrome. If the screening tests come back as high risk the woman if offered further testing. This involves taking a sample of fetal cells for karyotyping:
- Chorionic villus sampling (CVS) involves an ultrasound-guided biopsy of the placental tissue. This is used when testing is done earlier in pregnancy (before 15 weeks).-
- Amniocentesis involves ultrasound-guided aspiration of amniotic fluid using a needle and syringe. This is used later in pregnancy once there is enough amniotic fluid to make it safer to take a sample.
- Non-invasive prenatal testing (NIPT) testing is a new, non invasive test that examines fragments of DNA in the maternal blood, arising from the placental tissue to detect down’s. It is not a definitive test (like the invasive) but it is very good.

92
Q

lichen sclerosus is a risk factor for what?

A

Around 5% of women with lichen sclerosus get vulval cancer

93
Q

Key - Types of gynaecological malignancy, what are their relative incidences and in whom do they present

A

Endometrial - most common gynae cancer, often presents with post menopausal bleeding, or postcoital, intermenstrual
Cervical - next most common, tends to affect younger women (HPV is an STI), also abnormal bleeding
Ovarian - peaks around 60, non specific symptoms (appeptide, abdominal bloating, weight loss)
Vulval - elderly ladies (75+) bleeding and lumps

94
Q

What is vulval intraepithelial neoplasia - VIN? Management?

A

Similar to CIN for cervical cancer, VIN is a premalignant condition that can preceed vulval cancer

VIN affects the squamous epithilium.

High grade squamous intraepithelial lesion is a type of VIN associated with HPV infection that typically occurs in younger women aged 35 – 50 years.

Differentiated VIN is an alternative type of VIN associated with lichen sclerosus and typically occurs in older women (aged 50 – 60 years).

A biopsy is required to diagnose VIN. A specialist will coordinate management. Treatment options include:

Watch and wait with close followup
Wide local excision (surgery) to remove the lesion
Imiquimod cream
Laser ablation

95
Q

Management of vulva cancer - Ix (3) and Rx (4)

A

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)

The International Federation of Gynaecology and Obstetrics (FIGO) system is used to stage vulval cancer.

Management depends on the stage, and may involve:

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

96
Q

KEY UROGYNAE

Two main types of incontinence and the respective causes?

other causes of urgency and frequency

A

Urinary incontinence refers to the loss of control of urination

Stress incontinence- the involuntary leakage of urine when there is increased pressure on the bladder from exertion, sneezing or coughing (increased abdominal pressure with a weak pelvic floor).
Most often caused by weakness of the pelvic floor. Presents with leakage symptoms.
The pelvic floor consists of a sling of muscles that support the contents of the pelvic. There are three canals through the centre of the female pelvic floor: the urethral, vaginal and rectal canals. When the muscles of the pelvic floor are weak, the canals become lax, and the organs are poorly supported within the pelvis.

Urge incontinence - Urge incontinence is caused by overactivity of the detrusor muscle of the bladder. Urge incontinence is also known as overactive bladder. The typical description is of suddenly feeling the urge to pass urine, having to rush to the bathroom and not arriving before urination occurs.
Presents with urgency and frequency

Also overflow (obstructed outflow or urine -> retention -> incontinent) and mixed incontinence (Stress and Urge)

Other causes of urgency and frequency
- detrousser overactivity
- UTI - dipstick
- bladder masses
- small capacity bladder
- Gynae- fibroids, press onto the bladder
- Cystocele
- Diabetes

97
Q

Examination needed for incontinence or pelvic prolapse

A

Abdominal - Rule out any abdominal or pelvic masses that could be responsible for the symptoms

Speculum (+cough)

Bimanual - pelvic mass, prolapse, assess for pelvic tone (squeeze against fingers)

98
Q

Investigations for Urinary Incontinence

A

Simple

  • Urinaylsis
  • MSU
  • fluid volume chart- shows maximum capacity

Invasive:

  • Ultrasound - if suspect a pelvic mass, bladder scan to assess for incomplete emptying
  • Urodynamics- used if unsure whether due to stress or urge, especially before treatment (med or surgical) to get a definative diagnosis
  • cystoscopy
99
Q

Lifestyle advice for incontinence - 4?

A
  • weightloss
  • smoking cessation
  • reduced caffeine intake
  • avoidance of straining and constipation
100
Q

KEY, BIG BOY -Management of Stress vs Urge Incontinence

A

Treatment:

Stress incontinent:

  • conservative - physiotherapy (pelvic floor) for 3 months, lifestyle changes, continence pads

Surgery:
- Autologous fascial sling (support the urethra)
- colposuspension (anteori wall attaches to pubic synthesis to support the urethra)
- intramural urethral bulking

  • Medical - duloxetine (SNRIs) if surgery not preffered

Vaginal mesh has been baned because of issues with chronic pain, dypareunia, bower and bladder issues. Mesh is still used as part of prolapse repair in sacrohysteroplexy .

Urge Incontinence:

  • bladder retrianing
  • anticholinergic medication - oxybutynin, solifenacine, tolterodine
  • Mirabegron (Beta 3-agonist)
  • botulinum toxin type A injecitons into bladder wall
  • augmentation cystoplasty (enlarge bladder with section of bowel)
  • bypass/ urinary diversion to a urostomy bag.
101
Q

Congenital structural abdnormalities of teh female reproductive tract can lead to menstrual, sexual and reproductive problems.

What embryological structure forms the female pelvic organs?

A

TOM TIP: If you remember one thing about the embryology of the female reproductive system, remember the Mullerian ducts. Medical school exams are unlikely to test your knowledge of the embryology of the female reproductive system in detail (unless the exam is specific to that topic). However, they may refer to a congenital structural abnormality and ask what structure in the fetus this relates to. The answer is the Mullerian ducts. Equally, they may ask why males do not develop a uterus, and the answer is anti-Mullerian hormone, which suppresses the growth of teh paramesonephric ducts. The paramesonephric/mullerian ducts are a pair of passage eways along the outside of teh urogenital region that sure to form the upper third of the vegina, cervix, uterus and fallopian tubes (ovaries develop speerately).

102
Q

Name 4 congintal structural abormalities of the female reproductive tract

A

Bicornuate uterus - two horns (heart-shaoed uterus). Can be diagnosed on pelvic ultrasound scan and leads to complications in pregnancy (miscarraige, prematrue birth and malpresentaiton)

Imperforate hymen (the hymen at vaginal entrance does have an opening) -> menses are seaked in the vagina. surgical incision.

transverse vaginal septae - a septum/wall forms transversely across the vagina. Surgical correction.

vaginal hypoplasia (abnormally small vagina) and vaginal agenesis (absent vagina) - failure or mullerian ducts to properly develop. Surgical correction or dilators.

103
Q

What is an endometrial polyp and how does it present

A

It is an extreme form of macroscopic endometrial hyperplasia (tissue grows so fast that parts of the entrometrium enter the uterine cavity)

They present with menorrhagia (heavy periods) and post-menopausal bleeding

Management is Heavy bleeeding managment basically.

Diagosis is with endometrial biopsy or diagnostic hysteroscopy. TV USS scan may play a role in determinine endometrial thickeness. Polyps, need to be removed with hysteroscopy because of the risk of endometrial cancer.

Sidenote: Me guessing because no Z2F page, maybe just like with PCOS - reduce risk of endometrial hyperplasia with mirena coil, combined pill, cylical progesterones?

104
Q

What is a vaginal fistula?

A

A vaginal fistula is an abnormal opening between the vagina and other nearby organs in the pelvis, including the bladder or rectum. A fistula can cause many complications, such as urinary and fecal leakage, abnormal vaginal discharge, tissue damage, kidney infections and other irritative type symptoms.

Surgical repair is often required.

105
Q

What is premenstrual dysphoric disorder/premenstrual syndrome?

What causes it?

Presentation?

A

PMS describes a range of psychological and physical symptoms every month during the week or two before your period (the luteal phase). When features are severe and have a significant effect on quality of life, this is called premenstrual dysphoric disorder.

The symptoms of PMS resolve once menstruation begins. Symptoms are not present before menarche, during pregnancy or after menopause. These are key things to note when you take a history.

Premenstrual syndrome is though to the caused by fluctuation in oestrogen and progesterone hormones during the menstrual cycle. The exact mechanism is not known, but it may be due to increased sensitivity to progesterone or an interaction between the sex hormones and the neurotransmitters serotonin and GABA.

Presentation:
Low mood
Anxiety
Mood swings
Irritability
Bloating
Fatigue
Headaches
Breast pain
Reduced confidence
Cognitive impairment
Clumsiness
Reduced libido

These symptoms can also be caused by progesterone contraceptives sych as COCP.

106
Q

Premenstrual dysphoric disorder:
- diagnosis?
- management in primary and in secondary care?

A

Diagnosis:
- symptom diary demonstrates cyclical symptoms that occour before and resolve after the onset of menstruation
- A definitive diagnosis may be made, under the care of a specialist, by administering a GnRH analogues to halt the menstrual cycle and temporarily induce menopause, to see if the symptoms resolve.

Management in primary care:
- COCP
- SSRI antidepressants (in the luteual phase and during menstruation) and CBT

Specialist management:
- estrogen patches (with progestoerone to prevent endometrial hyperplasia)
- Severe cases GnRH - induce menopausal state and then HRT to mitagate oestoperosis and other adverse effects.
- hysterectomy severe and GnRH has not helped.
- danazol for cyclic breast pain

107
Q

Female Puberty:
Physiological cause?

What is the order of development of sexual characteristics?

age of onset and duration?

stagging system for puberty?

hormonal changes in puberty?

A

In childhood, girls have relatively little GnRH, LH, FSH, oestrogen and progesterone in their system. During puberty, these hormones start to increase sequentially, causing the development of female secondary sexual characteristics, the onset of the menstrual cycle and the ability to conceive children.

In girls, puberty starts with the development of breast buds, followed by pubic hair and finally the onset of menstrual periods. The first episode of menstruation is called menarche. Menstrual periods usually begin about two years from the start of puberty.

Puberty starts age 8 – 14 in girls and 9 – 15 in boys. It takes about 4 years from start to finish

Staging system - the tanner scale (Stage 1-5) is used to stage pubertal development based on the pubic hair and breast development.

Hormonal changes in puberty:
- Growth Hormonne increases initially which cuases an initial growth spurt
- Hypothalamus secretes GnRH
- GnRh stimulates the release of FSH and LH which stimulate the ovaries to produce oestrogen and progesterone (causing secondary sexual characteristic development).
- FSH levels plateau about a year before menarche, LH continues to rise and has a spike just before menarche.