cOGText: Gynaecological problems Flashcards

1
Q
  1. The length of a menstrual cycle is measured between which 2 days?
  2. Average ___ days but normal __-__ days.
  3. The menstrual cycle is typically most irregular when in life? why
A
  1. first day of menstrual bleeding of one cycle to the onset of menses of the next
  2. 28, 21-35
  3. around the extremes of reproductive life (menarche and menopause) due to anovulation and inadequate follicular development.
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2
Q

What are the two phases of the menstrual cycle and how long is each?

A
  • luteal phase: constant duration of 14 days.
  • follicular phase: varies, range from 10 - 16 days.
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3
Q

Control of the menstrual cycle

  1. The hypothalamus produces the peptide hormone, ______ which controls pituitary hormone secretion.
  2. GnRH must be secreted in what way to stimulate pituitary secretion of LH and FSH
A
  1. Gonadotrophin-releasing hormone (GnRH)
  2. a pulsatile fashion
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4
Q

The menstrual cycle is controlled by feedback systems:

  1. Moderate oestrogen levels: ____ feedback on the HPO axis
  2. High oestrogen levels (in the absence of progesterone): ____ feedback on the HPO axis
  3. Oestrogen in the presence of progesterone: ____ feedback on the HPO axis
  4. Inhibin: selectively inhibits ___ at the ____ pituitary
A
  1. negative
  2. positive
  3. negative
  4. FSH, anterior
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5
Q

what are the 3 events that occur in the ovaries during the menstrual cycle?

A

follicular phase

ovulation

luteal phase

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6
Q

Follicular phase

  1. ____ levels rise in the first days of the menstrual cycle when the oestrogen, progesterone and inhibin levels are low.
  2. Within the follicle, what are the 2 types of cells which are involved in oestrogen and progesterone synthesis? Which hormones does each respond to?
  3. Describe what LH stimulates the proction of in theca cells
  4. then the granulosa cells carry out what function
  5. T/F: Both FSH and LH are needed to generate a normal cycle with adequate oestrogen.
  6. As the follicles grow, there is a negative feedback by both ____ and ____ on the pituitary to decrease FSH secretion.
  7. What is the effect of this?
  8. Which follice will form the dominant follicle?
  9. The follicle with the most efficient ____ activity and highest concentration of FSH-induced __ receptors will be the most likely to survive as FSH levels drop and smaller follicles undergo _____.
  10. The dominant follicle will keep producing ____ and _____ which enhances androgen synthesis under ___ control.
  11. Inhibin in women is produced by the ____ cells where it feedbacks to the pituitary to downregulate ____ release and also enhances ____ synthesis.
  12. Activin has an opposite action but is also produced by the ____ cells and pituitary. It works to increase ____ binding in the follicles.
A
  1. FSH
  2. theca (LH) and the granulosa (FSH) cells
  3. LH > stimulates theca cells to produce androgens from cholesterol
  4. FSH > stimulates granulosa cells to convert androgens to oestrogen (by aromatisation)
  5. true
  6. oestrogen, inhibin
  7. results in selection of one follicle (the dominant follicle) to continue its development towards ovulation
  8. aromatase, LH, atresia
  9. oestrogen, inhibin, LH
  10. granulosa, FSH, androgen
  11. granulosa, FSH
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7
Q

Ovulation

  1. By the end of the follicular phase (which lasts an average ___ days), what has occurred?
  2. FSH induces LH receptors on the ____ cells to compensate for lower FSH levels and prepare for ovulation
  3. Production of oestrogen increases until it reaches the threshold to exert a ____ feedback effort on the hypothalamus and pituitary to cause what?
  4. This occurs over ___hours during which time the LH-induced luteinization of granulosa cells causes _____ to be produced, adding to the positive feedback for ___ secretion and small periovulatory rise in FSH as well.
  5. Androgens, made by ____ cells, also rise during ovulation. This is thought to have an important role in stimulating ____
  6. What is the best predictor of imminent ovulation?
  7. It also is involved in stimulating the resumption of ____ in the oocyte just before its release.
  8. ____ mediators are suspected to be involved in the extrusion of the oocyte from the follicle stimulating smooth muscle activity.
  9. How long after the LH surge does ovulation occur?
A
  1. 14, the dominant follicle has grown and matured.
  2. granulosa
  3. positive, LH surge
  4. 24-36, progesterone, LH
  5. theca, libido
  6. the LH surge (used in ovulation predictor tests)
  7. meiosis
  8. Inflammatory
  9. 12 hours (dominant follicle ruptures and releases the oocyte)
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8
Q

Luteal phase

  1. After release of the oocyte, the remaining granulosa and theca cells on the ovary form the ___ ___
  2. The ____ cells have a vacuolated appearance with a yellow pigment and form the corpus luteum which secretes ____ which begins the ____ phase of the endometrium.
  3. Ongoing pituitary LH secretion and granulosa cell ensures a supply of ____ which stabilises the endometrium in preparation for pregnancy.
  4. The high levels of progesterone during the luteal phase suppress secretion of what? Why is this important?
  5. How long does the rhe luteal phase last?
  6. In the absence of __ __ __ __ being produced from an implanting embryo, the corpus luteum will undergo luteolysis and regress.
  7. Progesterone secretion then decreases, resulting in what?
  8. A reduction in progesterone, oestrogen and inhibin feeding back to the pituitary cause an increase in _____ hormones, particularly ___ and new preantral follicles begin to be stimulated and the cycle begins again.
  9. Progesterone production peaks __ days before the start of the next menses. This has a clinical application in assessing ____ and checking for ovulation. For those with a 28day cycle, mid-luteal progesterone levels are checked on day ___ and for those with a 35day cycle, a mid-luteal progesterone level is checked on day __
A
  1. corpus luteum
  2. granulosa, progesterone, secretory
  3. progesterone
  4. FSH and LH - to prevent further follicular growth in the ovary
  5. 14 days
  6. beta human chorionic gonadotrophin
  7. endometrium sheds and menstruation occurs.
  8. gonadotrophin, FSH
  9. 7, infertility, 21, 28
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9
Q

Endometrial events

  1. The endometrium is under the influence of ___ steroids that circulate in females of reproductive age.
  2. Sequential exposure to oestrogen and progesterone will result in cellular ___ and ____ in preparation for embryo implantation followed by shedding and bleeding if the ___ ___ regresses.
  3. During the ovarian follicular phase, the endometrium undergoes its ___ phase and during the luteal phase is undergoes its ___ phase.
  4. In the proliferative phase, the endometrium changes from a single layer of ___ cells to a _____ epithelium with frequent mitoses.
  5. The secretory phase involves a period of endometrial glandular secretory activity. The endometrial glands will become more ____, ____ arteries will grow and fluid is secreted into glandular cells and into the uterine lumen.
  6. Later, progesterone induces the formation of the a temporary layer, the _____.
  7. What is decidualisation?
  8. What is menstruation (day 1)?
  9. A fall in oestrogen and progesterone on the endometrium approximately 14 days after ovulation leads what changes in the endometrium?
  10. How is haemostasis in the uterine endometrium different from elsewhere in the body?
  11. Enhanced ____ reduces clotting.
  12. There are multiple vasoconstrictors and vasodilators that are involved in endometrial shedding, including _____.
  13. This forms the basis for management of heavy periods e.g. what drugs?
A
  1. sex
  2. proliferation, differentiation, corpus luteum
  3. proliferative, secretory
  4. columnar, pseudostratified
  5. tortuous, spiral
  6. decidua
  7. The formation of a specialised glandular epithelium. Irreversible process, apoptosis occurs if no embryo implants
  8. shedding of the dead endometrium (ceases as the endometrium regenerates)
  9. loss of tissue fluids, vasoconstriction of spiral arterioles and distal ischaemia > tissue breakdown, loss of the upper layer + bleeding from the remaining arterioles (menstrual bleeding).
  10. doesn’t involve the process of clot formation and fibrosis.
  11. fibrinolysis
  12. prostaglandins
  13. NSAIDs e.g. mefenamic acid - a prostaglandin inhibitor widely used for heavy menstrual bleeding (acts by increasing the ratio of vasoconstrictor to the vasodilator)
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10
Q

Define:

  1. Menorrhagia
  2. Metrorrhagia
  3. Polymenorrhea
  4. Polymenorrhagia
  5. Menometrorrhagia
  6. Amenorrhea
  7. Oligomenorrhea
A
  1. Prolonged and increased (>80ml per period) menstrual flow (heavy menstrual bleeding)
  2. Regular intermenstrual bleeding
  3. Menses occurring at < 21 day interval
  4. Increased bleeding and frequent cycle
  5. Prolonged menses and intermenstrual bleeding
  6. Absence of menstruation >6months
  7. Menses at intervals of >35days OR ≤5 menstrual cycles over a year.
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11
Q

Causes of menorrhagia (local)?

A
  • Intrauterine contraceptive device (IUCD)
  • Endometrial hyperplasia
  • Endometriosis
  • Endocervical or endometrial polyp
  • Adenomyosis
  • Fibroids
  • Uterine/ cervical malignancy
  • Hormone producing ovarian tumours
  • Pelvic inflammatory disease (PID)
  • Arteriovenous malformation

(think inside uterus then work outwards >endometrium > myometrium > ovaries)

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12
Q

Causes of menorrhagia (systemic)?

A
  • Endocrine disorders (hyper/hypothyroism, DM, adrenal disease, prolactin disorders)
  • Haematological diseases (Von willebrand’s disease, immune thrombocytopenic purpura (ITP), factor II, V, VII and XI deficiency
  • Liver disorders – cirrhosis
  • Renal disease
  • Drugs – anticoagulants (warfarin, clopidrogel, rivaroxaban)
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13
Q

For causes of menorrhagia, also consider pregnancy complications e.g. …?

A

miscarriage, ectopic pregnancy, gestational trophoblastic disease, placenta praevia

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14
Q

In a patient presenting with menorrhagia, after history taking a clinical examination to look for signs of ___ and abdominal and pelvic examination is required.

At this stage, any pelvic masses can be palpated, the cervix visualised and what Ix are carried out?

A

anaemia

cervical smears if due and also swabs if PID suspected

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15
Q

what is non-organic menorrhagia?

A
  • Occurs in the absence of pathology
  • aka dysfunctional uterine bleeding
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16
Q

Dysfunctional uterine bleeding (DUB)

  1. It may be called “bleeding of ____ origin”
  2. Accounts for ___% of women with abnormal uterine bleeding
  3. Diagnosis is made how?
  4. what are the 2 subtypes?
A
  1. endometrial
  2. 50
  3. by exclusion of other diagnoses
  4. Anovulatory (85%) and ovulatory
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17
Q
  1. Anovulatory DUB accounts for __% of all cases. Occurs at what age? Presents with a regular/ irregular cycle. More frequent in what demographic of women?
  2. Ovulatory DUB is more common in women aged ___ years. How do they describe their periods? Due to what?
A
  1. 85, extremes of reproductive life, irregular, obese women.
  2. 35-45, Regular heavy, inadequate progesterone production by corpus luteum
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18
Q

Investigations for DUB?

A
  • Full blood count
  • TFTs if features of hypothyroidism (fatigue, weight gain, skin changes)
  • Coagulation screen if very heavy bleeding/ other signs of bleeding tendency
  • Renal/Liver function tests if other signs of systemic illness
  • Transvaginal ultrasound scan (Endometrial thickness, Presence of fibroids and other pelvic masses)
  • Endometrial sampling (Pipelle biopsies, Hysteroscopic directed endometrial biopsies under GA, Dilatation & curettage).
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19
Q

Management of dysfunctional uterine bleeding (medical)

A
  • First line: Mirena IUS (progesterone releasing). Best option if compliance concerns and avoids drug interactions.
  • COCP. Useful when contraception is required
  • Antifibrinolytics e.g. tranexamic acid; taken during menstruation only. Appropriate when the woman is considering conceiving.
  • NSAIDs e.g. mefenamic acid – taken during menstruation only. Appropriate when the woman is considering conceiving.
  • Oral progestogens e.g. Norethisterone and medroxyprogesterone acetate.
  • GnRH analogue/agonists e.g. Goserelin, Decapeptyl, Buserelin.
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20
Q

2 types of amenorrhoea

A
  1. Primary: failure of menstruation by 16 y/o
  2. Secondary: absence of menstruation for at least 6 months in a female of reproductive age with a history of regular cyclic bleeding that is not caused by pregnancy, lactation or menopause.
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21
Q

Causes of primary amenorrhoea?

A
  • Genital tract abnormalities e.g. imperforate hymen, vaginal agenesis or septa, cervical stenosis
  • Mullerian agenesis – congenital malformation > absent uterus, vaginal malformation
  • Premature ovarian failure/ insufficiency
  • Pituitary disorders e.g. adenoma (often prolactinomas), infiltrative disease (sarcoidosis)
  • Hypothalamic disorders e.g. Kallman’s syndrome
  • Endocrine causes – hypothyroidism, constitutional delay, congenital adrenal hyperplasia, PCOS, androgen secreting tumour
  • Genetic – Turner’s syndrome, pure gonadal agenesis, androgen insensitivity syndrome, 5-alpha reductase deficiency
  • Iatrogenic – chemotherapy or radiation
  • Autoimmune destruction

(start at the bottom, work up. Genital tract > mullerian duct > ovaries > pituitary > hypothalamus > general)

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22
Q

What is premature ovarian failure/ insufficiency?

A

cessation of periods <40 (could be due to chemo, radiotherapy, Turner’s syndrome. Often seen in patients with other autoimmune disorders)

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23
Q

What is Kallman’s syndrome?

A

genetic condition resulting in failure to go through puberty due to an absence or failure of respond to GnRH

Treatment = HRT

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24
Q

What might indicate that the cause of primary amenorrhoea is a genital tract abnormality? (e.g. imperforate hymen, vaginal agenesis or septa, cervical stenosis)

  1. examination
  2. USS
A
  1. primary amenorrhea but with secondary sexual characteristics
  2. distended uterus or vagina filled with blood (haematometra or haematocolpos respectively)
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25
Q

Causes of secondary amenorrhoea?

A
  • Ashermann’s syndrome: adhesions inside the uterus 2º to endometrial surgery/ infection. Prevents menstruation, causes other menstrual disturbances, reduced fertility and placental abnormalities.
  • Other uterine problems: endometrial atrophy, cervical stenosis from aggressive cervical cancer treatment.
  • Pituitary: Sheehan syndrome, Hyperprolactinaemia, haemochromatosis
  • Hypothalamic: excessive exercise, weight loss or stress, systemic disorders such as sarcoidosis
  • Endocrine: hypo/hyperthyroidism, PCOS
  • Autoimmune conditions
  • Iatrogenic: oophorectomy, radiation, chemotherapy, antidopaminergic drugs e.g. phenothiazines.
  • Physiological (lactation, pregnancy)

think uterus > pituitary > hypothalamus > endocrine > other

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26
Q

What is Sheehan syndrome?

A

damage to pituitary due to prolonged hypotension following a major obstetric haemorrhage causing hypoxia

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27
Q
  1. What should examination cover in someone presenting with amenorrhoea?
  2. What important investigation should be done in women of reproductive age presenting with amenorrhea?
A
  1. BMI, secondary sexual characteristics, signs of endocrine disorders (acne, abdominal striae, hirsutism, skin pigmentation changes). May need visual field tests if suggestive of a pituitary lesion. Examination of the external genitalia to detect any structural abnormalities
  2. Urine/ serum bHCG to exclude pregnancy
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28
Q

what is the climateric?

A

is the period around the beginning of the menopause (aka perimenopause).

marks the transition from reproductive > non-reproductive state

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29
Q

what is the menopause due to?

A

loss of ovarian follicular activity leading to a fall in oestradiol levels below that needed for endometrial stimulation

is a retrospective clinical diagnosis (FSH, LH, oestradiol levels not particularly useful unless pt is young with amenorrhea and signs of menopause)

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30
Q

what is premature menopause defined as?

how is a diagnosis confirmed?

A

menopause <45

2 measurements of FSH at least 2 weeks apart recommended to confirm menopause.

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31
Q

Menopause

  1. Due to cessation of follicular development and ripening, levels of which hormones decrease?
  2. T/F: a fall in oestradiol levels has effects on all oestrogen-responsive tissue in the body.
A
  1. oestradiol, progesterone, inhibin, androgens
  2. true
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32
Q

Effects of the menopause (Physical)

A
  • Vaginal dryness and soreness > dyspareunia
  • Urogenital prolapse
  • Recurrent UTI, urinary urgency
  • Joint aches and pains
  • Osteoporosis increasing risk of fractures
  • cardiovascular disease.
  • Vasomotor symptoms e.g. hot flushes and night sweats
  • Dementia
  • Dry and itchy skin
  • Hair changes

genitals > urethra > bones > heart and vessels > brain > skin > hair

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33
Q

Effects of the menopause (psychological)?

A
  • Labile mood, anxiety, tearfulness
  • Loss of concentration, poor memory
  • Loss of libido
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34
Q

Management of menopause

  1. good 1st step for symptom management?
  2. what other lifestyle modication can have a positive effect?
  3. what is the main medical management?
  4. can come in what different forms?
A
  1. lifestyle modification e.g. using fans and avoiding spicy foods
  2. Regular exercise: +ve effect on cardiovascular risk, reduce vasomotor symptoms, improve bone density, maintain muscle strength, joint flexibility and overall balance.
  3. HRT (replaces the hormones that are normally produced by the ovaries)
  4. patches, gel, tablets or implants.
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35
Q

HRT for menopause

  1. what is the main hormone contained in this
  2. NB: oestrogen only HRT is only given to which group of women?
  3. What form of oestrogen HRT is often considered better options for women with a personal or family history of venous thrombosis or known liver problems?
  4. Progesterone HRT also comes in many different forms e.g. ?
  5. HRT can be given in different cycles, e.g.?
  6. side effect of continuous combined systemic HRT?
  7. A 3rd hormone, _____, can be added in cases of reduced libido
  8. What other drug class is now being used as non-hormonal treatment in women with a history of breast cancer?
  9. what can be used to tackle the psychological effects of menopause?
  10. Improvement is usually seen how long after starting HRT?
  11. Women who have undergone premature ovarian insufficiency/premature menopause will need to take HRT until the age of at least ___ to protect ____ health.
  12. how long should other women take HRT?
  13. Contraception should continue for how long after the last menstrual period?
  14. T/F: HRT is also a contraceptive
A
  1. Oestrogen - can be given as a standalone or in combination with progestogen.
  2. those without a uterus
  3. oestrogen patches - it avoids first-pass metabolism reducing impact on the liver in terms of haemostatic and coagulation system.
  4. tablets, IUD, transdermal.
  5. continuous combined (often menopausal women, taken every day), cyclical combined (often perimenopausal women who still get periods, oestradiol tablet daily + progestogen tablet on the last 14 days of the month).
  6. erratic bleeding in the first 3-6months
  7. testosterone
  8. SSRIs e.g. fluoxetine (HRT still far more effective)
  9. CBT (labile moods, anxiety)
  10. 4-6 weeks
  11. 50, bone
  12. no limit - length of treatment based on how long the woman feels she benefits from HRT.
  13. 2 years if <50, 1 year if >50
  14. false - women with premature menopause can occasionally ovulate so contraception will be needed for those who are sexually active and don’t wish to conceive.
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36
Q
  1. Women who have undergone a premature menopause (cessation of ovarian function <40) are at increased risk of what?
  2. what type of hormone replacement is likely to reduce these risks in women with POI?
A
  1. cardiovascular disease, osteoporosis, cognitive impairment
  2. Sex steroid hormone replacement
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37
Q

Side effects of HRT

  1. Oestrogen related?
  2. progesterone related?
A
  1. Breast enlargement, leg cramps, dyspepsia, fluid retention, nausea, headaches (usually dose-related and settle with time)
  2. Fluid retention, breast tenderness, headaches, acne, mood swings, depression, irritability, constipation, increased appetite (similar to premenstrual symptoms)
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38
Q

Risks associated with HRT?

A

Breast cancer

VTE (and PE and stroke)

Endometrial cancer

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39
Q

Risk of VTE with HRT

  1. risk of VTE greatly increases with HRT
  2. This risk is further increased in what women?
  3. ____ HRT is preferred in these women
  4. T/F: the risk of VTE is lower than that associated with the COCP
A
  1. 2 fold increased risk but background risk is low so still v low risk
  2. obese, underlying thrombophilia e.g. factor V leiden, previous VTE
  3. Transdermal
  4. True. Also lower than that associated with pregnancy and puerperium
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40
Q

how is the risk of endometrial cancer in HRT decreased?

A

by adding progestogen therapy in menopausal women with a uterus

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41
Q

absolute contraindication to HRT?

A
  • Suspected pregnancy
  • Breast cancer
  • Endometrial cancer
  • Active liver disease
  • Uncontrolled hypertension
  • Known VTE
  • Known thrombophilia e.g. factor V leiden
  • otosclerosis
42
Q

relative contraindications to HRT?

A
  • Uninvestigated abnormal bleeding
  • Large uterine fibroids
  • Past history of benign breast disease
  • Unconfirmed personal history or a strong family history of VTE
  • Chronic stable liver disease
  • Migraine with aura
43
Q

What does ‘the vulva’ include?

A

labia majora, minora, clitoris and the fourchette.

44
Q

Causes of vulval pruritis?

A
  • Other skin conditions – eczema, atopic dermatitis, psoriasis, candida infection
  • Lichen sclerosus
  • Lichen planus
  • Infection e.g. candidiasis, trichomonas vaginalis.
  • Extramammary Paget’s disease of the vulva
45
Q
  1. How long should a woman take HRT?
  2. Contraception should continue for __ __ after the last menstrual period in women under 50 and for __ __ in women over 50.
  3. T/F: HRT not a contraceptive
A
  1. For as long as the woman feels she benefits.
  2. 2 years <50, 1 year >50
  3. True - women with premature menopause can occasionally ovulate so contraception will be needed for those who are sexually active and don’t wish to conceive.
46
Q

Lichen sclerosus

  1. What is it
  2. It can be found anywhere in the body but most commonly affects the ___ area in men and women at any age.
  3. Pts often have what comorbidities
  4. How does it present?
  5. Over time, with persistent inflammation and healing, what may form?
  6. Most commonly affected area?
  7. In advanced cases, how might the skin appear/ be described as?
  8. Splitting of the skin is common and often occurs at the posterior ___ leading to superficial dyspareunia.
A
  1. Chronic inflammatory condition characterised by areas of atrophy and systematic destruction to the skin cells including melanocytes and hair follicles.
  2. Genital
  3. Believed to be autoimmune - pts often have other autoimmune conditions e.g. thyroid disease, pernicious anaemia.
  4. Vulval pruritus and skin irritation. Hypopigmented and atrophied skin with hair loss> shiny appearance. Easily bleed, pinpoint vessels. White polygonal papules coalesce to form plaques.
  5. scarring > atrophy and fusion of the labia, stenosis of the introitus or difficulties in defecation. Without Rx, may also develop vulvar intraepithelial neoplasia (VIN), esp older women.
  6. Labia majora, extending into the labia minora and the anus, in a figure of 8 pattern.
  7. The affected area is shiny and wrinkled - ‘cigarette paper/parchment paper appearance’.
  8. fourchette
47
Q

Lichen sclerosus

  1. diagnosis?
  2. treatment?
  3. T/F: Lichen sclerosis is considered a precancerous condition
A
  1. Usually clinical, but biopsies may be useful
  2. emollients and topical high-dose steroids e.g. dermovate (3 month trial > 2nd line topical calcineurin inhibitor e.g. tacrolimus)
  3. True - increasing the risk of vulval carcinoma. In treatment resistant cases, a biopsy is needed to confirm diagnosis and rule out malignancy.
48
Q

Name a condition which presents similarly to lichen sclerosis but may have the characteristic Wickham’s striae to help differentiate it

A

Lichen planus

49
Q

Extra-mammary Paget’s disease of the vulva.

  1. Presentation?
  2. Additional Ix needed?
  3. Tumour cells are within the ____ and contain ____
A
  1. May extend towards the anus and presents as an erythematous, eczematous area with a crusting rash.
  2. Is often a sign of other malignancy in the body therefore a full body work-up is indicated in patients presenting with this condition.
  3. epidermis, mucin
50
Q

Which of the following are premalignant conditions

  • lichen sclerosis
  • lichen planus
  • vulval intra-epithelial neoplasia
A

All of them

5-10% risk of progression to cancer.

Regular review and early treatment will avoid this.

51
Q

Vaginal discharge

  1. Describe discharge during the most fertile days of the cycle (around ovulation)? This is due to the influence of which hormone?
  2. Describe normal vaginal discharge
  3. _____ is part of the normal vaginal flora and maintains acidity in the vagina which protects it from pathogens
  4. In pre-pubertal or postmenopausal women, vaginal pH may be LOWER/ HIGHER - consequence of this?
  5. Abnormal discharge can have an offensive odour and change in colour. Often due to infection, some of which include…?
A
  1. Thin and clear, to allow sperm to swim easier if intercourse occurs due to the high levels of oestrogen. As the cycle progresses the cervical mucus becomes thicker and more hostile to sperm.
  2. Clear, white/pale yellow and odourless
  3. Lactobacilli
  4. higher - presdisposing them to infections
  5. Bacterial vaginosis, Vulvovaginal candidiasis, STI (chlamydia, gonorrhea), Trichomoniasis
52
Q

Pelvic infection

  1. Some causes?
  2. Risk factors associated with pelvic infection?
  3. Consequences of an ascending genital tract infection?
  4. Pelvic infection due to PID may present how?
  5. Often, which Ix can help with the diagnosis.
A
  1. PID from STIs e.g. chlamydia or gonorrhea, insertion of intrauterine devices, or from organisms not sexually contracted e.g. mycoplasma genitalium, gardenella vaginalis
  2. Age <25years, Multiple sex partners, Unprotected sexual intercourse, Recent insertion of IUD, Recent change in sexual partner.
  3. Cervicitis, endometritis, salpingitis and may lead to the development of tubo-ovarian abscesses.
  4. Irregular menstrual bleeding, abnormal vaginal discharge, chronic pelvic pain or infertility.
  5. vaginal and endocervical swabs
53
Q

Pelvic inflammatory disease

  1. symptoms?
  2. signs?
  3. management?
A
  1. Fever, Lower abdominal pain, dysuria, Deep dyspareunia, Abnormal vaginal bleeding (intermenstrual, menorrhea, post-coital), Offensive vaginal discharge (fever, pain, discharge)
  2. Cervical motion tenderness, Adnexal tenderness
  3. Sepsis 6 if acutely unwell. Partner notification (with patient’s consent).
54
Q

Ovarian cysts

  1. T/F: Benign ovarian cysts are very common.
  2. Most benign ovarian cysts will be diagnosed how?
  3. what other Sx may they have?
  4. What is a benign ovarian cyst?
  5. Cysts can also present acutely, termed cyst ___ - what is this?
  6. Types of ovarian cysts?
  7. Functional cysts are common in what age group?
  8. __ __ tumours occur more common in young women while __ __ tumours occurs more common in older women.
  9. Most cysts will have non-suspicious features i.e. ..?
  10. Sometimes cysts that increase in size and have concerning features i.e. thick wall septa will need further investigation including?
  11. RCOG recommend which tests are performed for all pre-menopausal women with a complex ovarian cysts.
  12. Which imaging modalities may be used?
  13. Inflammatory markers such as CRP or white cell counts can be important if the differential diagnosis includes what?
A
  1. True
  2. by the presence of pelvic/abdominal mass by symptoms such as pain/ incidentally on ultrasound.
  3. Features of pressure on the bowel/ bladder. Disturbance in the menstrual cycle or virilisation may occur.
  4. <5cm in maximum diameter, are physiological and tend to resolve over 2-3 menstrual cycles.
  5. accidents; may be haemorrhage within the cysts, or the cysts may rupture or twist on itself (torsion).
  6. physiological/functional cysts, benign germ cell tumours, benign epithelial tumours and benign sex cord stromal tumours.
  7. young women in their reproductive years
  8. germ cell, benign epithelial
  9. Thin wall with no solid or papillary projections into the cyst cavity.
  10. Tumour markers including inhibin, AFP, b-HCG, CA125 which can also be used to follow-up and monitor progress.
  11. serum CA125, alpha fetoprotein and beta-HCG
  12. US (transabdominal or transvaginal), CT scans or MRI
  13. appendicitis or a tubo-ovarian abscess.
55
Q
  1. What are the commonest type of ovarian cysts.
  2. Appearance on US?
  3. how do they form?
  4. How long do they persist for?
  5. Name some types?
  6. Treatment?
A
  1. Functional ovarian cysts
  2. simple, uniloculated cysts >3cm (normal ovulatory follicles measure <3cm).
  3. Due to the non-rupture of the dominant follicle or failure of atresia in a non-dominant follicle.
  4. Often they will regress after several menstrual cycles.
  5. follicular, corpus luteal and theca luteal cysts.
  6. depends on symptoms – if asymptomatic, observe with sequential USS to assess change. If symptomatic, laparoscopic removal may be performed.
56
Q
  1. What is the most common benign ovarian tumour in women <30years
  2. Name a type of benign germ cell tumour
  3. Dermoid cysts are often lined with ____ tissue and hence may contain hair, teeth.
  4. As they tend to be very big, they are more likely to present with ____
A
  1. Benign germ cell tumours
  2. Dermoid cyst (aka mature cystic teratomas).
  3. epithelial
  4. torsion
57
Q

Benign epithelial ovarian tumours.

  • These arise from the ovarian surface epithelium
  • They include: (2)
A
  1. Cystadenoma
  2. Mucinous cystadenoma.
58
Q

Bartholin cysts/abscess

  1. Where are bartholin’s glands located?
  2. Sometimes these settle with antibiotics but may require a surgical procedure known as marsupialization.
A
  1. pair of glands located next to the vaginal entrance at 5 and 7 o’clock. Normally pea-sized but can become infected and enlarge > Bartholin’s abscess
59
Q

Acute abdominal/pelvic pain

  1. Wide DDx. General rule - any female of reproductive age presenting with abdominal pain should always have what test done?
  2. Gynaecological causes?
  3. Gastro/Genitourinary causes?
A
  1. Pregnancy test
  2. PID, Ovarian torsion, Ovarian cyst rupture or haemorrhage, Mittelschmerz – ovulation pain, Tubo-ovarian abscess, Ectopic pregnancy, Endometriosis, Fibroids, Miscarriage (ovaries > tubes > endometrium)
  3. Appendicitis, Diverticulitis, UTI, Bowel obstruction
60
Q

Uterine fibroids

  1. Symptoms?
  2. Ix
A
  1. Asymptomatic, Menorrhagia and dysmenorrhea, Lower abdominal pain during menstruation, Subfertility, Pressure symptoms (urinary symptoms)
  2. TV USS
  3. Mirena IUS (first line), Short-term GnRH analogues (e.g. goserelin), Uterine artery embolisation, Myomectomy, Hysterectomy (medical > pre-surgical > surgical)
61
Q

Endometriosis

  1. Signs and symptoms?
  2. Ix?
  3. Management?
A
  1. Dsymenorrhea, Deep dyspareunia, Subfertility, Non-gynaecological signs – dysuria, urgency, dyschezia
  2. Often diagnosed via laparoscopy. On pelvic examination – tender nodularity on posterior fournix
  3. Medical: symptomatic (NSAIDs, paracetamol), COCP or progestogens. Surgical – laparoscopic excision of lesions
62
Q

Ovarian torsion

  1. Signs and symptoms?
  2. Ix?
  3. Management?
A
  1. Sudden onset of deep colicky pain, Associated with vomiting and distress, Adnexal tenderness/ acute abdomen.
  2. USS: classical whirlpool sign
  3. Laparoscopy to untwist ovary and remove cyst. If ovary necrotic- removed.
63
Q

Pelvic inflammatory disease

  1. Signs and symptoms?
  2. Ix?
  3. Rx?
A
  1. Vaginal discharge, Bilateral lower abdominal pain
  2. FBC, High vaginal/ endocervical swabs. Pelvic imaging if doesn’t settle with Abx/ acute abdomen/ mass palpable
  3. Antibiotics (may have pelvic abscess requiring surgical drainage)
64
Q

Mittelschmerz

  1. What is this?
  2. Rx?
A
  1. Mid cycle pain
  2. Simple analgesics and reassurance
65
Q

Mefanamic acid - particularly useful for menorrhagia which is accompanied by ____

Contraindications?

A
  • dysmenorrhea
  • NSAIDs are contraindicated with a history of duodenal ulcers or severe asthma.
66
Q

GnRH analogue/agonists

  1. How do these help with menorrhagia?
  2. risks ass with long term use?
  3. Examples?
A
  1. Act on the pituitary to stop oestrogen production resulting in amenorrhea
  2. osteoporosis (unless combined with HRT) - therefore used in the short-term (<6 months).
  3. Goserelin, Decapeptyl, Buserelin.
67
Q

Advantages of non-surgical management for DUB?

A
  • Cheaper
  • No waiting lists
  • No anaesthetic risk
  • Adverse effects non-permanent
  • May not be effective
  • Fertility can be retained
68
Q

DUB - Surgical Management

  1. T/F: Normally offered to women in whom medical treatment has failed.
  2. T/F: is an appropriate option for women wishing to preseve fertility
  3. Advantages?
  4. Disadvantages?
A
  1. True
  2. false - they should be advised to use medical methods
  3. Very effective (amenorrhea with hysterectomy)
  4. More expensive, Waiting list, Anaesthetic risk presents, Complications are possible e.g. placenta accreta in future pregnancies (risk factor for PPH), Fertility lost
69
Q

Why is contraception required following endometrial ablation?

A

Due to the risk of prematurity or morbidly adherent placenta

women considering this must be sure their family is complete

70
Q

Endometrial ablation vs hysterectomy for DUB

A

Endometrial ablation:

  • Day-case, Shorter operating time + recovery, fewer complications,
  • Requires cervical smears, Combined HRT required.

Hysterectomy:

  • Major operation, Longer operating time + recovery, More complications, No cervical smears required (for total hysterectomies), Oestrogen only HRT (unless cervix retained), A definitive treatment (if total hysterectomy),
  • Infertility
71
Q
  1. What is intermenstrual bleeding?
  2. Causes?
  3. Ix?
A
  1. Bleeding in between clearly defined menses.
  2. PID and STI, pregnancy/ pregnancy complications, Hyatidiform molar disease, Endometrial polyps, Endometrial cancer, cervical ectropion, Cervical cancer, cervical polyps
  3. Tailored to suspected diagnosis e.g. vaginal swabs to exclude PID/ hysteroscopy for endometrial or cervical biopsies.
72
Q

Premenstrual syndrome

  1. What is it
  2. Features?
  3. What are the hallmark psychological changes?
  4. The contributing factors are decreased _____ synthesis and increased ____, _____, _____ and _____ synthesis during the luteal phase.
  5. Diagnosis?
A
  1. Occurrence of cyclical somatic, psychological and emotional symptoms that occur in the luteal (premenstrual) phase of the menstrual cycle and resolve by the time menstruation ceases.
  2. Bloating, Cyclical weight gain, Mastalgia, Abdominal cramps, Fatigue, Headache, Depression, Changes in appetite and increased craving, Irritability
  3. Depression, irritability and emotional lability
  4. progesterone, prolactin, oestrogen, aldosterone and prostaglandin
  5. Often clinical - cyclical pattern is the cornerstone. Ask pt to keep a menstrual diary of symptoms over at least 2 cycles.
73
Q

Premenstrual syndrome

  1. Management?
  2. How do GnRH analogues improve symptoms?
  3. Examples of GnRH analogues?
A
  1. Symptom relief is the goal. Severe symptoms: SSRI/ SNRI taken daily or during luteal phase. CBT for psychological syptoms. Mild symptoms: lifestyle changes e.g. stress reduction, alcohol and caffeine limitation, increased exercise. Medical: COCP, transdermal oestrogen, short-term GnRH anaolgues. Last resort: HBSO.
  2. Mimic GnRH. When given continuously, the GnRH receptors are constantly stimulated and densisitised. This downregulates the pituitary, decreasing FSH and LH release > decreases oestrogen and progesterone levels.
  3. buserelin and goserelin
74
Q

Postcoital bleeding (PCB)

  1. What is this?
  2. Causes?
  3. What is Cervical ectropion? (aka cervical erosion)
  4. Most common cause of cervical ectropion?
A
  1. Bleeding which is brought on by sexual intercourse
  2. Trauma, Cervical ectropion, Cervical carcinoma, Cervicitis secondary to STD, Polyps, Idiopathic, Atrophic vaginitis
  3. cervix develops a red, raw appearance that may bleed on contact.
  4. hormonal changes due to high oestrogenic states in pregnancy/ use of hormonal contraceptives (esp the combined pill)
75
Q

Postmenopausal bleeding (PMB)

  1. What is it?
  2. NB: some patients may be on which medication which causes cyclical bleeding
  3. A thorough history and ___ and ___ examination should be carried out to exclude more serious diagnosis such as ___ ___
  4. NICE guidelines for PMB in women >55?
  5. Causes of PMB? (inc most common)
A
  1. Defined as bleeding after the menopause.
  2. combined cyclical HRT - causes cyclical bleeding during the progesterone free period (should still be investigated to rule out other causes)
  3. abdominal, pelvic, endometrial cancer.
  4. should be investigated within 2 weeks by USS for endometrial cancer
  5. Atrophic vaginitis (most common. Benign condition where the epithelium thins and breaks down in response to low oestrogen), Vaginal cancer (rare), Cervical carcinoma Endometrial polyps/ hyperplasia/ carcinoma (10% of women with PMB), Ovarian cancer (esp oestrogen-secreting (theca cell) tumours)
76
Q

Postmenopausal bleeding

  1. Investigations? (inc first line)
  2. What is being assessed in particular on transvaginal USS?
  3. An exception to this rule is women on tamoxifen as ultrasound will not assist with diagnosis. Most women on tamoxifen will have a thickened, irregular and cystic endometrium. Direct visualisation of the cavity by hysteroscopy and an endometrial biopsy is indicated in this case.

Further imaging in secondary care includes a CT or MRI of the uterus, pelvis and abdomen.

A
  1. USS (transvaginal always 1st line, better sensitivity than transabdominal)
  2. Endometrial thickness - if <3mm, likelihood of endometrial cancer low, no further Ix needed. If >4mm, further Ix needed i.e. endometrial biopsy. If pt is taking HRT, the cut off is 5mm or less.
77
Q

Treatment for

  1. atrophic vaginitis?
  2. Endometrial hyperplasia –
A
  1. Topical oestrogen and vaginal lubricants for symptomatic relief. Consider HRT.
  2. Dilatation and curettage, progestogen treatment: Mirena IUS 1st line, oral progestogens can be used e.g. norethisterone.
78
Q

Most common cause of menstrual irregularity?

A

Polycystic ovarian syndrome (PCOS)

79
Q

Polycystic ovarian syndrome.

  1. What criteria is used to diagnose PCOS?
  2. Describe the components of this criteria
  3. Which clinical features may indicate hyperandrogenism?
  4. What indicates polycystic ovaries on USS?
A
  1. The Rotterdam criteria
  2. 2 of the following: evidence of hyperandrogenism; Polycystic ovaries on ultrasound scan; Oligo/amenorrhea.
  3. Hirsutism, acne; high free testosterone, low sex hormone binding globulin, high free androgen index respectively
  4. Increase in ovarian volume to >10cm3, at least 12 follicles in one ovary measuring 2-9mm in diameter.
80
Q

Features of PCOS? (oh caaam)

(some pts may be asymptomatic)

A
  • Obesity/overweight
  • Hypertension
  • Cardiovascular risk: insulin resistance, diabetes, lipid abnormalities
  • Acanthosis nigricans (thickening and pigmentation of the skin of the neck, axillae and intertriginous areas)
  • Acne and hirsutism (increased testosterone)
  • Alopecia
  • Menstrual irregularity
81
Q

PCOS is associated with an increased risk of which endometrial problem?

A

endometrial hyperplasia and carcinoma (due to oligo/amenorrhea in the presence of pre-menopausal levels of oestrogen)

82
Q

Hormonal changes in PCOS?

A

increase in the LH:FSH ratio

  • LH levels are very high
  • FSH levels are low/ normal.
83
Q

Management of PCOS: general

A
  1. Pepends on PC/ patient’s main concern. Health promotion: optimise BMI (weight loss 5-10%, exercise) & protect endometrium with hormonal contraception.
  2. First line: Clomifene. Adding metformin (insulin-sensitiser), improves glucose tolerance, decreases androgen levels and improves ovulation rate. Gonadotrophin injections if clomifene has no effect. Ovarian drilling (used to improve ovulation rates in women who fail to conceive with clomifene). IVF last resort, for cases where 1st or 2nd line hasn’t worked.
84
Q

Describe the process of ovarian drilling and how it may help in PCOS

A

diathermy to destroy ovarian stroma which reduces androgen-secreting tissue leading a restoration of the normal LH:FSH ratio and a fall in androgens.

85
Q

Management of PCOS: acne

A
  • Co-cyrprindol (Dianette): combo of cyproterone acetate and ethinylestraidol. Is effective to manage acne and hirsutism.
  • COCP: effects are inferior to co-cyprindol but allows withdrawal bleeds (needed to ensure endometrial protection)
86
Q

Cyproterone acetate mechanism of action?

A

an anti-androgen: blocks the action of androgens on the pilosebaceous glands, leading to a reduction in sebum production reducing acne and hirsutism.

87
Q

Management of PCOS: amenorrhea?

A
  • COCP
  • Alternative = cyclical medroxyprogesterone or insertion of Mirena IUS - can be helpful in managing the increased risk of endometrial hyperplasia and cancer
88
Q

Management of PCOS: infertility

A
  • First line: Clomifene.
  • Adding metformin (insulin-sensitiser), improves glucose tolerance, decreases androgen levels and improves ovulation rate.
  • Gonadotrophin injections if clomifene has no effect.
  • Ovarian drilling (used to improve ovulation rates in women who fail to conceive with clomifene).
  • IVF last resort, for cases where 1st or 2nd line hasn’t worked.
89
Q
  1. Clomifene mechanism of action?
  2. side effects?
A
  1. selective oestrogen receptor modulator -blocks oestrogen negative feedback effect on hypothalamus resulting in more pulsatile GnRH secretion and therefore FSH and LH
  2. Hot flushes and sweating, increased risk of multiple pregnancy and ovarian cancer (with long term use)
90
Q

Dysmenorrhea

  1. what is this?
  2. Primary vs secondary dysmenorrhoea?
  3. Excessive endometrial ____ production is thought to be partially responsible for primary dysmenorrhoea
  4. Compare the pain of primary to secondary amenorrhoea
A
  1. excessive pain during the menstrual period.
  2. Primary: no underlying pelvic pathology, affects up to 50% of menstruating women and usually appears within 1-2 years of the menarche. Secondary: results from underlying pathology. Typically develops many years after the menarche.
  3. prostaglandin
  4. Primary: usually starts just before or within a few hours of the period starting. Suprapubic cramping pains, may radiate to the back/ down the thigh. Secondary: usually starts 3-4 days before the onset of the period.
91
Q

What underlying pathology could be associated with secondary dysmenorrhoea?

A
  • Endometriosis (endometrial tissue in the peritoneum or pelvic cavity)
  • Adenomyosis (endometrium between the layers of the myometrium), uterus will often appear large and globular.
  • Pelvic inflammatory disease
  • Cu IUD.
  • Fibroids
92
Q

Which type of dysmenorrhea is being described here?

  • Pain precedes and accompanies menstruation
  • Onset with or shortly after menarche
  • Normal examination and investigations
A

Primary

93
Q

Which cause of secondary dysmenorrhea is being described:

  1. Associated with heavy periods and dyspareunia. O/E: Uterosacral nodularity and/or tenderness. Fixed retroverted uterus
  2. Associated with prolonged, heavy periods. O/E: large, globular uterus
  3. Menstrual pain, pressure effects on adjacent organs. O/E: pelvic mass
  4. Hx of STI, pain not limited to menstruation. O/E: Mucopurulent discharge, Cervicitis, Findings suggesting Fitz-Curtis-Hugh syndrome on laparoscopy
A
  1. endometriosis
  2. Adenomyosis
  3. fibroids
  4. PID
94
Q

what potential complication of fibroids can develop during pregnancy?

A

red degeneration (hemorrhagic infarction)

95
Q

Investigations for dysmenorhoea?

A
  • High vaginal and endocervical swabs: pelvic infection (Chlamydia or Gonorrhea)
  • Pelvic USSL endometriomas, adenomyosis, fibrids
  • Diagnostic laparoscopy: when other Ix normal but symptoms persist, or when Hx suggests endometriosis.
96
Q

Management of dysmenorrhea?

A
  • NSAIDs e.g. mefenamic acid, ibuprofen effective in up to 80% of women (work by inhibiting prostaglandin production)
  • COCP 2nd line
  • Levonogestrel IUS: for dysmenorrhea + menorrhagia
  • GnRH analogues: the best to manage symptoms, esp due to fibroids, when awaiting for hysterectomy
97
Q

what is the gold standard investigation for suspected endometriosis?

A

Laparoscopy (can be combined with biopsy and histological verification of endometrial glands and/or stroma)

98
Q

COG guidelines recommend which blood tests for all pre-menopausal women with a complex ovarian cysts?

A

serum CA125, alpha fetoprotein and beta-HCG

99
Q

The only definitive treatment for adenomyosis is _____.

A

hysterectomy

100
Q

What structural abnormality blocks passage of menses resulting in apparent amenorrhea without affecting development of secondary sexual characteristics?

A

An imperforate hymen

(trapped blood > cyclical pelvic pain and bloating with distention of the part of the vagina above the hymen (haematocolpos) and if severe enough, the uterus (haematometra).