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finals > gynae/breast > Flashcards

gynae/breast Flashcards

1
Q

featurs of benign breast lumps on examination

A

Soft, mobile, fluctuant, ?painful

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2
Q

features of a malignant breast lump on examination

A

Hard, irregular, painless, immobile, Tethered skin, skin dimpling, nipple retraction

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3
Q

triple assessment breast lumps

A

Hx + Exam
Imaging: Mammogram 🡪 US
+/- biopsy

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4
Q

2ww for breast lumps

A

aged 30 and over and have an unexplained breast lump with or without pain or
aged 50 and over with any of the following symptoms in one nipple only: discharge, retraction or other changes of concern

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5
Q

breast screening

A

NHS Breast Screening Programme is offered to women between the ages of 50-70 years. Women are offered a mammogram every 3 years. After the age of 70 years women may still have mammograms but are ‘encouraged to make their own appointments’.

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6
Q

features fibroadenoma

A

Mobile, firm breast lumps. No increase in risk of malignancy. ‘breast mice’. Common <30

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7
Q

mx fibroadenoma

A

If >3cm surgical excision is usual, Phyllodes tumours should be widely excised (mastectomy if the lesion is large)

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8
Q

features breast cyst

A

Usually presents as a smooth discrete lump (may be fluctuant). Small increased risk of breast cancer (especially if younger)

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9
Q

mx breast cyst

A

Cysts should be aspirated, those which are blood stained or persistently refill should be biopsied or excised

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10
Q

presentation fat necrosis

A

More common in obese women with large breasts
May follow trivial or unnoticed trauma
Initial inflammatory response, the lesion is typical firm and round but may develop into a hard, irregular breast lump

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11
Q

mx fat necrosis

A

Rare and may mimic breast cancer so further investigation is always warranted
Imaging and core biopsy

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12
Q

features duct papilloma

A

Usually present with nipple discharge. No increase risk of malignancy

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13
Q

mx duct papilloma

A

Microdochectomy

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14
Q

features lactational breast abscess

A

Infectious mastitis->accumulation of pus -> lactational breast abscess. Staphylococcus aureus

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15
Q

mx lactational breast abscess

A

Incision and drainage or needle aspiration, antibiotics according to local protocol

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16
Q

features puerperal mastitis

A

unilateral and typically presents 1 week postpartum. painful, tender, red and hot breast

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17
Q

mx puerperal mastitis

A

Continue breastfeeding. If sx don’t improve: flucloxacillin for 10-14 days

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18
Q

features fibroadenosis

A

Most common in middle-aged women
‘Lumpy’ breasts which may be painful. Symptoms may worsen prior to menstruation

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19
Q

mx fibroadenosis

A

supportive

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20
Q

features mammary duct ectasia

A

Dilatation of the large breast ducts
Most common around the menopause
May present with a tender lump around the areola +/- a green nipple discharge
If ruptures may cause local inflammation, sometimes referred to as ‘plasma cell mastitis

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21
Q

mx mammary duct ectasia

A

Patients with troublesome nipple discharge may be treated by microdochectomy (if young) or total duct excision (if older)

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22
Q

features cyclical mastalgia

A

Younger, varies in intensity according to the phase of the menstrual cycle

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23
Q

my cyclical mastalgia

A

supportive

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24
Q

predisposing factors for breast cancer

A

BRCA1, BRCA2 genes - 40% lifetime risk of breast/ovarian cancer,
1st degree relative premenopausal relative with breast cancer (e.g. mother)
nulliparity/1st pregnancy > 30 yrs (twice risk of women having 1st child < 25 yrs)
early menarche, late menopause
combined HRT (relative risk increase * 1.023/year of use)
combined oral contraceptive use
past breast cancer
not breastfeeding
ionising radiation
p53 gene mutations
obesity
previous surgery for benign disease (?more follow-up, scar hides lump)

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25
Q

presentation pagets disease of breast

A

intraductal carcinoma associated with a reddening and thickening (may resemble eczematous changes) of the nipple/areola

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26
Q

breast cancer staging

A

T1-4
N0-3
M0-1

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27
Q

types of breast cancer

A

Invasive ductal carcinomas are the most common type. Some may arise as a result of ductal carcinoma in situ (DCIS)
Other common types: invasive lobular carcinoma, ductal carcinoma in situ, lobular carcinoma in situ

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28
Q

medulary breast carcinoma

A

younger patients and those with BRCA1 mutations, often significant lymphocytic infiltration surrounding the tumour

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29
Q

malignant phyllodes tumour

A

fibroepithelial origin, commonly presents in women in their 40s or 50s. present similarly to fibroadenoma. On mammography-a round breast lesion with well-defined edges

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30
Q

inflammatory breast cancer

A

where cancerous cells block the lymph drainage resulting in an inflamed appearance of the breast. This accounts for around 1 in 10,000 cases of breast cancer

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31
Q

mx breast cancer

A

Surgery: offered to most patients. Mastectomy (multifocal tumour, central tumour, large lesion in small breast, DCIS>4) OR wide local excision (peripheral lesion, solitary lesion, small lesion in a big breast, DCIS<4cm) +/- axillary node clearance. Followed by reconstruction.

Radiotherapy: offered depending on tumour and surgery type

hormone therapy:

biological therapy:

Chemotherapy: may be used before or after surgery

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32
Q

tx for HER 2 +ve tumours

A

trastuzumab

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33
Q

tx for ER +ve tumours

A

tamoxifen in pre/peri-menopausal or anastrozole in post menopausal

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34
Q

cystocele

A

Prolapse of anterior vaginal wall involving the bladder

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35
Q

uterine prolapse

A

Prolapse of uterus, cervix and upper vagina

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36
Q

enterocele

A

Prolapse of upper posterior wall of vagina

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37
Q

rectocele

A

Prolapse of lower posterior wall of vagina, usually involving the anterior wall of rectum

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38
Q

stress incontinence

A

involuntary leakage of urine during increased intra-abdominal pressure

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39
Q

urge incontinence

A

overactive bladder syndrome - is the presence of urgency, usually with frequency and nocturia, in the absence of urinary tract infection or any other obvious pathology.

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40
Q

overflow incontinence

A

due tobladder outlet obstruction, e.g. due to prostate enlargement

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41
Q

functional incontinence

A

Causes include dementia, sedating medication and injury/illness resulting in decreased ambulation

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42
Q

RF for urinary incontinence

A

advancing age
previous pregnancy and childbirth
high body mass index
hysterectomy
family history

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43
Q

investigations for urinary incontinence

A

exclude infection of the urinary tract.
Frequency/volume charts: Stress – normal frequency and bladder capacity, Urge – increased frequency
Urodynamic studies – performed in stress urinary incontinence when considering surgery to confirm the diagnosis and rule out concomitant detrusor over-activity.

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44
Q

mx urge incontinence

A

bladder retraining(lasts for a minimum of 6 weeks, the idea is to gradually increase the intervals between voiding)
bladder stabilising drugs: antimuscarinics are first-line: oxybutynin (immediate release), tolterodine (immediate release) or darifenacin (once daily preparation). Immediate release oxybutynin should, however, beavoided in ‘frail older women’
mirabegron (abeta-3 agonist) may be useful if there is concern about anticholinergic side-effects infrail elderly patients

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45
Q

mx stress incontinence

A

pelvic floor muscle training: NICE recommend at least 8 contractions performed 3 times per day for a minimum of 3 months

surgical procedures: e.g. retropubic mid-urethral tape procedures

duloxetinemay be offered to women if they decline surgical procedures: mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced contraction

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46
Q

prolapse presentation

A

sensation of pressure, heaviness, ‘bearing-down’
urinary symptoms: incontinence, frequency, urgency
Rectocele often causes constipation rather than urinary sx

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47
Q

mx prolapse

A

if asymptomatic and mild prolapse then no treatment needed
conservative: weight loss, pelvic floor muscle exercises
ring pessary
Surgery: cystocele/cystourethrocele= anterior colporrhaphy, colposuspension, uterine prolapse = hysterectomy, sacrohysteropexy, rectocele = posterior colporrhaphy

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48
Q

didelphys

A

Total failure of fusion -> two uterine cavities and cervices

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49
Q

unicornate uterus

A

One duct failure

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50
Q

‘RUDIMENTARY HORN

A

One duct develops better than the other

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51
Q

phases of ovarian cycle

A

follicular
ovulation
luteal

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52
Q

follicular phase ovarian cycle

A

The follicular phase marks the beginning of a new cycle as follicles (oocytes surrounded by stromal cells) begin to mature and prepare to release an oocyte.

At the start of a new cycle (menses) there is little ovarian hormone production and the follicle begins to develop independently of gonadotropins or ovarian steroids. Due to the low steroid and inhibin levels, there is little negative feedback at the HPG axis, resulting in an increase in FSH and LH levels. These stimulate follicle growth and oestrogen production.

Only one dominant follicle can continue to maturity and complete each menstrual cycle. As oestrogen levels rise, negative feedback reduces FSH levels, and only one follicle can survive, with the other follicles forming polar bodies.

Follicular oestrogen eventually becomes high enough to initiate positive feedback at the HPG axis, increasing levels of GnRH and gonadotropins. However, the effect is only reflected in LH levels (the LH surge) due to the increased follicular inhibin, selectively inhibiting FSH production at the anterior pituitary. Granulosa cells become luteinised and express receptors for LH.

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53
Q

ovulation phase ovarian cycle

A

In response to the LH surge, the follicle ruptures and the mature oocyte is assisted to the fallopian tube by fimbria. Here it remains viable for fertilisation for around 24 hours.

Following ovulation, the follicle remains luteinised, secreting oestrogen and now also progesterone, reverting back to negative feedback on the HPG axis. This, together with inhibin (inhibits FSH) stalls the cycle in anticipation of fertilisation.

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54
Q

luteal phase ovarian cycle

A

The corpus luteum is the tissue in the ovary that forms at the site of a ruptured follicle following ovulation. It produces oestrogens, progesterone and inhibin to maintain conditions for fertilisation and implantation.

At the end of the cycle, in the absence of fertilisation, the corpus luteum spontaneously regresses after 14 days. There is a significant fall in hormones, relieving negative feedback, resetting the HPG axis ready to begin the cycle again.

If fertilisation occurs, the syncytiotrophoblast of the embryo produces human chorionic gonadotropin (HcG), exerting a luteinising effect, maintaining the corpus luteum. It is supported by placental HcG and it produces hormones to support the pregnancy. At around 4 months of gestation, the placenta is capable of production of sufficient steroid hormone to control the HPG axis.

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55
Q

phases of the uterine cycle

A

proliferative
secretory
menses

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56
Q

proliferative phase uterine cycle

A

Following menses, the proliferative phase runs alongside the follicular phase, preparing the reproductive tract for fertilisation and implantation. Oestrogen initiates fallopian tube formation, thickening of the endometrium, increased growth and motility of the myometrium and production of a thin alkaline cervical mucus (to facilitate sperm transport).

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57
Q

secretory phase uterine cycle

A

The secretory phase runs alongside the luteal phase. Progesterone stimulates further thickening of the endometrium into a glandular secretory form, thickening of the myometrium, reduction of motility of the myometrium, thick acidic cervical mucus production (a hostile environment to prevent polyspermy), changes in mammary tissue and other metabolic changes.

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58
Q

menses phase uterine cycle

A

Menses marks the beginning of a new menstrual cycle. It occurs in the absence of fertilisation once the corpus luteum has broken down and the internal lining of the uterus is shed. Menstrual bleeding usually lasts between 2-7 days with 10-80ml blood loss.

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59
Q

what does fsh do

A

binds to granulosa cells to stimulate follicle growth, permit the conversion of androgens (from theca cells) to oestrogens and stimulate inhibin secretion

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60
Q

what does lh do

A

theca cells to stimulate production and secretion of androgens

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61
Q

describe the main feedback systems in the menstrual cycle

A

Moderate oestrogen levels exert negative feedback on the HPG axis
High oestrogen levels (in the absence of progesterone) positively feedback on the HPG axis
Oestrogen in the presence of progesterone exerts negative feedback on the HPG axis
Inhibin selectively inhibits FSH at the anterior pituitary

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62
Q

what is menopause

A

Amenorrhoea (no menstruation) for 12 months

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63
Q

common perimenopausal sx

A

hot flushes, urinary incontinence and increased UTIs as well as irregular vaginal bleeding

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64
Q

premature ovarian insufficiency

A

women under the age of 40 and is characterised by low oestrogen, high gonadotropins and amenorrhoea.

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65
Q

levels of oestrogen post menopause

A

lower

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66
Q

changes after menopause

A

Vasomotor Changes: hot flushes. These occur with a red flush starting on the face and spreading down the neck and chest. These are associated with peripheral vasodilation and a transient rise in body temperature. is thought to be due to pulsatile LH release influencing central temperature control.

Urogenital Changes: The uterus and vagina are both tissues which are maintained by circulating oestrogen. After the menopause there is marked atrophy of the vagina and thinning of the myometrium. There is also thinning of vaginal walls and dryness, this can result in dyspareunia (pain during sex). The bladder and urethra share embryological derivation with the uterus and vagina and so these tissues also atrophy with the decrease in circulating oestrogen. This leads to symptoms of urinary incontinence and an increase in urinary tract infections.

Bone Density: Oestrogen protects bone mass and density through reducing the activity of oesteoclasts. With the drop in oestrogen this balance is tipped and there is an increase in bone reabsorption. This results in an acceleration of age related loss of bone density and an increased frequency in fractures, especially of the wrist and hip.

Ischaemic Heart Disease: Oestrogen offers a protective effect against heart disease. It is thought that oestrogen reduces levels of LDL cholesterol whilst raising HDL cholesterol. After the menopause women experience the same frequency of cardiovascular disease as men.

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67
Q

mx menopause

A

Lifestyle modifications: exercise, wt loss, sleep hygiene

Hormone replacement therapy (HRT)

Non-hormone replacement therapy: Vasomotor symptoms = fluoxetine, citalopram or venlafaxine, Vaginal dryness = vaginal lubricant or moisturiser, Psychological symptoms = self-help groups, cognitive behaviour therapy or antidepressants, Urogenital symptoms = if suffering from urogenital atrophy vaginal oestrogen

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68
Q

what is in HRT

A

Oestrogens (used to overcome oestrogen deficiency) – oral, transdermal, topical

Progestogen (endometrial protection from oestogen) – oral, transdermal, IUS (mirena

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69
Q

who can have oestrogen only HRT

A

women without a uterus

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70
Q

what are the types of combines HRT

A

Cyclically: perimenopausal women who are still having menstrual periods
Continuous: postmenopausal women who are not having menstrual periods

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71
Q

CI HRT

A

Breast cancer (current / past)
Undiagnosed vaginal bleeding
VTE
Active liver disease
Pregnancy
Thrombophilic disorder
Active / recent angina or MI
Smoking / smoking within 1 yr >35yrs

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72
Q

risks HRT

A

Breast cancer
Endometrial cancer (if oestrogen alone)
VTECardiovascular disease >60yrs

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73
Q

benefits HRT

A

Relief of vasomotor symptoms
Relief of urogenital symptoms
Reduced risk of osteoporosis

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74
Q

normal age of puberty

A

8-14 in females, and between the ages of 10-16 in males.

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75
Q

puberty in females

A

Thelarche: the beginning of breast development (thelarche). This typically occurs at around age 9-10

Pubarche: the second sign of puberty in girls is typically the growth of hair in the pubic area

Menarche is the first menstrual period and marks the beginning of the menstrual cycles. It normally occurs around 1.5-3 years after thelarche and is due to the increase in FSH and LH

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76
Q

puberty in males

A

Genital changes: The first sign of puberty in boys is the increase in testicular size

Pubarche: Another pubertal sign in boys is the growth of pubic hair at the base of the penis

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77
Q

tanner stages for male genitalia

A

Stage 1: Prepubertal
Stage 2: Enlargement of scrotum and testes; scrotum skin reddens
and changes in texture
Stage 3: Enlargement of penis (length at first); further growth of
testes
Stage 4: Increased size of penis with growth in breadth and
development of glans; testes and scrotum larger, scrotum
skin darker
Stage 5: Adult genitalia

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78
Q

tanner stages for breast development

A

Stage 1: Prepubertal
Stage 2: Breast bud stage with elevation of breast and papilla; enlargement of areola
Stage 3: Further enlargement of breast and areola; no separation of their contour
Stage 4: Areola and papilla form a secondary mound above level of breast
Stage 5: Mature stag

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79
Q

tanner stages for pubic hair

A

boys and girls
Stage 1: Prepubertal (can see velus hair similar to abdominal wall)
Stage 2: Sparse growth of long, slightly pigmented hair, straight or
curled, at base of penis or along labia
Stage 3: Darker, coarser and more curled hair and begins to extend
laterally
Stage 4: Hair adult in type, but covering smaller area than in adult; no
spread to medial surface of thighs
Stage 5: Adult in type an

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80
Q

tanner stages for growth

A

Stage 1: M 5-6cm per year, F 5-6cm per year
Stage 2: 5-6cm per year, 7-8cm per year
Stage 3: 7-8cm per year, 8cm per year
Stage 4: 10cm per year, 7cm per year
Stage 5: No further height
increase after 17 years, No further height
increase after 16 years

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81
Q

delayed puberty

A

Absence of secondary sexual characteristics by the age of 13 in girls or 16 in boys.

82
Q

causes of delayed puberty

A

Hypogondaotropic hypogonadism
Hypergondaotropic hypogonadism

83
Q

Hypogondaotropic hypogonadism

A

this is due to a disorder of either the hypothalamus or the pituitary gland. The disorder results in a deficiency in GnRH, LH or FSH.

84
Q

Hypergonadotropic hypogonadism

A

this is due to a disorder of the gonads (ovaries or testicles.) The disorder results in absent or reduced gonadal steroid secretion which results in high circulating levels of LH and FSH as there is minimal negative feedback from the gonadal steroids on the pituitary gland.

85
Q

conditions associated with delayed puberty

A

Turner’s Syndrome (45 XO): short, webbed neck, widely spaced nipples
Klinefelter’s Syndrome (47 XXY): primary gonadal failure in males. Develop breasts
Androgen Insensitivity Syndrome
Kallmann Syndrome: genetic defect that causes hypogonadism causing delayed puberty. Lack all secondary characterises and key feature is absence of smell

86
Q

precocious puberty

A

The appearance of secondary sexual characteristics before the age of 8 in girls or before the age of 9 in boys. There are a variety of causes/types:

87
Q

types of precocious puberty

A

Iatrogenic – this occurs as a result of exposure to exogenous oestrogens, e.g. via creams or lotions etc.

True/complete – due to early maturation of the HPG axis resulting in high levels of GnRH, FSH and LH. This may be due to CNS lesions near or in the posterior hypothalamus, CNS neoplasms, harmatomas, primary hypothyroidism.

Incomplete – due to increased levels of oestrogens in girls and androgens in boys that are independent of GnRH.

88
Q

androgen insensitivity syndrome

A

Androgen insensitivity syndrome is an X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype. Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome

89
Q

features androgen insensitivity syndrome

A

‘primary amenorrhoea’
little or no axillary and pubic hair
undescended testes causing groin swellings
breast development may occur as a result of the conversion of testosterone to oestradiol

90
Q

diagnosis androgen insensitivty syndrome

A

buccal smear or chromosomal analysis to reveal 46XY genotype
after puberty, testosterone concentrations are in the high-normal to slightly elevated reference range for postpubertal boys

91
Q

mx androgen insensitivity syndrome

A

counselling - raise the child as female
bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)
oestrogen therapy

92
Q

RF endometrial cancer

A

Anovulation: Early menarche and/or late menopause, Low parity, Polycystic ovarian syndrome, Hormone replacement therapy with oestrogen alone, Tamoxifen use
Age
Obesity
Hereditary Factors: hereditary non-polyposis colorectal cancer (Lynch syndrome)

93
Q

presentation endometrial cancer

A

Postmenopausal bleeding

94
Q

ix endometrial cancer

A

A transvaginal ultrasound scan
If an endometrial thickness of ≥4mm in a postmenopausal woman is identified, an endometrial biopsy
women over the age of 55 with postmenopausal bleeding should be investigated within two weeks by ultrasound for endometrial cancer

95
Q

staging endometrial cancer

A
  • FIGO I-IV
96
Q

mx endometrial cancer (stages)

A

Stage I – Total hysterectomy and bilateral salpingo-oophorectomy.

Stage II – Radical hysterectomy (whereby vaginal tissue surrounding the cervix is also removed, alongside the supporting ligaments of the uterus), and assessment and removal of pelvic lymph nodes (lymphadenectomy).
Women with confirmed carcinoma stage Ic or II may be offered adjuvant radiotherapy.

Stage III – Maximal de-bulking surgery (if possible)
Additional chemotherapy is usually given prior to radiotherapy.

Stage IV – Maximal de-bulking surgery (if possible)
In many stage IV patients, a palliative approach is preferred, e.g. with low dose radiotherapy, or high dose oral progestogens

97
Q

RF cervical cancer

A

HPV 16 and 18, CIN, Smoking, Other sexually transmitted infections, Long-term (> 8 years) combined oral contraceptive pill use, Immunodeficiency (e.g. HIV)

98
Q

presentation cervical cancer

A

abnormal vaginal bleeding (e.g post-coital, intermenstrual or post-menopausal). Other clinical features include vaginal discharge (blood-stained, foul-smelling), dyspareunia, pelvic pain and weight loss.
often asymptomatic – many cases are detected through routine screening.

99
Q

ix cervical cancer

A

Pre-menopausal – test for chlamydia trachomatis infection
Post-menopausal – urgent colposcopy and biopsy.
If the diagnosis of cervical cancer is confirmed, further investigations are required: Basic blood tests – such as full blood count, liver function tests and urea & electrolytes, CT Chest-Abdomen-Pelvis – looking for metastases, Further staging scans – e.g. MRI pelvis, PET.

100
Q

mx cervical cancer

A

Surgery: type dependent on stage. Radiotherapy, chemo

101
Q

CIN

A

dyskaryosis – mutations in the squamous cells in the transformation zone of the cervix

102
Q

mx CIN

A

high-grade dysplasia – CIN II or III should be treated. This can occur at the same time as colposcopy – ‘see and treat’ or at an additional time. The most common form of treatment is large loop excision of the transformation zone – a LLETZ biopsy

103
Q

screening for cervical cancer

A

Smear 25-49 3 yearly, 50-64 5 yearly
yearly if habe HIV

104
Q

RF ovarian cancer

A

Nulliparity, Early menarche, Late menopause, Hormone replacement therapy containing oestrogen only, Smoking, Obesity, BRCA1 & 2, Hereditary nonpolyposis colorectal cancer (Lynch II Syndrome)

105
Q

protective factors for ovarian cancer

A

Multiparity, Combined contraceptive methods, Breastfeeding

106
Q

what is the risk of malignancy index

A

for ovarian cancer
Ultrasound score x menopausal status x CA125 blood test
menopausal: 1 = pre, 3= post
USS: mulilocular cyst, solid areas, metastases, ascites, bilateral lesions. 1 = 1 feature, 3 = 2 or more

RMI >250 should be referred to a specialist gynaecologist

107
Q

presentation of ovarian cancer

A

Incidental and asymptomatic, pain, Bleeding per vagina, Bloating, Change in bowel habit, Change in urinary frequency, Weight loss

108
Q

ix ovarian cancer

A

blood tests included FBC, U&E, LFT, Ca125 and albumin. abdominal and pelvic ultrasound for pelvic masses, from which the RMI can be calculated.
In cases of confirmed cancer, chest x-ray and CT abdomen/pelvis should be undertaken

109
Q

mx ovarian cancer

A

Surgery – staging laparotomy for those with a high RMI with attempt to debulk the tumour.
Adjuvant chemotherapy – recommended for all patients apart from those with early, low grade disease and uses platinum based compounds.

110
Q

meigs syndrome

A

TRIAD: benign ovarian tumor with ascites and pleural effusion

111
Q

types of ovarian tumour

A

Epithelial tumours (90%): Serous cystadenomas (benign or malignant), Mucinous cystadenomas (benign or malignant), Endometrioid carcinoma (malignant), Clear cell carcinoma (malignant), Brenner tumour (benign)

Germ cell tumours (>30yrs): Dermoid cyst (benign), Solid teratoma (malignant), Dysgerminoma (malignant)

Sex cord tumours: Granulosa cell tumours (benign or malignant), Thecomas (usually benign), Fibromas (benign – risk of MEIG’S SYNDROME)

112
Q

vulval cancer type

A

squamous cell carcinomas

113
Q

presentation vulval cancer

A

pruritis, burning, soreness, bleeding, pain or a lum on the labia majora

114
Q

diagnosis vulval cancer

A

Keye’s punch biopsy

115
Q

mx vulval cancer

A

surgery

116
Q

vaginal cancer presentation

A

rare but can be post menopausal bleeding

117
Q

prolactinoma presentaion

A

Irregular periods or no periods, Reduced fertility, Reduced sex drive, galactorrhoea, Increased growth of hair on the face or body.

118
Q

mx prolactinoma

A

dopamine agonists are called bromocriptine, cabergoline, surgery

119
Q

adenomyosis

A

Functional endometrial tissue within the myometrium of the uterus. Seen towards the end of the reproductive years.

120
Q

RF adenomyosis

A

High parity, Uterine surgery e.g. any endometrial curettage, endometrial ablation, Previous caesarean section, potential genetic predisposition

121
Q

presentation adenomyosis

A

menorrhagia, dysmenorrhoea, deep dyspareunia and irregular bleeding
On examination: symmetrically enlarged tender uterus may be palpable.

122
Q

ix adenomyosis

A

definitive diagnosis: is histological, after hysterectomy.
Transvaginal ultrasound: globular uterine configuration, poor definition of the endometrial-myometrial interface, myometrial anterior-posterior asymmetry, intramyometrial cysts and a heterogeneous myometrial echo texture.
MRI – shows an ‘endo–myometrial junctional zone’

123
Q

mx adenomyosis

A

Conservative: hormone therapy (Combined oral contraceptives, Progestogens (oral or Intrauterine system e.g. Mirena), Gonadotropin-releasing hormone agonists, Aromatase inhibitors). Non-hormonal (uterine artery embolisation)
Definitive: hysterectomy

124
Q

fibroids

A

Lyeiomyotoma - benign smooth muscle tumours of the uterus

125
Q

RF fibroids

A

Obesity, Early menarche, Increasing age, Family history, Ethnicity (African-Americans are 3x more likely to develop fibroid than Caucasians)

126
Q

presentation fibroids

A

Asymptomatic, Pressure symptoms +/- abdominal distention (This includes urinary frequency or chronic retention), Heavy menstrual bleeding, Subfertility, Acute pelvic pain (red degeneration, torsion)
solid mass or enlarged uterus may be palpable on abdominal or bimanual examination. The uterus is usually non-tender.

127
Q

what is red degeneration of fibroids

A

in pregnancy.This is where the rapidly growing fibroid undergoes necrosis and haemorrhage.

128
Q

ix fibroids

A

Pelvic ultrasound, MRI

129
Q

mx fibroids

A

Medical: Tranexamic or mefanamic acid, Hormonal contraceptives (COCP, POP and Mirena IUS), GnRH analogues (Zolidex) - Suppresses ovulation, inducing a temporary menopausal state, Useful pre-operatively to reduce fibroid size and lower complications, Selective Progesterone Receptor Modulators (Ulipristal / Esmya) - Reduces size of fibroid and menorrhagia
Surgical: Hysteroscopy and Transcervical Resection of Fibroid (TCRF), Myomectomy - Option in women wanting to preserve their uterus, Uterine Artery Embolization, Hysterectomy

130
Q

complications fibrodis

A

Iron deficiency anaemia, Compression of pelvic organs (Recurrent urinary tract infections, Incontinence, Hydronephrosis, Urinary retention), Subfertility/infertility, Degeneration, Torsion

131
Q

PID cause

A

Chlamydia trachomatis and Neisseria gonorrhoea

132
Q

RF PID

A

Sexually active, Aged under 15-24, Recent partner change, Intercourse without barrier contraceptive protection, History of STIs, Personal history of pelvic inflammatory disease

133
Q

features PID

A

Asymptomatic, Lower abdominal pain, Deep dyspareunia, Menstrual abnormalities (e.g menorrhagia, dysmenorrhoea or intermenstrual bleeding), Post-coital bleeding, Dysuria (painful urination), Abnormal vaginal discharge (especially if purulent or with an unpleasant odour), fever
vaginal examination, there may be tenderness of uterus/adnexae or cervical excitation

134
Q

ix PID

A

Endocervical swabs should be taken to test for gonorrhea and chlamydia, and a high vaginal swab for trichomonas vaginalis and bacterial vaginosis. In the UK, testing is via nucleic acid amplification (NAAT).
Further ix: full STI screen, urine dipstick and MSU, pregnancy test

135
Q

mx PID

A

14d antibiotics - often Doxycycline, ceftriaxone and metronidazole
Hospital if: pregnant and especially if there is a risk of ectopic pregnancy., Severe symptoms: nausea, vomiting, high fever, Signs of pelvic peritonitis, Unresponsive to oral antibiotics, need for IV therapy, Need for emergency surgery

136
Q

complications PID

A

Ectopic pregnancy – due to narrowing and scarring of the fallopian tubes, Infertility, Tubo-ovarian abscess, Chronic pelvic pain, Fitz-Hugh Curtis syndrome – perihepatitis that typically causes right upper quadrant pain

137
Q

presentation ovarian cysts

A

: incidental finding, pain, bleeding

138
Q

mx pre-menopausal ovarian cycts

A

Lactate dehydrogenase, alphafetoprotein and hCG should be measured in all women under 40 due to the possibility of germ cell tumours.

Rescan a cyst in 6 weeks. If it is persistent then monitor with ultrasound an CA125 3-6 monthly and calculate RMI. If persistent or over 5cm consider laparoscopic cystectomy or oophorectomy.

139
Q

mx post menopausal ovarian cysts

A

Post-menopausal: Low RMI (less than 25): follow up for 1 year with ultrasound and CA125 if less than 5cm. Moderate RMI (25-250): bilateral oophorectomy and if malignancy found then staging is required (with completion surgery of hysterectomy, omentectomy +/- lymphadenectomy). High RMI (over 250): referral for staging laparotomy

140
Q

functional non neoplastic ovarian cysts

A

Follicular cysts – These are normally less than 3cm and represent the developing follicle in the first half of the menstrual cycle

Corpus luteal cysts – These are normally less than 5cm. These occur in the luteal phase of the menstrual cycle after the formation of the corpus luteum

141
Q

pathological non neoplastic pvarian cysts

A

Endometrioma – These are also called chocolate cysts and are present in those with endometriosis. There has been bleeding into the cyst resulting in the appearance.

Polycystic ovaries

Theca lutein cyst – These result as a consequence of markedly raised hCG e.g. molar pregnancy. They regress upon resolution of the raised hCG.

142
Q

epithelial tumours ovarian cysts (benign neoplastic)

A

Serous cystadenoma – reflects the most common type of malignant ovarian tumour and is usually unilocular with up to 30% being bilateral.

Mucinous cystadenoma – these are often multiloculated and usually unilateral.

Brenner tumour – unilateral with a solid grey or yellow appearance.

143
Q

benign germ cell tumours ovarian cysts

A

Mature cystic teratoma (Dermoid cysts) – 10% are bilateral, usually occur in young women and occur frequently in pregnancy. As germ cell in origin they can contain teeth, hair, skin and bone.

144
Q

sex cord stroma tumours ovarian cysts

A

Fibroma – the most common stromal tumour. Important to know about as up to 40% present with Meig’s syndrome which is the association between these tumours and ascites/pleural effusion.

145
Q

RF PCOS

A

diabetes, irregular menstruation and/or a family history of PCOS

146
Q

features PCOS

A

Oligomenorrhoea or amenorrhoea, Infertility, Hirsutism, Obesity, Chronic pelvic pain, Depression (and other psychological symptoms)

147
Q

diagnosis PCOS

A

Rotterdam Criteria- two out of three criteria are met: Oligo- and/or anovulation, Clinical and/or biochemical signs of hyperandrogenism, Polycystic ovaries on imaging (USS)

148
Q

mx PCOS

A

Management is catered to each woman’s needs:
Low dose combined oral contraceptive pill or dydrogesterone for oligo-/amenorrhoea
Exercise, orlistat for obesity
Clomifene for infertility
Cyproterone or spironolactone or finasteride and/or eflornithine for hirsutism.

149
Q

cause PCOS

A

unknown
theories:
Excess luteinising hormone (LH)– produced by the anterior pituitary gland in response to an increased GnRH pulse frequency. This stimulates ovarian production of androgens.

Insulin resistance– resulting in high levels of insulin secretion.

150
Q

endometriosis

A

endometrial tissueis located at sites other than the uterine cavity. It can occur in the ovaries, pouch of Douglas, uterosacral ligaments, pelvic peritoneum, bladder, umbilicus and lungs

151
Q

RF endometriosis

A

Early menarche, Family history of endometriosis, Short menstrual cycles, Long duration of menstrual bleeding, Heavy menstrual bleeding, Defects in the uterus or fallopian tubes

152
Q

presentation endometriosis

A

Cyclical pelvic pain - at time of menstruation, dysmenorrhoea, dyspareunia, dysuria, dyschezia (difficult, painful defecating), and subfertility.
bimanual examination, the clinician may note: A fixed, retroverted uterus, Uterosacral ligament nodules, General tenderness

153
Q

ix endometriosis

A

Pelvic USS, gold standard = laparosopy (Chocolate cysts, Adhesions, Peritoneal deposits)

154
Q

mx endometriosis

A

Pain: analgesia or NSAIDs. Follow the ‘analgesic ladder’ as appropriate.
Ovulation: A low dosecombined oral contraceptive pillor norethisterone can be used. Injected hormones or intrauterine devices such as the Mirena coil can also be used. The Mirena has the benefit of containing a low dose of hormone.
Surgery: if the symptoms seriously affect the patient’s life. Surgery such as excision, fulgaration andlaser ablation. Ultimate management may be a hysterectomy and removal of the ovaries

155
Q

causes endoemtriosis

A

unsure
retrograde menstruation

156
Q

primary amenorrohea

A

absence of menstrual periods. Primary– failure to commence menses (absence of menarche):
Girls aged 16+, in the presence of secondary sexual characteristics such as pubic hair growth and breast development
Girls aged 14+, in the absence of secondary sexual characteristics

157
Q

secondary amenorrhoea

A

cessation of periods for more than six months after the menarche (after excluding pregnancy).

158
Q

oligomenorrhoea

A

refers toirregular periods with intervals between menstrual cycles of more than 35 days and/or less than nine periods per year.

159
Q

causes amenorrhoea

A

hypothalamic: functional (eating disorders, exercise), thyroid, sarcoidosis, Kallmann syndrome
Pituitary: prolactinoma, other tumours, sheehans syndrome
Ovarian: PCOS, Turner’s syndrome, premature ovarian failure
Adrenal hyperplasia
Genital tract abnormalities: imperforate hymen, ashermann’s syndrome, Mayer-Rokitansky-Kuster-Hauser syndrome

160
Q

causes oligomenorrhoea/secondary amenorrhoea

A

PCOS, Contraceptive/Hormonal treatments, Perimenopause, Thyroid disease/Diabetes, Eating disorders/excessive exercise, Medications e.g. anti-psychotics, anti-epileptics

161
Q

ix amenorrhoea

A

Pregnancy test, Blood tests (Thyroid function tests (TFTS) and prolactin., FSH/LH/Oestradiol/Progesterone/Testosterone., 17 hydroxyprogesterone), Karyotyping, Ultrasound scan

162
Q

blood results in hypothalamic cause amenorrhoea

A

low GnRH
normal FSH
low or normal LH
low LH:FSH ratio
low oestrogen

163
Q

blood results pcos

A

normal FSH
high LH
high LH:FSH ratio
normal or high testosterone

164
Q

blood results in premature ovarian failure

A

high FSH and LH
low oestrogen

165
Q

dysmenorrhoea

A

painful periods
Primary– menstrual pain occurring with no underlying pelvic pathology.
Secondary– menstrual pain that occurs with an associated pelvic pathology.

166
Q

RF dysmenorrhoea

A

Early menarche, Long menstrual phase, Heavy periods, Smoking, Nuliparity

167
Q

causes secondary dysmenorrhoea

A

Endometriosis, Adenomyosis, Pelvic inflammatory disease, Adhesions

168
Q

features dysmenorrhoea

A

lower abdominal orpelvic pain, which can radiate to lower back or anterior thigh. Pain is crampy in nature. It usually lasts for48-72 hoursaround the menstrual period, and is characteristically worst at the onset of menses.

169
Q

mx dysmenorrhoea

A

Lifestyle: stop smoking
Pharmacological: analgesia first line = NSAIDs (ibuprofen, naproxen, mefenamic acid). Second line =COCP
Non-pharmacological: Local application of heat (water bottles or heat patch), Transcutaneous Electrical Nerve Stimulation (TENS)

170
Q

heavy menstrual bleeding

A

is a description of excessive menstrual loss which interferes with a woman’s quality of life
If no cause found = dysfunctional/abnormal uterine bleeding

171
Q

causes heavy menstrual bleeding

A

Structural: Polyp, Adenomyosis, Leiomyoma (Fibroid), Malignancy & hyperplasia
Non-structural: Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified

172
Q

ix heavy menstrual bleeding

A

Menstrual diary
Bloods: Full blood count, .Thyroid function test, Coagulation screen + test for Von Willebrand’s
Transvaginal USS
Swabs for infection

173
Q

mx heavy menstrual bleeding

A

Pharmacological: 3 tiered approach - Levonorgestral-releasing intrauterine system. Tranexamic acid, mefanamic acid or combined oral contraceptive pill.
Surgical: Endometrial ablation and (ii) Hysterectomy

174
Q

presentation ovarian torsion

A

sudden onset of deep seated colicky abdominal pain, vomiting and distress. Vaginal examination may reveal adnexial tenderness

175
Q

ix ovarian torsion

A

USS

176
Q

mx ovarian torsion

A

laparoscopy - diagnostic and therapeutic

177
Q

lichen sclerosis

A

is a chronic inflammatory skin disease of the anogenital region
potential to progress tosquamous cell carcinoma

178
Q

RF lichen sclerosis

A

genetic, other AI disorders

179
Q

features lichen sclerosis

A

white atrophic patches – figure of 8 distribution, itching

180
Q

mx lichen slcerosis

A

topical steroids - clobetasol propionate

181
Q

RF cervical ectropion

A

high oestrogen - Use of the combined oral contraceptive pill, Pregnancy, Adolescence, Menstruating age

182
Q

presentation cervical ectropion

A

asymptomatic, post-coital bleeding, intermenstrual bleeding, or excessive discharge

183
Q

mx cervical ectropion

A

none if no symptoms, stop COCP, ablation

184
Q

features atrophic vaginitis

A

vaginal dryness, dyspareunia and occasional spotting.

185
Q

mx atrophic vaginitis

A

vaginal lubricants and moisturisers - if these do not help then topical oestrogen cream can be used.

186
Q

bartholins cyst

A

soft, fluctuant and non-tender

187
Q

bartholins abscesss

A

tense and hard, with surrounding cellulitis
fluid-filled sac within one of the Bartholin’s glands of the vagina.

188
Q

RF bartholins cyst

A

personal hx, STIs,

189
Q

mx bartholins cyst

A

if pain - Word Catheteror marsupialisation

190
Q

ashermans syndrome

A

Intrauterine adhesions/scarring

191
Q

cause of ashermans syndrome

A

trauma e.g. dilation and curettage, CS

192
Q

presentation ashermans syndrome

A

: amenorrhoea, pain, infertility, recurrent miscarriage

193
Q

mx ashermans syndroem

A

hysteroscopy for adhesions

194
Q

cervical polyps

A

hyperplasia of thecolumnar epithelium

195
Q

presentation cervical polyps

A

asymptomatic, abnormal vaginal bleeding

196
Q

mx cervical polyps

A

removal and histological analysis

197
Q

types FGM

A
  1. Clitoridectomy – partial or total removal of the clitoris
  2. Excision – partial or total removal of the clitoris and labia minora +/- labia majora
  3. Infibulation - narrowing of the vaginal orifice by stiching the labia together
  4. All other harmful procedures to the female genitalia for non-medical purposes
198
Q

legalities of FGM

A

Illegal to perform FGM in England, Wales and northern Ireland
Illegal to assist in the carrying out of FGM (including helping them book the flights, taking them to have it done or even knowing about it and not doing anything)
If you see a child with FGM you need to phone the police

199
Q

gynae complications FGM

A

: Sexual dysfunction with anorgasmia, Chronic pain, Keloid scar formation, Dysmenorrhoea, Haematocolpos - period blood backs up in the uterus as it cannot get released during the period, Urinary outflow obstruction, Recurrent UTI, Difficulty conceiving – sexual intercourse can be very difficult, PTSD

200
Q

obstetric complications FGM

A

Fear of childbirth, Increased likelihood of C-section, PPH, episiotomy, severe vaginal lacerations and fistula formation, Extended hospital stay, Difficulty in – performing vaginal examinations in pregnancy, applying fetal scalp electrodes and FBS, Difficulty in catheterising the bladder. Best to try and reverse infibulation before the woman falls pregnant

finals (31 decks)

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