gynae/breast Flashcards
1
Q
featurs of benign breast lumps on examination
A
Soft, mobile, fluctuant, ?painful
2
Q
features of a malignant breast lump on examination
A
Hard, irregular, painless, immobile, Tethered skin, skin dimpling, nipple retraction
3
Q
triple assessment breast lumps
A
Hx + Exam
Imaging: Mammogram 🡪 US
+/- biopsy
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
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’.
6
Q
features fibroadenoma
A
Mobile, firm breast lumps. No increase in risk of malignancy. ‘breast mice’. Common <30
7
Q
mx fibroadenoma
A
If >3cm surgical excision is usual, Phyllodes tumours should be widely excised (mastectomy if the lesion is large)
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)
9
Q
mx breast cyst
A
Cysts should be aspirated, those which are blood stained or persistently refill should be biopsied or excised
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
11
Q
mx fat necrosis
A
Rare and may mimic breast cancer so further investigation is always warranted
Imaging and core biopsy
12
Q
features duct papilloma
A
Usually present with nipple discharge. No increase risk of malignancy
13
Q
mx duct papilloma
A
Microdochectomy
14
Q
features lactational breast abscess
A
Infectious mastitis->accumulation of pus -> lactational breast abscess. Staphylococcus aureus
15
Q
mx lactational breast abscess
A
Incision and drainage or needle aspiration, antibiotics according to local protocol
16
Q
features puerperal mastitis
A
unilateral and typically presents 1 week postpartum. painful, tender, red and hot breast
17
Q
mx puerperal mastitis
A
Continue breastfeeding. If sx don’t improve: flucloxacillin for 10-14 days
18
Q
features fibroadenosis
A
Most common in middle-aged women
‘Lumpy’ breasts which may be painful. Symptoms may worsen prior to menstruation
19
Q
mx fibroadenosis
A
supportive
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
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)
22
Q
features cyclical mastalgia
A
Younger, varies in intensity according to the phase of the menstrual cycle
23
Q
my cyclical mastalgia
A
supportive
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)
25
presentation pagets disease of breast
intraductal carcinoma associated with a reddening and thickening (may resemble eczematous changes) of the nipple/areola
26
breast cancer staging
T1-4
N0-3
M0-1
27
types of breast cancer
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
28
medulary breast carcinoma
younger patients and those with BRCA1 mutations, often significant lymphocytic infiltration surrounding the tumour
29
malignant phyllodes tumour
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
30
inflammatory breast cancer
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
31
mx breast cancer
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
32
tx for HER 2 +ve tumours
trastuzumab
33
tx for ER +ve tumours
tamoxifen in pre/peri-menopausal or anastrozole in post menopausal
34
cystocele
Prolapse of anterior vaginal wall involving the bladder
35
uterine prolapse
Prolapse of uterus, cervix and upper vagina
36
enterocele
Prolapse of upper posterior wall of vagina
37
rectocele
Prolapse of lower posterior wall of vagina, usually involving the anterior wall of rectum
38
stress incontinence
involuntary leakage of urine during increased intra-abdominal pressure
39
urge incontinence
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.
40
overflow incontinence
due to bladder outlet obstruction, e.g. due to prostate enlargement
41
functional incontinence
Causes include dementia, sedating medication and injury/illness resulting in decreased ambulation
42
RF for urinary incontinence
advancing age
previous pregnancy and childbirth
high body mass index
hysterectomy
family history
43
investigations for urinary incontinence
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.
44
mx urge incontinence
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, be avoided in 'frail older women'
mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patients
45
mx stress incontinence
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
duloxetine may 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
46
prolapse presentation
sensation of pressure, heaviness, 'bearing-down'
urinary symptoms: incontinence, frequency, urgency
Rectocele often causes constipation rather than urinary sx
47
mx prolapse
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
48
didelphys
Total failure of fusion -> two uterine cavities and cervices
49
unicornate uterus
One duct failure
50
‘RUDIMENTARY HORN
One duct develops better than the other
51
phases of ovarian cycle
follicular
ovulation
luteal
52
follicular phase ovarian cycle
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.
53
ovulation phase ovarian cycle
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.
54
luteal phase ovarian cycle
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.
55
phases of the uterine cycle
proliferative
secretory
menses
56
proliferative phase uterine cycle
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).
57
secretory phase uterine cycle
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.
58
menses phase uterine cycle
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.
59
what does fsh do
binds to granulosa cells to stimulate follicle growth, permit the conversion of androgens (from theca cells) to oestrogens and stimulate inhibin secretion
60
what does lh do
theca cells to stimulate production and secretion of androgens
61
describe the main feedback systems in the menstrual cycle
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
62
what is menopause
Amenorrhoea (no menstruation) for 12 months
63
common perimenopausal sx
hot flushes, urinary incontinence and increased UTIs as well as irregular vaginal bleeding
64
premature ovarian insufficiency
women under the age of 40 and is characterised by low oestrogen, high gonadotropins and amenorrhoea.
65
levels of oestrogen post menopause
lower
66
changes after menopause
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.
67
mx menopause
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
68
what is in HRT
Oestrogens (used to overcome oestrogen deficiency) – oral, transdermal, topical
Progestogen (endometrial protection from oestogen) – oral, transdermal, IUS (mirena
69
who can have oestrogen only HRT
women without a uterus
70
what are the types of combines HRT
Cyclically: perimenopausal women who are still having menstrual periods
Continuous: postmenopausal women who are not having menstrual periods
71
CI HRT
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
72
risks HRT
Breast cancer
Endometrial cancer (if oestrogen alone)
VTE Cardiovascular disease >60yrs
73
benefits HRT
Relief of vasomotor symptoms
Relief of urogenital symptoms
Reduced risk of osteoporosis
74
normal age of puberty
8-14 in females, and between the ages of 10-16 in males.
75
puberty in females
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
76
puberty in males
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
77
tanner stages for male genitalia
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
78
tanner stages for breast development
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
79
tanner stages for pubic hair
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
80
tanner stages for growth
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
81
delayed puberty
Absence of secondary sexual characteristics by the age of 13 in girls or 16 in boys.
82
causes of delayed puberty
Hypogondaotropic hypogonadism
Hypergondaotropic hypogonadism
83
Hypogondaotropic hypogonadism
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
Hypergonadotropic hypogonadism
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
conditions associated with delayed puberty
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
precocious puberty
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
types of precocious puberty
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
androgen insensitivity syndrome
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
features androgen insensitivity syndrome
'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
diagnosis androgen insensitivty syndrome
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
mx androgen insensitivity syndrome
counselling - raise the child as female
bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)
oestrogen therapy
92
RF endometrial cancer
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
presentation endometrial cancer
Postmenopausal bleeding
94
ix endometrial cancer
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
staging endometrial cancer
- FIGO I-IV
96
mx endometrial cancer (stages)
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
RF cervical cancer
HPV 16 and 18, CIN, Smoking, Other sexually transmitted infections, Long-term (> 8 years) combined oral contraceptive pill use, Immunodeficiency (e.g. HIV)
98
presentation cervical cancer
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
ix cervical cancer
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
mx cervical cancer
Surgery: type dependent on stage. Radiotherapy, chemo
101
CIN
dyskaryosis – mutations in the squamous cells in the transformation zone of the cervix
102
mx CIN
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
screening for cervical cancer
Smear 25-49 3 yearly, 50-64 5 yearly
yearly if habe HIV
104
RF ovarian cancer
Nulliparity, Early menarche, Late menopause, Hormone replacement therapy containing oestrogen only, Smoking, Obesity, BRCA1 & 2, Hereditary nonpolyposis colorectal cancer (Lynch II Syndrome)
105
protective factors for ovarian cancer
Multiparity, Combined contraceptive methods, Breastfeeding
106
what is the risk of malignancy index
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
presentation of ovarian cancer
Incidental and asymptomatic, pain, Bleeding per vagina, Bloating, Change in bowel habit, Change in urinary frequency, Weight loss
108
ix ovarian cancer
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
mx ovarian cancer
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
meigs syndrome
TRIAD: benign ovarian tumor with ascites and pleural effusion
111
types of ovarian tumour
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
vulval cancer type
squamous cell carcinomas
113
presentation vulval cancer
pruritis, burning, soreness, bleeding, pain or a lum on the labia majora
114
diagnosis vulval cancer
Keye’s punch biopsy
115
mx vulval cancer
surgery
116
vaginal cancer presentation
rare but can be post menopausal bleeding
117
prolactinoma presentaion
Irregular periods or no periods, Reduced fertility, Reduced sex drive, galactorrhoea, Increased growth of hair on the face or body.
118
mx prolactinoma
dopamine agonists are called bromocriptine, cabergoline, surgery
119
adenomyosis
Functional endometrial tissue within the myometrium of the uterus. Seen towards the end of the reproductive years.
120
RF adenomyosis
High parity, Uterine surgery e.g. any endometrial curettage, endometrial ablation, Previous caesarean section, potential genetic predisposition
121
presentation adenomyosis
menorrhagia, dysmenorrhoea, deep dyspareunia and irregular bleeding
On examination: symmetrically enlarged tender uterus may be palpable.
122
ix adenomyosis
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
mx adenomyosis
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
fibroids
Lyeiomyotoma - benign smooth muscle tumours of the uterus
125
RF fibroids
Obesity, Early menarche, Increasing age, Family history, Ethnicity (African-Americans are 3x more likely to develop fibroid than Caucasians)
126
presentation fibroids
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
what is red degeneration of fibroids
in pregnancy.This is where the rapidly growing fibroid undergoes necrosis and haemorrhage.
128
ix fibroids
Pelvic ultrasound, MRI
129
mx fibroids
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
complications fibrodis
Iron deficiency anaemia, Compression of pelvic organs (Recurrent urinary tract infections, Incontinence, Hydronephrosis, Urinary retention), Subfertility/infertility, Degeneration, Torsion
131
PID cause
Chlamydia trachomatis and Neisseria gonorrhoea
132
RF PID
Sexually active, Aged under 15-24, Recent partner change, Intercourse without barrier contraceptive protection, History of STIs, Personal history of pelvic inflammatory disease
133
features PID
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
ix PID
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
mx PID
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
complications PID
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
presentation ovarian cysts
: incidental finding, pain, bleeding
138
mx pre-menopausal ovarian cycts
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
mx post menopausal ovarian cysts
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
functional non neoplastic ovarian cysts
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
pathological non neoplastic pvarian cysts
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
epithelial tumours ovarian cysts (benign neoplastic)
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.
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benign germ cell tumours ovarian cysts
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.
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sex cord stroma tumours ovarian cysts
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.
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RF PCOS
diabetes, irregular menstruation and/or a family history of PCOS
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features PCOS
Oligomenorrhoea or amenorrhoea, Infertility, Hirsutism, Obesity, Chronic pelvic pain, Depression (and other psychological symptoms)
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diagnosis PCOS
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)
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mx PCOS
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.
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cause PCOS
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.
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endometriosis
endometrial tissue is 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
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RF endometriosis
Early menarche, Family history of endometriosis, Short menstrual cycles, Long duration of menstrual bleeding, Heavy menstrual bleeding, Defects in the uterus or fallopian tubes
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presentation endometriosis
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
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ix endometriosis
Pelvic USS, gold standard = laparosopy (Chocolate cysts, Adhesions, Peritoneal deposits)
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mx endometriosis
Pain: analgesia or NSAIDs. Follow the ‘analgesic ladder’ as appropriate.
Ovulation: A low dose combined oral contraceptive pill or 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 and laser ablation. Ultimate management may be a hysterectomy and removal of the ovaries
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causes endoemtriosis
unsure
retrograde menstruation
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primary amenorrohea
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
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secondary amenorrhoea
cessation of periods for more than six months after the menarche (after excluding pregnancy).
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oligomenorrhoea
refers to irregular periods with intervals between menstrual cycles of more than 35 days and/or less than nine periods per year.
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causes amenorrhoea
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
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causes oligomenorrhoea/secondary amenorrhoea
PCOS, Contraceptive/Hormonal treatments, Perimenopause, Thyroid disease/Diabetes, Eating disorders/excessive exercise, Medications e.g. anti-psychotics, anti-epileptics
161
ix amenorrhoea
Pregnancy test, Blood tests (Thyroid function tests (TFTS) and prolactin., FSH/LH/Oestradiol/Progesterone/Testosterone., 17 hydroxyprogesterone), Karyotyping, Ultrasound scan
162
blood results in hypothalamic cause amenorrhoea
low GnRH
normal FSH
low or normal LH
low LH:FSH ratio
low oestrogen
163
blood results pcos
normal FSH
high LH
high LH:FSH ratio
normal or high testosterone
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blood results in premature ovarian failure
high FSH and LH
low oestrogen
165
dysmenorrhoea
painful periods
Primary – menstrual pain occurring with no underlying pelvic pathology.
Secondary – menstrual pain that occurs with an associated pelvic pathology.
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RF dysmenorrhoea
Early menarche, Long menstrual phase, Heavy periods, Smoking, Nuliparity
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causes secondary dysmenorrhoea
Endometriosis, Adenomyosis, Pelvic inflammatory disease, Adhesions
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features dysmenorrhoea
lower abdominal or pelvic pain, which can radiate to lower back or anterior thigh. Pain is crampy in nature. It usually lasts for 48-72 hours around the menstrual period, and is characteristically worst at the onset of menses.
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mx dysmenorrhoea
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
heavy menstrual bleeding
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
causes heavy menstrual bleeding
Structural: Polyp, Adenomyosis, Leiomyoma (Fibroid), Malignancy & hyperplasia
Non-structural: Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified
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ix heavy menstrual bleeding
Menstrual diary
Bloods: Full blood count, .Thyroid function test, Coagulation screen + test for Von Willebrand’s
Transvaginal USS
Swabs for infection
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mx heavy menstrual bleeding
Pharmacological: 3 tiered approach - Levonorgestral-releasing intrauterine system. Tranexamic acid, mefanamic acid or combined oral contraceptive pill.
Surgical: Endometrial ablation and (ii) Hysterectomy
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presentation ovarian torsion
sudden onset of deep seated colicky abdominal pain, vomiting and distress. Vaginal examination may reveal adnexial tenderness
175
ix ovarian torsion
USS
176
mx ovarian torsion
laparoscopy - diagnostic and therapeutic
177
lichen sclerosis
is a chronic inflammatory skin disease of the anogenital region
potential to progress to squamous cell carcinoma
178
RF lichen sclerosis
genetic, other AI disorders
179
features lichen sclerosis
white atrophic patches – figure of 8 distribution , itching
180
mx lichen slcerosis
topical steroids - clobetasol propionate
181
RF cervical ectropion
high oestrogen - Use of the combined oral contraceptive pill, Pregnancy, Adolescence, Menstruating age
182
presentation cervical ectropion
asymptomatic, post-coital bleeding, intermenstrual bleeding, or excessive discharge
183
mx cervical ectropion
none if no symptoms, stop COCP, ablation
184
features atrophic vaginitis
vaginal dryness, dyspareunia and occasional spotting.
185
mx atrophic vaginitis
vaginal lubricants and moisturisers - if these do not help then topical oestrogen cream can be used.
186
bartholins cyst
soft, fluctuant and non-tender
187
bartholins abscesss
tense and hard, with surrounding cellulitis
fluid-filled sac within one of the Bartholin’s glands of the vagina.
188
RF bartholins cyst
personal hx, STIs,
189
mx bartholins cyst
if pain - Word Catheter or marsupialisation
190
ashermans syndrome
Intrauterine adhesions/scarring
191
cause of ashermans syndrome
trauma e.g. dilation and curettage, CS
192
presentation ashermans syndrome
: amenorrhoea, pain, infertility, recurrent miscarriage
193
mx ashermans syndroem
hysteroscopy for adhesions
194
cervical polyps
hyperplasia of the columnar epithelium
195
presentation cervical polyps
asymptomatic, abnormal vaginal bleeding
196
mx cervical polyps
removal and histological analysis
197
types FGM
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
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legalities of FGM
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
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gynae complications FGM
: 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
obstetric complications FGM
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
