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Phase 3a Finals > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

What is polycystic ovarian syndrome: pcos?

A

ovarian dysfunction

hyperinsulinaemia and high levels of luteinizing hormone.

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2
Q

features of pcos

A

subfertility and infertility
menstrual disturbance: oligomenorrhoea and amenorrhoea

hirsutism, acne (because of hyperandrogenism)
obesity
acanthasis nigricans (due to insulin resistance)
acne

hair loss in male pattern

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3
Q

how would you investigate pcos?

A

pelvic ultrasound - multiple cysts on ovaries
transvaginal uss - gold standard.
follicles around periphery of ovary (STRING OF PEARLES)

FSH,LH,PROLACTIN,TSH,TESTOSTEONE,SEX HORMONE BINDING GLOBULIN(SHBG)

raised lh:fsh ratio
prolactin: normal/mildly elvated
testosterone: poss normal/mildly elevated
SHBH - normal to low
raised lh

check for impaired glucose tolerance

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4
Q

what is the diagnostic criteria for pcos?

A

Rotterdam criteria: 2 of following 3

  1. infrequent or no ovulation
  2. clinical/biochemical signs of hyperandrogenism (hirsutism, acne, elevated levels of total/free testosterone)
  3. polycystic ovaries on uss scan - 12 or more follicles (2-9mm in diameter) in 1 or both ovaries and/or increased ovarian vol over 10cm^3
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5
Q

Management of pcos

A

weight reduction if poss. - orlistat : lipase inhibitor
combined oral contraceptive if need contraception - regulate her cycle and induce monthly bleed.

hirsutism and acne:
- COC pill. 3rd gen.- fewer androgenic effects or co-cyprindiol (has anti-androgen action) - both have VTE risk.
- if doesnt respond to COC : topical eflornithine
-spironolactone, flutamide, finasteride - specialist supervision

infertilityL
- weight reduction
- poss metformin,clomifene or combo to stimulate ovulation.
- use metformin either with clomifene or alone - esp in obese
-gonadotrophins

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6
Q

which drug poses risk of multiple pregnancies?

A

clomifene - antioestrogen therapy

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7
Q

how might a oral ccp help regulate cycle and induce monthly bleed?

A
  1. occupy hypothalamic oestrogen receptor without activating them.
  2. interferes with binding of oestradiol
  3. prevents negative feedback inhibition of FSH secretion.
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8
Q

comps of pcos

A

insulin resistance and diabetes
acanthosis nigricans
cv disease
hypercholestrolaemia
endometrial hyperplasia and cancer
obstructive sleep apnoea
depression and anxiety
sexual problems.

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9
Q

hirsutism can be caused by?

A

pcos
meds : phenytoin, ciclosporin, corticosteroids, testosterone, anabolic steroids

ovarian/adrenal tumours secreting androgens

cushings syndrome
congenital adrenal hyperplasia

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10
Q

how does insulin resistance play in pcos?

A

insulin resist pt, pancreas produces more insulin.
promotes release of androgens from ovaries and adrenal glands

insulin also suppresses SHBH production by liver. it would normally bind to androgens and suppress the function.

high insulin halt development of follicles in overaies = anovulation. and multiple partially developed follicles - Polycstic ovaries.

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11
Q

screening for pcos

A

OGTT
2 hr 75g
morning before breakfast.

impaired fasting glucose - 6.1-6.9
impaired glucose tolerance - plasma glucose at 2hrs 7.8-11.1
diabetes - plasma glucose at 2 hours over 11.1

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12
Q

how would you manage acne in pcos?

A

coc pill - 1st line.
co-cyprindiol antiandrogen effects - risk of vte.

topical adapalene
topical abx - clindamycin 1% with benzoyl peroxide 5%
topical azelaic acid 20%
oral tetracycle abx - lymecycline

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13
Q

how would you manage hirsutism?

A

weight loss

co-cyprindiol - COC pill - ANTI-ANDROGENIC. - vte risk.

topical eflornithine - facial hirsutism - 6-8 weeks. - will return 2 months after stopping.

other:
laser
electrolysis
spironolactine, finasteride, flutamide (non steroid antiandrogen), cyproterone acetate(antiandrogen and progestin)

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14
Q

i have heard you can do ovarian drilling for infertility in pcos women? explain?

A

laparoscopic surgery.
multiple holes in ovaries using diathermy/laser.

= regular ovulation and fertility.

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15
Q

when would you check for gestational diabetes?

A

ogtt before pregnancy and at 24-28 weeks gestation

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16
Q

what is pelvic inflammatory disease?

A

infection and inflammation of female pelvic organs including uterus falopian tubes ovaries and surrounding peritoneum.

usually due to ascending infection from endocervix

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17
Q

causative organisms of pelvic inflammatory disease

A

chlamydia trachomatis: MC

neisseria gonorrhoeae - causes more severe PID

mycoplasma genitalium

mycoplasma hominis

can be caused by non sti like:
- gardnerella vaginalis
-haemophilis influenzae
- e coli

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18
Q

features of pelvic inflammatory disease

A

lower abdo pain
fever
deep dyspareunia
dysuria and menstrual irregularities
vaginal/cervical discharge
cervical excitation
abnormal bleeding - intermenstrual or postcoital

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19
Q

how would you investigate for pelvic inflammatory disease?

A

pregnancy test - exclude ectopic pregnancy

high vaginal swab - often negative - you can see BV, candidiasis and trichomonas.

micrscope - pus cells from vagina/endocervix. absense of it excludes PID.
inflammatory markers crp esr - high.

screen for chlamydia and gonorrhoea - NAAT swabs and for mycoplasma genitalium if poss.
hiv test
syphilis test

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20
Q

how would you manage pelvic inflammatory disease?

A

low threshold for tx

1st line : stat IM ceftriaxone 1g (gonorhoea) + 14 days 100mg twice daily oral doxycyline (chla + mycoplasma genitalium) + oral metronidazole400mg 14 days twice daily - avoid fluoroquinolones where poss (cover anaerobes like gardnerella)

2nd line: oral ofloxacin + oral metronidazole

if mild case:
leave in intrauterine contraceptive. - now seen if you remove between outcomes.

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21
Q

potential complications of pelvic inflammatory disease

A

infertility - 10-20% after single episode
sepsis , abscess

chronic pelvic pain
ectopic pregnancy

perihepatitis (fitz-hugh curtis syndrome) - 10% of cases. - RUQ pain , could confuse with cholecystitis.

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22
Q

talk to me about fitz hugh curtis syndrome

A

perihepatitis

comp of PID

caused by inflammation and infection of liver capsule (glissons capsule) = adhesions between liver and peritoneum.

bacteria can spread from pelvis via peritoneal cavity, lymphatics or blood.

RUQ pain - referred right shoulder tip pain if diaphragmatic irritation.

laparscopy- visualise

adhesiolysis - treatment of adhesions

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23
Q

what is the connective tissue around the uterus called?

A

parametrium

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24
Q

what is an ovarian torsion? twist

A

partial/complete torsion of ovary on its supporting ligaments that may compromise blood supply.

if fallopian tube involved: adnexal (blood supply) torsion

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25
Q

risk factors of ovarian torsion

A

ovarian mass - 90% of torsion cases (Cyst/tumour)

being of reproductive age -before menarche if girl has longer infundibulopelvic ligaments twist easier.

pregnancy

ovarian hyperstimulation syndrome

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26
Q

features of ovarian torsion

On examination

A

sudden onset deep-seated colicky abdo pain unilateral. - progressive

vomiting and distress

fever in minority - poss secondary to adnexal necrosis.

occasionally : can be not that severe and ovary can twist and untwist intermittently, causing pain that comes and goes.

on exam: localised tenderness. poss palpable mass in pelvis. - absense of mass doesnt exclude the diagnosis.

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27
Q

investigations for ovarian torsion

A

pelvic us. preferably transvaginal but transabdominal can be used: free fluid in pelvis/oedema of ovary. or whirlpool sign

doppler studies - lack of blood flow.
vaginal exam: adnexial tenderness

definitive diagnosis: made with laparoscopic surgery

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28
Q

tx of ovarian torsion

A

laparoscopy - diagnostic and therapeutic:
untwist ovary and fix it in place - detorsion
remove affected ovary- oophorectomy

laparotomy - if large ovarian mass or malignancy

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29
Q

comps of ovarian torsion

A

loss of function of that ovary. doesnt affect fertility because you have other ovary.

if only functioning one : infertility and menopause

if necrotic ovary not removed: can get infected, develop abscess, sepsis. - could rupture = peritonitis and adhesions.

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30
Q

if i see an ovarian cyst in pre vs post menopausal women what should i be thinking?

A

pre - benign
post - malignancy

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31
Q

presentation of ovarian cysts

A

usually asx and found incidentally on pelvic uss scan.

if sx : vague:
pelvic pain
bloating
fullness in abdo
palpable pevlic mass - esp with very large cysts like mucinous cystadenomas

acute pelvic pain if: ovarian torsion, haemorrhage or rupture of cyst

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32
Q

tell me the 2 different types of functional cysts

A

follicular cysts - when developing follicle fails to rupture and release egg. - dissapear after a few menstrual cycles. - thin walls no internal structures.

corpus luteum cysts - fails to break down fills with fluid. pelvic discomfort pain or delayed menstruation. often seen in early pregnancy

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33
Q

name the other types of ovarian cysts

A

serous cystadenoma - benign tumour of epithelial cells

mucinous cystadenomia - benign tumour of epithelial cells. can be huge - takeup space in pelvis and abdo

endometrioma - lumps of endometrial tissue in ovary in endometriosis pt. - pain and disrupt ovulation

dermoid cysts - germ cell tumours - benign. teratomas - have skin teeth hair and bone. - associated with ovarian torsion.

sex cord stromal tumours - rare - benign/malignant. come from stroma or sex cords.

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34
Q

features that would suggest ovarian cyst malignancy

A

abdo bloating
reduce apetite
early satiety
weight loss
urinary sx
pain
ascites
lymphadenopathy

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35
Q

risk factors for ovarian malignancy

A

age
postmenopause
increased number of ovulations
obesity
hormone replacement therpay
smoking
breastfeeding - protective an so is prenancy and cocpill

fhx and brca1 and brca2 genes
increased ovulation

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36
Q

it is known the number of times a women has ovulated during her life correlates with her risk of ovarian cancer.

what factors reduce the number of ovulations?

A

later onset of periods- menarche
early menopause
any pregnancies
use of coc pill

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37
Q

what blood tests should you do in ovarian cysts?

A

premenopasual women with simple ovarian cyst less than 5 cm on USS - no further required

CA125 - tumour marker

women under 40 with complex ovarian mass require tumour markers for poss germ cell tumour
lactate dehydrogenase - ldh
alpha-fetoprotein - a-FP
human chorionic gonadotropin - HCG

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38
Q

what is ca125
causes of raised CA125

A

tumour marker for epithelial cell ovarian cancer.
not very specific.

endometriosis
fibrosis
adenomyosis
pelvic infection
liver disease
pregnancy

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39
Q

what is the risk of malignancy index

A

estimates risk of ovarian mass being malignant - takes account of:

menopausal status
uss findings
ca125 level

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40
Q

how would you manage ovarian cysts?

A

poss ovarian cancer - 2 week wait refer to gynae.

poss dermoid cyst - refer to gynae for surgery

simple ovarian cyst in premenopause:
- less than 5cm: will resolve within 3 cycles.
- 5-7cm : refer to gynae and annual uss.
- 7+cm - MRI or surgery.

postmenopause :
- correlate with ca125 and refer to gynae.
-if raised - 2 week wait.
- simple cyst under 5cm with normal ca125 - uss every 4-6 months.

persistent or enlarging cysts : SURGERY WITH LAPAROSCOPY. could be:
- ovarian cystectomy
- poss remove affected ovary - OOPHORECTOMY

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41
Q

what is meigs syndrome?

occurs in?

A

triad:
ovarian fibroma - benign ovarian tumour
pleural effusion
ascites

older women

removal of tumour = complete resolution of effusion and ascites.

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42
Q

complications of ovarian cysts - pt it’s acute onset pain think wha?

A

if pt presents with acute onset pain:
torsion
haemorrhage into cyst
rupture - bleeding into peritoneum

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43
Q

peak incidence of ovarian cancer.
prognosis
pathophysiology of ovarian cancer.

A

60 yrs old.
poor prognosis - late diagnosis - 80% of women have advanced disease at presentation.

90% epithelial in origin, 70-80% due to serous carcinomas.
- distal end of fallopian tube site of origin of many ovarian cancers.

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44
Q

risk factors of ovarian cancer (OC)

A

fhx - mutations of BRCA1 or BRCA2 gene

many ovulations: infertility tx increases risk of OC (COC pill reduces risk and so does having loads of pregnancies)
- early menarche
-late menopause
-nulliparity

reccurent use of clomifene
smoking
obesity

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45
Q

clinical features of ovarian cancer: albeit vague

how can ovarian mass cause hip/groin pain.

A

abdo distension and bloating - abdo/pelvic mass
ascites
abdo and pelvic pain
urinary sx: urgency/frequency
weight loss
early satiety
diarrhoea
loss of apetite

ovarian mass press on obturator nerve - hip/groin pain.

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46
Q

investigations of ovarian cancer

A

CA125 (over 35 IU/ml) - if raised then USS of abdo and pelvis
pelvic ultrasound

if asx dont do ca125.

diagnostic laparotomy

further ix:
ct - diagnosis and stage the cancer
histology- ct guided biopsy, laparoscopy or laparotomy
paracentesis (ascitic tap) - test for ascitic fluid for cancer cells.

women under 40 with complex ovarian mass require tumour markers for possible germ cell tumour:
- alpha-fetoprotein
-human chorionic gonadotropin

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47
Q

how would you manage ovarian cancer

A

combo of surgery and platinum based chemo

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48
Q

staging of ovarian cancer

A

FIGO

stage 1 - confined to ovary
2 - spread past ovary but inside pelvis
3 - spread past pelvis but inside abdo
4 - spread outside abdo

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49
Q

why might you get hip/groin pain with ovarian cancer?

A

ovarian mass press on obturator nerve.

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50
Q

types of ovarian cancer

A

epithelial cell tumour - serous tumour MC. endometrioid carcinoma,clear cell , mucinuous or undifferentiated tumours

dermoid cysts/germ cell tumours

sexcord stromal tumour

metastasis - from elsewhere. krukenberg tumour mets from gi cancer (Stomach). SIGNET RING cells on histology

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51
Q

factors that increase the number of ovulations increase the risk of ovarian cancer which include:

A

early onset of periods
late menopause
no pregnancies

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52
Q

higher number of lifetime ovulations increases the risk of ovarian cancer. factors that stop ovulation and reduce the number of lifetime ovulations reduce the risk which are:

A

coc pill
breastfeeding
pregnancy

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53
Q

what is prolactin?

primary function

A

hormone produced by anterior pituitary gland.

stimulate :
- glandular breast tissue development
- breast milk production

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54
Q

what factors stimulate prolactin production

A

nipple stimulation - suckling by baby

thyrotropin-releasing hormone (TRH) from hypothalamus

elevated oestrogen - during pregnancy

stress
sleep

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55
Q

what hormone inhibits prolactin effects on breast tissue?

A

progresterone.
prevents breast milk production during pregnancy.
after birth, progesterone levels fall rapid - allow prolactin to carry out its effects.

dopamin - inhibits prolactin secretion

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56
Q

what type of drug can cause prolactin to increase?

side effects

A

dopamine antagonist - antipsychotic meds

inhibit dopamine receptors

allow prolactin to rise

gyanaecomastia -
galactorrhoea - breast milk production

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57
Q

how does prolactin affect the breast tissue?

A

mamillary alveoli growth - where breastmilk is made and stored

breastmilk synthesis by epithelial cells of alveoli.

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58
Q

how does prolactin affect testes and ovaries?

A

prolactin inhibits gonadotropin-releasing hormone by hypothalamus.

inhibits HPA axis.
low GnRH = anterior pituitary produces less LH and FSH resulting in:

  • reduced stimulation of testes in men = low testosterone production
  • reduced stimulation of ovaries in women = absent ovulation, absent periods
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59
Q

is exclusively breastfeeding enough for contraception?

A

breastfeeding have high prolactin levels
cause anovulation and amenorrhoea

but just breastfeeding aint enough

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60
Q

causes of hyperprolactinaemia

A

pregnancy breastfeeding
prolactinomas - prolactin-secreting tumours of pit gland
hypothyroid
meds - dopamin antagonists
pcos
acromegaly: 1/3
stress,exercise,sleep

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61
Q

high prolactin sx

A

galactorrhoea
menstrual irregularities, amenorrhoea
infertility

reduced libido
ED
gynaecomastia

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62
Q

hypoprolactinaemia - side efects

causes

A

cant produce breastmild in postpartum.

tumours
surgery
radiotherapy
sheehans syndrome

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63
Q

what is sheehans syndrome

A

comp of postpartum haemorrhage
drop in circulating blood vol
avascular necrosis of pit gland.

low bp and reduced perfusion of pit gland = ischaemia in pit cells and cell death.

only affects anterior pit gland.

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64
Q

what is a prolactinoma?

classifying pit adenomas

A

type of pit adenoma - benign tumour of pit gland.

size - microadenoma less than 1cm and macroadenoma over 1cm

hormonal status - secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma doesnt produce hormone to excess

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65
Q

features of prolactinoma

A

excess prolactin in woman - amenorrhoea, infertility, galactorrhoea, osteoporosis.

excess prolactin in men - impotence, loss of libido, galactorrhoea

other sx may be seen with macroadenomas:
- headache
-visual disturbances - bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia
- sx and sx of hypopituitarism

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66
Q

how would you diagnose prolactinoma

A

MRI

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67
Q

how would you manage prolactinoma?

A

sx pts: dopamine agonist - cabergoline, bromocriptine - inhibit release of prolactin from pit gland

surgery: if cant tolerate or fail to respond to above.

trans-sphenoidal .

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68
Q

what drugs can cause raised prolactin?

A

metoclopramide, domperidone
phenothiazines
haloperidol

very rare: SSRI, opioids

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69
Q

What is a hydatidiform mole?

2 types

A

tumour grows like a pregnancy inside uterus.

complete mole - 2 sperm cells fertilise empty ovum with no genetic material. - no fetal material will form.

partial mole - 2 sperm cells + normal ovum at same time. 3 sets of chromosomes. some fetal material will form

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70
Q

hydatidiform mole?

differences from normal pregnancy

A

behaves like normal pregnancy
periods stop
hormonal changes or pregnancy will occur.

vs normal pregnancy?
- more severe morning sickness
-vaginal bleed
-increased enlargement of uterus
-abnormally high hCG
- thyrotoxicosis ( hCG mimic TSH and stimulate the thyroid to produce excess T3/T4)

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71
Q

would you diagnose hydatidiform mole?

A

ultrasound of pelvis - snowstorm appearance

histology of mole after evacuation

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72
Q

how would you manage hydatidiform mole?

A

evacuation of uterus

histology send to confirm.

refer pt to gestational trophoblastic disease centre.

hcg levels monitored until returned to normal.

sometimes mole can metastasise - if so systemic chemo

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73
Q

features of hydatidiform mole

A

vaginal bleeding
uterus size greater than expected for gestational age
abnormally high serum hCG
US: snow storm - mixed echogenicity

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74
Q

What are fibroids?
who they occur in more?
sensitive to what

4 types

A

benign tumours of smooth muscle of uterus.
20% white and 50% black women in later productive years

oestrogen sensitive

  • intramural - within myometrium (uterus muscle) - grown, change shape of uterus
  • subserosal - below outer layer of uterus. grow outwards become very large fill abdo cavity.
  • submucosal - below lining of uterus (endometrium)

-pedunculated - on a stalk

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75
Q

how would fibroids present?

rare feature and why?

A

often asx

heavy menstrual bleeding - MC - can lead to iron def anaemia
prolonged menstruation- longer than 7 days
lower abdo pain- worse during menstruation - cramping

bloating/feeling full in abdo
urinary/bowel sx - frequency due to pelvic pressure or fullness (larger)
subfertility

deep dyspareunia
reduced fertility

rare: polycythaemia - secondary to autonomous production of erythropoietin

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76
Q

what might a abdo and bimanual exam reveal in fibroids?

A

palpable pelvic mass or enlarged firm non-tender uterus.

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77
Q

how would you investigate fibroids?

A

hysteroscopy - initial - submucosal fibroids presenting with heavy menstrual bleeding.

pelvic uss - larger fibroids
transvaginal uss

MRI - before surgery - see size shape and blood supply of fibroid

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78
Q

how would you manage fibroids? if less than 3cm

A

if less than 3cm:
- mirena coil (levonorgestrel intrauterine system) - 1st line - no distortion of uterus and less than 3cm.
- sx mx : nsaids and tranexamic acid
- coc pill
- cyclical oral progesterones or injectale

surgery for smaller fibroids with heavy bleeding:
- endometrial ablation
-resection of submucosal fibroids during hysteroscopy
-hysterectomy

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79
Q

how would you manage fibroids if more than 3cm?

A

refer to gynae

sx : nsaids and tranexamic acid

mirena coil - depnds on size and shape of fibroids and uterus

COC PILL
cyclical oral progesterones

surgery:
uterine artery embolisation
myomectomy
hysterectomy

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80
Q

before surgery to remove fibroids what might you give the pt?

how it works?

A

GnRH agonist : goserelin or leuprorelin.

reduce the size of it.

induces menopause like state.(hot flushes, vaginal dryness) and loss of bone mineral density
reduces oestrogen.

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81
Q

what is a myomectomy?

A

surgery
remove fibroid laparoscopic or laparatomy.

improve fertility in fibroid pts.

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82
Q

what is endometrial ablation?

how does it work?

A

destroy endometrium.

baloon thermal ablation.

insert baloon into endometrial cavity
fill with high temp fluid.
burns endometrial lining

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83
Q

what is a hysterectomy?

A

remove uterus and fibroids

laparoscopy , laparotomy or vaginal approach.

may remove ovaries depends on pt preference , risk/benefits

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84
Q

what potential complications are there in fibroids?

A

heavy menstrual bleed : iron def anaemia

reduced fertility

pregnancy comps: miscarriage, premature labour, obstructive delivery

constipation
urinary outflow obstruction, uti

red degeneration of fibroid

torsion of fibroid - pedunculated more affected

malignant change to a leiomyosarcoma - very RARE

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85
Q

what does it mean by red degeneration of fibroids?

what size of fibroid does it affect more?

sx
mx

A

ischaemia infarction and necrosis of fibroid.

larger fibroids over 5 cm

2nd and 3rd trimeter of pregnancy.

happens when it gets bigger in pregnancy and outgrows its blood supply and becomes ischemic.

sx:
- severe abdo pai
-low grade fever
-tachy
-often vomiting.

mx:
- supportive
-rest-
-fluids and analgesia

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86
Q

What is endometriosis?

A

ectopic endometrial tissue outside the uterus.

lump of it = endometrioma - if in ovaries : chocolate cysts.

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87
Q

what does it mean by adenomyosis?

A

endometrial tissue in myometrium - muscle layer of uterus

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88
Q

aetiology of endometriosis

A

-genetic?

  • during menstruation, endometrial lining flow back through fallopian tubes and out into pelvis and peritoneum - RETROGRADE MENSTRUATION. - tissue then seeds itself around pelvis and peritoneal cavity.
  • cells outside uterus undergo metaplasia - from typical cells into endometrial cells
  • spread of endometrial cells through lymphatic system
  • embryonic cells remain in areas outside uterus during fetus development and later develop into ectopic endometrial tissue
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89
Q

Pathophysiology of endometrial tissue

A

Pelvic Pain : endometrial tissue sheds and bleeds regardless of whereit is. irritation and inflammation caused. CYCLICAL, DULL HEAVY OR BURNING PAIN.

deposits of endometriosis in bladder or bowel = blood in urine/stools

adhesions: scar tissue binding organs. chronic pain sharp stabbing.

fertility: issues due to blocked/damaged reproductive organs.

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90
Q

when you examine a pt with endometriosis what will be your findings?

A

endometrial tissue visible in vagina on speculum exam - particularly in posterior fornix (nodularity)

reduced organ mobility,

fixed cervix on bimanual exam

tenderness in vagina, cervix and adnexa

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91
Q

what sx would you see in endometriosis?

A

can be asx

cyclical abdo or pelvic pain
deep dyspaerunia
dysmenorrhoea
infertility/subfertility
cyclical bleeding from other sites: haematuria

cyclical sx:
- urinary sx - dysuria urgency
- bowel sx - dyschezia (painful bowel movement)

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92
Q

how would you be able to make a diagnosis of endometriosis?

A

Pelvic Ultrasound : large endometriomas and chocolate cysts. refer to gynae for laparoscopy

laparoscopic surgery : GOLD STANDARD.

definitive with biopsy of lesions during laparoscopy.
surgeon can remove deposits of it and potentially improve sx too.

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93
Q

how do you stage endometriosis?

A

ASRM

1 - small superficial lesions
2 - mild , deeper lesions than stage 1
3 - deeper lesions - lesions on ovaries and mild adhesions
4- deep and large lesions affect ovaries with extensive adhesions

94
Q

how would you manage endometriosis?

A

initial: ice , diagnose, explain, analgesia

hormonal mx before laparoscopy
COC pill
progesterone only pill
medroxyprogesterone acetate injection - depo-provera
nexplanon implant
mirena coil
GnRH agonist

surgical:
- laparoscopic surgery - excise or ablate endometrial tissue and remove adhesions(ahesiolysis)
- hysterectomy and bilateral sapingo-opherectomy - final surgery option. - removing ovaries induces menopause and stops the ectopic endometrial tissue responding to menstrual cycle.

95
Q

which tx in endometriosis improve fertility and which doesnt?

A

laparoscopic tx improves it.
hormonal might improve sx but not fertility .

96
Q

how do these tx options for endometriosis help?

A

cyclical pain tx with hormonalmeds - stop ovulation and reduce endometrial thickening.
it gets better when menopause happens so you can induce menopause using GnRH agonists like goserelin and leuprorelin

97
Q

give 2 examples of GnRH agonists and theyre function

side effects of what it induces?

A

goserelin
leuprorelin

induce menopause. - menopause like state.

shut down ovaries temporarily

side effects of menopause:
hot flushes
night sweats
risk of osteoporosis.

98
Q

what is endometrial cancer?

mc type

dependent on anything?

rf?

A

cancer of endometrium- lining of uterus.

mc: adenocarcinoma.

oestrogen dependent cancer.

obesity
diabetes
age
early onset of menstratuion
late menopause
oestrogen only HRT
no/fewer pregnancies (nulliparity)
PCOS
tamoxifen
hereditary non-polyposis colorectal carcinoma

99
Q

what is endometrial hyperplasia? (endometrial cancer)

2 types

tx

A

precancerous condition.
thickening of endometrium.

normally go back to normal over time.

2 types:
hyperplasia without atypia
atypical hyperplasia

tx: progesterones:
- intrauterine system - mirena coil
-continuos oral progesterones - medroxyprogesterone or levonorgestrel

100
Q

name 3 protective factors of endometrial cancer

A

multiparity
coc pill
smoking
mirena coil

101
Q

features of endometrial cancer

A

postmenopausal bleeding

if pre:
menorrhagia or intermenstrual bleeding
pain aint common - signifies extensive disease
vaginal discharge - UNUSUAL
haematuria , anaemia, raised platelet count

102
Q

how would you manage endometrial cancer?

A

surgery
localised: total abdo hysterectomy with bilateral salingo-oophorectomy

if high risk: postoperative radiotherapy

if frail elderly: progesterone therapy

103
Q

how would you investigate for endometrial cancer?

A

transvaginal uss - endometrial thickness - normal is less than 4mm post-menopause

pipelle biopsy : highly sensitive.

hysteroscopy+ endometrial biopsy

104
Q

what to use to stage endometrial cancer

A

FIGO

105
Q

on average how much blood do women lose during menstruation?

excessive would be?

how would you know its too much?

A

40ml

80ml

changing pads every1-2 hrs - bleeding lasting more than 7 days and passing large clots.

106
Q

causes of heavy menstrual bleeding

A

dysfunctional uterine bleeding - no identifiable cause
extremes of reproductive age
fibroids
endometriosis and adenomyosis
PID
contraceptives esp copper coil

anticoag meds
bleeding disorders - von willebrand

endo - dm and hypothyroid
connective tissue disorders

endometrial hypersplasia/cancer/pcos

107
Q

pt has heavy bleeding what investigations to do?

A

pelvic exam with speculum and bimanual - assess for fibroids, ascites, cancers

fbc - iron def anaemia

outpatient hysteroscopy: submucosal fibroids, endometrial pathology, intermenstrual bleeding

pelvic and transvaginal uss : - large fibroids, adenomyosis if hysterescopy declined

swabs - sti hx?
coagulation screen
ferritin
thyroid tests

108
Q

how would you manage treat heavy menstrual bleeding?

A

if doesnt want contraception:
tranexamic acid - if no pain - antifibrinolytic - reduces bleeding

below both 1st day of period:

mefenamic acid 500 mg tds - if pain - nsaid or tranexamic acid 500mg tds

if contraception accepted:
- mirena coil - 1st line
- coc pill
- cyclical oral progesterones - norethisterone 5 mg 3 time day from day 5-26. - VTE RISK AND PROGESTERONIC SE.

progesterone only contraception: suppress menstruation. -depo or implant

final option: endometrial ablation and hysterestomy.

109
Q

what can be used to stop heavy menstrual bleeding?

A

noresthisterone 5mg tds

short term

110
Q

MC type of cervical cancer

strong association with which virus.

when do kids gets vaccinated for it?

A

squamous cell carcinoma
adenocarcinoma

human papillomavirus

12-13

111
Q

HPV associated with which types of cancers?

2 important types and explain role in cancer.

A

anal
vulval
vaginal
penis
mouth
throat

type 16 and 18. p53 and pRb - tumour supressor genes. e6 inhibits p53 and e7 for pRb. e6 and e7 inhibits these tunour suppressors

112
Q

risk factors of cervical cancer

A

increased risk of catching hpv:
- early sex activity
- increase no. of partners.
-sexual partners who have had more partners
- not using condoms

non-engagement with cervical screenin.

smoking
hiv
coc pill - more than 5 yrs
increased full term pregnancies
fhx

exposure to diethylstilbestrol during fetal development

113
Q

presentation of cervical cancer

A

cervical smear for asx women

abnormal vaginal bleeding (intermenstrual, postcoital or post-menopausal)
vaginal discharge
pelvic pain
dyspareunia

these sx are non -specific so you exam cervix with speculum.
take swab to exclude infection

114
Q

what you see on colposcopy for cervical cancer?

A

ulceration
inflammation
bleeding
visible tumour

115
Q

what is cervical intraepithelial neoplasia?

how is it diagnosed?

how is it graded?

A

dysplasia - pre malignant of cervix.

colposcopy

1: mild - 1/3 thickness of epithelial layer affected - go back to normal without tx

2: moderate - 2/3 - likely to progress to cancer if untx.

    • severe : very likely to progress to cancer if untx.
116
Q

another way of CIN III (cervical intraepithelial neoplasia)

A

cervical carcinoma in situ

117
Q

how to screen for cervical cancer?

how is it done?

what is the process called?

A

smear test.

speculum exam and collect cells using brush and put into preservation fluid.

check for precancerous change (dyskaryosis)

called : LIQUID BASED CYTOLOGY

118
Q

when a smear test is done by liquid based cytology, what is the sample tested for?

A

high risk HPV. - if negative not examined.

119
Q

how often do you do cervical screen program

A

every 3 years aged 25-49

every 5 years 50-64

EXCEPTIONS:
- hiv - screen annually
- over 65 can request.
- previous CIN can require more tess

  • immunocomprised
  • pregnant women due should wait until 12 weeks post partum
120
Q

from cytology, ie a cervical smeer what results can come up?

A

inadequate
normal
borderline changes
low grade dyskaryosis
high grade dyskaryosis - mod/sevee
possible invasive squamous cell carcinoma
possible glandular neoplasia

can clock bv, candiadiasis and trichomonas on smear too

121
Q

what organisms can be found in women with intrauterine device on smeer?

tx

A

actinomyces-like organisms.

no tx unless sx.

if sx: remove device.

122
Q

mx based of cervical smeer results

A

inadequate - repeat after 3 months min

hpv negative - continue routine screening

hpv positive with normal cytology - repeat hpv test after 12 months

hpv positive with abnormal cytology - refer for colposcopy

123
Q

what is colposcopy?

A

insert speculum - then use colposcope to magnify cervix.

use
acetic acid: abnormal cells appear white. - acetwhite! - happens in CIN and cervical cancer cells.

schillers iodine test: iodine to stain cervix cells.
healthy cells : brown. abnormal wont stain

punch biopsy/large loop excision of transformational zone : done to get tissue sample

124
Q

what is a large loop excision of the transformation zone?

A

loop biopsy.
local anaesthetic.

loop of wear with electrical current to remove abnormal epithelial tissue on cervix. - cauterise tissue and stop bleeding.

125
Q

rules for large loop excision >

A

bleeding and abnormal discharge can occur for several weeks after.

intercourse and tampon use to be avoided.

126
Q

a consquence of large loop excision of transformation zone?

A

increase preterm labour risk

127
Q

what is a cone biopsy?

how its done?

main risks

A

tx of CIN.
general anaesthic.

cone shaped piece of cervix using scalpel removed. - assess for malignancy

pain,bleeding,infection,scar formation with stenosis of cervix, increased risk of miscarriage and premature labour

128
Q

staging of cervical cancer

A

figo

1a: confined to cervix visible my microscopy less than 7mm :
A1: less than 3mm deep
A2: 3-5MM deep

1b: confined to cervix visible clinically larger than 7 mm:
- B1: less than 4cm diameter
-B2: over 4cm

2: extension of tumour beyond cervix but not to pelvic wall:
A- upper2/3 of vagina
B - parametrial involvement

3: - extension of tumour beyond cervix and to pelvic wall
A - lower 1/3 of vagina
B= pelvic side wall.
(if causing hydronephrosis or nonfunctioning kidney its stage 3

4: extension of tumour beyond pelvis or involvement of bladder or rectum.
A: bladder or rectum involved
B - distant sites outside pelvis involved

129
Q

how would you manage cervical cancer? (1A)

A

gold: hysterectomy +/- lymph node clearance

if maintain fertility : cone biopsy with negative margins

for A2:
nodal clearance
node evaluation
radical thrachelectomy (poss)

130
Q

what is pelvic exenteration?

A

for advanced cervical cancer

remove most pelvic organs:
vagina
cervix
uterus
fallopian tubes
ovaries
bladder
rectum

implications of QoL

131
Q

what is bevacizumab (avastin?

what is it used for?

what cells does it target?

it treats something else too ? what is it?

A

monoclonal antibody

used with chemos to treat metastatic or reccurent cervical cancer.

targets vascular endothelial growth factor A - (VEGF-A) - development of new blood vessels.

wet age related macular degeneration

132
Q

HPV vaccine

when is it given

what is it called

which strains cause genital warts
which strains cause cervical cancer

A

girls and boys before they have sex.

prevent contracting and spreading it.

GARDASIL - protects on strains 6 11 16 18

6 and 11 - genital warts
16 18 - cervical cancer

133
Q

if endocervical cells are infected what cells can develop ?

tell me its characteristics?

A

koilocytes

enlarged nucleus

irregular nuclear membrane contour

nucleus stains darker than normal (hyperchromasia)

perinuclear halo poss

134
Q

how would you manage stage 1b tumours for cervical cancer?

A

B1: radiotherapy + chemo

radio: either bachytherapy or external beam

cisplatin - chemo

B2: radical hysterectomy with pelvi lymph node dissection

135
Q

how would you manage stage 2 and 3 cervical cancer tumours?

A

radiaiton+ chemo

if hydronephrosis: nephrostomy poss

136
Q

how would you manage stage 4 cervical cancer tumours?

A

ridation and or chemo

palliative chemo poss best option

137
Q

how would you manage cervical cancer recurring disease?

A

primary surgical tx: chemo or radiation

primary radiation: surgical therapy

138
Q

complications of cervical cancer tx surgeries?

A

standard:
bleeding
damage to local structures
infection
anaesthetic risk

cone biopsy and radical trachelectomy: increase risk of preterm birth in future pregnancy.

radical hysterectomy: poss ureteral fistula

139
Q

complications of radiotherapy

A

short:
- diarrhoea
- vaginal bleeding
-radiation burns
-pains on micturition
- tired/weak

long term:
- ovarian failure
-fibrosis of bowel skin bladder vagina
- lymphoeda.

140
Q

how would you treat endometrial cancer?

A

total abdominal hysterectomy with bilateral salpingo-ooporectomy : TAH and BSO : removal of uterus cervix and adnexa.

other:

radical hysterectomy : remove pelvic lymph nodes surrounding tissues and top of vagina

radio
chemo

progesterone: hormonal tx - slow cancer progression

141
Q

MC type of vulval cancer

risk factors for it?

A

squamous cell carcinoma.

less common malignant melanoma

rf:
- age over 75
-immunosuppressed
-hpv 16 and 18
herpes simples virus 2
- lichen sclerosus

142
Q

what is vulval intraepithelial neoplasia?

2 types

A

premalignant affecting squamous epithelium of skin .

high grade squamous intraepithelial lesion: associated with HPV - younger women 35-50

differentiated VIN: associated with lichen sclerosus and occurs in older women 5-60

143
Q

how would you diagnose VIN?

tx

A

biopsy punch or excisional for histology

hpv testing PCR or in situ hybridisation for high risk HPV DNA

watch and wait
wide local excision
imiquimod cream
5 Fluorouracil : topical chemo agent
laser ablation/wide local excision/partial vulvectomy if extensive.

monitor with colposcopy and biopsy if recurring

144
Q

how does vulval cancer present_

A

incidental finding during catheterisation in pt with dementia

vulval lump
ulceration
bleeding
pain
ithcing
lymphadenopathy in groin INGUINAL

145
Q

what area of the vulva does vulval cancer affect mostÑ

what appearance does it give_

A

labia majora

irregular mass
fungating lesion
ulceration
bleeding

146
Q

how would you investigate for vulval cancer_

A

2 week wait urgent refer

biopsy of lesion
sentinel node biopsy ‘ check lymph node spread

further imagine for staging ‘ CT ABDO AND PELVIS

147
Q

how do you stage vulval cancer

A

FIGO

148
Q

mx of vulval cancer

A

wide local excision
groin lymph node dissection
chemo
radio

149
Q

What is atrophic vaginitis?

why?

who does it happen in ?

A

dryness and atrophy of vaginal mucosa

lack of oestrogen

genitourinar sx of menopause.

occurs in women entering meno

150
Q

pathophysiology of atrophic vaginitis

A

epithelial lining of vagina and urinary tract responds to oestrogen by becoming thicker more elastic and producing secretions.

women enters meno
oestrogen levels fall
mucosa: thinner,less elastic dry.

prone to inflam.

vaginal ph change (ph over 4.5)
microbial flora change

151
Q

how does oestrogen help with atrophic vaginitis?

A

oestrogen helps maintain healthy connective tissue around pelvic organs

lack of oestrogen contribute to pelvic organ prolapse and stress incontinence.

152
Q

presentation of atrophic vaginitis

A

itching
dryness
dyspareunia
bleeding due to localised inflammation

occasional spotting

153
Q

women comes in with recurrent uti , stress incontinence or pelvic organ prolapse.

what am i thinking?

tx

A

atrophic vaginitis

tx: topical oestrogen

154
Q

examination of atrophic vaginitis pt will reveal?

A

pale mucosa
thin skin
reduced skin folds
erythema and inflammation
dryness
sparse pubic hair

155
Q

how would you manage atrophic vaginitis?

A

vaginal lubricants : help dryness - SYLK,REPLENS, YES.

topical oestrogen:
- estriol cream - syringe at night
- estriol pessaries - inset bedtime
- estradiol tabs - vagifem - once day.
- estradiol ring - estring - replace every 3 months

156
Q

topical oestrogen contraindicatiosn

A

same as systemic HRT

breast cancer
angina
VTE.

poss long term use: endometrial hyperplasia/cancer.

monitor annually

157
Q

What is lichen sclerosus?

presenttion : main

where is affects most:

associations:

how to confirm diagnosis?

A

chronic inflammatory skin condition

porcelain white shiny skin patches

labia, perineum,perianal skin. - axilla/thighs (women)

foreskin and glans (men)

autoimmune

t1dm
alopecia
hypothyroid
vitiligo

vulval biopsy

158
Q

presentation of lichen sclerosus

A

45-60 vulval itching and skin changes in vulva. can be asx or:

itching
soreness - pain worse at night
skin tightness
dyspareunia
erosions
fissures

159
Q

what is the koebner phenomenon?

happens with which condition?

what can make it worse?

A

signs and symptoms made worse by skin friction.

happens with lichen sclerosus

tight underwear that rubs skin, urinary incontinence and scratching

160
Q

Appearance of lichen sclerosus

A

changes affecting labia perianal and perineal skin.

associated fissures cracks erosions or haemorrhages under skin.

porcelain white colour
shiny tight thin
slightly raised
could be papules/pustules

161
Q

how would you manage lichen sclerosus?

A

cant be cured.

mx and followed up every 3-6 months.

potential topical steroids - clobetasol propionate (0.05% dermovate) - reduce risk of malignancy.

once a day for 4 weeks.
then reduce every 4 weeks to alternate days then twice weekly.

if flare start again .

30g tube should last 3 months min.

use emoilents too.

2nd line: topical calcineurin inhibitors
topical retinoids

162
Q

comps of lichen sclerosus

A

5% risk of getting squamous cell carcinoma of vulva.

pain and discomfort
sex dysfunction
bleeding
narrowing of vaginal or urethral openings

163
Q

What is Asherman’s Syndrome?

A

adhesions form in uterus - after damage to uterus.

164
Q

When might Asherman’s Syndrome occur?

A

after pregnancy related dilatation and currettage procedure eg in treatment of retained products of contraception.

uterine surgery - mymectomy

pelvic infection - endometritis

165
Q

how can endometrial curettage (scraping) cause asherman’s syndrome?

what happens when the adhesions are formed?

A

damage basal layer of endometrium.

damaged tissue might heal abnormal.
scar tissue - adhesions
connecting areas to uterus.

might bind uterine walls together or within endocervix sealing it shut.

form physical obstructions and distort pelvic organs -so you get menstruation abnormalities, infertility and recurrent miscarriages.

166
Q

presentation of ashermans syndrome

A

following recent dilatation and curettage, uterine surgery, endometritis with:

  • secondary amenorrhoea
    -significantly lighter periods
  • dysmenorrhoea

poss intertility.

167
Q

how would you diagnose ashermans syndrome?

A

hysteroscopy - gold : can involve dissection and tx of adhesions

hysterosalpingography - constrast injected into uterus and imaged with xrays

sonohysterography - uterus filled with fluid and a pelvic uss performed

MRI

168
Q

how would you manage ashermans syndrome?

reacurrance?

A

dissect adhesions during hysteroscopy.

reoccurance: common

169
Q

What is Adenomyosis?

more common in ?

A

endometrial tissue in myometrium - muscle layer of uterus

later reproductive years
several pregnancies.

hormone dependent.

sx resolve after menopause similar to endometriosis and fibroids

170
Q

presentation of adenomyosis

A

painful period - dysmenorrhoea

heavy periods - menorrhagia

pain during intercourse (dyspareunia)

1/3 asx
can present with infertility or pregnancy-related comps.

171
Q

what will examination of adenomyosis show?

A

ENLARGED AND TENDER UTERUS.

MORE SOFT THAN A UTERUS WITH FIBROIDS.

172
Q

how would you diagnosis adenomyosis?

A

transvaginal ultrasound of pelvis : 1st line

MRI and transabdominal uss - alternative if above not suitable.

gold: histological exam of uterus after hysterectomy.

173
Q

how would you manage adenomyosis?

A

if women dont want contraception : use these during menstruation for sx relief:

  • tranexamic acid - no associated pain

mefenamic acid - if pain

if contra acception:
- mirena - 1st line
-coc pill
- cyclical oral progesterone

progesterone only meds like pill,implant,depot poss good?

others:
endometrial ablation
uterine artery embolisation
hysterectomy
GnRH analogues - induce menopause-like state

174
Q

what is tranexamic acid?

A

antifibrinolytic - reduce bleeding

175
Q

what is mefenamic acid

A

nsaid - reduce bleeding and pain

176
Q

in terms of pregnancy what can happen with adenomyosis?

A

infertility
miscarriage
preterm birth
small for gestational age
preterm premature rupture of membranes

need for c section
postpartum haemorrhage

177
Q

what is menopause?

A

when menstruation stops in women.

12 months after last period in women over 50
24 months after last period before 50.

(effective contraception for both)

178
Q

Symptoms of menopause

change in periods
vasomotor
urogenital
psychological
longer term comps

A

sx seen in climacteric period are caused by reduced levels of female hormones : oestrogen mainly.

change in periods:
- change in length of menstrual cycles
- dysfunctional uterine bleeding

vasomotor: 80% women. daily and can continue for 5 yrs
- hot flushes
-night sweats

urogenital: 35%
- vaginal dryness and atrophy
- urinary frequency

psychological:
- anxiety + depression - 10%
short term memory impairement

longer term comps:
-osteoporosis
-increased risk of IHD

179
Q

different terms for menopause condition

A

menopause - when menstruation stops

post menopause - 12 months after final menstrual period

perimenopause - time around menopause experiencing vasomotor/irregular periods. last period to 12 months after. 45+

premature menopause -before 40. caused by premature ovarian insufficiency

180
Q

what is menopause caused by?

A

lack of ovarian follicular function

changes in sex hormones :

oestrogen and progesterone levels are low

LH and FSH are high - in response to absence of negative feedback from oestrogen.

181
Q

how would you manage perimenopausal sx?

A

vasomotor sx will resolve after 2-5 yrs without any tx.

mx:
- HRT
-Tibolone - synthetic steroid hormone - continous combined HRT - only after 12 months of amenorrhoea

  • CBT
    -SSRI eg fluoxetine or citalopram

-testosterone - reduced libido tx - gel/cream

-vaginal oestrogen cream/tablet - dryness and atrophy

vaginal moisturiser - SYLK,REPLENS,YES

  • clonidine - agonist of alpha adrenergic and imidazoline receptors
182
Q

good contraceptive options approaching menopause

A

barrier methods
mirena/copper coil
progesterone only pill

progesterone implant
progesterone depot injection (under 45)
sterilisation

coc pill : 40-50. containing norethisterone or levonorgestrel in women over 40. - low risk of VTE

183
Q

side effect of depot - contraception

A

weight gain
reduced bone mineral density - osteoporosis.

184
Q

in terms of contraception, when do women need to use it relative to menopause?

A

2 yrs after last menstrual period in women under 50.

1 yr after last menostrual period in women over 50.

185
Q

how would you diagnose menopause?

A

women over 45 with sx - no ix.

FSH blood test to help in:
women under 40 with premature

women 40-45 with menopausal sx or change in menstrual cycle.

186
Q

lack of oestrogen increases risk of what conditions?

A

cv disease and stroke

osteoporosis

pelvic organ prolapse

urinary incontinence

187
Q

HRT RISKS

A

VTE

stroke - with oral oestrogen hrt

coronary heart disease- combined hrt

breast cancer

ovarian cancer

188
Q

What is androgen insensitivity syndrome?

genetic

A

x linked recessive

end organ resistance to testosterone causing genotypically male children (46XY) to have female phenotype.

189
Q

features of androgen insensitivity syndrome

A

primary amenorrhoea

little/no axillary and pubic hir

undescended testes causing groin swellings

breast development - testosterone to oestradiol conversion

190
Q

how would you diagnose androgen insensitivity syndrome?

A

buccal smear or chromosomal analysis reveal - 46XY genotype

after puberty: testosterone conc high-normal to slightly elevate reference for postpubertal boys

191
Q

how would you manage androgen insensitivity syndrome?

A

counselling - raise child female

bilateral orchidectomy - testicular cancer risk bc of undescended testes

vaginal dilators or vaginal surgery - create adequate vaginal length.

oestrogen therapy

192
Q

if i was to do hormone test for androgen insensitivity syndrome what would come up?

A

raised lh
normal/raised fsh
normal/raised testosterone levels - male
raised oestrogen levels - male

193
Q

when and how does androgen insensitivity syndrome present?

A

in infancy

inguinal hernias containing testes.
or
puberty with primary amenorrhoea.

194
Q

what is partial androgen insensitivity syndrome?

presentation

A

cells partial response to androgens.

micropenis
clitoromegaly
bifid scrotum
hyposapdias
diminshed male characteristics

195
Q

what dont pts with androgen insensitivity have and what do they have?

A

have testes - in abdo or inguinal cancal

no uterus upper vagina cervix fallopian tube and ovaries.

196
Q

if androgen insensitivity syndrome why dont female internal organs develop?

A

testes produce anti-mullerian hormone.

prevents males from getting upper vagina uterus cervix fallopian tubes.

197
Q

Physiology of menopause

A

decline in development of ovarian follicles.

reduced oestrogen production.

negative feedback on pituitary gland not happening, so increased levels of LH and FSH.

anovulation

irregular menstrual cycles.

endometrium doesnt develop - amenorrhoea

198
Q

what is premature ovarian insuffiency?

A

onset of menopausal sx and high gonadotrophin levels before 40.

199
Q

causes of premature menopause

A

idiopathic - mc cause - fhx

bilateral oophorectomy - having hysterectomy with preservation of ovarian has also been shown to advance age of menopause

radio
chemo
infection: mumps
autoimmune
resistant ovary syndrome: due to fsh receptor abnormalities

200
Q

features of premature ovarian syndrome

A

climactreric sx: hot flushes , night sweats
infertility
secondary amenorrhoea

raised fsh,lh levels
fsh over 30
elevatred fsh on 2 blood samples 4-6 weeks apart.

low oestradiol : under 100 pmol/L

201
Q

how would you manage premature ovarian syndrome?

A

hrt or combined oral contraceptive - until 51 (menopase)

hrt doesnt give contraception in case sponaneous ovarian activity resumes.

202
Q

Explain the hypothalamic-pituitary gonadal axis in women

A

hypothalamus releases GnRH

that stimulates anterior pituitary to release lh and fsh

lh and fsh stimulate follicle development in ovaries.

cause theca granulosa cells to secrete oestrogen, which negatively feed back to hypothalamus and AP, reducing LH and FSH levels.

203
Q

What is oestrogen and what does it stimulate?

A

steroid sex hormone (17-beta oestradiol is main active version)

  • breast tissue development
  • growth and development of female sex organs (vulva,vagina,uterus) at puberty
  • blood vessel development in uterus
  • development of endometrium
204
Q

What is progesterone and what does it stimulate?

A

steroid sex hormone produced by corpus luteum after ovulation.

in pregnancy produced by placenta from 10 weeks gestation onwards.

acts on tissues previous stimulated by oestrogen?

  • thickens and maintains endometrium
    -thickens cervical mucus
    -increases body temp
205
Q

what age does puberty occur in girls, how long does it last and in what sequence do changes occur?also why does low weight delay puberty.

what staging is used

A

8-14 yrs
4yrs

growth spurt/breast buds, pubic hear, menarche

aromatase found in adipose tissue helps create oestrogen.

more aromatase (Fat) = earlier puberty. low birth weight, chronic disease/ED, athletic hence cause cause delays.

Tanner staging (under 10, no pubic hear or breasts =1 )

206
Q

2 phases of menstrual cycle

A

follicular phase - start of menstruation to ovulation - 1st 14 days

luteal phase - ovulation to start of menstruation - final 14 days

207
Q

what are ovarian follicles?

A

oocytes are cells that have potential to develop into eggs. surrounded by granulosa cells , forming follicles.

primary follicles are always maturing into primary and secondary follicles.

when they reach secondary, they grow FSH receptors, which when stimulated, cause granulosa cells to secrete oestradiol. (oestrogen)

208
Q

Describe the follicular phase

A

Low oestrogen and progesterone causes endometrium shedding and bleeding.

FSH stimulates secondary follicles, causing them to grow, and for surrounding granulosa cells to secrete oestrogen. This reduces LH and FSH production (negative feedback). Rising oestrogen also causes cervical mucus to become more permeable, allowing sperm to penetrate cervix around ovulation.

One follicle will develop more than the rest (dominant follicle) LH spike causes dominant follicle to release an ovum. Ovulation occurs 14 days before end of cycle.

Overall: FSH stimulates oestrogen, which spikes ~day 12. There is an LH spike right before ovulation causing an ovum to release.

209
Q

Describe luteal phase

A

The follicle that released the ovum collapses, becoming the corpus luteum. This secretes progesterone, maintaining the endometrial lining. It also causes the cervical mucus to become thick.

If pregnancy: the syncytiotrophoblast of the embryo secretes Human Chorionic Gonadotrophin (HCG), maintaining the corpus luteum.

Without fertilisation the corpus luteum degenerates and stops producing oestrogen and progesterone. This fall causes breakdown of the endometrium and menstruation. The stromal cells in the endometrium release prostaglandins, causing uterus contractions. The fall in Oestrogen and Progesterone causes an increase in LH and FSH, restarting the cycle.

Menstruation marks day 1 of the menstrual cycle.

210
Q

What is amenorrhoea? Give primary and secondary causes?

A

failure to establish menstruation at 15 with normal sexual development and 13 without.

Primary
- Gonadal dysgenesis (e.g. Turners)
- Hypogonadotrophic hypogonadism (deficiency of LH and FSH), Hypergonadotrophic hypogonadism (lack of response to LH and FSH by gonads)
- Pregnancy

Secondary - 3-6 months amenorrhoea when previously normal
- Hypothalamic (secondary stress, excessive exercise)
- PCOS
- Thyroid disease
- Hyperprolactinaemia

211
Q

mc gynae malignancy in developed world

A

endometrial carcinoma

90% adenocarcinomas

212
Q

endogenous and exogenous sources of unopposed oestrogen

A

Endogenous
- Chronic anovulation (e.g. PCOS)
- Aromatisation of androgens
- Granulosa cell tumours

Exogenous unopposed oestrogen
- HRT
- Selective oestrogen receptor modulators (tamoxifen)

213
Q

How can these cysts rupture, and what is a ruptured ovarian cyst

A

Can occur spontaneously or in response to physical activity such as vigorous exercise, intercourse, or trauma.

Common emergency characterised by sudden severe lower abdo pain.

214
Q

presentation of ruptured ovarian cyst

A

Severe unilateral sharp lower abdo/pelvic pain, radiates to back or thigh.
Rebound tenderness, guarding and rigidity
Haemodynamic instability, caused by intraperitoneal bleeding. (Tachycardia, hypotension, pallor, diaphoresis, syncope)
Fever
Nausea and Vomiting

215
Q

What cancers are caused by BRCA 1 and 2

A

BRCA1 - Breast/ovarian (Chromosome 17)
BRCA2 - Breast, Prostate, Ovarian (C13)

Autosomal dominant

216
Q

What guidelines are used to indicate whether a person is eligible for different types of contraception

A

The FSRH UKMEC (Faculty of Sexual and Reproductive Healthcare UK Medical Eligibility) Guidelines 2016.

1: No restriction
2: Benefits outweigh risks
3: Risks generally outweigh benefits
4: Unacceptable - Contraindicated

217
Q

What are the 3 most effective contraceptions

A

Surgery (sterilisation/vasectomy)
Coils (Copper coil/Mirena coil)
Progesterone only implant
> 99% Under both typical and perfect use

218
Q

What are some specific risk factors to keep an eye out for when prescribing contraception

A

Any hormonal contraception - Breast cancer
Any coil - Cervical/endometrial cancer
Copper coil - Wilsons disease

219
Q

What are some COCP contraindications (UKMEC 4)

A

Uncontrolled HTN (>160/100)
Migraine with aura
History of VTE or vascular disease/stroke
> 35y AND smoking >15 cigs
Major surgery with immobility
Liver cirrhosis
SLE/antiphospholipid syndrome
Heart disease/ AFib

220
Q

What are some contraception considerations in over 50s

A

After the last period keep contraception for 2 years if under 50 and 1 year if over 50
COCP can be used up to 50
Progesterone injection should be stopped <50y due to osteoporosis risk

221
Q

What does MEN 1 cause and what its pattern of inheritance?

A

Autosomal dominant

Parathyroid adenoma
Pituitary prolactinoma or acromegaly
Pancreatic endocrine tumours

222
Q

What does men2a cause

A

medullary thyroid cancer

pheochromocytoma

primary hyperparathyroidism

223
Q

what does men 2b cause

A

medullary thyroid cancer
pheochromocytoma
mucosal neuromas

224
Q

Risk factors of hyperemesis gravidarum

A

increased levels of beta-hcg:
- multiple pregnancies
-trophoblastic disease

nulliparity
obesity
fhx personal hx of NVP

SMOKING DECREASED INCIDENCE

225
Q

TRIAD OF HYPEREMESIS GRAVIDARUM

A

5% pre-pregnancy weight loss
dehydration
electrolyte imbalance

226
Q

Management of hyperemesis gravidarum

A

simple:
- rest avoid trigger
-bland plain food in morning
-ginger
- p6 wrist acupressure

1st line:
antihistamine : oral cyclizine or premethazine

phenothiazines: oral prochlorperazine or chlorpromazine.

2nd line:
- oral ondansetron
- oral metoclopramide or domperidone: max 5 days meto bc extrapyramidal se.

admission for iv hydraiton: normal saline with added potasium

227
Q

oral ondansetron as 2nd line tx of hyperemesis gravidarum - side effect

A

increased risk of cleft lip/palate.

228
Q

complications of hyperemesis gravidarum

A

dehydration
weight loss
electrolyte imbalances

aki
wernickes
oesophagitis, mallory weiss
vte

229
Q

when to consider admission for hyperemesis gravidarum?

A

n+ v continued - cant keep liquid or oral antiemetics down

continued n+ v with ketonuria and/or wt loss (over 5%) despite oral antiemetics

comorbidity? like cant tolerate abx for uti

230
Q

what is ovarian hyperstimulation syndrome?

A

seen in some infertility tx.

multiple leutinized cysts in ovaries = high oestrogen and progesterone and vegf.

increased membrane permeability and loss of fluid from intravascular compartment.

231
Q

when is ovarian hyperstimulation syndrome seen?

A

following gonadotropin or hcg tx.

1/3 of ivf women

232
Q

classifying ovarian hyperstimulation syndrome?

A

mild : abdo pain and bloating.

moderate. n+v and uss of ascites. + mild

severe: moderate + clinical ev of ascites.
oliguria.
haematocrit over 45%
hypoproteinemia

critical : severe. thromboembolism.

ards
anuria
tense ascites

Phase 3a Finals (25 decks)

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