Obs and Gynae Flashcards
(338 cards)
What are the phases of the menstrual cycle
Follicular phase
- Increasing FSH and LH - stimulate primary follicle growth, secretion + conversion of androgens to oestrogens and inhibin section.
- this increases oestrogen - starts to inhibit FSH - dominant follicle grows
- once reaches maturity oestrogen ↑↑ –> LH surge –> follicle rupture
Luteal phase
- remaining follicle become corpus luteum
- Progesterone ↑ - maintain conditions for fertilisation and implantation
- if not fertilised - corpus luteum spontaneously regresses (PG cut of blood supply) - ↓ Oest & prog –> menses
- if fertilised - syncytiotrophoblast of embryo will produce hCG –> maintain endometrium (prod progesterone)
Phases of the uterine cycle
Proliferative Phase (same time as follicular - prepare for fertilisation) - Oestrogen fallopian tube formation, thickening of endometrium, ↑ growth and motility of myometrium and produce thin alkaline cervical mucus (to facilitate sperm transport)
Secretory Phase (along luteal phase) - Progesterone further thickening of the endometrium (glandular secretory form + development of spiral A.) and the myometrium; ↓ of motility of the myometrium (don’t want contractions); thick acidic cervical mucus production (prevent polyspermy); ↓ fallopian tube motility, secretion and cilia activity; changes in mammary tissue and other metabolic changes; elevates basal body temperature.
What is the menopause
The end of the reproductive life - the ovarian follicles are depleted and there has been amenorrhoea for 12 months.
Usually between the ages of 45 and 55y/o.
2 FSH levels >30IU/L - suggestive
Symptoms of menopause
• Menstrual irregularity - cycles become anovulatory, before stopping
• Vasomotor disturbance—sweats, palpitations, and hot flushes (peripheral vasodilation and a transient rise in body temp)
• Atrophy of oestrogen-dependent tissues (genitalia, breasts, bladder and urethra) and skin. Vaginal dryness can lead to vaginal and urinary infection, dyspareunia, traumatic bleeding, stress incontinence, and prolapse.
• Osteoporosis: ↓ oestrogen –> ↑ osteoclast activity –> acceleration of age related loss of bone density and ↑ frequency in # - femur, neck, radius and vertebrae
• Oest. is protective effect against IHD (↓ LDL + ↑ HDL)
Other: Joint stiffness/soreness; dizzy; interrupted sleep; anxiety; reduced concentration; irritable/ mood swings
Management of menopause
Lifestyle
o Stop smoking, healthy diet, exercise + weight loss,↓ stress, ↓ caffeine/spicy food/ alcohol
o Stay cool at night; Vaginal lubrication
o Annual BP, breast checks
HRT
- oestrogen only (if had hysterectomy)
- cyclical - if still periods –>oestrogen every day then progesterone either last 14d of -cycle(reg)/ 3m (irreg)
- continous combined - if post-menopausal
o SSRI - for hot flushes
o Clonidine - ↓ hot flushes + night sweats (doesn’t affect hormone levels – no ↑ risk Ca)
SE –> dry mouth, drowsiness, depression and constipation
o Tibolone – agonist at oestrogen receptor – relieve symptoms (same risks HRT)
o Raloxifene (SERM) - protects bones, ↓ breast & endometrial ca risk (ineffective for flushes)
o Natural hormones not recommended as not regulated and effect not known
o Complementary therapies (be careful about ADR) Black cohost and st johns wart
o Alternative -acupuncture, reflexology, aromatherapy or homeopathy
o Psych - CBT - elevate low mood
Methods of administration, risks and benefits of HRT
Tablets; cream/pessary/ring (for vaginal dryness) ; transdermal e.g. patch/gel (dependent on skin conditions); implants (oestrogen/IUS)
Benefits
- Improves vaginal dryness and sexual function, reduces vaginal atrophy
- ↓ CV risk
- Improved QOL - Improves symptoms, sleep, mood, BMD, etc
- ↓ flushing frequency + severity
- ↓ CRC risk – combined
Risks
- ↑ Risk VTE (Stop 4 weeks pre-elective surgery)
- ↑ Risk ischaemic stroke (>60 y/o) – oral HRT
- ↑ Breast ca risk
(combined) ; after stopping HRT risk returns to normal. Encourage breast awareness. - Unopposed - ↑ Endometrial and ovarian Ca risk
CI and SE of HRT
CI
- Oestrogen-dependent Ca
- Past PE
- Undiagnosed PV bleeding
- LFT ↑
- Pregnancy
- Breastfeeding
- Phlebitis
SE
- Weight ↑
- ‘premenstrual’ syndrome
- cholestasis;
- vomiting
- muscle cramps
- irregular bleeding
What is an early menopause and what are the risk factors
Menopause - 40-45 y/o
Risk factors –> High BMI, FH, Early menarche, Low parity, hx oral contraceptive treatment
Ix and Mx of early menopause
Ix - FSH - > 40 Iµ/L x 2 (4-6 weeks apart)
Mx - HRT (may require higher oestrogen dose)
What is premature ovarian insufficiency and the cause.
Menopausal sx in women <40y/o - May be reversible
Cause - ↓ no. follicles at birth/ accelerated follicle atresia/ follicle or FSH R dysfunction
Sx, Ix, Mx and complications of POI
Sx - Amenorrhoea, ↑ gonadotrophins, ↓ Oestrogen (Hot flushes + vasomotor)
Ix - FSH x 2 raised (4-weeks apart) are diagnostic; Estradiol - low (<50 pmol/L)
o ? DEXA - Assess BMD and Tests for cause: Genetic karyotyping + Adrenal antibodies
Mx - MDT important to consider physical + psychological issues o Adcal D3 to prevent Osteoporosis and monitor CVD o HRT (cont/ cyclic) --> until age of natural menopause (~51 years old) with higher oest levels
Complications –> 80% greater chance of CV mortality, osteoporosis, Dementia
What are fibroids and describe the different types
benign growths of SM in the uterine myometrium
o Intramural (commonest) – confined to the myometrium of the uterus.
o Submucosal -immediately underneath the endometrium, protrudes into the uterine cavity.
o Subserosal - protrudes into and distort the serosal (outer) surface of the uterus. They may be pedunculated (on a stalk).
RF for fibroids
- Obesity
- Early menarche
- ↑ age
- FH
- African-American
Presentation of Fibroids
- Prolonged / HMB
- Pressure sx (e.g. urinary) ± abdo distension
- Chronic pelvic pain
- Subfertility (? Obstructive fibroid)
- Solid/ enlarged uterus – smooth, non-tender
Differentials of abnormal uterine bleeding
PALM - COEIN PALM: Structural Causes - Polyp (endometrial/cervical) - Adenomyosis - Leiomyoma (Fibroid) - Malignancy & hyperplasia
COEIN: Nonstructural Causes
Coagulopathy (esp vW)
Ovulatory dysfunction (↓ T3/4; PCOS; ↑ prolactin)
Endometriosis - <5%
Iatrogenic (IUD; TCA; warfarin; hormones)
Not yet classified (AV malformation)
Differential for enlarged uterus
Uterine Fibroids Pregnancy/ Molar pregnancy Haematoma Leiomyosarcoma/ endometrial carcinoma Adenomyosis
Extra-uterine Ovarian cyst Ovarian malignancy Ectopic pregnancy Pyosalpinx Hydrosalpinx Primary fallopian tube neoplasm Pelvic abscess CRC Bladder carcinoma
Investigations for enlarged uterus
- Pregnancy test/ ßHCG levels
- Bloods – FBC; iron studies, TFT; FSH+LH; oestrogen
- Pelvic USS – Confirm fibroids diagnosis and size
- ?MRI
Management of Fibroids
Medical - If Sx
- NSAIDs / Tranexamic acid/ mefenamic acid – may reduce bleeding
- Hormonal contraception –> COCP; POP; Mirena – control menorrhagia
- GnRH agonists – ↓ fibroid size within a few months – use pre-op– use 6m only (risk osteoporosis). Often recur after stopping the medication.
- Ulipristal acetate –>↓ size of fibroid and menorrhagia – use pre-op
Surgical
- Myomectomy (excise fibrois S.E blood loss; adhesions; C-section)
- Hysterectomy
- Hysteroscopy and transcervical resection of fibroid (submucosal fibroids)
Radiological
UAE (Uterine artery embolisation) - occlude vascular supply to fibroid
Complications of fibroids
- Recurrent miscarriage
- Iron deficiency anaemia
- Bladder / bowel symptoms
- Torsion (penduculated fibroid)
- Acute pelvic pain in pregnancy (red degeneration) - rapidly growing fibroid undergoes necrosis and haemorrhage
In pregnancy - Premature labour; PPH; Hydronephrosis; fetal malpresentation; IUGR
Pathophysiology of PCOS
Endocrine disorder –>excess androgen production and the presence of multiple immature follicles (“cysts”) within the ovaries.
↑ pulse frequency GnRH –> Excess LH –> ↑androgens –> testosterone)
o Suppress LH surge - no ovulation
o Follicles develop but arrested in early stage - ovarian cysts
o Unopposed oestrogen - ↑ risk endometrial hyperplasia
o Insulin resistance - ↑ levels insulin secretion –> suppress hepatic production SHBG –> higher levels of free circulating androgens.
RF and presentation of PCOS
Risk factors –> DM; Irregular menstruation; FH
Presentation
- Amenorrhoea / Oligomenorrhoea
- Weight gain/ obesity (+Insulin resistance
- -> Acanthosis nigricans)
- Masculinisation (Hirsutism, acne, male-pattern hair-loss)
- Chronic pelvic pain
- Depression (and other psychological symptoms)
- Infertility
Differentials for PCOS
- Hypothyroidisism
- Hyperprolactinaemia
- Cushing’s disease
- CAH
Ix for PCOS
Rotterdam Criteria - 2 out of 3
1) Oligo- ± anovulation
2) Clinical ± biochemical signs of hyperandrogenism
- ↑ test + LH and ↓ SHBG +prog
- ↑ 3:1 LH:FSH
3) USS –> Polycystic ovaries - ≥ 12 peripheral ovarian follicles ± ovarian volume >10 cm3 (string of pearls)
Consider oral glucose tolerance test (esp if BMI >30).
Mx of PCOS
Treat underlying DM; HTN; dyslipidaemia and OSA
Oligomenorrhoea/Amenorrhoea
• Low dose COCP – control bleeding and ↓ risk unopposed oestrogen
• Dydrogesterone – a progesterone analogue –> withdrawal bleed (~3monthly)
Obesity -Aim BMI <30 - will help trigger regular menstrual cycle.
- Healthy diet, exercise to ↑ insulin sensitivity, smoking cessation
- In severe cases –> orlistat (pancreatic lipase inhibitor) can be prescribed.
Hirsutism
- Cosmetically ± with anti-androgen medication (cyproterone, spironolactone or finasteride) - avoided during pregnancy as teratogenic.
- Eflornithine (topical cream) - ↓ growth rate of facial hair.
Fertility
• 50mg Clomifene (Selective oestrogen R modulator) –>induce ovulation- 50-60% conceive in 6m
- ↑ risk multiple pregnancies, ovarian hyperstimulation syndrome, ovarian Ca (limit to 6 cycles)
• ± Metformin improves insulin sensitivity, helps menstrual disturbance and ovulatory function (recommended up BMI >25 and want to conceive)
• Women with a normal BMI could also benefit from laparoscopic ovarian drilling ( reduce test, and increase FSH - ovulate)