Obs and gynae Flashcards
(321 cards)
1
Q
How does endometriosis present?
A
Infertility
Depends on location:
Pain (often chronic pelvic pain 6 months) - cyclical or constant due to adhesions, severe dysmenorrhoea (can be due to adenomyosis), deep dyspareunia (indicates involvement of uterosacral ligaments), dysuria, dyschezia and cyclic pararectal bleeding, fatigue
-oxford handbook
2
Q
What causes endometriosis?
A
The most popular theory is retrograde menstruation with adherence, invasion and growth of the tissue. Metaplasia of endometrial cells, systemic and lymphatic spread, and impaired immunity also contribute.
Most common sites are pelvis.
-oxford handbook
3
Q
How is endometriosis diagnosed?
A
Bimanual pelvic exam for adnexal masses (endometriomas) or tenderness
Transvaginal USS - endometriomas, urinary bladder/rectal involvement
Laparoscopy with biopsy - positive is confirmative, negative does not exclude.
4
Q
How is endometriosis treated?
A
Pain: COCP, NSAIDs
Fertility: surgical removal or endometriotic lesions.
5
Q
Give 5 causes of pelvic pain.
A
Obstetric: Ectopic pregnancy, fibroid red degeneration
Gynae: ovarian cyst accident eg torsion, PID, endometriosis, mittelschmerz, adhesions
GI - appendicitis, hernia strangulation, IBD, IBS
Urological - UTI, renal/bladder calculi
6
Q
Give 3 risk factors for ectopic pregnancy.
A
History of PID Prev ectopic IVF Gynae surgery tubal ligation IUD in situ Smoking Age >35 Black race Age <18 at first sexual intercourse
7
Q
Why is ectopic pregnancy a medical emergency?
A
Internal bleeding, severe pain and damage to the fallopian tube. The pregnancy pushes against the fallopian tube walls and can rupture. The blood irritates the peritoneum, which can cause referred pain to the shoulder.
8
Q
What investigations are done when ectopic pregnancy is suspected?
A
hCG - this doubles every 2 days in uterine pregnancy. Suboptimal rise is suspicious (not diagnostic) of EP. The rate of change is important.
Serum progesterone
Group and save
Rhesus
transvaginal ultrasound to look for uterine pregnancy, adnexal masses or free fluid.
9
Q
How is ectopic pregnancy managed?
A
If they are stable, asymptomatic, understand the symptoms and complications, can use expectant and medical management.
Expectant: body sorts it out. Repeat serum hCG 48hourly - should be falling.
Medical: methotrexate 50mg/m2 IM single dose.
Surgical: Laparotomy in haem unstable patients, salpingectomy (remove entire fallopian tube) if contralateral tube normal, salpingotomy if contalateral tube disease.
Anti-D in rhesus negative patients.
Admit if lives far away from hosp.
10
Q
What are the risk factors for pelvic inflammatory disease?
A
Young, poor, sexually active, multiple partners unprotected sex, nulliparous. Almost never occurs during viable pregnancy.
11
Q
What causes pelvic inflammatory disease?
A
Infection with chlamydia or gonococcus, 40% polymicrobial.
12
Q
How does PID present?
A
Chlamydia - asymptomatic, symptoms may be due to secondary infection, or present with subfertility or menstrual problems.
Gonococcus - acute.
Bilat lower abdo pain with deep dyspareunia, vaginal bleeding and discharge.
Peritonism –> bilateral adnexal tenderness, cervical excitation (pain on moving cervix during the exam).
If spread to the liver via the peritoneum, you get Fitz-Hugh-Curtis syndrome, cuases RUQ pain due to adhesions.
13
Q
How is PID diagnosed?
A
Clinical diagnosis supported by swabs and blood cultures if fever, raised WCC and CRP.
Pelvic USS excludes abscess or ovarian cyst
Laparoscopy with fimbrial biopsy and culture ‘gold standard’ but not typically performed.
14
Q
How would you manage PID? What about if the lady has a recently inserted IUS?
A
Analgesia
Broad spec: IM ceftriaxone (covers gonorrhea), oral doxycycline (covers chlamydia) and metronidazole (covers trichomonas). Dont delay for swabs.
Febrile –> IV therapy.
Review in 24 hours - if not improved, there may be pelvic abscess. Rupture can be life-threatening.
Admit if fever >38 degrees.
Coils:
Leave in a recently inserted coil. If there is no response within 48-72hrs to the antibiotics, remove the coil and prescribe any other necessary emergency contraceptives
15
Q
What are the non-pathological causes of amenorrhoea?
A
Primary (never had periods) - alway pathological
Secondary (periods stopped) pregnancy. lactation, menopause, contraceptives (COCP etc)
16
Q
What are the pathological causes of amenorrhea?
A
Primary - hypogonadism (either due to hypothalamus/pituitary (hypogonadotropic) or gonads (hypergonadotropic)
Secondary:
- PCOS
- Anorexia nervosa
- Hyperprolactinaemia (usually a pituitary adenoma, 30% have galactorrhea)
- Hypo/hyperthyroidism. Hypo = raised prolactin, amenorrhea
- Cushing’s syndrome
- Premature ovarian insufficiency
- Meds - antidepressants, antipsychotics
17
Q
How does PCOS present?
A
Galactorrhea, androgenic sx (eg facial hirsutism, weight gain, acne)
18
Q
What is Asherman’s syndrome?
A
Aka iatrogenic intrauterine adhesions, due to excessive curettage at evacuation of retained products of conception (ERPC) procedure following miscarriage or delivery.
19
Q
What is Turner’s syndrome? Give 3 features.
A
Absent X chromosome (45XO). short stature, poor secondary sexual characteristics, webbed neck, bicuspid aortic valve.
Normal intelligence.
20
Q
What are the clinical features of prolactinoma?
A
Amenorrhoea Galactorrhoea Headache Bitemporal hemianopia Diabetes insipidus --> polydipsia, polyuria.
21
Q
How is prolactinoma diagnosed?
A
Imaging using CT/MRI, raised serum prolactin levels.
22
Q
What can cause hyperprolactinaemia?
A
Pituitary tumour Hypothalamus or pituitary stalk lesion Normal breastfeeding/pregnancy Hypothyroidism Chronic renal failure Drugs: phenothiazines, metoclopramide, methyldopa.
23
Q
What is the management of hyperprolactinaemia?
A
Dopamine receptor agonists (bromocriptine, cabergoline) which reduce prolactin levels. Occasionally, surgery. These need to be stopped in pregnancy. Avoid pregnancy until tumour shrunk, due to risk of enlargement in pregnancy.
24
Q
What is the most common endocrine disorder in women?
A
PCOS
25
What are the diagnostic criteria for PCOS?
Rotterdam criteria:
- exclude other disorders and two out of:
- Cycle >42 days
- Hyperandrogenism - acne, hirsutism, alopecia
- Polycystic ovaries on pelvic USS - >12 antral follicles on one ovary.
- Ovarian volume >10 ml
26
What causes PCOS?
Hypersecretion of LH in 60%. LH stimulates androgen secretion from thecal cells. Elevated LH:FSH.
Genetics - familial clustering
Insulin resistance with compensatory hyperinsulinaemia - defect on insulin receptor.
Hyperandrogenism - elevated ovarian androgen secretion
Obesity - BMI >30 in 35-60%, central obesity, worsens insulin resistance
27
How is PCOS managed?
1. Lifestyle - even 5% wt loss can improve sx, restore ovulation and improve fertility
2. COCP - reduces serum androgen levels by increasing SHBG.
Metformin
depilatory cream for hirsutism, antiandrogens such as finasteride
Need withdrawal bleed every 3-4 months to reduce risk of endometrial hyperplasia and cancer. This is stimulated by regular COCP or medroxyprogesterone.
28
What is the most common type of malpresentation?
Breech - 3-4% of births. (ox handbook)
29
How would you diagnose breech presentation?
```
On examination:
Lie is longitudinal
Head can be palpated at the fundus
Presenting part is not hard
Fetal heart is best heard high up in the uterus.
```
USS confirms diagnosis and should also assess growth and anatomy because of the association with fetal abnormalities.
30
How would you manage breech presentation?
1. Wait - 8% of primiparous breech presentations will revert by 36 weeks.
2. After 36 weeks for primiparous/37 for multiparous, use external cephalic version (ECV). Success rate 50%. Absolute Contraindications: C-section indicated, APH, pre-eclampsia, rhesus isoimmunization, oligohydramnios, fetal compromise (so basically ECV is everything is otherwise fine)
3. Anti-D if Rh -ve.
4. Vaginal birth indicated if no fetal compromise, EFW <4kg, spontaneous onset of labour, extended breech, non-extended neck.
5. Elective CS if any of the above.
31
What is the most favourable position for vaginal delivery?
Occipito-anterior: cephalic, longitudinal, limbs and head flexed. 95% of births.
Occiput means the BACK of the baby's head so occipito-anterior is face-down.
32
What causes malpresentations? Give 3 risk factors.
Maternal: Multiparous (lax uterus), uterine abnormalities eg fibroids, tumour/mass
Fetal: Fetal abnormality, multiple pregnancy, preterm labour (not enough time to turn)
Placental: placenta praevia, polyhydramnios
33
What are the risk factors for endometrial cancer?
Postmenopausal
high estrogen to progesterone ratio - pregnancy and COCP are protective.
Unopposed estrogen (ie, no protective effect of progesterone). This can be endogenous (eg obesity causes peripheral conversion in adipose tissue of androgens to estrogens, nulliparity) or exogenous (eg tamoxifen)
Ox handbook
34
Which is the most common cancer of the genital tract?
Endometrial carcinoma. Prevalence is highest around 60 years of age. (Impey)
35
What is the most common histological type of endometrial carcinoma and what is the prognosis like?
>90% are adenocarcinomas of columnar endometrial gland cells. Prognosis same as ovarian cancer but usually presents early so often wrongly thought as benign. Prognosis is poorer for the rarer histology type, adenosquamous carcinoma (<10% of cases) (Impey)
36
What are the stages of endometrial carcinoma?
1. Myometrial invasion in uterus (1A= <1/2, 1B= >1/2 myometrium invaded)
2. Cervical stromal invasion
3. Uterus invasion (3A=adnexae, 3B=vaginal, 3Ci=pelvic nodes, 3Cb = para-aortic)
4. Spread outside uterus (4A= bowel/bladder, 4B = distant mets)
(Impey and child)
37
How is endometrial carcinoma treated?
```
Chemotherapy:
Carboplatin +/- paclitaxel
or
Doxorubicin + cisplatin
(Ox handbook)
```
38
What is the prognosis like for breast cancer? Does pregnancy have an effect?
Poorer in young women. Pregnancy itself has no effect on prognosis.
39
How is breast cancer in a pregnant woman managed?
Chemotherapy safe after 1st trimester (12 weeks)
Tamoxifen and trastuzumab are contraindicated in pregnancy
Radiotherapy contraindicated unless life-saving.
40
Which genes are associated with breast cancer?
BRCA1 and 2 (also in ovarian cancer), TP53, ERBB2 aka HER2.
41
How is breast cancer treated?
It depends on the type.
ER+ve, HER2-ve =most common.
Selective ER modulator eg tamoxifen/fulvestrant.. If postmenopausal, use aromatase inhibitor eg anastrozole.
42
What are the signs of malignant breast lumps?
Hard, painless lump, commonly upper outer quadrant., may have axillary lymph node involvement, dimpling
43
What is Paget's disease of the breast?
An infiltrating carcinoma of the nipple epithelium which represents about 1% of breast cancers. (Patient.info)
44
How does Paget's disease of the breast most commonly present?
Chronic eczematous change of one nipple: Itching, erythema, scales, erosions, nipple discharge including bleeding. Underlying lump usually indicates invasive nature.
45
What is the pathophysiology of Paget's disease?
Malignant cells infiltrate into the epidermis via the mammary duct epithelium. The cells proliferate leading to thickening of the affected skin.
[patient.info]
46
How is Paget's disease managed?
Usually mastectomy, although recent reports suggest excision may be just as good.
47
Which forms of breast cancer are associated with Paget's disease?
Higher histo grade, estrogen receptor -ve, progesterone receptor negative breast cancers.
48
What is the most common type of breast lump?
Fibroadenoma (benign). [patient.info]
49
What is a fibroadenoma?
Benign tumour common in women age 20-24. They arise in breast lobules and are composed of fibrous and epithelial tissue. HRT increases incidence.
50
How does a fibroadenoma present?
Firm, non-tender, highly mobile palpable lump.
51
How would you manage fibroadenoma?
It is an unexplained lump so refer to breast clinic for triple assessment.
Surgical excision may be done if the lump is large or cancer is not excluded. Complex and multiple fibroadenomas are asso with increased risk of breast cancer.
52
What is 'triple assessment' in breast clinic?
Examination
Imaging (USS <40, mammography >40)
Core needle biopsy
53
What is an abscess?
A collection of pus. Pus is a thick, yellow/green, smelly fluid that contains WBCs, dead tissue and bacteria. .
54
What can cause a breast abscess?
Mastitis (infection of the breast) can develop into an abscess. It is usually associated with lactation (puerperal mastitis). Breast ducts become blocked with milk, and bacteria (usually staph aureus) enter from cracks in the nipple.
55
How can you differentiate an abscess from other breast lumps?
There is inflammation, so the area is red, tender, and warm, and the cyst will be soft and filled with fluid.
56
How is puerperal mastitis managed?
First-line is reassurance, increase milk removal, and analgesia.
If no improvement after 24 hours, use penicillinase-resistant abx - flucloxacillin/erythromycin.
57
What is placental abruption?
Separation of part or all of the placenta from the uterine wall before delivery. This causes bleeding, further distress and separation.
58
Why does placental abruption occur?
The arteries of the decidua basalis degenerate which attach the placenta to the uterine wall. Risk factors: previous abruption, IUGR, pre-eclampsia, smoking, autoimmune disease, multiple pregnancy, high parity and age. Cocaine/amphetamines --> vasoconstriction --> high blood pressure, arterial rupture.
59
What are the complications of placental abruption?
Acute fetal distress, causing fetal death in 30%.
| Maternal death rarely occurs, due to transfusion, DIC and renal failure
60
How does placental abruption usually present?
Acute onset severe abdo pain, constant with exacerbations. Often dark blood (revealed) but in 20% there is no bleeding (concealed)
Bleeding amount does not correlate to abruption severity.
Shock: tachycardia, hypotension in late stage.
Uterine contractions, may be in labour, tender, late stage: woody and hard.
Fetal heart tones abnormal/absent
61
How is placental abruption managed?
Admit (all women with unexplained bleed/pain), CTG, USS, IV access, bloods (FBC, u+e, crossmatch, coag screen).
Then if no fetal distress, bleeding and pain stop, can consider delivery by term
If fetal distress/maternal compromise, resuscitate and deliver.
62
What are the 4 conditions needed for pregnancy to occur?
```
Ovulation
Sperm release
Sperm reach egg
Blastocyst implantation
(impey+child)
```
63
Give 3 causes of subfertility in a woman.
Ovarian - PCOS, POF
Hypothalamic - hypothalamic hypogonadism, Kallmann's syndrome - no GnRH-secreting neurones
Pituitary - hyperprolactinaemia.
Endometriosis (implantation problem)
Tubal damage causing fertilisation problem
Chlamydia - 12% will be infertile after having it once
Low/high BMI, smoking
64
How is ovulation best detected?
Regular cycles, discharge, pelvic pain are suggestive of ovulation. This is confirmed by high serum progesterone, ultrasound. Over-the-counter urine LH kits can also be used.
65
What are the causes of male factor subfertility?
```
Drugs
Varicocoele
Antisperm antibodies
Infection eg epididymitis
Klinefelter's syndrome - 47XXY karyotype
Smoking
Insufficient local cooling
Cystic fibrosis
```
66
What is clomifene used for and how does it work?
Induce ovulation in someone with PCOS as a fertility treatment. Anti-estrogen, works by blocking estrogen receptors in the hypothalamus and pituitary. Given AFTER lifestyle advice eg losing wt.
(Impey)
67
What is azoospermia?
No sperm in ejaculate. Usually managed with surgical IVF and intra cytoplasmic sperm injection (ICSI).
68
What hormone is elevated in testicular failure?
FSH
69
What initial investigations would you do for oligo/azoospermia?
CF screen: Check for congenital bilateral absence of the vas deference (CBAVD), due to CFTR mutation.
47XXY karyotype
hormone profile: FSH is elevated in testicular failure
70
How would you manage oligo/azoospermia?
Treat underlying conditions
Address lifestyle issues - alcohol, smoking
Review meds - antispermatogenic eg anabolic steroids, antiandrogenic (cimetidine, spironolactone), erectile/ejaculatory (a/b-blockers, antidepressants)
71
Give an example of an antispermatogenic substance.
Alcohol
Anabolic steroids
Sulfasalazine
72
Why might a man with heart failure have subfertility?
They may be on spironolactone which is anti-androgenic.
73
Give 3 drugs which can cause ejaculatory/erectile dysfunction.
Antidepressants eg sertraline
alpha or beta blockers
diuretics
metoclopramide (antiemetic)
74
How would you manage subfertility in a man with a varicocoele?
Surgery is not indicated as it does not improve pregnancy rates. Use other management.
75
What is Kallmann's syndrome?
Failure of the GnRH-secreting neurones to develop, causing hypogonadism.
76
What is IVF and what are the indications?
External (in vitro) fertilisation of the sperm and oocyte. Tubal disease, male factor subfertility, endometriosis, anovulation, unexplained
77
What is IUI and when is it done?
Intrauterine insemination. Mild male factor subfertility, same-sex, unexplained, coital difficulties.
78
What is ICSI and when is it done?
Intracytoplasmic sperm injection. Men with severely abnormal semen parameters.
79
What are the side-effects of induction of ovulation?
Risk of multiple pregnancy with gonadotrophins (FSH/LH) and clomifene, but not with metformin.
80
What causes functional cysts?
Follicular cysts are persistently enlarged follicles, lutein cysts are enlarged corpora lutea. In pregnancy, the CL continues to secrete progesterone, which inhibits LH. If there is no fertilisation, the CL should dissolve to become the corpus albicans. If the follicle fails to rupture (follicular) or ruptures but closes again (lutein) the CL does not dissolve so continues to make LH.
81
How do ovarian masses generally present?
They usually don't cause symptoms until there is an 'ovarian accident' like haemorrhage, rupture or torsion or they are detected on a scan.
82
What could cause intense acute pain in someone with an ovarian cyst?
Ovarian torsion - this could cause infarction to the ovary +/- tube, needs urgent surgery and 'detorsion' (untwisting).
Rupture - particularly with endometrioma or dermoid cyst
Haemorrhage - if into peritoneal cavity could cause hypovolaemic shock
83
How are primary ovarian tumours classified?
Not strictly split into benign vs malignancy because benign primary cysts can become malignant
a) epithelial:
- serous or mucinous cystadenoma (benign)
- serous or mucinous adenocarcinoma (malignant)
- Endometrioid carcinoma (malignant)
- Clear cell carcinoma (malignant)
b) Germ cell:
- Teratoma/dermoid cyst (benign, common)
- Dysgerminoma (malignant, rare/young women)
c) sex cord tumours:
- granulosa cell tumours (malignant but slow-growing)
- thecoma (benign)
- fibroma (benign)
84
What is meant by 'borderline malignancy'?
Unique to ovarian epithelial tumours, malignant histological features are evident but invasion is not. Surgery is advised but controversial.
[Impey]
85
Which type of ovarian tumour is most common in postmenopausal women?
Epithelial.
86
What is the most common malignant ovarian neoplasm?
Serous adenocarcinoma (50% of malignancies). Mucinous are less likely to be malignant (10%) but can become very large.
87
What is a clear cell carcinoma?
Malignant ovarian epithelial tumour, accounts for <10% of ovarian malignancies, poor prognosis.
88
Which kind of ovarian tumour secretes oestrogen and inhibin?
Granulosa cell tumours, a type of sex cord tumour. Post-menopausal women. Serum inhibin is used as a marker for recurrence. Usually malignant but slow-growing.
89
What is Meig's syndrome?
Rare syndrome associated with fibroma, where you get ascites and (usually) right pleural effusion with small ovarian mass (fibroma). The effusion is benign and cured by removal of the mass.
[Impey]
90
Which two cancers have a particularly high risk of mets to the ovary?
breast
| GI tract
91
What is a chocolate cyst?
Accumulation of old blood in endometrioma.
92
Which type of cysts are more likely in pre-menopausal women?
```
Functional cysts (follicular/lutein) only in pre-menopausal because they are enlarged follicles/corpora lutea.
Also dermoid cysts and endometriomas are more likely in pre-menopausal women.
```
93
How are functional cysts treated?
OCP inhibits ovulation so reduces risk
lutein cysts tend to cause more symptoms
If no symptoms, no treatment. However, malignancy is excluded by doing Ca125 if tumour persists beyond 2 months and is >5cm. Laparoscopy may be done to remove or drain the cyst.
94
Who is screened by the NHS breast screening programme?
High risk women eg those with BRCA
| All women over 50.
95
What is ductal carcinoma in situ?
A pre-malignant change.
'DCIS means that some cells in the lining of the ducts of the breast tissue have started to turn [cancerous] These cells are all contained inside the ducts.'
Cancer research UK.
96
What causes urinary incontinence?
1. URGE incontinence: overactivity of detrusor muscle
2. Stress incontinence: Weakness of pelvic floor and sphincter muscles causing LEAKS when coughing, laughing etc. Women
3. Mixed - address whichever is having the more significant impact first.
4. Overflow incontinence: have they been in retention? Males, anticholinergics, tumours, MS, DM, spinal cord injuries.
[Z2F]
97
What investigations would you do for urinary incontinence?
Bladder diary over at least 3 days
Urine dipstick
Post void residual bladder volume bladder scan - to assess for incomplete emptying
Urodynamic testing if not responding to treatment.
98
How is stress incontinence managed?
1. Avoid caffeine, diuretics, overhydration and dehydration, wt loss if appropriate
2. Supervised pelvic floor exercises 3 months
3. Surgery or Duloxetine (SNRI).
99
How is urge incontinence managed?
1. Bladder retraining
2. Anticholinergic - oxybutynin, solifenacin, tolterodine
3. Mirabegron (b-3 agonist - increases BP)
4. Invasive procedures eg botox, nerve stimulation, urinary diversion, bladder enlargement.
100
What is uterine prolapse?
A type of prolapse where the uterus descends into the vagina. Prolapse is due to weakness of pelvic ligaments and muscles.
101
What is vault prolapse?
Top of the vagina is called the vault. this descends into the vagina in women with no uterus (hysterectomy).
102
What is a rectocele?
Defect in POSTERIOR vaginal wall allowing RECTUM to prolapse forwards into vagina. Constipation, urinary retention, palpable lump in vagina that some women have to push back in order to open their bowels.
103
What is a cystocele?
Defect in the ANTERIOR vaginal wall allowing BLADDER to prolapse backwards into the vagina. Urethra prolapse = urethrocele. Both = cystourethrocele.
104
How would you investigate a pelvic organ prolapse?
Empty bladder and bowels.
Dorsal and left lateral position
Sims speculum (the U shaped one) - anterior wall, posterior wall.
Uterine prolapse: POP-Q grading 0-4
105
How is pelvic organ prolapse managed?
1. Conservative - physio (pelvic floor exercises), wt loss, lifestyle changes for stress incontinence, vaginal oestrogen cream
2. Vaginal pessary - ring, shelf, gellhorn. with estrogen cream to protect vaginal walls from irritation. change every 4 months.
3. Surgery
106
What is a fistula?
Abnormal connection between the urinary tract and other organs.
Urethro-vaginal,
Vesico(Bladder)-vaginal,
Vesico-uterine,
Uretero-vaginal.
Occur due to obstructed labour, surgery, radiotherapy or malignancy.
107
What investigation would you do in a woman presenting with urinary incontinence, labial swelling and urine coming form the vagina?
This could be urethral injury eg urethrovaginal fistula. CT urogram or cystoscopy.
[OH]
108
What are fibroids and how are they classified?
Common, benign tumours of the smooth muscle of the uterus, aka uterine leiomyomas. Estrogen-sensitive so they grow in response to estrogen.
1. Intramural: within the myometrium --> distort shape
2. Subserosal - outer layer of uterus, fill abdo cavity
3. Submucosal - inner lining of uterus
4. Pedunculated - on a little stalk so could be intra- or extra-uterine.
109
How would fibroids present and what are 3 risk factors to look for in the history?
Asymptomatic, HMB, long heavy painful periods, bloating, reduced fertility. Abdo/bimanual exam - mass or enlarged firm non-tender uterus.
Black women
Later reproductive years
110
What imaging is used to diagnose fibroids?
1. Hysteroscopy for submucosal fibroids presenting with HMB.
2. Pelvic USS for larger fibroids
(MRI before surgery to determine size, shape and blood supply)
111
How are fibroids managed?
1. < 3 cm - medical management as for HMB. IUS (Mirena). symptomatic - NSAIDs, tranexamic acid, COC, cyclical oral progesterones
2. Surgery - endometrial ablation, resection of submucosal fibroids during hysteroscopy, hysterectomy.
>3cm: as above (1) and refer to gynae.
GnRH agonists to reduce size before surgery.
Rx for HMB is different to rx for infertility. If treating for infertility, myomectomy is the only effective rx.
112
What are the important complications of fibroids?
```
Red degeneration
Torsion, especially with pedunculated fibroids.
Malignant change (rare)
HMB - iron def anaemia
reduced fertility
pregnancy complications, prem labour, miscarriage
Constipation
urinary outflow obstruction, UTIs
```
113
A woman is 24 weeks pregnant presenting with severe abdominal pain and low grade fever, tachycardia and vomiting. She was treated for fibroids in the past. What could be the diagnosis?
Red degeneration of the fibroid: ischemia, infarction and necrosis due to disrupted blood supply. In larger fibroids, 2nd and 3rd trimester of pregnancy. It enlarged during pregnancy, outgrowing its blood supply and becoming ischemic.
Rx: rest, fluids, analgesia.
Exclude torsion.
[Z to F]
114
What can cause vulval itching and shiny white patches on the labia, perinium and perianal area in a 50 year old woman?
Lichen sclerosis. This is due to chronic autoimmune inflammation. Associated with other autoimmune disease - T1DM, alopecia, hypothyroid and vitiligo.
Dx clinical but can do vulval biopsy to confirm.
115
What is the difference between lichen sclerosis, lichen simplex and lichen planus?
Lichen sclerosis = autoiummune disease causing white shiny skin patches especially on the genitals.
Lichen simplex = inflammation and irritation caused by scratching and rubbing the skin, causing plaques, scaling and thickened skin.
Lichen planus = autoimmune condition causing shiny, purplish flat-topped raised areas with white lines across the surface.
116
How is lichen sclerosis managed?
Potent topical steroids eg clobetasol propionate 0.05% (dermovate). Reduce risk of malignancy and symptoms.
Start daily then gradually reduce to twice weekly, titrate up again in flares.
+ Emollients.
117
What are the important complications of lichen sclerosis?
5% risk of developing squamous cell carcinoma of the vulva.
| Pain, discomfort, sexual dysfunction, bleeding, narrowing of the vaginal or urethral openings.
118
How is cervical cancer prevented?
Screening - majority diagnosed at stage 1, 90% survival.
| Vaccination against HPV high risk strains.
119
How is cervical cancer staged and treated?
FIGO I-IV.
Ia: LLETx/loop diathermy.
Ib: hysterectomy. consider age, fertility wishes, woman's choice.
II+ - radio, chemo, palliative.
120
Why is it important to examine older women with UTI not responding to treatment?
Examine the vulva/vagina for lichen sclerosis which may have progressed to vulval cancer. Ladies may not examine self esp if older.
121
How is vulval cancer treated?
Surgery
| Radiotherapy +/- chemo
122
What is the pathology of vulval cancer?
90% squamous cell carcinoma.
<10% malignant melanoma.
Rare. RFs: older age, immunosuppression, HPV, lichen sclerosus.
123
What investigations would you do in a 55 year old woman presenting with bloating, abdominal pain, and change in bowel habit?
```
Could be IBS but also could be ovarian cancer. Do Ca125, pelvic USS, ask about menopause.
Risk of malignancy index (RMI):
Menopausal status
USS findings
Ca125.
```
124
Give 3 risk factors for ovarian cancer.
More ovulation = higher risk. OLD NUNS would be at high risk.
Age, early menarche, late menopause, nulliparous, non breastfeeding, no contraception used, hysterectomy, clomifene excessive use, smoking.
125
How is ovarian cancer treated?
Surgery - if fit, may lead to permanent stoma. Late presentation - poor prognosis.
126
What is the aetiopathology of cervical cancer?
80% squamous cell carcinoma
<20% Adenocarcinoma
HPV 16 and 18.
Tumour suppressor genes: P53, pRb. HPV produces E6 and E7 which INHIBIT P52 and pRb respectively.
Ask about smears, number of sexual partners, FHx, smoking.
127
How is cervical cancer diagnosed?
Screening
but if someone presents with symptoms that you suspect could be cancer, do urgent colposcopy referral, NOT unscheduled smear/using the last smear.
128
What in cervical intraepithelial neoplasia (CIN)? What do each of the grades mean?
Grading system for dsyplasia (premalignant change) in cells of the cervix, diagnosed at colposcopy (not smear).
CIN I: mild dysplasia
CIN II: moderate dysplasia
CIN III: cervical carcinoma in situ. May still spontaneously return to normal, can recur after treatment, and can be associated with areas of CIN I in the same patient.
129
What is dyskaryosis?
Precancerous changes detected on cervical smear.
Graded as mild, moderate and severe.
If negative, reassessed to reduce risk of false negative
False positive can be due to benign abnormality.
130
What are the main outcomes of a smear test and how is each one managed?
Inadequate sample - repeat after 3 months
HPV neg - continue routine
HPV pos, normal cytology - repeat HPV test after 1 year
HPV pos, abnormal cytology - refer for colposcopy.
[z2f, PHE 2019]
131
What is the pathology of ovarian cancer?
1) Epithelial cell tumours - serous, mucinous.
2) dermoid cysts/germ cell - benign, teratomas. raised a-FB, hCG.
3) sex cord stromal tumours - rare.
4) Metastases - Krukenburg. Usually GI, stomach. Signet ring cells on histology.
132
What is vulval intraepithelial neoplasia and how is it treated?
Similar to CIN but premalignant cells of the vulval epithelium. Diagnose with biopsy. May need treatment with wide local excision, imiquimod cream or laser ablation, depending on biopsy, age etc.
133
What is the likely cause of a cancer in the vagina?
Metastasis from cervix or uterus, Primary is rare.
| HPV, older age.
134
What is a hydatidiform mole? What causes it?
A tumour that grows like a pregnancy inside the uterus. Aka molar pregnancy. 2 types:
Complete: 2 sperm cells fertilise an empty ovum (no genetic material). No fetal material will form, just a tumour.
Partial: 2 sperm cells fertilise a normal ovum at the same time, so the new cell has 3 sets of chromosomes. some fetal material may form.
135
When would you suspect molar pregnancy and how would you diagnose/exclude it?
Normal pregnancy plus severe morning sickness, vaginal bleeding, enlarged uterus, v high hCG, thyrotoxicosis as hCG stimulates thyroid.
USS: 'snowstorm appearance'.
Histology of the mole confirms dx.
136
How is molar pregnancy managed?
```
Evacuation to remove mole
Send for histology to confirm dx
Refer woman to GTD centre for follow up.
Monitor hCG until return to normal
Mole may metastasise in which case systemic chemo will be needed.
```
137
Give 5 causes of menorrhagia?
```
Dysfunctional uterine bleeding (idiopathic)
Just starting/finishing periods eg 13 year olds and 40 year olds
Fibroids
Endometriosis and adenomyosis
PID
Contraceptives - copper coil
Anticoagulants
VWF
Endocrine - DM, hyperthyroid
CTDs
Endometrial hyperplasia or cancer
PCOS
```
138
How is menorrhagia (HMB) managed?
```
Exclude or manage:
anaemia - FBC
fibroids - USS
bleeding disorders- coag screen
cancer - Ca125
Rx depends on womans choice.
Contraception - IUS (mirena) 1st line, COC, cyclical progesterones (VTE risk)
No contraception/fertility wishes: Antifibrinolytic eg tranexamic acid if no pain, NSAID eg mefenamic acid if pain.
[zero to finals]
```
139
What is adenomyosis?
Endometrial tissue (responsive to estrogen) in the myometrium. Common in later reproductive years, multiparous. Similar to endometriosis and fibroids, heavy painful periods and dyspareunia, sx resolve after menopause.
140
When is tranexamic acid used?
It is an antifibrinolytic, used for HMB without pain
141
When if mefenamic acid used?
NSAID used for heavy and painful periods.
| [zero to finals]
142
What is menopause and what is normal age for menopause?
Cessation of menstruation and ovarian function. Ovary becomes unresponsive to LH and FSH, production of estrogen and progesterone falls --> no negative feedback so LH and FSH levels rise. Mean age 51 years. Retrospectively diagnosed as 1 year period free.
143
What is perimenopause and how does it affect the body?
The time around the menopause up to 12 months from last period. Usually >45 years.
Less estrogen: osteoporosis, joint pain, heart disease, dementia, Vasomotor symptoms Vaginal dryness -> dyspareunia. Emotional lability. pelvic organ prolapse, urinary incontinence.
Less progesterone -> loss of libido, erratic bleeding, endometrial hyperplasia
144
What is premature menopause?
Menopause before 40 (or 45?) years due to premature ovarian insufficiency.
FSH levels to diagnose.
Iatrogenic - chemo, radio, oophorectomy.
145
How are perimenopausal symptoms managed?
Vasomotor sx resolve in 2-5 years. Rx individualised.
Sequential HRT: loweest effective dose estrogen daily, + progesterone in people with uterus.
CBT
SSRIs
Testosterone for reduced libido
146
A 48 year old lady asks you if she needs to use contraception any more as she is becoming perimenopausal. What can you tell her?
Fertility declines gradually after 40 years of age and is asso with increased risk and complications. You are still fertile until 2 years after the LMP in women under 50, or one year after the LMP in women over 50. Therefore this lady would need to use contraception until 2 years after her LMP. (STIs still exist though!)
147
What contraception can you offer to a 48 year old woman?
UKMEC1:
Barrier
Mirena/copper coil
Sterilisation
POP, implant but
NOT Depot because it causes wt gain and osteoporosis, therefore unsuitable for women >45 years.
UKMEC2: COC up to age 50. Norethisterone and levonorgestrol have lower risk of VTE than other COCs.
148
When might tibolone be used?
Synthetic steroid hormone which acts as continuous combined HRT. Post-menopausal sx. Not suitable within 12 months of LMP.
149
How does clonidine work and when would it be used?
A-adrenergic and imidazoline receptor agonist.
150
How is osteoporosis monitored?
Osteoporosis - DXA scan at 65 y/o, 60 for smokers
151
What is atrophic vaginitis?
Dryness and atrophy of the vaginal mucosa related to a lack of oestrogen. A GU sx of menopause. Changes in the vaginal pH and microbial flora contribute to localised infections.
152
How is atrophic vaginitis treated?
Topical oestrogen, vaginal lubricants. CI: breast ca, angina, VTE. Worth bringing up in consultations about other stuff - UTI, incontinence, prolapse, because women may not ask but it is easily treatable.
153
How is atrophic vaginitis diagnosed?
Examination will show pale mucosa, thin skin, reduced skin folds, erythema and inflammation, dryness, and sparse pubic hair.
154
What is normal menarche?
First periods. May be irregular at first as oestrogen secretion rises. Pregnancy is possible from first period. Average age is <16 years and increasing.
155
What is an intrauterine polyp?
A small, usually benign tumour of the uterine cavity, usually originating in the endometrium. Common in women aged 40-50 years, high estrogen, using tamoxifen for breast ca. Occasionally contain endometrial hyperplasia or carcinoma. Can cause HMB, IMB and prolapse through cervix.
156
How is a polyp diagnosed and treated?
If symptomatic, usually cause HMB, IMB, and diagnosed on USS or hysteroscopy. Resection of the polyp with cutting diathermy or avulsion normally cures bleeding problems.
157
What causes congenital uterine malformations?
Failure of fusion of the 2 Mullerian ducts at about 9 weeks gestation. Total failure = 2 uteruses, 2 cervices: didelphys.
Failure of 1 duct = unicornuate uterus.
158
What are the complications of uterine malformations, and how are they managed?
Check for renal anomalies.
25% cause pregnancy-related problems which lead to their discovery, eg malpresentation, recurrent miscarriage or preterm labour.
Only treat surgically if you are sure that is what is causing the problem. Bicornuate uteri are not treated surgically as risks outweigh benefits.
159
What is SROM, and is it a problem?
Spontaneous rupture of the amniotic sac, causing fluid to gush out. Completely normal.
160
What is PROM? It is a problem?
Pre-LABOUR rupture of membranes - amniotic sac ruptured before onset of labour after 37 weeks, occurs in 10% of women.
Cord prolapse may occur if transverse/breech lie.
Neonatal (ascending) infection risk - further increased by vaginal examination, group B strep and increased duration of membrane rupture.
Mx: Admit, monitor 4hrly - 80% labour in 24h. Induction of labour (IOL) in GBS+ve, suspected infection or meconium. Abx against GBS after 18hr.
Prolonged rupture of membranes: rupture >18hrs before delivery.
[Lissauer]
161
What is P-PROM and what is the significance?
Pre-TERM prelabour rupture of membranes- amniotic sac rupture <37 weeks. Complications: preterm delivery; infection of fetus (chorioamnionitis) or cord (funisitis); cord prolapse, if <24 wks, absent liquor --> pulmonary hypoplasia.
Dx by speculum exam - pooling of amniotic fluid.
162
PCOS increases the risk of which cancer and why?
Endometrial, because chronic anovulation --> more estrogen, less progesterone.
163
How is P-PROM managed?
Abx to prevent chorioamnionitis: erythromycin 250mg qds [NICE 2019]
IOL 34 weeks >.
Give abx for 10 days or until she is in labour, whichever is sooner. [PTS/RCOG]
164
What is miscarriage? How is it classified/defined?
Loss of pregnancy before 24 weeks gestation.
Early = <12 weeks
late = >24 weeks.
Missed = fetus dead, no sx.
Threatened: Alive, closed cervix, PV bleeding
Inevitable: PV bleed, open cervix
Incomplete: retained products of conception in the uterus after miscarriage
Complete: no POCs left
Anembryonic: empty gestational sac, no embryo.
165
How is miscarriage diagnosed?
TVUSS:
Fetal heartbeat visible = viable pregnancy.
Crown rump length >7mm without fetal heartbeat = non-viable
mean gestational sac diameter >25mm with no fetal pole = anembryonic
repeat scan after 1 week before diagnosing non viable or anembyronic miscarriage.
166
What is the management of a woman with positive pregnancy test and bleeding before 24 weeks?
Expectant: < 6 weeks, but no other pain, complications or RFs, no scan needed. repeat hCG after 7-10 days to ensure negative.
>6 weeks or prev ectopic/RFs: Exclude ectopic on scan
Expectant 1st line, repeat hcg, deterioration/more bleeding --> ?incomplete miscarriage, repeat USS.
Medical: Misoprostol (prostaglandin) to stimulate process of miscarriage. Can be vaginal or oral. It causes bleeding, pain, vomiting and diarrhoea.
Surgical: misoprostol first, then vacuum aspiration under local or general anaesthetic. Anti-D prophlaxis for Rh-ve women.
167
How is overflow incontinence diagnosed?
Hx: voiding symptoms eg straining, poor flow, incomplete emptying, suggest bladder outlet obstruction. This can be confirmed on urodynamics - HIGH voiding detrusor pressure,
LOW peak flow rate - indicates bladder outlet obstruction.
168
What is post-partum haemorrhage?
Blood loss >500ml.
Primary = within 24h of birth. Due to atony.
Secondary = 24h-12 weeks of birth. Due to retained placental tissue or endometritis.
169
What is the main cause of primary post partum haemorrhage?
An atonic uterus (lax uterus due to polyhdramnios/twins/macrosomia/grand multiparity; prev C section)
Other causes include genital trauma and clotting factors.
170
How is primary PPH managed?
ABC - 2 x 14-guage cannulae
IV syntocinon or ergometrine to contract the uterus
IM carboprost
During the 3rd stage of labour, perform cord traction and massage the uterus after delivery of placenta.
171
What is done at the booking visit at 8-12 weeks?
General info - diet, alcohol, folic acid etc
BP, urine dipstick, BMI
Bloods:
FBC, blood group, rh status, red cell alloantibodies, haemoglobinopathies (thalassemia for all, SCD if high risk);
hep B, syphilis, HIV offered
Urine culture to detect asymptomatic bacteriuria.
[passmed/NICE}
172
When should the early scan be done to confirm dates and exclude multiple pregnancy?
10-13+6 weeks
173
Explain the screening programme for Down's syndrome.
Ideally beta-HCG, low PAPP-A) + ultrasound nuchal translucency scan. >6mm in Down's (not the only cause)
14-20 weeks - Triple test. Maternal blood tests only. Raised b-hcg, low AFP, low oestriol.
Quadruple test = same but with Inhibin A (raised)
If risk >1 in 150 offer amniocentesis (USS guided aspiration via abdomen) or CVS.
NIPT new
174
What happens at 16 weeks in antenatal care?
Information on the anomaly and blood results
If Hb <11g/dl consider iron
Routine care: BP and urine dipstick
[passmed]
175
When is the anomaly scan meant to be?
18-20+6 weeks.
176
When is the first dose of anti-D given to rh negative women, and what else would be done at this point?
28 weeks:
routine - BP, urine dipstick, SFH
2nd screen for anaemia and atypical red cell alloantibodies
If Hb<10.5 g/dl consider iron
First dose anti-D prophylaxis to rh-ve women
177
When is the 2nd dose of anti-D given to rh -ve women?
34 weeks.
| Also do routine care (BP, urine, SFH) and info on labour and birth plan.
178
How often do women have to go for routine cervical smear tests?
Every 3 years if 25-49, every 5 years 50-64
179
What happens if a cervical smear is positive for hrHPV?
Cytology is done.
Abnormal cytology --> colposcopy --> detects cancer and dyskaryosis.
Normal cytology --> repeat HPV test at 12 months
--> HPV +ve? repeat 12 months later. If still +ve, colposcopy.
Otherwise return to normal recall (3 yrs for <50s, 5 yrs >50s)
180
How long does Nexplanon work for? What are the advantages and disadvantages?
3 years.
Efficacy: Most effective form of contraception
Estrogen: NONE so safe for migraine, VTE etc
Safe immediately after TOP
Disadvantages: Minor surgery to insert and remove, additional contraceptive methods needed for first 7 days.
Irregular/heavy bleeding, progestogen effects - headache ,nausea, breast pain
CI:
UKMEC 3 - IHD/stroke, suspicious PV bleed, liver cancer, past breast ca
UKMEC 4 - current breast ca
181
Give 3 risk factors for miscarriage.
```
Obesity
increased maternal age
Alcohol
Smoking
recreational drugs, caffeine
infections
health conditions eg hypertension, diabetes
Medicines eg ibuprofen, methotrexate and retinoids
```
182
Why should you measure urine HCG after termination of pregnancy? What would be an abnormal result?
To ensure the abortion has completed and there is no persistent trophoblast.
should decrease by 50% every 2 days.
Can remain positive for up to 4 weeks, but if still positive at 4 weeks this indicates incomplete abortion or persistent trophoblast.
[passmed]
183
What do you do if a woman is exposed to chicken pox during pregnancy?
Urgent blood test for varicella antibodies --> if positive, woman is non-immune so susceptible (risk of pneumonitis, fetal varicella syndrome). Give post-exposure prophylaxis, either IM VZIG or oral acyclovir.
BEFORE 20 weeks: immediately
AFTER 20 weeks: Day 7-14 post exposure.
184
Give three UKMEC-4 contraindications to the combined oral contraceptive pill.
```
These are ABSOLUTE CIs.
Migraine with aura
Breastfeeding <6 weeks postpartum
Age 35 and smoking >15/day
Vascular disease
Clot - stroke, VTE, IHD
```
185
How does endometrial hyperplasia present?
Post-menopausal, intermenstrual, heavy or irregular bleeding.
Also think RFs - high unopposed estrogen, obesity. Some will go on to develop endometrial cancer.
186
Give five things that are included in general lifestyle advice for pregnant women.
Folic acid from before pregnancy to 12 week (reduces neural tube defects)
Vitamin D
AVOID vitamin A/liver/pate - teratogenic at high doses
Dont drink alcohol (fetal alcohol syndrome)
Dont smoke (cleft, SIDS)
Avoid unpasteurised dairy (listeriosis)
Avoid undercooked or raw poultry (salmonella)
Avoid contact sports
Sex is safe
Flying increases risk of VTE
place seatbelts above and below the bump, not across it.
187
What result on the combined test would indicate higher risk of Down's syndrome?
high b-HCG, low PAPP-A.
188
What result on the quadruple test would indicate higher risk of Down's syndrome?
High b-HCG
High inhibin-A
Low AFP
Low serum oestriol
189
What would you offer a woman whose risk of having a fetus with Down's is more than 1 in 150?
Offer CVS or amniocentesis. Both take a sample of fetal cells for karyotyping for Downs.
Before 15 weeks:
Chorionic villus sampling (CVS) - USS-guided biopsy of placental tissue
Later:
Amniocentesis - USS-guided aspiration of amniotic fluid using needle and syringe. Needs to be later because then there is more amniotic fluid --> safer.
In some places: NIPT (non invasive prenatal testing) using a blood test which contains fragments of fetal DNA. not as definitive as karyotyping
[ztf]
190
How is hypothyroidism in pregnancy treated?
Treatment is still with levothyroxine (T4) but as this crosses the placenta, the dose needs to be increased during pregnancy by 25-50mg. Treatment is titrated based on the TSH level, aiming for a low-normal TSH.
Untreated or under-treated hypothyroidism in pregnancy -> miscarriage, anaemia, SGA, pre-eclampsia.
191
How do you manage women with pre-existing htn who get pregnant? Eg, should she come off her beta blocker?
STOP (risk of congenital abnormalities)
ACEi eg ramipril
ARB eg losartan
Thiazide and thiazide-like diuretics eg indapamide
OK to continue:
labetalol - 1st line for pre-eclamps*
CCBs eg nifedipine
A-blockers eg doxasin.
Other B-blockers can cause fetal growth restriction, hypoglycaemia in neonate, bradycardia in neonate.
[ztf]
192
How would you manage a lady with epilepsy who has become pregnant? Is levetiracetam okay?
OK to continue:
Levetiracetam
Lamotrigine
Carbamazepine
STOP
Sodium valproate (CI in all women as it causes neural tube defects and developmental delay)
Phenytoin (cleft lip+palate)
193
A lady with RA asks you if she is safe to conceive while taking naproxen. What can you tell her about the treatment of RA in pregnancy?
Ideally ensure RA is well controlled for 3 MONTHS before becoming pregnant, so advise her to wait if that is not the case. Sx of RA can IMPROVE during pregnancy but flare up after delivery.
AVOID:
Methotrexate (teratogenic, miscarriage, congenital abnormalities)
3rd tri:
NSAIDs (ibuprofen, naproxen) block prostaglandins.
PGs help maintain the ductus arteriosus, stimulate contractions and soften the cervix.
Therefore NSAIDS --> premature closure of ductus arteriosus and delay labour, so avoid in 3rd trimester but OK if really necessary before that.
Recommend:
Hydroxychloroquine (1st line)
Sulfasalazine
CS for flare ups (but avoid these)
194
A pregnant lady with hypertension asks you if she can continue her ramipril. What would you tell her?
Medications that block the renin-angiotensin system (ACEis and ARBs) can cross the placenta and enter the fetus --> affect fetal kidneys --> oligohydramnios, renal failure in neonate. Also cause
Hypocalvaria (= incomplete formation of skull bones); Miscarriage, fetal death, hypotension in neonate
Offer labetalol instead.
195
A 12-hour old fetus is noted to be irritable, tachypnoeic, pyrexic and not feeding well at the newborn baby check. You have no information about pregnancy so far or the mother. What should you consider/ask about?
Neonatal abstinence syndrome.
Ask about opiates primarily, also SSRIs, alcohol.
Presents 3-72hrs after birth.
196
A lady taking warfarin due to previous VTE has been told she cannot take this during pregnancy, but is concerned about having another thrombosis. What would you tell her?
Warfarin -> fetal loss, congenital malformations particularly craniofacial problems; bleeding during pregnancy, PPH, fetal haemorrhage, intracranial bleeding. Artificial metal valves are particularly prone to thrombosis and warfarin is used after the first 12 weeks, despite its fetal risks [Lissauer]
Pregnancy and especially postpartum is a hypercoagulable state.
Advise to mobilise, hydrate. If LMWH CI'd, use mechanical prophylaxis: stockings, intermittent pneumatic compression
LMWH if high risk or if VTE diagnosed. Eg enoxaparin, dalteparin, tinzaparin, continue to 6 weeks postnatally. Temporarily stopped during labour and started again after delivery, unless PPH/spinal/epidural.
[ztf]
197
You suspect a VTE in a lady who is 20 weeks pregnant. What investigations will you do? How will you treat her?
CXR, ABG, CT, VQ scanning, doppler.
LMWH - dose adjusted according to anti-factor Xa level, higher does needed due to placenta. If possible, stop treatment shortly before labour.
198
A lady with bipolar disorder wants to have a baby. What advice would you give her regarding lithium use in pregnancy?
Relative contraindication - only if other options have failed. Try and get her stable on an antipsychotic instead for a good amount of time before pregnancy.
Particularly avoid in first trimester - congenital cardiac abnormalities especially Ebstein's anomaly.
Monitor levels every 4 weeks then weekly from 36/40.
Avoid in breastfeeding as it enters breast milk and is toxic to infant.
199
What is Ebstein's anomaly?
Tricuspid valve is set lower on the R side of the heart (towards the apex) causing a bigger right atrium and a smaller right ventricle.
Risk factors: lithium
200
How is depression managed in pregnancy? Can you take sertraline?
SSRIs cross the placenta. Risks weighed up against benefits.
1st tri: congenital heart defects, paroxetine has strongest link with congenital malformations
3rd tri: persistent pulmonary hypertension in the neonate
Neonate withdrawal symptoms but usually mild with SSRIs.
201
A lady with severe acne comes asks you to remove her contraceptive implant as she wants to get pregnant. What medication would you particularly ask about?
Is she taking isotretinoin (roaccutane)? This is a retinoid medication which is highly teratogenic, causing miscarriage and congenital defects. Need contraception for 1 month before and after taking it.
202
Give 3 reasons why a cervical smear might be reported as 'inadaquate'.
Blood on the smear
Cervical inflammation
Age-related atrophic changes
(sperm -> NOT sufficiently problematic to count as inadequate)
203
Give 3 complications of the LLETZ prodecure.
It removes the transformation zone of the cervix, and ideally the whole CIN lesion.
Can cause scarring -> cervical stenosis -> future difficulty with smears
Cervical incompetence
Pyometria (uterine infection - less common now, cause of miscarriage in 2nd tri)
Incomplete excision needing further excision
Persistence of HPV -> further lesions
204
What causes raised ca-125 other than ovarian cancer?
aka mucin 16. tumour marker for ovarian cancer, but also raised in endometriosis, fibroid and pregnancy, after treatment, ascites, menstruation, breast cancer, ovarian torsion, endometrial cancer, liver disease, metastatic lung cancer
205
What is the Kleihauer test?
The Kleihauer test checks how much fetal blood has passed into the mother's blood during a sensitising event. This test is used after any sensitising event past 20 weeks, to assess whether further doses of Anti-D are required.
Acid+ mothers blood --> fetal hb more resistant --> fetal hb persists, mums is destroyed. The more cells left, the more fetal hb.
206
What is the different between SGA and FGR?
SGA = small for gestation age - small for the dates, not known why, could be constitutional or FGR (aka IUGR) ->
FGR = fetal growth restriction - there is a pathological reason, higher risk of morbidity and mortality.
[ztf]
207
Give 2 placenta-mediated and 2 non-placenta mediated causes of fetal growth restriction.
```
Placenta mediated (mothers problem):
Idiopathic
Pre-eclampsia
Maternal smoking
Maternal alcohol
Anaemia
Malnutrition
Infection
Maternal health conditions
```
```
Non-placenta medicated (fetal problem):
Genetic abnormalities
Structural abnormalities
Fetal infection
Errors of metabolism
```
208
What is SGA and how is it diagnosed/monitored?
small for gestational age = <10th centile for their gestational age.
Severe SGA = <3rd centile for GA
LBW = BW <2500g
Monitoring:
Low risk - SFH (symphysis-fundal height) at antenatal appointments >24 weeks. Customised growth charts allow for ethnic group, wt, height and parity.
If <10th centile or risk factors do
Serial growth scans to calculate growth velocity, using EFW (estimated fetal weight) and AC (fetal abdominal circumference), amniotic fluid vol
+ Umbilical artery doppler
209
Give 3 signs of IUGR.
```
Reduced amniotic fluid volume
Abnormal doppler studies
Reduced fetal movements
Abnormal CTGs
[ztf]
```
210
Give 2 short term and 2 long term complications of IUGR.
```
Short term:
Fetal death or stillbirth
Birth asphyxia
Neonatal hypothermia
Neonatal hypoglycaemia
```
```
Long term risk:
Cardiovascular disease, particularly hypertension
Type 2 diabetes
Obesity
Mood and behavioural problems
[ztf]
```
211
Give 3 risk factors for SGA/FGR
```
Previous SGA baby
Pre-preg BMI: <20 (according to PTS), or weight >75kg
Smoking
Diabetes
Existing hypertension
Pre-eclampsia
Maternal age <16 or ?35
Multiple pregnancy
Low pregnancy‑associated plasma protein‑A (PAPPA)
Antepartum haemorrhage
Antiphospholipid syndrome
Interpregnancy interval <6 months or >120 months
```
212
What is the management for SGA?
Prevention - identify those at risk, aspirin to those with pre-eclampsia, treat modifiable RFs eg smoking
Monitoring - serial growth scans
Delivery - early if growth stops or there are other concerns eg abnormal doppler. corticosteroids especially for c section (remember CS for CS). Paediatricians on hand for resus
Investigate cause:
- BP + urine (pre-eclampsia)
Uterine artery doppler (placental perfusion)
Fetal anatomy scan by fetal medicine
Karyotyping for chromosomal abnormalities
Infection screen - toxoplasmosis, CMV, syphilis, malaria
213
What is macrosomia?
aka LGA
birth weight >4.5kg
EFW >90th centile
214
Give 3 causes of macrosomia.
```
Constitutional
Maternal diabetes
Previous macrosomia
Maternal obesity or rapid wt gain
Overdue
Male baby
```
215
How can gestational DM lead to shoulder dystocia?
DM --> macrosomia --> birth injury, shoulder dystocia.
216
Give 2 maternal and 2 fetal complications of macrosomia.
```
Mother:
!!Shoulder dystocia (tear, bleeding)
Failure to progress
Perineal tears
Instrumental delivery or caesarean
Postpartum haemorrhage
Uterine rupture (rare)
```
```
Fetus:
Birth injury (Erbs palsy, clavicular fracture, fetal distress and hypoxia)
Neonatal hypoglycaemia
Obesity in childhood and later life
Type 2 diabetes in adulthood
```
217
What actions would you take if a baby measured on the 95th centile on the growth chart?
Investigate:
USS to exclude polyhydramnios and estimate fetal weight
Oral glucose tolerance test for gestational diabetes.
Main risk is shoulder dystocia.
Reduce the risk by:
delivery on a consultant led unit, experienced midwife/obstetrician, access to theatre if required, active management of 3rd stage, early decision for C-Section if required, and paediatrician attending the birth.
(Nb: NICE doesnt recommend induction just for macrosomia)
218
How would you determine what type of twins are present?
```
Monozygotic = identical, one zygote
Dizygotic = two zygotes
```
amnionicity and chorionicity differentiated using USS:
```
Monoamniotic = one amniotic sacs
Diamniotic = 2 sacs - 'T sign' on USS, membrane between the twins - membrane abruptly meets the chorion.
```
Monochorionic: single placenta, no membrane between them
Dichorionic: 2 placental, lambda/twin peak sign (triangle where chorion meets and blends partially into the membrane)
Best outcome is diamniotic dichorionic twins, as each fetus has their own nutrient supply.
219
Give 2 maternal and 2 fetal complications of multiple pregnancy.
```
Maternal:
Anaemia
Polyhydramnios
Hypertension
Malpresentation
Spontaneous preterm birth
Instrumental delivery or caesarean
Postpartum haemorrhage
```
```
Fetal:
Miscarriage
Stillbirth
Fetal growth restriction
Prematurity
Twin-twin transfusion syndrome
Twin anaemia polycythaemia sequence
Congenital abnormalities
```
220
What is twin-twin transfusion syndrome and how is it managed?
```
Monochorionic twins (share a placenta).
The 'recipient' fetus gets more blood than the 'donor' fetus. The recipient is worse off because they get fluid overload, heart failure, polyhydramnios.
The donor gets growth restricted, anaemia and oligohydramnios.
Management: tertiary care, laser treatment to destroy connection in severe cases.
```
221
What in twin anaemia polycythaemia sequence?
Similar to twin-twin transfusion but less acute, one twin becomes anaemia while other develops polycythaemia (raised hb).
222
What additional monitoring and management is needed in multiple pregnancy?
Specialist obstetric led care. Think more monitoring and earlier birth for mono, less monitoring for di, because of the blood supplies.
1. FBC at booking, 20 weeks and 28 weeks (anaemia)
2. USS: FGR, unequal growth, TTTS
Monochorionic -> 2-weekly from 16 weeks
Dichorionic -> 4-weekly from 20 weeks
```
3. Delivery:
Early to reduce risk of fetal death at:
32- 33+6 = monochorionic monoamniotic
36 and 36+6 = monochorionic diamniotic
37 and 37+6 = dichorionic diamniotic
If complications this may differ.
Give steroids to mature fetal lungs.
```
Monoamniotic- elective caesarean section at between 32 and 33 + 6 weeks.
Diamniotic - aim to deliver between 37 and 37 + 6 weeks, C section may be needed for the second twin, or if non-cephalic first twin.
[ztf]
223
What are the consequences of UTIs in pregnancy? How are these risks reduced?
Preterm delivery
Low birth weight
Pre-eclampsia
Risk reduction: testing for asymptomatic bacteria at booking and routinely throughout pregnancy - urine MC+S.
224
How would you differentiate pyrelonephritis from lower urinary tract infection?
LUTI: Dysuria, subrapubic pain, increased frequency of urination, urgency, incontinence, haematuria
Pyelo: Above plus higher fever and loin or back pain, vomiting, loss of appetite, renal angle tenderness on examination.
225
What does nitrites/leukocytes on the urine MC+S tell you?
Infection.
Nitrites are a more accurate indication of infection than leukocytes. They are produced by gram negs (eg E. coli) which break down nitrates in urine into nitrites.
Leukocytes (WBCs) usually present in small numbers, rise can be due to infection or inflammation. Urine dips test for leukocyte esterase, a product of leukocytes, which gives an indication to the number of leukocytes in the urine.
226
What are the 2 most common causative organisms of UTIs in pregnancy?
```
In order of likelihood:
E. coli
Klebsiella pneumonia
enterococcus
pseudomonal aeruginosa
staph saprophyticus
candida albicans
```
227
How are UTIs managed in pregnancy?
7 days abx:
Nitrofurantoin (not in 3rd tri - neonatal haemolysis)
Amoxicillin (only after sensitivities known)
Cefalexin
Nb avoid trimethoprim in 1st tri as it works as a folate antagonist -> neural tube defects (spina bifida).
228
What are the causes of anaemia in pregnancy?
Microcytic - iron def
Normocytic - Dilutional - plasma vol increases more than hb leading to reduction in hb concentration.
Macrocytic - b12/folate
Haemoglobinopathy
229
How would you identify anaemia in a pregnant woman?
It can be asymptomatic/harder to tell. SOB, fatigue, dizziness, pallor.
Hence screening at booking (<110g/L), 28 weeks (<105g/L) and postpartum (<100g/L).
Screened at booking for hb-opathies - thalassemia (all) and SCD (those at higher risk)
230
How is anaemia in pregnancy managed?
Iron - 200mg 3x daily
B12 - test for pernicious anaemia checking for intrinsic factor antibodies. Liaise with haematology for rx - options are IM hydroxocobalamin, and PO cyanocobalamin.
Folate - all women should take 400mcg per day, plus 5mg if folate deficient.
Hbopathy - specialist haematology, 5mg folic acid, monitoring, transfusions.
231
Give 5 risk factors for VTE in pregnancy.
| How many of these do you need before prophylaxis is indicated?
```
Smoking
Parity ≥ 3
Age > 35 years
BMI > 30
Reduced mobility
Multiple pregnancy
Pre-eclampsia
Gross varicose veins
Immobility
Family history of VTE
Thrombophilia
IVF pregnancy
```
RCOG:
prophylaxis from 28 wks if 3 or more RFs
from 1st tri if 4 or more RFs
(also if hosp admission, surgery, prev VTE, cancer/arthritis, high risk thrombophilias, or ovarian hyperstimulation syndrome)
232
How do DVTs present?
Unilat calf/leg swelling (>3cm difference between the legs, measure 10cm below tibial tuberosity and compare)
Dilated superficial veins
Calf tenderness, particularly over deep veins
oedema
colour changes to leg
233
How does PE present?
```
Have high index of suspicion as can be subtle.
SOB
Cough +/- haemoptysis
Pleuritic chest pain
hypoxia
tachycardia
raised resp rate
low-grade fever
haem instability -> hypotension
[ztf]
```
234
How is DVT diagnosed in pregnancy?
Doppler USS. If negative, repeat on day 3 and 7 if suspected DVT (RCOG 2015)
May want CXR/ECG for suspected PE.
*nb: Wells score not validated for use in pregnant women, and D dimer is raised in pregnancy anyway*
[ztf]
235
How do you diagnose PE?
Initial: Doppler USS for DVT. CXR, ECG
Definitive dx is with CTPA or VQ but these arent necessary if doppler shows DVT.
CTPA = CT pulmonary angiogram. usually more available, gives info about alternative dx such as pneumonia or malignancy. Risk of breast ca in mum.
VQ scan = ventilation-perfusion scan. Inhaled radioactive isotopes and gamma camera to compare ventilation with perfusion. PE = deficit in perfusion (V>Q) as thrombus blocks blood flow to lung tissue. Risk of childhood ca in fetus.
236
How is VTE in pregnancy?
LMWH (enoxaparin, tinzaparin, dalteparin) - start asap, empirically if delay in scan results.
Dose based on wt and height at booking
Continue for rest of preg, up to 6 months postnatally or 3 months in total, whichever is longer.
Can switch to warfarin or DOAC after delivery.
Massive PE + haemodynamic compromise is life threatening - ABCDE, unfractionated heparin, thrombolysis, surgical embolectomy.
[ztf]
237
What is pre-eclampsia?
```
New hypertension (>20 weeks GA)
plus end-organ dysfunction (proteinuria). Oedema may also be present.
Occurs due to abnormal formation of the spiral arteries/lacunae of the placenta, leading to high vascular resistance in these vessels. This causes poor perfusion of the placenta -> oxidative stress -> inflammatory chemicals released into systemic circulation -> systemic inflammation and impaired endothelial function in the blood vessels.
```
238
Give 2 maternal and 2 fetal complications of pre-eclampsia.
Maternal: organ damage, seizures, death
Fetal: IUGR, early labour, death
239
What is eclampsia? What is the acute management?
Seizures as a result of pre-eclampsia. Should be assumed as the cause of seizures in pregnancy until proven otherwise.
Rx with IV mag sulphate.
240
Give 2 high-risk and 2 moderate-risk factors for pre-eclampsia.
When would you give aspirin?
```
High:
Pre-existing htn
Prev htn in pregnancy
AI condition eg SLE
diabetes
CKD
```
```
Moderate:
Age >40
BMI >35
>10 yrs since prev pregnancy
multiple pregnancy
first pregnancy
FHx pre-eclampsia
```
ASPIRIN prophylaxis from 12 weeks till birth, if 1 high risk or 2+ moderate-risk.
241
Give 3 symptoms of pre-eclampsia.
```
Headache
Visual disturbance or blurriness
Nausea, vomiting
upper abdominal or epigastric pain (due to liver swelling)
Oedema
Oligouria
Brisk reflexes
```
242
What are the diagnostic criteria for pre-eclampsia?
BP >140/90
+ proteinuria (1+ on urine dipstick), organ dysfunction (raised creatinine, liver enzymes; seizures; thrombocytopaenia; haemolytic anaemia), or placental dysfunction (IUGR, abnormal doppler)
Proteinuria can be quantified using urine albumin creat ratio (>30mg/mmol) or protein:creatinine ratio (>8mg/mmol).
Placental growth factor (PlGF) stimulates development of new placental vessels. Can be tested once to rule-out pre-eclampsia between 20 and 35 weeks - it would be low in pre-eclampsia.
[NICE 2019, ztf]
243
How is pre-eclampsia managed?
Aspirin prophylaxis 12 wks - birth if 1 high risk factor or 2+ moderate risk factors.
Routine monitoring every appointment. BP, urine, sx.
Aim for BP <135/85, admit if >160/110, weekly urine and bloods - FBC, LFTs and U+Es (renal profile). Growth scans, PlGF testing once.
Labetalol 1st line antihypertensive.
Nifedipine 2nd-line
Methyldopa 3rd line (stop within 2 days of birth)
IV Mag sulphate during labour and 24h afterwards to prevent seizures
Fluid restriction if severe
Planned early birth may be necessary, give corticosteroids if this is the case.
Switch to enalapril after delivery (nifedipine in black African/Carribean pts), BP should return to normal over time.
244
What is HELLP syndrome?
A combination of features that occurs as a complication of pre-eclampsia and eclampsia.
Haemolysis
Elevated Liver enzymes
Low Platelets
245
Are sulfonamides safe in pregnancy?
Not in 3rd tri - associated with kernicterus.
246
Are tetracyclines safe in pregnancy?
No - staining of baby's teeth and problems with skeletal development.
247
Give 3 complications of delayed or recurrent PID.
Chronic pelvic pain
Ectopic pregnancies due to adhesions
Fitz Hugh Curtis syndrome - infection into peritoneum, scarring and 'violin sting adhesions'
Hydrosalpinx - fluid buildup in blocked fallopian tubes
Tubo-ovarian abscesses due to adhesions/advanced infection.
248
How are haemorrhagic ovarian cysts managed?
If patient is stable, admit and manage conservatively. Most cysts presenting acutely will present with lower abdominal pain, but without signs of peritonism or
systemic upset.
If vomiting, peritonism, or fever consider torsion and appendicitis.
[PTS]
249
How does BV present? How can you identify it from other causes of discharge?
FISHY smelling watery grey or white vaginal discharge
Otherwise asymptomatic but may have oc-occurring infection
Caused by depletion of normal flora using soap/douching.
Causative organisms: gardnerella vaginalis, m. hominis, prevotella species
Can confirm with vaginal swab -> microscopy -> clue cells.
250
How does thrush present?
Thick, white discharge, does not typically smell.
| Vulval and vaginal itching, irritation or dyscomfort.
251
How does chlamydia present? How is it diagnosed?
Often asymptomatic,
abnormal vaginal discharge, pelvic pain, IMB/PCB, dyspareunia, dysuria
Cannot be cultured or seen on microscopy because it is obligate intracellular.
Diagnosed with NAAT, nucleic acid amplification test - first catch urine sample. Urethral swab is also suitable but more invasive.
252
How does gonorrhea present? How is it diagnosed?
Odourless purulent discharge, green or yellow
Dysuria
pelvic pain
Men more likely to be asymptomatic
Gonorrhoea can be excluded by urine or urethral swab NAAT. If NAAT is positive for gonorrhoea, a urethral swab is needed for culture, to identify sensitivities before starting antibiotic treatment. If Gram negative diplococci are seen on microscopy, this is gonorrhoea, in the context of a urethral swab.[pts]
253
How does mycoplasma genitalium present?
STI which causes non-gonococcal urethritis.
Usually asymptomatic and similar to chlamydia. May have both.
Testing with NAAT
Do first urine sample in morning for men
Vaginal swabs for women
BASHH (2018)
254
How does trichomonas vaginalis present?
STI, parasite, protozoan.
50% asymptomatic, or non-specific symptoms.
Discharge - frothy, yellow-green, may be fishy.
Strawberry cervix
Itching, dysuria, dyspareunia, balanitis
255
How does genital herpes present?
```
Ulcers or blistering lesions on genital area
Neuropathic pain
Flu-like symptoms
dysuria
inguinal lymphadenopathy
```
256
How does syphilis present?
STI caused by bacteria treponema pallidum.
The incubation period between the initial infection and symptoms is 21 days on average
PRIMARY: chancre = painless ulcer, usually on genitals
SECONDARY syphilis presents with widespread rash, neurological symptoms and glomerulonephritis. Resolves in 3-12 weeks -> LATENT syphilis.
TERTIARY: gummatous (granulomatous) lesions, CVS, neuro.
NEUROsyphilis can occur at any stage. Tabes dosalis, ocular syphilis, argyll-robertson pupil - it accommodates but does not react ('prostitutes')
257
How is syphilis diagnosed?
PTS:
Treponemal antibody tests (TPHA) - positive indicates immunity - IgG.
VDRL - enzymes produced in active syphilis infection.
ztf:
Dark field microscopy
Polymerase chain reaction (PCR)
Rapid plasma reagin (RPR) and venereal disease research laboratory (VDRL) tests are two non-specific but sensitive tests used to assess for active syphilis infection. . These tests involve introducing a sample of serum to a solution containing antigens and assessing the reaction. A more significant reaction suggests a higher quantity of antibodies. The tests are non-specific, meaning they often produce false-positive results. There is a skill to both performing and interpreting the results of these tests.
258
Give 4 complications of congenital syphilis.
```
Generalised lymphadenopathy
Hepatosplenomegaly
Rash
Skeletal malformations
[pts]
```
259
What would you consider in someone with a pink rash, swelling of lymph glands behind the ears and mild fever?
Rubella.
260
What is TORCH syndrome? How does it present?
Cluster of symptoms caused by congenital infection with Toxoplasmosis, Other (zika, syphilis, VZV, parvoB19) Rubella, CMV, HIV, or Herpes.
Presentation: Hepatosplenomegaly, fever, lethargy, difficulty feeding, anaemia, petechiae, purpurae, jaundice and chorioretinitis.
261
What would be the consequences of antenatal rubella infection on the fetus?
```
20 weeks 0 risk
Fetal rubella syndrome:
learning disability.
Cataracts.
Deafness.
Heart defects.
Intrauterine growth restriction.
Inflammation of the brain, liver, lungs and bone marrow.
```
262
How is antenatal rubella infection managed? What investigations would you do?
Ix:
Rubella and parvovirus B19 blood tests (even if reported to be immune)
Serum IgG and IgM. Rising levels suggest recent infection (consult a virologist).
Mx:
Evidence of infection should be discussed with the patient with a view to considering termination if indicated and appropriate (consult a fetal medicine specialist).
Notifiable so report to health protection unit.
Prevention is by measles, mumps and rubella (MMR) vaccine in the second year of life plus a pre-school booster, with antenatal screening for rubella susceptibility.
263
What could cause fever, malaise and a pruritic maculopapular/vesicular rash?
Chickenpox/VZV.
264
A child has chicken pox, and her mother asks how infectious she is. What do you tell her and what hx do you need to know?
The incubation period is 7-21 days and the disease is infectious 48 hours before the rash appears, continuing to be infectious until the vesicles crust over (usually within 5-6 days of onset of illness). So she is infectious until the vesicles crust over.
265
A teacher comes to you saying she has had contact with a child with chickenpox at school. She is 14 weeks pregnant. What is her risk and the risk to the fetus?
If she has had chickenpox/has varicella IgG antibodies, the pregnancy won't be complicated as she should not be infected.
chickenpox is associated with greater morbidity - pneumonia (10% of pregnant women), hepatitis and encephalitis.
Infection in first tri (<20 weeks): no increased risk of miscarriage but risk of FVS:
Skin scarring in a dermatomal distribution.
Microphthalmia, chorioretinitis and cataracts.
Hypoplasia of the limbs.
Neurological abnormalities - eg, microcephaly, cortical atrophy, intellectual disability, and dysfunction of bowel and bladder sphincters.
The risk of FVS if a mother develops chickenpox is approximately 0.2% under 13 weeks of gestation, and 2% at 13-20 weeks of gestation
20-36 weeks: No adverse effects. Possible shingles in the first few years of infant life.
After 36 weeks:
Up to 50% of babies are infected and approximately 23% of these develop clinical varicella despite high titres of passively acquired maternal antibody.
The most severe chickenpox occurs if the infant is born within seven days of onset of the mother's rash.
266
How would you manage chickenpox exposure in a pregnant woman who has never had shingles or chickenpox herself?
Get urgent varicella-zoster IgG antibody titre.
Liaise with local microbiology for advice and to expedite results.
Varicella-zoster immunoglobulin (VZIG) may be indicated but NOT in established infection.
If infected:
Seek specialised obstetric advice - counselling on the risk of fetal complications, antiviral treatment and follow-up.
Monitor the patient and admit if:
Respiratory symptoms.
Neurological symptoms other than headache.
Haemorrhagic rash or bleeding.
Severe disease - eg, dense rash.
Significant immunosuppression, including systemic corticosteroids in the previous three months.
267
Which is the most common congenitally acquired infection in infants, and the leading infectious cause of congenital malformation?
CMV. Ask if woman has other children or works with young children - this may be the exposure
268
What are the consequences of antenatal CMV infection?
There is a 30-40% risk of intrauterine transmission, and a 20-25% risk of postnatal sequelae if the fetus has been infected.
```
Intrauterine growth restriction and low birth weight.
Hepatosplenomegaly.
Jaundice.
Thrombocytopenia.
Anaemia.
Hydrops and ascites.
Petechiae and/or purpura.
Microcephaly.
Intracranial calcifications.
Choroidoretinitis.
Deafness.
Speech defects.
General learning disability, which may appear later.
Psychomotor delay.
Visual impairment.
```
269
How is CMV transmitted?
breast-feeding, close contact, sexual activity, blood transfusion and organ transplantation.
Risk factors - exposure to young children eg daycare
270
How is antenatal CMV infection managed?
Diagnosis can be made antenatally by amniocentesis at least seven weeks after infection and after 21 weeks of gestation
If infection is confirmed, ultrasound is performed regularly to monitor for complications.
The effect on the fetus is more severe from a primary infection so establish if the mother has had it before using IgG titres
Prevention - hygiene, thorough hand washing after nappy changing, feeding a child or wiping their face or handling children's toys.
Not sharing food or utensils with a young child.
Avoiding kissing a child on or near the mouth.
271
Which one of the TORCH infections causes mild fever, red cheeks, generalised rash and arthropathy?
Parvovirus B19 (slapped cheek aka erythema infectiosum)
272
What are the consequences of antenatal Parvovirus B19 infection?
Infection in the first 20 weeks of pregnancy:
9% increase in the risk of intrauterine death
3% risk of hydrops fetalis. Of these, 50% die.
These events usually occur 3-5 weeks after the onset of maternal infection.
Generally the neonate is unaffected.
273
How is exposure to slapped cheek syndrome in pregnant women managed?
Parvovirus IgM and IgG testing should be done if there is suspicion of exposure or infection. Specialised advice should be sought.
Intrauterine transfusion for treatment of fetal anaemia reduces mortality rate in hydrops.
Serial USS/doppler
274
Explain the menstrual cycle.
GnRH is released from hypothalamus
Stimulates AP to produce LH and FSH
FSH stimulates follicles to produce estrogen in the ovary
Oestrogen reduces GnRH, LH and FSH production
Follicle becomes corpus luteum and produces progesterone which thickens the endometrium
If fertilised, egg produces HCG and uterus produces progesterone and oestrogen which inhibits LH and FSH, if not, dies and the cycle starts again.
275
Give 4 functions of the placenta.
1. Acts as the lungs of the fetus - fetal Hb has higher affinity for O2 than maternal, so maternal Hb passes on oxygen and takes away CO2 from fetal Hb
2. Acts as the kidney of the fetus - excretes waste products from fetus eg bicarb, H+, lactic acid, urea, creatinine
3. Nutrition - nutrients and glucose diffuse across placental membrane
4. Immunity- mother passes antibodies on to fetus
5. Endocrine hormones eg HCG, oestrogen and progesterone cause ligament and muscle softening and stretching.
276
Give 4 physiological hormonal changes in pregnancy.
The anterior pituitary gland produces more ACTH, prolactin and melanocyte stimulating hormone in pregnancy.
Higher ACTH levels cause a rise in steroid hormones, particularly cortisol and aldosterone. Higher steroid levels lead to an improvement in most autoimmune conditions and a susceptibility to diabetes and infections.
Increased prolactin acts to suppress FSH and LH, causing reduced FSH and LH levels.
Increased melanocyte stimulating hormone causes increased pigmentation of the skin during pregnancy, resulting in skin changes such as linea nigra and melasma.
TSH remains normal, but T3 and T4 levels rise.
HCG levels rise, roughly doubling every 48 hours until they plateau around 8 – 12 weeks, then gradually start to fall.
Progesterone levels rise throughout pregnancy. Progesterone acts to maintain the pregnancy, prevent contractions and suppress the mother’s immune reaction to fetal antigens. The corpus luteum produces progesterone until ten weeks gestation. The placenta produces it during the remainder of the pregnancy.
Oestrogen rises throughout pregnancy, produced by the placenta.
277
Give 4 physiological changes to the uterus, cervix and vagina in pregnancy.
Size of the uterus increases from around 100g to 1.1kg during pregnancy.
Hypertrophy of the myometrium and the blood vessels in the uterus.
Increased oestrogen may cause cervical ectropion and increased cervical discharge. Oestrogen also causes hypertrophy of the vaginal muscles and increased vaginal discharge. The changes in the vagina prepare it for delivery, however they make bacterial and candidal infection (thrush) more common.
Before delivery, prostaglandins break down collagen in the cervix, allowing it to dilate and efface during childbirth.
278
Give 4 physiological cardiovascular changes in pregnancy.
Increased blood volume
Increased plasma volume
Increased cardiac output, with increased stroke volume and heart rate
Decreased peripheral vascular resistance
Decreased blood pressure in early and middle pregnancy, returning to normal by term
Varicose veins can occur due to peripheral vasodilation and obstruction of the inferior vena cava by the uterus
Peripheral vasodilation also causes flushing and hot sweats
279
How does respiratory function change in pregnancy?
Tidal volume and respiratory rate increase in later pregnancy, to meet the increased oxygen demands.
280
Give 4 physiological renal changes in pregnancy.
Increased blood flow to the kidneys
Increased glomerular filtration rate (GFR)
Increased aldosterone leads to increased salt and water reabsorption and retention
Increased protein excretion from the kidneys (normal is up to 0.3g in 24 hours)
Dilatation of the ureters and collecting system, leading to a physiological hydronephrosis (more right-sided)
281
Give 4 haematological changes in pregnancy that you might see on bloods.
Increased RBC production --> higher iron, folate and B12 requirements
Plasma volume increases --> dilutional anaemia
Increased clotting factors such as fibrinogen and factor VII, VIII and X
Increased white blood cells
Decreased platelet count
Increased ESR and D-dimer
Increased alkaline phosphatase (ALP), up to 4 times normal, due to secretion by the placenta
Reduced albumin due to loss of proteins in the kidneys
Calcium requirements increase, but so does gut absorption of calcium, meaning calcium levels remain stable
282
Give 4 physiological skin/hair changes in pregnancy.
Increased skin pigmentation due to increased melanocyte stimulating hormone, with linea nigra and melasma
Striae gravidarum (stretch marks on the expanding abdomen)
General itchiness (pruritus) can be normal, but can indicate obstetric cholestasis
Spider naevi
Palmar erythema
Postpartum hair loss is normal, and usually improves within six months.
283
What are the 3 stages of labour and what do they involve?
1. Onset of labour (true contractions) until 10cm cervical dilatation
2. 10cm dilatation until delivery of baby
3. Delivery of baby until delivery of placenta
(Labour is 37-42 weeks normally)
284
What are the function of prostaglandins in labour?
Stimulate contractions
Role in ripening cervix
Prostaglandin E2 = dinoprostone pessary used to induce labour
285
What are braxton-hicks contractions?
Irregular contractions of uterus in 2nd and 3rd trimester, they do not progress or become regular, not indicative of labour. Stay hydrated and relax
286
What is effacement?
Thinning of the cervix from front to back to prepare for delivery.
287
What is the show or bloody show in labour?
Mucus plug (prevents bacteria from entering uterus) falling out.
288
What is the latent phase?
First phase of the 1st stage of labour, from 0-3cm dilation of the cervix, progressing at 0.5cm/hour, irregular contractions
289
What is the active phase?
Second phase of the 1st stage of labour, from 3-7cm dilation of the cervix, progressing at 1cm/hour, regular contractions.
290
What is the transition phase?
Third phase of the 1st stage of labour. From 7-10cm dilation, progressing at 1cm/hour, strong and regular contractions.
291
What are the 7 cardinal movements of labour in the 2nd stage?
```
Engagement
Descent
Flexion
Internal Rotation
Extension
Restitution and external rotation
Expulsion
```
292
What is descent and how is it measured?
Position of the baby's head in relation to the mother's ischial spines during the descent phase. Measured in cm from -5 (baby head at pelvic inlet), to +5 when fetal head has descended further out. Engagement is at 0cm (head at ischial spine).
293
What is active management of the third stage of labour?
Midwife/doctor assist in delivery of the placenta to reduce risk of bleeding. Indicated in >60 min delay in placental delivery or haemorrhage. Involves giving IM oxytocin to help uterus contract and expel placenta. Can cause nausea and vomiting.
294
What do you need to counsel patients about when starting the COCP? (ATHLETICS)
ATHLETICS:
Action - works by stopping ovulation, thickening mucus and thinning endometrium
Time: Take at same time every day
How to take: tablet, can take 21 d on, 7 d off, or tricycle = 3 packs on, 7 d off; or continuous.
Length of treatment: any length
Effect: contraception 99% perfect use, 82% typical use. Decreases risk of ca endometrium, ovary and colon, and benign ovarian cysts.
Time to take effect - 7 days unless day 1 of cycle
Interacts with enzyme inducing drugs eg anti-epileptics, antibiotics
CI - UKMEC4 - clots, cancer, migraine with aura, APLS, smoking >15/day AND BMI >35, uncontrolled hypertension, severe diabetes, 3 weeks postpartum, 6 weeks breastfeeding, 4 weeks pre-op, exclude pregnancy
Complications: increased risk breast and cervical cancer
SEs: spotting, breast pain, mood, headache, clots
Supplementary advice: missed pill (>24h) - take pill as soon as you remember and take today's pill, if week 1 (havent taken for 7 days continuously) need emergency contraception
D+V
Switching pills
295
What do you need to counsel patients about when starting the POP (cerazette)?
Traditional vs desogestrel only (cerazette). Cerazette:
Action: stop ovulation and thicken cervical mucus.
Time: take same time each day
How: orally, continuously
Length: as long as you want
Effect: contraception 91% effective (typical use). 1/3 amenorrhea, 1/3 irreg/worse bleeding, 1/3 reg bleeding
Time to take effect = 2 days unless day 1 of cycle
Interactions - enzyme inducers
CI - UKMEC4: current breast ca
Complications: slight increased risk breast ca (returns to normal 10 yrs after stopping), ovarian cysts
SE: headache, breast tenderness, acne
Supplementary: missed pills (>12 hrs/D+V) - take last pill + todays pill + use extra contraception for 2 days. Emergency needed if UPSI in 48 since missed pill.
296
How would you counsel someone for the progesterone only injection?
Action - DMPA (depot medroxyprogesterone acetate). This is a type of progestin. Stops ovulation by inhibiting FSH by pituitary.
Time to take it - 12-13 week intervals.
How: IM in clinic (Depo-Provera), SC self injection (Sayana Press)
Length: 12-13 weeks, can prevent fertility up to 1 yr after stopping injections
Effect: 99% perfect use, 94% typical use (forgetting to book in). Bleeding may become irregular/worse at first but usually stops after 1 yr.
Time to effect: 7 Days unless first 5 days of cycle. Reduces risk ovarian and endometrial ca, sickle cell crisis, and endometriosis sx.
Interactions - NOT affected by enzyme inducers
CI - active breast UK (UKMEC4).
Complications: osteoporosis - UKMEC2 in >45 yrs, ask about steroid use, slight increase risk breast and cervical cancer.
SEs: wt gain, acne, reduced libido, mood changes, headaches, flushes, alopecia, skin reaction at site. Problematic bleeding should be investigated and can be settled with COCP or mefenamic acid.
Supplementary advice: still need to protect against STIs
297
How would you counsel a patient for the progestogen only implant?
Eg Nexplanon - 68mg etonogestrel
Action - 4cm flexible plastic rod placed in upper arm below the skin, slowly releases progestogen into systemic circulation.
Time to take - Inserting takes ten mins
How - nurse inserts it into non-dominant upper arm 1/3 up medially. Lidocaine (local) used. You will feel it when you touch it but not otherwise. Removed also using lidocaine, contraception needed immediately after removal.
Length of treatment - 3 yrs
Effect: >99% effective, no room for user error.
Time to take effect: 7 days unless inserted on days 1-5 of cycle.
Interactions- Enzyme inducers
CI - Active breast cancer UKMEC4
Complications: Risks of procedure, bleeding, deep implantation.
SEs: 1/3 have infrequent bleeding, 1/4 have frequent/prolonged bleeding, 1/4 normal bleeding, 1/5 have no bleeding. May worsen acne
Safety net: If it becomes impalpable let us know (may need to scan it) and extra contraception is required until it is located.
298
How would you counsel someone for the IUD?
Aka Cu-IUD:
Action- Copper in uterus creates hostile environment for fertilisation.
Time taken - short procedure, may need a day to recover
How - minor operation. Bimanual exam to check position and size of uterus. Speculum inserted, specialised equipment used to fit the device. Obs monitored.
Removal: can't remove if pregnant so abstain/use condoms 7 days before removal. Pull the strings slowly to remove.
Length - long acting
Effect - >99%. Fertility returns immediately after removal. No hormones. May reduce risk endometrial and cervical cancer.
Time to effect: Immediate
Indications: Long acting/emergency
CI - PID/infection, immunosuppression, pregnancy, unexplained bleeding, pelvic cancer, uterine distortion eg by fibroids, Wilsons disease
Complications: bleeding, pain on insertion, vasovagal reactions, uterine perforation (1-2 in 1000, higher in breastfeeding women), PID (first 20 days), expulsion (first 3 months (1 in 20, increased risk under 20 yrs old)
A pregnancy is more likely to be ectopic, but still lower risk than no contraception.
SEs: cramps after insertion. NSAIDs may help.
Safety net: Come back in a month to check the threads, you should feel the strings to ensure it's still in place.
Non-visible threads could indicate expulsion/pregnancy/perforation. Use condoms until coil is located. May need USS --> X ray --> hysteroscopy.
299
How would you counsel a patient for the IUS?
Eg Mirena (most common) aka LNG-IUS.
Action: Progesterone into the uterus (levonorgestrel).
Time: About half an hour appointment, may need day off to recover.
How: Minor operation. Bimanual exam to check position and size of uterus. Speculum inserted, specialised equipment used to fit the device. Obs monitored
Length: Effective for 5 years apart from Jaydess which is only 3 years. Mirena is licensed for 5 years for contraception but 4 years for HRT.
Removal: can't remove if pregnant so abstain/use condoms 7 days before removal. Pull the strings slowly to remove.
Effect: 99% effective contraception, improve dysmenorrhea/endometriosis sx.
Time to work: 7 days unless inserted on day 1-7 of cycle.
Indications: Mirena: HRT and menorrhagia as well as contraception
CI: PID/infection, immunosuppression, pregnancy, unexplained bleeding, pelvic cancer, uterine distortion eg by fibroids
Complications: Risks of procedure, irregular bleeding, pelvic pain, cysts, may be systemic absorption causing acne, headaches or breast tenderness. Vasovagal reactions, uterine perforation (1-2 in 1000, higher in breastfeeding women), PID (first 20 days), expulsion (first 3 months (1 in 20, increased risk under 20 yrs old)
A pregnancy is more likely to be ectopic, but still lower risk than no contraception.
SEs: above
300
Give 5 causes of intermenstrual bleeding.
```
Hormonal contraception
Cervical ectropion, polyps or cancer
Sexually transmitted infection
Endometrial polyps or cancer
Vaginal pathology, including cancers
Pregnancy
Ovulation can cause spotting in some women
Medications, such as SSRIs and anticoagulants
```
301
Give 5 causes of dysmenorrhoea.
```
(painful periods)
Primary dysmenorrhea (no pathology)
Endometriosis or adenomyosis
Fibroids
PID
Copper coil
Cervical or ovarian cancer
```
302
Give 5 causes of postcoital bleeding.
```
(bleeding after sex)
Often idiopathic
Cervical cancer, ectropion or infection
Trauma
Atrophic vaginitis
Polyps
Endometrial cancer
Vaginal cancer
```
303
Give 5 causes of pruritus vulvae.
```
Itching of vulva and vagina.
Irritants - soaps, detergents, barrier conraception
Atrophic vaginitis
Infections - candidiasis (thrush), pubic lice
Skin conditions - eczema
Vulval malignancy
Pregnancy related discharge
Urinary or fecal incontinence
Stress
```
304
What is primary amenorrhea? How is it defined?
No periods by age 13 if no other evidence of pubertal development, or 15 if there are other signs of puberty eg breast buds.
305
When does puberty normally start?
Girls: 8-14. Boys: 9-15.
Girls have pubertal growth spurt earlier in puberty than boys.
Breast buds, pubic hair --> menstrual periods
306
Give 3 causes of hypogonadotropic hypogonadism.
Deficiency of LH and FSH (gonadotropins) from anterior pituitary --> ovaries don't secrete sex hormones. Can be due to:
Hypopituitarism
Damage to hypothalamus or pituitary eg radiotherapy/surgery
Chronic conditions - CF, IBD can delay puberty
Exercise + dieting
Constitional (not pathological)
Endocrine - GH deficiency, hypothyroidism, Cushing's, hyperprolactinaemia
Kallman syndrome (anosmia)
307
Give 3 causes of hypergonadotropic hypogonadism.
Gonads fail to respond to stimulation from FSH and LH. Can be due to:
Damage to gonads - torsion, cancer, infections eg mumps
Congenital absence of the ovaries
Turner's syndrome (XO)
308
What is congenital adrenal hyperplasia?
Congenital deficiency of 21-hydroxylase --> underproduction of cortisol and aldosterone, overproduction of androgens from birth.
309
What is the inheritance pattern of CAH?
Autosomal recessive (common for metabolic/endocrine conditions)
310
Give 3 complications of CAH.
If severe, neonatal hypoglycaemia and electrolyte disturbances (is this like adrenal crisis?)
Mild - tall, facial hair, amenorrhea, deep voice, early puberty
311
What is androgen insensitivity syndrome?
Tissues unable to respond to androgen hormones (eg testosterone) so typical male chalacteristics do not develop, in someone with XY chromosomes.
Female external genitalia and breast tissue with testes in abdomen or inguinal canal.
Absent: uterus, upper vagina, fallopian tubes and ovaries.
312
What structural pathology can cause amenorrhoea?
```
May cause cyclic abdo pain as menses build up
Imperforate hymen
Transverse vaginal septae
Vaginal agenesis
Absent uterus
FGM
```
313
How is secondary amenorrhoea defined? What is the most common cause?
No menstruation for more than 3 months after previous regular menstrual periods, or 6 months in those with irregular periods.
Pregnancy is the most common cause.
314
What is the management of hyperprolactinaemia?
May not need treatment
| Dopamine agonists eg bromocriptine/cabergoline can reduce prolactin production
315
Give 4 investigations would you do for secondary amenorrhea and why?
```
HCG - pregnancy
FSH - high in POF
LH - high in PCOS (high LH:FSH ratio)
Prolactin - hyperprolactinaemia --> MRI
TSH - hypo/hyperthyroidism
Testosterone - high in PCOS, AIS, CAH
Estrgen - if low, and amenorrhea >12 months, need to treat osteoporosis risk with vit D, Calcium, and estrogen (COCP or HRT)
```
316
What is pre menstrual syndrome (PMS)?
Psychological, emotional and physical symptoms in luteal phase of menstrual cycle (prior to bleed). Eg low mood, anxiety, mood swings, irritability, blarting, fatigue. Symptoms resolve once menstruation begins and aren't present before menarche, during pregnancy or after menopause. Caused by fluctuation in oestrogen and progesterone, possible increased sensitivity to progesterone or interaction between sex hormones and neurotransmitters (serotonin and GABA).
317
Can people without periods get PMS?
Yes because they are due to ovarian function so can still occur in hysterectomy, endometrial ablation, COCP, HRT containing progesterone
318
How is PMS diagnosed?
Symptom diary for 2 menstrual cycles shows cyclical symptoms occurring just before and resolving after menstruation. GnRH analogues improve symptoms by temporarily inducing menopause.
319
What is the management of PMS?
Lifestyle: Improving diet, exercise, alcohol, smoking, stress and sleep
COCP containing drospirenone (Yasmin) - antimineralocorticoid. Continous use.
SSRI
CBT
Continuous transdermal oestrogen + progesterogens to endometrial protection eg norethisterone/Mirena
GnRH analogues (cause osteoporosis so reserved for severe cases, give HRT to mitigate these effects)
Hysterectomy and bilateral oophorectomy + HRT
Breast pain - danazole and tamoxifen
Spironolactone for breast swelling, water retention and bloating
See NICE CKS May 2019
320
How is menorrhagia defined?
>80 ml blood loss during menstruation. (40ml is average in normal menstruation). This looks like changin pads more often than 2 hourly, bleeding lasting more than 7 days, and passing large clots.
321
What is the initial management of menorrhagia/HMB?
Exclude and treat pathology - anaemia, fibroids, bleeding disorders, cancer
Contraception wanted? -->
1. Mirena coil
2. COCP
3. Cyclical oral progestogens (risk VTE increased)
Contraception not wanted -->
Tranexamic acid - antifibrinolytic to reduce bleeding
Mefenamic acid - NSAID to reduce pain and bleeding
