Obs and Gynae anki 1 Flashcards
How can urinary incontinece be characterised?
- Overactive bladder/urge incontinence
- Stress incontinence
- Mixed incontinence
- Overflow incontince
- Functional incontinence
How is urinary incontinence investigated?
- Physical exam-in some cases to rule out pelvic organ prolapse and ability to contract pelvic floor muscles
- Bladder diary-minimum of 3 days
- Urinalysis-rule out infection
- Urodynamic studies-cystometry and cystogram
Describe the management of stress incontinence
Conservative: avoid caffeine and fizzy drinks and excessive fluid intake-
Pelvic floor exercises
Medical: Duloxetine-ONLY if conservative doesn’t work and patients doesn’t want surgery
Surgical: GS: Mid urethral slings
Other surgeries: Incontinence pessaries, bulking agents, colposuscpension and fascial slings
How do mid-urethral slings work to treat stress incontinence?
Compress the urethra against a supportive layer and assist in the closure of the urethral sphincter during increased intra-abdominal pressures
How does colposuspension and facial slings work in treating stress incontinence
Involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper
Describe the general conservative management of incontinence
Lifestyle advice: avoid caffeine and fizzy drinks, avoid excessive fluid intake
Pelvic floor exercises
Describe the medical management of urge incontinence
Anticholinergics(antimuscarinics): inhibit the parasympathetic action of the detrusor muscle-
Oxybutinin, tolterodine, etc
Describe the symptoms of a genital prolapse
Pelvic discomfort or a sensation of ‘heaviness’
Visible protrusion of tissue from the vagina
Urinary symptoms such as incontinence, recurrent urinary tract infections or difficulties voiding
Defecatory symptoms, including constipation or incomplete bowel emptying
Sexual dysfunction
Describe the management of a gential prolapse
If asymptomatic and mild: no treatment Conservative: Weight loss, smoking cessation, avoid heavy lifting, pelvic floor exercises
Ring pessary
Surgery
Describe the surgical management for a cystocele
Anterior colporrhaphy, colposuspension
Describe the symptoms of a vaginal fistula
Incontinence-especailly if vesicovaginal(bladder and vagina)
Also: diarrhoea, nausea, vomiting, weight loss
How is a vaginal fistula diagnosed?
Pelvic exam
Cystoscopy and urodynamic studies
Imaging
Describe the management of vaginal fistulas
Conservative: catheterisation, antibiotics to prevent/treat infection
Surgical: fistula repair, tissue grafts
Describe the aetiology of uterine fibroids
Unknown
Genetic, hormonal and environmental factors
How can uterine fibroids cause polycythaemia?
Secondary to autonomous production of erythropoeitin
How are uterine fibroids diagnosed
Trans-vaginal ultrasound: Used to assess the size and location of the fibroids
MRI: Used if ultrasound does not provide enough detail to assess the fibroid for surgery
Biopsy: May be taken if there is any doubt over the diagnosis to differentiate the fibroid from other conditions such as endometrial cancer
Describe the management of asymptomatic fibroids
No treatment, just review to monitor growth and size
Describe the management of menorrhagia secondary to fibroids
Levonorgestrel intrauterine system (LNG-IUS)-Mirena coil first line
Mefenamic acid and TXA
COCP and oral/injectable progesterone
How does red degeneration of fibroids present?
-Severe abdominal pain
-Low grade fever
-Tachycardia
-Vomiting
How is red degeneration of fibroids managed?
Supportive: rest, fluids and analgesia
Describe the aetiology of ovarian cysts
Hormonal imbalances, endometriosis, pregnancy and pelvic infections.
Describe some symptoms of an ovarian cyst
-Asymptomatic
-Acute unilateral pain
Bloating/fullness in the abdomen
-Intra-peritoneal haemorrhage with haemodynamic compromise
Describe the management of a simpole ovarian cyst in premenopausal women
<5cm: often resolve within 3 cycles
5-7cm: gynae referral and yearly US
>7cm: consider MRI or surgical evaluation-difficult to characterise with US
Describe the management of ovarian cysts in postmenopausal women
Post-menopausal-concerning for malignancy
Check Ca125 and referall to gynaecology
High Ca125: 2 week cancer list
Normal Ca125: if simple cyst and >5cm: mUS every 4-6 months
How are persistent or enlarging ovarian cysts treated?
Surgical intervention-laparoscopy->ovarian cystectomy, sometimes with affected oophorectomy
How can benign ovarian cysts becharacterised?
Physiological/functional cysts
Benign germ cell tumours
Benign epithelial tumours
Benign sex cord stromal tumours
Describe the features of follicular cysts
Represent the developing follicle
When these fail to rupture and release the egg the cyst can persist.
Typically on US they have thin walls and no internal structures
Describe the features of a corpus luteum cyst
Occur when the corpus luteum fails to break down and instead fills with fluid
They may cause symptoms such as pelvic discomfort, pain or delayed menstruation.
They are often seen in early pregnancy.
What is an endometrioma?
Lump of endometrial tissue within the ovary, occurring in patients with endometriosis.
They can cause pain and disrupt ovulation
Describe the features of dermoid cysts/germ cell tumours
Benign ovarian teratomas-
Come from germ cells
Can contain tissue types like skin, teeth hair and bone.
Torsion is more likely than with other ovarian tumours
Describe the pathophysiolgy of an ovarian torsion
Twisting of the adnexa and blood supply to the ovary leads to ischaemia. If the torsion persists, necrosis will occur, and the function of that ovary will be lost.
Describe the presentation of a patient with ovarian torsion
Sudden onset severe unilateral pelvic pain
Pain is constant and gets progressively worse
Associated with nausea and vomiting
Pain can also come and go if ovary twists and untwists intermittently
How is ovarian torsion diagnosed?
1st line: Pelvic US(transvaginal ideally, transabdominal as backup)->;’whirlpool sign’ free fluid in pelvis and oedema or ovary
Doppler-> reduced blood flow
Definitive->laparoscopic surgery
Describe the management of ovarian torsion
Urgent admission and gynae involvement
Laparoscopic surgery to:Untwist the ovary and fix it in place(de-torsion)
Remove the affected ovary (oophorectomy)
Laparotomy may be needed if large ovarian mass or malignancy is suspected
Describe the aetiology of lichen sclerosus
Thought to be autoimmune reaction-associated with T1DM
Also genetics and hormonal factors
Describe a typical presentation of a patient with lichen sclerosus
45-60yr old woman
Vulval itching
Soreness/pain
Skin tightness
Painful sex (superficial dyspareunia)
Erosions
Fissures
Koebner phenomenon
Describe the appearance of lichen sclerosus
“Porcelain-white” in colour
Shiny
Tight
Thin
Slightly raised
There may be papules or plaques
How is lichen sclerosus diagnosed?
Mostly clinical
Skin biopsy can be used to confirm the diagnosis-usually done if atypical features are present(e.g. doesn’t respond to treatment, clinical suspicion of cancer etc)
Blood tests to check for potential autoimmune conditions
Describe the management of lichen sclerosus
Topical corticosteroids(dermovate) to reduce inflammation and itching
Avoidance of soap in affected areas to prevent further irritation
Emollients to relieve dryness and soothe itching
Describe the role of tumour suppressor genes in cervical cancer
2 main tumour suppressor genes: P53 and pRb
HPV produces 2 main proteins: E6 and E7
E6 protein inhibits p53
E7 inhibits pRb
Therefore, HPV promotes the development of cancer by inhibiting tumour suppressor genes.
At what age are children vaccinated against HPV?
age 12-13 yrs
Describe the signs and symptoms of cervical cancer
Most commonly picked up on screening incidentally
Abnormal vaginal bleeding (intermenstrual, postcoital or post-menopausal bleeding)
Vaginal discharge
Pelvic pain
Dyspareunia (pain or discomfort with sex)
Urinary/bowel habit change
Abnormal white/red patches on cervix
Mass on PR exam
How is cervical cancer investigated and diagnosed?
-If symptoms-speculum exam and smear test
If abnormal appearance of cervix-urgent cancer referral for colposcopy
How is the cervical intraepithelial neoplasia determined?
Colposcopy NOT screening
Describe the grades of cervical intraepithelial neoplasia
CIN I::mild dysplasia, affecting 1/3 the thickness of the epithelial layer likely to return to normal without treatment
CIN II: moderate dysplasia, affecting 2/3 the thickness of the epithelial layer, likely to progress to cancer if untreated
CIN III: severe dysplasia, very likely to progress to cancer if untreated
What ages and how regularly is cervical cancer screening done in the UK
All women between ages 24-64
25-49 yrs: 3 yearly
50-64 yrs: 5 yearly
Describe the results obtained from cervical cancer screening cytology
Inadequate
Normal
Borderline changes
Low-grade dyskaryosis
High-grade dyskaryosis (moderate)
High-grade dyskaryosis (severe)
Possible invasive squamous cell carcinoma
Possible glandular neoplasia
What is a cone biopsy used for?
Treatment for cervical intraepithelial neoplasia(CIN) and very early-stage cervical cancer.
It involves a general anesthetic.
The surgeon removes a cone-shaped piece of the cervix using a scalpel
This sample is sent for histology to assess for& malignancy
How does Bevacizumab work for cancer treatment
Targets vascular endothelial growth factor A: which is responsible for the development of new blood vessels.
Reduces the development of new blood vessels
Where does endometrial cancer arise from
Endometrium of the uterus
What is the red flag symptoms for endometrial cancer
> 55yrs with post menopausal bleeding-suspected cancer pathway 2ww
How is endometrial cancer investigated?
1)Trans-vaginal ultrasound: endometrial thickness >4mm
2)Hysteroscopy with endometrial biopsy
How is endometrial cancer managed?
Surgery: hysterectomy with bilateral salpingo-oophorectomy-can be curative if limited
Radio/chemotherapy
Progesterone therapy sometimes used in frail elderly women not suitable for surgery
Describe the outcomes of endometrial hyperplasia
- Most return to normal
- 5% become cancer
How is endometrial hyperplasia treated?
Intrauterine system(mirena coil)
Continuous oral progesterones(levonorgestrel)
How does adipose tissue result in increased oestrogen levels?
Contains aromatase->converts androgens.
More adipose tissue->more androgens converted to oestrogen
How common is ovarian cancer?
5th most common malignancy in femals
What might epithelial ovarian tumours contain?
Partially cystic so can contain fluid
How do germ cell ovarian tumours typically spread?
Via lymphatics
Describe the presentation of ovarian cancer
Typically present late-non-specific symptoms
Abdominal pain
Bloating
Early satiety
Urinary frequency or change in bowel habits
Later stages:Ascites(vascular growth factors increasing vessel permeability)
Pelvic, back and abdominal pain
Palpable pelvic or abdominal mass
How is CA125 used to guide further investigations when investigting a patient for possible ovarian cancer?
Raised CA125(>=35IU/mL)-> urgent US of abdomen and pelvis
How is ovarian cancer treated?
Surgery:If early disease-remove uterus, fallopian tubes, ovaries and infracolic omentectomy
Advanced-debulking surgery
Pelvic exenteration if severe
Adjuvant/intraperitoneal chemotherapy
Biologics
Describe the prognosis of ovarian cancer
80% have advanced disease at presentation
All stage 5 year survival is 46%
Why might an ovarian mass result in pain elsewhere?
Presses on the obturator nerve-> referred hip or groin pain
How common is vulval cancer?
Rare-4% of gynae cancers
At what age are the majority of vulval cancers diagnosed?
>60 years
Describe the clinical features of a patient with vulval cancer
Lump on labia majora
Inguinal lymphadenopathy
Itching/discomfort in vulval area
Non healing ulcer
Changes in skin colour/thickening of vulva
Bleeding/discharge not related to the menstrual cycle
How is vulval cancer managed?
Surgery
Radical/wide local excision
Radical vulvectomy for multi-focal disease
Reconstructive surgery
Radiotherapy.chemo
What is a molar pregnancy?
AKA hydatidiform mole
Spectrum of disorders known as gestational trophoblastic disease
Imbalance in no of chromosomes originating from the mother and father during conception
How can molar pregnancies be characterised?
Complete
Partial
Describe the presentation of a patient with a hydatidiform mole
Vaginal bleeding
Enlargement of uterus beyond the expected size for gestational age
Nausea and hyperemesis gravidarum
Thyrotoxicosis
How can a molar pregnancy cause enlargement of the uterus?
Excessive growth of trophoblasts and retained blood
How can a molar pregnancy cause thryotoxicosis?
HCG closely related to TSH so able to activate receptors
How is a molar pregnancy diagnosed?
B-HCG-> higher than normal
Trans-vaginal US->‘snowstorm’ appearance, low resistance of blood vessel flow and absence of a foetus
How are molar pregnancies managed?
Specialist centre-> choriocarcinoma
Suction curettage
Hysterectomy if not fertility performed
Surveillance:
Partial mole, repeat hCG test is done 4 weeks later - if normal, discharge
Complete mole, monthly repeat hCG samples are sent for at least 6 months.
How common is endometriosis?
Common-10% of women in reproductive years
Describe the symptoms of endometriosis
Chronic pelvic pain
Dysmenorrhoea
Dyspareunia
Subfertility
Non-gynaecological-> dysuria, urgency, haematuria
Cyclical rectal bleeding, if endometrium-like tissue grows outside the female reproductive system
Describe the medical management of endometriosis
Analgesia-paracetemol/NSAIDs
Hormonal therapies-mirena coil, COCP, medroxyprogesterone acetate, Gonadotrophin releasing hormone agonists
Describe the surgical management of endometriosis
Laparoscopic excision or ablation plus adhesiolysis-> especially for fertility
Ovarian cystectomy(for endometriomas)
Bilateral oophorectomy(sometimes hysterectomy)
How do patients with adenomyosis typically present?
Asymptomatic
Dysmenorrhoea
Menorrhagia
Dyspareunia
Infertility or pregnancy-related complications
(Older then endo, often post-menopausal women-enlarged boggy uterus’)
Describe the management of adenomyosis
Symptomatic: TXA/mefenamic acid
Mirena coil(first line)
COCP
Cyclical oral progesterones
GnRH agonists
Uterine artery embolisation
Hysterecomy-definitive treatment
How is andorgen insensitivity syndrome diagnosed?
Buccal smear or chromosomal analysis to reveal 46XY genotype
After puberty: hormonal tests
Describe the presentation of a patient with atrophic vaginitis
Vaginal dryness and discharge
Dyspareunia
Occasional spotting
Loss of pubic hair
Urinary symptoms like dysuria and recurrent UTI
Describe the management of atrophic vaginitis
Lubricants and moisturisers
Topical HRT
Systemic HRT
Describe the management of a miscarriage
Conservative: Allow POC to pass naturally-> repeat scan/pregnancy test
Medical:
Missed: mifepristone and misoprostol
Incomplete: misoprostol only
How does vaginal misoprostol work as medical management for a msicarriage?
Stimulates cervical ripening and myometrial contractions
Describe the features of a threatened pregnancy
Painless vaignal bleeding <24 weeks(usually 6-9 weeks)
Bleeding but often less than menstruation
Cervical os closed
How is a threatened pregnancy treated?
ReassuranceIf heavy: admit and observe
If >12 weeks, and rhesus negative: Anti D
Describe the features of an inevitable pregnancy
Heavy bleeding
Clots
Pain
Cervical os open
How is an inevitable miscarriage treated?
Reassurance, if heavy bleeding then admit and observe
If >12 weeks and rhesus negative : Anti D
Likely to proceed to a complete/incomplete miscarriage
Describe the features of a missed/delayed pregnancy
Gestational sac containing a dead fetus <2 weeks without symptoms of expulsion
Cervical os closed
Asymptomatic, light bleeding, discharge, pregnancy symptoms which disappear
How is a missed/delayed miscarriage treated?
Missed: mifepristone then misoprostol 48 hours later
Describe the features of an incomplete miscarriage
POC partly expelled
Symptom of bleeding/clots
Cervical os open
How might a patient with a complete miscarriage present?
History of bleeding
Clots
POC
Pain
Symptoms settled
How are patients with complete miscarriages managed?
Discharged to GP
Describe the symptoms of a septic miscarriage
Infected POC
Rigors
Fever
Bleeding
Leukocytosis
Increased CRP
How is a septic miscarriage treated?
IV antibiotics and fluids
Medical/surgical treatment
Describe the symptoms of a patient with an ectopic pregnancy
Pelvic pain: can be unilateral
Shoulder tip pain-irritation of diaphragm by intra-abdominal bleeding
Vaginal discharge/bleeding-decidua breaking down
Describe the conservative management of an ectopic pregnancy
Close follow up and repeat B-HCG’s
Not usually done
Describe the medical management of an ecoptic pregnancy
IM methotrexate
Regular B-HCG checks : >15% decline by day 4/5 or repeat methotrexate
How does methotrexate work as treatment in a patient with an ectopic pregnancy?
Disrupts folate dependent cell division
Describe the surgical management of an ectopic pregnancy
Tubal ectopics: laparoscopic salpingectomy (remove ectopic and tube)
If only one tube left: salpingotomy (cut in fallopian tube and remove ectopic)
B-HCG follow up until <5iU(negative)-> check for residual trophoblast
How does amniotic fluid normally change throughout pregnancy?
Volune increases until 33 weeks
Platueaus at 33-38 weeks
Decreases at term to reach 500ml
Describe the normal physiological cycle of amniotic fluid
Fetus breathes and swallows fluid, processed and voided through the bladder
Predominantly fetal urine output with some fetal secretions and placenta
How does placental insufficiency cause oligohydramnios?
Blood flows to brain instead of kidneys so there is a lower fetal urine output
How do patients with oligohydramnios present?
Potter’s syndrome:
Fetal compression: clubbed feet, facial deformity, congenital hip dysplasia
Lack of amniotic fluid:
pulmonary hypoplasia in fetus
Describe the management of oligohydramnios
Treat underlying cause and optimise gestation of delivery
Maternal rehydration to increase amniotic fluid volume if mild
Amnioinfusion: saline into amniotic fluid to increase volume
Deliver: may be induced-C-section
Describe the prognosis of patients with oligohydramnios
If 2nd trimester: poor prognosis
If premature delivery and pulmonary hypoplasia: respiratory distress at birth
PLacental insufficiency: higher rate of preterm deliveries
Describe the aetiology of polyhdramnios
50-60%: Idiopathic
1) Escess production due to increased fetal urination:
-Maternal diabetes
-Fetal anaemia
-Fetal renal disorders
-Twin to twin transfusion syndrome
2)Insufficient removal due to decreased fetal swallowing:
-Oesophageal duodenal atresia
-Diaphragmatic hernia
-Anencephaly
-Chromosomal disorders
How is polyhdramnios diagnosed?
USS: Measure amniotic fluid: AFI/MPD
How fast does cervical dilation typicaly progress?
Primiparous: 1cm every 2 hours
Multiparous: 1cm every hour
Describe the physiology of the first stage of labour
Hormones(mostly prostaglandins and oxytocin) stimulate regular uterine contractions
That and pressure from presenting part of foetus->progressive dilation of the cervix
Describe the signs and symptoms of the first stage of labour
Regular, painful contractions
Progressive cervical dilation
Passage of blood stained mucus-‘show’
Rupture of membranes
Descent of foetal head into pelvis
How is the first stage of labour managed?
Pain relief-> epidural analgesia, nitrous oxide, opioids
Encourage mobility and changes in position to facilitate labour progression
Ensure hydration and nutritional support
Regular monitoring
How is the second stage of labour managed?
Instrumental delivery
C-section
How long does the third stage of labour usually last?
Natural: 30-60 minutes
With oxytocin: 5-10 minutes
How is the 3rd stage of labour managed?
Controlled cord traction->gently to avoid uterine inversion/PPH
If retained placenta: manual removal or curettage may be necessary
How is labour induction carried out?
Membrane sweep: insert finger into extenral os and separate membranes from cervix
Vaginal prostalgandins: Used to ripen cervix and induce contractions
Amniotony: artificial rupture of membranes
Ballon catheter: mechanically dilates cervix
Describe the aetiology of pre-term labour
Overstretching of uterus: multiple pregnancy, polyhydramnios
Foetal risk complications: pre-eclampsia, placental abruption
Uterus/cervical problems: fibroids, malformations
Infections: chorioamnionitis, sepsis, group B strep etc
Maternal co-morbidity: htn, diabetes etc
How might patients with pre term labour present?
Regular uterine contractsion/changes in cervical effacement or dilation/rupturing of membranes before onset of contractions
How is pre term labour managed?
Corticosteroids: betamethasone/dex to assist foetal lung maturation
IV abx if increased risk of infection(penicillin)
Tocolytic agents may be used(nifedipine), risk of side effects
How is menopause diagnosed?
Clinically: absence of menarche for 12 months in someone >45
If <40: test FSH etc
Describe the management of menopause
Conservative:
Lifestyle: regular exercise, weight loss, good sleep
Medical:HRT, SSRI’s
Vaginal lubricants/moisturisers
Clonidine for vasomotor
In terms of time frames, when can HRT be given?
Cyclically: perimenopausal women still having periods
Continuously: Post menopausal not having periods
How is HRT given cyclically?
Monthly: oestrogen every day of months and progesterone for last 14 days
Every 3 months: Oestrogen very day for 3 months and progesterone for the last 14 days
How can menopause result in dyspareunia?
Vaginal dryness from reduced oestrogen
How can menopause result in urinary incontinence?
Caused by epithelial thinning as a result of decline in oestrogen
Describe the feedback systems that control the menstrual cycle
Moderate oestrogen levels-> negative feedback on HPG
High oestrogen with no progesterone-> positive feedback on HPG
Oestrogen +progesterone-negative feedback on HPG
Inhibin selectively inhibits FSH at anterior pituitary
How much blood is usually lost during menses?
10-80ml
Describe the epidemiology of PCOS
Common
Affects up to 1/4 of women during reproductive years
Describe the aetiology of PCOS
Hormonal imblanaces-unknown?
Hyperandrogenism
Insulin resistance
Elevated levels of LH
Raised oestrogen
Describe the symptoms of PCOS
Oligomenorrhoea
Subfertility
Acne
Hirsutism
Obesity
Mood changes: depression, anxiety
Male pattern baldness
Acanthosis nigracans->secondary to insulin resistance
Describe the rotterdam diagnositc criteria
> =2 of:
Polycystic ovaries(>12 cysts on imaging or ovarian volume >10cubic cm)
Oligo/an ovulation
Clinical or biochemical features of hyperandrogenism
How is PCOS managed?
Conservative:Weight loss, exercise, educate on risks of diabetes.cvr.endometrial cancer
Medical for those not planning pregnancy:COCP
Metformin
Medical for those wanting to conceive:
Clomiphene-induces ovulation
Metformin
Gonadotrophins-induce ovulation
Surgical for those wanting to conceive:
Ovarian drilling: laparoscopic-damages hormone producing cells of ovary
How can endometrial curettage result in Asherman’s syndrome
Damages basal layer of endometrium->heals abnormally creating adhesions connecting areas of the uterus that aren’t normally connected
Adhesions can bind uterine walls together or might seal the endocervix shut
How do adhesions cause problems in Asherman’s syndrome?
Can cause physical obstruction and distort pelvic organs->menstrual abnormalities, infertility and recurrent miscarriages
How might patient with Asherman’s syndrome present?
Secondary amenorrhoea(absent periods)
Significantly lighter periods
Dysmenorrhoea
Infertility
In a patient with prior pelvic surgery
How is Asherman’s syndrome diagnosed?
Hysteroscopy: GS-can also treat adhesions
Hysterosalpingography
Sonohysterography
MRI
How is Asherman’s syndrome treated?
Dissect adhesions during hysteroscopy
How are congenital uterine abnormalities diagnosed?
USS
Hysterosapingography
MRI-considered best
How are congenital uterine abnormailites managed?
Surgical intervention
Give some examples of congenital uterine malformations
Complete failure of duct fusion:
double vagina, double cervix, double uterus
Septate uterus
arcuate uterus
Give some examples of congenital vaginal abnormalities
Vaginal agenesis
Vaginal atresia
Mullerian aplasia-normal external genitalia but absense of vagina
transverse vaginal septa
How might abnormalities of the hymen present?
Obstruciton of menstrual flow after puberty
Descriebe the pathogenesis of polyps
Involves oestrogen->stimulates endometrial growth
Can arise from hyperplasia of basal layer of endometrium
How are endometrial polyps diagnosed?
Speculum exam
USS
How are endometrial polyps managed?
ASX in premenopausal: monitor
Symptomatic/postmenopausal/atypical: removed via hysteroscopic polypectomy
Histology of removed polyp to exclude malignancy
Describe the presentation of a patient with PID
Bilateral abdominal pain
Vaginal discharge
Post-coital bleeding
Adnexal tenderness
Cervical motion tenderness
Fever
Dysuria and menstrual irregularities
How is Fitz Hugh Curtis syndrome diagnosed and treated?
Normal LFTs
US rule out stones
Definitive dx: laparoscopy
Tx: abx
How is PID managed?
IM ceftriaxone+14 days oral doxycycline+metronidazole
2nd line: oral ofloxacin+oral metronidazole
Consider removal of IUD
Avoid unprotected sexual intercourse
Describe the epidemiology of urinary tract stones
CommonM>F
>65 yrs
Can be both renal and ureteric
Describe the aetiology of renal stones
Calcium oxalate-mc
Calcium phosphate
Cystine
Uric acid
Struvite
Indinavir
How might patient with urinary tract calculi present?
Severe intermittent loin pain that can radiate ot the groin
Restlessness
Haematuria
N+V
Sedoncary infection of stone->fever/sepsis
How are renal stones managed?
Analgesia
Wait if <5mm
Medical expulsive therapy
Extracorporeal shockwave lithotripsy
Uteroscopy-pregnancy women
Prevention
How can pituitary adenomas be classified?
Size -micro(<1cm) or macro(>1cm)
Hormonal status (secretory vs non secretory)
Describe the symptoms of a prolactinoma in men
Macroadenomas:
Headache
Visual disturbance-bitemporal hemianopia
Hypopituitarism signs and sx
Excess prolactin:
Impotence
Loss of libido
Galactorrhoea
Describe the symptoms of prolacitnomas in women
Macroadenomas:
Headache
Visual disturbance-bitemporal hemianopia
Hypopituitarism signs and sx
Excess prolactin:
Amenorrhoea
Infertility
Galactorrhoea
Osteoporosis
How is a prolactinoma diagnosed?
MRI head
How are prolactinomas treated?
Dopamine agonists: cabergoline, bromocriptine(inhibits release of prolactin)
Trans-sphenoidal surgery: those who can’t tolerate therapy
Describe the surface anatomy of the breast
Lateral border of sternum at mid axillary line
2nd and 6th costal cartilages
Superficial to pectoralis major and serratus anterior muscles
Circular body
Axillary tail
Describe the mammary glands with regards to breast anatomy
Modified sweat glands-> ducts and secretory lobules
Each lobule consists of many alveoli drained by a lactiferous duct
Describe the connective tissue stroma with regards to breast anatomy
Fibrous and fatty component
Fibrous stroma condenses to form suspensory ligaments
Attach and secure breast to dermis and underlying pectoral fascia
Separate secretory lobules of breast
Describe the pectoral fascia with regards to breast anatomy
Flat sheet of connective tissue associated with pec major
Retromammaroy space-> layer of loose conective tissue between breast and pectoral fascia(used in reconstruction)
Describe the medial vasculature of the breast
Internal thoracic(mammary) artery->branch of subclavian
Describe the lateral vasculature of the breast
Lateral thoracic and thoracocromial branches-> axillary
Lateral mammary branches->posterior intercostal arteries
Mammary branch-> anterior intercostal artery
How does lymphatic drainage link into the presentation of patiens with breast cancer
Blockages of lymphatic drainage->lymph builds up in SC tissues->nipple deviation and retraction, peau d’orange
Metastasis can occur through lymph nodes->axillary mx, then can spread to liver, bones and ovary
Describe the nerve supply of the breast
Anterior and lateral cutaneous branches of 4th-6th IC nerves(autonomic and sensory nerve fibres)
Describe the epidemiology of fibroadenomas
Young women-early 20s
Describe the presentation of a patient with a fibroadenoma
Firm, non-tender breast mass
Rounded and smooth edges
Highly mobile on palpation-‘rubbery’ <3cm in diameter(mc 2.5cm)Usually slow growing and solitary
Describe the management of fibroadenomas
Conservative: Leave, usually regress naturally post menopause
Surgical excision: considered if large, growing, causing significant symptoms or diagnostic uncertainty
Describe the epidemiology of fibrocystic breast disease
Most common benign breast condition
20-50 years
Describe the aetiology of fibrocystic breast disease
Cumulative effect of cyclical hormone
Mostly oestrogen and progesterone-> multiple cysts and proliferative changes
Describe the presentation of a patient with fibrocystic breast disease
Bilateral ‘lumpy’ breasts, most commonly in upper outer quadrant
Breast pain
Sx worsen with menstrual cycle and peak 1 week before menstruation
Describe the management of fibrocystic breast disease
Encourage use of soft, well-fitting bra
Analgesia for pain relief
Most resolve after menopause
Describe the eppidemiology of breast cancer
Commonest cancer in UK in women
2nd most common cause of cancer deaths
Describe the pathophysiology of breast cancer
Genetic mutations and damaged cellular signalling-> generation of malignant cells-> metastasise
Describe how breast cancer cells metastasize
Invasion through basement membrane
Intravasation(entry into circulation)
Circulation
Extravasation
Colonisation
Describe the features of ductal carcinoma in situ
From epithelial cells
Confined to ducts
Describe the features of lobular carcinoma in situ
Area of abnormal cell growth that increases risk of developing invasive breask cancer later
Describe the features of invasive ductal carcinoma
Mc
Starts in epithelial cells in milk duct-> invades fatty tissue of breast
Describe the features of medullary carcinoma
Younger people
Higher grade than invasive ductal carcinoma
Describe some signs and symptoms of breast cancer
Unexplained breast/axillary mass in those >30 years
Nipple discharge
Nipple retraction
Skin changes-p’eau d’orange
Metastatic features: weight loss, bone pain, SOB
How is breast cancer diagnosed?
1st line: imaging:>30yrs and clinical suspicion: mammogram
<30yrs: USS of axilla
2nd line: biopsy
Fine needle aspiration and cytology
Others:
Oestrogen/progesterone receptor testing,
HER2 receptor testing
CT if metastatic disease suspected
Describe the stages of breast cancer
1A: <2cm, isolated to breast
1B: <2cm, minor axillary LN spread
2A: <2cm, spread to 1-3 ipsilateral lymph nodes
2B: 2-5cm, minor axillary node spread or >5cm with no nodal spread
3A: 4-9 ipsilateral LN spread/>5cm with 1-3 ipsilateral nodes
3B: Spread to skin, chest wall
3C: >10 axillary nodes/supraclavicular/parasternal/axillary spread
4: metastatic spread to other organs
How can bisphosphonates be used in the treatment of breast cancer?
Can help reduce recurrence in node-positive cancers
What are fibroadenomas?
Fibroadenomas-overgrowth of glandular and connective tissue resulting in blocked breast ducts and subsequent fluid accumulation
Describe the general management of benign breast disease
Reassurance: often only need monitoring
Antibiotics: for infections like mastitis
Analgesics
Surgery: e.g. large fibroadenomas, persistent cysts, symptomatic intraductal papillomas
Describe the epidemiology of Paget’s disease of the nipple
Rare: <5% of all breast cancer patients
Most common in postmenopausal women
Describe the aetiology of Paget’s disease of the nipple
2 theories:
Epidermotrophic: underlying breasst cancer cells migrate to the nipple
Intraepidermal origin: originates in nipple itself
Describe the signs and symptoms of a patient with Paget’s disease of the nipple
Eczema like rash on skin of nipple/areola(often crusty, red, inflamed, itchy)
Bloody nipple discharge
Non-healing skin ulcer
Changes to nipple-> retraction/inversion
Pain
Breast lump
How is Paget’s disease of the nipple diagnosed?
Mammography/US
Punch biopsy of affected skin, nipple discharge cytology
MRI for staging in uncertain cases
How is Paget’s disease of the nipple different to eczema of the nipple?
Paget’s involves the nipple primarily and only latterly spreads to the areolar(opposite way around in eczema)
How is Paget’s disease of the nipple treated?
Depends on underlying lesion
Simple mastectomy: remove entire breast and nipple and areeola
Modified radical mastectomy: remove some axillary lymph nodes
Lumpectomy
Chemo, radiation, hormonal
Describe the latent phase of labour
Contractions(may be irregular)
Mucoid plug
Cervix beginning to efface and dilate(0-4cm)
Can last up to 2-3 days
Describe the features of contractions
Starts in the fundus(pacemaker)
Retraction/shortenng of muscle fibres
Build in aplitude as labour progresses
Fetus forced down causing pressure on the cervix
Describe the features of a gynaecoid pelvis
Inlet is slightly transverse oval
Sacrum wide with average concavitiy and inclination
Side walls straight with blunt ischial spines
Wide suprapubic arch
How might midwives help with the delivery of the body stage of labour?
Gentle downward traction to assist with delivery of shoulder below suprapubic arch
Gentle upwads traction to assist delivery of posterior shoulder
Describe the anatomy of the placenta and how it is connected to the fetus
Lobes which attach to the uterine wall
Connected to fetus via umbilical cord whcih has 2 arteries and a vein
How is a ventouse used?
Cup is applied with centre over flexion point on fetal skull
During uterine contractons, traction applied perpendicular to cup
At what age gestation is non invasive prenatal testing available?
From 10 weeks
At what week gestation is CVS offered for?
11-14 weeks gestation
How many weeks gestatin would amniocentesis be performed?
>15 weeks
Describe the epidemiology of mastitis
Postpartum: 10-20% prevalence
Usually in first 6 weeks post birth
Increased risk in 1st time mothers and previous hx of mastitis
Describe the aetiology if mastitis
Milk stasis->inflammatory response and potential secondary infection
Cracked/sore nipples-> S.aureus-> infective mastitis
Describe the presentation of mastitis
Localised: painful, red, tender, hot breast
Systemic: fever, rigors, myalgia, fatigue nausea and headache
Usually unilateral-presents 1st week post partum
How is mastitis diagnosed?
Mostly clinical
US to ID if suspicion of abscess-> done in secondary care
How is mastitis managed?
Reassure lactating women they can continue to breastfeed
Advice on methods to faciliate milk expression
Analgesia
Oral/IV abx, surgery if abscess
Describe the aetiology of a breast abscess
S.aureus mc through crack in nipple/through milk duct
Accumulation of milk, trauma to nipple skin from incorrect latch/pump
Describe the presentation of a patient with a breast abscess
Fever/rigors
Malaise
Pain and erythema over an area of the breast
Possible presence of a fluctuant mass->might not be palpable
Hisotry of recent/ongoing mastitis
How is a breast abscess diagnosed/investigated?
Breast USS-> visualise abscess and guide drainage
Diagnostic needle aspiration-> culture organism and evacuation
How is a breast abscess managed?
Incision and drainage/needle aspiration(with/out US guidance)
Abx therapy targeted towards most likely causative organism
Describe the epidemiology of bacterial vaginosis?
Mc cause of abnormal dishcarge in women of childbearing age
More common in sexually active women but not an STI
Describe the pathophysiology of bacterial vaginosis
Disturbance of normal vaginal flora->decrease in number of lactobacilli bacteria
How is bacterial vaginosis managed in pregnanct/lactating women?
Screening done antenatally and quick treatment if needed
Lower doses of metronidazole in lactating women
Describe the epidemiology of vulvovaginal candidiasis
Highlyy prevalent: 20% of women/yr
Most women will experience it at some point in their lifetime
Describe the aetiology of vulvovaginal candidiasis
Candida albicans- replicated by budding
Opportunistic infection vs hypersensitivity reaction
Describe the symptoms of vulvovaginal candidiasis
Pruritus vulvae
Vaginal discharge-white, curd like
Dysuria
How is vulvovaginal candidiasis diagnosed/inveestigated?
Usually history/clinical
Vaginal smear and mc+s-> blastospores, pseudohyphae and neutrophils
Describe the management of vulvovaginal candidiasis
Oral fluconazole single dose
Clotrimazole pessayr if CI(including pregnancy)
Vulval sx: consider topical imidazole
How is vulvovaginal candidiasis treated in pregnancy?
Clotrimzole pessary
DO NOT use oral antifungals
Advise care with intravaginal treatment applicator
Saftynetting if not resolved in 7-14 days
Describe the epidemiology of chlamydia
Most common STD in UK
Highest prevalence in 15-24 yr olds
How is chlamydia transmitted?
Via unprotected vaginal, oral, anal sex
Skin to skin contact of genitalsVertical(mother to baby during delivery)
Describe the signs and symptoms of chlamydia in men
Often asymptomatic: incubation period 7-21 days
Urethritis: dysuria, urethral discharge
Epididymo-orchitis: testicular pain
Epididymal tenderness
Mucopurulent discharge
Describe the signs and symptoms of chlamydia in women
Asymptomatic often: incubation period 7-21 days
Dysuria
Discharge
Intermenstrual bleeding
Pain/tenderness
Describe the signs and symptoms of chlamydia in neonates
Pneumonia
Conjunctivitis
How is chlamydia diagnosed?
Women: vulvovaginal swab
Men: first catch urine sample
Analyze using nucleic acid amplification tests
Describe the management of chalmydia in non-pregnant people
Doxycycline: 100mg twice daily for 7 days
Describe the management of chlamydia in pregnant women
Azithromycin/erythromycin
Describe the management of neonates with chlamydia
Oral erythromycin
Describe the epidemiology of gonorrhoea
2nd most common STI after chlamydia-increased prevalence in 15-24yrs->Higher prevalence in MSM
How is gonorrhoea transmitted?
Unprotected vaginal/oral/anal sex
Vertical transmission
Describe the aetiology and pathology of gonorrhoea
Gram negative diplococcus neisseria gonorrhoea
Causes acute inflammation-> uterus, urethra, cervix, fallopian tube, ovaries, rectum, testicles, eyes, throat
How do patients with gonorrhoea present?
Males: urethral discharge, dysuria
Women: discharge, dysuria, dyspareunia, pain
Dishcarge tends to be thin, watery green/yellow
Asymptomoatic especially when rectal/pharyngeal infection
How is gonorrhoea diagnosed?
Females: endocervical/vaginal/urethral swab
Males: first pass urine(NAAT), urethral/meatal swab
Microsopcy, culture and NAAT
How is gonorrhoea treated?
Singled dose 1g IM ceftriaxone
Screen/treat other infections-test of cure recommended
Describe the symptoms of disseminated gonococcall infection
Tenosynovitis
Migratory polyarthritis
Dermatitis
How is gonorrhoea treated in pregnancy?
Prophylactic abx+tx in pregnancy->ceftriaxone
How are neonates with gonorrhoea managed?
Urgent referral and treatment
Long term damage and blindness
Describe the epidemiology of genital herpes
Very common
15-24yrs
Describe the pathophysiology of genital herpes
After infecting surface-> travels up to meet nearest ganglion and stays there until reactivated
Describe the presentation of a patient with a primary genital herpes infection
Asymptomatic
Small, painful red blisters around genitals, can form open sores
Vaginal/penile discharge, dysuria, urinary retention
Flu like sx-> fever ,muscle aches, malaise, headaches
After 20 days: lesions crust and heal-> end of viral shedding
Describe the presentation of a patient with an outbreak of a genital herpes infection
Usually shorter and less severe than initial infection
Burning, itching, painful red blisters
How is genital herpes diagnosed?
Clinical hz and exam
Swab from base of ulcer-> NAAT
Describe the management of genital herpes
Primary infection: aciclovir 400mgTD 5 days
Recurrent outbreaks: OTC analgesia, ice, topical lidocaine
Regular episodes: episodic aciclovir tx when sx begin
Describe the management of herpes in pregnancy
Low risk of transmission with vaginal birth
Referral to GUM clinic and treat with aiclovir if 1st time HSV infection
If contracted in last trimester: antibodies not developed-> C-section
Describe the features/management of neonatal herpes
Skin/eyes/mouth herpes(SEM)-antiviral tx
Disseminated herpes(DIS)-internal organs
CNS herpes-> encephalitis
DIS and CNS herpes associated with increased mortality
Describe the aetiology of genital warts
90% HPV 6/11-low risk, not associated with cancer
How do patients with genital warts typically present?
Asx
Painless warts of scrotum, penis, vagina, cervix, perianal skin, anus
Warts can be keratinised(hard) or non-keratinised(soft)
Extra-genital lesions: oral cavity, larynx, nasal cavity, conjunctivae
How are genital warts diagnosed/
Usually from clinical exam/hx
Proctoscopy/vaginal speculum exam to check for internal warts
Biopsy for atypical lesions/suspected intraepithelial neoplastic lesions
Describe the management of genital wwarts
Tx not always needed, can resolve spontaneously
Topical:Podophyllotoxin: antiviral to destroy clusters(BD 3 days then 4 days rest)
Imiquimod: immune response modifier for larger keratinised warts(3 times/week)
Physical:Cryotherapy
Surgical excisionElecrto/laser-surgery
How does pregnancy impact genital warts?
No risk to babies but maternal warts can multiply/enlarge during pregnancy
Describe the pathophysiology behind the HIV infection
Penetrates host CDD4 cell and empties its contents.
Single strands of viral RNA converted to double stranded DNA by reverse transcriptase and combined host DNA using integraseInfected cell divides, viral DNA read->creates viral protein chains and immature virus pushes out of cell, retaining some membranes
Virus matures when protease cuts viral protein chains and assemble to create a working virus, destroying a host cell
How do CD4 levels change over the course of the HIV infection?
Seroconversion(producing anti-HIV antiibodies during primary infection)->flu-like sx->decrease in CD4 levels due to initial rapid replication-> extremely infectious
Latent phase: months-yrs: initial asx but increased susceptibility to infections
How is HIV transmitted?
Unprotected sexual intercourse
Sharing needles
Medical procedures
Vertical transmission
Describe the symptoms of the seroconversion stage of HIV
2-6 weeks post exposure
Fever
Muscle aches
Malaise
Lymphadenopathy
Maculoapular rash
Pharyngitis
Describe the symptoms of the symptomatic stage of HIV
Weight loss
High temperature
Diarrhoea
Frequent opportunistic infections
Describe the symptoms of the AIDS defining illness stage
Advanced stage: immune system significantly weakened
Deveopment of AIDS defining illnesses/infections/malignancies
How is HIV diagnosed?
4th generation tests:ELISA-> test for serum/salivary HIV antibodies and p24 antigen
Reliable results 4-6 weeks post exposure
Contact tracing
Describe the management of HIV
HAART: highly active antiretroviral therapy >=3 drugs: usually 2 nRTIs and 1 PI/NNRTI
Decreases viral replication and reduces risk of viral resistance emerging
Describe the features of NNRTI’s
non-nucleoside reverse transcriptase inhibitors
E.g. nevirapineSE: P450 enzyme interaction, rashes
Describe the features of protease inhibitors
E.g. indinavir, nelfanivir
SE: diabetes, hyperlipidaemia, central obesity, P450 enzyme inhibitirion
Describe the features of integrase inhibitors
E.g. raltegravir, elvitegravir
Block the action of integrase(viral enzyme that inserts the viral genome into the DNA of the host cell)
How is HIV managed in pregnancy and why?
Can be transmitted in utero, at delivery and through breast-feeding
Risk reduction strategies
C-section non longer recommended if undetectable viral load
How is the risk of HIV transmission in pregnant women minimised?
Anttenatal antiretroviral therapy during pregnancy and delivery
Avoidance of breastfeeding
Neonatal post-exposure prophylaxis
How do patients with a threatened miscarriage present?
Painless vaginal bleeding <24 weeks(usually 6-9 weeks)
Bleeding often less than menstruation
How can the aetiology of polyhydramnios be classified?
Idiopathic
Excess production due to increased fetal urination
Insufficient removal due to decreased fetal swallowing
How might a patient with polyhydramnios present?
Uterus feels tense/large for dates
Difficult to feel fetal parts on abdominal palpation
How is polyhydramnios managed?
Usually no intervention needed
Treat underlying cause
Severe only: amnioreductionIndomethacin
How is indomethacin useful for treating polyhydramnios?
Enhances water retention and decreases fetal urine output
How is prolonged pregnancy managed?
Membrane sweeps-40 wks nulliparous, 41 wks in parous
Induction of labour-41/42 weeks gestation
If 2 declined: twice weekly CTG monitoring and US with amniotic fluid measurement to predict fetal distress.
Might need C-section
How do patients with placenta praevia present?
Painless bright red vaginal bleeding after 24 weeks
Sometimes pain if in labour
Can present with signs of shock if severe blood loss
Malpresentation of fetus due to abnormal placental position
Describe the management of acute presentation of placenta praevia
ABCDE approach
If bleeding not controlled/in labour: C-section
Anti-D within 72 hours of bleeding onset if rhesus D negative
How is placenta praevia managed if found in a 20 week scan
Placenta praevia minor: rpt scan at 36 weeks-likely to move
Major: rpt at 32 weeks and plan for delivery-> usually elective c-section
Advice about pelvic rest: no penetrative sexual intercourse and go hospital if major bleeding
Describe the pathophysiology of placental abruption
Rupture of maternal vessels in basal layer of endometrium-> blood gathers and splits placental attachment from basal layer
Detached portion unable to function-> rapid fetal compromise
How might patients with placental abruption present?
Painful vaginal bleeding
If in labour: may have pain between contractions
Abdominal pain: often sudden and severe
Hypovolaemic shock disproportionate to amount of vaginal bleeding visible
How is placental abruption managed?
ABCDE resus including anti D if rh D negative
Tx dependent on health of fetus
Emergency delivery: usually C section, even if in-utero death
Induction of labour at term to avoid further bleeding if haemodynamically stable
Describe the natural progressin of most breech babies
20% breech at 28weeks
Most revert to cephalic presentation spontaneously with only 3% still breech at term
How is breeech presentation diagnosed?
Clinical:Head felt in upper uteris, buttocks and legs in pelvis
Fetal heart auscultates higher on maternal abdomen on US
20% not diagnosed until labour
How might breech presentatin present at labour?
Fetal distress->meconium stained liquor
Vaginal exam: sacrum/foot felt through cervical opening
Describe the management of breech presentation
External cephalic version: offered at 37 weeks to primiparous women
C-section
Vaginal breech birth
How is abnormal fetal lie/malpresentation/malrotation diagnosed?
Abdominal exam
Confirm with US-> also ID predisposing abnormalities
Describe the management of abnormal fetal lie
External cephalic version(ECV)-> 36-38 weeks gestation
Describe the management of malpresentation
Breech: ECV before labour, vaginal birth, C section
Brow: c-section
Shoulder: c -section
Face: chin posterior: c section,
chin anterior: attempt normal labour
Describe the management of malposition
90% spontaneously rotate during labour
If not: operative vaginal delivery/C-section
Describe the pathophysiology of pre-eclampsia
High resistance, low flow uteroplacental circulation develops as constrictive muscular walls of spiral arterioles are maintained
Increase in BP, hypoxia-> systemic inflammatory response
Describe the symptoms of pre-eclampsia
Headaches
visual changes
Epigastric pain
Sudden onset non-dependent oedema
Hyper-reflexia
Describe the management of pre-eclampsia
Serial monitoring: BP, urinalysis, fetal growth scans, CTG
VTE-LMWH
Anti-hypertensives-labetalol, nifedipine, methyldopa
Delivery(give IM steroids if <35 weeks)
Post-natal: monitor for 24 hours post partum and BP for 5 days
Descrbe the split of eclamptic seizures in the post natal, antepartumand intrapartum periods
Post-natal: mc-44%
Antepartum: 38%
Intrapartum: 18%
Describe the symptoms of eclampsia
New onset tonic clonic seizure in presence of pre-eclampsia
Lasts 60-75 secs then post-ictal phase
May cause fetal distress and bradycardia
Describe the management of eclampsia
Rescuscitation
ABCDE approach
Pt lie in left lateral position and secure airway and O2 therapy
Seizure control:Magensium sulphate
Monitor for signs of magensium poisoning
BP control:IV labetalol and hydralazine
Delivery of baby and placenta:Usually C-section
Monitoring:Fluid balance: prevent pulmonary oedema and AKI
Monitor platelets, transaminases and creatinine
How long should a magnesium suflate drip be continued for after an eclamptic seizure?
48 hours after last seizure
How is trichomoniasis transmitted?
Predominanly sexual
Describe the epidemiology of trichomoniasis
Mc non-viral STI globally
Describe the signs and symptoms of trichomoniasis in women
Profuse, frothy, yellow vaginal discharge
Vulvovaginitis
Dyspareunia
Strawberry cervix-may be seen
pH>4.5
Asx
Describe the signs and symptoms of trichomoniasis in men
Usually asymptomatic
Non-gonococcal urethritis
How is trichomoniasis diagnosed?
Direct microscopy and culture of the causative organism-> motile trophozoites
pH>4.5
Test for other STIs
How is trichomoniasis treated?
Oral metronidazole for 5-7 days or single dose of 2g orally
Abstain from sex for a week
Screen for others
Contact tracing
Describe the epidemiology of chancroid
Global incidence decreasing
Mc in tropical areas and greenland
Describe the symptoms of chancroid
Painful genital ulcers which may bleed on contact-ulcers are sharply defined, ragged, undermined border
Painful inguinal lymphadenopathy
Sx 4-10 days after bacterium exposure
How is chancroid diagnosed?
Usually clinical
Can culture and use PCR
How is chancroid treated?
Antibiotics: ceftriaxone/azithromycin/ciprfloxacin
Analgesics
Incision/drainage of buboes
Describe the presentatin of a patient with lymphogranuloma venereum
Stage 1: small painless pustule which later forms an ulcer
Stage 2: painful ingional lymohadenopathy-may from fistulaitng buboes
Stage 3: proctocolitis(can include rectal pain and discharge)
How is lymphogranuloma venereum diagnosed?
PCR from swab of genital ulcer
How is lymphogranuloma venereum managed?
oral doxycuclin 100mg twice daily for 21 days
Can also use: tetracycline, erythromycin
How is lymphogranuloma venereum different to ‘normal’ chalmydia?
Normal chalmydia: urethritis and PID: Chlamydia trachomatis serovars D-> Klymphogranuloma venereum: serovards L1, L2, L3
Describe the aetiology of balanitis
Mc: infective: bacterial and candidal
Autoimmune causes
How is balanitis investigated/diagnosed?
Usually clinical-hx and exam
Swab for mc+s/PCR->bacteria or candida albicans
If doubt/extensive skin changes: biopsy
Describe the general treatment of balanitis
Gentle saline washes
Wash properly under foreskin
1%hydrocortisone for a short period
Treat underlying cause
How is balanitis due to dermatitis treated?
Mild potency steroid- hydocortisone
How is balanitis due to lichen sclerosus treated?
High potency topical steroids
Clobetasol
Circumcision can help
How is balanitis due to candidiasis treated?
Topical clotrimazole for 2 weeks
How is syphilis transmitted?
Direct contact with syphilis sores or rash during vaginal, anal or oral sex
Vertical: mother to child
Describe the features of primary syphilis?
Chancre-painless ulcer at the site of sexual contact
Local non-tender lymphadenopathy
Often not seen in women(lesion can be on the cervix)
Describe the lesion associated with the primary syphilis infection
Painless
Round, indurated base
Heals spontaneously within 3-8 eeks
Describe the features of secondary syphilis
Systemic: fevers, malaise etc
Rash on trunks, palms and sores buccal ‘snail track’ ulcers
Condylomata lata (painless warty lesions on genitalia)
Describe the features of tertiary syphilis
Gummas(granulomatous lesions of skin and bones)
Ascending aortic aneurysms
neurological: demenita, paresis, tabes dorsalis, argyll-robertson pupil)
Describe the features of congenital syphilis
Presents shortly after birth or later in infancy
Rash: palms/soles, mucous patches/leisons in motuh/nose/genitals
Feever
Blunted upper incisor teeth(Hutchinson’s teeth), ‘mulberry’ molars
Rhagaades( linear scars at angle of mouth)
Keratitis
Saber shins
Saddle nose
Neruological; seizures, developmental delay
How can serological tests for syphilis be divided?
Non-treponemal tests
Treponemal specific tests
Describe the features of non-treponemal tests for syphilis
Not-specific for syphilis: false positives
Based on reactivity of serum from infected patients to a cardiolipin cholesterol-lecithin antigen
Negative after treatment
Describe the features of treponemal specific tests?
More complex and expensive but sspecific for syphilis
Positive for life-even after treatment
Qualitative
Describe the treatment pf syphilis
IM benzathine penzylpenicillin
Tertiary/late latent: longer course of IM penicillin
Neurosyphilis: IV penicillin G for 10-14 days
Backup for penicillin allergy: doxycycline
How might patients with intraductal papilloma present?
Bloody discharge from the nipple
With/without a palpable mass
May have breast tenderness
How are intraductal papillomas treated?
Often surgery recommended
How can breast cysts be classified?
Microcysts: seen on imaging but too small to be felt
Macrocysts: 1-2cm: large enough to be felt
How might patients with mammary duct ectasia present?
Tender lump arounf areola +/- thick green nipple discharge
If ruptures: local inflammation-> ‘plasma cell mastitis’
Describe the treatment for mammary duct ectasia
Surgical intervention may be needed if symptomatic
Describe the epidemiology of HELLP syndrome
Rare
Significant cause of maternal and perinatal morbidity/mortality
Describe the aetiology of HELLP syndrome
Unknown
Related to abnormal placentation, endothelial cell injury and generalized inflammatory response
Describe the presentation of patients with HELLP syndrome
N+V
RUQ pain-> liver distention
Lethargy
Headaches
Blurred vision
Peripheral oedema
Describe the maangement of HELLP syndrome
Definitive: deliver baby
Steroids: accelerate fetal lung maturation
Blood transfusions to manage anaemia and thrombocytopenia
Describe the epidemiology of cord prolapse
Relatively rare
Higher risk in breech presentations and multiple pregnancies
Describe the pathology of cord prolapse
Usually membrane rupture-> amniotic fluid egress-> descent of umbilical cord
Cord compression-> against maternal soft tissues or bony pelvis->fetal hypooxia
How might patients with cord prolapse present?
Abnormal fetal heart rate: mc varibable/prolonged decelerations
Palpable umbilical cord
Sudden onset of sympotms post rupture of membranes
Patient reported sensation
How is a cord prolapse investigates/diagnosed?
Clinical
USS
Cardiotocoography(CTG)
Speculum exam
How is cord prolapse managed?
Immediate delivery of fetus-> instrumental or C section
‘knees chest’ or ‘all fours’ position to reduce pressure on cord
Elevation of presenting part
Avoid exposure and handling of cord, reducing into vagina
Use of tocolytics like terbutaline to stop uterine contractions
Describe the pathophysiology of vasa praevia
Fetal vessels run close to or over the internal cervical os-> prone to rupture when membranes rupture as not protected by umbilical cord or placental tissue->fetal haemorrhage/death
How can vasa praevia be classified?
Type 1 and Type 2
Ramified or funic
Describe the signs and symptoms of vasa praevia
Triad of:
Painless vaginal bleeding
Rupture of membranes
Fetal bradycardia/resulting fetal death
Also:Foetal anaemia
How is vasa praevia diagnosed?
Transabdominal/TV USS-most cases now diagnosed antenatally
Can use MRI and prenatal testing
How is vasa praevia managed?
Elective C-section prior to rupture of membranes: 35-36 weeks gestation
Emergency C-section if premature labour or membranes rupture
Prompt neonatal resus
Describe the epidemiology of peruperal psychosis
Rare: 1-2/1000 childbirths
Describe the aetiology of peurperal psychosis
Unknown
Hormonal changes post childbirth
Genetics
Psychosocial stressors
Sleep deprivation
Describe the signs and symptoms of peurperal psychosis
Paranoia
Delusions: Capgras
Hallucinations-command
Manic episodes
Depressive episodes
Confusion
How is peurperal psychosis diagnosed?
Clinical
Thorough psych evaluation
Rule out: thyroid disorders, sepsis etc
Describe the management of peurperal psychosis
Admit to mother/baby mental health unit: especially if Capgras/command hallucinations
Antipsychotics: olanzapine and quetiapine
Mood stabilisers in some cases
CBT
Describe the epidemiology of postpartum depression
Prevalent: 10-20% of mothers
Describe the aetiology of postpartum depression
Multifactorial
Biological: hormones, melatonin, cortisol, inflammatory processes, genetics
Psychological
Social
Describe the signs and symptoms of postpartum depression
Persistents low mood and anhedonia
Low energy
Sleep issues-important to distinguish between baby’s fault and depression
Poor appetite
Concerns relating to bonding with baby, caring for baby etc
How is baby blues different to postpartum depression?
MIlder: mood swings, irritability, anxiety and tearfullness
Sx present within first 2 weeks after birth and resolve spontaneously
How is postpartum depression diagnosed?
Clinical
Edinburgh postnatal depression scale >13
ule out risk of psychosis-risk assessment really important
Physical exam: anaemia, hypothyroidism to rule out organic causes
Describe the management of postpartum depression
Self-help, CBT, ITP(interpersonal therapy)
Antidepressants(SSRIs)-paroxetineand sertraline safe for breastfeeding
Severe: admission to mother baby mental health unit
How is baby blues managed?
Reassurance and support
Regular health visitor checks to check in with mother
Define pre-term labour
Onset of regular uterine contractions accompanied by cervical changes occuring before 37 weeks gestation
Define pre-term birth
Delivery of a baby 20-37 weeks gestation
Define premature rupture of membranes
Rupture of membranes at least one hour before onset of contracitons
Define prolonged premature rupture of membranes
Rupture of membranes over 24 hours before onset of labour
Define pre-term premature rupture of membranes
Early rupture of the membranes before 37 weeks gestation
Describe the epidemiology of preterm prelabour rupture of the membranees
Occurs in around 2% of all pregnancies
Associated with 40% of preterm delvieries
How is PPROM diagnosed?
Sterile speculum exam: look for pooling of amniotic fluid in posterior vaginal vault
Avoid digital exam: risk of infection
If no pooling: test fluid for placental alpha microglobulin protein(PAMG-1) or insulin like growth factor binding protein 1
USS-oligohydramnios
How is PPROM managed?
Admission
Regular observations to check for chorioamnionitis
Oral erythromycin for 10 days
Antenatal corticosteroids: reduce risk of respiratory distress syndrome
Delivery should be considered at 34 weeks gestation
Describe the aetiology of postpartum haemorrhage
4T’s:Tone: mc: uterine atony(failure of uterus to contract after delivery)
Trauma(tears)
Tissue(retained placenta etc)
Thrombin(clotting/bleeding disorder)
Describe the initial management of PPH
Life threatening emergency: ABCDE approach
2 14 gauge large bore peripheral cannulas
Lie flat
Bloods including group and save
Commence warm crystalloid infusion
Describe the mechancial strategies that can be used to manage postpartum haemorrhage
Palpate uterine fundus and rub it to stimulate contractions
Catheterisation to prevent bladder distention and monitor urine output
Describe the medical management of postpartum haemorrhage
IV oxytocin: slow IV injection then infusion; ergometrine slow IV(unless hx of htn)
carboprost IM(unless hx of asthma)
sublingual misprostol
Describe the surgical management of postpartum haemorrhage
If medical options fail to control bleeding:
Intrauterine balloon tamponde-if uterine atony as cause
B-lynch suture,
ligation of uterine/internal iliac arteries
If severe: hysterectomy as life-saving procedure
How is secondary postpartum haemorrhage managed?
24hrs-12 weeks
Depends on underlying cause
Abx for infection
Surgical evacuation for retained products of conception
Describe the pathophysiology of rhesus negative pregnancy
15% of mothers rhesus negative
If rh negative mother delivers a rh positive child, a leak of fetal red blood cells can occur
Causes anti D-IgG antibodies to form in mother
Maternal anti-D antibodies can cross placenta in subsequent pregnancies and cause rhesus haemolytic disease if baby is rhesus positive
Can also occur in first pregnancy due to leaks
Give some examples of sensitisation events in rhesus negative pregnancies
Antepartum haemorrhage
Placental abruption
Abdo trauma
ECV
Miscarriage if gestation >12 weeks
Termination of pregnancy
Delivery of rh positive infant
Ectopic pregnancy
Amniocentesis, CVS, fetal blood sampling
How is rhesus heamolytic disease prevented and screened for?
Test for D antibodies in all rhesus negative mothers at booking
Anti-D given to non-sensitised rh negative mothers at 28 and 34 weeks-prophylaxis(once sensitisation occurs can’t be undone)
How is rhesus negative pregnancy managed?
Screening/prevention strategies
Give Anti-D immunoglobulin as soon as possible but always within 72 hours when a sensitisation even occurs
Describe the medical management of termination of pregnancy
Mifepristone(first orally) then misoprostol 24-48 hours after
Misoprostol can be repeated 3 hourly(max 5) until expulsion
Takes time: hours to days
Pregnancy test required in 2 weeks: multi-level pregnancy test-measures level of HCG not just positive or negative
How is trichomoniasis vaginalis managed in pregnancy?
Same: oral metronidazole 400-500mg twicce a day for 5-7 days
High dose not recommended in pregnancy/breastfeeding(no 2g single dose)
Describe the symptoms of uterine rupture
Sudden severe abdominal pain which persists between contractions
Shoulder tip pain-diaphragmatic irritation)
Vaginal bleeding
Describe the signs of a uterine rupture
O/E: regression of presenting part
Abdominal palpation: scar tenderness and palpable fetal parts
Fetal monitoring: fetal distress/absent heart sounds
Significant haemorrhage: signs of shock: tachycardia, hypotension
Describe the management of a uterine rupture
ABCDE appproach
C-section
Uterus either repaired or removed
Decision-incision interval should be under 30 minutes
Define gestational diabetes
Glucose intolerance on OGTT with:
Fasting blood glucose >=5.6mmol/L
2 hour plasma glucose levels >=7.8mmol/L
Describe the epidemiology of gestational diabetes
5% of pregnancies
2nd most common medical disorder complicating pregnancies
How might patients with gestational diabetes present?
Often asx
Polyuria
Thirst
Fatigue
How is gestational diabetes diagnosed?
OGTT: fasting >=5.6, 2 hour: >=7.8-REMEMBER 5,6,7,8
HbA1c: distinguish between gestational and pre-existing diabetes early on
Urinalysis: check for glycosuria
Describe the management of gestational diabetes
Fasting glucose <7mmol/L: lifestyle : diet and exercise. Give it 1-2 weeks then metformin if targets not met, then insulin added
>=7mmol/L: start insulin (short acting not long acting)
6-6.9mmmol/L + complications like macrosomia or hydramnios: offer insulin
Glibenclamide only for women who can’t use metormin/doesn’t work and decline insulin
Describe the management of pre-existing diabetes in pregnancy
Weight loss if BMI >27
Stop oral hypoglycaemimcs except metformin and start insulin
Folic acid 5mg/day until 12 weeks
Detailed anomaly scan at 20 weeks including 4 chamber view of heart and outflow tracts
Tight glycaemic control reduces complication rates
Treat retinopathy: can worsen in pegnancy
Describe the normal changes in blood pressure in pregnancy
Usually falls in the 1st trimester and continues to fall until 20-24 weeks
After this: BP usually increases to pre-pregnancy levels by term
How should pregnant patients with hypertension be classified?
Pre-existing hypertension
Pregnancy induced hypertension/gestational hypertension
Pre-eclampsia
Describe the management of pre-existing hypertension in pregnancy
STOP ACE inhibitor or angiotensin 2 receptor
SWAP for alternative: labetalol whilst waiting specialist review
Nifedipine if asthmatic
Describe the features of pregnancy induced hypertension
Hypertension occuring in the 2nd half of pregnancy(after 20 weeks)
No proteinuria, no oedema5-7% of pregnancies
Describe the management of pregnancy induced hypertension
Oral labetalol/nifedipine/hydralazine
Typically resolves within 1 month after birth
Describe the features of pre-eclampsia
Pregnancy induced hypertension associated with proteinuria(>0.3g/24hrs)
Oedema may occur but less commonly used now as a criteria
5% of pregnancies
Describe the epidemiology of Group B strep infection
Mc asx commensal bacterium in GI and GU tracts
25% of pregnant women estimated to be carriers
Can cause severe illness to mother and infant during transmission during delivery
How might Group B strep infection be investigated?
No current routine screening test for pregnant women as colonisation status can change through pregnancy
GBS culture may be done in certain cirumstances
How is Group B strep infection managed?
Intrapartum antibiotic prophylaxis-benzylpenicillin
Abx IV during labour and delivery
Describe the management of obesity in pregnancy
5mg folic acid not 400mcg
Screening for gestational diabetes with OGTT at 24-28 weeks
BMI >35: Birth in consultant led obstetric clinicBMI>=40: Antenatal coonsultation with ostetric anaesthetist and plan made in advance
How is cephalopelvic disproportion managed?
Trial of labour
Instrumental vaginal delivery-may need episiotomy
C-section
How is prolonged labour managed?
ID causes and evaluate progress of labour
Medical:Artificial rupture of membranes
IV oxytpcin to augemnt contractions
Pian management: epidural, nitrous oxide etc
Surgical:Operative delivery
C-section
Postpartum:Monitor closely for infection
Active management of 3rd stage of labour: uterotonic agents
Ensure adequate analgesia
Describe the clinical features of obstetric cholestasis
Pruritus: intense-typically worst in palms, soles, abdomen
Jaundice: dark urine and pale stools in about 20% of patients
General fatigue and malaise
GI sx: nausea and appetite lossRUQ abdominal pain
Raised bilirubin in >90% of cases
How is obstetric cholestasis managed?
Chlorphenamine and emollients to reduce itching
Induction of labour at 37-38 weeks
Ursodeoxycholic acid
Vitamin K supplementation->minimise risk of bleeding
Describe the prognosis of obstetric cholestasis
High recurrence: 45-90% in subsequent pregnancies
Describe the aetiology of chorioamnionitis
Bacteria ascending from vagina into uterus
Mc: Group B strep, E.coli and anaerobic bacteria
How is chorioamnionitis diagnosed?
Usually clinical
Blood tests and cultures to confirm and ID causative organism
How is chorioamnionitis managed?
IV broad sectrum abx: sepsis 6 protocol
Monitoring of fetus and mother for complications
Early delivery might be needed-C section
Describe the management of FGM in the UK
Illegal in UK-immediate child protection referrral if child at risk
Anterior episiotomy during second stage of labour under local anaesthetic or regional block
Deinfibulation surgery: important to protect urethra
Describe the clinical features of shoulder dystocia
Difficult delivery of fetal face/chin
Retraction of fetal head-turtle neck sign
Failure of restitution
Failure of descent of fetal shoulders following delivery of head
Describe the management of shoulder dystocia
Immediately call for senior help
Do not apply fundal pressure-can lead to uterne rupture
McRoberts maneouevre
All fours position
Internal rotational manoeuvers
Episiotomy-won’t remove bony obstruction but will allow space for internal manoeuvers
Cleidotomy/symphysiotomy: not 1st line-associated with significant maternal morbidity]
Zavanelli manoeuvre-also dangerous
Define anaemia in pregnancy
Hb:1st trimester: <110g/L
2/3 triester: <105g/L
Postpartum: <100g/L
lDescribe some clinical features of anaemia
Asx
Dizziness, fatigue, dyspnoea: normal pregnancy
Pallor
Koilonychia
Angular cheilitis
How is anaemia diagnosed/investigated in pregnancy?
FBC
Folate to check for folate deficiency
Check for beta thalassaemia and sickle cell
Describe the risk of congenital rubella syndrome?
Risk high as 90% in first 8-10 weeks
Damage rare after 16 weeks
Describe the epidemiology of congenital rubella syndrome
Rare now due to MMR vaccine
How is rubella transmitted ot the fetus in congenital rubella syndrome?
Virus can cross the placenta and affect the developing fetus
How is congenital rubella syndrome diagnosed?
Serology to confirm rubella infection-IgM raised in women recently exposed to virus
Audiology tests for hearing impairment
Opthalmology for eye abnormalities
Echos for congenital heart defects
How is congenital rubella syndrome managed?
During pregnancy: discuss with local health protection unit
Advised to keep away from people who might have rubella
Offer MMR vaccine in post natal period
Neonates: primarily supprotive and symptomatic-monitor progress and manage long-term complications
How can perineal tears be classified?
1st, 2nd, 3rd, 4th degree
Describe the features of a first degree perineal tear
Superficial damage with no muscle involvement
Do not require any repair
Describe the features of a second degree perineal tear
Injury to perineal muscle but not involving the anal sphincter
Require suturing on ward by suitably experienced midwife or clinician
Describe the features of a third degree perineal tear
Injury to perineum involving the anal sphincter complex(external anal sphincter(EAS) and internal anal sphincter(IAS)
3a: <50% EAS thickness torn
3b: >50% EAS thickness torn
3c: IAS torn
Require repair in theatre by suitably trained clinician
Describe the features of a fourth degree perineal tear
INjury to perineum involving the anal sphincter complex(EAS and IAS) and rectal mucosa
Require repair in theatre by suitably trained clinician
Describe the management of perineal tearss
1st degree: no repair
2nd: suturing
3rd/4th: surgical repair under regional or general anaesthetic
Broad spectrum abx and laxatives given post surgery
Describe the epidemiology of amniotic fluid embolism
Rare but significant cause of maternal morbidity and mortality
Describe the aetiology of an amniotic fluid embolism
Not known fully
Amniotic fluid can enter maternal circulation and form embolism-> block circulation like a blood clot especially in lung
Fluid also triggers inflammatory response within mother’s immune system-> DIC
Describe the signs and symptoms of an amniotic fluid embolism
Tachypnoea
Tachycardia
Hypotension
Hypoxia
DIC
Cyanosis and MI
Chills, shivering, sweating, anxiety and coughing
How is an amniotic fluid embolism diagnosed?
Clinical
Exclude other causes-no definitive diagnostic test
Describe the management of an amniotic fluid embolism
Immediate transfer to ICU, MDT care
Oxygen, fluid resus
Correction of any coagulopathy
FFP if prolonged PT
Cryoprecipitate for low fibrinogen
Platelet transfusion for low platelets
Describe the management of hyperemesis gravidarum
Simple:Rest and avoid trigggers
Bland, plain food, ginger
P6(wrist) acupressure1st line meds:antihistamines: oral cyclyzine/promethazinephenothiazines: oral prochlorperazine or chlorppromazine
2nd line:Oral odansetron
Oral metoclopramide/domperidone-5 DAYS MAX
Thiamine and folic acid supplementation
Atacids
Thromboembolic stockings and LMWH -dehydration
How is hyperemesis gravidarum managed in hospital?
Normal saline with added potassium for rehydation
Antiemetics
Describe the management of hypothyroidism in pregnancy
Levothyroxine: usual dose increased by 25-50mcg due to increased metabolic demand
Describe the aetiology of acute fatty liver of pregnancy
LCHAS mutation->accumulation of fatty acid metabolites in placenta->shunted into maternal circulation and accumulate in maternal liver
How is acute fatty liver of pregnancy investigated/diagnosed?
Raised:AST/ALT
Bilirubin
Creatinine
Ammonia
Lactate
Serum uric acid
Leukocytosis,
low-normal platelets,
normocytic normochromic anaemia
Coagulopathy: prolonged PT, hypofibrinogenaemia and elevated D dimer
Describe the management of acute fatty liver of pregnancy
Curative: delivery of the fetus
Maternal stabilisation: correct hypoglycaemia, coagulopathy and hypertension
After delivery: close monitoring-if ongoing deteriorattion in liver function post birth-transfer to liver transplant facility
Describe the management of the thyrotoxic phase of postpartum thyroidits
Propanolol for sx control
Not usually treated with anti-thyroid drugs as thyroid not overactive
Describe the treatment of the hypothyroid phase of postpartum thyroidits
Usually treated with thyroxine
Describe the presentation of a patient with obstructed labour
Widest diameter of fetal sckull remains stationary above the pelvic brim
Prolonged labour: >12 hours
Premature rupture of membranes
Mother has abnormal vital signs
Bandls’ ring
Foul smelling meconium from mother’s vagina
Oedema of vulva/cervix
Caput
Malpresentation/malposition of fetus
Poor cervical effacement
Assess using vaginal exam
Describe the management of obstructed labour
Saline for dehydration
catheter to drain bladder
May need C section or instrumental delivery
Describe the epidemiology of intrauterine growth restriction
3-7% of newborns
Increased prevalence in low/middle income countries->maternal malnutrition and infection
Describe the signs and symptoms of intrauterine growth restriction
Decreased fetal movement
Abnormal fundal height for gestational age
Complications like pre-eclampsia and stillbirh
How is intrauterine growth restriction managed?
Close monitoring of fetal growth and wellbeing
Management of maternal conditions contributing
Consideration for early delivery if fetus is in distress/conditions worsens
Describe the aetiology of ovarian hyperstimulation syndrome
Excessive response to hormones->multiple follicles mature and enlarge->all transform into corpus luteum->overproduction of oestrogen, progesterone and local cytokines, especially vascular endothelial growth factor->increased membrane permeability and loss of fluid from intravascular compartment
Describe the signs and symptoms of ovarian hyperstimulation syndrome
Bloating
Abdo pain
Oedema
Pleural effusions
Ascites
Weight gain
How is ovarian hyperstimulation syndrome diagnosed?
Routine bloods: evaluate haemoconcentration and detect potential organ dysfunction
CXR: ID pleural effusion
Describe the management of ovarian hyperstimulation syndrome
Supportive-tailored to severity of condition
Simple analgesia for discomfort
Might need ICU and close monitoring if severe
Describe the features of fetal varicella syndrome
Skin scarring
Eye defects: microphthalmia
Limb hypoplasia
Microcephaly
Learning difficulties
Describe the management of chickenpox exposure in pregnancy
If doubt about previous infection: check blood urgently for varicella antibodies
Oral aciclovir now first choice for post exposure prophylaxis(used to be VZIG)-should be given day 7-14 after exposure not immediately
Describe the management of chickenpox in pregnancy
Seek specialist advice
Oral aciclovir >=20 weeks and presents within 24hrs of rash onset <20 weeks: aciclovir ‘considered with caution
Describe the pathophysiology of placental insufficiency?
Placental vascular remodeling is affected-> placental functioning progressively deteriorates.
This process affects the placental blood flow, leading to fetal hypoxemia, or low levels of oxygen in the blood, and restriction of fetal growth.
How might placental insufficiency present?
Usually no observable sx
Decreased fetal movement
Intrauterine growth restriction
Prematurity
Stillbirth
How is placental insufficiency diagnosed/investigated?
Doppler USS: evaluate fetal and placental circulations-> regular screening
MRI if inconclusive
Describe the management of placental insufficiency
<34 weeks: delay delivery: low dose aspirin, vitamin C and E, heparin
>34 weeks: prompt delivery
How is a pregnant women at high risk of VTE treated?
LMWH throughout antenatal period and input from experts
If a pregnant woman has 3 risk factors for VTE how should this be managed?
LMWH from 28 weeks and continued nutil 6 weeks postnatal
If a diagnosis of DVT is made shortly beefore delivery in a pregnant woman, how long should treatment be continued for?
At least 3 months
How can twin pregnancies be classified?
Zygosity
Chorionicity
Amnionicity
How can monozygotic twwins be further classified?
Dichorionic + daimniotic: 2 different sacs
Monochorionic + diamniotic: same outer sac, two inner sacs
Monochorionic + monoamniotic: same sacs
Describe the epidemiology of twins
2/3: dizygotic
1/3: monozygotic
^When conceived naturally
Describe the management of twins
Rest
USS for diagnosis and monthly checks
Additional iron and folate
More antenatal care(weekly when >30 weeks)
Precautions at labour(2 obstetricians present)
75% of twins deliver by 38 twins, if longer, most twins are induced at 38-40 weeks
Describe the aetiology of twin-to-twin transfusion syndrome
Precipitated by anastamoses of umbilical vessels betwween 2 fetuses in the placenta of monochorionic twins
How is twin-to-twin transfusion syndrome diagnosed?
Monochorionic twins: regular USS to monitor
Observe fluid levels in each amniotic sac, measure size of twins and assess blood flow in umbilical cord and placenta
Describe the management of twin-to-twin transfusion syndrome
Laser transection of problematic vessels in utero-can increase survival rate, high mortlaity for both twins without tx
Describe the symptoms of UTI in pregnancy
Frequent urination
Dysuria
Lower abdo pain
Fever
Haematuria
Describe the management of asymptomatic bacteriuria in pregnancy
Nitrofurantoin and cefalexin mc used
If Group B strep ID d: intrapartum prophylactic abx to reduce risk of transmission
Describe the treatment for a UTI in pregnant women
nitrofurantoin for 7 days(avoid at term)
Amoxicillin/cefalexin
Describe the symptoms of puerperal infection
Fever
Abdo pain
Tachycardia
Abnormal discharge
Foul smelling lochia(postpartum bleeding)
Tenderness/pain in pelvic area
Sepsis signs: hypotension, tachypnoea etc
Describe the maangement of puerperal infection
Abx-broad spectrum initially: ceftriaxone and metronidazole
Fluids
Analgesia
Prevention: good hygiene practices during childbirth and postpartum care
Close monitoring
Drainage of abscesses if needed
Describe LH and FSH in Turners
Raised LH
Raised FSH
Describe LH and FSH in Kallman’s
Low LH
Low FSH
Describe the general function of blood hormones
Oestrogen: sex development-females
Progesterone: uterine development
Testosterone: sex development males
FSH and LH: ovarian functionality
Describe the management of primary amenorrhoea
Primary hypo: COCP
Primary hyper: GnRH analogue
Descrieb the management of secondnary amenorrhoea
Lifestyle: stress/weight management
Treat underlying cause
Surgical: tumour/cyst removal
For how long/how frequently do a couple need to be having unrpotected sexual intercourse to be cnsidered infertile?
2 years despite sex 3-4 times/wweek
How can causes of infertility be classified?
Genetics
Ovulation/endocrine
Tubal abnormalities
Uterine abnormalities
Endometriosis
Cervical abnormalities
Testicular disorders
Ejaculatory disorders
Give some ovulation/endocrine disorders that can cause infertility
PCOS
Pituitary tumours
Sheehan’s syndrome
Hyperprolactinaemia
Cushing’s
Premature ovarian failure
Give some tubal abnormalities that can cause infertility
Congenital anatomical abnormalities
Adhesions
Can be secondary to PID(- gonorrhoea, chlamydia)
Give some uterine abnormalities that can cause infertility
Bicronate uterus
Fibroids
Asherman’s syndrome
How is infertility investigated in women?
Bedside:Thorough hx including PMH, sexual history and past pregnancies
Speculum and bimanual exam-e.g. fibroids
STI screen
Bloods:Serum progesterone testing
Prolactin
LH/FSH
Anti-mullerian hormone
TFTsImaging:
TV USS
Hysterosalpingography
Laparoscopy and dye
How is infertility investigated in men?
Bedside:Thorough hx including PMH, sexual history past children
Testicular exam: e.g. varicocele
Semen analysis: evaluate sperm count, motility and morphology
Bloods:Serum testosterone
LH/FSHTFTs
Describe the conservative management of infertility
Folic acid
Weight loss: BMI 20-25
Smoking cessation and alcohol advice
Stres reduction strategies
Advice sexual intercourse every 2-3 days
Describe the aetioloy of mastitis
Bacterial infection
What is an intraductal papilloma
Benign tumour of breast ducts
What is a radial scar
benign sclerosing breast lesion
Describe the aetiology of fat necrosis
response to adipose tissue damage
Describe the etiology of fibrocystic breast disease
Increased hormonal response response resulting in inflammation and fibrosis
Describe the aetiology of mammary duct ectasia
Inflammation and dilation of large breast ducts
