Selected Notes obgyn 1 Flashcards
How can urinary incontinece be characterised?
- Overactive bladder/urge incontinence<br></br>2. Stress incontinence<br></br>3. Mixed incontinence<br></br>4. Overflow incontince<br></br>5. 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<br></br>2. Bladder diary-minimum of 3 days<br></br>3. Urinalysis-rule out infection<br></br>4. Urodynamic studies-cystometry and cystogram
Describe the management of stress incontinence
Conservative: avoid caffeine and fizzy drinks and excessive fluid intake<br></br>-Pelvic floor exercises<br></br>Medical: Duloxetine-ONLY if conservative doesn’t work and patients doesn’t want surgery<br></br>Surgical: GS: Mid urethral slings<br></br>Other surgeries: Incontinence pessaries, bulking agents, colposuscpension and fascial slings
In the gold standard surgical management of stress incontinence, mid-urethral slings {{c1::compress the urethra against a supportive layer}} and assist in the {{c2::closure of the urethra}} during {{c3::increased intra-abdominal pressures}}
In the surgical management of stress incontinence, {{c1::colposuspension and fascial slings}} involve <span>s</span>{{c2::uspending the anterior vaginal wall}} <span>to the </span>{{c3::iliopectineal ligament of Cooper}}
Describe the general conservative management of incontinence
Lifestyle advice: avoid caffeine and fizzy drinks, avoid excessive fluid intake<br></br>Pelvic floor exercises
Describe the medical management of urge incontinence
Anticholinergics(antimuscarinics): inhibit the parasympathetic action of the detrusor muscle<br></br>-Oxybutinin, tolterodine, etc<br></br><br></br>
Describe the symptoms of a genital prolapse
<ul><li>Pelvic discomfort or a sensation of 'heaviness'</li><li>Visible protrusion of tissue from the vagina</li><li>Urinary symptoms such as incontinence, recurrent urinary tract infections or difficulties voiding</li><li>Defecatory symptoms, including constipation or incomplete bowel emptying</li><li>Sexual dysfunction</li></ul>
Describe the management of a gential prolapse
If asymptomatic and mild: no treatment <br></br>Conservative: Weight loss, smoking cessation, avoid heavy lifting, pelvic floor exercises<br></br>Ring pessary<br></br>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)<br></br>Also: diarrhoea, nausea, vomiting, weight loss<br></br>
How is a vaginal fistula diagnosed?
Pelvic exam<br></br>Cystoscopy and urodynamic studies<br></br>Imagin<br></br>
Describe the management of vaginal fistulas
Conservative: catheterisation, antibiotics to prevent/treat infection<br></br>Surgical: fistula repair, tissue grafts<br></br>
Describe the aetiology of uterine fibroids
Unknown<br></br>Genetic, hormonal and environmental factors<br></br>
How can uterine fibroids cause polycythaemia?
Secondary to autonomous production of erythropoeitin
How are uterine fibroids diagnosed
<ul><li>Trans-vaginal ultrasound: Used to assess the size and location of the fibroids</li><li>MRI: Used if ultrasound does not provide enough detail to assess the fibroid for surgery</li><li>Biopsy: May be taken if there is any doubt over the diagnosis to differentiate the fibroid from other conditions such as endometrial cancer</li></ul>
Describe the management of <b>asymptomatic</b> 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<br></br>Mefenamic and TXA<br></br>COCP and oral/injectable progesterone
How does red degeneration of fibroids present?
-Severe abdominal pain<br></br>-Low grade fever<br></br>-Tachycardia<br></br>-Vomiting
How is red degeneration of fibroids managed?
Supportive: rest, fluids and analgesia
Describe the aetiology of ovarian cysts
<span>Hormonal imbalances, endometriosis, pregnancy and pelvic infections.</span>
Describe some symptoms of an ovarian cyst
-Asymptomatic<br></br>-Acute unilateral pain<br></br>Bloating/fullness in the abdomen<br></br>-Intra-peritoneal haemorrhage with haemodynamic compromise<br></br>
Describe the management of a simpole ovarian cyst in premenopausal women
<5cm: often resolve within 3 cycles<br></br>5-7cm: gynae referral and yearly US<br></br>>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<br></br>Check Ca125 and referall to gynaecology<br></br>High Ca125: 2 week cancer list<br></br>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?
<ol><li>Physiological/functional cysts</li><li>Benign germ cell tumours</li><li>Benign epithelial tumours</li><li>Benign sex cord stromal tumours</li></ol>
Follicluar cysts represent {{c1::the developing follice.}} When these {{c1::fail to rupture and release the egg,}} the cyst can persist. Typically on US they have {{c1::thin walls and no internal structures}}
<b><i>Corpus luteum cysts</i></b><span> occur when the corpus luteum fails to break down and instead </span>{{c1::fills with fluid.}}<span> They may cause symptoms such as </span>{{c1::pelvic discomfort, pain or delayed menstruation.}}<span> They are often seen in </span>{{c1::early pregnancy.}}
An endometrioma is a <span>lump of </span>{{c1::endometrial tissue}} <span>within the ovary, occurring in patients with </span>{{c1::endometriosis.}} <span>They can cause </span>{{c1::pain}}<span> and disrupt</span> {{c1::ovulation.}}
Dermoid cysts/germ cell tumours are {{c1::benign ovarian teratoma}}s-> come from {{c1::germ cells}}. Can contain tissue types like {{c1::skin, teeth hair and bone.}} . {{c1::Torsion}} is more likely than with other ovarian tumours
Describe the pathophysiolgy of an ovarian torsion
<span>Twisting of the adnexa and blood supply to the ovary leads to </span><b><i>ischaemia</i></b><span>. If the torsion persists, </span><b><i>necrosis</i></b><span> will occur, and the function of that ovary will be lost.</span>
Describe the presentation of a patient with ovarian torsion
<ul><li>Sudden onset severe unilateral pelvic pain</li><li>Pain is constant and gets progressively worse</li><li>Associated with nausea and vomiting</li></ul>
<div>Pain can also come and go if ovary twists and untwists intermittently </div>
How is ovarian torsion diagnosed?
1st line: Pelvic US(transvaginal ideally, transabdominal as backup)->‘whirlpool sign’ free fluid in pelvis and oedema or ovary<br></br>Doppler-> reduced blood flow<br></br>Definitive-> laparoscopic surgery
Describe the management of ovarian torsion
<ul><li>Urgent admission and gynae involvemebt</li><li>Laparoscopic surgery to:</li></ul>
<div><ol><li>Untwist the ovary and fix it in place(de-torsion)</li><li>Remove the affected ovary (oophorectomy)</li></ol><div>Laparotomy may be needed if large ovarian mass or malignancy is suspected</div></div>
Describe the aetiology of lichen sclerosus
Thought to be autoimmune reaction-associated with T1DM<br></br>Also genetics and hormonal factors
Describe a typical presentation of a patient with lichen sclerosus
45-60yr old woman<br></br>Vulval itching<br></br>Soreness/pain<br></br>Skin tightness<br></br><ul><li>Painful sex (superficial dyspareunia)</li><li>Erosions</li><li>Fissures</li></ul>Koebner phenomenon
Describe the appearance of lichen sclerosus
<ul><li>“Porcelain-white” in colour</li><li>Shiny</li><li>Tight</li><li>Thin</li><li>Slightly raised</li><li>There may be papules or plaques</li></ul>
<div><img></img><br></br></div>
How is lichen sclerosus diagnosed?
<ul><li>Mostly clinical</li><li>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)</li><li>Blood tests to check for potential autoimmune conditions</li></ul>
Describe the management of lichen sclerosus
<ul><li>Topical corticosteroids(dermovate) to reduce inflammation and itching</li><li>Avoidance of soap in affected areas to prevent further irritation</li><li>Emollients to relieve dryness and soothe itching</li></ul>
Cervical cancer:<br></br>2 main tumour suppressor genes: {{c1::P53 and pRb}}<br></br>HPV produces 2 main proteins: {{c2::E6 and E7}}<br></br><br></br>E6 protein inhibits {{c2::p53}} and E7 inhibits {{c2::pRb}}<br></br><br></br><span>Therefore, HPV promotes the development of cancer by inhibiting tumour suppressor genes.</span>
At what age are children vaccinated against HPV?
age 12-13 yrs
Describe the signs and symptoms of cervical cancer
<ul><li>Most commonly picked up on screening incidentally</li><li>Abnormal vaginal bleeding (<b><i>intermenstrual</i></b>, <b><i>postcoital</i></b> or<b><i> post-menopausal bleeding</i></b>)</li><li>Vaginal discharge</li><li>Pelvic pain</li><li>Dyspareunia (pain or discomfort with sex)</li><li>Urinary/boewl habit change</li><li>Abnormal white/red patches on cervix</li><li>Mass on PR exam</li></ul>
How is cervical cancer investigated and diagnosed?
-If symptoms-> speculum exam and smear test<br></br>If abnormal appearance of cervice-> urgen cancer referral for colposcopy
How is the cervical intraepithelial neoplasia determined?
Colposcopy NOT screening
Grades of cervical intraepithelial neoplasia:<br></br><ul><li><b><i>CIN I</i></b>: {{c1::mild}} dysplasia, affecting {{c1::1/3 t}}he thickness of the {{c1::epithelial layer,}} likely to r{{c1::eturn to normal}} without treatment</li><li><b><i>CIN II</i></b>: {{c2::moderate}} dysplasia, affecting {{c2::2/3}} the thickness of the {{c2::epithelial layer}}, l{{c2::ikely to progress to cancer}} if untreated</li><li><b><i>CIN III</i></b>: {{c2::severe}} dysplasia, {{c2::very likely to progress}} to cancer if untreated</li></ul>
Cervical cancer screening:<br></br>Offered to all women between ages {{c1::25-64 years}}<br></br><ul><li>25-49yrs: {{c2::3}} yearly screening</li><li>50-64yrs: {{c3::5}} yearly screening</li></ul><div>Cannot be offered to women over {{c4::64 years}}</div>
Describe the results obtained from cervical cancer screening cytology
<ul><li>Inadequate</li><li>Normal</li><li>Borderline changes</li><li>Low-grade dyskaryosis</li><li>High-grade dyskaryosis (moderate)</li><li>High-grade dyskaryosis (severe)</li><li>Possible invasive squamous cell carcinoma</li><li>Possible glandular neoplasia</li></ul>
<div> </div>
<span>A cone biopsy is a treatment for </span>{{c1::<b><i>cervical intraepithelial neoplasia</i></b><span> (</span><b><i>CIN</i></b><span>) and very early-stage cervical cancer. </span>}}<span>It involves a general anaesthetic. The surgeon removes a cone-shaped piece of the cervix using a </span>{{c1::scalpel.}}<span> This sample is sent for histology to assess for </span>{{c1::malignancy.}}
<b><i>Bevacizumab</i></b><span> (</span><b><i>Avastin</i></b><span>) </span><span>targets</span>{{c1::<span> </span><b><i>vascular endothelial growth factor A</i></b><span> (</span><b><i>VEGF-A</i></b><span>),</span>}}<span> which is responsible for </span>{{c2::the development of new blood vessels.}}<span> Therefore, it </span>{{c3::reduces the development of new blood vessels}}<span>. </span>
Endometrial cancer is a malignancy that originates from the {{c1::endometrium}}-the {{c1::inner}} lining of the uterus
Endometrial cancer:<br></br>All women {{c1::>=55yrs}} presenting with {{c1::postmenopausal bleeding}} should be referred using the suspected cancer pathway
How is endometrial cancer investigated?
<ul><li>first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value</li><li>hysteroscopy with endometrial biopsy</li></ul>
How is endometrial cancer managed?
Surgery: hysterecotmy with bilateral alpingo-oophorectomy-can be curative if limited<br></br>Radio/chemotherapy<br></br>Progesterone therapy sometimes used in frail elderly women not suitable for surgery
Describe the outcomes of endometrial hyperplasia
- Most return to normal<br></br>2, <5% become cancer
How is endometrial hyperplasia treated?
<ol><li>Intrauterine system(mirena coil)</li><li>Continuous oral progesterones(levonorgestrel)</li></ol>
How does adipose tissue result in increased oestrogen levels?
<ul><li>Contains aromatase->converts androgens.</li><li>More adipose tissue->more androgens converted to oestrogen</li></ul>
How common is ovarian cancer?
5th most common malignancy in femals
Epithelial ovarian tumours are partically {{c1::cystic}} so can contain {{c1::fluid}}
How do germ cell ovarian tumours typically spread?
Via lymphatics
Describe the presentation of ovarian cancer
<ul><li>Typicall present layte-non-specific symptoms</li><li>Abdominal pain</li><li>Bloating</li><li>Ealry satiety</li><li>Urinary frequency or change in bowel habits</li></ul>
<div>Later stages:</div>
<div><ul><li>Ascites(vascular growth factors increasing vessel permeability)</li><li>Pelvic, back and abdominal pain</li><li>Palpable pelvic or abdominal mass</li></ul></div>
How is CA125 used to guide further investigations when investigting a patient for possible ovarian cancer?
<ul><li>Raised CA125(>=35IU/mL)-> urgent US of abdomen and pelvis</li></ul>
How is ovarian cancer treated?
Surgery:<br></br><ul><li>If early disease-remove uterus, fallopian tubes, ovaries and infracolic omentectomy</li><li>Advanced-debulking surgery</li></ul><div><br></br></div><div>Adjuvant/intraperitoneal chemotherapy</div><div>Biologics</div><br></br>
Describe the prognosis of ovarian cancer
80% have advanced disease at presentation<br></br>All stage 5 year survival is 46%
<span>An ovarian mass may press on the </span>{{c1::obturator}}<b><i> nerve</i></b><span> and cause referred </span>{{c2::<b><i>hip</i></b><span> or </span><b><i>groin</i></b>}}<b><i> pain</i></b><span>. </span>
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
<ul><li>Lump on labia majora</li><li>Inguinal lymphadenopathy</li><li>Itching/discomfort in vulval area</li><li>Non healing ulcer</li><li>Changes in skin colour/thickening of vulva</li><li>Bleeding/discharge not related to the menstrual cycle</li></ul>
How is vulval cancer managed?
Surgery<br></br><ul><li>Radical/wide local excision</li><li>Radical vulvectomy for multi-focal disease</li><li>Reconstructive surgery</li><li>Radioterhapy.chemo</li></ul>
<span>A molar pregnancy, also known as a </span>{{c1::hydatidiform mole}}<span>, forms part of a spectrum of disorders known as </span>{{c2::gestational trophoblastic disease}}<span>. It is characterized by an imbalance in the</span> {{c3::number of chromosomes}}<span> originating from the mother and father during conception.</span>
How can molar pregnancies be characterised?
<ul><li>Complete</li><li>Partial</li></ul>
Describe the presentation of a patient with a <span>hydatidiform mole</span>
<ul><li>Vaginal bleeding</li><li>Enlargement of uterus beyond the expected size for gestational age</li><li>Nausea and hyperemesis gravidarum</li><li>Thyrotoxicosis</li></ul>
How can a <font><span>molar pregnancy cause enlargement of the uterus?</span></font>
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 <br></br>Trans-vaginal US->‘snowstorm’ appearance, low resistance of blood vessel flow and absence of a foetus
How are molar pregnancies managed?
<ul><li>Immediate referral to a specialist centre for treatment is necessary to reduce the risk of potential complications such as choriocarcinoma or invasion.</li><li>As molar pregnancies are not viable, they are managed with suction curettage to remove them from the uterus.</li><li>When fertility preservation is not a concern, a hysterectomy may be performed.</li><li>Surveillance is recommended, including:<ul><li>Bimonthly serum and urine hCG testing until levels are normal.</li><li>In the case of a partial mole, a repeat hCG test is done 4 weeks later - if normal, the patient is discharged from surveillance.</li><li>In a complete mole, monthly repeat hCG samples are sent for at least 6 months.</li></ul></li></ul>
How common is endometriosis?
Common-10% of women in reproductive years
Describe the symptoms of endometriosis
<ul><li>Chronic pelvic pain</li><li>Dysmenorrhoea</li><li>Dyspareunia</li><li>Subfertility</li><li>Non-gynaecological-> dysuria, urgency, haematuria</li><li>Cyclical rectal bleeding, if endometrium-like tissue grows outside the female reproductive system</li></ul>
Describe the medical management of endometriosis
<ul><li>Analgesia->paracetemol/NSAIDs</li><li>Hormonal therapies-> COCP, medroxyprogesterone acetate, Gonadotrophin releasing hormone agonists</li></ul>
Describe the surgical management of endometriosis
<ul><li>Diathermy of lesions</li><li>Ovarian cystectomy(for endometriomas)</li><li>Adhesiolysis</li><li>Bilateral oophorectomy(sometimes hysterectomy)</li></ul>
How do patients with adenomyosis typically present?
<ul><li>Asymptomatic</li><li>Dysmenorrhoea</li><li>Menorrhagia</li><li>Dyspareunia</li><li>Infertility or pregnancy-related complications</li></ul>
Describe the management of adenomyosis
Symptomatic: TXA/mefenamic acid<br></br><ol><li>Mirena coil(first line)</li><li>COCP</li><li>Cyclical oral progesterones</li></ol><div><br></br></div><div>GnRH agonists</div><div>Uterine artery embolisation</div><div>Hysterecomy-definitive treatment</div>
How is andorgen insensitivity syndrome diagnosed?
<ul><li>Buccal smear or chromosomal analysis to reveal 46XY genotype</li><li>After puberty: hormonal tests</li></ul>
Describe the presentation of a patient with atrophic vaginitis
<ul><li>Vaginal dryness and discharge</li><li>Dyspareunia</li><li>Occasional spotting</li><li>Loss of pubic hair</li><li>Urinary symptoms like dysuria and recurrent UTI</li></ul>
Describe the management of atrophic vaginitis
<ul><li>Hormonal treatment:<ul><li>Systemic hormone-replacement therapy (oral or transdermal)</li><li>Topical oestrogen preparations</li></ul></li><li>Non-hormonal treatments:<ul><li>Lubricants, which provide short-term improvement to vaginal dryness, alleviating symptoms such as dyspareunia</li><li>Moisturisers, which should be used regularly</li></ul></li><li>Transvaginal laser therapy, although not currently recommended due to lack of evidence</li></ul>
Describe the management of a miscarriage
<ul><li>Conservative: Allow POC to pass naturally-> repeat scan/pregnancy test</li><li>Medical: vaginal misoprostol</li><li>Surgical</li></ul>
How does vaginal misoprostol work as medical management for a msicarriage?
<ul><li>Stimulates cervical ripening and myometrial contractions</li></ul>
Describe the features of a threatened pregnancy
<ul><li>Painless vaignal bleeding <24 weeks(usually 6-9 weeks)</li><li>Bleeding but often less than menstruation</li><li>Cervical os closed</li></ul>
How is a threatened pregnancy treated?
<ul><li>Reassurance</li><li>If heavy: admit and observe</li><li>If >12 weeks, and rhesus negative: Anti D</li></ul>
Describe the features of an inevitable pregnancy
<ul><li>Heavy bleeding</li><li>Clots</li><li>Pain</li><li>Cervical os open</li></ul>
How is an inevitable miscarriage treated?
<ul><li>Reassurance, if heavy bleeding then admit and observe</li><li>If >12 weeks and rhesus negative : Anti D</li><li>Likely to proceed to a complete/incomplete miscarriage</li></ul>
Describe the features of a missed/delayed pregnancy
<ul><li>Gestational sac containing a dead fetus <2 weeks without symptoms of expulsion</li><li>Cervical os closed</li><li>Asymptomatic, light bleeding, discharge, pregnancy symptoms which disappear</li></ul>
How is a missed/delayed miscarriage treated?
<ul><li>Reassurance, if heavy bleeding admit for observation</li><li>Low success rate</li></ul>
Describe the features of an incomplete miscarriage
<ul><li>POC partly expelled</li><li>Symptom of bleeding.clots</li><li>Cervical os open</li></ul>
How might a patient with a complete miscarriage present?
<ul><li>History of bleeding</li><li>Clots</li><li>POC</li><li>Pain</li><li>Symptoms settled</li></ul>
How are patients with complete miscarriages managed?
<ul><li>Discharged to GP</li></ul>
Describe the symptoms of a septic miscarriage
<ul><li>Infected POC</li><li>Rigors</li><li>Fever</li><li>Bleeding</li><li>Leukocytosis</li><li>Increased CRP</li></ul>
How is a septic miscarriage treated?
<ul><li>IV antibiotics and fluids</li><li>Medical/surgical treatment</li></ul>
Describe the symptoms of a patient with an ectopic pregnancy
<ul><li>Pelvic pain: can be unilateral</li><li>Shoulder tip pain-irritation of diaphragm by intra-abdominal bleeding</li><li>Vaginal discharge/bleeding-decidua breaking down</li></ul>
Describe the conservative management of an ectopic pregnancy
<ul><li>Close follow up and repeat B-HCG's</li><li>Not usually done</li></ul>
Describe the medical management of an ecoptic pregnancy
<ul><li>IM methotrexate</li><li>Regular B-HCG checks : >15% decline by day 4/5 or repeat methotrexate</li></ul>
How does methotrexate work as treatment in a patient with an ectopic pregnancy?
<ul><li>Disrupts folate dependent cell division</li></ul>
Describe the surgical management of an ectopic pregnancy
<ol><li>Tubal ectopics: laparoscopic salpingectomy (remove ectopic and tube)</li><li>If only one tube left: salpingotomy (cut in fallopian tube and remove ectopic)</li></ol>
<div>B-HCG follow up until <5iU(negative)-> check for residual trophoblast</div>
How does amniotic fluid normally change throughout pregnancy?
<ul><li>Volune increases until 33 weeks</li><li>Platueaus at 33-38 weeks</li><li>Decreases at term to reach 500ml</li></ul>
Describe the normal physiological cycle of amniotic fluid
Fetus breathes and swallows fluid, processed and voided through the bladder<br></br><ul><li>Predominantly fetal urine output with some fetal secretions and placenta</li></ul>
How does placental insufficiency cause oligohydramnios?
<ul><li>Blood flows to brain instead of kidneys so there is a lower fetal urine output</li></ul>
How do patients with oligohydramnios present?
Potter’s syndrome:<br></br><br></br><ol><li>Fetal compression: clubbed feet, facial deformity, congenital hip dysplasia</li><li>Lack of amniotic fluid: pulmonary hypoplasia in fetus</li></ol>
Describe the management of oligohydramnios
<ul><li>Treat underlying cause and optimise gestation of delivery</li><li>Maternal rehydration to increase amniotic fluid volume if mild</li><li>Amnioinfusion: saline into amniotic fluid to increase volume</li><li>Deliver: may be induced-C-section</li></ul>
Describe the prognosis of patients with oligohydramnios
If 2nd trimester: poor prognosis<br></br><ul><li>If premature delivery and pulmonary hypoplasia: respiratory distress at birth</li><li>PLacental insufficiency: higher rate of preterm deliveries</li></ul>
<b>Aetiology of polyhdramnios:</b><br></br><br></br><ul><li>50-60% of cases: {{c1::idiopathic}}<br></br></li></ul><div>Excess production due to {{c2::increased fetal urination:}}</div><div><ul><li>{{c2::</li><li>Maternal diabetes</li><li>Fetal anaemia</li><li>Fetal renal disorders</li><li>Twin to twin transfusion syndrome</li>}}<br></br></ul><div>Insufficient removal due to {{c3::decreased fetal swallowing:}}</div></div><div><ul><li>{{c3::</li><li>Oesophageal duodenal atresia</li><li>Diaphragmatic hernia</li><li>Anencephaly</li><li>Chromosomal disorders</li>}}<br></br></ul></div>
How is polyhdramnios diagnosed?
<ul><li>USS</li><li>Measure amniotic lfuid: AFI/MPD</li></ul>
<br></br>
How fast does cervical dilation typicaly progress?
<ul><li>Primiparous: 1cm every 2 hours</li><li>Multiparous: 1cm every hour</li></ul>
Describe the physiology of the first stage of labour
<ul><li>Hormones(mostly prostaglandinds and oxytocin) stimulate regular uterine contractions</li><li>That and pressure from presenting part of foetus-> progressive dilation of the cervix</li></ul>
Describe the signs and symptoms of the first stage of labour
<ul><li>Regular, painful contractions</li><li>Progressive cervical dilation</li><li>Passage of blood stainf mucus-'show'</li><li>Rupture of membranes</li><li>Descent of foetal head into pelvis</li></ul>
How is the first stage of labour managed?
<ul><li>Pain relief-> epidural analgesia, nitrous oxide, opioids</li><li>Encourage mobility and changes in position to facilitate labour progression</li><li>Ensure hydration and nutritional supprot</li><li>Regular monitoring</li></ul>
How is the second stage of labour managed?
<ul><li>Instrumental delivery</li><li>C-section</li></ul>
How long does the third stage of labour usually last?
<ul><li>Natural: 30-60 minutes</li><li>With oxytocin: 5-10 minutes</li></ul>
How is the 3rd stage of labour managed?
<ul><li>Controlled cord traction-> gently to avoid uterine inversion/PPH</li><li>If retained placenta: manual removal or curettage may be necessary</li></ul>
How is labour induction carried out?
<ul><li>Membrane sweep: insert finger into extenral os and separate membranes from cervix</li><li>Vaginal prostalgandins: Used to ripen cervix and induce contractions</li><li>Amniotony: artificial rupture of membranes</li><li>Ballon catheter: mechanically dilates cervix</li></ul>
Describe the aetiology of pre-term labour
<ul><li>Overstretching of uterus: multiple pregnancy, polyhydramnios</li><li>Foetal risk complications: pre-eclampsia, placental abruption</li><li>Uterus/cervical problems: fibroids, malformations</li><li>Infections: chorioamnionitis, sepsis, group B strep etc</li><li>Maternal co-morbidity: htn, diabetes etc</li></ul>
How might patients with pre term labour present?
<ul><li>Regular uterine contractsion/changes in cervical effacement or dilation/rupturing of membranes before onset of contractions</li></ul>
How is pre term labour managed?
<ul><li>Corticosteroids: betamethasone/dex to assist foetal lung maturation</li><li>IV abx if increased risk of infection(penicillin)</li><li>Tocolytic agents may be used(nifedipine), risk of side effects</li></ul>
How is menopause diagnosed?
<ul><li>Clinically: absence of menarche for 12 months in someone >45(generally>45)</li><li>If <40: test FSH etc</li></ul>
Describe the management of menopause
Conservative: <br></br><ul><li>Lifestyle: regular exercise, weight loss, good sleep</li></ul><div>Medical:</div><div><ul><li>HRT</li><li>SSRI’s</li><li>Vaginal lubricants/moisturisers</li><li>Clonidine for vasomotor</li></ul></div>
In terms of time frames, when can HRT be given?
<ul><li>Cyclically: perimenopausal women still having periods</li><li>Continuously: Post menopausal not having periods</li></ul>
How is HRT given cyclically?
<ul><li>Monthly: oestrogen every day of months and progesterone for last 14 days</li><li>Every 3 months: Oestrogen very day for 3 months and progesterone for the last 14 days</li></ul>
How can menopause result in dyspareunia?
<ul><li>Vaginal dryness from reduced oestrogen</li></ul>
How can menopause result in urinary incontinence?
<ul><li>Caused by epithelial thinning as a result of decline in oestrogen</li></ul>
Describe the feedback systems that control the menstrual cycle
<ul><li>Moderate oestrogen levels-> negative feedback on HPG</li><li>High oestrogen with no progesterone-> positive feedback on HPG</li><li>Oestrogen +progesterone-> negative feedback on HPG</li><li>Inhibin selectively inhibits FSH at anterior pituitary</li></ul>
How much blood is usually lost during menses?
<ul><li>10-80ml</li></ul>
Describe the epidemiology of PCOS
<ul><li>Common</li><li>Affects up to 1/4 of women during reproductive years</li></ul>
Describe the aetiology of PCOS
<ul><li>Hormonal imblanaces-unknown?</li><li>Hyperandrogenism</li><li>Insulin resistance</li><li>Elevated levels of LH</li><li>Raised oestrogen</li></ul>
Describe the symptoms of PCOS
<ul><li>Oligomenorrhoea</li><li>Subfertility</li><li>Acne</li><li>Hirsutism</li><li>Obesity</li><li>Mood changes: depression, anxiety</li><li>Male pattern baldness</li><li>Acanthosis nigracans-> secondary to insulin resistance</li></ul>
Describe the rotterdam diagnositc criteria
>=2 of:<br></br><ul><li>Polycystic ovaries(>12 cysts on imaging or ovarian volume >10cubic cm)</li><li>Oligo/an ovulation</li><li>Clinical or biochemical features of hyperandrogenism</li></ul>
How is PCOS managed?
Conservative:<br></br><ul><li>Weight loss, exercise, educate on risks of diabetes.cvr.endometrial cancer</li></ul><div>Medical for those not planning pregnancy:</div><div><ul><li>Co-cyprindrol</li><li>COCP</li><li>Metformin</li></ul><div>Medical for those wanting to conceive:</div></div><div><ul><li>Clomiphene-induces ovulation </li><li>Metformin</li><li>Gonadotrophins-induce ovulation</li></ul><div>Surgical for those wanting to conceive:</div></div><div><ul><li>Ovarian drilling: laparoscopic-damages hormone producing cells of ovary</li></ul></div>
How can endometrial curettage result in Asherman’s syndrome
<ul><li>Damages basal layer of endometrium-> heals abnormally creating adhesions connecting areas of the uterus that aren't normally connected</li><li>Adhesions can bind uterine walls together or might seal the endocervix shut</li></ul>
How do adhesions cause problems in Asherman’s syndrome?
<ul><li>Can cause physical obstruction and distort pelvic organs-> menstrual abnormalities, infertility and recurrent miscarriages</li></ul>
How might patient with Asherman’s syndrome present?
<ul><li>Secondary amenorrhoea(absent periods)</li><li>Significantly lighter periods</li><li>Dysmenorrhoea</li><li>Infertility</li></ul>
How is Asherman’s syndrome diagnosed?
<ul><li>Hysteroscopy: GS-can also treat adhesions</li><li>Hysterosalpingography</li><li>Sonohysterography</li><li>MRI</li></ul>
How is Asherman’s syndrome treated?
<ul><li>Dissect adhesions during hysteroscopy</li></ul>
How are congenital uterine abnormalities diagnosed?
<ul><li>USS</li><li>Hysterosapingography</li><li>MRI-considered best</li></ul>
How are congenital uterine abnormailites managed?
<ul><li>Surgical intervention</li></ul>
Give some examples of congenital uterine malformations
<ul><li>Complete failure of duct fusion: double vagina, double cervix, double uterus</li><li>Septate uterus</li><li>arcuate uterus</li><li><img></img><br></br></li></ul>
Give some examples of congenital vaginal abnormalities
<ul><li>Vaginal agenesis</li><li>Vaginal atresia</li><li>Mullerian aplasia-normal external genitalia but absense of vagina</li><li>transverese vaginal septa</li></ul>
How might abnormalities of the hymen present?
<ul><li>Obstruciton of menstrual flow after puberty</li></ul>
Descriebe the pathogenesis of polyps
<ul><li>Involves oestrogen-> stimulates endometrial growth</li><li>Can arise from hyperplasia of basal layer of endometrium</li></ul>
How are endometrial polyps diagnosed?
<ul><li>Speculum exam</li><li>USS</li></ul>
How are endometrial polyps managed?
<ul><li>ASX in premenopausal: monitor</li><li>Symptomatic/postmenopausal/atypical: removed via hysteroscopic polypectomy</li><li>Histology of removed polyp to exclude malignancy</li></ul>
Describe the presentation of a patient with PID
<ul><li>Bilateral abdominal pain</li><li>Vaginal discharge</li><li>Post-coital bleeding</li><li>Adnexal tenderness</li><li>Cervical motion tenderness</li><li>Fever</li><li>Dysuria and menstrual irregularitis</li></ul>
How is Fitz Hugh Curtis syndrome diagnosed and treated?
<ul><li>Normal LFTs</li><li>US rule out stones</li><li>Definitive dx: laparoscopy</li><li>Tx: abx</li></ul>
How is PID managed?
<ul><li>IM ceftriaxone+14 days oral doxycycline+metronidazole</li><li>2nd line: oral ofloxacin+oral metronidazole</li><li>Consider removal of IUD</li><li>Avoid unprotected sexual intercourse</li></ul>
Describe the epidemiology of urinary tract stones
<ul><li>Common</li><li>M>F</li><li><65 yrs</li><li>Can be both renal and ureteric</li></ul>
Describe the aetiology of renal stones
<ul><li>Calcium oxalate-mc</li><li>Calcium phosphate</li><li>Cystine</li><li>Uric acid</li><li>Struvite</li><li>Indinavir</li></ul>
How might patient with urinary tract calculi present?
<ul><li>Severe intermittent loin pain that can radiate ot the groin</li><li>Restlessness</li><li>Haematuria</li><li>N+V</li><li>Sedoncary infection of stone-> fever/sepsis</li></ul>
How are renal stones managed?
<ul><li>Analgesia</li><li>Wait if <5mm</li><li>Medical expulsive therapy</li><li>Extracorporeal shockwave lithotripsy</li><li>Uteroscopy-pregnanyt women</li><li>Prevention</li></ul>
How can pituitary adenomas be classified?
<ul><li>Size -micro(<1cm) or macro(>1cm)</li><li>Hormonal status (secretory vs non secretory)</li></ul>
Describe the symptoms of a prolactinoma in men
Macroadenomas:<br></br><ul><li>Headache</li><li>Visual disturbance-bitemporal hemianopia</li><li>Hypopituitarism signs and sx</li></ul><div>Excess prolactin:</div><div><ul><li>Impotence</li><li>Loss of libido</li><li>Galactorrhoea</li></ul></div>
Describe the symptoms of prolacitnomas in women
Macroadenomas:<br></br><ul><li>Headache</li><li>Visual disturbance-bitemporal hemianopia</li><li>Hypopituitarism signs and sx</li></ul><div>Excess prolactin:</div><div><ul><li>Amenorrhoea</li><li>Infertility</li><li>Galactorrhoea</li><li>Osteoporosis</li></ul></div>
How is a prolactinoma diagnosed?
<ul><li>MRI head</li></ul>
How are prolactinomas treated?
<ul><li>Dopamine agonists: cabergoline, bromocriptine(inhibits release of prolactin)</li><li>Trans-sphenoidal surgery: those who can't toelrate therapy</li></ul>
Describe the surface anatomy of the breast
<ul><li>Lateral border of sternum at mid axillary line</li><li>2nd and 6th costal cartilages</li><li>Superficial to pectoralis major and serratu anterior muscles</li></ul>
<div>Circular body</div>
<div>Axillary tail</div>
Describe the mammary glands with regards to breast anatomy
<ul><li>Modified sweat glands-> ducts and secretory lobules</li><li>Each lobule consists of many alveoli drained by a lactiferous duct</li></ul>
Describe the connective tissue stroma with regards to breast anatomy
<ul><li>Fibrous and fatty component</li><li>Fibrous stroma condenses to form suspensory ligaments</li><li>Attach and secure breast to dermis and underlying pectoral fascia</li><li>Separate secretory lobules of breast</li></ul>
Describe the pectoral fascia with regards to breast anatomy
<ul><li>Flat sheet of connective tissue associated with pec major</li><li>Retromammaroy space-> layer of loose conective tissue between breast and pectoral fascia(used in reconstruction)</li></ul>
Describe the medial vasculature of the breast
<ul><li>Internal thoracic(mammary) artery-> branch of subclavian</li></ul>
Describe the lateral vasculature of the breast
<ul><li>Lateral thoracic and thoracocromial branches-> axillary</li><li>Lateral mammary branches-> posterior intercostal arteries</li><li>Mammary branch-> anterior intercostal artery</li></ul>
How does lymphatic drainage link into the presentation of patiens with breast cancer
<div><ul><li>Blockages of lymphatic drainage-> lymph builds up in SC tissues-> nipple deviation and retraction, peau d'orange</li><li>Metastasis can occur through lymph nodes-> axillary mx, then can spread to liver, bones and ovary</li></ul></div>
Describe the nerve supply of the breast
<ul><li>Anterior and lateral cutaneous branches of 4th-6th IC nerves(autonomic and sensory nerve fibres)</li></ul>
Describe the epidemiology of fibroadenomas
<ul><li>Young women-early 20s</li></ul>
Describe the presentation of a patient with a fibroadenoma
<ul><li>Firm, non-tender breast mass</li><li>Rounded and smooth edges</li><li>Highly mobile on palpation-'rubbery' </li><li><3cm in diameter(mc 2.5cm)</li><li>Usually slow growing and solitary</li></ul>
Describe the management of fibroadenomas
<ul><li>Conservative: Leave, usually regress naturally post menopause</li><li>Surgical excision: considered if large, growing, causing significant symptoms or diagnostic uncertainty</li></ul>
Describe the epidemiology of fibrocystic breast disease
<ul><li>Most common benign breast condition</li><li>20-50 years</li></ul>
Describe the aetiology of fibrocystic breast disease
<ul><li>Cumulative effect of cyclical hormone</li><li>Mostly oestrogen and progesterone-> multiple cysts and proliferative changes</li></ul>
Describe the presentation of a patient with fibrocystic breast disease
<ul><li>Bilateral 'lumpy' breasts, most commonly in upper outer quadrant</li><li>Breast pain</li><li>Sx worsen with menstrual cycle and peak 1 week before menstruation</li></ul>
Describe the management of fibrocystic breast disease
<ul><li>Encourage use of soft, well-fitting bra</li><li>Analgesia for pain relief</li><li>Most resolve after menopause</li></ul>
Describe the eppidemiology of breast cancer
<ul><li>Commonest cancer in UK in women</li><li>2nd most common cause of cancer deaths</li></ul>
Describe the pathophysiology of breast cancer
<ul><li>Genetic mutations and damaged cellular signalling-> generation of malignant cells-> metastasise</li></ul>
Describe how breast cancer cells metastasize
<ol><li>Invasion through basement membrane</li><li>Intravasation(entry into circulation)</li><li>Circulation</li><li>Extravasation</li><li>Colonisation</li></ol>
Describe the features of ductal carcinoma in situ
<ul><li>From epithelial cells</li><li>Confined to ducts</li></ul>
Describe the features of lobular carcinoma in situ
<ul><li>Arise from epithelial cells</li><li>Neoplastic cell proliferation</li></ul>
Describe the features of invasive ductal carcinoma
<ul><li>Neoplastic proliferation of epithelial cells-> ductal basement membrane-> fatty tissue</li></ul>
Describe the features of medullary carcinoma
<ul><li>Younger people</li><li>Higher grade than invasive ductal carcinoma</li></ul>
Describe some signs and symptoms of breast cancer
<ul><li>Unexplained breast/axillary mass in those >30 years</li><li>Nipple discharge</li><li>Nipple retraction</li><li>Skin changes-p'eau d'orange</li><li>Metastatic features: weight loss, bone pain, SOB</li></ul>
How is breast cancer diagnosed?
1st line: imaging<br></br><ul><li>>30yrs and clinical suspicion: mammogram</li><li><30yrs: USS</li><li>US of axilla</li></ul><div>2nd line: biopsy</div><div><ul><li>Fine needle aspiration and cytology</li></ul><div>Others:</div></div><div><ul><li>Oestrogen/progesterone receptor testing, HER2 receptor testing</li><li>CT if metastatic disease suspected</li></ul></div>
<b>Breast cancer staging:</b><br></br><ul><li>1A: {{c1::<2cm, isolated to breast}}<br></br></li><li>1B: {{c2::<2cm, minor axillary LN spread}}</li><li>2A: {{c3::<2cm, spread to 1-3 ipsilateral lymph nodes}}</li><li>2B: {{c4::2-5cm, minor axillary node spread/>5cm with no nodal spread/2-5cm with 103 ipsilateral LN spread}}</li><li>3A: {{c5::4-9 ipsilateral nodes/>5cm with 1-3 ipsilateral nodes}}</li><li>3B: {{c6::Spread to skin/chest wall}}</li><li>3C{{c7::: >10 axillary nodoes/supraclavicular/parasternal/axillary spread}}</li><li>4: {{c8::metastatic spread to other organs}}</li></ul>
How can bisphosphonates be used in the treatment of breast cancer?
<ul><li>Can help reduce recurrence in node-positive cancers</li></ul>
<b>Aetiology of benign breast disease:</b><br></br><ul><li>Fibroadenomas: {{c1::overgrowth of glandular and connective tissue resulting in blocked breast ducts and subsequent fluid accumulation}}</li><li>Mastitis: bacterial infection-> {{c2::breaks in skin around nipple}}</li><li>Intraductal papilloma: {{c3::benign tumour of breast ducts}}</li><li>Radial scar: {{c4::benign sclerosing breast lesion}}</li><li>Fat necrosis: {{c5::response to adipose tissue damage}}</li><li>Fibroycstic breast disease: {{c6::increased hormonal response resulting in inflammation and fibrosis}}</li><li>Mammary duct ectasia: {{c7::inflammation and dilation of large bresat ducts}}</li></ul>
Describe the general management of benign breast disease
<ul><li>Reassurance: often only need monitoring</li><li>Antibiotics: for infections like mastitis</li><li>Analgesics</li><li>Surgery: e.g. large fibroadenomas, persistent cysts, symptomatic intraductal papillomas</li></ul>
Describe the epidemiology of Paget’s disease of the nipple
<ul><li>Rare: <5% of all breast cancer patients</li><li>Most common in postmenopausal women</li></ul>
Describe the aetiology of Paget’s disease of the nipple
2 theories:<br></br><ul><li>Epidermotrophic: underlying breasst cancer cells migrate to the nipple</li><li>Intraepidermal origin: originates in nipple itself</li></ul>
Describe the signs and symptoms of a patient with<b> </b>Paget’s disease of the nipple
<ul><li>Eczema like rash on skin of nipple/areola(often crusty, red, inflamed, itchy)</li><li>Bloody nipple discharge</li><li>Non-healing skin ulcer</li><li>Changes to nipple-> retraction/inversion</li><li>Pain</li><li>Breast lump</li></ul>
How is Paget’s disease of the nipple diagnosed?
<ul><li>Mammography/US</li><li>Punch biopsy of affected skin, nipple discharge cytology</li><li>MRI for stagin in uncertain cases</li></ul>
How is Paget’s disease of the nipple different to eczema of the nipple?
<ul><li>Paget's involves the nipple primarily and only latterly spreads to the areolar(opposite way around in eczema)</li></ul>
How is Paget’s disease of the nipple treated?
<ul><li>Depends on underlying lesin</li><li>Simple mastectomy: remove entire breast and nipple and areeola</li><li>Modified radical mastectomy: remove some axillarry lymph nodes </li><li>Lumpectomy</li><li>Chemo, radiation, hormonal</li></ul>
Describe the latent phase of labour
<ul><li>Contractions(may be irregular)</li><li>Mucoid plug</li><li>Cervix beginning to efface and dilate(0-4cm)</li><li>Can last up to 2-3 days</li></ul>
Describe the features of contractions
<ul><li>Starts in the fundus(pacemaker)</li><li>Retraction/shortenng of muscle fibres</li><li>Build in aplitude as labour progresses</li><li>Fetus forced down causing pressure on the cervix</li></ul>
Describe the features of a gynaecoid pelvis
<ul><li>Inlet is slightly transverse oval</li><li>Sacrum wide with average concavitiy and inclination</li><li>Side walls straight with blunt ischial spines</li><li>Wide suprapubic arch</li></ul>
<div><br></br></div>
<div><img></img><br></br></div>
How might midwives help with the delivery of the body stage of labour?
<ul><li>Gentle downward traction to assist with delivery of shoulder below suprapubic arch</li><li>Gentle upwads traction to assist delivery of posterior shoulder</li></ul>
<div><img></img><br></br></div>
Describe the anatomy of the placenta and how it is connected to the fetus
<ul><li>Lobes which attach to the uterine wall</li><li>Connected to fetus via umbilical cord whcih has 2 arteries and a vein</li></ul>
How is a ventouse used?
<ul><li>Cup is applied with centre over flexion point on fetal skull</li><li>During uterine contractons, traction applied perpendicular to cup</li></ul>
At what age gestation is non invasive prenatal testing available?
<ul><li>From 10 weeks</li></ul>
At what week gestation is CVS offered for?
<ul><li>11-14 weeks gestation</li></ul>
How many weeks gestatin would amniocentesis be performed?
<ul><li>>15 weeks</li></ul>
Describe the epidemiology of mastitis
<ul><li>Postpartum: 10-20% prevalence</li><li>Usually in first 6 weeks post birth</li><li>Increased risk in 1st time mothers and previous hx of mastitis</li></ul>
Describe the aetiology if mastitis
<ul><li>Milk stasis-> inflammatory response and potential secondary infection</li><li>Cracked/sore nipples-> S.aureus-> infective mastitis</li></ul>
Describe the presentation of mastitis
<ul><li>Localised: painful, red, tender, hot breast</li><li>Systemic: fever, rigors, myalgia, fatigue nausea and headache</li><li>Usually unilateral-presents 1st week post partum</li></ul>
How is mastitis diagnosed?
<ul><li>Mostly clinical</li><li>US to ID if suspicion of abscess-> done in secondary care</li></ul>
How is mastitis managed?
<ul><li>Reassure lactating women they can continue to breastfeed</li><li>Advice on methods to faciliate milk expression</li><li>Analgesia</li><li>Oral/IV abx, surgery if abscess</li></ul>
Describe the aetiology of a breast abscess
<ul><li>S.aureus mc through crack in nipple/through milk duct</li><li>Accumulation of milk, trauma to nipple skin from incorrect latch/pump</li></ul>
Describe the presentation of a patient with a breast abscess
<ul><li>Fever/rigors</li><li>Malaise</li><li>Pain and erythema over an area of the breast</li><li>Possible presence of a fluctuant mass-> might not be palpable</li><li>Hisotry of recent/ongoing mastitis</li></ul>
How is a breast abscess diagnosed/investigated?
<ul><li>Breast USS-> visualise abscess and guide drainage</li><li>Diagnostic needle aspiration-> culture organism and evacuation</li></ul>
How is a breast abscess managed?
<ul><li>Incision and drainage/needle aspiration(with/out US guidance)</li><li>Abx therapy targeted towards most likely causative organism</li></ul>
Describe the epidemiology of bacterial vaginosis?
<ul><li>Mc cause of abnormal dishcarge in women of childbearing age</li><li>More common in sexually active women but not an STI</li></ul>
Describe the pathophysiology of bacterial vaginosis
<ul><li>Disturbance of normal vaginal flora-> decrease in number of lactobacilli bacteria</li></ul>
How is bacterial vaginosis managed in pregnanct/lactating women?
<ul><li>Screening done antenatally and quick treatment if needed</li><li>Lower doses of metronidazole in lactating women</li></ul>
Describe the epidemiology of vulvovaginal candidiasis
<ul><li>Highlyy prevalent: 20% of women/yr</li><li>Most women will experience it at some point in their lifetime</li></ul>
Describe the aetiology of vulvovaginal candidiasis
<ul><li>Candida albicans-> replicated by budding</li><li>Opportunistic infection vs hypersensitivity reaction</li></ul>
Describe the symptoms of vulvovaginal candidiasis
<ul><li>Pruritus vulvae</li><li>Vaginal discharge-white, curd like</li><li>Dysuria</li></ul>
How is vulvovaginal candidiasis diagnosed/inveestigated?
<ul><li>Usually history/clinical</li><li>Vaginal smear and mc+s-> blastospores, pseudohyphae and neutrophils</li></ul>
Describe the management of vulvovaginal candidiasis
<ul><li>Intravaginal antifungal-> clotrimazole pessary</li><li>Oral antifungal-> fluconazole</li><li>Vulva/topical steroid-> topical imidazole</li></ul>
How is vulvovaginal candidiasis treated in pregnancy?
<ul><li>DO NOT use oral antifungals</li><li>Advise care with intravaginal treatment applicator</li><li>Saftynetting if not resolved in 7-14 days</li></ul>
Describe the epidemiology of chlamydia
<ul><li>Most common STD in UK</li><li>Highest prevalence in 15-24 yr olds</li></ul>
How is chlamydia transmitted?
<ul><li>Via unprotected vaginal, oral, anal sex</li><li>Skin to skin contact of genitals</li><li>Vertical(mother to baby during delivery)</li></ul>
Describe the signs and symptoms of chlamydia in men
<ul><li>Often asymptomatic: incubation period 7-21 days</li><li>Urethritis: dysuria, urethral discharge</li><li>Epididymo-orchitis: testicular pain</li><li>Epididymal tenderness</li><li>Mucopurulent discharge</li></ul>
Describe the signs and symptoms of chlamydia in women
<ul><li>Asymptomatic often: incubation period 7-21 days</li><li>Dysuria</li><li>Discharge</li><li>Intermenstrual bleeding</li><li>Pain/tenderness</li></ul>
Describe the signs and symptoms of chlamydia in neonates
<ul><li>Pneumonia</li><li>Conjunctivitis</li></ul>
How is chlamydia diagnosed?
<ul><li>Women: vulvovaginal swab</li><li>Men: first catch urine sample</li></ul>
<div>Analyze using nucelic acid amplification tests</div>
Describe the management of chalmydia in non-pregnant people
<ul><li>Doxycycline: 100mg twice daily for 7 days</li></ul>
Describe the management of chlamydia in pregnant women
<ul><li>Azithromycin/erythromycin</li></ul>
Describe the management of neonates with chlamydia
<ul><li>Oral erythromycin</li></ul>
Describe the epidemiology of gonorrhoea
<ul><li>2nd most common STI after chlamydia</li><li>increased prevalence in 15-24yrs</li><li>Hihger prevalence in MSM</li></ul>
How is gonorrhoea transmitted?
<ul><li>Unrpotected vaginal/oral/anal sex</li><li>Vertical transmission</li></ul>
Describe the aetiology and pathology of gonorrhoea
<ul><li>Gram negative diplococcus neisseria gonorrhoea</li><li>Causes acute inflammation-> uterus, urethra, cervix, fallopian tube, ovaries, rectum, testicles, eyes, throat</li></ul>
How do patients with gonorrhoea present?
<ul><li>Males: urethral discharge, dysuria</li><li>Women: discharge, dysuria, dyspareunia, pain</li><li>Dishcarge tends to be thin, watery green/yellow</li><li>Asymptomoatic especially when rectal/pharyngeal infection</li></ul>
How is gonorrhoea diagnosed?
<ul><li>Females: endocervical/vaginal/urethral swab</li><li>Males: first pass urine(NAAT), urethral/meatal swab</li></ul>
<div>Microsopcy, culture and NAAT</div>
How is gonorrhoea treated?
<ul><li>Singled soe 1g IM ceftriaxone</li><li>Screen/treat other infections</li><li>test of cure recommended</li></ul>
Describe the symptoms of disseminated gonococcall infection
<ul><li>Tenosynovitis</li><li>Migratory polyarthritis</li><li>Dermatitis</li></ul>
How is gonorrhoea treated in pregnancy?
<ul><li>Prophylactic abx+tx in pregnancy-> ceftriaxone</li></ul>
How are neonates with gonorrhoea managed?
<ul><li>Urgent referral and treatment</li><li>Long term damage and blindness</li></ul>
Describe the epidemiology of genital herpes
<ul><li>Very common</li><li>15-24yrs</li></ul>
Describe the pathophysiology of genital herpes
<ul><li>After infecting surface-> travels up to meet nearest ganglion and stays there until reactivated</li></ul>
Describe the presentation of a patient with a primary genital herpes infection
<div><ul><li>Asymptomatic</li><li>Small, painful red blisters around genitals, can form open sores</li><li>Vaginal/penile discharge, dysuria, urinary retention</li><li>Flu like sx-> fever ,muscle aches, malaise, headaches</li><li>After 20 days: lesions crust and heal-> end of viral shedding</li></ul></div>
Describe the presentation of a patient with an outbreak of a genital herpes infection
<ul><li>Usually shorter and less severe than initial infection</li><li>Burning, itching, painful red blisters</li></ul>
How is genital herpes diagnosed?
<ul><li>Clinical hz and exam</li><li>Swab from abse of ulcer-> NAAT</li></ul>
Describe the management of genital herpes
<ul><li>Primary infection: aciclovir 400mgTD 5 days</li><li>Recurrent outbreaks: OTC analgesia, ice, topical lidocaine</li><li>Regular episodes: episodic aciclovir tx when sx begin</li></ul>
Describe the management of herpes in pregnancy
<ul><li>Low risk of transmission with vaginal birth</li><li>Referral to GUM clinic and treat with aiclovir if 1st time HSV infection</li><li>If contracted in last trimester: antibodies not developed-> C-section</li></ul>
Describe the features/management of neonatal herpes
<ul><li>Skin/eyes/mouth herpes(SEM)-antiviral tx</li><li>Disseminated herpes(DIS)-internal organs</li><li>CNS herpes-> encphalitis</li></ul>
<div>DIS and CNS herpes associated with increased mortality</div>
Describe the aetiology of genital warts
<ul><li>90% HPV 6/11-low risk, not associated with cancer</li></ul>
How do patients with genital warts typically present?
<ul><li>Asx</li><li>Painless warts of scrotum, penis, vagina, cervix, perianal skin, anus</li><li>Warts can be keratinised(hard) or non-keratinised(soft)</li><li>Extra-genital lesions: oral cavity, larynx, nasal cavity, conjunctivae</li></ul>
How are genital warts diagnosed/
<ul><li>Usually from clinical exam/hx</li><li>Proctoscopy/vaginal speculum exam to check for internal warts</li><li>Biopsy for atypical lesions/suspected intraepithelial neoplastic lesions</li></ul>
Describe the management of genital wwarts
Tx not always needed, can resolve spontaneously<br></br><br></br>Topical:<br></br><ul><li>Podophyllotoxin: antiviral to destroy clusters(BD 3 days then 4 days rest)</li><li>Imiquimod: immune response modifier for larger keratinised warts(3 times/week)</li></ul><div>Physical:</div><div><ul><li>Cryotherapy</li><li>Surgical excision</li><li>Elecrto/laser-surgery</li></ul></div>
How does pregnancy impact genital warts?
<ul><li>No risk to babies but maternal warts can multiply/enlarge during pregnancy</li></ul>
Describe the pathophysiology behind the HIV infection
<ol><li>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 integrase</li><li>Infected cell divides, viral DNA read-> creates viral protein chains and immature virus pushes out of cell, retaining some membranes</li><li>Virus matures when protease cuts viral protein chains and assemble to create a working virus, destroying a host cell</li></ol>
How do CD4 levels change over the course of the HIV infection?
<ul><li>Seroconversion(producing anti-HIV antiibodies during primary infection)-> flu-like sx-> decrease in CD4 levels due to initial rapid replication-> extremely infectious</li><li>Latent phase: months-yrs: initiay asx but increased susceptibility to infections</li></ul>
How is HIV transmitted?
<ul><li>Unprotected sexual intercourse</li><li>Sharing needles</li><li>Medical procedures</li><li>Vertical transmission</li></ul>
Describe the symptoms of the seroconversion stage of HIV
<ul><li>2-6 weeks post exposure</li><li>Fever</li><li>Muscle aches</li><li>Malaise</li><li>Lymphadenopathy</li><li>Maculoapular rash</li><li>Pharyngitis</li></ul>
Describe the symptoms of the symptomatic stage of HIV
<ul><li>Weight loss</li><li>High temperature</li><li>Diarrhoea</li><li>Frequent opportunistic infections</li></ul>
Describe the symptoms of the AIDS defining illness stage
<ul><li>Advanced stage: immune system significantly weakened</li><li>Deveopment of AIDS defining illnesses/infections/malignancies</li></ul>
How is HIV diagnosed?
4th generation tests:<br></br><ul><li>ELISA-> test for serum/salivary HIV antibodies and p24 antigen</li><li>Reliable results 4-6 weeks post exposure</li></ul><div>Contact tracing</div>
Describe the management of HIV
HAART: highly active antiretroviral therapy<br></br>>=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
<ul><li>non-nucleoside reverse transcriptase inhibitors</li><li>E.g. nevirapine</li><li>SE: P450 enzyme interaction, rashes</li></ul>
Describe the features of protease inhibitors
<ul><li>E.g. indinavir, nelfanivir</li><li>SE: diabetes, hyperlipidaemia, central obesity, P450 enzyme inhibitirion</li></ul>
Describe the features of integrase inhibitors
<ul><li>E.g. raltegravir, elvitegravir</li><li>Block the action of integrase(viral enzyme that inserts the viral genome into the DNA of the host cell)</li></ul>
How is HIV managed in pregnancy and why?
<ul><li>Can be transmitted in utero, at delivery and through breast-feeding</li><li>Risk reduction strategies(separate flashcard)</li><li>C-section non longer recommended if undetectable viral load</li></ul>
How is the risk of HIV transmission in pregnant women minimised?
<ul><li>Anttenatal antiretroviral therapy during pregnancy and delivery</li><li>Avoidance of breastfeeding</li><li>Neonatal post-exposure prophylaxis</li></ul>
How do patients with a threatened miscarriage present?
<ul><li>Painless vaginal bleeding <24 weeks(usually 6-9 weeks)</li><li>Bleeding often less than menstruation</li></ul>
How can the aetiology of polyhydramnios be classified?
<ul><li>Idiopathic</li><li>Excess production due to increased fetal urination</li><li>Insufficient removal due to decreased fetal swallowing</li></ul>
How might a patient with polyhydramnios present?
<ul><li>Uterus feels tense/large for dates</li><li>Difficult to feel fetal parts on abdominal palpation</li></ul>
How is polyhydramnios managed?
<ul><li>Usually no intervention needed</li><li>Treat underlying cause</li><li>Severe only: amnioreduction</li><li>Indomethacin</li></ul>
How is indomethacin useful for treating polyhydramnios?
<ul><li>Enhances water retention and decreases fetal urine output</li></ul>
How is prolonged pregnancy managed?
<ol><li>Membrane sweeps-40 wks nulliparous, 41 wks in parous</li><li>Induction of labour-41/42 weeks gestation</li></ol>
<div>If 2 declined: twice weekly CTG moniotring and US with amniotic fluid measurement to predict fetal distress. Might need C-section</div>
How do patients with placenta praevia present?
<ul><li>Painless bright red vaginal bleeding after 24 weeks</li><li>Sometimes pain if in labour</li><li>Can present with signs of shock if severe blood loss</li><li>Malpresentation of fetus due to abnormal placental position</li></ul>
Describe the management of acute presentation of placenta praevia
<ul><li>ABCDE approach</li><li>If bleeding not controlled/in labour: C-section</li><li>Anti-D within 72 hours of bleeding onset if rhesus D negative</li></ul>
How is placenta praevia managed if found in a 20 week scan
<ul><li>Placenta praevia minor: rpt scan at 36 weeks-likely to move</li><li>Major: rpt at 32 weeks and plan for delivery-> usually elective c-section</li><li>Advice about pelvic rest: no penetrative sexual intercourse and go hospital if major bleeding</li></ul>
Describe the pathophysiology of placental abruption
<ul><li>Rupture of maternal vessels in basal layer of endometrium-> blood gathers and splits placental attachment from basal layer</li><li>Detached portion unable to funciton-> rapid fetal compromise</li></ul>
How might patients with placental abruption present?
<ul><li>Painful vaginal bleeding</li><li>If in labour: may have pain between contractions</li><li>Abdominal pain: often sudden and severe</li><li>Hypovolaemic shock disproportionate to amount of vaginal bleeding visible</li></ul>
How is placental abruption managed?
<ul><li>ABCDE resus including anti D if rh D negative</li><li>Tx dependednt on health of fetus</li><li>Emergency delivery: usually C section, even if in-utero death</li><li>Induction of labour at term to avoid further bleeding if haemodynamically stable</li></ul>
Describe the natural progressin of most breech babies
<ul><li>20% breech at 28weeks</li><li>Most revert to cephalic presentation spontaneously witih onlly 3% still breech at term</li></ul>
How is breeech presentation diagnosed?
Clinical:<br></br><ul><li>Head felt in upper uteris, buttocks and elgs in pelvis</li><li>Fetal heart auscultates higher on maternal abdomen on US</li><li>20% not diagnosed until labour</li></ul>
How might breech presentatin present at labour?
<ul><li>Fetal distress-> meconium stained liquor</li><li>Vaginal exam: sacrum/foot felt through cervical opening</li></ul>
Describe the management of breech presentation
<ul><li>External cephalic version: offered at 37 weeks to primiparous women</li><li>C-section</li><li>Vaginal breech birth</li></ul>
How is abnormal fetal lie/malpresentation/malrotation diagnosed?
<ul><li>Abdominal exam</li><li>Confirm with US-> also ID predisposing abnormalities</li></ul>
Describe the management of normal fetal lie
<ul><li>External cephalic version(ECV)-> 36-38 weeks gestation</li></ul>
Describe the management of malpresentation
<ul><li>Breech: ECV before labour, vaginal birth, C section</li><li>Brow: c-section</li><li>Shoulder: c -section</li><li>Face: chin posterior: c section, chin anterior: attempt normal labour</li></ul>
Describe the management of malposition
<ul><li>90% spontaneously rotate during labour</li><li>If not: operative vaginal delivery/C-section</li></ul>
Describe the pathophysiology of pre-eclampsia
<ul><li>High resistance, low flow uteroplacental circulation develops as constrictive muscular walls of spiral arterioles are maintained</li><li>Increase in BP, hypoxia-> systemic inflammatory response</li></ul>
Describe the symptoms of pre-eclampsia
<ul><li>Headaches</li><li>visual changes</li><li>Epigastric pain</li><li>Sudden onset non-dependent oedema</li><li>Hyper-reflexia</li></ul>
Describe the management of pre-eclampsia
<ul><li>Serial monitoring: BP, urinalysis, fetal growth scans, CTG</li><li>VTW-LMWH</li><li>Anti-hypertensives-labetalol, nifedipine, methyldopa</li><li>Delivery(give IM steroids if <35 weeks)</li><li>Post-natal: monitor for 24 hours post partum and BP for 5 days</li></ul>
Descrbe the split of eclamptic seizures in the post natal, antepartumand intrapartum periods
Post-natal: mc-44%<br></br>Antepartum: 38%<br></br>Intrapartum: 18%
Describe the symptoms of eclampsia
<ul><li>New onset tonic clonic seizure in presence of pre-eclampsia</li><li>Lasts 60-75 secs then post-ictal phase</li><li>May cause fetal distress and bradycardia</li></ul>
Describe the management of eclampsia
Rescuscitation<br></br><ul><li>ABCDE approach</li><li>Pt lie in left lateral position and secure airway and O2 therapy</li></ul><div>Seizure control:</div><div><ul><li>Magensium sulphate</li><li>Monitor for signs of magensium poisoning</li></ul><div>BP control:</div></div><div><ul><li>IV labetalol and hydralazine</li></ul><div>Delivery of baby and placenta:</div></div><div><ul><li>Usually C-section</li></ul><div>Monitoring:</div></div><div><ul><li>Fluid balance: prevent pulmonary oedema and AKI</li><li>Monitor platelets, transaminases and creatinine</li></ul></div>
How long should a magnesium suflate drip be continued for after an eclamptic seizure?
<ul><li>48 hours after last seizure</li></ul>
How is t<span>richomoniasis transmitted?</span>
<ul><li>Predominanly sexual</li></ul>
Describe the epidemiology of t<span>richomoniasis</span>
<ul><li>Mc non-viral STI globally</li></ul>
Describe the signs and symptoms of t<span>richomoniasis in women</span>
<ul><li>Profuse, frothy, yellow vaginal discharge</li><li>Vulvovaginitis</li><li>Dyspareunia</li><li>Starwberry cervix-may be seen</li><li>pH>4.5</li><li>Asx</li></ul>
Describe the signs and symptoms of t<span>richomoniasis in men</span>
<ul><li>Usually asymptomatic</li><li>Non-gonococcal urethritis</li></ul>
How is t<span>richomoniasis diagnosed?</span>
<ul><li>Direct microscopy and culture of the causative organism-> motile trophozoites</li><li>pH>4.5</li><li>Test for other STIs</li></ul>
How is t<span>richomoniasis treated?</span>
<ul><li>Oral metronidazole for 5-7 days or single dose of 2g orally</li><li>Abstain from sex for a week</li><li>Screen for others</li><li>Contact tracing</li></ul>
Describe the epidemiology of chancroid
<ul><li>Global incidence decreasing</li><li>Mc in tropical areas and greenland</li></ul>
Describe the symptoms of chancroid
<ul><li>Painful genital ulcers which may bleed on contact-ulcers are sharply defined, ragged, undermined border</li><li>Painful inguinal lymphadenopathy</li><li>Sx 4-10 days after bacterium exposure</li></ul>
<div><img></img><br></br></div>
How is chancroid diagnosed?
<ul><li>Usually clinical</li></ul>
<div>Can culture and use PCR</div>
How is chancroid treated?
<ul><li>Antibiotics: ceftriaxone/azithromycin/ciprfloxacin</li><li>Analgesics </li><li>Incision/drainage of buboes</li></ul>
Describe the presentatin of a patient with l<span>ymphogranuloma venereum</span>
<ul><li>Stage 1: small painless pustule which later forms an ulcer</li><li>Stage 2: painful ingional lymohadenopathy-may from fistulaitng buboes</li><li>Stage 3: proctocolitis(can include rectal pain and discharge)</li></ul>
<div><img></img><br></br></div>
How is lymphogranuloma venereum diagnosed?
<ul><li>PCR from swab of genital ulcer</li></ul>
How is lymphogranuloma venereum managed?
<ul><li>oral doxycuclin 100mg twice daily for 21 days</li><li>Can also use: tetracycline, erythromycin</li></ul>
How is lymphogranuloma venereum different to ‘normal’ chalmydia?
<ul><li>Normal chalmydia: urethritis and PID: Chlamydia trachomatis serovars D-> K</li><li>lymphogranuloma venereum: serovards L1, L2, L3<br></br></li></ul>
Describe the aetiology of balanitis
<ul><li>Mc: infective: bacterial and candidal</li><li>Autoimmune causes</li></ul>
How is balanitis investigated/diagnosed?
<ul><li>Usually clinical-hx and exam</li><li>Swab for mc+s/PCR-> bacteria or candida albicans</li><li>If doubt/extensive skin changes: biopsy</li></ul>
Describe the general treatment of balanitis
<ul><li>Gentle saline washes</li><li>Wash properly under foreskin</li><li>1%hydrocortisone for a short period</li><li>Treat underlying cause</li></ul>
How is balanitis due to dermatitis treated?
<ul><li>Mild potency steroid- hydocortisone</li></ul>
How is balanitis due to lichen sclerosus treated?
<ul><li>High potency topical steroids</li><li>Clobetasol</li><li>Circumcision can help</li></ul>
How is balanitis due to candidiasis treated?
<ul><li>Topical clotrimazole for 2 weeks</li></ul>
How is syphilis transmitted?
<ul><li>Direct contact with shyphilis sores or rash during vaginal, anal or oral sex</li><li>Vertical: mother to child</li></ul>
Describe the features of primary syphilis?
<ul><li>Chancre-painless ulcer at the site of sexual contact</li><li>Local non-tender lymphadenopathy</li><li>Often not seen in women(lesion can be on the cervix)</li></ul>
Describe the lesion associated with the primary syphilis infection
<ul><li>Painless</li><li>Round, indurated base</li><li>Heals spontaneously within 3-8 eeks</li></ul>
Describe the features of secondary syphilis
<ul><li>Systemic: fevers, malaise etc</li><li>Rash on trunks, palsm and sores</li><li>buccal 'snail track' ulcers</li><li>Condylomata lata ( painless warty lesions on genitalia)#</li></ul>
<div><img></img><br></br></div>
Describe the features of tertiary syphilis
<ul><li>Gummas(granulomatous lesions of skin and bones)</li><li>Ascending aortic aneurysms</li><li>neurological: demenita, paresis, tabes dorsalis, argyll-robertson pupil)</li></ul>
Describe the features of congenital syphilis
<ul><li>Presents shortly after birth or later in infancy</li><li>Rash: palms/soles, mucous patches/leisons in motuh/nose/genitals</li><li>Feever</li><li>Blunted upper incisor teeth(Hutchinson's teeth), 'mulberry' molars</li><li>Rhagaades( linear scars at angle of mouth)</li><li>Keratitis</li><li>Saber shins</li><li>Saddle nose</li><li>Neruological; seizures, developmental delay</li></ul>
How can serological tests for syphilis be divided?
<ul><li>Non-treponemal tests</li><li>Treponemal specific tests</li></ul>
Describe the features of non-treponemal tests for syphilis
<ul><li>Not-specific for syphilis: false positives</li><li>Based on reactivity of serum from infected patients to a cardiolipin cholesterol-lecithin antigen</li><li>Negative after treatment</li></ul>
Describe the features of treponemal specific tests?
<ul><li>More complex and expensive but sspecific for syphilis</li><li>Qualitative</li></ul>
Describe the treatment pf syphilis
<ul><li>IM benzathine penzylpenicillin</li><li>Tertiary/late latent: longer course of IM penicillin G</li><li>Neurosyphilis: IV penicillin G for 10-14 days</li></ul>
<div>Backup for penicillin allergy: doxycycline</div>
How might patients with intraductal papilloma present?
<ul><li>Bloody discharge from the nipple</li><li>With/without a palpable mass</li><li>May have breast tenderness</li></ul>
How are intraductal papillomas treated?
<ul><li>Severe cases might need surgery</li></ul>
How can breast cysts be classified?
<ul><li>Microcysts: seen on imaging but too small to be felt</li><li>Macrocysts: 1-2cm: large enough to be felt</li></ul>
How might patients with mammary duct ectasia present?
<ul><li>Tender lump arounf areola +/- thick green nipple discharge</li><li>If ruptures: local inflammation-> 'plasma cell mastitis'</li></ul>
Describe the treatment for mammary duct ectasia
<ul><li>Surgical intervention may be needed if symptomatic</li></ul>
Describe the epidemiology of HELLP syndrome
<ul><li>Rare</li><li>Significant cause of maternal and perinatal morbidity/mortality</li></ul>
Describe the aetiology of HELLP syndrome
<ul><li>Unknown</li><li>Related to abnormal placentation, endothelial cell injury and generalized inflammatory response</li></ul>
Describe the presentation of patients with HELLP syndrome
<ul><li>N+V</li><li>RUQ pain-> liver distention</li><li>Lethargy</li><li>Headahces</li><li>Blurred vision</li><li>Peripheral oedema</li></ul>
Describe the maangement of HELLP syndrome
<ul><li>Definitive: deliver baby</li><li>Steroids: accelerate fetal lung maturation</li><li>Blood transfusions to manage anaemia and thrombocytopenia</li></ul>
Describe the epidemiology of cord prolapse
<ul><li>Relatively rare</li><li>Higher risk in breech presentations and multiple pregnancies</li></ul>
Describe the pathology of cord prolapse
<div><ul><li>Usually membrane rupture-> amniotic fluid egress-> descent of umbilical cord</li><li>Cord compression-> against maternal soft tissues or bony pelvis-> fetal hypooxia</li></ul></div>
How might patients with cord prolapse present?
<ul><li>Abnormal fetal heart rate: mc -> varibable/prolonged decelerations</li><li>Palpable umbilical cord</li><li>Sudden onset of sympotms post rupture of membranes</li><li>Patient reported sensation</li></ul>
How is a cord prolapse investigates/diagnosed?
<ul><li>Clinical</li><li>USS</li><li>Cardiotocoography(CTG)</li><li>Speculum exam</li></ul>
How is cord prolapse managed?
<ul><li>Immediate delivery of fetus-> instrumental or C section </li><li>'knees chest' position to reeduce pressure on cord</li><li>Avoid exposure and handling of cord, reducing into vagina</li><li>Use of tocolytics like terbutaline to stop uterine contractions</li></ul>
Describe the pathophysiology of vasa praevia
<ul><li>Abnormal placental development</li><li>Fetal membrane development: persistence of membranous vessels</li><li>Fetal vessel vulnerability: prone to rupture</li></ul>
How can vasa praevia be classified?
<ul><li>Type 1 and Type 2</li><li>Ramified or funic</li></ul>
Describe the signs and symptoms of vasa praevia
<ul><li>Painless vaginal bleesin</li><li>Rupture of membranes</li><li>Fetal bradycardia/resulting fetal death</li></ul>
<div><br></br></div>
<div>Also:</div>
<div><ul><li>Foetal anaemia</li></ul></div>
How is vasa praevia diagnosed?
<ul><li>Transabdominal/TV USS-most cases now diagnosed antenatally</li></ul>
<div>Can use MRI and prenatal testing</div>
How is vasa praevia managed?
<ul><li>Elective C-section prior to rupture of membranes: 35-36 weeks gestation</li><li>Emergency C-section of premature labour or membranes rupture</li><li>Prompt neonatal resus</li></ul>
Describe the epidemiology of peruperal psychosis
<ul><li>Rare: 11-2/1000 childbirths</li></ul>
Describe the aetiology of peurperal psychosis
<ul><li>Unknown</li><li>Hormonal changes post childbirth</li><li>Genetics</li><li>Psychosocial stressors</li><li>Sleep deprivation</li></ul>
Describe the signs and symptoms of peurperal psychosis
<ul><li>Paranoia</li><li>Delusions: Capgras</li><li>Hallucinations-command </li><li>Manic episodes</li><li>Depressive episodes</li><li>Confusion</li></ul>
How is peurperal psychosis diagnosed?
<ul><li>Clinical</li><li>Thorough psych evaluation</li><li>Rule out: thyroid disorders, sepsis etc</li></ul>
Describe the management of peurperal psychosis
<ul><li>Admit to mother/baby mental health unit: especially if Capgras/command hallucinations</li><li>Antipsychotics: olanzapine and quetipaine</li><li>Mood stabilisers in some cases</li><li>CBT</li></ul>
Describe the epidemiology of postpartum depression
<ul><li>Prevalent: 10-20% of mothers</li></ul>
Describe the aetiology of postpartum depression
<ul><li>Multifactorial</li><li>Biological: hormones, melatonin, cortisol, inflammatory processes, genetics</li><li>Psychological </li><li>Social</li></ul>
Describe the signs and symptoms of postpartum depression
<ul><li>Persistents low mood and anhedonia</li><li>Low energy</li><li>Sleep issues-important to distinguish between abby's fault and depression</li><li>Poor appetite</li><li>Concerns relating to bonding with baby, caring for baby etc</li></ul>
How is baby blues different to postpartum depression?
<ul><li>MIlder: mood swings, irritability, anxiety and tearfullness</li><li>Sx present within first 2 weeks after birth and resolve spontaneously</li></ul>
How is postpartum depression diagnosed?
<ul><li>Clinical</li><li>Edinburgh postnatal depression scale</li><li>Rule out risk of psychosis-risk assessment really important</li></ul>
<div>Physical exam: anaemia, hypothyroidism to rule out organic causes</div>
Describe the management of postpartum depression
<ul><li>Self-help, CBT, ITP(interpersonal therapy)</li><li>Antidepressants(SSRIs)</li><li>Severe: admission to mother baby mental health unit</li></ul>
How is baby blues managed?
<ul><li>Reassurance and support</li><li>Regular health visitor checks to check in with mother</li></ul>
Define pre-term labour
<ul><li>Onset of regular uterine contractions accompanied by cervical changes occuring before 37 weeks gestation</li></ul>
Define pre-term birth
<ul><li>Delivery of a baby 20-37 weeks gestation</li></ul>
Define premature rupture of membranes
<ul><li>Rupture of membranes at least one hour before onset of contracitons</li></ul>
Define prolonged premature rupture of membranes
<ul><li>Rupture of membranes over 24 hours before onset of labour</li></ul>
Define pre-term premature rupture of membranes
<ul><li>Early rupture of the membranes before 37 weeks gestation</li></ul>
Describe the epidemiology of preterm prelabour rupture of the membranees
<ul><li>Occurs in around 2% of all pregnancies</li><li>Associated with 40% of preterm delvieries</li></ul>
How is PPROM diagnosed?
<ul><li>Sterile speculum exam: look for pooling of amniotic fluid in posterior vaginal vault</li><li>Avoid digital exam: risk of infection</li><li>If no pooling: test fluid for placental alpha microglobulin protein(PAMG-1) or insulin like growth factor binding protein 1</li><li>USS-oligohydramnios</li></ul>
How is PPROM managed?
<ul><li>Admission</li><li>Regular observations to check for chorioamnionitis</li><li>Oral erythromycin for 10 days</li><li>Antenatal corticosteroids: reduce risk of respiratory distress syndrome</li><li>Delivery should be considered at 34 weeks gestation</li></ul>
Describe the aetiology of postpartum haemorrhage
4T’s:<br></br><ul><li>Tone: mc: uterine atony(failure of uterus to contract after delivery)</li><li>Trauma</li><li>Tissue(retained placenta etc)</li><li>Thrombin(clotting/bleeding disorder)</li></ul>
Describe the initial management of PPH
<ul><li>Life threatening emergency: ABCDE approach</li><li>2 14 gauge large bore peripheral cannulas</li><li>Lie flat</li><li>Bloods including grooup and save</li><li>Commence warm crystalloid infusion</li></ul>
Describe the mechancial strategies that can be used to manage postpartum haemorrhage
<ul><li>Palpate uterine fundus and rub it to stimulate contractions</li><li>Catheterisation to prevent bladder distention and monitor urine output</li></ul>
Describe the medical management of postpartum haemorrhage
<ul><li>IV oxytocin: slow IV injection then infusion </li><li>ergometrine slow IV(unless hx of htn)</li><li>carboprost IM(unless hx of asthma)</li><li>sublingual misprostol</li></ul>
Describe the surgical management of postpartum haemorrhage
If medical options fail to control bleeding:<br></br><ul><li>Intrauterine balloon tamponde-if uterine atony as cause</li><li>B-lynch suture, ligation of uterine/internal iliac arteries</li><li>If severe: hysterectomy as life-saving procedure</li></ul>
How is secondary postpartum haemorrhage managed?
<ul><li>Depends on underlying cause</li><li>Abx for infection</li><li>Surgical evacuation for retained products of conception</li></ul>
Describe the pathophysiology of rhesus negative pregnancy
<ul><li>15% of mothers rhesus negative</li><li>If rh negative mother delivers a rh positive child, a leak of fetal red blood cells can occur</li><li>Causes anti D-IgG antibodies to form in mother</li><li>Maternal anti-D antibodies can cross placenta in subsequent pregnancies and cause rhesus haemolytic disease if baby is rhesus positive</li><li>Can also occur in first pregnancy due to leaks</li></ul>
Give some examples of sensitisation events in rhesus negative pregnancies
<ul><li>Anteepartum haemorrhage</li><li>Placental abruption</li><li>Abdo trauma</li><li>ECV</li><li>Miscarriage if gestation > 12 weeks</li><li>Termination of pregnancy</li><li>Delivery of rh positive infant</li><li>Ectopic pregnancy</li><li>Amniocentesis, CVS, fetal blood sampling</li></ul>
How is rhesus heamolytic disease prevented and screened for?
<ul><li>Test for D antibodies in all rhesus negative mothers at booking</li><li>Anti-D given to non-sensitised rh negative mothers at 28 and 34 weeks-prophylaxis(once sensitisation occurs can't be undone)</li></ul>
How is rhesus negative pregnancy managed?
<ul><li>Screening/prevention strategies</li><li>Give Anti-D immunoglobulin as soon as possible but always within 72 hours when a sensitisation even occurs</li></ul>
Describe the medical management of termination of pregnancy
<ul><li>Mifepristone(first orally) then misoprostol 24-48 hours after</li><li>Misoprostol can be repeated 3 hourly(max 5) until expulsion</li><li>Takes time: hours to days</li><li>Pregnancy test required in 2 weeks: multi-level pregnancy test-measures level of HCG not just positive or negative</li></ul>
How is trichomoniasis vaginalis managed in pregnancy?
<ul><li>Same: oral metronidazole 400-500mg twicce a day for 5-7 days</li><li>High dose not recommended in pregnancy/breastfeeding(no 2g single dose)</li></ul>
Describe the symptoms of uterine rupture
<ul><li>Sudden severe abdominal pain which persists between contractions</li><li>Shoulder tip pain-diaphragmatic irritation)</li><li>Vaginal bleeding</li></ul>
Describe the signs of a uterine rupture
<ul><li>O/E: regression of presenting part</li><li>Abdominal palpation: scar tenderness and palpable fetal parts</li><li>Fetal monitoring: fetal distress/absent heart sounds</li><li>Significant haemorrhage: signs of shock: tachycardia, hypotension</li></ul>
Describe the management of a uterine rupture
<ul><li>ABCDE appproach</li><li>C-section</li><li>Uterus either repaired or removed</li><li>Decision-incision interval should be under 30 minutes</li></ul>
Define gestational diabetes
<ul><li>Glucose intolerance on OGTT with:</li><li>Fasting blood glucose >=5.6mmol/L</li><li>2 hour plasma glucose levels >=7.8mmol/L</li></ul>
Describe the epidemiology of gestational diabetes
<ul><li>5% of pregnancies</li><li>2nd most common medical disorder complicating pregnancies</li></ul>
How might patients with gestational diabetes present?
<ul><li>Often asx</li><li>Polyuria</li><li>Thirst</li><li>Fatigue</li></ul>
How is gestational diabetes diagnosed?
<ul><li>OGTT: fasting >=5.6, 2 hour: >=7.8-REMEMBER 5,6,7,8</li><li>HbA1c: distinguish between gestational and pre-existing diabetes early on</li><li>Urinalysis: check for glycosuria</li></ul>
Describe the management of gestational diabetes
<ul><li>Fasting glucose <7mmol/L: lifestyle : diet and exercise. Give it 1-2 weeks then metformin if targets not met, then insulin added</li><li>>=7mmol/L: start insulin (short acting not long acting)</li><li>6-6.9mmmol/L + complications like macrosomia or hydramnios: offer insulin</li><li>Glibenclamide only for women who can't use metormin/doesn't work and decline insulin</li></ul>
Describe the management of pre-existing diabetes in pregnancy
<ul><li>Weight loss if BMI >27</li><li>Stop oral hypoglycaemimcs except metformin and start insulin</li><li>Folic acid 5mg/day until 12 weeks </li><li>Detailed anomaly scan at 20 weeks including 4 chamber view of heart and outflow tracts</li><li>Tight glycaemic control reduces complication rates</li><li>Treat retinopathy: can worsen in pegnancy</li></ul>
Describe the normal changes in blood pressure in pregnancy
<ul><li>Usually falls in the 1st trimester and continues to fall until 20-24 weeks</li><li>After this: BP usually increases to pre-pregnancy levels by term</li></ul>
How should pregnant patients with hypertension be classified?
<ul><li>Pre-existing hypertension</li><li>Pregnancy induced hypertension/gestational hypertension</li><li>Pre-eclampsia</li></ul>
<div><br></br></div>
Describe the management of pre-existing hypertension in pregnancy
<ul><li>STOP ACE inhibitor or angiotensin 2 receptor</li><li>SWAP for alternative: labetalol whilst waiting specialist review</li><li>Nifedipine if asthmatic</li></ul>
Describe the features of pregnancy induced hypertension
<ul><li>Hypertension occuring in the 2nd half of pregnancy(after 20 weeks)</li><li>No proteinuria, no oedema</li><li>5-7% of pregnancies</li></ul>
Describe the management of pregnancy induced hypertension
<ul><li>Oral labetalol/nifedipine/hydralazine</li><li>Typically resolves within 1 month after birth </li></ul>
Describe the features of pre-eclampsia
<ul><li>Pregnancy induced hypertension associated wwith proteinuria(>0.3g/24hrs)</li><li>Oedema may occur but less commonly used now as a criteria</li><li>5% of pregnancies</li></ul>
Describe the epidemiology of Group B strep infection
<ul><li>Mc asx commensal bacterium in GI and GU tracts</li><li>25% of pregnant women estimated to be carriers</li><li>Can cause severe illness to mother and infant during transmission during delivery</li></ul>
How might Group B strep infection be investigated?
<ul><li>No current routine screening test for pregnant women as colonisation status can change through pregnancy</li><li>GBS culture may be done in certain cirumstances</li></ul>
How is Group B strep infection managed?
<ul><li>Intrapartum antibiotic prophylaxis-benzylpenicillin</li><li>Abx IV during labour and delivery</li></ul>
Describe the management of obesity in pregnancy
<ul><li>5mg folic acid not 400mcg</li><li>Screening for gestational diaebetes with OGTT at 24-28 weeks</li><li>BMI >=35: Birth in consultant led obstetric clinic</li><li>BMI>=40: Antenatal coonsultation with ostetric anaesthetist and plan made in advance</li></ul>
How is cephalopelvic disproportion managed?
<ul><li>Trial of labour</li><li>Intrumental vaginal delivery-may need episiotomy</li><li>C-section</li></ul>
How is prolonged labour managed?
<ul><li>ID causes and evaluate progress of labour</li></ul>
<div>Medical:</div>
<div><ul><li>Artificial rupture of membranes</li><li>IV oxytpcin to augemnt contractions</li><li>Pian management: epidural, nitrous oxide etc</li></ul><div>Surgical:</div></div>
<div><ul><li>Operative delivery</li><li>C-section</li></ul><div>Postpartum:</div></div>
<div><ul><li>Monitor closely for infection</li><li>Active management of 3rd stage of labour: uterotonic agents</li><li>Ensure adequate analgesia</li></ul></div>
Describe the clinical features of obstetric cholestasis
<ul><li>Pruritus: intense-typically worst in palms, soles, abdomen</li><li>Jaundice: dark urine and pale stools in about 20% of patients</li><li>General fatigue and malaise</li><li>GI sx: nausea and appetite loss</li><li>RUQ abdominal pain</li><li>Raised bilirubing in >90% of acses</li></ul>
How is obstetric cholestasis managed?
<ul><li>Chlorphenamine and emollients to reduce itching</li><li>Induction of labour at 37-38 weeks</li><li>Ursodeoxycholic acid</li><li>Vitamin K supplementation-> minimise risk of bleeding</li></ul>
Describe the prognosis of obstetric cholestasis
<ul><li>Hihg recurrence: 45-90% in subseqquent pregnancies</li></ul>
Describe the aetiology of chorioamnionitis
<ul><li>Bacteria ascending from vagina into uterus</li><li>Mc: Group B strep, E.coli and anaerobic bacteria</li></ul>
How is chorioamnionitis diagnosed?
<ul><li>Usually clinical</li><li>Blood tests and cultures ot confirm and ID causative organism</li></ul>
How is chorioamnionitis managed?
<ul><li>IV broad sectrum abx: sepsis 6 protocol</li><li>Monitoring of fetus and mother for complications</li><li>Early delivery might be needed-C section</li></ul>
Describe the management of FGM in the UK
<ul><li>Illegal in UK-immediate child protection referrral if child at risk</li><li>Anterior episiotomy during second stage of labour under local anaesthetic or regional block</li><li>Deinfibulation surgery: important to protect urethra</li></ul>
Describe the clinical features of shoulder dystocia
<ul><li>Difficult delivery of fetal face/chin</li><li>Retraction of fetal head-turtle neck sign</li><li>Failure of restitution</li><li>Failure of descent of fetal shoulders following delivery of head</li></ul>
Describe the management of shoulder dystocia
<ul><li>Immediately call for senior help</li><li>Do not apply fundal pressure-can lead to uterne rupture</li><li>McRoberts maneouevre</li><li>All fours position</li><li>Internal rotational manoeuvers</li><li>Episiotomy-won't remove bony obstruction but will allow space for internal manoeuvers</li><li>Cleidotomy/symphysiotomy: not 1st line-associated with significant maternal morbidity]</li><li>Zavanelli manoeuvre-also dangerous</li></ul>
Define anaemia in pregnancy
Hb:<br></br><ul><li>1st trimester: <110g/L</li><li>2/3 triester: <105g/L</li><li>Postpartum: <100g/L</li></ul>
Describe some clinical features of anaemia
<ul><li>Asx</li><li>Dizziness, fatigue, dyspnoea: normal pregnancy</li><li>Pallor</li><li>Koilonychia</li><li>Angular cheilitis</li></ul>
How is anaemia diagnosed/investigated in pregnancy?
<ul><li>FBC</li><li>Folate to check for folate deficiency</li><li>Check for beta thalassaemia and sickle cell</li></ul>
Describe the risk of congenital rubella syndrome?
<ul><li>Risk high as 90% in first 8-10 weeks</li><li>Damage rare after 16 weeks</li></ul>
Describe the epidemiology of congenital rubella syndrome
<ul><li>Rare now due to MMR vaccine</li></ul>
How is rubella transmitted ot the fetus in congenital rubella syndrome?
<ul><li>Virus can cross the placenta and affect the developing fetus</li></ul>
How is congenital rubella syndrome diagnosed?
<ul><li>Serology to confirm rubella infection-IgM raised in women recently exposed to virus</li><li>Audiology tests for hearing impairment</li><li>Opthalmology for eye abnormalities</li><li>Echos for congenital heart defects</li></ul>
How is congenital rubella syndrome managed?
<ul><li>During pregnancy: discuss with local health protection unit</li><li>Advised to keep away from people who might have rubella</li><li>Offer MMR vaccine in post natal period</li><li>Neonates: primarily supprotive and symptomatic-monitor progress and manage long-term complications</li></ul>
How can perineal tears be classified?
<ul><li>1st, 2nd, 3rd, 4th degree </li></ul>
Describe the features of a first degree perineal tear
<ul><li>Superficial damage with no muscle involvement</li><li>Do not require any repair</li></ul>
Describe the features of a second degree perineal tear
<ul><li>Injury to perineal muscle but not involving the anal sphincter</li><li>Require suturing on ward by suitably experienced midwife or clinician</li></ul>
Describe the features of a third degree perineal tear
<ul><li>Injury to perineum involving the anal sphincter complex(external anal sphincter(EAS) and internal anal sphincter(IAS)</li><li>3a: < 50% EAS thickness torn</li><li>3b: >50% EAS thickness torn</li><li>3c: IAS torn</li><li>Require repair in theatre by suitably trained clinician</li></ul>
Describe the features of a fourth degree perineal tear
<ul><li>INjury to perineum involving the anal sphincter complex(EAS and IAS) and rectal mucosa</li><li>Require repair in theatre by suitably trained clinician</li></ul>
Describe the management of perineal tearss
<ul><li>1st degree: no repair</li><li>2nd: suturing</li><li>3rd/4th: surgical repair under regional or general anaesthetic</li><li>Broad spectrum abx and laxatives given post surgery</li></ul>
Describe the epidemiology of amniotic fluid embolism
<ul><li>Rare but significant cause of maternal morbidity and mortality</li></ul>
Describe the aetiology of an amniotic fluid embolism
<ul><li>Not known fully</li><li>Amniotic fluid can enter maternal circulation and form embolism-> block circulation like a blood clot especially in lung</li><li>Fluid also triggers inflammatory response within mother's immune system-> DIC</li></ul>
Describe the signs and symptoms of an amniotic fluid embolism
<ul><li>Tachypnoea</li><li>Tachycardia</li><li>Hypotension</li><li>Hypoxia</li><li>DIC</li><li>Cyanosis and MI</li><li>Chills, shivering, sweating, anxiety and coughing</li></ul>
How is an amniotic fluid embolism diagnosed?
<ul><li>Clinical</li><li>Exclude other causes-no definitive diagnostic test</li></ul>
Describe the management of an amniotic fluid embolism
<ul><li>Immediate transfer to ICU, MDT care</li><li>Oxygen, fluid resus</li><li>Correction of any coagulopathy</li><li>FFP if prolonged PT</li><li>Cryoprecipitate for low fibrinogen</li><li>Platelet transfusion for low platelets</li></ul>
Describe the management of hyperemesis gravidarum
Simple:<br></br><ul><li>Rest and avoid trigggers</li><li>Bland, plain food, ginger</li><li>P6(wrist) acupressure</li></ul><div>1st line meds:</div><div><ul><li>antihistamines: oral cyclyzine/promethazine</li><li>phenothiazines: oral prochlorperazine or chlorppromazine</li></ul><div>2nd line:</div></div><div><ul><li>Oral odansetron</li><li>Oral metoclopramide/domperidone-5 DAYS MAX</li></ul><div><br></br></div></div><div><br></br></div><div><ul><li>Thiamine and folic acid supplementation</li><li>Atacids</li><li>Thromboembolic stockings and LMWH -dehydration </li></ul></div><div><br></br></div><div><br></br></div><div><br></br></div><div><br></br></div><div><br></br></div><div><ul><li><br></br></li></ul></div>
How is hyperemesis gravidarum managed in hospital?
<ul><li>Normal saline with added potassium for rehydation</li><li>Antiemetics</li></ul>
Describe the management of hypothyroidism in pregnancy
<ul><li>Levothyroxine: usual dose increased by 25-50mcg due to increased metabolic demand</li></ul>
Describe the aetiology of acute fatty liver of pregnancy
<ul><li>LCHAS mutation-> accumulation of fatty acid metabolites in placenta-> shunted into maternal circulation and accumulate in maternal liver</li></ul>
How is acute fatty liver of pregnancy investigated/diagnosed?
Raised:<br></br><ul><li>AST/ALT</li><li>Bilirubin</li><li>Creatinine</li><li>Ammonia</li><li>Lactate</li><li>Serum uric acid</li></ul><div>Leukocytosis, low-normal platelets, normocytic normochromic anaemia</div><div>Coagulopathy: prolonged PT, hypofibrinogenaemia and elevated D dimer</div>
Describe the management of acute fatty liver of pregnancy
<ul><li>Curative: delivery of the fetus</li><li>Maternal stabilisation: correct hypoglycaemia, coagulopathy and hypertension</li><li>After delivery: cloese monitoring-if ongoing deteriorattion in liver function post birth-transfer to liver transplant facility</li></ul>
Describe the management of the thyrotoxic phase of postpartum thyroidits
<ul><li>Propanolol for sx control</li><li>Not usually treated with anti-thyroid drugs as thhryroid not overactive</li></ul>
Describe the treatment of the hypothyroid phase of postpartum thyroidits
<ul><li>Usually treated with thyroxine</li></ul>
Describe the presentation of a patient with obstructed labour
<ul><li>Widest diameter of fetal sckull remains stationary above the pelvic brim</li><li>Prolionged labour: >12 hours</li><li>Premature rupture of membranes</li><li>Mother has abnormal vital signs</li><li>Bandls' ring</li><li>Foul smelling meconium from mother's vagina</li><li>Oedema of fulva/cervix</li><li>Caput</li><li>Malpresentation/malposition of fetus</li><li>Poor cervical effaceemnt</li></ul>
<div><br></br></div>
<div>Assess using vaginal exam</div>
Describe the management of obstructed labour
<ul><li>Saline for dehydration</li><li>catheter to drain bladder</li><li>May need C section or instrumental delivery</li></ul>
Describe the epidemiology of intrauterine growth restriction
<ul><li>3-7% of newborns</li><li>Increased prevalence in low/middle income countries-> maternal malnutrition and infection</li></ul>
Describe the signs and symptoms of intrauterine growth restriction
<ul><li>Decreased fetal movement</li><li>Abnormal fundal height for gestational age</li><li>Complications like pre-eclampsia and stillbirh</li></ul>
How is intrauterine growth restriction managed?
<ul><li>Close monitoring of fetal growth and wellbeing</li><li>Management of maternal conditions contributing</li><li>Consideration for early delivery if fetus is in distress/conditions worsens</li></ul>
Describe the aetiology of ovarian hyperstimulation syndrome
<ul><li>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</li></ul>
Describe the signs and symptoms of ovarian hyperstimulation syndrome
<ul><li>Bloating</li><li>Abdo pain</li><li>Oedema</li><li>Pleural efffusions</li><li>Ascites</li><li>Weight gain</li></ul>
How is ovarian hyperstimulation syndrome diagnosed?
<ul><li>Routine bloods: evaluate haemoconcentration and detect potential organ dysfunction</li><li>CXR: ID pleural effusion</li></ul>
Describe the management of ovarian hyperstimulation syndrome
<ul><li>Supportive-tailored to severity of condition</li><li>Simple analgesia for discomfort</li><li>Might need ICU and close monitoring if severe</li></ul>
Describe the features of fetal varicella syndrome
<ul><li>Skin scarring</li><li>Eye defects: microphthalmia</li><li>Limb hypoplasia</li><li>Microcephaly</li><li>Learning difficulties</li></ul>
Describe the management of chickenpox <b>exposure</b> in pregnancy
<ul><li>If doubt about previous infection: check blood urgently for varicella antibodies</li><li>Oral aciclovir now first choice for post exposure prophylaxis(used to be VZIG)-should be given day 7-14 after exposure not immediately</li></ul>
Describe the management of chickenpox in pregnancy
<ul><li>Seek specialist advice</li><li>Oraal aciclovir if >=20 weeks and presents within 24hrs of rash onset</li><li>If <20 weeks: aciclovir 'considered with caution</li></ul>
Describe the pathophysiology of placental insufficiency?
<ul><li><span>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. </span></li></ul>
How might placental insufficiency present?
<ul><li>Usually no observable sx</li><li>Decreased fetal movemennt</li><li>Intrauterine growth restriction</li><li>Prematurity</li><li>Stillbirth</li></ul>
How is placental insufficiency diagnosed/investigated?
<ul><li>Doppler USS: evaluate fetal and placental circulations-> regulare screening</li><li>MRI if inconclusive</li></ul>
Describe the management of <span>placental insufficiency</span>
<ul><li><34 weeks: delay delivery: low dose aspirin, vitamin C and E, heparin</li><li>>34 weeks: prompt delivery</li></ul>
How is a pregnant women at high risk of VTE treated?
<ul><li>LMWH throughout antenatal period and input from experts</li></ul>
If a pregnant woman has 3 risk factors for VTE how should this be managed?
<ul><li>LMWH from 28 weeks and continued nutil 6 weeks postnatal</li></ul>
If a diagnosis of DVT is made shortly beefore delivery in a pregnant woman, how long should treatment be continued for?
<div><ul><li>At least 3 months</li></ul></div>
How can twin pregnancies be classified?
<ul><li>Zygosity</li><li>Chorionicity</li><li>Amnionicity</li></ul>
How can monozygotic twwins be further classified?
<ul><li>Dichorionic + daimniotic: 2 different sacs</li><li>Monochorionic + diamniotic: same outer sac, two inner sacs</li><li>Monochorionic + monoamniotic: same sacs</li></ul>
Describe the epidemiology of twins
<ul><li>2/3: dizygotic</li><li>1/3: monozygotic</li></ul>
<div>^When conceived naturally</div>
Describe the management of twins
<ul><li>Rest</li><li>USS for diagnosis and monthly checks</li><li>Additional iron and folate</li><li>More antenatal care( weeekly when >30 weeks)</li><li>Precautions at labour(2 obstetricians present)</li><li>75% of twins deliver by 38 twins, if longer, most twins are induced at 38-40 weeks</li></ul>
Describe the aetiology of twin-to-twin transfusion syndrome
<ul><li>Precipitated by anastamoses of umbilical vessels betwween 2 fetuses in the placenta of monochorionic twins</li></ul>
How is twin-to-twin transfusion syndrome diagnosed?
<ul><li>Monochorionic twins: regular USS to monitor</li><li>Observe fluid levels in each amniotic sac, measure size of twins and assess blood flow in umbilical cord and placenta</li></ul>
Describe the management of twin-to-twin transfusion syndrome
<ul><li>Laser transection of problematic vessels in utero-can increase survival rate, high mortlaity for both twins without tx</li></ul>
Describe the symptoms of UTI in pregnancy
<ul><li>Frequent urination</li><li>Dysuria</li><li>Lower abdo pain</li><li>Fever</li><li>Haematuria</li></ul>
Describe the management of asymptomatic bacteriuria in pregnancy
<ul><li>Nitrofurantoin and cefalexin mc used</li><li>Ig Group B strep ID d: intrapartum prophylactic abx to reduce risk of transmission </li></ul>
Describe the treatment for a UTI in pregnant women
<ol><li>nitrofurantoin for 7 days(avoid at term)</li><li>Amoxicillin/cefelexin</li></ol>
Describe the symptoms of puerperal infection
<ul><li>Fever</li><li>Abdo pain</li><li>Tahycardia</li><li>Abnormal discharge</li><li>Foul smellinf lochia(postpartum bleeding)</li><li>Tenderness/pain in pelvi area</li><li>Sepsis signs: hypotension, tachypnoea etc</li></ul>
Describe the maangement of puerperal infection
<ul><li>Abx-broad spectrum initially: ceftriaxone and metronidazole</li><li>Fluids</li><li>Analgesia</li><li>Prevention: good hygiene practices during childbirth and postpartum care</li><li>Close monitoring</li><li>Drainage od abscesses if needed</li></ul>
Describe LH and FSH in Turners
<ul><li>Raised LH</li><li>Raised FSH</li></ul>
Describe LH and FSH in Kallman’s
<ul><li>Low LH</li><li>Low FSH</li></ul>
Describe the general function of blood hormones
<ul><li>Oestrogen: sex development-females</li><li>Progesterone: uterine development</li><li>Testosterone: sex development males</li><li>FSH and LH: ovarian funcitonality</li></ul>
Describe the management of primary amenorrhoea
<ul><li>Primary hypo: COCP</li><li>Primary hyper: GnRH analogue</li></ul>
Descrieb the management of secondnary amenorrhoea
<ul><li>Lifestyle: stress/weight managemenet</li><li>Treat underlying cause</li><li>Surgical: tumour/cyst removal</li></ul>
For how long/how frequently do a couple need to be having unrpotected sexual intercourse to be cnsidered infertile?
<ul><li>2 years despite sex 3-4 times/wweek</li></ul>
How can causes of infertility be classified?
<ul><li>Genetics</li><li>Ovulation/endocrine</li><li>Tubal abnormalities</li><li>Uterine abnormalities</li><li>Endometriosis</li><li>Cervical abnormalities</li><li>Testricular disorders</li><li>Ejaculatory disorders</li></ul>
Give some ovulation/endocrine disorders that can cause infertility
<ul><li>PCOS</li><li>Pituitary tumours</li><li>Sheehan's syndrome</li><li>Hyperprolactinaemia</li><li>Cushing's</li><li>Premature ovarian failure</li></ul>
Give some tubal abnormalities that can cause infertility
<ul><li>Congenital anatomical abnormalities</li><li>Adhesions</li><li>Can be secondary to PID(-> gonorrhoea, chlamydia)</li></ul>
Give some uterine abnormalities that can cause infertility
<ul><li>Bicronate uterus</li><li>Fibroids</li><li>Asherman's syndrome</li></ul>
How is infertility investigated in women?
Bedside:<br></br><ul><li>Thorough hx including PMH, sexual history and past pregnancies</li><li>Speculujm and bimaual exam-e.g. fibroids</li><li>STI screen</li></ul><div><br></br></div><div>Bloods:</div><div><ul><li>Serum progesterone testing</li><li>Prolactin</li><li>LH/FSH</li><li>Anti-mullerian hormone</li><li>TFTs</li></ul><div>Imaging:</div></div><div><ul><li>TV USS</li><li>Hysterosalpingography</li><li>Laparoscopy and dye</li></ul></div>
How is infertility investigated in men?
Bedside:<br></br><ul><li>Thorough hx including PMH, sexual history past children</li><li>Testicular exam: e.g. varicocele</li><li>Semen analysis: evaluate sperm count, motility and morphology</li></ul><div>Bloods:</div><div><ul><li>Serum testosterone</li><li>LH/FSH</li><li>TFTs</li></ul></div>
Describe the conservative management of infertility
<ul><li>Folic acid</li><li>Weight loss: BMI 20-25</li><li>Smoking cessation and alcohol advice</li><li>Stres reduction strategies</li><li>Advice sexual intercourse every 2-3 days</li></ul>
