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>
