Selected Notes obgyn 1 Flashcards

(474 cards)

1
Q

How can urinary incontinece be characterised?

A
  1. Overactive bladder/urge incontinence<br></br>2. Stress incontinence<br></br>3. Mixed incontinence<br></br>4. Overflow incontince<br></br>5. Functional incontinence
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2
Q

How is urinary incontinence investigated?

A
  1. 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
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3
Q

Describe the management of stress incontinence

A

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 

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4
Q

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}}

A
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5
Q

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}}

A
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6
Q

Describe the general conservative management of incontinence

A

Lifestyle advice: avoid caffeine and fizzy drinks, avoid excessive fluid intake<br></br>Pelvic floor exercises

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7
Q

Describe the medical management of urge incontinence

A

Anticholinergics(antimuscarinics): inhibit the parasympathetic action of the detrusor muscle<br></br>-Oxybutinin, tolterodine, etc<br></br><br></br>

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8
Q

Describe the symptoms of a genital prolapse

A

<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>

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9
Q

Describe the management of a gential prolapse

A

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

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10
Q

Describe the surgical management for a cystocele

A

Anterior colporrhaphy, colposuspension

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11
Q

Describe the symptoms of a vaginal fistula

A

Incontinence-especailly if vesicovaginal(bladder and vagina)<br></br>Also: diarrhoea, nausea, vomiting, weight loss<br></br>

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12
Q

How is a vaginal fistula diagnosed?

A

Pelvic exam<br></br>Cystoscopy and urodynamic studies<br></br>Imagin<br></br>

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13
Q

Describe the management of vaginal fistulas

A

Conservative: catheterisation, antibiotics to prevent/treat infection<br></br>Surgical: fistula repair, tissue grafts<br></br>

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14
Q

Describe the aetiology of uterine fibroids

A

Unknown<br></br>Genetic, hormonal and environmental factors<br></br>

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15
Q

How can uterine fibroids cause polycythaemia?

A

Secondary to autonomous production of erythropoeitin

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16
Q

How are uterine fibroids diagnosed

A

<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>

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17
Q

Describe the management of <b>asymptomatic</b> fibroids

A

No treatment, just review to monitor growth and size

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18
Q

Describe the management of menorrhagia secondary to fibroids

A

Levonorgestrel intrauterine system (LNG-IUS)-Mirena coil first line<br></br>Mefenamic and TXA<br></br>COCP and oral/injectable progesterone

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19
Q

How does red degeneration of fibroids present?

A

-Severe abdominal pain<br></br>-Low grade fever<br></br>-Tachycardia<br></br>-Vomiting

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20
Q

How is red degeneration of fibroids managed?

A

Supportive: rest, fluids and analgesia

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21
Q

Describe the aetiology of ovarian cysts

A

<span>Hormonal imbalances, endometriosis, pregnancy and pelvic infections.</span>

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22
Q

Describe some symptoms of an ovarian cyst

A

-Asymptomatic<br></br>-Acute unilateral pain<br></br>Bloating/fullness in the abdomen<br></br>-Intra-peritoneal haemorrhage with haemodynamic compromise<br></br>

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23
Q

Describe the management of a simpole ovarian cyst in premenopausal women

A

<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

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24
Q

Describe the management of ovarian cysts in postmenopausal women

A

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

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25
How are persistent or enlarging ovarian cysts treated?
Surgical intervention-laparoscopy-> ovarian cystectomy, sometimes with affected oophorectomy
26
How can benign ovarian cysts becharacterised?
  1. Physiological/functional cysts
  2. Benign germ cell tumours
  3. Benign epithelial tumours
  4. Benign sex cord stromal tumours
27
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}}
28
Corpus luteum cysts occur when the corpus luteum fails to break down and instead {{c1::fills with fluid.}} They may cause symptoms such as {{c1::pelvic discomfort, pain or delayed menstruation.}} They are often seen in {{c1::early pregnancy.}} 
29
An endometrioma is a lump of {{c1::endometrial tissue}} within the ovary, occurring in patients with {{c1::endometriosis.}} They can cause {{c1::pain}} and disrupt {{c1::ovulation.}}
30
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
31
Describe the pathophysiolgy of an ovarian torsion
Twisting of the adnexa and blood supply to the ovary leads to ischaemia. If the torsion persists, necrosis will occur, and the function of that ovary will be lost.
32
Describe the presentation of a patient with ovarian torsion
  • Sudden onset severe unilateral pelvic pain
  • Pain is constant and gets progressively worse
  • Associated with nausea and vomiting
Pain can also come and go if ovary twists and untwists intermittently 
33
How is ovarian torsion diagnosed?
1st line: Pelvic US(transvaginal ideally, transabdominal as backup)->'whirlpool sign' free fluid in pelvis and oedema or ovary
Doppler-> reduced blood flow
Definitive-> laparoscopic surgery
34
Describe the management of ovarian torsion
  • Urgent admission and gynae involvemebt
  • Laparoscopic surgery to:
  1. Untwist the ovary and fix it in place(de-torsion)
  2. Remove the affected ovary (oophorectomy)
Laparotomy may be needed if large ovarian mass or malignancy is suspected
35
Describe the aetiology of lichen sclerosus
Thought to be autoimmune reaction-associated with T1DM
Also genetics and hormonal factors
36
Describe a typical presentation of a patient with lichen sclerosus
45-60yr old woman
Vulval itching
Soreness/pain
Skin tightness
  • Painful sex (superficial dyspareunia)
  • Erosions
  • Fissures
Koebner phenomenon
37
Describe the appearance of lichen sclerosus
  • “Porcelain-white” in colour
  • Shiny
  • Tight
  • Thin
  • Slightly raised
  • There may be papules or plaques

38
How is lichen sclerosus diagnosed?
  • Mostly clinical
  • Skin biopsy can be used to confirm the diagnosis-usually done if atypical features are present(e.g. doesn't respond to treatment, clinical suspicion of cancer etc)
  • Blood tests to check for potential autoimmune conditions
39
Describe the management of lichen sclerosus
  • Topical corticosteroids(dermovate) to reduce inflammation and itching
  • Avoidance of soap in affected areas to prevent further irritation
  • Emollients to relieve dryness and soothe itching
40
Cervical cancer:
2 main tumour suppressor genes: {{c1::P53 and pRb}}
HPV produces 2 main proteins: {{c2::E6 and E7}}

E6 protein inhibits {{c2::p53}} and E7 inhibits {{c2::pRb}}

Therefore, HPV promotes the development of cancer by inhibiting tumour suppressor genes.
41
At what age are children vaccinated against HPV?
age 12-13 yrs
42
Describe the signs and symptoms of cervical cancer
  • Most commonly picked up on screening incidentally
  • Abnormal vaginal bleeding (intermenstrualpostcoital or post-menopausal bleeding)
  • Vaginal discharge
  • Pelvic pain
  • Dyspareunia (pain or discomfort with sex)
  • Urinary/boewl habit change
  • Abnormal white/red patches on cervix
  • Mass on PR exam
43
How is cervical cancer investigated and diagnosed?
-If symptoms-> speculum exam and smear test
If abnormal appearance of cervice-> urgen cancer referral for colposcopy
44
How is the cervical intraepithelial neoplasia determined?
Colposcopy NOT screening
45
Grades of cervical intraepithelial neoplasia:
  • CIN I: {{c1::mild}} dysplasia, affecting {{c1::1/3 t}}he thickness of the {{c1::epithelial layer,}} likely to r{{c1::eturn to normal}} without treatment
  • CIN II: {{c2::moderate}} dysplasia, affecting {{c2::2/3}} the thickness of the {{c2::epithelial layer}}, l{{c2::ikely to progress to cancer}} if untreated
  • CIN III: {{c2::severe}} dysplasia, {{c2::very likely to progress}} to cancer if untreated
46
Cervical cancer screening:
Offered to all women between ages {{c1::25-64 years}}
  • 25-49yrs: {{c2::3}} yearly screening
  • 50-64yrs: {{c3::5}} yearly screening
Cannot be offered to women over {{c4::64 years}}
47
Describe the results obtained from cervical cancer screening cytology
  • Inadequate
  • Normal
  • Borderline changes
  • Low-grade dyskaryosis
  • High-grade dyskaryosis (moderate)
  • High-grade dyskaryosis (severe)
  • Possible invasive squamous cell carcinoma
  • Possible glandular neoplasia
 
48
A cone biopsy is a treatment for {{c1::cervical intraepithelial neoplasia (CIN) and very early-stage cervical cancer. }}It involves a general anaesthetic. The surgeon removes a cone-shaped piece of the cervix using a {{c1::scalpel.}} This sample is sent for histology to assess for {{c1::malignancy.}}
49
Bevacizumab (Avastintargets{{c1:: vascular endothelial growth factor A (VEGF-A),}} which is responsible for {{c2::the development of new blood vessels.}} Therefore, it {{c3::reduces the development of new blood vessels}}
50
Endometrial cancer is a malignancy that originates from the {{c1::endometrium}}-the {{c1::inner}} lining of the uterus
51
Endometrial cancer:
All women {{c1::>=55yrs}} presenting with {{c1::postmenopausal bleeding}} should be referred using the suspected cancer pathway
52
How is endometrial cancer investigated?
  • first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
  • hysteroscopy with endometrial biopsy
53
How is endometrial cancer managed?
Surgery: hysterecotmy with bilateral alpingo-oophorectomy-can be curative if limited
Radio/chemotherapy
Progesterone therapy sometimes used in frail elderly women not suitable for surgery
54
Describe the outcomes of endometrial hyperplasia
1. Most return to normal
2, <5% become cancer
55
How is endometrial hyperplasia treated?
  1. Intrauterine system(mirena coil)
  2. Continuous oral progesterones(levonorgestrel)
56
How does adipose tissue result in increased oestrogen levels?
  • Contains aromatase->converts androgens.
  • More adipose tissue->more androgens converted to oestrogen
57
How common is ovarian cancer?
5th most common malignancy in femals
58
Epithelial ovarian tumours are partically {{c1::cystic}} so can contain {{c1::fluid}}
59
How do germ cell ovarian tumours typically spread?
Via lymphatics
60
Describe the presentation of ovarian cancer
  • Typicall present layte-non-specific symptoms
  • Abdominal pain
  • Bloating
  • Ealry satiety
  • Urinary frequency or change in bowel habits
Later stages:
  • Ascites(vascular growth factors increasing vessel permeability)
  • Pelvic, back and abdominal pain
  • Palpable pelvic or abdominal mass
61
How is CA125 used to guide further investigations when investigting a patient for possible ovarian cancer?
  • Raised CA125(>=35IU/mL)-> urgent US of abdomen and pelvis
62
How is ovarian cancer treated?
Surgery:
  • If early disease-remove uterus, fallopian tubes, ovaries and infracolic omentectomy
  • Advanced-debulking surgery

Adjuvant/intraperitoneal chemotherapy
Biologics

63
Describe the prognosis of ovarian cancer
80% have advanced disease at presentation
All stage 5 year survival is 46%
64
An ovarian mass may press on the {{c1::obturator}} nerve and cause referred {{c2::hip or groin}} pain
65
How common is vulval cancer?
Rare-4% of gynae cancers
66
At what age are the majority of vulval cancers diagnosed?
>60 years
67
Describe the clinical features of a patient with vulval cancer
  • Lump on labia majora
  • Inguinal lymphadenopathy
  • Itching/discomfort in vulval area
  • Non healing ulcer
  • Changes in skin colour/thickening of vulva
  • Bleeding/discharge not related to the menstrual cycle
68
How is vulval cancer managed?
Surgery
  • Radical/wide local excision
  • Radical vulvectomy for multi-focal disease
  • Reconstructive surgery
  • Radioterhapy.chemo
69
A molar pregnancy, also known as a {{c1::hydatidiform mole}}, forms part of a spectrum of disorders known as {{c2::gestational trophoblastic disease}}. It is characterized by an imbalance in the {{c3::number of chromosomes}} originating from the mother and father during conception.
70
How can molar pregnancies be characterised?
  • Complete
  • Partial
71
Describe the presentation of a patient with a hydatidiform mole
  • Vaginal bleeding
  • Enlargement of uterus beyond the expected size for gestational age
  • Nausea and hyperemesis gravidarum
  • Thyrotoxicosis
72
How can a molar pregnancy cause enlargement of the uterus?
Excessive growth of trophoblasts and retained blood
73
How can a molar pregnancy cause thryotoxicosis?
HCG closely related to TSH so able to activate receptors
74
How is a molar pregnancy diagnosed?
B-HCG->higher than normal 
Trans-vaginal US->'snowstorm' appearance, low resistance of blood vessel flow and absence of a foetus
75
How are molar pregnancies managed?
  • Immediate referral to a specialist centre for treatment is necessary to reduce the risk of potential complications such as choriocarcinoma or invasion.
  • As molar pregnancies are not viable, they are managed with suction curettage to remove them from the uterus.
  • When fertility preservation is not a concern, a hysterectomy may be performed.
  • Surveillance is recommended, including:
    • Bimonthly serum and urine hCG testing until levels are normal.
    • In the case of a partial mole, a repeat hCG test is done 4 weeks later - if normal, the patient is discharged from surveillance.
    • In a complete mole, monthly repeat hCG samples are sent for at least 6 months.
76
How common is endometriosis?
Common-10% of women in reproductive years
77
Describe the symptoms of endometriosis
  • Chronic pelvic pain
  • Dysmenorrhoea
  • Dyspareunia
  • Subfertility
  • Non-gynaecological-> dysuria, urgency, haematuria
  • Cyclical rectal bleeding, if endometrium-like tissue grows outside the female reproductive system
78
Describe the medical management of endometriosis
  • Analgesia->paracetemol/NSAIDs
  • Hormonal therapies-> COCP, medroxyprogesterone acetate, Gonadotrophin releasing hormone agonists
79
Describe the surgical management of endometriosis
  • Diathermy of lesions
  • Ovarian cystectomy(for endometriomas)
  • Adhesiolysis
  • Bilateral oophorectomy(sometimes hysterectomy)
80
How do patients with adenomyosis typically present?
  • Asymptomatic
  • Dysmenorrhoea
  • Menorrhagia
  • Dyspareunia
  • Infertility or pregnancy-related complications
81
Describe the management of adenomyosis
Symptomatic: TXA/mefenamic acid
  1. Mirena coil(first line)
  2. COCP
  3. Cyclical oral progesterones

GnRH agonists
Uterine artery embolisation
Hysterecomy-definitive treatment
82
How is andorgen insensitivity syndrome diagnosed?
  • Buccal smear or chromosomal analysis to reveal 46XY genotype
  • After puberty: hormonal tests
83
Describe the presentation of a patient with atrophic vaginitis
  • Vaginal dryness and discharge
  • Dyspareunia
  • Occasional spotting
  • Loss of pubic hair
  • Urinary symptoms like dysuria and recurrent UTI
84
Describe the management of atrophic vaginitis
  • Hormonal treatment:
    • Systemic hormone-replacement therapy (oral or transdermal)
    • Topical oestrogen preparations
  • Non-hormonal treatments:
    • Lubricants, which provide short-term improvement to vaginal dryness, alleviating symptoms such as dyspareunia
    • Moisturisers, which should be used regularly
  • Transvaginal laser therapy, although not currently recommended due to lack of evidence
85
Describe the management of a miscarriage
  • Conservative: Allow POC to pass naturally-> repeat scan/pregnancy test
  • Medical: vaginal misoprostol
  • Surgical
86
How does vaginal misoprostol work as medical management for a msicarriage?
  • Stimulates cervical ripening and myometrial contractions
87
Describe the features of a threatened pregnancy
  • Painless vaignal bleeding <24 weeks(usually 6-9 weeks)
  • Bleeding but often less than menstruation
  • Cervical os closed
88
How is a threatened pregnancy treated?
  • Reassurance
  • If heavy: admit and observe
  • If >12 weeks, and rhesus negative: Anti D
89
Describe the features of an inevitable pregnancy
  • Heavy bleeding
  • Clots
  • Pain
  • Cervical os open
90
How is an inevitable miscarriage treated?
  • Reassurance, if heavy bleeding then admit and observe
  • If >12 weeks and rhesus negative : Anti D
  • Likely to proceed to a complete/incomplete miscarriage
91
Describe the features of a missed/delayed pregnancy
  • Gestational sac containing a dead fetus <2 weeks without symptoms of expulsion
  • Cervical os closed
  • Asymptomatic, light bleeding, discharge, pregnancy symptoms which disappear
92
How is a missed/delayed miscarriage treated?
  • Reassurance, if heavy bleeding admit for observation
  • Low success rate
93
Describe the features of an incomplete miscarriage
  • POC partly expelled
  • Symptom of bleeding.clots
  • Cervical os open
94
How might a patient with a complete miscarriage present?
  • History of bleeding
  • Clots
  • POC
  • Pain
  • Symptoms settled
95
How are patients with complete miscarriages managed?
  • Discharged to GP
96
Describe the symptoms of a septic miscarriage
  • Infected POC
  • Rigors
  • Fever
  • Bleeding
  • Leukocytosis
  • Increased CRP
97
How is a septic miscarriage treated?
  • IV antibiotics and fluids
  • Medical/surgical treatment
98
Describe the symptoms of a patient with an ectopic pregnancy
  • Pelvic pain: can be unilateral
  • Shoulder tip pain-irritation of diaphragm by intra-abdominal bleeding
  • Vaginal discharge/bleeding-decidua breaking down
99
Describe the conservative management of an ectopic pregnancy
  • Close follow up and repeat B-HCG's
  • Not usually done
100
Describe the medical management of an ecoptic pregnancy
  • IM methotrexate
  • Regular B-HCG checks : >15% decline by day 4/5 or repeat methotrexate
101
How does methotrexate work as treatment in a patient with an ectopic pregnancy?
  • Disrupts folate dependent cell division
102
Describe the surgical management of an ectopic pregnancy
  1. Tubal ectopics: laparoscopic salpingectomy (remove ectopic and tube)
  2. If only one tube left: salpingotomy (cut in fallopian tube and remove ectopic)
B-HCG follow up until <5iU(negative)-> check for residual trophoblast
103
How does amniotic fluid normally change throughout pregnancy?
  • Volune increases until 33 weeks
  • Platueaus at 33-38 weeks
  • Decreases at term to reach 500ml
104
Describe the normal physiological cycle of amniotic fluid
Fetus breathes and swallows fluid, processed and voided through the bladder
  • Predominantly fetal urine output with some fetal secretions and placenta
105
How does placental insufficiency cause oligohydramnios?
  • Blood flows to brain instead of kidneys so there is a lower fetal urine output
106
How do patients with oligohydramnios present?
Potter's syndrome:

  1. Fetal compression: clubbed feet, facial deformity, congenital hip dysplasia
  2. Lack of amniotic fluid: pulmonary hypoplasia in fetus
107
Describe the management of oligohydramnios
  • Treat underlying cause and optimise gestation of delivery
  • Maternal rehydration to increase amniotic fluid volume if mild
  • Amnioinfusion: saline into amniotic fluid to increase volume
  • Deliver: may be induced-C-section
108
Describe the prognosis of patients with oligohydramnios
If 2nd trimester: poor prognosis
  • If premature delivery and pulmonary hypoplasia: respiratory distress at birth
  • PLacental insufficiency: higher rate of preterm deliveries
109
Aetiology of polyhdramnios:

  • 50-60% of cases: {{c1::idiopathic}}
Excess production due to {{c2::increased fetal urination:}}
  • {{c2::
  • Maternal diabetes
  • Fetal anaemia
  • Fetal renal disorders
  • Twin to twin transfusion syndrome
  • }}
Insufficient removal due to {{c3::decreased fetal swallowing:}}
  • {{c3::
  • Oesophageal duodenal atresia
  • Diaphragmatic hernia
  • Anencephaly
  • Chromosomal disorders
  • }}
110
How is polyhdramnios diagnosed?
  • USS
  • Measure amniotic lfuid: AFI/MPD

111
How fast does cervical dilation typicaly progress?
  • Primiparous: 1cm every 2 hours
  • Multiparous: 1cm every hour
112
Describe the physiology of the first stage of labour
  • Hormones(mostly prostaglandinds and oxytocin) stimulate regular uterine contractions
  • That and pressure from presenting part of foetus-> progressive dilation of the cervix
113
Describe the signs and symptoms of the first stage of labour
  • Regular, painful contractions
  • Progressive cervical dilation
  • Passage of blood stainf mucus-'show'
  • Rupture of membranes
  • Descent of foetal head into pelvis
114
How is the first stage of labour managed?
  • Pain relief-> epidural analgesia, nitrous oxide, opioids
  • Encourage mobility and changes in position to facilitate labour progression
  • Ensure hydration and nutritional supprot
  • Regular monitoring
115
How is the second stage of labour managed?
  • Instrumental delivery
  • C-section
116
How long does the third stage of labour usually last?
  • Natural: 30-60 minutes
  • With oxytocin: 5-10 minutes
117
How is the 3rd stage of labour managed?
  • Controlled cord traction-> gently to avoid uterine inversion/PPH
  • If retained placenta: manual removal or curettage may be necessary
118
How is labour induction carried out?
  • Membrane sweep: insert finger into extenral os and separate membranes from cervix
  • Vaginal prostalgandins: Used to ripen cervix and induce contractions
  • Amniotony: artificial rupture of membranes
  • Ballon catheter: mechanically dilates cervix
119
Describe the aetiology of pre-term labour
  • Overstretching of uterus: multiple pregnancy, polyhydramnios
  • Foetal risk complications: pre-eclampsia, placental abruption
  • Uterus/cervical problems: fibroids, malformations
  • Infections: chorioamnionitis, sepsis, group B strep etc
  • Maternal co-morbidity: htn, diabetes etc
120
How might patients with pre term labour present?
  • Regular uterine contractsion/changes in cervical effacement or dilation/rupturing of membranes before onset of contractions
121
How is pre term labour managed?
  • Corticosteroids: betamethasone/dex to assist foetal lung maturation
  • IV abx if increased risk of infection(penicillin)
  • Tocolytic agents may be used(nifedipine), risk of side effects
122
How is menopause diagnosed?
  • Clinically: absence of menarche for 12 months in someone >45(generally>45)
  • If <40: test FSH etc
123
Describe the management of menopause
Conservative: 
  • Lifestyle: regular exercise, weight loss, good sleep
Medical:
  • HRT
  • SSRI's
  • Vaginal lubricants/moisturisers
  • Clonidine for vasomotor
124
In terms of time frames, when can HRT be given?
  • Cyclically: perimenopausal women still having periods
  • Continuously: Post menopausal not having periods
125
How is HRT given cyclically?
  • Monthly: oestrogen every day of months and progesterone for last 14 days
  • Every 3 months: Oestrogen very day for 3 months and progesterone for the last 14 days
126
How can menopause result in dyspareunia?
  • Vaginal dryness from reduced oestrogen
127
How can menopause result in urinary incontinence?
  • Caused by epithelial thinning as a result of decline in oestrogen
128
Describe the feedback systems that control the menstrual cycle
  • Moderate oestrogen levels-> negative feedback on HPG
  • High oestrogen with no progesterone-> positive feedback on HPG
  • Oestrogen +progesterone-> negative feedback on HPG
  • Inhibin selectively inhibits FSH at anterior pituitary
129
How much blood is usually lost during menses?
  • 10-80ml
130
Describe the epidemiology of PCOS
  • Common
  • Affects up to 1/4 of women during reproductive years
131
Describe the aetiology of PCOS
  • Hormonal imblanaces-unknown?
  • Hyperandrogenism
  • Insulin resistance
  • Elevated levels of LH
  • Raised oestrogen
132
Describe the symptoms of PCOS
  • Oligomenorrhoea
  • Subfertility
  • Acne
  • Hirsutism
  • Obesity
  • Mood changes: depression, anxiety
  • Male pattern baldness
  • Acanthosis nigracans-> secondary to insulin resistance
133
Describe the rotterdam diagnositc criteria
>=2 of:
  • Polycystic ovaries(>12 cysts on imaging or ovarian volume >10cubic cm)
  • Oligo/an ovulation
  • Clinical or biochemical features of hyperandrogenism
134
How is PCOS managed?
Conservative:
  • Weight loss, exercise, educate on risks of diabetes.cvr.endometrial cancer
Medical for those not planning pregnancy:
  • Co-cyprindrol
  • COCP
  • Metformin
Medical for those wanting to conceive:
  • Clomiphene-induces ovulation 
  • Metformin
  • Gonadotrophins-induce ovulation
Surgical for those wanting to conceive:
  • Ovarian drilling: laparoscopic-damages hormone producing cells of ovary
135
How can endometrial curettage result in Asherman's syndrome
  • Damages basal layer of endometrium-> heals abnormally creating adhesions connecting areas of the uterus that aren't normally connected
  • Adhesions can bind uterine walls together or might seal the endocervix shut
136
How do adhesions cause problems in Asherman's syndrome?
  • Can cause physical obstruction and distort pelvic organs-> menstrual abnormalities, infertility and recurrent miscarriages
137
How might patient with Asherman's syndrome present?
  • Secondary amenorrhoea(absent periods)
  • Significantly lighter periods
  • Dysmenorrhoea
  • Infertility
138
How is Asherman's syndrome diagnosed?
  • Hysteroscopy: GS-can also treat adhesions
  • Hysterosalpingography
  • Sonohysterography
  • MRI
139
How is Asherman's syndrome treated?
  • Dissect adhesions during hysteroscopy
140
How are congenital uterine abnormalities diagnosed?
  • USS
  • Hysterosapingography
  • MRI-considered best
141
How are congenital uterine abnormailites managed?
  • Surgical intervention
142
Give some examples of congenital uterine malformations
  • Complete failure of duct fusion: double vagina, double cervix, double uterus
  • Septate uterus
  • arcuate uterus

143
Give some examples of congenital vaginal abnormalities
  • Vaginal agenesis
  • Vaginal atresia
  • Mullerian aplasia-normal external genitalia but absense of vagina
  • transverese vaginal septa
144
How might abnormalities of the hymen present?
  • Obstruciton of menstrual flow after puberty
145
Descriebe the pathogenesis of polyps
  • Involves oestrogen-> stimulates endometrial growth
  • Can arise from hyperplasia of basal layer of endometrium
146
How are endometrial polyps diagnosed?
  • Speculum exam
  • USS
147
How are endometrial polyps managed?
  • ASX in premenopausal: monitor
  • Symptomatic/postmenopausal/atypical: removed via hysteroscopic polypectomy
  • Histology of removed polyp to exclude malignancy
148
Describe the presentation of a patient with PID
  • Bilateral abdominal pain
  • Vaginal discharge
  • Post-coital bleeding
  • Adnexal tenderness
  • Cervical motion tenderness
  • Fever
  • Dysuria and menstrual irregularitis
149
How is Fitz Hugh Curtis syndrome diagnosed and treated?
  • Normal LFTs
  • US rule out stones
  • Definitive dx: laparoscopy
  • Tx: abx
150
How is PID managed?
  • IM ceftriaxone+14 days oral doxycycline+metronidazole
  • 2nd line: oral ofloxacin+oral metronidazole
  • Consider removal of IUD
  • Avoid unprotected sexual intercourse
151
Describe the epidemiology of urinary tract stones
  • Common
  • M>F
  • <65 yrs
  • Can be both renal and ureteric
152
Describe the aetiology of renal stones
  • Calcium oxalate-mc
  • Calcium phosphate
  • Cystine
  • Uric acid
  • Struvite
  • Indinavir
153
How might patient with urinary tract calculi present?
  • Severe intermittent loin pain that can radiate ot the groin
  • Restlessness
  • Haematuria
  • N+V
  • Sedoncary infection of stone-> fever/sepsis
154
How are renal stones managed?
  • Analgesia
  • Wait if <5mm
  • Medical expulsive therapy
  • Extracorporeal shockwave lithotripsy
  • Uteroscopy-pregnanyt women
  • Prevention
155
How can pituitary adenomas be classified?
  • Size -micro(<1cm) or macro(>1cm)
  • Hormonal status (secretory vs non secretory)
156
Describe the symptoms of a prolactinoma in men
Macroadenomas:
  • Headache
  • Visual disturbance-bitemporal hemianopia
  • Hypopituitarism signs and sx
Excess prolactin:
  • Impotence
  • Loss of libido
  • Galactorrhoea
157
Describe the symptoms of prolacitnomas in women
Macroadenomas:
  • Headache
  • Visual disturbance-bitemporal hemianopia
  • Hypopituitarism signs and sx
Excess prolactin:
  • Amenorrhoea
  • Infertility
  • Galactorrhoea
  • Osteoporosis
158
How is a prolactinoma diagnosed?
  • MRI head
159
How are prolactinomas treated?
  • Dopamine agonists: cabergoline, bromocriptine(inhibits release of prolactin)
  • Trans-sphenoidal surgery: those who can't toelrate therapy
160
Describe the surface anatomy of the breast
  • Lateral border of sternum at mid axillary line
  • 2nd and 6th costal cartilages
  • Superficial to pectoralis major and serratu anterior muscles
Circular body
Axillary tail
161
Describe the mammary glands with regards to breast anatomy
  • Modified sweat glands-> ducts and secretory lobules
  • Each lobule consists of many alveoli drained by a lactiferous duct
162
Describe the connective tissue stroma with regards to breast anatomy
  • Fibrous and fatty component
  • Fibrous stroma condenses to form suspensory ligaments
  • Attach and secure breast to dermis and underlying pectoral fascia
  • Separate secretory lobules of breast
163
Describe the pectoral fascia with regards to breast anatomy
  • Flat sheet of connective tissue associated with pec major
  • Retromammaroy space-> layer of loose conective tissue between breast and pectoral fascia(used in reconstruction)
164
Describe the medial vasculature of the breast
  • Internal thoracic(mammary) artery-> branch of subclavian
165
Describe the lateral vasculature of the breast
  • Lateral thoracic and thoracocromial branches-> axillary
  • Lateral mammary branches-> posterior intercostal arteries
  • Mammary branch-> anterior intercostal artery
166
How does lymphatic drainage link into the presentation of patiens with breast cancer
  • Blockages of lymphatic drainage-> lymph builds up in SC tissues-> nipple deviation and retraction, peau d'orange
  • Metastasis can occur through lymph nodes-> axillary mx, then can spread to liver, bones and ovary
167
Describe the nerve supply of the breast
  • Anterior and lateral cutaneous branches of 4th-6th IC nerves(autonomic and sensory nerve fibres)
168
Describe the epidemiology of fibroadenomas
  • Young women-early 20s
169
Describe the presentation of a patient with a fibroadenoma
  • Firm, non-tender breast mass
  • Rounded and smooth edges
  • Highly mobile on palpation-'rubbery' 
  • <3cm in diameter(mc 2.5cm)
  • Usually slow growing and solitary
170
Describe the management of fibroadenomas
  • Conservative: Leave, usually regress naturally post menopause
  • Surgical excision: considered if large, growing, causing significant symptoms or diagnostic uncertainty
171
Describe the epidemiology of fibrocystic breast disease
  • Most common benign breast condition
  • 20-50 years
172
Describe the aetiology of fibrocystic breast disease
  • Cumulative effect of cyclical hormone
  • Mostly oestrogen and progesterone-> multiple cysts and proliferative changes
173
Describe the presentation of a patient with fibrocystic breast disease
  • Bilateral 'lumpy' breasts, most commonly in upper outer quadrant
  • Breast pain
  • Sx worsen with menstrual cycle and peak 1 week before menstruation
174
Describe the management of fibrocystic breast disease
  • Encourage use of soft, well-fitting bra
  • Analgesia for pain relief
  • Most resolve after menopause
175
Describe the eppidemiology of breast cancer
  • Commonest cancer in UK in women
  • 2nd most common cause of cancer deaths
176
Describe the pathophysiology of breast cancer
  • Genetic mutations and damaged cellular signalling-> generation of malignant cells-> metastasise
177
Describe how breast cancer cells metastasize
  1. Invasion through basement membrane
  2. Intravasation(entry into circulation)
  3. Circulation
  4. Extravasation
  5. Colonisation
178
Describe the features of ductal carcinoma in situ
  • From epithelial cells
  • Confined to ducts
179
Describe the features of lobular carcinoma in situ
  • Arise from epithelial cells
  • Neoplastic cell proliferation
180
Describe the features of invasive ductal carcinoma
  • Neoplastic proliferation of epithelial cells-> ductal basement membrane-> fatty tissue
181
Describe the features of medullary carcinoma
  • Younger people
  • Higher grade than invasive ductal carcinoma
182
Describe some signs and symptoms of breast cancer
  • Unexplained breast/axillary mass in those >30 years
  • Nipple discharge
  • Nipple retraction
  • Skin changes-p'eau d'orange
  • Metastatic features: weight loss, bone pain, SOB
183
How is breast cancer diagnosed?
1st line: imaging
  • >30yrs and clinical suspicion: mammogram
  • <30yrs: USS
  • US of axilla
2nd line: biopsy
  • Fine needle aspiration and cytology
Others:
  • Oestrogen/progesterone receptor testing, HER2 receptor testing
  • CT if metastatic disease suspected
184
Breast cancer staging:
  • 1A: {{c1::<2cm, isolated to breast}}
  • 1B: {{c2::<2cm, minor axillary LN spread}}
  • 2A: {{c3::<2cm, spread to 1-3 ipsilateral lymph nodes}}
  • 2B: {{c4::2-5cm, minor axillary node spread/>5cm with no nodal spread/2-5cm with 103 ipsilateral LN spread}}
  • 3A: {{c5::4-9 ipsilateral nodes/>5cm with 1-3 ipsilateral nodes}}
  • 3B: {{c6::Spread to skin/chest wall}}
  • 3C{{c7::: >10 axillary nodoes/supraclavicular/parasternal/axillary spread}}
  • 4: {{c8::metastatic spread to other organs}}
185
How can bisphosphonates be used in the treatment of breast cancer?
  • Can help reduce recurrence in node-positive cancers
186
Aetiology of benign breast disease:
  • Fibroadenomas: {{c1::overgrowth of glandular and connective tissue resulting in blocked breast ducts and subsequent fluid accumulation}}
  • Mastitis: bacterial infection-> {{c2::breaks in skin around nipple}}
  • Intraductal papilloma: {{c3::benign tumour of breast ducts}}
  • Radial scar: {{c4::benign sclerosing breast lesion}}
  • Fat necrosis: {{c5::response to adipose tissue damage}}
  • Fibroycstic breast disease: {{c6::increased hormonal response resulting in inflammation and fibrosis}}
  • Mammary duct ectasia: {{c7::inflammation and dilation of large bresat ducts}}
187
Describe the general management of benign breast disease
  • Reassurance: often only need monitoring
  • Antibiotics: for infections like mastitis
  • Analgesics
  • Surgery: e.g. large fibroadenomas, persistent cysts, symptomatic intraductal papillomas
188
Describe the epidemiology of Paget's disease of the nipple
  • Rare: <5% of all breast cancer patients
  • Most common in postmenopausal women
189
Describe the aetiology of Paget's disease of the nipple
2 theories:
  • Epidermotrophic: underlying breasst cancer cells migrate to the nipple
  • Intraepidermal origin: originates in nipple itself
190
Describe the signs and symptoms of a patient with Paget's disease of the nipple
  • Eczema like rash on skin of nipple/areola(often crusty, red, inflamed, itchy)
  • Bloody nipple discharge
  • Non-healing skin ulcer
  • Changes to nipple-> retraction/inversion
  • Pain
  • Breast lump
191
How is Paget's disease of the nipple diagnosed?
  • Mammography/US
  • Punch biopsy of affected skin, nipple discharge cytology
  • MRI for stagin in uncertain cases
192
How is Paget's disease of the nipple different to eczema of the nipple?
  • Paget's involves the nipple primarily and only latterly spreads to the areolar(opposite way around in eczema)
193
How is Paget's disease of the nipple treated?
  • Depends on underlying lesin
  • Simple mastectomy: remove entire breast and nipple and areeola
  • Modified radical mastectomy: remove some axillarry lymph nodes 
  • Lumpectomy
  • Chemo, radiation, hormonal
194
Describe the latent phase of labour
  • Contractions(may be irregular)
  • Mucoid plug
  • Cervix beginning to efface and dilate(0-4cm)
  • Can last up to 2-3 days
195
Describe the features of contractions
  • Starts in the fundus(pacemaker)
  • Retraction/shortenng of muscle fibres
  • Build in aplitude as labour progresses
  • Fetus forced down causing pressure on the cervix
196
Describe the features of a gynaecoid pelvis
  • Inlet is slightly transverse oval
  • Sacrum wide with average concavitiy and inclination
  • Side walls straight with blunt ischial spines
  • Wide suprapubic arch


197
How might midwives help with the delivery of the body stage of labour?
  • Gentle downward traction to assist with delivery of shoulder below suprapubic arch
  • Gentle upwads traction to assist delivery of posterior shoulder

198
Describe the anatomy of the placenta and how it is connected to the fetus
  • Lobes which attach to the uterine wall
  • Connected to fetus via umbilical cord whcih has 2 arteries and a vein
199
How is a ventouse used?
  • Cup is applied with centre over flexion point on fetal skull
  • During uterine contractons, traction applied perpendicular to cup
200
At what age gestation is non invasive prenatal testing available?
  • From 10 weeks
201
At what week gestation is CVS offered for?
  • 11-14 weeks gestation
202
How many weeks gestatin would amniocentesis be performed?
  • >15 weeks
203
Describe the epidemiology of mastitis
  • Postpartum: 10-20% prevalence
  • Usually in first 6 weeks post birth
  • Increased risk in 1st time mothers and previous hx of mastitis
204
Describe the aetiology if mastitis
  • Milk stasis-> inflammatory response and potential secondary infection
  • Cracked/sore nipples-> S.aureus-> infective mastitis
205
Describe the presentation of mastitis
  • Localised: painful, red, tender, hot breast
  • Systemic: fever, rigors, myalgia, fatigue nausea and headache
  • Usually unilateral-presents 1st week post partum
206
How is mastitis diagnosed?
  • Mostly clinical
  • US to ID if suspicion of abscess-> done in secondary care
207
How is mastitis managed?
  • Reassure lactating women they can continue to breastfeed
  • Advice on methods to faciliate milk expression
  • Analgesia
  • Oral/IV abx, surgery if abscess
208
Describe the aetiology of a breast abscess
  • S.aureus mc through crack in nipple/through milk duct
  • Accumulation of milk, trauma to nipple skin from incorrect latch/pump
209
Describe the presentation of a patient with a breast abscess
  • Fever/rigors
  • Malaise
  • Pain and erythema over an area of the breast
  • Possible presence of a fluctuant mass-> might not be palpable
  • Hisotry of recent/ongoing mastitis
210
How is a breast abscess diagnosed/investigated?
  • Breast USS-> visualise abscess and guide drainage
  • Diagnostic needle aspiration-> culture organism and evacuation
211
How is a breast abscess managed?
  • Incision and drainage/needle aspiration(with/out US guidance)
  • Abx therapy targeted towards most likely causative organism
212
Describe the epidemiology of bacterial vaginosis?
  • Mc cause of abnormal dishcarge in women of childbearing age
  • More common in sexually active women but not an STI
213
Describe the pathophysiology of bacterial vaginosis
  • Disturbance of normal vaginal flora-> decrease in number of lactobacilli bacteria
214
How is bacterial vaginosis managed in pregnanct/lactating women?
  • Screening done antenatally and quick treatment if needed
  • Lower doses of metronidazole in lactating women
215
Describe the epidemiology of vulvovaginal candidiasis
  • Highlyy prevalent: 20% of women/yr
  • Most women will experience it at some point in their lifetime
216
Describe the aetiology of vulvovaginal candidiasis
  • Candida albicans-> replicated by budding
  • Opportunistic infection vs hypersensitivity reaction
217
Describe the symptoms of vulvovaginal candidiasis
  • Pruritus vulvae
  • Vaginal discharge-white, curd like
  • Dysuria
218
How is vulvovaginal candidiasis diagnosed/inveestigated?
  • Usually history/clinical
  • Vaginal smear and mc+s-> blastospores, pseudohyphae and neutrophils
219
Describe the management of vulvovaginal candidiasis
  • Intravaginal antifungal-> clotrimazole pessary
  • Oral antifungal-> fluconazole
  • Vulva/topical steroid-> topical imidazole
220
How is vulvovaginal candidiasis treated in pregnancy?
  • DO NOT use oral antifungals
  • Advise care with intravaginal treatment applicator
  • Saftynetting if not resolved in 7-14 days
221
Describe the epidemiology of chlamydia
  • Most common STD in UK
  • Highest prevalence in 15-24 yr olds
222
How is chlamydia transmitted?
  • Via unprotected vaginal, oral, anal sex
  • Skin to skin contact of genitals
  • Vertical(mother to baby during delivery)
223
Describe the signs and symptoms of chlamydia in men
  • Often asymptomatic: incubation period 7-21 days
  • Urethritis: dysuria, urethral discharge
  • Epididymo-orchitis: testicular pain
  • Epididymal tenderness
  • Mucopurulent discharge
224
Describe the signs and symptoms of chlamydia in women
  • Asymptomatic often: incubation period 7-21 days
  • Dysuria
  • Discharge
  • Intermenstrual bleeding
  • Pain/tenderness
225
Describe the signs and symptoms of chlamydia in neonates
  • Pneumonia
  • Conjunctivitis
226
How is chlamydia diagnosed?
  • Women: vulvovaginal swab
  • Men: first catch urine sample
Analyze using nucelic acid amplification tests
227
Describe the management of chalmydia in non-pregnant people
  • Doxycycline: 100mg twice daily for 7 days
228
Describe the management of chlamydia in pregnant women
  • Azithromycin/erythromycin
229
Describe the management of neonates with chlamydia
  • Oral erythromycin
230
 Describe the epidemiology of gonorrhoea
  • 2nd most common STI after chlamydia
  • increased prevalence in 15-24yrs
  • Hihger prevalence in MSM
231
How is gonorrhoea transmitted?
  • Unrpotected vaginal/oral/anal sex
  • Vertical transmission
232
Describe the aetiology and pathology of gonorrhoea
  • Gram negative diplococcus neisseria gonorrhoea
  • Causes acute inflammation-> uterus, urethra, cervix, fallopian tube, ovaries, rectum, testicles, eyes, throat
233
How do patients with gonorrhoea present?
  • Males: urethral discharge, dysuria
  • Women: discharge, dysuria, dyspareunia, pain
  • Dishcarge tends to be thin, watery green/yellow
  • Asymptomoatic especially when rectal/pharyngeal infection
234
How is gonorrhoea diagnosed?
  • Females: endocervical/vaginal/urethral swab
  • Males: first pass urine(NAAT), urethral/meatal swab
Microsopcy, culture and NAAT
235
How is gonorrhoea treated?
  • Singled soe 1g IM ceftriaxone
  • Screen/treat other infections
  • test of cure recommended
236
Describe the symptoms of disseminated gonococcall infection
  • Tenosynovitis
  • Migratory polyarthritis
  • Dermatitis
237
How is gonorrhoea treated in pregnancy?
  • Prophylactic abx+tx in pregnancy-> ceftriaxone
238
How are neonates with gonorrhoea managed?
  • Urgent referral and treatment
  • Long term damage and blindness
239
Describe the epidemiology of genital herpes
  • Very common
  • 15-24yrs
240
Describe the pathophysiology of genital herpes
  • After infecting surface-> travels up to meet nearest ganglion and stays there until reactivated
241
Describe the presentation of a patient with a primary genital herpes infection
  • Asymptomatic
  • Small, painful red blisters around genitals, can form open sores
  • Vaginal/penile discharge, dysuria, urinary retention
  • Flu like sx-> fever ,muscle aches, malaise, headaches
  • After 20 days: lesions crust and heal-> end of viral shedding
242
Describe the presentation of a patient with an outbreak of a genital herpes infection
  • Usually shorter and less severe than initial infection
  • Burning, itching, painful red blisters
243
How is genital herpes diagnosed?
  • Clinical hz and exam
  • Swab from abse of ulcer-> NAAT
244
Describe the management of genital herpes
  • Primary infection: aciclovir 400mgTD 5 days
  • Recurrent outbreaks: OTC analgesia, ice, topical lidocaine
  • Regular episodes: episodic aciclovir tx when sx begin
245
Describe the management of herpes in pregnancy
  • Low risk of transmission with vaginal birth
  • Referral to GUM clinic and treat with aiclovir if 1st time HSV infection
  • If contracted in last trimester: antibodies not developed-> C-section
246
Describe the features/management of neonatal herpes
  • Skin/eyes/mouth herpes(SEM)-antiviral tx
  • Disseminated herpes(DIS)-internal organs
  • CNS herpes-> encphalitis
DIS and CNS herpes associated with increased mortality
247
Describe the aetiology of genital warts
  • 90% HPV 6/11-low risk, not associated with cancer
248
How do patients with genital warts typically present?
  • Asx
  • Painless warts of scrotum, penis, vagina, cervix, perianal skin, anus
  • Warts can be keratinised(hard) or non-keratinised(soft)
  • Extra-genital lesions: oral cavity, larynx, nasal cavity, conjunctivae
249
How are genital warts diagnosed/
  • Usually from clinical exam/hx
  • Proctoscopy/vaginal speculum exam to check for internal warts
  • Biopsy for atypical lesions/suspected intraepithelial neoplastic lesions
250
Describe the management of genital wwarts
Tx not always needed, can resolve spontaneously

Topical:
  • Podophyllotoxin: antiviral to destroy clusters(BD 3 days then 4 days rest)
  • Imiquimod: immune response modifier for larger keratinised warts(3 times/week)
Physical:
  • Cryotherapy
  • Surgical excision
  • Elecrto/laser-surgery
251
How does pregnancy impact genital warts?
  • No risk to babies but maternal warts can multiply/enlarge during pregnancy
252
Describe the pathophysiology behind the HIV infection
  1. 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
  2. Infected cell divides, viral DNA read-> creates viral protein chains and immature virus pushes out of cell, retaining some membranes
  3. Virus matures when protease cuts viral protein chains and assemble to create a working virus, destroying a host cell
253
How do CD4 levels change over the course of the HIV infection?
  • Seroconversion(producing anti-HIV antiibodies during primary infection)-> flu-like sx-> decrease in CD4 levels due to initial rapid replication-> extremely infectious
  • Latent phase: months-yrs: initiay asx but increased susceptibility to infections
254
How is HIV transmitted?
  • Unprotected sexual intercourse
  • Sharing needles
  • Medical procedures
  • Vertical transmission
255
Describe the symptoms of the seroconversion stage of HIV
  • 2-6 weeks post exposure
  • Fever
  • Muscle aches
  • Malaise
  • Lymphadenopathy
  • Maculoapular rash
  • Pharyngitis
256
Describe the symptoms of the symptomatic stage of HIV
  • Weight loss
  • High temperature
  • Diarrhoea
  • Frequent opportunistic infections
257
Describe the symptoms of the AIDS defining illness stage
  • Advanced stage: immune system significantly weakened
  • Deveopment of AIDS defining illnesses/infections/malignancies
258
How is HIV diagnosed?
4th generation tests:
  • ELISA-> test for serum/salivary HIV antibodies and p24 antigen
  • Reliable results 4-6 weeks post exposure
Contact tracing
259
Describe the management of HIV
HAART: highly active antiretroviral therapy
>=3 drugs: usually 2 nRTIs and 1 PI/NNRTI-> Decreases viral replication and reduces risk of viral resistance emerging
260
Describe the features of NNRTI's
  • non-nucleoside reverse transcriptase inhibitors
  • E.g. nevirapine
  • SE: P450 enzyme interaction, rashes
261
Describe the features of protease inhibitors
  • E.g. indinavir, nelfanivir
  • SE: diabetes, hyperlipidaemia, central obesity, P450 enzyme inhibitirion
262
Describe the features of integrase inhibitors
  • E.g. raltegravir, elvitegravir
  • Block the action of integrase(viral enzyme that inserts the viral genome into the DNA of the host cell)
263
How is HIV managed in pregnancy and why?
  • Can be transmitted in utero, at delivery and through breast-feeding
  • Risk reduction strategies(separate flashcard)
  • C-section non longer recommended if undetectable viral load
264
How is the risk of HIV transmission in pregnant women minimised?
  • Anttenatal antiretroviral therapy during pregnancy and delivery
  • Avoidance of breastfeeding
  • Neonatal post-exposure prophylaxis
265
How do patients with a threatened miscarriage present?
  • Painless vaginal bleeding <24 weeks(usually 6-9 weeks)
  • Bleeding often less than menstruation
266
How can the aetiology of polyhydramnios be classified?
  • Idiopathic
  • Excess production due to increased fetal urination
  • Insufficient removal due to decreased fetal swallowing
267
How might a patient with polyhydramnios present?
  • Uterus feels tense/large for dates
  • Difficult to feel fetal parts on abdominal palpation
268
How is polyhydramnios managed?
  • Usually no intervention needed
  • Treat underlying cause
  • Severe only: amnioreduction
  • Indomethacin
269
How is indomethacin useful for treating polyhydramnios?
  • Enhances water retention and decreases fetal urine output
270
How is prolonged pregnancy managed?
  1. Membrane sweeps-40 wks nulliparous, 41 wks in parous
  2. Induction of labour-41/42 weeks gestation
If 2 declined: twice weekly CTG moniotring and US with amniotic fluid measurement to predict fetal distress. Might need C-section
271
How do patients with placenta praevia present?
  • Painless bright red vaginal bleeding after 24 weeks
  • Sometimes pain if in labour
  • Can present with signs of shock if severe blood loss
  • Malpresentation of fetus due to abnormal placental position
272
Describe the management of acute presentation of placenta praevia
  • ABCDE approach
  • If bleeding not controlled/in labour: C-section
  • Anti-D within 72 hours of bleeding onset if rhesus D negative
273
How is placenta praevia managed if found in a 20 week scan
  • Placenta praevia minor: rpt scan at 36 weeks-likely to move
  • Major: rpt at 32 weeks and plan for delivery-> usually elective c-section
  • Advice about pelvic rest: no penetrative sexual intercourse and go hospital if major bleeding
274
Describe the pathophysiology of placental abruption
  • Rupture of maternal vessels in basal layer of endometrium-> blood gathers and splits placental attachment from basal layer
  • Detached portion unable to funciton-> rapid fetal compromise
275
How might patients with placental abruption present?
  • Painful vaginal bleeding
  • If in labour: may have pain between contractions
  • Abdominal pain: often sudden and severe
  • Hypovolaemic shock disproportionate to amount of vaginal bleeding visible
276
How is placental abruption managed?
  • ABCDE resus including anti D if rh D negative
  • Tx dependednt on health of fetus
  • Emergency delivery: usually C section, even if in-utero death
  • Induction of labour at term to avoid further bleeding if haemodynamically stable
277
Describe the natural progressin of most breech babies
  • 20% breech at 28weeks
  • Most revert to cephalic presentation spontaneously witih onlly 3% still breech at term
278
How is breeech presentation diagnosed?
Clinical:
  • Head felt in upper uteris, buttocks and elgs in pelvis
  • Fetal heart auscultates higher on maternal abdomen on US
  • 20% not diagnosed until labour
279
How might breech presentatin present at labour?
  • Fetal distress-> meconium stained liquor
  • Vaginal exam: sacrum/foot felt through cervical opening
280
Describe the management of breech presentation
  • External cephalic version: offered at 37 weeks to primiparous women
  • C-section
  • Vaginal breech birth
281
How is abnormal fetal lie/malpresentation/malrotation diagnosed?
  • Abdominal exam
  • Confirm with US-> also ID predisposing abnormalities
282
Describe the management of normal fetal lie
  • External cephalic version(ECV)-> 36-38 weeks gestation
283
Describe the management of malpresentation
  • Breech: ECV before labour, vaginal birth, C section
  • Brow: c-section
  • Shoulder: c -section
  • Face: chin posterior: c section, chin anterior: attempt normal labour
284
Describe the management of malposition
  • 90% spontaneously rotate during labour
  • If not: operative vaginal delivery/C-section
285
Describe the pathophysiology of pre-eclampsia
  • High resistance, low flow uteroplacental circulation develops as constrictive muscular walls of spiral arterioles are maintained
  • Increase in BP, hypoxia-> systemic inflammatory response
286
Describe the symptoms of pre-eclampsia
  • Headaches
  • visual changes
  • Epigastric pain
  • Sudden onset non-dependent oedema
  • Hyper-reflexia
287
Describe the management of pre-eclampsia
  • Serial monitoring: BP, urinalysis, fetal growth scans, CTG
  • VTW-LMWH
  • Anti-hypertensives-labetalol, nifedipine, methyldopa
  • Delivery(give IM steroids if <35 weeks)
  • Post-natal: monitor for 24 hours post partum and BP for 5 days
288
Descrbe the split of eclamptic seizures in the post natal, antepartumand intrapartum periods
Post-natal: mc-44%
Antepartum: 38%
Intrapartum: 18%
289
Describe the symptoms of eclampsia
  • New onset tonic clonic seizure in presence of pre-eclampsia
  • Lasts 60-75 secs then post-ictal phase
  • May cause fetal distress and bradycardia
290
Describe the management of eclampsia
Rescuscitation
  • ABCDE approach
  • Pt lie in left lateral position and secure airway and O2 therapy
Seizure control:
  • Magensium sulphate
  • Monitor for signs of magensium poisoning
BP control:
  • IV labetalol and hydralazine
Delivery of baby and placenta:
  • Usually C-section
Monitoring:
  • Fluid balance: prevent pulmonary oedema and AKI
  • Monitor platelets, transaminases and creatinine
291
How long should a magnesium suflate drip be continued for after an eclamptic seizure?
  • 48 hours after last seizure
292
How is trichomoniasis transmitted?
  • Predominanly sexual
293
Describe the epidemiology of trichomoniasis
  • Mc non-viral STI globally
294
Describe the signs and symptoms of trichomoniasis in women
  • Profuse, frothy, yellow vaginal discharge
  • Vulvovaginitis
  • Dyspareunia
  • Starwberry cervix-may be seen
  • pH>4.5
  • Asx
295
Describe the signs and symptoms of trichomoniasis in men
  • Usually asymptomatic
  • Non-gonococcal urethritis
296
How is trichomoniasis diagnosed?
  • Direct microscopy and culture of the causative organism-> motile trophozoites
  • pH>4.5
  • Test for other STIs
297
How is trichomoniasis treated?
  • Oral metronidazole for 5-7 days or single dose of 2g orally
  • Abstain from sex for a week
  • Screen for others
  • Contact tracing
298
Describe the epidemiology of chancroid
  • Global incidence decreasing
  • Mc in tropical areas and greenland
299
Describe the symptoms of chancroid
  • Painful genital ulcers which may bleed on contact-ulcers are sharply defined, ragged, undermined border
  • Painful inguinal lymphadenopathy
  • Sx 4-10 days after bacterium exposure

300
How is chancroid diagnosed?
  • Usually clinical
Can culture and use PCR
301
How is chancroid treated?
  • Antibiotics: ceftriaxone/azithromycin/ciprfloxacin
  • Analgesics 
  • Incision/drainage of buboes
302
Describe the presentatin of a patient with lymphogranuloma venereum
  • Stage 1: small painless pustule which later forms an ulcer
  • Stage 2: painful ingional lymohadenopathy-may from fistulaitng buboes
  • Stage 3: proctocolitis(can include rectal pain and discharge)

303
How is lymphogranuloma venereum diagnosed?
  • PCR from swab of genital ulcer
304
How is lymphogranuloma venereum managed?
  • oral doxycuclin 100mg twice daily for 21 days
  • Can also use: tetracycline, erythromycin
305
How is lymphogranuloma venereum different to 'normal' chalmydia?
  • Normal chalmydia: urethritis and PID: Chlamydia trachomatis serovars D-> K
  • lymphogranuloma venereum: serovards L1, L2, L3
306
Describe the aetiology of balanitis
  • Mc: infective: bacterial and candidal
  • Autoimmune causes
307
How is balanitis investigated/diagnosed?
  • Usually clinical-hx and exam
  • Swab for mc+s/PCR-> bacteria or candida albicans
  • If doubt/extensive skin changes: biopsy
308
Describe the general treatment of balanitis
  • Gentle saline washes
  • Wash properly under foreskin
  • 1%hydrocortisone for a short period
  • Treat underlying cause
309
How is balanitis due to dermatitis treated?
  • Mild potency steroid- hydocortisone
310
How is balanitis due to lichen sclerosus treated?
  • High potency topical steroids
  • Clobetasol
  • Circumcision can help
311
How is balanitis due to candidiasis treated?
  • Topical clotrimazole for 2 weeks
312
How is syphilis transmitted?
  • Direct contact with shyphilis sores or rash during vaginal,  anal or oral sex
  • Vertical: mother to child
313
Describe the features of primary syphilis?
  • Chancre-painless ulcer at the site of sexual contact
  • Local non-tender lymphadenopathy
  • Often not seen in women(lesion can be on the cervix)
314
Describe the lesion associated with the primary syphilis infection
  • Painless
  • Round, indurated base
  • Heals spontaneously within 3-8 eeks
315
Describe the features of secondary syphilis
  • Systemic: fevers, malaise etc
  • Rash on trunks, palsm and sores
  • buccal 'snail track' ulcers
  • Condylomata lata ( painless warty lesions on genitalia)#

316
Describe the features of tertiary syphilis
  • Gummas(granulomatous lesions of skin and bones)
  • Ascending aortic aneurysms
  • neurological: demenita, paresis, tabes dorsalis, argyll-robertson pupil)
317
Describe the features of congenital syphilis
  • Presents shortly after birth or later in infancy
  • Rash: palms/soles, mucous patches/leisons in motuh/nose/genitals
  • Feever
  • Blunted upper incisor teeth(Hutchinson's teeth), 'mulberry' molars
  • Rhagaades( linear scars at angle of mouth)
  • Keratitis
  • Saber shins
  • Saddle nose
  • Neruological; seizures, developmental delay
318
How can serological tests for syphilis be divided?
  • Non-treponemal tests
  • Treponemal specific tests
319
Describe the features of non-treponemal tests for syphilis
  • Not-specific for syphilis: false positives
  • Based on reactivity of serum from infected patients to a cardiolipin cholesterol-lecithin antigen
  • Negative after treatment
320
Describe the features of treponemal specific tests?
  • More complex and expensive but sspecific for syphilis
  • Qualitative
321
Describe the treatment pf syphilis
  • IM benzathine penzylpenicillin
  • Tertiary/late latent: longer course of IM penicillin G
  • Neurosyphilis: IV penicillin G for 10-14 days
Backup for penicillin allergy: doxycycline
322
How might patients with intraductal papilloma present?
  • Bloody discharge from the nipple
  • With/without a palpable mass
  • May have breast tenderness
323
How are intraductal papillomas treated?
  • Severe cases might need surgery
324
How can breast cysts be classified?
  • Microcysts: seen on imaging but too small to be felt
  • Macrocysts: 1-2cm: large enough to be felt
325
How might patients with mammary duct ectasia present?
  • Tender lump arounf areola +/- thick green nipple discharge
  • If ruptures: local inflammation-> 'plasma cell mastitis'
326
Describe the treatment for mammary duct ectasia
  • Surgical intervention may be needed if symptomatic
327
Describe the epidemiology of HELLP syndrome
  • Rare
  • Significant cause of maternal and perinatal morbidity/mortality
328
Describe the aetiology of HELLP syndrome
  • Unknown
  • Related to abnormal placentation, endothelial cell injury and generalized inflammatory response
329
Describe the presentation of patients with HELLP syndrome
  • N+V
  • RUQ pain-> liver distention
  • Lethargy
  • Headahces
  • Blurred vision
  • Peripheral oedema
330
Describe the maangement of HELLP syndrome
  • Definitive: deliver baby
  • Steroids: accelerate fetal lung maturation
  • Blood transfusions to manage anaemia and thrombocytopenia
331
Describe the epidemiology of cord prolapse
  • Relatively rare
  • Higher risk in breech presentations and multiple pregnancies
332
Describe the pathology of cord prolapse
  • Usually membrane rupture-> amniotic fluid egress-> descent of umbilical cord
  • Cord compression-> against maternal soft tissues or bony pelvis-> fetal hypooxia
333
How might patients with cord prolapse present?
  • Abnormal fetal heart rate: mc -> varibable/prolonged decelerations
  • Palpable umbilical cord
  • Sudden onset of sympotms post rupture of membranes
  • Patient reported sensation
334
How is a cord prolapse investigates/diagnosed?
  • Clinical
  • USS
  • Cardiotocoography(CTG)
  • Speculum exam
335
How is cord prolapse managed?
  • Immediate delivery of fetus-> instrumental or C section 
  • 'knees chest' position to reeduce pressure on cord
  • Avoid exposure and handling of cord, reducing into vagina
  • Use of tocolytics like terbutaline to stop uterine contractions
336
Describe the pathophysiology of vasa praevia
  • Abnormal placental development
  • Fetal membrane development: persistence of membranous vessels
  • Fetal vessel vulnerability: prone to rupture
337
How can vasa praevia be classified?
  • Type 1 and Type 2
  • Ramified or funic
338
Describe the signs and symptoms of vasa praevia
  • Painless vaginal bleesin
  • Rupture of membranes
  • Fetal bradycardia/resulting fetal death

Also:
  • Foetal anaemia
339
How is vasa praevia diagnosed?
  • Transabdominal/TV USS-most cases now diagnosed antenatally
Can use MRI and prenatal testing
340
How is vasa praevia managed?
  • Elective C-section prior to rupture of membranes: 35-36 weeks gestation
  • Emergency C-section of premature labour or membranes rupture
  • Prompt neonatal resus
341
Describe the epidemiology of peruperal psychosis
  • Rare: 11-2/1000 childbirths
342
Describe the aetiology of peurperal psychosis
  • Unknown
  • Hormonal changes post childbirth
  • Genetics
  • Psychosocial stressors
  • Sleep deprivation
343
Describe the signs and symptoms of peurperal psychosis
  • Paranoia
  • Delusions: Capgras
  • Hallucinations-command 
  • Manic episodes
  • Depressive episodes
  • Confusion
344
How is peurperal psychosis diagnosed?
  • Clinical
  • Thorough psych evaluation
  • Rule out: thyroid disorders, sepsis etc
345
Describe the management of peurperal psychosis
  • Admit to mother/baby mental health unit: especially if Capgras/command hallucinations
  • Antipsychotics: olanzapine and quetipaine
  • Mood stabilisers in some cases
  • CBT
346
Describe the epidemiology of postpartum depression
  • Prevalent: 10-20% of mothers
347
Describe the aetiology of postpartum depression
  • Multifactorial
  • Biological: hormones, melatonin, cortisol, inflammatory processes, genetics
  • Psychological 
  • Social
348
Describe the signs and symptoms of postpartum depression
  • Persistents low mood and anhedonia
  • Low energy
  • Sleep issues-important to distinguish between abby's fault and depression
  • Poor appetite
  • Concerns relating to bonding with baby, caring for baby etc
349
How is baby blues different to postpartum depression?
  • MIlder: mood swings, irritability, anxiety and tearfullness
  • Sx present within first 2 weeks after birth and resolve spontaneously
350
How is postpartum depression diagnosed?
  • Clinical
  • Edinburgh postnatal depression scale
  • Rule out risk of psychosis-risk assessment really important
Physical exam: anaemia, hypothyroidism to rule out organic causes
351
Describe the management of postpartum depression
  • Self-help, CBT, ITP(interpersonal therapy)
  • Antidepressants(SSRIs)
  • Severe: admission to mother baby mental health unit
352
How is baby blues managed?
  • Reassurance and support
  • Regular health visitor checks to check in with mother
353
Define pre-term labour
  • Onset of regular uterine contractions accompanied by cervical changes occuring before 37 weeks gestation
354
Define pre-term birth
  • Delivery of a baby 20-37 weeks gestation
355
Define premature rupture of membranes
  • Rupture of membranes at least one hour before onset of contracitons
356
Define prolonged premature rupture of membranes
  • Rupture of membranes over 24 hours before onset of labour
357
Define pre-term premature rupture of membranes
  • Early rupture of the membranes before 37 weeks gestation
358
Describe the epidemiology of preterm prelabour rupture of the membranees
  • Occurs in around 2% of all pregnancies
  • Associated with 40% of preterm delvieries
359
How is PPROM diagnosed?
  • Sterile speculum exam: look for pooling of amniotic fluid in posterior vaginal vault
  • Avoid digital exam: risk of infection
  • If no pooling: test fluid for placental alpha microglobulin protein(PAMG-1) or insulin like growth factor binding protein 1
  • USS-oligohydramnios
360
How is PPROM managed?
  • Admission
  • Regular observations to check for chorioamnionitis
  • Oral erythromycin for 10 days
  • Antenatal corticosteroids: reduce risk of respiratory distress syndrome
  • Delivery should be considered at 34 weeks gestation
361
Describe the aetiology of postpartum haemorrhage
4T's:
  • Tone: mc: uterine atony(failure of uterus to contract after delivery)
  • Trauma
  • Tissue(retained placenta etc)
  • Thrombin(clotting/bleeding disorder)
362
Describe the initial management of PPH
  • Life threatening emergency: ABCDE approach
  • 2 14 gauge large bore peripheral cannulas
  • Lie flat
  • Bloods including grooup and save
  • Commence warm crystalloid infusion
363
Describe the mechancial strategies that can be used to manage postpartum haemorrhage
  • Palpate uterine fundus and rub it to stimulate contractions
  • Catheterisation to prevent bladder distention and monitor urine output
364
Describe the medical management of postpartum haemorrhage
  • IV oxytocin: slow IV injection then infusion 
  • ergometrine slow IV(unless hx of htn)
  • carboprost IM(unless hx of asthma)
  • sublingual misprostol
365
Describe the surgical management of postpartum haemorrhage
If medical options fail to control bleeding:
  • Intrauterine balloon tamponde-if uterine atony as cause
  • B-lynch suture, ligation of uterine/internal iliac arteries
  • If severe: hysterectomy as life-saving procedure
366
How is secondary postpartum haemorrhage managed?
  • Depends on underlying cause
  • Abx for infection
  • Surgical evacuation for retained products of conception
367
Describe the pathophysiology of rhesus negative pregnancy
  • 15% of mothers rhesus negative
  • If rh negative mother delivers a rh positive child, a leak of fetal red blood cells can occur
  • Causes anti D-IgG antibodies to form in mother
  • Maternal anti-D antibodies can cross placenta in subsequent pregnancies and cause rhesus haemolytic disease if baby is rhesus positive
  • Can also occur in first pregnancy due to leaks
368
Give some examples of sensitisation events in rhesus negative pregnancies
  • Anteepartum haemorrhage
  • Placental abruption
  • Abdo trauma
  • ECV
  • Miscarriage if gestation > 12 weeks
  • Termination of pregnancy
  • Delivery of rh positive infant
  • Ectopic pregnancy
  • Amniocentesis, CVS, fetal blood sampling
369
How is rhesus heamolytic disease prevented and screened for?
  • Test for D antibodies in all rhesus negative mothers at booking
  • Anti-D given to non-sensitised rh negative mothers at 28 and 34 weeks-prophylaxis(once sensitisation occurs can't be undone)
370
How is rhesus negative pregnancy managed?
  • Screening/prevention strategies
  • Give Anti-D immunoglobulin as soon as possible but always within 72 hours when a sensitisation even occurs
371
Describe the medical management of termination of pregnancy
  • Mifepristone(first orally) then misoprostol 24-48 hours after
  • Misoprostol can be repeated 3 hourly(max 5) until expulsion
  • Takes time: hours to days
  • Pregnancy test required in 2 weeks: multi-level pregnancy test-measures level of HCG not just positive or negative
372
How is trichomoniasis vaginalis managed in pregnancy?
  • Same: oral metronidazole 400-500mg twicce a day for 5-7 days
  • High dose not recommended in pregnancy/breastfeeding(no 2g single dose)
373
Describe the symptoms of uterine rupture
  • Sudden severe abdominal pain which persists between contractions
  • Shoulder tip pain-diaphragmatic irritation)
  • Vaginal bleeding
374
Describe the signs of a uterine rupture
  • O/E: regression of presenting part
  • Abdominal palpation: scar tenderness and palpable fetal parts
  • Fetal monitoring: fetal distress/absent heart sounds
  • Significant haemorrhage: signs of shock: tachycardia, hypotension
375
Describe the management of a uterine rupture
  • ABCDE appproach
  • C-section
  • Uterus either repaired or removed
  • Decision-incision interval should be under 30 minutes
376
Define gestational diabetes
  • Glucose intolerance on OGTT with:
  • Fasting blood glucose >=5.6mmol/L
  • 2 hour plasma glucose levels >=7.8mmol/L
377
Describe the epidemiology of gestational diabetes
  • 5% of pregnancies
  • 2nd most common medical disorder complicating pregnancies
378
How might patients with gestational diabetes present?
  • Often asx
  • Polyuria
  • Thirst
  • Fatigue
379
How is gestational diabetes diagnosed?
  • OGTT: fasting >=5.6, 2 hour: >=7.8-REMEMBER 5,6,7,8
  • HbA1c: distinguish between gestational and pre-existing diabetes early on
  • Urinalysis: check for glycosuria
380
Describe the management of gestational diabetes
  • Fasting glucose <7mmol/L: lifestyle : diet and exercise. Give it 1-2 weeks then metformin if targets not met, then insulin added
  • >=7mmol/L: start insulin (short acting not long acting)
  • 6-6.9mmmol/L + complications like macrosomia or hydramnios: offer insulin
  • Glibenclamide only for women who can't use metormin/doesn't work and decline insulin
381
Describe the management of pre-existing diabetes in pregnancy
  • Weight loss if BMI >27
  • Stop oral hypoglycaemimcs except metformin and start insulin
  • Folic acid 5mg/day until 12 weeks 
  • Detailed anomaly scan at 20 weeks including 4 chamber view of heart and outflow tracts
  • Tight glycaemic control reduces complication rates
  • Treat retinopathy: can worsen in pegnancy
382
Describe the normal changes in blood pressure in pregnancy
  • Usually falls in the 1st trimester and continues to fall until 20-24 weeks
  • After this: BP usually increases to pre-pregnancy levels by term
383
How should pregnant patients with hypertension be classified?
  • Pre-existing hypertension
  • Pregnancy induced hypertension/gestational hypertension
  • Pre-eclampsia

384
Describe the management of pre-existing hypertension in pregnancy
  • STOP ACE inhibitor or angiotensin 2 receptor
  • SWAP for alternative: labetalol whilst waiting specialist review
  • Nifedipine if asthmatic
385
Describe the features of pregnancy induced hypertension
  • Hypertension occuring in the 2nd half of pregnancy(after 20 weeks)
  • No proteinuria, no oedema
  • 5-7% of pregnancies
386
Describe the management of pregnancy induced hypertension
  • Oral labetalol/nifedipine/hydralazine
  • Typically resolves within 1 month after birth 
387
Describe the features of pre-eclampsia
  • Pregnancy induced hypertension associated wwith proteinuria(>0.3g/24hrs)
  • Oedema may occur but less commonly used now as a criteria
  • 5% of pregnancies
388
Describe the epidemiology of Group B strep infection
  • Mc asx commensal bacterium in GI and GU tracts
  • 25% of pregnant women estimated to be carriers
  • Can cause severe illness to mother and infant during transmission during delivery
389
How might Group B strep infection be investigated?
  • No current routine screening test for pregnant women as colonisation status can change through pregnancy
  • GBS culture may be done in certain cirumstances
390
How is Group B strep infection managed?
  • Intrapartum antibiotic prophylaxis-benzylpenicillin
  • Abx IV during labour and delivery
391
Describe the management of obesity in pregnancy
  • 5mg folic acid not 400mcg
  • Screening for gestational diaebetes with OGTT at 24-28 weeks
  • BMI >=35: Birth in consultant led obstetric clinic
  • BMI>=40: Antenatal coonsultation with ostetric anaesthetist and plan made in advance
392
How is cephalopelvic disproportion managed?
  • Trial of labour
  • Intrumental vaginal delivery-may need episiotomy
  • C-section
393
How is prolonged labour managed?
  • ID causes and evaluate progress of labour
Medical:
  • Artificial rupture of membranes
  • IV oxytpcin to augemnt contractions
  • Pian management: epidural, nitrous oxide etc
Surgical:
  • Operative delivery
  • C-section
Postpartum:
  • Monitor closely for infection
  • Active management of 3rd stage of labour: uterotonic agents
  • Ensure adequate analgesia
394
Describe the clinical features of obstetric cholestasis
  • Pruritus: intense-typically worst in palms, soles, abdomen
  • Jaundice: dark urine and pale stools in about 20% of patients
  • General fatigue and malaise
  • GI sx: nausea and appetite loss
  • RUQ abdominal pain
  • Raised bilirubing in >90% of acses
395
How is obstetric cholestasis managed?
  • Chlorphenamine and emollients to reduce itching
  • Induction of labour at 37-38 weeks
  • Ursodeoxycholic acid
  • Vitamin K supplementation-> minimise risk of bleeding
396
Describe the prognosis of obstetric cholestasis
  • Hihg recurrence: 45-90% in subseqquent pregnancies
397
Describe the aetiology of chorioamnionitis
  • Bacteria ascending from vagina into uterus
  • Mc: Group B strep, E.coli and anaerobic bacteria
398
How is chorioamnionitis diagnosed?
  • Usually clinical
  • Blood tests and cultures ot confirm and ID causative organism
399
How is chorioamnionitis managed?
  • IV broad sectrum abx: sepsis 6 protocol
  • Monitoring of fetus and mother for complications
  • Early delivery might be needed-C section
400
Describe the management of FGM in the UK
  • Illegal in UK-immediate child protection referrral if child at risk
  • Anterior episiotomy during second stage of labour under local anaesthetic or regional block
  • Deinfibulation surgery: important to protect urethra
401
Describe the clinical features of shoulder dystocia
  • Difficult delivery of fetal face/chin
  • Retraction of fetal head-turtle neck sign
  • Failure of restitution
  • Failure of descent of fetal shoulders following delivery of head
402
Describe the management of shoulder dystocia
  • Immediately call for senior help
  • Do not apply fundal pressure-can lead to uterne rupture
  • McRoberts maneouevre
  • All fours position
  • Internal rotational manoeuvers
  • Episiotomy-won't remove bony obstruction but will allow space for internal manoeuvers
  • Cleidotomy/symphysiotomy: not 1st line-associated with significant maternal morbidity]
  • Zavanelli manoeuvre-also dangerous
403
Define anaemia in pregnancy
Hb:
  • 1st trimester: <110g/L
  • 2/3 triester: <105g/L
  • Postpartum: <100g/L
404
Describe some clinical features of anaemia
  • Asx
  • Dizziness, fatigue, dyspnoea: normal pregnancy
  • Pallor
  • Koilonychia
  • Angular cheilitis
405
How is anaemia diagnosed/investigated in pregnancy?
  • FBC
  • Folate to check for folate deficiency
  • Check for beta thalassaemia and sickle cell
406
Describe the risk of congenital rubella syndrome?
  • Risk high as 90% in first 8-10 weeks
  • Damage rare after 16 weeks
407
Describe the epidemiology of congenital rubella syndrome
  • Rare now due to MMR vaccine
408
How is rubella transmitted ot the fetus in congenital rubella syndrome?
  • Virus can cross the placenta and affect the developing fetus
409
How is congenital rubella syndrome diagnosed?
  • Serology to confirm rubella infection-IgM raised in women recently exposed to virus
  • Audiology tests for hearing impairment
  • Opthalmology for eye abnormalities
  • Echos for congenital heart defects
410
How is congenital rubella syndrome managed?
  • During pregnancy: discuss with local health protection unit
  • Advised to keep away from people who might have rubella
  • Offer MMR vaccine in post natal period
  • Neonates: primarily supprotive and symptomatic-monitor progress and manage long-term complications
411
How can perineal tears be classified?
  • 1st, 2nd, 3rd, 4th degree 
412
Describe the features of a first degree perineal tear
  • Superficial damage with no muscle involvement
  • Do not require any repair
413
Describe the features of a second degree perineal tear
  • Injury to perineal muscle but not involving the anal sphincter
  • Require suturing on ward by suitably experienced midwife or clinician
414
Describe the features of a third degree perineal tear
  • Injury to perineum involving the anal sphincter complex(external anal sphincter(EAS) and internal anal sphincter(IAS)
  • 3a: < 50% EAS thickness torn
  • 3b: >50% EAS thickness torn
  • 3c: IAS torn
  • Require repair in theatre by suitably trained clinician
415
Describe the features of a fourth degree perineal tear
  • INjury to perineum involving the anal sphincter complex(EAS and IAS) and rectal mucosa
  • Require repair in theatre by suitably trained clinician
416
Describe the management of perineal tearss
  • 1st degree: no repair
  • 2nd: suturing
  • 3rd/4th: surgical repair under regional or general anaesthetic
  • Broad spectrum abx and laxatives given post surgery
417
Describe the epidemiology of amniotic fluid embolism
  • Rare but significant cause of maternal morbidity and mortality
418
Describe the aetiology of an amniotic fluid embolism
  • Not known fully
  • Amniotic fluid can enter maternal circulation and form embolism-> block circulation like a blood clot especially in lung
  • Fluid also triggers inflammatory response within mother's immune system-> DIC
419
Describe the signs and symptoms of an amniotic fluid embolism
  • Tachypnoea
  • Tachycardia
  • Hypotension
  • Hypoxia
  • DIC
  • Cyanosis and MI
  • Chills, shivering, sweating, anxiety and coughing
420
How is an amniotic fluid embolism diagnosed?
  • Clinical
  • Exclude other causes-no definitive diagnostic test
421
Describe the management of an amniotic fluid embolism
  • Immediate transfer to ICU, MDT care
  • Oxygen, fluid resus
  • Correction of any coagulopathy
  • FFP if prolonged PT
  • Cryoprecipitate for low fibrinogen
  • Platelet transfusion for low platelets
422
Describe the management of hyperemesis gravidarum
Simple:
  • Rest and avoid trigggers
  • Bland, plain food, ginger
  • P6(wrist) acupressure
1st line meds:
  • antihistamines: oral cyclyzine/promethazine
  • phenothiazines: oral prochlorperazine or chlorppromazine
2nd line:
  • Oral odansetron
  • Oral metoclopramide/domperidone-5 DAYS MAX


  • Thiamine and folic acid supplementation
  • Atacids
  • Thromboembolic stockings and LMWH -dehydration 






423
How is hyperemesis gravidarum managed in hospital?
  • Normal saline with added potassium for rehydation
  • Antiemetics
424
Describe the management of hypothyroidism in pregnancy
  • Levothyroxine: usual dose increased by 25-50mcg due to increased metabolic demand
425
Describe the aetiology of acute fatty liver of pregnancy
  • LCHAS mutation-> accumulation of fatty acid metabolites in placenta-> shunted into maternal circulation and accumulate in maternal liver
426
How is acute fatty liver of pregnancy investigated/diagnosed?
Raised:
  • AST/ALT
  • Bilirubin
  • Creatinine
  • Ammonia
  • Lactate
  • Serum uric acid
Leukocytosis, low-normal platelets, normocytic normochromic anaemia
Coagulopathy: prolonged PT, hypofibrinogenaemia and elevated D dimer
427
Describe the management of acute fatty liver of pregnancy
  • Curative: delivery of the fetus
  • Maternal stabilisation: correct hypoglycaemia, coagulopathy and hypertension
  • After delivery: cloese monitoring-if ongoing deteriorattion in liver function post birth-transfer to liver transplant facility
428
Describe the management of the thyrotoxic phase of postpartum thyroidits
  • Propanolol for sx control
  • Not usually treated with anti-thyroid drugs as thhryroid not overactive
429
Describe the treatment of the hypothyroid phase of postpartum thyroidits
  • Usually treated with thyroxine
430
Describe the presentation of a patient with obstructed labour
  • Widest diameter of fetal sckull remains stationary above the pelvic brim
  • Prolionged labour: >12 hours
  • Premature rupture of membranes
  • Mother has abnormal vital signs
  • Bandls' ring
  • Foul smelling meconium from mother's vagina
  • Oedema of fulva/cervix
  • Caput
  • Malpresentation/malposition of fetus
  • Poor cervical effaceemnt

Assess using vaginal exam
431
Describe the management of obstructed labour
  • Saline for dehydration
  • catheter to drain bladder
  • May need C section or instrumental delivery
432
Describe the epidemiology of intrauterine growth restriction
  • 3-7% of newborns
  • Increased prevalence in low/middle income countries-> maternal malnutrition and infection
433
Describe the signs and symptoms of intrauterine growth restriction
  • Decreased fetal movement
  • Abnormal fundal height for gestational age
  • Complications like pre-eclampsia and stillbirh
434
How is intrauterine growth restriction managed?
  • Close monitoring of fetal growth and wellbeing
  • Management of maternal conditions contributing
  • Consideration for early delivery if fetus is in distress/conditions worsens
435
Describe the aetiology of ovarian hyperstimulation syndrome
  • Excessive response to hormones-> multiple follicles mature and enlarge-> all transform into corpus luteum-> overproduction of oestrogen, progesterone and local cytokines, especially vascular endothelial growth factor-> increased membrane permeability and loss of fluid from intravascular compartment
436
Describe the signs and symptoms of ovarian hyperstimulation syndrome
  • Bloating
  • Abdo pain
  • Oedema
  • Pleural efffusions
  • Ascites
  • Weight gain
437
How is ovarian hyperstimulation syndrome diagnosed?
  • Routine bloods: evaluate haemoconcentration and detect potential organ dysfunction
  • CXR: ID pleural effusion
438
Describe the management of ovarian hyperstimulation syndrome
  • Supportive-tailored to severity of condition
  • Simple analgesia for discomfort
  • Might need ICU and close monitoring if severe
439
Describe the features of fetal varicella syndrome
  • Skin scarring
  • Eye defects: microphthalmia
  • Limb hypoplasia
  • Microcephaly
  • Learning difficulties
440
Describe the management of chickenpox exposure in pregnancy
  • If doubt about previous infection: check blood urgently for varicella antibodies
  • Oral aciclovir now first choice for post exposure prophylaxis(used to be VZIG)-should be given day 7-14 after exposure not immediately
441
Describe the management of chickenpox in pregnancy
  • Seek specialist advice
  • Oraal aciclovir if >=20 weeks and presents within 24hrs of rash onset
  • If <20 weeks: aciclovir 'considered with caution
442
Describe the pathophysiology of placental insufficiency?
  • Placental vascular remodeling is affected-> placental functioning progressively deteriorates. This process affects the placental blood flow, leading to fetal hypoxemia, or low levels of oxygen in the blood, and restriction of fetal growth. 
443
How might placental insufficiency present?
  • Usually no observable sx
  • Decreased fetal movemennt
  • Intrauterine growth restriction
  • Prematurity
  • Stillbirth
444
How is placental insufficiency diagnosed/investigated?
  • Doppler USS: evaluate fetal and placental circulations-> regulare screening
  • MRI if inconclusive
445
Describe the management of placental insufficiency
  • <34 weeks: delay delivery: low dose aspirin, vitamin C and E, heparin
  • >34 weeks: prompt delivery
446
How is a pregnant women at high risk of VTE treated?
  • LMWH throughout antenatal period and input from experts
447
If a pregnant woman has 3 risk factors for VTE how should this be managed?
  • LMWH from 28 weeks and continued nutil 6 weeks postnatal
448
If a diagnosis of DVT is made shortly beefore delivery in a pregnant woman, how long should treatment be continued for?
  • At least 3 months
449
How can twin pregnancies be classified?
  • Zygosity
  • Chorionicity
  • Amnionicity
450
How can monozygotic twwins be further classified?
  • Dichorionic + daimniotic: 2 different sacs
  • Monochorionic + diamniotic: same outer sac, two inner sacs
  • Monochorionic + monoamniotic: same sacs
451
Describe the epidemiology of twins
  • 2/3: dizygotic
  • 1/3: monozygotic
^When conceived naturally
452
Describe the management of twins
  • Rest
  • USS for diagnosis and monthly checks
  • Additional iron and folate
  • More antenatal care( weeekly when >30 weeks)
  • Precautions at labour(2 obstetricians present)
  • 75% of twins deliver by 38 twins, if longer, most twins are induced at 38-40 weeks
453
Describe the aetiology of twin-to-twin transfusion syndrome
  • Precipitated by anastamoses of umbilical vessels betwween 2 fetuses in the placenta of monochorionic twins
454
How is twin-to-twin transfusion syndrome diagnosed?
  • Monochorionic twins: regular USS to monitor
  • Observe fluid levels in each amniotic sac, measure size of twins and assess blood flow in umbilical cord and placenta
455
Describe the management of twin-to-twin transfusion syndrome
  • Laser transection of problematic vessels in utero-can increase survival rate, high mortlaity for both twins without tx
456
Describe the symptoms of UTI in pregnancy
  • Frequent urination
  • Dysuria
  • Lower abdo pain
  • Fever
  • Haematuria
457
Describe the management of asymptomatic bacteriuria in pregnancy
  • Nitrofurantoin and cefalexin mc used
  • Ig Group B strep ID d: intrapartum prophylactic abx to reduce risk of transmission 
458
Describe the treatment for a UTI in pregnant women
  1. nitrofurantoin for 7 days(avoid at term)
  2. Amoxicillin/cefelexin
459
Describe the symptoms of puerperal infection
  • Fever
  • Abdo pain
  • Tahycardia
  • Abnormal discharge
  • Foul smellinf lochia(postpartum bleeding)
  • Tenderness/pain in pelvi area
  • Sepsis signs: hypotension, tachypnoea etc
460
Describe the maangement of puerperal infection
  • Abx-broad spectrum initially: ceftriaxone and metronidazole
  • Fluids
  • Analgesia
  • Prevention: good hygiene practices during childbirth and postpartum care
  • Close monitoring
  • Drainage od abscesses if needed
461
Describe LH and FSH in Turners
  • Raised LH
  • Raised FSH
462
Describe LH and FSH in Kallman's
  • Low LH
  • Low FSH
463
Describe the general function of blood hormones
  • Oestrogen: sex development-females
  • Progesterone: uterine development
  • Testosterone: sex development males
  • FSH and LH: ovarian funcitonality
464
Describe the management of primary amenorrhoea
  • Primary hypo: COCP
  • Primary hyper: GnRH analogue
465
Descrieb the management of secondnary amenorrhoea
  • Lifestyle: stress/weight managemenet
  • Treat underlying cause
  • Surgical: tumour/cyst removal
466
For how long/how frequently do a couple need to be having unrpotected sexual intercourse to be cnsidered infertile?
  • 2 years despite sex 3-4 times/wweek
467
How can causes of infertility be classified?
  • Genetics
  • Ovulation/endocrine
  • Tubal abnormalities
  • Uterine abnormalities
  • Endometriosis
  • Cervical abnormalities
  • Testricular disorders
  • Ejaculatory disorders
468
Give some ovulation/endocrine disorders that can cause infertility
  • PCOS
  • Pituitary tumours
  • Sheehan's syndrome
  • Hyperprolactinaemia
  • Cushing's
  • Premature ovarian failure
469
Give some tubal abnormalities that can cause infertility
  • Congenital anatomical abnormalities
  • Adhesions
  • Can be secondary to PID(-> gonorrhoea, chlamydia)
470
Give some uterine abnormalities that can cause infertility
  • Bicronate uterus
  • Fibroids
  • Asherman's syndrome
471
How is infertility investigated in women?
Bedside:
  • Thorough hx including PMH, sexual history and past pregnancies
  • Speculujm and bimaual exam-e.g. fibroids
  • STI screen

Bloods:
  • Serum progesterone testing
  • Prolactin
  • LH/FSH
  • Anti-mullerian hormone
  • TFTs
Imaging:
  • TV USS
  • Hysterosalpingography
  • Laparoscopy and dye
472
How is infertility investigated in men?
Bedside:
  • Thorough hx including PMH, sexual history past children
  • Testicular exam: e.g. varicocele
  • Semen analysis: evaluate sperm count, motility and morphology
Bloods:
  • Serum testosterone
  • LH/FSH
  • TFTs
473
Describe the conservative management of infertility
  • Folic acid
  • Weight loss: BMI 20-25
  • Smoking cessation and alcohol advice
  • Stres reduction strategies
  • Advice sexual intercourse every 2-3 days
474