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B TO REVISE - PHASE 3A > WOMENS EXTRA CONDITIONS > Flashcards

WOMENS EXTRA CONDITIONS Flashcards

1
Q

1* AMENORRHOEA
What is primary amenorrhoea?

A

Absence of menstruation by –
- 14y if no secondary sexual characteristics (more indicative of a chromosomal abnormality)
- 16y with secondary sexual characteristics (breast buds)

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2
Q

1* AMENORRHOEA
What is the difference between hypogonadotrophic hypogonadism and hypergonadotrophic hypogonadism?

A
  • Deficiency in gonadotrophins (LH + FSH) stimulating ovaries due to abnormal hypothalamus or pituitary means they do not respond by producing sex hormones (oestrogen)
  • Gonads fails to respond to stimulation of gonadotrophins meaning no negative feedback + increasing amounts of FSH/LH
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3
Q

1* AMENORRHOEA
What are some causes of hypogonadotrophic hypogonadism?

A
  • Constitutional delay (temporary delay, no pathology, ?FHx)
  • Hypopituitarism
  • Kallmann’s (failure to start puberty + anosmia)
  • Excessive exercise, dieting or stress causes hypothalamic failure
  • Endo = Cushing’s, prolactinoma, thyroid
  • Damage (cancer, surgery)
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4
Q

1* AMENORRHOEA
What are some causes of hypergonadotrophic hypogonadism?

A
  • Turner’s syndrome XO
  • Congenital absence of ovaries
  • Previous damage to gonads (torsion, cancer, infections like mumps)
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5
Q

1* AMENORRHOEA
What are some other causes of primary amenorrhoea and how may they present?

A
  • Congenital adrenal hyperplasia (tall, deep voice, facial hair)
  • Androgen insensitivity syndrome (46XY but female phenotype)
  • Congenital malformations of genital tract (if ovaries unaffected = secondary sexual characteristics but no menses)
  • Gonadal dysgenesis (no ovaries or uterus form)
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6
Q

1* AMENORRHOEA
What are some first line investigations for primary amenorrhoea?

A
  • Examination = signs of puberty, PV exam, BMI, visual fields
  • FBC + ferritin (anaemia), U+E for CKD, anti-TTG for coeliac, urinary beta-hCG crucial
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7
Q

1* AMENORRHOEA
What hormonal blood tests would you do for primary amenorrhoea?

A
  • FSH + LH (low or high)
  • TFTs, prolactin (if indicated)
  • Free androgens raised in PCOS, AIS + CAH
  • Insulin-like growth factor I used for screening for GH deficiency
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8
Q

1* AMENORRHOEA
What other investigations may be useful for primary amenorrhoea?

A
  • XR of wrist to assess bone age + Dx constitutional delay
  • Pelvic USS for structural causes
  • ?MRI head if pituitary
  • Karyotyping for Turner’s syndrome, AIS
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9
Q

1* AMENORRHOEA
What is the management of…

i) constitutional delay?
ii) ovarian causes (PCOS, damage/absence of ovaries)
iii) genital tract abnormalities?
iv) pituitary tumour?
v) stress?

A

i) May only require reassurance + observation
ii) COCP can induce regular menstruation + prevent Sx of oestrogen deficiency
iii) Surgery
iv) Surgery, chemo, radio or bromocriptine if prolactinoma
v) CBT, healthy weight gain, stress reduction

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10
Q

1* AMENORRHOEA
What is the management of hypogonadotrophic hypogonadism?

A
  • Pulsatile GnRH can induce ovulation, menstruation + potentially fertility
  • COCP if pregnancy not wanted to replace sex hormones, induce regular menstruation + prevent Sx of oestrogen deficiency
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11
Q

2* AMENORRHOEA
What is secondary amenorrhoea?
What is oligomenorrhoea?

A
  • Previously normal menstruation ceases for >3m in a non-pregnancy woman
  • Where menses are >35d apart (up to 6m), can be ovarian normality but exclude PCOS
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12
Q

2* AMENORRHOEA
What are the causes of secondary amenorrhoea?

A
  • Pregnancy (most common), breastfeeding, menopause (physiological)
  • Iatrogenic (contraception)
  • Hypothalamic/pituitary
  • Ovarian causes (PCOS, POI)
  • Thyroid, uterine pathology (Asherman’s)
  • Excessive exercise, stress or eating disorders
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13
Q

2* AMENORRHOEA
What are the hypothalamic or pituitary causes of secondary amenorrhoea?

A
  • Sheehan’s syndrome = pituitary necrosis following PPH
  • Pituitary tumour like prolactinoma leading to hyperprolactinaemia which prevents GnRH
  • Trauma, radiotherapy or surgery
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14
Q

2* AMENORRHOEA
How does excessive stress or eating disorders cause secondary amenorrhoea?

A
  • Hypothalamus reduces GnRH in times of stress > hypogonadotrophic hypogonadism to prevent pregnancy in adverse situations
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15
Q

2* AMENORRHOEA
What hormonal tests would you do in secondary amenorrhoea?

A
  • Urine/blood beta-hCG
  • High FSH (POI)
  • Low FSH/LH (hypgonadotrophic hypogonadism)
  • High LH or LH:FSH ratio suggests PCOS
  • Free androgen raised in PCOS
  • Mid-luteal (day 21) progesterone to check ovulation happened
  • Prolactin + TFTs if indicated
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16
Q

2* AMENORRHOEA
What other investigations may you do in secondary amenorrhoea?

A
  • Pelvic USS to Dx PCOS
  • MRI head if ?pituitary tumour
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17
Q

2* AMENORRHOEA
What is the management of…

i) hyperprolactinaemia?
ii) hypothalamic failure?

A

i) Bromocriptine or cabergoline (dopamine agonists)
ii) GnRH replacement

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18
Q

CERVICAL ECTROPION
What is cervical ectropion?
What is it associated with?

A
  • Columnar epithelium of endocervix extends out to ectocervix
  • Endocervix cells more fragile so prone to trauma + to bleed (post-coital)
  • High oestrogen > young women, COCP, pregnancy
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19
Q

CERVICAL ECTROPION
How does cervical ectropion present?

A
  • Increased vaginal discharge
  • Abnormal PV bleeding (IMB + PCB)
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20
Q

CERVICAL ECTROPION
How does cervical ectropion present on speculum?

A
  • Well-demarcated border between redder, velvety columnar epithelium extended from os + pale pink squamous epithelium of ectocervix
  • ‘Red ring’ around cervical os (transformation zone)
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21
Q

CERVICAL ECTROPION
What is the management of cervical ectropion?

A
  • Problematic bleeding = cauterisation (silver nitrate or cold coagulation during colposcopy)
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22
Q

POI
What is premature ovarian insufficiency (POI)?

A
  • Premature menopause before the age of 40
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23
Q

POI
What are some causes of POI?

A
  • Majority idiopathic
  • Iatrogenic (chemo/radio, oophorectomy)
  • Autoimmune (coeliac, T1DM)
  • Genetic (FHx, Turner’s)
  • Infections (mumps, TB, CMV)
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24
Q

POI
What is the clinical presentation of POI?

A
  • Secondary amenorrhoea (or irregular) + typical peri-menopause Sx before age 40
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25
Q

POI
What are some investigations for POI?

A
  • Clinically = menopausal Sx in woman <40y with 4m of amenorrhoea
  • FSH level = >25IU/L on 2 samples >4w apart
  • Hypergonadotrophism + hypoestrogenism
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26
Q

POI
What are the complications of POI?

A
  • Higher risk of conditions due to lack of oestrogen > CVD, stroke, osteoporosis, dementia + cognitive impairment + Parkinsonism
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27
Q

POI
What is the management of POI?

A
  • HRT imperative until at least average age of menopause to reduce risks
  • HRT or COCP can be used
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28
Q

POI
What is the difference between traditional HRT and COCP in POI?

A
  • Traditional HRT associated with lower BP than COCP
  • COCP may be more socially acceptable if younger + acts as contraceptive
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29
Q

POI
Are there the same risks of HRT in POI as in menopause?

A
  • No increase in breast cancer risk as women normally produce these hormones at that age
  • Slight increased risk of VTE but reduced by transdermal patch
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30
Q

FGM
What is female genital mutilation (FGM)?

A
  • All procedures involving partial or total removal of female external genitalia or injury to female organs for non-medical reasons, often pre-pubertal
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31
Q

FGM
What is the WHO classification for the types of FGM?

A
  • 1 = partial or total clitoridectomy
  • 2 = excision
  • 3 = infibulation
  • 4 = all other non-medical harmful procedures incl. pricking, piercing, incising
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32
Q

FGM
What is…

i) excision?
ii) infibulation?

A

i) Partial or total removal of clitoris + labia minora ± excision of labia majora
ii) Narrowing/closing of vaginal orifice with creation of a covering seal (stitch labia together)

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33
Q

FGM
What are some potential reasons for FGM?

A

Based on customs –
- It will bring status + respect to family (social norm)
- Rite of passage + being part of woman
- Preserves girls’ virginity so acceptable for marriage
- Cleanses + purifies girl with perceived religious requirement

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34
Q

FGM
What are some acute complications of FGM?

A
  • Pain
  • Bleeding
  • Infection (BBV)
  • Sepsis
  • Swelling
  • Urinary retention
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35
Q

FGM
What are some chronic complications of FGM?

A
  • Dyspareunia
  • Dysmenorrhoea
  • Infertility + pregnancy issues
  • Keloid scar
  • Haematocolpos (period backs up in uterus as cannot be released)
  • PTSD
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36
Q

FGM
What is the initial management of suspected or confirmed FGM?

A
  • Report ANY FGM in <18 to police + Record in notes (consider in >18 after risk assessment e.g. others at risk like unborn children)
  • Educate pts + relatives that FGM is illegal + health consequences
  • Services = social, safeguarding, paeds, counselling, FGM specialists
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37
Q

FGM
What is the overall management of FGM?

A
  • De-infibulation by specialist in FGM in some type 3 to try restore function
  • Re-infibulation may be requested after childbirth but this is illegal
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38
Q

MACROSOMIA
What is…

i) large for gestational age (LGA)?
ii) macrosomia?

A

i) Estimated foetal weight above the 90th centile for their gestational age
ii) Baby with a weight >4kg regardless of gestational age

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39
Q

MACROSOMIA
What are the causes of macrosomia?

A
  • Constitutionally large or familial (parental height + weight)
  • Maternal diabetes, previous macrosomia, obesity or rapid weight gain
  • Overdue
  • Male baby
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40
Q

MACROSOMIA
What are some complications of macrosomia?

A
  • Maternal = failure to progress, perineal tears, instrumental/c-section, PPH, uterine rupture (rare)
  • Foetal = shoulder dystocia, neonatal hypoglycaemia, obesity in childhood + later life
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41
Q

MACROSOMIA
How do you diagnose and manage macrosomia?

A
  • OGTT to screen for diabetes
  • SFH + EFW from USS to plot on growth chart + >90th centile = Dx
  • Regular growth scans to assess progress + check amniotic fluid index levels to exclude polyhydramnios
  • Most vaginal delivery, consider c-section if v large or signs of distress
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42
Q

CHORIOAMNIONITIS
What is chorioamnionitis?
What is a major factor in the condition?

A
  • Acute inflammation of amnion + chorion membranes due to ascending bacterial infection in setting of membrane rupture
  • PPROM
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43
Q

CHORIOAMNIONITIS
What is the clinical presentation of chorioamnionitis?

A
  • Uterine tenderness
  • Evidence of foetal distress on CTG
  • Foul odour, purulent/offensive PV discharge (yellow/brown)
  • Maternal infection (fever, abdo pain, maternal + foetal tachycardia)
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44
Q

CHORIOAMNIONITIS
What are some investigations for chorioamnionitis?

A
  • FBC, CRP (raised WCC + CRP)
  • Swabs (high + low vaginal swabs), MSU
  • USS for foetal presentation, EFW + liquor volume
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45
Q

CHORIOAMNIONITIS
What is the management of chorioamnionitis?

A
  • Steroids <34w
  • Deliver foetus (whatever gestation, often c-section)
  • IV Abx
46
Q

INFECTIONS + PREGNANCY
What is Parvovirus?
What are the adverse effects?
What is the management?

A
  • Parvovirus B19 can give viral Sx then ‘slapped cheeks’ (erythema infectiosum)
  • Worse <20w = suppresses foetal erythropoiesis causing anaemia + foetal hydrops, death, pre-eclampsia-like (mirror) syndrome in women
  • Maternal IgM + IgG, supportive, refer to foetal medicine to monitor
47
Q

INFECTIONS + PREGNANCY
What is toxoplasmosis?
How is it spread?
What is the clinical presentation?
What is the management

A
  • Toxoplasma gondii protozoan
  • Cat poo, eating infected meat
  • Glandular fever-like illness (fever, rash, eosinophilia)
  • TORCH screen (IgM + IgG), proven infection use spiramycin
48
Q

INFECTIONS + PREGNANCY
What is the management of Hep B in pregnancy?

A
  • Babies born to Hep B +ve mothers should be vaccinated within 24h of birth as well as other times recommended on vaccination schedule
  • No breastfeeding transmission in contrast to HIV
49
Q

INFECTIONS + PREGNANCY
What are the risks of rubella in pregnancy?
What is the management?

A
  • Congenital rubella syndrome in first 8–10w (sensorineural deafness, CHD like PDA + PS, congenital cataracts, cerebral palsy)
  • Live vaccines like MMR avoided in pregnancy (offer postnatally if no immunity), avoid contacts
50
Q

INFECTIONS + PREGNANCY
What is the management of HIV in pregnancy?

A
  • Normal vaginal delivery if viral load <50 copies/ml if. not c-section (IV zidovudine 4h before)
  • Neonatal zidovudine PO if maternal viral load <50 if not triple ART, both for 4–6w
  • Breastfeeding C/I
51
Q

ASTHMA + PREGNANCY
What are the complications of asthma in pregnancy?

A
  • Foetal growth restriction due to inadequate placental perfusion
  • Premature delivery (usually due to maternal deterioration)
52
Q

ASTHMA + PREGNANCY
What is the management of asthma in pregnancy?

A
  • Optimise control pre-conception
  • All drugs for asthma safe
  • Risk of exacerbation, esp in third trimester as baby grows it can press up on lungs > in asthma attack, prioritise mum
53
Q

ACUTE FATTY LIVER
What is acute fatty liver of pregnancy?

A
  • Rapid accumulation of fat within the hepatocytes that occurs in the third trimester of pregnancy
  • Rare cause of hepatitis in pregnancy
54
Q

ACUTE FATTY LIVER
What is the clinical presentation of acute fatty liver in pregnancy?

A

Vague Sx like –
- Abdo pain
- N+V
- Jaundice
- Anorexia
- Ascites

55
Q

ACUTE FATTY LIVER
What is the management of acute fatty liver?

A
  • LFTs show elevated liver enzymes, esp. ALT
  • Stabilise, admit + deliver foetus as high risk of liver failure + mortality (for both)
56
Q

THYROID + PREGNANCY
How common is hyperthyroidism in pregnancy?
How does hyperthyroidism present?
What are some complications?

A
  • Uncommon, often improves after 1st trimester
  • May present with excessive vomiting
  • Maternal = thyroid crisis with cardiac failure
  • Foetal = thyrotoxicosis due to transfer of thyroid stimulating antibodies
57
Q

THYROID + PREGNANCY
What is the management of hyperthyroidism in pregnancy?

A
  • Propylthiouracil is choice in 1st trimester (associated with maternal hepatic injury)
  • Carbimazole C/I until 2nd trimester as causes foetal abnormalities
  • If mother has stimulating antibodies, monitor foetal growth with USS
58
Q

THYROID + PREGNANCY
Is hypothyroidism in pregnancy common?
What is the prognosis of untreated hypothyroidism in pregnancy?
What is the management?

A
  • Yes
  • Early foetal loss + congenital hypothyroidism leading to impaired neurodevelopment
  • Aim for adequate replacement with levothyroxine (safe), especially in 1st trimester
59
Q

THYROID + PREGNANCY
What is post-partum thyroiditis?

A

3 stages –
- Thyrotoxicosis (3m)
- Hypothyroidism (3–6m)
- Normal thyroid function
Sx control of thyrotoxicosis, treat hypothyroidism with levothyroxine
Just need TFTs to Dx if within 12m of giving birth + Sx

60
Q

EPILEPSY + PREGNANCY
What pre-conception advice should be given for women with epilepsy?

A
  • 5mg folic acid
  • Determine if medication required or if it can be rationalised
  • Aim for monotherapy > carbamazepine + lamotrigine safest
  • Valproate can cause NTD + phenytoin can cause cleft lip + palate
61
Q

PREMATURITY
What are the WHO definitions of prematurity?

A
  • Birth before 37w
  • Extreme preterm = <28w
  • Very preterm = 28–32w
  • Mod-late preterm = 32–37w (term >37w)
62
Q

PREMATURITY
When are babies considered non-viable?

A
  • <24w so if no signs of life = no resus
  • From 24w chances improve so full resus
63
Q

PREMATURITY
What are the classifications of prematurity?

A
  • Spontaneous (70%) = PPROM, cervical weakness, amnionitis
  • Iatrogenic = induced due to some complication
64
Q

PREMATURITY
What are the risk factors of prematurity?

A
  • 50% none
  • Multiple pregnancy
  • Complications (IUGR, pre-eclampsia)
  • APH
  • Previous cervical surgery
  • Previous preterm
  • Polyhydramnios
  • Infection
  • Maternal diseases
65
Q

PREMATURITY
What is the clinical presentation of prematurity?

A
  • Persistent uterine activity WITH change in cervical dilatation ± effacement
  • Preterm labour with intact membranes if no ruptured amniotic sac
  • Increase or change in PV discharge or bleeding
66
Q

PREMATURITY
What are the investigations for prematurity?

A
  • Speculum (assess cervical dilatation, look for amniotic fluid) can Dx if <30w
  • TVS if >30w to measure cervical length (<15mm + contractions = Dx)
  • OR foetal fibronectin (Actim Partus, acts as glue between chorion + uterus + found in vagina during birth) test >50ng/ml = early labour
67
Q

PREMATURITY
What are the complications of prematurity?

A
  • Maternal = infection
  • Neonatal = necrotising enterocolitis, apneoa of prematurity, RDS, intraventricular haemorrhage, retinopathy of prematurity, jaundice, hearing issues, chronic lung disease
68
Q

PREMATURITY
What is the prophylaxis for prematurity and how do they work?

A
  • Progesterone gel or pessary decreases activity of myometrium + prevents cervix remodelling in preparation for delivery
  • Cervical cerclage = ≥1 sutures to strengthen + keep cervix closed
  • ‘Rescue’ cerclage to halt delivery
69
Q

PREMATURITY
What are the indications for…

i) progesterone prophylaxis?
ii) cervical cerclage?
iii) ‘rescue’ cerclage?

A

i) Cervical length <25mm on TVS at 16–24w
ii) Cervical length <25mm on TVS at 16–24w, previous premature birth or cervical trauma (colposcopy, cone biopsy)
iii) Cervical dilatation without ROM at 16–27+6 with no infection, bleeding or contractions

70
Q

PREMATURITY
What is the acute management of prematurity?

A
  • Senior obs + neonate input
  • Foetal monitoring (CTG)
  • Tocolytics
  • Corticosteroids
  • IV magnesium sulfate
  • Consider delayed cord clamping or cord milking (increases circulating blood volume + Hb in baby)
71
Q

PREMATURITY
What are tocolytics?
Why are they used?
Who for?
Examples?

A
  • Drugs to delay uterine contractions
  • Administer 2x steroids or transfer to more specialist unit (with neonatal ICU)
  • Those 24–33+6w
  • CCBs like nifedipine or oxytocin receptor antagonist like atosiban if C/I, terbutaline (SABA)
72
Q

PREMATURITY
What are corticosteroids used for?
Who for?
Give examples

A
  • Aids surfactant production so helps develop + protect baby’s lungs
  • Those <34w
  • Dexamethasone, betamethasone
73
Q

PREMATURITY
What is magnesium sulfate used for?
What is the regime?

A
  • Neuroprotection + reduced risk of cerebral palsy
  • Bolus + infusion for up to 24h or until birth in <34w
74
Q

PROLONGED PREGNANCY
What is a prolonged pregnancy?
What are some investigations?

A
  • Pregnancy exceeding 42w from LMP
  • USS assessment of growth + amniotic fluid volume
  • Daily CTGs after 42w + Advised to report any decreased foetal movements
75
Q

PROLONGED PREGNANCY
What are some complications of prolonged pregnancy for the foetus?

A
  • Macrosomia (+ dystocia)
  • Oligohydramnios
  • Reduced placental perfusion
  • May have meconium stained liquor (foetal distress), beware of aspiration as can cause severe pneumonitis
76
Q

PROLONGED PREGNANCY
What are the maternal complications of prolonged pregnancy?
What is the management?

A
  • Anxiety, more interventions (induction, operative delivery)
  • Confirm EDD, offer one membrane sweep at 41w + induction at 41–42w to prevent this
77
Q

AMNIOTIC EMBOLISM
What is an amniotic fluid embolism?

A
  • Amniotic fluid/foetal cells enter mother’s blood stream causing an immune reaction from the mother’s immune system > systemic illness
78
Q

AMNIOTIC EMBOLISM
What are some risk factors for amniotic fluid embolism?
Presentation?

A
  • Increasing maternal age + ARM
  • Often around time of labour + delivery but can be postpartum
  • Sx = SOB, sweating, anxiety, seizures, haemorrhage
  • Signs = hypoxia, tachycardia + hypotension, may lead to cardiac arrest
79
Q

AMNIOTIC EMBOLISM
What is the management of amniotic fluid embolism?

A
  • Supportive + requires involvement from critical care (maternal A-E resus)
80
Q

MATERNAL SEPSIS
What is sepsis?
What is septic shock?
What is the importance of sepsis?

A
  • Life-threatening organ dysfunction from dysregulated host response to infection
  • Persistent tissue hypoperfusion despite adequate fluid replacement
  • One of top direct causes of maternal death in UK
81
Q

MATERNAL SEPSIS
What are some causes of sepsis?

A
  • Pyelonephritis
  • Chorioamnionitis
  • Wound infection (c-section, episiotomy)
  • GBS
  • Pneumonia
  • Cellulitis
  • Basically any infection
82
Q

MATERNAL SEPSIS
What are some risk factors for sepsis?

A
  • Immunosuppressed
  • Obesity
  • DM
  • Hx of pelvic infection
  • Amniocentesis + CVS
  • Cervical stitch
  • Prolonged ROM (>18h in prems, >24h in term)
83
Q

MATERNAL SEPSIS
What is the clinical presentation of sepsis?

A
  • Pyrexia OR hypothermia, rigors, non-blanching rash
  • Tachycardia + hypotension (shock)
  • Oliguria, hypoxia, impaired consciousness
  • Failure to respond to treatment
84
Q

MATERNAL SEPSIS
What are the investigations for maternal sepsis?

A
  • Monitor Maternal Early Obstetric Warning Score (MEOWS)
  • Warning signs of sepsis (3Ts white with sugar)
85
Q

MATERNAL SEPSIS
What are the warning signs of sepsis?

A

3Ts white with sugar –
- Temp <36 or >38
- Tachycardia >90bpm
- Tachypnoea >20bpm
- WCC >12 or <4
- Hyperglycaemia >7.7mmol/L in absence of diabetes

86
Q

MATERNAL SEPSIS
How can maternal sepsis be prevented?

A
  • All pregnant ladies get seasonal flu vaccine
  • Broad-spec IV Abx then alter with sensitivities
  • Involve senior team + experts early
  • SEPSIS 6 within first hour
  • Consider delivery + VTE prophylaxis
87
Q

MATERNAL SEPSIS
What are the SEPSIS 6 components?

A

BUFALO (3 in, 3 out) –
- Blood cultures (out)
- Urine output by catheter (hourly, out)
- Fluids resus (IV, in)
- Abx (IV broad-spec, in)
- Lactate (ABG, out)
- Oxygen (high flow SpO2 >94%, in)

88
Q

MATERNAL SEPSIS
What is puerperal pyrexia?
What are the causes?
What is the management

A
  • Temp >38 in first 14d postpartum
  • Endometritis #1, UTI, mastitis, wound infections, VTE
  • Endometritis = hospital for IV Abx (clindamycin/gent) until afebrile >24h
89
Q

MATERNAL SEPSIS
What is the clinical presentation of endometritis?
What can cause it?
How should you investigate it?

A
  • Foul-smelling discharge or lochia, bleeding gets heavier or does not improve with time, lower abdo pain
  • Commonly after c-section (give prophylactic Abx), can be caused by STIs
  • Vaginal swabs + urine MC&S
90
Q

PUERPERIUM
What is the puerperium?
What does it involve?

A
  • Delivery of placenta to 6w following birth
  • Return to pre-pregnant state, initiation/suppression of lactation + transition to parenthood
91
Q

PUERPERIUM
What is the postnatal period?

A
  • Period under which woman + baby are still under midwife care, usually at least 10d + for as long as midwife feels necessary
92
Q

PUERPERIUM
What is…

i) maternal death?
ii) direct maternal death?
iii) indirect maternal death?

A

i) Death of a woman during or up to 6w after her pregnancy (may or not have been aggravated by pregnancy)
ii) Mother dying as a result of an obstetric complication
iii) Mother dying as a result of a pre-existing disease or disease that developed during pregnancy, but not as a direct obstetric cause

93
Q

PUERPERIUM
What are some direct and indirect causes of maternal death?

A
  • Direct = VTE (#1), haemorrhage, HTN disorders, suicide
  • Indirect = cardiac disease
94
Q

PUERPERIUM
What are some major and minor post-natal problems?

A
  • Major = sepsis, PPH, pre-eclampsia, VTE, uterine prolapse, breast abscess, MH issues
  • Minor = fatigue, anaemia, mastitis, baby blues
95
Q

PUERPERIUM
What changes happen during the puerperium?

A
  • Big decrease in serum placental hormones (hPL, hCG, oestrogen + progesterone)
  • Uterus involutes from 1kg > 100g + cervix firm after 3d
  • Decidua is shed as lochia
  • Milk replaces colostrum after 3d
  • Breast engorgement (swollen, red + tender) after 3d
96
Q

PUERPERIUM
What are the different types of lochia?

A
  • Rubra (red) 0–4d (blood cervical discharge, meconium)
  • Serosa (yellow) 4–10d (mucus, exudate, foetal membrane, WBCs)
  • Alba (white) 10–28d (cholesterol, fat, leukocytes, mucus)
97
Q

PUERPERIUM
What is the difference between colostrum and breast milk?

A
  • Colostrum at birth = yellow fluid, first form of milk with high proteins (IgA, lactoferrin), low sugar + fat
  • Milk = lactose, protein, fat + water
98
Q

PUERPERIUM
What is the physiology of breast feeding?

A
  • Baby suckles so sensory impulses from nipple > brain
  • Prolactin secreted by ant. pit > breasts via blood + lactocytes produce milk
  • Oxytocin secreted by post. pit > breasts via blood causes myometrial cell contraction to expel milk
99
Q

PUERPERIUM
When else is prolactin secreted and why?

A
  • More at night
  • Suppresses ovulation
  • Levels peak after feed to produce more for next feed
100
Q

PUERPERIUM
What stimulates oxytocin secretion?
What hinders it?

A
  • Sight, sound + smell of baby (conditioned over time)
  • Hindered by anxiety, stress + pain
101
Q

PUERPERIUM
What is lactoferrin?

A
  • Multifunctional protein in milk but loads in colostrum
  • Regulates iron absorption in intestines + delivery of iron to cells
  • Prevention against infections
  • Regulation of bone marrow function + boosts immune system
102
Q

PUERPERIUM
What are some drug contraindications in breastfeeding?

A
  • Abx (ciprofloxacin, tetracyclines, chloramphenicol)
  • Psych drugs (lithium, BDZs)
  • Amiodarone, aspirin
  • Carbimazole, methotrexate
  • Sulfonylureas
  • Cytotoxic drugs
103
Q

PUERPERIUM
What are the pros + cons of breast feeding?

A
  • Readily available good nutrition, cheaper, contraceptive effect, decrease childhood infections (gastroenteritis), decrease in necrotising enterocolitis
  • Feed more often, uncomfortable + pain (mastitis)
104
Q

PUERPERIUM
What contraception can be offered to women?

A
  • POP + implant safe in breastfeeding, start any time
  • COCP UKMEC4 <6w + UKMEC2 >6w, avoid in breastfeeding
  • IUD/IUS inserted <48h OR >4w but is UKMEC3 between
105
Q

PUERPERIUM
What is mastitis?
What can cause it?

A
  • Inflammation of breast tissue
  • Obstruction of ducts + accumulation of milk (prevent by expressing regularly)
  • Infection enter at nipple>duct (commonly S. aureus)
106
Q

PUERPERIUM
How does mastitis present?
What can it lead to?

A
  • Breast pain + tenderness, erythema, local inflammation
  • Breast abscess if untreated
107
Q

PUERPERIUM
How does breast abscess present?
What is the management?

A
  • Unilateral erythema, tenderness, fever, palpable mass + tender/enlarged LNs in axilla
  • Requires surgical incision + drainage
108
Q

PUERPERIUM
What is the management of mastitis?

A
  • Milk MC&S if ?infection
  • Analgesia
  • Continue feeding or expressing
  • Flucloxacillin 10–14d if systemically unwell, nipple fissure, Sx>24h, infection
109
Q

SHEEHAN’S SYNDROME
What is Sheehan’s syndrome?

A
  • Drop in circulating blood volume leads to avascular necrosis of the pituitary gland
  • Ischaemia + infarction of anterior pituitary cells as supplied by hypothalamo-hypophysial portal system which is susceptible to rapid drops in BP after PPH
110
Q

SHEEHAN’S SYNDROME
How does Sheehan’s syndrome present?
What is the management?

A
  • Reduced lactation (lack of prolactin)
  • Amenorrhoea (lack of LH + FSH > HRT)
  • Hypothyroidism (lack of TSH > levothyroxine)
  • Adrenal insufficiency (lack of ACTH > hydrocortisone)

B TO REVISE - PHASE 3A (9 decks)

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