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Y4 ObGyn > Medical conditions during pregnancy > Flashcards

Medical conditions during pregnancy Flashcards

1
Q

What is pre- eclampsia and what causes it?

A
  • one of several hypertensive disorders which can occur during pregnancy
  • exact mechanism unknown but thought to be due to poor placental perfusion secondary to abnormal placentation
  • normally trophoblast invades myometrium and spiral arteries, destroying the tunica muscularis media which renders the spiral arteries dilated and unable to constrict, giving it a large blood supply
  • in preeclampsia the remodelling of spiral arteries is incomplete leading to high resistance requiring high blood pressure. The high blood pressure + hypoxia and oxidative stress from the inadequate uteroplacental perfusion lead to systemic inflammatory response and endothelial dysfunction
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2
Q

List 5 high and 5 moderate risk factors for pre eclampsia?

A 
high:
- chronic HTN
- HTN, eclampsia or preeclampsia in previous pregnancy
- pre- existing CKD
- DM
- autoimmune disease eg SLE or antiphospholipid syndrome
Moderate:
- nulipartity
- age >40
- BMI > 35
- fhx pre eclampsia
- pregnancy interval >10 yrs
- mutliple pregnancy
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3
Q

Who gets aspirin 150mg OD prophylaxis for preclampsia in the uk?

A
  • all women with 1 high risk factor or 2 or more moderate risk factors
  • this should be continued from 12 weeks gestation until birth
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4
Q

Describe the three criteria needed for diagnosis of pre- eclampsia and what other symptoms they may present with?

A
  • HTN (>140mmhg or >90 diastolic, on two occasions at least 4 hrs apart)
  • significant proteinuria (>30mg/mmol urinary protein/ creatinine)
  • in a woman >20 weeks gestation
  • may be asymptomatic or may have: headaches, visual disturbances, epigastric pain (due to hepatic capsule distension/ infarct), sudden onset odema, hyper- reflexia
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5
Q

Describe the classification of pre- eclampsia?

A

mild: bp 140/90- 149/99
moderate: 150/100-159/109
Severe: >160/110 + proteinuria >0.5g/ day OR bp >140/ 90 + proteinuria + symptoms

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6
Q

State 5 maternal and 3 fetal complications complications of pre-eclampsia?

A
  • HELLP syndrome (haemolysis, elevated liver enzymes, low platelets)
  • eclampsia
  • DIC
  • AKI
  • ARDS
  • hypertension post partum
  • cerebrovascular haemorrhage
  • death
  • fetal complications inc: prematurity, IUGR, placental abruption, intrauterine fetal death
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7
Q

Give 3 differentials for hypertension in pregnancy

A
  • essential HTN: HTN prior to 20 weeks gestation
  • pregnancy induced HTN: new onset HTN after 20 weeks gestation but without significant proteinuria
  • eclampsia: pre- eclampsia + seizures (emergency)
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8
Q

How should pre-eclampsia be investigated?

A
  • do protein dip first but then do 24 hr urinary collection or ACR to quantify
  • monitor for organ dysfunction
  • FBC: low hb and platelets
  • U+E: high urea, creatinine and urate, low urine output
  • LFT: high ALT, AST
  • USS for fetal growth, CTG, amniotic fluid level etc for fetal monitoring
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9
Q

How should pre- eclampsia be managed?

A
  • monitor frequently with bloods, urinalysis, bp, fetal growth scans, CTG- more severe the disease = more frequent monitoring
  • VTE prevention
  • antihypertensives (reduces risk of hemorrhagic stroke but doesn’t alter disease course)
  • delivery: only definitive cure, but prolonging pregnancy is only for the benefit of the fetus and decision for when to delivery should be made on individual basis
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10
Q

What antihypertensives are reccommended for use in pregnancy?

A
  • 1st line= labetalol (B blocker)- may cause postural hypotension, fatigue, headache, N+v
  • nifedipine (CCB)- may cause peripheral odema, dizziness, flushing, constipation
  • methyldopa (alpha agonist)- may cause drowsiness, headache, odema, Gi disturbance, dry mouth, bradycardia, hepatotoxic)
  • ACEi are CONTRAINDICATED in pregnancy due to association with congenital abnormalities
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11
Q

How should pre- eclampsia be managed post partum?

A
  • monitor mother for at least 24 hrs post partum as still at risk of seizures
  • generaly by day 5 theyre considered safe
  • BP monitored daily for first 2 days then at least once after 3-5 days and the need for antihypertensives reassessed
  • advice women of risk in subsequent pregnancies
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12
Q

What is hyperemesis gravidarum/ when can it be diagnosed?

A
  • N+V of pregnancy normally starts between 4 and 7 weeks gestation, peaks in 9th week and settles by week 20 usually
  • Hyperemesis gravidarum is diagnosed when prolonged and severe NVP with:
  • more than 5% pre pregnancy weight loss
  • dehydration
  • electrolyte imbalance
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13
Q

What is thought to cause hyperemesis gravidarum?

A
  • n+v thought to be due to rapidly increasing levels of bHCG which is released by the placenta
  • it stimulates chemoreceptor trigger zone in the brainstem which feeds into vomiting centre
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14
Q

give 3 rfs for hyperemesis gravidarum?

A
  • 1st pregnancy
  • past HG
  • raised BMI
  • multiple pregnancy
  • hydratidiform mole
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15
Q

What objective scoring system can be used to classify severity of N+V

A

pregnancy- unique quantification of emesis (PUQE) score

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16
Q

give 4 differentials for n+v in pregnancy?

A
  • gastroenteritis
  • cholecystitis
  • hepatitis
  • pancreatitis
  • peptic ulcers
  • UTI/ pyelonephritis
  • metabolic conditions
  • neurological disorders
  • drug induced
  • these should be particularly considered if symptoms start after 10+6 weeks gestation
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17
Q

How should N+V be investigated?

A
  • weight
  • urine dip
  • MSU
  • FBC, U+E, glucose
  • lft, amylase, tft, abg if severe
  • uss may be used to confirm viability, confirm gestation, excude multiple pregnancies and trophoblastic disease
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18
Q

How should mild, moderate and severe hyperemesis gravidarum be managed?

A

mild: oral antiemetics, oral hydration, dietary advice, reassurance
- moderate: ambulatory day care- IV fluids, parenteral antiemetics and thiamine, manage until ketonuria resolves
Severe: inpt management with Iv fluids, PPI, thiamine (prevents wernickes encephalopathy in prolonged vomiting), thromboprophylaxis if admitted

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19
Q

What antiemetics are recommended 1st, 2nd and 3rd line?

A

1st: cyclizine, prochlorperazine, promethazine, chlorpromazine
2nd: metoclopramide, domperidone, ondansetron
3rd: hydrocortisone IV, when symptoms improve can swap to PO pred and gradually reduce dose until lowest maintenance is reached

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20
Q

What is the definition of gestational diabetes?

A

any degree of glucose intolerance with onset or first recognition during pregnancy

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21
Q

What is the cause of glucose intolerance during pregnancy

A
  • it occurs when the body is unable to produce enough insulin to meet demands of the pregnancy
  • in pregnancy there is progressive insulin resistance so more insulin is needed in response to increases in glucose
  • a woman with poor pancreatic reserve is unable to respond to increased insulin requirement leading to transient hyperglycaemia
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22
Q

give 3 RFs for gestational diabetes

A
  • BMI >30
  • asian
  • previous gestational diabetes
  • 1st degree relative w/ diabetes
  • PCOS
  • previous macrosomic baby
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23
Q

Give 5 complications of gestational diabetes for the fetus

A

Leads to increased glucose and causes fetus to make more insulin also:

  • macrosomia
  • organomegaly (esp cardio)
  • erythropoiesis -> polycythaemia
  • polyhydramnios
  • increased rates of prem
  • hypoglycaemia (babies insulin remains high after birth)
  • increased risk still birth at term (why they tend to delivery early)
  • more insulin= reduced pulmonary phospholipids= reduced surfactant = increased risk transient tachypnoea of newborn (lungs are roughly 3 weeks behind normal development)
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24
Q

How is gestational diabates diagnosed?

A
  • oral glucose tolerance test (plasma glucose measured, then 75g glucose given, then measured again after 2hrs)
  • fasting glucose >5.6 or 2hrs after test >7.8 is diagnostic
  • test is offered at booking if previous GD, at 24-28 weeks if RFs present of previous GD and at any point if 2+ glycosuria or symptoms
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25
Q

How should gestational diabetes be managed?

A
  • sometime diet and exercise advice alone can be sufficient
  • cap glucose monitoring QDS- aim for BM <5.4 before meals and <7.8 after
  • metformin is safe
  • glibenclamide if metformin not tolerated
  • consider insulin at diagnosis if fasting glucose >7 or later if baby getting really big
  • monitor for complications with scans at 28,32 and 36 weeks (can do 2 weekly, and 2 weekly CTG is common)
  • deliver at 39-40 weeks by IOL or C section if on diet control and 38 weeks if metformin/ insulin
  • stop meds immediatly after delivery and check glucose before discharge
  • do fasting glucose test at 6-13 weeks, and yearly due to increased risk T2DM
  • check hba1c at 13 weeks postnatally and yearly thereafter
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26
Q

What is the most common virus transmitted to the fetus during pregnancy?

A

cytomegalovirus (herpes virus 5)

  • 1 in 100 women get it and 1/3 are transmitted to fetus
  • but only 5% fetal infections cause CMV related damage, risk is highest in 1st trimester
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27
Q

What symptoms, if any, may CMV cause?

A
  • usually asymptomatic if immunocompetent
  • Occasionally causes mild flu like illness
  • rarely can cause mononucleosis syndrome similar to EBV, w/ fever, splenomegaly and impaire liver function
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28
Q

How can CMV infection be confirmed?

A
  • viral serology for IgM and IgG

- fetal CMV infection diagnoses with amniocentesis and PCR after 21 weeks gestation

29
Q

how should CMV infections be managed?

A
  • mother required no treatment if immunocompetent
  • if fetal CMV infection confirmed, termination of pregnancy should be offered
  • if woman decided to continue, serial USS should be used to asses for manifestations of congenital CMV
  • promising results for trials using CMV specific hyperimmune globulin
30
Q

What problems are associated with intrauterine CMV infections?

A
  • IUGR
  • hepatosplenomegaly
  • TTP
  • jaundice
  • microencephaly
  • 20-30% mortality if symptomatic usually due to DIC or hepatic dysfunction
  • if no symptoms initially, have a 10-15% change of sequalae within 2 years such as: sensorineural hearing loss, psychomotor development delay, visual impairment
31
Q

25% of women have group b strep as a commensal in the vagina or rectum, what RFs are there for this bacteria being transmitted to the fetus?

A
  • GBS infection in previous baby
  • prematurity <37 weeks
  • rupture of membranes >24 hrs before delivery
  • pyrexia during labour
  • positive tests for GBS in mother
  • mother diagnosed with UTI found to be GBS during pregnancy
32
Q

Describe the clinical features of group B strep infection (in mother and neonate)

A
  • mother: UTI, Chroioamnioitis (fever, lower abdo tenderness, foul discharge, maternal/ fetal tachycardia during intrapartum) or endometritis (fever, lower abdo pain, intermenstraul bleeding, foul discharge- occurs post partum)
  • neonate infection/ sepsis: pyrexia, cyanosis, difficulty feeding and breathing, floppiness
33
Q

How should group B strep be diagnosed?

A
  • swabs (vaginal then rectal), PCR of culture
  • urine culture if UTI
  • screening only if high risk
34
Q

What is used to prevent group b strep infection and who gets the prevention?

A 
- High dose penicillins eg benzylpenicillin
Indicated if:
- GBS swab positive
- UTI caused by GBS during pregnancy
- pyrexia during labour
- previous baby with GBS infection
- labour onset <37 weeks
- rupture of membranes >18 hrs 
- if rupture of membranes in a woman >37 weeks and confirmed GBS +ve, they will be induced immediatly to reduce fetal exposure
35
Q

Describe the clinical features of parovirus B19 infection?

A
  • usually asymptomatic
  • symmetrical arthralgia, often proximal
  • in a child: upper RTI, malaise, headaches, low grade fever, erythema infectiosum (slapped cheek)
  • pink reticular macular rash
36
Q

How can parvovirus B19 infection be confirmed?

A
  • viral serology
37
Q

What can parvovirus b19 infection cause in the fetus?

A
  • fetal hydrops: abnormal accumulation of fluid in two or more fetal compartments (eg ascites, subcut odema, pleural effusion, pericardial effusion etc)
  • caused by virus attacking erythroid system leading to anaemia causing high cardiac output and hepatic erythropoesis (portal HTN and hypoprotinaemia)
  • can lead to spontaneous miscarriage and intrauterine disease in 9% infected pregnancies
  • diagnosed with USS
38
Q

How is fetal parvovirus infection managed?

A
  • fetal medicine specialist
  • no treament needed for mum
  • serial USS and doppler assessment starting 4 weeks post infection or at least 16 weeks, repeated every 1-2 weeks until 30 weeks gestation
  • if evidence of hydrops, sent to specialist centre for intrauterine erythrocyte transfusion
39
Q

Describe the clinical features of rubella ?

A
  • maternal rubella usually asymptomatic
  • fine maculopapular rash starts behind ears and spreads to face neck and then body
  • koplik spots
  • lethargy
  • headache
  • coryza
  • lymphadenopathy
40
Q

Describe the clinical features of congenital rubella syndrome

A 
At birth:
- sensorineural deafness
- cardiac defects
- retinopathy, congenital cateracts
- learning disability, microencephaly
- thrombocytopaenia, blueberry muffin appearance
Late onset:
- DM
- throiditis
- growth hormone abnormalities
- behaviour disorders
41
Q

how is rubella infection in pregnancy managed?

A
  • no treatment needed for mum
  • if <12 weeks, theres a 90% change of multiple defects, terminate pregnancy
  • at 12-20 weeks, prenatal diagnosis of fetal rubella infection required by amniocentesis and PCR, if transmitted can terminate or opt for USS surveillance
  • at >20 weeks there is no additional risk, no action required
42
Q

How can suspected varicella zoster infection be confirmed?

A
  • clinical diagnosis so dont need tests
  • can do PCR for VZV dna
  • immunofluorescence of basal epithelial cells scraped form vesicle
43
Q

How is maternal suspected varicella contact managed?

A
  • if theyve had chicken pox before you can assume immunity (IgG positive) and do nothing
  • if no previsou infection, do varicella IgG testing to confirm immunity status
  • if not immune, give varicella zoster immunoglobulin within 10 days of contact and before any rash appears (no benefit after)
44
Q

how should maternal chicken pox be managed?

A
  • give aciclovir within first 24 hrs if >20 weeks gestation- avoid is <20 weeks
  • counsel about symptoms of pneumonia, neurological signs and haematological rash- tell them to go to hospital if they occur
  • refer to fetal med specialist for serial USS from 5 weeks post infection to monitor for fetal abnormalities
45
Q

What complications may occur due to varicella zoster infection?

A
  • maternal: pneumonitis, hepatitis, ecephalitis (2% mortality)
  • varicella of newborn: if maternal infection in last 4 weeks pregnancy, treat with varicella- zoster immunoglobulin +/- aciclovir
  • fetal varicella syndrome: reactivation of virus in utero, occurs when maternal infection before 20 weeks. Characterised by: hypoplasia of limbs, skin scarring, eye defects, neuro abnormalities such as microencephaly, horners and seizures
46
Q

Define anaemia in pregnancy

A
  • Hb <110 in first trimester
  • Hb <105 in 2nd/ 3rd trimester
  • Hb <100 post partum
47
Q

Give 3 RFs for anaemia in pregnancy?

A
  • haemoglobinopathies eg thalassaemia or sickle cell disease
  • increasing maternal age
  • anaemia during previous pregnancy
  • poor diet
  • low socioeconomic status
48
Q

Give 5 causes of macrocytic anaemia

A
  • folate deficiency (common during pregnancy)
  • b12 deficiency
  • alcohol consumption
  • reticulocytosis
  • hypothyroidism
49
Q

How can beta thalassaemia and sickle cell disease be diagnosed?

A
  • haemoglobin electrophoresis
  • HbA2 or A1 low (one or both), increased or normal (either A1 or A2 or both will be decreased), high HbF= B thala
  • HbA absent, 80-95% HbSS and 2-20%HbF= sickle cell
50
Q

Should anaemia be screened for during pregnancy?

A

yes- at booking and at 28 weeks

In multiple pregnancies they also get it between 20-28 weeks

51
Q

how is iron deficiency anaemia managed in pregnancy?

A
  • give 100-200mg iron, retest FBC in 2 weeks, if Hb increase this is also diagnostic
  • parenteral iron transfusion should be considered if compliance is poor or evidence of malformation
52
Q

How should folate defiency, B thalassaemia and sickle cell be managed during pregnancy?

A

Folate deficiency: 5mg folic acid OD, increase to TDS if required
Beta Thalassaemia: folate supplement and blood transfusions, aim for Hb >80 and 100 at delivery
Sickle cell: folate and iron supplement if lab evidence of deficiency

53
Q

What is anti phospholipid syndrome?

A

An autoimmune condition in which antibodies are targeted against phospholipid- binding proteins. Characterised by vascular thrombosis and/ or adverse pregnancy outcomes, APS is a major treatable cause of recurrent miscarriage.
May occur as primary disease or secondary to other autoimmune conditions like SLE, RA or SS

54
Q

Why do obstetric complications arise from antiphospholipid syndrome?

A
  • inhibition of trophoblastic (precursor to placenta) function and differentiation
  • activation of complement pathways at maternal- fetus interface
  • thrombosis of the uteroplacental vasculature (late pregnancy)
55
Q

Describe the clinical features of antiphospholipid syndrome

A
  • Thrombosis formation and/ or recurrent pregancy loss
  • thrombosis: arterial (ischaemic stroke), venous (DVT) or microvascular. PE, MI, renal are rarer
  • Recurrent miscarriage may be at any stage
  • other features may be: IUGR, pre- eclampsia, livedo reticularis (red/purple/ blue reticular pattern on trunk, arms or legs), valvular heart disease, renal impairment, thrombocytopenia
56
Q

What is catastrophic antiphospholipid syndrome?

A
  • rare complication
  • acute formation of microthrombosis which cause infarction in multiple organs
  • exact mechanism unknown, but 20% triggered by major surgery, trauma or infection
  • 50% mortality rate
57
Q

Describe the diagnostic criteria for antiphospholipid syndrome

A

Need one clinical and one lab criteria minimum.
Clinical:
-1 or more eps of vascular thrombosis
- pregnancy morbidity (3 or more unexplained consecutive spontaneous abortions before 10 weeks or 1 prem birth before 34 weeks due to eclampsia or 1 or more unexplained deaths of morphologically normal fetuses after 10 weeks
Lab:
- lupus anti coagulant present on 2 or more occasions >12 weeks apart
- anticardiolipid antibody: in medium or high titre on 2 or more occasions >12 weeks apart
- anti B2 glycoproteinI- present in serum or plasma in high titre on 2 occasions >12 weeks apart

58
Q

How is antiphospholipid syndrome managed?

A
  • if presents with recurrent miscarriage: LMWH and low dose aspirin thoughout next pregnancies
  • presents with previous pre- eclampsia or IUGR: low dose aspirin throughout next pregnancies
  • presents w/ vascular thrombosis: long term anticoagulation, switch to LWMH if pt becomes pregnant or trying to conceive
59
Q

What is the increase in risk of VTE during pregnancy and why does it occur?

A
  • risk increases 4-5x
  • changes in levels of some proteins in clotting cascade ( increased fibrinogen and decreased protein S)
  • risk increases throughout and peaks post partum
60
Q

Give 4 obstetric specific RFs for VTE

A
  • multiple pregnancies
  • c section
  • prolonged labour
  • still birth
  • prem
  • PPH >1L
  • preeclampsia
61
Q

How should DVT and PE be investigated during pregnancy?

A
  • routine bloods
  • rise in D dimer is normal in pregnancy so this test is of little value
  • duplex USS for DVT, if negative but suspicion remains high can do a repeat 1 week later
  • PE: ECG and CXR, ABG may be helpful to assess severity. CTPA or V/Q scan
  • If presents with DVT and PE together, dont need todo CTPA or V/Q scan, just confirm DVT w/ USS and save the radiation exposure
  • if cardiogenic shock due to massive PE: A-E resus, consider thrombolysis and IV unfractionated heparin
62
Q

how should VTE be managed during pregnancy?

A
  • LMWH started immediatly until diagnosis excluded
  • titrate dose against pts weight
  • maintain until 6-12 weeks post partum and omit dose 24hrs before planned induction of c section or if they think theyre going into labour
  • if VTE presents at term, use IV unfractioned heparin and discontinue 6 hrs before planned induction of labour or c section (compared to 24hrs for LMWH)
63
Q

When should VTE prophylaxis be used in pregnancy

A
  • if they have >3 RFs in first 2 trimesters, >2 in 3rd or >1 in post partum period
  • 10 days LMWH considered in all having a C section esp if emergency
  • if previous VTE or known thrombophilia theyre very high risk and should be managed in collab with a haematologist
64
Q

What management is needed for ladies who are diabetic and wish to be pregnant?

A
  • optomise hba1c before pregnancy
  • give follic acid (3 months before and 12 weeks after)
  • stop teratogenic meds such as statins
  • do retinal scan, repeat at 28 weeks if normal or earlier if not
  • renal assessment- U+e, egfr, proteinuria
  • detailed/ cardiac scan at 18 weeks
  • USS scans at 28, 32, 36 weeks
  • monitor hba1c throughout
  • asiprin 75mg after 12 weeks gestation
  • loose weight
  • vit d supplements if BMI >35
  • joint MDT clinic every 1-2 weeks
  • if no complications, deliver at 37/38 weeks by IOL or C section, do earlier if complications
65
Q

What is obstetric cholestasis?

A
  • mutlifactoral cholestasis
  • presents with pruritis but no rash (starts on palms and soles, often worse at night), abnormal LFTs (increased bile acids, mildly increased bilirubin, increased GGT, ALP, ALT)
  • no other cause
  • resolves after birth
66
Q

How should obsetric cholestasis be investigated?

A
  • LFTs (raised , ALT, ALP, GGT, alk phos, mildly raised bilirubin, bile acids increase up to 100 fold), bile acid
  • viral screen (hepatitis, EBV, CMV)
  • liver autoimmune screen
  • USS abdo- liver- also excludes gall stones
67
Q

What are the risk asssociated with obstetric cholestasis

A

Maternal: vit k deficiency, increased risk PPH
Fetal: fetal distress, meconium, preterm labour, intracranial haemorrhage, still birth

68
Q

How is obestric cholestasis managed?

A
  • maternal vit k (esp if prolonged PT time)
  • neonatal vit k
  • fetal surveillance
  • emollients (diprobase) ursodeocycholic acid, antihistamine and calamine can reduce itching
  • LFTs every 2 weeks
  • if severe biochemical abnormalities they may be offered IOL/ C section after 37 weeks- but the evidence for this is poor
  • follow up LFTs 2 weeks after delivery, 2 weekly until normal (should resolve by 6-8 weeks)#
69
Q

Give 3 new onset/ reversible RFs for VTE that may occur during pregnancy

A
  • bone fractures
  • surgical procedure
  • hyperemesis, dehydration
  • OHSS, ART
  • immobility >3 days
  • long haul travel >4hrs
  • current systemic infection

Y4 ObGyn (8 decks)

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