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Paediatric Biochemistry > Pregnancy Monitoring > Flashcards

Pregnancy Monitoring Flashcards

1
Q

What are forms of Pregnancy Monitoring?

A

Non-biochemical monitoring

  • US, foetal heartbeat, bp, weight gain

Biochemistry

  • Monitoring of at-risk patients for diabetes, thyroid disease, liver disease
  • Testing in pregnancy for ectopic pregnancy, hydatidiform mole and choriocarcinoma
  • Monitoring pre-existing conditions during pregnancy
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2
Q

What are the implications of Pregnancy on Reference ranges?

A
  • Increased volume of distribution
  • Increased binding proteins
  • Increased requirements
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3
Q

What happens to calcium in Pregnancy?

A
  • Total calcium falls due to physiological hypoalbuminaema
  • Free ionised calcium does not change
  • Placenta produces 1,25-dihydroxyvitamin D resulting in increased absorption of calcium from the gut
  • Calcium is actively transported across the placenta, facilitated by PTH-rP
  • Foetal calcium homeostasis depends mostly on PTHrP
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4
Q

Who are the patients that need to be monitored in Pregnancy?

A
  • Diabetes
  • Thyroid disease
  • Liver disease
  • Pre-eclampsia syndrome

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5
Q

What is Gestational Diabetes?

A
  • Any degree of glucose intolerance resulting in hyperglycaemia with the onset during pregnancy
  • Screen at 24-28 weeks
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6
Q

What are risk factors for Gestational Diabetes?

A
  • Weight BMI>30 kg/m2
  • Family history of DM (1o relative)
  • Previous macrosomic baby >4.5 kg
  • Ethnic origin esp Asian, Black Caribbean
  • Previous GDM
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7
Q

How is Gestational Diabetes diagnosed?

A
  • Patients with risk factor oGTT at 24-28 weeks
  • (prev GDM, initial oGTT, rpt at 24-28 wks if normal)
  • Definition of GDM includes previous categories of gestational impaired glucose tolerance and GDM
  • Fasting glucose >5.6; 2hr glucose >7.8 mmol/L (N.B. can’t use HbA1c for diagnosis, or fasting glucose)
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8
Q

What is the treatment for Gestational Diabetes?

A
  • Diet, exercise, metformin, insulin as required
  • Weight loss advice for BMI >28 kg/m2
  • Maintain fasting glucose <5.3mmol/l, 2hr post- prandial <7.8mmol/L
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9
Q

What are possible causes of Gestational Diabetes Mellitus?

A

Human placental lactogen (hPL) – rises from 6th week of pregnancy to peak at approx 23 weeks

  • Increases breakdown of maternal fat to increase fatty acids as energy source (glucose for foetus)
  • Increase in insulin release from pancreas (poss increase in peripheral resistance)
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10
Q

What are thyroiid diseases in Pregnancy?

A

Hyperthyroidism - differential diagnosis:

  • Hyperemesis gravidarum
  • Thyroid disease (Usually Graves, affects approx 1:1500 pregnancies)

Hypothyroidism

  • Hashimoto’s thyroiditis

N.B. Post partum thyroiditis

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11
Q

What is Post Partum Thyroiditis?

A
  • Develops within a couple of months of birth
  • Transient hyperthyroid followed by hypothyroid state, resolves spontaneously without treatment
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12
Q

Whya re thryoid hormones affected by Pregnancy?

A

hCG

  • Weak thyroid stimulating action of hCG due to structural similarity with TSH. The beta subunit of both molecules are similar. Has 1/10,000th of activity of TSH
  • See clinical effects if hCG>200 U/L for several weeks (note hCG>25U/L consistent with pregnancy)
  • Can see slightly low TSH, high normal free T4/T3 in first trimester when hCG highest

TBG

  • Total T4/T3 affected by increased TBG in pregnancy caused by oestrogen
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13
Q

Why does hCG have the same effect as some Pituitary Hormones?

A
  • hCG, TSH, LH, FSH have common alpha subunit
  • hCG and TSH structurally similar beta subunit
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14
Q

What is Hyperemesis Gravidarum?

A
  • Excessive vomiting in pregnancy”
  • Usually first trimester
  • Asians greater incidence than caucasians
  • Believed to be related to high hCG, aetiology unknown
  • Most cases spontaneously resolve by second trimester
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15
Q

How is Hyperemesis Gravidarum differentiated from other thyroid disorders?

A
  • Can be difficult to distinguish between HG and thyrotoxicosis as 2/3 are transiently biochemically hyperthyroid
  • TRABs negative in HG, positive in Graves’ disease
  • Generally managed with fluid replacement, rarely require beta blockers or anti-thyroid meds
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16
Q

What are features of Obstetric cholestasis?

A
  • Liver disorder unique to pregnancy; describes association between liver dysfunction and pruritus
  • Occurs in third trimester but pathogenesis still unknown.
  • Genetic element
  • Role of oestrogen as highest in third trimester – cases also described
  • Affects approx 0.7 % pregnancies, (1.2-1.5% Asian pregnancies)
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17
Q

What are symptoms and investigations of Obstetric Cholestasis?

A
  • Pruritus (itch) common in pregnancy (23% affected)
  • Obstetric cholestasis should be suspected in cases of pruritus of unexplained origin in absence of a rash, esp palms of hands or soles of feet, with abnormal LFTs and/or raised bile acids
  • If LFT/bile acids normal repeat 1-2 weekly as pruritis may predate rise.
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18
Q

What are risk factors for Obstetric Cholestasis?

A
  • Previous history (45-90% recurrence)
  • Family history
  • Multiple pregnancies
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19
Q

What are adverse foetal outcomes for Obstetric Cholestasis?

A
  • Increased intrauterine mortality
  • Increased spontaneous (and iatrogenic) premature birth
  • Increase intracranial haemorrhage secondary to vitamin K deficiency (fat soluble vitamins affected by disordered bile acid metabolism)
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20
Q

What is the treatment for Obstetric Cholestasis?

A
  • Topical
  • Antihistamines
  • Ursodeoxycholic acid (+vit K)
  • Conservative management (monitoring weekly)
  • Consider elective delivery from 37 weeks
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21
Q

What happens post partum in Obstetric Cholestasis?

A

Repeat 2wks, if LFT/bile acids still increased at 8wks refer

22
Q

Describe Bile Acid biochemistry

A
  • Family of acidic sterole based of C24 cholaninc Acid.
  • Synthesised from cholesterol in the liver to form primary bile acids
  • 7-alpha hydroxylation is rate limiting tep in bile acid synthesis
  • Amphilic compounds – hydrophilic underside & hydrophobic topside
  • Conjugated with glycine or taurine (decrease pKa)
23
Q

What is the function of Bile Acids?

A

Function as biological detergents:

  • Solubilise cholesterol & lipids in bile
  • Emulsification & absorption of dietary fat (Vit K)
24
Q

What are Biochemistry results for patients with Obstetric Cholestasis?

A
  • Bile acids >14 umol/L
  • AST/ALT/γGT may be raised
  • bilirubin usually normal (jaundice rare)
  • ALP rise due to pregnancy isoform
  • In absence of other cause of liver disease e.g. pre eclampsia, viral esp hep C, alcohol, gallstones, autoimmune
  • Other investigations viral hep A,B,C, EBV,CMV; AMA, ASMA; urine PCR; bp; liver US
25
Q

What is HELLP syndrome?

A
  • Haemolysis
  • Elevated Liver Enzymes
  • Low Platelets)
26
Q

What are features of HELLP syndrome?

A
  • Affects 0.2-0.6% pregnancies
  • Affects 10-20% women with pre eclampsia
  • Cause unknown ?separate condition or severe form of pre eclampsia
  • Usually presents at >37 weeks but may present post partum
  • 1:4 risk of recurrence with future pregnancies
27
Q

What are the biochemistry results for HELLP syndrome?

A
  • Haemolysis: Fractured red cells on blood film (LDH >600 IU/L) [Ref range 20-220IU/L]
  • Liver Enzymes: AST/ALT >70 IU/L, (increases morbidity/mortality if >150) [Ref range 5-45 U/L]
  • Bilirubin: often increased
  • Low Platelets: need to distinguish from gestational thrombocytopenia where platelet count drops to 7-150 x 109/L in 2nd/3rd trimester

CT scan may show bleeding in liver

28
Q

What are complications of HELLP syndrome?

A
  • DIC (disseminated intravascular coagulation)
  • Pulmonary oedema
  • Renal failure
  • Liver haemorrhage and failure
  • Placental abruption
29
Q

What is the treatment for HELLP syndrome?

A
  • Delivery, may require transfusion
  • Affects may continue post partum
30
Q

What are features of Acute Fatty Liver of Pregnancy?

A
  • Rare life-threatening disorder presenting in 3rd trimester or post-partum
  • Thought to be due to disordered metabolism of fatty acids caused by a deficiency in the mitochondrial LCHAD (long chain 3-hydroxyacyl coenzyme A dehydrogenase) enzyme
  • Mortality 10-20% maternal, 20-30% foetal
31
Q

What is the biochemstry of Acute fatty liver of pregnancy?

A
  • Bilirubin increased
  • Liver enzymes (AST/ALT): typically, >1000 IU/L (may be 300-500)
  • May also present with hypoglycaemia, raised WCC
  • Liver US may show fat deposition in liver
32
Q

What is Pre eclampsia syndrome?

A
  • Maternal syndrome of hypertension, proteinuria and oedema part of a severe systemic inflammatory response.
  • Although mechanism remains unclear, a major cause is the failure to develop an adequate blood supply to the placenta, leading to placental oxidative stress.
  • (See a rapid disappearance of clinical signs or symptoms following delivery of the placenta
33
Q

How is diagnosis of Pre-Eclampsia syndrome made?

A
  • Proteinuria (300 mg/d mild to severe >5g/d) [Ref range <150mg/d] or urine PCR>30mg/mmol [Ref <3]
  • with blood pressure >140 mmHg systolic; or >90 mmHg diastolic on 2 separate occasions

Other associated findings are Hyperuricaemia

34
Q

How are Placental Biomarkers produced?

A
  • Biomarkers produced by the trophoblastic cells of the placenta and pass into the maternal bloodstream where they can exert effects on the maternal metabolism.
  • Production of the placental biomarkers may be altered in placental dysfunction, so the concentration in maternal serum has the potential to be used clinically in the investigation of patients.
35
Q

What are some Placental Biomarkers?

A
  • PlGF (placental growth factor)
  • sFlt-1 (soluble fms-like tyrosine kinase-1)
  • sFlt-1:PlGF ratio
36
Q

What are features of PlGF (placental growth factor)?

A
  • Angiogenic hormone, 46-50kDa, involved in remodelling of arteries in uterus to increase blood supply to placenta (angiogenesis = growth of blood vessels)
  • In normal pregnancy, rises in maternal circulation peaking at 26-30 weeks, falling towards delivery
  • Lower concentrations associated with pre eclampsia
  • Can be measured with sFlt-1 (soluble fms-like tyrosine kinase-1
37
Q

What are features of sFlt-1 (soluble fms-like tyrosine kinase-1)?

A
  • Anti-angiogenic protein.
  • Truncated form of the VEGF receptor-1 (Flt-1) (VEGF= vascular endothelial growth factor)
  • Flt-1 binds both VEGF and PlGF
  • sFlt is important in blood vessel regulation in tissues such as kidney, uterus and cornea
  • Found to be abnormally increased in pre-eclampsia
38
Q

What does sFlt-1:PlGF ratio tell us?

A

High concentrations both of sFlt and sFlt:PlGF ratio associated with pre-eclampsia

39
Q

How does Pre-Eclampsia develop?

A
  • Placental ischemia results in the release of antiangiogenic factors (sFtl-1), which bind to vascular endothelial growth factor (VEGF) and placental growth factor (PlGF)
  • This prevents their interaction with their native high affinity kinase receptors on the vascular endothelium.
  • The resultant endothelial dysfunction prevents the development of an adequate blood supply.
  • Pre-eclampsia may be mediated, in part, by this imbalance of circulating angiogenic factors.
40
Q

What is Ectopic Pregnancy?

A
  • When foetus develops outside uterus usually in Fallopian tube
  • Affects approx 1% pregnancies
41
Q

What are the risk factors of Ectopic Pregnancy?

A
  • IUDs, progesterone only OCP, tubal ligation
  • Previous ectopic pregnancy (10-20% recurrence)
  • Pelvic, abdominal, tubal surgery
  • Previous PID
  • IVF, Ovulation induction
42
Q

How does Ectopic Pregnancy present?

A
  • 30% present prior to missed period
  • Pain (lower abdo)
  • May have positive pregnancy test
  • If ruptured then profuse bleeding into pelvis, vaginal bleeding insignificant leading to hypovolaemic shock (deaths in UK 0.2% of ectopic pregnancies, 2015)
  • Suspect if any of risk factors present
43
Q

How is an Ecotpic Pregancy Diagnosed?

A
  • Vaginal ultrasound can detect intrauterine pregnancy
  • In absence of intrauterine pregnancy may be miscarriage (vaginal bleeding should proceed pain) or ectopic pregnancy
  • hCG typically <1000 IU/L although can present higher
  • Normally at least double every 2.3d, lack of increase (but no decrease) suggests ectopic
  • Progesterone suggested (cut-off <48 or <70 nmol/L) as low in ectopic, negative predictive value poor
44
Q

What is the treatment for Ectopic Pregnancy?

A
  • Spontaneous abortion or degenerating ectopic usually managed conservatively
  • Methotrexate can be used to halt foetal growth
  • Surgical laparotomy may be required
  • Emergency if rupture- surgery plus fluid replacement
45
Q

What are features of Hydatidiform mole (gestational) and Choriocarcinoma trophoblastic neoplasia?

A
  • After surgery to remove mole 20% complete moles require further surgery or chemotherapy
  • Can develop into invasive moles or choriocarcinoma (8%)
  • Choriocarcinoma most frequently develops from complete moles but can occur after normal pregnancy or early foetal loss
  • More likely to metastasize
  • All moles go on National Hydatidiform Register (monitor hCG 99% sensitivity and specificity)
46
Q

What are features of Gestational trophoblastic neoplasia (GTN)?

A
  • Tumours which develop in the trophoblast cells surrounding the embryo
  • Can develop following a molar pregnancy or a normal pregnancy
  • Molar pregnancy cannot produce normal foetus
  • Suspect in bleeding in early pregnancy or in cases of persistent bleeding post delivery
47
Q

What is the most common types of GTN?

A
  • Hydatidiform mole (molar pregnancy)
  • <16 and >40 yrs most common, approx 1:1000
  • Moles are villi resembling bunches of grapes
48
Q

What are complete and partial moles?

A
  • Complete mole: When sperm fertilises an empty egg containing no nucleus or DNA
  • Partial mole: When 2 sperm fertilise an egg (too much DNA). Rarely become malignant or require further treatment
49
Q

How is Diagnosis of Hydatidiform mole (molar pregnancy) made?

A
  • High serum hCG (can be up to 6,000,000 IU/L)
  • Ultrasound
50
Q

How are pre-existing conditions monitored during pregnancy?

A
  • Any drug therapies stopped if contra-indicated or alternatives found
  • Monitoring of long term conditions more closely as pregnancy may exacerbate disorder. Increased volume of distribution or requirements
51
Q

How is Diabetes monitored as an example?

A
  • Increased risk to mother of pre eclampsia, miscarriage, preterm labour; risk to foetus of congenital defects, macrosomia, birth injury, perinatal mortality.
  • Advise HbA1c <48 mmol/mol (<6.5%) pre conception
  • Fasting blood glucose 5-7mmol/L, other times of day 4-7mmol/L
  • Stop oral hypoglycaemics, replace with metformin or insulin

Paediatric Biochemistry (31 decks)

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