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Kira - Mat Med > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Discuss Addison’s in pregnancy
-Pathophysiology
-Presentation
-Diagnosis
-Effect of pregnancy on Addison’s
-Effect of Addison’s on pregnancy
-Management in pregnancy

A
  1. Pathophysiology
    -Autoimmune destruction of adrenal gland leading to deficiency in (glucocorticoid) cortisol and (mineralcorticoids) aldosterone.
  2. Presentation
    -Hypotension, salt wasting, skin pigmentation, weight loss
    -Associated with other autoimmune disease - T1DM, Graves
  3. Diagnosis
    -Loss of cortisol response to ACTH (Synacthen test)
    -Hyperkalemia, hyponatremia, hypocalcemia
    -Low morning cortisol (can be WNL in pregnancy)
  4. Effect of pregnancy on Addison’s
    -May mask symptoms but doesn’t generally affect it
    -May deteriorate PP
  5. Effect of Addison’s on Pregnancy
    -No effect
    -Adrenal antibodies do cross placenta but very rare to have adrenal insufficiency
  6. Management in pregnancy
    -Need to replace glucocorticoids and mineralocorticoids (hydrocortisone and fludrocortisone)
    -Need stress dosing if hyperemesis, infection, stressful events
    -Need stress dosing for labour
    -Watch for profound hypotension with fluid shifts and diuresis PP. Manage with IV Saline
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2
Q

Discuss Conns in pregnancy
-Pathophysiology
-Presentation
-Diagnosis
-Management in pregnancy

A
  1. Pathophysiology
    -Caused by primary hyperaldosteronism due to adrenal hyperplasia/adenoma/carcinoma
  2. Presentation
    -Hypertension, hypokalemia
  3. Diagnosis
    -High aldosterone
    -Hypernatremia, hypokalemia
  4. Management in pregnancy
    -Control BP - manage same as chronic HTN
    -Replace potassium
    -Avoid ACEi and spironolactone as cause feminisation of male fetus.
    -Defer surgery until after pregnancy
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3
Q

Discuss congenital adrenal hyperplasia in pregnancy
-Pathophysiology
-Presentation
-Diagnosis
-Effect of CAH on pregnancy
-Effect of pregnancy on CAH
-Management in pregnancy

A
  1. Pathophysiology
    -Autosomal recessive condition with lack of adrenal enzymes.
    -90% caused by lack of 21-hydrolase enzyme. Results in low cortisol and aldosterone and high androgens
  2. Presentation for classic
    -Masculinisation of female fetus, salt wasting crisis as neonate
  3. Diagnosis
    -17 hydroxyprogesterone levels are elevated
    -Synacthen test. Cortisol will not respond to ATCH
  4. Effects of CAH on pregnancy
    -Increased miscarriage rates
    -IUGR
    -CS due to CPD from android pelvis
    -PET, GDM
  5. Effects of pregnancy on CAH
    -Increased risk of female fetus having CAH and virilisation of genitalia
  6. Management in pregnancy
    -Pre-pregnancy counselling for genetics
    -Continue fludrocortisone and hydrocortisone replacement in pregnancy
    -Stress dose for hyperemesis, infection, labour
    -Monitor for PET
    -Consider dexamethasone from early pregnancy (before 6 weeks) to avoid virilisation of female fetus genitalia. Stop once sex known to be male as don’t need or CVS/Amnio show fetus not affected. Dexamethasone is not without fetal complications. Needs careful counselling
    -Growth scans
    -OGTT
    -MDT - MFM, endocrinologists
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4
Q

Discuss management of phaeochromocytoma in pregnancy
-Pathophysiology
-Presentation
-Diagnosis
-Effects of phaeo on pregnancy
-Effects of pregnancy on phaeo
-Management

A
  1. Pathophysiology
    -Tumour of the adrenal medulla producing excess catecholamines
  2. Presentation
    -Paroxysms of hypertension
    -Headache
    -Palpitations
    -Sweating
    -Anxiety
    -Can mimic PET
  3. Diagnosis
    -Raised 24hr urinary catecholamines
    -USS or MRI (best) to localise tumour (10% extramedullary)
  4. Effects of phaeo on pregnancy
    -Increased maternal and fetal mortality (25-60% if undiagnosed)
    -Increased risk of arrythmia, CVA, pulmonary oedema, cardiogenic shock
    -Increased risk GDM
    -IUGR, acute/ chronic hypoxia, Abruption
  5. Effect of pregnancy on Phaeo
    -Potentially fatal HTN crises stimulated by labour, delivery, or pressure of gravid uterus on tumour when supine
  6. Management
    -MDT - endocrine, obstetrics, anaesthetics, neonatologist, surgeons
    -Alpha blockade with prazosin / phenoxybenzamine
    -Beta blockade for arrythmia but only once alpha blockers used.
    -Cautions with meds which increase BP - metocloprimide, phenothiazides
    -Surgical removal either <23 weeks or PP
    -Delivery by CS. Half the risk of maternal mortality
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5
Q

What are the mechanisms in pregnancy which increase risk of DKA (4)

A

-Increased insulin resistance from placental hormones (human placental lactogen, cortisol, prolactin and progesterone)
-Increased carbohydrate absorption with reduced gut motility
-Predisposition for starvation with increased metabolic demands from utero-placental unit resulting in decreased fasting glucose and predisposition to ketoacidosis
-Limited buffering in blood with reduced bicarb (Increased renal loss), Predominance of respiratory alkalosis

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6
Q

What are the possible causes of DKA in pregnancy (5)

A
  1. Insulin withdrawal - faulty pump, non compliance
  2. New T1DM
  3. Increased metabolic demands - sepsis, trauma
  4. Reduced absorption - hyperemesis, fasting
  5. Drugs - beta mimetics, steriods
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7
Q

Discuss gestational diabetes
-Definition
-Incidence
-Risk factors (7)

A
  1. Definition
    Impaired glucose tolerance with onset or first recognition in pregnancy.
  2. Incidence
    -10%
  3. Risk factors
    -PCOS
    -FHx of >1 first degree relative with diabetes
    -Previous GDM or macrosomia
    -Medications - steroids, antipsychotics
    -Obesity >30 BMI
    -Ethnicity - Asian, Indian, Maori, Pacific, Aboriginal
    -Advanced maternal age >40
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8
Q

Describe antenatal screening for GDM
-RANZCOG recommendation
-Australian cut offs for GDM
-Time for testing - high risk, and average risk

A
  1. RANZCOG recommendations
    -2hr 75g diagnostic test (no screening test)
  2. Australian cut offs
    -Fasting glucose >5.1
    -1Hr Glucose >10
    -2Hr Glucose >8.5
  3. Time for testing
    -Women at high risk - OGTT at first opportunity after conception and if negative 24-28 weeks
    -Average risk women - OGTT 26-28weeks
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9
Q

Describe the New Zealand diagnostic pathway for GDM
-First antenatal HbA1c
-Screening cut off
-Diagnostic cut off

A
  1. First antenatal HbA1c
    -HbA1c >=50 - probable undiagnosed diabetes. Immediate referral to specialist diabetes clinic. (WHO says >=48)
    -HbA1c < = 40 - GCT
    -HbA1c 41-49 - OGTT
  2. GCT
    -Positive if >=7.8 - proceed to OGTT
    - >11.1 = diagnostic for GDM
  3. OGTT
    -Fasting >= 5.5
    -2 hr >= 9.0
    - Do OGTT directly if: BMI >30, Prev GDM, 1st degree relative with DM
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10
Q

Discuss risks associated with GDM
-Risk to mother during pregnancy (5)
-Risk to fetus
-Risk to mother PP

A
  1. Risk during pregnancy.
    -HTN, PET, CS, SD, Birth injury, PPH
    -At risk of all same issues as T2DM but to a much lesser degree
  2. Risks to fetus
    -IUGR, Macrosomia, NICU admissions, neonatal hypoglycemia,
    -Not associated with congenital abnormalities
  3. Maternal risks PP
    -40-60% chance of developing T2DM in 10-15yrs
    -30% risk of recurrent GDM
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11
Q

Discuss antenatal management of GDM
-Lifestyle advice
-Aim for glucose
-Medical management
-Fetal surveillance
-Maternal surveillance

A
  1. Lifestyle advice
    -Dietary - reduce fat, increase fibre, low GI foods
    -Moderate exercise 30mins / day
    -Weight gain - if BMI >30 aim 5-9kg
  2. Glucose targets
    -Fasting <5
    -1hr post food <7.4
    -2hrs post food <6.7
  3. Medical management
    -If levels persist above target for >2weeks consider medical
    -Metformin: contra-indicated in IUGR, PET, Inadequate maternal wt gain. Crosses placenta. Not teratogenic
    -Short acting insulin to bring down post parandial levels
    -Intermediate acting to bring down high fasting levels
  4. Fetal surveillance
    -GS at time of diagnosis and 36-37 weeks
  5. Maternal monitoring
    -PET - BP and urinalysis
    -BGL
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12
Q

Discuss timing of delivery for GDM

A
  1. If GDM without complications - IOL at 40/40
  2. If GDM with co-morbidities Aim IOL 38-39/40 (Macrosomia +/- poorly controlled diabetes)
  3. If GDM and EFW >4.5kg offer CS
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13
Q

Discuss labour and postpartum management of GDM
-Labour management
-Postpartum management

A
  1. Labour management
    -Stop insulin when in labour
    -If high BSL consider GIK
    -Hourly BSL should be 4-7
  2. Postpartum management
    -Following delivery stop insulin and all oral agents
    -Monitor BSL for 24hrs to make sure no ongoing hyperglycemia
    -Monitor baby’s BSL 1-2hrs after birth
    -Discuss risk of GDM recurrence and T2DM in later life (up to 90%)
    -HbA1c 3 months PP
    -HBA1c or OGTT two yearly
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14
Q

What are the parameters for diagnosis of DM
-HbA1c parameters (2)
-Glucose levels (3)

A
  1. -HbA1c 41-49 = pre diabetes
    -HbA1c 50 or more = diabetes
  2. Glucose levels
    -Random glucose >11
    -Fasting glucose >7
    -2 hr 75mg OGTT >11
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15
Q

What are the effects of pregnancy on diabetes (9 effects)

A
  1. Increased insulin requirements - 2x higher in term T1DM
  2. Increased risk of diabetic nephropathy - 30% if HTN
    -If mild pre-existing nephropathy often reversible. If severe not reversible
  3. Increased risk of progression to retinopathy
    -T1DM >T2DM
    -10% increased risk of progression if mild retinopathy
    -50% increased risk of progression if proliferative retinopathy
  4. Increased risk of HTN
  5. Increased risk of hypoglycemia
    -Better control
    -Increased insulin sensitivity in first trimester
    -Increased unawareness of hypoglycemia
  6. Diabetic ketoacidosis.
    -Rare in pregnancy
    -Triggered by infection, steroid use, hyperemesis
  7. Worsening of autonomic neuropathy
  8. Worsening of Gastric paresis
  9. Normocytic normochromic anaemia
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16
Q

What are the effects of diabetes on pregnancy for mothers (6 effects)

A
  1. Increased miscarriage
  2. HTN and PET 3-4 x risk
  3. Infections
  4. Mode of delivery - more IOL and CS
  5. Increased perineal injury
  6. PPH if macrosomic
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17
Q

What are the effects of diabetes on pregnancy for fetus (11 effects)

A
  1. Congenital abnormalities
    -4% incidence. 2 fold increase. 22% chance
    -Cardiac 3 times risk
    -NT defects 3 x risk
    -Sacral agenesis - rare but specific to DM
    -Situs inverts, renal anomalies
    -Increased risk with increased HBA1c
  2. Macrosomia
    -Related to blood sugar control but can still have with excellent control
  3. Polyhydramnios
    -Related to fetal polyuria
    -Increased risk of PTL, PPROM, Cord prolapse
  4. Sudden intrauterine fetal demise - 5 fold increase
    -Due to chronic hypoxia from accelerated metabolism
    -High O2 requirements
    -Uteroplacental vasculopathy
    -Highest risk at term. RR 7.2
    -CTG, BPP and doppler don’t predict
  5. PTD - 5 times more likely to be born before 37/40
  6. Shoulder dystocia - 8% vs 3% in general population. Increased risk at any weight
  7. Fetal distress in labour
  8. Jaundice - polycythemia
  9. Respiratory distress syndrome
  10. Erbs palsy - 10 times risk
  11. IUGR from impaired placental perfusion
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18
Q

Discuss management of women with diabetes: preconception (9 points)

A
  1. Basic advice: smoking, exercise, optimise wt, immunisations
  2. Optimise BSL. Aim for HbA1c <48. Advise better outcomes with better control (miscarriage, anomilies, macrosomia, IUFD)
  3. Stop sulphonylureas. Switch to insulin
  4. Retinal screening - treat if proliferative retinopathy
  5. Renal function - BP, Cr, Urinalysis. If Cr >125 advise against pregnancy
  6. Assess cardiovascular risk.
  7. Stop statins and ACEi / switch if required
  8. Commence on 5mg folic acid
  9. Advise against pregnancy if IHD, untreated proliferative retinopathy, severe gastroparesis, severe renal impairment
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19
Q

What is the risk of a child having T1DM if:
1. The mother has it
2. The father has it
3. Both parents have it

A
  1. 2-3%
  2. 6-9%
  3. 20-30%
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20
Q

Discuss antenatal care for women with diabetes (7)

A
  1. MDT based care with obstetrician, physician, dietician, diabetic educator
  2. Education on diet and physical exercise.
  3. BSL monitoring
    -HBA1c once a trimester
    -Aim 4.0-5.3 fasting BSL
    -Aim <7.8 1 hr post parandial
  4. Hypoglycemia management
    -Discuss risks
    -Avoid starvation
    -Educate partner
    -Have hypo kits available
  5. Pre-eclampsia prevention
    -Aspirin 100mg PO OD 12-36 weeks
    -Calcium 1.5 g PO OD 12 weeks onwards
    -BP and urinalysis each visit
  6. Retinal screening in first trimester +/- 3rd trimester
  7. Renal screening - serum Cr and PCR each trimester
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21
Q

Discuss fetal monitoring in diabetic women (6)

A
  1. Early dating scan for accurate dating
  2. Nuchal translucency - can help for cardiac anomalies
  3. Detailed anatomy 18-20. Can consider at 16/40 in addition to 20/40 anatomy scan if high risk or obese
  4. Fetal echo 24/40
  5. Growth scans at minimum 28,32,36 weeks
  6. Weekly CTG from 34/40
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22
Q

Discuss intrapartum care of diabetic women
1. Mode of delivery
2. Timing of delivery
3. BSL control

A
  1. Mode of delivery
    -Aim for vaginal birth
    -If EFW >4.5kg offer CS - risk of shoulder dystocia
  2. Timing
    -By term in DM without complications
    -After 37 weeks depending on situation
    -If delivering before 34 weeks may need GIK infusion with steroids
    -Need to consider risk and benefits of delivery/prematurity
  3. BSL control
    -Hourly BSL monitoring aiming for 4-7 BSL
    -Sliding scale of short acting insulin and dextrose infusions
    -Give reduced long acting (1/2 to 1/3) and stop short acting insulin in labour or pre CS
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23
Q

Discuss post-partum care for diabetic women
1. T1DM women
2. T2DM women
3. Other PP care

A
  1. T1DM women
    -Half insulin infusion after delivery if T1DM.
    -Once eating normally can recommence pre-pregnancy sub cut regimen
    -If breast feeding insulin dose reduced
  2. T2DM women
    -Recommend pre-pregnancy medications
    -May need insulin if breast feeding
  3. Other care
    -Check neonatal BSL at hr and pre feeds
    -Contraceptive advice
    -Life style advice
    -Biannual diabetes FU
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24
Q

Describe the physiological changes in pregnancy regarding calcium metabolism
-Is pregnancy hypocalcemic or hypercalcemic state?
-How does that state occur
-How is that state counter balanced

A
  1. Pregnancy is a relatively hypocalcemic state
  2. Hypocalcemia is driven by:
    -Increased fetal uptake of calcium
    -Increased maternal renal losses
    -Reduced serum albumin so reduced protein bound calcium
  3. Hypocalcemia is counter balanced by:
    -Increased PTH
    -PTH reduces renal clearance from kidneys
    -PTH increase intestinal absorption of vit D
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25
Q

Describe hyperparathyroid in pregnancy
-Epidemiology
-Causes
-Clinical features
-Diagnosis

A
  1. Incidence
    -Third most common endocrine disorder
    -Rare in pregnancy 8:100,000
    -Complications to mother 70%, complications to fetus 80%
  2. Causes
    -Adenomas, hyperplasia
  3. Clinical features
    -thirst, fatigue, constipation, depression, renal calculi, pancreatitis, HTN
  4. Diagnosis
    -Raised calcium, Raised PTH
    -USS of the neck to look for adenomas
26
Q

How does pregnancy affect hyperparathyroidism (3)

A
  1. Improvement in hypercalcemia as pregnancy is a hypocalcemic state
  2. Increased risk of pancreatitis
  3. Risk of acute hypercalcemic crisis especially post-partum due to abrupt end to calcium transfer to fetus
27
Q

How does hyperparathyroidism affect the pregnancy (8)

A
  1. Increase in miscarriage
  2. IUFD
  3. PTL
  4. HTN and PET
  5. Polyhydramnios
  6. Suppression of fetal PTH by high maternal calcium can lead to fetal hypocalcemia and tentany
  7. Acute neonatal hypocalcemia
  8. IUGR
28
Q

How should hyperparathyroid be manged in pregnancy

A
  1. Surgery
  2. If mild and asx can be conservative
    -Encourage low calcium diet and increase PO fluid intake
  3. Forced diuresis to increase renal clearance
    -Loop diuretics- frusemide
    -Dialysis if hypercalcemia is very severe
29
Q

Discuss hypoparathyroid disorder in pregnancy
-Cause
-Diagnosis
-Impact of pregnancy on hypoparathyroidism
-Impact of hypoparathyroidism on pregnancy
-Management

A
  1. Cause
    -Autoimmune disease or complication of thyroid surgery
  2. Diagnosis
    -Low Ca and PTH
  3. Effect of pregnancy on hypoparathyroism
    -Increased demand for vit D cannot be met. Need supplements
  4. Effect of hypoparathyroid on pregnancy
    -Increased miscarriage
    -Fetal hypocalcemia
    -Secondary hyperparathyroidism
    -Bone demineralisation and ricketts
  5. Management
    -Vit D and calcium supplements
    -Calcium and albumin levels monthly
    -Reduced vit D dose PP
    -Refer to endocrine
    -D/W Neonatologists for PP testing
30
Q

Discuss vitamin D deficiency
-Levels and severity (3)
-Risk factors (10)

A
  1. Levels and severity
    -Profound deficiency - <25nmol/L
    -deficient - <50nmol/L
    -Insufficient <75nmol/L
  2. Risk factors
    -Vegan diet
    -Pigmented skin
    -Covered skin
    -Regular sun screen use
    -Obesity >30 BMI
    -Antiepileptic drugs
    -Liver or renal impairment
    -Alcoholism
    -Short birth interval
    -Malabsorption
31
Q

What is the impact of low vitamin D levels of pregnant women (7)

A
  1. Increased risk of reduced weight gain
  2. Hypocalcemia
  3. Osteomalcia
  4. GDM
  5. PET
  6. HTN
  7. CS delivery
32
Q

What is the impact to the fetus of low vit D levels

A
  1. Poor fetal bone health
  2. Hypocalcemia and neonatal tetany
  3. Childhood asthma
  4. SGA
33
Q

What are the RANZCOG guidelines for vit D supplementation (5)

A
  1. Do not test for vit D levels as part of routine AN screening unless maternal risk factors
  2. Do not re-test vit D in pregnancy irrespective of level
  3. Advise all women to take 400IU of vit D daily during pregnancy
  4. Advise women about safe sun exposure
  5. Exclusively breastfed infants should be given 400IU daily of vit D for at least the first 6 months of life. Not required in formula fed.
34
Q

What does the research show regarding vit D supplementation (2 points)

A
  1. 2 big RCT found no improvement to neonatal or obstetric outcomes with supplementation
  2. Does improve wheeze in children up to 3 yrs
35
Q

Discuss hyperprolactinemia in pregnancy
-Epidemiology
-Causes (3 groups)
-Clinical features
-Diagnosis

A
  1. Epidemiology
    -Prolactin adenomas are the most common type of pituitary tumour in pregnancy
    -Prolactinoma’s are rare 1:4500 pregnancies
  2. Causes of hyperprolactinemia
    -Decreased dopamine antagonism
    -Dopamine antagonists (metocloprimide, phenothiazides)
    -Increased prolactin production
    -Pituitary micro/macroadenomas
    -Increased lactotrophs
    -Breastfeeding
    -Decreased prolactin clearance
    -Chronic liver and renal disease
  3. Clinical features
    -Menstrual irregularities
    -Galactorrhoea
    -Infertility
    -Frontal headache, visual field changes
  4. Diagnosis
    -High serum prolactin (not reliable in pregnancy)
    -Visual field testing
    -Brain MRI
36
Q

What is the effect of pregnancy on prolactinomas (2)

A
  1. Risk of enlargement during pregnancy
    -Highest risk with untreated macroadenomas
  2. Regression following cessation of breast feeding
37
Q

What is the effect of prolactinomas on pregnancy (3)

A
  1. Infertility - treatment with dopamine agonist can help conception
  2. No impact on pregnancy
  3. No impact on lactation
38
Q

Discuss management of prolactinomas in pregnancy
-Pre-conception
-Antenatal
-Intrapartum
-Postnatal

A
  1. Pre-conception
    -Treat with dopamine receptor agonist or surgery
    -Avoid pregnancy until treated (Meds not tetarogenic)
  2. Antenatal
    -If microadenomas - stop dopamine agonists
    -If macroadenomas - continue. Can use carbergoline or bromocryptine.
    -If develop sx for visual field testing and MRI
  3. Intrapartum
    -Nil changes to routine care
  4. Postpartum
    -Dopamine agonists may suppress lactation
    -Lactation is safe
39
Q

Discuss the fetal pituitary thyroid axis
-Fetal metabolism T4
-Fetal reliance on maternal T4
-Fetal reliance on maternal iodine

A
  1. Maternal T4 crosses the placenta and the fetus converts T4 to T3 in the brain
  2. Fetus needs T4 until 12/40 then limited transfer of maternal thyroid hormones
  3. Fetus thyroid control becomes independent of mother by 12/40
  4. Fetus needs maternal iodine for whole pregnancy
40
Q

What thyroid hormones, thyroid medications and antibodies:
-Cross the placenta (4)
-Don’t cross the plalcenta (3)

A
  1. Cross the placenta
    -TSI (thyroid stimulating immunoglobulin - Graves)
    -Small T3/T4 until 12/40
    -PTU (less than carbimazole)
    -Carbimazole
  2. Doesn’t cross the placenta
    -TSH
    -TPO (Thyroid peroxidase antibody - (Hashimoto’s or Graves)
    -Thyroxine
41
Q

Discuss hyperthyroid disease in pregnancy
-Incidence in pregnancy
-Causes (4)
-Clinical presentation
-Diagnosis

A
  1. Incidence = 0.2%
  2. Causes
    -Graves -85% of cases - autoimmune disorder with TSI stimulating TSH receptor on thyroid gland
    -Toxic multi nodular goitre
    -Thyroiditis
    -Thyroid cancer
    -Drugs - amiodarone, lithium, iodine
    -TSH producing adenoma, HCG producing tumor, teratoma
  3. Clinical presentation
    -Can look like pregnancy - heat intolerance, palpitations, vomiting, tachycardia, palmar erythema
    -Discriminating features - weight loss, tremor, lid lag, exopthalmus (Graves)
  4. Diagnosis
    -Low TSH high free T4
    -Difficult to diagnosis in early pregnancy secondary to biochemical supression of TSH by HCG
    -TSI positive suggests graves
    -TRAB (Thyroid receptor antibodies) - Graves
42
Q

What is the effect of pregnancy on hyperthyroidism (4)

A
  1. Exacerbation in first trimester (Increased HCG or decreased absorption of medication)
  2. Improvement in 2nd and 3rd trimester due to immunosuppression
  3. Postpartum - may have exacerbation
  4. Labour, CS or infection can precipitate a thyroid storm
43
Q

What is the effect of hyperthyroidism on pregnancy
-Maternal effects (6)
-Fetal effects (7)

A
  1. Maternal effects
    -If well controlled outcomes are good
    -If poorly controlled: HTN, PET, Abruption
    -Subfertility
    -Tachycardia and heart failure
    -Thyroid storm especially around delivery
    -Retrosternal goitre causing tracheal obstruction and difficult intubation
  2. Fetal effects
    Untreated hyperthyroidism
    -Miscarriage
    -Congenital abnormalities - oesophageal atresia, aplasia cutis
    -Fetal goitre
    -Fetal tachycardia, hydrops and cardiac failure
    -IUGR
    -PTD
    -Perinatal mortality
    -Antithyroid medication (Carbimazole >PTU) can cross the placenta and cause fetal hypothyroidism, agranulocytosis
    -Carbimazole can cause aplasia cutis
    -TSI can cross the placenta and cause fetal hyperthyroidism
44
Q

Describe the management of hyperthyroidism in pregnancy
-Pre-conception (2)
-Antenatal (9)
-Intrapartum (1)
-Postpartum - fetal monitoring (3) and maternal monitoring (2)

A
  1. Pre-conception
    -Aim for euthyroid for 3 months before conception
    -Smoking cessation - makes exopthalmus worse
  2. Antenatal
    -Continue medication if pre-existing disease at lowest does to maintain euthyroid status with T4 at upper limit of normal
    -If new diagnosis in pregnancy treat with high dose PTU daily for 4-6 weeks then reduce to lowest dose to maintain
    -If new diagnosis in pregnancy consider propranalol for sympathetic control
    -Monitor maternal TFTs monthly to three monthly
    -Monitor LFTs monthly if on PTU (can cause liver toxicity)
    -Monitor fetal growth, heart rate
    -Scan for fetal goitre
    -Measure maternal TSI/TRAB early and late in pregnancy(high levels associated with fetal hyperthyroidism)
    -Radioactive iodine in pregnancy and breastfeeding is contra-indicated
    -Consider thyroidectomy if resistant to medical intervention or sx of airway obstruction
  3. Intrapartum
    -Monitor for sx of a thyroid storm
  4. Postpartum
    -Cord bloods for TFTs and TRAB
    -Monitor fetal sx for signs of hyperthyroidism
    -Treat with anti thyroid medication. Self limiting until TSI cleared
    -Monitor maternal TFT 6 weeks and3 months
    -Encourage breastfeeding. Safe with carbimazole and PTU at low doses. PTU preferrable
45
Q

Discuss hypothyroidism in pregnancy
-Incidence (2)
-Causes (4)
-Symptoms
-Diagnosis

A
  1. Incidence
    -Subclinical hypothyroidism 3%
    -Overt hypothyroidism 1%
  2. Causes
    -Autoimmune causes - TPO antibodies (Thyroid peroxidase antibodies). Hashimoto’s thyroiditis (Most common cause), atrophic thyroiditis
    -Iodine deficiency (Second most common cause)
    -Iatrogenic - post surgery, drugs
    -Secondary - Sheenan’s syndrome
    -Transient - subacute de Quervains or postpartum thyroiditis
  3. Symptoms
    -Overlap with pregnancy - weight gain, lethargy, hair loss, dry skin, constipation, fluid retention, goitre
    -Discriminatory - cold intolerance, bradycardia
  4. Diagnosis
    -TSH levels most important.
    -TSH of 4 is the upper limit of normal in all trimesters
    -Overt - TSH >2.5 + low T4 or TSH >10
    -Subacute TSH 2.5-10 normal T4
    -TPO antibodies confirms autoimmune cause but also present in 20% of normal population
46
Q

Effect of pregnancy on hypothyroidism (1)

A
  1. No effect
47
Q

Effect of hypothyroidism on pregnancy
-When well controlled
-Maternal effects if untreated (5)
-Fetal effects if untreated (6)

A
  1. Effects to pregnancy when well controlled
    -Nil effects if treated and euthyroid
  2. Effects to mother if untreated
    -Subfertility
    -Miscarriage
    -PET
    -Abruption
    -PPH / Anemia
    -Postpartum depression
    -Prematurity, perinatal mortality
  3. Fetal effects - if untreated - very rare
    -Growth restriction/ LBW
    -Still birth
    -Reduced neurodevelopment and IQ
    -Cretinism
    -Miscarriage
    -Fetal goitre
48
Q

Discuss management of hypothyroidism in pregnancy
-Pre-conception (4)
-Antenatal (5)
-Postpartum (4)

A
  1. Management preconception
    -Check TFTs and optimise control
    -Advise delay of pregnancy until good control is achieved
    -Routine screening and treatment for subclinical hypothyroidism not recommended. No difference to outcomes
    -Screen women with T1DM or lupus as high correlation
  2. Antenatal management
    -If pre-existing disease: Continue thyroxine to maintain euthyroid state
    -If newly diagnosed commence on 100cmg of levothyroxine
    -Check TFTs each trimester and 4-6 weeks post dose adjustment
    -Test TSI/TRAb if iatrogenic hypothyroid and previously managed for graves as still have Abx and can cross to fetus causing hyperthyroidism
    -Monitor fetal growth
  3. Postpartum care
    -Check TFT
    -Up to 75% with TPO develop postpartum thyroiditis
    -Monitor for postpartum depression
    -Screen neonate for TSH
49
Q

Discuss post partum thyroiditis
-Incidence (2)
-Causes (2)
-Clinical features
-Diagnosis

A
  1. Incidence
    -5-10% of pregnancies
    -3x higher in women with T1DM
  2. Causes
    -Autoimmune destruction of the thyroid gland
    -Occurs in 50 -75% of women with TPO antibodies
  3. Clinical features
    -Usually presents 3-6months postpartum
    -Sx often vague
    -Biphasic with transient hyperthyroidism then prolonged hypothyroidism
    -50% have small painless goitre
  4. Diagnosis
    -TFTs
    -Check TSI/TRAb to distinguish from Graves flare
    -Radioactive iodine scan - increased uptake in graves. Reduced uptake in postpartum thyroiditis. (Avoid Breastfeeding for 24hrs)
50
Q

How should postpartum thyroiditis be managed (4) and what is the prognosis

A
  1. Management
    -Spontaneous recovery by 1 yrs
    -Treatment depends on sx not TFTs
    -If Hyperthyroidism - beta blockers
    -If hypothyroidism - thyroxine. Withdraw after 6-9 months to check recovery. If ongoing high TSH for 5yrs treatment
    -Yearly TFT to determine if developing hypothyroidism
  2. Prognosis
    -3-4% remain hypothyroid
    -10-25% have recurrent postpartum thyroiditis
    -20-40% with TPO Abx develop overt hypothyroidism within 5 yrs
51
Q

What are the RANZCOG recommendations for hypothyroid management in pregnancy (7)

A
  1. Women should take 150mcg iodine daily if planning pregnancy, are pregnant and are breastfeeding
  2. Targeted testing for overt hypothyroidism is recommended in pregnancy
  3. Women who have a personal history of thyroid disease or T1DM should be tested with TSH and T4
  4. Overt hypothyroidism should be treated in pregnancy
  5. Overt hypothyroidism is defined as TSH above the reference range with a decreased T4 or TSH >10mIU/L irrespective of T4 levels
  6. Screening for subclinical hypothyroidism or TPO antibodies and subsequent treatment with levothyroxine is not recommended
  7. Treatment of TPO antibodies in Euthyroid women does not reduce miscarriage rate and is not recommended
52
Q

Discuss the HAPO trial
-Primary aim
-Study type
-Study population / inclusion criteria
-Study methodology

A
  1. Primary aim
    To investigate the impact of maternal hyperglycemia less severe than overt DM on adverse pregnancy outcomes
  2. Study type
    Cohort
    3.Study population
    -23,000 pregnant women at 15 centers in 9 countries
    ->18 yrs, Sure of dates
    -No pre-exisiting DM, IVF/ART, HIV/HEP, singleton pregnancy
    4.Study methodology
    -Undertook OGTT (75g) between 24-32/40
    -Results were blinded unless high fasting and 2 hr glucose readings
    -Categorised glucose levels into 7 categories of increasing BSL for fasting, 1hr PP and 2hrs PP
  3. Primary outcomes
    -BW >90%
    -Primary CS delivery
    -Neonatal hypoglycemia
    -Cord blood C peptide >90% (Measure of neonatal beta cell function/ hyperinsulinemia)
  4. Secondary outcomes
    -Delivery before 37/40
    -Shoulder dystocia
    -Birth injury
    -PET
    -Hyperbillirubinemia
    -Admission to NICU
53
Q

Discuss the HAPO trial results
-Primary outcomes
-Secondary outcomes

A

Primary outcomes
-Increasing risk of all primary outcomes with increasing glucose category for fasting 1hr PP and 2hrs PP
-Significant association with increasing BSL at all three times and BW >90% dose response and Serum C peptide (dose response) (strongest association) for highest BSL category
-Significant association with fasting and 1hr PP and CS -weak and without clear dose response
-No clear association with neonatal hypoglycemia and BSL of any category at any time
Secondary outcomes
-Incremental increase in BSL associated with increased risk for PTB, Shoulder dystocia/birth injury, NICU admission, Hyperbillirubinemia, PET
-Strongest associations seen with PET and shoulder dystocia
-No association with perinatal death in any of the 3 time categories but not powered to asses

54
Q

What are the limitations of the HAPO study (3)

A
  1. Observational study so cannot link outcomes to BSL
  2. Some confounders not measured so not controlled for in MVA - weight gain in pregnancy
  3. Participation was only 54%
55
Q

Discuss the ACHIOS study
-Primary aim (1)
-Study type (2)
-Inclusion criteria (2)
-Exclusion criteria (3)

A
  1. Primary aim
    To investigate if treatment of GDM reduces risk of perinatal complications
  2. Study type
    RCT - multicentre in Australia
    Randomised to routine care (GDM dx not disclosed) vs monitoring and management of BSL as per standard GDM care
  3. Inclusion criteria
    -Singleton/twins 16-30wks with RF or +ve polycose and + OGTT 24-34 weeks
  4. Exclusion criteria
    More severe glucose intolerance,
    Active chronic disease except ess HTN
    Previous GDM
56
Q

Discuss the ACHIOS study
-Primary outcomes (6)
-Secondary outcomes (6)

A
  1. Primary outcomes
    -Composite measure of serious fetal complications (Still birth, SD, nerve palsy, fracture)
    -IOL
    -CS
    -Admission to NICU
    -Neonatal Jaundice
    -Maternal 3/12 QoL
  2. Secondary outcomes
    -Birth weight (LGA, macrosomia)
    -Mode of delivery
    -Pregnancy induced HTN
    -Perineal trauma, PPH
    -Number of clinic visits
57
Q

Discuss the ACHIOS study
-Number in study
-Results of primary outcomes (stat sig ones - 6)
-Results of secondary outcomes (stat sig ones - 3)

A
  1. Number in study
    -Approx 500 in each group
    -No loss to FU
  2. Results of primary outcomes
    -Increase in serious fetal complications in routine care group 4% vs 1% RR 0.33 NNT 34
    -Increase in NICU admissions in intervention group 71% vs 61% RR 1.13 (Rx for hypoglycemia same)
    -Increase in IOL in intervention group 39% vs 29% RR 1.36
    -CS rates the same and for similar indications
    -Lower rates of depression as per EPNDS in intervention group 8% vs 17% RR 0.46
    -No difference in shoulder dystocia rates
  3. Results of the secondary outcomes
    -Less macrosomia in intervention group 10% vs 21% RR 0.47
    -Less PET in intervention group 12% vs 18% RR0.7
    -No difference in PPH/perineal trauma
58
Q

Discuss the TARGET study
-Aim (1)
-Study design (2)
-Primary outcomes (1)
-Secondary outcomes (6)

A
  1. Aim
    To assess whether tighter glycemic control of GDM lead to reduced perinatal and maternal morbidity
  2. Study design
    -Step wedge cluster RCT in 10 NZ hospitals
    -Roll out of tighter glycemic control every 4 months (Fasting <5, 1hr <7.4 2hr <6.7)
  3. Primary outcome
    -Incidence of LGA babies
  4. Secondary outcomes
    -Composite measure of neonatal outcomes (Death, birth trauma, shoulder dystocia)
    -Composite measure of PPH, coagulopathy, emboilism, obstetric complications)
    -PET
    -IOL
    -CS
    -Need for pharmacological treatment for GDM
59
Q

Discuss the results of the TARGET study
-Number of women recruited
-Results of primary outcomes
-Results of secondary outcomes

A
  1. Number of women recruited
    -1000
  2. Results from primary outcome
    -No difference in rates of LGA between groups 14.7% vs 15.1% RR 0.96
  3. Results for secondary outcomes
    -Reduced serious neonatal health outcomes in tight control group RR 0.23 NNT 47
    -Reduced length of NICU stay in tight control
    -Increased serious health outcomes for women in tight control group RR 2.28 NNTH 27)
    -No difference in CS, IOL, PET
    -Increased need for pharmacological input int he tighter control group
60
Q

Discuss the MiG study
-Aim
-Methods
-Primary outcomes (1)
-Secondary outcomes (5)

A
  1. Aim
    -To determine the efficacy and safety of metformin in the management of GDM
  2. Methods
    -Open RCT
    -Metformin or metformin and insulin vs insulin
    -Women between 20-33 weeks with GDM
  3. Primary outcomes
    -Composite measure of: Neonatal hypoglycemia, respiratory distress, Apgar scores, need for photo therapy, birth trauma and prematurity
  4. Secondary outcomes
    -Anthropromorphic measures
    -Maternal glycemic control
    -Maternal HTN complications
    -Acceptability of Rx
    -PP glucose tolerance
61
Q

Discuss MiG study
-Number included in study
-Results from primary outcome
-Results to secondary outcomes

A
  1. Number included in the study
    750
  2. Results from primary outcome
    -No difference in composite outcome between groups 30 vs 32%
  3. Results from secondary outcomes
    -Higher acceptability in the metformin group for treatment (SS)
    -No SS difference for other outcomes
    -No SAE with metformin

Kira - Mat Med (14 decks)

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