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M2 Endo/Repro > Maternal & Fetal Health - Sood > Flashcards

Maternal & Fetal Health - Sood Flashcards

1
Q

Why and how do T3 & T4 levels increase during pregnancy?

A
  • Increased thyroxin binding globulin (TBG) levels cause a decrease in free T3/T4
    • Decreased clearance of TBG (due to estrogen[?])
    • Increased liver production of TBG
  • Pituitary senses low free T3/T4 and increases TSH production
  • Placenta also stimulates T3/T4 release via hCG
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2
Q

How would placental production of hCG affect TSH levels?

A

hCG stimulates T3/T4 release from the thyroid, which would decrease TSH release via negative feedback.

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3
Q

Review:

Name three thyroid antigens which autoantibodies can be produced against in the context of autoimmune thyroid diease. Which antigen can have blocking and stimulating antibodies raised against it?

A
  • Thyroglobulin (Tg, aka colloidal antigen)
  • Thyroid peroxidase (TPO)
  • TSH receptor
    • Abs can be blocking (e.g. autoimmune thyroiditis) or stimulating (Graves’)
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4
Q

How common are Tg or TPO autoantibodies in women of child-bearing age?

A

10-20%

[Wiki states Hashimoto’s has a prevalance of ~1:1000. The lecture goes on to state that most women with autoabs do not suffer sufficient thyroid destruction to cause hypothyroidism. So it seems having the autoabs does not imply a clinically significant disease.]

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5
Q

What are the side effects of iodine deficiency in a pregnant woman?

A
  • Goiter in the mother
  • If severe, neurocognitive impairment / mental retardation / deaf-mutism in the offspring
  • (Keep in mind - higher dietary requirement in pregnancy)
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6
Q

What complications of pregnancy are noted in women with Tg or TPO autoabs?

A

Associated with pregnancy loss, recurrent miscarraiges, and preterm delivery

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7
Q

Your patient is a 27yo pregnant female in her 1st trimester of pregnancy, presenting with heat intolerance, palpitations, increased sweating, and anxiety. She denies nausea or vomiting. You suspect Graves’ disease, but anti-TSH receptor autoAbs are negative.

  1. What other process might be responsible for her symptoms?
  2. If the patient instead presented with a CC of nausea & vomiting, and you saw that she was no longer gaining weight at a normal rate despite her pregnancy, what would you suspect?
A
  1. Gestational Hyperthyroidism
    • Transient & observed in first half of pregnancy
    • 1-3% of pregnancies
    • Due to excess production or activity of hCG
  2. Hyperemesis Gravidarum
    • Nausea, vomiting & weight loss
    • 0.05% to 1% of pregnancies
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8
Q

What are the symptoms of a thyrotoxic crisis?

What are potential consequences of this condition?

A
  • aka Thyroid Storm
    • fever
    • tachycardia
    • seizures
    • restlessness / confusion
    • diarhhea
    • vomiting
    • cardiac arrythmia
  • Can result in shock, coma, or death
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9
Q

What are 5 potential complications of Grave’s disease in the context of pregnancy?

A
  • Increased abortion risk
  • Preterm labor
  • Low birth weight
  • Stillbirth
  • Preeclampsia
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10
Q

What advice would you give a young woman recently diagnosed Graves’ Disease if she told you she planned on becoming pregnant soon?

A
  • The disease needs to be treated several months before pregnancy
    • Circulating autoAbs that cross the placenta pose serious risk to the fetus
    • These Abs persist for months following surgical or radioactive thyroid ablation
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11
Q

What is the cause of Sheehan Syndrome?

Where is it most common?

A
  • Ischemic injury to the hypothalamic-pituitary axis following severe hemorrhage and hypotension at delivery
  • Susceptibility is due to increased size of the pituitary during pregnancy and the low-flow, low-pressure nature of the portal circulation
  • Most common in parts of the world where deliveries are not performed in healthcare facilities
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12
Q

If a woman developed Sheehan Syndrome shortly following delivery, what symptoms might she notice quickly and thus present with?

A
  • Failure of lactation
  • Failure of hair growth over areas shaved for delivery
  • Poor wound healing following a cesarean delivery
  • Weakness
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13
Q

Why does some healthy pregnant women develop a temporary loss of vision in the outer halves of their left and right visual fields?

A

Bitemporal hemianopia

  • Lactrotroph cells of pituitary increase 20-60% by the 3rd trimester
  • Entire pituitary gland also increases in wieght by 30%
  • Increased size places pressure on the optic chiasm, which causes the visual disturbance.
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14
Q

In general terms, what are the major hemodynamic (vessel) changes of pregnancy?

A
  • Increased capacity and reduced resistance
    • Decreased vascular resistance
    • Arterial compliance
    • Vascular capacitance
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15
Q

What changes in renal function occur during pregnancy?

(Hint: Think of the hemodynamic changes)

A
  • Increased renal blood flow
  • Increased glomerular filtration
  • Increased RAAS activation
    • ​Note: causes reduced response to infused pressor compounds
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16
Q

Define gestational hypertension.

A

Typical criteria of HTN (>140mmHg systolic and/or >90mmHg diastolic) in a pregnant woman.

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17
Q

What are ~7 symptoms of preeclampia?

What additional symptom makes for a diagnosis of eclampsia?

A
  • Severe HTN (>160mmHg systolic / >110mmHg diastolic)
  • Proteinuria (not always present but useful in making the Dx when present)
  • “End organ dysfunction”
  • Visual distubances & Headaches
  • Epigastric pain
  • Thrombocytopenia
  • Abnormal liver function
  • Seizures in the context of preeclampsia makes for a Dx of eclampsia
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18
Q

What are the defining criteria of HELLP syndrome?

A
  • Severe HTN plus:
  • Hemolysis
  • Elevated Liver enzymes (hepatic dysfunction)
  • _L_ow _P_latelet count (thrombocytopenia <100,000/ul)
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19
Q

What are **seven **potential maternal sequelae of severe HTN disorders during pregnancy?

A
  1. Pulmonary edema
  2. Stroke
  3. Liver failure
  4. Renal failure
  5. Seizures
  6. Death
  7. Long-term risk to develop HTN and/or related disorders (outside of pregnancy)
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20
Q

What are four potential fetal sequelae of severe HTN disorders during pregnancy?

A
  1. Growth restriction in utero and small birth weight
  2. Oligohydramnios (reduced amniotic fluid)
  3. Indicated preterm delivery
  4. Long term risk to develop metabolic and/or cardiovascular disorders
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21
Q

What are five emerging hypotheses regarding

the pathophysiology of preeclampsia?

A
  • Think decreased blood flow to the fetus/placenta
    • Placental hypoperfusion
    • Placental release of anti-angiogenic factors (sFlt1, sEng)
    • Defective trophoblast differentiation
      • Cells of the placenta that are important for implantation and interaction with the maternal uterus
    • Angiotensin autoantibodies
    • Incomplete spiral artery remodeling
22
Q

What are five risk factors for preeclampsia?

A
  1. Primiparity (woman who is pregnant for the first time)
  2. Past history / Family history
  3. Preexisting medical conditions
    • Diabetes, BMI >26.1, Kidney Disease, aPLs (antiphospholipid Abs)
  4. Multiple gestation
  5. Maternal age <20 or >35
23
Q

What is the only known cure for preeclampsia?

A

Delivery.

Thus, timing of potentially required induced labor or cesarean section is decided baced on disease severity.

24
Q

What drug is given for seizure prophylaxis in pregnant women at risk for eclampsia?

A

Magnesium sulfate

25
Q

If a woman needs to undergo pre-term induced labor due to severe preeclampsia, what drug can be given to develop the infant’s lungs?

Is the drug given **antenatally **or postnatally?

A

Betamethasone, a glucocorticoid

Given antenatally. Beneficial up to 34 weeks into pregnancy.

26
Q

What is mechanism of action of magnesium sulfate?

A
  • Unknown
  • Alters Ca2+ metabolism so affects CV and neuro functions
  • May act as a vasodilator, reducing cerebral edema.
  • Likely acts at the level of the NMJ
  • Conveniently, also crosses the placenta and is neuroprotective for the fetus - useful for preterm births
27
Q

What are side effects of magnesium sulfate?

A
  • Common & minor:
    • Warmth
    • Flushing
    • Nausea
    • Vomiting
  • Rare but serious:
    • Loss of patellar reflex
    • Respiratory depression
28
Q

How is magenium sulfate excreted?

A

Kidneys

29
Q

What is the mechanism of action of betamethasone?

A

Glucocorticoid that accelerates development of type 1 and type 2 pneumocytes. The resulting structural and biochemical changes (including surfactant production) improve lung mechanics.

30
Q

What are side effects of betamethasone?

A
  • Maternal fluid retention
  • Transient increase in fetal heart rate
31
Q

What phenomenon may help explain why some adult diseases like metabolic syndrome are seen intergenerationally in families despite having no simple genetic inheritance pattern?

A

“Prenatal programming” of adult disease

A pregnant woman with, for example, metabolic syndrome will have dysregulated nutrient transport to her fetus, stimulating fetal overgrowth. Fetal overgrowth is known to increase the risk of adult metabolic disease later in life. This may be a contributing factor for the development of several chronic syndromes.

32
Q

What does hemochorial mean?

What does this mean for the human placenta?

A

Direct contact between the blood and the chorion

It means that the mother’s blood directly bathes the vili, and hormones/chemicals from the fetus/mom can affect each other

33
Q

What are some metabolic changes that occur during pregnancy?

What is the basis of all these changes?

A

Hyperinsulinemia

Insulin Resistance

Hyperlipidemia

Hypertriglyceridemia

Hyperketonemia

These changes give the fetus the most access to glucose and amino acids.

34
Q

What three changes are seen regarding insulin in pregnancy?

A

Higher circulating glucose in fed state

Hyperinsulinemia

Insulin Resistance

35
Q

What changes are seen in the following organs during pregnancy?

Pancreas

Adipose Tissue

Brain

Liver

A

Pancreas- hyperplasia of beta cells, hyperinsulinemia

Adipose Tissue- accelerated lipid catabolism

Brain- leptin resistance

Liver- insulin resistance, minimal protein catabolism, and hyperketonemia

36
Q

What nutrients are transported to the fetus?

How are they transported?

A

Amino acids- active transport

Glucose- facilitated diffusion

Fatty acids- diffusion/placental metabolism

37
Q

Why does the simulated diabetic state of pregnancy benefit the fetus?

A

The fetal glucose transporter has a very high affinity for glucose and saturates at 360 mg/dL. With a higher need for nutrients and a higher affinity transporter, the fetus benefits greatly from the diabetic state.

38
Q

What causes gestational diabetes?

A

Pregnancy is a stress test. If the mother already has glucose abnormalities, pregnancy might push her over the edge.

Pre-existing Insulin resistance worsened

Hyperinsulinemia from lowered capacity for production

Circulating antibody changes

39
Q

What effect does diabetes have on the fetus?

What problems could this cause as a neonate?

A

Hyperglycemia causes the fetus to become hyperinsulinemic. The extra glucose is stored as fat and causes macrosomia. Early in the pregnancy, it can lead to congenital abnormalities.

As a neonate outside of a hyperglycemic environment, the blood sugar can crash causing hypoglycemia in an hyperinsulinemic baby.

40
Q

What are some risk factors for congenital diabetes?

Who should be tested and when?

A
  • Obesity
  • Hx of diabetes
  • Family Hx
  • Non-white

All pregnanct women should be tested; at the first prenatal visit for high risk women and between weeks 24-28 for everyone.

41
Q

Gestational Diabetes

What are some implications for the fetus?

What are some implications for the mother?

A

Fetus

  • Macrosomia
  • Polyhydramnios
  • neonatal hypoglycemia
  • risk of birth trauma
  • metabolic disorders

Mother

  • Future risk of diabetes
42
Q

Why are statistics on pregnancy and maternal health important?

A
  • Sentinel indicators of a communities quality of healthcare
  • Poor fetal care may lead to disease as an adult
  • Maternal organ malfunctions in pregnancy indicate latent pathology that could cause disease later
43
Q

What constitutes direct maternal death?

What consitutes indirect maternal death?

A

A death resulting directly from pregnancy, labor, delivery, post-partum conditions, or pregnancy (75-80%)

A death caused by an aggrevation of an underlying condition because physiological stress of pregnancy

44
Q

What is the maternal mortality rate?

What is the maternal mortality ratio?

A

Rate

MM Rate= (# of deaths)/(# of women of reproductive age)* 10000

MM Ratio= (# of deaths)/ (# of live births) * 10000

45
Q

What is the leading cause of maternal mortality world wide?

What is the leading cause in the United States?

A

Hemorrhage, hypertensive disorders, infections/sepsis

Cardiovascular disease, infection/sepsis, and “non-cardiovascular disease”

Incidence of coronary syndromes are increasing due to increased obesity, diabets, hypertension, and older age at pregnancy

46
Q

What is the definition of a post-partum hemorrhage?

What can cause it?

A

Blood loss >500mL in a vaginal birth or >1000mL in a C section

Uterine Atony -80%

Congenital or Acquired Coagulation Defects

Trauma

Placenta Accreta

47
Q

What can cause antepartum hemorrhage?

A

Placental Abruption- 30%

Vasa previa- rare

Uterine Rupture- rare

Placenta previa- 20%

48
Q

How do you calculate the following:

Infant Mortality Rate

Fetal Mortality Rate

Neonate Mortality Rate

Perinatal Mortality Rate

A

IMR=(# of infant deaths)/(# of live births) *1000

FMR= (# of fetal deaths)/(# of total births) *1000

NMR= (# of neonatal deaths)/(# of live births) *1000

PMR=(# of neonatal deaths)+(# of stillbirths)/ (# of total births) *1000

Notice that for statistics involving death around birth, TOTAL births are used in the denominator.

49
Q

Which vaccines should be updated for women hoping to get pregnant?

What other things should be included in preconception care?

A

Varicella, Rubella, Hepatitis B

Get chronic diseases undercontrol, start folic acid, assess for tetratogen exposure, genetic counseling

50
Q
A

M2 Endo/Repro (57 decks)

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