Thyroid Flashcards
what are adverse outcomes associated with thyroid disorders
- miscarriage, fetal loss
- gestational hypertension, pre-eclampsia
- intrauterine growth restriction [IUGR]
- compromised fetal neurocognitive development
- fetal distress
- stillbirth
- premature birth
- lactation difficulty
- postnatal depression
- thyroid storm
- maternal congestive heart failure
normal production of thyroid hormones [T3 and T4] is dependent on
- an adequate supply of dietary iodine
- a normally functioning thyroid gland
- a functioning pituitary gland producing adequate TSH
- a functioning hypothalamus producing adequate TRH
where is iodine found
in seafood, vegetables grown in iodine-rich soil, and iodized table salt.
clinical picture of hyperthyroidism [high T3 and T4]
- increased basal metabolic rate
- weight loss with good appetite
- anxiety, physical restlessness, nervousness, excessively emotional
- hair loss
- fast pulse, heart palpitations
- intolerance to heat, warm sweaty skin
- diarrhea
- exophthalmos [protrusion of the eyes] in Graves’ disease
- oligomenorrhea or amenorrhea
what is the clinical presentation of hypothyroidism [low T3 and T4]
- decreased basal metabolic rate
- weight gain and poor appetite. easily fatigues
- mental sluggishness, depression, lethargy, psychosis
- dry skin, brittle hair
- slow, weak pulse
- dry cold skin, poor tolerance to cold. puffy appearance on face hands and feet [myxedema]
- constipation
- anovulation
what are some of the changes to maternal thyroid function in pregnancy
- a marked increase of TBG
- Increased T3 and T4
fetal requirements for thyroid hormone in first trimester - increased demand for iodine
- hCG has a thyroid- stimulating effect
- de-iodination of thyroid hormones in the placenta to facilitate passage of iodine to the fetus
- thyroid function tests are difficult to interpret
What thyroid hormone crosses the placenta
iodine crosses the placenta and thyroxine [T4] is transferred, but only in the 1st trimester. T3 and TSH do not cross at all
when does the fetal thyroid begin functioning
at the end of the 1st trimester, and prior to that the fetal brain development is dependent on maternal supply of T4, which is converted intracellularly to T3. during this time thyroid hormones are most important to fetal brain development.
what is fetal intellectual development dependent on
adequate amounts of thyroid hormone. Deficiencies can lead to impaired growth and irreversible intellectual disability.
what happens in women with severe iodine deficiency during pregnancy
trapping mechanisms override fetal demand, conserving iodine for maternal use but this results in congenital iodine deficiency syndrome [poor growth and intellectual deficiency ]
why might hCG cause transient biochemical hyperthyroidism
hCG and TSH share a similar structure and have similar receptors, giving hCG thyroid-stimulating features. hCG stimulates the thyroid gland during early pg. In situations with high hCG like multi-fetal pg, molar pg, and HG hCG may overstimulate the TSH receptors causing the transient hyperthyroidism
what is the thyroid activity in labor and birth
the levels of total and free T3 increase in response to the increase energy requirement of the contracting uterine muscles.
what happens to the thyroid during pp
delivery of placenta and consequent reduction in estrogen, the production of TBG decreases, as does the renal excretion of iodine. gradually over 4-6 weeks the changes to thyroid function of pg are reversed.
when is the diagnosis of thyroid disorders ideal
pre-conception as some diagnostic tools and treatments are inadvisable in pg
how can hyperthyroidism affect pregnancy
lead to hypertensive disease of pg, cardiac disease, infection, IUGR, stillbirth, abruption or preterm labor, and thyroid storms