Thyroid Flashcards
T hyroxin(T4), Triiodothyronine (T
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Normal thyroid gland function is very important and critical for
• Neurocognitive development
• Physical growth throughout childhood and adolescence.
• Increases basal metabolic rate
• Increases cardiac output, heart rate, and ventilation rate.
• Potentiates the effects of catecholamines (i.e. increases sympathetic activity)
T hyroid hormone synthesis
Iodide uptake by thyroid follicular cells via the
sodium-iodide symporter (NIS)
The TPO-mediated iodination of tyrosine residues
on thyroglobulin (Tg) forms mono- and
diiodotyrosines (MIT and DIT)
• mono- and diiodotyrosines (MIT and DIT) couple
to form T3 (1 MIT plus 1 DIT) or T4 (2 DITs).
• T3 and T4 attached to Tg are stored as colloid in
the follicular lumen.
Pathophysiology
• Congenital hypothyroidism may be secondary to mutations in multiple genes
associated with thyroid malformation and migration failure (Thyroid
Dysgenesis) or thyroid hormone biosynthesis (Thyroid dyshormonogenesis )
• Autoimmune hypothyroidism (Hashimoto thyroiditis) is usually associated
with antibodies against TPO and/or TG. These autoantibodies indicate immune
activation against the thyroid gland and damage to thyroid follicular cells.
• Autoimmune hyperthyroidism (Graves disease), thyroid-stimulating
immunoglobulins (TSIs) bind to the TSH receptor resulting in dysregulated
overproduction of T3 and T4.
Iodine
• Iodine is essential in the production of thyroid hormone.
• Dietary sources of iodine include milk, meat, vitamin preparations, and iodized salt.
• The recommended daily intake of iodine is 100 μg for adults and adolescents, 60 μg to 100 μg
for children, and 30 to 40 μg for infants less than one year.
• Although it is rare in Saudi Arabia , iodine deficiency is the leading cause of hypothyroidism
worldwide.
• Its effects are most pronounced if iodine deficiency is present early in life, when it results in
intellectual impairment. (Cretinism)
Etiology
Of CH
Permanent hypothyroidism or transient hypothyroidism
• The most common cause of primary CH is thyroid dysgenesis , 80% to 85% of all cases. (permanent
hypothyroidism)
• Defects in thyroid hormone biosynthesis or secretion known as thyroid dyshormonogenesis 15% . (permanent
hypothyroidism)
• Central hypothyroidism associated with additional pituitary hormone deficiencies.
• Exogenous or environmental etiologies of CH include maternal thyrotropin(TSH) receptor blocking antibodies,
antithyroid drug use ( transient)
• Iodine deficiency (transient)
Clinical features of CH
• Newborns with CH are typically asymptomatic at birth.
• Fetuses are protected from the effects of hypothyroidism by the placental transfer of
maternal thyroid hormone and because they commonly have some functioning thyroid tissue.
• Classic symptoms of untreated CH include prolonged jaundice, lethargy, poor feeding,
constipation, and a hoarse cry.
• The most common signs are umbilical hernia, macroglossia, and mottled skin.
• Occasionally, bradycardia, wide posterior fontanelle, coarse facies, and hypotonia with
delayed reflexes.
Diagnosis of CH
The mainstay tool for diagnosis is newborn screening by doing TSH level or
thyroxine (T4) testing with heel-prick samples obtained between 2 and 5 days
of life, or from umbilical cord.
• False positives may occur if the newborn screening is performed before 48
hours of life due to the thyrotropin (TSH) surge that occurs shortly after birth.
• In premature infants (<28 weeks’ gestation and/or weighing <1500 g) and
acutely ill-term newborns, an elevation in TSH is frequently delayed until 2 to 6
weeks after delivery ( False negative)
There are 3 screening strategies for the detection of congenital hypothyroidism
• Primary TSH measurement with backup thyroxine (T4) determination in infants with high TSH levels
• Primary T4 measurement with backup TSH assessment in infants with low T4 levels
• Simultaneous measurement of T4 and TSH levels (preferred)
Second screening for the following infants
• Preterm, low-birth weight (LBW) and very low-birth weight (VLBW) neonates
• Infants admitted to neonatal intensive care units (NICU)
• Infants originally tested within the first 24 hours of life
• Multiple births (particularly same-sex twins)
Normal findings in screening
normal TSH is less than 20 mU/L
• Any infant with a low T4 concentration and TSH concentration greater than 40 mU/L is considered
to have primary hypothyroidism.
• Confirmatory serum testing should be performed to verify the diagnosis and treatment initiated
immediately and before the results of the confirmatory tests are available.
•TSH levels in the mid-range of 20 to 40 mU/L (often reflect transient hypothyroidism), require prompt further evaluation by performing a confirmatory serum testing.
Additional testing can be considered to define the underline cause
of the hypothyroidism
• Ultrasonography of the thyroid can confirm thyroid hypoplasia or aplasia.
• Thyroglobulin (Tg) level could help in the diagnosis of thyroid agenesis.
• Thyroid radionuclide scan (scintigraphy), administering either iodine 123 or
sodium pertechnetate technetium Tc 99m, can demonstrate an ectopic gland or
thyroid aplasia.
• Thyroid scintigraphy should be performed within 1 week of initiating thyroid
hormone replacement therapy; however, treatment should not be delayed
while obtaining these imaging tests.
X- ray of knee
A lateral radiograph of the knee may be obtained to look for the distal femoral epiphysis.
• This ossification center appears at about 36 weeks’ gestation.
• Its absence in a term or post term infant indicates prenatal effects of hypothyroidism.
Dignosis صورة
Treatment with Thyroid hormone replacement
• Should be started no later than the first 2 weeks of life.
• The goal of therapy is to normalize thyroid hormone levels as early as possible to optimize
neurocognitive outcome.
• Frequent laboratory monitoring can decrease the likelihood of prolonged periods of sub
physiologic and supraphysiologic thyroid hormones.
• Treatment of choice for CH is levothyroxine at a starting dose of 10 to 15 μg/kg administered
once daily
• The tablet form should be crushed and then administered via a spoon with a few milliliters of
water, formula, or breast milk.
Calcium, iron, and soy , are known to interfere with the absorption of
levothyroxine and should be administered at a different time of the
day, separated by several hours.
• When an infant with CH is switched to soy formula, thyroid tests
should be performed 2 to 3 weeks afterward to determine whether an
increase in the levothyroxine dose is needed.
T he goal of treatment
• Normalize the T4 level within 2 weeks of starting levothyroxine, to normalize the
thyrotropin TSH level within 1 month, and to maintain the T4 level within the upper half
of the normal range.
• Monitoring thyroid hormone levels every 2 weeks until the thyrotropin level normalizes,
then every 1 to 3 months during the first year of life, and every 2 to 4 months between 1
and 3 years of age.
• Transient CH, a reevaluation of treatment with levothyroxine can be considered after they
reach 3 years of age.
• At that time most of brain development has been completed therefore we can avoid the
mental retardation
Autoimmune hypothyroidism
Autoimmune hypothyroidism (Hashimoto thyroiditis) is the most common cause of acquired hypothyroidism in children, adolescents, and adults. • The prevalence of autoimmune hypothyroidism in childhood is an estimated 1% to 2% with a 4:1 female predominance. • Approximately 50% of cases have a family history of autoimmune thyroid disease. • Several syndromes are associated with an increased risk for developing autoimmune hypothyroidism, including Down syndrome and Turner syndrome. • Other Autoimmune disorder in the same patient is also associated with an increased risk, most commonly diabetes, alopecia, vitiligo, and celiac disease ( autoimmune polyglandular syndrome)
