Thyroid Flashcards
most sensitive indicator of mild thyroid dysfunction
MEASUREMENT OF TSH LEVELS (better marker than T4); most are primary disorders, with inverse relationship btw TSH and T4
- Hyperthyroidism: Low TSH
- Primary hypothyroidism: High TSH
TSH can be misleading if:
- TSH dependent hyperthyroid (i.e., at level of hypothalamus or pituitary): elevated T4 due to elevated TSH
- Secondary Hypothyroid: low T4 due to low TSH
Clinical situations in which TBG is increased (thereby increasing amount of bound T4)
Clinical situations where TBG is decreased
Increased TBG:
- Estrogen: i.e., pregnancy or OCPs
- Hepatitis: b/c TBG is made in the liver
Decreased TBG:
- Chronic liver failure
- chronic malnutrition
- protein loss
In general terms, a change in the TBG level will be associated with a change in the total thyroid levels, but not in amount of free/functional T4
- i.e., change in TBG levels does not cause hyper or hypothyroid
Thyroid Uptake and Scan
- Administer tracer dose of radioactive iodine-123
- measure the amount of iodide that the thyroid extracts from the blood as a percent of the total dose
- uptake of iodide is dependent on TSH
- can also see the distribution of Iodide in the gland and evaluate regional abnormalities
cold vs hot nodules
Cold Nodules: Do not take up iodine
Hot Nodules: Take up iodine
Causes of Increased Radioiodine Uptake
- Iodine deficiency
- Stimulation of the thyroid
» Thyroid stimulating immunoglobulins (Graves Disease)
» TSH
» hCG
• Autonomously functioning thyroid nodules
• Recovery phase of thyroiditis
Causes of Decreased Radioiodine Uptake
- Iodine excess • Defect in iodine uptake mechanism • Thyroid failure or ablation • Exogenous suppression of TSH • Active phase of thyroiditis
Thyroid Storm vs. Thyrotoxicosis
- Stress-induced catecholamine surge leading to death by arrhythmia
- a serious complication of Grave’s disease or other hyperthyroid disoders
CNS: Agitation, delerium, coma (vs. restlessness/tremor)
CV: Arrythmias, congestive heart failure (vs. tachycardia, a-fib)
Thermo: Hyperthemia (vs. heat intolerance)
GI: Diarrhea, vomiting, jaundice (vs. frequent defecation)
Etiology of Hyperthyroidism
Common:
- Graves disease
• Toxic multinodular goiter
• Solitary toxic nodule
Rare: - Neonatal Graves disease • Infantile “Familial” thyrotoxicosis • TSH-dependent thyrotoxicosis • CG-secreting neoplasm
- Hyperthyroidism responds to antithyroid drugs or radioiodine ablation
Graves Disease
- an autoimmune hyperthyroidism with thyroid-stimulating immunoglobulins
- presents with diffuse, painless goiter
- Elevated radioiodine uptake with diffuse
distribution of tracer
• Detectable thyroid stimulating
immunoglobulin (TSI); TSI is an IgG; could cross placenta and cause hyperthyroid in the fetus
Extra-thyroid symptoms (unique to Graves):
» Orbitopathy (Propotosis, EOM swelling)
» Pretibial myxedema
Treatment:
- surgery (b/c there is slight increase risk of thyroid cancer)
- radioactive iodide (contraindicated in pregnancy) (permanent hypothyroid is common)
- anti-thyroid drugs
Neonatal Graves Disease
- a pregnant woman with Graves disease passes TSI (IgGs) through the placenta to the baby –> baby develops form of Graves disease as a result of maternal antibodies
- can be treated with anti-thyroid drugs
- would expect condition to resolve as maternal antibodies are cleared
Toxic Multinodular Goiter
- Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor (constitutively active) –> increased release of T3/T4
- Hot nodules (rarely malignant), with patches of cold nodules (compensating for the hot nodules)
- Peak age 5th -7th decade
• Insidious onset, may initially be present
as “sub-clinical hyperthyroidism”:
suppressed TSH, normal free T4
• May be exacerbated by acute iodine load,
for example IV contrast (Jod-Basedow phenomenon)
Subacute Thyroiditis
- Self-limited hypothyroidism, often following a flu-like illness
- may be hyperthyroid early in course
» Hard, tender, painful thyroid gland
» Constitutional symptoms
» Sedimentation rate elevated
Histo: granulomatous inflammation
Treatment
» Beta adrenergic blocking agents
» Anti-inflammatory drugs
» May require temporary thyroxine replacement during hypothyroid phase
Silent Thyroiditis
- Early hyperthyroidism, followed by hypothyroidism
- May be a variant of chronic (Hashimoto) thyroiditis
» Painless, non-tender thyroid
» Often noted in post-partum women (“postpartum thyroiditis”); may recur following
subsequent pregnancies
» High risk of permanent hypothyroidism
» Anti-thyroid peroxidase antibody often
detectable - Treatment: Beta adrenergic blocking agents
Etiology of Hypothyroidism
Goitrous
- Chronic thyroiditis
• Dyshormonogenesis
• Iodine deficiency
Non-Goitrous - Post-ablative • Atrophic thyroiditis • Developmental defects • Central hypothyroidism
Hashimoto’s Thyroiditis
- Most common cause of hypothyroidism
- An autoimmune disorder, with antibodies against thyroid peroxidase and and thyroglobulin
- presents with firm, irregular goiter
- May be associated with other autoimmune diseases, e.g., SLE, rheumatoid arthritis
- Associated with HLA-DR5
Histo:
- HURTHLE CELLS: cuboidal cells that ling the follicles, with abundant mitochondria, giving them a pink, granular appearance in sections
- lymphocytic infiltrate with germinal centers
Tx: administer PURE T4 to normalize TSH
Course: development of lymphoma of the thyroid
