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Laboratory test most useful in screening for thyroid dysfunction
TSH (thyrotropin assay), 3rd generation
What is the pathway to thyroid hormone synthesis & secretion?
Hypothalamus releases TRH (thyrotropin- releasing hormone) to the anterior pituitary which releases TSH (thyroid stimulating hormone/thyrotropin) which attaches to receptors on thyroid gland in response to low circulating thyroid hormone (T4/T3) - Negative feedback loop.
What is thyroid peroxidase?
An enzyme in the thyroid gland that oxidizes iodide to iodine to be used in the making of T4/T3.
Which of the thyroid hormones is more potent and therefore more biologically active?
T3 - 3-5x more potent than T4. Most of this hormone is actually from the peripheral tissue conversion of T4 to T3. Only 20% is actually synthesized in the thyroid gland.
T or F : Thyroid hormones are mostly in bound form to carrier proteins such as TBG (thyroxine binding globulin), thyroxine-binding prealbumin (TBPA, transthyretin) and albumin.
TRUE, All but 0.03% of T4 and 0.3% of T3 is protein bound. The free concentration is responsible for biologic effects of the thyroid hormones.
Other laboratory methods in thyroid testing...
Measurement of thyroid gland autoantibodies (anti-thyroid peroxidase (TPOab), antithyroglobulin), and antibodies against the thyrotropin receptor.
When an abnormal TSH is received, what is the next test?
free T4 level - shows an inverse correlation to the serum thyrotropin level.
With a normal TSH, but abnl serum FT4 result, what can be the cause?
abnormality in protein binding of thyroid hormone.
What is a better way to monitor treatment of hyperthyroidism, at least in the beginning?
FT4 - level normalizes much sooner and is a better marker to gauge effectiveness of the therapy in the first few months of treatment. TSH levels may take many months to respond.
Normal adult thyrotropin levels
Normal Total T4 (adult)
Normal Free T4 (adult)
Normal Total T3 (adult)
Normal Free T3 (adult)
elevated TSH, low T4
More prevalent in women
Caused by loss of functional thyroid tissue from infiltrative diseases to thyroid (bacterial, viral), autoimmune thyroiditis, thyroid sx, radiation injury to neck, defects in synthesis caused by iodine deficiency, antithyroid drugs, medications (steroids), congenital defects of enzymes.
causes outside of thyroid gland itself
- less common
- deficiency in pituitary hormone secretion or hypothalamic disease
Symptoms of hypothyroidism
fatigue, lethargy, cold intolerance, slowed speech & intellectual functions, slowed reflexes, periorbital edema, thickened/coarse/dry skin.
Symptoms of hyperthyroidism
pre-tibial edema, nervousness, heart palpitations, rapid pulse, fatigability, muscle weakness, weight loss/gain, diarrhea, heat intolerance, sweating, variable eye changes, gland enlargement.
Most common cause of hyperthyroidism in the U.S.
- autoimmunce disease that afflicts women to men 5:1.
characterized by antibodies to the thyrotropin receptor which causes autonomous stimulation of thyroid gland
Other causes of primary hyperthyroidism
diffuse and multinodular goiter
Other causes (less common): acute/subacute thyroiditis, thyroid cancer, iatrogenic intake of thyroid meds. or iodide, or drug-induced thyrotoxicosis.
- can be caused by thyrotropin-secreting pituitary adenoma
Diagnosis of primary hyperthyroidism
elevated free T4, low or undetectable TSH (together confirmatory)
If a patient has low or undetectable TSH but normal FT4, checking a FT3 may suggest T3 thyrotoxicosis.
Thyroid levels suggestive of pituitary tumor
S&S of hyperthyroidism
nl or increased levels of serum thyrotropin (TSH)
Characteristics of Graves' Disease
Hyperthyroidism (low TSH, high T4)
Goiter (diffuse) & FIRM
Opthalmopathy (lid lag, excessive lacrimationbulging from increased deposition of retroorbital fat, enlarged orbital musculature)
Dermopathy (shiny, hairless skin, hyperpigmented)
- - Peak age 20-40
- - onset can be stress: pregnancy, illness
15-20% of cases
glandular inflammation and follicular cell destruction - thought to occur after viral illness.
Causes release of stored hormone, therefore, early is hyperthyroid state, while late is hypothyroid.
Present w/ firm, painful, enlarged thyroid, possibly low-grade fever. Pain may mean degeneration or hemorrhage into a thyroid nodule, or suppurative thyroiditis.
low uptake of radioactive iodine
Tx: self-limiting and tx with anti-inflammatory agents and prednisone (20-40mg BID). In late stage of hypothyroidism, pts. will need temporary TH replacement.
(silent thyroiditis - gland moderately enlarged and non-tender)
Diagnosis of Graves' disease
antithyroglubulin and antimicrosomal antibodies elevated
TSH-Rab (TSH-receptor antibody) elevated
NM I123 to assess functional status.
RAIU - high, diffuse uptake
Management of Graves' Disease
3 treatment options: antithyroid drugs (PTU, MMI), radioactive iodine ablation, surgery (most successful, but rarely done unless anatomic problem).
Symptomatic relief: beta-blockers
tx of hyperthyroidism
50-150mg PO TID
May take 2-8 weeks to see effect.
Rarely used for long-term treatment.
S.E./adverse reactions: pruritis, drowsiness, allergic dermatitis, N/V, arthralgia, rare: agranulocytosis.
Peak: 4-10 weeks
tx of hyperthyroidism
10-40mg PO/PR daily. Titrate q3-4weeks.
Not used long-term.
May take 2-8 weeks to see effect.
S.E./adverse effects: pruritis, drowsiness, allergic dermatitis, nausea, parotitis, arthralgia, rare: agranulocytosis (report fever, malaise, sore throat, or mouth sores).
Peak: 4-10 weeks.
Radioactive Iodine Ablation, I123
Treatment of choice in U.S., middle-aged or older adults for hyperthyroidism
24-hr dose given orally, which concentrates in the overactive tissue, radiates that tissue causing inflammation and destruction.