Thyroid Flashcards
HPT Axis
Hypothalamus makes TRH–> goes to anterior pituitary makes TSH–> Thyroid releases T3 or T4 converted to T3 in tissues
Differential diagnosis of Hypothyroidism
Primary hypothyroidism-
#1- chronic lymphocytic thyroditis (hastimotos thyroditis)
Partial or total thyroidectomy
Reversible autoimmune thyroiditis (silent and postpartum thyroiditis)
Thyroid irradiation
Infiltrative and infectious disease, thyroid dysgenesis, idine deficieny, iodine excess (Wolff Chaikoff effect), drugs (antithyroid agents, lithium)
Pathogenesis of chronic lymphocytic thyroiditis (hashimotos thyroiditis)
- Sensitization of the hosts own lymphocytes to various thyroidal antigens (thyroglobulin, thyroid peroxidase, the TSH receptor)
- Antibodies to one or more of the antigens can be detected in many patients
- Initiation of Autoimmune response: environmental factors (viral or bacterial infection, or high iodine intake), Genetic factors (defects in suppressor T cells)
- Cytokine release and inflammation ultimately result in glandular destruction
Secondary/tertiary hypothyroidism
aka Central hypothyroidism: tumors, trauma (surgery, irradiation, head injury), infiltrative diseases (sarcoidosis, hemochromatosis), drugs (dopamine, glucocorticoids), inactivating mutation in genes that code for various proteins involved in regulation of the hypothalamic pituitary thyroid axis
hypothyroidism clinical features
Hairloss, fatigue, depression, shortness of breath, weight gain, constipation, menstrual irregularities, infertility, muscle cramps, joint pain, cold intolerance
Periorbital puffness, loss of outer 3rd of eyebrow, pallor, macroglossia, hoarseness, bradycardia, hypoventilation, absent or decreased bowel sounds, non pitting edema, delayed relaxation or ankle jerks, peripheral neuropathy, cool/rough/dry skin, hypothermia
TSH is more sensitive
myxedema coma
very severe hypothyroidism
Essentially low T4–> low T3–> CNS (Altered mental status)
low thermogenesis, hypothermia, decreased sensitivity to hypercapnia and hypoxia, respiratory insufficiency, cerebral anoxia
CV–> shock
Fluid balance
treatment of hypothyroidism
usually just give levothyroxineT 4 very long half life and liothyronine (T3)
hyperthyroidism Different forms of Primary
The TSH is always low
Thyroiditis: Decreased TSH, increased T4
Graves disease: Decreased TSH, increased T4
Toxic multinodular goiter: decreased TSH, increased T4
Solitary Toxic nodule: decreased TSH, increased T4
In secondary: the TSH will be high or normal bc theres a tumor secreting it
Pathogenesis of Graves disease
Pathogenesis of Graves Disease: Ag are shared in fibroblasts in the eyes and skin etc
inhibitor of IGF receptor
Symptoms of hyperthyroidism (thyrotoxicosis)
Alertness, emotional lability, nervousness, irritability
Poor concentration, muscular weakness, fatigability, palpitations, voracious appetite, weight loss
increased frequency of bowel movements
heat intolerance
Signs: hyperkinesia, rapid speech, Proximal muscle weakness, fine tremor, fine moist skin, fine abundant hair, onycholysis, pretibial skin thinkening, lid lag, stare, chemosis, periorbital edema, proptosis
accentuated first heart sound, tachycardia, atriral fibrillation, widened pulse pressure, dyspnea
pathogenesis of thyroid storm
Increased thyroid hormone–> increased Cardiac output (A fib, CHF (increased inotropy, increased chronotropy)
Increased Basal metabolic rate–> increased heat production and hyperthermia, CNS effects (Agitation, psychosis, delerium seizure, coma
Radiotracer uptake and scan- Graves whole thyroid lights up, in solitary toxic (only one side), multi nodular (everywhere
Hyperthyroid pharmachology
Methimazole: therapeutic use (treatment of hyperthyroidism), MOA: inhibits the synthesis of thyroid hormones by blocking the oxidation of iodine in the thyroid gland, SE: Relatively low incidency of SE, rash, joint pain, headache, reversible agranulocytosis, liver toxicity, and birth defect aplasia cutis can occur.
Propylthiouracil: therapy (adjuctive therapy for hyperthyroidism who are intolerant of methimazole and in pregnant pts. MOA: inhibits the synthesis thyroid hormones by blocking the oxidation of iodine in the thyroid gland, it also partially inhibits the peripheral deiodination of T4 to T3
SE: same as Methimazole, w/ liver toxicity
giving iodine to hyperthyroidism
therapeutic use- treatment of pts with hyperthyroidism ana are in preop in prep for thyroidectomy, and in conjuction with anti thyroid drugs and propranolol, in the treatment of thyrotoxic crisis, another use of iodide is to protect the thyroid from radioactive iodine fallout following a nuclear accident
mOa: idodide inhibits hormone release, wolffchaikoff effect iodides decrease the vascularity, size and fragility of a hyperplastic gland, making the drugs valuable as preoperative prepfor surgery
SE: acute sensitivity reaction (IV or IP ) including angioedema and laryngeal edema, serum sickness like effects, mild iodism stimulates a head cold
Radioactive iodine
Therapeutic use- thyroid destruction of an overactive or enlarged thyroid and in thyroid cancer for thyroid ablation and treatment of metastatic disease
MOA: I is trapped by the thyroid, incorporated into the iodoamino acids, and deposited in the colloid of the follicles, I has a t.5 of 8 days and emits both gamma rays and beta particles, the beta particles destroy the parenchymal cells of the thyroid
SE: high incidence of delayed hypothyroidism
B- adrenergic blocking agents (propranolol)
use- reduce adrenergic effects of thyroid hormone (palpitations, tachycardia, tremulousness, anxiety, heat intolerance)
MOA: Competitvely blocks response to B adrenergic stimulation which results in decreases in heart rate, myocardial contractility, blood pressure, and myocardial oxygen demand, propranolol may also inhibit the peripheral deiodination of T 4 and T3
SE: brady cardia, hypotension, syncope, bronchospasm, wheezing
