Thyroid Clinical Flashcards
hyperthyroidism - defined
*too much thyroid hormone
*elevated T3 and T4
*low TSH
hyperthyroidism - symptoms
- metabolism: heat intolerance, diaphoresis, weight loss, restlessness, hyperactivity, anxiety
- CV/resp: tachycardia, palpitations, arrhythmias, chest pain
- derm: warm, moist skin, onycholysis
- GI: diarrhea
- MSK: muscle weakness, hand tremors, osteoporosis
- neuropsych: anxiety, insomnia, psychosis, pressured speech
- repro: oligomenorrhea, amenorrhea, decreased libido, decreased fertility
causes of hyperthyroidism
- Graves’ Disease (most common cause)
- other causes include:
-hyperfunctioning “toxic” adenoma (Plummer’s disease)
-multinodular goiter
-thyroiditis
-hCG-related [pregnancy, cancer]
-Jod-Basedow phenomenon
-factitious/iatrogenic use of thyroid hormone
-TSH secreting adenoma
Graves’ disease - overview
*an autoimmune cause of hyperthyroidism; most common cause of hyperthyroidism
*hallmark: + thyroid stimulating immunoglobulins (TSI) or TSH receptor antibodies (TRAb); autoantibodies bind the TSH receptor and stimulate hormone synthesis
Graves’ disease - exophthalmos
*exophthalmos (bulging eyes) - only occurs in Graves’ disease
*pathogenesis: TSI activates T cells → lymphocytic infiltration of the retroorbital space which increases inflammatory cytokines → orbital fibroblasts secrete GAGs to increase osmotic muscle swelling/inflammation and adipocyte build up → exophthalmos
*note - exophthalmos associated with HLA-DR3 and HLA-B8
Graves’ disease - clinical features
*exophthalmos
*periorbital edema
*lid lag (upper eyelid is high in downward gaze; increased sympathetic stimulation of superior tarsal muscle)
*smooth goiter
*pretibial myxedema (TSI stimulate pretibial dermal fibroblasts → skin thickening)
*Pemberton sign (goiter obstructs jugular venous flow as the thyroid is forced downward with raised arms)
Graves’ disease diagnosis - ultrasound
*US shows significantly increased blood flow to the thyroid
nuclear uptake & scan (Tc-99 pertechnetate thyroid scintigraphy) - overview
*give pt pertechnetate, which looks a lot like iodine (but isn’t used to make thyroid hormone)
*gets taken up into the thyroid cells
*uptake = gives us a % of how much pertechnetate is taken up
*scan = gives us a picture of where the pertechnetate is taken up
Graves’ disease diagnosis: nuclear uptake & scan (Tc-99 pertechnetate thyroid scintigraphy)
*scan reveals pattern of uptake similar to that of a normal thyroid, but much higher % of uptake in Graves’ disease
*homogenous distribution of uptake throughout the thyroid
Graves’ disease - treatment
- medications: inhibit thyroid peroxidase enzyme → blocks thyroid peroxidase → less tyrosine iodination and coupling → prevents formation of T3/T4
-options for meds: methimazole, propylthiouracil (PTU)
-ADEs: hepatic failure, agranulocytosis - beta blockers (decrease hyperadrenergic sx) = INITIAL therapy to control symptoms
- other: thyroidectomy, radioactive iodine ablation
methimazole - MOA, ADEs
*MOA: inhibit thyroid peroxidase enzyme → less tyrosine iodination and coupling → prevents formation of T3/T4
*ADEs:
-hepatic failure (jaundice, abdominal pain, elevated LFTs)
-agranulocytosis (low absolute neutrophil count, fever, sore throat)
-teratogenic (avoid in pregnancy)
toxic adenoma / toxic multinodular goiter - nuclear uptake & scan (Tc-99 pertechnetate thyroid scintigraphy)
*nodular locations of uptake on scan
*focal patches of follicular cells become hyperfunctioning → hypersecretion of T3/T4 independent of TSH
thyroiditis - overview
*inflammation (damage) to the thyroid gland causes premade/stored thyroid hormone to leak into the bloodstream
subacute granulomatosis thyroiditis - overview
*aka de Quervain thyroiditis
*usually preceded by infection
*PAINFUL inflammation of the thyroid
*lab trends: hyperthyroid state → euthyroid → hypothyroid state → euthyroid
*typically self-resolves in several weeks
postpartum thyroiditis
*a mild, self-limiting variant to Hashimoto thyroiditis < 1 year after delivery