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 → increased 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
*used to treat Graves’ disease
*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
Riedel thyroiditis
*aka invasive fibrous thyroiditis
*can be due to IgG4 → progressive fibrosis of the thyroid gland and surrounding structures
*slowly enlarging, hard, fixed, non-tender thyroid gland
*may lead to hypothyroidism
*treatment = surgery; monitor parathyroid function
thyroiditis - treatment
*mostly transient process, so does not require methimazole or PTU
*beta blocker may be used to help with symptoms until thyroiditis resolves
*NSAIDs for pain if needed
hCG-mediated hyperthyroidism - overview
*TSH, hCG, LH, and FSH all share the same alpha subunit, but have different beta subunits
*at high levels, hCG can bind to TSH receptors
*human chorionic gonadotropin (hCG) is made almost exclusively by the placenta but also by some neoplasms; therefore, seen in pregnancy, molar pregnancy, choriocarcinoma
*transient, no treatment needed
Jod-Basedow phenomenon - overview
*iodine-induced hyperthyroidism
*occurs when a pt with an underlying thyroid disorder is given excess iodine → excess hormone production by an abnormal thyroid gland that doesn’t respond to normal regulation
*pertinent history: excess source of iodine, such as administration of IV contrast, amiodarone, iodine supplements
other causes of hyperthyroidism
- iatrogenic use of thyroid hormone
- TSH secreting adenoma (very rare, sx of pituitary mass with hyperthyroidism, tx = surgery)
- struma ovarii (thyroid hormone-secreting ovarian teratoma: hyperthyroidism + pelvic mass)
thyroid storm - overview
*rare but life-threatening complication of hyperthyroidism (untreated or incompletely treated hyperthyroidism + acute stressor such as infection, trauma, surgery)
*presentation: agitation, delirium, fever, coma, tachyarrhythmias
*treatment:
-beta blocker
-PTU or methimazole
-glucocorticoids
-iodine
hypothyroidism - defined
*too little thyroid hormone
*low T4 and T3
*elevated TSH
hypothyroidism - symptoms
- metabolism: cold intolerance, weight gain, hyponatremia, hyperlipidemia
- CV/pulm: bradycardia, dyspnea on exertion
- derm: dry, cool skin, coarse brittle hair, alopecia
- GI: constipatiion
- MSK: proximal muscle weakness, carpal tunnel, myoedema
- neuropsych: fatigue/lethargy, depression, hyporeflexia
- repro: abnormal uterine bleeding, decreased libido, infertility
hypothyroidism - features
*periorbital edema
*edema, tongue swelling
*goiter
*Queen Anne’s sign (thinning of distal 1/3 of the eyebrow)
causes of hypothyroidism
*Hashimoto thyroiditis (most common)
*congenital hypothyroidism
*central hypothyroidism
*iodine deficiency
*medication-induced
*surgery/radiation
Hashimoto thyroiditis - overview
*most common cause of hypothyroidism in iodine-sufficient countries
*an autoimmune cause of hypothyroidism
Hashimoto thyroiditis - pathogenesis
*thyroid peroxidase (TPO) antibodies destroy follicular cells → decreased thyroid hormone production
*initial normal/high thyroid hormone levels followed by permanent hypothyroidism
Hashimoto thyroiditis - risk factors
*female
*PMH/FHx of autoimmune disease
*Down Syndrome, Turner Syndrome
*HLA-DR5 haplotype
congenital hypothyroidism - overview
*most common cause worldwide = iodine deficiency
*most common cause in USA = thyroid dysgenesis/agenesis
*thyroid hormone affects axon proliferation, dendrite branching, synaptogenesis, myelination, cell migration, growth, skeletal development
*undiagnosed/untreated congenital hypothyroidism → irreversible intellectual disability
-this is an emergency; newborn screening programs essential
congenital hypothyroidism - clinical presentation
*aka cretinism
*classically presents with 6 P’s: pot-bellied, pale, puffy-faced child with protruding umbilicus, protuberant tongue, and poor brain development
*undiagnosed/untreated, leads to irreversible intellectual disability
central hypothyroidism - overview
*thyroid gland is normal but signal from pituitary/hypothalamus is absent, so thyroid hormone isn’t produced
*labs = low TSH and low T4
*less common than primary hypothyroidism
*look for hx of pituitary disorders
other causes of hypothyroidism
- iodine deficiency: no iodine → no organification → no T3/T4 production
- medication induced: amiodarone, lithium inhibits thyroid hormone synthesis + release
- surgery/radiation
hypothyroidism - treatment
*goal = replace thyroid hormone
1. levothyroxine = T4 (Synthroid is the brand name)
2 liothyronine = T3; can add to levothyroxine regimen, but not prescribed alone
myxedema coma - overview
*severe, potentially fatal complication of hypothyroidism
*hypothyroid state + stressor (infection, MI, stroke, surgery)
*severe hypothyroidism → decreased mental status, hypothermia, hypoglycemia, hyponatremia, hypoventilation, bradycardia, puffy hands/face
*elderly pts with hypothyroidism have highest risk
amiodarone & thyroid
*amiodarone: class III anti-arrhythmic drug rich in iodine; can do anything to the thyroid:
-hypothyroidism: decreased conversion of T4 to T3
-hyperthyroidism: trigger autoimmune hyperthyroidism
-thyroiditis: can cause destruction of thyroid gland
