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What is a goiter?
abn enlargement of the thyroid gland; often painless
What is the most common cause of goiters world-wide?
lack of iodine
What is the most common cause of goiters in the US?
over/under production of thyroid hormones
How does lack of iodine contribute to goiter formation?
no T3/T4 production → no inhibition of TRH/TSH → overstimulation of thyroid → enlargement
What is thyrotoxicosis?
state of thyroid hormone excess, large amount in circulation
What is hyperthyroidism?
thyroid hormone excess resulting form excessive thyroid gland function, large amount in circulation
What labs are seen in Hyperthyroidism?
high T3/T4; low TSH
What are examples of Primary Hyperthyroidism?
Graves, toxic nodular goiter, toxic thyroid adenoma, functioning thyroid cancer, iodine excess
What is the most common cause of hyperthyroidism?
Graves’ disease
What are examples of secondary hyperthyroidism?
TSH-secreting pituitary adenoma, ovarian tumor containing ectopic thyroid tissue
What are examples of Iatrogenic hyperthyroidism?
medications: interferon, amiodarone
What are some examples of Thyrotoxicosis w/o hyperthyroidism?
ingestion of excess thyroid hormone, thyroid destructive processes, subacute thyroiditis (painful), silent thyroiditis, damage to thyroid causing release of T3/T4 w/o inc production
Who does Graves’ disease primarily affect?
young adult women (10:1 F-M); +FHx inc risk
What is the pathophysiology behind Graves’ disease?
TSH receptor auto-Ab TSH-R stimulates thyroid follicular cells to produce excessive amounts of T3/T4 → thyroid becomes hyperplastic and very vascular → inc in T3/T4 shuts down TSH, but Auto-Ab continue T3/T4 production
What are the S/sx associated w/ Graves’ disease?
irritable, nervous, poor concentration, tremor, hyperreflexia, exophthalmos, ptosis, heat intolerance, wt loss, palpitations, tachycardia, diarrhea
What effects can hyperthyroidism have on the cardiovascular system?
inc HR and contractility, dec PVR, inc CO, pulse pressure inc, tachycardia, CHF
What metabolic effects can hyperthyroidism cause?
inc hepatic gluconeogenesis, wt loss, inc need for vitamins, inc bone fragility, inc defecation
What GU/GYN effects can hyperthyroidism cause?
W: oligomenorrhea w/ dec fertility
M: dec fertility and impotence
What ocular effects can hyperthyroidism cause?
proptosis, fibrotic EOMS, restricted ocular mobility, diplopia
What effects can hyperthyroidism have on the skin?
warm, sweaty, velvety, non-pitting edema of LE, nodular plaques, clubbing, hyperpigmentation of LE & nail beds, pretibial myxedema or thyrotoxic dermopathy (skin thickening, orange peel texture)
What is a complication of hyperthyroidism?
Thyroid storm -rare, but emergency
What can cause a Thyroid Storm?
often precipitated by another illness or a surgical emergency
What S/sx are associated w/ a Thyroid storm?
tachycardia, HTN, fever, agitation, N/V/D, restlessness, psychosis, CHF, hypotension, shock, can be fatal
What is another term for Hypothyroidism?
Myxedema
What is Hypothyroidism characterized by?
low serum T4/T3, elevated serum TSH
What causes primary hypothyroidism?
damage to the thyroid gland
What are some examples of primary hypothyroidism?
Cretinism, Hashimoto’s, iodine deficiency, thyroidectomy, drugs (amio)
What causes secondary hypothyroidism?
deficiency of TSH secretion from the pituitary
What are some examples of secondary hypothyroidism?
hypopituitarism, hypothalamic disease
What is Cretinism?
congenital hypothyroidism -evident at birth or w/in a few months
What are the clinical manifestation of Cretinism?
persistent jaundice, hoarse cry, delay in development, short stature, protruding tongue, broad flat nose, wide set eyes, dry skin
What happens if Cretinism goes untreated?
leads to mental retardation
What S/sx are associated w/ hypothyroidism?
fatigue, cold intolerance, boggy facies, puffy eyelids, edema of hands and feet (myxedema), hoarseness, trouble concentrating, slow movements, menorrhagia, wt gain, constipation
What is a complication of long-standing hypothyroidism?
Myxedema coma -high mortality rate
What causes a Myxedema coma?
often precipitated by infection (sepsis), stroke, sedative-hypnotic meds
What are S/sx of a Myxedema coma?
sx of hypothyroidism + dec level of consciousness, possibly seizures
What is the most common form of hypothyroidism?
Hashimoto’s thyroiditis
Who is more likely to be effected by Hashimoto’s?
3x more common in women, 3rd-5th decade
What helps distinguish Hashimoto’s from other forms of hypothyroidism?
presence of anti thyroidperoxidase (antiTPO) and antithyroglobulin antibodies (Tg Ab)
What is one of the first sx of Hashimoto’s?
painless enlarged goiter-lymphocytic infiltrate
What is the pathophysiology behind Hashimoto’s?
T cell mediated follicular cell destruction + Anti-TSH block TSH action + Anti-TPO blocks peroxidase → no synthesis of T4/T3 + Tg Ab don’t allow for storage of T3/T4
What signs may be present on the PE in pts w/ Hashimoto’s?
painless, symmetric enlarged thyroid, can impair swallowing, may be only one firm palpable lobe/nodule due to atrophy
What labs would be seen in pts w/ Hashimoto’s?
90% have anti-TPO, 50% have Tg Ab, cell membrane Ab, can have normal T4 and TSH; no T3
What are the neurological signs associated w/ Hashimoto’s?
slowed mentation, forgetfulness, dec hearing, ataxia, sluggish DTRs, paresthesias
What MSK sx are associated w/ Hashimoto’s?
muscle weakness, cramps, stiffness
What cardiac sx are associated w/ Hashimoto’s?
dec CO, bradycardia
What other sx are associated w/ Hashimoto’s?
inc incidence of sleep apnea, inc cholesterol & TGs, Normo normo anemia, constipation, brittle hair, loss of body hair
What skin sx are associated w/ Hashimoto’s?
cool, dry, diffuse non-pitting edema, puffy face w/ coarse features
What is Nodular Disease characterized by?
disordered growth of thyroid cells → gradual development of fibrosis
Who is more likely to develop a nontoxic multinodular goiter?
females, inc incidence w/ age, develop over many yrs
What S/sx are associated w/ nontoxic multinodular goiters?
Asx, often felt on PE, ± dysphagia
What complications can arise from nontoxic mulinodular goiters?
sudden pain → hemorrhage or malignancy ± hoarseness if laryngeal nerve involved
What is a toxic Nodular goiter?
enlarged thyroid gland w/ nodules that produce too much thyroid hormone
Who is more likely to develop a toxic Nodular goiter?
elderly, develop from a simple goiter over yrs
How might a pt w/ a toxic Nodular goiter present?
A fib, palpitations, tachycardia, nervousness, tremor, wt loss
What can cause a toxic Nodular goiter?
receiving IV or oral iodine, medicines that contain iodine (amio)
What is a toxic Adenoma?
single solitary nodule that autonomously produces thyrotoxicosis
What would be seen on the PE of a pt w/ a toxic Adenoma?
large enough to palpate nodule, No S/sx of Grave’s dz
What would a thyroid scan show in pts w/ a toxic Adenoma?
focal uptake in the hyper-functioning nodule and diminished uptake in the remainder of the gland; “HOT nodule“
What are the tumor characteristics of a toxic Adenoma?
rapidly enlarging nodule, vocal cord involvement, fixed hard nodule, cervical LAD, dysphagia, stridor
What risk factors increase the likelihood of someone developing a toxic Adenoma?
radiation exposure (head/neck radiation, nuclear disaster/test sites), FMHx of papillary or medullary thyroid cancer, male