deck_5762361 Flashcards
thyroid anlage
thickened foregut endodermsite where thyroid devpt begins
thyroid devptal pathology
most congenital hypothyroidism linked to abnl thyroid gland devpt maldescent → lingual thyroid, retrosternal thyroid thyroglossal duct cysts
hum over active thyroidwhy?
incr venous blood flow from hyperplastic/hypertrophic gland
euthyroidhypothyroidhypertyroid thyrotoxicosissubclinical
euthyroid : normal thyroid hormone actionhypothyroid : underactive thyroid gland, clinical evidence of deficient thyroid hormone actionhyperthyroid : overactive thyroid gland & clinical evidence of excess thyroid hormone action thyrotoxicosis : clinical evidence of excess thyroid hormone actionsubclinical : only lab evidence of hormone excess/def
fx of thyroid hormone
controls metabolic rate
congenital hypothyroidism causesclnical findings
causes * thyroid gland dysgenesis * inborn errors of TH synthesis * TSH-receptor blocking ab from mom clinical findings * jaundice * feeding troubles * enlarged tongue * umbilical hernia * delayed bone maturation majority identified by newborn blood screening!
endemic cretinism
hypothyroidism → issues with brain devpt * mental retardation (MBP) * movement disorders (PCP2)
goiter
enlarged thyroid most common cause: IODINE DEFICIENCY
hypothyroidism signs and sx (juvenile vs adult)
juvenile * mental retardation, learning disabilities * short stature adult * CNS : delayed deep tendon reflexes, mental slowness * CV: bradycardia, weakness * periorbital and peripheral edema * dry coarse hair, orange skin (keratin), decr BMR, cold intolerance, weight gain * repro: menorrhagia * GI: constipation
classification of hypothyroidism x3 and causes
PRIMARY hypothyroidism : TSH high Hashimoto’s aka chronic lymphocytic thyroiditis (95% cases in US) * drug induced (Li, I) * TH synthesis defects (ex. thyroperoxidase issues) * lingual thyroid (devpt defect) * iodine def * infiltrative disease (amyloid, fibrous replacement) CENTRAL hypothyroidism (TSH nl, low) * pituitary or hypothalamic disease (rad, tumor, infiltrative) TRANSIENT hypothyroidism (TSH variable → can progress to permanent) postpartum or silent thyroiditis (painless, related to lymphocytic) * after preg, woman has a flareup of autoimmunity * subacute thyroiditis (deQuervain’s or painful thyroiditis, viral in origin)
primary hypothyroidism
LACK OF HORMONE FOR NEGATIVE FEEDBACK may or may not present with goiter
Hashimoto’s thyroiditisakachronic lymphocytic thyroiditis
most common cause of permanent hypothyroidismautoimmune disase assoc with DR5 and antiTPO antibodies * high prevalence: women, Japanese (maybe high I diet) * “Hashitoxicosis”: early thyrotoxic phase due to follicular rupture (rare presentation) * end-stage? atrophic thyroiditis * assoc with incr risk of thyroid lymphoma
central hypothyroidism
low hormone levels due to INADEQUATE CENTRAL STIMULATION normal or small thyroid gland
transient hypothyroidism
most common causes of transient hypothyroidism: subacute (painful) thyroiditis * referred jaw pain, viral in origin, confused with pharyngitis postpartum (painless) thyroiditis * can recur with subsequent pregs or progress to Hashimoto can result in a triphasic response (destruction, repair, normal) destruction: TSH suppressed * no radioactive update during destructive phase * repair: TSH high * repairED: TSH normal
thyrotoxicosis signs/sxjuvenile vs adult
prenatal/juvenile * cranial synostosis (premature fusion of cranial sutures) adult * tachycardia, afib, dyspnea, palps/angina * inability to concentrate, active CTRs, tremor * thyroid bruit, eye, skin complaints (Graves disease) * pain in neck or jaw → subacute thyroiditis * velvety, moist skin, incr BMR, wt loss * oligomenorrhea (light/infreq periods) * diarrhea * osteoporosis
effect of thyroid hormone on basal metabolism
thyroid hormone increases cell membrane permeability to Na and K → incr in Na/K ATPase activity making ATP is not totally efficient → some energy is released as heat
effect of excess thyroid hormone on CV function
T3 incr alphaMHC gene, Ca ATPase * increase cardiac O2 demand * incr systolic bp (incr pulse pressure) vasodilation * decr diastolic bp (incr pulse pressure) * incr RAAS incr beta adrenergic signaling angina + palpitations + tachycardia/atrial arrhythmias
classification of thyrotoxicosis
HYPERTHYROIDISM (TSH undetectable) Graves’ disease (most common, 60% cases) * toxic adenoma (solitary overactive nodule) toxic multinodular goiter (TMNG common, many overactive nodules aka Plummer’s disease) THYROID DESTRUCTION (TSH variable) subacute or painful thyroiditis (common) postpartum thyroiditis (common) * Hashitoxicosis : transient thyrotoxicosis phase of Hashimoto’s thyroiditis * atypical causes (rare)
hyperthyroidism
HIGH HORMONE LEVELS and HIGH NEGATIVE FEEDBACK goiter may be diffuse (Graves) or nodular depending on cause
thyrotoxicosisvshyperthyroidism
thyrotoxicosis: increased thyroid hormone and evidence of TH excess no matter what the cause
Graves Disease triad
most common cause of thyrotoxicosis * goiter * opthalmopathy dermopathy * aka pretibial myxedema incr activity of T helpers → causes B cells to become active → production of oligoclonal TSH receptor abs * abs bind to TSH receptor and activate it (as if TSH were bound) →→→ growth and overactivity prevalence: 2% females, 0.2% malesrisk factors: genetics, smoking, postpartum pd
euthyroid sick syndrome
seen in systemically ill peopleadaptive hypometabolic state * low free T3 * TSH, total T4, free T4 are normal cause: defect in peripheral deiodination of T4 → T3
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