deck_5762361

Question 1

thyroid anlage

Answer 1

thickened foregut endodermsite where thyroid devpt begins

Question 2

thyroid devptal pathology

Answer 2

most congenital hypothyroidism linked to abnl thyroid gland devpt maldescent → lingual thyroid, retrosternal thyroid thyroglossal duct cysts

Question 3

hum over active thyroidwhy?

Answer 3

incr venous blood flow from hyperplastic/hypertrophic gland

Question 4

euthyroidhypothyroidhypertyroid thyrotoxicosissubclinical

Answer 4

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

Question 5

fx of thyroid hormone

Answer 5

controls metabolic rate

Question 6

congenital hypothyroidism causesclnical findings

Answer 6

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!

Question 7

endemic cretinism

Answer 7

hypothyroidism → issues with brain devpt * mental retardation (MBP) * movement disorders (PCP2)

Question 8

goiter

Answer 8

enlarged thyroid most common cause: IODINE DEFICIENCY

Question 9

hypothyroidism signs and sx (juvenile vs adult)

Answer 9

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

Question 10

classification of hypothyroidism x3 and causes

Answer 10

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)

Question 11

primary hypothyroidism

Answer 11

LACK OF HORMONE FOR NEGATIVE FEEDBACK may or may not present with goiter

Question 12

Hashimoto’s thyroiditisakachronic lymphocytic thyroiditis

Answer 12

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

Question 13

central hypothyroidism

Answer 13

low hormone levels due to INADEQUATE CENTRAL STIMULATION normal or small thyroid gland

Question 14

transient hypothyroidism

Answer 14

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

Question 15

thyrotoxicosis signs/sxjuvenile vs adult

Answer 15

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

Question 16

effect of thyroid hormone on basal metabolism

Answer 16

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

Question 17

effect of excess thyroid hormone on CV function

Answer 17

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

Question 18

classification of thyrotoxicosis

Answer 18

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)

Question 19

hyperthyroidism

Answer 19

HIGH HORMONE LEVELS and HIGH NEGATIVE FEEDBACK goiter may be diffuse (Graves) or nodular depending on cause

Question 20

thyrotoxicosisvshyperthyroidism

Answer 20

thyrotoxicosis: increased thyroid hormone and evidence of TH excess no matter what the cause

Question 21

Graves Disease triad

Answer 21

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

Question 22

euthyroid sick syndrome

Answer 22

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

Question 23

summary