Thyroid Dysfunction Flashcards

1
Q

Treatments for Graves

A

Meds, radioactive iodine (I131– kills off cells), surgery

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2
Q

medications for Graves

A
  • antithyroid drugs–inhibit synthesis of thyroid hormone (methimazole, propylthiouracil)
  • beta blockers - reduce systemic hyperadrenergic symptoms and effects (tremor, palpitations)
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3
Q

preferred antithyroid drug

A

methimazole preferred due to PTU effects on liver

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4
Q

when might you use propylthiouracil instead of methimazole in Graves?

A

pregnant women

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5
Q

what symptom common between hypothyroid and hyperthyroid

A

fatigue

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6
Q

when to treat hypothyroidism with TSH

A

almost all will treat with TSH >10. WHether to treat between 5-10 mIU/L controversial

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7
Q

preferred medication for hypothyroid treatment

A

levothyroxine- synthetic T4

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8
Q

treatment goal for hypothyroidism

A

between 1-2.5

- somewhere in nl range

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9
Q

Myxedema coma

A

extreme hypothyroidism so severe it can progress to death unless diagnosed promptly and treated vigorously

  • usually inciting event
  • high mortality– endocrine emergency
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10
Q

Sxs of myxedema coma

A

decreased cardiac output, bradycardia, respiratory depression, edema, altered mental status, hypothermia, metabolic derangements

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11
Q

Does the thyroid produce more T3 or T4

A

T4 (80-100 micrograms/day compared to 3-6 micrograms per day)

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12
Q

Which thyroid hormone is more active

A

T3

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13
Q

Deiodinase

A

converts T4 to T3

types 1 and 2 convert T4 to T3, but type 3 converts T4 to rT3 (inactive)

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14
Q

how is thyroid hormone transported

A

in blood, most is bound to proteins (TBG, TBPA, albumin)

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15
Q

is there a higher concentration of T3 or T4 in the blood

A

T3 (0.2% total TH vs 0.02%)

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16
Q

proteins binding T4 in blood

A

thyroxine binding globulin(TBG), thyroid binding prealbumin (TBPA), albumin

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17
Q

proteins binding T3 in blood

A

Thyroxine binding globulin, albumin

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18
Q

halflives of T3 vs T4

A

T3 = 1 day vs 7 days for T4

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19
Q

Causes of increased total T4 and total T3

A
  • hyperthyroidism/thyrotoxicosis
  • increased binding proteins (i.e. Estrogen increased like in pregnancy)
  • thyroid hormone resistance (rare)
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20
Q

causes of increased free T4 and free T3

A

hyperthyroid/thyrotoxicosis and thyroid hormone resistance

** binding protein issues not important

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21
Q

causes of decreased total or free T4 and T3

A
  • hypothyroidism
  • decreased serum protein binding
  • Euthyroid sick syndrome (nonthyroidal illness)
  • drugs
  • liver or kidney disease (total T4, total T3)—mostly has to do with binding proteins
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22
Q

Euthyroid sick syndrome/nonthyroidal illness

A

pt is sick for some other reason and not underlying thyroid disease; have elevated circulating cortisol, free fatty acids, cytokines that cause upregulation or type 3 deiodinase, so you get inactivation of thyroid hormone
- also have mild central hypothyroidism– have nl to decreased TSH at pituitary

  • abnormal thyroid labs with inappropriately low TH (esp T3)and low or nl TSH
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23
Q

nl TSH level

A

0.4-4.0

24
Q

what test do we use to look at thyroid function

A

TSH level - single best screening test for thyroid dysfunction
- indicates person’s thyroid hormone ‘set point’

25
Q

what is the relative level of TSH in primary hypothyroidism

A

elevated (lack of negative feedback)

26
Q

what is the relative level of TSH in primary hyperthyroidism

A

suppressed (excess negative feedback)

27
Q

when is TSH not reliable

A

abnormal pituitary (panhypopituitarism, TSHoma, idiopathic central hypothyroidism)

28
Q

sxs of hyperthyroidism

A

nervousness, weight loss, change in appetite – normally increased, fatigue, tremor, heat intolerance, palpitations, hyperdefecation, trouble sleeping, diaphoresis

29
Q

Labs in Overt hyperthyroidism/thyrotoxicosis

A

increased free T4 and free T3 but low TSH

30
Q

subclinical hyperthyroidism

A

low TSH but nl free T3 and T4

31
Q

thyrotoxicosis

A

high levels of circulating thyroid hormone

- can be due to overproduction of T3, T4 or high release of preformed/stored T3 adn T4 (not true hyperthyroidism)

32
Q

How to determine cause of thyrotoxicosis

A
  • thyroid uptake and perhaps radioactive iodine scan
  • If TSH suppressed, should be no iodine uptake since TSH stimulates iodine uptake/synthesis of T3/T4
  • “normal” or elevated iodine uptake in setting of low TSH is abnormal– autonomous production – True hyperthyroid
  • low uptake - hormone excess due to high release of preformed thyroid hormone
33
Q

radioactive iodine uptake

A

gives info on category of hyperthyroidism/thyrotoxicosis

34
Q

What does high iodine uptake in setting of low TSH mean

A

true hyperthyroid– pattern gives info on etiology (Graves’ vs hot nodule vs multinodular goiter)

35
Q

Etiologies of Low uptake Hyperthyroidism

A
  • Subacute thyroiditis (granulomatous thyroiditis (viral); de Quervain’s)
  • Chronic lymphocytic thyroiditis (Hashimoto’s), postpartum thyroiditis,
  • radiation-induced thyroiditis,
  • infectious thyroiditis, -Drug-induced thyroiditis,
  • ectopic thyrotoxicosis (factitious or struma ovarii)
36
Q

etiology of high uptake hyperthyroidism with low TSH

A
  • Thyrotropin receptor Ab (Graves’; Hashitoxicosis)
  • Thyroid autonomu (toxic adenoma, toxic multinodular goiter—MNG)
  • HCG (hydatidiform mole, choriocarcinoma)
  • TSH (TSH-oma –pit tumor, thyroid hormone resistance
37
Q

which hyperthyroidism conditions are painful

A

Granulomatous thyroiditis, radiation-induced thyroiditis, infectious thyroiditis

38
Q

Graves disease

A

type of hyperthyroidism where you have Ab to TSH receptor, constantly activating it to make more thyroid hormone

39
Q

Destructive thyroiditis

A

examples = subacute/granulomatous and postpartum

40
Q

clinical course of destructive thyroiditis

A

have initial hyperthyroid phase with high free T4 and low TSH then transition to low free T4 with high TSH

  • about 20-25% remain hypothyroid
41
Q

labs in overt hypothyroidism

A

elevated TSH, low free T4

42
Q

subclinical hypothyroidism

A

high TSH but nl free T4; small decrease in T4 can have a large increase in TSH

43
Q

sxs of hypothyroidism

A

mental slowness, weight gain, appetite change- usually decreased, fatigue, muscle cramps, cold intolerance, bradycardia, constipation, hypersomnia, dry skin

44
Q

main categories of hypothyroidism

A

primary and central (secondary/tertiary)

45
Q

etiologies of primary hypothyroidism

A
  • Chronic autoimmune (Hashimoto’s) thyroiditis
  • Transient hypothyroidism (silent or postpartum thyroiditis, subaute or granulomatous thyroiditis)
  • iatrogenic (thyroid surgery/thyroidectomy, radioactive iodine, external neck irradiation)
  • iodine deficiency or excess
  • drugs
  • infiltrative diseases
  • infections
  • congenital
46
Q

drugs that can cause hypothyroidism

A

antithyroid, lithium, amiodarone, tyrosine kinase inhibitors, Fe, cholestyramine, phenytoin, carbamazepine

47
Q

infiltrative diseases causing hypothyroidism

A

hemochromatosis, sarcoidosis, amyloidosis, fibrous (Reidel’s) thyroiditis, scleroderma

48
Q

infections that can cause hypothyroidism

A

M. tuberculosis, P. carinii

49
Q

Hashimoto’s thyroiditis

A

autoimmune condition where you have antibodies that destroy the thyroid’s ability to make thyroid hormone

50
Q

Thyroid autoantibodies in Hashimotos

A

TPO (thyroid peroxidase)
Tg (thyroglobulin)
- some have anti- TSHR Ab
(thyroid stimulating hormone receptor Ab)

51
Q

is hypothyroidism more common in males or females

A

females

52
Q

what thyroid antibodies are present in Graves’ disease

A
  • most have Anti-TSHR Ab

- some also have Anti-TG (50-80%)and Anti-TPO (50-80%)

53
Q

what other conditions besides Graves and Hashimoto’s might you see thyroid antibodies

A
  • normal population (TG, TPO)
  • relatives of those with autoimmune thyroiditis (TG, TPO)
  • Type I DM (TG, TPO)
  • Pregnant women (TG, TPO)
54
Q

positive thyroid Ab with elevated TSH, what proportion develop hypothyroidism

A

rate of 5% per year. If just Abs alone ~2% per year

55
Q

hypothyroid treatment goal

A

~ 0.5-3