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REI Written Boards > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What stimulates and inhibits TSH?

A
  • Stimulated by TRH

- Inhibited by somatostatin and dopamine

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2
Q

What is the active thyroid hormone?

A

T3 is active thyroid hormone

3-5x more potent than T4

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3
Q

What is secreted at a higher rate? T3 or T4?

A

T4 is secreted at higher rate (x20) than T3

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4
Q

How is the majority of T3 made?

A

T3 is made primarily from peripheral conversion of T4 in the liver and kidney

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5
Q

Where is the thyroid hormone receptor?

A

Nucleus

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6
Q

What are the two key thyroid hormone receptors?

A

Nuclear steroid receptor; two types: alpha (chromosome 17), beta (chromosome 3)

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7
Q

Describe the implications of an inactivating mutation of the thyroid hormone receptor?

A

Inactivating mutation causes thyroid resistance syndrome

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8
Q

What is Hashimoto’s thyroiditis?

A

Most common cause of hypothyroidism in iodine-sufficient areas of the world is chronic autoimmune thyroiditis, which is caused by cell- and antibody-mediated destruction of thyroid tissue

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9
Q

What are the laboratory findings of primary hypothyroidism?

A

high TSH, low free T4

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10
Q

What are the main causes of primary hypothyroidism?

A
  • Hashimoto’s thyroiditis

- Iatrogenic disease (thyroidectomy, radiation, etc)

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11
Q

Describe thyroid physiology in the setting of anorexia

A
  • Similar to sick euthyroid state
  • TSH normal or slightly low
  • Low T3, high reverse T3
  • Normal or low T4, but normal free T4
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12
Q

Describe Subacute (viral/deQuervain) thyroiditis:

A
  • Subacute thyroiditis (subacute granulomatous thyroiditis) is characterized by neck pain or discomfort, a tender diffuse goiter, and a predictable course of thyroid function evolution
  • Hyperthyroidism followed by euthyroidism, hypothyroidism, and ultimately restoration of normal thyroid function
  • Low iodine uptake; high T3, low TSH
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13
Q

Describe secondary hypothyroidism

A
  • TSH deficiency
  • Hypopituitarism (tumor, Sheehan, trauma)
  • TSH-R mutation
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14
Q

Describe tertiary hypothyroidism

A
  • TRH deficiency
  • Damage to hypothalamus or portal blood flow
  • TRH-R mutation
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15
Q

Describe Graves Disease

A
  • Autoimmune disease consisting of hyperthyroidism, goiter, eye disease (orbitopathy), dermopathy (pretibial or localized myxedema)
  • Hyperthyroidism is the most common feature, affecting nearly all patients, and is caused by thyroid-stimulating hormone (TSH, thyrotropin)-receptor antibodies (TRAb) that activate the receptor, thereby stimulating thyroid hormone synthesis and secretion as well as thyroid growth (causing a diffuse goiter)
  • High iodine uptake; high T3, low TSH
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16
Q

How do you work up a thyroid nodule?

A
  • Serum TSH (higher TSH, higher risk of malignancy)
  • Thyroid ultrasound
  • FNA (if TSH is high and nodules meets sonographic criteria for sampling)
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17
Q

What is thyroid storm?

A

Rare, life-threatening condition characterized by severe clinical manifestations of thyrotoxicosis

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18
Q

Describe the treatment for thyroid storm?

A
  • Beta blocker to control the symptoms and signs induced by increased adrenergic tone
  • A thionamide to block new hormone synthesis
  • An iodine solution to block the release of thyroid hormone
  • An iodinated radiocontrast agent (if available) to inhibit the peripheral conversion of T4 to T3
  • Glucocorticoids to reduce T4-to-T3 conversion, promote vasomotor stability, possibly reduce the autoimmune process in Graves’ disease, and possibly treat an associated relative adrenal insufficiency
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19
Q

What happens to TSH in pregnancy?

A

TSH – decreases in first trimester (secondary to HCG), then normalizes

20
Q

What happens to total T4 in pregnancy?

A

Total T4 – increases; increased overall requirement (increased metabolic rate and some transfer to fetus)

21
Q

What happens to free T4 in pregnancy?

A

Free T4 – decreases; due to increased TBG

22
Q

What happens to TBG in pregnancy?

A

TBG – increase; secondary to increased estrogen levels

23
Q

When does fetal synthesis begin?

A

8-10 weeks

24
Q

When is fetal thyroid development is complete?

A

12- 14 weeks

25
Q

Does TSH cross the placenta?

A

No

26
Q

What thyroid hormones can cross the placenta?

A

TRH, T4, and T3

27
Q

Describe normal fetal thyroid physiology

A
  • Fetus dependent on maternal thyroid hormone in first 20 weeks of pregnancy
  • Fetal TSH plateaus at 28 weeks
  • Increases production of T4 is compensated by peripheral conversion to RT3 (to conserve caloric expenditure)
28
Q

What is a risk associated of PTU?

A

Agranulocytosis, check CBC

29
Q

What is a risk associated with methimazole?

A

Aplasia cutis (congenital absence of skin)

30
Q

What is the preferred treatment of hyperthyroidism during pregnancy?

A

PTU

31
Q

Describe hyperthyroidism during pregnancy. What is the most common cause?

A
  • Graves’ disease is the most cause of thyrotoxicosis in pregnancy
  • Clinical triad: Goiter, thyroid ab, TSH-R Ab
  • TSH-R antibodies can cross placenta
  • PTU is preferred treatment
32
Q

How does PTU affect the fetus?

A

Increases fetal TSH in newborns (lowers T4)

33
Q

Describe treatment issues of treating hypothyroidism in pregnant women

A
  • Will likely need increase in thyroid treatment in hypothyroid women who become pregnant
  • Don’t check sooner than 8 weeks
  • Increased intravascular volume (dilutes thyroid)
  • Placental transport to fetus
  • Increase in TBG (Estrogen induces increases in TBG)
34
Q

Describe recommendations for post postpartum management of hypothyroidism

A
  • Post-partum, return to pre-pregnancy dosing

- Follow closely for 6 months with TSH levels due to high incidence of postpartum thyroiditis

35
Q

How you titrate hypothyroid medications in pregnancy

A

Recommendations are to increase by 30%, then check monthly and adjust treatment based on TSH values (using pregnancy specific reference ranges)

36
Q

When does thyroidal hyperactivity disappear in neonatal physiology?

A

After 3-4 weeks

37
Q

Describe normal neonatal physiology of TSH

A

TSH: peaks 30 min, fall to baseline by 48-72h (response to TRH surge due to rapid neonatal cooling)

38
Q

Describe normal neonatal physiology of free/total T4

A

Free/Total T4: Peak by 24-48h

39
Q

Describe normal neonatal physiology of T3

A

T3: Peak by 24h

40
Q

Describe normal neonatal physiology of RT3

A

RT3: High pregnancy levels continue for 3-5d, fall to normal by 2 weeks

41
Q

What are causes of goiter in the neonate?

A
  • Inborn errors of thyroid hormone production
  • Maternal thyroid antibodies
  • Blocking antibodies cause fetal hypoT and rare goiter
  • Stimulating TSHR antibodies are classic to cause goiter + hyperthyroidism
  • Maternal antithyroid drugs (PTU) or iodine rich drugs like amiodarone
  • Activating TSH-R mutation (autosomal dominant)
  • McCune Albright Syndrome
42
Q

Describe fetal/neonatal physiology when mother is take PTU or iodine rich drugs like amiodarone.

A

Fetus: Increased TSH, reduced T4
Newborn: Labs normalize by DOL4-5 -> euthyroid

43
Q

How common is postpartum thyroiditis?

A

Common (5-10%) auto-immune phenomenon after delivery

44
Q

What are risk factors for postpartum thyroiditis?

A
  • Personal or family history of autoimmune disease
  • Previous PP episode
  • Insulin-requiring DM (25% develop)
  • Presence of thyroid Abs, also associated with postpartum depression
45
Q

What are the rates of transient thyrotoxicosis followed by hypothyroidism for both transient hyper and hypothyroidism?

A

33% transient hyperthyroidism alone

44% transient hypothyroidism alone

46
Q

What is associated with postpartum thyroiditis?

A

Associated with thyroid microsomal antibodies (like Hashimoto’s)

47
Q

What proportion of patients with postpartum thyroiditis require long-term treatment?

A

10%; recurrence in subsequent pregnancy is high

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