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
Does TSH cross the placenta?
No
26
What thyroid hormones can cross the placenta?
TRH, T4, and T3
27
Describe normal fetal thyroid physiology
- 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
What is a risk associated of PTU?
Agranulocytosis, check CBC
29
What is a risk associated with methimazole?
Aplasia cutis (congenital absence of skin)
30
What is the preferred treatment of hyperthyroidism during pregnancy?
PTU
31
Describe hyperthyroidism during pregnancy. What is the most common cause?
- 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
How does PTU affect the fetus?
Increases fetal TSH in newborns (lowers T4)
33
Describe treatment issues of treating hypothyroidism in pregnant women
- 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
Describe recommendations for post postpartum management of hypothyroidism
- Post-partum, return to pre-pregnancy dosing | - Follow closely for 6 months with TSH levels due to high incidence of postpartum thyroiditis
35
How you titrate hypothyroid medications in pregnancy
Recommendations are to increase by 30%, then check monthly and adjust treatment based on TSH values (using pregnancy specific reference ranges)
36
When does thyroidal hyperactivity disappear in neonatal physiology?
After 3-4 weeks
37
Describe normal neonatal physiology of TSH
TSH: peaks 30 min, fall to baseline by 48-72h (response to TRH surge due to rapid neonatal cooling)
38
Describe normal neonatal physiology of free/total T4
Free/Total T4: Peak by 24-48h
39
Describe normal neonatal physiology of T3
T3: Peak by 24h
40
Describe normal neonatal physiology of RT3
RT3: High pregnancy levels continue for 3-5d, fall to normal by 2 weeks
41
What are causes of goiter in the neonate?
- 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
Describe fetal/neonatal physiology when mother is take PTU or iodine rich drugs like amiodarone.
Fetus: Increased TSH, reduced T4 Newborn: Labs normalize by DOL4-5 -> euthyroid
43
How common is postpartum thyroiditis?
Common (5-10%) auto-immune phenomenon after delivery
44
What are risk factors for postpartum thyroiditis?
- 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
What are the rates of transient thyrotoxicosis followed by hypothyroidism for both transient hyper and hypothyroidism?
33% transient hyperthyroidism alone | 44% transient hypothyroidism alone
46
What is associated with postpartum thyroiditis?
Associated with thyroid microsomal antibodies (like Hashimoto’s)
47
What proportion of patients with postpartum thyroiditis require long-term treatment?
10%; recurrence in subsequent pregnancy is high