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DEMS III > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is the primary constituent of the colloid of the thyriod gland?

A

Thryroglobulin (TG)

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2
Q

What do parafollicular cells (C cells) secrete?

A

Calcitonin

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3
Q

Which is considered the “thyroid hormone:” T3 or T4?

A

T3

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4
Q

Which is considered the “prohormone:” T3 or T4?

A

T4

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5
Q

What are the two ingredients for thyroid hormone (TH)?

A

Iodide and tyrosine

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6
Q

What anion acts as a competitive inhibitor or iodide uptake?

A

Perchlorate (ClO4)

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7
Q

Where does organification of iodide occur?

A

At the follicular cell-colloid interface

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8
Q

Which enzyme catalyzes iodination of thyroglobulin?

A

Thyroperoxidase

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9
Q

Where is thyroglobulin produced?

A

In the follicular cell

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10
Q

What is the source of the tyrosine used to make thyroid hormone?

A

Thyroglobulin

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11
Q

Where do all of the iodination and coupling reactions of TH synthesis occur?

A

On tyrosyl residues of TG

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12
Q

Is most TH carried in bloodstream bound or unbound? To what is it bound?

A

99% exists bound to TBG

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13
Q

Which inhibitory compound leads to goiter?

A

Thiourea drugs

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14
Q

Why is T3 considered to be the active form of TH?

A

Because its affinity for the Th receptor is 10 fold greater for T3 than for T4

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15
Q

What is the main action of TH?

A

Maintain basal metabolic rate

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16
Q

What can congenital hypothyroidism lead to in a neonate?

A

Severe and irreversible mental retardation

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17
Q

Define cretinism

A

Severely stunted physical and mental growth due to congenital hypothyroidism

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18
Q

What are the CV effects of TH?

A

Upregulates beta adrenergic activity

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19
Q

How does T3 provide negative feedback?

A

Free T3 and T4 can influence the response of the anterior pituitary to TRH (high levels reduce response, low levels sensitize response)

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20
Q

Describe the Wolff-Chaikoff effect

A

Iodine deficient diets will lead to a decrease in TH synthesis, but paradoxically, a short term effect of high doses of iodine will also lead to a decrease in TH release. This is the Wolff-Chaikoff effect. This happens because high iodide will diminish the response to TSH.

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21
Q

Is high iodide intake used for chronic management of hyperthyroidism?

A

No, because the Wolff-Chaikoff effect is only transient

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22
Q

What is the pathophysiology of Graves’ Disease?

A

Autoantibodies mimic actions of TSH leading to hyperthyroidism

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23
Q

Does the thyroid produce more T4 or T3?

A

Much more T4, but then T4 is later converted to T3

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24
Q

In cases of severe illness, stress, or starvation, is more or less T3 produced?

A

Much less; advantageous to have a lower BMR

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25
Q

What is the half-life of T4?

A

7 days

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26
Q

What is the half-life of T3?

A

1 day

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27
Q

What is the main cause of increased TOTAL (not free) T4 and T3?

A

Increased binding proteins

28
Q

What is the main cause of increased FREE T4 and T3?

A

Hyperthyroidism/Thyrotoxicosis

29
Q

What is the main cause of decreased TOTAL T4 and T3?

A

Hypothyroidism

30
Q

How can liver disease cause low total or free T3/T4?

A

Liver produces the binding proteins. Less binding proteins means less hormone.

31
Q

How can kidney disease cause low total or free T3/T4?

A

Proteins can leak out in urine. Less binding proteins means less hormone.

32
Q

The level of what is the primary indicator of someone’s thyroid status (aka what do you check)?

A

TSH

33
Q

Is TSH elevated or reduced in primary hypothyroidism?

A

Elevated

34
Q

Is TSH elevated or reduced in primary hyperthyroidism?

A

Reduced

35
Q

When can we not rely on the TSH?

A

Anytime there is an abnormal pituitary gland

36
Q

Define thyrotoxicosis

A

High circulating levels of TH (does not always mean it’s hyperthyroidism)

37
Q

What is true hyperthyroidism/

A

OVERPRODUCTION of T4 and T3

38
Q

How can radioactive iodine uptake and scan help us distinguish between true hyperthyroidism and thyrotoxicosis?

A

When TSH is low, there should be no uptake of iodine. A normal or elevated uptake of iodine in the setting of a low TSH indicated true hyperthyroidism.

39
Q

What is the most common cause of thyrotoxicosis?

A

Hashimoto’s thyroiditis

40
Q

What are the most common causes of true hyperthyroidism?

A

Graves’ disease and toxic nodules

41
Q

What is the pathophysiology of Graves’ ophthalmopathy?

A

There are fibroblasts behind the eye that express TSH receptors. Binding of auto-antibodies to these receptors can cause the fibroblasts to differentiate into adipocytes.

42
Q

What is the skin finding of Graves’ disease?

A

Pretibial myxedema

43
Q

What are the two medications used to treat Graves’ disease? What is their mechanism?

A

Methimazole adn propylthiouracil; inhibit synthesis of thyroid hormone. Beta blockers to counteract systemic effects.

44
Q

What are other ways to treat Graves’ disease?

A

Radioactive iodine and surgery

45
Q

What is the pathophysiology of Hashimoto’s?

A

Autoantibodies against thyroid peroxidase and thyroglobulin

46
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (synthetic T4)

47
Q

What is myxedema coma?

A

An extreme form of hypothyroidism. Life-threatening. High mortality rate.

48
Q

What is the most common type of malignant tumor of the thyroid?

A

Papillary

49
Q

What percentage of nodules are cancer?

A

10-15%

50
Q

What kind of spread does papillary thyroid cancer have?

A

Lymph node spread

51
Q

Define central hypothyroidism

A

A reduction in TH as a result of inadequate stimulation of a normal thyroid gland by TSH and may be secondary, due to pituitary disease, or tertiary, due to hypothalamic dysfunction.

52
Q

What is the prognosis of a papillary carcinoma of the thyroid?

A

Excellent

53
Q

Optically clear nuclei is indicative of which type of thyroid cancer?

A

Papillary carcinoma

54
Q

What is the prognosis of a anaplastic carcinoma of the thyroid?

A

Poor

55
Q

What are the three patterns of anaplastic carcinoma of the thyroid?

A

Spindle cell, giant cells, and squamoid cells

56
Q

What are the two types of follicular/hurthle cell carcinoma of the thyroid?

A

Minimally invasive and widely invasive

57
Q

What is the most common pathway that is messed up in thyroid cancer?

A

MAP kinase pathway

58
Q

What is the most common mutation in all thyroid cancer?

A

BRAF - leads to papillary carcinoma

59
Q

The thyroid gland arises from what?

A

Originates as a proliferation of endodermal epithelial cells on median surface of pharyngeal floor between 1st and 2nd arches

60
Q

85% of cases of congenital hypothyroidism are caused by what?

A

Abnormal development of the thyroid gland (dysgenesis)

61
Q

Those with congenital hypothyroidism due to mutation in PAX8 may also present with what abnormality?

A

Renal agenesis

62
Q

Those with congenital hypothyroidism due to mutation in TITF2 may also present with what abnormality?

A

Bamforth-Lazarus syndrome (very rare)

63
Q

Those with congenital hypothyroidism due to mutation in TITF2 may also present with what abnormality?

A

Respiratory distress and neurologic disorders

64
Q

Those with congenital hypothyroidism due to mutation in SCL26A4 also present with what?

A

Pendred syndrome - Aut rec disorder characterized by sensorineural congenital deafness and goiter

65
Q

What do THOX1 and THOX2 encode?

A

NADPH oxidases which are involved in H2O2 generation in the thyroid; H2O2 is an essential cofactor for iodination and coupling reactions

DEMS III (7 decks)

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