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Endocrine System > The Pathology of Thyroid Gland > Flashcards

The Pathology of Thyroid Gland Flashcards

1
Q

What is the structure of the thyroid like?

A

The thyroid has a right and left lofe, which are connected by a narrow isthmus

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2
Q

Can a NORMAL thyroid be palpated during a physial examination?

A

It cannot easily be palpated

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3
Q

What is the epithelium of the thyroid gland?

A

Lined by a cuboidal epithelium and filled with pink, homogenous colloid

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4
Q

What does the interstitium of the thyroid contain?

A

C cells, but it is not prominent

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5
Q

What is hyperthyroidism?

A

Increased levels of circulating thyroid hormone

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6
Q

What are the main types of hyperthyroidism? (3)

A
  1. Abnormal thyroid stimulator –> Grave’s disease
  2. Intrinsic disease of the thyroid gland –> Toxic multinodular Goiter or functional adenoma
  3. Excess TSH production by the pituitary adenoma (rare)
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7
Q

What is thyrotoxicosis?

A

Hypermetabolic state due to elevated circulating levels of T3 and T4

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8
Q

What are the primary causes of hyperthyroidism? (4)

A
  1. Diffuse toxic hyperplasia (Grave’s disease)
  2. Hyperfunctioning multinodular goiter
  3. Hyperfunctioning adenoma
  4. Iodine-induced hyperthyroidism
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9
Q

What are the secondary causes of hyperthyroidism?

A

TSH-secreting pituitary adenoma (rare)

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10
Q

What do the signs and symptoms of hyperthyroidism reflect?

A

A hypermetabolic state of target tissues

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11
Q

What are the constitutional symptoms of hyperthyroidism?

A

Skin: soft, warm, and flushed –> heat intolerance and excessive sweating
Increased sympathetic activity and hypermetabolism –> weight loss despite an increase in appetite

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12
Q

What are the GI symptoms of hyperthyroidism?

A

Stimulation of the gut:
Hypermotility –> fat malabsorption & diarrhea

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13
Q

What are the cardiac symptoms of hyperthyroidism?

A

Palpitations and tachycardia
Older adult patients with pre-existing heart disease may develop congestive heart failure

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14
Q

What are the neuromuscular symptoms of hyperthyroidism?

A

Nervousness, tremor, and irritability (sympathetic overactivity)
Nearly 50% of patients develop proximal muscle weakness (thyroid myopathy)

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15
Q

What are the ocular manifestations of hyperthyroidism?

A

Wide, staring gaze and lid lag

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16
Q

What is Grave’s disease?

A

The most common cause of endogenous hyperthyroidism (diffuse toxic goiter)

Autoimmune disorder resulting in increased synthesis & release of thyroid hormones

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17
Q

What is the ratio of women to men developing Grave’s disease?

A

Female: Male
8:1

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18
Q

What is the common age group for developing Grave’s disease?

A

20 to 40 years of age

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19
Q

What is the triad of manifestation for Grave’s disease?

A

Thryrotoxicosis
Infiltrative ophtalmopathy
Localized, infiltrative dermopathy –> sometimes designated pretibial myxedema

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20
Q

What causes thyrotoxicosis in Grave’s diseasE?

A

Diffusely enlarged, hyper-functional thyroid

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21
Q

What is the result of infiltrative ophthalmopathy in Grave’s disease?

A

Exophthalmos

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22
Q

What % of patients with Grave’s disease present with thyrotoxicosis?

A

100% –> All of the patients

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23
Q

What % of patients with Grave’s disease present with infiltrative ophthalmopathy?

A

40%

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24
Q

What is Grave’s disease caused by?

A

Autoantibodies against TSH receptor that bind to, and stimulate, thyroid follicular cells independent of endogenous trophic hormones

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25
Q

What is the pathogenesis of Grave’s disease?

A
  1. Breakdown in self-tolerance to thyroid autoantigens (TSH receptor)
  2. Production of multiple autoantibodies
  3. Thyroid-stimulating immunoglobulin –> IgG antibody binds to TSH receptor and mimics the action of TSH, stimulating adenyl cyclase –> Increased release of thyroid hormones
    OR
    Thyroid-growth stimulating immunoglobulin –> Abs directed against TSH receptor –> Proliferation of thyroid follicular epithelium
    OR
    TSH binding inhibitor immunoglobulins –> Anti-TSH receptor antibodies prevent TSH from binding to its thyroid epithelial cels –> Inhibit thyroid cell function
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26
Q

What is the pathogenesis of Grave’s disease ophthalmopathy?

A

The volume of retroorbital connective tissues and extraocular muscles is increased

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27
Q

What causes the increased volume of retroorbital connective tissue and extraocular muscles? (4)

A
  1. Marked infiltration of the retroorbital space by mononuclear cells (predominantly T cells)
  2. Inflammatory edema and swelling of extraocular muscles
  3. Accumulation of extracellular matrix components, specifically hydrophilic glycosaminoglycans
  4. Increased number of adipocytes (fatty infiltration)
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28
Q

What are examples of glycosaminoglycans?

A

Hyaluronic acid and chondroitin sulfate

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29
Q

What are the gross features of Grave’s disease?

A

The thyroid gland is symmetrically enlarged (35 –> 100g)
The cut surface: firm & dark red

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29
Q

What is the effect of Grave’s opthalmopathy?

A

Changes displace the eyeball forward, potentially interfering with the function of the extraocular muscles

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30
Q

What are the microscopic features of Grave’s disease?

A

Follicular epithelial cells: tall, columnar, and more crowded than usual
Colloid within follicular lumen: pale, with scalloped margins
Interstitium: lymphoid infiltrates (consisting predominantly of T cells, with fewer B cells and mature plasma cells)

31
Q
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32
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33
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33
Q
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34
Q

What is cretinism?

A

Hypothyroidism developing in infancy or early childhood

35
Q

What are the different types of cretinism?

A

Endemic cretinism
Sporadic cretinism

36
Q

What is endemic cretinism?

A

Dietary iodine deficiency is endemic (mountainous areas)

37
Q

What is sporadic cretinism?

A

Enzyme defects that interfere withy thyroid hormone synthesis

38
Q

What is cretinism characterised by? (5)

A
  1. Mental retardation
  2. SHort stature with skeletal abnormalities
  3. Coarse facial features
  4. Enlarged tongue
  5. Umbilical hernia
39
Q

Why is mental retardation a sign of cretinism?

A

Cretinism –> hypothyroidism –> low levels of thyroid hormones in the mother –> decreased levels of T3 and T4 passing through the placenta onto the fetus

40
Q

What is myxedema?

A

Also known as Gull disease
Hypothyroidism in older children or adults

41
Q

What are the clinical features of Myxedema? (9)

A

Decreased basal metabolic rate and decreased stimulation of sympathetic nervous system:
1. Accumulation of glycosaminoglycans in skin and soft tissue
2. Weight gain despite the loss of appetite
3. Slowing of mental activity
4. Muscle weakness
5. Cold intolerance with decreased sweating
6. Bradycardia with decreased cardiac output, leading to shortness of breath and fatigue
7. Oligomenorrhea
8. Hypercholesterolemia
9. Constipation

42
Q

What will the accumulation of glycosaminoglycans in skin and soft tissue cause in cases of myxedema?

A

Deepening of the voice and large tongue

43
Q

What is thyroiditis?

A

Heterogenous group of inflammatory disorders if the thyroid gland

44
Q

What are the most common examples of Thyroiditis? (3)

A
  1. Hashimoto thyroiditis (chronic lymphocytic thyroiditis)
  2. Granulomatous thyroiditis
  3. Subacute lymphocytic thyroiditis
45
Q

What is Granulomatous thyroiditis?

A

Self-limited disease, probably secondary to viral infection like influenza or adenovirus

46
Q

What characterizes Granulomatous thyroiditis?

A

Pain and the presence of granulomatous inflammation in the thyroid

47
Q

What is Subacute lymphocytic thyroiditis?

A

Self-limited disease, occurs after pregnancy (postpartum thyroiditis)

48
Q

What characterizes Subacute lymphocytic thyroiditis?

A

Typically painless, characterized by lymphocytic inflammation in the thyroid

49
Q

What is Hashimoto thyroiditis?

A

Gradual thyroid failure secondary to autoimmune destruction of the thyroid gland

50
Q

What is the most common cause of hypothyroidism?

A

Hashimoto thyroiditis

51
Q

What is the female: male ratio of Hashimoto thyroiditis?

A

Female: male –> 10:1
Older Female: male –> 20:1

52
Q

What is the age group affected by Hashimoto thyroiditis?

A

45 to 65

53
Q

Can Hashimoto thyroiditis occur in chidlren?

A

Yes but it is less common

54
Q

What is the pathogenesis of Hashimoto thyroiditis?

A

Circulating autoantibodies against thyroid agents –> the immune response leads to progressive depletion of thyroid epithelial cells (thyrocytes) –> and replacement by mononuclear cell infiltration and fibrosis

55
Q

What activates the CD4 lymphocytes sensitized to thyroid antigens?

A

Initiated by viral and bacterial infection, which leads to the proliferation of autoreactive cytotoxic CD8+

56
Q

What do the activated CD4 cells also recruit in Hashimoto thyroiditis?

A

They recruit autoreactive B cells to produce antibodies against thyroid agents

57
Q

What are the antithyroid antibodies?

A

Antithyroglobulin
Antithyroid peroxidase antibodies

58
Q

What are the gross features of Hashimoto thyroiditis?

A

Diffusely & symmetrically enlarged gland (6 0 to 200g)

59
Q

What is the cut surface of Hashimoto’s thyroiditis?

A

Pale and grey-tan and fleshly with vaguely nodular pattern

60
Q

What are the microscopic examination of Hashimoto thyroiditis like?

A

The parenchyma: infiltration of mononuclear inflammatory (small lymphocytes, plasma cells, and well-developed germinal centres)

The follicles: atrophic, metaplasia of epithelial cells (abundant eosinophilic, granular cytoplasm –> Hurthle or oxyphil cells)

61
Q

What are Hurthle cells like?

A
  1. Abundant eosinophilic cytoplasm
  2. Round central nuclei
  3. Single prominent nucleus
62
Q

What are the clinical presentations of Hashimoto thyroiditis?

A

Painless enlargement of the thyroid, usually associated with some degree of hypothyroidism, which develops gradually often seen in middle-aged women

63
Q

What may Hashimoto thyroiditis be preceded by?

A

Transient thyrotoxicosis is caused by disruption of thyroid follicles, with the secondary release of thyroid

During this phase, free T4 and T3 concentrations are elevated, TSH is diminished and radioactiveiodine uptake is decreased

64
Q

What happens as hypothyroisism seupervenes?

A

T3 and T4 levels progressively fall, accompanied by a compensatory increase in TSH

65
Q

What does neoplasm of the thyroid usually present as?

A

As a distinct, solitary nodule

66
Q

Which nodule types are more likely to be neoplastic?

A
  1. Solitary nodules rather than multiple nodules
  2. Nodules in younger patients than those in older patients
  3. Nodules in males than those in females
67
Q

Where is increased uptake “hot” nodule seen?

A

In Grave’s disease or nodular goiter

68
Q

Where is decreased uptake “cold” nodule seen?

A

In adenoma and cracinoma

69
Q

What are adenomas of the thyroid?

A

Benign neoplasms derived from follicular epithelium (Follicular adenoma)
Typically is solitary encapsulated neoplasms

70
Q

Which age group do adenomas of the thyroid appear in?

A

40 to 50 year olds

71
Q

What is the female: male ratio of adenomas of the thyroid?

A

Female: male
7:1

72
Q

What is the pathogenesis of the adenomas of the thyroid?

A

Driver mutations in the TSH receptor signaling pathway play an important role in the pathogenesis of toxic adenomas:
1. Activating (gain-of-function) somatic mutations in the gene encoding the TSH receptor itslef or alpha-subunit of Gs
2. Follicular cells secrete thyroid hormone independent of TSH stimulation (thyroid autonomy)
3. Symptomatic hyperthyroidism, with a “hot” thyroid nodule seen on imaging

73
Q
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74
Q
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Endocrine System (11 decks)

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