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Pathology Block C > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is this?

A

normal thyroid gland

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2
Q

What is this?

A

Normal thyroid (usu 10-30gm)

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3
Q

What is the function of TSH?

A

1) stimulates T3/T4 production via Iodination of Thyroglobulin
2) stimulates release of T3/4 (by cleavage from Iodinated Thyroglobulin), it than binds Thyroid Binding Globulin in serum

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4
Q

What is the function of Thyroid Peroxidase?

A

1) responsible for the iodination of thyroglobulin
2) readies the Iodine into Iodide

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5
Q

Where do thyroid hormones (T3/T4) carry out its function?

A

It passes to cells where it works intranuclearly: binding the Thyroid Hormone receptor forming a complex

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6
Q

What does the complex of thyroid hormone with thyroid hormone receptor goes on to do?

A

binds Thyroid Response Elements (TRE) in the genome, thereby upregulating transcription (despite it being a peptide derivative!!!)

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7
Q

How does goitrogens affect the thyroids?

A

lead to thyroid enlargment

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8
Q

How does goitrogen work?

A

Inhibit thyroid hormone release in the blood

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9
Q

Explain the two mechanisms for how goitrogens work.

A

1) One mechanism (Iodides) prevents cleavage of thyroglobulin, thus Iodinated Thyroglubulin continues to be stored in the colloid, and low serum T3/T4 leads to increased TSH secretion promoting proliferation of thyroid tissue-> goiter! {includes both Drugs & certain foods}
2) Another mechanism is preventing of Iodine uptake -> leads to Goitrous Hypothyroid

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10
Q

What are the 3 broad classifications of thyroid disease?

A

Hyperparathyroidism

Hypothyroidism

Mass Lesions

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11
Q

How is thyrotoxicosis and hyperthyroidism similar?

A

Thyrotoxicosis is the hypermetabolic state of excess T3/T4; it is most commonly caused by hyperfunction of the Thyroid gland itself (=Hyperthyroidism, thus often used interchangeably)

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12
Q

Contrast thyrotoxicosis and hyperthyroidism.

A

Thyrotoxicosis may also be due to increased release of hormone (as in Thyroiditis) or even extra-thyroidal source (tumor); thus, strictly, hyperthyroidism is a FORM of thyrotoxicosis

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13
Q

What are the most common causes of thyrotoxicosis and hyperthyroidism?

A

Diffuse Hyperplasia (eg: Graves), Hyperfuctional Multinodular Goiter, Hyperfunctionnal Adenoma of Thyroid

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14
Q

What generally happens with elevated thyroid hormones?

A

Increased basal metabolic rate (BMR), sweating, warm skin, weight loss, decreased appetite, lymphandenopathy

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15
Q

What happens cardiovascularly with elevated thyroid hormones?

A

Palpitations, Tachycarddia, arrythmia, even CHF in patients w/ previous CHD

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16
Q

What happens neuromuscularly with elevated thyroid hormones?

A

anxious, tremor, hyperactive, proximal muscle weakness, poor concentration, insomnia

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17
Q

What happens gastrointestinally with elevated thyroid hormone?

A

SNS hyperstimulation -> increased motility, diarrhea, reduced absorption (-> weight loss)

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18
Q

What happens ocularly with elevated thyroid hormone?

A

exopthalmia (more specific to Graves)

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19
Q

What happens skeletally with elevated thyroid hormones?

A

increased bone resorption & osteoporosis (if chronic)

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20
Q

What is a thyroid storm?

A

abrupt onset of hyperthyroidism (elevated thyroid hormone); febrile & tachy; occurs due to underlying disease (graves & stress); medical emergency, can die of arrhythmia

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21
Q

What are 3 causes of thyrotoxicosis?

A

Hyperthyroid, T3/4 Spilling, Tumor

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22
Q

List 5 primary causes of excess thyroid hormone.

A
  1. Diffuse Toxic Hyperplasia (Graves)
  2. Hyperfxning Multinodular Goiter
  3. Hyperfxning Thyroid Adenoma
  4. Hyperfxning Thyroid Carcinoma
  5. Iodine-Induced Hyperthyroidism

*all of these have down-regulated TSH*

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23
Q

What leads to neonatal thyrotoxicosis?

A

associated w/ Maternal Hyperthyroid/Thyrotoxic Disease

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24
Q

What is a secondary cause of elevated thyroid hormone?

A

TSH Secreting Pituitary Adenoma (rare); in this case TSH will be elevated along w/ high T3/T4

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25
Q

What is primary hyperthyroidism?

A

Primary is associated w/ increased T3/T4 due to thyroid overproduction; Low TSH

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26
Q

What is secondary hyperthyroidism?

A

Secondary is associated w/ increased T3/T4 due to upregulation of thyroid; extrinsic to thyroid; High TSH

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27
Q

How effective is TSH as a screening test for hyperthyroidism?

A

TSH is the best measure as it is lowered (by neg feedback) even in the very early stages of disease; this is assoc w/ an incrd T4/T3 level {TSH could be high if TSH tumor though!}

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28
Q

What comes up after TSH as a screening procedure?

A

Follow up w/ radioactive Iodine studies to determine etiology

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29
Q

What’s the link between iodine and Grave’s disease?

A

whole gland increased Iodine uptake

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30
Q

What’s the link between iodine and adenoma?

A

single region of increased Iodine uptake (increased assumes Hyperfunction adenoma)

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31
Q

What’s the link between iodine and adenocarcinoma?

A

single cold spot (Follicular can be hot)

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32
Q

What’s the link between iodine and thyroiditis?

A

decreased Iodine uptake; T3/4 spilling & overproduction is not the issue

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33
Q

What is primary hypothyroidism?

A

due to failure of the Thyroid itself

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34
Q

What is secondary hypothyroidism?

A

due to failure of the Pituitary to make TSH

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35
Q

What is tertiary hypothyroidism?

A

due to failure of the Hypothalamus to make TRH (Rare)

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36
Q

List the major causes of hypOthyroidism.

A

Developmental (thyroid dysgenesis: due to PAX-8, TFF-2, or TSH receptor mutations)

Congenital biosynthetic defect in T3/T4 synthesis

Thyroid Hormone Resistance Syndrome (TR-beta mutation at tissues)

Ablative (Qx/Removal, Radioactive Iodine, Radiation exposure)

Autoimmune (Hashimoto’s)

Iodine Deficiency (3rd world countries)

Drugs (Iodides, a Goitrogen)

Pituitary Defect (secondary Hypo)

Hypothalamic defect (tertiary Hypo)

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37
Q

What is cretinism?

A

Cretinism is hypothyroidism that develops in infancy or early childhood; may be due to iodine deficiency or defective synthesis (congenital enzyme defect as above)

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38
Q

What are the clinical features of cretinism?

A

impaired development of skeleton & CNS: mental retardation, short stature, coarse fascies, protruding tongue, umbilical hernia

degree of abnormality varies based on maternal levels early (normal is high) & late (normal is low) in pregnancy

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39
Q

What is myxedema?

A

Hypothyroidism occurring in older child or adult; thus, often acquired

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40
Q

What are some clinical features of myxdema?

A

Features include slowed mental & physical activity; which may be more apparent in child & indolent in adult (long course for clinical suspicion); other traits are opposite of those seen in Hyperthyroidism along with: edema, coarse features, deepened voice, enlarged tongue-> all due to GAG & Hyaluronic Acid deposition

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41
Q

How is hypothyroidism diagnosed?

A

TSH levels are also important for diagnosis; it will be high in primary hypo, but low in 2ndry or 3ry hypo

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42
Q

What are the 3 most common and clinically significant forms of thyroiditis?

A

Hashimoto’s (Chronic Lymphocytic)

Subacute Granulomatous

Subacute Lymphocytic

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43
Q

List the typical age of onset, male:female ratio, and HLA associations of Hashimoto thyroiditis.

A

45-65yrs, 10:1 or even 20:1 Female:Male; HLA-DR3 & HLD-DR5

44
Q

Patients with Hashimoto’s Disease have _________ risk of developing (exocrine and non-exocrine) autoimmune diseases.

A

increased

45
Q

What other diseases will patients with Hashimoto’s be at risk for?

A

Endocrine autoimmune (Type I DM)

non-endocrine autoimmune (SLE, Myasthenia, Sjogren)

Non-Hodgkin’s Lymphoma

NO specific link to thyroid neoplasms

46
Q

What are 3 autoantibodies produced by B lymphocytes in Hashimoto thyroiditis?

A

Anti-TSH Receptor, Anti-Thyroglobulin, Anti-Thyroid Peroxidase

47
Q

Three mechanisms of Thyrocyte Death

A
  1. CTL mediated cell death
  2. CD4 mediated cytokine release (INF-γ) that activates Macros leading to cell death
  3. Anti-Thyroid Antibodies mediated cell death
48
Q

What are the functions of anti-thyroid antibodies?

A

All three lead to Ab-Dependent Cell-mediated Cytotoxicity (ADCC)

They will all alter T3/T4 production & release, and Anti-TSH-R blocks TSH

49
Q

What is this?

A

Hashimoto’s Thyroditis

50
Q

What do you expect to see on micro slide for Hashimoto’s thyroiditis?

A

Thyroid gland w/ Lymphoid Follicles (mononuclear cells); Atrophic Thyroid follicles; Hurthle Cells

In addition, Fibrous variants may demonstrate broad, kelloid like fibrosis

51
Q

What are Hurthle cells?

A

cells w/ eosinophilic granular cytoplasm found in Hashimoto’s thyroiditis

52
Q

Describe the clinical course of Hashimoto thyroiditis.

A

Gradual autoimmune destruction of the thyroid gland; it is the most common cause of hypothyroidism where Iodine intake is sufficient; it presents painlessly,

Initial Thyrotoxicosis/Hashitoxicosis (incrd T3/4 & decrd TSH) -> Euthyroid -> Hypothyroid (decrd T3/4 & incrd TSH)

53
Q

List the typical age of onset and male:female ratio of Granulomatous Thyroiditis

A

30-50 yrs; 3:1 or 5:1 Female:Male (again women favored)

54
Q

Discuss the proposed etiology of Granulomatous Thyroiditis

A

Occurs secondary to antecedent viral infection (cocksackie, mumps, measles, adenovirus), w/ a summer predilection

One hypothesis is that viral infection leads to release of an Ag (viral or thyroid is unclear) that leads to CTL mediated attack on Thyrocytes (follicular cells); this is in contrast to Auto-immune diseases due to the viral induced component

55
Q

What’s the most common cause of endogenous hyperthyroidism? What’s its frequency?

A

Graves Disease

It occurs in 1.5-2% of women in US; w/ incr’d incidence in families

56
Q

What’s the “Classic Triad” of Grave’s disease?

A
  1. Hyperthyroidism (leads to Hyperplasia of thyroid)
  2. Opthalmopathy – Exopthalamus
  3. Dermatopathology – Localized & infiltrative: Pretibial Myxedema in some ptnts
57
Q

What’s the difference between myxdema or pretibial myxdema?

A

Myxedema refers to Adult HYPOthyroid, but Pretibial Myxedema can occur in Graves (disease of hyperthyroidism)

58
Q

List the typical age of onset, Male:female ratio, and HLA associations of Graves disease

A

20-40 yrs; 7:1 Female:Male; HLA-B8 & HLA-DR3; CTLA-4 defects have also been noted (CTLA-4 normally reduces response of T-cells to self-Ag, binds B7)

59
Q

State the underlying etiology of Graves disease

A

Various Auto-Ab may be present in the serum, most important of which is the TSH Receptor stimulating Ab (opp of TSH-R blocking Ab, 1 of 3 seen in Hashimoto’s)

60
Q

What are the 3 autoantibodies found in Grave’s disease (similar to Hashimoto’s)?

A

Auto-Abs targeted against TSH receptors, thyroid peroxidase, and thyroglobulin

61
Q

What are the auto-antibodies reserved for Grave’s disease?

A

(All three binds to TSH receptors)

  1. Thyroid Stimulating Immunoglobulin
  2. Thyroid Growth Stimulating Immunoglobulin (stimulates growth of tissue itself)
  3. TSH-Binding Inhibitor Immunoglobulins (blocking TSH from binding - stim or inhib - may be related to the presence of spontaneous hypothyroidism sometimes seen in Graves)
62
Q

Compare and contrast Hashimoto’s with Grave’s.

A

Opposite extremes of the autoimmune disease spectrum (Hashimoto’s - hypO; Grave’s - hypER)

Hashimoto’s occur later (55s) than Grave’s (30s)

Both can have CROSSOVER during progress (patient may be concurrently both diseases).

Also, both have a strong link with other autoimmune diseases and intrathyroidal lymphoid infiltrate

63
Q

What’s expected grossly in Graves?

A

>80g; smooth and soft

64
Q

What’s expected microscopically with Graves?

A

“Too Many Cells”; hypertrophied follicles, w/ tall columnar epi, scalloped edge colloid, and papillary-like insertions of epithelium into the colloid due to overgrowth; as above, Intrathyroidal Lymphoid Infiltrate (T’s, B’s, Plasma) & even germinal centers (as in Hashimoto’s)

65
Q

What’s particularly special about the eyes in Graves?

A

exopthalamos! eyeballs will show edema

66
Q

Describe clinical course of Graves.

A

General changes assoc w/ Thyrotoxicosis apply, but also…

Hyperplasia of thyroid, Opthalmopathy, Dermatopathology (eg: pretibial myxedema - thickening, peau d’orange, induration, slight pigmentation)

Weakened extraocular muscles due to Exopthalmia (persists even w/ Graves treatment)

67
Q

Lab findings of Graves?

A

elevated T3/4 w/ low TSH; incrd & diffuse uptake of Radioactive Iodine

68
Q

Treatment of Graves?

A

ablation of tissue: Qx/removal, Propylthiouracil (a goitrogen), radioiodine

69
Q

Why do we get goiters?

A

thyroids enlarged due to compensatory hyperplasia in attempt to maintain euthyroid state when there’s impaired synthesis of thyroid hormone (GRAVE’S EXCEPTION)

*MOST COMMON MANIFESTATION OF THYROID DISEASE*

70
Q

What’s goitrous hypothyroidism?

A

when the compensation of a goiter is insufficient

71
Q

Define diffuse goiter.

A

the goiter formation is diffuse within the thyroid & no nodularity; assoc w/ Endemic or Sporadic Goiter

72
Q

Define multinodular goiter.

A

chronic cycles of hyperplasia & involution lead to irregular enlargement of the thyroid; arise from diffuse (simple) goiters which recur, thus can also be assoc w/ Endemic or Sporadic; cause the largest goiters, and may be confused for neoplasia

73
Q

What’s endemic goiter?

A

Areas where 10% of the population has a goiter related to poor availability of Iodine in the soil, water, & food (mountainous areas like: Alps, Andes, Himalayas)

In these areas, Goitrogenic foods (cassava, cabbage, brussel sprouts, turnips) may exacerbate

74
Q

What’s the accepted theory of multinodular goiter development?

A

Due to variations in responsiveness of follicular cells to growth factors (eg: trophic hormones, mutations in TSH response pathway proteins may be involved) - some cells may have a growth advantage and may even become autonomous (similar to thyroid Adenomas)

nodules may be poly & monoclonal; uneven growth may lead to rupture of follicles & vessels, which can create fibrosis & perpetuate a 2nd rupture

75
Q

What’s seen grossly in multinodular goiter?

A

Asymmetric, nodular hyperplasia of thyroid; 2,000g’s is possible

Large size may impede on neck & mediastinal structures (Mass Lesion)

76
Q

What’s seen microscopically in multinodular goiter?

A

colloid filled follicles, w/ low columnar epi & hyperplastic epi; hemorrhage, fibrosis, calcification, & cysts are signs of degenerative change (grow so fast!)

77
Q

Describe clinical course of goiter.

A

For both types, main problem is Mass Effect on structures of neck, thoracic outlet, and mediastinum

Both show high TSH (trying to maintain euthyroid) and increased radioiodine uptake in “Hot” zones of hyperplasia

Most cases are euthyroid (a few mutlinodular can be hyper or hypothyroid)

*if hyperthyroid - does not have opthalmopathology or dermatopathology*

78
Q

Discuss the male:female ratio and clinical significance of a Solitary Thyroid Nodule.

A

4:1 Female:Male; it is a palpable mass in an otherwise normal thyroid

Possibility of neoplasia in a solitary nodule is a major concern when detected; luckily 10:1; benign:malig

79
Q

State the frequency and general overall prognosis of thyroid malignancy

A

Rare ; good prognosis

80
Q

What are the 5 clinical criteria of thyroid nodule?

A
  1. Solitary vs. Multiple (solitary more likely neoplastic)
  2. Young (more likely neoplastic)
  3. Males (more likely neoplastic)
  4. Radiation of head and neck (increased risk of neoplasm)
  5. Hot nodules (more likely BENIGN - exception is follicular carcinoma which may be hot or cold - think: INFLAMMATION)

Summary: Solitary “Cold” nodule in a young male with a history of radiation is most likely to be neoplastic

81
Q

Describe the derivation of typical thyroid adenoma.

A

derived from follicular epithelium, aka: Follicular Adenomas

A small portion may produce T3/4 autonomously, aka Multinodular Goiters

82
Q

What’s grossly seen in typical thyroid adenoma?

A

grey-white to yellow-brown; encapsulated; can be reminiscent of Multinodular Goiter w/ calcification, hemorrhage, fibrosis, & cystic change; normally a single foci & will compress adjacent tissue (both v. Multinodular Goiter)

83
Q

What’s seen microscopically in typical thyroid adenoma?

A

distinct pattern of clonal follicular cells; NO papillary arrange (suggests malig!)

84
Q

What’s seen clinically in thyroid adenoma?

A

Painless Cold Nodule

Sx may include dysphagia due to mass effect; possibility of Hyperfxnal or Toxic Adenoma (rare Hot Nodule)

They take up less Radioactive Iodine = Cold nodules (differ from Multinodular goiter); but, not all cold nodules are adenoma (some cold nodules may be malignant, 10%)

85
Q

What’s important in the diagnosis of thyroid adenoma?

A

Fine needle aspiration & most importantly surgical specimen (tell if benign/malignant)

86
Q

What’s the significance of a “cold” thyroid nodule?

A

takes up LESS Radioactive Iodine than normal tissue

87
Q

What’s the significance of a “hot” thyroid nodule?

A

takes up MORE Radioactive Iodine than normal tissue

88
Q

List and rank by frequency the 4 major subtypes of thyroid cancer.

List and rank by prognosis the 4 major subtypes of thyroid cancer.

A

frequency: papillary > follicular > medullary > anaplastic

“please forgive my aunt”

THE EXACT OPPOSITE for prognosis

89
Q

What are the 3 proven/suspected risk factors for thyroid carcinoma?

A

genetics, radiation exposure, long standing multinodular goiter (growth factor response)

90
Q

List the typical age of onset and risk factors for Papillary Carcinoma of the thyroid.

A

20-40yrs (same as Graves), most commonly assoc w/ exposure to Ionizing Radiation

91
Q

What’s seen microscopically in papillary carcinoma?

A
  1. Papillary appearance w/ Fibrovascular core (infiltrating or fairly well delimited)
  2. Clear to Empty look of the nuclei (Orphan Annie Eye Nuceli)
  3. Psammoma Bodies – concentrically calcified structures w/in the lesion; used for discrimination from Follicular v. Medullary Carcinoma
  4. Lymphatic invasion is common, blood vessel invasion is not
92
Q

What is this?

A

papillary carcinoma

93
Q

What is this?

A

Papillary Carcinoma

94
Q

What’s the classic presentation of papillary carcinoma?

A

most are asymp thyroid nodules; may show up as metast to cervical node, but still good prog; Mass Effect if big (eg: dysphagia); possible lung metast also

95
Q

What are the Scintscan findings of papillary carcinoma?

A

most are “Cold” lesions; Fine needle aspiration is also useful (Orphan Annie)

96
Q

What’s the prognosis of papillary carcinoma?

A

GOOD

10yr survival 95%; 5-20% recur; 10-15% metast; also depends on Age (>40 is worse), extrathyroidal extension, & metastasis

97
Q

List the typical age of onset and proposed risk factors for Follicular Carcinoma.

A

40-50yr old women most common; possibly assoc w/ Nodular Goiters in endemic iodine deficient regions; ras mutations correlate Follicular Adenoma & Carcinoma

98
Q

Discuss the significance of a thyroid malignancy presenting as a “Hot” nodule.

A

This is a hyperfxnal lesion, and thus may lead to Thyrotoxicosis (hyperthyroidism)

99
Q

What carcinoma is a neuroendocrine tumor?

A

Medullary Carcinoma, as it is derived from the Parafollicular or C-cells; assoc w/ MEN2

100
Q

What’s the most typical secretory product of Medullary Carcinoma

A

Calcitonin (although, VIP, SS, 5HT also possible)

101
Q

What is acellular amyloid deposits associated with?

A

medullary carcinoma

102
Q

ID the clinical course of medullary carcinoma.

A

Present as mass in neck, sometimes w/ mass effect; may demonstrate 1st as Paraneoplastic Syndrome due to VIP, SS, 5HT; but surprisingly, Hypocalcemia is NOT common!

103
Q

Identify the prognosis of Anaplastic Carcinoma of the thyroid gland

A

BAD

No effective therapy, almost uniformly fatal w/in a year due to rapid growth & Mass Effect compressing vital neck structures; it is the worst of the Thyroid Carcinomas

104
Q

State the most common clinically significant congenital anomaly of the thyroid gland

A

Thyroglossal Duct Cysts

105
Q

What’s the clinical significance of thyroglossal duct cyst?

A

May convert into abscess cavities, and in rare instances can demonstrate premalignant potentional

Pathology Block C (7 decks)

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