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Gabe's Endocrinology > Thyroid pathology > Flashcards

Thyroid pathology Flashcards

1
Q

How much does the thyroid weigh?

A

Around 20g, ± 5-10g

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2
Q

What comprises the normal thyroid histology?

A
  • Round-to-oval follicles of various sizes
  • Lined by epithelial cells
  • Filled with colloid (thyroglobulin)(pink stuff)
  • Thin fibrous septa with rich blood supply
  • C Cells (“parafollicular cells”) are a little different - neuroendocrine origin
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3
Q

What surrounds the colloid?

A

Follicular cells

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4
Q

What does the colloid contain?

A

Thyroglobulin

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5
Q

What do the C cells do?

A

They sit in the interstitial spaces, secreting calcitonin for calcium metabolism.

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6
Q

What is the difference between inactive and active thyroid glands?

A
  • Inactive: low cuboidal cells, follicle filled with colloid.
  • Active: Tall cuboidal to columnar cells, scalloping of colloid.
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7
Q

What are the signs and symptoms of a hypometabolic state?

A
  • Cold intolerance; cold thickened skin; alopecia
  • Weight gain (despite decreased appetite); fatigue
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8
Q

What are the signs and symptoms of sympathetic nervous system underactivity?

A
  • Bradycardia, angina, CHF; slow-relaxing reflexes
  • GI (constipation); decreased mood, concentration; other…
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9
Q

What are the consequences of hypothyroidism in children?

A
  • Developmental abnormalities, cretinism
  • children are the most susceptible/affected
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10
Q

What will happen to TSH and fT4 levels in hypothyroidism?

A

Decreased (generally)

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11
Q

What are there inadequate levels of in hypothyroidism?

A

fT3 and fT4

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12
Q

What are the most common primary causes of hypothyroidism?

A
  • Autoimmune hypothyroidism (Hashimoto thyroiditis)
  • Iodine deficiency
  • Drugs (lithium, iodides, p-aminosalicylic acid)
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13
Q

What is thyrotoxicosis (including hyperthyroidism)?

A

Elevated circulating fT3 and fT4 leading to a hypermetabolic state, sympathetic nervous system overactivity and TSH descreases and fT4 increases.

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14
Q

What is hypothyroidism?

A

Inadequate circulating fT3 and fT4 leading to hypometabolic state, sympathetic nervous system underactivity and increased TSH and fT4.

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15
Q

What are the signs and symptoms of a hypermetabolic state?

A
  • Heat intolerance; warm flushed skin; fatigue
  • Weight loss (despite increased appetite); osteoporosis
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16
Q

What are the signs and symptoms of sympathetic nervous system overactivity?

A
  • Palpitations, atrial fibrillation, cardiomegaly, CHF
  • Tremor, anxiety, insomnia, emotional lability
  • GI (diarrhoea), MSK, ocular (lid lag), other…
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17
Q

What are the causes of thyrotoxicosis (including hyperthyroidism)?

A

Diffuse hyperplasia (Grave’s disease) and hyperfunctioning (“toxic”) multinodular goitre.

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18
Q

What is the most common manifestation of thyroid disease?

A

Enlargement of the thyroid, or goitre, is the most common manifestation of thyroid disease

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19
Q

What do diffuse and multinodular goitres reflect?

A

Increased synthesis of thyroid hormone

20
Q

What is a goitre?

A
  • A non-specific term that is used to describe any enlargement of the thyroid.
  • A goiter is an enlarged thyroid gland, and it may be diffuse or nodular.
  • A goitre may extend into the retrosternal space, with or without substantial anterior enlargement.
  • Goiter refers to abnormal growth of the thyroid gland. Adults may have goitres that are diffuse or nodular, and the goitres may be associated with normal, decreased, or increased thyroid hormone production.
21
Q

What is diffuse non-toxic (“simple”) goitre?

A
  • Reflects impaired synthesis of thyroid hormone
  • Low thyroid hormone causes elevation of TSH
  • A compensatory response
  • Usually euthyroid
  • TSH to slightly increase, fT4 (generally)
  • Will “involute” if TSH and thyroid hormone levels return to normal
22
Q

What have thyroid cells done in response to increased TSH, histologically?

A
  • Hyperplastic: “increased number of cells”
  • Follicles lined by crowded cells
  • Some follicles are larger than others, may have large colloid-filled cysts
  • With resolution of high TSH, follicles involute →low cuboidal epithelium and abundant colloid with persistent high TSH, some follicles rupture or haemorrhage and others grow larger
23
Q

What will simple goitre become?

A
  • Multinodular
  • Over time, with cycles of hyperplasia and involution, some follicles become large nodules, while others rupture and fibrose.
24
Q

What can multinodular goitre be?

A
  • “Toxic multinodular goitre” (TMNG)
  • Nodules can be autonomous
  • Patient may be hyperthyroid
  • (Nodule will be “hot” on a NM scan)
25
Q

What is mass effect?

A

Reddening of the face when arms are raised due to a substernal goitre blocking off the thoracic inlet.

26
Q

How is simple goitre managed?

A
  • Iodine or thyroid hormone replacement therapy
    • Diffuse goitre: regression over 3-6months
    • Multinodular goitre: less than a third regress
  • Surgery to relieve compressive symptoms (and for cosmetic effect)
27
Q

What are the histopathological findings of Hashimoto’s disease (hypothyroidism)?

A
  • Formation of lymphoid follicles
  • Marked changes in thyroid epithelial cells
  • Extensive formation of new connective tissue
  • Diffuse “round cell” infiltration
28
Q

What is the histopathology of Hashimoto’s thyroditis?

A
  • Mononuclear inflammatory infiltrate
    • Lymphocytes (equal proportions of T and B cells)
    • Plasma cells
    • Germinal centres
  • Thyroid cells show changes
    • With “abundant, eosinophilic, granular cytoplasm” (‘Hürthle cells’)
  • Increased interstitial connective tissue
    • Fibrosis/scarring: chronic inflammation
29
Q

What are the gross pathological findings of Hashimoto thyroiditis?

A
  • Enlarged at first, eventually atrophic gland;
  • Cut surface: firm, tan-yellow (similar to lymph nodes) pale (fibrotic), somewhat nodular
  • Incision like “cutting through an unripe pear”
30
Q

How does the breakdown of tolerance to thyroid tissues cause damage?

A
  • CD8+ cytotoxic cell-mediated cell death
  • Cytokine-mediated cell death (e.g. IFN-γ, Fas)
  • Antibody-dependent cell-mediated cytotoxicity
  • TSH-blocking ABs further reduce thyroid function
31
Q

Why is there a breakdown of tolerance to thyroid tissues in Hashimoto’s disease?

A
  • “Inciting events not fully elucidated”
  • Treg abnormalities
  • Exposure of normally sequestered thyroid antibodies
32
Q

What are the blood levels seen in Hashimoto’s thyroditis?

A

Increased TSH

Decreased fT4

Increased thyroglobulin antibodies

Highly increased anti-TPO antibodies

33
Q

What will FNA of Hashimoto’s thyroiditis show?

A

Huerthle cells with mixed population of lymphocytes

34
Q

How is Hashimoto’s disease managed?

A
  • Thyroxine replacement
  • Monitor closely if elderly or pregnant
35
Q

What is the triad of findings in Grave’s disease?

A
  1. Hyperthyroidism due to diffuse, hyperfunctional enlargement of the thyroid
  2. Infiltrative ophthalmopathy with resultant exophthalmos
  3. Localised infiltrative dermopathy (“pretibial myxoedema”) in a minority of patients
  • All caused by stimulatory antibodies to TSH receptor!!!
36
Q

What is the histopathology of Grave’s disease?

A
  • Follicular cells are tall and more crowded: Diffuse hypertrophy and hyperplasia
    • May form papillae in follicle lumen
  • Widespread scalloping of colloid
    • Colloid is often paler-staining
  • Lymphocytic infiltrates
37
Q

What is the gross pathology of Grave’s disease?

A
  • Diffuse symmetrical enlargement (cf: multinodular goitre)
  • Cut surface is “soft, meaty”
38
Q

What is the autoimmunity in Grave’s disease against?

A

TSH receptor

39
Q

Which antibody binds and stimulate the TSH receptor in Grave’s disease?

A

Thyroid stimulating thyroglobulin (TSI)

40
Q

What do thyroid growth-stimulating immunoglobulins do?

A

Bind and stimulate TSH receptor

41
Q

What do TSH-binding inhibitor immunoglobulins?

A
  • Stimulate or inhibit TSH receptor
    • Can develop or even present with hypothyroidism
42
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

43
Q

What are the clinical signs of Grave’s disease?

A
  • Symptoms of thyrotoxicosis, possibly a goitre
    • Associated non-thyroid changes
  • Ophthalmopathy (30-50%), pretibial myxoedema (~5%)
  • TSH ↓, fT4 ↑, Anti TPO ABs ↑, TSI↑ (diagnostic)
  • Scintiscan (if necessary) should show diffuse increased uptake
44
Q

What is myxoedema?

A
  • Mucopolysaccharides deposition in the dermis, resulting in in swelling of the affected area.
  • Due to severe hypothyroidism.
45
Q

What opthalmology is associated with Grave’s disease?

A
  • Retro-orbital hydrophilic mucopolysaccharides, oedema, lymphocytes, fibrosis, and fat
  • Fibroblasts seem to be target and effector cells
    • Express TSH-like antigens
    • Produce more hyaluronic acid (GAG: osmotic++)
    • Transform into adipocytes
46
Q

How is Grave’s disease managed?

A
  • Reduce elevated thyroid function:
    • Antithyroid drugs (carbimazole)
    • (18 month regime may result in remission in <50%)
    • Surgery: subtotal thyroidectomy
    • Radioactive iodine ablation
  • Reduce sympathetic overactivity
    • Beta blockers
47
Q

What is the difference between T-cell vs. B-cell autoimmunity?

A
  • B-cell autoimmunity: antibody mediated
    • Type II hypersensitivity
    • Graves disease: an unusual example of increased function caused by antibodies
  • T-cell autoimmunity: cell mediated
    • Type IV “delayed type” hypersensitivity
    • Hashimoto disease

Gabe's Endocrinology (17 decks)

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