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09. Thyroid Pathology > 4. Thyroiditis > Flashcards

4. Thyroiditis Flashcards

1
Q

Definition of thyroiditis

A

Inflammatory conditions of the thyroid gland

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2
Q

Types of thyroiditis

A
  1. Subacute (granulomatous) thyroiditis
  2. Subacute lymphocytic (painless) thyroiditis
  3. Reidel thyroiditis
  4. Hashimoto thyroiditis
  5. Graves disease
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3
Q

What is Subacute (granulomatous) thyroiditis all known as?

A

DeQuervain thyroiditis

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4
Q

Epidemiology & associations with Subacute (granulomatous) thyroiditis

A
  1. Female > male
  2. Most common between ages 40 & 50
  3. Viral infections (mumps, coxsackievirus, adenovirus)
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5
Q

Pathogenesis of Subacute (granulomatous) thyroiditis

A
  1. Inciting agent is probably a viral infection or post-viral inflammatory process which damages thyroid follicular cells, releasing a normally sequestered antigen
  2. This incites cytotoxic T cell mediated injury
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6
Q

Morphology of subacute (granulomatous) thyroiditis

A
  1. [Grossly]
    - Enlarged firm thyroid gland which may be uni or bilateral
    - Patchy appearance (pale yellowish areas intervening with normal brown parenchyma)
  2. [Histologically]
    - Initially, neutrophilic infiltrate, microabscesses
    - Later on, mononuclear infiltrate (lymphocytes, plasma cells, histiocytes) around damaged follicles
    - Multinucleated giant cells engulfing pools of colloid
    - Note that the picture varies with the stage & area sampled (as inflammation affects different parts of the gland at different points in time)
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7
Q

Clinical features of subacute (granulomatous) thyroiditis

A
  1. Sudden/gradual presentation of symptoms
    - Painful goitre (jaw, throat, ears, occasional nodule)
    - Systemic: fever, malaise, anorexia, myalgia
    - Period of disease & recovery lasts 14 weeks
    - Usually self-limiting (not self-perpetuating)
  2. Laboratory test
    - Initial 2-6 weeks: transient mild hyperthyroidism (high T3 & T4, low TSH) due to released of preformed colloid following follicular damage
    - Later 2-8 weeks: transient asymptomatic hypothyroidism
    - Radioiodine uptake diminished
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8
Q

Epidemiology & Associations of Subacute Lymphocytic (Painless) Thyroiditis

A
  1. Female > male

2. Most common in middle age women, post-partum

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9
Q

Pathogenesis of Subacute Lymphocytic (Painless) Thyroiditis

A

Possibly autoimmune etiology

- Occasionally evolves into overt autoimmune disease

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10
Q

Morphology of Subacute Lymphocytic (Painless) Thyroiditis

A
  1. Grossly:
    - Normal/minimal diffuse enlargement
  2. Histologically:
    - Hyperplastic reactive lymphoid nodules
    - No Hurthle cell change or fibrosis (distinguishing factor from Hashimoto thyroiditis)
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11
Q

Clinical features of Subacute Lymphocytic (Painless) Thyroiditis

A
  1. Mild diffuse goitre (condition lasts 2-8 weeks in total)

2. Hyperthyroidism lasting 1-2 weeks

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12
Q

Pathogenesis of Reidel thyroiditis

A

Unknown etiology (postulated to be autoimmune)

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13
Q

Clinical Features of Reidel thyroiditis

A

Extensive fibrosis of thyroid & surrounding structures in the neck, presenting as a hard fixed mass in the neck
- Can mimic thyroid carcinoma

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14
Q

Definition of Hashimoto thyroiditis

A

Autoimmune destruction of thyroid leading to gradual thyroid failure

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15
Q

Epidemiology & Associations with Hashimoto thyroiditis

A
  1. Female > male (females 10-20x more)
  2. Most common between ages of 45 & 65
  3. HLA-DR3, HLA-DR5 (weak association)
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16
Q

Pathogenesis of Hashimoto thyroiditis

A
  1. Cell-mediated cell death by CD8+ cytotoxic T cells
  2. Cytokine-mediated cell death by CD4+ TH1 cells
  3. Antibody-mediated cytotoxicity by antithyroid autoantibodies
    - Anti-thyroglobulin
    - Anti-thyroperoxidase (anti-TPO)
    - Anti-TSH receptor
17
Q

Clinical features of Hashimoto thyroiditis

A
  1. Painless goitre (often diffuse, may be localized)
  2. Laboratory tests
    - Initial transient hyperthyroidism/Hashitoxicosis (high T3 & T4, low TSH)
    - Progressive hypothyroidism (low T3 & T4, high TSH)
    - Detection of autoantibodies
  3. Complications
    - Associated autoimmune disorders (Sjögren syndrome, SLE, type I diabetes mellitus)
    - Extranodal marginal zone B cell lymphoma
18
Q

Morphology of Hashimoto thyroiditis

A
  1. [Grossly]
    - Pale, enlarged thyroid (most commonly diffuse, may be localized)
    - Pale yellow firm cut surface with or without nodules
  2. [Histologically]
    - Lymphocytic infiltrate comprising lymphocytes & plasma cells
    - Reactive lymphoid follicles
    - Atrophic thyroid follicles
    - Follicular cells may display Hurthle cell change (cells with abundant eosinophilic cytoplasm; a metaplastic change in response to ongoing injury)
    - Fibrosis confined within thyroid capsule (does not extend beyond to adjacent structures unlike in Reidel thyroiditis)
19
Q

Definition of Graves disease

A

Can be considered both a hyperplastic thyroid condition as well as a form of thyroiditis; leads to hyperthyroidism

20
Q

Epidemiology & Associations with Graves disease

A
  1. Female > male (females 7x more)
  2. Most common between the ages 20 & 40
  3. HLA-B8, HLA-DR3
21
Q

Pathogenesis of Graves disease

A

Breakdown in self-tolerance to thyroid auto-antigens, resulting in the production of multiple autoantibodies:

  • Thyroid-stimulating immunoglobulin (TSI)
    i. Binds to TSH receptor & mimics TSH action
    ii. Induces release of thyroid hormones
  • Thyroid growth-stimulating immunoglobulin (TGI)
    i. Binds to TSH receptor
    ii. Induces proliferation of follicular cells
  • TSH-binding inhibitor immunoglobulin (TBH)
    i. Binds to TSH receptor to block normal TSH binding to TSH receptors
    ii. Some TBH are agonistic (mimic TSH action)
    iii. Some TBH are antagonistic (inhibit TSH action)
    iv. May explain why Graves patients may experience episodes of hypothyroidism
22
Q

Morphology of Graves disease

A
  1. [Grossly]
    - Symmetrical diffuse goitre
    - Cut surface is soft & meat/beaf-steak like (deep red appearance)
  2. [Histologically]
    - Follicular cells are tall & overcrowded, giving rise to pseudopapillae (also seen in simple & multinodular goitre)
    - Pale scalloped colloid (due to active colloid reabsorption)
    - Lymphocytic infiltration, reactive lymphoid follicles
23
Q

Clinical Features of Graves disease

A

Clinical triad:
1. Hyperthyroidism

  1. Infiltrative ophthalmopathy
    - Exophthalmos (anterior bulging of eyes)
    - Due to marked infiltration of retro-orbital space by lymphocytes (predominantly T cells) as orbital periadipocytes express TSH receptors
    - Causes inflammatory edema & swelling of extraocular muscles
    - Fatty & extracellular matrix accumulation
  2. Infiltrative dermopathy (pretibial myxedema)
    - Scaly thickening & induration of skin over shins
    - Due to lymphocytic infiltration & deposition of extracellular matrix proteins

Physical examination

  1. Diffusely enlarged thyroid gland
  2. May have bruit on auscultation of thyroid gland (due to increased blood flow through gland)

Laboratory tests

  1. Hyperthyroidism (high T3 & T4, low TSH)
  2. Detection of serum TSI
  3. Radioiodine uptake is diffusely increased

Treatment

  1. Propylthiouracil + beta-blockers
  2. Radioiodine ablation, surgical intervention

09. Thyroid Pathology (6 decks)

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