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MBBS II ERS > L09 – Autoimmune Thyroid Disorders and Thyroiditis > Flashcards

L09 – Autoimmune Thyroid Disorders and Thyroiditis Flashcards

1
Q

3 common causes of hyperthyroidism?

A

 Graves’ disease
 Toxic multinodular goiter
 Toxic adenoma

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2
Q

2 causes of Transient hyperthyroidism?

A

 Initial phase of Hashimoto thyroiditis

 Subacute granulomatous thyroiditis

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3
Q

List symptoms of hyperthyroidism? think increased sympathetic activity

A

 Irritability, nervousness/anxiety  Heat intolerance, excessive sweating warm flushed skin
 Tremors
 Palpitations, tachycardia
 Weight loss despite increase in appetite
 Hypermotility of intestines&raquo_space; steatorrhea
 Proptosis (Graves’ disease)
 Fatigue

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4
Q

List some primary, congenital causes of Hypothyroidism?

A

 Thyroid dysgenesis
 Dyshormonogenetic goiter
 Enzyme defects in thyroid hormone synthesis

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5
Q

Most common cause of hypothyroidism?

A

Autoimmune: Hashimoto thyroiditis

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6
Q

List some iatrogenic causes of hypothyroidism?

A

surgical / radiation-induced ablation

Drug-induced, e.g.: lithium, iodides

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7
Q

What diseases cause secondary hypothyroidism?

A

hypothalamic / pituitary diseases

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8
Q

List some clinical manifestations of hypothyroidism in children?

A

cretinism:

 Severe mental retardation
 Short stature
 Coarse facial features, protruding tongue
 Umbilical hernia

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9
Q

List some clinical manifestations of hypothyroidism in older children and adults? think decreased sympathetic activity

A
  • Constipation
  • Cool, pale skin with decreased sweating
  • Fatigue, reduced exercise capacity and weak pulse
  • Apathy
  • Mental sluggishness
  • Non-pitting peripheral edema
  • Broad and coarse facial features with enlargement of tongue and deepening voice
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10
Q

Explain how hypothyroidism causes reduced cardiac outut?

A

Low thyroid hormones = decreased transcription of Sarcolemmal genes (Ca-ATPase)/ SERCA = decreased cardiac output efficiency

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11
Q

List the 3 autoantibodies made in Grave’s disease?

A
  1. Thyroid-stimulating immunoglobulins (TSI) = stimulatory *****
  2. Thyroid growth-stimulating immunoglobulins (TGSI) = stimulatory
  3. TSH-binding inhibitor immunoglobulins (TBII) = inhibitory
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12
Q

Explain why some patients with Grave’s can exp. hypothyroidism?

A

Stimulating and inhibiting immunoglobulins may coexist

> > spontaneously develop episodes of hypothyroidism

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13
Q

Compare the effects of TSI and Thyroid growth stimulating Ab?

A

TSI = IgG binds to TSH receptor&raquo_space; mimics TSH&raquo_space; Stimulate adenyl cyclase&raquo_space; release thyroid hormones

TGSI = also targets TSH&raquo_space; proliferation of thyroid follicular epithelium

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14
Q

Effect of TSH-binding inhibitor Ab?

A

Prevent TSH from binding to its receptor on thyroid follicular epithelial cells = inhibit thyroid cell function

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15
Q

3 clinical presentation signatures of Grave’s?

A
  1. Diffuse symmetrical enlargement of gland (goiter)
  2. thyrotoxicosis and related symptoms
  3. infiltrative ophthalmopathy/ Exophthalmos
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16
Q

Describe the gross changes to the thyroid gland in Grave’s disease? P/E result?

A
  • Diffuse symmetrical enlargement: congested/ haemorrhagic
  • Prominent vascularity, increased blood flow = Bruit
  • Soft, Spongy, without well- defined nodules
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17
Q

3 pathological changes associated with infiltrative ophthalmopathy?

A
  1. Increase in inflammatory cells (mainly T cells)
  2. Accumulation of extracellular matrix = myxoid ground substance
  3. Increase in number of adipocytes (fatty infiltration)

> > > edema of retro-orbital tissue and extraocular muscles
displace eye forward

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18
Q

Complications of infiltrative opthalmopathy?

A
  • Opthalmoplegia: extraocular muscles weaken over time

- Exophthalmos > corneal injury

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19
Q

Pathological changes seen in infiltrative dermatopathy?

A

Pretibial Myxedema:
- Dermis expanded due to Mucopolysaccharide deposits on skin over shins ***
» Pigmented nodules with Orange peel texture

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20
Q

Epidemiology and genetic mutations of Grave’s disease?

A
  • Women predominant, 20-40
  • HLA- DR9 in Chinese
  • Polymorphism of Inhibitory T-cell receptor CTLA-4 & Tyrosine phosphatase PTPN22
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21
Q

Thyroid hormone level changes in Grave’s?

A

 Elevated serum free T4, T3
 Suppressed serum TSH
 Serum autoantibodies

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22
Q

Radiological test for Grave’s?

A

I-123 scan: radioactive iodine uptake is diffusely increased

Ultrasound or CT scans

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23
Q

Describe the histological appearance of thyroid gland in Grave’s disease?

A
  • Small thyroid follicles with PAPILLARY INFOLDINGS (loss of colloid content)
  • Follicular cell hyperplasia
  • SCALLOPING of colloid (pushed to periphery of follicles)
  • Patchy LYMPHOCYTIC infiltration
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24
Q

Treatment options for Grave’s disease?

A

1)
i) Anti-thyroid drugs (e.g. methimazole, propylthiouracil, carbimazole)
ii) β-blockers e.g. propranolol = control/relieve the cardiac symptoms)

2) Nonradioactive iodine (inhibit T3/T4 release and peripheral conversion)
3) Refractory = Radioactive Iodine Ablation + lifelong T4 supplement
4) Refractory = Thyroidectomy

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25
Q

Ddx of Grave’s disease? think about the metrics and P/E exam (5)

A

Adenomatous nodules (nodular hyperplasia)

Toxic multinodular goiter (hyperthyroidism w/o autoAb)

Early Hashimoto thyroiditis = ‘Hashitoxicosis’

PAPILLARY thyroid CARCINOMA

Dyshormonogenetic goiter (inherited defect in T4/T3 metaolism)

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26
Q

Complications of treatments for Grave’s disease?

A

Radioactive iodine = follicular destruction, fibrosis, and dystrophic calcification = hypothyroidism

Anti-thyroid drugs = hyperplastic changes (degenerative, not malignant) + loss of colloid

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27
Q

Which condition resembles Grave’s histologically but has opposite thyroid hormone levels?

A

Dyshormonogenetic goiter

Low T3/T4 but high TSH = opposite to Grave’s

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28
Q

Name the most common carcinoma of the thyroid and list 3 histological features?

A

Papillary thyroid carcinoma

Papillary architecture
cells with nuclear grooves
+ pseudonuclear inclusions

29
Q

Ddx Grave’s from Toxic multinodular goiter?

A

Toxic Multinodular goiter:
- Also Hyperthyroidism

  • NO Auto-Ab
  • Multinodular vs no defined nodules in Grave’s
  • Abundant colloid vs reduced colloid in Grave’s
30
Q

Ddx Adenomatous nodules and Grave’s?

A

Adenomatous nodules:

  • No AutoAb
  • Multinodular asymmetrical goiter* vs symmetrical, diffuse goitre in Grave’s
  • Abundant colloid vs reduced colloid in Grave’s
31
Q

Pathogenesis of Hashimoto thyroiditis?

A
  • Anti-thyroglobulin autoAb + Anti-thyroid peroxidase microsomal antibodies bind to thyroid antigens

> > ADCC + Activation of CD4 Th1

> > Progressive depletion/ fibrosis of thyroid epithelial cells

32
Q

Clinical presentation of Hashimoto’s?

A
  • Painless, symmetrical, diffusely enlarged thyroid
  • Hypothyroidism symptoms
  • Transient thyrotoxicosis (Hashitoxicosis)
33
Q

Hashimoto’s predispose to development of which cancer?

A

primary thyroid non-Hodgkin lymphomas

34
Q

Which conditions are associated with hashimoto’s?

A

Other autoimmune diseases:

Pernicious anemia
Type II diabetes mellitus
SLE
Thrombotic thrombocytopenic purpura

35
Q

Epidemiology and genetic predisposition of Hashimoto’s

A

Women predom, 45-65

HLA-DR3 and -DR5

CTLA4 polymorphism

High familial clustering

36
Q

Which dietary deficiencies can lead to Hashimoto’s?

A

iodine, selenium deficiency

37
Q

Thyroid hormone levels in Hashimoto’s?

A

 Suppressed T4 / T3

 Elevated TSH

38
Q

Which Ab in Hashimoto’s is more specific?

A

 Antithyroglobulin antibody in >60% of patients

 Antithyroid microsomal antibodies** in 95% of patients

39
Q

Gross changes to thyroid in Hashimoto’s?

A

symmetrically enlarged (2-3 times the size of normal)

Bosselated (with protuberance)/ irregular surface

Prominent pyramidal lobe

40
Q

Overall changes to the thyroid parenchyma in Hashimoto’s?

A
  • Accentuated LOBULATION
  • Diffuse lymphoplasmacytic/ Chronic inflammatory cell infiltration
  • FIBROSIS of parenchyma = yellow
41
Q

Typical Histological changes to thyroid in Hashimoto’s?

A
  • REACTIVE LYMPHOID follicles *** with prominent germinal center formation
  • ATROPHIC*** THYROID follicles
  • Follicular cells show prominent **Hürthle cell change **
42
Q

Describe Hürthle cell changes?

A

Cellular enlargement

Increased number of mitochondria

eosinophilic, granular cytoplasm

43
Q

Histological changes seen in Fibrotic variant of Hashimotos?

A

Prominent acellular, KELOID- LIKE FIBROSIS
Does NOT extend beyond gland = Ddx from Riedel’s Thyroiditis

FOLLICULAR ATROPHY

Chronic inflammatory cell infiltrate

44
Q

Treatment options for Hashimotos?

A
  • Levothyroxine (lifelong)
  • immunosuppressive therapy (e.g. steroids)
  • Unresponsive/ malignant/ compressive = Surgery
45
Q

DDx of Hashimoto thyroiditis?

A
  • Lymphocytic thyroiditis
  • Riedel thyroiditis/ IgG4- related thyroiditis
  • Papillary thyroid carcinoma
  • Lymphoma
46
Q

Pathogenesis of subacute lymphocytic thyroiditis?

A

Initial inflammation and destruction of thyroid follicles = 4-8 weeks thyrotoxicosis

Thyroid depleted of colloid = hypothyroidism after 2 months

47
Q

2 theories for pathogenesis of Riedel’s thyroiditis?

A

1) Anti-thyroid antibodies&raquo_space; autoimmune

2) SLE/ Scleroderma&raquo_space; IgG4-related sclerosing disease&raquo_space; dense thyroid fibrosis

48
Q

Clinical presentation of Riedel’s thyroiditis?

A
  • Usually EUTHYROID, subsequent hypothyroidism
  • ‘Sudden’ onset of enlarged, painless neck mass
  • dysphagia, dyspnoea, and stridor
  • Non-tender, HARD GLAND on palpation
49
Q

Explain why Riedel’s thyroiditis cause dysphonea?

A

Fibrosis of thyroid cause compression and excasement of recurrent laryngeal nerve

50
Q

Thyroid hormone levels in Riedel thyroiditis? Antibodies?

A

anti-thyroglobulin antibodies and anti microsomal antibodies (similar to Hashimoto’s)

Usually euthyroid, 30-40% develop subsequent hypothyroidism

51
Q

Gross morphology of thyroid in Reidel thyroiditis?

A
  • Avascular, woody, tan-grey with loss of lobulation
  • Extensive fibrosis

HARD GLAND

52
Q

Histological appearance of Riedel’s thyroiditis?

A

Similar to Fibrotic Variant of Hashimotos

  • KELOID-LIKE FIBROSIS replace follicles
  • Extension of fibrosclerotic process to extrathyroidal soft tissue and parathyroid gland Ddx from Fibrotic variant of Hashimoto
  • lymphocytes, plasma cells infiltration
53
Q

Treatment options for Riedel thyroiditis?

A

steroids, tamoxifen

Hypothyroid = hormone replacement

Systemic fibrosis = Mycophenolate mofetil

Compressive symptoms = Surgery

54
Q

Name 2 conditions morphologically similar to Riedel thyroiditis?

A

Fibrotic Variant of Hashimoto’s**
IgG4-related thyroiditis

Only Riedel’s thyroiditis fibrotic process extend beyond gland

55
Q

Gross morphology, histology of IgG4-related thyroiditis?

A

WHITE with lobulations + fibrotic

STROMAL FIBROSIS + FOLLICULAR ATROPHY

lymphocytes, plasma cells infiltration

Fibrosis does NOT extend to extrathyroid tissue Ddx Riedel’s

56
Q

Dx of IgG4- related thyroiditis?

A

↑ IgG4+/IgG+ plasma cells (>40%) histologically

57
Q

Epidemiology of Subacute granulomatous thyroiditis?

A

Women predom, 30-50

58
Q

Causes of Subacute granulomatous thyroiditis (de Quervain’s thyroiditis)?

A

preceding URTI &raquo_space; inflammatory rxn

After anti-viral therapy (interferon) (rare)

59
Q

List some viral infectons that precede Subacute granulomatous thyroiditis?

A

Measles, influenza, adenovirus, Epstein-Barr virus, Coxsackie virus, mumps, HIV, H1N1

60
Q

Symptoms of Subacute granulomatous thyroidits?

A

6-8 weeks:
neck pain, sore throat and difficulty in swallowing, low-grade fever, malaise

initial ‘thyroid storm’ followed by hypothyroidism

Enlarged, tender thyroid

61
Q

Thyroid levels in subacute granulomatous thyroiditis?

A

Initial - High T3/T4, low TSH (Thyroid storm)

Mid-phase = hypothyroidism

Late = euthyroid

62
Q

Gross appearance of subacute granulomatous thyroiditis?

A

Firm, glossy, intact capsule

unilaterally or bilaterally enlarged

63
Q

Histology of subacute granulomatous thyroiditis?

A

Disruption of thyroid follicles, extravasation of colloid

MULTINUCLEATED GIANT CELLS to engulf colloid

64
Q

DDx of subacute granulomatous thyroiditis?

A

Other foreign body type granulomatous reactions:

  • Mycobacterium
  • Fungus
  • Sarcoidosis
65
Q

List some pathogens that can cause infectious thyroiditis?

A

Streptococcus haemolyticus, staphylococcus aureus, pneumococcus

(actinmyces, candida spp., pneumocystis jirovecii)

66
Q

Pathogenesis of infective thyroiditis?

A

NEUTROPHILIC infiltration and cytotoxicity

ABSCESS formation and follicle extravasation&raquo_space;> Graulomatous reaction

67
Q

Histological appearance of radiological thyroiditis? (e.g. after radiotherapy for head and neck squamous cell carcinoma)

A

 DISRUPTED ARCHITECTURE

 Parenchymal FIBROSIS, vascular sclerosis

 Chronic (lymphocytic) inflammation

68
Q

What is the cause and reaction of palpation thyroiditis?

A

vigorous clinical palpation of the thyroid

Colloid is leaked from traumatized follicles into the surrounding stroma
» foreign body type granulomatous reaction

69
Q

List some drugs that can induce thyroiditis? Effect on thyroid activity?

A

Iodide, lithium, anticonvulsants, amiodarone

> > Painless enlargement of thyroid gland
Hyper- / hypo-thyroidism

MBBS II ERS (37 decks)

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