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M2 Endocrine > thyroid pathology > Flashcards

thyroid pathology Flashcards

1
Q

causes of diffuse goiter

A

Graves disease, Hashimoto Thyroiditis, DeQuervain thyroiditis, simple goitre

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2
Q

causes of localized swelling/nodular goitre

A

nodular goitre, neoplasms, thyroiditis

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3
Q

causes of hyperthyroidism/thyrotoxicosis

A

Graves disease, hyperplasia, nodular goitre, neoplasms

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4
Q

causes of hypothyroidism

A

Hashimoto Thyroiditis, congenital abnormalities

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5
Q

causes of euthyroid derangement

A

nodular goitre, neoplasms

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6
Q

hyperthyroid symptoms

A

weight loss, heat intolerance, oligomenorrhea, diarrhoea, irritable mental state, increased appetite

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7
Q

symptoms of hypothyroidism

A

weight gain, cold intolerance, menorrhagia, constipation, mental slowness, poor appetite

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8
Q

hyperthyroidism signs

A

loss of weight, staring gaze, lid lag, *exophthalmos, warm and sweaty skin, tachycardia, atrial fibrillation, *pretibial myxedema, proximal myopathy

*: only in Graves

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9
Q

hypothyroidism signs

A

weight gain, peaches and cream skin, dry cool skin, bradycardia, pericardial effusion, proximal myopathy

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10
Q

congenital thyroid diseases

A
  1. thyroglossal duct cyst
  2. abnormal development of thyroid gland
  3. ectopic thyroid tissue
  4. thyroid dyshormonogenesis
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11
Q

causes of diffuse and multinodular goitre

A

due to iodine deficiency or dyshormonogenetic goitre causing a compensatory increase in TSH –> hypertrophy and hyperplasia of follicular cells

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12
Q

progression of disease of diffuse non-toxic non-hyperfunctioning goitre

A
  1. hyperplastic stage: diffuse mild enlargement, crowded columnar cells, pseudopapillae
  2. colloid involution stage: flattened cuboidal epithelium, abundant colloid
  3. multinodular goitre stage: extreme irregular enlargement, cystic change, haemorrhage, compression on trachea and recurrent laryngeal nerve
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13
Q

Hashimoto Thyroiditis risk factors

A

female, 45-60yo, HLA-DR3/DR5 genes, other autoimmune diseases

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14
Q

Hashimoto Thyroiditis pathogenesis

A
  1. sensitisation of CD4+ Th cells to thyroid antigens
  2. cytotoxic CD8+ T cell mediated cell death
  3. cytokine (IFN-γ) mediated cell death - ADCC via autoantibodies against thyroglobulin, TSH receptor and thyroid peroxidase
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15
Q

morphology of Hashimoto Thyroiditis

A

grossly: pale diffusely enlarged gland, pale yellow firm cut surface ± nodules

microscopically: infiltrates including reactive lymphoid follicles, lymphocytes, plasma cells, thyroid follicles that are atrophic, Hurthle cell change, larger eosinophilic granular cytoplasm, fibrosis

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16
Q

Graves disease risk factors

A

female, 20-40yo, family history of HLA-B8/DR3 genes, other autoimmune conditions

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17
Q

clinical triad for Graves disease

A
  1. hyperthyroidism
  2. infiltrative ophthalmopathy
  3. infiltrative dermopathy (pretibial myxedema)
18
Q

pathogenesis of Graves disease

A
  1. breakdown in Th cell tolerance
  2. autoantibodies to TSH receptors (thyroid stimulating immunoglobulin, TSH-binding inhibitor immunoglobulin)
  3. overstimulation of thyroid gland, leading to thyrotoxicosis, diffuse goitre ±bruit, ophthalmopathy and dermopathy due to Th cells cytokines attacking retro orbital tissue
19
Q

morphology of Graves disease

A

grossly: symmetrical diffuse enlargement, soft reddish meaty cut surface

microscopically: tall columnar crowded follicular cells with pseudopapillae, pale scalloped colloid, lymphoid infiltrates and reactive lymphoid follicles

20
Q

risk factors for DeQuervain thyroiditis

A

female, 30-50yo, short history (weeks), self limiting, recent URTI

21
Q

pathogenesis of DeQuervain thyroiditis

A

virus-induced cytotoxic T-cell response to thyroid antigens leading to follicular cell damage, neck pain, and goitre

22
Q

DeQuervain thyroiditis morphology

A

grossly: enlarged firm gland, patchy (firm yellow pale atead with intervening normal parenchyma)

microscopically: destruction of follicles, neutrophilic invasion, microabscesses, lymphocytes, plasma cells, histiocytes around damaged follicles, multinucleated giant cells engulfing pools of colloid

23
Q

IgG4 related thyroiditis pathogenesis

A

assoc with IgG4-related fibroscleretic disease, increase with serum IgG4 increase, mimics malignancy with progressive fibrosis, enlargement and adherence to neck structures

24
Q

morphology of IgG4-related thyroiditis

A

microscopically: lymphoplasmacytic infiltration, fibrosis, obliterative thrombophlebitis

25
Q

types of benign follicular neoplasms

A

follicular adenoma and oncocytic (Hurthle cell) adenoma

26
Q

morphology of benign follicular cells adenomas (follicular adenoma and oncocytic Hurthle cell adenoma)

A

grossly: rounded, encapsulated and well demarcated nodule with an intact capsule, bulges from the cut surface

microscopically: completely surrounded by an intact capsule with no capsular or vascular invasion (follicular adenoma: no oncocytic change, Hurthle cell adenoma: oncocytic change)

27
Q

follicular carcinoma risk factors

A

female, RAS family mutations, PPARγ/PAX8 rearrangements

28
Q

clinical presentation (and subtypes) of follicular carcinoma

A

slow growing painless cold nodule, metastasis through bloodstream to lungs and bone

WHO subtypes:
1. minimally invasive (capsular invasion only)
2. encapsulated angioinvasive
3. widely invasive with gross extension into extrathyroidal tissues

29
Q

oncocytic carcinoma presentation and cells

A

(similar to follicular carcinoma)
slow growing painless cold nodule, metastasises through bloodstream to lungs and bone

oncocytic cells present in capsular and vascular invasion

30
Q

papillary carcinoma risk factors

A

20-40yo or children, exposure to ionising radiation, RET/PTC gene rearrangements, BRAF mutations

31
Q

papillary carcinoma presentation

A

cold painless nodule, enlarged cervical lymph nodes, metastasis via lymph nodes: hoarseness, cough, dysphagia

32
Q

classic papillary carcinoma vs follicular variant papillary carcinoma

A

branching well formed papillae with fibrovascular core vs non-encapsulated infiltrative follicular growth pattern

cells have psammoma bodies, fibrosis, calcifications, lymphatic invasion vs finely dispersed chromatin with ground glass / orphan annie eye nuclei, nuclear grooves, pseudoinclusions

33
Q

morphology of papillary carcinoma

A

grossly: solitary or multifocal masses, encapsulated or infiltrative whitish nodules, cystic change, calcifications, fibrosis

microscopically: differs based on classic vs follicular papillary carcinoma

34
Q

poorly differentiated thyroid carcinoma mutations

A

TP53, TERT promoter mutations + low grade mutations

35
Q

morphology of poorly differentiated thyroid carcinoma

A

grossly: usually invasive

microscopically: trabecular/insular growth in large islands, high mitotic count and tumour necrosis

36
Q

risk factors for anaplastic thyroid carcinoma

A

65yo, underlying multinodular goitre/well differentiated thyroid adenocarcinoma, TP53 / TERT promoter mutations

37
Q

clinical presentation of anaplastic thyroid carcinoma

A

rapidly enlarging bulky thyroid mass, compressive symptoms of dyspnoea, dysphagia, hoarseness, metastasis to lungs

38
Q

morphology of anaplastic thyroid carcinoma

A

grossly: bulky mass

microscopically: highly pleomorphic and barely recognisable cells, giant tumour cells, spindle cells, small anaplastic cells

39
Q

medullary carcinoma risk factors

A

40-50yo, RET proto-oncogene mutation, MEN 2A/2B hereditary genes

RET mutant tumours more likely to respond to RET-inhibitor treatment, MEN 2B tumours more aggressive

40
Q

medullary carcinoma clinical presentation

A

grey white infiltrative mass, paraneoplastic syndromes, raised serum calcitonin, MEN syndrome related tumours

41
Q

medullary carcinoma morphology

A

microscopically: epithelioid or spindled cells, salt and pepper chromatin, nests, trabeculae, follicles, stain of Congo Red and C cell hyperplasia

42
Q

thyroid lymphoma types

A

B cell non-Hodgkin lymphoma, MALT lymphomas, large B cell lymphomas

M2 Endocrine (3 decks)

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