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Endocrinology > Thyroid Pathology > Flashcards

Thyroid Pathology Flashcards

1
Q

is thyroid bigger in men or women

A

slightly larger in women

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2
Q

what level is the thyroid

A

C5/6-T1

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3
Q

describe the embryological development of the thyroid gland

A

develops from evagination of pharyngeal epithelium

descends from foramen caecum to normal location along the thryoglossal duct

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4
Q

what are the three common embryological abnormalities of the thryoid

A

failure of descent (lingual thyroid)
excessive descent (retrosternal location in mediastinum)
thyroglossal duct cyst

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5
Q

what makes up the thyroid

A

composed of follicles that are surrounded by flat cuboidal follicular epithelial cells

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6
Q

what is in the centre of each follicle

A

dense amorphic pink material containing thryoglobulin

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7
Q

what cells are scattered throughout the thyroid gland

A

C cells (parafollicular)- have slightly larger with clearer cytoplasms

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8
Q

what do C cells produce

A

calcitonin- lowers serum Ca

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9
Q

what cells produce thyroid hormones

A

thyroid follicular epithelium cells

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10
Q

describe how TSH works

A

binds to TSH surface receptor on surface of thyroid epithelial cells. G proteins activated with conversion of GTP to GDP and production of cAMP which stimulates production and release of T3 and 4, circulate in bound and free forms

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11
Q

what happens when T3 binds to receptors in target cells

A

complex translocates to the nucleus, binds to thyroid response elements on target genes, stimulates transcription of these genes- increase BMR

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12
Q

what can cause a thyroid gland to shrink in size

A

atrophy- presentation of reduced function a

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13
Q

what can a mass effect if an enlarged thyroid gland be

A

airway obstruction

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14
Q

polymorphisms in what genes are associated with autoimmune thyroid problems

A

CTLA-4 (negative regulator of T cell responses)

PTPN-22 (inhibits T cell function)

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15
Q

what are causes of inflammation in the thyroid

A

autoimmune disordersm infection, palpation, subacute lymphocytic, de Quervains, riedels

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16
Q

what does riedels do to the thyroid

A

makes it hard, claggy

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17
Q

what autoimmune disease causes hypothyroidism

A

hashimotos thyroiditis

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18
Q

what autoimmune disease causes 8% of hyperthyroidism cases

A

graves disease

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19
Q

what is thyrotoxoicosis

A

hyperthyroidism

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20
Q

what else can cause hyperthyroidism

A

hyperfunctioning nodules, tumours (adenomas, carcinomas)
TSH secreting pituitary adenomas (rare),
thyroditis, ectopic production (struma ovarii)

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21
Q

is graves more common in men or women

A

women 10:1

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22
Q

what age to people gets graves

A

20-40 years old

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23
Q

what is the triad of symptoms seen in graves

A

hyperthyroidism with diffuse enlargement of the thryoid
eye changes (exophthalamos),
partial myxoedema

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24
Q

what autoantibodies are seen in graves

A

Antibodies to TSH receptor, thyroid peroxisomes and thyroglobulin.

Anti TSH receptor antibodies: thyroid stimulating immunoglobulin, thyroid growth stimulating immunilogbulin,
TSH binding inhibitor immunoglobulins

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25
Q

what do the antibodies in graves do

A

stimulate thyroid hormone to function- except TSH binding inhibitor which causes episodes of hypofunction seen in graves

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26
Q

what is seen histologically in graves

A

thyroid follicles lack the ‘pink collar’ of follicular cells aka scalloping due to uptake of colloid

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27
Q

what causes symptoms in hypothyroidism

A

lack of thyroid hormones

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28
Q

who gets hashimotos

A

middle aged women

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29
Q

what genes is hashimotos associated

A

HLA- DR3 and DR5

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30
Q

what else can cause hypothyroidism

A

iodine deficiency, drugs (lithium), post therapy (surgery, irradiation), congenital abnormalities

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31
Q

what is hashimotos thyroiditis

A

autoimmune disease which causes gradual failure of thyroid function

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32
Q

what antibodies are in hashimotos thyroiditis

A

anti thyroid antibodies
(anti thyroglobulin and anti peroxidase)
when bound cause anti body dependent cell mediated cytotoxicity

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33
Q

what cells mediate hashimotos thyroiditis

A

CD8 +ve cells (destroy cell epithelium)
cytokine mediated cell death (gamma interferon from T cell activation recruits macrophages that may damage thyroid follicles)

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34
Q

what is the histology of hashimotos

A

follicles that remain dont have scalloping as retention of thyroid hormone
inflammatory infiltrate

35
Q

what might hashimotos thyroiditis be preceded by

A

transient hyperfunction (hashitoxicosis)

36
Q

what cancer is at increased risk in hashimotos thyroiditis

A

B cell non hogkins lymphoma

37
Q

what is a goitre

A

any enlargement of the thyroid gland

38
Q

what commonly causes goitres

A

lack of dietary, reduced T3/4 production causing rise in TSH which stimulates gland enlargement

39
Q

who gets diffuse goitres

A

females more than men, puberty and young adults

40
Q

what causes a diffuse goire

A

ingestion of substances limiting T3/4 production, dyshormogenesis, idiopathic (most)

41
Q

what are the usual symptoms of a goitre

A

usually euthyroid

presents with mass effects- cosmesis, airway obstruction, dysphagia, compresses vessels

42
Q

what can dyshormogenesis cause in children

A

cretinism

43
Q

what is seen in blood test in diffuse goitres

A

normal thyroid hormones but increase or upper side of normal TSH

44
Q

what causes a multinodular goitre

A

recurrent hyperplasia and involution, mutations in TSH, rupture of follicles, haemorrhage, scarring, calcification

45
Q

what do many multi nodular goitres develop

A

autonomous nodule- hyperthyroid

46
Q

describe the structure of a thyroid adenoma

A

discrete solitary mass, encapsulated by a surrounding collagen cuff, composed of neoplastic thyroid follicles (follicular adenoma)

47
Q

are thyroid adenomas benign

A

yes

48
Q

what is it hard to differentiate a thyroid adenoma from

A

dominant nodule in multinodular goitre, follicular carcinoma

49
Q

what are the effects of an adenoma

A

mass effects

usually non functional- can secrete thyroid hormones (thyrotoxicosis)- are TSH independent

50
Q

what mutations are seen in thyroid adenomas

A

<20% have mutant ras or PIK3CA

mutations of TSHR signalling pathway in functional adenomas
-activating TSHR, G proteins which increases cAMP levels

51
Q

what cells do thryoid malignancies come from

A

follicular epithelium (medullary from C cells)

52
Q

list the thyroid malignancies from most to least common

A

papillary (75-85%), follicular, medullary, anaplastic

53
Q

what is the aetiology of each of the thryoid cancers

A

environment-radiation (papillary), iodine deficiency (follicular)

genetics-
papillary- activate MAP kinase pathway, activation of BRAF, mutation in ras
follicular- mutations in ras family
anaplastic- above + p53 and beta-catenin mutations
medullary- MEN2

54
Q

what is the most common thyroid malignancy

A

papillary

55
Q

what is the usual structure of papillary carcinomas

A

usually solitary, can be mutlifocal, often cystic, may be calcified (psammoma bodies)

56
Q

do papillary carcinomas spread via the lymph

A

yes

if find thyroid tissue or psammoma body in a lymph node look for occult papillary carcinoma

57
Q

how do papillary carcinomas present

A

lesion in thyroid gland or cervical lymph node mass (metastasis)

local effects:
-hoarseness
-dysphagia
-cough 
-dyspnoea 
(all suggest locally advanced disease)
58
Q

do papillary carcinomas spread via the lung

A

not usually- if they do its commonly to the lung

59
Q

what is the second most common thyroid carcinoma

A

follicular

60
Q

who gets follicular carcinomas

A

F>M, older than papillary (40s and 50s)

61
Q

when is there not a female predominance in thyroid carcinomad

A

childhood and old age

62
Q

what are the survival rates for papillary carcinoma

A

95% at 10 years

63
Q

follicular carcinomas: onset, character and spread

A

slowly enlarging, painless, non functional, invasive growth pattern

dont spread via the lymph (unlike papillary) but spread haematogenous spread to the bones lungs and liver

64
Q

describe the structure of widely invasive follicular carcinomas

A

more solid architecture, less follicular architecture, more mitotic activity

65
Q

describe the structure of minimally invasive follicular carcinomas

A

follicular architecture (well differentiated), may have surrounding capsule, hard to distinguish from adenoma

66
Q

what is the difference between follicular adenoma and carcinoma

A

carcinoma need vascular or capsular invasion

67
Q

what is the prognosis for follicular carcinoma

A

depends on extent of invasion and stage of presentation

if high stage at presentation 50% mortality at 10 years

less invasive 90% at 10 years

68
Q

what is autoimmune thyroiditis

A

hashimotos

69
Q

what type of tumour is a medullary thyroid carcinoma

A

neuoendocrine (derived from C cells)

70
Q

what can medullary thyroid carcinoma secrete

A

calcitonin

71
Q

what are the forms of medullary thyroid carcinoma

A

can be specific, associated with multiple endocrine neoplasm, familial

72
Q

what type of medullary thyroid carcinoma can arise in very young patients

A

MEN cases

73
Q

who gets sporadic and familial medullary thyroid carcinoma

A

40s-50s

74
Q

what form do sporadic medullary carcinomas take

A

solitary nodules

75
Q

what form do familial medullary carcinomas take

A

bilateral/ multicentric (c cell hyperplasia)

76
Q

what is the histology of medullary carcinomas

A

spindle or polygonal cells arranged in nests, trabeculae or follicles
associated amyloid deposition

77
Q

what paraneoplastic syndromes are seen in medullary carcinomas

A

diarrhoea (VIP production)

cushings (ACTH production)

78
Q

what is the treatment for medullary carcinoma

A

total thyroidectomy

79
Q

what is the survival rates for medullary carcinoma

A

70-80% in 5 years

80
Q

what are the good prognostic factors for medullary carcinoma

A

young, female, familial setting, tumour size, confined to the gland

81
Q

what histological features suggest a tumour with more aggressive behavior

A

necrosis, many mitosis, small cell morphology

82
Q

describe anaplastic carcinomas

A

undifferentiated and aggressive tumours

rapid growth an involvement of neck structure and death

83
Q

who gets anaplastic carcinomas

A

older patients

people with a history of differentiated thyroid cancer

Endocrinology (46 decks)

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