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Endocrine > Thyroid Pathology > Flashcards

Thyroid Pathology Flashcards

1
Q

Where does the thyroid gland originate from?

A

Develops from evagination of the pharyngeal epithelium = descends from foramen caecum to normal location along thyroglossal duct

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2
Q

What are some embryological abnormalities of the thyroid gland?

A

Failure to descend = lingual thyroid
Excessive descent = retrosternal location in mediastinum
Thyroglossal duct cyst

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3
Q

What is the thyroid composed of?

A

Follicles = each follicle is surrounded by flat to cuboidal follicular epithelial cells

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4
Q

What is at the centre of each follicle in the thyroid?

A

Dense amorphic pink material containing thyroglobulin

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5
Q

What is the other name for C cells?

A

Parafollicular cells = slightly larger cells with clearer cytoplasm, secrete calcitonin (results in lower serum Ca)

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6
Q

Where does TSH bind to on the thyroid?

A

To TSH receptor on the surface of thyroid epithelial cells

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7
Q

What does activation of G-proteins cause?

A

Conversion of GTP to GDP and production of cAMP

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8
Q

What does cAMP increase the production of?

A

T3 and T4 = both circulate in free and bound forms

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9
Q

What does the binding of T3 and T4 to the receptors on target cells cause?

A

Complex translocates to nucleus and binds to thyroid response elements on target genes = stimulates transcription of these genes (increases BMR)

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10
Q

What are some features of autoimmune thyroiditis?

A

Increased incidence in family members, concordance rate high in monozygotic twins, susceptibility associated with HLA haplotype, linked to other autoimmune things

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11
Q

What are some polymorphisms of immune regulation associated genes that cause autoimmune thyroiditis?

A 
CTLA-4 = negative regulator of T cell responses
PTPN-22 = inhibits T cell function
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12
Q

What kind of polymorphisms in CTLA-4 are linked with autoimmune diseases?

A

Polymorphisms that cause reduced protein level or function

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13
Q

What do they symptoms and signs of thyrotoxicosis occur as a result of?

A

Excess T3 and T4

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14
Q

What is the main cause of thyrotoxicosis?

A

Hyperthyroidism = 85% due to Grave’s disease, hyperfunctioning nodules, adenomas, carcinomas, TSH secreting pituitary adenoma (rare)

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15
Q

What are other causes of thyrotoxicosis?

A

Thyroiditis, ectopic production (struma ovarii), factitious (exogenous intake)

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16
Q

Who gets Grave’s disease?

A

10 times more common in women, affects those most often aged 20-40

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17
Q

What is Grave’s disease?

A

Autoimmune disorder = antibodies to TSH receptor, thyroid peroxisomes and thyroglobulin

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18
Q

What are some anti-TSH receptor antibodies linked with Grave’s disease?

A

Thyroid stimulating immunoglobulin = relatively specific
Thyroid growth stimulating immunoglobulin
TSH binding inhibitor immunoglobulin = may explain episodes of hypofunction

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19
Q

What is the triad of features that Grave’s disease presents with?

A

Hyperthyroidism with diffuse enlargement of the thyroid, eye changes (exophthalmos), pretibial myxoedema

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20
Q

What causes the eye changes in Grave’s disease?

A

Fibroblasts (etc) expressing TSH receptors

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21
Q

What causes the symptoms and sings of hypothyroidism?

A

Low levels of T3 and T4

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22
Q

What are some causes of hypothyroidism?

A

Most causes due to Hashimoto’s thyroiditis

Iodine deficiency, drugs, post therapy, congenital abnormalities, inborn errors of metabolism

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23
Q

What are some rare causes of hypothyroidism?

A

Secondary (pituitary) and tertiary (hypothalamus) pathology

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24
Q

What is Hashimoto’s thyroiditis?

A

Gradual failure of thyroid function = autoimmune destruction of thyroid tissue

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25
Q

Who gets Hashimoto’s thyroiditis?

A

10-20 times more common in women, aged 45-60, associated with HLA-DR3 and DR5, polymorphisms in CTLA-4 and PTPN-22 may be present

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26
Q

What are some anti-thyroid antibodies involved in Hashimoto’s thyroiditis?

A

Anti-thyroglobulin and anti-peroxidase = cause antibody cell mediated cytotoxicity when bound

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27
Q

What are some immune cells involved in Hashimoto’s thyroiditis?

A

CD8 positive cells may mediate destruction of thyroid epithelium

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28
Q

How does cytokine mediated cell death occur in Hashimoto’s thyroiditis?

A

Gamma interferon from T cell activation recruits macrophages that may damage thyroid follicles

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29
Q

What may precede Hashimoto’s thyroiditis?

A

Transient hyperfunction (Hashitoxicosis)

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30
Q

What does Hashimoto’s thyroiditis put patients at risk of?

A

Other autoimmune diseases and development of B cell NHL in the affected gland

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31
Q

What is a goitre?

A

Any enlargement of the thyroid gland

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32
Q

What may cause a goitre to develop?

A

Lack of dietary iodine or lack of bio-availability of iodine

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33
Q

How does reduced T3/T4 production cause goitres?

A

Causes rise in TSH, stimulating gland enlargement = may maintain euthyroid state, if compensation fails then patients have goitrous hypothyroidism

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34
Q

What are the types of diffuse goitres?

A

Endemic = >10% of population affected

Sporadic

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35
Q

What are some features of sporadic diffuse goitres?

A

More common in women, occur in puberty and young adults, most causes have unknown cause, may be due to ingestion of substances limiting T3/T4 production or inborn errors of metabolism (dyshormonogenesis)

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36
Q

What are some features of diffuse goitres?

A

Usually euthyroid = present with mass effects
T3 and T4 normal but TSH high
In children dyshormonogenesis may cause cretinism

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37
Q

How do multinodular goitres arise from long standing simple goitres?

A

Recurrent hyperplasia and involution = enlargement can be impressive, differential diagnosis is thyroid neoplasm

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38
Q

How do multinodular goitres arise?

A

Variations of response in follicular cells to external stimuli = mutations in TSH signalling pathway

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39
Q

What can multinodular goitres cause?

A

Follicle rupture, haemorrhage, scarring, calcification

40
Q

What are the mass effects of multinodular goitres?

A

Cosmetic, airway obstruction, dysphagia, vessel compression

41
Q

What may develop form multinodular goitres?

A

Autonomous nodules = may cause hyperthyroid, occur in 10% after ten years, low risk of malignancy

42
Q

What are adenomas?

A

Discrete solitary swelling encapsulated by surrounding collagen cuff = composed of neoplastic thyroid follicles

43
Q

What can adenomas be confused with?

A

Dominant nodule in multinodular goitre or follicular carcinoma

44
Q

What are some features of adenomas?

A

Usually non-functional

Can secrete thyroid hormones = cause thyrotoxicosis (TSH independent)

45
Q

What mutations cause adenomas?

A

<20% have mutant ras or PIK3CA

Mutations of TSHR signalling pathway in functional adenomas (10-75%)

46
Q

What are some features of carcinomas?

A

1.5% of all cancers, can affect any age group, more common in females (except childhood and elderly)

47
Q

Where are most carcinomas derived from?

A

Most are well differentiated and are derived from follicular epithelium (medullary from C cells)

48
Q

What are the types of thyroid carcinomas, from most to least common?

A

Papillary, follicular, medullary, anaplastic

49
Q

What are some environmental associations of carcinomas?

A

Ionising radiation = papillary

Iodine deficiency = follicular

50
Q

What are some genetic features of papillary carcinomas?

A

Activate MAP kinase pathway = rearrangements of RET or NTKR1, mutations of ras, activating point mutation in BRAF

51
Q

What mutations cause follicular carcinomas?

A

Mutations in PI3K or AKT pathways, mutations in ras family (usually N-ras), translocation involving Pax8 and PPAR gamma

52
Q

What are some additional mutations that cause anaplastic carcinomas?

A

p53 and beta catenin mutations

53
Q

Abnormalities in what cause medullary carcinomas?

A

MEN2 = germline RET mutations

54
Q

What are papillary carcinomas?

A

Usually solitary nodule = can be multifocal, often cystic, may be calcified (psammoma bodies)

55
Q

How do papillary carcinomas sometimes present?

A

Lymph node metastases = if thyroid tissue or psammomas body in lymph node then search for occult papillary carcinoma

56
Q

What are local effects of papillary carcinomas that suggest locally aggressive disease?

A

Hoarseness, dysphagia, cough, dyspnoea

57
Q

Can papillary carcinomas spread haematogenously?

A

Yes - rarely spread this way, but when they do it is most often to the lungs

58
Q

What is the prognosis of papillary cancer?

A

Overall good survival = 95% at 10 years

Worse prognosis with age >40, extra-thyroid extension and distant metastases

59
Q

How do follicular carcinomas present?

A

More common in females, patient in 40s-50s, usually single nodule = slowly enlarging, painless, non-functional

60
Q

How do follicular carcinomas spread?

A

Rarely lymphatic spread

Most commonly spread haematogenously to the bone, lungs and liver

61
Q

What kind of growth pattern do follicular carcinomas have?

A

Invasive

62
Q

What are some features of a widely invasive follicular carcinoma?

A

More solid and less follicular architecture, more mitotic activity

63
Q

What are some features of a minimally invasive follicular carcinoma?

A

Follicular architecture (well-differentiated), may have part of surrounding capsule, difficult to distinguish from follicular adenoma (need capsular/vascular invasion)

64
Q

What does the prognosis of follicular carcinoma depend on?

A

Extent on invasion and stage at presentation:
High stage at presentation = 50% mortality at 10 years
Minimally invasive lesions = >90% survival at 10 years

65
Q

What are medullary thyroid carcinomas (MTC)?

A

Relatively rare tumour = derived from C cells, can secret calcitonin

66
Q

What are the types of medullary thyroid carcinomas?

A

Sporadic = 70%, solitary nodule
Associated with Multiple Endocrine Neoplasia = MEN IIA or IIB)
Familial medullary carcinoma = bilateral/multicentric

67
Q

Who gets medullary thyroid carcinomas?

A

MEN cases are in very young patients

Sporadic and familial cases are seen in adults aged 40s-50s

68
Q

What are some features of medullary thyroid carcinomas?

A

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

69
Q

How do medullary thyroid carcinomas present?

A

Neck mass with local effects = dysphagia, hoarseness, airway compromise
Paraneoplastic syndrome = diarrhoea (VIP production), Cushing’s (ACTH production)

70
Q

What is the prognosis of medullary thyroid carcinomas?

A

Treated with total thyroidectomy = local recurrence in 35%, 5 year survival is 70-80%

71
Q

What are some good prognostic indicators for medullary thyroid carcinomas?

A

Young, female, familial type, tumour size, confined to gland

72
Q

What are some indicators of aggressive behaviour in medullary thyroid carcinomas?

A

Necrosis, many mitoses and small cell morphology

73
Q

What are some features of anaplastic carcinomas?

A

Undifferentiated and aggressive tumours, usually older patients, rapid growth and involvement of neck structures and death

74
Q

Having a history of what can predispose patients to anaplastic carcinomas?

A

Differentiated thyroid cancer

75
Q

Who are samples taken for thyroid cytology?

A

Aspirates are taken and interpreted without architecture = provides a minimally invasive assessment of the likelihood of malignancy

76
Q

What is the grading of thyroid tissue?

A 
Thy 1 = insufficient/uninterpretable
Thy 2 = benign
Thy 3 = atypia probably benign/equivocal
Thy 4 = atypia suspicious of malignancy
Thy 5 = malignant
77
Q

What type of carcinoma can be well assessed using the grading of thyroid tissue?

A

Papillary carcinomas

78
Q

Why are all follicular lesions given a Thy 3 grading?

A

Features can be difficult to interpret as relationship to capsule isn’t assessed

79
Q

What are some features of the parathyroid gland?

A

Usually four glands, but 10% only have two or three

Variable position

80
Q

What cell makes up the parathyroid glands?

A

Chief cells = secret PTH, act on calcium homeostasis, round cells with moderate cytoplasm and round central nuclei

81
Q

What cells support the chief cells in the parathyroid glands?

A

Oxyphil cells = slightly larger cells with acidophilic cytoplasm

82
Q

What is the most common cause of hyperparathyroidism?

A

Small adenomas

Hyperplasia is responsible for 5-10% and carcinomas for about 1%

83
Q

What can hyperplasia of the parathyroid glands be associated with?

A

Both MEN I and MEN IIa

84
Q

What are some features of hyperparathyroidism caused be adenomas?

A

Single gland involved (weighing 0.5-5g), other glands atrophic, microscopically resembles normal parathyroid, may see fibrous connective tissue capsule with adjacent rim of compressed parathyroid tissue

85
Q

What occurs in hyperparathyroidism caused by hyperplasia?

A

Typically involves all glands = collectively weigh rarely >1.0g

86
Q

What occurs in hyperparathyroidism caused by secondary causes?

A

Secondary = chronic hypocalcaemia causes compensatory over-activity (renal failure, low Ca intake, vitamin D deficiency)

87
Q

What occurs in tertiary hyperparathyroidism?

A

Parathyroid activity becomes autonomous = associated with hypercalcaemia

88
Q

What are some bone and GI complications of hyperparathyroidism?

A

Bone disease = pain, fracture, osteoporosis, osteitis fibrosa cystica
GI = nausea, constipation, peptic ulcer, pancreatitis, gallstones

89
Q

What are some CNS and CVS complications of hyperparathyroidism?

A 
CNS = depression, lethargy, seizures
CVS = calcification of aortic and mitral valves
90
Q

What are some other complications of hyperparathyroidism?

A 
Nephrolithiasis = renal stones and complications
Neuromuscular = weakness, fatigue
91
Q

What are some causes of hypoparathyroidism?

A

Very rare = usually post-op, rarely congenital absence (DiGeorge syndrome), familial variant exisits

92
Q

What are some associations of familial hypoparathyroidism?

A

Primary adrenal insufficiency and mucocutaneous candidiasis

93
Q

How can hypoparathyroidism alter the mental state of a patient?

A

Emotional lability, anxiety, depression, confusion, psychosis

94
Q

What is tetany?

A

Caused by hypoparathyroidism = neuromuscular irritability (spasms), confirmed by Chvostek’s and Trousseau’s signs

95
Q

How can hypoparathyroidism affect the heart and the eyes?

A

Prolongation of the OT interval on ECG

Calcification of lens and cataract formation in eyes

96
Q

When can dental abnormalities occur due to hypoparathyroidism?

A

If there was hypocalcaemia during development

97
Q

What are some complications of hypoparathyroidism?

A

Basal ganglia calcification, Parkinson’s raised ICP, papilloedema

Endocrine (42 decks)

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