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Endocrine > Pathology of the thyroid gland > Flashcards

Pathology of the thyroid gland Flashcards

1
Q

What does the thyroid gland develop from embryologically?

A

an evagination of pharnygeal epithelium

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2
Q

What causes inlgual thyroid?

A

failure of descne of thyroid from tongue

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3
Q

How do you tell a thyroglossal duct cyst?

A

will move on swallowing; in the midline of the neck

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4
Q

What type of cells surrounds each follicle?

A

flat to cuboidla follicaular epithelial cells

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5
Q

What does TSH bind to in the thyroid?

A

TSH receptor on surface of thyroid epithelial cells

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6
Q

How does binding to the TSH receptor induce release of T3 and T4?

A

G proteins stimulate production of cAMP which increases production and release of T3 and T4

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7
Q

What do T3 and T4 bind to the nucleus?

A

thyroid response elements

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8
Q

Aside from Grave’s, what else can cause hyperthyroidism?

A

hyperfunctioning nodules/ tumours, thyroiditis; TSH secreting pituitary adenoma; ectopic production (struma ovarii); factitious (exogenous intake)

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9
Q

What are the 2 autoimmune diseases affecting the thyroid gland?

A

Hashimoto’s thyroiditis and Grave’s disease

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10
Q

What are antibodies produced against in Grave’s disease?

A

TSH receptor; thyroid peroxisomes; thyroglobulin

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11
Q

What are the types of anti-TSH receptor antibody in Grave’s disease?

A

thyroid stimulaating immunoglobulin; thyroid growth stimulating immunoglobulin; TSH biding inhibitor immunoglobulin

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12
Q

What is the most specific Ab for Grave’s?

A

thyroid stimulating immunoglobulin

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13
Q

What might the presesnce of TSH binding inhibitor immunoglobulin hlpe explain?

A

episodes of hypofunction

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14
Q

What are the triad of features seen with Grave’s disease?

A

hyperthyroidisim with diffuse enlargement of the thyroid; eye changes; pretibial myxoedema

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15
Q

What do the eye changes in Grave’s result from?

A

fibroblasts etc. expressing TSH receptors

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16
Q

What are the antibodies found in Hashimoto’s thyroiditis?

A

anti-thyroglobulin and anti-peroxidase

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17
Q

What is the difference in antibodies in Hashimoto’s and Grave’s and why does this cause differences in clinical picture?

A

the main antibody in Grave’s is anti-TSH receptor antibody, which stimulates the receptor to produce more T3 and T4 but is not affected by the feedbakc loop. In Hashimoto’s, the main antibodies are made against thyroglobulin- a precursor of T3 and T4 and peroxidase- an ezyme used to make T3 and T4

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18
Q

What is Hashitoxicosis?

A

transient hyperfunction before decrease in function in Hashimoto’s

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19
Q

What are pts with Hashimoto’s more at risk of developing in the thyroid?

A

B cell NHL (lymphoma)

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20
Q

What causes diffuse goitre?

A

reduced T3/T4 production causes rise in TSH stimulating gland enlargement to maintain euthyroid state

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21
Q

What can cause diffuse goitre?

A

ingestion of substances limiting T3/T4 production; inborn errors of metabolism (dyshormonogenesis)

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22
Q

What is seen on blood tests in patients with diffuse goitre?

A

T3/T4 normal but TSH high or upper limit of normal

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23
Q

What do patients usually present with with diffuse goitre?

A

mass effects (usually euthyroid)

24
Q

What can dyshormonogenesis lead to in children?

A

cretinism

25
Q

What does multi-nodular goitre develop from?

A

long-standing simple goitre- recurrent hyperplasia and involution

26
Q

What should you suspect in patients with multi-nodular goitre?

A

thyroid neoplasm

27
Q

Why can people with multi-nodular goitre develop hyperthyroidism?

A

may develop an autonomous nodule

28
Q

What is the type of adenoma seen with thyroids?

A

follicular adenoma

29
Q

What types of carcinoma are seen in the thyroid?

A

papillary; follicular; medullary; anaplastic

30
Q

What are the features of a follicular adenoma?

A

discrete solitary mass; encapsulated by a surroudning collagen cuff; compaosed of neoplastic thyroid follicles

31
Q

What can an adenoma be difficult to distinguish from?

A

dominant nodule in multinodular goitre; follicular carcinoma

32
Q

Are thyroid carcinomas more common in females or males?

A

females

33
Q

What age group gets thyroid carcinoma?

A

early adulthood

34
Q

What type of carcinoma is associated with ionising radiation?

A

papillary carcinoma

35
Q

What type of carcinoma is associated with iodine deficiency?

A

follicular carcinoma

36
Q

What is the most common form of thyroid cancer?

A

papillary carcinoma

37
Q

How does papillary carcinoma usually present?

A

solitary nodule- can be mulitofcal; often cystic; may be calcified- Psammoma bodies on biopsy

38
Q

What is the difference between the spread of papillary and follicular carcinoma?

A

papillary goes through lymph whereas follicular tends to spread haematogenously

39
Q

How do you distinguish between follicular carcinoma and adenoma?

A

carcinoma will have vascular or capsular invasion

40
Q

What cells are medullary thyroid carcinomas derived from?

A

c-cells

41
Q

What does amyloid represent?

A

deposition of an abnormally folded protein

42
Q

What is anaplastic carcinoma?

A

undifferentiated and aggressive tumours- may arise in patients with a Hx of differentiated thyroid chancer whic hhas then dedifferentiated

43
Q

How many parathyroid glands do most people have?

A

4

44
Q

What type of cells are parathyroid glands composed of?

A

chief cells

45
Q

How do chief cells appear?

A

roudn cells with moderate cytoplasm and bland roudn central nuclei

46
Q

What type of cell suppports the chief cells in the parathyroid?

A

oxyphil cells

47
Q

What type of cytoplams do oxyphil cells have?

A

acidophilic

48
Q

What does PTH do?

A

acts on calcium homeostasis

49
Q

What does hyperparathyroidism normally result from?

A

small adenomas

50
Q

What else can causes hyperparathyroidism?

A

hyperplasia; carcinoma

51
Q

What is the difference between an adenoma nad hyperplasia in the parathyroid glands?

A

adenoma is a single gland involved but hyperplasia typically involves all the glands

52
Q

What causes secondary hyperparathyroidism?

A

chronic hypocalcaemia

53
Q

What is tertiary hyperparathyroidism?

A

when parathyroid activity becomes autonomous - hypercalcaemia

54
Q

What are the consequences of hyperparathyroidism?

A

bone disease; nephrolithiasis; GI complications- constipation; nausea; peptic ulcer disease; pancreatitis; glla stones; CNS- depression; lethargy; seizures; calcification of aortic and mitral valves; wekaness anf fatigue

55
Q

What congenital problem can cause hypoparathyroidism?

A

diGeorge syndrom

56
Q

What is seen with hypoparathyroidism?

A

tetany; altered mental state; parkinsonism; calcification of lens and cataract formation; prolonged QT interval in ECG

Endocrine (27 decks)

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