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Endocrine > Thyroid pathology > Flashcards

Thyroid pathology Flashcards

1
Q

Why are biopsies not usually performed on the thyroid gland?

What is the alternative?

A

Thyroid gland is very vascular

Do FNA instead

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2
Q

Describe the normal appearance of the thyroid gland?

A

Fleshy, mahogany coloured

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3
Q

Describe the origin of the cells of the thyroid gland?

A

C cells are neuroendocrine in origin

Rest are of epithelial origin

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4
Q

Describe the normal histology of the thyroid gland?

A

Round/oval follicles, various sizes

Epithelial cells line follicles

Follicles filled with colloid

Thin, fibrous septa with rich vascular supply

C cells (difficult to distinguish in H&E)

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5
Q

Describe the different histological appearance of inactive and active thyroid follicles?

A

Inactive: low cuboidal cells, follicle filled with colloid

Active: tall cuboidal/columnar cells, scalloping of colloid (cells taking up colloid)

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6
Q

Describe the metabolic symptoms of hypothyroidism?

A

Hypometabolic state:

cold intolerance

alopecia

cold, thickened skin

weight gain

fatigue

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7
Q

Describe the effects of hypothyroidism on the nervous system and the consequences of this?

A

Sympathetic nervous system underactivity > bradycardia, angina, slow reflexes, constipation, decreased mood and concentration

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8
Q

Which population is most affected by hypothyroidism?

A

Children

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9
Q

What are the most common causes of hypothyroidism?

A

Iodine deficiency

Hashimoto’s disease

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10
Q

What is thyrotoxicosis?

A

Elevated circulating fT3 and fT4

Includes hyperthyroidism

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11
Q

Describe the metabolic effects of hyperthyroidism?

A

Hypermetabolic state:

heat intolerance

warm, flushed skin

fatigue

weight loss

osteoporosis

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12
Q

Describe the effects of hyperthyroidism on the nervous system, and the consequences of this?

A

Sympathetic nervous system overactivity > palpitations, AF, cardiomegaly, tremor, anxiety, insomnia, diarrhoea

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13
Q

What are the major causes of thyrotoxicosis?

A

Graves disease

Hyperfunctioning toxic multinodular goiter

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14
Q

Describe the cause of a simple goiter?

A

Impaired synthesis of thyroid hormone > TSH elevation > thyroid growth stimulated

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15
Q

Describe the thyroid hormone levels in a simple goiter?

A

Usually euthyroid, with slightly high TSH

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16
Q

What is the most common cause of simple goiter?

A

Iodine deficiency

17
Q

Describe the histological appearrance of a simple goiter?

A

Hyperplasia

Crowded cells line follicles

Some follicles largr than others

Large colloid-filled cysts may be present

18
Q

Describe what happens to the thyroid follicles in a simple goiter with:

a) TSH resolution
b) TSH persistence

A

a) Follicles incolute
b) Follicles rupture, haemorrhage or grow larger

19
Q

Describe what can happen to a simple goiter over time?

A

Cycles of hyperplasia and involution > follicles can become large nodules > multinodular goiter

20
Q

What can multinodular goiter progress to?

What are the consequences of this?

A

Nodules can be autonomous (secrete thyroid hormone without TSH) > toxic multinodular goiter

Patient may become hyperhtyroid

21
Q

What is Pemberton’s sign?

When does it occur?

A

Enlarged thyroid > compresses SVC when arms raised > blood backlog in SVC

22
Q

Describe the histological appearrance of Hashimoto’s thyroiditis?

A

Mononuclear inflammatory infiltrate: lymphocytes, plasma cells, germinal centres

Hurthle cells: thyroid cells with abundant, eosinophilic, granular cytoplasm

Increased interstitial connective tissue: fibrosis/scarring

23
Q

Describe the gross pathology of Hashimoto’s thyroiditis?

A

Enlatge at first > atrophic

Cut surface: firm, tan-yellow, pale, nodular

24
Q

Describe the cause of Hashimoto’s thyroiditis?

A

Breakdown of tolerance to thyroid tissues

Damage by: CD8 cytotoxic cell-mediated death, cytokine-mediated cell death, TSH-blocking Abs

25
Q

Which population is most affected by Hashimoto’s thyroiditis?

A

Females

45-65 yo

26
Q

Describe the clinical presentation of Hashimoto’s thyroiditis?

A

Hypothyroidism

Goiter

High Anti-g Abs

Very high Anti-TPO

High TSH, low fT4

27
Q

Describe the triad of clinical findings in Graves disease?

A

1) Hyperhtyroidism due to diffuse, hyperfunctional enlargement of the thyroid
2) Infiltrative opthalmopathy > exopthalmos
3) Localised infiltrative dermopathy (pretibial myxoedoma)

28
Q

What is the cause of Graves disease?

A

Stimulatory auto-Ab to TSH receptor

29
Q

Describe the histological appearance of Graves disease?

A

Tall, crowded follicular cells > papillae

Diffuse hypertrophy and hyperplasia

Widespread scalloping

Lymphocytic infiltrates

30
Q

Describe the gross pathology of Graves disease?

A

Diffuse symmetrical enlargement of thyroid

Soft, meaty cut surface

31
Q

Name the auto-Abs that stimulate the TSH receptor in Graves disease?

A

Thyroid stimulating immunoglobulins (TSI)

32
Q

Which population is most susceptible to Graves disease?

A

Females

20-50 yo

33
Q

Describe the blood findings in a Graves disease patient?

A

Low TSH, high fT4

High Anti TPO Abs

High TSI

34
Q

Describe what causes the opthalmopathy seen in Graves disease?

A

Retro-orbital hydrophilic mucopolysaccharides, oedema, lymphocytes, fibrosis and fat

Fibroblasts are target and effector cells

35
Q

How can the symptoms of Graves disease be managed?

A

Beta blocker to reduce sympathetic overactivity

36
Q

Which type of hypersensitivites are Hashimoto’s thyroiditis and Grave’s disease?

A

Hashimoto’s: T-cell mediated > Type IV

Graves: B-cell mediated > Type II

37
Q

Describe the thyroid hormone levels in a patient with simple goiter?

A

Euthyroid

Endocrine (17 decks)

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