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MD1 Endocrine > Thyroid Pathology > Flashcards

Thyroid Pathology Flashcards

1
Q

How much does the normal thyroid gland weigh?

A

20 g +/- 5-10 g

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2
Q

Why can’t you do a biopsy of the thyroid gland?

A

Very vascular

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3
Q

Can you do a fine needle aspirate of the thyroid gland?

A

Yes

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4
Q

What is the colour of the thyroid gland?

A

Fleshy

Mahogany

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5
Q

What does thyroid stimulating hormone (TSH) stimulate?

A

Increased proliferation
Increased cell size
Increased calcitonin function
Increased thyroid hormone synthesis and release

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6
Q

Where are the follicular cells in the thyroid gland?

A

Surround colloid

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7
Q

What is the colloid?

A

Glycoprotein mix

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8
Q

What does the colloid contain?

A

Thyroglobulin

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9
Q

Where are the C cells?

A

In interstitial space

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10
Q

What do the C cell secrete?

A

Calcitonin

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11
Q

What is calcitonin involved in?

A

Calcium metabolism

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12
Q

What is normal thyroid histology with H&E stain?

A

Round to oval follicles of various sizes
Lined by thyroid epithelial cells
Filled with colloid = pink
Thin fibrous septa with rich blood supply

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13
Q

What is the origin of C cells?

A

Neuroendocrine

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14
Q

What does an inactive thyroid gland look like histologically?

A

Low cuboidal cells

Follicle filled with colloid

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15
Q

What does an active thyroid gland look like histologically?

A

Tall cuboidal to columnar cells

Scalloping of colloid

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16
Q

Does a hypo-/eu-/hyperthyroid state give a definitive diagnosis?

A

No, as possible in any condition

Give indication of disease

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17
Q

What is hypothyroidism?

A

Inadequate circulating T3 and T4

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18
Q

What does inadequate T3 and T4 lead to?

A 
Hypometabolic state
- Cold intolerance
- Cold thickened skin
- Alopecia
- Weight gain with decreased appetite
- Fatigue
Autonomic effects
- Bradycardia
- Angina
- Slow relaxing reflexes
- Constipation
- Low mood and concentration
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19
Q

What does hypothyroidism in children lead to?

A

Developmental abnormalities

Cretinism

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20
Q

What are the hormone test results generally in hypothyroidism?

A

Increased TSH

Decreased T4

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21
Q

What is the difference between thyrotoxicosis and hyperthyroidism?

A 
Thyrotoxicosis = too much thyroid hormone circulating
Hyperthyroidism = thyroid gland working too hard to make hormone
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22
Q

What do elevated circulating levels of T3 and T4 lead to?

A 
Hypermetabolic state
- Heat intolerance
- Warm flushed skin
- Fatigue
- Weight loss with increased appetite
- Osteoporosis
Autonomic effects
- Palpitations
- Arrhythmias
- Cardiomyopathy
- Tremor
- Anxiety
- Insomnia
- Emotional lability
- Diarrhoea
- Lid lag
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23
Q

What are the hormone tests generally in thyrotoxicosis?

A

Decreased TSH

Increased T4

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24
Q

What is a goitre?

A

Thyroid bigger than usual

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25
Q

Who dos goitre affect more: males or females?

A

Females

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26
Q

What does a diffuse non-toxic (simple) goitre reflect?

A

Impaired synthesis of thyroid hormone

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27
Q

What is the most common cause of impaired synthesis of thyroid hormone?

A

Dietary iodine deficiency

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28
Q

What happens to TSH in response to low thyroid?

A

Increases

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29
Q

Are people with a simple goitre usually hypothyroid, euthyroid, or hyperthyroid?

A

Euthyroid

  • TSH normal to slightly high
  • T4 generally normal
30
Q

Will the goitre regress if TSH and thyroid hormones return to normal>

A

Yes

31
Q

Where is dietary iodine deficiency most common?

A

Mountainous areas away from sea

32
Q

When does goitre become endemic?

A

If more than 10% of population has it

33
Q

What are other causes of simple goitre?

A

Congenital biosynthetic defects

Goitrogens in certain foods

34
Q

What does a simple goitre look like histologically?

A

Hyperplastic
Follicles lined by crowded cells
Some follicles larger than others
Can have large colloid-filled cysts

35
Q

What can happen to thyroid follicles with persistent high TSH?

A

Some can rupture/haemorrhage

Others grow larger

36
Q

How does a simple goitre become multinodular?

A

Cycles of hyperplasia and involution > some follicles become large nodules > others rupture and fibrose

37
Q

How does a multinodular goitre feel on palpation?

A

Hard and fibrosed

38
Q

What might be seen histologically with a multinodular goitre?

A

Haemosiderin
Calcification
Cholesterol clefts

39
Q

Is it common for a multinodular goitre to become a toxic multinodular goitre?

A

No

40
Q

What happens in toxic multinodular goitre?

A

Nodules can become autonomous

41
Q

Are patients with a multinodular goitre hypothyroid, euthyroid, or hyperthyroid?

A

Can become hyperthyroid

42
Q

What is the management of a simple goitre?

A

Iodine/thyroid hormone replacement therapy
Surgery to relieve compressive symptoms and cosmetic effect
If autonomous nodule, assess if malignant > remove

43
Q

How long does a diffuse goitre take to regress?

A

3-6 months

44
Q

How long does a multinodular goitre take to regress?

A

Less than 1/3 regress

45
Q

What is the histopathology of Hashimoto thyroiditis?

A

Mononuclear inflammatory infiltrate
- Lymphocytes with T cells = B cells
- Plasma cells
Germinal centres
Thyroid cells have abundant, eosinophilic granular cytoplasm = Hurthle cells
Increased interstitial connective tissue
- Chronic inflammation > fibrosis/scarring

46
Q

What is the gross pathology of Hashimoto thyroiditis?

A 
Enlarged at first > eventually atrophies
Cut surface
- Firm
- Pale
- Fibrotic
- Somewhat nodular
- Tan-yellow colour
47
Q

What causes the damage in Hashimoto thyroiditis?

A

CD8 T cell mediated cell death
Cytokine mediated cell death
Antibody dependent cell mediated cytotoxicity

48
Q

What causes further reduced thyroid function in Hashimoto thyroiditis?

A

TSH-blocking Abs

49
Q

What is the prevalence of Hashimoto thyroiditis?

A

5-10% of women with increasing age

50
Q

What is the most common autoimmune disease?

A

Hashimoto thyroiditis

51
Q

What is the female predominance of Hashimoto thyroiditis?

A

10-20:1

52
Q

Is there a strong genetic component with Hashimoto thyroiditis?

A

Yes

53
Q

Is there an associated susceptibility to other autoimmune conditions in Hashimoto thyroiditis?

A

Yes

54
Q

Which cancer is there an associated risk with in Hashimoto thyroiditis?

A

B-cell non-Hodgkin lymphoma

55
Q

What is the clinical presentation of Hashimoto thyroiditis?

A 
Gradual onset of hypothyroidism and/or goitre
Increased TSH
Decreased T4
Increased thyroglobulin Abs
Massive increase in anti TPO Abs
Fine needle aspirate will show
- Hurthle cells
- Mixed population of lymphocytes
56
Q

What is the management of Hashimoto thyroiditis?

A

Thyroxine replacement

Monitor closely if elderly or pregnant

57
Q

What are the clinical features of Graves disease?

A

Hyperthyroidism due to diffuse, hyperfunctional enlargement of thyroid
Infiltrative ophthalmology > exophthalmos
Localised infiltrativ dermopathy in minority of patients

58
Q

What is the cause of Graves disease?

A

Stimulatory Abs to TSH receptor

  • Thyroid stimulating Igs (TSI)
  • Thyroid growth-stimulating Igs
  • TSH-binding inhibitor Igs
    • Can stimulate/inhibit
59
Q

What is the histopathology of Graves disease?

A 
Follicular cells tall and more crowded
- Diffuse hypertrophy and hyperplasia
- May form papillae in follicle lumen
Widespread excessive scalloping of colloid
- Colloid paler staining
Lymphocytic infiltrates
- Mostly T cells
- Sometimes germinal centres
60
Q

What is the gross pathology of Graves disease?

A

Diffuse symmetrical enlargement

Cut surface soft and meaty

61
Q

What is Hashitoxicosis?

A

Thyrotoxic Hashimoto disease

If Abs attack thyroid gland very specifically > follicles rupture > release thyroid hormones

62
Q

What is the prevalence of Graves disease?

A

0.5-2%

63
Q

What is the female predominance of Graves disease?

A

5-8:1

64
Q

What is there an association with in Graves disease?

A

Genetics

Association with smoking

65
Q

What is the most common cause of hyperthyroidism?

A

Graves disease

66
Q

What are the hormone and serology results in Graves disease?

A

Decreased TSH
Increased T4
Increased Anti TPO Abs
Increased TSI = diagnostic

67
Q

Why do you get ophthalmopathy in Graves disease?

A

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

68
Q

What is the role of fibroblasts in exophthalmos in Graves disease?

A

Target and effector cells
Express TSH-like Ags
Produce more hyaluronic acid
Transform into adipocytes

69
Q

What eye problems can exophthalmos cause?

A 
Problems with
- Cornea
- Optic nerve
- Venous drainage
- Cosmetic
Diplopia
70
Q

What is the management of Graves disease?

A 
Reduce sympathetic overactivity
- Beta blockers
Reduce elevated thyroid function
- Antithyroid drugs; eg: carbimaozole
- 18 month course results in remission in

MD1 Endocrine (18 decks)

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