L7 Thyroid Hormones 2 Flashcards

1
Q

Toxic multinodular goitre usually occurs in…

A

older patients with longstanding euthyroid multinodular goitre

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2
Q

Presentations of toxic multinodular goitre

A
  • tachycardia, heart failure or arrhythmia
  • sometimes weight loss, nervousness, weakness, tremors & sweats
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3
Q

Laboratory findings of toxic multinodular goitre

A

suppressed TSH, elevated serum T3 levels, less striking elevation of serum T4

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4
Q

Toxic multinodular goitre management

A
  • control of the hyperthyroid state with anti-thyroid drugs, followed by radioiodine (therapy of choice)
  • if goitre is very large, thyroidectomy is considered if patient is a good surgical candidate
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5
Q

What is amiodarone?

A

an anti-arrhythmic drug that contains 37.3% iodine by weight

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6
Q

Two types of amiodarone-induced thryotoxicosis

A

Type 1: thyrotoxicosis due to excess iodine
Type 2: amiodarone-induced thyroiditis, with inflammation and release of stored hormone into the bloodstream, causing thyrotoxicosis

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7
Q

Which type of AIT typically develops after more prolonged amiodarone use?

A

Type 2 - thyroiditis

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8
Q

Treatment for AIT

A
  • iodine-induced thyrotoxicosis can be controlled with methimazole/carbimazole and beta blockers
  • treatment with potassium perchlorate to block further iodine uptake requires careful monitoring because it has been associated with pernicious anaemia
  • prednisone therapy for drug-induced thyroiditis
  • mixed form of disease is treated with both thioamides and prednisone
  • total thyroidectomy is curative - may be needed in patients who are non-responsive to pharmacologic therapy
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9
Q

What is non-toxic goitre?

A

Goitre not associated with hyperthyroidism, can be diffuse or nodular

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10
Q

What is the most common cause of non-toxic goitre?

A

Iodine deficiency

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11
Q

Development of NTG in patients with impaired hormone synthesis or severe iodine deficiency causes an increase in __ secretion.

A

TSH

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12
Q

TSH-induced diffuse thyroid hyperplasia causes…

A

focal hyperplasia with necrosis and haemorrhage, and development of new areas of focal hyperplasia

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13
Q

Focal or nodular hyperplasia may or may not be able to…

A

concentrate iodine or synthesise TG

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14
Q

Initially, the hyperplasia is dependent upon…

A

TSH, but later the nodules become TSH-independent

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15
Q

Mutations of which gene have been found in a high proportion of nodules from patients with multinodular goitre?

A

gsp oncogene

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16
Q

Chronic activation of which protein results in thyroid cell proliferation and hyperfunction, even when TSH is suppressed?

A

the Gs protein

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17
Q

Patients with NTG usually present with?

A

thyroid enlargement, may be diffuse or multinodular

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18
Q

What indicates obstruction to jugular venous flow?

A

Positive Pemberton sign: facial flushing and dilation of cervical veins on lifting the arms over the head

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19
Q

The vast majority of patients with NTG are __.

A

euthyroid

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20
Q

Thyroid enlargement in NTG probably represents __ __.

A

compensated hypothyroidism

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21
Q

NTG treatment

A
  • with the exception of those due to neoplasm, the current management of NTG consists simply of observation, without any specific therapy
  • thyroid hormone suppression therapy rarely results in clinically significant decrements in goitre size
  • T4 therapy may be required to suppress serum TSH levels (but could cause harm to elderly patients)
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22
Q

TSH-independent/autonomous NTGs will not decrease in size and may contribute to…

A

iatrogenic hyperthyroidism

23
Q

Subacute thyroiditis is also known as…

A

De Quervain thyroiditis or granulomatous thyroiditis

24
Q

What is subacute thyroiditis?

A

An acute inflammatory disorder of the thyroid gland, most likely due to viral infection

25
Q

Examples of viruses that have been implicated in subacute thyroiditis

A
  • mumps virus
  • coxsackievirus
  • adenoviruses
26
Q

Histological features of subacute thyroiditis

A

destruction of thyroid parenchyma, presence of many phagocytic cells (including giant cells)

27
Q

Who is more susceptible to subacute thyroiditis?

A

women, and individuals who are HLA-Bw35 positive

28
Q

Signs & symptoms of subacute thyroiditis

A
  • fever, malaise, soreness in the anterior neck
  • initially, patient may have symptoms of hyperthyroidism, with palpitations, nervousness & sweats
  • clinical signs of thyrotoxicosis (tachycardia, tremor, hyperreflexia) may be present
29
Q

Treatment of subacute thyroiditis

A
  • NSAIDs
  • patients who do not respond to NSAIDs - glucocorticoid treatment e.g. prednisone (daily for 7-10 days) to reduce inflammation
  • beta blockers to treat hyperthyroid symptoms
  • T4 if hypothyroid symptoms are present. T4 therapy may also prevent exacerbations of inflammation due to elevated TSH levels
30
Q

Chronic thyroiditis is also known as…

A

Hashimoto’s disease/thyroiditis or lymphocytic thyroiditis

31
Q

What is the most common cause of hypothyroidism and goitre in the US?

A

Hashimoto’s disease

32
Q

Example of an end stage of Hashimoto thyroiditis?

A

Idiopathic myxoedema, with total destruction of the gland

33
Q

Most common signs/symptoms of Hashimoto thyroiditis

A
  • fatigue & sluggishness
  • increased sensitivity to cold
  • unexplained weight gain
  • enlarged & inflamed underactive thyroid (goitre)
34
Q

What is Hashimoto’s disease?

A

An immunologic disorder in which lymphocytes become sensitised to thyroidal antigens and auto-antibodies are formed that react with these antigens. The thyroid gland is gradually destroyed.

35
Q

The 3 most important thyroid auto-antibodies

A

TG Ab, TPO Ab, TSH-R-blocking Ab

36
Q

Which auto-antibody is be present for many years?

A

TPO Ab

37
Q

What are Hurthle cells?

A

In Hashimoto thyroiditis, the follicular epithelial cells of the thyroid gland are frequently enlarged and contain an eosinophilic cytoplasm laden with mitochondria. These are known as Hurthle cells.

38
Q

What happens following destruction of the thyroid gland in Hashimoto thyroiditis?

A

a fall in serum T3 and FT4 and a rise in TSH

39
Q

What is Schmidt syndrome?

A

consists of Hashimoto thyroiditis, idiopathic adrenal insufficiency, and commonly, T1DM. The phenomenon has also been called the autoimmune polyglandular syndrome.

40
Q

Indications for Hashimoto’s disease treatment

A

goitre or overt hypothyroidism (symptoms are usually mild)

41
Q

When is surgery considered for Hashimoto thyroiditis?

A

Rarely, but occasionally when goitre does not regress and continues to cause compressive symptoms

42
Q

Dyslipidaemia associated with Hashimoto’s disease can be ameliorated by…

A

T4 therapy

43
Q

What is administered to normalise TSH and allow regression of the goitre in Hashimoto’s disease?

A

sufficient T4

44
Q

Agenesis of one lobe of the thyroid, with hypertrophy of the other, can produce benign thyroid nodules. Which lobe is more likely to fail to develop?

A

It is usually the left lobe of the thyroid that fails to develop, and the hypertrophy occurs in the right lobe (presents as a mass in the neck and mimics a nodule)

45
Q

Examples of benign areas of hyperplasia and neoplasms in the thyroid that present as thyroid nodules

A

follicular adenomas, and Hurthle cell adenomas (also called oxyphil adenomas)

46
Q

Examples of rare benign thyroidal lesions

A

teratomas, lipomas, haemangiomas

47
Q

Diagnosis of a thyroid nodule

A

A patient with a thyroid nodule should have a serum TSH and thyroid ultrasound performed. If TSH is low, radionuclide thyroid scanning should be done.

48
Q

What happens when a nodule is cytologically malignant?

A

the patient is generally referred for thyroid surgery

49
Q

What happens when the nodule is classified as cytologically benign?

A

only reassessment of nodule size in 6-18 months by physical examination and/or ultrasound is required

50
Q

Types of thyroid cancer

A
  • papillary carcinoma (80%)
  • follicular carcinoma (10%)
  • medullary carcinoma (5%)
  • undifferentiated (anaplastic) carcinomas (3%)
  • miscellaneous e.g. lymphoma, teratoma, fibrosarcoma (1%)
51
Q

Most common type of thyroid cancer

A

papillary carcinoma

52
Q

Management of thyroid cancer (low risk patients)

A
  • Lobectomy or total thyroidectomy
  • radioiodine not given to most low risk patients
  • thyroxine for life with maintenance of low normal serum TSH
  • monitor with serum TG and neck ultrasound every 6-12 mnths for first 1-5 yrs
53
Q

Management of thyroid cancer (high risk patients)

A
  • surgery
  • radioiodine therapy given to most intermediate and all high risk patients
  • thyroxine for life with maintenance of suppressed serum TSH
  • monitor with serum TG and neck US every 6-12 mnths for 3-5 yrs
  • repeat radioiodine scan and measure serum stimulated thyroglobulin