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Systems: Endocrine AB > Clinical Thyroid Disease > Flashcards

Clinical Thyroid Disease Flashcards

1
Q

GIve 4 examples of thyroid disease.

A
  • Hyperthyroidism
  • Hypothyroidism
  • Goitre
  • Thyroid Cancer
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2
Q

What can hypothyroidism present with?

A
  • Weight Gain
  • Lethargy
  • Feeling cold
  • Constipation
  • Heavy periods
  • Dry Skin/Hair
  • Bradycardia
  • Slow reflexes
  • Goitre
  • Severe (puffy face, large tongue, hoarseness, coma)
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3
Q

What can hyperthyroidism present with?

A
  • Weight Loss
  • Anxiety/Irritability
  • Heat Intolerance
  • Bowel frequency
  • Light periods
  • Sweaty palms
  • Palipitations
  • Hyperreflexia/Tremors
  • Goitre
  • Thyroid eye symptoms/signs
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4
Q

What will TFT results for primary hypothyroidism be?

A
  • Raised TSH
  • Low T4
  • Low T3
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5
Q

What will TFT results for subclinical (compensated) hypothyroidism?

A
  • Raised TSH
  • Normal T4
  • Normal T3
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6
Q

What will TFT results for secondary hypothyroidism be?

A
  • Low TSH
  • Low T4
  • Low T3
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7
Q

What is the prevalence of hypothyroidism?

A

Commonest endocrine condition after diabetes

  • 1.9% in women
  • O.1% in men
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8
Q

How many people are affected by subclinical hypothyroidism?

A

What is the incidence of congenital hypothyroidism?

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9
Q

What are the congenital causes of hypothyroidism?

A

Developmental
-agenesis / maldevelopment

Dyshormonogenesis
-trapping / organification / dehalogenase

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10
Q

What are the acquired causes of primary hypothyroidism?

A

-Autoimmune thyroid disease Hashimotos / atrophic
-Iatrogenic
Postoperative / post- radioactive iodine
External RT for head and neck cancers
Antithyroid drugs, Amiodarone, Lithium, Interferon
-Chronic iodine deficiency
-Post-subacute thyroiditis
Post partum thyroiditis

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11
Q

What are the causes of secondary/tertiary hypothyroidism?

A

Pituitary / hypothalamic damage

  • Pituitary tumour -Craniopharyngioma
  • Post pituitary surgery or radiotherapy
  • Sheehan’s syndrome
  • Isolated TRH deficiency
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12
Q

How should hypothyroidism be investigated?

A
  • TSH / fT4
  • Autoantibodies: TPO (Thyroid peroxidase antibodies)
  • (FBC (MCV increased))
  • (Lipids for hypercholesterolemia)
  • (Hyponatremia due to SIADH)
  • (Increased muscle enzymes, ALT, CK)
  • (Hyperprolactinaemia)
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13
Q

How should hypothyroidism be treated?

A
  • Levothyroxine (T4) tablets
  • (Liothyronine (T3))
  • Combination of T4 & T3: no benefit in studies
  • Initial dose Levothyroxine 50mcg/day, increase after 2 weeks to 100mcg
  • Increase dose until TSH normal (or fT4 in normal range in secondary)
  • Half-life of T4 is 7 days
  • After stabilisation annual testing of TSH
  • Compliance
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14
Q

How should hypothyroidism be treated in ischaemic heart disease?

A

Start at lower dose 25mcg and increase cautiously; risk of precipitating angina

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15
Q

How should hypothyroidism be treated in pregnancy?

A

Most patients need an increase in LT4 dose

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16
Q

How should hypothyroidism be treated in postpartum thyroiditis?

A

Trial withdrawal and measure TFT’s in 6 weeks

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17
Q

How should hypothyroidism be treated in myxoedema coma?

A

Very rare emergency, may need IV T3 (steroid)

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18
Q

When should treatment for subclinical hypothyroidism be considered?

A
  • Consider treatment TSH > 10
  • TSH > 5 with positive thyroid antibodies
  • TSH elevated with symptoms (Trial of therapy for 3 to 4 months and continue if symptomatic improvement)
  • If planning pregnancy or already pregnant
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19
Q

What are the risks of treatment of subclinical hypothyroidism?

A
  • Osteopenia

- AF

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20
Q

What is the risk of thyroid disease progression with positive TAb only?

A

1.3%/year

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21
Q

What is the risk of thyroid disease progression with raised TSH only?

A

1.6%/year

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22
Q

What is the risk of thyroid disease progression with raised TSH and positive TAb?

A

2.3%/year

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23
Q

What can inadequately treated hypothyroidism lead to during pregnancy?

A

Inadequately treated hypothyroidism linked with increased foetal loss and Lower IQ

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24
Q

What should be done for hypothyroid individuals when they become pregnant?

A
  • Increase LT4 dose by about 25% and monitor closely

- Aim to keep TSH in low normal range (<2.5mU/l) and FT4 in high normal range

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25
Q

When are levothyroxine requirements increased?

A

During pregnancy

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26
Q

What are the causes of Goitre?

A 
-Physiological
   Puberty
   Pregnancy
-Autoimmune
   Graves’ disease
   Hashimoto’s disease
-Thyroiditis
   Acute (de Quervain’s )
   Chronic fibrotic (Reidel’s)
-Iodine deficiency (endemic goitre)
-Dyshormogenesis
-Goitrogens
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27
Q

What are the different types of goitre?

A

-Multinodular Goitre
-Diffuse goitre
Colloid
Simple
-Cysts
-Tumours
Adenomas
Carcinoma
Lymphoma
-Miscellaneous
Sarcoidosis,
Tuberculosis

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28
Q

When is there a risk of malignancy in solitary thyroid nodule?

A
  • Child
  • Adults less than 30 or over 60 years
  • Previous head and neck irradiation
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29
Q

What should be investigated in multinodular goitre?

A

Large dominant nodule

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30
Q

What is the chance of malignancy in solitary thyroid nodules?

A

5%

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31
Q

How should solitary thyroid nodules be investigated?

A

-Thyroid function test
(solitary toxic nodule)
-Isoptope scanning if low TSH: Hot nodule
-Ultrasound: useful in differentiating benign vs malignant
-Fine needle aspiration (FNA)
-Chest and thoracic inlet Xrays if large retrosternal extensions

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32
Q

What are the different types of differentiated thyroid cancers?

A
  • Papillary

- Follicular

33
Q

What are the characteristics of papillary thyroid cancer?

A
  • Commonest
  • Multifocal, local spread to lymph nodes
  • Good prognosis
34
Q

What are the characteristics of follicular thyroid cancer?

A
  • Usually single lesion
  • Metastases to lung/bone
  • Good prognosis if resectable
35
Q

When is thyroid cancer prognosis poor?

A
  • <16
  • > 65
  • Tumour size is large
  • Spread outside thyroid capsule
  • Metastases
  • TNM stage advanced
36
Q

What management options are there for thyroid cancer?

A
  • Near Total Thyroidectomy
  • High dose radioiodine (Ablative)
  • Long term suppressive doses of thyroxine
  • Follow up with thyroglobulin (Whole body iodine scanning following 2-4 weeks of thyroxine withdrawal)
37
Q

Why does anaplastic thyroid cancer have a very poor prognosis?

A
  • Do not respond to radioiodine

- External RT may help but only briefly

38
Q

How does anaplastic thyroid cancer behave?

A

Aggressive, locally invasive

39
Q

What percentage of thyroid cancers are anaplastic?

A

<5%

40
Q

What may lymphomas arise from?

A

Pre-existing Hashimoto’s thyroiditis

41
Q

What is the treatment for lymphoma?

A

-External RT more helpful combined with chemotherapy.

42
Q

Where do medullary thyroid tumours arise from?

A

Para follicular C cells

43
Q

What are medullary thyroid cancers often associated with?

A

MEN 2 (pheochromocytoma and hyperparathyroidism)

44
Q

What serum level is raised in medullary thyroid cancer?

A

Calcitonin

45
Q

What is the prognosis of medullary thyroid cancer?

A

Variable

46
Q

What is the treatment for medullary thyroid cancer?

A

Total thyroidectomy. No role for radioiodine

47
Q

What are the primary causes of thyrotoxicosis?

A
  • Grave’s disease (70%)
  • Toxic Multinodular Goitre (20%)
  • Toxic adenoma
48
Q

Give an example of a secondary cause of thyrotoxicosis.

A

Pituitary adenoma secreting TSH

49
Q

What can cause thyrotoxicosis without hyperthyroidism?

A
  • Destructive thyroiditis (post-partum, subacute [de Quervain’s], amiodarone-induced
  • Excessive thyroxine administration
50
Q

What is the incidence and prevalence of Grave’s disease?

A
  • 70-80% of all cases of hyperthyroidism
  • Incidence 2-3 per 1000 per year (Sex ratio 5:1)
  • Prevalence 1.9% female, 0.16% male
51
Q

What is Grave’s disease?

A

Autoimmune driven condition

  • Thyroid peroxidase Antibodies
  • TSH receptor Antibodies
  • Review personal/family history for concurrent autoimmune disease
52
Q

How is a diagnosis of Grave’s disease made?

A
  • Hyperthyroidism

- Thyroid antibodies (TSH receptor antibodies)

53
Q

What is the most common cause of thyrotoxicosis in the elderly?

A

Multi-nodular goitre

54
Q

What is multi-nodular goitre characterised by?

A
  • Characteristic goitre

- Absence of Grave’s disease

55
Q

Will multi-nodular goitre resolve by itself?

A

No. It will not go into spontaneous remission

56
Q

Who does Subacute (de Quervain’s) thyroiditis usually affect?

A

Generally younger patients <50 years

57
Q

What usually triggers subacute (de Quervain’s) thyroiditis?

A

Viral trigger (eg enteroviruses, coxsackie)

58
Q

How does subacute (de Quervain’s) thyroiditis usually present?

A
  • Often recall painful goitre +/- fever/myalgia; ESR increased
  • Thyrotoxicosis 3-6 weeks followed by hypothyroidism for 3-6 months
59
Q

What might subacute (de Quervain’s) thyroiditis require treatment wise?

A

May require short term steroids and NSAIDs

60
Q

How can hyperthyroidism be managed?

A
  • ATD
  • RAI
  • Surgery
  • B blockers for symptomatic management
61
Q

Give 2 examples of antithyroid drugs.

A
  • Carbimazole

- Propylthioracil

62
Q

How can ATD be administered?

A
  • Titration regimen

- Block-replace

63
Q

Describe the effectiveness of titration regimen in the treatment of hyperthyroidism.

A
  • 50% cure

- 30% hypothyroidism

64
Q

Describe the effectiveness of block-replace in the treatment of hyperthyroidism.

A
  • 50% cure
  • 30% hypothyroidism
  • High side effects
65
Q

What is a potentially fatal side effect of ATDs.

A

Agranulocytosis

66
Q

How are ATDs usually administered?

A

Usually titration regimen, 12-18 months

67
Q

In what selected cases are ATDs used long term in low doses?

A
  • Elderly
  • Cardiac complications
  • Unwilling for RAI
68
Q

How can radioiodine be administered?

A
  • High dose ablative

- Variable calculated

69
Q

Describe the effectiveness of high dose ablative radioiodine.

A
  • 90% cure

- 70% hypothyroid

70
Q

Describe the effectiveness of variable calculated radioiodine.

A
  • 60-80% cure

- Less Hypothyroidism

71
Q

How is radioiodine usually given?

A

High ablative dose

72
Q

What is there a 70% risk of in RAI?

A

Hypothyroidism

73
Q

When is RAI avoided?

A

Severe eye disease

74
Q

When is ATD used with RAI?

A

Treat with ATD (stop 4-7 days before and after)

  • Elderly
  • Risk of cardiac problems
75
Q

What is supressed in subclinical hyperthyroidism?

A

TSH

76
Q

What are the levels of free thyroid hormones in subclinical hyperthyroidism?

A

Normal

77
Q

What concerns are there in subclinical hyperthyroidism?

A
  • Bone: decreased bone density in postmenopausal; No clear fracture data
  • AF: 3 fold increased risk in over 60s
78
Q

When is treatment considered in subclinical hyperthyroidism?

A

Treatment considered ATD/RAI if persistent especially in elderly or those with increased cardiac risk

Systems: Endocrine AB (25 decks)

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