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endocrinology lectures phase 2 > thyroid diseases > Flashcards

thyroid diseases Flashcards

1
Q

what are the commonest endocrine disorders

A

thyroid disorders

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2
Q

prevalence of hyperthyroidism

A

2.5%

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3
Q

prevalence of hypothyroidism

A

5%

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4
Q

prevalence of goitre

A

5 - 15%

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5
Q

examples of thyroid autoimmunity

A
  • focal thyroditis and/or positive TPO and thyroglobulin antibodies
  • post partum thyroidits
  • auto immune hypothyroidism
  • graves’ disease
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6
Q

why are autoimmune thyroid diseases important

A

they are the first auto immune diseases to be described

they are associated with other serious autoimmune disorders

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7
Q

which antibodies are found in almost all patients with autoimmune hypothyroidism

A

thyroglobulin and thyroid peroxidase (TPO) antibodies

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8
Q

do healthy patients have thyroid autoantibodies

A

low levels are present in healthy individuals who are at risk of thyroid or other autoimmune disease

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9
Q

mechanism of thyroid cell destruction

A

cytotoxic t cell cd8+ mediated

thyroglobulin and TPO antibodies may case secondary damage, but have no effect alone

uncommonly - antibodies against the TSH receptor may block the effects of TSH

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10
Q

nomenclature of TSH receptor (TSH-R) antibodies

A

originally called long acting thyroid stimulates - LATS

now called thyroid stimulating antibodies

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11
Q

what causes graves’ disease

A

thyroid stimulating antibodies

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12
Q

can TSH-R antibodies cause hypothyroidism

A

Some TSH-R antibodies do not stimulate the receptor; instead they block the effects of TSH - these (rarely) can cause hypothyroidism

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13
Q

biggest risk fasvtor to thyroid autoimmunity

A

being female

onset o disease is common postpartum

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14
Q

which gene contribute to thyroid autoimmunity

A

HLA-DR3 and other immunoregulatory genes contribute (25% monozygotic twins concordant)

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15
Q

environmental factors that cause thyroid autoimmunity

A

stress, high iodine intake, smoking

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16
Q

some examples of autoimmune diseases associated with thyroid autoimmunity

A

• Type 1 diabetes mellitus
• Addison’s disease
• Vitiligo
• Alopecia areata
• Coeliac disease/ dermatitis herpetiformis
• Chronic active hepatitis
• Rheumatoid arthritis/ SLE/ Sjogren’s syndrome
• Myasthenia gravis (Graves’ disease)

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17
Q

where is thyroid associated opthalmopathy present

A

in most Graves and some autoimmune hypothyroidism patients

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18
Q

what is thyroid associated opthalmopathy

A

swelling in extraocular muscles

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19
Q

what causes thyroid associated opthalmopathy

A

Most likely due to an autoantigen in the extraocular muscle that cross reacts with, or is identical to, a thyroid autoantigen

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20
Q

what is GOITRE

A

palpable and visible thyroid enlargement

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21
Q

causes of GOITRE

A

variety
commonly sporadic or autoimmune

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22
Q

where is GOITRE endemic

A

in iodine deficient area

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23
Q

what is the commonest endocrine disorder (specific)

A

sporadic non toxic goitre

8.6% prevalence thyroid enlargement

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24
Q

define hyperthyroidism

A

excess of thyroid hormones in bloo

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25
Q

what are the 3 mechanisms of hyperthyroidism

A

a. overproduction thyroid hormone
b. leakage of preformed hormone from
thyroid
c. ingestion of excess thyroid hormone

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26
Q

3 common causes of hyperthyroidism

A

Graves’ disease (75- 80% of all cases)

Toxic multinodular goitre

Toxic adenoma

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27
Q

what can cause drug induced hyperthyroidism

A

• Iodine
• Amiodarone
• Lithium ?
• Radiocontrast agents

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28
Q

clinical features of hyperthyroidism

A

• Weight loss
• Tachycardia
• Hyperphagia
• Anxiety
• Tremor
• Heat intolerance
• Sweating
• Diarrhoea
• Lid lag + stare
• Menstrual disturbance

29
Q

specific signs for grave disease

A

Diffuse goitre

Thyroid eye disease (infiltrative)

Pretibial myxoedema Acropachy

30
Q

MNG specific signs

A

multinodular goitre

31
Q

adenoma specific signs

A

solitary nodule

32
Q

how to confirm biochemical hyperthyroidism

A

thyroid function tests

diagnosis of underlying cause - because treatment varies

33
Q

are physical signs sufficient for diagnosis of hyperthyroidism.

A

yes

34
Q

results of thyroid funciton tests for primary hyperthyroidism

A

increase in free t4

increase in free T3

suppresssed TSH

35
Q

results of thyroid function tests in secondary hyperthyroidism

A

increased free T4

increased free T3

inappropriately high TSH

36
Q

supporting investigations for hyperthyroidism

A

thyroid antibodies: TPO, Th, TRAb

isotope uptake scan

37
Q

treatment for hyperthyroidism

A
  • anti thyroid drugs (course or long term)
  • radioidione 131I
  • surgery (partial, subtotal thyroidectomy)
38
Q

what are anti thyroid drugs

A

thionamides

decrease synthesis of new thyroid hormone
but do not treat underlying cause of hyperthyroidism

39
Q

benefits of anti thyroid drug

A

immune modifying effects are seen (decrease IL6) and reduction in antibody titres

40
Q

what are the regimens for thionamides

A

titration regimen: 12 - 18 months

block and replace regimen with T4: 6 - 12 months for graves’ disease

OR
short course to render euthyroid before 131I and surgery

OR
long-term treatment in patients unwilling to have131I or surgery

41
Q

remission rates for anti thyroid drugs

A

30-50%

42
Q

what are poor prognosis factors for anti thyroid drugs ie who is more likely to relapse

A
  • severe biochemical hyperthyroidism
  • large goitre
    TRAb +ve at end of course of ATD
  • male sex
  • young age of disease onset
43
Q

side effects of thionamides

A

Common side effect:
- rash
• Less common:
- arthralgia
- hepatitis
- neuritis
- thrombocytopenia
- vasculitis

44
Q

most serious side effects of thionamides

A

agranulocytosis

manifests as sore throat, fever, mouth ulcers

45
Q

what is essential for thyroid hormone production

A

iodine

46
Q

how is iodine transported

A

• I actively transported by Na/I symporter into thyroid follicular cells

47
Q

what is 131i

A

• One of 20 isotopes of I (127I stable)
• Ideal for ablation
• Emits large B particles of moderate energy
• B particles non penetrating and deliver 90% of energy within a 1-2 mm zone to follicular cells
• Some gamma ray emission
• Half-life 8.1 days

48
Q

how does 131I work

A

• Emission of B particles results in ionization of thyroid cells
• Direct damage to DNA and enzymes
• Indirect damage via free radicals

49
Q

early effects of 131I

A

necrosis follicular cells
vascular occlusion
occur over weeks to months

50
Q

long term effects of 131I

A

• shorter cell survival
• impaired replication cells
• atrophy and fibrosis
• chronic inflammation resembling Hashimoto’
• late hypothyroidism

51
Q

what surgery for graves’ disease and MNG

A

near total thyroidectomy

52
Q

what surgery for toxic adenoma

A

near total thyrodiuectomy/ love to my

53
Q

define hypothyroidism

A

thyroid hormones levels abnormally low

54
Q

3 types of hypothyroidism

A

primary
secondary
tertiary

55
Q

what is primary hypothyroidism

A
  • absence / dysfunction thyroid gland
    1
  • most cases due to Hashimoto’s thyroiditis
56
Q

what is secondary/tertiary hypothyroidism

A

pituitary / hypothalamic dysfunction

57
Q

causes of primary hypothyroidism

A

Hashimoto’s thyroiditis
131I therapy Thyroidectomy
Postpartum thyroiditis
Drugs
Thyroiditides
Iodine deficiency
Thyroid hormone resistance

58
Q

causes of secondary/tertiary hypothyroidism

A

pituitary disease

hypothalamic disease

59
Q

what’s drugs cause hypothyroidism

A

Iodine, inorganic or organic iodide
iodinated contrast agents amiodarone
Lithium
Thionamides
Interferon - a

60
Q

causes of hypothyroidism in kids

A

Neonatal hypothyroidism
- Thyroid agenesis
- Thyroid ectopia
- Thyroid dyshormonogenesis
- Others

Resistance to thyroid hormone

Isolated TSH deficiency

61
Q

clinical features of hypothyroidism

A

• Fatigue
• Wt gain
• Cold intolerance
• Constipation
• Menstrual disturbance
• Muscle cramps
• Slow cerebration
• Dry, rough skin
• Periorbital oedema
• Delayed muscle reflexes
• Carotenaemia • Oedema

62
Q

describe thyroid levels in primary hypothyroidism investigation

A

increase TSH - most sensitive market

usually decreased free T4 and T3

T4/T3 may be low normal in mild hypothyroidism

positive titre of tpo antibodies in hashimotos

63
Q

describe thyroid levels in secondary hypothyroidism investigation

A

TSH inapppuatelyt low for reduced T3/T4 levels

64
Q

treatment for hypothyroidism

A

• Treatment of choice synthetic L-thyroxine (T4)
• Older treatments - dessicated thyroid (pig and beef extracts) - inconsistent from batch to batch
• ? T3 / T4 combination

• young adults - usual full replacement of
100 ig ugly ug

65
Q

how to monitor treatment in primary hypothyrisum

A

dose titrated until TSH normalises
T4 half-life is long - check levels 6-8 weeks after dose adjustment

66
Q

how to monitor treatment in secondary/tertiary hypothyroidism

A

TSH will always be low
T4 is monitored

67
Q

are TPO and thyroglobulin antibodies specific

A

no they are sensitive but not specific

68
Q

what causes graves’ disease

A

thyroid stimulating antibodies that may cross the placenta

endocrinology lectures phase 2 (17 decks)

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