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Y2 LCRS Endocrinology > thyroid > Flashcards

thyroid Flashcards

hyperthyroidism: list the causes of hyperthyroidism; recall the clinical features, explain the diagnosis, explain treatment options including mechanism of action, side effects, interactions and special circumstances (e.g. pregnancy); explain how to differentiate between Graves' disease and other causes of hyperthyroidism; recall the clinical features of a thyroid storm

1
Q

4 classes of drugs used in treatment of hyperthyroidism

A

thionamides (thiourylenes; anti-thyoid drug), potassium iodide, radioiodine, B-blockers

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2
Q

2 examples of thionamides

A

propylthiouracil (PTU), carbimazole (CBZ)

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3
Q

what do thionamides (thiourylenes; anti-thyoid drug), potassium iodide and radioiodine classes attempt to do

A

reduce thyroid hormone symptoms

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4
Q

what does B-blocker class attempt to do

A

help with symptoms

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5
Q

3 clinical uses of thionamides

A

daily treatment of hyperthyroid conditions, treatment prior to surgery, reduction of symptoms while waiting for radioactive iodine to act

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6
Q

2 causes of hyperthyroidism

A

Graves’ disease, toxic thyroid nodule (Plummer’s disease)/toxic multinodular goitre

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7
Q

thyroid hormone synthesis

A

I- enters thyroid follicular cell from blood and passes into colloid via active transport -> coupling reaction occurs using peroxidase transaminase -> iodination of thryoglobulin occurs using thyroperoxidase and H2O2 -> T3 and T4 stored in colloid -> endocytosed and secreted

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8
Q

how do thionamides work to prevent T3 and T4 synthesis and secretion

A

inhibit thyroid peroxidase

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9
Q

thionamides: biochemical effect duration

A

hours

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10
Q

thionamides: clinical effect duration

A

weeks (colloid contains stored thyroxine)

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11
Q

thionamides: why might the treatment regimen include propranolol (B-blocker)

A

rapidly reduces tremor and tachycardia before clinical effect of thionamide

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12
Q

2 mechanisms of action of thionamides

A

may suppress antibody production in Graves’ disease, reduces conversion fo T4 to T3 in peripheral tissues (specifically propylthiouracil (PTU))

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13
Q

2 unwanted actions of thionamides

A

agranulocytosis (usually reduction in neutrophils; rare and reversible on withdrawal of drug), rashes (relatively common)

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14
Q

4 pharmacokinetic features of thionamides

A

orally active, carbimazole is pro-drug so must first be converted to methimazole, can cross placenta (pregnancy relevant) and are secreted in breastmilk (carbimazole (CBZ) more so than propylthiouracil (PTU)), metabolised in liver and excreted in urine

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15
Q

thionamides: follow up (duration and review)

A

usually aim to stop anti-thyroid drug treatment after 18 months, review patient periodically including thyroid function tests for remission (euthyroid) or relapse

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16
Q

anti-thyroid drug clinical effects

A

reduced tumour, slower heart rate, less anxiety

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17
Q

duration before anti-thyroid drugs have clinical effects

A

several weeks

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18
Q

what is used to achieve same clinical effects in interim before anti-thyoid drugs have clinical effect

A

non-selective (B1 and B2) B-blockers e.g. propranolol so all symptoms treated; less so with selective B1 blockers e.g. atenolol which only slow heart rate

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19
Q

when is iodide (usually KI, with doses x30 average daily requirement) used (2 conditions)

A

preparation of hyperthyroid patients for surgery, severe thyrotoxic crisis (thyroid storm) so quicker action required

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20
Q

2 KI mechanisms of action

A

inhibits iodination of thyroglobulin; inhibits H202 generation and thyroperoxidase (Wolff-Chaikoff effect)

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21
Q

what is the Wolff-Chaikoff effect

A

autoregulatory effect when thyroid hormone synthesis and secretion are both inhibited in presence of large doses of iodine

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22
Q

with KI, when do hyperthyroid symptoms reduce within

A

1-2 days

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23
Q

with KI, when does vascularity and size of thyroid gland reduce within

A

10-14 days

24
Q

KI unwanted action

A

allergic reaction e.g. rashes, fever, angio-oedema

25
Q

pharmacokinetic feature of KI (administration and duration before maximal effects)

A

given orally (Lugol’s solution; aqueous iodine), with maximum effects after 10 days of continuous administration

26
Q

what is radioiodine chemically

A

131 I in high doses

27
Q

what 2 things does radioiodine treat

A

hyperthyroidism, thyroid cancers

28
Q

how does radioiodine work

A

accumulates in colloid, emiting B particles and destroying follicular cells; switches it off for good (e.g. 6 months before pregnancy so don’t have to take anti-thyroid drugs during pregnancy or for 18 months); then treat with thyroxine as if they were hypothyroid

29
Q

prior to radioiodine treatment what must happen

A

anti-thyroid drugs must be discontinued for 7-10 days

30
Q

how is radioiodine administered a) for Graves’ disease and b) for thyroid cancer

A

both as a single oral dose, but Graves’ disease: approx 500 MBq, and thyroid cancer: approx 3000 MBq

31
Q

what is radioiodine’s radioactive half life, and when is it’s radioactivity negligible after

A

8 days half life, with radioactivity negligible after 2 months

32
Q

2 cautions when using radioiodine

A

avoid close contact with small children for several weeks after receiving radioiodine; contra-indicated in pregnancy and breast feeding

33
Q

what version of radioiodine is used at very low, tracer doses

A

technetium 99 pertechnetate

34
Q

how is thryoid gland pathology (e.g. toxic nodule, thyroiditis vs Graves’) tested (2 tests)

A

administer i.v., negligible cytotoxicity

35
Q

Graves’ disease: type and pathophysiology

A

autoimmune; antibodies bind to and stimulate TSH receptor in thyroid

36
Q

2 effects of Graves’ disease

A

goitre (smooth thyroid) and hyperthyroidism (which causes lid lag)

37
Q

signs and symptoms of Graves’ disease

A

makes B receptors more sensitive: pretibial myxoedema, exophthalmos, goitre (smooth swellling of neck due to diffuse enlargement and engorgement of thyroid gland by antibodies binding)

38
Q

how does Graves’ disease cause exophthalmos

A

antibodies bind to muscles behind the eye (measure antibodies to confirm diagnosis); can get double vision or lose vision due to swelling and pressure on optic nerves; approx. 1 year after goitre

39
Q

in Graves’ disease, what else can other antibodies cause

A

pretibial myxoedema (hypertrophy)

40
Q

what is pretibial myxoedema

A

swelling (non-pitting) that occurs on shins due to growth of soft tissue caused by antibody binding (NOT MYXOEDEMA - that’s primary hypothyroidism)

41
Q

thyroid scan in Graves’ disease

A

very big with smoothly increased uptake of radioactive iodine

42
Q

what is Plummer’s disease and pathophysiology

A

toxic nodular goitre (not smooth so lump on one side) due to overactive thyroxine-making benign adenoma

43
Q

Plummer’s disease vs Graves’ disease

A

not autoimmune, no pretibial myxoedema, no exophthalmos

44
Q

histology of Plummer’s disease

A

hyperfunctioning adenoma; pituitary therefore doesn’t make TSH so rest of thyroid shrinks, but adenoma continues to grow

45
Q

thyroid scan in Plummer’s disease

A

hot nodule

46
Q

how does thryoxine cause apparent sympathetic activation

A

sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline

47
Q

clinical effects of thyroxine due to sentisation of beta adrenoceptors

A

tachycardia, palpitations, tremor in hands, lid lag

48
Q

what is lid lag

A

where upper eyelid is higher than normal with globe in downgaze; eyelid is delayed when eyeball goes down (see white of eye above iris, as adrenaline holds back eyelid)

49
Q

clinical presentation of hyperthyroidism

A

weight loss despite increased appetite, breathlessness, palpitations, tachycardia, sweating, heat intolerance, diarrhoea, lid lag and other sympathetic features; family history

50
Q

thyroid storm: what is it, mortality if untreated and blood results

A

very high thyroxine level; 50% mortality if untreated; bood results confirm hyperthyroidism

51
Q

5 clinical features of a thyroid storm (2 on top of thyroxine = thryoid storm)

A

hyperpyrexia > 41°C (increased basal metabolic rate); accelerated tachycardia/arrhythmia, cardiac failure, delirium/frank psychosis, hepatocellular dysfunction; jaundice

52
Q

3 treatment options for thyroid storm

A

surgery (thyroidectomy), radioiodine, drugs

53
Q

4 features of viral (de Quervain’s) thyroiditis

A

painful dysphagia, hyperthyroidism, pyrexia, raised erythrocyte sedimentation rate (ESR)

54
Q

5 clinical presentations of viral (de Quervain’s) thyroiditis

A

malaise, dysphagia, pain radiating to ear, thyroid gland visible enlarged (more on one side) whilst being tender and palpable, tender pretracheal lymph nodes

55
Q

natural history of viral (de Quervain’s) thyroiditis

A

virus attacks thyroid gland causing pain and tenderness -> thyroid stops making thyroxine and makes viruses instead -> no iodine uptake

56
Q

effect of viral (de Quervain’s) thyroiditis on stored thyroxine

A

as radioiodine uptake is zero, stored thyroxine is released, so is toxic with zero uptake; after 4 weeks, stored thyroxine is exhausted, so hypothyroid

57
Q

what happens after a further month of having viral (de Quervain’s) thyroiditis, after hypothyroid

A

resolution occurs (as with all viral diseases), so patient becomes euthyroid again

Y2 LCRS Endocrinology (37 decks)

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