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brs (phase 1b) > (endo) hyperthyroidism > Flashcards

(endo) hyperthyroidism Flashcards

1
Q

how is thyroxine stored in thyroid follicular cells?

A

bound to thyroid globulin

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2
Q

what is the main function of thyroxine?

A

increases basal metabolic rate

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3
Q

what is the main function of TSH?

A

activates iodide uptake to stimulate thyroxine release

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4
Q

what is thyroid globulin?

A

binds thyroxine in the colloid when it is stored

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5
Q

describe how thyroid activity is controlled

A

reduced plasma thyroxine levels stimulate thyrotrophs to increase TSH release and stimulate the hypothalamus to increase TRH release

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6
Q

what level of TSH will you find in a patient with primary hypothyroidism, where the thyroid gland has been destroyed by the immune system?

A

(low fT4 causes) high TSH

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7
Q

how does thyroxine replacement work?

A

give patient w primary hypothyroidism thyroxine tablet and monitor TSH levels

increase the thyroxine dose accordingly until TSH levels are in the desired range

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8
Q

what is Graves’ disease?

A

autoimmune disease where the antibodies bind to and stimulate the TSH receptor in the thyroid

= hyperthyroidism and goitre (smooth)

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9
Q

what are the main symptoms of Graves’ disease?

A

hyperthyroidism and smooth goitre

(can also cause exophthalmos, pretibial myxedema

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10
Q

why does hyperthyroidism occur in Graves’ disease?

A

antibodies bind to the TSH receptors on thyroid gland and cause excess thyroxine release

exacerbated by growth of thyroid gland

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11
Q

how do patients with Graves’ disease present?

A

palpitation, elevated pulse/heart rate, smooth goitre, exophthalmos, diarrhoea (increased bowel movements)

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12
Q

what are the symptoms of Graves’ disease caused by?

A

increased basal metabolic rate

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13
Q

how does Graves’ disease cause exophthalmos?

A

antibodies bind to and stimulate growth receptors behind the eye causing the muscles to grow = exophthalmos

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14
Q

how does Graves’ disease cause pretibial myxoedema?

A

antibodies bind to receptors of the soft tissue causing hypertrophy and swelling of the lower limb

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15
Q

what is pretibial myxoedema?

A

the swelling (non-pitting) that occurs on the shins/lower limbs of patients with Graves’ disease causing growth of soft tissue

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16
Q

differentiate between pitting and non-pitting oedema

A

pitting oedema is caused in heart failure and is due to a fluid build-up

non-pitting oedema is caused in Graves’ disease and is due to accumulation of excess glycosaminoglycans in the skin

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17
Q

differentiate between pretibial myxoedema and myxoedema

A

myxoedema refers to a severe form of hypothyroidism that occurs when the condition is left untreated

pretibial myxoedema refers to swelling and hypertrophy of the soft tissue in the lower limbs in Graves’ disease

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18
Q

what is smooth goitre?

A

diffuse enlargement and engorgement of the thyroid gland

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19
Q

how can Graves’ disease be detected on a scan?

A

in Graves’ disease = enlarged thyroid gland (smooth goitre)

give radioactive iodine so follicular cells that take it up become radioactive and can be detected

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20
Q

what is Plummer’s disease?

A

toxic nodular goitre

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21
Q

differentiate between Graves’ disease and Plummer’s disease

A

Graves’ disease = autoimmune damage to thyroid gland, presents w exophthalmos and pretibial myxoedema

Plummer’s disease = not autoimmune, overactive thyroxine-producing benign adenoma but cannot present w exophthalmos and pretibial myxoedema

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22
Q

differentiate between toxic multinodular goitre and single goitre

A

single goitre = single nodule making the extra amount of thyroid hormone (also be referred to as a ‘toxic adenoma’ - Plummer’s disease)

toxic multinodular goiter = more than one nodule producing an extra amount of thyroid hormone

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23
Q

what are the effects of thyroxine on the sympathetic nervous system and why?

A

sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline

= apparent sympathetic activation

so tachycardia, palpitations, tremor in hands, lid lag

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24
Q

what is lid lag?

A

delay in moving the eyelid as the eye moves downwards

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25
Q

why does thyroxine cause sympathetic activation?

A

sensitises beta-adrenoreceptors to ambient levels of adrenaline and noradrenaline = apparent sympathetic activation

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26
Q

why are beta adrenoreceptors more sensitive due to thyroxine?

A

thyroxine sensitises beta adrenoreceptors SO normal amount of adrenaline does MORE than usually because adrenergic receptors are more sensitive

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27
Q

what are the symptoms of hyperthyroidism?

A

breathlessness

weight loss despite increased appetite

palpitations

tachycardia

heat intolerance

diarrhoea

lid lag ( + other sympathetic features such as tremors)

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28
Q

what is a thyroid storm?

A

a medical emergency w 50% mortality if wherein the blood results confirm hyperthyroidism = must be treated urgently and aggressively

should have confirmed hyperthyroidism and two of the following:

hyperpyrexia (> 41 degrees)

accelerated tachycardia/arrhythmia

cardiac failure

delirium/frank psychosis

heaptocellular dysfunction/jaundice

29
Q

what is hyperpyrexia?

A

condition where the body temperature goes above 41.5 degrees

30
Q

what treatment options are available for thyroid storm?

A

surgery (thyroidectomy)
radioiodine
drugs

31
Q

what are the four classes of drugs used to treat hyperthyroidism?

A

thionamides (PTU, CBZ) = anti-thyroid drugs

potassium iodide

radioiodine

beta blockers

32
Q

how do beta blockers treat hyperthyroidism?

A

target the sympathetic symptoms

33
Q

how do thionamides, potassium iodide and radioiodine treat hyperthyroidism?

A

block thyroid hormone synthesis

34
Q

name the two main thionamides

A

propylthiouracil (PTU)

carbimazole (CBZ)

35
Q

what are thionamides used for clinically?

A

daily treatment of hyperthyroid conditions

e.g. Graves’ + toxic multinodular goitre/toxic thyroid nodule

36
Q

what are the four components of thyroid hormone synthesis?

A

uptake of iodide (active transport)

iodination

coupling reaction + storage in colloid

endocytosis + secretion

37
Q

what is the mechanism of action of thionamides?

A

inhibition of thyroid peroxidase

= inhibits both T3 and T4 synthesis and secretion

38
Q

describe the biochemical and clinical effect of thionamides

A

biochemical = hours

clinical = weeks

39
Q

which drug is usually given alongside thionamides?

A

propanolol

= rapidly acts to reduce tremors, tachycardia + other sympathetic effects (as the ATDs tend to take much longer to do the same)

40
Q

why are beta blockers usually given in hyperthyroidism?

A

to reduce the sympathetic effects RAPIDLY (tremors, tachycardia, lid lag)

= need to be given as the ATDs do have the same reducing effect but take muuuch longer

41
Q

what are the unwanted actions of thionamides?

A

agranulocytosis (reduction in neutrophil count = rare & reversible on withdrawal of drug)

rashes (relatively common)

42
Q

how is thionamide administration followed up on?

A

usually aim to stop treatment after 18 months

continue w regular thyroid function tests to ensure there is no relapse or remission

43
Q

what is thyrotoxicosis?

A

excess thyroid hormone present in the body

44
Q

differentiate between thyrotoxicosis and hyperthyroidism

A

hyperthyroidism = increased thyroid hormone synthesis and secretion from the thyroid gland

thyrotoxicosis = clinical manifestations of inappropriately high thyroid hormone action in tissues

45
Q

what is the role of beta blockers in thyrotoxicosis?

A

act more rapidly than the anti-thyroid drugs to reduce the sympathetic symptoms of hyperthyroidism (tremor, tachycardia)

= relieves symptoms while ATDs take longer to do the same

46
Q

what kind of beta blockers are used to treat thyrotoxicosis?

A

non-selective beta blockers (B1, B2)

e.g. propanolol

= relieves the sympathetic symptoms in the meantime

47
Q

at which doses is potassium iodide usually given to hyperthyroid patients?

A

x30 of the average daily requirement

48
Q

when is potassium iodide most commonly given to hyperthyroid patients?

A

to prepare hyperthyroid patients for surgery

OR

in a severe thyrotoxic crisis (thyroid storm)

49
Q

what is the mechanism of action of potassium iodide in hyperthyroid patients?

A

inhibits the iodination of thyroglobulin

inhibits H2O2 generation and thyroperoxidase activity

= inhibiting thyroid hormone synthesis + secretion

50
Q

what is the Wolff-Chaikoff effect?

A

an autoregulatory phenomenon

= large amounts of ingested iodine acutely inhibits thyroid hormone synthesis within the follicular cells (regardless of TSH levels)

51
Q

how does potassium iodide affect hyperthyroidism?

A
  • hyperthyroid symptoms reduce within 1-2 days

- vascularity and size of gland reduce within 10-14 days

52
Q

what are the risks of a thyroidectomy?

A

risk of voice change

risk of losing the parathyroid glands

scar

anaesthesia

53
Q

describe how radioiodine therapy works

A

swallow a capsule containing about 370 MBq (10 mCi) of the isotope I-131 which targets the thyroid gland

taken up by the thyroid follicular cells, and destroys the cells in the thyroid gland

= reduced thyroxine production + size of the thyroid gland

54
Q

can radioiodine be given to anyone?

A

no, contraindicated in pregnant women

so if you receive radioiodine, should self-isolate AND stay away from pregnant women + children

55
Q

what is viral thyroiditis?

A

painful swelling of the thyroid gland thought to be triggered by a viral infection

56
Q

what are the signs of viral (de Quervain’s) thyroditis?

A

painful dysphagia
hyperthyroidism
pyrexia
thyroid inflammation

57
Q

explain briefly how viral thyroiditis occurs

A

virus attacks thyroid gland causing pain and tenderness

gland stops making thyroxine and all the stored thyroxine is released and makes viruses instead

= therefore, no iodine uptake

58
Q

explain why thyroiditis leads to

A

infection = rapid thyroid cells damage

so they release all the stored thyroxine causing a rapid increase in plasma thyroxine levels

59
Q

what is the radioiodine uptake in viral thyroiditis?

A

zero = no uptake

due to elevated plasma thyroxine = because of the release of pre-formed stores of thyroxine as a result of infection

60
Q

how does the thyroid hormone level vary in viral thyroiditis?

A

begins with hyperthyroidism and can progress into hypothyroidism

61
Q

explain how viral thyroiditis can lead to hypothyroidism

A

hyperthyroidism = RAPID release of stored thyroxine from the damaged thyroid follicular cells

hypothyroidism = four weeks following the infection, when all stored thyroxine in the non-damaged thyroid follicular cells exhausted

62
Q

how and when is viral thyroiditis resolved?

A

after two months following initial infection, resolution occurs + patient becomes euthyroid

63
Q

what are the fT3, fT4 and TSH levels in viral thyroiditis?

A

all stored thyroxine released = fT4 levels rise + TSH levels drop

= remains like this for a month BUT no new thyroxine is synthesised (making viruses instead so no iodine uptake)

64
Q

what happens to the nick in viral thyroiditis?

A

neck stiffness

65
Q

what happens to thyroid levels in the second month of viral thyroiditis?

A

(HYPOTHYROIDISM)
gland stops making thyroxine so no new thyroxine produced

all stored thyroxine is exhausted SO patient is now hypothyroid for a month

(slow recovery after 3 months)

66
Q

what happens to thyroid levels in the first month of viral thyroiditis?

A

(HYPERTHYROIDISM)
all stored thyroxine released = fT4 levels rise + TSH levels drop

= remains like this for a month BUT no new thyroxine is synthesised

67
Q

when and how do patients recover form viral thyroiditis?

A

slow recovery after 3 months

68
Q

what is postpartum thyroiditis?

A

similar to viral thyroiditis but no pain + only occurs after pregnancy

(inflammation of the thyroid gland after giving birth - immune system modulated during pregnancy)

69
Q

name four causes of an overactive thyroid gland

A

automimmune Graves’ disease

nodular thyroid disease

viral (de Quervain’s thyroiditis)

post-partum thyroiditis

brs (phase 1b) (71 decks)

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