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(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
why does thyroxine cause sympathetic activation?
sensitises beta-adrenoreceptors to ambient levels of adrenaline and noradrenaline = apparent sympathetic activation
26
why are beta adrenoreceptors more sensitive due to thyroxine?
thyroxine sensitises beta adrenoreceptors SO normal amount of adrenaline does MORE than usually because adrenergic receptors are more sensitive
27
what are the symptoms of hyperthyroidism?
breathlessness weight loss despite increased appetite palpitations tachycardia heat intolerance diarrhoea lid lag ( + other sympathetic features such as tremors)
28
what is a thyroid storm?
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
what is hyperpyrexia?
condition where the body temperature goes above 41.5 degrees
30
what treatment options are available for thyroid storm?
surgery (thyroidectomy) radioiodine drugs
31
what are the four classes of drugs used to treat hyperthyroidism?
thionamides (PTU, CBZ) = anti-thyroid drugs potassium iodide radioiodine beta blockers
32
how do beta blockers treat hyperthyroidism?
target the sympathetic symptoms
33
how do thionamides, potassium iodide and radioiodine treat hyperthyroidism?
block thyroid hormone synthesis
34
name the two main thionamides
propylthiouracil (PTU) | carbimazole (CBZ)
35
what are thionamides used for clinically?
daily treatment of hyperthyroid conditions e.g. Graves' + toxic multinodular goitre/toxic thyroid nodule
36
what are the four components of thyroid hormone synthesis?
uptake of iodide (active transport) iodination coupling reaction + storage in colloid endocytosis + secretion
37
what is the mechanism of action of thionamides?
inhibition of thyroid peroxidase = inhibits both T3 and T4 synthesis and secretion
38
describe the biochemical and clinical effect of thionamides
biochemical = hours clinical = weeks
39
which drug is usually given alongside thionamides?
propanolol = rapidly acts to reduce tremors, tachycardia + other sympathetic effects (as the ATDs tend to take much longer to do the same)
40
why are beta blockers usually given in hyperthyroidism?
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
what are the unwanted actions of thionamides?
agranulocytosis (reduction in neutrophil count = rare & reversible on withdrawal of drug) rashes (relatively common)
42
how is thionamide administration followed up on?
usually aim to stop treatment after 18 months continue w regular thyroid function tests to ensure there is no relapse or remission
43
what is thyrotoxicosis?
excess thyroid hormone present in the body
44
differentiate between thyrotoxicosis and hyperthyroidism
hyperthyroidism = increased thyroid hormone synthesis and secretion from the thyroid gland thyrotoxicosis = clinical manifestations of inappropriately high thyroid hormone action in tissues
45
what is the role of beta blockers in thyrotoxicosis?
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
what kind of beta blockers are used to treat thyrotoxicosis?
non-selective beta blockers (B1, B2) e.g. propanolol = relieves the sympathetic symptoms in the meantime
47
at which doses is potassium iodide usually given to hyperthyroid patients?
x30 of the average daily requirement
48
when is potassium iodide most commonly given to hyperthyroid patients?
to prepare hyperthyroid patients for surgery OR in a severe thyrotoxic crisis (thyroid storm)
49
what is the mechanism of action of potassium iodide in hyperthyroid patients?
inhibits the iodination of thyroglobulin inhibits H2O2 generation and thyroperoxidase activity = inhibiting thyroid hormone synthesis + secretion
50
what is the Wolff-Chaikoff effect?
an autoregulatory phenomenon = large amounts of ingested iodine acutely inhibits thyroid hormone synthesis within the follicular cells (regardless of TSH levels)
51
how does potassium iodide affect hyperthyroidism?
- hyperthyroid symptoms reduce within 1-2 days | - vascularity and size of gland reduce within 10-14 days
52
what are the risks of a thyroidectomy?
risk of voice change risk of losing the parathyroid glands scar anaesthesia
53
describe how radioiodine therapy works
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
can radioiodine be given to anyone?
no, contraindicated in pregnant women | so if you receive radioiodine, should self-isolate AND stay away from pregnant women + children
55
what is viral thyroiditis?
painful swelling of the thyroid gland thought to be triggered by a viral infection
56
what are the signs of viral (de Quervain's) thyroditis?
painful dysphagia hyperthyroidism pyrexia thyroid inflammation
57
explain briefly how viral thyroiditis occurs
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
explain why thyroiditis leads to
infection = rapid thyroid cells damage so they release all the stored thyroxine causing a rapid increase in plasma thyroxine levels
59
what is the radioiodine uptake in viral thyroiditis?
zero = no uptake | due to elevated plasma thyroxine = because of the release of pre-formed stores of thyroxine as a result of infection
60
how does the thyroid hormone level vary in viral thyroiditis?
begins with hyperthyroidism and can progress into hypothyroidism
61
explain how viral thyroiditis can lead to hypothyroidism
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
how and when is viral thyroiditis resolved?
after two months following initial infection, resolution occurs + patient becomes euthyroid
63
what are the fT3, fT4 and TSH levels in viral thyroiditis?
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
what happens to the nick in viral thyroiditis?
neck stiffness
65
what happens to thyroid levels in the second month of viral thyroiditis?
(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
what happens to thyroid levels in the first month of viral thyroiditis?
(HYPERTHYROIDISM) all stored thyroxine released = fT4 levels rise + TSH levels drop = remains like this for a month BUT no new thyroxine is synthesised
67
when and how do patients recover form viral thyroiditis?
slow recovery after 3 months
68
what is postpartum thyroiditis?
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
name four causes of an overactive thyroid gland
automimmune Graves' disease nodular thyroid disease viral (de Quervain’s thyroiditis) post-partum thyroiditis

brs (phase 1b) (71 decks)

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