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YR2 LCRS Endocrinology > 5. Hyperthyroidism > Flashcards

5. Hyperthyroidism Flashcards

1
Q

what are the 2 causes of hyperthyroidism?

A
  1. Grave’s disease

2. nodular goitre (Plummer’s disease)

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2
Q

describe grave’s disease

A

an autoimmune disease where the whole gland is smoothly enlarged and the whole gland is overactive

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3
Q

how does grave’s disease trigger hyperthyroidism?

A

the immune system produces an antibody pretending to be TSH which binds to the TSH receptor and the thyroid gland becomes overactive

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4
Q

what are the 2 major symptoms of grave’s disease?

A
  1. exophthalmos

2. pretibial myxoedema

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5
Q

describe exophthalmos

A

thyroxine makes b-receptors more sensitive and makes your eyes wider than normal and other antibodies bind the muscles behind the eye, pushing the eye forward

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6
Q

describe pretibial myxoedema

A

antibodies stimulate the growth of soft tissue on the skin (hypertrophy)

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7
Q

how might a patient present with grave’s disease?

A
  • exophthalmos
  • localised myxoedema
  • lid lag
  • perspiration
  • facial flush
  • muscle wasting
  • shortness of breath
  • loss of weight
  • rapid pulse
  • warm, moist palms
  • increased appetite
  • tremor
  • clubbing of fingers
  • muscular weakness/fatigue
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8
Q

what is a scintigram?

A

a scan where radioactive iodine is given. the thyroid gland takes up iodine and can be visualised on the scan

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9
Q

describe plummer’s disease

A

toxic nodular goitre which is not autoimmune but the result of a benign adenoma that is overactive and produces too much thyroxine

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10
Q

what are the main differences you can see between grave’s disease and plummer’s disease?

A

in plummer’s disease there will only be a lump on one side not a smoothly enlarged thyroid

there are no autoimmune features (pretibial myxodeoma/exophthalmos) in plummer’s disease

the scintigram will show a hot nodule as opposed to the whole thyroid gland being enlarged

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11
Q

what are some clinical features of plummer’s disease due to the actions of throxine?

A
  • increased BMR
  • weight loss
  • overheating
  • increased sensitivity of the sympathetic NS
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12
Q

what are the effects of thyroxine on the sympathetic NS?

A

sensitises beta adrenoreceptors to low levels of adrenaline and NA so there is more sympathetic activation even when small amounts of adrenaline are released

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13
Q

what is thyroid storm?

A

hyperthyroidism when it becomes life threatening (medical emergency)

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14
Q

what are the features of thyroid storm?

A
  • hyperpyrexia (temperature >41 degrees C)
  • accelerated tachycardia (>170bpm)
  • cardiac failure
  • delirium/psychosis
  • hepatocellular dysfunction, jaundice

2 or more symptoms are necessary for it to be a medical emergency

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15
Q

what are the aggressive treatment options for thyroid storm?

A
  • surgery (thyroidectomy)
  • radioiodine
  • drugs
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16
Q

what drugs are used in the treatment of hyperthyroidism?

A
  1. thionamides (1st line treatment) e.g. propylthiouracil (PTU) and carbimazole (CBZ)
  2. potassium iodide
  3. radioiodine
  4. beta-blockers (to help symptoms)
17
Q

why might drugs be given for reasons other than direct treatment?

A
  • to prepare a patient for a thyroidectomy (lower heart rate)
  • to reduce symptoms while waiting for radioactive iodine to act
18
Q

what is the role of thyroid peroxidase in the production of thyroid hormones?

A

iodinates thyroglobulin and is involved in the coupling of mono/di-iodothyronines to make T3 or T4

19
Q

how do thionamides work?

A

they inhibit thyroperoxidase enzyme, preventing the thyroid gland from making hormones

20
Q

why do the clinical effects of thionamides take so long to show?

A

there is a store of thyroid hormones in the colloid so the biochemical effect takes hours and clinical effects are seen after several weeks

21
Q

what is given to reduce side effects in the short-term?

A

propranolol (non-selective beta blocker) to reduce tremor and tachycardia

a cardio-selective beta blocker would only overcome palpitations, not the tremor

22
Q

what are the other mechanisms of propylthiouracil (thionamide)?

A
  • suppresses anti-TSH antibody production in Grave’s disease
  • reduces the conversion of T4 to T3 in peripheral tissues
23
Q

what are the unwanted actions of thionamides?

A
  • agranulocytosis - fall in WBC count (usually reduction in neutrophils) however is rare and reversible
  • rashes
24
Q

describe the pharmacokinetics of thionamides

A
  • drugs are in tablet form and are orally active
  • carbimazole is a pro-drug so must be converted to methimazole first
  • grave’s disease affects young people so women of reproductive age should be warned against pregnancy until dose is low because thionamides cross the placenta and are secreted in breast milk
  • aim is to stop treatment after 18months
25
Q

why is iodide (usually in the form of potassium iodide) given in the treatment of hyperthyroidism?

A

in preparation for surgery and in severe thyrotoxic crisis (thyroid storm)

inorganic iodide inhibits iodothyronine release (wolff-chaikoff effect) and reduces hyperthyroid symptoms within 1-2 days. it also reduces the size and vascularity of the thyroid gland

26
Q

what is hypothesised as the way KI switches off thyroid hormone production?

A
  1. inhibiting iodination of tyrosine residues on thyroglobulin
  2. inhibiting thyroid peroxidase with hydrogen peroxide
27
Q

what is the wolff-chaikoff effect?

A

inhibition of thyroid hormone synthesis and secretion

28
Q

what are the unwanted actions of KI?

A

allergic reactions e.g. rashes, fever

29
Q

describe the pharmacokinetics of KI

A
  • given orally as tablets or lugol’s solution (aq. iodine)

- maximum effects are seen after 10 days continuous administration

30
Q

why might radioiodine be given in the treatment of hyperthyroidism?

A

to treat hyperthyroidism or thyroid cancer

radioiodine accumulates in the colloid and emits beta particles (beta radiation) which destroys thyroid follicular cells so the thyroid gland is effectively switched off. thyroxine can then be given as a supplement

31
Q

how is radioiodine given, in what dose is it given and what must be done before giving it?

A

given as a tablet

graves disease: 500MBg, thyroid cancer: 3000MBg

discontinue anti-thyroid drugs 7-10 days prior to treatment so the thyroid gland sucks up all the radioiodine

32
Q

what must you be cautious of with radioiodine?

A

avoid close contact with small children for several weeks after receiving treatment

33
Q

how can radioiodine be used in scintigraphy?

A

to map out the thyroid gland

administered intravenously, has a negligible cytotoxicity

34
Q

what is viral (de Quervain’s) thyroiditis?

A

thyroid gland is infected by a virus resulting in painful dysphagia (difficulty swallowing)

damage to the thyroid follicles leading to a huge release of thyroxine (hyperthyroidism) as well as an immune response leading to pyrexia (fever)

35
Q

what is the main clinical feature of viral (de Quervain’s) thyroiditis?

A

raised erythrocyte sedimentation rate (ESR)

36
Q

what does a scintigram of someone with viral thyroiditis show and why?

A

blank scintigram

the virus hijacks the follicular cells and the cells make viruses instead of thyroxine. the patient has released the stored thyroxine and become hyperthyroid quickly but is not making any new thyroxine to store in the colloid so there is 0 iodine uptake

37
Q

how can you tell the difference between viral thyroiditis and graves disease?

A

in viral thyroiditis the thyroid gland is painful

in viral thyroiditis the hyperthyroid is short-term, in 3-4 weeks the patient will become hypothyroid (cold and lethargic) because the stored thyroxine is exhausted

YR2 LCRS Endocrinology (18 decks)

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