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Endocrinology Year 2 > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

State two common causes of hyperthyroidism

A

Graves’ Disease

Plummer’s Disease (toxic nodular goitre)

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2
Q

What type of disease is Graves’? Describe its mechanism.

A

Autoimmune

Antibodies bind to and stimulate the TSH receptor in the thyroid

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3
Q

Describe the appearance of the thyroid gland in Graves’ disease

A

Smoothly enlarged thyroid gland (goitre); moves up and down when swallowing

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4
Q

What are two defining features of Graves’ and what are they caused by?

A

Other antibodies bind to muscles behind the eye and cause EXOPHTHALMOS (maybe with chemosis as well)

Other antibodies cause (non-pitting) PRETIBIAL MYXOEDEMA (hypertrophy of soft tissue)

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5
Q

Describe the appearance of a thyroid gland of a Graves’ patient in a thyroid scan using radioactive iodine.

A

Gland is overactive so there is increased uptake of radio-iodine (dark black area)

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6
Q

What causes Plummer’s Disease?

A

It is caused by a benign adenoma in the thyroid gland that is overactive at making thyroxine

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7
Q

How does Plummer’s disease differ from Graves’?

A

NO pretibial myxoedema
NO exophthalmos
NOT autoimmune
Nodular goitre

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8
Q

What will a technetium or iodine scan of the thyroid show in a patient with Plummer’s Disease?

A

All the iodine will be taken up by the overactive, tumorous part of the thyroid so you will see a hot nodule appear.
The rest of the thyroid gland will not be seen because the high thyroxine production will decrease TSH release from the anterior pituitary and so the rest of the thyroid gland that is responding to TSH will not produce any thyroxine and will not take up iodine

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9
Q

Describe the effects of thyroxine on the sympathetic nervous system

A

Thyroxine sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline => symptoms of having high adrenaline (e.g. tachycardia, palpitations, tremor)

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10
Q

List the general features associated with hyperthyroidism

A
  • Weight loss despite increased appetite
  • Breathlessness
  • Palpitations
  • Tachycardia
  • Sweating
  • Heat intolerance
  • Diarrhoea
  • Lid lag
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11
Q

What is lid lag and what causes it?

A

Upper eyelid is higher than normal; caused by high adrenaline

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12
Q

What is thyroid storm (thyrotoxic crisis) and what are the features of thyroid storm?

A

This is a medical emergency that is a rare but important complication of hyperthyroidism that requires aggressive treatment

  • Hyperpyrexia (>41)
  • Accelerated tachycardia/arrhythmia
  • Cardiac failure
  • Delirium/frank psychosis
  • Hepatocellular dysfunction, jaundice
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13
Q

Briefly summarise the treatment options for thyroid storm

A

Surgery (thyroidectomy)
Radioiodine
Drugs

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14
Q

What is viral (de Quervain’s) thyroiditis?

A
  • Virus attacks thyroid gland causing pain and tenderness
  • Thyroid stops making thyroxine and makes viruses instead
  • Therefore any stored thyroxine is released and radio iodine uptake is zero (not visible on thyroid uptake scan)
  • Four weeks later, stored thyroxine is exhausted => hypothyroid
  • After a further month, resolution occurs => patient becomes euthyroid
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15
Q

State the four classes of drugs used in the treatment of hyperthyroidism

A
  1. Thionamides (thiourylenes; anti-thyroid drugs)
  2. Potassium Iodide
  3. Radioiodine
  4. Beta Blockers (only to help with symptoms)
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16
Q

Name two thionamides

A

Propylthiouracil (PTU)

Carbimazole (CBZ)

17
Q

Which types of hyperthyroidism can thionamides be used to treat? When might they be used?

A

Graves’ disease
Plummer’s disease

  • Used as a daily treatment
  • Used as a treatment prior to surgery
  • Used to reduce symptoms while waiting for radioactive iodine to act
18
Q

What is the mechanism of action of thionamides?

A

Thionamides inhibit thyroid peroxidase

This prevents the iodination of thyroglobulin and coupling of MIT and DIT.

19
Q

What is the duration of thionamide’s biochemical and clinical effect? Give a reason for this difference.

A

Biochemical effect = hours
Clinical effect = weeks

Thionamides are quick in inhibiting synthesis of thyroid hormone but it does nothing to the thyroid hormone that has already been synthesised and is stored in the colloid ready for release.
So there is a big delay between the biochemical effects and the clinical effects

20
Q

Other than its main function in inhibiting thyroperoxidase, what else do thionamides do?

A
  • Suppress antibody production in Graves’ disease

- Reduces conversion of T4 to T3 in peripheral tissues (PTU)

21
Q

What would you give the patient temporarily whilst waiting for the thionamides to have their clinical effect?

A

Non-selective beta-blockers (e.g. propranolol)

are co-administered to reduce the effects of beta adrenoceptor sensitisation by thyroxine

22
Q

State some unwanted effects of thionamides

A
  • Agranulocytosis (usually reduction in neutrophils): rare and reversible on withdrawal of drug.
  • Rashes (relatively common)
23
Q

Outline the pharmacokinetics of a thionamide such as carbimazole

A

Carbimazole is an orally active pro-drug which first has to be converted to methimazole.
It is metabolised in the liver and excreted in urine

24
Q

Outline the follow up for thionamide treatment

A
  • Usually aim to stop treatment after 18 months

- Review patient periodically including thyroid function tests for remission/relapse

25
Q

How does the dosage of thionamide change in the case for a pregnant patient?

A

Thionamides can cross the placenta and is present in breast milk so it can cause foetal hypothyroidism
This means that you would want to give as low a dose as possible to a patient who is trying to conceive.
Note that PTU does this less than CBZ

26
Q

When might potassium iodide be used to treat hyperthyroidism?

A
  • Preparation of hyperthyroid patients for surgery

- Severe thyrotoxic crisis (thyroid storm)

27
Q

What is the mechanism of action of potassium iodide? State the name given to this effect

A

If you give a massive dose of iodine (at least 30 times the average daily requirement) turns off thyroid hormone synthesis & secretion.
It inhibits the iodination of thyroglobulin, the production of hydrogen peroxide, and thyroperoxidase.

WOLFF-CHAIKOFF effect (presumed auto-regulatory effect)

28
Q

What are the clinical effects of potassium iodide treatment?

A
  • Hyperthyroid symptoms reduce within 1-2 days

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

29
Q

State some unwanted actions of potassium iodide

A

Allergic reaction eg. rashes, fever, angio-oedema

30
Q

In what form is potassium iodide given?

A

Given orally as Lugol’s Solution or Aqueous iodine, with maximum effects after 10 days continuous administration

31
Q

Radioiodine (131 I) may be used to treat which types of hyperthyroidism?

A

Graves’ disease

Plummer’s disease (=toxic nodular disease)

Thyroid cancers

32
Q

How does radioiodine work in suppressing thyroxine synthesis and secretion?

A

It accumulates in the colloid, and emits β particles,

destroying follicular cells

33
Q

Summarise the clinically relevant pharmacokinetic details associated with radioiodine use

A
  • Discontinue anti-thyroid drugs 7-10 days prior to radioiodine treatment
  • Administer as a single oral dose (note: Graves’ disease = approx 500 MBq; Thyroid cancer = circa 3,000 MBq)
  • Radioactive half life of 8 days
  • Radioactivity negligible after 2 months
34
Q

What are some of the important cautions related to radioiodine treatment?

A
  • Avoid close contact with small children for several weeks after receiving radioiodine
  • Contraindicated in pregnancy and breast feeding
35
Q

What test can be used to confirm the thyroid gland pathology?

A

Radioiodine or technetium 99 pertechnetate is administered i.v. in very low, tracer doses (negligible toxicity)

36
Q

State some symptoms of viral thyroiditis (de Quervain’s thyroiditis).

A
  • Painful dysphagia
  • Pyrexia
  • Hyperthyroidism
  • Raised ESR
37
Q

What substances would you check for in the blood test of a patient suffering from hyperthyroidism?

A

fT4, TSH, TSH receptor antibodies

Endocrinology Year 2 (18 decks)

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