hyperthyroidism Flashcards

1
Q

Give two causes of hyperthyroidism?

A

Graves’ disease, Plummer’s disease.

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2
Q

Outline the pathology of Graves’ disease.

A

Autoimmune condiiton.

Antibodies bind to and stimulate thyroid TSH receptor.

Causes goitre (smooth) and hyperthyroidism.

Lid lag.

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3
Q

Give some symptoms of hyperthyroidism.

A

Perspiration.

Muscle wasting.

SOB.

Rapid pulse.

Weight loss.

Moist palms.

Localsed myoxedema.

Exopthalmos.

Goiter.

Palpitations/tachycardia.

Tremor

Increased appetite.

Diarrhea.

Clubbing of fingers.

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4
Q

What is Graves’ exophthalmos?

A

Protusion of eyes due to growth of soft tissue behind eyes (another antibody).

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5
Q

What is pretibial myxoedema?

A

Swelling on shins of Graves’ patients - growth of soft tissue (another hormone).

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6
Q

Why does the thyoid grow in Graves’ disease?

A

Antibodies bind to TSH receptors - they work harder and grow.

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7
Q

How can Graves’ disease be distinguished from other hyperthyroidism forms?

A

Measure antibody.

Radioactive iodine scan.

Feel their neck.

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8
Q

What causes Plummer’s disease?

A

Begign overactive adenoma in thyroid making thyroxine.

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9
Q

How does Plummer’s disease differ from Graves’ disease?

A

Not autoimmune.

Nodular not smooth goitre.

No pretibial myxoedema.

No exopthalmos.

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10
Q

How does the thyroid appear in Plummer’s disease?

A

Thyroid shrinks due to low TSH (negative feedback due to high Thyroxine) - except for adenoma.

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11
Q

What does a radioactive iodine scan of Plummer’s yield?

A

A hot nodule - small area of highly active thyroid cells.

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12
Q

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

A

Sensitises B adrenoceptors to ambient levels of NA and A.

–> apparent sympatheticv activation.

–> Tachycardia, palpitations, tremor in hands, lid lag.

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13
Q

What is a thyroid storm? Why is it concerning?

A

The consequences of very high levels of thyroxine. Mismanagement can lead to death.

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14
Q

What are the features of a thyroid storm?

A
  • Hyperpyrexia > 41oC
  • accelerated tachycardia / arrhythmia
  • cardiac failure
  • delirium / frank psychosis
  • hepatocellular dysfunction; jaundice

High thyroxine and 2 of these features = thyroid storm.

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15
Q

What are the treatment options for a thyroid storm?

A

Surgery (thyroidectomy)

Radioiodine

Drugs.

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16
Q

What are the classes of drugs used in hyperthyroidism treatment?

A
  1. thionamides (thiourylenes; anti-thyroid drugs)
    - propylthiouracil (PTU)
    - carbimazole (CBZ)
  2. Potassium iodide
  3. radioiodine.
  4. Beta blockers.
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17
Q

How are Beta blockers different to other hyperthyroidism drugs?

A

They don’t reduce thyroxine, they help with symptoms.

18
Q

Why might thioamines be used?

A
  1. daily treatment of hyperthyroid conditions.
  2. treatment prior to surgery
  3. reduction of symptoms while waiting for radioiodine to take effect.
19
Q

How do thioamides work?

A

inhibition of thyroid peroxidase and hence T3/4 synthesis and secretion.

20
Q

Why don’t thioamides not have a clinical effect for a long period of time?

A

Although biochemical effect in inhibiting synthesis and secretion is quick (hours), lots of thyroxine in colloid and blood (T4 half life = 6 days) which must be used up.

21
Q

Why might propanolol be included in a treatment regimen of thioamide?

A

Treat symptoms, e.g. reducing tremor and tachycardia while waiting for thioamide to take effect.

22
Q

What other 2 mechanisms of action do thioamides have?

A

Suppress antibody production of Graves’ disease.

Reduce conversion of T4 –> T3 in peripheral tissues (PTU).

23
Q

What are the potential side effects of thioamides?

A

Agranulocytosis (neutrophil reduction) - rare, reversible with drug withdrawal.

Rashes - common.

24
Q

How are thionamides administered?

A

Orally. Tablets.

25
Q

What is the name of the active drug synthesised from the pro-drug carbimazole?

A

methimazole.

26
Q

Why my pregnancy be a concern when administering Thionamines.

A

They can cross the placenta and be secreted in breast milk.

27
Q

How are thioamides removes from the body?

A

Metabolised in liver, excrered in urine.

28
Q

How is thioamide treatment followed up?

A

Aim to stop anti-thyroid drug treatment after 18 months.

Review patient periodically with thyroid function tests to check for remission/relapse.

29
Q

Why are non-selective Beta blockers used to hyperthyroidism symptom control?

A

A widespread effect is desired.

30
Q

When is potassium iodide used?

A

To prepare patients for surgery or manage a thyroid storm - rapid reduction in thyroxine.

31
Q

How does Potassium Iodide reduce thyroxine.

A

Inhibits thyroxine synthesis rather than stimulates it - counterintuitive.

Wolff - Chaikoff effect - large dose of KI shuts down thyroid gland and stops it working (autoregulatory effect).

Thyroxine reduction in a couple of days.

32
Q

What are the effects of potassium iodide?

A

Hyperthyroidism symptoms reduce within 1-2 days (makes anaethetic easier).

Vascularly and size of gland reduce within 10-14 days (makes surgery easier)

33
Q

What side effects of potassium iodide treatment may arise?

A

Allergic reaction e.g. rashes.

34
Q

How is potassium iodide administered?

A

Orally - Lugol’s solution.

35
Q

What is the mechanism of action of Radioiodine (131I)?

A

Accumulates in colloid, emits beta particles which destroy follicular cells.

36
Q

When is radioiodine administered?

A

When anti-thyroid drug treatment is unsuccessful (discontinue 7-10 days before)

Women intending to be pregnant since thionamides can cross placenta.

37
Q

How is radioiodine administered?

A

Orally.

38
Q

How much radioiodine is administered for Graves’ disease and Thyroid cancer respectively?

A

Graves’ approx. 500 MBq

Thyroid cancer approx. 3,000Mbq

39
Q

131I

A

8 days

40
Q

At what point is the radioactivity of radioiodine treatment negligable?

A

2 months

41
Q

What considerations must be taken before administering it?

A

Contact with small children must be avoided for several weeks.

Contra-indicated in pregnancy and breast feeding.

42
Q
A