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
What is the name of the active drug synthesised from the pro-drug carbimazole?
methimazole.
26
Why my pregnancy be a concern when administering Thionamines.
They can cross the placenta and be secreted in breast milk.
27
How are thioamides removes from the body?
Metabolised in liver, excrered in urine.
28
How is thioamide treatment followed up?
Aim to stop anti-thyroid drug treatment after 18 months. Review patient periodically with thyroid function tests to check for remission/relapse.
29
Why are non-selective Beta blockers used to hyperthyroidism symptom control?
A widespread effect is desired.
30
When is potassium iodide used?
To prepare patients for surgery or manage a thyroid storm - rapid reduction in thyroxine.
31
How does Potassium Iodide reduce thyroxine.
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
What are the effects of potassium iodide?
Hyperthyroidism symptoms reduce within 1-2 days (makes anaethetic easier). Vascularly and size of gland reduce within 10-14 days (makes surgery easier)
33
What side effects of potassium iodide treatment may arise?
Allergic reaction e.g. rashes.
34
How is potassium iodide administered?
Orally - Lugol's solution.
35
What is the mechanism of action of Radioiodine (131I)?
Accumulates in colloid, emits beta particles which destroy follicular cells.
36
When is radioiodine administered?
When anti-thyroid drug treatment is unsuccessful (discontinue 7-10 days before) Women intending to be pregnant since thionamides can cross placenta.
37
How is radioiodine administered?
Orally.
38
How much radioiodine is administered for Graves' disease and Thyroid cancer respectively?
Graves' approx. 500 MBq Thyroid cancer approx. 3,000Mbq
39
131I
8 days
40
At what point is the radioactivity of radioiodine treatment negligable?
2 months
41
What considerations must be taken before administering it?
Contact with small children must be avoided for several weeks. Contra-indicated in pregnancy and breast feeding.
42