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Endocrinology > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

State causes of hyperthyroidism. (2)

A 
Common causes:
- Grave's disease
- Plummer's disease 
But also ... 
- Early stages of De Quervain's thyroiditis
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2
Q

What is Grave’s disease? (2)

A
  • An autoimmune disease
  • An autoimmune antibody is produced that behaves like TSH and binds to the TSH receptor on the thyroid gland
  • Antibody stimulates thyroid hormone production
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3
Q

What does a thyroid gland look like in Graves’ Disease? (1)

A

Diffuse goitre: the thyroid gland is smoothly enlarged and the whole gland is active

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4
Q

State some features of Graves’ Disease. (4)

A 
Anything from diagram on page 18 is fine
Rapid pulse 
Warm (heat-intolerance)
Localised pretibial myxoedema 
Exophthalmos 
Lid lag
Excitability/nervousness/tremor
Loss of weight 
Muscle wasting 
Oligomenorrhoea/amenorrhoea/diarrhoea
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5
Q

How does Grave’s disease give rise to pretibial myxoedema and exophthalmos? (2)

A
  • Antibodies that bind to growth receptors

- Promote growth of soft tissue e.g. in the shins or behind the eye leading to bulging

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6
Q

What are two defining features of Graves’ and what is it caused by? (2)

A
  • Localised pretibial myxoedema
  • Exophthalmos
    Antibodies cause both of these
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7
Q

What is decompensation in the context of Grave’s disease? (1)

A

Initially patients have increased cognitive speed, more active, losing weight, but eventually decompensate, because cannot sleep so constantly feel tired, leading to emotional instability and lose ability to focus

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8
Q

Describe the appearance of a thyroid gland of a Graves’ patient in a thyroid scan using radioactive iodine. (1)

A

The whole gland is smoothly enlarged and the whole gland is overactive

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9
Q

What can be used instead of iodine in the production of thyroid scintigrams? (1)

A

Technetium (cheaper)

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10
Q

Describe the levels of TSH and T3/T4 in Grave’s disease. (1)

A

High T3/T4 (OBVIOUSLY)

Low TSH

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11
Q

What is Plummer’s disease? (1)

A

A benign adenoma of the thyroid that is overactive at making thyroxine

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12
Q

How does Plummer’s disease differ from Graves’? (2)

A
  • No autoimmune antibodies
  • No pretibial myxoedema
  • No exophthalmos
  • On a scinitigram in Plummer’s observe a hot nodule as it is only a specific part of the thyroid gland that is overactive
  • Histology different (e.g. diffuse hyperplasia in Grave’s whereas outside of the adenoma in Plummer’s get involution of the gland)
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13
Q

What will a technetium or iodine scan of the thyroid show in a patient with Plummer’s Disease? (1)

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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14
Q

Describe the effects of thyroxine on the sympathetic nervous system. (2)

A
  • Thyroxine sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline. So you get symptoms of having high adrenaline (or sympathetic over-activation)
  • Tachycardia, lid-lag and palpitations all arise due to sensitivity to adrenaline
  • Exercise: small amounts of exercise = small increases in adrenaline, as a result get huge amount of anxiety, massive increase in heart rate
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15
Q

What is thyroid storm? (1)

A

A rare medical emergency - potentially life threatening complication of hyperthyroidism (50% mortality if untreated)

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16
Q

What are the biochemical features of thyroid storm? (3)

A
  • Hyperpyrexia > 41oC (pyrexia = fever)
  • Accelerated tachycardia / arrhythmia (i.e. fast and irregular heart beat)
  • Cardiac failure (when the heart is unable to pump sufficiently to meet body needs)
  • Delirium / frank psychosis
  • Hepatocellular dysfunction; jaundice
17
Q

How is thyroid storm treated? (2)

A
  • Surgery
  • Radioiodine
  • Drugs
18
Q

What is viral (de Quervain’s) thyroiditis? (2)

A
  • Virus takes over thyroid gland: release of all stored thyroxine
  • But because cell machinery now dedicated to producing viral particles no more uptake of iodine
  • Goes from hyperthyroid to hypothyroid after ~4 weeks as thyroxine stores are depleted
19
Q

How can viral thyroiditis be distinguished from Grave’s disease? (3)

A
  • Thyroid gland does not show any iodine or technetium uptake
  • Patients complain of pain
  • General features of inflammation
  • Eventually developing hypothyroidis
  • Lack of TSH antibody (cf. Grave’s)
20
Q

List the key clinical features of viral thyroiditis. (2)

A
  • Hyperpyrexia
  • Painful dysphagia
  • Raised ESR
21
Q

State the classes of drugs used in the treatment of hyperthyroidism. (2)

A
  • Thionamides
  • Potassium iodide
  • Radioiodine
  • Beta blockers (improves symptoms - the other 3 block thyroxine production)
22
Q

Name two thionamides. (1)

A

Carbimazole & propylthiouracil

23
Q

When are thionamides used? (3)

A
  • In hyperthyroidism:
  • 1) Daily management of disease
  • 2) Prior to surgery
  • 3) Reduction of symptoms whilst waiting for other treatment to come in
24
Q

What is the mechanism of action of thionamides? (3)

A
  • i) Inhibition of thyroid peroxidase
  • :. no oxidation of iodide to atomic iodine (a free radical) nor does the coupling reaction (also catalysed by thyroperoxidase) take place
  • ii) may suppress antibody production in Grave’s disease
  • iii) Reduces conversion of T4 to T3
25
Q

Why do thionamides have a delayed effect on thyroid hormone levels? (2)

A
  • 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 (hours) and the clinical effects (weeks)
26
Q

What would you give the patient temporarily whilst waiting for thethionamides to have their clinical effect? (1)

A

Non-selective beta-blockers e.g. propanolol

This will reduce the effects of beta sensitisation by thyroxine

27
Q

State some unwanted effects of thionamides. (1)

A

Agranulocytosis

Rashes

28
Q

Carbimazole is a pro-drug. What is it converted to become active? (1)

A

Methimazole

29
Q

In what circumstances are propylthiouracil preferred to carbimazole? (1)

A

Breast-feeding mothers/pregnancy

PTU crosses placenta/concentrates in breastmilk much less

30
Q

What is the mechanism of action of potassium iodide treatment? (1)

A

If you give a massive dose of iodine it can turn off the thyroid gland
It inhibits the iodination of thyroglobulin and inhibits the production of hydrogen peroxide

31
Q

What is the Wolff-Chaikoff effect? (1)

A

The temporary reduction in thyroid hormones following ingestion of a large amount of iodine

32
Q

When is potassium iodide used in hyperthyroidism? (1)

A

In hyperthyroidism to reduce the size/vascularity of the thyroid gland in preparation for surgery
OR
in thyroid storm (severe thyrotoxicosis)

33
Q

State some unwanted actions of potassium iodide. (1)

A

Rashes
Fever
Angioedema

34
Q

What is the mechanism of action of radioiodine treatment in hyperthyroidism? (1)

A

Taken up by the follicular cells and transported to the colloid where it accumulates; consequently emits ß-particles destroying follicular cells

35
Q

What cautions need to be taken with radioiodine treatment? (2)

A

Avoid close contact with small children for several weeks after receiving radioiodine
Contra-indicated in pregnancy and breast-feeding
Be wary when travelling

Endocrinology (27 decks)

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