Hyperthyroidism Flashcards
(39 cards)
State two common causes of hyperthyroidism.
Graves’ Disease Plummer’s Disease (toxic nodular goitre)
What type of disease is Graves’? Describe its mechanism.
Autoimmune An autoimmune antibody is produced that behaves like TSH and binds to the TSH receptor thus stimulating thyroid hormone production Another antibody causes pretibial myxoedema another antibody binds to muscles behind eye causing exophthalmos as the muscles grow
What does a thyroid gland look like in Graves’ Disease?
The thyroid gland is smoothly enlarged and the whole gland is active
State some features of Graves’ Disease.
Antibodies causing:
Goitre (smooth enlargement)
Pretibial myxoedema
Exophtalmos
Sensitises beta receptors to adrenaline and NA leading to sympa activation:
•Tachycardia
- palpitations,
- tremor in hands,
- lid lag
- increased sweating
Others- everything speeds up:
- weight loss despite inreased appetite
- Heat intolerance
- Diarrhoea
What are two defining features of Graves’ and what is it caused by?
Localised pretibial myxoedema Exophthalmos Antibodies cause both of these
Describe the appearance of a thyroid gland of a Graves’ patient in a thyroid scan using radioactive iodine.
The whole gland is smoothly enlarged and the whole gland is overactive
slide 11
What causes Plummer’s Disease?
It is caused by a benign adenoma in the thyroid gland
How does Plummer’s disease differ from Graves’?
NO pretibial myxoedema NO exophthalmos NOT autoimmune
What will a technetium or iodine scan of the thyroid show in a patient with Plummer’s Disease?
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
Describe the effects of thyroxine on the sympathetic nervous system.
Thyroxine sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline So you get symptoms of having high adrenaline
What causes lid lag?
superior tarsal muscle (an eyelid elevator) is partly innervated by Sympa NS and
Thyroxine sentises beta receptors to adrenaline and noradrenaline in the sympathetic nervous system.
What is thyroid storm (thyrotoxic crisis) and what are the clinical features of thyroid storm?
•Extreme hyperthyroidism, this happens when patients dontpresent early enough
Clinical features
- Hyperpyrexia (high fever, not just fever)> 41oC
- accelerated tachycardia / arrhythmia
- cardiac failure
- delirium / frank psychosis (really confused
- hepatocellular dysfunction (liver problems); jaundice
State four drugs used during the treatment for hyperthyroidism.
Thionamides (also called thiourylenes; anti-thyroid drugs)
Potassium Iodide
Radioiodine
Beta Blockers
State two thionamides.
- propylthiouracil (PTU)
- carbimazole(CBZ)
What are thionamides used to treat and when would you use it?
Graves’ Disease
Plummer’s Disease
- You can use it before thyroidectomy to stabilise the patient (you wouldn’t want to give general anaesthetic to someone who is tachycardic with a labile heart rate)
- It can be used after radioiodine treatment while you’re waiting for the clinical effects of the radioiodine to come in to reduce the symptoms that the patient is facing from hyperthyroidism
Describe the synthesis of thyroxine by follicular cells.
Thyroglobulin is a protein produced by the follicular cells Iodine is taken up by the follicular cells Thyroid peroxidase, in the presence of hydrogen peroxide, iodinates the tyrosyl residues on the thyroglobulin to produce monoiodotyrosine or diiodotyrosine Peroxidase transaminase then couples MIT and DIT to form T3 and T4, which is stored in the colloid
What is the mechanism of action of thionamides?
Thionamides inhibit thyroperoxidase This prevents the iodination of thyroglobulin and coupling of MIT and DIT It also inhibits peroxidase transaminase
Why do thionamides have a delayed effect on thyroid hormone levels?
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. When these are released, they also have a long half life so it takes time for the effects to wear off So there is a big delay between the biochemical effects and the clinical effects.
What would you give the patient temporarily whilst waiting for thethionamides to have their clinical effect?
Non-selective beta-blockers
It takes timeforantithyroid drugs to come into effect and so in the mean time, you give beta blockers to deal with the symptoms caused by excess Beta receptor stimulation (thyroxine sensitisesbeta receptor to adrenaline etc).
you use non selective beta blocker so it deals with all the symptoms associated with excess Beta stimulation rather than only the symptoms associated with subgroups of beta receptors
Other than its main function in inhibiting thyroperoxidase, what else do thionamides do?
Suppress antibody production (in Graves’)
Reduces deiodination of T4 to T3 in peripheral tissues (propylthiouracil/PTU)
State some unwanted effects of thionamides.
Agranulocytosis/granulocytopenia (rare and reversible with withdrawal of the drug)
rashes (common)
Agranulocytosis acute condition involving a severe and dangerous leukopenia (lowered white blood cell count), most commonly of neutrophils causing a neutropenia in the circulating blood.
Carbimazole is a pro-drug. What is it converted to become active?
Methimazole
What are the implications of thionamides in pregnancy?
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 and is taking thionamides Both drugs cross into breast milk but PTU does this less than CBZ It is metabolised in the liver and excreted in the urine
What is the mechanism of action of potassium iodide treatment?
If you give a massive dose of iodine it can turn off the thyroid gland - Wolff Chaikoff effect
- High KI Inhibits H2O2 generation + thyoperoxidase
- hence High KI Inhibits iodination of thyroglobulin
