Hyperthyroidism Flashcards
State two common causes of hyperthyroidism
Graves’ Disease
Plummer’s Disease (toxic nodular goitre)
What type of disease is Graves’? Describe its mechanism.
Autoimmune
Antibodies bind to and stimulate the TSH receptor in the thyroid
Describe the appearance of the thyroid gland in Graves’ disease
Smoothly enlarged thyroid gland (goitre); moves up and down when swallowing
What are two defining features of Graves’ and what are they caused by?
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)
Describe the appearance of a thyroid gland of a Graves’ patient in a thyroid scan using radioactive iodine.
Gland is overactive so there is increased uptake of radio-iodine (dark black area)
What causes Plummer’s Disease?
It is caused by a benign adenoma in the thyroid gland that is overactive at making thyroxine
How does Plummer’s disease differ from Graves’?
NO pretibial myxoedema
NO exophthalmos
NOT autoimmune
Nodular goitre
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 => symptoms of having high adrenaline (e.g. tachycardia, palpitations, tremor)
List the general features associated with hyperthyroidism
- Weight loss despite increased appetite
- Breathlessness
- Palpitations
- Tachycardia
- Sweating
- Heat intolerance
- Diarrhoea
- Lid lag
What is lid lag and what causes it?
Upper eyelid is higher than normal; caused by high adrenaline
What is thyroid storm (thyrotoxic crisis) and what are the features of thyroid storm?
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
Briefly summarise the treatment options for thyroid storm
Surgery (thyroidectomy)
Radioiodine
Drugs
What is viral (de Quervain’s) thyroiditis?
- 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
State the four classes of drugs used in the treatment of hyperthyroidism
- Thionamides (thiourylenes; anti-thyroid drugs)
- Potassium Iodide
- Radioiodine
- Beta Blockers (only to help with symptoms)
Name two thionamides
Propylthiouracil (PTU)
Carbimazole (CBZ)
Which types of hyperthyroidism can thionamides be used to treat? When might they be used?
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
What is the mechanism of action of thionamides?
Thionamides inhibit thyroid peroxidase
This prevents the iodination of thyroglobulin and coupling of MIT and DIT.
What is the duration of thionamide’s biochemical and clinical effect? Give a reason for this difference.
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
Other than its main function in inhibiting thyroperoxidase, what else do thionamides do?
- Suppress antibody production in Graves’ disease
- Reduces conversion of T4 to T3 in peripheral tissues (PTU)
What would you give the patient temporarily whilst waiting for the thionamides to have their clinical effect?
Non-selective beta-blockers (e.g. propranolol)
are co-administered to reduce the effects of beta adrenoceptor sensitisation by thyroxine
State some unwanted effects of thionamides
- Agranulocytosis (usually reduction in neutrophils): rare and reversible on withdrawal of drug.
- Rashes (relatively common)
Outline the pharmacokinetics of a thionamide such as carbimazole
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
Outline the follow up for thionamide treatment
- Usually aim to stop treatment after 18 months
- Review patient periodically including thyroid function tests for remission/relapse
