Hyperthyroidism Flashcards
Hyperthyroidism has more than one cause. What are these two diseases?
- Graves’ disease
- Nodular Goitre (benign tumour making a bit too much thyroxine), aka Plummer’s disease
What kind of disease is Graves’ disease, what happens to cause the problems and what does it cause?
- Autoimmune
- Antibodies bind to and stimulate the TSH receptor in the thyroid
- Causes goitre and hyperthyroidism (causes lid lag)
What effect does thyroxine have on beta receptors in the heart?
Increase the sensitivity - method of increasing heart rate
What do other antibodies bind to and cause in Graves’ disease?
- Muscles behind the eye - causes exophthalmos (different antibody to thyroid-targeting one)
- Cause pretibial myoedema (hypertrophy of soft tissue around shin) (different antibody to both the others, 3 total antibodies)
What is pretibial myxoedema?
Swelling that occurs on the shins of patients with Graves’ disease, growth of soft tissue
NOT to be confused with myxoedema = hyPOthyroidism
What is a goitre?
Smooth, enlarged thyroid gland
What is Plummer’s disease?
Toxic nodular goitre
- Benign adenoma that is overactive, lump on one side of thyroid gland
- Thyroid gland atrophies due to excess thyroxine negative feedback on TSH production, so on scan you see a lump
What 3 methods can you use to distinguish between Graves’ and Plummer’s disease?
- Examine patient carefully for lump
- Measure antibodies
- Radio-labelled Iodine scan will show hot nodule instead of Graves’ disease
What are the effects of thyroxine on the sympathetic nervous system?
- Sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline
- Thus apparent sympathetic activation
- Causes tachycardia, palpitations, tremor in hands, lid lag
What is lid lag and what is behind it?
Usually when an eye is following a finger the eyelid follows it very accurately
- if you have too much thyroxine on board, the eyelid is held open by adrenaline and this is lid-lag
Why is it potentially important if the patient mentions they have a family history of hyperthyroidism?
Certainly strengthens the possibility that they have Graves’ disease since autoimmune disease is heritable where tumours are not.
That said, doesn’t guarantee this, could be an extremely unlikely case where both people had independent tumours but it’s something worth remembering
What are the features of hyperthyroidism?
- Weight loss despite increased appetite
- Breathlessness
- Palpitations, tachycardia
- Sweating
- Heat intolerance (feeling hot)
- Diarrhoea
- Lid lag and other sympathetic features
What is a thyroid storm and what are some of its features?
An extreme version of hyperthyroidism
- 50% mortality
- hyperpyrexia >41oC temperature
- accelerated tachycardia/arrhythmia
- cardiac failure
- delirium/frank psychosis
- hepatocellular dysfunction, jaundice
Must be treated AGGRESSIVELY otherwise they’ll die
What are the treatment options for hyperthyroidism?
- Surgery (thyroidectomy)
- Radioiodine
- Drugs
What are the 4 classes of drugs used in the treatment of hyperthyroidism?
Thionamides (anti-thyroid drugs) - e.g. proprylthiouracil and carbimazole Potassium Iodide Radioiodine Beta-blockers
- The first 3 classes reduce thyroid hormone synthesis
- Beta blockers help with symptoms
What are the clinical uses of thionamides (e.g. propylthiouracil and carbimazole)?
- (mainly) daily treatment of both major hyperthyroid conditions
- treatment prior to surgery
- reduction of symptoms while waiting for radioactive iodine to act
What are the 4 target phases of thyroid hormone synthesis?
1) uptake of iodide, active transport
2) iodination
3) coupling reaction, storage in colloid
4) endocytosis and secretion
How do thionamides inhibit thyroid hormone synthesis and how long does it take to act both biochemically and clinically?
Block thyroid peroxidase and hence T3/4 synthesis and secretion
Biochemical effect - hours
Clinical effect - weeks (because yes there’s no synthesis but there’s both the large storage of T3/4 in the colloid and T4’s long half-life)
What may also be administered with thionamides to reduce symptoms while waiting for clinical effect of thionamides to take place?
Treatment regimen may include propranolol (non-selective beta blockers)
- rapidly reduces tremor and tachycardia
What additional effects, besides inhibition of thyroid hormone synthesis, do thionamides have?
- May suppress atibody production in Graves’ disease
- Reduces conversion of T4 to T3 in peripheral tissues
What are the unwanted actions of drug treatment of hyperthyroidism?
- Agranulocytosis (usually reduction in neutrophils), reduction in white blood cells - very rare (<1%) and reversible on withdrawal of the drug
- Rashes (relatively common)
What are the pharmacokinetics of anti-hyperthyroid drugs?
- Orally active
- Carbimazole is a pro-drug which first has to be converted to methimazole
- Cross placenta, secretted in breastmilk (PTU over carbimazole in pregnant patient)
What is the course of follow-up actions on a course of drugs?
- Usually aim to stop anti-thyroid drug treatment after 18 months
- Review patient periodically including thyroid function tests for remission/relapse (50/50 chance)
What is the role of beta blockers in treating thyrotoxicosis?
- It takes several weeks for anti-thyroid drugs (ATDs) to have clinical effects
- Reduces tremor, slows heart rate, reduces anxiety
- Non-selective beta blocker e.g. propranolol achieves these effects while ATDs are waiting to take effect
