Hyperthyroidism Flashcards
How does TSH interact with the thyroid follicular cell?
What is the thyroid follicular cell (TFC) and how much thyroxine does it store?
What are the functions of TSH on the TFCs?
Pituitary gland releases TSH, which travels in the blood stream to the thyroid follicular cell - this activates the uptake of iodine into the thyroid gland
The iodine is added onto tyrosine to make thyroxine
Thyroxine is stored within the (TFCs)
Stored enough thyroxine for a month
TSH stimulates the uptake and formation of thyroxine, but also activates proteolytic enzymes that make holes into the TFCs that then release the Thyroxine into the blood circulation
How does thyroxine affect metabolic activity?
High thyroxine levels = increased metabolic activity
Low thyroxine levels = decreased metabolic activity
How is thyroid acitivity controlled?
Hypothalamic-pituitary-thyroid axis
Thyroxine inhibits TRH and TSH
TRH stimulates TSH, which then stimulates thyroxine production and release from the thyroid gland
In primary hypothyroidism, due to autoimmune reasons, what occurs to the TSH levels?
High TSH to try stimulate thyroxine
What is the treatment for primary thyroidism?
Tablet with thyroxine - adjust dosage according to TSH levels until they return to reference range
What is Graves’ Disease? What is it caused by?
Autoimmune condition
Antibodies bind to and stimulate the TSH receptor in the thyroid
Causes smooth goitre and hyperthyroidism
How does Graves’ Disease present clinically?
Sweaty Young Often female Menstrual disturbance Bulgy eyes (exophthamos) Goitre Blood circulates through the thyroid gland - overactive Swollen shins and ankles Tremor Diarrhoea (everything speeds up due to too much thyroxine production)
Exophthalmos is found in some Graves’ disease patients?
What causes exophthamos?
Growth factor antibody binds to muscles behind the eyes and causes them to grow - causes difficult eye issues
Pretibial myxoedema is also found in some Graves’ disease patients.
What is pretibial myxoedema?
Swelling that occurs on the shins of patients - growth of soft tissue
What is pretibial myxodema VS myxoedema?
Pretibial myxoedema = swollen shins from growth of soft tissue
Myxoedema = hypothyroidism
How can Graves’ disease be investigated and diagnosed?
Patient is given radio-iodine - thyroid gland takes up all the iodine and shows up black on the scan = Graves’ disease
Abs continuously activating and binding to thyroid gland causes growth of the thyroid gland = smooth goitre (swollen and symmetrical)
What is Plummer’s disease? What is it caused by?
How is Plummer;s disease different in clinical presentation?
Benign adenoma that is overactive in making thyroxine
Toxic nodular goitre (usually not symmetrical, growth only on the adenoma)
Not autoimmune
They DO NOT have pretibial myxoedema or exophthalmos
Why does it matter to distinguish between Plummer’s and Graves’?
Different treatment plans given
How can Plummer’s disease be investigated and diagnosed clinically?
How is it different from diagnosing Graves’ disease?
Patient is given radioactive iodine - tumour takes up most of the iodine for thyroxine production
Due to excess thyroxine production by the tumour, TSH is suppressed so the actual thyroid gland that isn’t part of the tumour is suppressed from release thyroxine so some iodine still goes to the rest of the body
Does look like a bit like Graves’ on scan but less black and only on adenoma, not whole PTG
How does thyroxine affect the sympathetic nervous system?
Sensitises B-adrenoreceptors (more sensitive)
Therefore, ambient levels of adrenaline and noradrenaline cause quick and excessive sympathetic activation e.g. tachycardia, palpitations, tremors, lid lags etc.
How does hyperthyroidism present clinically?
Increased adrenaline sensitivity causes many of the symptoms Weightloss despite increased appetite Breathlessness Palpitations, tachycardia Sweating Heat intolerance Diarrhoea Examine their thyroid gland Check their eyes - current overactive thyroidism shows lid lag, eyes held open by sympathetic innervation
What is a thyroid storm?
Sudden hyperthyroidism - happens in patients with undiagnosed Graves' Hyperpyrexia (high fever) >41 degrees C Accelerated tachycardia / arrhthymia Cardiac failure Delirium Jaundice
2 or more symptoms = thyroid storm = medical emergency or death
What are the 3 treatment options of thyroid storm?
- Drug treatments
- Radio-iodine
- Surgery - thyroidectomy
What are the 4 drug options? How do they work?
- Thionamides: PTU or CBZ (anti-thyroid drugs) slow the uptake / activation of iodine by blocking the enzyme thyroid peroxidase
- Potassium iodide - a stable form of iodine that blocks uptake of iodine into the thyroid
- Radio-iodine
- Beta blockers - blocks beta receptors make you feel better (from the adrenaline sensitivity)
What are thionamides given with?
What are the side effects of thianamides?
Beta blockers to make them feel better
Suppresses immune system too much - agranulocytosis = reduction in neutrophils
Rashes = common, creams settle it down
What is the follow-up from drug treatment for thyroid storms / hyperthyroidism?
An anti-thyroid drug for 18 months
Afterwards: 50% chance it resolves itself or thyroid surgery (thyroidectomy)
Why is potassium iodide useful? Why is it used before a thyroidectomy?
Inhibits thyroid hormone synthesis
Given to hyperthyroid patients before surgery to make sure there is zero thyroxine production - so there is no increased adrenaline sensitivity or during a thyroid storm
How did thyroid surgery used to be done before? How is it different to now?
Used to partially take out thyroid
Now fully take out thyroid and give thyroxine tablets
What are the issues with thyroid surgery?
Recurrent laryngeal surgery may be hurt - risk of voice change / losing voice
Risk of losing PTG
Scars
