hyperthyroidism Flashcards

1
Q

What is grave’s disease?

A

autoimmune disease which causes hyperthyroidism

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2
Q

What are the actions of the antibodies which are produced in Grave’s disease?

A
  1. Antibodies bind to and stimulate the TSH receptor in the thyroid.

The thyroid gland will grow- will form a smooth goiter

  1. They bind to muscles behind the eyes, making them bulge and swollen. This puts pressure on the optic nerve, causing blurred vision or blindness. This is called exopthalmos.
  2. Antibodies cause localised pretibial sweeling/ hypertrophy of the shins (non-pitting oedema)
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3
Q

Grave’s disease and adrenaline

A

People with Grave’s disease have increased sensitivity to adrenaline (increased beta adrenoreceptor sensitivity). This is responsible for lid lag.

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4
Q

What is Plummer’s disease?

A

Not an autoimmune cause of hyperthyroidism but results due to a benign adenoma.

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5
Q

Characteristics of someone with Plummer’s disease

A
  • Toxic nodular goitre (lump in the throat)
  • The adenoma is overactive and is making thyroxine
  • There is no pretibial myxoedema
  • No exophthalmos
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6
Q

What are some of the general symptoms of someone with hyperthyroidism?

A
  • Weight loss despite increased appetite
  • Breathlessness,
  • palpitations, tachycardia
  • Sweating
  • Heat intolerance
  • Diarrhea
  • Lid lag and other sympathetic features- thyroxine sensitizes beta-adrenoreceptors to ambient levels of adrenaline and noradrenaline. This leads to SNS activation when there doesn’t need to be. Responsible for the palpitations and tachycardia.
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7
Q

What is viral thyroiditis?

A

Virus (infectious) attacks the thyroid gland. The virus then lyses the cell, releasing a lot of thyroxine in the bloodstream.

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8
Q

What are the cycles of hyperthyroidism/ hypothyroidism in viral thyroiditis?

A

At first, patients will appear to have hyperthyroidism.

Painful/ tender dysphagia, pyrexia (fever).

There will be high levels of WBC present in a blood sample from these patients.

After around a month, the patients will develop hypothyroidism. This is because the virus has been dealt with, but the thyroid gland can’t release thyroxine (because all of the stores have been used up). There will zero iodine uptake on scans.

After the bout of hypothyroidism, the patient will return back to normal.

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9
Q

what is a thyroid storm?

A

When patients have a really high level of thyroxine- people can die if untreated

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10
Q

What are the features of someone in an episode of thyroid storm?

A

Hyperpyrexia- increase in BMR- arrythmia, tachycardia, temperature above 41 degrees

Cardiac failure

Psychosis

Hepatic failure and jaundice

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11
Q

what are the treatment options of hyperthyroidism?

A
  1. The thionamides (anti-thyroid drugs)- PTU (propylthiouracil) and carbimazole (CBZ)
  2. Potassium iodide
  3. Radioiodine
  4. Beta blockers

Surgery can also be done to remove the thyroid gland (thyroidectomy)

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12
Q

Thionamides- why would they be given?

A

Daily treatment of hyperthyroid conditions- Grave’s or targeting thyroid nodule.

Can also be used as treatment prior to surgery- prepare them before the surgery so they are stable.

Drugs can be used to manage symptoms before radioiodine takes place.

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13
Q

Mechanism behind Thionamides

A

Mechanisms of action:

  • Inhibits TPO and peroxidase transaminase
  • Supresses antibody production in Grave’s
  • Reduces T4 to T3 conversion in peripheral tissue (PTU)
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14
Q

Why does the clinical effects of thionamides take long?

A

The clinical effect takes weeks.

You cannot do anything about the hormones that have already been made by the colloid cells- there is a large store of normal thyroxine in the thyroid gland.

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15
Q

Unwanted side effects of thionamides

A

Agranulocytosis- loss of white cells (specifically neutrophils) rare and reversible on withdrawal of the drug.

Rashes too can occur. Patients can tolerate one drug better than the other.

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16
Q

Pharmacokinetics behind CBZ and PTU

A

CBZ and PTU are orally active.

Carbimazole is a pro-drug which has to be converted to methimazole. If patient with hyperthyroidism is pregnant there can be placenta cross over (and secreted in breast milk)- CBZ more than PTU.

Plasma half-life is around 6-15 hours.

Metabolised in the liver and excreted in the urine.

17
Q

Why would you use beta blockers like propanolol?

A

Overall treatment of symptoms (palpitations, arrythmias and tremors)

18
Q

How can potassium iodide be used to treat hyperthyroidism?

A

Instead of the gland using the iodide to make T3 and T4, the high dose of iodide give will shut down the thyroid gland. The hydrogen peroxide generation will be inhibited. This is called the WOLFF-CHAIKOFFeffect. Potassium iodide also reduces the vascularity of the thyroid gland and the size of the gland which is important for surgery.

19
Q

How is potassium iodide administered?

A

Potassium iodide is given as a tablet.

Symptoms reduce in 1-2 days and the size of the gland reduces in 10-14 days.

You can have allergic reactions to KI however.

20
Q

How can radioiodine be used to treat hyperthyroidism?

A

The radioiodine (I 131) accumulates in the colloid cells- emits beta particles and destroys follicular cells.

After this give them a daily dose of thyroxine to replace what they can’t make anymore.

21
Q

When would you the radioiodine?

A

For patients with hyperthyroidism that cannot really be controlled with drugs. Also used to treat thyroid cancers.

You use this also for patients that want to get pregnant- treat it once and for all.

Safety- stay away from children/ partners for around a week

22
Q

Pharmacokinetics of radioiodine

A

Administered as a single dose orally.

Graves- 500MBq

Thyroid cancer-3000Mbq

The radioiodine has a radioactive half-life of 8 days and is negligible after 2 months.

23
Q
A