Hyperthyroidism Flashcards

1
Q

Hyperthyroidism has more than one cause. What are these two diseases?

A
  • Graves’ disease

- Nodular Goitre (benign tumour making a bit too much thyroxine), aka Plummer’s disease

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2
Q

What kind of disease is Graves’ disease, what happens to cause the problems and what does it cause?

A
  • Autoimmune
  • Antibodies bind to and stimulate the TSH receptor in the thyroid
  • Causes goitre and hyperthyroidism (causes lid lag)
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3
Q

What effect does thyroxine have on beta receptors in the heart?

A

Increase the sensitivity - method of increasing heart rate

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4
Q

What do other antibodies bind to and cause in Graves’ disease?

A
  • 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)
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5
Q

What is pretibial myxoedema?

A

Swelling that occurs on the shins of patients with Graves’ disease, growth of soft tissue

NOT to be confused with myxoedema = hyPOthyroidism

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6
Q

What is a goitre?

A

Smooth, enlarged thyroid gland

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7
Q

What is Plummer’s disease?

A

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
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8
Q

What 3 methods can you use to distinguish between Graves’ and Plummer’s disease?

A
  • Examine patient carefully for lump
  • Measure antibodies
  • Radio-labelled Iodine scan will show hot nodule instead of Graves’ disease
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9
Q

What are the effects of thyroxine on the sympathetic nervous system?

A
  • Sensitises beta adrenoceptors to ambient levels of adrenaline and noradrenaline
  • Thus apparent sympathetic activation
  • Causes tachycardia, palpitations, tremor in hands, lid lag
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10
Q

What is lid lag and what is behind it?

A

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

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11
Q

Why is it potentially important if the patient mentions they have a family history of hyperthyroidism?

A

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

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12
Q

What are the features of hyperthyroidism?

A
  • Weight loss despite increased appetite
  • Breathlessness
  • Palpitations, tachycardia
  • Sweating
  • Heat intolerance (feeling hot)
  • Diarrhoea
  • Lid lag and other sympathetic features
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13
Q

What is a thyroid storm and what are some of its features?

A

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

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14
Q

What are the treatment options for hyperthyroidism?

A
  • Surgery (thyroidectomy)
  • Radioiodine
  • Drugs
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15
Q

What are the 4 classes of drugs used in the treatment of hyperthyroidism?

A
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
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16
Q

What are the clinical uses of thionamides (e.g. propylthiouracil and carbimazole)?

A
  • (mainly) daily treatment of both major hyperthyroid conditions
  • treatment prior to surgery
  • reduction of symptoms while waiting for radioactive iodine to act
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17
Q

What are the 4 target phases of thyroid hormone synthesis?

A

1) uptake of iodide, active transport
2) iodination
3) coupling reaction, storage in colloid
4) endocytosis and secretion

18
Q

How do thionamides inhibit thyroid hormone synthesis and how long does it take to act both biochemically and clinically?

A

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)

19
Q

What may also be administered with thionamides to reduce symptoms while waiting for clinical effect of thionamides to take place?

A

Treatment regimen may include propranolol (non-selective beta blockers)
- rapidly reduces tremor and tachycardia

20
Q

What additional effects, besides inhibition of thyroid hormone synthesis, do thionamides have?

A
  • May suppress atibody production in Graves’ disease

- Reduces conversion of T4 to T3 in peripheral tissues

21
Q

What are the unwanted actions of drug treatment of hyperthyroidism?

A
  • Agranulocytosis (usually reduction in neutrophils), reduction in white blood cells - very rare (<1%) and reversible on withdrawal of the drug
  • Rashes (relatively common)
22
Q

What are the pharmacokinetics of anti-hyperthyroid drugs?

A
  • 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)
23
Q

What is the course of follow-up actions on a course of drugs?

A
  • Usually aim to stop anti-thyroid drug treatment after 18 months
  • Review patient periodically including thyroid function tests for remission/relapse (50/50 chance)
24
Q

What is the role of beta blockers in treating thyrotoxicosis?

A
  • 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
25
Q

What are the uses of potassium iodide in treatment of hyperthyroidism?

A
  • Preparation of hyperthyroid patients for surgery, without it they can be very unstable under anaesthetic
  • Severe thyrotoxic crisis (thyroid storm)
26
Q

What is the mechanism of action of potassium iodide?

A

Inhibits iodination of thyroglobulin (not what we’d expect)

  • The large dose of iodine actually switches off the iodination
  • Inhibits thyroperoxidase and H2O2 generation
  • Wolff-Chaikov effect, presumed autoregulatory effect, body’s protection of itself instead of just blindly making tons of thyroid hormone
27
Q

How quickly do different types of symptoms, vascularity and size of gland become reduced?

A
  • Hyperthyroid symptoms reduced within 1-2 days
  • Vascularity and size of gland reduced within 10-14 days

POINT IS that it’s fast-acting which makes it useful with ATDs taking so long to have their clinical effect

28
Q

What are the unwanted effects of potassium iodide?

A

Allergic reaction

- e.g. rashes, fever, angio-oedema

29
Q

What is the administration route and after how long are the maximum effects seen?

A
  • Given orally (Lugol’s solution, aqueous iodine)

- Maximum effects after 10 days continuous administration

30
Q

What is the clinical use of radioiodine (131i)?

A

Used if patient has tried other options like 18 months of ATDs and it hasn’t helped
- Treats both types of hyperthyroidism and thyroid cancers

31
Q

What is the mechanism of action of radioiodine?

A

Taken up into thyroid follicular cell, accumulates in the colloid, emits beta particles which destroys follicular cells

32
Q

What is the administration method of radioiodine, when is anti-thyroid drug treatment discontinued, what is the radioactive half life and when does the radioactivity become negligible?

A
  • Single oral dose
  • Discontinue ATDs 7-10 days prior to radioiodine treatment
  • Radioactive half-life 8days
  • Radioactivity negligible after 2 months
33
Q

What are the cautions of and reasons why radioiodine cannot be used in some patients?

A
  • Avoid close contact with small children for several weeks after receiving radioiodine (not suitable for those with small children)
  • Contra-indicated in pregnancy and breast-feeding (so if planning for pregnancy, don’t have radioiodine)
34
Q

What interesting interaction at airports does radioiodine cause?

A

Sets off alarms since patient is effectively radioactive
- Patients still under the effects of radioiodine carry a small card that goes in the wallet so they can show it to security/airline

35
Q

What is radioiodine used for in very low, tracer doses and how is it administered?

A

Tests of thyroid gland pathology e.g. differentiating between toxic nodule, thyroiditis, and Graves

  • Administered intravenously
  • Negligible cytotoxicity
36
Q

What is viral thyroiditis?

A

Viral attack on the thyroid gland

- results in hyperthyroidism

37
Q

What are signs and symptoms of viral thyroiditis?

A
  • Painful dysphagia
  • Hyperthyroidisim
  • Pyrexia (fever)
  • Raised ESR
38
Q

What happens in viral thyroiditis?

A
  • Virus attacks thyroid gland causing pain and tenderness
  • Thyroid stops making thyroxine and makes viruses instead
  • Thus there is no iodine uptake (zero)
39
Q

What would you see in a thyroid scan of someone with viral thyroiditis?

A

Blank, no uptake going on so no shape on scan

40
Q

What is the timeline of viral thyroiditis symptoms?

A

One month of hyperthyroidism

After which, stored thyroxine has been exhausted so they experience one month of hypothyroidism

41
Q

What is the course of treatment in cases of viral thyroiditis?

A

Do the scan to assess what type of hyperthyroidism it is

  • If blank then viral thyroiditis can be suspected
  • In which case, you don’t do anything, let the virus take its course, let the patient go from hyper to hypo, then the virus will be cleared naturally and the patient will become euthyroid again (normal thyroid function restored)