Endocrine: Hyperthyroidism Flashcards

1
Q

what is hyperthyroidism?

A

Hyperthyroidism is where there is over-production of thyroid hormones

  • LOW TSH
  • HIGH FREE T4 / T3
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2
Q

what is primary hyperthyroidism?

A

Primary Hyperthyroidism is due to thyroid pathology.

It is the thyroid itself that is behaving abnormally and producing excessive thyroid hormone.

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3
Q

what is secondary hyperthyroidism?

A

Secondary hyperthyroidism is the condition where the thyroid is producing excessive thyroid hormone as a result of overstimulation by thyroid stimulating hormone.

The pathology is in the hypothalamus or pituitary, e.g TSH secreting tumour

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4
Q

what TFTs would you expect with sub-clinical hyperthyroidism?

A

TSH is suppressed but FT4 and FT3 concentrations are within the normal reference range.

  • low or undetectable TSH
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5
Q

what signs might you find on examination for a patient with hyperthyroidism?

A

Agitation / fine tremor / warm moist skin / palmar erythema / tachycardia / AF / hair thinning / brisk reflexes / goitre

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6
Q

what are the causes of primary hyperthyroidism?

A
  • Graves disease
  • toxic multi nodular goitre
  • toxic thyroid nodule (adenoma)
  • certain drugs e.g. amiodarone
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7
Q

what are the causes of secondary hyperthyroidism?

A

High levels of human chorionic gonadotrophin

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8
Q

what are some risk factors of primary hyperthyroidism?

A
  • female
  • family history of thyroid disease
  • smoking
  • low iodine intake
  • autoimmune disease
  • radiation exposure
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9
Q

what are some clinical features of hyperthyroidism?

A
polyuria 
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
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10
Q

which conditions present in a similar way to hyperthyroidism?

A
Toxic nodular goitre.
Painless postnatal thyroiditis.
Gestational hyperthyroidism. 
Subacute thyroiditis.
Iodine-induced hyperthyroidism.
TSH-producing pituitary adenoma.
Thyroid hormone resistance.
Inflammatory eye conditions, myasthenia gravis. 
Factitious ingestion of thyroid hormones (thyrotoxicosis factitia).
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11
Q

what investigations would you do to confirm a diagnosis of hyperthyroidism?

A

TSH level

expected result: - LOW TSH
- HIGH FREE T4 / T3

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12
Q

what diagnosis would you give for TFTs that show:

  • low TSH
  • Raised FT4/FT3
A

primary hyperthyroidism

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13
Q

what diagnosis would you give for TFTs that show:

  • low TSH
  • low FT3
A

A low TSH and low FT3 may be caused by non-thyroid illness,although usually the FT3 alone is low.

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14
Q

what diagnosis would you give for TFTs that show:

  • low TSH
  • thyroid pain
A

thyroiditis.

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15
Q

what diagnosis would you give for TFTs that show:

  • low TSH
  • PMH of levothyroxine
  • normal FT3/FT4
A

usually indicates over-treatment of hypothyroidism

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16
Q

what diagnosis would you give for TFTs that show:

  • high TSH
  • high FT3/FT4
A

TSH-secreting pituitary adenoma(very rare)

17
Q

what diagnosis would you give for TFTs that show:

  • persistently low TSH on repeat testing
A

subclinical hyperthyroidism

18
Q

what is the treatment for Graves’ disease?

A

ABC-I

(ABC-I: Antithyroid, beta-blocker, corticosteroid and iodine solution).

19
Q

what is the treatment for Toxic multi nodular goitre?

A

First line: Radioactive iodine therapy WITH High-dose antithyroid drugs: thiamazole.

Second line: Thyroid surgery (NB: subsequent hypothyroidism likely).

20
Q

what is the treatment for Toxic adenoma?

A

First line: Radioactive iodine therapy WITH High-dose antithyroid drugs: thiamazole.

Second line: Subtotal thyroidectomy (complications incl recurrent laryngeal nerve damage).

21
Q

what is the treatment for a subacute granulomatous thyroiditis?

A

NB: Many patients have only mild symptoms of hyperthyroidism that do not require treatment. However, if symptoms are troublesome, then beta-blockers or calcium-channel blockers can be beneficial.

Analgesic e.g. ibuprofen or naproxen.
AND
Beta-blocker e.g. propranolol.

22
Q

what are the complications of hyperthyroidism?

A
Graves' orbitopathy.
Thyroid storm (thyrotoxic crisis).
Atrial fibrillation.
Heart failure.
Reduced bone mineral density.
Increased mortality rate.
23
Q

What is graves disease?

A

Grave’s Disease is an autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism.

These TSH receptor antibodies are abnormal antibodies produced by the immune system that mimic TSH and stimulate the TSH receptors on the thyroid.

This is the most common cause of hyperthyroidism.

24
Q

what is a toxic multinodular goitre?

A

Toxic Multinodular Goitre (also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thyroid hormone.

25
Q

what are some clinical features of graves disease?

A

Bilateral Exopthalmos (eyes bulging)

Pretibial Myxoedema (muchin deposits on skin givesdiscoloured, waxy, oedematous appearance to the skin on the shins)

Diffuse Goitre (without nodules)

Graves Eye Disease

26
Q

what is De Quervain’s Thyroiditis?

A

the presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism.

There is a hyperthyroid phase followed by hypothyroid phase as the TSH level falls due to negative feedback.

It is a self-limiting condition and supportive treatment with NSAIDs for pain and inflammation and beta blockers for symptomatic relief of hyperthyroidism is usually all that is necessary.

27
Q

what is a thyroid storm?

A

Thyroid storm is a rare presentation of hyperthyroidism. It is also known as “thyrotoxic crisis”.

It is a more severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium.

It requires admission for monitoring and is treated the same way as any other presentation of thyrotoxicosis, although they may need supportive care with fluid resuscitation, anti-arrhythmic medication and beta blockers.

28
Q

name some anti-thyroid drugs?

A

first line: Carbimazole
- Complete remission and the ability to stop taking carbimazole is usually achieved within 18 months of treatment.

second line: Propylthiouracil
- There is a small risk of severe hepatic reactions, including death, which is why carbimazole is preferred.

29
Q

how does radioactive iodine treatment work for hyperthyroidism?

A

Treatment with radioactive iodine involves drinking a single dose of radioactive iodine. This is taken up by the thyroid gland and the emitted radiation destroys a proportion of the thyroid cells. This reduction in functioning cells results in a decrease of thyroid hormone production and thus remission from the hyperthyroidism. Remission can take 6 months and patients can be left hypothyroid afterwards and require levothyroxine replacement.

There are strict rules where the patient:
- Must not be pregnant and are not allowed to get pregnant within 6 months
- Must avoid close contact with children and pregnant women for 3 weeks (depending on the dose)
Limit contact with anyone for several days after receiving the dose.

30
Q

which is the best beta-blocker to use to block the adrenalin related symptoms of hyperthyroidism?

A

Propranolol
- it non-selectively blocks adrenergic activity as opposed to more “selective” beta blockers the work only on the heart.

NB: They do not actually treat the underlying problem but control the symptoms whilst the definitive treatment takes time to work. They are particularly useful in patients with thyroid storm.

31
Q

what are some implications of a total thyroidectomy?

A

the patient will be left hypothyroid post thyroidectomy and require levothyroxine replacement for life.