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Y4 - CCC & PC > Hyperthyroidism & Graves Disease > Flashcards

Hyperthyroidism & Graves Disease Flashcards

1
Q

What is the definition of hyperthyroidism?

A

an over-production of thyroid hormone by the thyroid gland

hyperthyroidism is also sometimes called thyrotoxicosis

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2
Q

What is the definition of thyrotoxicosis?

A

an abnormal and excessive quantity of thyroid hormone in the body

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3
Q

What is the difference between primary and secondary hyperthyroidism?

A

primary:
* this is due to thyroid pathology

  • the thyroid gland is producing excessive levels of thyroid hormone

secondary:
* the thyroid is producing excessive thyroid hormone as a result of overstimulation by TSH

  • the pathology is within the hypothalamus or pituitary gland
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4
Q

What is Grave’s disease and how does it produce symptoms?

A
  • an autoimmune condition in which TSH receptor antibodies cause a primary hyperthyroidism
  • TSH receptor antibodies are produced by the immune system
  • they mimic TSH and stimulate TSH receptors on the thyroid

this is the most common cause of hyperthyroidism

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5
Q

What is toxic multinodular goitre (Plummer’s disease) and how does it cause symptoms?

A
  • multiple nodules develop on the thyroid gland
  • the nodules all act independently of each other and the normal feedback system
  • they continuously produce excessive thyroid hormone
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6
Q

What is meant by exopthalmos?

Why does it occur?

A
  • the bulging of the eyeball out of the socket caused by Grave’s disease
  • due to inflammation, swelling and hypertrophy of the tissue behind the eyeball
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7
Q

What is meant by pretibial myxoedema and why does it occur?

A
  • there are deposits of mucin under the skin on the anterior aspect of the leg
  • this produces a discoloured, waxy, oedematous appearance
  • it is specific to Grave’s disease and is a reaction to TSH receptor antibodies
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8
Q

Who is typically affected by Grave’s disease?

A

women aged 30 - 50

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9
Q

What are the 4 main causes of hyperthyroidism?

A
  • Grave’s disease
  • toxic multinodular goitre
  • solitary toxic thyroid nodule
  • thyroiditis (e.g. Hashimoto’s / De Quervain’s)
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10
Q

What are the universal features of hyperthyroidism?

A
  • sweating / heat intolerance
  • tachycardia
  • frequent loose stools
  • sexual dysfunction
  • fatigue
  • weight loss
  • anxiety / irritability
  • oligomenorrhea
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11
Q

What features of hyperthyroidism are specific to Grave’s disease?

A
  • diffuse goitre (without nodules)
  • bilateral exophthalmos
  • pretibial myxoedema
  • thyroid acropachy
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12
Q

What is thyroid acropachy?

A

a triad of:

  • digital clubbing
  • soft tissue swelling of the hands and feet
  • periosteal new bone formation

this occurs in < 1% patients with Grave’s disease

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13
Q

What features are unique to toxic multinodular goitre?

Who tends to be affected?

A
  • most patients are aged > 50
  • goitre with many firm nodules

this is the second most common cause of hyperthyroidism

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14
Q

What is a solitary toxic thyroid nodule?

A
  • there is a single abnormal thyroid nodule that acts alone to release thyroid hormone
  • usually a benign adenoma
  • treated with surgical removal of the nodule
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15
Q

What are the features of De Quervain’s thyroiditis?

A

there is a presentation of a viral infection with:

  • fever
  • neck pain + tenderness
  • dysphagia
  • features of hyperthyroidism
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16
Q

What is the course of De Quervain’s thyroiditis typically like?

A
  • initially there is a hyperthyroid phase
  • TSH levels fall due to negative feedback
  • this results in a subsequent hypothyroid phase
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17
Q

What is the treatment for De Quervain’s thyroiditis?

A
  • the condition is self-limiting
  • supportive treatment with NSAIDs for pain / inflammation
  • beta-blockers may be given for symptomatic relief of hyperthyroidism
18
Q

What is meant by “thyroid storm”?

A
  • a rare and more severe presentation of hyperthyroidism
  • it presents with pyrexia, tachycardia and delirium

this is life-threatening if not treated

19
Q

How is thyroid storm managed?

A
  • patient needs admission for monitoring
  • it is treated in the same way as any other presentation of thyrotoxicosis
  • supportive care with IV fluids, beta-blockers and antiarrhythmic medications may be required
20
Q

Why does thyroid storm occur?

A

it occurs as a result of uncontrolled hyperthyroidism due to a major stress:

  • infection
  • trauma
  • untreated / undertreated hyperthyroidism
  • PE / CHF
  • severe emotional distress
  • DKA
  • stroke
21
Q

What is the first line treatment for hyperthryoidism (including Grave’s disease)?

A

carbimazole 40mg

  • euthyroidism is typically achieved after 4-8 weeks
  • the patient is then given a maintenance dose of carbimazole
22
Q

When giving the maintenance dose of carbimazole, what 2 methods can be used for titration?

A

“titration-block”:
* the dose of carbimazole is titrated down from 40mg gradually to maintain euthyroidism

block-and-replace:
* a dose is given that is sufficient to block all thyroid hormone production

  • the patient is given levothyroxine which is titrated to effect
23
Q

How long must a patient take carbimazole for?

A

complete remission and the ability to stop taking carbimazole is usually achieved within 18 months

block and replace treatments tend to last for 6-9 months

24
Q

What is the main side effect associated with carbimazole?

A

agranulocytosis

  • a deficiency of granulocytes (i.e. neutrophils) in the blood
  • this results in increased vulnerability to infection
25
Q

What is the second-line treatment for hyperthyroidism?

A

propylthiouracil

  • used in a similar way to carbimazole
  • small risk of severe hepatic reactions, including death

carbimazole is preffered due to risk of severe hepatic reactions

26
Q

How can radioactive iodine be used to treat hyperthyroidism?

A
  • a single dose of radioactive iodine is drunk
  • the radiation destroys a portion of cells within the thyroid
  • the reduction in functioning cells results in decreased thyroid hormone production

this is usually used when patients relapse after ATD treatment or are resistant to it

27
Q

What are the drawbacks of using radioactive iodine?

A
  • remission can take up to 6 months
  • patients can be left hypothyroid afterwards and require levothyroxine replacement
28
Q

What are the rules that are in place when radioactive iodine treatment is used?

A
  • must not be pregnant or get pregnant within 6 months
  • must be > 16 years
  • must avoid contact with children / pregnant women for 3 weeks after
  • must avoid contact with anyone for several days after
29
Q

When are beta-blockers used for the management of hyperthyroidism?

A
  • used for symptomatic relief of adrenaline-related symptoms
  • propanolol is preffered as it is non-selective
  • treat the symptoms whilst the underlying treatment takes time to work
  • particularly useful in thyroid storm
30
Q

What is the only definitive treatment option for hyperthyroidism?

A
  • surgery to remove the whole thyroid or any toxic nodules
  • the patient will be left hypothyroid as thyroid hormone production is stopped
  • they require life-long levothyroxine replacement
31
Q

What drugs can cause hyperthyroidism?

A

amiodarone

32
Q

What would you expect to see on TFTs in hyperthyroidism?

A
  • low TSH
  • high levels of T4 and T3

this is in primary hyperthyroidism

33
Q

What are the 4 phases of De Quervain’s thyroiditis?

A

phase 1:

  • hyperthyroidism, painful goitre, raised ESR
  • lasts 3-6 weeks

phase 2:
* euthyroid for 1-3 weekw

phase 3:
* hypothyroid for weeks - months

phase 4:
* thyroid structure / function returns to normal

34
Q

What investigation can be performed in De Quervain’s thyroiditis?

A

thyroid scintigraphy

  • shows globally reduced uptake of iodine-131
35
Q

What can rarely cause thyrotoxicosis in patients with pre-existing thyroid disease?

A

contrast

  • patients with pre-existing thyrotoxicosis should not receive iodinated contrast
  • this results in a large iodine load to the thyroid and hyperthyroidism developing over 2-12 weeks
36
Q

What is meant by thyroid eye disease and why does it occur?

A
  • there is an autoimmune response to an autoantigen (TSH receptor)
  • this results in retro-orbital inflammation
  • inflammation results in glycosaminoglycan and collagen deposition in the muscles

this affects 25-50% of patients with Grave’s disease

37
Q

What risk factors increase the likelihood of thyroid eye disease?

A
  • smoking is the most important modifiable RF
  • radioiodine treatment may increase inflammatory symptoms (prednisolone reduces risk)
38
Q

What are the features of thyroid eye disease?

A
  • exophthalmos
  • conjunctival oedema
  • optic disc swelling
  • ophthalmoplegia
  • inability to close the eyelids results in sore, dry eyes

if this is untreated, there is a risk of exposure keratopathy

patients may be hypo-, eu- or hyperthyroid at time of presentation

39
Q

What is exposure keratopathy?

A

damage to the cornea that occurs from prolonged exposure of the ocular surface to the outside environment

  • can lead to ulceration, keratitis and permanent vision loss from scarring
40
Q

What is involved in the management of thyroid eye disease?

A
  • topical lubricants prevent corneal inflammation caused by exposure
  • steroids (prednisolone)
  • radiotherapy
  • surgery
41
Q

For patients with established thyroid eye disease, what red flag symptoms prompt urgent review by an opthalmologist?

A
  • unexplained deterioration in vision
  • obvious corneal opacity
  • cornea still visible when eyes are closed
  • disc swelling
  • history of globe subluxation (eye suddenly popping out)
  • awareness of change in intensity or quality of colour vision

Y4 - CCC & PC (34 decks)

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