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CP3 @ UoN - Medicine & Surgery > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

What is a Goitre?

A

Painless enlargement of the thyroid gland

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2
Q

What are the key characteristics of a goitre to comment on?

A

Diffuse vs nodular
Simple vs toxic (secreting)
Benign vs malignant

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3
Q

What is the ddx for a diffuse goitre?

A 
Physiological - Puberty, pregnancy
Autoimmune - Grave's, Hashimoto's
Thyroiditis - De Quervain's , Riedel's
Endemic - Iodine deficiency
Drugs - Anti-thyroid drugs, lithium, amiodarone, iodine excess
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4
Q

What is the ddx for a nodular goitre?

A

Multinodular - Toxic multinodular, subacute thyroiditis
Solitary - Follicular adenoma, benign nodule, malignancy, lymphoma met
Infiltration - TB, sarcoid

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5
Q

What is the main local complication of a goitre?

A

Retrosternal extension

Pressure sx on trachea, oesophagus or vv

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6
Q

What investigations are appropriate when a pt presents with a goitre?

A 
FBC (anaemia)
ESR
TFTs
Thyroid autoantibodies
CT
USS
FNAC
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7
Q

What determines the management of a goitre?

A

Whether the pt is hyper/hypothyroid

If eu-thyroid do not need to treat

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8
Q

What is Thyrotoxicosis?

A

Clinical disorder resulting from raised circulating levels of thyroid hormone

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9
Q

How common is Thyrotoxicosis?

A

1% of population

5:1 female preponderance

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10
Q

What are the common causes of Thyrotoxicosis?

A

Grave’s disease

Toxic multinodular goitre

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11
Q

What are the less common causes of Thyrotoxicosis?

A 
Solitary toxic adenoma (Plummer's)
Thyroiditis
Drug induced (Amiodarone, levothyroxine)
Excess iodine
Hashitoxicosis
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12
Q

What are the rare causes of Thyrotoxicosis?

A

2o causes

  • TSH secreting pituitary adenoma
  • Resistance to thyroid hormone
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13
Q

What is Grave’s disease?

A

Autoimmune condition where IgG autoantibodies stimulate thyroid follicular cells
Out of control of normal feedback mechanism

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14
Q

What is Toxic Multinodular Goitre?

A

Several hyperactive nodules develop
Outside of TSH control
Common in older women

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15
Q

What are the sx of Thyrotoxicosis?

A 
Anxiety/irritability
Heat intolerance/sweating
Increased appetite
Palpitations
Wt loss
Tremor
Loose motions
Fatigue/weakness
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16
Q

What are the signs of Thyrotoxicosis?

A 
Lid retraction/lag
Systolic HTN
Tachycardia/AF
Tremor
Hyper-reflexia
Warm peripheries
Proximal weakness
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17
Q

What signs of Thyrotoxicosis are unique to Grave’s disease?

A

Grave’s ophthalmopathy
Goitre/bruit
Acropachy
Pre-tibial myxoedema

18
Q

What is Grave’s ophthalmopathy?

A

Lagopthalmos (unable to close eyes completely)
Exopthalmos/proptosis (bulging eyes)
Ophthalmoplegia (up & lat)
Periorbital oedema

19
Q

What is acropachy?

A

Dermopathy associated w/ Graves
Soft tissue swelling of hands
Clubbing of fingers

20
Q

What is pre-tibial myxoedema?

A

Dermopathy associated w/ Graves

Swelling of lower legs

21
Q

What is Thyroid crisis/storm?

A

Rare presentation occurring in periods of stress in people w/ untreated hyperthyroidism

22
Q

How does Thyroid crisis/storm present?

A 
Hyperpyrexia
Severe tachycardia
Profuse sweating
Confusion/psychosis
Coma/death
23
Q

How should Thyroid crisis/storm be managed?

A

Propylthiouracil
Propranolol
Sodium Iodide
High dose steroids

24
Q

What investigations are appropriate in suspected Thyrotoxicosis?

A 
TSH (suppressed)
T3/T4 (elevated)
TRAb (elevated in Grave's)
Technetium uptake scan
CT/MRI of orbit
25
Q

What are the management options for Thyrotoxicosis in primary care?

A

Non-selective B-blocker (propranolol)-
-20-40mg t.d.s.
Refer to endocrinologist

26
Q

What are the management options for Thyrotoxicosis in secondary care?

A

Antithyroid drugs
Radioacive Iodine
Surgical management

27
Q

What antithyroid drugs are available?

A

Carbimazole (1st line)

Propylthiouracil (2nd line)

28
Q

What is the main complication of Propylthiouracil?

A

Risk of severe liver injury (1/10000)

29
Q

How do antithyroid drugs work?

A

Act as substrates for TPO

Prevent thyroid hormone synthesis

30
Q

What are the main s/e of antithyroid drugs?

A 
Skin rashes
Severe agranulocytosis (mouth ulceration, sore throat, fever)
31
Q

What is the main complication of Carbimazole?

A

Can cause cholestatic jaundice

32
Q

How are antithyroid drugs introduced?

A

Intermediate course to induce remission (6-18mo)
Titration (starting high, titrating down to euthyroid)
Block & replace (maintain high, add thyroxine once T3/T4 controlled)

33
Q

What is the success rate of anithyroid medications?

A

50%

34
Q

When are antithyroid drugs most commonly used?

A

Grave’s disease mainly

35
Q

When is Radio-active Iodine (RAI) therapy used?

A

1st line in non-Grave’s pathology

Grave’s where drug therapy failed

36
Q

How does RAI therapy work?

A

Taken up by thyroid cells

Induces DNA damage & cell death

37
Q

When is RAI contraindicated?

A

Pregnancy
Active Grave’s ophthalmopathy
If anti-thyroid drugs not discontinued/discontinued <1wk

38
Q

What are the complications of RAI treatment?

A

Initial worsening of sx/thyroid storm (rare)

Small increased risk of thyroid cancer

39
Q

What advice should pts receiving RAI be given re. children?

A

Avoid prolonged contact w/ children for 3/52 after treatment
Avoid conceiving for 6mo
No effect on fertility/congenital malformations

40
Q

What are the surgical options for Thyrotoxicosis?

A

Total/sub-total thyroidectomy

41
Q

When is surgical management indicated?

A

When drug therapy/RAI have failed or are contraindicated
If there is a suspicion of malignancy
If there is a large, toxic goitre

42
Q

What are the potential post-op complications of surgical management for Thyrotoxicosis?

A

Haematoma causing asphyxia (emergency removal of sutures required)
Hypothyroidism (10%)
Hypocalcaemia (transient, due to hypoparathyroidism)
Vocal cord paresis (damage to recu larnygeal)

CP3 @ UoN - Medicine & Surgery (135 decks)

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