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
What are the management options for Thyrotoxicosis in primary care?
Non-selective B-blocker (propranolol)- -20-40mg t.d.s. Refer to endocrinologist
26
What are the management options for Thyrotoxicosis in secondary care?
Antithyroid drugs Radioacive Iodine Surgical management
27
What antithyroid drugs are available?
Carbimazole (1st line) | Propylthiouracil (2nd line)
28
What is the main complication of Propylthiouracil?
Risk of severe liver injury (1/10000)
29
How do antithyroid drugs work?
Act as substrates for TPO | Prevent thyroid hormone synthesis
30
What are the main s/e of antithyroid drugs?
``` Skin rashes Severe agranulocytosis (mouth ulceration, sore throat, fever) ```
31
What is the main complication of Carbimazole?
Can cause cholestatic jaundice
32
How are antithyroid drugs introduced?
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
What is the success rate of anithyroid medications?
50%
34
When are antithyroid drugs most commonly used?
Grave's disease mainly
35
When is Radio-active Iodine (RAI) therapy used?
1st line in non-Grave's pathology | Grave's where drug therapy failed
36
How does RAI therapy work?
Taken up by thyroid cells | Induces DNA damage & cell death
37
When is RAI contraindicated?
Pregnancy Active Grave's ophthalmopathy If anti-thyroid drugs not discontinued/discontinued <1wk
38
What are the complications of RAI treatment?
Initial worsening of sx/thyroid storm (rare) | Small increased risk of thyroid cancer
39
What advice should pts receiving RAI be given re. children?
Avoid prolonged contact w/ children for 3/52 after treatment Avoid conceiving for 6mo No effect on fertility/congenital malformations
40
What are the surgical options for Thyrotoxicosis?
Total/sub-total thyroidectomy
41
When is surgical management indicated?
When drug therapy/RAI have failed or are contraindicated If there is a suspicion of malignancy If there is a large, toxic goitre
42
What are the potential post-op complications of surgical management for Thyrotoxicosis?
Haematoma causing asphyxia (emergency removal of sutures required) Hypothyroidism (10%) Hypocalcaemia (transient, due to hypoparathyroidism) Vocal cord paresis (damage to recu larnygeal)