Graves' disease Flashcards

1
Q

How can thyrotoxic storm manifest?

A

Abdominal pain

Infective colitis, or possibly pseudomembranous colitis, following antibiotic treatment should be considered and diabetic ketoacidosis can present with sweating, pyrexia and abdominal pain. Must also rule out acute pancreatitis/perforated viscus.

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2
Q

Which types of hyperthyroidism usually present with painful midline neck lump?

A

Hashimotos thyroiditis and de Quervain’s subacute thyroiditis are usually painful

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3
Q

How do beta blockers help with hyperthyroidism?

A

Beta blockers will inhibit peripheral conversion of T4 to T3 (active form).

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4
Q

True or false: In thyroid crisis you should do a radioisotope investigation of the thyroid urgently.

A

Radioiodine can precipitate/worsen thyroid crisis but can be useful for later management (possible focal hot nodule or diffuse uptake).

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5
Q

Which of these are triggers for a thyroid crisis?

  • Thyroid surgery
  • Infection
  • Type 2 diabetes mellitus
  • Myocardial infarction
  • Diabetic ketoacidosis
  • Radioactive iodine administration
  • Hip replacement
A
  • Thyroid surgery
  • Infection
  • Myocardial infarction
  • Diabetic ketoacidosis
  • Radioactive iodine administration
  • Hip replacement

Type 2 diabetes has not been shown to be a precipitants of thyroid crisis but the type 1 diabetes complication DKA does.

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6
Q

Name some eye signs of thyroid disease.

A

proptosis and conjunctival oedema

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7
Q

Which of these are symptoms of thyrotoxicosis?

  • Anorexia (loss of appetite)
  • Heat intolerance
  • A distorted body image
  • Dysphagia (difficulty swallowing)
  • Oligo- or amenorrhoea (i.e. few / no periods)
  • Polyuria & polydipsia
A

Heat intolerance

Oligo or amenorrhoea

Other: thyrotoxicosis causes weight loss with hyperphagia (increased appetite). Goitres rarely cause dysphagias. Type 1 diabetes should be excluded in a young person with weight loss.

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8
Q

Define Graves’ disease.

A

Graves’ disease is an autoimmune thyroid condition associated with hyperthyroidism. TSH receptor antibodies cause the hyperthyroid syndrome.

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9
Q

How common is Graves’ disease?

A

In iodine sufficient parts of the world: 0.2-1.3%

Graves is the most common cause of hyperthyroidism

Usually seen in women aged 30-50yrs

In areas of iodine deficiency and endemic goitre: toxic multinodular goitre

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10
Q

What is the pathophysiology of Graves’ disease?

A

Autoimmunity - anti-TSH receptor antibodies stimulate the thyroid and cause hormone overproduction and hypertrophy of thyroid follicular cells

Other thyroid antibodies can also occur antithyroglobulin (Tg), antithyroid peroxidase (TPO) and antibodies to NaI transporter

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11
Q

What are the clinical features of Graves’?

A

Eye signs - exophthalmos, ophthalmoplegia

Pretibial myxoedema

Thyroid acropathy - triad of: digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation.

Signs and symptoms:

  • heat intolerance
  • sweating
  • weight loss
  • palpitations - AF/SVTs
  • irritability
  • scalp hair loss
  • generalised proximal muscle weakness
  • menstrual irregularities, gynaecomastia, ED
  • tremor
  • tachycardia, wide pulse pressure
  • diffuse goitre
  • orbitopathy - bilateral proptosis, lid retraction, inflammation, diplopia.
  • cardiac flow murmur - from increased flow of blood through heart valves
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12
Q

What are the risk factors for Graves’ disease?

A
  • FH of AI thryoid disease
  • female sex - x4-9 more common
  • tobacco use
  • high iodine intake
  • biological/cytokine therapies
  • radiation
  • radioiodine therapy for benign nodular goitre
  • stress
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13
Q

What investigations would you do for Graves’ disease?

A
  • TSH - suppressed <0.01 mIU/L
  • T4 - elevated (good for monitoring therapy)
  • Total T3/T4 or FT3/FT4 ratio - high compared to thyroiditis. May be helpful to distinguish Graves’ from toxic nodular goitre.
  • Radioactive iodine or technetium-99 uptake scan - diffuse uptake
  • Anti-TSHr, anti-TPO - positive
  • Thyroid US - large, highly vascular, diffuse
  • CT/MRI scan of orbit - shows muscle thickening
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14
Q

How do you manage Graves’?

A

Aim to normalise thyroid function by antithyroid meds, radioactive iodine ablation or surgery, depending on patient.

  • Symptomatic therapy - propranolol - normalises peripheral thyroid hormone levels [alternatively: CCB]
  • Antithyroid drugs (1st line) - PTU/carbimazole/ thiamazole - given for 12-18 months with aim of achieving remission. Start with higher doses then titrate to lower maintenance.
  • Radioactive iodine - reserved for patients who prefer these approaches. Although NICE recommends this first line, but this is CI in thyroid orbitopathy.
  • Surgery - for those planning pregnancy or with large goitres
  • Orbitopathy - stop smoking, lubricant eye drops, IV methylprednisolone, immune modulation (MMF) and immunosuppression
  • Dermopathy - topical corticosteroids
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15
Q

Which of these (1) is seen in all thyrotoxicosis cases, not just Graves?

  • Proptosis
  • Periorbital oedema
  • Lid retraction and lid lag
  • Diplopia due to extraocular muscle dysfunction
  • Grittiness with increased tear production
A

Lid retraction and lid lag

All others are seen in Graves’ only

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16
Q

Which lifestyle factor increases risk of ophthalmopathy in Graves?

A

Ophthalmopathy is more common in smokers

17
Q

What tachycardias can vagal manoeuvres and Adenosine be used for?

A

Vagal manoeuvres and Adenosine are used in narrow complex (i.e. supraventricular) tachycardias other than AF. They both work by causing atrioventricular node block which shows the underlying atrial rhythm. In addition, adenosine may convert a junctional rhythm to sinus rhythm. It has a short half-life of 10-15 seconds, although this can be potentiated by dipyridamole.

18
Q

Name 4 side effects of carbimazole.

A
  • Maculopapular rash
  • BM suppression leading to agranulocytosis
  • Pruritus
  • Jaundice
19
Q

What are the side effects of Graves’ management?

A
  • Nausea
  • headache
  • Fever
  • Malaise
  • Arthralgia
  • Jaundice
  • BM suppression (agranulocytosis also presents with sore throat- Carbimazole and PTU)
  • Pancreatitis (Carbimazole)
  • Rash
  • Birth defects if used in the first trimester of pregnancy (Carbimazole)
  • Liver damage (PTU)
20
Q

What is first line treatment for Graves?

A

Carbimazole (pancreatitis, not in pregnant women)

Propylthiouracil - second line (particlarly in pregnancy) risk of liver failure

21
Q

What are the two regimens for Graves’ hormone replacement?

A
  1. Block and replace - high dose of antithyroid drugs given continuously; after 4-8 weeks when the patient becomes euthyroid, levothyroxine is also added.
  2. Titration - initially high dose of antithyroid drugs is given and this is titrated down to a lower maintenance dose.
22
Q

Which antithyroid treatment regimen for Graves’ is preferred and why?

A

Titration of doses is better

NB: ‘block and replace’ is the other regimen but this can cause more side effects because of continuously high doses given even when euthyroid. This is associated with pancreatitis, congenital malformations. PTU can cause hepatic toxicity and birth defects.

23
Q

Why is thyrotoxicosis associated with glucose derangement?

A

Causes hypercalcaemia due to increased hepatic glucose production as well as glycogenolysis

24
Q

What is shown on each radioisotope scan?

A
25
Q

What is shown?

A

Pretibial myxoedema - non pitting oedema

26
Q

What eye signs are shown?

A

Lid retraction

Mild proptosis

Mild chemosis

27
Q

What is the management of Graves’ in pregnancy?

A

Antithyroid drugs at lowest doses should be given - PTU is used in the first trimester

Radioactive iodine is contraindicated

Surgery may be offered only once thyroid hormone levels are in range

28
Q

How do you treat AF in Graves’?

A

High risk (>150bpm with ongoing chest pain +/- critical perfusion)

  • Heparinisation +
  • With immediate cardioversion to sinus rhythm to restore cardiac output by synchronised DC shock - needs to be done under sedation/GA
  • Or IV amiodarone 300mg over 1hr

Low risk (<100bpm, mild or no symptoms)

  • If onset known <24hrs - heparinisation and attempted chemical cardioversion with amiodarone
  • >24hr - heparin and warfarin should be commenced with view to elective cardioversion at a later date

Intermediate risk (100-150bpm, no known structural heart disease) timing of onset determines if rate control/DC:

  • Rate control - if any risk that onset was >24hrs and there is theoretical risk of cardiac thrombus formation which may be dislodges during cardioversion.
  • So use IV BBs, oral or IV verapamil or digoxin. Cardioversion after appropriate cardioversion.