Hyperthyroidism Flashcards

1
Q

What is hyperthyroidism?

A

pathologically increased thyroid hormone production + secretion by the thyroid gland

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2
Q

What is thyrotoxicosis?

A

Clinical manifestation of excess circulating thyroid hormones due to any cause

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3
Q

List 6 causes of thyrotoxicosis

A

Graves’ disease (most common)
Toxic multi nodular goitre
Acute phase of de Quervain’s thyroiditis
Acute phase of postpartum thyroiditis
Acute phase of Hashimoto’s thyroiditis
Amiodarone

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4
Q

What is primary hyperthyroidism?

A

Thyrotoxicosis caused by abnormality of the thyroid gland e.g. Graves’ disease or nodular goitre

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5
Q

What are the 2 subtypes of primary hyperthyroidism?

A

Overt: TSH < normal, T3/T4 > normal

Subclinical: TSH < normal, T3/T4 normal

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6
Q

List 4 risk factors for development of hyperthyroidism

A

F > M
FH
Smoking
Other AI disease e.g. T1DM

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7
Q

What is Graves’ disease?

A

AI disorder mediated by TSH receptor antibodies
TRAbs timulate TSH receptor, leading to thyroid hyperplasia + unregulated excessive production + secretion of thyroid hormone

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8
Q

List 3 signs specific to Graves’ and not seen in other causes of thyrotoxicosis

A

Eye signs (30%)
Pretibial myxoedema
Thyroid acropachy

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9
Q

What eye signs may be seen in Graves’ disease?

A

Exophthalmos
Ophthalmoplegia
Conjunctival oedema
Optic disc swelling
Inability to close eyelids may lead to sore, dry eyes (risks exposure Keratopathy)

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10
Q

What is thyroid acropachy?

A

Triad of:
Digital clubbing
Soft tissue swelling of hands + feet
Periosteal new bone formation

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11
Q

What is the most important modifiable risk factor for thyroid eye disease in Graves’ disease?

A

Smoking

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12
Q

How does radio iodine affect thyroid eye disease?

A

Increases inflammatory Sx of thyroid eye disease

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13
Q

Which antibodies may be found in Graves’ disease?

A

TSH receptor stimulating antibodies (90%)
Anti-thyroid peroxidase antibodies (75%)

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14
Q

Describe Thyroid Scintigraphy in Graves’ disease

A

Diffuse, homogenous, increased uptake of radioactive iodine

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15
Q

Describe initial management of Graves’ disease

A

Propanolol to block adrenergic effects (palpitations, tremor, tachycardia)
Refer
Specialists: ATD e.g. Carbimazole (if Sx not controlled by propranolol)

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16
Q

What are anti-thyroid drugs aka? Give 2 examples

A

Thionamides
Carbimazole
Propylthiouracil

17
Q

Describe the titration regime of carbimazole for Graves’ disease

A

Start Carbimazole 40mg
Reduce gradually to maintain euthyroidism
Continued for ~12-18 months

18
Q

What is the ‘block and replace’ regime of Carbimazole for Graves’ disease?

A

Start Carbimazole 40mg
Add Thyroxine when patient is euthyroid
Tx lasts ~6-9 months

19
Q

Compare the regimes of carbimazole use in Graves’ disease

A

ATD titration regime suffer fewer side-effects than those on block-and-replace regime

20
Q

What is the main adverse effect of carbimazole?

A

Agranulocytosis

21
Q

What is the main risk of propylthiouracil?

A

Severe liver injury

22
Q

When is propylthiouracil used first line in Graves’ disease?

A

Pre-pregnancy/ 1st Trimester
(Carbimazole a/w congenital abnormalities)

23
Q

When is radio-iodine used in Graves’ disease?

A

Relapse following ATD therapy
Resistance to primary ATD Tx

24
Q

What are the contraindications to radio-iodine for Graves’ disease?

A

Pregnancy (+ avoid for 4-6 months following Tx)
Age < 16y .

Relative CI: Thyroid eye disease- may worsen the condition

25
What proportion of patients receiving radio-iodine for Graves' become hypothyroid?
Depends on dose Majority require thyroxine supplementation after 5y
26
Describe management of thyroid eye disease
TOP lubricants: help prevent corneal inflammation caused by exposure Steroids: Prednisolone Orbita irradiation Rehabilitative surgery
27
For patients with established thyroid eye disease, which 6 features indicate the need for urgent review by ophthalmology?
Unexplained deterioration in vision Awareness of change in intensity or quality of colour vision in 1/ both eyes Hx of eye suddenly 'popping out' (globe subluxation) Obvious corneal opacity Cornea still visible when eyelids are closed Disc swelling
28
What is Toxic Multinodular Goitre?
Thyroid gland containing a number of autonomously functioning thyroid nodules resulting in hyperthyroidism (2nd most common cause)
29
Describe nuclear scintigraphy in Toxic multi nodular goitre
Patchy uptake.
30
Describe management of Toxic multinodular goitre
Radioiodine therapy
31
What is Thyrotoxicosis without hyperthyroidism?
Thyrotoxicosis without thyroid gland overactivity Usually transient
32
List 3 causes of thyrotoxicosis without hyperthyroidism
Postpartum thyroiditis Subacute (de Quervain's) thyroiditis Drug induced: Amiodarone induced thyrotoxicosis
33
List features of thyrotoxicosis by system
General: WL, 'Manic', restlessness, Heat intolerance Cardiac: Palpitations, tachycardia high-output HF (elderly), reversible cardiomyopathy (rare) Skin: Sweating, Pretibial myxoedema, Thyroid acropachy GI: Increased appetite, Diarrhoea Gynae: Oligomenorrhea, sub fertility Neurological: Anxiety, Tremor
34
What is pretibial myxoedema?
Erythematous, oedematous lesions above the lateral malleoli
35
What is thyroid storm?
Rare but life-threatening complication of thyrotoxicosis. Typically seen in those with established thyrotoxicosis, rarely seen as presenting feature
36
List 4 precipitating events of thyroid storm
Thyroid or non-thyroidal surgery Trauma Infection Acute iodine load e.g. CT contrast media
37
List 7 clinical features of thyroid storm
Fever > 38.5ºC Tachycardia Confusion + agitation N+V HTN Heart failure Abnormal LFTs +/or jaundice
38
Describe management of thyroid storm
High dose Anti-thyroid drugs: Carbimazole or propylthiouracil + Hydrocortisone IV (reduce peripheral conversion of T4 to the more active T3) + B-blockers: IV propranolol + Lugol's iodine + Symptomatic Tx e.g. paracetamol Tx of underlying precipitating event
39
Why may colestyramine be considered in management of thyroid storm?
= bile acid-sequestering agent Reduces enterohepatic circulation of thyroid hormones.