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YR6: ENDO > Hyperthyroidism > Flashcards

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
Q

What proportion of patients receiving radio-iodine for Graves’ become hypothyroid?

A

Depends on dose
Majority require thyroxine supplementation after 5y

26
Q

Describe management of thyroid eye disease

A

TOP lubricants: help prevent corneal inflammation caused by exposure
Steroids: Prednisolone
Orbita irradiation
Rehabilitative surgery

27
Q

For patients with established thyroid eye disease, which 6 features indicate the need for urgent review by ophthalmology?

A

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
Q

What is Toxic Multinodular Goitre?

A

Thyroid gland containing a number of autonomously functioning thyroid nodules resulting in hyperthyroidism (2nd most common cause)

29
Q

Describe nuclear scintigraphy in Toxic multi nodular goitre

A

Patchy uptake.

30
Q

Describe management of Toxic multinodular goitre

A

Radioiodine therapy

31
Q

What is Thyrotoxicosis without hyperthyroidism?

A

Thyrotoxicosis without thyroid gland overactivity
Usually transient

32
Q

List 3 causes of thyrotoxicosis without hyperthyroidism

A

Postpartum thyroiditis
Subacute (de Quervain’s) thyroiditis
Drug induced: Amiodarone induced thyrotoxicosis

33
Q

List features of thyrotoxicosis by system

A

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
Q

What is pretibial myxoedema?

A

Erythematous, oedematous lesions above the lateral malleoli

35
Q

What is thyroid storm?

A

Rare but life-threatening complication of thyrotoxicosis.
Typically seen in those with established thyrotoxicosis, rarely seen as presenting feature

36
Q

List 4 precipitating events of thyroid storm

A

Thyroid or non-thyroidal surgery
Trauma
Infection
Acute iodine load e.g. CT contrast media

37
Q

List 7 clinical features of thyroid storm

A

Fever > 38.5ºC
Tachycardia
Confusion + agitation
N+V
HTN
Heart failure
Abnormal LFTs +/or jaundice

38
Q

Describe management of thyroid storm

A

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
Q

Why may colestyramine be considered in management of thyroid storm?

A

= bile acid-sequestering agent

Reduces enterohepatic circulation of thyroid hormones.

YR6: ENDO (17 decks)

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