Thyrotoxicosis + hyperthyroidism

Question 1

Causes of thyrotoxicosis?

Answer 1

Graves disease – younger
Thyroiditis (have an overactice and underactive phase)
Multinodular goitre (small nodules) – older
Single nodule goitre
Iatrogenic (Iodine, Amiodarone)
Lithium

Question 2

Primary hyperthyroidism

Answer 2

• due to thyroid pathology → thryoid itself behaving abnormally and producing excessive thyroid hormone
• Graves disease, toxic multinodular goitre

Question 3

Secondary hypethyroidism

Answer 3

• thyroid is producing excessive thyroid hormone as a result of overstimualtion by TSH
• pathology is in the hypothalamus or pituitary

Question 4

Graves disease pathophysiology

Answer 4

circulating IgG autoanibodies binding to and activating G-protein-coupled thyrotropin receptors, which cause smooth thyroid enlargement and increased hormone production, and react with orbital autoantigens.

Question 5

Graves disease key points

Answer 5

2/3rds most common cause of hyperthyroidism/thyrotoxicosis

• autoimmune where TSH receptor antibodies cause a primary hyperthyroidism → mimic TSH and stimulate TSH receptors in the thyroid.
• 9:1 female to male
• typical age: 40-60

Question 6

Toxic multinodular goitre (Plummer’s disease) mainly seen in?

Answer 6

• seen in the elderly and in iodine-deficient areas
• there are nodules that secrete thyroid hormones

Question 7

graves disease triggers?

Answer 7

• stress
• infection
• childbirth
• associated with other autoimmune diseases: vitiligo, type 1 DM, addison’s

Question 8

Clinical presentation: universal hyperthyroidism?

Answer 8

• Anxiety and irritability
• Sweating and heat intolerance
• Tachycardia
• Weight loss
• Fatigue
• Frequent loose stools
• Sexual dysfunction
• Oligomennorhoea, or amennohoea

Question 9

Unique features of Grave’s disease?

Answer 9

(all relate to the presence of TSH receptor antibodies)

• Diffuse goiture (without nodules)
• Graves eye disease
• Bilateral exopthalmos
• Pretibial myxoedema: oedematous swellings about lateral malleoli
• Clubbing, painful finger and toe swelling, periosteal reaction to limb bones

Question 10

Unique features of toxic multinodular goitre

Answer 10

Unique features of toxic multinodular goitre

Question 11

De Quervain’s Thyroiditis: clinical presentation unique features

Answer 11

• presentation of a viral infection with fever, neck pain and tenderness
• dysphagia

Question 12

Thyroid storm “thyrotoxic crisis” presentation?

Answer 12

• rare presentation of hyperthyroidism
• severe
• pyrexia, tachycardia and delirium

Question 13

Investigation/Diagnosis thyrotoxicosis?

Answer 13

main investigations:

• TSH suppressed
• T4 and T3 high
• erythrocyte sedimentation rate
  (ESR) high
• Ca2+ high
• Liver function test (LFT) high

additional tests:

• check autoantibodies
• isotope scan if the cause is unclear, to detect nodular disease or subacute thyroiditis
• if opthalmopathy, test visual fields, acuity, and eye movements

may be:

• mild normocytic anaemia
• mild neutropenia (in Graves)

Question 14

Beta blockers for thyrotoxicosis?

Answer 14

Beta blockers for rapid control of symptoms (e.g. propranolol 40mg/6h).

Propranolol is good as it selectively blocks adrenergic activity as opposed to more selective beta blockers which only work on the heart.

Question 15

Carbimazole treatment?

Answer 15

first line anti-thyroid drug, usually successful in treating Grave’s disease, leaving them with normal thyroid function after 4-8 weeks. Once the patient has normal thyroid hormone levels they continue on maintenance carbimazole and either: block and replace with levothyroxine or dose is carefully titrated to maintain normal levels known as titration-block.

Question 16

Propylthiouracil

Answer 16

second line treatment. used in similar was to carbimazole.

Question 17

Administer anti-thyroid medication either by:

Answer 17

• Titration → carbimazole (20/40mg/24h po for 4wks), reduce according to TFTs ever 1-2 months
• Block & replace → give carbimazole + levothyroxine simultaneously (less risk of iatrogenic hypothyroidism)

Question 18

Complete remission and the ability to stop taking anti-thyroids is usually achieved within?

Answer 18

18 months of treatment

Question 19

Radioactive iodine treatment?

Answer 19

• invovles drinking a single dose of radioactive iodine
• taken up by thyroid gland and emitted radiation destroys a proportion of the thyroid cells
• remission can take 6 months and patients can be left hypothyroid afterwards and require levothyroxine replacement

Question 20

Thyroidectomy?

Answer 20

• definitive option to remove whole thyroid or toxic nodules
• patient will be left hypothyroid post thryoidectomy and require levothyroxine replacement for life.

Question 21

Complications of antithryoids?

Answer 21

Carbimazole SE: agranulocytosis → decrease in neutrophils → sepsis (sore throat and mouth ulcers signs stop immediately)

• Propylthiouracil → small risk of severe hepatic reactions, including death, which is why carbimazole is preferred.
• iatrogenic hypothyroidism from antithyroid medication (esp with just titration instead of block and replace)
• In graves → 50% will relapse after stopping treatment → requiring radioidine or surgery

Question 22

Complications of radioactive iodine treatment

Answer 22

• can be left hypothyroid afterwards
• Must not be pregnant and are not allowed to get pregnant within 6 months
• Must avoid close contact with children and pregnant women for 3 weeks (depending on the dose)
• Limit contact with anyone for several days after receiving the dose

Question 23

What is De Quervian’s thyroiditis?

Answer 23

Subacute thyroiditis (also known as De Quervain’s thyroiditis and subacute granulomatous thyroiditis) is thought to occur following viral infection and typically presents with hyperthyroidism.

This presentation of hyperthyroidism and painful goitre following an upper respiratory tract infection is typical of De Quervain’s thyroiditis.

Question 24

Pathophysiology of De Quervian’s thyroiditis?

Answer 24

De Quervain’s thyroiditis: initial hyperthyroidism, painful goitre and globally reduced uptake of iodine-131

Question 25

Clinical presentation of De Quervian’s thyroiditis?

Answer 25

There are typically4 phases;

• phase 1 (lasts 3-6 weeks): hyperthyroidism,painful goitre,raised ESR
• phase 2 (1-3 weeks): euthyroid
• phase 3 (weeks - months): hypothyroidism
• phase 4: thyroid structure and function goes back to normal

Question 26

Investigation/ diagnosis of De Quervian’s thyroiditis?

Answer 26

• thyroid scintigraphy:globally reduced uptake of iodine-131

Investigation results expected in De Quervain’s thyroiditis include:

• Raised erythrocyte sedimentation rate (ESR) and C reactive protein (CRP)
• Raised T3 and T4
• Reduced TSH - Eventually resulting in hypothyroid period
• Normal thyroid autoantibodies
• Mild leukocytosis
• Diffusely reduced uptake of radioactive iodine-131

Question 27

Treatment of De Quervian’s thyroiditis?

Answer 27

• usually self-limiting - most patients do not require treatment
• thyroid pain may respond to aspirin or otherNSAIDs
• in more severe cases steroids are used, particularly if hypothyroidism develops