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Endocrinology > Hyperthyroidism + Graves > Flashcards

Hyperthyroidism + Graves Flashcards

1
Q

Definition of hyperthyroidism

A

common endocrine condition caused by an overactive thyroid gland causing an excess of thyroid hormone and thyroxtoxicosis

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2
Q

What is thyrotoxicosis

A

refers to an excess of thyroid hormone, having an overactive thyroid gland is not a prerequisite (e.g.consumption of thyroid hormone).

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3
Q

Epidemiology of hyperthyroidism

A
  • The overall prevalence of hyperthyroidism is approximately 1.3% and increases to 4-5% in older women
  • Affects 2-5% of all women at some time
  • Mainly between 20-40yrs
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4
Q

Aetiology of hyperthyroidism

A

Primary:
Graves
Toxic multinodular goitre
Toxic adenoma
Subclinical hyperthyroidism
Thyroiditis

Secondary:
Pituitary adenoma
ectopic tumour
hypothalamic tumour

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5
Q

RF Hyperthyroidism

A
  • Family history
  • Auto-immune disease e.g. vitiligo, type 1 diabetes, Addison’s disease
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6
Q

Primary hyperthyroidism pathophysiology

A

involves an excessive production of T3/T4 by the thyroid gland due to pathology affecting the thyroid gland itself.
Increased metabolic rate and sympathetic NS activation
More common subtype

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7
Q

Secondary hyperthyroidism

A

occurs due to excessive stimulation of the thyroid gland by TSH, secondary to pituitary or hypothalamic pathology, or from an ectopic source such as a TSH-secreting tumour.

Rarer

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8
Q

Key presentation pneumonic

A

THYROIDISM

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9
Q

Thyroidism pneumonic for key presentation

A

tremor, heart rate increase, yawning, restless, oligomenorrhoea, irritability, diarrhoea, intolerance to heat, sweating, muscle wasting (weight loss).

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10
Q

Signs of Hyperthyroidism

A
  • Postural Tremor
  • Palmar erythema
  • Hyperreflexia
  • Sinus tachycardia/ arrhythmia
  • Goitre
  • Lid lag and retraction
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11
Q

Symptoms of hyperthyroidism

A
  • Weight loss
  • Anxiety
  • Fatigue
  • Reduced libido
  • Heat intolerance
  • Palpitations
  • Menstrual irregularity
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12
Q

1st line investigation for Hyperthyroidism

A

Thyroid function tests
Graves : Low TSH High T4
Subclinical hyperthyroidism: Low TSH normal T4
Secondary hyperthyroidism: High TSH High T4

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13
Q

Other investigations for hyperthyroidism

A

Antibodies;
Anti TSH receptors 95% common in graves
Anti TPO
Anti thyroglobulin

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14
Q

1st line therapy for hyperthyroidism

A
  • Beta blocker e.g. propranolol for symptomatic relief
  • Anti-thyroid medication: preferred in mild disease - 1st line is carbimazole
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15
Q

Radiodine treatment

A

first line treatment in more than mild Graves’ or toxic multinodular goitre

Contraindicated inpregnancy, age < 16 years old, when breastfeeding or those with established eye disease as can make eye symptoms worse

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16
Q

Complications of management

A
  • Surgery complications - risk of hypothyroidism, hypoparathyroidism, and recurrent laryngeal nerve palsy resulting in a hoarse voice, trachael compression from post-operative bleeding
  • Anti-thyroid drugs - agranulocytosis and neutropenia or hepatotoxicity
17
Q

Complications

A
  • Cardiovascular: heart failure, atrial fibrillation
  • Musculoskeletal:osteoporosis, proximal myopathy
  • Thyrotoxic crisis/ thyroid storm
18
Q

What is Thyrotoxic crisis/ thyroid storm

A
  • Rapid T4 increase. Medical emergency!
    • Features include hyperpyrexia, tachycardia, extreme restlessness
      and eventually delirium, coma and death
    • Treated with large doses of carbimazole, propranolol, potassium iodide, IV hydrocortisone to stop conversion of T4 to T3
19
Q

Iatrogenic complications due to treatment

A
  • Agranulocytosis and neutropaenic sepsis: secondary to carbimazole
  • Hepatotoxicity: secondary to propylthiouracil
  • Congenital malformations: carbimazole in first trimester
  • Foetal goitre and hypothyroidism: any antithyroid medication in pregnancy at high doses
20
Q

Graves disease definition

A

Graves’ disease is the most common cause of hyperthyroidism worldwide. It is an autoimmune induced excess production of thyroid hormone

21
Q

Epidemiology of Graves disease

A
  • This is the MOST COMMON CAUSE of hyperthyroidism (2/3rds of cases)
  • More common in FEMALES than males
  • Typically presents at 40-60yrs (appears earlier if maternal family history)
22
Q

Aetiology of Graves

A
  • Serum IgG antibodies, specific for Graves’ disease, known as TSH receptor stimulating antibodies (TSHR-Ab) bind to TSH receptors in the thyroid
  • Thereby stimulating thyroid hormone production (T3 & T4) - essentially they behave like TSH
  • Resulting in excess secretion of thyroid hormones and hyperplasia of thyroid follicular cells resulting in hyperthyroidism and diffuse goitre
  • Persistent high levels predict a relapse
    when drug treatment is stopped
  • Similar auto antigen can also result in retro-orbital inflammation - graves opthalmopathy
23
Q

RF 4 Graves

A
  • Family history
  • Female
  • Autoimmune disease
  • Stress
  • High iodine intake
  • Radiation
  • Tobacco use
24
Q

Pathophysiology of Graves

A

Involves anti-TSH antibodies causing increased thyroid hormone production through stimulation of the TSH receptor.

Of note, anti-TSH antibodies react with orbital antigens in fat and connective tissue, causing retro-orbital inflammation which leads to thyroid eye disease.

25
Q

S + S of Graves

A
  • Thyroid acropachy - clubbing, swollen fingers and periosteal bone formation
  • Thyroid bruit - continuous sound heard over thyroid mass
  • Pretibial myxoedema - raised, purple-red symmetrical skin lesions over the anterolateral aspects of the shin
  • Eye signs
    • Exophthalmos - protruding eye
    • Ophthalmoplegia - paralysis or weakness of eye muscles
26
Q

1st line investigation for Graves Disease

A

TFT’s: raised T3 and T4, reduced TSH.
All other aspects of investigation and management are the same as generic hyperthyroidism

Endocrinology (17 decks)

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