Hyperthyroidism + Graves Flashcards
Definition of hyperthyroidism
common endocrine condition caused by an overactive thyroid gland causing an excess of thyroid hormone and thyroxtoxicosis
What is thyrotoxicosis
refers to an excess of thyroid hormone, having an overactive thyroid gland is not a prerequisite (e.g.consumption of thyroid hormone).
Epidemiology of hyperthyroidism
- 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
Aetiology of hyperthyroidism
Primary:
Graves
Toxic multinodular goitre
Toxic adenoma
Subclinical hyperthyroidism
Thyroiditis
Secondary:
Pituitary adenoma
ectopic tumour
hypothalamic tumour
RF Hyperthyroidism
- Family history
- Auto-immune disease e.g. vitiligo, type 1 diabetes, Addison’s disease
Primary hyperthyroidism pathophysiology
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
Secondary hyperthyroidism
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
Key presentation pneumonic
THYROIDISM
Thyroidism pneumonic for key presentation
tremor, heart rate increase, yawning, restless, oligomenorrhoea, irritability, diarrhoea, intolerance to heat, sweating, muscle wasting (weight loss).
Signs of Hyperthyroidism
- Postural Tremor
- Palmar erythema
- Hyperreflexia
- Sinus tachycardia/ arrhythmia
- Goitre
- Lid lag and retraction
Symptoms of hyperthyroidism
- Weight loss
- Anxiety
- Fatigue
- Reduced libido
- Heat intolerance
- Palpitations
- Menstrual irregularity
1st line investigation for Hyperthyroidism
Thyroid function tests
Graves : Low TSH High T4
Subclinical hyperthyroidism: Low TSH normal T4
Secondary hyperthyroidism: High TSH High T4
Other investigations for hyperthyroidism
Antibodies;
Anti TSH receptors 95% common in graves
Anti TPO
Anti thyroglobulin
1st line therapy for hyperthyroidism
- Beta blocker e.g. propranolol for symptomatic relief
- Anti-thyroid medication: preferred in mild disease - 1st line is carbimazole
Radiodine treatment
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
Complications of management
- 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
Complications
- Cardiovascular: heart failure, atrial fibrillation
- Musculoskeletal:osteoporosis, proximal myopathy
- Thyrotoxic crisis/ thyroid storm
What is Thyrotoxic crisis/ thyroid storm
- 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
- Features include hyperpyrexia, tachycardia, extreme restlessness
Iatrogenic complications due to treatment
- 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
Graves disease definition
Graves’ disease is the most common cause of hyperthyroidism worldwide. It is an autoimmune induced excess production of thyroid hormone
Epidemiology of Graves disease
- 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)
Aetiology of Graves
- 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
RF 4 Graves
- Family history
- Female
- Autoimmune disease
- Stress
- High iodine intake
- Radiation
- Tobacco use
Pathophysiology of Graves
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.
S + S of Graves
- 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
1st line investigation for Graves Disease
TFT’s: raised T3 and T4, reduced TSH.
All other aspects of investigation and management are the same as generic hyperthyroidism
