Thyroids Flashcards
Thyroid gland introduction
Largest pure endocrine gland
Located in the anterior neck
2 lobes connected by an isthmus
Controls metabolism via thyroid hormones
Anatomy of the thyroid
Physiology of thyroid gland
Made up of 2 types of cells
Closely packed follicular- iodine containing thyroid hormones T3 and T4-majority of the tissue
Parafollicular cells- Calcitonin
Follicular cells take up iodide an amino acids from circulation on the basolateral side -synthesise thyroglobulin and thioperoxidase from A. acids
These are then secreted into thyroid follicles together with iodide
Follicular cells then take up iodinated thyroglobulin from follicles by endocytosis, extract thyroid hormones into blood.
Thyroid hormones are transported throughout the body where they control metabolism
Normally 80% T4 and 20% T3 is produced
Categories and effect of thyroid glands
Diseases of the thyroid
Congenital
Inflammation
Functional abnormality
Goitres
neoplasia
Goitres
Thyroid disease may present as a swelling, a disordered metabolism or a combination-7% of the world’s population has a goitre, mostly as a result of iodine deficiency.
Thyroid swellings can be classified as follows:
• Diffuse goitre
• Multinodular goitre
• Solitary thyroid nodule
Patients may present with any combination of a normal or large thyroid coupled with hypo-, eu or hyperthyroidism
Treatment
Medical:thyroxine analogues –levothyroxine
Conservative-cosmesis concerns
Surgical –thyroidectomy
Indications for surgery of a multinodular goitre
Local symptoms, eg significant or symptomatic retrosternal extension, dysphagia, tracheal deviation or
Stenosis
• Enlarging dominant nodule, unless unequivocally benign
• RLN palsy
• Cosmesis
• Hyperthyroidism
Thyroid cancers
70% papillary carcinoma: affects young people; 95%+ survival
• 20% follicular carcinoma: not able to diagnose on FNAC; 95%+ survival
• 5%medullary carcinoma: C-cell multifocal cancer. May be part of MEN syndrome; genetic testing is required
• <5%anaplastic carcinoma: terrible prognosis. Seen in older patients
• Lymphoma: needs chemotherapy under the care of the haemato-oncologists. Good prognosis
Treatment:surgery,radiotherapy
Inflammatory thyroiditis
Acute thyroiditis: bacterial cause (usually streptococci)
• Subacute thyroiditis (de Quervain’s thyroiditis): viral cause (Epstein–Barr virus [EBV], mumps, measles)
• Chronic thyroiditis (Hashimoto’s thyroiditis): autoimmune cause
Hypothyroidism (myxoedema)
Iatrogenic causes (90% cases) include:
• Post-iodine-131 therapy
• Post-thyroidectomy
• Post-radiotherapy
• Drugs:
Carbimazole and propylthiouracil: used as treatment of hyperthyroidism to block thyroid
peroxidase enzyme
• Amiodarone: used as treatment for atrial fibrillation; contains iodine and can cause
hyperthyroidism and hypothyroidism. Thyroid function tests (TFTs) should be checked every 6 months
• Lithium: used as mood stabiliser in bipolar affective disorder
Idiopathic myxoedema
Autoimmune diseases: eg Hashimotos thyroiditis
Iodine deficiency
Hypopituitarism
Tumour infiltration
Treatment of hypothyroidism
Oral T4 for life.
T4 has a predictable biological activity and is cheap. It has a long half-life (1 week).TFTs can be checked to ensure that the patient is euthyroid.
Emergency
Myxoedema coma Elderly patients with undiagnosed hypothyroidism, or those who have not taken their medication,can present with:
altered mental status
coma
bradycardia
hypothermia
hypoglycaemia.
TFTs should always be checked in patients with this clinical picture. Patients should be resuscitated on ITU with fluids, gentle rewarming, and T3 and T4 supplementation. Ventilation may be necessary.
Hyperthyroidism
Three causes account for 99% of cases:
• Graves’ disease (autoimmune) accounts for 90% of cases
• Toxic adenoma
• Toxic multinodular goitre (Plummer’s disease)
Other causes of hyperthyroidism
Drugs such as thyroxine (the Jod–Basedow effect is induction of thyrotoxicosis in a previously
euthyroid individual by the over-treatment of multinodular goitre with iodine)
Carcinoma (rare)
Iodine-131 treatment
Hyperfunctioning ovarian teratoma
(struma ovarii)
Subacute/acute thyroiditis
TSH-secreting tumour (eg hydatidiform mole, choriocarcinoma, pituitary tumour)
Graves disease
Graves’ disease is an immunological disorder of unknown aetiology characterised by stimulation of TSH receptors by immunoglobulins or antibodies.
It is classically seen in women aged 20–40 years.
Pathophysiology of Graves’ disease
Thyroid-stimulating immunoglobulins or thyroid-receptor antibodies attach to TSH receptors on the surface of the thyroid follicular cell and cause excess secretion of T3 and T4
Clinical features of Graves disease
• Hyperthyroidism
• 85% have eye signs
• Diffuse goitre
• Thyroid acropachy (similar to clubbing)
• Pretibial myxoedema
• Thyroid bruit on auscultation due to increased vascularity
Eye disease in hyperthyroidism
Three-quarters of patients with Graves’ disease have associated eye signs.
1.Exophthalmos is due to:
Proptosis: caused by increased retrobulbar orbital fat and enlarged intraorbital muscles
infiltrated with lymphocytes and containing increased water and mucopolysaccharide
2. Lid retraction: due to a direct effect of thyroxine on the orbital muscles
3. Orbital oedema
Erythema of the conjunctiva is seen in association with the lid retraction. In severe cases,
paralysis of the ocular muscles can lead to squint, diplopia and, rarely, optic nerve damage.
Treatment of Graves’ disease
medical
carbimazole
Propylthiouracil and carbimazole are thionamides that inhibit thyroid peroxidase and hence block the organification and coupling process in the thyroid follicular cell, and thus reduce thyroid hormone synthesis
radioiodine
surgical
