The thyroid – examination and testing

C M Dayan

Consultant Senior Lecturer, University of Bristol

Endocrine Nurses Training Course 9-11 September 2004
Wills Hall, Stoke Bishop, Bristol, BS9 1AE

Thyroid

Where is it?

The thyroid is the largest of the endocrine organs weighing 15-20g. It is a bilobed structure with each lobe approx 2 x 2 x 2cms. It lies below the tracheal cartilage (“Adams’ apple”) anterior to the trachea. The normal gland can be palpated in most people especially women. The isthmus typically lies in front of the 2nd and 3rd tracheal rings

Feeling it

Physical Examination of the thyroid: The key to finding the gland is to feel methodically down the trachea from the thyroid cartilage (“Adams apple”) until you find the isthmus. The lobes of the thyroid will then be on either side of this and should move upwards on swallowing. Complete examination includes

1. Assessing the patient for hyper- or hypothyroidism
2. Examining the eyes for thyroid eye disease (Graves’ disease)
3. Feeling for lymph glands in the neck esp if cancer is suspected

Useful things to know about the thyroid anatomy/physiology

• The right lobe is usually bigger than the left
• The nerve to the voice box (larynx) – the recurrent laryngeal nerve – runs along the outer edge of the thyroid.
  It is therefore easily damaged during thyroidectomy causing a hoarse voice
• It has a very high blood flow – in Graves’ disease it can receive 20% of the whole cardiac output
• It is made up of spherical follicles
• The thyroid also contains C- cells that make calcitonin. This has nothing to do with thyroid hormone. Calcitonin can lower calcium levels but the loss of calcitonin after thyroidectomy seems to make no difference to calcium levels
  Cancer of the C cells is called medullary carcinoma and secreted calcitonin
• The thyroid cells have an iodide pump ( the Na+/iodide symporter. NIS) on the outside that can concentrate iodide 50 - 100X
  We can use radioactive iodine to image the thyroid
  The NIS is one of the 4 thyroid-specific proteins
• The thyroid contains 90% of the iodine in the body
  Radioiodine only damages the thyroid gland
• 60ug of iodine are required each day to make thyroid hormones
  Lower intakes of iodine cause the thyroid to enlarge (goitre) and can lead to hypothyroidism
• On the other membrane (the side next to the centre of the follicle) the thyroid cells have the enzyme thyroid peroxidase (TPO) which attaches iodine atoms to tyrosine amino-acids in the huge molecule, thyroglobulin (Tg 2748 amino-acids)
  1. TPO (previously called the thyroid microsomal antigen) and Tg are two more thyroid specific proteins to which antibodies can arise in Graves’ Hashimoto’s disease
  2. Carbimazole acts by blocking TPO and hence blocks thyroid hormone production
• Each tyrosine can carry 2 iodine molecules; two iodinated tyrosines together from either T4 (if there are 4 iodines) or T3 (if there are only 3). The T4 is stored attached to thyroglobulin molecules in the form of the “colloid” at the centre of the follicle. The thyroid stores enough thyroxine for around 50days supply! Some of the thyroglobulin leaks into the blood and can be detected.
  After the thyroid has been removed, thyroglobulin levels in the blood can be used to detect regrowth – eg regrowth of thyroid cancer
• Thyroid stimulating hormone (TSH) from the pituitary stimulates iodine uptake, synthesis of more TPO enzyme and release of thyroid hormone.
  The receptor for TSH on the thyroid – TSHR - is the 4^th thyroid specific protein: antibodies to the TSHR cause thyroid gland overactivity in Graves’ disease
• 99.9% of thyroid hormone in the blood is bound to proteins in the blood
  Blood tests can now measure Free T4or T3 rather than total T4 or T3
• T3 is the active form of the hormone. 80% of T3 is made from T4 in the tissues of the body AFTER it leaves the thyroid by Deiodinase enzymes
  Does this explain why some people are unhappy on T4??
• Comparison of T3 and T4 inc half-life
  T4 can be given daily and even weekly
• Thyroid hormone levels are tightly controlled by a feedback loop involving the hypothalamus/pituitary and TSH.
  TSH levels can be used to monitor thyroid activity
• Thyroid hormone have many actions including:
  Nervous system development - lack causes cretinism
  Promote growth in children (& differentiation in tadpoles) - lack in children causes short stature
  Increase metabolic rate - can cause weight loss
  Stimulate the heart - causing fast pulse and sometimes atrial fibrillation
  Increase bone turnover - uncontrolled thyrotoxicosis may cause osteoporosis

What can go wrong with the thyroid?

A. Swelling/enlargement “goitre”:

Diffuse goitre – eg iodine deficiency, Hashimoto’s disease
Multinodular goitre
Solitary nodule can be a cancer in 5-10% of cases (NB thyroid cancer generally has a very good prognosis)
Cyst (can also be malignant)

B. Overactive thyroid gland (3 main causes)

Graves’ disease – an autoimmune condition
Toxic Nodule
Toxic Multinodular goitre

Rarer causes include – viral inflammation of the thyroid – “viral thyroiditis” or an autoimmune reaction after pregnancy –postpartum thyroiditis

C. Underactive thyroid gland (1 main cause)

Hashimoto’s disease – autoimmune condition – “autoimmune thyroiditis”. Up to 10% of women have this to a mild degree
Doctor – induced: ie after surgery or radioiodine

Rarer cause: congenital abnormalities, iodine deficiency (common in some areas)

Thyroid function tests

• These consist of sensitive TSH (first line test), T4 (or free T4), T3 (or free T3).
  NB TSH misleading in pituitary disease – use T4
• Other blood tests are: anti-thyroid antibodies (anti-TPO – previously called anti-thyroid microsomal antibody, anti-Thyroglobulin, anti-TSH receptor), and thyroglobulin (used as a marker in thyroid cancer)
• Thyroid imaging – ultrasound, radionucleotide scan (Tc99 or I-123)
• HYPERTHYROIDISM – low TSH, raised T3, raised T4
• SUB-CLINICAL HYPERTHYOIDISM – low TSH, normal T3/T4
• HYPOTHYOIDISM – high TSH, low T4 (and sometimes T3)
• SEB-CLINICAL HYPOTHYOIDISM (v. common) - Raised TSH, normal T3/T4.
• Cases will be discussed in the session.

The opinions expressed in this paper are those of the speaker and do not necessarily reflect the views of the Society