The thyroid gland

Thyroid lump or Thyroid swelling or Goiter

A common thyroid problem, affecting about 5% of the population that present as a lump in the neck or sometimes present with acute painful enlargement Can be divided to 3 main types
1- Diffuse goiter
2- Multinodular goitre
3- Solitary nodule.

1- Diffuse goitre

A- Simple goitre This form of goitre usually presents between the ages of 15 and 25 years,,
It occurs sporadically and is of unknown aetiology.
The goitre is soft and symmetrical and the thyroid is enlarged to two or three times its normal size.
There is no tenderness, overlying bruit lymphadenopathy.

T3,T4 and TSH are normal and no thyroid autoantibodies are detected.

A diffuse goitre rarely needs further treatment and in most cases the
goitre regresses unless it is very large and causing cosmetic symptoms or
compression of other local structures (resulting in stridor or dysphagia).
Thyroxine therapy is some times justified in an attempt to shrink the goitre.

In some, however, the unknown stimulus

to thyroid enlargement persists and, as a result of recurrent episodes of hyperplasia and involution during
the following 10–20 years, the gland becomes multinodularwith areas of autonomous function (Multinodular goitre).

B- Hashimoto’s thyroiditis

Thyroiditis refers to an inflammation of the thyroid.
Hashimoto’s thyroiditis is characterised by destructive lymphoid infiltration of the thyroid, leading to a varying degree of fibrosis and thyroid enlargement.
Hashimoto’s thyroiditis increases in incidence with age and affects more women than men.

Many present with a moderately sized diffuse goitre, which is characteristically

firm or rubbery in consistency. It is sometimes impossible to differentiate it from simple goitre by palpation alone. Around 25% of patients are hypothyroid at presentation. the others are normal, but these patients are at risk of developing overt hypothyroidism in future years.

Anti-thyroid peroxidase antibodies are present in the serum in more than 90% of patients with Hashimoto’s thyroiditis. Thyroxine therapy is indicated as treatment for hypothyroidism, and also to shrink an associated goitre.
Although rare there is an increased risk of thyroid lymphoma.
Spontaneous atrophic hypothyroidism Term used for hypothyroid patients

without a goitre in whom TSH receptor-blocking antibodies

may be more important than anti-peroxidase antibodies.
However, these syndromes can both be considered as variants of the same underlying disease process, and sometimes are given the nomenclature of autoimmune hypothyroidism.


C- Transient thyroiditis
i- Subacute (de Quervain’s) thyroiditis
Is a transient inflammation of the thyroid gland occurring after infection with Coxsackie, mumps or adenoviruses.
There is pain in the region of the thyroid that radiate to the jaw, the ears, and is made worse by swallowing, coughing and movement of the neck.
The thyroid is usually palpably enlarged and tender.

Systemic upset is common. Affected patients are usually females

aged 20–40 years.
ii- Silent thyroiditis
Is other form of Subacute but Painless transient thyroiditis, also occur after viral infection and in patients with underlying
autoimmune disease.
iii- Drug-induced thyroiditis
The condition can also be precipitated
by drugs,

Including amiodarone, interferon-α and lithium. Symptoms continue as long as the drug is taken.

In all these forms, inflammation in the thyroid gland occurs and is associated with release of colloid and stored thyroid hormones, with damage to follicular cells and impaired synthesis of new thyroid hormones. As a result, T4 and T3 levels
are raised for 4–6 weeks until the

preformed colloid is depleted. There after, there is usually a period of hypothyroidism of variable severity until follicular cells recover and normal thyroid function is restored within
4–6 months. During this time there is negligible radioisotope uptake, because the damaged follicular cells are unable to trap iodine and because TSH secretion is suppressed.


Low-titre thyroid autoantibodies appear transiently in the serum, and the ESR is usually raised.
The pain if present usually respond to (NSAIDs). Occasionally, it may be
necessary to prescribe prednisolone 40 mg daily for 3–4 weeks.
The thyrotoxicosis is mild and treatment
with a β-blocker is usually adequate. Antithyroid drugs are of no benefit because

thyroid hormone synthesis is

impaired rather than enhanced. Thyroxine can be prescribed temporarily in the hypothyroid phase.

iv- Acute thyroiditis (also called suppurative thyroiditis)

Caused by bacteria. Symptoms include a painful thyroid, generalized illness and occasionally symptoms of mild hypothyroidism.

Symptoms improve after treatment of the infectious cause.

v- Post-partum thyroiditis
The maternal immune response, which is depressed during pregnancy to allow survival of the fetus, is enhanced after delivery and may unmask previously unrecognized subclinical autoimmune thyroid disease.

Symptoms of thyroid dysfunction

are rare . However, symptomatic thyrotoxicosis presenting
for the first time within 12 months of childbirth is likely to be due to post-partum thyroiditis and the diagnosis is
confirmed by a negligible radioisotope uptake.
The clinical course and treatment are similar to painless subacute thyroiditis.



Post-partum thyroiditis tends to recur after subsequent pregnancies and eventually patients progress over a period of years to permanent
hypothyroidism.

D- Iodine-associated thyroid disease

i- Iodine deficiency
Thyroid enlargement is extremely common in certain mountainous parts of the world, where there is dietary iodine

deficiency (endemic goitre). Most patients are euthyroid with normal or raised TSH levels, although
hypothyroidism can occur with severe iodine deficiency.
Iodine supplementation programmes have abolished this condition in most developed countries.

ii- Iodine-excess thyroid dysfunction

Iodine has complex effects on thyroid function.
1- Very high concentrations for short periods, iodine inhibit thyroid hormone release (as in iodine treatment of thyroid storm and prior to subtotal thyroidectomy).
2- Lower concentrations of iodine effects varies according to whether the patient

Iodine-deficient diet or

Underlying thyroid disease.
Duration
In iodine-deficient parts of the world, transient thyrotoxicosis may be precipitated by prophylactic iodinsation programmes.
In iodine sufficient areas, thyrotoxicosis can be precipitated by Iodine-excess in individuals who have underlying thyroid disease predisposing to thyrotoxicosis,


such as multinodular goitre or Graves’ disease in remission.
Induction of thyrotoxicosis
by iodine is called the Jod–Basedow effect.
Chronic excess iodine administration can, however, result in hypothyroidism. Increased iodine within the thyroid gland down-regulates iodine trapping, so that uptake is low in all circumstances.

Amiodarone

The anti-arrhythmic agent amiodarone affect the thyroid by
Has a structure that is analogous to T4
Contains huge amounts of iodine.
Cytotoxic effect on thyroid follicular cells.
Inhibits conversion of T4 to T3.
Only 20% of patients receiving amiodarone develop hypothyroidism or thyrotoxicosis and so thyroid function

should be monitored regularly.

The thyrotoxicosis can be classified as either:
• type I: a Jod–Basedow effect in patients with underlying thyroid disease, or
• type II: thyroiditis due to cytotoxicity, resulting in a transient thyrotoxicosis.
These patterns can overlap and can be difficult to distinguish



There is no widely accepted management algorithm,
Antithyroid drugs may be effective in
type I form, Prednisolone is beneficial in type II form. Potassium perchlorate can also be used to inhibit iodine trapping in the thyroid. If the cardiac state
allows, amiodarone should be discontinued.

2- Multinodular goitre

Patients with diffuse thyroid enlargement in the absence of thyroid dysfunction or positive autoantibodies (i.e. ‘simple goitre’) may progress to develop nodules. These nodules grow at varying rates and start to secrete thyroid hormone ‘autonomously’, thereby
suppressing TSH-dependent growth and function in the rest of the gland.

Ultimately, complete suppression of

TSH occurs in about 25% of cases leading to (toxic multinodular goitre).
There are reports that the prevalence of foci of thyroid cancer is increased in multinodular goitres, but for practical purposes patients can be reassured that it is a benign condition and malignancy need only be considered in patients with a large ‘dominant’ nodule that is ‘cold’ (i.e. does not take up radioisotope).

diffuse and multinodular goitre has a 1:20 chance of malignancy

Clinical features and investigations
Multinodular goitre present with either
Thyrotoxicosis, or
Large goitre or
Sudden painful swelling caused
by haemorrhage into a nodule or cyst.
Very large goitres may cause mediastinal compression with stridor, dysphagia and


obstruction of the superior vena cava.
Hoarseness due to recurrent laryngeal nerve palsy can occur, but is far more suggestive of thyroid carcinoma.
The diagnosis can be confirmed by a radioisotope thyroid scan and/or ultrasonography.
In those with a ‘dominant’, ‘cold’ nodule, fine needle aspiration is indicated
to exclude thyroid cancer.

Management

If the goitre is small and non toxic, no treatment is necessary, but follow up.
Partial thyroidectomy is indicated for large Goitres, or 131I for the old.
Thyroxine therapy is of no benefit in shrinking multinodular goitres.
In toxic multinodular goitre treatment is usually with 131I.

3- Solitary thyroid nodule

It is important to determine whether the nodule is benign or malignant. It is rarely possible to make this distinction
on clinical grounds alone, although the presence of
Cervical lymphadenopathy
Presenting in childhood / adolescence,
Past history of head and neck irradiation,
Presenting in the elderly

Very occasionally, a secondary

deposit from a renal, breast or lung carcinoma presents as a painful, rapidly growing solitary thyroid nodule.
Investigations
Serum T3, T4 and TSH.
The finding of undetectable TSH is very suggestive of a benign autonomously
functioning thyroid follicular adenoma, For euthyroid patients, the most useful investigation

is FNA of the nodule.

Cytological examination can differentiate benign (80%) from definitely malignant or indeterminate nodules(20%), of which 25–50% are confirmed as cancer at surgery.
Management
Solitary nodules with a solid component in which cytology either is inconclusive or shows malignant cells are treated by surgical excision.

Thyroid malignancy

Primary thyroid malignancy is rare, accounting for less than 1% of all carcinomas,
With the exception of medullary carcinoma, thyroid cancer is
more common in females.

Papillary carcinoma

This is the most common of the malignant thyroid tumours and accounts for 90% of irradiation-induced
thyroid cancer.
It may spread is to regional lymph nodes.
Follicular carcinoma
This is always a single encapsulated lesion. rare metastases to LN bec metastases are blood-borne

and are most often found in bone, lungs and brain.

Management for Both
This is usually by total thyroidectomy followed by a large dose of 131I to ablate any remaining thyroid tissue, normal or malignant.
Thereafter, long-term treatment with thyroxine in a dose sufficient to suppress TSH (usually 150–200 μg daily)
is important, as there is evidence that


growth of differentiated thyroid carcinomas is TSH-dependent. Follow up
is by measurement of serum thyroglobulin, which should be undetectable in patients whose thyroid has been ablated and who are taking a suppressive dose of thyroxine.
Prognosis
Most patients have an excellent prognosis when treated appropriately.

Medullary carcinoma

This tumour arises from the parafollicular C cells In addition to calcitonin, the tumour may
secrete 5-hydroxytryptamine (5-HT, serotonin), tachykinin peptides, ACTH and prostaglandins.
As a consequence, carcinoid syndrome and Cushing’s syndrome may occur.
Patients usually present in middle age with a firm thyroid mass.


Cervical lymphadenopathy involvement is common, but distant metastases are rare initially.
Serum calcitonin levels are raised and are useful in monitoring response to
treatment .
Treatment is by total thyroidectomy. Since the C cells do not concentrate
iodine, there is no role for 131I therapy.

Medullary carcinoma of the thyroid may occur sporadically, or in families as part of the MEN type 2 syndrome.

Riedel’s thyroiditis

This is not a form of thyroid cancer, but the presentation is similar and the differentiation can usually only be made by thyroid biopsy. It is very rare condition of unknown aetiology in which there is
extensive infiltration of the thyroid and


Surrounding structures with fibrous tissue. There may be associated mediastinal and retroperitoneal fibrosis. Presentation is with a slow-growing goitre which is irregular and
stony-hard. There is usually tracheal and oesophageal compression.
Other recognised complications include recurrent laryngeal nerve palsy, hypoparathyroidism and eventually
hypothyroidism.