The term goiter (from the Latin gutter = the throat) is used to describe generalized

enlargement of the thyroid gland.

A discrete swelling (nodule) in one lobe with no palpable abnormality elsewhere is termed
an isolated (or solitary) swelling. Discrete swellings with evidence of abnormality
elsewhere in the gland are termed dominant.
Deficiency of circulating thyroid
Iodine deficiency
hormone due to the deficiency
(Most common)
of inborn errors of metabolism (Daily requirement: 0.10.15mg)
1. Very low iodide content in
the water and food
2. Although iodides in food
and water may be adequate,
failure of intestinal absorption
EXCESSIVE RELEASE OF
THYROID STIMULATING
HORMONE (TSH)
The natural history of simple goiter
Stages in goiter formation are:
Persistent growth stimulation causes diffuse hyperplasia; all
lobules are composed of active follicles and iodine uptake is

Goitrogenic agents
1. The vegetables of the
brassica family (cabbage,
kale and rape), which contain
thiocyanate
2. Drugs such as paraaminosalicylic acid (PAS) and
the antithyroid drugs.
3. Consumption of iodine in
large quantities
Improper synthesis of thyroid
and
hormones Thiocyanates
results in defective
interfere with
negativeperchlorates
feedback mechanism
to
iodide
trapping;
carbimazole
the anterior pituitary
and thiouracil compounds
interfere with the oxidation of
iodide and the binding of
iodine to tyrosine

Hyperplasia represents the response of the thyroid to TSH, other growth factors, or circulating
stimulatory antibodies. The hyperplasia may compensate for thyroid hormone deficiency. The
epithelium is tall and columnar; the follicles are collapsed and contain only scanty
colloid. When the hyperplastic stage is extreme and prolonged, there may be confusion with
carcinoma because of the degree of cellularity and the presence of enlarged cells. The nuclei
are enlarged, hyperchromatic, and even bizarre. Because of follicular collapse and epithelial
hyperplasia and hypertrophy, papillary changes can be seen.
uniform. This is a diffuse hyperplastic goiter, which may persist for a long time but is reversible
if stimulation ceases.

Later, as a result of fluctuating stimulation, a mixed pattern develops with areas of active
lobules and areas of inactive lobules.
Thyroid follicles may not remain in a state of continuous hyperplasia, but instead undergo
involution, with the hyperplastic follicles re-accumulating colloid. The epithelium becomes
low cuboidal or flattened and resembles that of the normal gland. Some follicles become
much larger than normal, contain excessive colloid, and are lined with flat epithelium. The
gland is diffusely enlarged, soft, and has a glistening cut surface because of the excess of
stored colloid. In addition to large follicles filled with colloid, there are foci in the gland where
hyperplasia is still evident.This phase of nontoxic goiter is often termed colloid goiter.

 Active lobules become more vascular and hyperplastic until hemorrhage occurs, causing
central necrosis and leaving only a surrounding rind of active follicles.
Patients with long-standing thyroid deficiency typically develop nodular goiters that result
from over distention of some involuted follicles, and persistence of regions of epithelial
hyperplasia. The new follicles form nodules and may be heterogeneous in their appearance, in
their capacity for growth and function, and in their responsiveness to TSH. The vascular
network is altered through the elongation and distortion of vessels, leading to
hemorrhage, necrosis, inflammation, and fibrosis. These localized degenerative and reparative

changes produce some nodules that are poorly circumscribed, and others that are well
demarcated and resemble true adenomas. Because the nodules distort the vascular supply to
some areas of the gland, some zones will contain larger-than-normal amounts of colloid and/or
iodide, and others will have relative colloid and/or iodide deficiency. Growth of goiters
therefore may be related to focally excessive stimulation by TSH, stimulation by
Necrotic lobules coalesce to form nodules filled either with iodine-free colloid or a mass of new
but inactive follicles.
Continual repetition of this process results in a nodular goiter. Most nodules are inactive, and
active follicles are present only in the internodular tissues.
Diagnosis
Diagnosis is usually straightforward. The patient is euthyroid, the nodules are palpable and often
visible; they are smooth, usually firm and not hard, and the goiter is painless and moves freely
on swallowing. Hardness and irregularity, due to calcification, may simulate carcinoma. A painful
nodule, sudden appearance, or rapid enlargement of a nodule raises suspicion of carcinoma but
is usually due to hemorrhage into a simple nodule. Differential diagnosis from autoimmune
thyroiditis may be difficult and the two conditions frequently coexist.
Investigations
1. Thyroid function tests---- to exclude mild hyperthyroidism
2. the presence of circulating thyroid antibodies tested to differentiate between autoimmune
thyroiditis
3. Plain radiographs of the chest and thoracic inlet will rapidly demonstrate clinically
significant tracheal deviation or compression
4. Ultrasound and CT give more detailed images but rarely influence clinical management.
5. FNAC is only required for a dominant swelling in a generalized goiter.
Treatment
In the early stages, a hyperplastic goiter may regress if thyroxine is given in a
dose of 0.150.2 mg daily for a few months.
Although the nodular stage of simple goiter is irreversible, more than half of benign
nodules will regress in size over ten years.
Most patients with multinodular goiter are asymptomatic and do not require operation.
Operation may be indicated on cosmetic grounds, for pressure symptoms or in response
to patient anxiety.
Retrosternal extension with actual or incipient tracheal compression is also an indication
for operation, as is the presence of a dominant area of enlargement that may be
neoplastic.
There is a choice of surgical treatment in multinodular goitre: total thyroidectomy with
immediate and lifelong replacement of thyroxine, or some form of partial resection, to
conserve sufficient functioning thyroid tissue to subserve normal function while reducing
the risk of hypoparathyroidism that accompanies total thyroidectomy.
Subtotal thyroidectomy involves partial resection of each lobe, removing the bulk of the
gland, leaving up to 8 g of relatively normal tissue in each remnant.

The technique is essentially the same as described for toxic goiter, as are the
postoperative complications. More often, however, the multinodular change is
asymmetrically distributed, with one lobe more significantly involved than the other.
In these circumstances, particularly in older patients, total lobectomy on the more
affected side is the appropriate management with either subtotal resection (Dunhill
procedure) or no intervention on the less affected side. In many cases, the causative
factors persist and recurrence is likely. Reoperation for recurrent nodular goiter is more
difficult and hazardous and, for this reason, an increasing number of thyroid surgeons
favor total thyroidectomy in younger patients. However, when the first operation
comprised unilateral lobectomy alone for asymmetric goiter, reoperation and completion
total thyroidectomy is straightforward if required for progression of nodularity in the
remaining lobe.
Total lobectomy and total thyroidectomy have the additional advantage of being
therapeutic for incidental carcinomas