THYROID GLAND

DR SALAH SHAHEEN
Prof of General Surgery
Faculty of Medicine, Cairo University
SURGICAL ANATOMY
• The thyroid gland develops from a median bud that descends from an opening at
base of the tongue (foramen caecum) as thyroglossal duct. The lower end of the duct
grows and divided into two lobes. The thyroglossal duct disappears and a remnant
remains as a pyramidal lobe.
• Gland weighs about 20-25 grams.
• It is situated in lower part of the front of the neck (both muscular triangles). It has
right and left lobes connected by an isthmus.
• Enclosed between the two layers of the pretracheal fascia which is attached above to
the thyroid cartilage. So, the thyroid gland moves up and down on swallowing.
• It has a rich blood supply.
• Thyroid gland is related to superior laryngeal nerve and recurrent laryngeal nerve on
each side (both are branches of vagus nerve).
• Parathyroid glands lie on the posterior aspect of the thyroid gland.
THYROID GLAND ANATOMY
SURGICAL PHYSIOLOGY
• Follicular cells secrete hormones; triiodothyronine (T3) and tetraiodothyronine (T4).
Parafollicular cells (C-cells) secrete thyrocalcitonin.
• Synthesis of thyroid hormones starts by trapping of inorganic iodide from blood
followed by oxidation of iodide to iodine. Then binding of iodine with tyrosine to
form iodotyrosine; mono (MIT) or diiodotyrosine (DIT). Finally, coupling of MIT and
DIT to form T3 or between two DIT to form T4.
• T3 and T4 are then attached to thyroglobulin in the thyroid gland. On requirement,
they are released in blood and get bound to serum proteins. A small amount of
hormone remains free in the serum and is biologically active.
• There is a feedback mechanism between thyroid hormones and TSH produced by
the anterior pituitary.
GOITER
CLASSIFICATION

Goiter is an enlargement of the thyroid gland.

1. Simple e.g. physiological, colloid and nodular goiter.
2. Toxic e.g. diffuse toxic (Grave’s disease), toxic nodular and toxic
nodule.
3. Neoplastic e.g. benign and malignant.
4. Thyroiditis e.g. autoimmune (Hashimoto’s), fibrosing (Reidel’s)
and granulomatous (de Quervains) thyroiditis. Rarely bacterial
SIMPLE GOITER
PHYSIOLOGICAL GOITER

• usually seen at times of increased physiological demands i.e. stress

e.g. puberty, menstruation, pregnancy, lactation.
• diffuse thyroid hyperplasia
• Thyroid enlargement is diffuse (butterfly), symmetrical, smooth
surface, soft in consistency
• Reversible process. If disturbed → simple nodular goiter
COLLOID GOITER

• Last stage of physiological goiter especially with iodine intake

• Gland is larger and becomes firm
SIMPLE NODULAR GOITER (SNG)
OR
MULTINODULAR GOITER (MNG)
ETIOLOGY
• Environmental; iodine deficiency in endemic areas.
• Familial; enzyme deficiency
• Goitrogen e.g. cabbage, drugs
• In physiological goiter, fluctuating stimulation results in a
mixed pattern of areas of active lobules and areas of
inactive lobules ending in nodular goiter.
CLINICAL MANIFESTATIONS

• Usually female, middle age

• Thyroid function is usually normal
• Localized or diffuse asymmetrical enlargement of the gland, nodular
surface, moves up and down with swallowing, heterogenous
consistency (hard if calcified and cystic if degenerated).
• Carotid artery may be displaced if gland is huge. Trachea may be
displaced or kinked.
• May present by asymptomatic neck mass
MULTINODULAR GOITER
COMPLICATIONS

• Hemorrhage in a cyst (respiratory embarrassment).

• Secondary thyrotoxicosis, usually internodular tissue.
• Carcinoma, usually follicular.
• Retrosternal extension.
INVESTIGATIONS

• Thyroid profile (T3, T4, TSH) normal

• Ultrasonography
• Indirect laryngoscopy before surgery
TREATMENT

• Surgery is indicated for

• Cosmetic reasons
• Pressure manifestation or retrosternal extension
• Complications
• Risk of malignant transformation
• Surgery done ranges from lobectomy to total thyroidectomy.
TOXIC GOITER
TYPES
Hyperthyroidism means excess circulating thyroid hormones. Thyrotoxicosis is
overproduction from the thyroid gland.
Clinical types are:
• Primary thyrotoxicosis or diffuse toxic goiter (Graves’ disease)
• Secondary thyrotoxicosis or toxic nodular goiter (Plummer’s disease)
• Toxic nodule
• Thyroiditis in early stages
• Other rare types
ETIOLOGY AND PATHOGENESIS

• Graves’ disease is an autoimmune disorder due to thyroid stimulating

immunoglobulins. The whole gland is active and produce thyroid hormones.
The gland is enlarged, symmetrical, smooth and soft. May be firm on taking
antithyroid drugs due to accumulation of colloid.
• In toxic nodular goiter, the internodular follicles are active.
• Toxic nodule is autonomously hyperactive with inactivity of the rest of gland.
• Break down of follicles with release of thyroid hormones early in thyroiditis.
CLINICAL PICTURE
• Intolerance to heat.
• Weight loss despite increased appetite.
• Nervousness, anxiety, insomnia and emotional instability.
• Warm moist skin.
• Fine tremors of the hands.
• Eye manifestations e.g. exophthalmos, diplopia, blurring of vision.
These symptoms and signs are mostly in Graves’ disease.
• Cardiovascular manifestations e.g. tachycardia, fibrillation,
hypertension with big pulse volume, heart failure. More frequent
with secondary type.
Primary thyrotoxicosis (Grave’s disease)
Grave’s disease
COMPLICATIONS

• Thyrotoxic heart failure.

• Thyroid storm or crisis; it is a state of severe hypermetabolism.
It is life- threatening complication. It occurs when patient stops
medications or got infection. It may complicate surgery.
INVESTIGATIONS

• Elevated thyroid hormones with low TSH.

• Thyroid scan is very valuable.
TREATMENT
• Medical treatment mainly especially in Graves’ hoping for remission.
• Medical treatment as preparation for surgery in secondary type. Total
thyroidectomy may be justified.
• Medical treatment is beta blocker e.g. inderal plus anti thyroid drugs
e.g. carbimazole. Antithyroid drugs are contraindicated if there is
retrosternal extension. Complications include agranulocytosis.
• Radioactive iodine is ideal in toxic nodule, but it is contraindicated
below 45y, pregnancy and lactation.
Left hemithyroidectomy
Total thyroidectomy
THYROID NEOPLASM
CLASSIFICATION
❑Benign
Follicular adenoma; present as a solitary nodule. 10 – 20% are
malignant. The treatment is lobectomy.
❑Malignant
• Differentiated;
➢Papillary carcinoma
➢Follicular carcinoma
➢Hürthle cell carcinoma
• Undifferentiated (anaplastic)
• Medullary carcinoma
• Malignant lymphoma
• Secondaries
ETIOLOGY

• Neck irradiation during childhood (gene mutation).

• Autoimmune thyroiditis
• Long standing nodular goiter
PATHOLOGY
• Papillary carcinoma; the commonest, characteristic papillary projection inside
follicles, Orphan Annie eye (empty) nucleus and psammoma bodies, grows slowly,
spread early by lymphatics.
• Follicular carcinoma; second most common, in patient with iodine deficiency,
grows and invade fibrous capsule, invade blood vessels with metastasis to lung,
bones, liver and brain, not by lymph node.
• Anaplastic carcinoma; rare, most aggressive, local infiltration is marked.
• Medullary carcinoma; arise from C cells, due to spontaneous RET oncogene
mutation, may be inherited mutation in familial type, may be part of multiple
endocrinal adenopathy (MEA) type 2A and 2B, aggressive malignancy with bad
prognosis, early lymphatic and hematogenous spread.
CLINICAL MANIFESTATIONS
• Mostly females, usually above 40
• Papillary at younger age (two peaks; at 10 and 20y)
• Most often, the first sign may be solitary painless nodule
• Hard and immobile nodules are highly malignant
• Usually non-functioning, so no hypo or hyperthyroidism
• Long standing nodular goiter with recent rapid increase in size and becomes hard
(follicular)
• Pain referred to the ear through Arnold’s branch of vagus
• Enlarged cervical lymph nodes (papillary, medullary)
• Evidences of local infiltration of nearby structures e.g. carotid, esophagus, RLN,
larynx and trachea (anaplastic)
• Diarrhea due to vasoactive peptide and flushing due to serotonin (medullary)
• Metastasis to skull, lungs and bones
Follicular carcinoma developing in long standing multinodular goiter
Multiple cervical lymph nodes appearing two years after
thyroidectomy for papillary carcinoma thyroid
INVESTIGATIONS AND DIAGNOSIS

• US; cyst or solid, suspicious nodules, lymphadenopathy

• Calcitonin; high in medullary
• Radioiodine scan for cold nodules
• Fine needle aspiration biopsy
TREATMENT

Total or near total thyroidectomy, preserve at least one

parathyroid gland, role of block neck dissection, role of
radioactive iodine, investigate for metastasis, full
thyroxine replacement after thyroidectomy.
Solitary thyroid nodule of right lobe