Thyroid Gland

Located in the central part of the neck. 2 lobes on both sides of trachea and central isthmus

weight: 20 to 25 gm.

Blood supply: The sup. pedicle (artery, vein) runs with it, the laryngeal
nerve, so ligation must be done close to the thyroid.
1. Superior thyroid artery – a branch from external carotid artery
2. Inferior thyroid artery – from the subclavian artery. It crosses the recurrent laryngeal n.

Venous drainage: Veins are large, so you have to make

sure the ligatures won't slid.
1. Superior thyroid vein---- to jugular vein.

2. Middle thyroid vein--- to jugular vein.

3. Inferior thyroid vein --- to brachiocephalic vein.

Lingual thyroid

Lateral abbarent thyroid a lymph node metastasis from

papillary thyroid carcinoma.
Median ectopic thyroid (tongue)

Thyroglossal cyst

Thyroglossal fistula

Physiology of thyroid gland:

Thyroid hormones T3 (tri-iodothyronine) and L-thyroxine (t4) are bound to thyroglobulin within the
colloid.

Synthesis of these hormones is controlled by several enzymes in several steps:

1. Trapping of inorganic iodide from the blood.

2. Oxidation of iodide to iodine.

3. Binding of iodine with tyrosine to form iodo-tyrosine.

4. Coupling of (mono-iodo-tyrosine) and (Di-iodo-tyrosine) to form T3 and T4.

A lingual thyroid is a specific type of ectopic thyroid, and results from lack of normal caudal migration of
the thyroid gland.
Synthesis and liberation of thyroid hormones from the thyroid is controlled by TSH and secretion of TSH
depends on the level of circulating of thyroid hormones.

Test of thyroid function:

1. Serum TSH.

2. T3 and T4 (Total).

3. Free T3 and Free T4.

4. Essay of thyroid stimulating Antibodies.

5. Isotop scanning (I 123, Tc99m) to demonstrate the distribution of activity in the gland.

Its’ principle value is in the toxic patient with a nodule or multi nodularity of the gland.

6. Essay of thyroid autoantibodies, they’re antibodies against thyroid peroxidase (PTO) and against
Thyroglobulin.

Diseases of Thyroid Gland:

1. Hypothyroidism:

Cretinism (Fetal or infantile Hypothyroidism).

Adult hypothyroidism.
Eu- or Hypo- thyroid --> Iodine, or thyroxine.

2. Thyroid Enlargement:

A. diffuse hyperplastic goiter (simple goiter):

1. due to stimulation of thyroid gland by TSH in response to low levels of thyroid hormones.
2. the most important factor in endemic goiter is dietary deficiency of iodine.
3. Defective hormone synthesis account for many sporadic goiters.
4. Enzyme deficiencies may be responsible for many sporadic goiters also. Only thyroxine is beneficial.
5. Goitrogenes , like vegetables of the brassica (cabbage, Kale, rape) which contain thyocyanate . Drugs
such as (PAS) and Anti thyroid drugs. And Iodine in large quantities can also be goitrogenic.
4-Aminosalicylic acid, also known as para-aminosalicylic acid (PAS) is an antibiotic
primarily used to treat tuberculosis
The goiter appears in childhood in endemic areas but it usually occurs at puberty when metabolic
demands are high.
If TSH stimulation ceases, the goiter may regress.
The goiter is soft diffuse and may become large enough to cause discomfort.
A colloid goiter is a late stage of diffuse hyperplasia when TSH stimulation has fallen of and when many
follicles are inactive and full of colloid.
 If MNG is euthyroid, small, with small nodules (less than 1 cm), with no suspicion of malignancy -->
Monitor.
...........
MNG and solitary nodule have the same risk of malignancy so it requires FNA.
...........
US should be done in MNG.
B. Nodular goiter: ...........
Any nodule greater than 1 cm is suspicious of malignancy.
Is the end result of the changes that occur due to fluctuating stimulation by TSH where active lobules
become more vascular and hyperplastic until hemorrhage occurs causing central necrosis and leaving
only a surrounding rim of active follicles, then necrotic lobules coalesce to form nodules filled either
with iodine free colloid or a mass of a new but inactive follicles.

Continual repetition of this process results in a nodular goiter.

Most nodules are inactive and active follicles are present in the inter-nodular tissue.

Clinically the patient is Euthyroid , the nodules are palpable and often visible , smooth and firm but not
hard . The goiter is painless and move freely on swallowing.

Thyroid function should be assessed to exclude mild toxicity and the presence of circulating thyroid
antibodies should be tested to exclude autoimmune thyroiditis.

Complications: The trachea doesn't collapse, but the veins get

obstructed and edema develops.
1. Multinodular goiter might get very big in size to cause tracheal obstruction due to gross lateral
displacement or compression in a lateral or antero-posterior plane by retrosternal extension of the
goiter.

2. Secondary thyrotoxicosis, transient episodes of mild hyperthyroidism are common occurring in up to

30% of patients.

3. Carcinoma, dominant or rapidly growing nodules in long standing goiters are suspicious for
malignancy.

Prevention and treatment:

In endemic areas, the incidence of simple goiter can be reduced by the introduction of iodized salt to the
diet. In the early stages, a hyperplastic goiter may regress if thyroxine is given in a dose of 0.15 to 0.2 mg
daily for few months.

Although the nodular stage of simple goiter is irreversible, more than half of the nodules will regress in
size over 10 years.

Asymptomatic small nodular goiter do not require operation, operation may be indicated for cosmotic
reasons or for pressure symptoms or in response to patient’s anxiety.

Retrosternal extension with tracheal compression is also indication for operation.

The presence of a dominant area of enlargement that may be neoplastic is also indication for surgery.
The type of surgery is either Total thyroidectomy, Near total thyroidectomy or subtotal thyroidectomy.
After all these surgeries, thyroxine should be given for replacement or prevention of recurrence in
subtotal resection.

Solitary thyroid nodule:

The importance of solitary nodules lies in the risk of neoplasia. 15% of isolated nodules prove to be
malignant and an additional 30-40% is follicular adenomas, the remainder is non-neoplastic largely
consisting of areas of colloid degeneration, thyroiditis or cysts.

Investigations:

1. Thyroid function test: TSH, T3 and T4. To diagnose toxic adenomas. Itsigns
is done to all patients with goiter even if there are no
or symptoms because some cases are subclinical.

2. Autoantibody titers: to diagnose chronic lymphocytic thyroiditis.

3. Isotope scan: to determine the functional activity relative to the surrounding gland according to the
isotope uptake. On scanning, swellings are classified as hot (over active) , warm ( active) or Cold Especially
important in MNG.
(underactive). About 80% of solitary nodules are cold but only 15% prove to be malignant.

4. Ultrasonography: can differentiate between cyst, adenomas and as adjunct to aspiration cytology.

5. FNAC (Fine Needle Aspiration Cytology): is the investigation of choice in the discrete thyroid nodule. It
can differentiate between colloid nodules, thyroiditis, papillary carcinoma, medullary carcinoma,
anaplastic carcinoma and lymphoma. When there is a suspicion of malignancy.

It cannot differentiate between benign follicular adenoma and follicular carcinoma.

6. Chest and Thoracic inlet radiographs.

Because the difference lies in
the invasion of the capsule.
7. CT and MRI, second line. Detect retrosternal
extension, LN. assessment,
8. Indirect laryngoscopy. vascularity, diffuse or
nodular?
9. Large bore needle (Trucut) Biopsy.
Radical Neck Dissection (RND) - removal of all ipsilateral cervical
lymph node groups from levels I through V, together with SAN, SCM
and IJV.
Thyrotoxicosis:
1. Diffuse Toxic goiter (grave’s disease ) .

2. Toxic nodular goiter . Toxic MNG is due to the activity of a single toxic adenoma, and if not, then it is due to the activity of
the normal intervening tissue when it becomes out of control.
To differentiate between the two causes, thyroid scan must be done.
3. Toxic nodule.

4. Hyperthyroidsm due to rare causes: early stage hashimoto's thyroiditis or pituitary microadenoma

Diffuse toxic goiter (Grave’s disease) :

Vascular goiter occurs usually in young women and frequently associated with eye signs, it is a primary
thyrotoxicosis. 50% of patients have family history of autoimmune endocrine diseases.

The whole functioning thyroid tissue is involved and hypertrophy and hyperplasia are due to abnormal
thyroid stimulating antibodies (TSH- R Abs) that bind to TSH receptor sites and produce a
disproportionate and prolonged effect.

Toxic nodular goiter:

A simple nodular goiter is present for a long time before the hyperthyroidism appears. Usually in the
middle aged or elderly . The syndrome is that of secondary thyrotoxicosis .Eye signs are rare but cardiac
signs are frequent .

In many cases the nodules are inactive and the activity is in the inter-nodular thyroid tissue however in
some cases one or more nodules are overactive (toxic adenoma).

Toxic nodule:

It may be true toxic adenoma or part of generalized nodularity, the cause of toxicity is unknown and a
single nodule in the gland becomes overactive and produce high level of thyroxine causing suppression
of all surrounding thyroid tissue and suppression of TSH.

Eye disease is unusual

Clinical features of thyrotoxicosis:

Symptoms:-
Tiredness, emotional liability, heat intolerance, weight loss, increased appetite, palpitations,
early morning diarrhea, and increased sweating

Signs:-
Tachycardia, hot moist palms, agitation, bruit over the gland, exophthalmus and other eye
signs(lid lag, lid retraction and ophthalmoplegia), proximal myopathy, pretibial myxoedema

*in primary thyrotoxicosis eye signs are more prominent while in secondary thyrotoxicosis cardiac signs
are more common.

Management of thyrotoxicosis:-
The common principle is to make all patients euthyroid before any further action.

1. Antithyroid drugs:

Those in common use are carbimazole and propylthiouracil.

carbimazole and related drugs block thyroid peroxidase and inhibit thyroxine synthesis.
The response is slow and 4-8 weeks may be required to reduce the effect of thyrotoxicosis.
These drugs are used to restore the patient to an euthryoid state and to maintain this for a
prolonged period in the hope that a permanent remission will occur (i: e the production of TSH
antibodies will be diminished.

It should be noted that antithyroid drugs cannot cure a toxic nodule.

The disadvantage is that the treatment is prolonged (6 months to 2 years) and failure rate is at
least 50%.

Side effects are very rare :-agranulocytosis or aplastic anaemia.

The daily dose is 30-40mg (10 mg tds) .When the patient becomes biochemically euthyroid a
3 times a day
maintenance dose of 5 mg 2-3 times aday is given for 6-24 months.
Start with high dose, and after 8 weeks reduce it but no less than 10 mg (5 mg in the morning, 5 mg at night). If
hypothyroidism develops, then give replacement therapy.
 beta adrenergic blocking agents:-

These are effective in reducing the effect of T4 on sympathetic system to control

thyrotoxic clinical manifestations. Propranolol (inderal) is most commonly used in a dose of 20-
40 mg tds for 2-3 weeks.

Management of specific causes of thyrotoxicosis:-

1. Grave’s disease:

A. Non operative treatment: The possibility of spontaneous remission makes non

operative treatment preferable.

Antithyroid drugs are continued for 6-24 months. Half of those treated become
permanently euthyroid . Antithyroid drugs are preferred in young patients with small
gland, while radio-active iodine is preferred in older patients (above 45 years).

B. Operation is indicated for

*Patients unwilling to undergo prolonged drug treatment.

*relapse after drug therapy

*large goiter after effective medical therapy

*failure of compliance and intractable side effects.

Complications of thyroidectomy in graves disease include recurrence of thyrotoxicosis

(3%), or hypothyroidism (10%).

2. Multinodular toxic goiter Because there is fibrosis, so the

treatment won't work.
A. Non operative treatment : antithyroid drugs very uncommonly induce remission.
Radioactive iodine is the definitive treatment in those with small goiters, absence of
pressure symptoms, contraindications to surgery, or those who refuse surgery.

B. operation is indicated in large goiters, with pressure symptoms and it is the treatment
of choice in toxic MNG. Total or near total thyroidectomy usually leads to permanent
hypothyroidism which requires replacement therapy by thyroxine for life.

3. Solitary toxic nodule:

Radioactive iodine is the best option especially for those above 45 years because only
the nodule will take iodine and the remainder of the gland will remain functioning.

Surgery is indicated is indicated in younger patients where it involves excision of the

nodule together with lobe in which it is contained.

Thyrotoxicosis during pregnancy :

Radio iodine is strictly contraindicated.

Surgery during second trimester is safe.

Antithyroid drugs used carefully are usually safe.

Preparation of thyrotoxic patient for surgery

1. carbimazole 30-40 mg /day is given alone for 8-12 weeks until the patient becomes euthryoid
clinically and hormones level s (T3 , T4 , TSH) return to normal .

2. carbimazole 30-40mg /day + proranolol 40-80mg/ day for 10-14 days prior to surgery

3. propranolol 40-80 mg/day for 10-14 days prior to surgery. Propranolol wil abolish the clinical
manifestation of the toxic state by acting on target organs and not on the gland itself.

Preoperative investigations that should be done before thyroid surgery

1. thyroid function tests

2. indirect larngoscopy

3. thyroid antibodies

4. serum calcium estimation

5. an isotope scan in toxic MNG

postoperative complications

1. early:

a. hemorrhage : lead to tension hematoma deep to the cervical fascia. Usually due to slipping of
ligature on the sup. Thyr. Art. . the patient should be taken to theater and operation should be
 Permanent hypocalcemia -->removal of the glands.
Temporary hypocalcemia --> spasm of aa.

done under GA to control bleeding. A milder form of bleeding leading to subcutaneous

hematoma or seroma could be aspirated or evacuated under local anesthesia.

b. Respiratory obstruction; mostly due to laryngeal edema which the consequence of tension
hematoma. Very rarely obstruction is due to collapse or kink of trachea . trauma to the larynx
by the anesthesia tube or surgical manipulation are contributaory factors. Treatment by
steroids and reintubation for few days or tracheostomy.

c. Laryngeal nerve paralysis: may unilat or bilat. , transient or permanent .

Periorbital numbness d. Parathyroid insufficiency: 0.5% this is due to surgical removal of parathyroid glands or
(earliest), carpopedal
spasm, Trouesse's sign, infarction due to injury to its end artery. Present after 2-5 days after operation.
Chvostek's sign.
e. Thyrotoxic crisis: acute exacerbation of hyperthyroidism. It occurs when thyrotoxic patient is
not adequately prepared for surgery. Clinically the patient becomes dehydrated, restless and
hyperpyrexic. Treatment by cold iv fluids, cooling the patient, administration of O2 , diuretics
for heart failure, digoxin for uncontrolled atrial fibrillation, sedation and intravenous
hydrocortisone. Specific treatment by carbimazole and Lugol"s iodine 10 drops 8-hourly by
mouth. Propranolol could be given as 40 mg 6 hourly orally or iv 1-2mg slowly.

f. Wound infection
Incomplete injury --> adduction of vocal cords --> change in voice.
2. Late complications : Complete injury --> abduction of vocal cords --> aspiration during feeding.

a. hypertrophic or keloid scar.

Incomplete injury --> tracheostomy is needed.
b. stitch granuloma Complete injury --> Teflon mesh.

c. hypothyroidism

thyroiditis

hashimotos's thyroiditis

autoimmune disease of unknown cause . the thyroid is diffusely infiltrated by lymphoid and
plasma cells . in the early stages there may be thyrotoxicosis but usually end with hypothyroidism.
The gland is diffusely enlarged ,firm with irregular surface. Titers of Abs against thyroglobulin and
thyroid microsome are markedly elevated. FNA is used to cinfirm diagnosis. Management by
lifelong thyroxine replacement.

De Quervain's thyroididtis Patients are afraid of death! (because it is painful).

Some patients undergo surgery to relieve pain. (surgery is very difficult).
Viral infection leading to acute inflammatory reaction with histeocytes, multinucleated giant cells
and granuloma formation. Clinically there is acute pain in the neck and tender enlarged gland. It is
selflimiting and treated by analgesic and NSAIDs

Reidel's thyroiditis Localized nodules.

 Neoplasm of thyroid gland
Benign :

follicular adenoma present as solitary nodule. The only difference between follicular adenoma
and carcinoma is the invasion of the capsule , so the diagnosis depend on hitological examination .
treatment by wide local excision ( lobectomy.

Malignant tumors

1. Differentiated ( origin from follicular cells) Give Iodine after surgery (to kill metastasized cells)

Papillary carcinoma- 60%

Follicular carcinoma – 20%

2. undifferentiated ( anaplastic)- 10%

3. medullary carcinoma ( origin from parafollicular cells )-5%

4. lymphoma- 5%

5. secondary
The only treatment is total thyroidectomy. (to avoid
papillary carcinoma giving iodine in partial thyroidectomy, which will
destruct the normal tissues first and then you have to
give more to kill the cancer cells).
slow growing with good prognosis. Mostly related to irradiation before 5 years of age. Related to
ret/PTC1 or ret/PTC3 Ags.

The growth is multifocal with finger like tumor papillae are present histologically . there are typical
psammoma bodies. The tumor invades lymphatics and over 50% of patients have cervical lymph
node involvement at presentation. Blood born metastasis is unusual

The patient is euthryoid, and ultrasound shows a solid lesion with enlarged cervical lymph nodes .
The diagnostic investigation is FNA which shows papillary configuration.

Management:

1-the minimal procedure is total thyroid lobectomy with resection of the isthmus followed by
thyroid suppression by the thyroxine

2- Total thyroidectomy followed by Iodine 131 for therapeutic ablation.

Incase of cervical lymph node metastasis all the pretracheal , paratracheal or lymph nodes in the
jugular chain should be removed. If the jugular nodes are extensively involved, amodified neck
dissection should be carried out.
It is standard practice to give thyroxine in a dose of 0.1 to 0.2 mg daily to suppress TSH production.

Following surgery a whole body radio-iodine scan should be done to detect metastatic lesions which
are treated by large doses of radio-iodine.

Follicular Carcinoma:

Usually solitary nodule with invasion of the capsule and lymph node involvement is much less
common than in papillary carcinoma, blood-born metastases are twice as common as in papillary
carcinoma.

Management:

1. Lobectomy and resection of the isthmus with ablation with radio iodine and permanent thyroxine
replacement.

2. Total or near total thyroidectomy followed by radio-iodine ablation and thyroxine replacement.

Most differentiated tumors produce thyroglobulin therefore it is useful as a postoperative tumor

marker. Therefore annual measurement of thyroglobulin is used by many centers for follow up.

Undifferentiated carcinoma:

Usually occur in elderly women and are believed to arise from previously unrecognized
differentiated tumors, they are more common in endemic goiter areas.

Clinically there may be along standing goiter which has recently increased in size with possibly
pressure symptoms , the gland is hard woody with fixation to the surrounding structures , can be
diagnosed by FNAC or Open Biopsy with excision of as much as possible of the tumor especially the
isthmus and treated by external beam radiotherapy.

It has a very poor prognosis.

Medullary Carcinoma : Positron emission tomography

Tumors of the parafollicular ( C-cells ) derived from the neural crest which means that they produce
calcitonin ( more than 0.08 ng/ml ) which is considered as a very good tumor marker in the follow up
of those patients.

75% of these tumors are sporadic while 25% have genetic basis.

And it is inherited in an autosomal dominant manner and often multifocal and associated with other
endocrine disorders (MEN II ) usually presented as thyroid nodule or lymph node enlargement in the
neck and blood examination shows raised calcitonin and the diagnosis is confirmed by FNAC .

Management by total thyroidectomy and thyroid replacement therapy.

** Some notes about Thyroglossal cyst :

Normally the thyroid gland descends early in life from the

base of the tongue towards its position in the lower neck
with the isthmus lying over the 2nd and 3rd tracheal rings .
this cyst represent a persistence of this track and may
therefore be found anywhere in or adjacent to the midline
from the tongue base to the thyroid isthmus .

Clinical features
Classically the cyst moves upwards on swallowing and with
tongue protrusion due to attachment to the hyoid bone .
Thyroglossal cysts may become infected and rupture onto
the skin of the neck
presenting as a discharging sinus , although they often
occur in children they may also present in adults , even as
late as the sixth or seventh decade of life .

Treatment
Excision of the whole tract , which involves removal of the
body of the hyoid bone
and suprahyoid tract through the tongue base to the vallecula
at the site of the
primitive foramen caecum , together with a core of tissue on
either side . this
operation is known as Sistrunk’s operation and prevents
recurrence which might
occur from small branches of the original cyst .
Previous years questions about the thyroid gland

● Discuss the management of solitary thyroid nodule ?

● Discuss the management of diffuse goiter ?
● How would you prepare a patient with thyrotoxicosis for surgery ?
● Write on the postoperative complications of thyroid surgery ?
● Discuss the management of toxic multinodular goiter ?
● Write on each of the following :
A- Thyroglossal cyst B- Papillary CA of the thyroid gland
● Write short notes about the management of simple goiter ?
● Enumerate the various methods of treatment of toxic goiter ?
● What is the differential diagnosis of a solitary right thyroid nodule , write on the
methods of investigation to reach the diagnosis ?
● Enumerate only types of malignant thyroid gland tumors & discuss the
management of only one of them ?