THYROID DISEASE

PRESENTATION BY: PIMUNDU VICENT

AUDO RITAH
TUTOR: DR. FUALAL JANE
OBJECTIVES
 To discuss the anatomy of the thyroid gland.
 To discuss the embryology of the thyroid gland.
 To discuss the histology and physiology of the thyroid gland.
 To discuss the congenital anomalies affecting the thyroid
gland, their clinical features, diagnosis and treatment.
 To discuss the classification of goitre, the clinical features,
diagnosis and treatment of goitre.
 To discuss hypothyroidism and hyperthyroidism,
investigations and their management.
ANATOMY
 The thyroid gland weighing 20-40g lies deep to the sternothyroid and
sternohyoid muscles, located anteriorly in the neck at the level of the C5–
T1 vertebrae. It is butterfly shaped consisting primarily of the right and left
lobes anterolateral to the larynx and trachea, the two lobes connected by a
relatively thin isthmus that lies over the trachea(usually around the 2 nd &3rd
tracheal rings). Each lobe is 5 × 3 × 1.5 cm in size, extends from the middle
of thyroid cartilage to 6th tracheal ring and the right lobe is larger than the
left. It is surrounded by a thin fibrous capsule that sends septa deep into the
gland. External to the capsule is a loose sheath formed by the visceral
portion of the pretracheal layer of deep cervical fascia. The sheath attaches
the gland to the trachea and larynx.
Continuation…
 Pyramidal lobe is upward extension as fibrous strands or muscular strands from
the junction of the isthmus and left lateral lobe. It is seen in 30% of individuals.
 Berry’s ligament is a strong condensed vascular connective tissue between the
lateral lobe and cricoid cartilage on each side.
 The gland is highly vascularized, supplied by the superior and inferior thyroid
arteries which lie between the fibrous capsule and fascial sheath. The superior
thyroid artery supplies the anterosuperior aspect of the gland, the inferior supplies
the posteroinferior aspect and inferior pole of the gland. The right and left
superior and inferior thyroid arteries anastomose extensively within the gland
ensuring supply and also potential collaterals between the subclavian and external
carotid vessels. The thyroid ima artery supplies the isthmus of the gland.
VENOUS DRAINAGE
 Three pairs of veins that form venous plexus on the anterior aspect of the thyroid

gland and anterior to the trachea drain the gland.

 The superior thyroid vein, which drains into the internal jugular vein

 The middle thyroid vein, which drains into the internal jugular vein.

 The inferior thyroid veins drain into the left brachiocephalic vein in the thorax

LYMPH DRAINAGE
 The lymph from the thyroid gland drains mainly laterally into the superior and

inferior deep cervical lymph nodes.

 A few lymph vessels descend to the pre-tracheal, paratracheal and pre-laryngeal

lymph nodes, which eventually drain into the deep cervical lymph nodes
NERVE SUPPLY
 Superior, middle, and inferior cervical sympathetic ganglia reach the gland through

the cardiac and superior and inferior thyroid peri-arterial plexuses that accompany
the thyroid arteries. Nerve supply is vasomotor not secretory.
RELATIONS OF THYROID GLAND

 ANTEROLATERALLY : The sternothyroid, the superior

belly of the omohyoid, the sternohyoid, and the anterior
border of the sternocleidomastoid.

 POSTEROLATERALLY: The carotid sheath with the

common carotid artery, the internal jugular vein, and the
vagus nerve.

 MEDIALLY :
Organs – larynx, pharynx, trachea and oesophagus
Nerves – external laryngeal and recurrent laryngeal

 POSTERIORLLY : superior and inferior parathyroid glands

and the anastomosis between the superior and inferior
thyroid arteries.
 EMBRYOLOGY
 The thyroid gland develops from the endodermal lining of the floor of the
primitive pharynx.
 It appears as an epithelial proliferation in the floor of the pharynx between the
tuberculum impar and the copula at a point later indicated by the foramen cecum.
 Subsequently the thyroid descends in front of the pharyngeal gut as a bi-lobed
diverticulum .
 During this migration, the thyroid remains connected to the tongue by a narrow canal,
the thyroglossal duct.
 This duct later disappears. With further development, the thyroid gland descends in
front of the hyoid bone and the laryngeal cartilages.
 It reaches its final position in front of the trachea in the 7 th week .
 By then it has acquired a small median isthmus and two lateral lobes and a portion of
the duct forms pyramidal lobe.
 The thyroid begins to function at approximately the end of 3 rd month, at which time
the first follicles containing colloid become visible.
 Follicular cells produce the colloid that serves as a source of thyroxine(T4) and
triiodothyronine(T3).
 HISTOLOGY
 The thyroid gland is composed of large numbers of closed follicles (100 to
300 mm in diameter)
 They are filled with a secretory substance called colloid and lined with
cuboidal epithelial cells that secrete into the interior of the follicles.
 The major constituent of colloid is the large glycoprotein thyroglobulin,
which contains the thyroid hormones.
 Once the secretion has entered the follicles, it must be absorbed back through
the follicular epithelium into the blood before it can function in the body.
 The thyroid gland has a blood flow about 5 times the weight of the gland
each minute, which is grater than any other area of the body, with the possible
exception of the adrenal cortex.
 The thyroid gland also contains C cells that secrete calcitonin, a hormone that
contributes to regulation of plasma calcium ion concentration.
 PHYSIOLOGY
Thyroid gland has two secretory cells:
1. Follicular cells—secretes thyroid hormones (Thyroxine (T4), Tri-iodothyronine (T3).
2. Parafollicular cells (‘C’ cells)—secretes calcitonin.
 The hypothalamus-pituitary-thyroid axis regulates thyroid hormone production and release in a classic feedback
system.
 TRH is a regulatory hormone from hypothalamus and TSH is a regulatory hormone from anterior pituitary
Thyroid Hormone Synthesis
 Ninety per cent of body iodide uptake is in the thyroid gland, whose uptake into the follicular cells is regulated
by TSH and follicular iodide content.
 The hormones tri-iodothyronine (T3) and thyroxine (T4) are bound to thyroglobulin within the colloid.
Synthesis within the thyroglobulin complex is controlled by several enzymes, in distinct steps:
 trapping of inorganic iodide from the blood;
 oxidation of iodide to iodine;
 binding of iodine with tyrosine to form iodotyrosine;
 coupling of monoiodotyrosines and di-iodotyrosines to form T3 and T4.
When hormones are required, the complex is resorbed into the cell and thyroglobulin is broken down. T3 and T4 are
liberated and enter the blood, where they are bound to serum proteins: albumin, thyroxine-binding globulin (TBG) and
thyroxine-binding prealbumin (TBPA). The small amount of hormone that remains free in the serum is biologically active.
 CONGENITAL ANOMALIES
Athyrosis
 It is total absence of lateral lobes and isthmus (non-visualised thyroid glands) with

hypothyroidism.
 This is rare but can be clinically important.

 It leads to confusion in diagnosis, as it can be confused with ectopic thyroid glands,

ectopic thyroid glands and thyroid hypoplasia.

ECTOPIC THYROID
 Failure of the thyroid fails to descend from the thyroid anlage region to its final

location in front of the trachea is called an ectopic thyroid.

  Ectopic thyroid can present at any position from the foramen caecum at the base of

the tongue or in the upper part of the neck in midline, or intrathoracic region
 Carcinoma develops more commonly in ectopic thyroid tissue than normal thyroid

 The most common thyroid location in the ectopic cases is the Lingual thyroid
LINGUAL THYROID

It is a thyroid swelling in the posterior third of tongue, at the foramen

caecum, presenting as rounded swelling (pink round strawberry like
mass).
Lingual thyroid may cause :
a. Dysphagia, pain, speech impairment, stomatolalia (speech with
clogged nostrils), foreign body sensation, cough, snoring, sleep apnea.
b. Respiratory obstruction, hemorrhage.
c. 70% present as hypothyroidism, 10% as cretinism.
d. Common in females (3:1).
e. Symptoms coincide with puberty, pregnancy.
Any diseases which can occur in normal thyroid can also occur in lingual
thyroid, i.e. nodularity, toxicity, malignancy (If turns malignant, follicular
carcinoma is more common, papillary carcinoma is very rare).
.
DIAGNOSIS
 Radioisotope study.

 Ultrasound neck has to be done to see the absence of

thyroid in normal location.

 MRI is very useful in lingual thyroid.

 Endoscopy guided FNAC/tissue biopsy is done to

confirm or lingual thyroid is suspected to be

pathological.
 Thyroid function tests should be done. Commonly, it

is hypothyroid but rarely can be toxic.

TREATMENT
 L-thyroxine is given daily orally.

 Surgical excision is indicated in a large lingual thyroid

with obstructive features, bleeding, ulceration, cystic

degeneration or malignant transformation
 Radioisotope therapy for ablation is also often used.
THYROGLOSSAL CYST
 Thyroglossal cyst is a swelling occurring in the neck or in any part along the line of thyroglossal
tract.
 It is due to failure of the thyroglossal duct/tract to obliterate completely; there will be persistent
duct at certain part forming cystic swelling containing mucus fluid.
 Sometimes, thyroid may not be present in the normal site but may be present in the wall of the
thyroglossal cyst.
 It is a tubulodermoid type of cyst.
Possible sites for thyroglossal cyst:
a. Beneath the foramen caecum
b. In the floor of mouth
c. Suprahyoid
d. Subhyoid—commonest site
e. On the thyroid cartilage—2nd common site.
CLINICAL FEATURES
 Swelling in the midline, towards the left.
 Moves with deglutition as well as with the protrusion of tongue.
 Non-tender, mobile, often transilluminant.
 Thyroid fossa is empty, if there is no thyroid in normal location.
 Thyroglossal cyst can get infected and may form an abscess.
 Cyst wall contains lymphatic tissue and so infection is common.
 Malignancy can develop in thyroglossal cyst (papillary carcinoma)—1%. Cyst will be harder, fixed, with
palpable neck nodes.
 If biopsy report is papillary carcinoma, then complete thyroidectomy.
 If neck nodes are present, node dissection, and radioactive iodine therapy with suppressive dose of L thyroxine
0.3 mg OD is needed.
 Incidence is equal in both sexes.
Investigations
a. Radioisotope study.
b. Ultrasound neck; T3, T4, TSH estimation.
c. FNAC from the cyst.
Treatment
a. Sistrunk operation: Excision of cyst and also full tract up to the foramen caecum is done along with removal
of central part of the hyoid bone, as the tract passes through it.
b. b. If there is no normal thyroid gland after the surgery, maintenance dose of L-thyroxine 0.1 mg OD is given
life long.
Note: If tract is not completely excised, it will result in thyroglossal fistula.
THYROGLOSSAL FISTULA
 It is not a congenital condition. It is acquired.
 It either follows infection of thyroglossal cyst which bursts open or after inadequate removal of the cyst.
 It is lined by columnar epithelium, discharges mucous and is a seat of recurrent inflammation.
 “Hood sign” is characteristic
 Peculiar crescentic appearance is called as semilunar sign.
 It secretes mucus discharge.
 Site of the fistula is just below the hyoid bone commonly; in infants it may be much lower.
Investigations: Radioisotope study and fistulogram.
Treatment: Sistrunk operation.
Note: One more Sistrunk operation is done in case of lymphoedema.
Lateral Aberrant Thyroid
 It is at present considered as a misnomer.

 It is a mass of tissue having the structure of a normal or

pathologic thyroid gland situated at a definite distance from

the normal thyroid gland with which it has no connection.
 They occur as a result of an anomaly in the development of the

thyroid gland
 It is the metastasis into cervical lymph node from a papillary

carcinoma of thyroid.
 Histologically these tumours are not composed of normal

thyroid tissue but have a papillary structure indistinguishable

from that of papillary tumors of the thyroid.
 FNAC has to be done and treated as papillary carcinoma of

thyroid.
Goitre
 The term goitre 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.
Thyrotoxicosis and hyperthyroidism
Thyrotoxicosis is the clinical, physiological and biochemical effect of thyroid hormone excess on target
tissues.
Hyperthyroidism is a syndrome associated with excess thyroid hormone production. It is always associated
with thyrotoxicosis BUT THE REVERSE IS NOT TRUE!!

 Symptoms f hyperthyroidism
Gastrointestinal symptoms :weight loss in spite of increase appetite ,diarrhea
Cardiovascular symptoms: include palpitations, shortness of breath on min. exertion or rest, angina,
cardiac irregularity, cardiac failure in elderly.
Genitourinary symptom: including oligo- or amenorrhea and occasional urinary frequency
integumentary symptoms : hair loss , pruritus , palmar erythema
Psychiatry: irritability ,nervousness, insomnia
Neuromuscular: undue fatigue and muscle weakness, tremor
Signs of thyrotoxicosis
Eye signs :
 Stellwag’s sign – Absence of normal blinking.

 Lid lag’s sign – It is inability of the upper eyelid to keep pace with the eyeball when

it looks downward to follow the examiner finger.

 Joffroy’s sign – Absence of wrinkling on forehead when patient looks up.

 Moebius sign- Lack of convergence of eyeball

Cardiac: tachycardia, wide pulse pressure, persistent atrial fibrillation

Myopathy: weakness of proximal muscles occurs i.e. the front thigh muscles, arm
muscles
Clinical types of thyrotoxicosis
 Diffuse toxic Goitre-(Graves disease)
 Toxic multinodular goitre-(Plummer disease)
 Toxic nodule
 Thyrotoxicosis due to rarer causes:-
a. iodine induced thyrotoxicosis (Jod-Basedow phenomenon)
b. Sub acute thyroiditis ( de Quervian thyroididtis)
c. Postpartum thyroiditis
d. Thyroid adenomas
Investigations for thyrotoxicosis

• Thyroid hormone panel , TSH T3, T4

• Radioactive iodine uptake
• Thyroid antibody estimation, anti-TPO, anti-Trab
• Ultrasound scan for nodular masses.
• ECG for atrial fibrillation
• X-ray bones/ bone scan for osteoporosis
Histology of thyrotoxicosis

In hyperthyroidism there is hyperplasia of acini, which are lined by high columnar

epithelium. Many of them are empty, and others contain vacuolated colloid with a
characteristic ‘scalloped’ pattern adjacent to the thyrocytes
Treatment
 Anti thyroid drugs.
 Antithyroid drugs are used to restore the patient to a euthyroid state and to maintain
this for a prolonged period in the hope that a permanent remission will occur.
Carbamizole and propylthiouracil are commonly used. The anti thyroid drugs cant
cure a toxic nodule.

 Advantages. No surgery and no use of radioactive materials.

 Disadvantages. Treatment is prolonged and the failure rate is at least 50%. The
duration of treatment may be tailored to the severity of the toxicity, with milder cases
being treated for only 6 months and severe cases for 2 years before stopping therapy.
 Treatment

 Radioiodine
Radioiodine destroys thyroid cells and reduces the mass of functioning thyroid tissue to
below a critical level.
● Advantages. No surgery and no prolonged drug therapy.
● Disadvantages. Isotope facilities must be available. The patient must be quarantined
while radiation levels are high and avoid pregnancy and close physical contact,
particularly with children. Eye signs may be aggravated.

 Surgery
In diffuse toxic goitre and toxic nodular goitre with overactive internodular tissue,
surgery cures by reducing the mass of overactive tissue by reducing the thyroid below a
critical mass.
There are however, the long-term risks of recurrence and eventual thyroid failure.
 THYROIDECTOMY
1. Hemithyroidectomy: Along with removal of one lobe, entire isthmus is removed. It is done in benign diseases of only
one lobe. It is also done in follicular neoplasm involving only one lobe. Solitary toxic or nontoxic nodule, thyroid cyst
are other indications.

2. Subtotal thyroidectomy commonly done in toxic thyroid either primary or secondary and also often for nontoxic
multinodular goitre. Here about 8 grams, or a tissue, size of pulp of finger is retained on lower pole, on both sides and rest of
the thyroid gland is removed. It is also done in MNG.

3. Partial thyroidectomy (By Thomas) is removal of the gland in front of trachea after mobilization. It is done in nontoxic
multinodular goitre. Its role is controversial.

4. Near total thyroidectomy: Here both lobes except the lower pole (one or other sides) which is very close to recurrent
laryngeal nerve and parathyroid is removed (To retain blood supply to parathyroids). It is done in case of papillary
carcinoma of thyroid. Here less than 2 grams of thyroid tissue is left behind near its lower pole on one side usually opposite
side of the diseased, occasionally on both sides.

5. Total thyroidectomy: Entire gland is removed. It is done in case of follicular carcinoma of thyroid, medullary carcinoma
of thyroid.

6. Hartley Dunhill operation is removal of one entire lateral lobe with isthmus and partial/subtotal removal of opposite
lateral lobe. It is done in non-toxic multinodular goitre. 4 grams of tissue is left behind only on one side.
Complications of thyroidectomy
Metabolic
 Hypoparathyroidism

• Temporary hypoparathyroidism
• Temporary hypocalcaemia without hypoparathyroidism (hungry bone syndrome) Permanent
hypoparathyroidism
• Spurious hypoparathyroidism (total calcium is less but ionized calcium is normal) Thyroid crisis
• Hypothyroidism/thyroid failure/myxedema

Intraoperative
• Hemorrhage; – primary and reactionary

• Vascular complications which include hematoma formation and Compromised tracheo-oesophageal blood

supply.
• Nerve injuries; External laryngeal nerve injury – pitch of the voice is lost, Recurrent laryngeal nerve injury
Complications of thyroidectomy
Immediate postoperative
 Hematoma, Laryngeal oedema, Respiratory obstruction – stridor, Hypoparathyroidism,

RLN injury and its problems

Late postoperative
• Hypothyroidism
• Recurrent nodule
• Recurrent toxicity
• Wound infection
• Granuloma/keloid
Other complications; Hypothyroidism, Recurrent nodule, Recurrent toxicity, Wound
infection Granuloma/keloid
 HYPOTHYROIDISM
Failure of the thyroid gland to produce sufficient thyroid hormones to meet the metabolic demands of the body
Types of hypothyroidism:
Primary: Is due to thyroid diseases or removal of the thyroid
Secondary: Occurs when hypothalamic-pituitary axis is damaged, e.g. Pituitary adenoma, Tumors impinging
on the hypothalamus, Sheehan syndrome, Drugs e.g. dopamine, prednisolone, opioids, TRH resistance, TRH
deficiency
Tertiary : due to hypothalamic diseases
Causes
• Thyroidectomy
• Agenesis or dysgenesis
• Enzyme deficiency
• Iodine deficiency
• Hashimoto’s thyroiditis
• Antithyroid drugs
• Radioiodine
• Drugs: Lithium, amiodarone
Clinical features
General: Tiredness, weight gain, cold intolerance, goitre, hyperlipidaemia
Cardiovascular: Bradycardia, angina, cardiac failure, pericardial effusion.
 Hematological: Anaemia.
Dermatological: Dry skin, vitiligo, alopecia, erythema.
 Reproductive: Infertility, menorrhagia, galactorrhoea.
 Gastrointestinal: Constipation, ileus.
 Developmental: Growth and mental retardation, delayed puberty.
 Other features: Carpal tunnel syndrome, myalgia, hoarseness,
deafness, ataxia, depression, psychosis (Myxedema madness).

Investigations
T3, T4 estimation.
TSH level estimation which is higher.

Treatment
 Replacement with L-thyroxine 100 to 150 µg/day. In old patients with ischemic heart disease initial
therapy is with 25–50 µg/day and then gradually increased up to the required dose.
 Initial rapid response can be achieved by giving L iodothyronine 20 μg tid.
Thyroid gland neoplasms
Benign Follicular adenoma
Malignant Primary Follicular epithelium Follicular ( 10%)
– Papillary( 80%)
differentiated
Follicular epithelium Anaplastic ( 5%)
_
poorly differentiated

Parafollicular cells Medullary ( 2.5%)

Lymphoid cells Lymphoma ( 2.5%)

Secondary Metastatic especially from renal

cell carcinoma
Local infiltration (from pharynx and
esopahgus)
Benign tumors
 Follicular adenomas
 present as clinically solitary nodules and the distinction between a
follicular carcinoma and an adenoma can only be made by
histological examination; in the adenoma there is no invasion of the
capsule or of pericapsular blood vessels. For this reason, FNA, which
provides cytological detail but not tissue architecture, cannot
differentiate between benign and malignant follicular lesions.
Diagnosis and treatment is therefore, by wide excision, i.e. total
lobectomy.
Malignant tumors
 Vast majority of primary malignancies are carcinomas derived from the follicular
cells. Such tumors were thought of as differentiated (papillary, follicular and
Hürthle cell) and undifferentiated (anaplastic).
 Lymph node and blood-borne metastases of thyroid cancer occur primarily to
bone and lung and may be the mode of presentation.
 Etiology
 Papillary carcinomas often are due to irradiation. The incidence of follicular
carcinoma is high in endemic goitrous areas, possibly due to TSH stimulation.
Malignant lymphomas sometimes develop in autoimmune thyroiditis, and the
lymphocytic infiltration in the autoimmune process may be an etiological factor.
Papillary carcinoma
 It is the most common thyroid malignancy
 At autopsy of people who died of causes other than thyroid disease,
up to 40% of individuals have deposits of PTC suggesting that many
people live with the disease undetected.
 Has a high propensity for lymph node metastases especially among
the young patients, but doesn’t affect excellent survival.
 Papillary micro carcinomas( <10mm lesions of PTC) are commonly
found in excised tissue from benign thyroid resections. However, they
don’t confer recurrence and progression of disease.
Follicular carcinoma
 It has to be differentiated from follicular adenoma by cytology.
 Multiple foci of follicular carcinoma are seldom seen and lymph node
involvement is much less common than in papillary carcinoma.
 Blood-borne metastases are more common and the eventual mortality
rate, although still low, is twice that of papillary cancer.

 Prognosis of both papillary and follicular carcinomas is generally

excellent. Older patients, those with large tumors, distant metastases
and extra-thyroid extension have worse outcomes.
 Follicular carcinoma

Capsule and blood vessel invasion

Anaplastic carcinoma
 The most aggressive malignancies in humans. Thankfully it is rare.
 It may develop de novo, or present as Dedifferentiation of a papillary or
poorly differentiated carcinoma.
 The disease is characterized by rapid growth, visceral invasion and distant
metastases.
 Thyroid lymphoma can be incorrectly diagnosed as anaplastic cancer and so
biopsy is critical. This can be done using a core or open technique.
 Management is controversial. Almost all patients will be dead within 6
months. Radiotherapy and chemotherapy have not been shown to improve
survival.
Medullary carcinoma
 These are tumors of the parafollicular (C cells).
 The cells have a characteristic amyloid stroma is seen on histological
analysis.
 Tumors are not TSH dependent and do not take up radioactive iodine
 High levels of serum calcitonin and carcinoembryonic antigen are produced
by many medullary tumors, which should be tested for in suspected cases.
Calcitonin levels fall after resection and rise again with recurrence, making it
a valuable tumor marker in the follow-up of patients with this disease.
 Diarrhea is a feature in 30% of cases and this may be due to 5-
hydroxytryptamine or prostaglandins produced by the tumor cells.
Continuation
 The familial form of the disease frequently affects children and young adults, whereas
the sporadic cases occur at any age with no sex predominance.
 Medullary carcinoma may occur in combination with adrenal phaeochromocytoma and
hyperparathyroidism (HPT) (usually due to hyperplasia) in the syndrome known as
multiple endocrine neoplasia type 2A (MEN-2A).
 When the familial form is associated with prominent mucosal neuromas involving the
lips, tongue and inner aspect of the eyelids, with a Marfanoid habitus, the syndrome is
referred to as MEN type 2B.
 The prognosis is variable and depends on the stage at diagnosis. Any nodal involvement
virtually eliminates the prospect of cure and, unfortunately, even small tumors confined
to the thyroid gland may have spread by the time of diagnosis, particularly in familial
cancers.
References
 Bailey and love’s short practice of surgery 27th edition
 SRB Manual of surgery 5E 2016