Surgery (thyroid)

Anatomy: anterior triangle of neck. Below and lateral to the thyroid cartilage,
anterior to the cricoid cartilage. 2 lateral lobes (which cover the anterolateral
surfaces of the trachea, the cricoid cartilage, and the lower part of the thyroid
cartilage), isthmus (connects the lateral lobes and crosses the anterior surfaces of the
second and third tracheal cartilages) and pyramid.
Composed of follicles; an epithelial layer of cells encircling a lake of fluid that
contains a protein-rich follicular fluid. Principle protein component: “thyroglobulin.”

Lying deep to the sternohyoid, sternothyroid, and omohyoid muscles, it is in the

visceral compartment of the neck. This compartment includes the pharynx, trachea,
and esophagus and is surrounded by the pretracheal layers of fascia.

Embryology: follicular cells from foraemen caecum in the tongue, a median

outgrowth from the floor of the pharynx near the base of the tongue. During
embryological development, descends in midline to larynx, where it buds laterally. A
contribution of neural crest cells arising from the 4th branchial cleft gives rise to the C
cells of the thyroid.

The foramen caecum of the tongue indicates the site of origin and the thyroglossal
duct marks the path of migration of the thyroid gland to its final adult location. The
thyroglossal duct usually disappears early in development, but remnants may persist
as a cyst or as a connection to the foramen caecum (i.e. a fistula).
There may also be remains of the thyroid gland:
associated with the tongue (a lingual thyroid);
along the path of migration; or,
upward from the gland along the path of the thyroglossal duct (a pyramidal lobe).

Function: follicular cells produce, store and release thyroxine T4 and tri-
iodothyronine T3. C-cells produce calcitonin (calcium lowering)
Physiology: T3 & T4 are formed by iodination of tyrosine residues on the
thyroglobulin molecule and are thus part of the primary thyroglobulin molecule.
T4 and T3 remain part of thyroglobulin in the follicle lumen until thyroid secretion is
stimulated. It undergoes endocytosis by the follicular cell and is degraded within the
lysosomes of these cells
T4 is tightly bound to one of several binding proteins. It is carried to its sites of action
(nearly all the cells in the body). In the process of this transport, the liver and other
tissues take up some of the T4 and partially deiodinate it to T3; this T3 can then re-
enter the circulation.
Both T3 and T4 enter target cells and bind to cytosolic and nuclear receptors.
T3 has higher affinity than T4 for the thyroid hormone receptor. Even though it
accounts for only approximately 5% of the circulating thyroid hormone, T 3 is probably
the main effector of thyroid hormone signalling.
Comprises numerous follicles, filled with colloid and lined by follicular cells. These
follicular cells are responsible for the trapping of iodine and the synthesis of
thyroglobulin, which contains thyroid hormone as part of its primary structure. These
cells also secrete thyroglobulin-the major protein of the thyroid colloid-into the
lumen of the follicle. The thyroglobulin protein that is stored in the follicular lumen
contains numerous iodinated tyrosines and thyronines, which are derivatives of the
amino acid tyrosine. On command, the follicular cells take up the thyroglobulin and
release the thyroid hormones triiodothyronine (T3) and thyroxine, or
tetraiodothyronine (T4), into the blood

T3 is far more active than T4

Reverse T3 (rT3) has no known biologic activity. It has two iodines on its outer benzyl
ring, rather than two on its inner ring, as is the case for T3
All three compounds derive from the ether linkage of a tyrosine molecule to the
benzyl group of a second tyrosine molecule; one or two iodine atoms are attached to
each benzyl group.

Pathology: thyroid function (hypo/hyper), thyroid structure (nodular goiture, thyroid

neoplasms)

1. Disorders of embryological development

a. PATHOLOGY:
i. Remnants left along the thyroglossal tract
ii. Some respiratory epithelium may remain “thyroglossal duct
cyst”
 iii. Non-cystic benign thyroid nodule or thyroid cancer
b. PRESENTATION:
i. Childhood / adolescence
ii. Midline swelling with movement on protrusion of tongue
iii. Inflammation: abscess / fistula
c. INVESTIGATIONS
i. Exam, FNAC (but may precipitate inflammation)
d. TREATMENT
i. Surgery and skin crease incision
ii. Prevent recurrence: remove cyst and thyroglossal tract (excise
mid-portion of hyoid bone)
2. Benign thyroid nodules
a. PATHOLOGY:
i. 30-40% are a dominant nodule in a multinodular goitre
ii. Rest are benign nodules (simple thyroid cyst, solitary colloid
nodules, or benign follicular adenoma)
iii. 7% cancer, rest nodularity within thyroiditis
b. PRESENTATION:
i. Asymptomatic swelling
ii. Moves on swallowing
iii. Local pressure symptoms (dysphagia, cough, stridor, change in
voice, SVCO of thoracic inlet)
c. INVESTIGATIONS
i. TFT: TSH, free T3, T4 ?subclinical thyrotoxicosis or
autonomously functioning nodule
ii. FNAC: cannot distinguish adenoma from carcinoma – find
capsular or vascular invasion on histology
iii. USS / nuclear medicine in thyrotoxicosis or thyroiditis
iv. CT: define anatomy, retrosternal extension or compressive
symptoms

d. TREATMENT
i. Asymptomatic benign – active surveillance
 ii. Indications for surgery: obstructive symptoms, thyrotoxicosis,
findings of malignancy or atypical changes on FNAC or
cosmetic conditions
iii. Lobectomy
iv. Not thyroxine suppression
3. Multinodular goitre
a. PATHOLOGY:
i. Repeated cycles of hyperplasia, nodule formation,
degeneration and fibrosis
ii. Dominant nodule – hyperplastic or colloid nodule
iii. 7% cancer
iv. Familial incidence
v. Where iodine is deficient
b. PRESENTATION:
i. Asymptomatic
ii. Obstruction to trachea, oesophagus, RLN, SVC
iii. Thyrotoxicosis
c. INVESTIGATIONS
i. TFT
ii. FNAC
iii. CT
d. TREATMENT
i. Surgery: indications: obstruction, thyrotoxicosis, suspicions or
malignant changes on FNAC, presence of retrosternal
extension or hx or head and neck irradiation. If young:
cosmetic reasons. Surgical excision – total thyroidectomy
preferred, removes all tissue, later recurrence if subtotal is
30%
ii. Lifelong thyroxine
4. Thyroid cancer
a. PATHOLOGY:
i. From follicular cells, C cells or other cells e.g. lymphocytes or
stromal cell
ii. Papillary ca in 85%, 20-40yo, often multifocal, spreads to local
LN, good prognosis, 10 year survival 90%
iii. Follicular: older, 40-60yo, single tumour, metastasise by blood
stream, worse prognosis than papillary (10 year 75%)
iv. Anaplastic, undiff, in elderly – rapidly enlarging diffuse mass,
spreads locally (10 year 5%)
v. C cells – medullary ca, secretes calcitonin, MEN with phaeo
and hyperPTH (10 year 35%)
vi. Lymphoma in thyroid: arise in lymphocytes, often associated
with pre-existing Hashiomoto’s thyroiditis
vii. Squamous, sarcoma, mets
b. PRESENTATION:
i. Single thyroid nodule or dominant nodule in multi-nodular
goitre
 ii. Mets – follicular  bone; papillary  lymphangitic lung
involvement
c. INVESTIGATIONS
i. Exam, FNAC
ii. CT / MRI
iii. Serum calcitonin
d. TREATMENT
i. High / low risk
ii. PAPILLARY: risk based on prognostic scoring systems on age,
tumour size, invasiveness, presence of mets
iii. FOLLICULAR: histological – degree of capsular and vascular
invasiveness
iv. High risk: total, removal of nodes. Radioactive iodine I131 and
thyroxine suppression allows for detection and ablation of
mets
v. Low risk: lobectomy
vi. Medullary: total thyroidectomy, central lymph node dissection.
Does not respond to radio-ablation.
vii. Lymphoma: radioTx, chemoTx
viii. Anaplastic: radioTx
5. Thyrotoxicosis
a. PATHOLOGY:
i. Diffuse hypersecretory goitre (Graves’), toxic multinodular
(Plummer’s), toxic follicular adenoma, thyroiditis
ii. TSH pituitary tumour, struma ovarii
iii. Graves’: autoimmune, antibodies to TSH receptor
iv. Toxic nodular goitre results from autonomous activity in
hyperplastic / neoplastic nodule
b. PRESENTATION:
i. Thyrotoxicosis
ii. Graves’ – exopthalmos, pre-tibial myxoedema
iii. Local pressure / obstruction
c. INVESTIGATIONS
i. TFT, T3, T4
ii. Exam
iii. Nuclear scans
d. TREATMENT
i. Render euthyroid by antithyroid medication – propylthiouracil,
carbinazole (present coupling of iodotyrosine)
ii. Graves’ – medications 12-18m, ablation with radioactive iodine
(>40, teratogenic), subtotal thyoidectomy. Surgery only if
relapse or non-compliance.
6. Thyroiditis
a. PATHOLOGY:
i. Lymphocytic (Hashiomoto’s), subacute (de Quervain’s – post-
viral), acute (bacterial), fibrosing (Riedel’s)
b. PRESENTATION:
 i. Lymphocytic thyroiditis may be hyperthyroidism (early),
hypothyroidism (late) or may present with nodular or diffuse
goitre
ii. Subacute thyroiditis: tender, enlarged, firm thyroid gland,
systemic headache, malaise, weight loss
c. INVESTIGATIONS
i. TFT
ii. Nuclear medicine scan – patchy lymphocytic thyroiditis uptake
d. TREATMENT
i. Subacute: high dose steroids, aspirin therapy (takes 3-6m to
fully resolve)
ii. Lymphocytic thyroiditis may respond to thyroxine suppression.
iii. Surgery of persistent, suspicions, pressure

Damage to RLN, external br of sup laryngeal nerves, PTH

Physiology