Thyroid Gland summarised review

1. Hiba Hamid
THYROID
Surgical anatomy
 Normal thyroid gland weighs 20-25 g.
 Functioning unit is the lobule, supplied by a single arteriole, has 24-40 follicles lined with
cuboidal epithelium. Follicle contains colloid which stores thyroglobulin.
 Normal parathyroid gland weighs about 50 mg. Has a characteristic orange / brown colour.
Physiology
Thyroxine
 Hormones tri-iodothyronine (T3) and ʟ-thyroxine (T4) are bound to thyroglobulin within the
colloid.
 Synthesis consists of following distinct steps:
 Trapping of inorganic iodide from the blood
 Oxidation of iodide to iodine
 Binding of iodine with tyrosine to form iodotyrosines
 Coupling of mono-iodotyrosine and di-iodotyrosine to form T3 and T4
 T3 and T4 when entered into the blood, bind to serum proteins:
 Albumin
 Thyroxine binding globulin (TBG)
 Thyroxine binding prealbumin (TBPA)
 Small amt. of free circulating hormone is biologically active
 Metabolic effects of thyroid hormones are due to the free unbound T3 and T4.
 T3 is more important physiological hormone. Also produced peripherally by conversion of
T4 to T3.
 T3 is quick acting = within a few hours
 T4 acts more slowly = 4-14 days
Parathormone
 Secreted by parathyroid glands
 Is 84-amino acid peptide

2. Hiba Hamid
 Controls level of serum calcium in ECF
 PTH is released in response to low serum calcium level, or high serum magnesium level.
 PTH:
 Activates osteoclasts to resorb bone
 Increases calcium reabsorption from urine
 Renal activation of Vit. D
 Subsequent increased gut absorption of calcium
 Renal excretion of phosphate also increased
Calcitonin
 Produced by parafollicular C cells
 They are of neuro-endocrine in origin and arrive in thyroid via ultimobranchial body
 Produce calcitonin, which is a serum marker for recurrence of medullary thyroid cancer
Pituitary-Thyroid axis
 Synthesis and production of thyroid hormones from thyroid is controlled by thyroid
stimulating hormone (TSH) from anterior pituitary
 Secretion of TSH is controlled by circulating thyroid hormones and is modified in a classic
negative feedback manner
 In hyperthyroidism = hormone levels in blood are high and TSH levels are suppressed
 Opposite is true in hypothyroidism
 Regulation of TSH is also controlled by action of thyrotrophin releasing hormone (TRH)
from hypothalamus.
Tests of Thyroid Function
Serum Thyroid Hormones
 Serum TSH
 TSH levels can be measured accurately down to very low serum levels with an
immunochemiluminometric assay

3. Hiba Hamid
 When serum TSH is within normal range, it is considered redundant to measure T3
and T4 levels.
Thyroid functional
state
TSH (0.3-3.3 mU/L) Free T4 (10-30
nmol/L)
Free T3 (3.5-7.5
µmol/L)
Euthyroid normal normal normal
Thyrotoxic undetectable high high
Myxoedema high low low
Suppressive T4
therapy
undetectable high high (often normal)
T3 toxicity low / undetectable normal high
 Euthyroid state: T3, T4, and TSH are normal
 Florid thyroid failure: depressed T3 and T4 levels, gross elevation of TSH
 Incipient / developing thyroid failure: low normal values of T3 and T4, elevation of
TSH
 Toxic states: TSH levels are suppressed and undetectable
 Thyroxine (T4) and Tri-iodothyronine (T3)
 Transported in plasma bound to specific proteins
 Only a small fraction is free and physiologically active. (0.03% of T4 and 0.3% of
T3)
Thyroid Auto-antibodies
 Serum levels of antibodies against thyroid peroxidase (TPO) is useful in determining cause
of thyroid dysfunction and swellings
 Autoimmune thyroiditis may be associated with:
 Thyroid toxicity
 Thyroid failure
 Euthyroid goiter

4. Hiba Hamid
 Levels above 25 units/mL for TPO antibody, titres of greater than 1:100 for antithyroglobulin
are considered significant.
 TSH receptor antibodies are often present in Graves’ disease. They are largely produced
within the thyroid gland itself.
Summary
Thyroid investigations
Essential
 Serum: TSH (is T3 and T4 are abnormal); thyroid autoantibodies
 FNAC of palpable discrete swellings; ultrasound guidance
Optional
 Corrected serum calcium
 Serum calcitonin
 Imaging: CXR and thoracic inlet if tracheal deviation / retrosternal goiter; U/S, CT, and
MRI scan for known cancer, come re-operations and some retrosternal goiters; isotope
scan if discrete swelling and toxicity coexist
Thyroid Imaging
Chest and thoracic inlet x-rays
 To confirm presence of significant retrosternal goitre and clinically important degrees of
tracheal deviation and compression
 Pulmonary metastasis may also be detected.
Ultrasound scanning
 Gives good anatomical images of thyroid and other surrounding structures
 Drawback may be that it may reveal thyroid swellings that are not clinically relevant leading
to unnecessary investigations, interventions and patient anxiety
 If done by experienced sonologists, can reduce number of unsatisfactory FNAC samples by
permitting more targeted sampling

5. Hiba Hamid
 Very reliable in identifying nodes involved in thyroid cancer and identification of larger
parathyroid adenomas.
Computed Tomography (CT), Magnetic Resonance Imaging (MRI), and Positron Emitted
Tomography (PET) Scanning
 Routine CT and MRI reserved for assessment of known malignancies, assess extent of
retrosternal goitre and occasionally recurrent goitres.
Isotope scanning
 Uptake by thyroid of low dose of either radiolabelled iodine or the cheaper technetium
demonstrates activity in whole gland.
 Routine isotope imaging is unnecessary and inappropriate for distinguishing benign from
malignant tumours because majority (80%) of ‘cold’ swellings are benign and some (5%)
functioning or ‘warm’ swellings are malignant
 Principal value is in a toxic patient with a nodule or nodularity in the thyroid.
 Localization of overactivity within the thyroid will differentiate between toxic nodule with
suppression of the rest of the gland, and toxic multinodular goitre with several areas of
increased uptake
 Whole body scanning is used for metastasis demonstration, but pt. must have all normally
functioning thyroid tissue ablated either by surgery or radioiodine before scan is performed.
Fine needle aspiration cytology (FNAC)
 FNAC is investigation of choice in discrete thyroid swellings.
 Excellent patient compliance
 Simple and quick to perform in OPD
 Is readily repeated
 Results reported using standard terminology as follows:
Classification of fine-needle aspiration cytology reports
Thy1 non-diagnostic
Thy1c non-diagnostic cystic

6. Hiba Hamid
Thy2 non-neoplastic
Thy3 follicular
Thy4 suspicious of malignancy
Thy5 malignant
HYPOTHYROIDISM
Classification of Hypothyroidism
Autoimmune thyroiditis (chronic
lymphocytic thyroiditis)
Non-goitrous: primary myxoedema
Goitrous: Hashimoto’s disease
Iatrogenic After thyroidectomy
After radioiodine therapy
Drug induced (antithyroid drugs, para-
aminosalicylic acid and iodides in excess)
Dyshormonogenesis
Goitrogens
Secondary to pituitary or hypothalamic
disease
Thyroid agenesis
Endemic cretinism often goitrous and due to iodine deficiency
Cretinism (Fetal / Infantile Hypothyroidism)
 Consequence of inadequate thyroid hormone production during fetal / neonate development
 Endemic cretinism is due to dietary iodine deficiency
 Sporadic cases are due either to an inborn error of thyroid metabolism or complete / partial
agenesis of the gland.
 Hoarse cry, macroglossia, and umbilical hernia in a neonate along with features of thyroid
failure suggest the diagnosis.
 Immediate diagnosis and treatment with thyroxine is essential to prevent progressive mental
and physical developmental damage.
 Women taking antithyroid drugs may give birth to hypothyroid infants

7. Hiba Hamid
 Radioactive iodine must never be given to pregnant women.
Adult hypothyroidism
 The term myxoedema should be reserved for severe thyroid failure
 Signs of thyroid deficiency:
 Bradycardia
 Cold extremities
 Dry skin and hair
 Periorbital puffiness
 Hoarse voice
 Bradykinesis, slow movements
 Delayed relaxation phase of ankle jerks (most useful clinical sign in making the
diagnosis)
 Symptoms of thyroid deficiency are:
 Tiredness
 Mental lethargy
 Cold intolerance
 Weight gain
 Constipation
 Menstrual disturbance
 Carpal tunnel syndrome
 Thyroid function tests:
 Show low T3 and T4 levels
 High TSH (except in rare event of pituitary failure)
 High serum levels of TPO antibodies = characteristic of autoimmune disease
 Treatment:
 Oral thyroxine (0.10-0.20 mg) once daily is curative
 Caution required in elderly and those with cardiac disease. Replacement dose is
commenced at 0.05 mg daily and increased cautiously.
 If rapid dose required, tri-iodothyronine 20 µg three times a day is used

8. Hiba Hamid
 Myxoedema:
 Signs and symptoms of hypothyroidism are accentuated
 Supraclavicular puffiness
 Malar flush
 Yellow tinge to the skin
 Myxoedema coma: altered mental state, hypothermia, and precipitating medical
condition like cardiac failure or infection, can be fatal
 Treatment: thyroid replacement, either bolus of 0.50 mg T4 or 10 µg T3
intravenously or orally every 4-6 hours.
 If body less than 30 degrees C, patient must be warmed slowly
 IV broad spectrum antibiotics and hydrocortisone recommended
Dyshormonogenesis
 Genetic deficiencies of enzymes controlling synthesis of thyroid hormones account for
minority of cases of neonatal hypothyroidism and goitre
 Inherited in autosomal recessive pattern
 Family history is common
 If biochemical effect is moderate, thyroid enlargement is the only manifestation, and
dyshormonogenesis should be only considered in young patients with Euthyroid goitre
THYROID ENLARGEMENT
 Normal thyroid gland is impalpable
 Goitre: generalized enlargement of the thyroid gland

9. Hiba Hamid
Classification of thyroid swellings
Simple goitre (euthyroid) Diffuse hyperplastic
Multinodular
Physiological
Pubertal
Pregnancy
Toxic Diffuse (Graves’ disease)
Multinodular
Toxic adenoma
Neoplastic Benign
Malignant
Inflammatory Autoimmune
Granulomatous
Fibrosing
Infective
Other
Chronic lymphocytic thyroiditis.
Hashimoto’s disease.
De Quervain’s thyroiditis.
Riedel’s thyroiditis.
Acute (bacterial thyroiditis, viral
thyroiditis, subacute thyroiditis).
Chronic (tuberculous, syphilitic).
Amyloid
Simple goitre
Etiology
 Develops as a result of overstimulation of the thyroid gland by TSH as a result of
inappropriate secretion from a microadenoma from anterior pituitary, or chronically low
levels of circulating thyroid hormones.
 Important factor in endemic goitre is iodine deficiency.
 Daily requirement of iodine is about 0.1-0.15 mg.
 All types of simple goitre are more common in females than males owing to the presence of
oestrogen receptors in the thyroid tissue

10. Hiba Hamid
Diagnosis
 Usually straightforward
 Patient is euthyroid
 Nodules are palpable and often visible
 They are smooth, usually firm, not hard, goitre is painless, moves freely on swallowing
 Hardness and irregularity, due to calcification, may simulate carcinoma
 Painful nodule, sudden appearance or rapid enlargement of nodule raises suspicion of
carcinoma, but is usually due to hemorrhage into a simple nodule
Investigations
 Thyroid function to exclude mild hyperthyroidism, and presence of circulating antibodies
tested to differentiate from autoimmune thyroiditis.
 Plain radiographs of chest and thoracic inlet to demonstrate significant tracheal deviation or
compression.
 FNAC only required for dominant swelling in generalized goitre.
Complications
 Acute respiratory obstruction
 Secondary thyrotoxicosis
 Carcinoma
Prevention and treatment of simple goitre
 In early stages, hyperplastic goitre may regress if thyroxine is given in doses of 0.15-0.2 mg
daily for a few months
 Although nodular stage of simple goitre is irreversible, more than half of benign nodules
regress in size over a ten year period
 Most pts. with multinodular goitre are asymptomatic and don’t require operation
 Operation may be indicated:
 On cosmetic grounds
 for pressure symptoms

11. Hiba Hamid
 in response to pt. anxiety
 retrosternal extension with actual / incipient tracheal compression
 presence of dominant area of enlargement that may be neoplastic
 choice of surgical treatment in multinodular goitre:
 total thyroidectomy with immediate and lifelong replacement of thyroxine, or some
form of partial resection to conserve normal functioning thyroid tissue
 Subtotal thyroidectomy involves partial resection of each lobe, removal of bulk of
gland, leaving up to 8 g of normal tissue in each remnant.
 More often, multinodular change is asymmetrically distributed, which results in
getting a total lobectomy on the more affected side with either subtotal resection
(Dunhill procedure) or no intervention of the less affected side. However causative
factors persist and recurrence is common, also reoperation of recurrent nodular goitre
is more difficult and hazardous, therefore total thyroidectomy is performed.
 After subtotal resection, it is customary to give thyroxine to suppress TSH secretion
to prevent recurrence
Retrosternal goitre
Clinical features
 Often symptomless and discovered on routine chest radiographs
 Some severe symptoms if present include:
 Dyspnea, particularly at night, cough and stridor (harsh sound on inspiration)
 Dysphagia
 Engorgement of facial, neck, and superficial chest wall veins; in severe cases,
obstruction of superior vena cava
 Recurrent nerve paralysis is rare; goitre may also be malignant or toxic
 Chest and thoracic inlet radiographs show soft tissue shadow in superior mediastinum,
sometimes with calcification, often deviation or compression of trachea
 CT scan gives most accurate, and dramatic visualization

12. Hiba Hamid
HYPERTHYROIDISM
Thyrotoxicosis
Clinical types include:
 Diffuse toxic goitre (Graves’ disease)
 Toxic nodular goitre
 Toxic nodule
 Hyperthyroidism due to rare causes
Diffuse toxic goitre
 Graves’ disease, a diffuse vascular goitre appearing at the same time as hyperthyroidism
 Usually occurs in younger women
 Frequently associated with eye signs
 Syndrome is that of primary thyrotoxicosis
 50% of pts. have family history of autoimmune endocrine diseases
 Whole of the functioning thyroid tissue is involved
 Hypertrophy and hyperplasia are due to abnormal thyroid-stimulating antibodies that bind to
TSH receptors and produce disproportionate and prolonged effect
Toxic nodular goitre
 Simple nodular goitre is present for a long time before hyperthyroidism
 Usually in middle aged or elderly
 Very infrequently associated with eye signs
 Syndrome is that of secondary thyrotoxicosis
 Nodules are inactive, it is the internodular thyroid tissue which is overactive
 In some toxic nodular goitres, one or more nodules are overactive and here the
hyperthyroidism is due to autonomous thyroid tissue as in toxic adenoma
Toxic nodule
 A solitary overactive nodule

13. Hiba Hamid
 Nodule may be part of a generalized nodularity or toxic adenoma
 Autonomous
 Hypertrophy and hyperplasia are not due to thyroid stimulating antibodies
 TSH secretion is suppressed by high levels of circulating thyroid hormones
 Normal thyroid tissue surrounding the nodule itself is suppressed and inactive
Clinical features
 Tiredness
 Emotional liability
 Heat tolerance
 Weight loss
 Excessive appetite
 Palpitations
The signs of thyrotoxicosis are:
 Tachycardia
 Hot, moist palms
 Exophthalmos
 Eyelid lag / retraction
 Agitation
 Thyroid goitre and bruit
Symptomatology
 Thyrotoxicosis is eight times more common in women than men
 May occur at any age
 Significant symptoms include loss of weight despite a good appetite, recent preference for
cold, and palpitations
 Significant signs are the excitability of the pt., presence of a goitre, exophthalmos,
tachycardia or cardiac arrhythmia
 The goitre in primary thyrotoxicosis:

14. Hiba Hamid
 Is diffuse and vascular
 May be large or small
 Firm or soft
 A thrill and a bruit may be present
 Onset is abrupt, but remissions and exacerbations are not infrequent
 Hyperthyroidism is usually severe than in secondary thyrotoxicosis, but cardiac
failure is rare
 Manifestations of thyrotoxicosis not due to hyperthyroidism per se, for example
orbital proptosis, ophthalmoplegia and pretibial myxoedema, may occur in primary
thyrotoxicosis
 In secondary thyrotoxicosis:
 Goitre is nodular
 Onset is insidious and may present with cardiac failure or atrial fibrillation
 Hyperthyroidism is not severe
 Eye signs other than lid lag and lid spasm (due to hyperthyroidism) is very rare
Cardiac rhythm
 Fast heart rate, which persists during sleep, is characteristic
 Cardiac arrhythmias are superimposed on the sinus tachycardia as disease progresses
 More common in older pts. with thyrotoxicosis because of prevalence of coincidental heart
disease
 Stages of development of thyrotoxic arrhythmias:
 Multiple extrasystoles
 Paroxysmal atrial tachycardia
 Paroxysmal atrial fibrillation
 Persistent atrial fibrillation, not responsive to digoxin
Myopathy
 Weakness of proximal limb muscles
 Severe muscular weakness (thyrotoxic myopathy) resembling myasthenia gravis, occurs
occasionally

15. Hiba Hamid
 Recovery proceeds as hyperthyroidism is controlled
Eye signs
 Some degree of exophthalmos is common
 May be unilateral
 True exophthalmos is a proptosis of the eye, caused by infiltration of retrobulbar tissues with
fluid and round cells, varying degree of retraction or spasm of the upper eyelid
 Lid spasm occurs because levator palpebrae superioris muscle is partly innervated by
sympathetic fibres
 Results in widening of palpebral fissure so that sclera may be seen clearly above the upper
margin of the iris and cornea, above the ‘limbus’
 Spasm and retraction usually disappear when hyperthyroidism is controlled
 May be improved by beta-adrenergic blocking drugs, for e.g. guanethidine eye drops
 Edema of the eyelids, conjunctival injection and chemosis are aggravated by compression of
ophthalmic veins
 Weakness of extraocular muscles results in diplopia
 In severe cases, papilloedema and corneal ulceration result. When severe and progressive, it
is known as malignant exophthalmos
 Exophthalmos tends to improve with time. Sleeping propped up will help protect the eye but
will not prevent progression. Hypothyroidism increases proptosis by a few millimetres and
should be avoided.
 Improvement reported with massive doses of prednisone.
 Intraorbital injections of steroids is dangerous because of venous congestion
 When eye is in danger, orbital decompression may be required
 Thyroid dermopathy (pre-tibial myxedema) is a rare condition, characterized by thickening
of skin in areas of trauma due to deposition of hyaluronic acid in dermis and subcutis. Occurs
after some years of thyrotoxicosis onset, usually responds to treatment of underlying thyroid
disorder and topical steroids

16. Hiba Hamid
Diagnosis of thyrotoxicosis
 Most cases diagnosed clinically
 Difficulty arises in differentiating between mild hyperthyroidism from an anxiety state when
goitre is present
 TRH test is rarely indicated
 Thyroid scan is required to diagnose an autonomous toxic nodule and differentiate it from a
dominant swelling in a toxic multinodular goitre
 Thyrotoxicosis should always be considered in:
 Children with a growth spurt, behavior problems or myopathy
 Tachycardia or arrhythmia in elderly
 Unexplained diarrhea
 Loss of weight
Principles of treatment of thyrotoxicosis
 Non-specific measures are rest and sedation
 Anti-thyroid drugs, surgery, and radio-iodine
Anti-thyroid drugs
 In common use are carbimazole and propylthiouracil
 Β-adrenergic blockers, including propranolol and nadolol, used to block cardiovascular
effects of T4.
 Iodides, which reduce the vascularity of thyroid, should only be used in the immediate pre-
operative preparation in the 10 days before surgery
 Anti-thyroid drugs are used to restore the pt. to a euthyroid state, to maintain this period for a
prolonged period of time in the hopes of the occurrence of a permanent remission.
 Anti-thyroid drugs do not cure a toxic nodule.
 Overactive thyroid tissue is autonomous. Recurrence of hyperthyroidism is certain when the
drug is discontinued
 Advantages: no surgery. No use of radioactive materials.

17. Hiba Hamid
 Disadvantages: treatment is prolonged. Failure rate at least 50%. Duration of treatment may
be tailored to severity of the toxicity with milder cases being treated for only six months and
severe for two years before stopping therapy
Surgery
 In diffuse toxic goitre and toxic nodular goitre with overactive internodular tissue, surgery
cures by reducing mass of overactive tissue.
Neoplasms of the thyroid gland
Classification of thyroid neoplasms
Benign Follicular adenoma
Malignant Primary Follicular epithelium – differentiated: Follicular,
Papillary
Follicular epithelium – undifferentiated: Anaplastic
Parafollicular cells: Medullary
Lymphoid cells: Lymphoma
Secondary Metastatic
Local Infiltration
Benign tumours
 Follicular adenomas present as clinically solitary nodules
 Distinction between follicular carcinoma and adenoma can only be made on histological
examination
 In adenoma, there is no invasion of capsule or peri-capsular blood vessels.
 Treatment is wide excision i.e. lobectomy.
 The remaining thyroid tissue is normal so no follow up is necessary in the long run
 However, all papillary tumors should be considered malignant even if encapsulated
Malignant tumours

18. Hiba Hamid
 Metastases to thyroid from kidney and breast are rare
 Lymph node and blood-borne metastases to bone and lung occur and may be the mode of
presentation
Etiology of malignant thyroid tumours
 Single most important etiological factor in differentiated thyroid carcinoma, particularly
papillary, is irradiation of the thyroid under five years of age.
 Malignant lymphomas sometimes develop in autoimmune thyroiditis. Lymphocytic
infiltration in the autoimmune process may be an etiological factor.
Clinical features of thyroid cancers
 Sex ratio is 3 females to one male
 The most common presenting symptom is a thyroid swelling
 Enlarged cervical lymph nodes may the presentation of papillary carcinoma
 Recurrent laryngeal nerve paralysis is very suggestive of locally advanced disease.
 Anaplastic growths are usually hard, irregular and infiltrating.
 A differentiated carcinoma may be suspiciously firm and irregular, often indistinguishable
from a benign swelling
 Small papillary tumors may be impalpable, even when lymphatic metastases is present
 Pain, often referred to the ear, is frequent in infiltrating growths
Papillary carcinoma
 If any papillary structure or characteristic cytology is present, the tumour will behave in a
predictable fashion as a papillary carcinoma
 Histologically, the tumour shows papillary projections and characteristic pale, empty nuclei
(Orphan Annie-eyed nuclei)
 Papillary carcinomas are very seldom encapsulated
 Multiple foci may occur in the same lobe as primary tumour, or less commonly in both lobes.
 Spread to lymph nodes is common, but blood borne metastases is unusual unless the tumour
is extra-thyroidal.

19. Hiba Hamid
Follicular carcinoma
 Appear to be encapsulated macroscopically
 Microscopically, there is invasion of the capsule and of the vascular spaces in the capsular
region.
 Multiple foci are seldom seen
 Lymph node involvement is much less common than in papillary carcinoma
 Blood borne metastases are more common
 Eventual mortality rate is twice that of papillary cancer
 Hurthle cell tumours are a variant of follicular neoplasm in which oxyphil (Hurthle) cells
predominate histologically. Hurthle cell cancers have a poorer prognosis and all Hurthle cell
cancers are malignant.
Lymph nodelevels in the neck
Lymph nodes in the neck have been divided into sevenlevels, generally for the purpose
of squamous cell carcinoma staging. However, this is not all inclusive as several groups such as
the supraclavicular, parotid and retropharyngeal space nodes are not accounted for in this
system.
Level I
 below mylohyoid muscle and above the lower margin of the hyoid bone
 anterior to the posterior border of the submandibular glands
o level Ia: submental nodes - between the anterior bellies of the digastric muscles
o level Ib: submandibular nodes - posterolateral to the anterior belly of the digastric
muscles
Level II
 internal jugular (deep cervical) chain
 base of skull to inferior border of hyoid bone
 anterior to the posterior border of sternocleidomastoid (SCM) muscle

20. Hiba Hamid
 posterior to the posterior border of the submandibular glands
o level IIa: anterior, lateral, or medial to the vein or posterior to the internal jugular
vein and inseparable from it
o level IIb: posterior to the internal jugular vein and have a fat plane separating the
nodes and the vein
Level III
 internal jugular (deep cervical) chain
 lower margin of hyoid to lower margin of cricoid cartilage
 anterior to the posterior border of SCM
 lateral to the medial margin of the common carotid artery (CCA)/internal carotid
artery (ICA)
Level IV
 internal jugular (deep cervical) chain
 lower margin of cricoid cartilage to level of the clavicle
 anterior and medial to an oblique line drawn through the posterior edge of the
sternocleidomastoid muscle and the posterolateral edge of the anterior scalene muscle 4
 lateral to the medial margin of the CCA
Level V
 posterior triangle (spinal accessory) nodes
o level Va: superior half, posterior to levels II and III (between base of skull and
inferior border of cricoid cartilage)
o level Vb: inferior half, posterior to level IV (between inferior border of cricoid
cartilage and the level of clavicles)
Level VI
 prelaryngeal/pretracheal/Delphian node
 anterior to visceral space
 from inferior margin of hyoid bone to manubrium
 anterior to of levels III and IV
Level VII
 superior mediastinal nodes
 between CCAs, below superior aspect of manubrium

21. Hiba Hamid