Clemen, Venalyn A.

OVERVIEW

ANATOMY

HISTOLOGY

PHYSIOLOGY

THYROID DISORDERS (benign and malignant)

-CLINICAL PRESENTATION
-DIAGNOSTIC STUDIES
-TREATMENT
-PROGNOSIS
 Thyroid gland= Gr. Thyreoeidis

Shield-shaped
 Outpouching of the primitive foregut at the 3rd week AOG

 Originates at the base of the tongue -> foramen cecum

 Descends ventrally in the midline of the neck in close

proximity with the hyoid bone

 Connected via an epithelial-lined tube  thyroglossal duct

Resorbs @ 10th week

AOG
 Most commonly encountered cervical anomalies

 Cx: persistence of thyroglossal duct

 Midline mass/ 2 cm from the midline

 80%- at or just below the hyoid bone

 Asymptomatic, infected by oral bacteria, 1% malignant (85%-

papillary CA)
Thyroglossal duct sinuses

 Result from infection of the cyst secondary to spontaneous

surgical drainage of the cyst

 Minor inflammation of the surrounding skin

 Dx: 1- to 2-cm, smooth, well-defined midline neck mass that

moves upward with tongue protrusion

 Thyroid scintigraphy and Ultrasound- presence of normal

thyroid tissue
En bloc cystectomy
 Tx: “Sistrunk operation”—> Central hyoid bone excision
 Cx: failure of median thyroid anlage to descend normally

 May be the only thyroid tissue present

 Obstructive symptoms intervention

 Tx:
Exogenous thyroid hormone- to suppress TSH

RAI ablation hormone replacement

Surgical excision (rare)- preceded by

evaluation of normal thyroid tissue to
avoid hypothyroidism
 Normal thyroid tissue found anywhere in the central neck
compartment
 Cx: thyroglossal duct remains as a fibrous band, instead of
being atrophied (normal)

 50% projects up from the isthmus lying just to the L or R of the

midline

 may not be palpable/ may be palpable

 20 g (varies with body weight or
iodine intake)

 Brown in color; firm in consistency

 Posterior to the “strap” muscles

 Thyroid lobes

-adjacent to the thyroid cartilage

-connected in the midline- isthmus

-inferior to the cricoid cartilage

Blood Supply

aorta
or brachiocephalic
 Note:
The inferior thyroid artery
crosses the RLN,
necessitating identification
of RLN before arterial
branches can be ligated.
Blood Supply

aorta
or brachiocephalic
Nerves

RLN- innervates all intrinsic muscles of the larynx except cricothyroid

muscles-> external laryngeal nerves
 Injury to one RLN (unilateral)-> paralysis of the ipsilateral vocal
cord= paramedian or abducted position

Paramedian- normal; weak voice

Abducted- hoarse voice; ineffective cough

 Bilateral RLN injury-> airway obstruction (tracheostomy); loss of

voice

Both cords in abducted position- air movement can occur

- ineffective cough

-RTI from aspiration

 Superior laryngeal nerves- from vagus nerve

Internal branch- sensory to supraglottic larynx

- injury (rare); aspiration

External branch - innervates cricothyroid muscle

 Injury:

 inability to tense ipsilateral vocal cord– difficulty “hitting high

notes”

 difficulty projecting voice

 voice fatigue during prolonged speech

 The type 2a variant, in which
the nerve crosses below the tip
of the thyroid superior pole
(20%), places the nerve at a
greater risk of injury.
Lymphatic System
 Lobules- 20 to 40 follicles

 Spherical, 30 um in diameter

 Central store of colloid

 C-cells or parafollicular cells-

calcitonin
Ave. daily iodine requirement= 0.1 mg

a. Iodide trapping from blood to thyrocyte (cell)

ATP dependent via Na+/I- symporter

b. Oxidation of Iodide to Iodine (follicle-colloid)

Iodination of tyrosine residues to MIT and DIT thru
tyrosine peroxidase

c. Coupling (follicle-colloid)
DIT + DIT= tetraiodotyrosine (T4)
MIT + DIT= triiodotyrosine (T3) and Rt3
Conjugation with thyroglobulin (Tg+T4 , Tg + T3)

d. Hydrolysis of Tg to release MIT, DIT, T3, T4 (cell)

e. Release of hormones (T3, T4) to the blood

 Bound thyroid hormones (majority)
Carrier proteins:
T4-binding globulin

T4-binding prealbumin

albumin

 Free/unbound thyroid hormones-physiologically

active (0.02%)
 T3 T4
circulating plasma level circulating plasma level
potency (3-4x) potency
less tightly bound more tightly bound
half life- 1 day half life- 1 week
 Autoregulation= allows to modify its function independent of
TSH

 Wolff-Chaikoff effect- excessively large doses of iodide may

lead to initial increased organification, followed by suppression

 Estrogen
stimulate
HCG

 Glucocorticoid- inhibit
TESTS OF THYROID FUNCTION

 Serum TSH levels (Normal 0.5-5 Uu/mL)

-reflect the ability of the anterior pituitary to detect free T4

levels

TSH assay- is the most sensitive and specific test for the
diagnosis of hyper- and hypothyroidism and for optimizing
T4 therapy.
TESTS OF THYROID FUNCTION

 Total T4 (Ref. Range 55-150 nmol/L) and T3 (Ref. Range 1.5-3.5

nmol/L)

-Total T4 levels- output from the thyroid gland

 Increased:  Decreased:
Hyperthyroid px Hypothyroid px
Elevated Tg levels secondary to Decreased Tg levels due to
pregnancy, anabolic steroid use, nephrotic
estrogen/progesterone use, syndrome
congenital diseases

-T3 levels- peripheral thyroid hormone metabolism

-Total T3 levels- important for T3 thyrotoxicosis
TESTS OF THYROID FUNCTION

 Free T4 (Ref. Range 12-28 pmol/L) and Free T3 (3-9 pmol/L)

-sensitive and accurate measurement of biologically active

thyroid hormone

-Refetoff’s syndrome- end-organ resistance to T4

- T4 levels; normal TSH levels

 Thyrotopin- Releasing Hormone

-evaluate pituitary TSH secretory function

-500 ug of TRH IV measuring TSH levels after 30-60 mins.

 Thyroid antibodies (anti-Tg, anti-microsomal, anti-TPO, TSI)

-may indicate the underlying disorder, autoimmune thyroiditis

 Serum Thyroglobulin

- is for monitoring patients with differentiated thyroid cancer

for recurrence, after total thyroidectomy and RAI ablation

 Serum Calcitonin (0-4 pg/mL Basal)

-is a sensitive marker for MTC

THYROID IMAGING

 Radionuclide imaging
Iodine 123- low dose radiation

Iodine 131- high dose radiation

screen and treat patients with differentiated

thyroid cancers for metastatic disease

 size and shape

 distribution of functional activity

“cold”- trap less radioactivity,

malignancy (20%)

“hot”- increased trapping,

malignancy (<5%)
THYROID IMAGING

 Radionuclide imaging
 Technetium Tc 99m pertechnetate

- taken up by the thyroid gland; for evaluation

 Advantages:

-shorter half-life; minimizes radiation exposure

-sensitive for nodal metastases

 F-fluorodeoxyglucose (FDG) PET combined w/ CT

-screen metastases in thyroid CA, whom other imaging studies

are negative
 Ultrasound
-noninvasive, portable, no radiation exposure

- evaluate thyroid nodules; distinguishing solid from cystic; size and multicentricity

-assessing cervical lymphadenopathy; guide FNAB

 CT/MRI Scan
-excellent imaging of the thyroid gland and adjacent nodes

-evaluate the extent of large, fixed, or substernal goiters

-noncontrast CT for those w/ subsequent RAI therapy

 excess of circulating thyroid hormones
 autoimmune disease

 familial predisposition

 female preponderance (5:1); ages of 40 and 60

 - Postpartum state
 exact etiology is unknown
- Iodine excess
 conditions as possible triggers - Lithium therapy
- Bacterial and viral
infections

 genetic factors: assctd.w/ certain HLA haplotypes

 polymorphisms of the CTLA-4

Hallmark: antibodies stimulate thyrocytes to grow and synthesize excess thyroid

hormone
 Gross:
 Diffusely and smoothly enlarged
 Increase in vascularity
 Microscopic:
 Hyperplastic
 Epithelium is columnar w/ minimal
colloid present
 Nuclei exhibit mitosis
 Papillary projections of epithelium
 Lack of suppressor T
Genetic TH2 activates B
cells; Helper T cells
predisposition, cells; production of
differentiate to TH2
viral infection autoantibodies
cells

Increased synthesis
Antibodies stimulate
of thyroid hormones;
TSH receptors
Hyperplasia

Hyperthyroidism
Diffuse enlargement

Adrenergic
stimulation

Grave’s disease- Pathogenesis of Hyperthyroidism

 Grave’s opthalmopathy (50%)
-orbital fibroblasts and muscles
share a common antigen, TSH-R

-result from inflammation caused

by cytokines released from
sensitized killer T lymphocytes
and cytotoxic Ab

 Dermopathy (1-2%)
-deposition of
glycosaminoglycans, leading to
thickened skin in the pretibial
region and dorsum of the foot
 T cells produce
inflammatory cytokines

Cytokines- growth and

TSHR antibodies bind to
proliferation of
TSH receptors in retro-
fibroblasts-secrete
orbital/dermis in legs
glycosaminoglycans

Swelling of connective
Shin tissue thickens tissue and muscle
behind eyes

PRETIBIAL MYXEDEMA OPTHALMOPATHY

Grave’s disease- Pathogenesis of Extrathyroid Manifestations

 Darlymples- lid retraction
 Von Graffe’s- lid lag on down
gaze
 Enroth’s- lower lid edema
 Joffroy’s- absent forehead
creases
 Kocher’s- spasmodic retraction
of upperlid
 Mobius- defective convergence
 Stellawag’s- infrequent blinking
PE findings:

Thyroid gland- diffusely and symmetrically enlarged; enlarged

pyramidal lobe

Bruit or thrill

Diagnostic tests:

 TSH with or w/out an free T4 or T3 level

 Eye signs (+)- other tests not needed

 Eye signs (-)- Iodine 123 uptake and scan- elevated uptake, with
a diffusely enlarged gland

 Free T4 levels are normal, free T3 levels should be determined

in early Grave’s disease or
T3 toxicosis
elevated TSH-R or TSAB (90%)
 Treatment:
 Antithyroid drugs-given in preparation for RAI ablation or
surgery
Propylthiouracil (100 to 300 mg, TID) reduce the production by inhibiting the
Methimazole (10 TO 30 mg, TID then OD) organic binding of iodine and the coupling

 PTU- inhibits peripheral conversion of T4 to T3; thyroid storm

- preferred in pregnant and breastfeeding
 Methimazole- congenital aplasia

 AE: reversible granulocytopenia, rashes, fever, peripheral

neuritis, polyarteritis, hepatitis, agranulocytosis, aplastic
anemia

 High relapse rate (40-80% recurrence after a 1 to 2 yr course)

 B-blockers - Propanolol (20-40 QID)

-catecholamine response ; decreasing peripheral T4 to T3

-Recommended: elderly; w/ cardiac disease; resting HR >90 bpm

!!!! Asthmatics!!!!

-If CI: use Calcium channel blockers

 Radioactive Iodine Therapy

A: avoidance of surgical procedure, ease of treatment, reduced

overall treatment costs

-leads to Grave’s opthalmopathy (33% after RAI vs 16% after

surgery)

 Absolute CI:  Relative CI:

 Pregnant (planning
pregnancy w/in 6 mos. of tx)
 breastfeeding
 Young patients
 w/ thyroid nodules
 w/ opthalmopathy
 Lack of access to a high-
volume thyroid surgeon

hypothyroidism
 Surgery
 Rec. when RAI is contraindicated:
a. Confirmed CA or suspicious thyroid nodules
b. Young
c. Desire to conceive (<6 mos.)
d. Severe reaction to antithyroid meds
e. Large goiters (>80g)
f. Reluctant to undergo RAI
g. PREGNANCY unless…at 2nd trimester

 Px should be rendered euthyroid before operation

(antithyroid drugs until the day of surgery)

 Lugol’s iodide sol. or saturated potassium iodide (beginning 7-10 days

preop, 3 drops 2x daily)

 Beta blockade and potassium iodide for urgent and allergy

cases
 Surgery
 Total or near total thyroidectomy

 Rec. for: -w/ coexistent thyroid CA

- who refused RAI therapy

- severe opthalmopathy (improve)

- life-threatening AE

 Subtotal thyroidectomy (4-7g remnant)- prone to recurrence

Bilateral subtotal thyroidectomy

Total lobectomy
 in older individuals w/ prior hx of a nontoxic multinodular goiter

 Autonomy

 (+) presentations when low TH suppression

 S/S are similar to GD, but extrathyroidal manifestations are --

Diagnostic studies:
 TSH level and free T4 and T3 levels

 RAI uptake- increased, showing multiple nodules with increased

uptake and suppression of the remaining gland
Treatment:
 Surgical resection

near or total thyroidectomy to avoid recurrence

 RAI therapy- larger doses

-elderly patients

-w/ poor operative risks

-no airway compression

-CA is not a concern

 hyperthyroidism from a single hyperfunctioning nodule

 younger patients who note recent growth of long standing

nodule w/ symptoms of hyperthyroidism (3cm)

Somatic mutations in the TSH-R gene and G-protein-stimulating gene

PE findings:
 solitary thyroid nodule without palpable thyroid tissue on the
contralateral side
Diagnostic:
 RAI scanning- “hot” nodule with suppression of the rest of the
thyroid gland

-rarely malignant

Treatment:
 smaller nodules- antithyroid medications and RAI

 larger nodules- higher doses; hypothyroidism

surgery (lobectomy and isthmusectomy) for

young patients
 condition of hyperthyroidism accompanied by fever, CNS agitation or
depression, CVS and GI dysfunction, hepatic failure

 precipitated by: abrupt cessation of antithyroid meds, infection,

thyroid/non-thyroid surgery, trauma in px with untreated
thyrotoxicosis

Treatment:
 beta blockers
 oxygen supplementation and hemodynamic support
 nonaspirin compounds-pyrexia
 Lugol’s iodine or sodium ipodate (IV)-dec. iodine uptake and TH
secretion
 Corticosteroids- X adrenal exhaustion
 deficiency in circulating levels of thyroid hormone
 Cretinism- neonates, with neurologic impairment and mental
retardation
 Pendred’s and Turner’s syndromes
Laboratory findings:
 T4 and T3

 TSH levels-primary thyroid failure

 TSH levels-secondary hypothyroidism

 Thyroid autoantibodies in autoimmune disease

 ECG- decreased voltage w/ flattening or inversion of T waves

Treatment:

 T4, dosages from 50 to 200 ug/day px size and condition

 Starting doses of 100 ug of T4 daily, well tolerated

 elderly patients (w/ heart disease and profound

hypothyroidism)- started with lower doses 25 to 50 ug/day

(assctd. hypercholesterolemia and atherosclerosis); dose

titered

 baseline ECG in severe hypothyroid before T4 tx

 Myxedema coma- large doses of IV T4 (300 TO 400 ug)in ICU

 a.k.a suppurative thyroiditis

 infection via hematogenous/lymphatic route, direct spread,

penetrating trauma, immunosupression

 Streptococcus and anaerobes (70%)

 > children, preceded by URTI or otitis media

 Complications: systemic sepsis, tracheal or esophageal

rupture, laryngeal chondritis, perichondritis
Diagnosis:
 Leukocytosis on CBC

 FNAB for Gram’s stain, culture and cytology

 CT scans- extent of infection and abscess detection

 persistent pyriform sinus fistula suspected in children w/ recurrence

Treatment:
 Parenteral antibiotics

 Drainage-abscess

 Thyroidectomy-persistent abscess and failure of open drainage

 Px w/ pyriform sinus fistulae- complete resection of the sinus tract

inc. the area of tract termination in thyroid gland
 a.k.a DeQuervain’s, Granulomatous thyroiditis

 Painful form

- viral in origin or from a postviral inflammatory response

- Women, 30-40-yr-old

- Hx of preceding URTI

CP:

- Sudden or gradual onset of neck pain mandible or ear

PE:

- enlarged gland, tender and firm

Diagnosis: TSH; Tg, T4, T3 levels

ESR >100 mm/h

RAIU-decreased

Treatment:

Self-limited; primarily symptomatic

Aspirin and other NSAIDs- pain relief; steroids-

severe

Thyroidectomy- px w/ prolonged course, recurrent

and non-responsive to meds
 Painless form
-autoimmune; postpartum period (6 wks)

-women, 30 and 60 yrs old

PE:

-normal sized or minimally enlarged, slightly firm, nontender gland

Diagnosis:

-lab tests and RAIU similar to painful except for a normal ESR

Treatment:

beta blockers and thyroid hormone replacement

thyroidectomy or RAI ablation- px w/ recurrent, disabling

episodes
Lymphocytic (Hashimoto’s) thyroiditis
 struma lymphomatosa- transformation of thyroid tissue to
lymphoid tissue

 most common inflammatory disorder of thyroid

 leading cause of hypothyroidism

 women>men (1:10 to 20), 30 and 50 yrs. old

 inherited predisposition
Pathogenesis:

Activation of CD4+ T (helper) lymphocytes w/ specificity for thyroid

antigens

Activated T cells recruit cytotoxic CD8+T cells

Pathogenesis:
 Apoptosis

 Inc. intake of iodine; medications: interferon-a,

lithium, amiodarone
 Gross:
 Mildly enlarged
 Pale, gray-tan cut surface
 Granular, nodular, firm
 Microscopic:
 Infiltrated by small
lymphocytes and plasma cells
 Well-developed germinal
centers
 Thyroid follicles smaller than
normal w/ reduced amounts of
colloid and inc. interstitial
connective tissue
 Pathognomonic: Hurthle or Azkanazy cells
PE:

min. or mod. enlarged firm gland

painless anterior neck mass

palpable pyramidal lobe

20%-hypothyroidism

5%-hyperthyroidism (Hashitoxicosis)

Diagnostic studies:

 TSH; presence of autoantibodies

 FNAB with ultrasound guidance w/ solitary suspicious nodule

or rapidly enlarging goiter
Treatment:

 Thyroid hormone replacement therapy- hypothyroid px

 Levothyroxine

-TSH levels >10uIU/ml

-TSH levels 5-10 uIU/ml in the presence of goiter or anti-TPO

antibodies

 Surgery

-suspicion of malignancy; goiters causing compressive

symptoms; cosmetic deformity

Riedel’s struma or invasive fibrous thyroiditis

 replacement of all or part of the thyroid parenchyma by

fibrous tissue, w/c also invades adjacent tissues

 autoimmune

 assctd. with other focal sclerosing syndromes

 symptoms of hypo/hyperthyroidism as the gland becomes

fibrotic
 Gross:
 Tan / gray, woody/ “stony
hard” and avascular, no
lobules apparent
 Microscopic:
 No normal lobular pattern
 Follicles are obliterated or
compressed by extensive dense
fibrous tissue, which also
infiltrates adjacent skeletal
muscle
CP:

women, 30 and 60 y.o.

painless, hard anterior neck mass

compressive symptoms

Symptoms of hypothyroidism and hypoparathyroidism

PE:

hard, “woody” thyroid gland with fixation to

surrounding tissues

Diagnostic studies:

FNAB is inadequate open thyroid biopsy

Treatment:

Surgery-mainstay

Goal: decompress the trachea by wedge excision of

thyroid isthmus and make a tissue diagnosis

thyroid hormone replacement-hypothyroid px

corticosteroids and tamoxifen

Mycophenolate mofetil- attenuate inflammatory

process
 any enlargement of the thyroid gland

 Diffuse, uninodular, or multinodular

 non-toxic goiters- result from TSH stimulation secondary to

inadequate TH synthesis
 Familial goiters, w/ inherited deficiencies in enzymes (TH
synthesis)

 Endemic goiter in proportion of individuals in a particular

geographic region

Iodine deficiency

-90%, Central Asia, South America, Indonesia

Kelp, cassava, cabbage

o Sporadic goiters, no obvious cause

CP:

 nontoxic- asymptomatic, pressure sensation in the neck

 Large- compressive symptoms

 Catarrh (clear throat frequently)

 Dysphonia from RLN (rare) except when malignant

 Pemberton’s sign-obstruction of venous return at the thoracic

inlet from a substernal goiter

facial flushing and dilatation of cervical veins upon rising the arms above the head

 Hemorrhage, acute pain

PE:

 Soft, diffusely enlarged gland (simple)

 nodules of various size and consistency (multinodular)

 Deviation or compression of the trachea

Diagnostic:

 euthyroid- normal TSH and low-normal or normal free T4 levels

 RAI uptake-patchy uptake w/ areas of hot and cold nodules

 FNAB-dominant, painful or enlarging nodule

 CA, in 5-10% of multinodular goiters

 CT scans- retrosternal extension and airway compression

Treatment:
 Euthyroid (small, diffuse goiters) – tx not required
 exogenous thyroid hormone-large goiters
 iodine- endemic goiters
 Surgery
Reserved for:
a. cont. to inc. despite T4 suppression
b. Obstruction
c. Substernal extension
d. Malignancy suspected or FNAB proven
e. Cosmetically unacceptable
near-total or total thyroidectomy w/ lifelong t4 therapy
 US- thyroid CA accounts for <1% (2% women; 0.5% men)

 Most rapidly increasing CA in women

 6 deaths/million persons annually

 Palpable swelling (neck)

Assessed:

History

PE

FNAB
 Oncogenes and thyroid suppressor genes- thyroid
tumorigenesis

 RET proto-oncogene (chromosome 10)- pathogenesis of

thyroid CA

 Mutations of p53 (tumor suppressor gene) are rare in PTCs

but common in undifferentiated thyroid CA and thyroid CA
cell lines

 p15 and p16, mutated more commonly in thyroid CA cell lines

than in primary tumors
 80%

 predominant thyroid CA in children and individuals

exposed to external radiation

 women>men (2:1), 30 to 40 y.o.

CP:
 most are euthyroid
 slow-growing painless mass
 compressive symptoms-locally advanced invasive disease
 lymph node metastases: common
Diagnosis:
 FNAB of mass or lymph node
If thyroid CA in FNAB:
 Neck UTZ- evaluate the contralateral lobe for LN metastases in
central and lateral neck compartments
 Distant metastases (uncommon, 20%)
lungs>bone>liver>brain
 Gross:  Microscopic:
 Papillary projections
 Hard, whitish, flat
 Nuclear cellular features:
 Macroscopic
 Cells are cuboidal w/ pale, abundant
calcification, necrosis
cytoplasm, crowded nuclei that may
or cystic change demonstrate “grooving”, and
intranuclear cytoplasmic inclusions
(ORPHAN ANNIE)
 Multifocality (85%)

Increased risk of cervical nodal metastases

Trachea, esophagus, RLNs

 Other variants: tall cell, insular, columnar, diffuse sclerosing,

clear cell, trabecular, poorly differentiated types (1%)

-Worse prognosis
Treatment:

 Surgical treatment

near-total or total thyroidectomy-

-high-risk tumors or bilateral tumors

- >1 cm unless there are contraindications

RAI- residual thyroid tissue

serum Tg level-sensitive marker of recurrent or persistent

disease

thyroid lobectomy, isthmusectomy, or removal of any

pyramidal lobe or adjacent LN- px w/ nodules suspicious for
CA
 Thyroid lobectomy- small (<1 cm), incidentally discovered,
low-risk, unifocal, intrathyroid CA

 Central neck nodes removed (therapeutic central-

compartment, level VI)

 Prophylactic (ipsilateral or bilateral) dissection (2009, ATA

guidelines)

Advanced (T3 or T4) papillary CA

Small (T1 and T2) tumors, node –

 Modified radical or functional neck dissection

 Biopsy proven LN metastases detected clin. or by imaging in the
lateral neck of px
 Excellent prognosis, >95% 10-yr survival rate

 AGES scoring system

 Predict the risk of dying

 Age, histologic Grade, Extrathyroidal invasion, and metastases

and tumor Size
 Low risk:  High risk:
Young, w/ well- Older, w/ poorly
differentiated tumors differentiated tumors
No metastases Local invasion
Small primary lesions Distant metastases
Large primary lesions
 MACIS scale

 Postoperative system modified from the AGES scale

 distant Metastases, Age at presentation (<40 or >40 yrs old),

Completeness of original surgical resection (in cm),

extrathyroidal Invasion, and Size of original lesion (in cm)

 4 risk groups
 AMES system

 Classify into low- and high- risk groups

 Age (men <40 yrs old, women <50 yrs old), Metastases,

Extrathyroidal spread, and Size of tumors (< or > 5cm)

 TNM system to determine prognosis

 Tumor, Nodal status, Metastases

 4 groups:

 Class I (intrathyroidal)

 Class II (cervical nodal metastases)

 Class III (extrathyroidal invasion)

 Class IV (distant metastases)

 10%

 Occur more commonly in iodine-deficient

areas

 women>men (3:1), 50 y.o.

CP:
 usually solitary
 rapid size increase, long standing goiter
 painless unless hemorrhagic
 lymph node metastasis: uncommon (5%)
 distant metastases: present
 vascular or capsular invasion

 Hyperfunctioning thyrotoxicosis

Diagnosis:
 FNAB is unable to distinguish benign from follicular
CA
 metastases
 large follicular tumor (>4cm) older men, malignant
  Gross:  Microscopic:
 Solitary lesions  Follicles are present
 encapsulated  Lumen may be devoid of
colloid

 Minimally invasive  Widely invasive

 Encapsulated
 Unencapsulated
 Microscopic invasion thru
tumor capsule w/o extension  Broad areas of tumor invasion
into parenchyma through the capsule
 Invasion into small to med.
sized vessels in or  Large vessel invasion
immediately outside the
capsule
Treatment:
 Surgical

total thyroidectomy-
older w/ follicular lesions (>4cm); risk of CA (50%)

Atypia on FNA

Family history

Radiation exposure

Follicular CA w/ angioinvasion w/ or w/o capsular invasion

prophylactic nodal dissection- not needed, unless in rare px

with nodal metastases

Prophylactic central neck dissection-large tumor

 Poor long term prognosis

 Mortality:

15% at 10 yrs.

30% at 20 yrs.
 3%

 presents w/ vascular or capsular invasion

 cannot be diagnosed by FNAB

 more often multifocal and bilateral (30%)

 do not take up RAI (5%)

 metastases to local nodes (25%) and distant sites

Management:

 similar to follicular CA

 lobectomy and isthmusectomy- unilateral Hurthle cell

adenomas

 total thyroidectomy-invasive CA

 routine central neck node removal

when lateral neck nodes are
palpable
 modified radical neck dissection
 5%

 arises from parafollicular/C cells

 most are sporadic

 occurs with other inherited syndromes: familial MTC, MEN2a,

MEN2b (25%)

 mutation in RET proto-oncogene

 women>men (1.5:1), between 50 and 60 yrs. old

CP:

 neck mass

 pain or aching

 local invasion produces

obstructive symptoms

Histology:

 sheets of infiltrating
neoplastic cells separated by
collagen and amyloid
Diagnosis:
 history and PE
 serum calcitonin or CEA
Calcitonin- more sensitive tumor marker
CEA- better predictor of prognosis
 FNAB cytology
Treatment:
 neck UTZ is recommended
 total thyroidectomy
 Tumor debulking- locally recurrent or widely metastatic disease
Prognosis:
 10-year survival rate: 80%
 45%- lymph node involvement
 Worst prognosis for MEN2B (35%
survival)
 1%

 women>men, 7th and 8th decade of life

CP:
 Long-standing neck mass, rapidly enlarges
 painful
 assctd. w/ obstructive symptoms
 Tumor- large w/ ulceration and necrosis
 LN palpable at presentation
Diagnosis:
 FNAB- giant and multinucleated cells
Treatment and Prognosis:

 one of the most aggressive

 few patients surviving 6 months

 all forms of treatments have been disappointing

 total or near-total thyroidectomy w/ LN dissection -

intrathyroidal mass

 En bloc resection- extrathyroidal extension

 Cytotoxic chemotherapy (comb. of Taxane, Anthracycline,

Platinum)- prolonged survival

 <1%

 Non-hodgkin’s B-cell type

 most develop in px w/ chronic lymphocytic thyroiditis

CP:

 rapidly enlarging neck mass

 painless

Diagnosis:

 UTZ =well-defined hypoechoic mass

 FNAB- nondiagnostic

 Needle core open biopsy- definitive dx

Treatment:

 CHOP (Cyclophosphamide, Doxorubicin, Vincristine,

Prednisone)

 Radiotherapy + Chemotherapy

 Thyroidectomy and nodal resection- alleviate obstructive

symptoms

Prognosis:

 5-year survival rate: 50%

 Metastases:
kidney
breast
lung
melanoma

Diagnosis: Treatment:

 clinical examination  thyroid resection = Lobectomy

 px history (depending on the status)

 FNAB- definitive
diagnosis
1. Patient is positioned supine, w/ a sandbag between the scapulae. Head is
placed in a donut cushion and the neck extended to provide maximal
exposure.

1. A Kocher transverse collar incision, typically 4 to 5 cm in length, is placed in

or parallel to a natural skin crease 1 cm below the cricoid cartilage, although
longer incisions maybe needed.
3. Subcutaneous fat and Platysma (triangle sheet of muscle at both sides of the
neck) are divided, and a subplatysmal dissection is made above the incision up to
the level of the thyroid cartilage above, and the sternal notch, but remaining
superficial to the anterior jugular veins.

4. The fascia between the sternohyoid, omohyoid and sternothyroid muscles (strap
muscles ) is divided along the midline and the muscles retracted laterally. This is
an avascular plane but care must be taken not to injure small veins crossing
between the anterior jugular veins.
5. The thyroid gland is rotated medially (using the surgeons fingers). The important
vascular structure to identify is the middle thyroid vein (it will be tightly stretched
by the medial rotation of the gland), which is then ligated. This permits
further mobilization of the gland and moving the bulk of the lobe out the wound.

6. Identify the superior laryngeal artery as close to the superior pole of the
thyroid parenchyma as possible. Great care should be taken while ligating the
superior laryngeal artery so as to avoid injury to the external laryngeal nerve.
7. The superior parathyroid gland is normally located in a posterior position, at the
level of the upper two thirds of the thyroid and approximately 1 cm above the
crossing point of the recurrent laryngeal nerve and the inferior thyroid artery.

8. The inferior parathyroid glands are normally located between the lower pole of
the thyroid and the isthmus, most commonly on the anterior or
the posterolateral surface of the lower pole of the thyroid. Care must be taken to
preserve it in situ and to avoid damaging its inferior thyroid artery.
9. The recurrent laryngeal nerve is located between the common carotid artery
laterally, the esophagus medially, and the inferior thyroid artery superiorly.

10. When doing a thyroid lobectomy, the isthmus, which is crossing between the two
thyroid lobes, is divided.
 Endoscopic thyroidectomy via axillary incisions
 Injury to RLN may occur by severance, ligation, or traction. It

is most vulnerable to injury during the last 2 to 3 cm of its

course.

 20% are at risk of injury to the external branches of SLN.

 The cervical sympathetic trunk may be injured= Horner’s

syndrome

 Transient hypocalcemia (50%)

 Postoperative hematomas or bleeding- emergency

reoperation to evacuate hematoma

 Bilateral cord dysfunction w/ airway compromises- immediate

reintubation and tracheostomy

 Seromas- aspiration
 Brunicardi, C.F. 2015. Schwartz’s Principles of Surgery. 10th
edition. Pp. 1521-1556.

Images:
 Kumar, A.A. 2015. Robbin’s and Cotran Pathologic Basis of
Disease. 9th edition. Pp. 1084-1100.