Thyroid

Ddx Neck Mass:

! 50% thyroid
! Inflammatory lesions
! Other malignancy (lymphoma, mets from head and neck), thyroglossal duct, branchial cleft cyst.
! Congenital lesion.

Anatomy:
! located in the neck, anterior to the trachea, between cricoid cartilage and suprasternal notch.
! 2 lobes connected by an isthmus at the second tracheal ring.
! 12-20g in size, highly vascularized, soft.
! Blood supply is from superior thyroid (branch of ext carotid) and inferior thyroid (branch of thyrocervical
trunk off subclavian). Venous drainage is through the sup, mid, inferior thyroid veins.
! Borders:
! Anterior: platysma, skin
! Anterolat: SCM, sternohyoid, sternothyroid mms
! Post: parathyroid glands.
! 4 parathyroid glands are located in the posterior region of each pole of the thyroid.
! Inferior glands:
" From 3
rd
brachial pouch (along with thymus)
" Position is more variable, 60% of time in lower 1/3
rd
of gland 1cm from lower pole
" Near inferior thyroid artery
! Superior Glands:
" From 4
th
brachial pouch
" More consistent location close to where recurrent laryngeal nn enters larynx.
! Recurrent laryngeal nns traverse the lateral borders of the thyroid gland (if injured vocal cord paralysis).
Ride in tracheoesophageal groove posterior to the thyroid.
! Mature Gland Composition: 2 major cell types
! Thyroid Medullary C cells or Parafollicular cells make calcitonin lowers Ca by inhib
osteoclasts. Does not play major role in regulating serum Ca and is not missed when thyrod is
removed.
! Numerous spherical follicles composed of thyroid follicular cells surrounding secreted colloid.
" Colloid = proteinaceous fluid that contains large amounts of thyroglobulin (protein precursor
to thyroid horomones).
" Thyroid follicular cells are polarized:
! Basolateral surface is apposed to the blood stream
! Apical surface is apposed to follicular lumen/ follicle.

Development:
! Thyroid comes from primitive pharynx during the 3
rd
week of gestation: gland migrates from the foramen
cecum (at the base of the tongue) along the thyroglossal duct, passing ventral to hyoid bone and thyroid
cartilage to reach its final location. Duct disappears by gest day 50, but may persist along its path as a
pyramidal lobe of thyroid or as thyroglossal duct cyst.
! Thyroid hormone synthesis begins at 11 wks gestation.
! Neural crest derivatives from ultimobranchial body (from 4
th
pharyngeal pouch) give rise to thyroid medullary
C cells produce calcitonin (lowers Ca). C Cells are interspersed throughout the thyroid, but are most dense
at junction b/w upper 1/3
rd
and lower 2/3rds.
! Gland development controlled by transcription factors: TTF1, TTF2, PAX8 these orchestrate thyroid cell
development and the induction of thyroid-specific genes (thyroglobulin (tg), thyroid peroxidase (tpo), sodium
iodide symporter (NIS), TSH-R. Mutations in these genes (or downstream target genes) responsible for
congenital hypothyroidism.

Regulation of Thyroid Axis:
! Hypothalamus releases TRH stimulates thyrotropic cells of anterior pituitary to release TSH TSH binds
TSHRs on the basolateral surface of thyroid follicular cells to stimulate hormone production/release thyroid
hormones have negative feedback on TRH and TSH.
! TSH:
! Most useful physiologic marker of thyroid hormone action.
! Alpha and beta sub-units: alpha is similar to other glycoprotein hormones (LH, FSH, hCG), beta
subunit is unique to TSH.
! Peak TSH occurs 15 min after admin of exogenous TRH
! GC, somatostatin and DA inhib TSH release, but not at physiologic doses.
! Released in pulsatile manner and exhibits diurnal rhythm highest levels at night.
! Half-life = 50 min.
! Binds to TSH-R: G-protein coupled R inc adenylate cyclase inc cAMP.

Thyroid Hormones:
! Thyroxine (T4) gets converted to other two forms via deiodinases; half-life = 7d
! Tri-iodothyronine (T3) (deiodinase 1 or 2); most active; half-life = 18h
! Reverse T3 (deiodinase 3); inactive
! Conversion of T4-T3 is impaired with fasting, oral contrast agents, systemic illness, acute trauma, variety of
meds ( PTU, propanolol, amiodarone, glucocorticoids).

Thyroid Hormone Synthesis:
! Iodide Metabolism and Transport:
! Ingested iodide is bound to proteins (albumin) or if unbound, excreted in urine.
! Na/I- Symporter (NIS) on basolateral surface of follicular cells takes up iodide. Rate limiting step.
(NIS is highly selective for thyroid, low levels present in salivary glands, lactating breast, and
placenta).
! Pendrin (iodide transporter) on apical surface of follicular cells, mediates efflux of iodide into lumen.
Defect in PENDRIN gene causes Pendred Syndrome (d/o characterized by defective organification of
iodine, goiter and sensorineuro deafness).
! Iodine deficiency: central Africa, central South America, northern Asia. (can lead to Cretinism
mental and growth retardation).
! Organification, Coupling, Storage and Release:
! Iodide enters the thyroid follicle cells via NIS, is trapped and transported to apical membrane of
thyroid follicular cells.
! Organification: On apical membrane iodide is oxidized to iodine in a rxn that involves membrane
bound enzyme, thyroid peroxidase (TPO).
! Tg is a lg glycoprotein that is synthesized in the follicular cells and secreted into follicles.
! Reactive iodine atom is added to tyrosine residues of Tg, making MIT (monoiodotyrosine) and DIT
(diiodotyrosine).
! DIT and MIT couple to form T3 (MIT + DIT) and T4 (DIT + DIT) in a rxn that is also catalyzed by
TPO. This iodinated Tg is the storage forms of TH kept in follicle.
! TSH stimulate thyroid to release hormone. Tg is taken back into follicular cell by endocytosis. Within
the cell it is hydrolized in lysosomes to release T3 and T4, let into circulation.
! Uncoupled mono and diiodotyrosines are deiodinated by the enzyme dehalogenase iodine is
recycled.
! Factors that influence Thyroid Synthesis/Release:
! TSH number one!
! IGF-I, epidermal growth factor, TGF-B, endothelins, various cytokines.

Thyroid Hormone Transport and Metabolism:
! T4 is secreted from thyroid in >20 fold excess over T3. (80% released hormone from thyroid is T4).
! Nearly 100% of T3 and T4 are bound to plasma proteins: thyroxine-binding globulin (TBG), transthyretin
(TTR), albumin. More T3 is unbound than T4. Only unbound hormones are active.
! TBG is low in concentration, but has high affinity for thyroid hormones (T4>T3) and carries 80%
! Albumin has low affinity, but higher concentration carries 10% of bound T4 and 30% bound T3.
! TTR carries 10% T4, very little T3.
! Increased Levels of binding-protein:
! Estrogen: inc TGB increases total T3 and T4 levels, but not unbound levels euthyroid.
! Circulating factors associated with acute illness sick euthyroid syndrome
! Meds.
! Androgens and nephritic syndrome dec TBG.

Thyroid Hormone Action:
! Nuclear Thyroid Hormone Rs:
! Thyroid hormone Rs (a and b) are nuclear.
! TRs contain central DNA-binding domain and a C-terminal ligand domain. They bind to thyroid
response elements (TREs) in promoter regions of target genes and either promote or inhibit gene
transcription.
! T3 binds with 10-15 times greater affinity than T4.
! Thyroid Hormone Resistance:
! Resistance to thyroid hormone (RTH) is and AD d/o characterized by elevated TH levels and
inappropriately nl or elevated TSH. These pts dont exhibit classic s/sx of hypothyroidism b/c
resistance is partially compensated for by increased levels of TH. Clinical features: goiter, ADD, mild
dec in IQ, delayed skeletal maturation, Inc HR, impaired metabolic responses to TH. Mutant Rs have
dominant negative effect.

Lab Evaluation:
! Measuring Thyroid Hormones:
! TSH: first test to order.
! TRH stimulation test: obsolete b/c failure of TSH to rise after a 200-400 IV bolus of TRH has the
same implications as a suppressed basal TSH.
! Total T3 and Total T4 (can be altered in many different circumstances).
! Free T3 and Free T4 (more useful than total). In most cases fT4 level is sufficient to confirm dx of
thyrotoxicosis, but in 2-5% pts fT4 is nl and only fT3 is elevated.
! T3 resin-uptake test: determines the distribution of radiolabeled T3 b/w resin and the unoccupied
thyroid hormone binding proteins in the sample.
" The binding of labeled T3 to resin is increased when: there are fewer unoccupied binding sites
on endogenous binding proteins (ie TBG deficiency) OR when there is increased total
thyroid hormone in the sample.
" T3 RU is decreased when there are more unoccupied binding sites on endogenous binding
protein OE when total levels of thyroid hormone in the sample are decreased.
! Free T3 or T4 index: product of thyroid hormone binding ratio and total T3 or T4. Index corrects for
anomalous total hormone values caused by abnl in hormone-protein binding.
! Tests to determine etiology of thyroid dysfunction:
! Autoimmune Thyroid Dz:
" measure circulating abs against TPO and Tg (Tg auto-abs rarely occur alone so it is sufficient
to just check TPO abs).
" TSI: auto-abs that stim the TSH-R in Graves Dz.
! Tg: levels are inc in all types of thyrotoxicosis except in thyrotoxicosis factitia (caused by self-admin
of TH). Main role for this test is s/p total thyroidectomy and radioablation levels should be
undetectable. If levels >1-2 suggests incomplete ablation or recurrent cancer.
! Radioiodine Uptake and Thyroid Scanning:
" I 123, 125, 131 and Tc99m pertechnetate.
" Graves: homogenous distribution of increased uptake
" Toxic adenomas: focal areas of increased uptake with suppressed uptake in remainder of gland
" Toxic multinodular goiter: gland is enlarged with distorted architecture, multiple areas of
relatively inc or dec uptake.
" Subacute thyroiditis: very low uptake b/c follicular cell dmg and TSH suppression.
" Thyrotoxicosis factitia: low uptake.
" Cold nodules vs. Hot:
! Cold: dec uptake, usually benign, but more likely to be malignant than hot
! Hot: never malignant.
" Also used in f/u of thyroid cancer: look for mets s/p ablation or surgical removal of thyroid.
This is done after TH w/d so that TSH levels are increased.
! FNA:
! U/S:
" Detects nodules and cysts >3mm
" Useful for detecting thyroid nodules, guiding FNA, aspiration of cysts.

HYPOTHYROIDISM:
Causes:
! Primary: top 3 are MCCs.
! Autoimmune: Hashimotos
! Iatrogenic: I131 tx, thyroidectomy, external radiation of neck
! Iodine def: MCC worldwide
! Drugs: iodine excess (incl contrast media and amiodarone), Li, antithyroid rx
! Congenital hypothyroidism: absent or ectopic gland, dyshormonogenesis, TSH-R mutation
! Infiltrative d/o: amyloidosis, sarcoidosis, hemochromatosis, scleroderma
! Overexpression of deiodinase 3 in infantile hemangioma.
! Transient:
! Silent thyroiditis (incl post-partum)
! Subacute thyroiditis
! W/d of thyroxine tx in pts with intact thyroid
! After I131 or subtotal thyroidectomy in pts with graves
! Secondary:
! Hypopituitarism: tumors, irradiation or surgery, infiltrativ d/o, sheehans, trauma
! Isolated TSH def or inactivity
! Hypothalamic dz: tumors, trauma, infiltrative d/o, idiopathic.

Autoimmune Hypothyroidism:
! may be associated with a goiter (hashimotos) or n later stages may have minimal residual thyroid tissue
(atrophic thyroiditis)
! Prevalence:
! 4:1000 women and 1:1000 men
! MC in Japanese
! Mean age dx is 60y
! Annual risk of developing clinical hypothyroidism is 4% when subclinical hypothyroidism is
associated with + TPO abs.
! Pathogenesis:
! Marked lymphocytic infiltration of thyroid with germinal center formation, atrophy of follicles,
absence of colloid, and fibrosis.
! Tg and TPO abs a re good markers of autoimmune activity, but dont act alone only amplify
ongoing process (dont affect fetal thyroid).
! Genetics:
" HLA-DR 3, 4 and 5 associated with inc risk in white people.
" CTLA-4: t-cell regulating gene is also associated.
" Related to other autoimmune dzs: Addison, pernicious anemia, vitiligo, DM1.
! MC presenting sx: goiter

Signs/Symptoms: (in descending order of frequency)
Symptoms:
! tired, weak
! dry skin
! cold intolerance
! hair loss
! difficult concentrating or poor memory
! constipation
! wt gain with poor appetite
! dyspnea (due to pleural effusion, impaired resp mm func, dec ventilatory drive, sleep apnea)
! hoarse voice (fluid accum in vocal cords and tongue)
! menorrhagia (late stages amenorrhea)
! paresthesias
! impaired hearing (conductive hearing loss secondary to serous fluid accum in middle ear).

Signs:
! dry coarse skin, cool peripheral ext
! puffy face, hands and feet myxedema
! diffuse alopecia
! bradycardia
! peripheral edema
! delayed DTR relaxation
! carpal tunnel syndrome
! serous cavity effusions.

Treatment:
! Levothyroxine (T4): (dont replace w T3 b/c the half life is so short it would necessitate 3-4 times daily
dosing).
! 1.6ug/kg
! Adult pts without evidence heart probs can be started on 50-100 ug daily with dose titrated according
to TSH levels. TSH responses are slow and should only be measured 2m after dose adjustment.
! Pts may not experience sx relief until 3-6 months after nl TSH level achieved.
! Inc dosing in pregnant women; dec dose with elderly.
! Myxedema coma:
! Reduced LOC, sz, hypothermia, hypoglycemia, hyponatremia
! Tx: levothyroxine 500 bolus then 50-100/daily. OR T3 Q8-12h (this is rec b/c T4T3 conversion is
impaired in coma).

THYROTOXICOSIS
Prevalence:
! lifetime risk hyperthy is 5% women and 1% men,

Causes:
! Primary Hyperthyroidism:
! Graves
! Toxic Multinodular Goiter (Plummers Dz): surgery is tx of choice.
! Toxic Adenoma: solitary tumor produces excess TH, malignancy is rare.
! Functioning thyroid carcinoma mets
! Activating mutation of TSH R
! Activating mutation of G-protein R (McCune-Albrights)
! Stuma Ovarii (ovarian teratoma or dermoid).
! Drugs: iodine excess
! Thyrotoxicosis without Hyperthyroidism:
! Subacute thyroiditis
! Silent thyroiditis
! Other causes of thyroid destruction: amiodarone, XRT, infarction of adenoma
! Ingestion of excess TH
! Secondary Hyperthyroidism:
! TSH-secreting pit adenoma
! TH resistance syndrome
! Chorionic Gonadotropin-secreting tumors
! Gestational thyrotoxicosis.

Signs/Symptoms:
! Symptoms:
! Hyperactivity, irritability
! Heat intolerance and sweating
! Palpitations
! Fatigue and weakness
! Wt loss with increased appetite
! Diarrhea
! Polyuria
! Oligomenorrhea and dec libido

! Signs:
! Inc HR; afib in elderly
! Tremor
! Goiter
! Warm, moist skin
! Mm weakness, proximal myopathy
! Lid retraction or lag
! Gynecomastia.
! hyperreflexia

Graves Dz:
! Prevalence:
! Accts for 60-80% thyrotoxicosis
! d/o rarely begins before adolescents, typically b/w 20-50y and in elderly.
! Pathogenesis:
! Genetics: HLA-DR and CTLA-4 polymorphisms make pts more susceptible; 20-30% mono-twin
concordance.
! Environmental factors play big role: smoking slightly inc risk, def inc risk for ophthalmopathy; sudden
inc in iodine intake.
! Hyperthyroidism is due to TSI (thyroid stim immunoglobins) that are synth in thyroid gland, BM and
LNs. The name of the ab is TSAb (an IgG).
! TSI can cross placenta and cause neonatal thyrotoxicosis.
! Specific Clinical Findings:
! Thyroid diffusely enlarged to 2-3 times nl size, firm consistency, may be a thrill or bruit b/c inc
vascularity
! Graves Ophthalmopathy: continuum from stare with lid lag, to proptosis, to deformity/edema of
periorbital tissue with optic nn involvement and complete loss of vision.
! Pretibial myxedema (thyroid dermopathy): noninflamed, indurated plaque with deep pink/purple color
and an orange skin appearance.
! Thyoid acropachy: clubbing
! Labs:
! Measure TSH, total T4 and T3 levels and TBG (to assure that increases in total levels arent due to inc
TBG) OR just get TSH and fT4, fT3.
! Tx:
! Antithyroid drugs:
" Thionamides: 1/3
rd
of pts who tolerate rx remain in remission 6-12months after tx. Other
2/3rds need more definitive tx.
! Propylthiouracil (PTU), carbimazole, methimazole (active metabolite of carbimazole).
! All inhib the TPO thus reduce oxidation of iodine and the organification.
! PTU also inhibits conversion T4 to T3.
! Common SEs: rash, urticaria, fever, arthralgia.
! Rare ADRs: hepatits, SLE-like syndrome, agranulocytosis.
" Propanolol: control adrenergic sx, blocks conversion of T4-T3.
! Subtotal thyroidectomy:
" Careful control of thyrotoxicosis with anti-thyroid rx, followed by K-iodide is impt prior to
surgery to prevent thyrotoxic crisis and reduce gland vascularity. Iodide, admin as K-iodide
or as Lugols solution temp inhibits the release of TH (Wolff-Chaikoff effect). Reason for this
are not understood.
" Complications:
! Bleeding
! Laryngeal edema
! Hypoparathyroidism
! Dmg to recurrent laryngeal nn
! Radioiodination:
" Causes progressive destruction of thyroid cells.
" Small risk of thyrotoxic crisis minimized by pre-tx with levothyroxine.
" Antithyroid drugs must be stopped 3-4d prior to tx to maximize iodine uptake.
" Hyperthyroidism can persist for 2-3 months, during this time use antithyroid rx and beta-block
" Pregnancy is safe 6 months after therapy. Breast feeding not safe either.
" May exacerbate ophthalmopalegia (esp in smokers) give CS.
! Pros and Cons for Surgery vs Medical Tx:
" Surgery is faster
" Surgery can trigger thyroid storm
" Surgical risks: dmg to PTH, nns
" PTU/MTZ allows for Graves to spont remit
" PTU/MTZ takes several months to work
! In pregnancy:
! PTU has less placental crossover than other anti-thyroid drugs. Can usually stop tx in 3
rd
trimester b/c
TSH-R abs tend to dec in pregnancy.
! Surgery in 2
nd
trimester only (1
st
developmental problems, 3
rd
premature labor)

Toxic Adenoma:
! solitary tumor of thyroid that produces excess TH.
! Malignancy is rare! (no ophthamopathy or pretibial myxedema b/c not an autoimmune phenomenon).
! Clinical Pres:
! High T3 and T4, low TSH.
! Thyroid is nl or small in size with palpable nodule that is hot (functional) on thyroid scan.
! Tx:
! Initial tx as per Graves, definitive tx usually surgery b/c resolution after tx with rx is rare.
! Pre-op prep with propanolol and one of thionamides, then lobe with hot nodule resected via lobectomy
and isthectomy.
! Not radiation for this or for toxic multinodular goiter (Plummers Dz).

Thyroid Carcinoma:
Prevalence:
! annual incidence of thyroid carcinoma is 36-60 cases per 1 million people.
! 2:1 women: men
! Usually 25-65y
! Types: can arise from any cell type
! Follicular cells:
" papillary well-differentiated cancers.
" follicular well-differentiated cancers.
" Hurthle cell or oxyphil cell tumors are a variant of follicular neoplasms and arise from
follicular cells.
" Anaplastic tumors
! Parafollicular (C cells): medullary
! Lymphoid cells: lymphoma.

General Principles of Tx:
! surgery unless anaplastic or lymphoma.
! Prognosis:
! Papillary and follicular: good, usually doesnt alter life expectancy

Papillary Carcinoma:
! MC thyroid malignancy, occurs in 70-80% of cases (tumors with mix of pap and follicular are classified as
pap)
! Clinical Pres:
! Concentric layers of calcium (psammoma bodies) found in the stalk formation that give this cancer its
name. Pseudonuclear inclusions, orphan Annie eye nuclei
! Slow growing
! Good prognosis
! Worse prognosis associated with:
" Male
" >50y
" Primary tumor >4cm
" Less-well-differentiated cells
" Locally invasive of distant met dz (mets usually to local LNs although this finding is not
associated with poorer prognosis, partic in young women).
! Distant mets usually to lungs and bones (can be identified and txed with radioiodine
only if all thyroid is removed). Bones need XRT as well.
! Tx:
! Good prognosis lesions: lobectomy and isthectomy or TT
! Poor prognosis: TT
! Risk stratification systems:
" AMES (age, mets, extent of dz , tumor size)
" AGES (age, grade, extent, size)
! Current data:
" For lesions >1cm TT and post-op radioablation
" Removal of obviously involved LN is advocated, but random sampling plays little role in
planning therapy and has no place in tx of thyroid cancer.
" All pts get replacement TH, with goal to keep TSH levels low to avoid potential trophic
effects of TSH on residual cancer cells.
! No well documented effects of chemo for pts with mets.

Follicular Carcinoma:
! 10-20% of thyroid cancers
! Clinical Pres:
! Monotonous, uniform appearance of microfollicles without complex papillations as seen in papillary
carcinoma. Closely resemble follicular adenomas on cytologic and frozen section examination. On
permanent section they are distinguished from follicular adenomas by their capsular and vascular
invasion.
! Slow growing, good prognosis is minimally invasive.
! Poor prognosis:
" Age >45
" Local invasion to contiguous neck structures
" Distant mets.
! Tx:
! As per papillary carcinoma.

Medullary Carcinoma (MTC):
! 7% of thyroid cancers; 20% pts with MTC have genetically transmitted, AD inheritance pattern associated
with either familial medullary carcinoma or MEN 2A or 2B. SECRETES CALCITONIN.
! Clinical Pres:
! In pts with familial MTC or MEN, tumor is always present in both lobes. Sporadic version is usually
unilateral.
! Worse prognosis than follicular or pap carcinoma. 50% pts with 10y survival.
! Dx: elevated plasma Calcitonin levels or by screening with Ca and Pentagastrin infusion test that
shows elevated Calcitonin.
! Tendency to have early LN and bloodborne mets
! Tx:
! TT and central LN dissection (removal of cervical nodes medial to both recurrent laryngeal nns and
carotid arteries)
! Modified radical LN dissection is performed only if there is LN involvement.

Anaplastic Carcinoma:
! VERY aggressive neoplasm
! Arises from follicular cells, but is nearly completely undifferentiated.
! Surgerical resection only provides palliative airway relief. XRT and chemo equally ineffective.
! Prognosis is dismal. Pts are considered to have Stage IV dz at presentation and few survive >2y.

Lymphoma:
! Can present as thyroid mass lesion and is treated similarly to lymphomas in other sites.
! To distinguish lymphoma from Hashimotos thyroiditis core need bx or open bx may be necessary.

Thyroid Nodule:
! Prevalence:
! 4% popn in US, 50% single, 50% multiple. (autopsy suggests true incidence is much higher)
! Thyroid cancer MC in women, but a nodule in a man is more likely to be malign than a comparable
nodule in woman.
! Ddx:
! Carcinoma
! Multinodular goiter MC
! Adenoma MC
! Hashimotos
! Mets (melanoma, breast, RCC)
! Hx:
! Duration
! Local sx:
" pain, pressure, hoarseness may suggest local invasiveness
" compression, dyspnea, dysphagia due to size
! S/Sx of thyrotoxicosis
! Fam Hx:
" MEN (multiple endocrine neoplasias)
! Hx XRT (risk beginning with dose as low as 200. >2000 rad actually destroys thyroid tissue).
! Chernobyl (pts from Ukraine or Gomel region of Belorussia).
! PE:
! Palpate thyroid
! LNs
! Pembertons Sign: retrosternal mass. Pt raises hands above head venous compression at thoracic
inlet, less VR engorged head feeling of strangulation.
! Signs of thyrotoxicosis.
! Studies:
! Indirect laryngoscopy indicated when hoarsenss or when s/sx suggest malignancy.
! Labs:
" TSH then other TFTs as needed.
" Serum Ca: parathyroid dz or MEN.
" Medullary thyroid cancer: elevated calcitonin
" Elevated Tg levels in pts with papillary or follicular carcinomas, or also in benign dz.
" Pts with hx of:
! XRT: measure Ca
! MEN II: urinary catecholamine to screen for pheo.
! U/S;
" Cystic vs. solid
! if mass cystic its drained, cytology examined if benign no further tx. Recurrent
cyst drained again and re-eval cytology.
! Solid nodule: requires FNA or bx
" Number of nodules and size of nodules.
" Multiple nodules usually benign, difficult to eval with percutaneous FNA and may require
resection to obtain dx.
! FNA:
" Single most impt study in eval thyroid mass.
" Only 3% FNs, 85% nodules identified as malignant are cancerous at resection.
" Difficulty arises in pts with indeterminate FNA result usually this happens in pts with
follicular neoplasms. Distinction b/w follicular adenoma and carcinoma rests on detection of
capsular and vascular invasion these arent identifiable by FNA cytology. In these cases
surgical resection is needed to obtain dx.

Draw in Algorithm here (pg 402):








! Tx:
! Solid nodules:
" Benign by FNA:
! Observation for 3-6 months while being treated with oral T4 to suppress TSH
stimulated growth of nodule.
! If nodule remains same size redo FNA
! If shrinks cont suppressive tx
! If grows higher risk of being malignant and must be excised.
" If working dx is cancer:
! Surgery: thyroid lobectomy and isthectomy to remove ipsilat lobe and isthmus.
! If specimen is not cancer: no further tx.
! If specimen is cancer: total thyroidectomy as indicated:
Dx Incidence
(%)
Age (y) Size Extra-
thyroid
Invasion
LN Surgery
Well-
differentiated
70-80 <45 < 2cm None +/- Thyroid
lobectomy and
isthmusectomy
or total
thyroidectomy
Papillary
Follicular
10-20 >45 >1cm Often +/- Total
thyroidectomy
(TT)
Medullary 7 Any Any +/- +/- TT and
median LN
dissection
Anaplastic 3 Any Any +/- +/- Nonsurgical
Tx.

! Surgical resection should be definitive b/c repeat surgery poses greater risk to
nn and parathyroids
! In performing lobectomy or TT great care taken to preserve parathys and
blood supply (from branches off inf thyroid arts) occasionally autografting
of parathy to SCM is necessary if bl supply is injured during procedure.
! NN injury:
" One recurrent laryngeal ipsilateral loss of vocal cord control raspy
voice
" Both recurrents total loss of speech and requires tracheostomy for
airway control

MEN Syndromes:
MEN1:
! AD dz with high penetrance, but variable expressivity.
! Gene: TSG on csome 11 that encode protein menin.
! Pituitary adenoma, Parathyroid hyperplasia, Pancreatic islet cell tumors

MEN IIA:
- AD: ret gene
- pheochromocytoma, MTC, parathyroid hyperplasia

MEN IIB:
- AD: ret gene
- pheo, MTC, characteristic phenotype.

Random Collachio Facts:
! Radiation causes papillary cancer, thus NOT hyperthyroidism (b/c only follicular cancers cause inc TH).
! Toxic adenoma: tx with surgical removal only b/c we cant tell if it is cancerous or just an adenoma until it is
removed.
! Herthle cell tumors: cannot tx with radioablation b/c doesnt take up iodine.