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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 1 of 11

THYROID AND PARATHYROIDS

Not Lectured

OUTLINE

I. Congenital Lesions

II. Evaluation of Thyroid Disease III. Goiter

IV. Hyperthyroidism/Thyrotoxicosis V. Toxic Goiter

VI. Non-toxic Goiter VII. Thyroiditis VIII. Thyroid Cyst

IX. Being Tumors X. Malignant Tumors XI. Parathyroid Glands

REFERENCES 1. PPT (2015 Lecture) 2. 2016A Trans 3. 2015B Trans 4. Schwart’z/Sabiston CONGENITAL LESIONS

 Unlike the abdomen and thoracic cavity, the neck is a relatively superficial so it’s easier to diagnose thyroid disease, usually presenting with an ANTERIOR NECK MASS

 Normally, the thyroid gland should not be palpated

Embryologic life of the thyroid gland: it starts at the base of the tongue and goes down the neck where it lies during the adult life

Any problem with the descent of the thyroid gland to the neck will cause congenital abnormalities

THYROGLOSSAL DUCT ANOMALIES (Cyst, Sinus, Fistula) Thyroglossal duct (lifted from 2015B Trans)

o The tract from the base of the tongue all the way to the neck o Supposed to disappear after the thyroid goes down

 Thyroglossal duct cysts are the most commonly encountered CONGENITAL CERVICAL anomalies

Typically midline masses in childhood  80% below hyoid bone

ELEVATES with tongue protrusion

o Upon protrusion, the thyroid gland goes up through the patent thyroglossal duct

 During the embryologic life, the thyroid gland originates from the foramen cecum at the base of the tongue. From there, it will descend and will split into two forming the 2 lobes of the thyroid gland. The thyroglossal duct is supposed to degenerate upon birth. If it persists → thyroglossal duct problems

 Clinical Importance: distinguish thyroglossal duct from simple cyst because they have different treatment

Cyst → excise

Thyroglossal duct cyst → Sistrunk Procedure

If the thyroglossal duct cyst is simply excised, it will recur  No external sinuses but may infect

Treatment: SISTRUNK Procedure – removal of the mass and the entire tract all the way to the base of the tongue, until the hyoid bone  This procedure consists of en bloc cystectomy and excision of the

central hyoid bone to minimize recurrence

Figure 1. Thyroglossal Duct

PYRAMIDAL LOBE  50 % of individuals

Distal end of thyroglossal duct persists

 Projecting up from the isthmus, lying just to the left or right of the midline.

Very common, and of no clinical significance, unless a surgeon decides to do a total thyroidectomy

 No pathologic problem most of the time

 When the thyroid gland enlarges, the pyramidal lobe can also enlarge

Figure 2. Pyramidal Lobe ECTOPIC THYROID

Failure of the thyroid to descend completely into the neck Results to thyroid tissue anywhere along the tract

LINGUAL / SUBLINGUAL THYROID Mass or thyroid found at the base of the tongue  If you excise it, the patient will no longer have a thyroid

 Represents a failure of the median thyroid anlage to descend normally and may be the only thyroid tissue present

 S/Sx:

o Hypothyroid symptoms o Obstructive symptoms

o Choking, dysphagia, airway obstruction  Treatment:

 If small in size, Exogenous thyroid hormone to suppress TSH  Radioactive iodine (RAI) ablation followed by hormone

replacement

 Surgical excision is rarely needed, but if required, should be preceded by an evaluation of normal thyroid tissue in the neck to avoid inadvertently rendering the patient hypothyroid (If big)

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 2 of 11

EVALUATION OF THYROID DISEASE

Thyroid problems usually appear as anterior neck masses  Usually, a thyroid mass moves up with swallowing

Figure 4. Hypothalamus – Pituitary – Thyroid Axis. The hypothalamus releases TRH, stimulating the anterior pituitary gland to secrete TSH, which

stimulates the thyroid to produce thyroid hormones with iodine. Excess in thyroid hormones will produce a negative feedback mechanism which

suppresses the production of TSH. Also, If TSH is increased, there is a negative feedback to the hypothalamus which will decrease TRH secretion.

THYROID FUNCTION TESTS MOST ACCURATE TESTS of thyroid function

o SERUM TSH (Thyroid Stimulating Hormone)

 The most sensitive and specific test for determining thyroid function

 Reflect the ability of the anterior pituitary to detect free T4 levels

 There is an inverse relationship between free T4 levels and the logarithm of TSH concentration – small changes in in free T4 lead to a large shift in TSH levels

o FREE T4 & FREE T3 ASSAY (FT4 & FT3)

 Measure the biologically active thyroid hormones which cause the clinical manifestations

 FT4 is not performed as a routine screening tool in thyroid disease. Use of this test is confined to cases of early hyperthyroidism

 FT3 is most useful in confirming the diagnosis of early hyperthyroidism

Table 1. Interpreting Thyroid Function Tests (Memorize) SERUM TSH FT4 AND FT3 ASSAY DIAGNOSIS

High Low Hypothyroid

High Normal Subclinical Hypothyroid

Low High Hyperthyroid

Low Normal Subclinical Hyperthyroid *If the patient can only avail one test, request for TSH

 Others:

o Total T4 & T3

 Both are measured by radioimmunoassay

 Measure both the free and bound components of the hormones

 T4 levels reflect the output from the thyroid gland

 T3 levels in the non-stimulated thyroid gland are more indicative of peripheral thyroid hormone metabolism; not generally suitable for as a general screening test

o Thyroid antibodies

 Include anti-Tg, antimicrosomal, or anti-TPO and thyroid-stimulating immunoglobulin

 indicate underlying disorder, usually an autoimmune thyroiditis

 High in 80% of patients with Hashimoto’s thyroiditis and may also be elevated in Grave’s disease, multinodular goiter, and thyroid neoplasms (occasionally)

o Thyroglobulin

 Increases dramatically in destructive processes of the thyroid gland (i.e. thyroiditis, Grave’s disease, toxic multinodular goiter)

 Most important use is in monitoring patients with differentiated thyroid cancer for recurrence

INITIAL WORK-UP Initial diagnostic modality is thyroid function test

o TSH, FT4, FT3 If euthyroid o Ultrasound o FNABC  If hyperthyroid o Thyroid scan

 Hot / warm nodule: treat as toxic nodule  Cold nodule: FNABC

ULTRASOUND Main advantage: determine consistency of mass

o Simple cyst = thyroid cyst (purely fluid)

o Complex cyst = goiter (has both cystic and solid components) o Solid nodule = tumor

 Noninvasive, no radiation exposure  Monitoring nodule size (for non-operative tx)  Size & multicentricity: can detect masses even 1mm  Detects non-palpable masses

 Cervical lymphadenopathy

 Guide fine-needle aspiration (FNA) biopsy

 Evaluating substernal goiters (extent, tracheal compression)  Characteristics associated w/ CA

o Hypoechogenicity o Irregular margins

o Increased nodular flow (Doppler)

Hypervascular → increased blood flow o Invasion / regional lymphadenopathy

Figure 5. Ultrasound Results

SOLID COMPLEX

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 3 of 11 FINE NEEDLE ASPIRATION BIOPSY CYTOLOGY (FNABC)

 Performed after ultrasound

Single most useful diagnostic modality for diagnosing thyroid nodules in euthyroid patients

 Diagnostic: Cytopathologic Diagnosis (cells)  Therapeutic: Thyroid Cyst

o If it’s a thyroid cyst, you can just aspirate the contents then the cyst will be gone

 Limitations

o Technical expertise of the surgeon and the pathologist o Differentiating Follicular CA vs Benign Adenoma o Small nodule (hard to hit)

 Do ultrasound-guided FNA

o Drawbacks of FNABC in “toxic” patients (hyperthyroid), not accurate

 More vascular which can lead to Increased bleeding, cells are actively dividing and can be mistaken for CA, so you do not do FNA for nodules that are hot or warm

 If hyperthyroid – you do a thyroid scan o Increased false positive result

o Hypertrophic cells mistaken for CA

RADIONUCLIDE IMAGING / THYROID SCAN

 Iodine-123 (123I), iodine-131 (131I), or Technetium-99m (99mTc) pertechnetate

Iodine is preferred because it is more accurate

o Preferably I123 or 131 because 3-8% of warm nodules are cold on pertechnetate scan

 Iodine-123 - emits low dose radiation, half-life of 12 to 14 hours, and is used to image lingual thyroids or goiters

 Iodine-131 - half-life of 8 to 10 days and leads to higher-dose radiation exposure, used to screen and treat patients with differentiated thyroid cancers for metastatic disease

 Technetium-99m pertechnetate

 Increasingly being used for thyroid evaluation  Taken up by the mitochondria, but is not organified

 Advantage of having a shorter half-life and minimizes radiation exposure

 Particularly sensitive for nodal metastases

 Thyroid gland is the only organ in the body that takes up iodine. If you give radioactive iodine, expect all of the iodine to be imbibed in the thyroid.

 Shows size and shape of the gland and distribution of functional activity  COLD

o Areas that trap less radioactivity than the surrounding gland  MALIGNANCY IS HIGHER (20%)

HOT

o Areas that demonstrate increased activity

Figure 6. Thyroid Scan

 More recently, 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) combined with computed tomography (CT) is being increasingly used to screen for metastases in patients with thyroid cancer in whom other imaging studies are negative.

OTHER DIAGNOSTICS  Not routinely used, only for completion  Neck CT Scan

o For lesions of borderline resectability

If not sure if mass is resectable (preferably use double contrast)

Laryngoscopy

o Hoarseness or s/s of compression of recurrent laryngeal nerve Metastatic Work-Up

o Symptom-Directed

 Chest / Liver / Bone / Brain  Work-up for MEN: for medullary cancer

o Suspect if w/ family history of Multiple Endocrine Neoplasia Type 2 (MEN 2A) or Medullary Thyroid Cancer (MTC)

o High basal serum CALCITONIN - virtually diagnostic for MTC

o Further work-up for primary hyperparathyroidism & pheochromocytoma

 CT/MRI provide excellent imaging of the thyroid gland and adjacent nodes and are particularly useful in evaluating the extent of large, fixed, or substernal goiters (which cannot be evaluated by ultrasound) and their relationship to the airway and vascular structures.

 Non-Contrast CT Scans should be obtained for patients who are likely to require subsequent RAI therapy.

 PET-CT scans - for Tg-positive, RAI-negative tumors

GOITER

 Most common thyroid disease in Filipinos

 More than 80% of thyroid nodules of Filipinos turn out to be goiter  Moves with swallowing

 Can be classified whether nodular vs. diffuse and toxic vs. nontoxic NODULAR VS DIFFUSE

Figure 7. (Left) Nodular Goiter: unilateral enlargement

(Right) Diffuse Goiter: bilaterally symmetrical enlargement; like a “scrotum” in the neck

 Any enlargement of the thyroid gland

 Endemic goiter - occurrence of a goiter in a significant proportion of individuals in a particular geographic region

o In the past, dietary iodine deficiency was the most common cause of endemic goiter

o Dietary goitrogens (kelp, cassava, and cabbage) also participate in formation

 Elevated TSH levels induce diffuse thyroid hyperplasia, followed by focal hyperplasia, resulting in nodules that may or may not concentrate iodine, colloid nodules, or microfollicular nodules. The TSH-dependent nodules progress to become autonomous.

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 4 of 11 TOXIC GOITER

Figure 8. Toxic Goiter

 Despite the normal thyroid hormone levels, there’s still production by either a tumor or the thyroid itself

S/Sx: Thyrotoxic symptoms

NON-TOXIC GOITER

Figure 9. Non-Toxic Goiter

 Most are thought to result from TSH stimulation secondary to inadequate thyroid hormone synthesis and other paracrine growth factors

 Signs and Symptoms: o ASYMPTOMATIC (80%)

 There’s just a mass that moves up with swallowing  Pressure sensation at the back (in the neck from the book) o Compressive Symptoms (as they become large)

 Dysphagia, orthopnea (dyspnea in the book)  Catarrh - frequent clearing of throat  Dysphonia – hoarseness

 From RLN injury is rare, except when malignancy is present

PEMBERTON SIGN

▫ Facial flushing and dilatation of cervical veins on raising the arms above the head

▫ Rarely seen

 Caused by obstruction of venous return at the thoracic inlet from a substernal goiter

MEMORIZE! Came out in the board exam

 Sudden enlargement of nodules or cysts due to hemorrhage may cause acute pain

 Physical Exam

o Soft, diffusely enlarged gland (simple goiter) or nodules of various size and consistency in case of a multinodular goiter

o Deviation or compression of the trachea may be apparent  Diagnostic Tests

o Patients are usually Euthyroid with normal TSH and low-normal or normal free T4 levels.

o RAI uptake often shows patchy uptake with areas of hot and cold nodules.

o FNAB is recommended in patients who have a dominant nodule or one that is painful or enlarging, as carcinomas have been reported in 5% to 10% of multinodular goiters.

o CT scans are helpful to evaluate the extent of retrosternal extension and airway compression.

 Treatment

o Most euthyroid patients with small, diffuse goiters do not require treatment

o Exogenous thyroid hormone to reduce the TSH stimulation of gland growth for large goiters

 May result in decrease and/or stabilization of goiter size  Most effective for small diffuse goiters

o Endemic goiters are treated by iodine administration o Surgical resection is reserved for goiters that:

a. Continue to increase despite T4 suppression b. Cause obstructive symptoms

c. Have substernal extension

d. Have malignancy suspected or proven by FNAB e. Are cosmetically unacceptable

Near-total or total thyroidectomy is the treatment of choice, and patients require lifelong T4 therapy

Table 2. Etiology of Non-Toxic Goiter

CLASSIFICATION SPECIFIC ETIOLOGY

Endemic Iodine Deficiency, Dietary Goitrogens (Cassava, Cabbage) Medications Iodide, Amiodarone, Lithium

Thyroiditis Subacute, Chronic (Hashimoto’s)

Familial Impaired Hormone Synthesis From Enzyme Defects

Neoplasm Adenoma, Carcinoma

Resistance to Thyroid Hormone

HYPERTHYROIDISM/THYROTOXICOSIS

 Clinical manifestations result from an excess of circulating thyroid hormone

 Clinical Manifestations

o Heat intolerance, sweating & thirst, weight loss, palpitations, atrial fibrillation

o Resting Tachycardia : most reliable sign

o Nervousness, fatigue, emotional lability, hyperkinesis, fine tremors, muscle wasting, proximal muscle group weakness with hyperactive tendon reflexes

o Amenorrhea, decreased fertility o Facial flushing, warm & moist skin o Ophthalmopathy (eye signs)

o Dermopathy (thickened skin in pretibial region)

 It is important to distinguish disorders such as Graves’ disease and toxic nodular goiters that result from increased production of thyroid hormone from those disorders that lead to a release of stored hormone from injury to the thyroid gland (thyroiditis) or from other non-thyroid gland–related conditions.

 Graves’ disease, toxic multinodular goiter, and solitary toxic nodule are most relevant to the surgeon

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 5 of 11 Table 3. Differential Diagnosis of Hyperthyroidism

INCREASED HORMONE SYNTHESIS (INCREASED RAIU)

RELEASE OF PREFORMED HORMONE (DECREASED RAIU)  Graves’ Disease (Diffuse Toxic

 Goiter)

 Toxic Multinodular Goiter  Toxic Adenoma  Drug Induced—Amiodarone, Iodine  Thyroid Cancer  Struma Ovarii  Hydatidiform Mole

 TSH-Secreting Pituitary Adenoma

 Thyroiditis - Acute Phase of Hashimoto’s Thyroiditis,  Subacute Thyroiditis  Factitious (Iatrogenic)  Thyrotoxicosis

 “Hamburger Thyrotoxicosis” RAIU = radioactive iodine uptake; TSH = thyroid-stimulating hormone

TOXIC GOITER

GRAVES DISEASE Diffuse toxic goiter

o Familial predisposition o Females 40-60 yrs  Possible “triggers”

o Postpartum state, iodine excess, lithium therapy, and bacterial & viral infections

 Etiology

o Autoimmune

o Antibodies directed against the thyroid hormone receptor o Stimulate thyrocytes to produce excessive thyroid hormone  Etiology is autoimmune that stimulates the thyroid to produce

excessive hormone  Clinical Features:

o Can be divided into those related to hyperthyroidism and those specific to Graves’ disease.

o Hyperthyroid symptoms:  Heat intolerance

 Increased sweating and thirst

 Weight loss despite adequate caloric intake o Symptoms of increased adrenergic stimulation

o The most common GI symptoms include increased frequency of bowel movements and diarrhea

o 50% of patients will develop clinically evident ophthalmopathy  Diagnosis

o High FT4 and/or FT3 o Low TSH

o Diffusely “Hot” uptake on radionuclide scan o Auto-antibodies against:

 Thyrotropin receptor  Thyroglobulin  Peroxidase

Figure 10. Thyroid Radionuclide Scan of Graves’ Disease  Treatment

o Anti-Thyroid drugs

 To prepare patient for definitive treatment  High relapse rate if discontinued

 Types

Propylthiouracil (PTU, 100-300mg TID) Methimazole (10-30mg TID)

 Definitive treatment:

o Radioactive Iodine Ablation Therapy (RAI)  Mainstay treatment in North America

 Causes progressive development of hypothyroidism (over 70% in 11 years), requiring lifelong thyroxine

Has been shown to lead to progression of opthalmopathy Takes 3-6 months to achieve Euthyroid

Absolute contraindications include women who are pregnant breastfeeding

o Surgery (thyroidectomy)

 Surgery is recommended when RAI is contraindicated: ▫ Confirmed cancer or suspicious thyroid nodule Young

Pregnant

Had severe reactions to anti-thyroid medications Have large goiters with compressive symptoms Reluctant to undergo RAI therapy

Indications for Treatment o Surgery

Compressive symptoms (e.g. dysphagia, orthopnea) Large nodules

Require high amounts of RAI Resistant to treatment Suspicions for malignancy

Immediate resolution of thyrotoxicosis is needed

 The patient needs to be euthyroid before surgery ( through anti-thyroid drugs for 3-4 week) to prevent thyroid storm and decrease vascularity of the gland

o RAI

Small goiters (<100mL)

Without suspected malignant potential Previous thyroidectomy

High surgical risk

Table 4. Comparison of Surgery and RAI

SURGERY RAI

Immediate ablation Gradual ablation (40% in 1 year)

Complete relief of symptoms Relief of most toxic symptoms in 3-6 months

(except ophthalmopathy) Definitive histologic diagnosis

Need to render euthyroid first Permanent hypothyroidism in 10 years

Surgical risk “radiation” effects Table 5. Adverse Effects of Surgery vs RAI

SURGERY RAI  Hemorrhage <5%  RLN (recurrent laryngeal nerve) injury 3-8%  Hypo-parathyroidism 2-5%  Hypothyroidism 10% in 5 yrs  Neck edema, thyroiditis 5-10%  Sialadenitis 11.5%

 Vocal cord paralysis <5%  GIT complaints 67%

 Acute radiation sickness 30-50%  Impaired fertility 10-45%  Bone marrow suppression 3-35%  Taste dysfunction 37%

 Parathyroid dysfunction 5-60%  Leukemia, bladder cancer <5%  Nodule consistency hardening

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 6 of 11 TOXIC MULTI-NODULAR GOITER

Usually older than 50 years of age

 Often has; prior history of a non-toxic multi-nodular goiter

 Over several years the thyroid nodules become autonomous to cause hyperthyroidism

 Diagnosis:

o TSH, FT4, FT3, thyroid scan  Treatment:

o Thyroidectomy

Figure 11. Toxic Multi-Nodular Goiter

NON-TOXIC GOITER

 Result from iodine deficiency and/or TSH stimulation, or idiopathic  Nowadays, it’s very hard to have iodine deficiency since a lot of food

are fortified

 Most of the time idiopathic

 May be diffuse, uninodular, multinodular

 Familial goiters result from enzyme deficiencies necessary for thyroid hormone synthesis

 Endemic goiter refers to occurrence of a goiter in a significant proportion on individuals in a particular geographic region (*you should know - mountain area where no seafood)

 Diagnosis: o TSH, FT4, FT3 o Ultrasound o FNAB

 If multinodular do FNAB on dominant nodule and/or any suspicious nodule on ultrasound

 Treatment (Suppression vs. Surgery):

o TSH suppression (conservative treatment)

 Give high dose exogenous thyroid hormone at levels that will suppress TSH

o Thyroidectomy

Table 6. Indications for TSH suppression vs. Thyroidectomy

TSH SUPPRESSION THYROIDECTOMY

Patients from geographic areas

with iodine deficiency Large goiters Young patient with small nodule Compressive symptoms Nodular goiter with no evidence

of functional anatomy Suspicious nodules Contraindication of TSH suppression

 Post-menopausal  Older than 60 y/o  Osteoporosis

 Cardiovascular disease Failure of medical treatment

SUMMARY – GOITER

 Most common thyroid disease in Philippines (85% of thyroid disease)  Types o Diffuse nontoxic o Nodular nontoxic o Diffuse toxic o Nodular toxic  Diagnosis o TSH, FT4, FT3

 If toxic : Thyroid scan  Non-toxic : Ultrasound, FNAB  Treatment

o Toxic: surgery, RAI, anti-thyroid drug o Non-toxic: none, TSH suppression, surgery

THYROIDITIS

Inflammatory disorder of the thyroid gland

May cause initial hyperthyroidism, then progress over time to hypothyroidism

 Thyroiditis usually is classified into acute, subacute, and chronic forms, each associated with a distinct clinical presentation and histology

ACUTE (SUPPURATIVE) THYROIDITIS Infectious cause

 The thyroid gland is inherently resistant to infection due to its extensive blood and lymphatic supply, high iodide content, and fibrous capsule.  Infectious agents can seed it via:

o Hematogenous or lymphatic route

o Direct spread from persistent pyriform sinus fistulae or thyroglossal duct cysts

o Result of penetrating trauma to the thyroid gland o Immunosuppression.

 Streptococcus and anaerobes account for about 70% of cases

 More common in children often preceded by an upper respiratory tract infection or otitis media

 Characterized by

o Severe neck pain radiating to the jaws or ear, fever, o Chills

o Odynophagia o Dysphonia  Diagnosis

o Established by leukocytosis on blood tests and FNAB for Gram’s stain, culture, and cytology

o CT scans may help to delineate the extent of infection

o A persistent pyriform sinus fistula should always be suspected in children with recurrent acute thyroiditis

o Barium swallow demonstrates the anomalous tract with 80% sensitivity

 Treatment

o Parenteral antibiotics and drainage of abscesses

o Patients with pyriform sinus fistulae require complete resection of the sinus tract, including the area of the thyroid where the tract terminates, to prevent recurrence.

SUBACUTE THYROIDITIS Self-limiting

o Remission in 2-4 months  Subtypes

o Granulomatous (De Quervain’s) o Lymphocytic

o Postpartum

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 7 of 11 Table 7. Painful and Painless Subacute Thyroiditis

PAINFUL PAINLESS

ONSET Gradual

AGE 30-40 years old women 30-60 years old women HISTORY Upper respiratory tract

infection Autoimmune; occurs in postpartum period (<6 weeks) PE Gland is enlarged, exquisitely tender, and firm

Normal sized or minimally enlarged, slightly firm,

non-tender gland

DIAGNOSIS

Early stages: TSH decreased; Tg, T4, and T3 levels are elevated due to the release of preformed thyroid hormone from

destroyed follicles TREATMENT

Aspirin and steroids; Thyroidectomy if non responsive to medical

treatment

B-blockers and thyroid hormone replacement for

symptomatic CHRONIC THYROIDITIS

LYMPHOCYTIC (HASHIMOTO’S) THYROIDITIS Autoimmune

 MOST COMMON INFLAMMATORY DISORDER OF THE THYROID and the leading cause of hypothyroidism

 Antibodies develop against thyroid antigens o Anti-thyroid peroxidase (anti-TPO) antibodies o Anti-thyroglobulin (anti-Tg) antibodies

o Must check for serum assays of anti-TPO and anti-TG antibodies  Others

o TSH receptor-blocking antibodies, Thyroid stimulating Ab, Cytotoxic Ab

 Clinical Presentation

o More common in women between ages of 30 and 50

o Most common presentation is that of a minimally or moderately enlarged firm granular gland discovered on routine physical examination or the awareness of a painless anterior neck mass o 20% of patients present with hypothyroidism

o 5% presents with hyperthyroidism

o Classically, presents with diffusely enlarged, firm gland, which also is lobulated.

 Diagnostic Studies

o When suspected clinically, an elevated TSH and the presence of thyroid autoantibodies usually confirm the diagnosis.

o FNAB is indicated in patients who present with a solitary nodule or a rapidly enlarging goiter

 Treatment

o Thyroid hormone replacement

RIEDEL’S THYROIDITIS

Chronic inflammatory disease causing dense fibrosis of the gland  Fibrosis may extend beyond thyroid capsule to the neck

 May be mistaken for CA

 Causes intense fibrosis and presents as a hard mass on the neck, so this is the one most operated on

 The Etiology of this disorder is controversial, and it has been reported to occur in patients with other autoimmune diseases.

 This association, coupled with the presence of lymphoid infiltration and response to steroid therapy, suggests a primary autoimmune etiology.  Typically presents as a painless, hard anterior neck mass, which

progresses over weeks to years to produce symptoms of compression, including dysphagia, dyspnea, choking and hoarseness.

 Physical exam reveals a hard, “woody” thyroid gland with fixation to surrounding tissues.

 Diagnosis is confirmed by open thyroid biopsy, because the firm and fibrous nature of the gland renders FNAB inadequate.

 Surgery is the mainstay of the treatment TREATMENT OF THYROIDITIS  Medical Treatment

Indications for surgery

o Malignancy cannot be ruled out o Significant signs of compression o Failure of medical treatment

 Serial monitoring of thyroid function as indicated

THYROID CYST

 Exact cause is unknown  Theories:

o Lack of iodine in the diet

o Autoimmune disorder that causes inflammation of the thyroid (Hashimoto’s disease)

o Genetic defect

o Exposure to radiation in childhood

 Treatment: needle aspiration +/- TSH suppression

BENIGN TUMORS

FOLLICULAR ADENOMA  Hard to differentiate from follicular carcinoma

o Only histologic difference from follicular carcinoma is absence of capsular & blood vessel invasion

o Do a preoperative biopsy

PLUMMER DISEASE (TOXIC ADENOMA)  Hyperthyroidism from a single hyperfunctioning nodule  Typically occurs in younger patients

 Diagnostics: RAI scan; “hot” nodule

 Treatment: Thyroidectomy after control of hyperthyroidism

MALIGNANT TUMORS  Well-differentiated o Papillary o Follicular  Medullary  Anaplastic  Others

Table 8. Frequency of Thyroid Carcinomas. 90-95% of thyroid carcinomas are well differentiated cancers

PATHOLOGY FREQUENCY (%) *Papillary 80 Follicular 10 Hurthle cell 3 Medullary 5 Anaplastic 1 Others 1 CLINICAL MANIFESTATIONS  Initially asymptomatic  Usually euthyroid  Progressive growth  Invasion of structures

o Recurrent laryngeal nerve, esophagus, trachea,  Neck node enlargement

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 8 of 11 PAPILLARY CARCINOMA

 Relatively benign course  Compatible with long life

 30-45% metastasis to lymph nodes (but this had no impact on survival)  Accounts for 80% of all thyroid malignancies in iodine-sufficient areas

and is the predominant thyroid cancer in children and individuals exposed to external radiation

 Papillary carcinoma is the MOST COMMON OF THE THYROID NEOPLASMS and is usually associated with an excellent prognosis, particularly in female patients younger than 40 years

 2:1 female-to-male ratio, and the mean age at presentation is 30 to 40 years

Most patients are euthyroid and present with a slow-growing painless mass in the neck

Diagnosis: FNAB

o If malignant, complete neck ultrasound is strongly recommended to evaluate the contralateral lobe and for lymph node metastases in the central and lateral neck compartments

Preference for LYMPHATIC SPREAD  1-2% distant metastasis

 Common radiation induced CA  90-95% cure rate

Cells with intranuclear cytoplasmic inclusions = ORPHAN ANNIE NUCLEI Calcified deposits = PSAMOMMA BODIES

 Most patients with papillary carcinoma can expect an excellent prognosis, with the 10-year survival rate approaching 95% for the most favorable stages

SUBTYPES

 The pathologic diagnosis of papillary carcinoma depends on the cytologic findings of well-recognized papillary cytomorphology

 Pure papillary, papillary follicular, follicular variant

 Tall cell, columnar, diffuse sclerosing, clear cell, trabecular, Hurthle cell variant and poorly differentiated

o They are trying to find out which types are aggressive compared to the rest, which is why there are so many subtypes

FORMS Minimal/Occult/Microcarcinoma

o < 1cm o Non-palpable

o Detected only by ultrasound

Intrathyroidal has NOT gone beyond the thyroid capsule Extrathyroidal has extended into the neck and nearby structures

TREATMENT

Total or near-total thyroidectomy for high risk or bilateral tumors and for primary cancers >1 cm unless with contraindications.

 The 2009 ATA guidelines for thyroid cancer management suggest that prophylactic (ipsilateral or bilateral) dissection may be performed in patients with advanced (T3 or T4) papillary thyroid carcinoma, whereas the procedure is not needed for small (T1 and T2) tumors that are clinically node negative

 Biopsy-proven lymph node metastases – modified radical or functional neck dissection

FOLLICULAR CARCINOMA  Relatively benign course

Common in iodine-deficient areas

Malignancy is defined by presence of capsular and vascular invasion  5-20% metastasis to lymph nodes

Spreads via BLOODSTREAM/HEMATOGENOUS SPREAD (in comparison to papillary which spreads via lymphatic system)

 2-5% distant metastasis  Associated with goiter in 10-15%

 70-80% cure rate (papillary type still has a higher cure rate)  Follicular and Papillary are relatively indolent

 3:1 female-to-male ratio (2015B)

 Mean age presentation: 50 years old (2015B)

 Cumulative mortality: 15% at 10 years and 30% at 20 years

PROGNOSTIC INDICATORS FOR WELL-DIFFERENTIATED CARCINOMA DAMES (Cady and Rossi)

D DNA content measured by flow cytometry A Age: men <40 years old, women <50 years old M Metastases

E Extrathyroid spread

S Size of tumors (less than or >5 cm)  AGES (Hay)

A Age

G Histologic Grade E Extrathyroidal invasion S Metastatic tumor size  MACIS (Hay)

M Metastases A Age of presentation

C Completeness of original resection I Extrathyroidal invasion

S Size of original lesion  Laudico, dela Peña, De Vera PGH

o Age

o Histology (nodal metastasis had no impact)

 Predictors of thyroid nodules malignancy, Ampil, Cortex, SIRF 1998 Age 56 +/- 15 years

Size 4.5 +/-1.4 cm especially if solitary

Consistency Hard especially if solitary (Histology and multicentricity had no impact)

o There is no consensus on methods to classify which are aggressive and which are not

Table 9. Prognostic Risk Classification for Patients with Well-Differentiated Thyroid Cancer (AMES or AGES) 

LOW RISK HIGH RISK

AGE <40 years >40 years

SEX Female Male

EXTENT No local extension, intrathyroidal, no capsular invasion Capsular invasion, extrathyroidal extension

METASTASIS None Regional or distant

SIZE <2 cm >4 cm

GRADE Well differentiated Poorly differentiated E. STAGING FOR WELL-DIFFERENTIATED CARCINOMA Primary tumor (T)

Tx Primary tumor cannot be assessed T0 No evidence of primary tumor

T1 Tumor ≤2 cm in diameter, limited to thyroid

T2 Tumor >2 cm but <4 cm in diameter, limited to thyroid

T3 Tumor >4 cm in diameter, limited to thyroid, or any tumor with minimal extrathyroidal invasion

T4a

Any size tumor extending beyond capsule to invade subcutaneous soft tissue, larynx, trachea, esophagus, or recurrent laryngeal nerve, or intrathyroidal anaplastic cancer

T4b Tumor invading pre-vertebral fascia, or encasing carotid artery or mediastinal vessels; or extrathyroidal anaplastic cance

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 9 of 11 Regional lymph nodes (N)—include central, lateral cervical, and upper

mediastinal nodes

Nx Regional lymph nodes cannot be assessed N0 No regional lymph node metastasis N1 Regional lymph node metastasis

N1a Metastases to level VI (pretracheal, paratracheal, and prelaryngeal/Delphian lymph nodes)

N1b Metastases to unilateral, bilateral, or contralateral cervical or superior mediastinal lymph nodes

Distant metastasis (M)

Mx Distant metastases cannot be assessed M1 No distant metastasis

Table 10. TNM Classification of Thyroid Tumors PAPILLARY OR FOLLICULAR TUMORS (WELL-DIFFERENTIATED)

STAGE TNM < 45 years I Any T, any N, M0 II Any T, any N, M1 ≥ 45 years I T1, N0, M0 II T2, N0, M0 III T3, N0, M0; T1–3, N1a, M0 Iv a T4a, N0–1a, M0; T1–4a, N1b, M0 IV b T4b, any N, M0

IV c Any T, any N, M1

Notice that in younger than age 45 years, the staging is only up to stage II

In younger than age 45 years old, notice that even if there is a metastasis it is still considered as stage II

 It signifies that it isn’t that aggressive when it is present for ages <45 years old

This is the only cancer that has age as a factor

TREATMENT OF WELL-DIFFERENTIATED CARCINOMA  Surgery

o < 1.0 cm (microcarcinoma), solitary: Total lobectomy + Isthmusectomy

o >1.0 cm, multicentric: Total Thyroidectomy (Schwartz’s it is >4 cm) Extrathyroidal Spread

o Total thyroidectomy + Central neck dissection  (+) Lymph Node Metastasis

o Total thyroidectomy + Modified radical neck dissection  Extent of Thyroidectomy

Figure 12. A diagram showing thyroid lobectomy to be done on <1cm WDC adenoma with a contralateral normal lobe. For all other types especially if

there are bilateral nodules, we do total thyroidectomy. Subtotal thyroidectomy is not indicated anymore.

COMPLICATION OF THYROIDECTOMY Bleeding - because it is a vascular area

Recurrent Laryngeal nerve injury – causes hoarseness. If both recurrent laryngeal nerve injury the vocal cords will both close necessitating tracheostomy

Superior Laryngeal nerve injury – decrease volume of voice Hypocalcaemia – inadvertent involvement of the parathyroids Thyroid storm – occurs if the patient was not euthyroid to begin with

Figure 13. Location of the parathyroid glands on the thyroid. Proximity of the parathyroid causes it to be excised along with thyroid upon thyroidectomy

causing symptoms of hypocalcaemia. You only need ½ -1 to maintain parathyroid function.

Figure 14. Borders of the Central Neck. Superior: Thyroid Cartilage. Medial: TE Groove. Lateral: Carotid Sheath. Inferior: Suprasternal Notch

ADJUVANT THERAPY  Radioactive iodine ablation

 TSH suppression (Target serum TSH = 0)  NO ROLE: Chemotherapy/radiation therapy

MONITORING AND FOLLOW-UP

Figure 15. Algorithm for Monitoring

We monitor Serum Thyroglobulin (Tg) after thyroidectomy. Ideally it should be decreased or 0 after the procedure because it is produce by the thyroid gland

 Tg levels in patients who have undergone total thyroidectomy should be <2 ng/mL when the patient is taking T4 , and <5 ng/mL when the patient is hypothyroid

 A Tg level >2 ng/mL is highly suggestive of metastatic disease or persistent normal thyroid tissue

 Approximately 95% of patients with persistent or recurrent thyroid cancer of follicular cell origin will have Tg levels >2 ng/mL

 Tg and anti-Tg antibody levels should be measured initially at 6-month intervals and then annually if the patient is clinically disease free

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 10 of 11  If serum Tg is still present after 6 months, we assume recurrence

 If it is still positive, we work up the patient with a whole body can. Areas with iodine will light up

WHOLE BODY IODINE-131 SCAN

In cases where there is still positive serum thyroglobulin (Tg) 6-12 months after total thyroidectomy for a high risk well-differentiated carcinoma, one must suspect recurrence since Tg is produced only by the thyroid

 When this happens, work up the patient and what is usually done is Whole Body Iodine-131 Scan. It works in a similar principle to RAI scan, but it is applied for the whole body. The distant metastatic lesions will imbibe iodine and will light up

Treatment for metastatic sites: Radioactive Iodine Tablets HURTHLE CELL CARCINOMA

Subtype of follicular CA

More often multifocal and bilateral (30 %), usually do not take up RAI (5 %), more likely to metastasize, associated with higher mortality rate (20% at 10 years).

It DOES NOT respond to RAI.

Treatment: lobectomy and isthmusectomy MEDULLARY CARCINOMA More aggressive than papillary/follicular carcinoma Arise from parafollicular or C cells of the thyroid

o C cells secrete calcitonin

o 25% occur within the spectrum of several inherited syndromes (germline mutations in the RET ) proto-oncogene

 Familial medullary thyroid cancer, MEN2A & B  Diagnosis

o Raised serum calcitonin levels – this finding clinches the diagnosis o FNA cytology – confirms the diagnosis

o Once diagnosed, all new patients with MTC should be screened for RET point mutations, pheochromocytoma, & hyperparathyroidism  Treatment

o Minimum is total thyroidectomy + central neck dissection ANAPLASTIC CARCINOMA

Most aggressive of all Rapidly enlarging

o Doctor’s experience: A patient with anaplastic carcinoma was admitted once, but whose surgery was delayed for 1 month because of financial constraints. The tumor was observed to be growing bigger and bigger every day before their very eyes  Treatment:

o Tracheostomy + Radiotherapy (RT provides only 30% success rate)

Most of the time, because of the immense size of the mass, thyroidectomy/resection may not be possible. Thus, tracheostomy is done to address the obstruction of airways. o Total thyroidectomy / Chemotherapy / Radiotherapy

 Done if the tumor is still resectable o Palliative treatment

J. OTHER RARE CANCERS Sarcoma

Lymphoma

 The diagnosis is considered in patients with a goiter, especially one that has apparently grown significantly in a short period.

 Other initial symptoms include hoarseness, dysphagia, and fever.  There is also an increased association between lymphoma and

Hashimoto's thyroiditis.

 Ultrasound may demonstrate a classic pseudocystic pattern.

 FNA can be diagnostic

 The use of flow cytometry for monoclonality can confirm diagnosis  Neck, chest, abdominal CT or MRI to assess extrathyroidal spread.  Most thyroid lymphomas are B cell in origin

 Use of the CHOP regimen (cyclophosphamide, hydroxydaunomycin [doxorubicin], vincristine, and prednisolone) has been associated with excellent survival.

Metastatic cancer

o Kidney, breast, lung, and melanoma  FNAB usually provides definitive diagnosis.

 Resection of the thyroid, usually lobectomy, may be helpful in many patients, depending on the status of their primary tumor

PARATHYROID GLANDS

CALCIUM HOMEOSTASIS Parathyroid hormone (PTH): increases serum calcium

Vitamin D: increases serum calcium by stimulating the absorption of calcium and phosphate from the gut.

o The first hydroxylation at carbon 25 occurs in the liver

o The second hydroxylation at carbon 1 occurs in the kidney in response to increased PTH levels.

o 1,25(OH)2D3 increases calcium and phosphate resorption from the

gastrointestinal tract and stimulates bone resorption, which raises calcium levels

Calcitonin: decreases serum calcium

Table 10. Actions of Major Calcium-Regulating Hormones 

BONE KIDNEY INTESTINE

PARA-THYROID HORMONE Stimulates resorption of calcium and phosphate Stimulates resorption of calcium and conversion of

25(OH)D3; inhibits resorption of phosphate and bicarbonate No direct effects VITAMIN D Stimulates transport of calcium Inhibits resorption of calcium Stimulates calcium and phosphate absorption CALCITONIN Inhibits resorption of calcium and phosphate Inhibits resorption of calcium and phosphate

No direct effects

Figure 16. Calcium homeostasis and parathyroid hormone (PTH). 1,25(OH)2D3, 1,25-dihydroxycholecalciferol. 

HYPERPARATHYROIDISM There is excess PTH, thus there is hypercalcemia Primary (PHPT)

o From abnormal parathyroid glands, usually due to a tumor  Secondary

o A compensatory response to hypocalcemic states  Chronic renal failure

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The L-team | Kheita, Jean, Renan, Ikey, Bea, James, Sher, Lori, Aleya Page 11 of 11 Tertiary

o Chronically stimulated glands become autonomous, resulting in persistence or recurrence of hypercalcemia after successful renal transplantation

o Even though serum calcium is elevated, PTH is still being continuously secreted.

PRIMARY HYPERTHYROIDISM (PHPT)

Arises from increased PTH production from abnormal parathyroid glands and results from a disturbance of normal feedback control exerted by serum calcium.

PHPT is characterized by increased parathyroid cell proliferation and PTH secretion that is independent of calcium levels

 Causes

o Parathyroid hyperplasia (20%)

o Adenoma (80% single if single adenoma) o Carcinoma (1%)

o Low dose ionizing radiation  Latency: 30 to 40 years

 Higher PTH levels and a higher incidence of concomitant thyroid neoplasms than those who did not have exposure o Family history

 MEN1, MEN2A, isolated familial HPT, and familial HPT with jaw-tumor syndrome

 PHPT is the most common primary presentation of MEN1 (80%)

 Signs and Symptoms

o Due to increased serum calcium o “Classic” pentad of symptoms

 Kidney stones (80%), painful bones(15 to 20%), abdominal groans, psychic moans & fatigue

o Minimally symptomatic

 Weakness, fatigue, polydipsia, polyuria, nocturia, bone & joint pain, constipation, decreased appetite, nausea, heartburn, pruritus, depression, & memory loss

o Asymptomatic  Diagnosis

o High serum calcium

 First done if suspicion of PHPT is raised because of signs and symptoms. If serum calcium is high, do serum PTH.

o High serum PTH assay

 A high serum PTH suggests the pathology is indeed primarily located in the parathyroids. Thus perform a parathyroid scan. o Parathyroid scan

 Presence of abnormal growth confirms the diagnosis, thus, do parathyroidectomy.

o Radiology

 Bone involvement

Pathognomonic signs seen best on hand X-ray: Subperiosteal resorption (most apparent on the radial aspect of the middle phalanx of the second and third fingers), bone cysts, and tufting of the distal phalanges

Treatment: Parathyroidectomy o Subtotal

 If dealing with an adenoma, usually, just one needs to be removed, since not all parathyroids will be enlarged.

 If dealing with hyperplasia, the problem is that all 4 glands will be enlarged. You can’t remove all four. Thus, do a three-and-one-half parathyroidectomy, leaving ½ of one

parathyroid in place.

o Total parathyroidectomy with autotransplantation or transfer of a gland to a neck or forearm muscle

 Alternative to 3 ½ parathyroidectomy.

HYPOPARATHYROIDISM  Causes

o Di George’s syndrome - congenitally absent parathyroid o Neonatal hypoparathyroidism - from hyperparathyroid mother o THYROID SURGERY: leading to injury to the parathyroid, most

common cause, 95% of cases (total thyroidectomy)

Temporary hypoparathyroidism – occurs in 90% of all thyroidectomy cases. In the course of thyroid gland dissection, edema of the parathyroids is unavoidable thus it temporarily becomes dysfunctional and cannot produce PTH.  Permanent hypoparathyroidism – remaining 5-10%. Means

the surgeon has inadvertently removed the parathyroids.  Signs and Symptoms

o Hypocalcemia causing increased neuromuscular excitability o Circumoral and fingertip numbness and tingling

o Mental symptoms: anxiety, confusion, and depression

o (+) CHVOSTEK SIGN: Contraction of facial muscles elicited by tapping on the facial nerve anterior to the ear

o (+) TROUSSEAU SIGN: Carpopedal spasm, which is elicited by occluding blood flow to the forearm with a blood pressure cuff for 2–3 min

o Tetany

o These signs and symptoms must be monitored in a patient who has undergone thyroidectomy.

 Diagnosis

o Decreased serum ionized calcium levels  Treatment

o Calcium tablets or IV infusion o Vitamin D supplements

I can't think of a single reason why I should be a surgeon, but I can think of a thousand reasons why I should quit. They make it hard on purpose. There are lives in our hands. There comes a moment when it's more than just a game, and you either take that step forward or turn around and walk away. I could quit but here's the thing, I love the playing field. –Dr. Meredith Grey (Grey’s Anatomy)

LAST TRANS FOR SURGERY!!! The L-team now signing off :)) See you clerkship! God bless for the upcoming exams!! :D

Editor’s note: Good luck to everyone!! Last push for third year!!

DO

n’t qu

IT

!!

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