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Head and Neck > Thyroid Anatomy + Non-Neoplastic Pathology > Flashcards

Thyroid Anatomy + Non-Neoplastic Pathology Flashcards

1
Q

Describe the embryology of the thyroid gland

A

SUMMARY (Cummings)
- Medial thyroid derives from the ventral diverticulum of the endoderm of the first and second pharyngeal pouches of the foramen cecum
- 4-7 GA: Diverticulum descends from the base of tongue to the pretracheal position. Proximal portion then retracts and degenerates into a fibrous stalk (persistence = TGDC)
- Lateral thyroid arise from fourth and fifth pharyngeal pouch and descend to join the medial portion
- Parafollicular C-cells arise from the neural crest of the fourth pharyngeal pouch as ultimobranchial bodies and infiltrate the upper portion of the thyroid lobes

DETAILS:
4 weeks GA:
- Endoderm on the floor of the pharynx between the 1st and 2nd arches invaginates and descends into the mesenchyme of the neck - this diverticulum is situated between the tuberculum impar (forms the oral tongue along with the lingual swellings) and the copula (forms the base of tongue)

4.5 weeks GA:
- Connection between the ventral thyroid diverticulum and the floor of the pharynx (foramen cecum) disappears
- Diverticulum develops into the median thyroid anlage

6-10 weeks GA:
- Thyroglossal duct has completed degenerated
- Cellular proliferation results in the right and left thyroid lobes, separated by an isthmus
- In up to 40-50% of individuals, the distal aspect of the duct persists as a pyramidal lobe
- The ultimobranchial body of the 4th arch fuses and is incorporated into the supero-lateral aspects of the thyroid lobes, and forms the parafollicular c-cells which secrete calcitonin

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2
Q

What are the two types of capsules of the thyroid?

A
  1. True capsule: Peripheral condensation of the glandular tissue, gives rise to septa deep within thyroid parenchyma
  2. False capsule: Pre-tracheal layer of deep cervical fascia encapsulating thyroid
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3
Q

What is the structural and functional unit of the thyroid?

A

FOLLICLES:
- A thyroid lobule is made up of aggregation of follicles

Histology:
- Follicles are lined by follicular cells, resting on a basement membrane, and have a cavity filled with colloid (homogenous gelatinous material)
- Colloid is composed of THYROGLOBULIN (protein made by thyroid gland, used to make T3/T4)
- Spaces between follicles = tissue stroma, capillaries, lymphatics

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4
Q

Regarding follicular cells, discuss:
1. What are they?
2. What phases could follicular cells be in at any time?
3. What do follicular cells secrete?
4. What does the electron microscopy of a follicular cell look like?

A

FOLLICULAR CELLS:
- Lining cells of a thyroid follicle
- Follicular cells can have different levels of activity within the same thyroid tissue

PHASES:
1. Resting (inactive) phase: flat, squamous, abundant colloid within cavity
2. High active phase: columnar, scanty colloid
3. Moderately active phase: Cuboidal, reasonable colloid

FUNCTION (Secretes the following, influenced by TSH):
1. T3 (more active)
2. T4

ELECTRON MICROSCOPY:
1. Apical microvilli
2. Abundant granular endoplasmic reticulum
3. Supranuclear Golgi complex
4. Lysosomes
5. Microtubules
6. Microfilaments

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5
Q

Regarding parafollicular C-cells, discuss:
1. What are alternative names?
2. Describe their structure and histology
3. Function
4. Electron microscopy

A

PARAFOLLICULAR C-CELLS:
- aka. Clear cells, light cells
- C stands for calcitonin (or clear)

STRUCTURE:
1. Polyhedral, pale-staining cells with oval and eccentric nuclei
2. Distributed BETWEEN follicular cells and their basement membrane; can also lie between adjoining follicular cells but do not reach the lumen; can also be seen between the follicles

FUNCTION:
- Secretes calcitonin (responsive to serum calcium levels)
- Other organs also secrete calcitonin: lungs, GI tract

ELECTRON MICROSCOPY:
1. Electron-dense secretory granules (100-200nm in diameter) of hormone calcitonin

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6
Q

Regarding the anatomy of the thyroid, discuss:
1. Describe the lobes and size of the thyroid
2. What is Berry’s ligament?

A

THYROID GLAND:
- Two lateral lobes connected by a central isthmus
- 40% with a pyramidal lobe arising from either lobe, or midline isthmus and extends superiorly
- 15-25g in adults, ~4cm tall x 1.5cm width x 2cm depth

BERRY’S LIGAMENT:
- The middle layer of the deep cervical fascia posterior to the thyroid
- Condenses to form the posterior suspensory ligament (aka Berry’s), which connects the lobes of the thyroid to the cricoid cartilages and first 2 tracheal rings

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7
Q

Describe the blood supply to the thyroid

A

TWO PAIRED ARTERIES PLUS IMA:
1. Inferior thyroid artery x 2
2. Superior thyroid artery x 2
3. Arteria Thyroidea Ima

Inferior thyroid artery:
- Arises from thyrocervical trunk (first branch of subclavian)
- Extends along anterior scalene and crosses beneath the long axis of the common carotid artery
- Lies anterior to RLN in 70% patients (landmark to find RLN at the tracheoesophageal groove - feel for the pulse)
- Main blood supply for parathyroid glands

Superior thyroid artery:
- First branch of the external carotid artery, courses along the inferior constrictor muscle and superior thyroid vein
- Courses posterolateral to the external SLN branch as it enters the cricothyroid muscle

Arteria Thyroidea Ima:
- May arise from the innominate, carotid, or aortic arch
- Supplies the thyroid gland near the midline

THREE PAIRS OF VEINS: All lead to internal jugular or innominate veins
1. Superior thyroid vein x 2
2. Middle thyroid vein x 2 (no arterial counterpart)
3. Inferior thyroid vein

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8
Q

Regarding the recurrent laryngeal nerve, discuss:
1. Function
2. Embryology
3. What is a non-recurrent laryngeal nerve? When does this usually occur?

A

FUNCTION:
1. Motor supply to larynx
2. Some sensory supply to upper trachea and subglottis

EMBRYOLOGY:
- Inferior laryngeal nerves derive from sixth branchial arch
- Originate from the vagus under the sixth aortic arch
- RLN dragged caudally by the lowest persisting aortic arches
1. Right side - recurs around the 4th arch (subclavian)
2. Left side - recurs around the 6th arch (ligamentum arteriosum)
- Left RLN takes a more medial course (near the tracheoesophageal groove) compared to the right RLN (~2cm more lateral to trachea)

NON-RECURRENT LARYNGEAL NERVES:
- Usually occurs only on the right side, and enters a lateral course
- In almost all cases, an aberrant retroesophageal subclavian artery (Arteria lusoria) and other congenital malformation of vascular rings is present

See Laryngology notes for further details

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9
Q

Regarding the superior laryngeal nerve, discuss:
1. What does the internal and external branches supply?
2. What does it typically travel with?

A
  • Internal branch enters posterior thyrohyoid membrane to supply sensation to the supraglottis
  • External branch extends medially along inferior constrictor muscle to enter the cricothyroid muscle
  • Travels with the superior thyroid artery and vein
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10
Q

What are the tubercles of Zuckerkandl?

A

Posterior extensions of each thyroid lobe

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11
Q

Regarding the physiology of the thyroid gland, discuss:
1. What are the major hormones? What derivatives are they from?
2. What is the general pathway of thyroid hormone production?
3. Where is thyroid hormone storeed within the thyroid?

A

MAJOR HORMONES = Iodinated derivatives of tyrosine
1. T3: 3,5,3’-triiodothyronine
2. T4: Thyroxine; 3,5,3’,5’-tetraiodothyronine

PATHWAY:
Iodide + thyroglobulin = thyroid hormone

STORAGE: Within follicular lumen (storage of hormone and their derivatives)

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12
Q

What are the 8 main steps in thyroid metabolism?

A
  1. Uptake of iodine by thyroid (stimulated by TSH)
    - Requires at least 100µg of iodine per day
    - Pendrin: Apical membrane protein that release iodide into follicular lumen (Pendred Syndrome = mutation of pendrin causing mild hypothyroidism, goiter, hearing loss)
  2. Coupling of iodine to Thyroglobulin Tg (organification) –> makes Monoiodotyrosine (MIT) and diiodotyrosine (DIT)
    - Thyroglobulin = glycoprotein that serves as matrix for hormone synthesis from iodine and vehicle for storage
    - Occurs through: oxidation of iodide, then transfer of oxidized iodide to thyrosyl residues on thyroglobulin
  3. Storage of MIT/DIT in colloid (fills the follicles)
  4. Re-absorption of MIT/DIT
  5. MIT/DIT link together to form T3 + T4
    - Catalyzed by THYROPEROXIDASE (TPO)
    - MIT + DIT = T3
    - DIT + DIT = T4
  6. Release of T3 and T4 into serum (90% released as T4)
    - THYROXINE-BINDING GLOBULIN (TBG): Binds 75% of circulating hormone (< 1% of circulating hormone is free); contains one hormone binding site and has a higher affinity for T4
    - TRANSTHYRETIN: Binds ~10% of circulating hormone; contains two hormone binding sites; first site has lower affinity than TBG, second site even lower than the first
    - ALBUMIN: Binds ~10-20% of circulating hormone; overall low affinity thyroid binding protein
    - Unbound (0.2% T4, 0.3% T3) - Higher amount of T3 is unbound, given lower affinity to TBG
  7. Liver, kidney, muscle, and anterior pituitary convert T4 to T3
    - T4 must be converted to T3 to exert biologic actions; enzymes are:
    - Type I Deiodinase: Primary source of circulating T3; found in kidney, liver, thyroid; INHIBITED by Prophylthiouracil (PTU)
    - Type II Deiodinase: Found primarily in CNS, pituitary, placenta, and skin; mainly involved in local T3 production
    - Type III Deiodinase: Inactivates T3/T4, role in protecting tissues from excess thyroid hormone; found in brain, skin, placenta, and high levels in fetal tissues
  8. Breakdown of T3 and T4 release iodine
    - Feedback to TRH/TSH (T3 causes negative feedback)
    - T3 causes negative feedback
    - TSH/TRH causes positive feedback
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13
Q

What is the percentage of thyroid hormone that is T4? Which thyroid hormone is more active?

A

98% T4

T3 is four times more active than T4

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14
Q

Regarding T3 and T4, discuss:
1. What are the half lives of each?
2. Where are they converted?
3. What are the synthetic compounds?

A

T3:
- Half life 1 day
- Converted peripherally
- Much more active than T4 (6 weeks)
- Liothyronine (Cytomel) is manufactured T3

T4:
- Half life 5-7 days
- 80% bound to TBG (Thryoxine binding globulin)
- Levothyroxine is manufactured T4 (2 weeks)

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15
Q

How long prior to RAI treatment should you withdraw thyroxine and cytomel?

A

Levothyroxine = 6 weeks
Liothyronine = 2 weeks

Note: rhTSH (Recombinant TSH) is used to stimulate TSH for patients on thyroid hormone suppression therapy
- Useful for preparing for RAI ablation and monitoring for recurrence of thyroid cancer
- Does NOT need to be stopped prior to RAI

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16
Q

What increases your levels of thyroxine binding globulin? What decreases it?

A

INCREASES:
1. Estrogen

DECREASES:
1. Steroids
2. Liver failure

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17
Q

Describe the Hypothalamus-pituitary axis with respect to control of thyroid function.

What are the effects of TSH on the thyroid? List 6.

A

HYPOTHALAMUS: Secretes TRH (Thyrotropin-releasing hormone)

ANTERIOR PITUITARY: Secretes TSH (aka. Thyrotropin; thyroid-stimulating hormone)

THYROID: Thyroid hormone (provides negative feedback to system above)

EFFECTS OF TSH ON THYROID:
1. Increase iodide uptake into cells
2. Increase organification (forming MIT/DIT)
3. Increase Tg synthesis and proteolysis
4. Alters distribution of iodoamino acids within Thyroglobulin (hydrolysis) to release MIT to DIT and T3 to T4, and release these into circulation
5. Increases intrathyroidal converstion of T4 to T3 by Type I/II deiodinases
6. Improves storage of T3 + T4 in the gland as colloid
Maintains structure of thyroid cells, and stimulates gland size and vascularity

Note: Prolonged iodine deficiency = goiter (increased cell stimulation)

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18
Q

What are the effects of thyroid hormone on fetal and neonatal development? What can develop if there is a deficiency in thyroid hormone in the fetus? What about an excess?

A
  1. Maturation of CNS, muscle, bone and lung

Cretinism: Severe deficiency of thyroid hormone during fetal development, resulting in mental retardation, deafness, mutism, and stunted growth

Excess of thyroid hormone in fetal development can result in neurologic abnormalities

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19
Q

What are the general actions of thyroid hormone on the body? List 9.

A
  1. Increase metabolism of protein, carbohydrates, and fats
  2. Modulation of several enzyme activities
  3. Increase Cardiac output and heart rate
  4. Increase heat production
  5. Increase RBC mass
  6. Increase O2 consumption
  7. Increase metabolic rate (calorigenesis)
  8. Epinephrine potentiation
  9. Decrease cholesterol
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20
Q

What are the 3 broad classes of anti-thyroid agents?

A
  1. Inhibits TH synthesis
  2. Inhibit TH secretion
  3. Inhibit TH metabolism
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21
Q

What are the different types of thyroid function studies that can be performed?

A
  1. Thyroid hormone measurement
  2. Serum TSH measurement
  3. Serum thyroglobulin measurement
  4. Thyroid antibody status
  5. Radioactive iodine uptake test
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22
Q

Regarding the measurement of thyroid hormone, discuss:
1. What is measured?
2. What are the indications to obtain T3 level?

A

MEASUREMENTS USING RADIOIMMUNOASSAY:
1. T4 (most commonly obtained)
2. T3

INDICATIONS FOR SERUM T3 LEVEL:
1. Determine severity of hyperthyroidism
2. Confirm diagnosis of suspected thyrotoxicosis in cases of normal Serum T4 levels
3. Evaluate patients with autonomously functioning thyroid adenomas (may have normal T4 and suppressed TSH)

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23
Q

What are the indications to obtain TSH measurement?

A
  1. Diagnosis of primary hypothyroidism (elevated TSH; degree may be determined by obtaining T4)
  2. Diagnosis of hyperthyroidism / subclinical hyperthyroidism
  3. Guidance of thyroid hormone replacement therapy
  4. Determination of TSH suppression in treating thyroid cancer
  5. Determination of suppressive therapy for nodular goiter (not commonly used in US)
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24
Q

What is the utility of serum thyroglobulin measurement? What is the main indication?

A

Elevated in almost all types of thyroid disorders, thus not that useful of a test

Main indication:
- Monitoring well-differentiated thyroid carcinoma (elevated or increasing level after initial surgical or ablation therapy suggests persistence or recurrence of tumor)

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25
Q

What are thyroid antibodies that can be measured? What are their indications?

A

ANTIBODIES: Present in autoimmune thyroid disease
1. Antithyroid antibodies (ATAs)
2. Antimicrosomal antibodies (AMAs)
3. Thyroid stimulating antibodies

AMA = Anti-TPO
- ~100% Hashimoto thyroiditis
- ~80% Graves disease
- Also positive in many other autoimmune diseases (e.g. lupus, RA, Sjogrens, T1DM, Addison’s disease)
- ATA less sensitive, but more specific (not as useful in autoimmune thyroid disease detection)

Measurement of Thyroid-Stimulating Antibodies
- Thyroid-stimulating immunoglobulin detectable in 90-95% of hyperthyroid Graves’ disease patients
- No indicated for routine diagnostic evaluation of suspected Graves’, but useful if diagnosis if not evident

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26
Q

Regarding the Radioactive Iodine uptake test, discuss:
1. How does the procedure work?
2. What are the indications?
3. What is normal uptake?

A

RAI UPTAKE:
- Oral administration of iodine-123, followed by measurement of % in thyroid gland after 24 hours

INDICATIONS:
1. Differentiating high vs. low-uptake hyperthyroidism
2. Not as useful now for differentiation hypo vs. hyperthyroidism

Normal Uptake ~15-20%

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27
Q

What are the symptoms of hypothyroid? List as many as you can think of

A
  1. General:
    - Weakness and fatigue
    - Cold intolerance
    - Weight gain
    - Hair loss
    - Edema of hands and face
    - Thick, dry skin and dry hair
    - Decreased tendency to sweat
  2. GI symptoms:
    - Constipation
    - Anorexia
    - Intermittent nausea and vomiting
    - Dysphagia (more common if external compression)
    - Bloating
  3. GU symptoms:
    - Menstrual disorders
    - Polyuria
  4. CVS symptoms:
    - Bradycardia
    - Hypertension
    - Intermittent angina
    - Pericardial effusion
    - Peripheral edema
  5. CNS symptoms:
    - Daytime somnolence, nighttime insomnia
    - Mental and physical slowness
    - Headaches and dizziness
    - Delayed reflexes
    - Psychologic symptoms - depression, anxiety
  6. MSK symptoms:
    - Arthritis
    - Stiffness of joints
    - Muscle cramps
  7. OHNS symptoms:
    - Hearing loss
    - Dizziness
    - Tinnitus
    - Voice aberrations (vocal cords may be thickened and polypoid along edges, causing harsh raspy voice)
    - Middle ear effusion
    - Slurred speech with enlarged tongue
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28
Q

What are the symptoms of hyperthyroidism? List as many as you can think of

A
  1. General:
    - Palpitations / Tachycardia with or without arrhythmia
    - Irritability
    - Anxiety
    - Easy fatigue
    - Increased bowel movements with weight loss
    - Heat intolerance
    - Warm, moist skin
    - Fine tremor of fingers
  2. Ocular symptoms:
    - Lid lag
    - Eyelid retraction
    - Exophthalmos
29
Q

What are the symptoms of compressive goiter?

A
  • Dysphagia
  • Dyspnea
  • Voice aberration
  • Vocal cord paralysis
  • Horner’s syndrome (ptosis, miosis, anhidrosis)
  • Superior vena cava syndrome
  • Pericardial or pleural effusion
30
Q

Aside from symptomology of thyroid disease, what other key history points are required?

A
  • History of thyroid/head and neck surgery
  • Laryngeal cancer or laryngectomy
  • Radiation to the head/neck
  • Hashimoto thyroiditis
  • Inflammatory thyroid conditions
31
Q

In addition to the physical exam features of hypo/hyperthyroid elicited on history, what are some special tests that can be performed for thyroid disorders?

A
  1. Pemberton Sign
    - Extend both arms above head and observe for facial erythema, swelling, or distention of the jugular veins, indicating cervicothoracic inlet obstruction
  2. Rule out lingual thyroid gland (guttural voice quality may signify obstruction of the aerodigestive passage)
  3. Texture of thyroid may suggest etiology:
    - Cobblestone-like / Bosselated thyroid: Autoimmune thyroid disease
    - Smooth nodularity: Colloid goiter
  4. Rule out vocal fold paralysis prior to surgical intervention (voice may sound normal even if paralyzed)
    - Paralysis usually indicates infiltration of nerve by malignancy, but can also indicate compression
32
Q

Regarding Hypothyroidism, discuss:
1. What is the prevalence/epidemiology?
2. What are the risk factors?
3. Clinical presentation? Specific ENT findings?
4. Management? How does this change with specific situations (e.g. pregnancy)?

A

PREVALENCE:
1. F>M (4-6x greater in female)
2. Increases prevalence with age
3. 11.3% have TPO antibodies

RISK FACTORS
- Older age
- Female
- Graves’
- Hashimoto disease
- Autoimmune disease (e.g. T1DM, Adrenal insufficiency, vitiligo)
- Post-thyroidectomy
- Goiter
- Prior neck irradiation
- Laryngectomy
- External radiation
- Drugs (e.g. lithium, amiodarone, iodine-containing compounds, PPI, sulfa, steroids)

CLINICAL PRESENTATION:
- See previous card on symptoms
- Severity depends on severity of deficiency, rapidity of onset, and in elder patients

ENT MANIFESTATIONS:
1. Hearing loss (more frequently in congenital hypothyroid)
- Cretinism: may have anomalous ossicles, or atrophy of organ of Corti
2. Vertigo (60%) without ENG changes or hearing loss
3. Macroglossia
4. Hoarseness: Mucopolysaccharide infiltration of vocal cords, tissue edema in ambiguous nucleus or cricothyroid muscles

MANAGEMENT:
1. Oral synthetic levothyroxine (T4)
- GI absorption 81%
- Half-life of T4 is 6.7 days
- Dosage: 1.6-1.7 µg/kg/day, may need up to 2.1µg/kg/day for surgical thyroidectomy patients
- Monitor TSH and adjust dose every 4-6 weeks (4-6 half lives)
- Thyroid hormone requirements increased during pregnancy by ~45% (estrogen-mediated increase in TBG, fetal T4 transfer, and increased T4 clearance)

33
Q

Describe the classification of hypothyroidism, and the etiology of each.

A

CLASSIFICATION:
1. Primary (Gland)
2. Secondary (Pituitary)
3. Tertiary (Hypothalamus)
4. Peripheral Resistance

PRIMARY HYPOTHYROIDISM: ETIOLOGY (4)
1. Thyroid Agenesis
2. Destruction of thyroid tissue
- Most common in iodine-sufficient world: Chronic Autoimmune (Hashimoto) Thyroiditis
- Surgical removal
- Therapeutic irradiation
- Cancer/infiltrative disease (e.g. amyloidosis, scleroderma)
- Post-thyroiditis (Acute or subacute)
- Post-laryngectomy or External Radiation (within 4 months)

  1. Inhibition of thyroid hormone synthesis, release, or both
    - Most common worldwide: Iodine Deficiency
    - Iodine administration in underlying autoimmune thyroiditis patients (e.g. Amiodarone, Lugol’s)
    - Medications with antithyroid action (e.g. Lithium, Interferon alpha/beta, IL-2, bile acid sequestrants, PPI, Raloxifene, Ciprofloxacin, soy products)
    - Inherited enzyme defects
  2. Transient hypothyroidism
    - Post-operatively
    - Post-partum
    - Recovery from thyroiditis
    - Autoimmune thyroiditis (Hashimoto)
    - Withdrawal of thyroid hormone in euthyroid patients
34
Q

Discuss the diagnosis of hypothyroidism, with respect to findings of T4/T3 and TSH:
1. Overt
2. Subclinical
3. Pituitary (secondary)
4. Hypothalamic (tertiary)

A
  1. Overt
    - T4/T3: NL or Low
    - TSH: High
  2. Subclinical
    - T4/T3: NL
    - TSH: High
  3. Pituitary (secondary)
    - T4: Low or NL
    - TSH: NL, low, or slightly high
  4. Hypothalamic (tertiary)
    - T4/T3: Low or NL
    - TSH: NL, low, or slightly high
35
Q

Regarding subclinical hypothyroidism, discuss:
1. How is this diagnosed?
2. Clinical presentation?
3. Risk factor of progression to overt?
4. Treatment?

A

Diagnosis:
- Elevated TSH with normal T3/T4

Clinical presentation:
- Goiter
- Possibly mild symptoms of hypothyroid, may progress to overt hypothyroidism

Risk factor of progression to overt:
- Positive TPO antibodies
- TSH > 10
- Radiation history

Treatment: (can prevent progression to overt, especially with above risks)
1. Low dose thyroid hormone, titrate to normal TSH
2. Benefits with improving cholesterol levels

36
Q

What is Sick Euthyroid syndrome?

A
  • Often seen in non-thyroid illness (e.g. ICU patients, trauma)
  • TSH elevation (mild), with normal or decreased T4 levels
37
Q

Regarding Hashimoto’s disease/thyroiditis, discuss:
1. What is this?
2. What antibodies are present?
3. Clinical presentation?

A

HASHIMOTO’S THYROIDITIS:
- Autoimmune disease of the thyroid

ANTIBODY PRESENCE:
- Anti-TPO (90%)
- Anti-Tg (50%)
- Anti-microsomal Ab (90%)
- Anti-TSH Ab

CLINICAL PRESENTATION:
1. Goiter
2. 10% transient hypothyroidism only

38
Q

Regarding Myxedema Coma, discuss:
1. What is it?
2. Etiology?
3. Clinical presentation?
4. Treatment?

A

MYXEDEMA COMA:
- Definition: Late manifestation of severe hypothyroidism characterized by coma or precoma with severe symptoms of myxedema (hypothyroidism), mortality up to 50%

ETIOLOGY:
- Infection
- Chronic illness
- Medication
- Precipitating source

CLINICAL PRESENTATION:
- Hypothermia
- Hypotension, Bradycardia
- Shock that doesn’t respond well to vasoconstrictors
- Pleural and pericardial effusion
- Hyponatremia
- Hypoventilation and respiratory acidosis
- Hypoxia, sleep apnea
- Upper airway obstruction (oropharyngeal muscle dysfunction, tissue infiltration with mucopolysaccharide)
- von Willebrand disease-like defect - bleeding (resolves with desmopressin temporarily until T4 corrected)
- Focal or generalized seizures preceding coma

TREATMENT:
- IV T4 (obtain diagnostic certainty prior this)
- Hydrocortisone (Adrenal insufficiency implicated in thyroid storm)
- Supportive care: ICU/ventilation, warming, support BP
- Treat underlying cause

39
Q

What are the indications for endocrinology consult for patients with hypothyroidism?

A
  • Children/infants
  • Difficult to maintain euthyroid state
  • Pregnancy or fertile women planning to conceive
  • Cardiac disease
  • Goiter, nodule, or other thyroid structural changes
  • Other Endocrine diseases (adrenal, pituitary)
  • Unusual thyroid function test results
  • Hypothyroidism caused by medications or other unusual presentations
40
Q

Regarding thyrotoxicosis, discuss:
1. What is it? How does it differ from the term “hyperthyroidism”? What does overt and subclinical thyrotoxicosis mean?
2. Epidemiology/prevalence?
3. Etiology?
4. Pathophysiology?
5. Symptoms?

A

THYROTOXICOSIS:
- Definition: Clinical and biochemical syndrome that results from exposure to excessive thyroid hormone concentration
- Whereas hyperthyroid = type of thyrotoxicosis, strictly meaning elevated endogenous thyroid hormone (used interchangeably, but technically different)
- Overt thyrotoxicosis: High serum T4 and T3 with low serum TSH
- Subclinical thyrotoxicosis: Normal T4 and T3 with low serum TSH, often no symptoms or signs of disease

EPIDEMIOLOGY:
- Onset: sudden or gradual
- Duration: transient or persistent
- Prevalence: 0.5-1 in 1000 (0.1%) in US, ~1-4% in Europe
- Women > Men (10:1), especially overt
- Increases with age

ETIOLOGY:
- Graves’ disease (60-85%) - ~30-60yo
- Toxic multinodular goiter (10-30%) - higher in areas of lower iodine intake, ~40-70yo
- Toxic thyroid adenoma (2-20%) - higher in areas of lower iodine intake ~40-70yo
- Thyroiditis (subacute, silent, postpartum, radiation induced)
- Exogenous thyrotoxicosis (thyroid hormone induced, iodine induced, drug and cytokine induced)
- Autosomal-dominant and sporadic thyrotoxicosis (e.g. McCune-Albright syndrome)
- Ectopic thyrotoxicosis (e.g. struma ovarii - monodermal teratoma composed of mature thyroid tissue)
- Thyroid carcinoma
- Thyrotropin-dependent thyrotoxicosis
- Pregnancy-related thyrotoxicosis (Gestational Thyrotoxicosis, Trophoblastic tumors)

PATHOPHYSIOLOGY:
- Generally, increased T3 production compared to T4
- T3 Thyrotoxicosis: Significant increased T3 concentrations compared to T4 (some have normal T4), more common in toxic thyroid adenoma or recurrent Graves’ disease
1. Unregulated release of T4 and T3
- Increased hormone synthesis and release 2o intrinsic thyroid disease
- Excessive TSH
- Excessive TRH
- Production of other TSH (e.g. autoantibody, chorionic gonadotropin)
- Destruction of thyroid tissue causing release of stored hormone

  1. Ingestion of excessive amounts of T3/4

SYMPTOMS:
- See previous list of all hyperthyroid symptoms
- Pertinent questions: 1) Duration of symptoms, 2) Degree and pattern of thyroid enlargement, 3) Presence or absence of thyroid pain and tenderness

41
Q

Regarding Graves’ disease, discuss:
1. Pathophysiology
2. Clinical Characteristics
3. Natural course
4. How is it typically diagnosed?

A

GRAVES’ DISEASE = Most common cause of thyrotoxicosis

PATHOPHYSIOLOGY:
- Autoimmune disease (IgG autoantibodies) against thyrotropin receptor (TSH receptor) causing activation of the receptor and autonomous production of thyroid hormones
- T-lymphocyte infiltration into orbital tissues –> fibroblast deposit Glycosaminoglycan (GAGs) and Collagen in the Extraocular muscles –> Fibrosis and Ophthalmoplegia

CLINICAL CHARACTERISTICS:
1. Hyperthyroidism symptoms (with thyrotoxicosis) - see above cards
2. Diffuse thyroid enlargement - hypertrophy and hyperplasia of thyroid follicular cells
3. Infiltrative ophthalmopathy (exophthalmos)
4. Infiltrative dermopathy: Localized/pretibial myxedema (Swelling of skin, appears waxy)
5. Thyroid acropachy (thickening of extremities including nail clubbing, swelling of hands/feet; often associated with ophthalmopathy and dermatopathy)

NATURAL COURSE:
1. Variable:
- Single episode of thyrotoxicosis that subsides spontaneously in a few months/years; OR
- Lifelong thyrotoxicosis with recurrent remission and relapses

  1. Associations: Increase risk of well-differentiated thyroid cancer (twice the prevalence compared to normal population)
    - More aggressive
    - More local regional LN metastases

DIAGNOSIS:
1. Confirm hyperthyroidism (low TSH)
2. Measure thyroid-stimulating immunoglobulin (TSI) or TSHR-Ab; positive = Graves’
3. If #2 negative, perform radioactive iodine uptake scan; positive = Graves’
- Normal uptake ~15-20%

42
Q

What is the Wolff-Chaikoff effect?

A

Autoregulatory phenomenon that inhibits organification when there is excess iodine circulating (protective mechanism to prevent overproduction where there is an abundance of iodine)

43
Q

What are the different types of medical management options that can be used for Graves’ disease?

A
  1. Antithyroid medications (Thionamides) - oral use only, especially indicated in young patients
    - Propylthiouracil
    - Methimazole
  2. Inorganic Iodine (Lugol’s solution)
  3. Radioactive Iodine Ablation (I-131)
  4. Beta blockers
44
Q

Regarding Propylthiouracil for the treatment of thyrotoxicosis, discuss:
1. Mechanism of action?
2. What are the indications?
3. Side effects?
4. Pregnancy Status?

A

MECHANISM OF ACTION:
1. Inhibit TPO (oxidation and organification of iodine)
2. Inhibits couplings of iodotyrosines
3. Inhibits peripheral conversion of T4 to T3 (inhibits Type I deiodinase)
4. Reduce intrathyroidal T-cells and inhibit lymphocyte function (immunosuppressive action)

INDICATIONS:
- No longer recommended as primary treatment by ATA guidelines (due to side effects)
- Exceptions:
1. First trimester pregnancy
2. Thyroid storm
3. Sensitivity/intolerance to Methimazole

Pregnancy status: Class D (evidence of human fetal risk) but used in life threatening situation

SIDE EFFECTS:
1. General (5%)
- Pruritus, urticaria, rashes
- Arthralgia or myalgia
- Fever
- Dysgeusia

  1. Rare but severe, life-threatening side effects
    - Hepatocellular hepatitis
    - Lupus-like vasculitis
    - Agranulocytosis (< 0.2%)
    - Aplastic anemia
    - Thrombocytopenia
45
Q

Regarding Methimazole, discuss:
1. What is the MOA?
2. Side effects?

A

Mechanism of action:
1. Inhibit TPO (oxidation and organification of iodine)
2. Inhibits couplings of iodotyrosines
3. Reduce intrathyroidal T-cells and inhibit lymphocyte function (immunosuppressive action)
4. NO PERIPHERAL ACTION LIKE PTU

SIDE EFFECTS:
1. General (5%)
- Pruritus, urticaria, rashes
- Arthralgia or myalgia
- Fever
- Dysgeusia

  1. Rare, but severe life-threatening side effects
    - Cholestatic hepatitis
    - Lupus-like vasculitis
    - Agranulocytosis (< 0.2%)
    - Aplastic anemia
    - Thrombocytopenia
46
Q

Regarding Inorganic iodine / Lugol’s solution in the treatment of thyrotoxicosis, discuss:
1. MOA and effects
2. Dosage
3. Indications
4. Contraindications

A

MECHANISM OF ACTION:
1. Inhibits thyroglobulin proteolysis
2. Inhibits thyroidal iodine transport, oxidation and organification (uses the Wolff-Chaikoff effect)
3. Decreases vascularity to thyroid (can be used pre-thyroidectomy)

DOSAGE:
1. Lugol solution 5-10 drops of saturated potassium iodide several times daily (only need a few mg daily); OR
2. Lithium carbonate 300mg TID/QID (shown to be similar to iodine)

INDICATIONS:
1. Most useful in thyroid storm

CONTRAINDICATIONS:
1. Hyperkalemia
2. Rheumatoid arthritis
3. Active TB

47
Q

Regarding radioactive iodine ablation (I-131) in the treatment of thyrotoxicsosi, discuss:
1. Mechanism of action
2. Primary indications
3. Contraindications
4. Advantages
5. Side effects/complications
6. Additional considerations prior to RAI

A

MECHANISM OF ACTION:
1. Reduces amount of functioning thyroid tissue

PRIMARY INDICATIONS (for thyrotoxicosis):
1. Most commonly used for Adults with Graves’
2. Children when thionamides fail
3. Patient does not respond to thionamides

CONTRAINDIATIONS:
1. Pregnancy (crosses placenta, can destroy fetal thyroid)

ADVANTAGES:
1. Single dose usually enough
2. Reduces thyroid size to normal
3. Safe with minimal side effects
4. Effective for 2-4 months

SIDE EFFECTS/ COMPLICATIONS:
1. Radiation-induced thyroiditis within 1-2 weeks
- Transient exacerbation of thyrotoxicosis, rarely precipitates thyroid storm
- Problematic for severe thyrotoxic or elderly patients
2. Early hypothyroidism (occurring within 1 year after treatment) caused by destructive effects of I-131 (more common in higher dosages)
3. Can worsen ophthalmopathy (increase tissue edema)

ADDITIONAL CONSIDERATIONS:
- Thionamides should be stopped ~3 days before and after RAI therapy

48
Q

Regarding beta blockers for hyperthyroidism, discuss:
1. What is its role in hyperthyroidism?
2. What are the indications?
3. What are the contraindications?

A

ROLE: Minimizes sympathetic overdrive symptoms

INDICATIONS (Often adjunct to primary treatments):
1. Reducing symptoms before and for several weeks after ablative iodine therapy
2. Prior to subtotal thyroidectomy
3. Thyroiditis
4. Thyroid storm

CONTRAINDICATIONS:
1. Severe thyrotoxic cardiomyopathy
2. Heart failure (unless due to afib)

49
Q

What are medical options for Graves’ disease in pregnant patients?

A
  1. PTU in 1st trimester
  2. Methimazole in 2/3rd trimesters
  3. Surgery is procedure of choice in pregnancy from severe thyrotoxicity
50
Q

Regarding thyroidectomy for the treatment of Graves, discuss:
1. What are the options of thyroidectomy?
2. Absolute indications?
3. Other indications?
4. Discuss the surgical preparation required

A

THYROIDECTOMY FOR GRAVES’:
- Procedure of choice
- ATA guidelines 2016: Total thyroidectomy, with lifelong thyroid supplementation
- Other options (also discussed in ATA)
1. Near-total thyroidectomy - leave 2-4g remnants bilaterally
2. Subtotal thyroidectomy (8% chance of recurrence) - Leave < 7g remnant for unilateral

ABSOLUTE INDICATIONS:
1. Significant adverse reactions to thionamide drugs
2. Neoplasm/suspicious nodule
3. Very large thyroid gland >75g

RELATIVE INDICATIONS:
1. Young women of child-bearing age requiring anti-thyroid medications (wishing to bear children soon, or lactating)
2. Severe Ophthalmopathy (can be worsened with RAI due to tissue edema)
3. Failed medical treatment (medications or RAI)
4. Non-compliance to medication
5. Compressive symptoms
6. Patient preference

SURGICAL PREPARATION:
1. Suppressive therapy with Thionamides (PTU, methimazole, carbimazole) used until patient normothyroid (start ~4-6 weeks prior)
2. Iodides, lithium used 10-14 days prior to surgery once normothyroid to inhibit synthesis & release of hormone
3. Βeta blockers used 48-72 hours before surgery to suppress sympathetic manifestations of thyrotoxicosis (should be continued after thyroidectomy, as half-life of T4 is long)

51
Q

Regarding thyroiditis, discuss:
1. What is it?
2. What is the natural course?
3. What are the different types of thyroiditis?

A

THYROIDITIS:
- Definition: Inflammation of the thyroid and disruption of the thyroid follicles causing T4 and T3 release from Tg resulting in thyrotoxicosis

NATURAL COURSE:
- Transient thyrotoxocosis (Tg stores limited)
- Inflammatory/Thyrotoxic Phase: 4-6 weeks
- Transient hypothyroidism Phase: following inflammation and depletion of Tg stores (Permanent hypothyroidism is rare)

TYPES OF THYORIDITIS:
1. Autoimmune/Hashimoto’s thyroiditis
2. Subacute (De Quervain’s) thyroiditis
3. Silent/painless or subacute lymphocytic thyroiditis
4. Radiation-induced thyroid follicular necrosis
5. Acute suppurative thyroiditis
6. Subacute lymphocytic thyroiditis
7. Riedel’s thyroiditis (IgG-4 related)
8. Granulomatous thyroiditis

52
Q

What is autoimmune / Hashimoto’s thyroiditis?

A

Most common cause of thyroiditis

Clinical presentation:
- Painless goiter
- Slow growth

53
Q

Regarding Subacute (De Quervain’s) thyroiditis, discuss:
1. What is it?
2. Etiology?
3. Clinical presentation?
4. Physical exam?
5. Investigations?
6. Treatments?

A

Subacute (De Quervain’s) thyroiditis:
- Most common cause of painful thyroiditis

ETIOLOGY:
1. Viral illness
- Mumps
- Influenza
- Adenovirus

CLINICAL PRESENTATION:
- Non-specific systemic inflammation: fever, malaise, myalgias
- Thyroid pain
- 50% recent URTI preceding illness
- Symptoms of thyrotoxicosis

PHYSICAL EXAM:
- Firm and hard thyroid
- Tender on palpation

INVESTIGATIONS:
- Thyroid radionuclide uptake scan: Low uptake
- U/S Thyroid: Thyroid hypoechogenicity

TREATMENTS:
- Symptom management (NSAIDs for pain)
- Severe pain/not improving quickly: Prednisone 40mg/day x 3-4 weeks then taper
- Beta-blocker x 1-2 weeks if significant thyrotoxicosis symptoms

54
Q

Regarding silent/painless or subacute lymphocytic thyroiditis, discuss:
1. What is it?
2. Clinical presentation?
3. Natural course?

A

Silent/painless or subacute lymphocytic thyroiditis:
- Uncommon cause of thyrotoxicosis
- Possibly variant of chronic autoimmune thyroiditis

Clinical presentation:
- Thyroid inflammation in absence of pain
- Often no history of URTI

Natural course:
- Thyrotoxicosis x 2-6 weeks, then transient hypothyroidism x 2-8 weeks
- Most develop longterm goitrous autoimmune thyroiditis/hypothyroid

55
Q

What is the clinical presentation and natural course of radiation-induced thyroid follicular necrosis?

A
  • Common after I-131 therapy
  • May or may not have thyroid pain
  • Natural course: occurs 1-2 weeks post-treatment, last 1-2 weeks, then subside spontaneously
56
Q

Regarding Acute Suppurative Thyroiditis, discuss:
1. Causes?
2. Pathophysiology?
3. Treatment?

A

ACUTE SUPPURATIVE THYROIDITIS:
- Rare cause of thyroiditis

COMMON CAUSES:
1. Staph Aureus
2. Hemolytic Streptococcus
3. Strep pneumo
4. Fusobacterium
5. Haemophilus

PATHOPHYSIOLOGY:
- Result of trauma, distant infection seeding, or direct extension from DNSI
- Usually localized to single lobe, but abscess may rupture into mediastinum
- Common in children with prodrome URTI
- Generally don’t develop thyrotoxicosis

TREATMENT:
- IV antibiotics (at least 2 weeks after any surgical drainage)
- FNA to aspirate abscess, surgical drainage usually required afterwards (partial thyroidectomy)

57
Q

Regarding subacute lymphocytic thyroiditis, discuss:
1. When does it typically occur?
2. Symptoms

A
  • Commonly post-partum
  • Often painless
58
Q

How does Reidel’s thyroiditis (IgG4) typically present? How is it treated?

A

Firm, fibrotic gland

Synthroid or remove gland if compressive

59
Q

What causes granulomatous thyroiditis? Describe the natural course

A

ETIOLOGY:
1. Coxsackie virus
2. Paramyxoma virus

NATURAL COURSE:
1. Rapid thyrotoxicosis followed by hypothyroidism
2. Often eventually returns to normal in 90%

60
Q

CHART

Regarding Hashimoto’s Thyroiditis, Painless/postpartum thyroiditis, Subcute De Quervain’s thyroiditis, acute suppurative thyroiditis, and riedel’s thyroiditis, compare and contrast:

  1. Age of onset
  2. Sex raio F:M
  3. Incidence
  4. Etiology
  5. Genetic predisposition
  6. Pathology
  7. Prodrome
  8. Goiter
  9. Thyroid function
  10. Fever/malaise
  11. Thyroid antibody
  12. Relapse
  13. Permanent Hypothyroiditism
A

HASHIMOTO’S THYROIDITIS:
1. Age of onset - all ages, peaks 30-5
2. Sex raio F:M - 8-9F > 1M
3. Incidence - 10% population
4. Etiology - Autoimmune
5. Genetic predisposition - Moderate; HLA DR3, DR5, B8
6. Pathology - Lymphocytic infiltration, germinal centres, fibrosis
7. Prodrome - None
8. Goiter - Nonpainful, persistent
9. Thyroid function - Hypothyroid
10. Fever/malaise - No
11. Thyroid antibody - High titer, persistent
12. Relapse - Persistent
13. Permanent Hypothyroiditism - Frequent

PAINLESS/POSTPARTUM THYROIDITIS:
1. Age of onset - Painless: all ages, peak 30-40; post-partum: child-bearing years
2. Sex raio F:M: Silent - 2:1
3. Incidence - Postpartum - 2-21%; Silent - unknown
4. Etiology - Autoimmune
5. Genetic predisposition - Low
6. Pathology - Lymphocytic infiltration
7. Prodrome - Pregnancy
8. Goiter - Nonpainful, persistent
9. Thyroid function - Thyrotoxicosis, followed by hypo
10. Fever/malaise - no
11. Thyroid antibody - high titer, persistent
12. Relapse - Common with subsequent pregnancies
13. Permanent Hypothyroiditism - Common

SUBACUTE THYROIDITIS (DE QUERVAINS):
1. Age of onset - 20-60 (peak 30-50)
2. Sex raio F:M - 5:1
3. Incidence - Common
4. Etiology - URTI (?Viral)
5. Genetic predisposition - Moderate, HLA Bw-35, DRw8
6. Pathology - Giant cells, granulomas
7. Prodrome - Viral illness
8. Goiter - Painful, transient
9. Thyroid function - Thyrotoxicosis, followed by hypo
10. Fever/malaise - yes
11. Thyroid antibody - low titer/absent; transient
12. Relapse - rare
13. Permanent Hypothyroiditism - occasionally

ACUTE SUPPURATIVE THYROIDITIS:
1. Age of onset - Children, 20-40
2. Sex raio F:M - 1:1:
3. Incidence - Rare
4. Etiology - Infectious organisms
5. Genetic predisposition - Low
6. Pathology - Abscess formation
7. Prodrome - Viral illness
8. Goiter - Painful, transient
9. Thyroid function - Euthyroid
10. Fever/malaise - Yes
11. Thyroid antibody - Absent
12. Relapse - Common only with left pyriform sinus fistula
13. Permanent Hypothyroiditism - Rare

RIEDEL’S THYROIDITIS:
1. Age of onset - 30-60
2. Sex raio F:M - 3-4:1
3. Incidence - Extremely rare
4. Etiology - Unknown
5. Genetic predisposition - Low
6. Pathology - Dense fibrosis
7. Prodrome - None
8. Goiter - Nonpainful
9. Thyroid function - Euthyroid
10. Fever/malaise - No
11. Thyroid antibody - Present in majority
12. Relapse - Persistent
13. Permanent Hypothyroiditism - Occasionally

61
Q

Regarding exogenous thyrotoxicosis, discuss:
1. What is the classic clinical presentation?

A

CLINICAL PRESENTATION:
1. Thyrotoxicosis in absence of thyroid enlargement
2. Normal or low T4 (if patient taking T3)
3. Low RAI uptake, low Tg concentration

62
Q

What is the Jod-Basedow Phenomenon?

A

JOD-BASEDOW PHENOMENON:
- Development of overt hyperthyroidism in subclinical hyperthyroid patients due to exogenous iodide administration
- Usually presents in patients from a geographical area deficient in iodine and who have underlying thyroid disease (toxic MNG, autonomous nodule, euthyroid Graves’) and who get excess iodine from:
1. Iodine containing medications (e.g. Amiodarone)
2. Topical antiseptics
3. Dietary supplements
4. Contrast

63
Q

Regarding toxic thyroid adenoma, discuss:
1. What does it do?
2. How is it diagnosed?
3. Treatment?

A

TOXIC THYROID ADENOMA:
- Functioning thyroid neoplasm
- 20% thyrotoxicosis
- 20% subclinical thyrotoxicosis

Diagnosis:
- Solitary thyroid nodule
- Radionuclide uptake imaging shows intense nuclear uptake at the nodule, and near complete absence of uptake in remainder of the thyroid

Treatment (required as will not resolve)
1. Surgical resection (Pre-op antithyroid drug x 4-6 weeks and iodine therapy 7-10 days prior)
2. 131-I ablation (risk of post-tx hypothyroidism)
3. Ethanol injection into adenoma - U/S guidance (common in Europe)

64
Q

Regarding toxic multinodular goiter, discuss:
1. Classic clinical presentation?
2. Treatment?

A

CLINICAL PRESENTATION:
- Women in 50s
- Commonly long-standing thyroid goiter, insidious subclinical disease, then overt thyrotoxicosis

Treatment:
- 131-I preferred (surgical would need total thyroidectomy)
- Similar to Graves’ surgical treatment

65
Q

Regarding Ectopic Thyrotoxicosis, discuss:
1. What are the possible causes?
2. Clinical presentation?

A

ETIOLOGY:
1. Struma Ovarii (specialized or monodermal teratoma predominantly composed of mature thyroid tissue)
- Ovary Dermoid tumors
- Ovary teratomas

CLINICAL PRESENTATION:
- Most commonly also have Graves’ or MNG in addition to struma ovarii

66
Q

Regarding subclinical thyrotoxicosis, discuss:
1. Biochemical characteristics
2. Natural course
3. Clinical presentation
4. Treatment

A

BIOCHEMICAL CHARACTERISTICS:
- Normal serum T4 and T3
- Low TSH

NATURAL COURSE, 1 of 3 possibilities:
- Resolution within weeks to years; or
- Maintain subclinical state; or
- ~10% overt thyrotoxicosis (Higher risk of progression in presence of thyroid adenoma, MNG, or Graves’ disease

Clinical presentation
- Mostly asymptomatic

TREATMENT:
- Generally not required since asymptomatic, but can surgically/RAI treat if there is nodular disease

67
Q

Regarding thyroid storm, discuss:
1. What is it?
2. Etiologies?
3. SIgns and symptoms?
4. Diagnosis?
5. Treatment?

A

THYROID STORM:
- Severe, life-threatening thyrotoxicosis, usually in a pre-existing hyperthyroid/thyrotoxic patient that develops an insult
- Mortality 15-20%

ETIOLOGY:
- Spontaneous
- Infection
- Medical illness (e.g. DKA)
- Trauma
- Major surgery
- Radioactive iodine
- Pregnancy or after childbirth
- Discontinuation of antithyroid medication

SIGNS AND SYMPTOMS:
1. Fever > 38.5
2. Tachycardia
3. CNS abnormality
- Anxiety
- Agitation / delirium
- Psychosis
- Seizures
- Coma
4. Cardiovascular events
- CHF
- Afib

DIAGNOSIS:
- T3/T4 values often high but not moreso than regular thyrotoxicosis patients

TREATMENT:
1. ICU admission
2. Antithyroid medication: PTU 800-1000mg NG daily
3. Propranolol IV (block adrenergic effect, block peripheral conversion)
4. Glucocorticoids (e.g. Hydrocortisone 50mg, Dex 2mg IV q6-8h) (suppresses HPT axis - hypothalmic-pituitary-thyroid axis that maintains normal thyroid hormone, prevents peripheral hormone conversion of T4 to T3 by inhibiting deiodases)
5. Sodium Iodide 1g IV or Inorganic Iodine 50-100mg QID (inhibit release of T4 and T3 into bloodstream)
6. Supportive care: Antipyrexic medication, Fluid and electrolyte replacement, cooling blankets
7. Plasmapheresis (last line)

68
Q

Describe the overall classification of benign thyroid disease

A

A. NON-TOXIC: Diffuse, Nodular goiter
- Iodine deficient –> Increased TSH –> chronic stimulation leads to hyperplasia

B. TOXIC:
1. High RAI uptake
- Grave’s (6% malignancy)
- Toxic MNG (16% malignancy)
- Toxic adenoma

  1. Low RAI uptake
    - Subacute thyroiditis (5% hypothyroid, 50% transient hypothyroid)
    - Throtoxicosis Factitia (due to ingestion of thyroid hormone)
    - Iodine toxicosis
69
Q

What are the indications for surgery in euthyroid goiter?

A

15% Malignancy
1. Symptoms: compressive (airway, esophagus), recurrent painful hemorrhage
2. Diagnosis: inability to exclude cancer on FNA
3. Cosmesis

Head and Neck (15 decks)

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