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MS2 Endocrine > 10/8- Disease of the Thyroid I > Flashcards

10/8- Disease of the Thyroid I Flashcards

1
Q

What is a goiter?

A

Chronic enlargement of the thyroid gland not due to neoplasm

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2
Q

What is an endemic goiter?

  • Epidemiology
A
  • Areas where > 5% of children 6-12 years of age have goiter
  • Common in China and central Africa, Himalayan foothills, Andes
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3
Q

What is a sporadic goiter?

A
  • Occurs in areas where < 5% of children 6-12 yo have goiter
  • Multinodular goiter often denotes the presence of multiple nodules rather than gross gland enlargement
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4
Q

What are possible etiologies behind goiter?

A
  • Hashimoto’s thyroiditis
  • Graves’ disease
  • Chronic Iodine excess
  • Medications: Lithium
  • Neoplasm
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5
Q

Describe the possible goiter in Hashimoto’s thyroiditis

A
  • Goiter may be present in early stages only, late stages show atrophic changes
  • May present with hypo, hyper, or euthyroid state
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6
Q

What causes goiter in Graves’ disease?

A

Chronic stimulation of TSH receptor

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7
Q

How does chronic iodine excess cause goiter?

A

Iodine excess leads to increased colloid formation and can prevent hormone release

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8
Q

How dose lithium cause goiter?

A

Lithium prevents release of hormone, causes goiter in 6% of chronic users

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9
Q

What is the pathogenesis behind goiter in iodine deficient vs. replete areas?

A

Iodine deficient areas:

  • Heterogeneous response to TSH
  • Chronic stimulation leads to multiple nodules

Iodine replete areas

  • Thyroid follicles are heterogeneous in their growth and activity potentia
  • Autopsy series show MNG - 30%.
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10
Q

What evaluation should be done if a pt has a goiter?

A

Determination of thyroid state is key in determining treatment!

Thyroid function evaluation:

  • TSH, T4, T3
  • Overt hyperthyroidism (TSH low, T3/T4 high)
  • Subclinical hyperthyroidism (TSH low, T3/T4 normal)
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11
Q

What should be screened for with non-toxic MNG (multi-nodular goiter)?

A

Longstanding MNG has a risk of malignancy identical to solitary nodules FNA in MNG

  • Negative FNA can be followed with annual US
  • Insufficient FNA’s should be repeated
  • Inconclusive FNA or papillary cytology warrants excision
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12
Q

What are treatment options for a non-toxic goiter not causing compressive symptoms?

A
  • US follow-up to monitor for progression
  • Thyroid suppression therapy has been used historically
  • May be used for progressive growth
  • Goiter re-growth occurs rapidly following therapy cessation
  • Surgery
  • Suspicious neck lymphadenopathy
  • History of radiation to the cervical region
  • Rapid enlargement of nodules
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13
Q

What are treatment options for a non-toxic goiter that is causing compressive symptoms?

A

RAI (radio-active iodine) ablation

  • Not a treatment of choice due to SLOW process
  • Volume reduction
  • Improvement of dysphagia or dyspnea
  • Post RAI hypothyroidism (pretty inevitable)
  • Need for additional ablation depends on size of gland, number of nodules and dose of original ablation

Surgery

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14
Q

How are types of thyroid nodules determined?

A

Based on uptake scan and on USS

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15
Q

What is the prevalence of thyroid nodules?

A

10-15% of US population

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16
Q

Approach to the thyroid nodule?

A
  • Labs
  • USS
  • RAIUS
  • FNA
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17
Q

Pathophysiology of Nodules

  • Benign
  • Malignant
A

Benign (~95%):

  • MNG
  • Hashimoto’s
  • Cysts
  • Adenomas
  • Hurthle-cell adenoma

Malignant (~5%):

  • Primary carcinoma
  • Lymphoma
  • Mets
18
Q

A single nodule should raise the possibility of what?

Especially if what association?

A

A single nodule, especially if associated with a cold defect, should always raise the possibility of malignancy

~ 15-20 % of cold nodules are malignant

19
Q

What do hot nodules reflect?

A

Hyperfunction causing hyperthyroidism

20
Q

Which nodules have higher malignancy potential, solid or cystic?

A

Solid nodules have a higher malignancy potential, but cystic nodules >4cm also pose cancer risk

21
Q

When do you suspect malignancy in nodular thyroid disease?

A
  • Age : children; nodules in young patients, or new nodules in the older patient (age under 30 or over 60)
  • Gender : though all forms of thyroid disease are more common in women, malignancy is more likely in the male patient with a thyroid nodule
  • Rapid enlargement in size
  • Hard nodules
  • Family history of thyroid cancer
  • Previous head and neck irradiation
  • Cold defects
22
Q

What are the FNA guidelines for diagnosing a thyroid nodule?

A
  • All hypoechoic nodules ≥ 10 mm
  • Irregular margins
  • Chaotic intra-nodular vascular spots
  • Micro-calcifications
23
Q

What may cause thyroiditis/what are the different types?

A
  • Hashimoto’s thyroiditis
  • Subacute thyroiditis
  • Silent / Post-partum thyroiditis
  • Acute thyroiditis
  • Riedel’s thyroiditis
24
Q

What is the most common cause of goiter and hypothyroidism in the US?

A

Hashimoto’s thyroiditis

25
Q

What causes Hashimoto’s thyroiditis?

  • Gland size
A
  • Result of antibodies to TPO, TBG
  • AI disease with progressive gland destruction
  • Gland size varies from goitrous enlargement to an impalpable gland
26
Q

Hashimoto’s thyroiditis typically presents in what population?

A

Females 30-50 yrs.

27
Q

What are clinical features of Hashimoto’s thyroiditis?

  • Physical exam findings
  • Lab studies
A

Clinical features

  • Reflect a hyper- or hypothyroid state depending on the natural progression of the disease.

Physical:

  • Usually non-tender and asymptomatic

Lab studies

  • Hypothyroidism (elevated TSH)
  • Abs are typically positive
  • Anti TPO antibodies (90%)
  • Anti Thyroglobulin antibodies (20-50%)
  • Acute Hyperthyroidism (5%)
28
Q

Treatment for Hashimoto’s thyroiditis?

A

Levothyroxine if hypothyroid

  • Replace thyroid hormone
29
Q

What is Subacute (de Quervains) Thyroiditis?

  • Prognosis
A
  • Self limiting disease of variable duration & severity
  • Most common cause of a (exquisitely) painful thyroid gland, likely secondary to an antecedent viral infection
30
Q

How to diagnose Subacute (de Quervains) Thyroiditis?

A
  • Elevated ESR
  • Low TSH, elevated T4 > T3
  • Low anti-TPO/Tgb
  • Low RAI uptake (same as silent thyroiditis)
31
Q

What is the course of Subacute (de Quervains) Thyroiditis?

A
  • Pain and thyrotoxicosis (3-6 weeks)
  • Asymptomatic euthyroidism
  • Hypothyroid period (weeks to months)
  • Recovery (complete in 95% after 4-6 months)
32
Q

Treatment during the early painful stage of Subacute (de Quervains) Thyroiditis includes what?

A
  • NSAID’s and salicylates.
  • Oral steroids in severe cases (powerful anti-inflammatory effect)
  • Beta blockers for symptoms of hyperthyroidism (thyroid hormones act through B adrenergic receptors; provide relief from tachycardia, palpitations, etc.)
  • Thionamides NOT indicated since excess hormone results from leak instead of hyperfunction
  • Symptoms can recur requiring repeat treatment
33
Q

What is silent thyroiditis?

  • Clinical features
A
  • “Post-partum thyroiditis” if it occurs within 1 yr of delivery

Clinically:

  • PAINLESS
  • Hyperthyroid symptoms at presentation
  • Progression to euthyroidism followed by hypothyroidism for up to 1 year.
  • Hypothyroidism generally resolves
34
Q

How is silent thyroiditis diagnoses complicated?

A

May be confused with post-partum Graves’ relapse

35
Q

Treatment for silent thyroiditis?

A
  • Beta blockers during toxic phase
  • No anti-thyroid medication indicated
  • Iodinated Rx for severe hyperthyroidism
  • Thyroid hormone during hypothyroid phase.
36
Q

What is the very broad progression of thyroid function in thyroiditis (pretty much all types)?

A

Hyperthyroid -> transient euthyroid -> possibly hypothyroid

37
Q

What are causes of acute thyroiditis?

A

Infection

  • Bacterial (S aureus, S pyogenes) (68%)
  • Fungal (15%)
  • Mycobacterial (9%)
  • Common in HIV

Secondary to:

  • Pyriform sinus fistulae
  • Pharyngeal space infections
  • Persistent thyroglossal remnants
  • Thyroid surgery wound infections (rare)
38
Q

How is acute thyroiditis diagnosed?

A
  • Warm, tender, enlarged thyroid (don’t confuse with subacute thyroiditis)
  • FNA to drain abscess, obtain culture
  • RAIU normal
  • Pretty much just infection of euthyroid/normally functioning thyroid
  • Contrast to decreased function in DeQuervain’s
  • CT or US if infected TGDC suspected
39
Q

Treatment for acute thyroiditis?

A
  • High mortality without prompt treatment
  • IV Antibiotics
  • Search for pyriform fistulae (BA swallow, endoscopy)
  • Recovery is usually complete
40
Q

What is Reidel’s thyroiditis?

A

Rare disease causing fibrosis of the thyroid gland

41
Q

How is Riedel’s Thyroiditis diagnosed?

A
  • Thyroid Ab’s present in 2/3
  • Painless goiter “woody”
  • Open biopsy often needed to diagnose
  • Associated with focal sclerosis syndromes (retroperitoneal, mediastinal, retroorbital, and sclerosing cholangitis)
42
Q

Treatment for Riedel’s Thyroiditis?

A
  • Resection for compressive symptoms
  • Steroids may be effective
  • Thyroid hormone only if hypothyroidism

MS2 Endocrine (25 decks)

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