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Endocrine Exam > Thyroid Gland Pathology > Flashcards

Thyroid Gland Pathology Flashcards

1
Q

What are some probable causes of primary hyperthyroidism?

A
  • Diffuse hyperplasia (Graves disease)
  • Hyperfunctioning multinodular goiter
  • Hyperfunctioning thyroid adenoma
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2
Q

What is a probable cause of secondary hyperthyroidism?

A
  • Pituitary adenoma
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3
Q

What can be looked at to determine primary from secondary hyperthyroidism ?

A
  • TSH levels
  • Low TSH means primary
  • High TSH means secondary
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4
Q

What may prompt someone with hyperthyroidism to go see the doctor?

A
  • Palpitations or tachycardia
  • Perspiration
  • Facial flushing
  • Exophthalmos
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5
Q

What is apathetic hyperthyroidism?

A
  • Older adults with masked symptomatology
  • Unexplained weight loss
  • Cardiovascular disease
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6
Q

What is regular hyperthyroidism?

A
  • Symptoms as seen in the hyperthyroidism
  • Jittery
  • Palpitations
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7
Q

What is thyroid storm?

A
  • Abrupt onset of thyrotoxicosis
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8
Q

What is seen in thyroid storm?

A
  • Fever
  • Cardiac manifestations
  • GI symptoms
  • Precipitating history
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9
Q

What cardiac manifestations may be seen in a thyroid storm?

A
  • Tachycardia

- CHF

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10
Q

What GI symptoms may be seen in a thyroid storm?

A
  • Diarrhea

- Jaundice

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11
Q

What precipitating history may cause a thyroid storm?

A
  • Pregnancy/postpartum
  • Hemithyroidectomy
  • Drugs: amiodarone
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12
Q

What are some treatment options of thyroid storm?

A
  • Beta blockers
  • High doses of iodide
  • Thioamide
  • Radioiodine ablation
  • Surgery
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13
Q

What is Graves disease characterized by?

A
  1. Hyperthyroidism with gland enlargement
  2. Infiltrative ophthalmopathy
  3. Pretibial myxedema
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14
Q

What is the pathogenesis of Graves disease?

A
  1. Lymphocytes invade preorbital space
  2. Fibroblasts have TSH receptors
  3. EOM swelling
  4. Matrix accumulates
  5. Adipocytes expand
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15
Q

What is pretibial myxedema?

A
  • Infiltrative dermopathy

- Scaly, indurated skin

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16
Q

What are the serum levels of thyroid hormones in Graves disease?

A
  • T3/T4: HIGH
  • TSH: LOW
  • TSI: HIGH
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17
Q

What is the presentation of congenital hypothyroidism?

A
  • Mental retardation
  • Growth retardation
  • Coarse facial features
  • Umbilical hernias
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18
Q

Where is congenital hypothyroidism seen?

A
  • Where there is endemic areas without iodine supplementation
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19
Q

What is myxedema?

A
  • Hypothyroidism in the adult/older child
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20
Q

What is the clinical presentation of myxedema?

A
  • Mental and physical sluggishness (slowing)
  • Weight gain
  • Cold intolerance
  • Cardiac effect (lower output and hypercholesterolemia)
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21
Q

What causes hashimoto thyroditis?

A
  • Autoantibodies against Thyroglobulin and Thyroid Peroxidase (TPO)
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22
Q

What is the progression to hypothyroidism in Hashimoto thyroiditis?

A
  • Immune mediated insult –> hyperactivity and enlargement –> follicular cell exhaustion causing hypothyroidism
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23
Q

What is seen on histology in Hashimoto thyroiditis?

A
  • Lymphocytic infiltrate with germinal centers

- Atrophic follicle cells with eosinophilic change (Hürthle cell metaplasia)

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24
Q

What is subacute lymphocytic thyroiditis?

A
  • Typically a transient period of thyroid hormone irregularities
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25
Q

What is Granulomatous thyroiditis?

A
  • Painful
  • Granulomata
  • Viral in origin??
  • Sometimes lumped in with subacute thyroiditis
26
Q

What is Riedel thyroiditis?

A
  • Fibrosing process

- Extends from the thyroid into adjacent tissue

27
Q

What is the cause of Riedel thyroiditis?

A
  • Unknown (IgG4-related)
28
Q

What is the thyroid state in Riedel thyroiditis?

A
  • Euthyroid
29
Q

What causes endemic goiters?

A
  • Iodine deficiency
30
Q

What are some goitrogens?

A
  • Cassava root

- Brassicaceae (broccoli, cauliflower, cabbage)

31
Q

Who is most likely to have a sporadic goiter?

A
  • Females
32
Q

What are some symptoms of a goiter due to mass effect?

A
  • Dysphagia
  • Hoarseness
  • Stridor
  • SVC syndrome
33
Q

Why are there multinodular goiters?

A
  • Hyperplasia, regression (involution) cycle
  • Varied response of nodules to stimuli
  • Neoplastic nature of some nodules (adenomas)
34
Q

What is radioisotope scanning?

A
  • A modality to determine if a specific nodule is responsible for hyperfunction
35
Q

What is a hot nodule? How is it treated?

A
  • Hyperfunctioning nodule

- Treated with radioactive iodide or excised

36
Q

What is a cold neoplasm? How is it treated?

A
  • Could be a neoplasm

- Need to do further workup like U/S

37
Q

What are some benign neoplasms of the thyroid?

A
  • Hyperplastic (adenomatoid) nodules

- Follicular adenomas

38
Q

What are some malignant neoplasms of the thyroid?

A
  • Papillary thyroid carcinoma
  • Follicular/Hürthle cell carcinoma
  • Anaplastic carcinoma
  • Medullary carcinoma
39
Q

What is a follicular adenoma?

A
  • Discrete clonal population of follicular cells with ‘Thyroid autonomy”
  • Benign but need to make sure there is an intact capsule
  • No nuclear features of papillary carcinoma
40
Q

What is a papillary thyroid carcinoma?

A
  • Majority of malignant tumors of the thyroid glands

- Most occur between 25-50

41
Q

How does a papillary thyroid carcinoma present?

A
  • Typically without symptoms
  • Palpable nodule
  • Ultrasound
42
Q

What does histology show for a papillary thyroid carcinoma?

A
  • Enlarged nuclei with “clear” appearance

- “Orphan Annie Eye nuclei”

43
Q

What is the follicular variant of PTC?

A
  • Follicular architecture, but nuclear features of papillary carcinoma
  • Fewer cases have RET-PTC rearrangements or BRAF mutations
  • More cases with RAS mutations
44
Q

What is the tall cell variant of PTC?

A
  • Older patients

- Aggressive

45
Q

What is the diffuse sclerosing variant of PTC?

A
  • Kids and young adults
  • Greater incidence of distant metastasis to lung, brain, bone, and liver
  • Shorter periods of disease-free survival
  • Mortality rate isn’t that bad despite the likelihood of distant metastasis
46
Q

What is follicular carcinoma?

A
  • Follicular neoplasm with invasive properties
  • Less common than papillary
  • More common in areas with goiter from iodide deficiency
47
Q

What mutations are seen in follicular carcinoma?

A
  • RAS mutations - not specific

- PAX8/PPARG mutations - more characteristic

48
Q

What are the two types of invasion seen with follicular carcinoma?

A
  • Invasion of the capsule (mushroom cloud)

- Angioinvasion

49
Q

What are some therapeutic options for differentiated thyroid carcinoma?

A
  • Surgery
  • Radioactive iodine
  • If refractory: chemotherapy or tyrosine kinase inhibitors
50
Q

What is special about using radioactive iodine in differentiated thyroid carcinoma?

A
  • The radioactive iodine will even target the metastasis due to the similar cell components
51
Q

What is anaplastic carcinoma?

A
  • Uncommon
  • Tend to occur in elderly patients
  • Highly aggressive
  • Present with mass effect
  • Die within a year of local invasion
52
Q

What are the genetics with papillary carcinoma?

A
  • RET/PTC rearrangements –> constitutive tyrosine kinase activity
  • BRAF gain of function mutations –> MAP kinase signaling
53
Q

What are the genetics with follicular carcinoma?

A
  • PAX8-PPARG
54
Q

What are the genetics with follicular neoplasms?

A
  • RAS

- PTEN

55
Q

What are the genetics with anaplastic carcinoma?

A
  • TP53
56
Q

What are C cells responsible for?

A
  • Calcitonin secretion
57
Q

What stain is done to help identify C cells?

A
  • Calcitonin immunohistochemistry
58
Q

What is medullary carcinoma?

A
  • Neuroendocrine carcinoma derived from C cells
  • Blue cells with dispersed chromatin
  • Amyloid
  • C cell hyperplasia
59
Q

What is the sporadic form of MTC?

A
  • 70-80% of all MTCs
  • Unifocal tumors
  • Mean age is 50
  • Aggressive
60
Q

What is the familial form of MTC?

A
  • BEST prognosis of all forms
  • Multifocal
  • Mean age is 43
61
Q

What proto-oncogene is associated with MTC?

A
  • RET on chromosome 10

Endocrine Exam (11 decks)

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