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Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

1
Q

For thyroid cancer, which molecular/genetic DNA mutation is associated with metastasis?

A

TERT promoter gene

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2
Q

what molecular markers have very high positive predictive value for malignancy for papillary thyroid cancer?

A

BRAFV600E, RET/PTC, and TERT fusions

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3
Q

PAX8/PPARG fusion is more commonly seen in?

A

follicular adenoma, follicular thyroid carcinoma, and follicular variant PTC

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4
Q

Prophylactic surgery for medullary thyroid cancer (timeline):
1. mutations in codon 900-800s (918, 922, 883)
2. mutations in codon 600s’s (609, 611, 618, 620, 630, 634)
3. mutation in codon 790

A
  1. first month to first year of life
  2. before age 5 years
  3. (lowest risk) - can defer if calcitonin levels are normal, cervical US is normal, and no family history of aggressive medullary thyroid cancer
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5
Q

Medullary thyroid cancer:
RET mutations - two most common?

A

M918T (highest risk) and M888
also remember codon 634 (familial MTC)

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6
Q

Additional features of MEN2A

A

-cutaneous lichen amyloidosis (hyperpigmented plaques)
-Hirschsprung disease

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7
Q

TSH resistance
1. TFT results?
2. pathogenesis. Pattern of inheritance?
3. treatment?
3. How is this different from resistance to thyroid hormone?

A
  1. similar to subclinical hypothyroidism, but no goiter, findings on thyroid US, or TPO Ab positivity
  2. inactivating pathogenic variants in the gene encoding the TSH receptor, which cause TSH resistance. Autosomal dominant.
  3. If euthyroid, nothing. If hypothyroid, levothyroxine with goal to normalize TSH.
  4. thyroid hormones (FT4 and T3) are elevated, rather than normal
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8
Q

For thyroid cancer,
a nonstimulated postoperative thyroglobulin concentration less than [ ? ] after a hemithyroidectomy is consistent with an excellent response to therapy

A

30 ng/ml

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9
Q
  1. What medication is currently approved for use in advanced medullary thyroid cancer?
  2. What about for differentiated thyroid cancer?
A
  1. vandetanib and cabozantinib (MEN in a van and cab)
  2. sorafenib and lenvatinib (sorab and len are different)
    - sorafenib and lenvatinib target: VEGFR 1, 2
    - additionally sorafenib also targets: BRAF
    - lenvatinib also targets: RET, FGFR 1-4, PDGFR (platelet derived growth factor)
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10
Q

treatment of medullary thyroid cancer
1. non-selective RET inhibitors
2. selective RET inhibitor
3. for diarrhea (due to secretion of calcitonin)

A
  1. cabozantinib and vandetanib (“cab and van”)
  2. selpercatinib
  3. somatostatin analogs
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11
Q

subclinical hypothyroidism in pregnancy:
1. recommendations for starting treatment with LT4?
2. weak evidence for starting LT4 treatment

A
  1. TSH above the reference range and + TPO Ab
  2. TSH between 4 and 10, and - TPO Ab
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12
Q
  1. medullary thyroid cancer can also produce other neuropeptide hormones such as?
  2. presentation?
  3. lab findings?
A
  1. ACTH, causing ectopic ACTH syndrome.
  2. weakness, hypokalemia, HTN, elevated glucose/diabetes, weight gain, diarrhea
  3. elevated ACTH and cortisol
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13
Q
  1. what is the definition of minimally invasive follicular thyroid cancer?
A
  1. capsular invasion only
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14
Q

teprotumumab

  1. what is it?
  2. indications for use?
  3. side effects?
A
  1. a fully human IGF-1 receptor inhibitory monoclonal antibody
  2. active, moderate thyroid eye disease, esp for patients with significant proptosis
  3. (high cost); worsening glucose control in DM and hearing impairment. Also IGF-1 can increase during treatment due to MOA, but pt without features of acromegaly.
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15
Q

treatment for thyroid eye disease:
1. active, moderate
2. inactive
3. mild, active
4. moderate to severe, active *with soft tissue inflammation and diplopia

A
  1. teprotumumab
  2. surgical intervention, including orbital decompression surgery
  3. selenium
  4. high dose IV glucocorticoids

a CAS score of greater than or equal to 4 is predictive of response to immunosuppresive treatment

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16
Q

thyroglobulin antibodies:
1. a decline means?
2. a stable level means?
3. increasing level

A
  1. reassuring, no indications of residual disease
  2. also reassuring, may indicate persistent disease
  3. progression of residual disease or disease recurrence
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17
Q
  1. TSH resistance: features? VS
  2. Resistance to Thyroid Hormone?
A
  1. A.D., looks like subclinical hypothyroidism picture
  2. looks like hyPERthyroidism due to elevated levels of thyroid hormone
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18
Q

For thyroid cancer, what Tg levels are considered acceptable responses to therapy?

  1. unstimulated
  2. stimulated
A
  1. Tg < 1.0 ng/ml
  2. Tg < 10 ng/ml
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19
Q

For a symptomatic goiter, what additional management approach is recommended when surgery is contraindicated?

A

radioiodine therapy with rhTSH

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20
Q

What is the classic description of a parathyroid cyst?

A

clear, colorless, liquid

contains extremely high PTH levels

can be functioning (in which surgery is recommended) or

nonfunctioning (in which conservative therapy, aspiration, sclerotherapy, or surgery can be pursued)

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21
Q

Bethesda system for reporting thyroid cytopathology:
I (% risk of malignancy) –> usual management
II
III
IV
V
VI

A

I - Nondiagnostic (1-4%) –> repeat FNA
II - Benign (0-3%) –> clinical F/U
III - Atypia of undetermined significance/AUS or Follicular Lesion of Undetermined Significance/FLUS (5-15%) –> repeat FNA
IV - Follicular Neoplasm/FN or suspicious for follicular neoplasm; includes Hurthle-cell neoplasm or suspicious for Huthle cell neoplasm (15-30%) –> Lobectomy, TTx
V - Suspicious for malignancy (60%) –> Lobectomy, TTx
VI - Malignant (99%) –> TTx

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22
Q

Nodules with indeterminate results include which Bethesda classes?

A

3-5
III (AUS/FLUS), IV (FN/SFN), V (SMC) —> can send these for molecular testing

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23
Q

Medullary thyroid cancer:
1. Required workup preoperatively?
2. If baseline calcitonin concentration is < 500 pg/ml, what does this suggest?
3. If + for s/s of distant mets, what additional imaging is indicated?

A
  1. physical exam, calcitonin and CEA levels, RET testing, and thyroid US (to assess for the presence of local mets)
  2. distant metastases will NOT be present
  3. chest CT to detect lung or mediastinal mets, and imaging with MRI or 3-phase contrast-enhanced multidetector CT to detect liver mets.
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24
Q

what is the pathogenesis of a solitary hot nodule?

A

**somatic activating **variant in the gene encoding the TSH receptor or the Gs alpha subunit

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25
Q

American Thyroid Association thyroid nodule classifications:
risk of malignancy (%) and characteristics –> when to FNA?
1. high suspicion
2. intermediate
3. low
4. very low
5. benign

A
  1. > 70-90%: *microcalcifications, hypoechoic, irregular margin, *taller than wide, *extrathyroidal extension, suspicious *lymph node –> FNA >/= 1 cm
  2. 10-20%: hypoechoic, solid, irregular margin –> FNA >/= 1 cm
  3. 5-10%: hyper/isoechoic, solid, regular margin, partially cystic –> FNA >/= 1.5 cm
  4. < 3%: spongiform, partially cystic no suspicious features –> FNA >/= 2 cm
  5. < 1%: cyst –> FNA not required
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26
Q

In nondiagnostic FNAB results with suspicious features on ultrasound, the risk of malignancy is?

A

25%
Treatment is thyroid surgery

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27
Q

Nonivasive Follicular Thyroid Neoplasm with Papillary-like Nuclear Features (NIFTP)
1. Formerly known as?
2. lack of?
3. management?

A
  1. encapsulated follicular variant of papillary thyroid carcinoma
  2. BRAF V600E variant or other high-risk variants in TERT or TP53
  3. LT4 therapy with a low-normal TSH target
28
Q

CEA elevation can occur in?

A

MTC (though not a specific biomarker)

Benign conditions: smoking, pancreatitis, PUD, heterophilic antibodies, hypothyroidism)

29
Q

Is medullary thyroid cancer TSH responsive?
What do not work?

A

NO
RAI scan and RAI tx do NOT work

30
Q

Imaging for MTC
1. 3-6 months postoperatively
2. when is PET-CT indicated?

A
  1. neck US
  2. very high calcitonin level >1000 pg/ml
31
Q

The finding of cribriform-morular variant of papillary thyroid cancer (CMVPTC) should prompt genetic testing for what inherited condition?

A

familial adenomatous polyposis (FAP)

32
Q

management of differentiated thyroid cancer (in order, 1-4)

A
  1. surgery
  2. RAI treatment (high risk FTC and some intermediate risk)
  3. thyroid hormone suppressive tx

for progressive, non-iodine avid disease: use I131 whole body scan SPECT CT or FDG PET/CT
4. external beam radiation tx with/wo TKIs

33
Q

Diffuse sclerosing variant of papillary thyroid carcinoma (DSVPTC):
1. accounts for what percentage of thyroid cancer?
2. seen mostly in?
3. features?
4. typical US findings?
5. pathology findings?

A
  1. only 6% of PTC
  2. young women
  3. more aggressive than classic PTC, with LN mets, extrathyroidal extension, structural recurrences.
  4. hyperechogenicity, thyroidal enlargement, numerous calcifications
  5. abundant psamomma bodies, squamoid metaplasia, fibrosis, calcification, lymphocytic infiltration
34
Q

Subclinical hyperthyroidism

  1. when is treatment indicated?
  2. when is treatment considered?
  3. when do you check TRAb?
  4. How about thyroid US?
A
  1. when TSH < 0.1 in ALL PATIENTS 65 YO or older; AND in younger patients with symptoms, known cardiac disease, or significant risk factors in postmenopasual women (osteoporosis; not on estrogen, bisphosphonates/other antiresorptive agents)
  2. all patients 65 YEARS AND OLDER and TSH 0.1-0.4; AND in younger patients with TSH < 0.1.
  3. if treatment is planned
  4. not routinely recommended in patients with hyperthyroidism, unless looking for amiodarone-induced thyrotoxicosis, or to correlate findings on nuclear imaging for thyroid nodular disease
35
Q

what is the standard surgical management of thyroglossal duct cysts?

A

Sistrunk procedure

36
Q

in chronic illness (such as anorexia and low body weight), what happens to thyroid physiology?

A

reduced: TRH gene expression, TSH secretion, pulsatility, type 1 deiodinase activity (liver) - 1 is DOWN
increased: type 3 deiodinase activity (liver) and type 2 diodinase activity (muscle)

37
Q

how does thyroid stimulating immunoglobulin (TSI) effect differentiated cancer prognosis?

A

differentiated thyroid cancer may be more aggressive

38
Q

how does thyroid stimulating immunoglobulin (TSI) effect differentiated cancer prognosis?

A

differentiated thyroid cancer may be more aggressive and may antagonize the effects of TSH suppression

39
Q

Thyroiditis:
1. Findings: Tg and RAI?
2. treatment options?

A
  1. elevated thyroglobulin or absent uptake on RAI uptake and scan
  2. therapy must be directed at removing circulating thyroid hormones: cholestyramine, surgery, plasmapheresis, plasma exchange, charcoal hemoperfusion
40
Q

how do tyrosine kinase inhibitors effect thyroid hormone levels

A

Can lead to hypothyroidism/increase levothyroxine dose requirement. Therefore, check TSH.

41
Q

Anaplastic thyroid cancer:
1. how do tumor characteristics influence survival?
2. how does tumor resection influence survival? Best tx combo?

A

background: anaplastic thyroid cancer arise from differentiated thyroid cancer that has progressively accumulated chromosomal alterations. Therefore, it is common to see areas of papillary or follicular thyroid cancer within anaplastic thyroid cancer.

  1. advanced tumor stage and metastatic disease at presentation adversely affect prognosis.
  2. most studies show a beneficial effect of complete tumor resection. RT and chemotherapy can then be used. (Best outcomes with this trimodal therapy)
42
Q

Noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP)
1. Criteria (3)
2. type of mutation present?

A
  1. encapsulated, follicular growth pattern with (< 1% papilla, no psammoma bodies, 30% solid growth pattern), No vascular/capsular invasion
  2. RAS mutations in 30%
43
Q
  1. Features of a TSH secreting adenoma (3)
  2. What test can you use? How do the results differ from Resistance to TH?
A
  1. normal TSH with an elevated TH, elevated alpha glycoprotein, and elevated SHBG
  2. TRH stim test: TSH secreting adenoma has a blunted response, whereas resistance to thyroid hormone has an increasing TSH
44
Q

Autoimmune polyglandular syndromes:
1. APS 1 (gene affected): features:
2. APS 2
3. APS 3

A

APS 1 in manifest in children; APS 2 and 3 manifest in adults

  1. (AIRE): aka autoimmune polyendocrinopathy candidiasis-ectodermal-dystrophy; A.R. Presents in childhood with the presence of 2/3: chronic mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency
  2. Addison disease + either T1DM and/or autoimmune thyroid failure
  3. autoimmune thyroid disease + autoimmune disorders other than Addison disease or hypoparathyroidism. Non-endocrine autoimmune diseases (Sjogren and alopecia areata) are more common.
45
Q

Cowden syndrome

  1. due to pathogenic variants in what gene?
  2. associated with what thyroid problems?
  3. also elevated risk of what other types of cancer?
  4. clinical features?
A
  1. PTEN gene (phosphatase and tensin homolog gene)
  2. increased risk of benign thyroid nodules, as well as papillary and follicular thyroid carcinoma (70-fold increased risk)
  3. breast, endometrial, and renal cancer
  4. colonic polyps usually hamartomas, macrocephaly, learning disabilities, and autism
46
Q

thyrotoxic periodic paralysis
1. what pump is stimulated?
2. tx to prevent recurrent episodes

A
  1. Na-K-ATPase –> intermittent hypokalemia during attacks
  2. propranolol: inhibits adrenergic stimulation of the Na-K-ATPase pump
47
Q

In thyroid nodules that have repeatedly nondiagnostic cytopathology (d/t inadequate number of cells) with suspicious features, what is the next step in management?

A

lobectomy
- molecular testing cannot be done due to inadequate number of cells for analysis

48
Q

hCG concentrations greater than what are required to cause sufficient thyroid stimulation of thyroid hormone production to result in suppressed TSH?

A

400,000 to 500,000 mIU/mL

49
Q

What is thyroglobulin “washout”?

A

Measuring thyroglobulin in the fluid obtained from FNAB aspirates of lymph nodes. FNA biopsy alone, without thyroglobulin washout, may fail to diagnose thyroid cancer in up to 20% of cases. (Q19)

50
Q
  1. Tall cell variant of papillary thyroid cancer is associated with?
  2. For non iodine avid PTC, what is the treatment?
A
  1. An aggressive presentation. May often not be iodine avid.
  2. External beam radiation therapy (tumoricidal) vs tyrosine kinase inhibitor therapy (benefits are transient)
51
Q
  1. Cytopathology showing uniform-appearing lymphocytes may be consistent with either?
  2. What is typically needed to confirm a diagnosis of lymphoma?
  3. Treatment of thyroid lymphoma?
A
  1. Hashimoto thyroiditis or thyroid lymphoma 2. FNAB with flow cytometry 3. Chemotherapy with or without radiation
52
Q

When evaluating patients with recurrent miscarriage, with or without infertility, what should be measured?

A

TPO antibody

53
Q
  1. What is Riedel thyroiditis?
  2. First line treatment?
  3. Second line treatment?
A
  1. a rare fibrotic condition that results in destruction of the thyroid and overgrowth of progressively fibrosing connective tissue. Histologically defined by the presence of inflammation. Primary hypothyroidism and positive antithyroid antibodies are present in most patients. Commonly associated with compressive symptoms.
  2. High dose glucocorticoids
  3. Tamoxifen Debulking surgery is effective but usually limited to isthmusectomy due to complications such as hypoparathyroidism and recurrent laryngeal nerve damage.
54
Q

What is the treatment for myxedema coma?

A

IV levothyroxine with a LOADING DOSE of 200-400 mcg (lower doses for smaller/older pts or with h/o CAD or arrhythmia). Then daily MAINTENANCE LT4 dose of 1.6 mcg/kg body weight reduced by 25% while on IV. A LOADING DOSE of liothyronine 5-20 mcg can be given, followed by a MAINTENANCE dose of 2.5-10 mcg q8h.

55
Q

What monoclonal antibody has recently been shown to effectively improve symptoms of active moderate-to-severe Graves ophthalmopathy?

A

TEPROTUMUMAB

56
Q

how does nephrotic syndrome cause an increase in LT4 dosage requirement?

A

due to large loss of thyroid-binding proteins (with thyroid hormone still bound) in the urine

57
Q

Histologic findings of papillary thyroid carcinoma

A
  1. orphan Annie nuclei
  2. psamomma bodies
  3. nuclear inclusions and grooves
  4. papillary architecture
58
Q

Familial dysalbuminemic hyperthyroxinemia
1. etiology?
2. clinical presentation
3. labs?

A
  1. genetic disorder associated with mutant albumin molecules with low affinity but high capacity for T4 but not T3
  2. patients are euthyroid
  3. high TT4; TSH and T3 normal
59
Q

Breastfeeding mom with hyperthyroidism.
1. max dose methimazole?
2. max dose PTU?

A
  1. 20 mg daily
  2. 450 mg daily
60
Q

If patient has two known autoimmune conditions (thyroid and something else), and presents with an elevated TSH despite increasing LT4 dose, you should be suspicious for?

A

a third autoimmune condition:
adrenal insufficiency - obtain a morning cortisol
(cortisol exerts a negative feedback on TSH)

61
Q

what biotin dose can impair TSH assays?

A

> 5,000 mcg/day

62
Q

Malignant struma ovarii (metastatic): what is the treatment?

A

total thyroidectomy followed by I131 RAI therapy

63
Q

pregnant mother with Graves’ disease s/p total thyroidectomy on a stable dose of LT4. Fetus with hyperthyroidism. Tx?

A

Tx mother with methimazole, no change in LT4 dose.

64
Q

FDG-PET and incidental thyroid nodules
1. focal uptake: malignancy rate?
2. diffuse uptake: malignancy rate? additional lab?

A
  1. 35%
  2. 4.4% get a TPO Ab since 60% of cases had hypothyroidism or autoimmune thyroiditis
65
Q

What TFT results would sugget that thyrotoxicosis is from an exogenous and not endogenous source of thyroid hormone?

A

elevated T3, but T4 is normal

66
Q

amiodarone-induced thyrotoxicosis: type 1 vs type 2.
What test is the best to distinguish the two? What is seen in T1 vs T2?

A

Color flow Doppler sonography
Type 1 has INCREASED vascularity, whereas type 2 has ABSENT vascularity

Endocrinology (8 decks)

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