front 1 Parathyroid glands share embryologic origin with the: | back 1 C. Thymus |
front 2 The parathyroid gland is composed of which two main cell
types? | back 2 A. Chief cells and oxyphil cells |
front 3 The primary function of the parathyroid gland is regulation
of: | back 3 D. Calcium homeostasis |
front 4 Vitamin D is biologically active primarily in which form? | back 4 B. Dihydroxy form |
front 5 A patient with elevated PTH is expected to have increased urinary
excretion of: | back 5 B. Phosphate |
front 6 Primary hyperparathyroidism is most commonly caused by a
parathyroid: | back 6 D. Adenoma |
front 7 Overexpression of cyclin D1 in primary hyperparathyroidism is
classically driven by: | back 7 A. CCDN1 gene inversion |
front 8 The CCDN1 inversion associated with primary hyperparathyroidism
occurs on chromosome: | back 8 C. 11 |
front 9 A common cause of sporadic parathyroid adenomas is loss of the tumor
suppressor: | back 9 B. Menin (MEN1) |
front 10 CDC73 abnormalities are implicated in: | back 10 A. Hyperparathyroidism-jaw tumor syndrome |
front 11 An oxyphil cell parathyroid adenoma most resembles which thyroid
tumor type? | back 11 D. Hurthle cell tumor |
front 12 Based on these notes, which statement matches gland
involvement? | back 12 C. Carcinomas one; adenomas multiple |
front 13 The common skeletal manifestations of primary hyperparathyroidism
include: | back 13 A. Osteoporosis brown tumors osteitis fibrosa |
front 14 Severe hyperparathyroidism most characteristically causes: | back 14 B. Metastatic calcification |
front 15 The most common cause of secondary hyperparathyroidism is: | back 15 C. Renal failure |
front 16 Chronic renal insufficiency is associated with decreased: | back 16 D. Phosphate secretion |
front 17 Which enzyme is necessary to synthesize the active form of vitamin
D? | back 17 B. Alpha1-hydroxylase |
front 18 In secondary hyperparathyroidism, parathyroid glands are
typically: | back 18 C. Hyperplastic |
front 19 Hypoparathyroidism is rare and is most often due to: | back 19 D. Surgery |
front 20 Autoimmune hypoparathyroidism most commonly involves mutations
in: | back 20 A. AIRE |
front 21 Autosomal dominant hypoparathyroidism is classically caused
by: | back 21 C. CASR gain-of-function |
front 22 CASR gain-of-function causes hypoparathyroidism because it: | back 22 B. Heightens calcium sensing, lowers PTH |
front 23 Familial isolated hypoparathyroidism is most classically due
to: | back 23 A. Autosomal recessive GCM2 loss-of-function |
front 24 The GCM2 gene is necessary for: | back 24 D. PTH maturation |
front 25 The hallmark clinical feature of hypoparathyroidism is: | back 25 A. Tetany |
front 26 Positive Chvostek and Trousseau signs most strongly suggest: | back 26 C. Hypoparathyroidism |
front 27 The CDC73 gene encodes: | back 27 D. Parafibromin |
front 28 Osteitis fibrosa cystica is also called: | back 28 B. von Recklinghausen bone disease |
front 29 A lytic skeletal lesion classically seen in primary
hyperparathyroidism is: | back 29 D. Brown tumor |
front 30 Menin is encoded by which gene? | back 30 B. MEN1 |
front 31 With CASR gain-of-function, the receptor “believes” serum calcium
is: | back 31 C. Higher than actual |
front 32 Defective alpha1-hydroxylase most directly reduces: | back 32 A. Dihydroxy vitamin D |
front 33 Tapping a nerve causes facial twitching and eye muscle contractions.
This is: | back 33 C. Chvostek sign |
front 34 The Chvostek sign is elicited by tapping the: | back 34 A. Facial nerve |
front 35 In a positive Chvostek sign, tapping induces: | back 35 D. Eye muscle contractions |
front 36 The Trousseau sign is best described as: | back 36 B. Carpal spasm with cuff |
front 37 Thyroid function can be inhibited by agents called: | back 37 A. Goitrogens |
front 38 Propylthiouracil most directly acts by: | back 38 D. Inhibiting iodide oxidation |
front 39 Calcitonin lowers serum calcium primarily by: | back 39 B. Promoting skeletal calcium uptake |
front 40 The most common cause of thyrotoxicosis is: | back 40 C. Graves disease |
front 41 Hyperthyroidism is typically associated with increased: | back 41 C. Sympathetic tone |
front 42 Abrupt onset of severe hyperthyroidism in Graves is termed: | back 42 D. Thyroid storm |
front 43 Radioiodine uptake confined to one nodule most suggests: | back 43 B. Toxic adenoma |
front 44 Worldwide congenital hypothyroidism is most often due to: | back 44 C. Iodine deficiency |
front 45 Most autoimmune hypothyroidism is caused by: | back 45 A. Hashimoto disease |
front 46 Drugs like methimazole and propylthiouracil generally: | back 46 B. Inhibit thyroid secretion |
front 47 A common lipid abnormality in hypothyroidism is high: | back 47 D. LDL |
front 48 Nonpitting edema in hypothyroidism is due to deposition of: | back 48 C. Glycosaminoglycans and hyaluronate |
front 49 Hashimoto thyroiditis commonly features antibodies against: | back 49 A. Thyroglobulin and TPO |
front 50 Hashimoto genetic predisposition is linked to: | back 50 B. CTLA4 PTPN22 IL2RA |
front 51 Hashimoto thyroiditis is characterized histologically by: | back 51 D. Hurthle cells |
front 52 Painless nodules with anti-TPO, grossly normal, and large germinal
centers suggests: | back 52 B. Hashimoto thyroiditis |
front 53 Subacute lymphocytic thyroiditis typically shows fibrosis and Hurthle
metaplasia that: | back 53 C. Are absent |
front 54 Granulomatous thyroiditis is most often: | back 54 B. Viral |
front 55 Granulomatous thyroiditis commonly shows: | back 55 D. Multinucleate giant cells |
front 56 A classic Graves triad feature is: | back 56 B. Pretibial myxedema |
front 57 A classic Graves triad eye finding is: | back 57 A. Exophthalmos |
front 58 The best description of thyroid storm is: | back 58 C. Abrupt severe hyperthyroidism |
front 59 A scan shows uptake only in one solitary hot nodule. Most likely
cause: | back 59 D. Adenoma |
front 60 High LDL plus nonpitting edema is most consistent with: | back 60 D. Hypothyroidism |
front 61 A patient with Graves develops proptosis. The most common mechanism
is: | back 61 C. Retroorbital GAG deposition |
front 62 To dampen increased sympathetic tone in Graves disease,
prescribe: | back 62 A. Beta-blockers |
front 63 Diffuse nontoxic goiter typically: | back 63 D. Does not produce nodularity |
front 64 Two phases of diffuse nontoxic goiter are: | back 64 B. Hyperplastic, colloid involution |
front 65 Persons with simple goiters most often remain: | back 65 A. Clinically euthyroid |
front 66 Recurring episodes of goiter most often produce: | back 66 C. Multinodular goiter |
front 67 Long-standing goiter develops an autonomous nodule causing
hyperthyroidism. Diagnosis: | back 67 B. Plummer syndrome |
front 68 A solitary thyroid nodule in a younger male is more likely: | back 68 D. Neoplastic |
front 69 Gain-of-function mutations implicated in thyroid adenomas
include: | back 69 C. TSHR EZH1 GNAS |
front 70 EZH1 encodes a: | back 70 A. Histone methyltransferase |
front 71 The hallmark of follicular adenoma is: | back 71 D. Well-formed intact capsule |
front 72 Compared with follicular carcinomas, follicular adenomas have
capsules that: | back 72 B. More intact, less invasion |
front 73 Most thyroid carcinomas arise from: | back 73 C. Thyroid follicular epithelium |
front 74 Most mutations causing follicular carcinoma involve: | back 74 A. RTK pathway components |
front 75 Conventional papillary thyroid carcinoma is characterized by: | back 75 B. RET-NTRK fusion, BRAF mutations |
front 76 The RET gene is located on: | back 76 D. Chromosome 10 |
front 77 In papillary thyroid carcinoma, RET most commonly fuses with: | back 77 A. PTC1 and PTC2 |
front 78 Most BRAF-mutant conventional papillary carcinomas have: | back 78 C. V600E |
front 79 Follicular neoplasms are commonly associated with: | back 79 B. RAS gain-of-function |
front 80 Anaplastic thyroid carcinoma commonly shows mutations in: | back 80 D. TP53 CTNNB1 TERT |
front 81 Medullary thyroid carcinoma is commonly seen in: | back 81 A. MEN-2 |
front 82 In Graves orbitopathy, the deposited material is primarily: | back 82 C. Glycosaminoglycans |
front 83 In Graves exophthalmos, GAG deposition occurs in the: | back 83 D. Retroorbital space |
front 84 The early proliferative phase of diffuse nontoxic goiter is: | back 84 B. Hyperplastic phase |
front 85 The later involutional phase of diffuse nontoxic goiter is: | back 85 C. Colloid involution phase |
front 86 A patient with a simple goiter is most likely: | back 86 A. Euthyroid |
front 87 A thyroid tumor with RET-NTRK fusion is most consistent with: | back 87 D. Conventional papillary carcinoma |
front 88 A thyroid nodule with gain-of-function TSHR mutation most
suggests: | back 88 B. Thyroid adenoma |
front 89 A solitary thyroid nodule that is encapsulated and intact is most
consistent with: | back 89 A. Follicular adenoma |
front 90 Compared with follicular adenoma, follicular carcinoma more often
shows: | back 90 C. Capsular invasion prominent |
front 91 The pathway most often implicated in follicular carcinoma mutations
is: | back 91 B. Receptor tyrosine kinase pathway |
front 92 A thyroid tumor with BRAF V600E most strongly supports: | back 92 D. Conventional papillary carcinoma |
front 93 A thyroid tumor with RAS gain-of-function most suggests a: | back 93 A. Follicular neoplasm |
front 94 TP53 + CTNNB1 + TERT mutations most support: | back 94 D. Anaplastic carcinoma |
front 95 MEN-2 association most strongly points to: | back 95 B. Medullary carcinoma |