Endocrine I

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Endocrine I
2011-04-21 19:56:13
Endocrine Path

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  1. What's the most likely cause of a warm/cold/hot thyroid nodule?
    • Warm = normal
    • Cold = hypofuncitonal (possibly mallignant)
    • Hot = hyperfunctional (benign)
  2. Which lesions are more worrisome (Sold/Cystic)?
    Solid; Cystic are probably adenomatour nodules underoging cystic degeneration
  3. Are papillary carcinomas more likely to be solid or cystic? Encapsulated or Unencapsulated?
    Sold (cystics aren't a big deal); unencapsulated (vs. follicular)
  4. What's the low power histological appearance of papillary carcinoma of thyroid?
    Papillary formations of tumor cells
  5. What's the characteristic high-power (cellular) histological characteristic for Papillary Carcinoma of thyroid?
    Opticlaly clear (orpahn annie nuclei); nucelar groove (intranuclear cytoplasmic inclusions); ; overlappting nuclei; even without papillae
  6. What type of thyroid carcinoma appears with Psammoma bodies?
    Papillary Thyroid Carcinoma (pathognomonic); calcified structure as fossilized tips of papillae
  7. What are risk factors specific for papillary thyroid carcinomas?
    • Irradiation of head/neck in first 2 decades of life
    • Hashimoto thyroiditis
  8. A thyorid nodule with a thick and irregular capsule is characteristic of what type of carcinoma?
  9. What histological pattern is charactersitic of follicular carcinoma of thyroid?
    • Small closely packed follicles of colloid
    • Absence of papillary structures (psammoma bodies; ground glass nuclei; grooves)
  10. How do you distinguish follicular adenoma from carcinoma?
    Invasion into capsule or blood vessles; metastases
  11. What genetic alterations are seen in papillary carcinoma?
    RET; BRAF mutations
  12. What genetic alterations are seen in medullary carcinoma?
    RET mutations
  13. What's included in MEN IIA Syndrome?
    Pheochromocytoma; parathyroid hyperplasia/adenoma; medullary carcinoma
  14. What's included in MEN IIB Syndrome?
    Pheochromocytoma; mucocutaneous neuromas; skeletal abnormalities; medullary carcinoma
  15. What cell type is the origin of medullary carcinoma?
    C-cells of thyroid (parafollicualr cells)
  16. What's the cell marker for Papillary/Follicular Carcinoma?
  17. What's the cell marker for Medulalr Carcinoma?
  18. What's the metastasis pattern for Papillary vs. Follicular vs. Anaplastic thyroid carcinoma?
    • Papillary/Anaplastic - Lymphatic spread
    • Follicular/Medullary - Hematogenous spread
  19. What's the prognosis comparison between types of thyroid carcinomas?
    Papillary (90%) > Follicular (65%) > Medullary (50%) > Anaplastic (0%)
  20. What type of histological pattern is most common in medullary thyroid carcinoma?
    Lobar pattern
  21. What thyroid carcinoma typically has amyloid present?
    Medullary Carcinoma of Thyroid
  22. What's the most common type of thyroid carcinoma to spread and where does it go?
    Papillary thyroid carcinoma to a lymph nodule
  23. What's the usuall gross features of Hashimoto Thyroditis?
    • Diffusely enlarged thyroid that's firm and rubbery
    • Red-brown --> yellow brown
  24. What are the histological characteristics of Hashimoto's Thyroiditis?
    • destruction of follicles
    • Lymphatic & plasmacytic infliltration --> lymphoid follicles and germinal centers
  25. What's the pathogenesis of Hashimoto's disease?
    CD4 T-cells targeting thyroid Ag's are activated post infectionB cell stimulation -> CD8 cells destroy gland
  26. What are Hurthle cells and when are they seen?
    • Oxyphilic cells from metaplasia of follicular epithelium (increased mitochondria)
    • Hashimoto Thyroiditis
  27. What autoantibodies are present in Hashimoto Thyroidits?
    Anti- TPO; thyroglobuli; TSH receptor
  28. What are clinical features of Hypothyroidism?
    Generalized Myxedema; cardiomegally; psychiatric issues
  29. What does Hashimoto's increase risk for ?
    B-cell lymphomas (MALToma)
  30. What is the cause for a multinodular goiter?
    Compensation for:Iodine deficiency; Thyroid hormone synthesis defect; decreased TH synthesis; long standing disease
  31. What are common complications associated with goiter?
    Cosmetic; airway obstruction; dysphagia; SVC syndrome
  32. What is Plummer Syndrome and when does it present?
    Multinodular Goiter
  33. When do you see pretibial Myxedema?
  34. What's the diagnostic test for the cause of Cushing's syndome?
    24-urine collection; dexamenthasone suppression test
  35. What would you expect to find from plasma ACTH and high dose dexemethasone suppresion in: Pituitary induced adrenal hyperplasia?
    Elevated ACTH; suppression only at high dose
  36. What would you expect to find from plasma ACTH and high dose dexemethasone suppresion in: Adrenal Adenoma?
    Low plasma ACTH; no ACTH suppression
  37. What would you expect to find from plasma ACTH and high dose dexemethasone suppresion in: Adrenal Carcinoma
    • Plasma ACTH - Low
    • No suppression
    • Large adrenal neoplasm on CT
  38. What would you expect to find from plasma ACTH and high dose dexemethasone suppresion in: Ectopic ACTH (SC CA)
    • Plasma ACTH: very high
    • No Suppression
  39. What's the most common cause of Cushing's syndrome?
    Steroid treatment
  40. What's the etiology of Cushing's Disease?
    Pituitary caused ACTH adenoma
  41. What factors increase the probablility of malignancy in Cushing's Syndome?
  42. What's the most common endogenous cause of Cushing's desease?
    Pituitary adenoma
  43. What is Conn's syndrome?
    Primary Hyperaldosteronism due to adrenal cortical adenoma (#2 cause of hyperaldosteronism)
  44. What's the most common cause of hyperaldosteronism?
    Adrenal Hyperplasia
  45. What features are charactersitic of secondary hyperaldosteronism?
    Increased aldosterone & increased Renin
  46. What features distinguish adrenal adenoma vs. carcinoma?
  47. What do adrenal tumors look like histologically?
    Clear; lipid-laden tumor cells in nests (like RCC)
  48. What's the characteristic clinical triad for Hyperparathyrodism?
    Painful bones; stones; abnominal groans; psychic moans
  49. What's the predominat cell type of parathyroid adenoma?
    Chief cells
  50. What's the most common cause of hyperparathyrodism?
  51. What are the causes of hypercalcemia?
    • Ca injestion; hyperthyroid; hyperparathyroid; Iatrogenic; Multiple Myeloma; Paget disease; Addison's; Neoplasia (Squamous Cell); Zollinger-Ellizon; Extra Vit D; Extra Vit A; Sacroidosis
  52. What's the most common causes of primary hyperparathyrodism?
    • 80% - solitary adenoma
    • 15% - PTH gland hyperplasia
  53. What do you expect to see histologically in the parathyroid?
    Fat cells (they're not present in hyperparathyroidism)
  54. What are common clinical features of hyperparathyroidism?
    Peptic Ulcers; Pancreatitis; Kidney Stones (post-renal renal failure)
  55. What's the most common cuase of secondary hyperparathyrodisim?
    Renal Failure
  56. What's the role of vitamin D?
    Stimulates absorption of calcium in gut & bone
  57. What's the etiology of renal failure causing hyperparathyroidism?
    Decreased phosphate re-absorption (↑ P); decreased vit D activation; decreased Ca absorption (↓ Ca)
  58. What's the difference between secondary and tertiary hyperPTHism?
    Tertiary: automatous PTH hyperfunction following secondary hyperPTHism for a while
  59. What are clinical symptoms of hypoparathyroidism?
    Hypocalcemia: increased irritibility; hyperreflexia; Chevostek & Trousseau signs; Cataracts; depression; paranoia; intracranial HTN; arrythmias