Endocrine3- Parathyroid Patho Ca Disorders

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Mawad
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310826
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Endocrine3- Parathyroid Patho Ca Disorders
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2015-11-04 19:14:35
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vetmed endocrine3
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vetmed endocrine3
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  1. How is serum PTH level controlled?
    PTH is constantly produced and stored in secretory vesicles; the amount secreted and degraded controls serum level
  2. Low ________ stimulates PTH release; _____ also to a lesser extent.
    iCa2+; Mg2+
  3. PTH stimulates _________ from the kidney, a negative regulator, and _________.
    calcitriol; active Vit D
  4. On histopath, more cytoplasm in PTG chief cells means _________; this can be caused by _________.
    more PTH production; chronic hypocalcemia
  5. How does acute hypercalcemia affect the PTG?
    secretory granules accumulate and are degraded
  6. How does chronic hypercalcemia affect the PTG?
    chief cells atrophy, decreased number of cells
  7. Causes of primary hypoparathyroidism. (2)
    [primary is rare] immune-mediated lymphocytic parathyroiditis, nodular regenerative chief cell hyperplasia
  8. How does nodular regenerative chief cell hyperplasia cause primary HYPOparathyroidism?
    a few cells proliferate and try to save the PTG, but they are all eventually killed
  9. The vast majority of parathyroid chief cell neoplasms are _________, leading to _______; a primary clinical sign associated with this is _______.
    functional; hypercalcemia; PU/PD
  10. Secondary C cell (thyroid gland) hyperplasia occurs secondarily to __________; there is an increase in _________ to try and combat _________.
    functional PTH neoplasia; calcitonin; hypercalcemia
  11. Primary hyperparathyroidism is usually caused by a _________; clinical signs include.... (5)
    tumor; PU/PD, weakness, generalized fibrous osteodystrophy (bone resorption), soft tissue mineralization, renal calculi
  12. Describe fibrous osteodystrophy.
    increase in poorly mineralized bone in an attempt to stabilize bone that has been resorbed
  13. Non-functional chief cell adenomas are ________ and are common in __________.
    subclinical; old rats
  14. Less common form of primary hyperparathyroidism that is usually functional and may require removal of multiple glands.
    multifocal hyperplasia
  15. Diffuse hyperplasia of the parathyroid gland occurs secondarily to _________; some less common causes are... (3)
    CKD; lack of dietary Ca2+, too much dietary Ph, or lack of dietary Vit D
  16. Secondary hyperparathyroidism to CKD occurs due to... (2)
    lack of calcitriol and increased FGF-23.
  17. Secondary hyperparathyroidism in reptiles is caused by... (3)
    CKD, lack of UV light, poor diet.
  18. Cancer-associated hypercalcemia can be caused by what kinds of cancer in animals? (4)
    anal sac, lymphoma, stomach SCC (horses), SCC {all produce PTHrP}
  19. Describe humoral hypercalcemia of malignancy.
    PTHrP has norma functions, but it is NOT usually secreted into circulation (except in cancer)
  20. Describe the synthesis and secretion of calcitonin.
    produced and sits in cytoplasm; released in the event of hypercalcemia
  21. What clinical conditions are associated with excess or deficient calcitonin?
    NONE
  22. Multiple endocrine neoplasia occurs due to __________.
    a genetic defect
  23. Corrected calcium is __________; the best indicator of systemic status is ___________.
    unreliable; iCa2+
  24. How do you collect a sample to measure iCa2+?
    serum tube or heparinized tube; NOT EDTA- falsely decreases Ca2+
  25. What increases Ca2+?
    PTH, PTHrP, Vit D
  26. Actions of PTH in the bone? (2)
    increase Ca2+ resorption, increase Ph resorption
  27. Actions of PTH in the kidney? (3)
    increased Ca2+ reabsorption, increased Ph excretion, activates Vit D by calcitriol
  28. Actions of PTH in the GI tract? (2)
    increased Ca2+ absorption, increased Ph absorption
  29. Classic role of Vit D? Other roles? (3)
    Classic: Ca-Ph homestasis; Other: immune system, RAAS, cardiovascular system
  30. What species cannot perform Vit D conversion in the skin?
    dogs and cats
  31. Dietary Vit D of plant origin.
    vit D2
  32. Dietary Vit D of animal origin.
    Vit D3
  33. What decreases Ca2+? (1)
    calcitonin
  34. Differentials for hypercalcemia.
    • Hyperparathyroidism
    • Addison's
    • Renal Failure
    • D Vit Excess
    • Idiopathic
    • Osteolytic
    • Neoplastic
    • Spurious/ systemic granulomatous dz
  35. Which differentials for hyperCa2+ have the higher Ca2+ values? (top 3)
    • 1- neoplasia
    • 2- primary hyperparathyroidism
    • 3- Vit D toxicity
  36. Top 4 differentials for hyperCa2+ in dogs? (in order)
    • 1- neoplasia
    • 2- renal disease
    • 3- hyperparathyroidism
    • 4- addison's disease
  37. What are the 2 most common neoplasias causing hyperCa2+ in dogs?
    lymphosarcoma, anal sac adenocarcinoma
  38. Top 3 differentials for hyperCa2+ in cats? (in order)
    • 1- neoplasia
    • 2- renal disease
    • 3- urolithiasis
  39. What are the 2 most common neoplasias causing hyperCa2+ in cats?
    lymphoma, squamous cell carcinoma
  40. Marked increase in Ca2+, marked decrease in phosphorous supports _____(2)_____.
    primary hyperparathyroidism, neoplasia
  41. Increase, normal, or decrease in Ca2+, marked increase in phosphorous supports __________.
    CKD
  42. Moderate increase in Ca2+ and phosphorous support __________.
    vit D toxicity
  43. Mild increase in Ca2+ and phosphorous support __________.
    Addison's disease
  44. Describe the txt of hyperCa2+. (4)
    treat underlying cause, diuresis, corticosteroids, bisphosphonates
  45. Why is diuresis a part of txt for hyperCa2+?
    causes Ca2+ excretion from kidneys
  46. How do bisphosphonates work?
    decrease number and action of osteoclasts, decrease bone resorption
  47. Clinical signs of hypoCa2+? (6)
    tremors/twitching, weakness, fasciculations, facial rubbing, seizures, anorexia
  48. Differential that causes the most profound hypoCa2+?
    hypoparathyroidism
  49. Differentials for hypoCa2+? (8)
    hypoparathyroidism, hypoalbuminemia, intestinal malabsorption, eclampsia/lactation; less common: acute pancreatitis, kidney disease, nutrition, ethylene glycol toxicity
  50. Emergency therapy for tetany?
    calcium gluconate IV slowly until Ca2+ level is LOW NORMAL
  51. Cardiotoxicity caused by rapid IV Ca2+ infusion causes _________.
    bradycardia
  52. If you suspect a hyperCa2+ disorder, what test should you order?
    malignancy panel- PTH, iCa2+, PTHrP
  53. You can only interpret PTH in light of ________.
    iCa2+
  54. Treatment for primary hyperparathyroidism.
    surgical removal of parathyroid gland
  55. Post-op risks associated with parathyroidectomy?
    risk for hypocalcemia- give Ca2+ and/or Vit D to maintain calcium in the low normal range
  56. Primary hyperparathyroidism is usually caused by a __________, causing...
    single adenoma; excessive synthesis and secretion of PTH.
  57. Primary hyperparathyroidism usually occurs in dogs __________ [age].
    middle-age to older (10yrs)
  58. Biochem changes that occur with primary hyperparathyroidism. (2)
    hypercalcemia, hypophosphatemia
  59. UA changes with primary hyperparathyroidism.
    USG<1.020, +/- crystalluria
  60. Why are hypercalcemic animals PU/PD?
    Ca2+ interferes with ADH, causing nephrogenic DI
  61. Definitive diagnosis of primary hyperparathyroidism is achieved by...
    paired PTH and iCa2+ measurements.
  62. Normally, if iCa2+ is high, PTH is _______.
    low
  63. What is the prognosis for primary hyperparathyroidism?
    excellent
  64. How do you diagnose idiopathic hyperCa2+?
    rule out all other causes
  65. Idiopathic hyperCa2+ typically occurs in __________.
    young to middle-aged cats
  66. With idiopathic hyperCa2+, Ca2+ is usually __________ increased.
    mildly to moderately
  67. 50% of cats with idiopathic hyperCa2+ will have __________ clinical signs.
    no
  68. Treatment for idiopathic hyperCa2+. (3)
    dietary modification, medical therapy with Prednisolone (promote calciuresis), bisphosphonates
  69. What are the nutritional goals when treating idiopathic hyperCa2+? (3)
    lower Ca2+ diet, avoid excess vit D (salmon), increase water consumption
  70. 3 causes of hypercalcemia with cancer.
    humoral hyperCa2+ (mediated by PTHrP), cancer in BM (osteolysis), tumor metastasis to bone
  71. 2 common causes of hematologic malignancy to BM.
    lymphoma, multiple myeloma
  72. HyperCa2+ of malignancy is typically not from primary __________, such as __________.
    bone tumors; osteosarcoma
  73. Clinical signs of hyperCa2+ of malignancy.
    lethargy, anorexia, GI signs, PU/PD
  74. Hypoparathyroidism is usually due to ____________; it is most common in ____________.
    immune-mediated destruction; young to middle-aged dogs (~4-5yrs)
  75. Clinical signs of hypoparathyroidism. (4)
    [may wax and wane] muscle tremors, seizures, tetany, facial rubbing
  76. What biochem abnormalities may you find with primary hypoparathyroidism? (2)
    hypocalcemia, hyperphosphatemia
  77. How do you definitively diagnose primary hypoparathyroidism?
    paired PTH and iCa2+: hypoCa2+ and low or low normal PTH
  78. Acute treatment for primary hypoparathyroidism- hypocalcemic tetany? (2)
    calcium gluconate IV slowly, monitor ECG for bradycardia/VPCs
  79. Long-term treatment of primary hypoparathyroidism? (2)
    calcitriol (vit D), goal is to keep total Ca2+ low normal
  80. What is the prognosis for hypoparathyroidism with proper treatment?
    excellent
  81. When and why does eclampsia occur?
    first 3 weeks of lactation due to excessive calcium loss into milk without proper nutrition/supplementation
  82. Eclampsia most commonly affects _________ with __________.
    small dogs; large litters
  83. What is the acute therapy for eclampsia? (2)
    calcium gluconate IV slowly, monitor ECG for bradycardia/VCPs
  84. What is the long-term treatment of eclampsia?
    calcium carbonate oral supplements until puppies are weaned
  85. Hyperparathyroidism can occur secondarily to... (2)
    renal failure, nutritional
  86. Clinical signs of renal secondary hypoparathyroidism? (2)
    PU/PD, GI signs (consistent with CKD)
  87. CBC and biochem abnormalities with secondary renal hypoparathyroidism? (4)
    mild anemia of chronic disease, azotemia, hyperphosphatemia, high/N/low tCa2+
  88. UA findings associated with renal secondary hypoparathyroidism? (3)
    isosthenuria, +/- proteinuria, +/- active sediment
  89. Treatment of renal secondary hypoparathyroidism. (6)
    calcitriol, treat CKD: dietary and medical management- low Ph diet, GI protectants, SQ fluids, antihypertensive, manage proteinuria
  90. Nutritional secondary hyperparathyroidism results from... (3)
    diet deficient in Ca2+, diet deficient in vit D, diet excessive in Ph
  91. Nutritional hyperparathyroidism causes __________; mineral is replaced by __________, a process called ____________.
    skeletal Ca2+ depletion; fibrous connective tissue; fibrous osteodystrophy
  92. Clinical signs of nutritional secondary hyperparathyroidism. (4)
    orthopedic disease- lameness, limb deformities in young animals; radiograph- decreased bone density, fractures
  93. How do you treat nutritional secondary hyperparathyroidism? (2)
    confinement to reduce risk of fracture, complete and balanced diet (increase Ca:Ph ratio)
  94. What is the prognosis for nutritional hyperparathyroidism?
    good, unless there are marked deformities

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