ERM2 - Calcium and Bone

Card Set Information

Author:
jknell
ID:
184755
Filename:
ERM2 - Calcium and Bone
Updated:
2012-11-21 00:32:02
Tags:
Endocrine Reproductive Pathology
Folders:

Description:
Endocrine and Reproductive Pathology
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user jknell on FreezingBlue Flashcards. What would you like to do?


  1. Vitamind D processing
    • 1. VitD hydroxylated in liver to 25vitD
    • 2. 25VitD hydroxylated in kidney to 1,25(OH)2VitD
    • -positive: PTH and hypophosphatemia
    • -negative: FGF23
  2. Ca inhibits PTH secretion
    • -negative feedback
    • -normal Ca = 10
  3. Calcium Metabolism
    • -major regulator of intestinal absorption: vitD
    • -major regulator of kidney reabsorption: PTH
    • -major regulator of bone resporption: PTH
  4. Functions of Vitamin D
    • -increase gut absorption of Ca
    • -increase kidney reabsorption of Ca
    • -increased resorption and formation of bone
  5. Functions of PTH
    • -increase gut absorption of Ca
    • -increase kidney reabsorption of Ca
    • -decrease bone formation
    • -increase bone resorption

    --> increase serum Ca
  6. Functions of Calcitonin
    • -decrease gut absorption of Ca
    • -decrease kidney reabsorption of Ca
    • -increase bone formation
    • -decrease bone resorption

    --> decrease serum Ca
  7. PTH and bone effects
    • 1. sustained PTH elevation --> bone resorption
    • 2. intermittent PTH elevation --> bone formation (ie: injections)
  8. Calcitonin tachyphylaxis
    • -eventually there is central downregulation of CT effets
    • -chronic changes in CT don't effect Ca homeostasis
  9. PTH Regulation
    • -iCa signals through CaSR to inhibit PTH and stimulate CT secretion
    • -most ppl have 4 parathyroid glands (can vary)
    • -supplied by inferior thyroid artery
  10. Milk Alkali Syndrome
    -peptic ulcers allow excess absorption of Ca into blood (milk, CaCO3)
  11. Primary Hyperparathyroidism: Epidemiology
    -more Ca required to affect a given degree of PTH suppression (right shift)

    -1/500 women, 1/2000 men
  12. Primary Hyperparathyroidism: Symptoms
    -asypmtomatic

    • -stones
    • -bones (painful resorption of bones = osteoitis)
    • -groans (peptic ulcer, pancreatitis)
    • -moans (fatigue, depression)
    • -CV
  13. Primary Hyperparathyroidism: Causes
    • 1. Parathyroid Hyperplasia
    • 2. Familial Hypocalciuric Hypercalcemia (FHH)
    • 3. Lithium use
  14. Parathyroid Hyperplasia
    • -too many parathyroid cells
    • -typically signal parathyroid adenoma
    • -sometimes four gland hyperplasia
    • -rarely carcinoma

    -urine Ca is high (at risk for kidney stones)
  15. Familial Hypocalciuric Hypercalcemia (FHH)
    • -CaSR mutation
    • -inability of Ca signaling to inhibit PTH
    • -Urine Ca is low (same CaSR mutation): not at risk for stones
  16. Lithium induced Hyperparathyroidism
    -inhibits signaling downstream of CaSR
  17. PTH levels in Hyperparathyroidism
    • -may be in the upper half of normal
    • -inappropriate in the face of hypercalcemia
  18. Hypercalcemia: Causes
    • 1. Artifactual (hyperproteinemia)
    • 2. Malignancy
    • 3. Drugs
    • 4. Renal Disease
    • 5. Endocrine
    • 6. Granulomatous Disease
    • 7. Immobilization
  19. Artifactual Hypercalcemia
    -iCa is normal, protein is elevated

    • Causes
    • -venous stasis
    • -hyperalbuminemia (increased protein consumption)
    • -hypergammaglobulinema (myeloma)
  20. Malignancy Hypercalcemia
    • -bone mets/myeloma
    • -PTHrP production
  21. Drug induced Hypercalcemia
    • -VitD and VitA
    • -Milk alkali syndrome
    • -Li
    • -Thiazides
  22. Renal Disease Hypercalcemia
    • -ARF
    • -tertiary hyperparathyroidism
  23. Endocrine Hypercalcemia
    • 1. Primary hyperparathyroidism
    • 2. FHH
    • 3. hyperthyroidism
    • 4. adrenal insufficiency
  24. Granulomatous Disease Hypercalcemia
    • sarcoidosis
    • coccidiomycosis
    • TB
    • histoplasmosis
    • berrylliosis
  25. Immoblization Hypercalcemia
    • -Paget's disease
    • -adolescence
  26. Hypercalcemia: treatment
    • 1. hydration (protect kidneys)
    • 2. CT injections (quick but temporary)
    • 3. hemodialysis
    • 4. Parathyroidectomy
    • 5. Bisphosphonates/tumor resection
    • 6. Glucocorticoids
  27. Anti-resorptive tx in osteoporosis
    -increase BMD while decreasing bone formation
  28. proformation tx in osteoporosis
    -increase BMD while increasing bone resorption
  29. Cushing's and osteoporosis
    -decreased bone formation is paradoxically coupled to increased resorption

    --> double whammy for osteoporosis
  30. Bone Turnover Markers
    • 1. Formation Markers (osteoblast origin)
    • -alk phos
    • -osteocalcin

    • 2. Resorption Markers (osteoclast origin)
    • -NTx, CTx
  31. Coupling of bone turnover has a lag time
    • -in high turnover states (adolescence and Paget's disease) immobilization leads to a sudden arrest of formation
    • -ongoing resorption is unopposed
    • --> hypercalcemia and kidney stones
  32. Hungry Bone Syndrome
    in PT adenoma resection can have a sudden arrest of resorption and ongoing formation goes on unopposed --> hypocalcemia and hypophospatemia
  33. Adynamic bone
    • -turnover too slow
    • -increased risk of fracture

    • Causes
    • 1. excessive use of bisphosphonates (block resorption)
    • 2. hypophosphatemia (TNSAP mutation)
    • 3. excessive use of 1,25D in renal failure (can over suppress PTH)
  34. More lytic bone lesions
    • Myeloma
    • renal
    • melanoma

    • --> lead to hypercalcemia
    • -cold on bone scan
  35. More blastic bone lesions
    • prostate
    • breast
    • lung

    • --> lead to hypocalcemia and elevated alk phos
    • -hot lesions
  36. Osteomalacia and Rickets
    • -impaired mineralization due to:
    •      -XLR
    •      -renal failure
    •      -D deficiency
    •      -hypophosphatemia

    • -dense bones
    • -plates wide and jagged
    • -richitic rosary beads
  37. X-linked hypophosphatemic rickets (XLR)
    • males less than 3yrs, with short bowed legs
    • -not nutritional defect
    • -PHEX protease mutation --> elevated FGF23
    • -phosphate wasting in urine (hypophosphatemia)
    • -low 1,25D
  38. Renal Osteodystrophy
    1. osteoitis fibrosa cystica: secondary hyperparathyroidism (decreased Ca --> increased PTH --> osteoclast activity)

    2. Osteomalacia (low Ca)

    3. adynamic bone disease (tx with 1,25D)

    4. osteoporosis

    Tx: low phosphate diet
  39. Primary Hyperparathyroidism
    • -PTH driven hypercalcemia
    • -usually single gland adenoma
  40. Secondary Hyperparathyroidism
    • -increased PTH due to compensatory response
    •      -Vit D deficienc
    •      -renal failure
    •      -PTH resistancce
    • -blood calcium low or normal
    • -typically 4 gland hyperplasia
  41. Tertiary Hyperparathyroidism
    • -when secondary hyperparathyroidism pick up mutations and become autonomous
    • -hypercalcemia
    • -very rare complication of renal failure

What would you like to do?

Home > Flashcards > Print Preview