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Endocrine Unit Phase 1 > Calcium and Bone Metabolism > Flashcards

Calcium and Bone Metabolism Flashcards

1
Q

What is Ca2+ bound to in the blood?

A

40% albumin, 15% to other anions (Po3-)

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2
Q

What happens when blood is acidic?

A

Acid means there are a lot of H+ in blood, will competitively bind to anions and lead to increase in free Ca2+

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3
Q

What is the relationship between alkalosis/acidosis and serum Ca2+?

A

alkalosis –> hypocalcemia

acidosis –> hypercalcemia

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4
Q

Where is Ca2+ found?

A

99% in bone, <1% in blood

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5
Q

What states can Ca2+ be in blood?

A

Free (ionized) 45%
Bound to albumin 40%
Bound to other anions (PO3-) 15%

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6
Q

How does Ca2+ enter our body? What does this process require

A

Via absorption from gut (requires vitamin D)

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7
Q

Besides Ca2+, what other molecules are highly dependent on bone metabolism?

A

PO3- and Alk Phos

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8
Q

What does Ca2+ and PO3- form in bone?

A

Hydroxyapatite

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9
Q

What happens to PO3- if Ca2+ released from bone?

A

Ca2+ bound to PO3- to form hydroxyapatite in bone so if need to increase serum Ca2+, will need to breakdown hydroxyapatite = increased serum PO3-

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10
Q

What are the 2 main hormones that regulate Ca2+ homeostasis?

A

PTH and VD

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11
Q

What is the action of VD?

A

Regulates Ca2+ and PO3- absorption from gut

Stops K from secreting Ca2+

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12
Q

On which bone cell(s) does PTH bind to?

A

Osteoblast and osteocyte

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13
Q

What is the pathway that is activated when RANK-L binds to RANK? What does it result in?

A

transcription factor pathway NFKB –> increased osteoclast activity leading to increased release of Ca2+ and pO3- from bone

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14
Q

What is the action of PTH on Kidney?

A

Increases Ca2+ reabsorption, decreases renal PO3- reabsorption, stimulates active VD (calcitriol) formation in K

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15
Q

How is bone mineralized? Which hormone is involved?

A

VD provides osteoblasts with Ca2+ and PO3-, allowing for spontaneous mineralization

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16
Q

What is PTH stimulated by?

A

low Ca2+, high PO3-, low Mg2+

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17
Q

What happens with low Mg2+? What about really low Mg2+?

A

Low Mg2+ = increased PTH secretion, will correct itself

Severely low Mg2+ = dHoecreases PTH secretion, hypoparathyroidism

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18
Q

How does MG2+ wasting present?

A

diarrhea, diuretics, alcohol abuse, and aminoglycosides

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19
Q

How does PTH increase PO3- secretion by K?

A

Blocks reabsorption of PO3- by inhibiting Na+/PO3- cotransporter in PCT

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20
Q

What happens with elevated PTH?

A

hypercalcemia, hypophosphatemia

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21
Q

What are examples of Secondary hyperparathyroidism?

A

Vitamin D deficiency, gut malabsorption, and CKD (most common)

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22
Q

How do we get tertiary hyperparathyroidism?

A

as a result of long-standing secondary hyperparathyroidism that progresses to autonomous oversecretion of PTH by the parathyroid gland, despite correction of the hypocalcemia

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23
Q

What are general sxs of HPT?

A

fatigue, irritability, depression, and memory pbs

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24
Q

What are the 3 possible causes of PHPT?

A

parathyroid adenoma, hyperplasia, carcinoma

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25
Q

What are the symptoms of hypercalcemia?

A 
Painful bones (bone pain, osteitis fibrosa cystica, osteoporosis, weakness), renal stones (nephrolithiasis nephrocalcinosis, and nephrogenic diabetes insipidus), abdominal groans (abdominal pain, ulcers, constipation, acute pancreatitis), psychiatric moans (confusion, depression, seizures, stupor, coma)
Can also cause hyporeflexia and weakness (Na+ channels excessively blocked so threshold rises)
HTN, cardiomyopathy (Ca2+ deposits in heart), shortened QT interval and ST segment elevation (shortening of myocardial AP)
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26
Q

What is osteitis fibrosa cystica? What is it caused by? What can we see with it?

A

von Recklinghausen disease of bone, due to increased bone resoprtion due to chronic HPT. See cystic bone lesions (brown tumors)

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27
Q

With what do we see brown tumors? What causes this brown color?

A

Osteitis fibrosa cystica, brown from hemosiderin deposition into fibrous stroma. Due to hemorrhage into cystic space

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28
Q

What do we see in the urine with hypercalcemia (has to do with bone breakdown)

A

hydroxyproline in urine due to breakdown of collagen in bone

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29
Q

What happens in nephrogenic diabetes insipidus? What is it associated with?

A

when K can’t respond to ADH so polyuria, associated with hypercalcemia (HPT etc…)

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30
Q

What are the GI symptoms associated with hypercalcemia caused by?

A

Ca2+ deposits in GI system or pancreas

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31
Q

What is the pathophysiology of chronic K disease leading to secondary HPT?

A

Damaged proximal tubule cells, reduced 1alpha-hydroxylase activity –> VD precursor not converted to active VD (calcitriol) –> decreased serum Ca2+ –> increased PTH secretion

High serum PO3- due to inadequate secretion by K –> binds to serum Ca2+ –> decreased serum Ca2+ –> increased PTH secretion

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32
Q

What are the sxs of 2ndary HPT?

A

renal osteodystrophy = bone and joint pain, bone deformities and fractures, decreased mobility

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33
Q

What causes renal osteodystrophy due to CKD?

A

CKD –> 2ndary HPT
chronic PTH levels = increased bone turnover = osteitis fibrosa cystica + osteomalacia
Renal tubular acidosis (acidic serum, hydroxyapatite dissolves = demineralization)

34
Q

With what population is tertiary HPT common in?

A

pts w/ end stage renal disease who receive dialysis and have long-standing 2ndary HPT

35
Q

what are the sxs associated with 3ary HPT?

A

musculoskeletal pain, itchiness, lethargy, fractures, subperiosteal thinning of radial aspects of proximal and middle phalanges of 2nd and 3rd finger

36
Q

What is the serum BUN and CR expected to be for PHPT? What about urine Ca2+, PO3-?

A

Serum BUN and Cr normal since not K pb. urine Ca2+ and phosphate high

37
Q

What is the treatment for PHPT?

A

Surgical removal, may result in hypoparathyroidism and hypocalcemia so can require long-term Ca2+ replacement
Medical management - bisphosphonates (alendronate and cinacalcet)

38
Q

What is alendronate? What is it specifically used to treat?

A

Bisphosphonate, primary medical tx for PHPT, inactivates osteoclasts.

39
Q

What is Cinacalcet?

A

Bisphosphanate, calcimimetic that binds to Ca2+ R on PG/ and “fools” it into turning off PTH secretion

40
Q

What is the tx for Secondary HPT caused by CKD?

A

Synthetic Calcitriol to increase calcitriol (VD) levels + restrict dietary PO3- + gut PO3- binders to lower serum PO3-
Dialysis: relieves acidosis

41
Q

What is the tx for tertiary HPT?

A

surgical parathyroidectomy

42
Q

What are normal Ca2+ levels?

A

8.4-10.2

43
Q

What are the hormones that regulate Ca2+?

A

PTH, Calcitriol (VD), Calcitonin (C-cells of thyroid)

44
Q

What is the mechanism of action of calcitonin?

A

inhibits osteoclast activity and renal tubular reabsorption of Ca2+ –> lowers serum Ca2+

45
Q

What are the 4 ways that PTH increases serum Ca2+?

A

increased osteoclast activity, increased renal reabsorption of Ca2+, increased active VD formation via activation of 1alpha hydroxylase in PCT, decreased renal PO3- reabsorption so less available to bind Ca2+ in blood

46
Q

What are the possible causes of hypercalcemia?

A

HPT (most common), Cancer, Granulomatous Disorders, Meds, Prolonged Immobility, Familial Hypocalciuric Hypercalcemia

47
Q

What types of cancers cause hypercalcemia?

A
  • paraneoplastic syndromes, ex: PTHrP (breast and squamous cell lung cancers)
  • metastatic bone invasion (Multiple Myeloma)
  • Increased VD formation (ectopic 1alpha-hydroxylase, lymphomas)
48
Q

What is a granuloma? How does it lead to hypercalcemia?

A

area of chronic inflammation w/ aggregation of macrophage. Macrophage express 1alpha-hydroxylase resulting in excessive VD which stimulates gut absorption of Ca2+

49
Q

What are conditions that cause granulomas?

A

Sarcoidosis, Tb, fungal infections (coccidiomycosis), occupational diseases (berylliosis)

50
Q

What medications cause hypercalcemia?

A

thiazide diuretics (chlorthalidone), lithium (1st line tx for bipolar disorder), excessive Ca2+ or VD supplements (for bone health)

51
Q

What is Chlorthalidone? What is its mechanism of action? What can it lead to?

A

Thiazide diuretic, increases renal reabsorption of Ca2+ in DCT, can lead to hypercalcemia

52
Q

How does prolonged immobility result in hypercalcemia?

A

excessive bone resorption and demineralization

53
Q

What is Familial Hypocalciuric Hypercalcemia (FHH)? What are the sxs? What makes it different from the other hypercalcemia causes?

A

rare inherited disorder due to defects in Ca2+ sensing R in parathyroids and renal tubules, results in persistent hypercalcemia (>10.2) yet usually asymptomatic. Only cause to show low urine Ca2+ excretion

54
Q

What is the function of Ca2+ in cells?

A

blocks Na+ channels and inhibits depolarization of nerves and muscles

55
Q

What sxs are usually seen w/ chronic hypercalcemia? What pt population does this usually affect? What about acute hypercalcemia?

A

asymptomatic, PHPT patients

acute - usually pts w/ cancer,

56
Q

How do you measure free (ionized) Ca2+?

A

Corrected Ca2+ = measured total serum Ca2+ + (0.8 x (4-[albumin])

57
Q

What is the treatment for asymptomatic hypercalcemia?

A

no immediate action required, avoid thiazide diuretics, lithium, high Ca2+ diet, volume depletion, prolonged immobility

58
Q

What is the treatment for symptomatic hypercalcemia?

A

volume repletion w/ IV 0.9% saline + loop diuretics (furosemide) + Bisphosphonates if mild to moderate hyperC resists to fluids and loop diuretics + Calcitonin if severe acute hyperC w/ hx of renal failure + Glucocorticoids (prednisone) in granulomatous diseases

59
Q

Why give IV 0.9% saline in symptomatic hypercalcemia patients?

A

dilutes Ca2+ and increases renal Ca2+ excretion

60
Q

What is furosemide? What is its mechanism of action? For what patients is this given?

A

Loop diuretic, increases Ca2+ excretion in K so given to patients w/ hypercalcemia

61
Q

How do bisphosphonates work? What are 3 examples of drugs?

A

inhibit bone Ca2+ resorption by binding to hydroxyapatite (Ca2+ & PO3-) and inhibiting OC activity = alendronate, zoledronate, pamidronate

62
Q

Why is Calcitonin a possible therapy for hyperC? For what pts? What must we keep in mind?

A

severe, acute hyperC and hx of renal failure, inhibits renal tubular reabsorption of Ca2+ + inhibits osteoclast activity in bones. Cannot be used long term, high risk for calcitonin resistance

63
Q

Why is prednisone a possible therapy for hyperC? For what pts? What type of drug is this?

A

Glucocorticoid, decreases Ca2+ by inhibiting production of calcitriol by macrophages, can be used in pts w/ granulomatous diseases and some lymphomas

64
Q

What is a drug that can treat hyperC due to overactivity of osteoclasts? What is its mechanism of action? What pt does it copy MOA?

A

Denosumab - monoclonal Ab, blocks maturation of OC by binding to RANK-L –> same action as OPG

65
Q

What does yellow bone marrow store?

A

Fat and mesenchymal cells (precursors to bone, fat, cartilage, and muscle cells)

66
Q

What is the at birth? What happens with aging? What is the structure <25 y.o., <25 y.o.( final adult)

A

@ birth = filled w/ red bone marrow
aging = some of it converted to yellow bone marrow
<25 y.o. = diaphysis contains yellow BM, epiphysis and metaphysisis contain red BM
>25 y.o.= red BM axial skeleton, yellow BM in diaphysis of long bones

67
Q

Where are Osteoblasts found in the bone? What do they look like? What do they synthesize?

A

Small, line surface of bony trabeculaem synthesize components of matrix: type I collagen, hydroxyapatite, osteopontin, osteocalcin

68
Q

What do osteoclasts look like? From what lineage are they descended? Where are they found?

A

huge, multinucleated - are related to monocyte/macrophage cell lineage. Found on surface of bone in Howship lacunae (indentations on surface)

69
Q

What is an osteon? What does it look like? What does it contain?

A

functional unit of cortical bone formed by several layers of osteocytes - form tree-like structure w/ intervening bone matrix (lamellae) wrapped around central canal containing Haversian canal which communicate are interconnected by periosteal vessels via Volkmann canal

70
Q

What are the 2 pathways for bone formation?

A

Endochondral ossification & Intramembranous ossification

71
Q

What is the lineage from which osteoblasts arise from? What about osteocytes?

A

Mesenchymal stem cells, become osteocytes when get trapped in the osteoid they secrete

72
Q

What is released into the blood as bone is resorbed?

A

Ca2+, PO3-, Mg2+

73
Q

What is the action of PTH, Calcitonin, VD3, and IL-6 on osteoclast activity? What other hormones/pts regulate bone modeling, and how?

A

PTH and IL-6 = increase activity
Calcitonin and VD3 = decreases
Estrogen = prevents OB apoptosis, promotes OC apoptosis
OPG = RANK-L decoy R produced by OB, binds circulating RANK-L

74
Q

From what is collagen formed?

A

from mesenchymal ccells that differentiate into chondroblasts

75
Q

What secretes cartilage matrix? What happens to these cells?

A

Chondroblasts secrete matrix and become chondrocytes once entrapped in lacunae

76
Q

What are the different types of cartilage?

A

hyaline cartilage, elastic cartilage, fibrocartilage

77
Q

What is the histology for hyaline cartilage? elastic cartilage? Fibrocartilage?

A 
Hyaline = chondroitin sulfate + type II collage
Elastic = // + elastic fibers
Fibrocartilage = type I collagen
78
Q

Progression of bone formation in endochondral ossification vs. membranous ossification?

A

Cartilage –> Woven bone –> lamellar bone

Woven bone –> lamellar bone

79
Q

Where is type 1 collagen found? Type 2?

A

1 –> bone

2 –> collagen

80
Q

What does Alk Phos increase w/?

A

bone breakdown and biliary obstruction

Endocrine Unit Phase 1 (5 decks)

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