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Therapeutics I > Block 4: Ca2+ and P > Flashcards

Block 4: Ca2+ and P Flashcards

1
Q

What is the function of Ca2+?

A
  1. Muscle contraction
  2. Membrane action potential
  3. Coagulation cascade
  4. Bone metabolism
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2
Q

Where is Ca2+ stored?

A
  1. Bone
  2. Serum
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3
Q

How is calcium regulated?

A

Vitamin D: carrier of Ca2+
Mg increases the absorption of Ca2+ (PTH)
PTH: ↑ Ca2+ → ↑ calcitonin →↓ Ca2+ absorption

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4
Q

How much of Ca2+ is in the body?

A

99% in bone
1% EC (40% is bound to albumin and rest is free calcium)

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5
Q

How do you calculate corrected calcium?

A

Corrected Calcium = Measured Ca + 0.8 (4- albumin)

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6
Q

What is normal serum total calcium?

A

8.4-10.2 mg/dL (2.1 to 2.55 mmol/L)

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7
Q

What is the normal serum ionized calcium?

A

4.48 to 5.32 mg/dL (1.12 to 1.33 mmol/L)

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8
Q

Describe the homeostasis of Ca2+

A
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9
Q

What is hypercalcemia?

A

> 10.2 mg/dL

Mild to moderate: 10.2 - 13 mg/dL
Severe: >13 mg/dL
Crisis: > 15 mg/dL

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10
Q

What are the causes of hypercalemia?

A
  1. Primary hyperPT
  2. Cancer secretions
  3. Immobilization
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11
Q

What drugs induce hypercalcemia?

A

Thiazides, Vit D, Lithium

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12
Q

What mechanisms are affected by hypercalcemia?

A
  1. Bone resorption (cancer, HPT)
  2. Increases calcium absorption in GIT (Vit D)
  3. Tubular reabsorption (thiazide, lithium)
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13
Q

What are the indications of mild to moderate Hyper calcemia?

A

<13
Asymptomatic
Drug induced or primary hyperparathyroidism

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14
Q

What are the indications of severe hypercalcemia (acute and chronic)?

A

> 13
Acute: N/V, constipation, polyuria, polydipsia
Chronic: calcification, nbephrolithiasis

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15
Q

What are the indications from hypercalcemic crisis?

A

> 15
AKI, Lethargy → chronic can lead to coma and life-threatening arrhythmias

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16
Q

Describe the treatment plan for hypercalcemia?

A
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17
Q

What is the first line for hypercalcemia?

A

0.9% NS
Loop diuretics

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18
Q

What are 1st lines for cancer associated hypercalcemia?

A

Pamidronate
Zoledronate

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19
Q

What should be used during refractory to bisphosphonate?

A

Denosumab (Xgeva not Prolia)

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20
Q

What is the function of calcitonin?

A

Inhibits bone resorption of Ca2+, inhibit absorption by intestine

Effectiveness can be increased if CS are added

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21
Q

CI of calcitonin? ADRs?

A

CHF, renal failure

Flushing, N/V, allergic reactions

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22
Q

What do you need to do prior to giving calcitonin?

A

10 units SQ test dose prior to starting therapy → continue with dosing if no erythema within 15 minutes

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23
Q

What is the MOA of bisphosphate?

A

Block bone resorption and inhibit osteoclast precursors

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24
Q

What are the first line for hypercalcemia caused by cancer?

A

Bisphosphates

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25
Q

Types of bisphosphates and dosing?

A

Pamidronate 30-90 mg IV over 2-24 hr

Zoledronic acid 4 mg IV over 15 minutes

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26
Q

ADR of using bisphosphates? CI? Warning?

A

ATN, jaw osteonecrosis

Severe renal impairment requiring dosing mod

Get dental work before use

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27
Q

What is the MOA of Denosumab? When should it be used?

A

Inhibitor principal mediator of osteoclast survival

If bisphosphates don’t work

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28
Q

ADR of Denosumab?

A

Jaw osteonecrosis, hungry bone, severe hypocalemiaW

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29
Q

How do the brands of denosumab differ?

A

Prolia (osteoporosis)

Xgeva (hypercalcemia if bisphosphate failed)

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30
Q

What is the GC indication? MOA?

A
  1. hypercalemia of myeloma, leukemia, lymphoma, sarcoidosis, combo with calcitonin

Can prevent tachyphylaxis of salmon calcitonin

Reduce GI absorption of calcium

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31
Q

ADRs of GC?

A

Hyperglycemia, osteoporosis, infection risk

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32
Q

How should GC be dosed for hypercalcemia?

A

Dosing: 200-400 mg HC equivalents IV daily, then pred 10-20 mg daily x 7 days

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33
Q

What is cinacalcet? Indication?

A

A calcimimetic that increases CaSr sensitivity resulting in lower PTH and serum Ca

Primary/secondary hyperPT

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34
Q

How do you dose cinacalcet?

A

Titrate Q2-4w in 30 mg increments

Max dose 90mg PO QID

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35
Q

What is the treatment of hypercalcemia in patients without heart or kidney impairment?

A

NS +/- loop diuretic for hydration and return to normal calcium level within 24-48 hr

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36
Q

What is the treatment of hypercalcemia in patients with renal and HF?

A

Hemodialysis
Calcitonin
≥4 months: body can develop antibody → ↓ effect of calcitonin
Add prednisone

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37
Q

What is the treatment of hypercalcemia in patients with primary/secondary hyperPT or parathyroid carcinoma?

A
  1. Cinacalcet (PO)
  2. Etelcalcetide (IV): for secondary (5 mg IV blood 3xwk at the end of dialysis
38
Q

What is the treatment of hypercalcemia in cancer patients?

A
  1. Bisphosphate: Pamidronate and zoledronic acid (more potent and better response)
  2. Denosumab in refractory to bisphosphate (cost more)
39
Q

What is hypocalcemia?

A
  1. Serum <8.6
  2. Ionized <4.4
40
Q

What are the causes of hypocalcemia?

A
  1. low PTH from Operations and Mg def
  2. Vitamin D def
  3. Drugs
41
Q

What drugs cause hypocalcemia?

A
  1. Sodium phosphate
  2. Phenobarbital, phenytoin, ketoconazole (CYP3A4)
  3. Furosemide
  4. Calcitonin
  5. Cinacalcet
  6. Bisphosphate and denosumab
42
Q

What are the the acute symptoms of hypocalcemia?

A
  1. Tetany
  2. Paresthesias
  3. Seizure
43
Q

What are the the chronic symptoms of hypocalcemia?

A

Depression and confusion

44
Q

What are the the dermatologic symptoms of hypocalcemia?

A

Hairloss, grooved and brittle nails

45
Q

What is the daily dose of elemental Ca?

46
Q

What are the ADRs of PO calcium?

A

Constipation

47
Q

What are the PO calcium salts and amount of elemental Ca?

A

Carbonate 40%
Acetate 25%
Citrate 21%

48
Q

What are the IV Ca salts and mEq?

A

Chloride: 1g CaCl = 13.6 mEq Ca
Gluconate: 1g of CaG = 4.6 mEQ Ca

Preferred in alert patients

49
Q

How often should IV calcium be monitored?

50
Q

What is the hypocalcemia treatment if the corrected Ca <8.5 mg/dL

51
Q

What is the hypocalcemia treatment is patient is symptomatic-acute with <7 Ca?

52
Q

What is the function of phosphorus?

A
  1. Source of ATP
  2. Regulate cell metabolism
  3. Bone and teeth health
  4. Blood buffer system
53
Q

How is phosphorus regulated?

A

PTH, FGF 23

54
Q

Describe the homeostasis of phosphorus?

55
Q

What are the normal values of phosphorus?

A

3-4.5 mg/dL

56
Q

What is hyperphosphatemia? What are the causes?

A

> 4.5
1. Renal failure
2. Tumor lysis
3. Hemolysis
4. Rhabdo
5. HypoPT
6. Acidosis

57
Q

What are the presentations of hyperphosphatemia?

A
  1. N/V
  2. Lethargy
  3. Seizures
  4. EV calcifications
  5. Nephrolithiasis
  6. Hypocalcemia from low PTH
  7. Red eye and pruritus (chronic)
58
Q

Why does P increase when Ca decreases?

A

PTH compensates with lack of Ca by increasing P release

59
Q

How do you treat hyperP in hypocalcemia patients?

A

IV calcium

60
Q

How do you treat hyperP if norm or hyper calcemic?

A

Phosphate binders

61
Q

How do you treat hyperP if symptomatic and failed other therapies?

A

Hemodialysis

62
Q

What are the types of phosphate binders?

A
  1. Calcium based (Carbonate and acetate)
  2. Resins (Sevelamer HCl and carbonate)
  3. iron based (ferric citrate and sucroferric oxyhydroxides)
  4. Lanthanum carbonate
63
Q

Out of the the iron based phosphate bind which ↑ Fe levels?

A

Ferric citrate

Sucroferric oxyhydroxides doesn’t effect Fe or Ca

64
Q

What is the difference between phosphate binding resins?

A

Sevelamer HCl worsens acidosis
Carbonate: basic

65
Q

When should calcium based Phosphate binders not be used?

A

Hypercalcemia

66
Q

What are the ADRs of phosphate binders?

A
  1. Constipation
  2. NVD
  3. Hypercalcemia with Ca-based
  4. Iron overload with ferric citrate
67
Q

What is the max elemental Ca?

A

1500mg/day

68
Q

How do you dose calcium carbonate?

A

1 tab (500mg) TID w/ meals (200 mg of elemental)

69
Q

What are the counseling points of calcium carbonate?

A
  1. Drug interactions with acid suppressors
  2. Give prior to meals to increase solubility
70
Q

How do you dose calcium acetate?

A

2 cap (667mg) PO TID with melas (169 of elemental)

71
Q

How does calcium acetate differ from carbonate?

A
  1. Bids 2x better to P
  2. Less affected by gastric pH
72
Q

What are the similarities of resin binders?

A

Initial Dose: 800 mg TID with meals

Decreases LDL and ↑ HDL

Cost the same

73
Q

What is the difference between sevelamer HCl and carbonate?

A

HCl: risk of metabolic acidosis
Carbonate comes in powder form

74
Q

Dosing of ferric citrate? Counseling points?

A

2 tabs TID with meals

Increases iron levels

75
Q

How does sucroferric oxyhydrate differ from ferric citrate?

A

500 mg TID with meals
1. Chewable formatin
2. Lower pill burdern
3. Longer effects
4. Doesn’t ↑ iron

76
Q

How does lanthanum differ from other P binders?

A

Dosing: 500 mg TID with meals
Chewable and powder formulations
High binding capacity
Poor GI absorption: localized
Cost is higher

77
Q

What are causes of hypophosphatemia?

A
  1. Reduced GI absorption
  2. Reduced tubular reabsorption
  3. Cellular redistribution
78
Q

What are causes of reduced GI absorption of P?

A
  1. Alcholism
  2. Diarrhea, anorexia
  3. Phosphate binders
79
Q

What are causes of reduced tubular reabsorption of P?

A
  1. Diuretics, GC, sodium bicarbonate, ferric carboxymaltose
  2. HyperPT
80
Q

What are causes of cellular redistribution of P?

A

Refeeding
Dextrose, glucagon, insulin, calciton

81
Q

What are the presentations of hypophosphatemia?

A
  1. Neuromuscular: weakness, paralysis (respiratory failure)
  2. Rhabdomyolysis
  3. Asymptomatic unless <1.5 mg/dL
82
Q

What is hypophophatemia?

A

<2.7 mg/dL

83
Q

What is referring syndrome?

84
Q

When would IV P be used?

A

<1.5 or symptomatic
Weight based: 0.32-0.64 mmol/kg

85
Q

What are the salt forms of IV P?

A

Sodium phosphate 1mmol=4mEq Na

Potassium phosphate
1mmol =4.4 mEq K

86
Q

ADRs of IV P?

A

Ca/P product deposition, hypocalcemia

87
Q

When is PO P used?

A

1.5-3 and asymptomatic

88
Q

ADRs of PO P?

89
Q

What PO P is for high sodium and K levels?

A

K-Phos No2

90
Q

What PO P is for low K levels?

A

Phos-NaK packet

91
Q

What are the dangers of using Ca/P IV?

A

Cal (mEq/L) x Phosphate (mEq/L) > 55-60 results in precipitation and deposition of complexes in vasculature

  1. Careful with admixtures
  2. Less risk with gluconate

Therapeutics I (32 decks)

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