Disorders Of Phosphate Hyperphosphatemia Flashcards

1
Q

What is hyperphosphatemia defined as?

A

Serum [Pi] > 4.5 mg/dL

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2
Q

What is the term for a spurious increase in serum [Pi]?

A

Pseudohyperphosphatemia

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3
Q

In which conditions has pseudohyperphosphatemia been described?

A
  • Hyperglobulinemia
  • Hypertriglyceridemia
  • Hyperbilirubinemia
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4
Q

What causes the spurious increase in serum phosphate levels?

A

Interference of proteins and triglycerides in the colorimetric assay of phosphate

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5
Q

What are the three major categories of true hyperphosphatemia causes?

A
  • Addition of phosphate from ICF to ECF compartment
  • Decrease in kidney excretion of phosphate
  • Drugs
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6
Q

What are the most significant causes of hyperphosphatemia in clinical practice?

A

Acute and chronic kidney diseases

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7
Q

What is one endogenous cause of phosphate addition to the ECF compartment?

A

Hemolysis

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8
Q

What is a cause of phosphate addition to the ECF compartment that is exogenous?

A

Oral intake or through IV route

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9
Q

What condition involves the release of phosphate from muscle cells?

A

Rhabdomyolysis

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10
Q

What syndrome involves the release of phosphate from tumor cells due to chemotherapy?

A

Tumor lysis syndrome

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11
Q

Fill in the blank: Chronic kidney disease G4 and G5 leads to decreased kidney excretion of _______.

A

phosphate

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12
Q

What is the effect of excess vitamin D on phosphate levels?

A

Increased gastrointestinal absorption of phosphate

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13
Q

What is the mechanism of action for bisphosphonates regarding phosphate?

A

Decreased phosphate excretion, cellular shift

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14
Q

True or False: Diabetic ketoacidosis causes a shift of phosphate from ICF to ECF.

A

True

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15
Q

What genetic mutations are associated with familial tumor calcinosis?

A
  • GALNT3
  • FGF-23
  • KLOTHO
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16
Q

What can lead to phosphate absorption from enemas?

A

Phosphate-containing enemas (Fleet enema)

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17
Q

What are immune checkpoint inhibitors associated with in terms of phosphate levels?

A

Tumor lysis syndrome (release from tumor cells)

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18
Q

What serum phosphate levels are common in patients with Acute Kidney Injury (AKI)?

A

Between 5 and 10 mg/dL

In cases of AKI caused by rhabdomyolysis, tumor lysis syndrome, hemolysis, or severe burns, levels may reach as high as 20 mg/dL.

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19
Q

List the mechanisms for hyperphosphatemia in Acute Kidney Injury (AKI).

A
  • Decreased kidney excretion
  • Release from injured muscle
  • Movement of phosphate out of cells during acute metabolic acidosis
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20
Q

What happens to phosphate homeostasis in early stages of Chronic Kidney Disease (CKD)?

A

It is maintained by progressive increase in phosphate excretion by surviving nephrons

This results in an increase of ( ext{FE}_{ ext{PO4}} ) > 35 %.

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21
Q

What role does FGF-23 play in phosphate excretion in early CKD?

A

It inhibits 1,25(OH)$_2$D$_3$ production, stimulating PTH secretion which increases phosphate excretion.

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22
Q

What is the GFR in CKD stages G4 and G5?

A

Less than 30 mL/min

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23
Q

How does Klotho deficiency contribute to hyperphosphatemia in CKD G4 and G5?

A

It causes resistance to FGF-23 action on phosphate excretion, leading to decreased phosphate excretion.

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24
Q

What is the result of the cycle involving Klotho deficiency and FGF-23 in CKD?

A

Hyperphosphatemia

25
Q

What are the electrolyte abnormalities commonly observed with oral sodium phosphate (OSP) use?

A
  • Hyperphosphatemia
  • Hypocalcemia
  • Hyponatremia
  • Hypokalemia
  • Hypernatremia
26
Q

What is Familial Tumor Calcinosis (FTC)?

A

A rare autosomal recessive disorder characterized by hyperphosphatemia and deposition of calcium phosphate crystals.

27
Q

What mutations are associated with Familial Tumor Calcinosis (FTC)?

A
  • GALNT3
  • FGF-23
  • KLOTHO
28
Q

What are the normal serum levels in patients with Familial Tumor Calcinosis (FTC)?

A
  • Serum Ca(^{2+})
  • PTH
  • Alkaline phosphatase
29
Q

What is Tumor Lysis Syndrome (TLS)?

A

An oncologic emergency that occurs following chemotherapy or spontaneously due to heavy tumor burden.

30
Q

What are the important electrolyte disturbances in Tumor Lysis Syndrome (TLS)?

A
  • Hyperkalemia
  • Hyperphosphatemia
  • Hyperuricemia
  • Hypocalcemia
31
Q

What are the symptoms of Tumor Lysis Syndrome (TLS)?

A
  • Nausea
  • Vomiting
  • Poor appetite
  • Dark and reduced urine output
  • Seizures
  • Palpitations
32
Q

What is the treatment for Tumor Lysis Syndrome (TLS)?

A
  • Volume replacement with normal saline
  • Uricosuric drugs (e.g., allopurinol, febuxostat, rasburicase)
  • Kidney replacement therapies if necessary
33
Q

True or False: Rhabdomyolysis behaves similarly to Tumor Lysis Syndrome (TLS).

A

True

Except for the presence of myoglobinuria due to muscle necrosis in rhabdomyolysis.

34
Q

What is the goal for maintaining phosphate levels in hyperphosphatemia treatment according to KDIGO?

A

PO₄ 3.5-5.5 mg/dL

KDIGO stands for Kidney Disease: Improving Global Outcomes, which provides guidelines for kidney disease management.

35
Q

What are the key strategies for managing hyperphosphatemia?

A
  • Dietary restriction
  • Phosphate binders
  • Dialysis optimization
  • Treat underlying cause
36
Q

What should be avoided in the dietary management of hyperphosphatemia?

A
  • Processed foods (additive phosphates)
  • Dairy products
  • Nuts/legumes
  • Colas (phosphoric acid)
37
Q

What types of proteins are recommended for dietary management in hyperphosphatemia?

A

Plant-based proteins (lower bioavailability)

38
Q

What are examples of calcium-based phosphate binders?

A
  • Ca carbonate
  • Ca acetate
39
Q

What are the pros and cons of calcium-based phosphate binders?

A
  • Pros: Low cost
  • Cons: ↑ Vascular calcification, hypercalcemia
40
Q

What is a key advantage of Sevelamer as a non-calcium based phosphate binder?

A

↓ LDL and ↓ vascular calcification

41
Q

What are the cons of using Sevelamer?

A

GI side effects, expensive

42
Q

What is the benefit of using Iron-based phosphate binders?

A

↑ Iron stores (benefit in anemia)

43
Q

Which phosphate binder is limited by diarrhea?

A

Magnesium carbonate

44
Q

What is the purpose of conventional hemodialysis in managing hyperphosphatemia?

A

Removes 700-900 mg/session

45
Q

What is a limitation of conventional hemodialysis?

A

Limited by rebound from tissue stores

46
Q

What are some enhanced removal techniques for dialysis?

A
  • Nocturnal HD
  • Daily HD
  • Increased session duration
47
Q

What is a treatment for acute hyperphosphatemia when PO₄ >10 mg/dL?

A

Emergent dialysis

48
Q

What should be combined with binders in CKD-MBD treatment?

A
  • Vitamin D analogs
  • Calcimimetics (cinacalcet)
49
Q

What parameters should be monitored monthly in dialysis patients?

A
  • Serum PO₄
  • Ca²⁺
  • PTH
50
Q

What is the target Ca×PO₄ product in hyperphosphatemia management?

A

<55 mg²/dL²

51
Q

What mnemonic can help remember key points about phosphate binders?

52
Q

What does the ‘B’ in the mnemonic ‘BINDERS’ stand for?

A

Balance Ca-PO₄

53
Q

What does the ‘C’ in the mnemonic ‘CLASH’ stand for regarding binder types?

A

Calcium-based

54
Q

What is the first-line treatment for hyperphosphatemia?

A

Dietary restriction + non-Ca binder

55
Q

In which scenario should calcium-based binders be avoided?

A

If vascular calcification present

56
Q

What is a clinical pearl regarding ferric citrate?

A

Ideal for patients with iron deficiency

57
Q

What investigational agent may reduce binder pill burden in the future?

58
Q

What is crucial for phosphate control in hyperphosphatemia?

A

Dialysis adequacy