Calcium and Phosphate Disorders Flashcards

1
Q

what hormones are released in response to hyper/hypo calcemia?

A
  • high blood Ca++: causes release of calcitonin
    • calcitnon promotes deposition of blood Ca++, thus lowering blood Ca++
  • low blood Ca++: promotes release of PTH
    • PTH promotes:
      • Ca+ reabsorption at the distal tubule
      • Ca++ absorption from bone/gut
      • relase of calitriol, which:
        • increases synthesis of CPB
        • promotes Ca++ absorption from gut/bone
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2
Q

what would increase Ca++ absorption from the gut?

A
  • puberty
  • pregnancy/lactation
  • Vitamin D excess
  • acromegaly
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3
Q

what would decrease Ca++ absorption of gut?

A

High vegetable & high fat diet

Steroids

Senescence

Gastrectomy

Malabsorption

Diabetes

Renal Failure

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4
Q

how does acidosis/alkalosis effect presence of calcium in the urine

A
  • acidosis: hypercalciuria
  • alkalosis: hypercalciuria
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5
Q

which diruetic corresponds to which level urine Ca++ level

A

Loop - hypercalciuria

Mannitol – hypercalciuria

Thiazides – hypocalciuria

Amiloride - hypocalciuria

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6
Q

false hypercalcemia vs true hypercalcemia

A

False Hypercalcemia: Increase total Ca++ resulting from increase total proteins

True Hypercalcemia: Increase in free plasma Ca++. This leads to clinically relevant hypercalcemia

  • if free plasma Ca++ not known: obtain plasma albumin level to estimate total calcium
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7
Q

what are the major causes of hypercalcemia?

A

“chimpanzees”

-Calcium supplementation

  • Hyperparathyroidism
  • Idiopathic
  • Milk-alkali syndrome
  • Paget’s disease
  • Addison’s disease
  • Neoplastic disease
  • Zollinger-Ellison syndrome
  • Excessive vitamin A
  • Excessive vitamin D
  • Sarcoidosis-think granulomatous disease
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8
Q

what are major clinical manifestations of hypercalcemia?

A
  • bones, stones, grones, psychiatric overtones
    • bones = abnormal bone remodeling/fracture risk
    • stones = increased risk for kidney stones
    • groans = abdominal cramping, nausea, ileus, coonstipation
    • psychiatric overtones
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9
Q

treatments for hypercalcemia:

A
  • Saline Infusion (0.9% NS)
  • Loop Diuretics once rehydrated
  • Dialysis
  • Calcitonin (promotes calcium deposition) – short term effects
  • for cancer:
    • Steroids – beneficial in cancer
    • IV Bisphosphonates – treatment of choice in cancer
      • Inhibit bone reabsorption, inhibits calcitriol synthesis (calcitriol synthesis is usually stimulated by PTH and increases plasma Ca++)
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10
Q

major causes of hypocalcemia

A

Chronic and acute renal failure

Vitamin D deficiency-can lead to osteoporosis

Magnesium deficiency

Acute pancreatitis

Hypoparathyroidism and pseudohypoparathyroidism

Infusion of phosphate, citrate, or calcium-free albumin

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11
Q

nueromuscular manifestations of hypocalcemia

A
  • troesseu’s sign: pt is unable to control finger movements when a blood pressure cuff is placed on their arm
  • Chostek’s sign: facial switch
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12
Q

cardiovascular manifestations of hypocalcemia

A
  • Hypotension
  • Decreased Cardiac Output
  • Ventricular ectopic activity
  • QT interval prolongation - monitor this patient with an EKG closeley
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13
Q

symptoms of hypocalcemia

A

Most patients will be asymptomatic or report symptoms of intermittent paresthesia (numbness and tingling) of the hands and feet or perioral numbness

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14
Q

general treatment for hypocalcemia

A
  • leafy greens
  • calcium supplements (1-3 g/day)
  • IV
    • only indicated in patients with symptomatic hypocalcemia OR ionized calcium levels below 0.65 mmol/L
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15
Q

major causes of hyperphosphatemia:

A
  • enhanced metabolism
    • hemolysis
    • rhabdomyolysos
    • malignant hyperthermia
  • neoplastic disease
    • leukemia, lymphoma
  • renal failure
  • hypothyroidism, psuedohypothyroidism
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16
Q

major clinical manifestations of hyperphosphatemia

A
  • formation of insoluble calcium-phosphate complexes that deposit in:
    • soft tissues
    • joints (should in picture)
    • kidneys
  • hyperphosphatemia can actually cause acute hypocalcemia, resulting in:
    • seizures
    • tetany
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17
Q

treatment for hyperphosphatemia

A
  • Oral phosphate binders
    • Aluminum Salts (up to 3gms/daily)
    • Calcium Salts (up to 8gms/daily) - dont give in someone with hypercalcemia
      • PhosLo
    • Non-Calcium Binders
      • Renagel of Fosrenal
    • Magnesium Salts (up to2-3gms/day) - dont give in someone with hypermagnesemia
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18
Q

what is considered severe moderate/severe hypophosphatemia

A
  • moderate: decrease of 2.5- 1 mg/dl
  • severe: decrease of less than 1.0 mg/dl
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19
Q

causes of hypophosphatemia

A
  • low intake
    • this is rarely due to patients diet.
    • if patient does have hypophosphatemia due to low diet, is it likely indicative of a malabsorption issue
  • increased excretion:
    • likely due to PTH
      • (in phys we learned that the combined effects of PTH leads ot no change in plasma phosphate, idk)
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20
Q

clinical manifestations of hypophosphatemia

A

Metabolic Encephalopathy

2) RBC dysfunction – may cause hemolysis
3) Leukocyte dysfunction
4) Thrombocytopenia
5) Decreased muscle strength and myocardial contractility.

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21
Q

treatment of hypophosphatemia

A

1) 2)

Oral phosphate salts Neutraphos

IV phosphorus

a) Severe (<1.0mg/dl) in critically ill – 0.08-0.16mmol/kg IV over 2-6 h
b) Moderate (1.0-2.5mg/dl) on ventilator – 0.08-0.16mmol/kg IV over 2-6 h
c) Moderate (1.0-2.5mg/dl) not on ventilator – oral treatment with 1,000 mg/day
d) Mild – treat with oral 1,000 mg/day

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22
Q

major causes of hypermagnesemia

A
  • renal insufficiency
  • hemolysis
    • concentration in erythrocytes - 3x greater than the serum
    • will rise 0.1/ mEqL for every 250 mL of erythrocytes
    • expected only in massive hemolysis
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23
Q

clinical manifestations of hypermagnesemia

A
  • cardiac conduction delays
  • depressed contractility
  • vasodilation
  • early symptoms include loss of deep tendon reflexes (hyporeflexia) and can progress to flacid paralysis
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24
Q

treatment for hypomagnesimia

A

Hemodialysis - treatment of choice

■ IV calcium gluconate (1 g IV over 2 to 3 minutes)

■ Fluids + furosemide

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