Disorders of Calcium and Phosphorus SA Flashcards

1
Q

what forms of calcium are in circulation?

A

iCa or free ionized calcium (55%): biologically active

protein bound calcium (35%): albumin and globulins

complexed calcium (10%): bound to phosphate, bicarb, citrate, lactate, oxalate

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2
Q

what are the main factors that influence calciums distribution?

A
  • iCa is tightly regulated by interacting feedback loops involving iCa, PTH, calcitriol and calcitonin
  • PTH related protein binds to PTH receptors in bone and kidneys
  • phosphorus absorption and excretion are regulated with calcium
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3
Q

if phosphorus x tCa > 60-70 =

A

tissue mineralization

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4
Q

main differential dx of hypocalemia in dogs

A

hypoalbuminemia
chronic renal failure
acute pancreatitis
eclampsia or puerperal tetany

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5
Q

main differential dx of hypercalcemia in dogs

A
  • primary hyperparathyroidism
    hypercalcemia of malignancy
  • hypercalcemia of malignancy: hurmoral or local
  • chronic renal failure
  • hypervitaminosis D
  • granulomatous Dz
  • idiopathic hypercalcemia (cats)
  • hypoadrenocorticism
  • non-malignant osteolyic lesions
  • acute renal injury
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6
Q

hypoalbuminemia

A

Low tCa, normal iCa; clinically insignificant

can mask hypercalcemia

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7
Q

acute pancreatitis

A

precipitation of calcium in peripancreatic fat +/- hypomagnesemia and calcitonin release

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8
Q

chronic renal failure

A

decreased renal phosphate clearance resulting in hyperPhos and Ca-Phos precipitation in tissues

decreased renal synthesis of 1-alpha-hydroxylase leading to decreased calcitriol

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9
Q

eclampsia or puerperal tetany

A

increased Ca mobilization for fetal skeletons and milk production +/- poor diet intake or parathyroid atrophy from Ca supplementation

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10
Q

if Ca is low and Phos is high

A

chronic kidney disease, acute kidney injury, urinary tract obstruction, hypoparathyroidism, phosphate-containing enema, or other causes of hyperphos

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11
Q

clinical signs of hypocalcemia

A

muscle tremors/fasiculations
facial rubbing
seizures
tachycardia/arrhythmias

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12
Q

treatment of hypocalcemia

A

acute/emergent: calcium gluconate 10%

subacute/chronic: calcium supplements and vitamin D metabolites

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13
Q

primary hyperparathyroidism

A

excesssive PTH from parathyroid gland tumor

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14
Q

hypercalcemia of humoral malignancy

A

tumor distant from bone, secretion of PTHrP, calcitriol, and/or cytokines

Lymphoma is common and AGASACA is less common

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15
Q

hypercalcemia of local malignancy

A

tumor in the bone, secretion of PTHrP and/or cytokines, osteolysis

lymphoma is common and multiple myelomas are less common

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16
Q

chronic renal failure

A

renal secondary hyperparathyroidism from decreased calcitriol production and hypocalcemia from Ca-Phos tissue precipitation

17
Q

hypervitaminosis D

A

typically from toxin ingestion ex. rodenticide, anti psoriasis cream, lilles

18
Q

granulomatous disease

A

-activate macrophages synthesize calcitriol
-fungal, parasitic, sterile nodular pancreatitis

19
Q

If high Ca and low-normal Phos

A

primary hyperparathyroidism, HyperCa of malignancy (humoral)

20
Q

If both Ca and Phos are high

A

hypervitaminosis D, chronic renal failure, hypadrenocorticism, hyperCa of malignancy (local, osteolytic)

21
Q

if concurrent azotemia with hypercalcemia

A

CKD, AKI, hypervitaminosis D, hyperadrenocorticism, hyperCa of malignancy, granulomatous disease

22
Q

what clinical signs are associated with hypercalcemia?

A
  • renal: pu/pd (ADH inhibition), tubular damage (mineralization)
  • neuromuscular (depressed cell membrane excitability); weakness, twitching, seizures
  • gastrointestinal (direct effects on chemoreceptor trigger zone)
  • cardiac; bradyarrhythmias, cardiac arrest
23
Q

treatment of acute/emergent hypercalcemia

A

hypercalcemia - induced renal failure, high risk of tissue mineralization

  • IV Fluids (NaCl 0.9% ideal)
  • Furosemide
  • glucocorticoids
  • sodium bicarb (save for lifethreatening)
24
Q

treatment of subacute/chronic hypercalcemia

A

furosemide, glucocorticoids, biphosphonates (decrease osteoclastic activity)

25
Q

common causes and clinical signs of hypophosphatemia

A

common causes:

  • primary hyperparathryroidism
  • malignancy- associated hypercalcemia
  • diabetic ketoacidosis

clinical signs:

  • if severe, hemolysis, rhabdomyolysis, respiratory disease, and neurologic abnormalities
26
Q

hypophosphatemia treatment

A
  • prevent with proactive monitoring and supplementation
  • emergent treatment is indicated for severe symptomatic hypophos and asymptomatic animals at risk for developing symptoms
  • potassium phosphate IV CRI
27
Q

hyperphosphatemia common causes and clinical signs

A

common causes:

  • chronic or acute kidney injury
  • hypervitaminosis D
  • hypoparathyroidism
  • young growing animals

clinical signs: rare

28
Q

hyperphosphatemia treatment

A

emergent (rare):
- IV fluids and parenteral glucose +/- insulin

chronic tx:
- dietary restriction (low protein diet)
- oral phosphate binders