Disorders of Calcium and Phosphorus SA Flashcards
what forms of calcium are in circulation?
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
what are the main factors that influence calciums distribution?
- 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
if phosphorus x tCa > 60-70 =
tissue mineralization
main differential dx of hypocalemia in dogs
hypoalbuminemia
chronic renal failure
acute pancreatitis
eclampsia or puerperal tetany
main differential dx of hypercalcemia in dogs
- 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
hypoalbuminemia
Low tCa, normal iCa; clinically insignificant
can mask hypercalcemia
acute pancreatitis
precipitation of calcium in peripancreatic fat +/- hypomagnesemia and calcitonin release
chronic renal failure
decreased renal phosphate clearance resulting in hyperPhos and Ca-Phos precipitation in tissues
decreased renal synthesis of 1-alpha-hydroxylase leading to decreased calcitriol
eclampsia or puerperal tetany
increased Ca mobilization for fetal skeletons and milk production +/- poor diet intake or parathyroid atrophy from Ca supplementation
if Ca is low and Phos is high
chronic kidney disease, acute kidney injury, urinary tract obstruction, hypoparathyroidism, phosphate-containing enema, or other causes of hyperphos
clinical signs of hypocalcemia
muscle tremors/fasiculations
facial rubbing
seizures
tachycardia/arrhythmias
treatment of hypocalcemia
acute/emergent: calcium gluconate 10%
subacute/chronic: calcium supplements and vitamin D metabolites
primary hyperparathyroidism
excesssive PTH from parathyroid gland tumor
hypercalcemia of humoral malignancy
tumor distant from bone, secretion of PTHrP, calcitriol, and/or cytokines
Lymphoma is common and AGASACA is less common
hypercalcemia of local malignancy
tumor in the bone, secretion of PTHrP and/or cytokines, osteolysis
lymphoma is common and multiple myelomas are less common
chronic renal failure
renal secondary hyperparathyroidism from decreased calcitriol production and hypocalcemia from Ca-Phos tissue precipitation
hypervitaminosis D
typically from toxin ingestion ex. rodenticide, anti psoriasis cream, lilles
granulomatous disease
-activate macrophages synthesize calcitriol
-fungal, parasitic, sterile nodular pancreatitis
If high Ca and low-normal Phos
primary hyperparathyroidism, HyperCa of malignancy (humoral)
If both Ca and Phos are high
hypervitaminosis D, chronic renal failure, hypadrenocorticism, hyperCa of malignancy (local, osteolytic)
if concurrent azotemia with hypercalcemia
CKD, AKI, hypervitaminosis D, hyperadrenocorticism, hyperCa of malignancy, granulomatous disease
what clinical signs are associated with hypercalcemia?
- 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
treatment of acute/emergent hypercalcemia
hypercalcemia - induced renal failure, high risk of tissue mineralization
- IV Fluids (NaCl 0.9% ideal)
- Furosemide
- glucocorticoids
- sodium bicarb (save for lifethreatening)
treatment of subacute/chronic hypercalcemia
furosemide, glucocorticoids, biphosphonates (decrease osteoclastic activity)
common causes and clinical signs of hypophosphatemia
common causes:
- primary hyperparathryroidism
- malignancy- associated hypercalcemia
- diabetic ketoacidosis
clinical signs:
- if severe, hemolysis, rhabdomyolysis, respiratory disease, and neurologic abnormalities
hypophosphatemia treatment
- 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
hyperphosphatemia common causes and clinical signs
common causes:
- chronic or acute kidney injury
- hypervitaminosis D
- hypoparathyroidism
- young growing animals
clinical signs: rare
hyperphosphatemia treatment
emergent (rare):
- IV fluids and parenteral glucose +/- insulin
chronic tx:
- dietary restriction (low protein diet)
- oral phosphate binders