Minerals Flashcards
Clinical signs of calcium disturbances
-Synaptic neural signal transmission
-Skeletal muscle contraction
-Cardiovascular muscle function
Clinical signs of Hypocalcemia
-Generalized weakness
-Muscle twitching, seizures
-Behavior changes
-Recumbency/paresis (cattle)
-Synchronous diaphragmatic flutter (equine)
Clinical signs of hypercalcemia
-Ileus, abdominal pain, constipation, anorexia, nausea, vomiting
-generalized weakness and muscle pain
-Arrhythmias
-PU/PD
-Increased soft tissue mineralization (> 70mg/ml of Ca and P)
Hypercalcemia effect on kidneys
Interfere with renal tubular ADH
Kidney injury and decreased function: vasoconstriction (decreased GFR), mineralization (damage nephrons), volume depletions worsen
Serum calcium
this is 1% of Ca in the body and can be spit into three fractions:
-Free ionized
-Protein bound
-Complexed
Free ionized Ca
Biologically active form
Tightly regulated and alterations associated with clinical signs, have to specifically request to look at this on analysis if concerned
Protein bound Ca
Mostly bound to albumin and small amount to globulin
Complexed Ca
Non protein anions like citrate, lactate, phosphate, and bicarb are bound
Most common cause of hypocalcemia
Hypoalbuminemia
Decreased protein binding
Affects of pH on Ca
Ca occupies 3-4 binding sites on albumin at normal pH but shifts occur in that fraction in response to pH changes: Acidemia-> increased ionized Ca, alkalemia-> decreased ionized Ca.
Total Ca not affected
Handling samples for Ca measurements
- Decrease exposure to air
- Process immediately
- Avoid anticoagulants that chelate Ca (EDTA and Citrate)
Phosphate and ATP
Phosphate needed to form ATP and without it can not live. Phosphate moved from ECF to ICF (transcellular shifting) to undergo cellular respiration
Transcellular shifting associated with alkalosis
Decreased CO2 stimulates glycolysis and Pi shifts intracellular and decreased extracellular Pi. Usually from respiratory alkalosis not really metabolic
Severe hypophosphatemia
Intravascular hemolysis due to decreased ATP and loss of RBC membrane integrity
Hypophosphatemia signs
-generalized weakness and muscle pain
-Anorexia, nausea, ileus, vomiting
-tremors ataxia
-Behavior changes
Hyperphosphatemia clinical signs
-Anorexia, nausea, vomiting
-Weakness, tetany, seizures
-Increased complexing with CA
Storage of Mg
-Bone (majority)
-Intracellular/soft tissues mostly muscle: needed for NT release and reactions with ATP
-Extracellular fluid (1%): has three fractions
Effect of PTH
Increase fCA and Mg
Decrease Pi
Vitamin D effect
Increase f Ca and Pi
Calcitonin effect
Decrease fCa and Pi
What stimulates PTH
Low free ionized C
Low vitamin D
Major organs targeted by PTH
Bone- resorption of Ca and P
Kidney-Renal reabsorption of Ca (DCT) and decrease resorption of Pi (PCT), activate vitamin D (PCT)
PTH on bone
Binds to receptors on bones and stimulates osteoblasts to release RANKL to activate osteoclasts to free fCa and Pi
