Exam 2 - Disorders of Mineral Metabolism Flashcards
_____ is the biologically active form of calcium
ionized calcium (Ca2+)
___ is the form of calcium that is closely regulated in the body
Ca2+
roles of Ca2+ in NMJ function
- dampens effects of Na+ channels which decreases excitability of axon
- promotes fusion of vesicle containing ACh to synaptic membrane to release ACh into NMJ
- propagation of AP through muscles (initiates actin-myosin coupling in muscle)
what does metabolic acidosis lead to?
signs of low [Ca2+] because acidosis renders bone mineral more soluble so Ca2+ is released more readily from bone increasing concentration in blood
- long term acidosis leads to demineralization of bone (osteoporosis)
as pH _____ bone resorption (Ca2+ release) ______
decreases (acidic)
increases
Calcitonin net effect
reduces [Ca+2] in ECF by promoting the deposition of calcium in bone & loss in urine
PTH effects on kidney
- increases Ca2+ reabsorption by nephrons (increase Ca)
- PO4 in saliva/urine (less complexing with calcium)
- conversion to vitamin D3 (the active form of vitamin D)
vitamin D effect
increases calcium & PO4 by 1) promoting bone resorption and 2) increase absorption of Ca and P from gut
purpose of a 2:1 Ca:P ratio
P inhibits Ca so need more Ca
what can cause severe metabolic alkalosis?
repetitive vomiting (loss of HCl)
forms Ca-albumin complex = less ionized Ca2+ (unavailable)
hypocalcemia in dogs/cats
during/after pregnancy; small breeds with big litters –>
- Puerperal eclampsia (tetanic seizures)
- Risus sardonicus (uncontrolled mm contractions of facial mm)
hypocalcemia in horses
“lactational tetany” - eclampsia (similar to dogs,cats,humans); more common in draft breeds bc higher lactation rate
hypocalcemia in ruminants
milk fever/periparturient hypocalcemia
difference between stage I, II and III milk fever
stage I: Irritable, hyperesthetic, tongue protrusion with jaw open, trembling, jerking, motions, spasms, brief duration
stage II: S shape body (head to flank), reduced GI motility, bloat, constipation, urine retention, dilated pupils & rapid, weak pulse & decreased extremities temp*
stage III: coma, death
treatment of milk fever/periparturient hypocalcemia
Ca2+ salts SLOWLY IV
Mg function in neuromuscular transmission
key component for AChE –> reduces ACh in synaptic cleft
dampens Ca influx in axon terminal –> preventing ACh release –> relaxation of muscle
what can cause hypermagnesemia
renal failure or poor renal function because Mg excreted by kidneys
ruminantts grazing a lush grass pasture will cause _____________
hypomagnesemia “grass tetany” aka “wheat pasture poisoning”
hypomagnesemia “grass tetany”
low Mg = ACh left in the synaptic cleft (no AChE) or Ca response not dampened = sustained muscle contractions = rigid tetany
how can you prevent grass tetany
feed/soil influence Mg absorption so you can feed Mg supplement in springtime or soil with Mg
nutritional secondary hyperparathyroidism “bran disease in horses”
high phosphorus in diet = competes with Ca for intestinal uptake = decrease Ca in the blood = chronic elevation of PTH to try to increase Ca = bone mineralization = lameness, bone remodeling with fibrous tissue (especially mandible)
renal secondary hyperparathyroidism
kidney failure = hyperphosphatemia (reduced excretion of PO4) = Ca absorption inhibited = less Ca in the blood = chronic elevations in PTH to increase Ca levels = low grade metabolic acidosis = osteoporosis
Describe the nutritional basis for struvite urolithiasis in ruminants fed high-grain diets.
feedlot cattle are often fed high grain diets (high P low Ca) which lead to phosphatic urinary calculi (PO4 containing urolith) –> urethral obstruction
how can hypophosphatemia be caused
1) insulin treatment because insulin drives PO4 into cells
2) high PTH
