what is the most common cause of hypoP?
complication of *periparturient hypocalcemia* - fails to respond to conventional therapy/relapses - alert but unable to stand (creeper cow)
how is hypoP treated?
- IV phosphorous = sodium monophosphate
- Fleet enema diluted in sterile water IV
- oral therapy via stomach tube for 5 days
how does prolonged hypoP affect RBCs?
depletes RBC 2,3DPG - friable - intravascular hemolysis = *postparturient hemoglobinuria*
who is most commonly affected by postparturient hemoglobinuria? how is it treated?
- dairy cattle
- oral and IV sodium monophosphate
- grain/P-rich and dicalcium phosphate feed to follow up
- blood transfusion if PCV <10% or severe signs
what is seen on CBC with postparturient hemoglobinuria? what other deficiencies are usually concurrent?
- anemia with Heinz bodies (kidney values affected from pigment nephropathy)
- copper and selenium deficiency (so low antioxidants)
What is cause of spontaneous fractures, lameness, and enlarged epiphysis in young, growing animals?
rickets due to *chronic dietary deficiency* of P and vit. D
what is string of pearls lesion? how is it prevented?
- costochondral junction enlargement seen w/deficiency in vit D and P
- adequate diet and exposure to UV light
where is phosphorous absorbed?
- small intestine
- (low levels stim. vit.D for increased absorption of Ca/P)
what is effect of PTH on phosphorous levels?
increases P loss through saliva/feces and urine
what are main losses/drains for P?
- fetal skeleton, formation of milk
- rumen metabolism/ATP
what is normal phosphorous level in adults?
4-8mg/dl (slightly higher in young)
what is serum P level with rickets (chronic dietary deficiency)?
what is serum P with postparturient hemoglobinuria? what about with severe acute hypoP (milk fever)?
- hemoglobinuria: <2
- severe, acute <1
what are functions of Mg?
- cofactor for enzymes (ATPase, kinases)
- bone mineral (released w/Ca)
- needed for PTH synthesis/release
- opposes Ca at neuromuscular jx
what is role of Mg at neuromuscular jx? what is result of hypoMg here? what is hyperMg?
- cofactor for acetylcholinesterase
- inhibits Ach release from axon (opposite Ca)
hypoMg: build up of Ach/incr. Ach release - prolonged contraction/spasm
hyperMg: neuromusc. blockade - weakness
what is main condition seen with hypoMg? Who is commonly effected?
- Grass Tetany
- beef cattle grazing rapidly growing pastures in spring/fall
where is Mg absorbed? where is it lost?
- absorbed from GI but not efficiently (excess = laxative)
- modest loss in milk, deposited in fetal bone/soft tissue
- excreted via kidney
what are two compounds that impair GI absorption of Mg? When are these elements higher in soil?
- nitrogen and potassium
- -heavily fertilized and rapidly growing
- cereal grains also low in Mg
- (add P to soil helps mg uptake)
what is mechanism for Mg homeostasis?
- NO hormone mechanisms
- must ingest/absorb (GIT tract main source - rumen for adults; small intestine for young)
what happens to Mg levels with renal failure or impaired renal perfusion? what will be signs in patient as a result?
hyperMg (fails to excrete) - somnolence
what are early signs of grass tetany? what are Ca levels?
- low Mg: spasms, goose stepping, nervous, aggressive
- without Mg - impaired PTH so Ca drops (stage 1)
what are late signs of grass tetany?
- lower Mg: recumbency, convulsions, paddling
- "dirt angel" from repetitive mm. contractions
- low CSF concentration of Mg
what is cause of transport tetany?
low Mg due to stress - catecholemines move Mg into cells; worsened by low Mg diet
what is cause of milk tetany?
low Mg because milk low in Mg already, growing calf outgrows the Mg supply by 4-6wks
what is cause of winter tetany?
low Mg in late gestation when inadequate crops available (eating mostly corn stalks/straw)
what is cause of wheat pasture tetany?
- cereal forage so naturally low in Mg
- (concurrently hypoCa so resembles milk fever)
how is hypoMg reliably diagnosed postmortem?
- low Mg in vitreous humor for 24-48hrs
- low Mg in CSF
- (serum levels not reliable)
how is hypoMg treated?
- immediately minimize stress (AceP) + IV Ca/Mg salts
- relapse common - follow up w/oral or SQ
- can do Mg enema as well (careful rectal slough)
how is diet managed to prevent hypoMg?
- feed legumes (good source of Mg/Ca) and cool season grasses - avoid rapid growing grass
- salt/molasses blocks, supplement drinking water
what is main function of K?
maintenance of resting membrane potential
what were 3 factors in common with all cows reported to have hypoK syndrome?
- hx of mod-severe ketosis
- parturition w/in 30 days
- isoflupredone acetate given
what are clinical signs seen w/HypoK?
- muscle fasciculations and profound flaccidity
- recumbent, unable to hold up head
- cardiac arrhythmias, atrial fibrillation, Vtach
what clinical pathology is consistent with hypoK syndrome?
- hypoK (<2)
- mild elevation in CPK
what are causes of hypoK?
- anorexia, ketosis
- incr. urination of K from steroids/mineralcorticoids like isoflupredone
- alkalosis - drives K into cell for H
- insulin/glucose tx drive K intracellular
how is hypoK treated?
- *IV + oral* K (IV alone not effective)
- do not excede 0.5mEq/kg/hr IV