FA Q4, Endocrine II

  1. 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)
  2. how is hypoP treated?
    • IV phosphorous = sodium monophosphate
    • Fleet enema diluted in sterile water IV
    • oral therapy via stomach tube for 5 days
  3. how does prolonged hypoP affect RBCs?
    depletes RBC 2,3DPG - friable - intravascular hemolysis = *postparturient hemoglobinuria*
  4. 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
  5. 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)
  6. 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
  7. 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
  8. where is phosphorous absorbed?
    • small intestine
    • (low levels stim. vit.D for increased absorption of Ca/P)
  9. what is effect of PTH on phosphorous levels?
    increases P loss through saliva/feces and urine
  10. what are main losses/drains for P?
    • fetal skeleton, formation of milk
    • rumen metabolism/ATP
    • saliva
  11. what is normal phosphorous level in adults?
    4-8mg/dl (slightly higher in young)
  12. what is serum P level with rickets (chronic dietary deficiency)?
  13. what is serum P with postparturient hemoglobinuria? what about with severe acute hypoP (milk fever)?
    • hemoglobinuria: <2
    • severe, acute <1
  14. 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
  15. 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)
  16. hypoMg: build up of Ach/incr. Ach release - prolonged contraction/spasm
    hyperMg: neuromusc. blockade - weakness
  17. what is main condition seen with hypoMg? Who is commonly effected?
    • Grass Tetany
    • beef cattle grazing rapidly growing pastures in spring/fall
  18. 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
  19. 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)
  20. what is mechanism for Mg homeostasis?
    • NO hormone mechanisms
    • must ingest/absorb (GIT tract main source - rumen for adults; small intestine for young)
  21. 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
  22. 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)
  23. what are late signs of grass tetany?
    • lower Mg: recumbency, convulsions, paddling
    • "dirt angel" from repetitive mm. contractions
    • low CSF concentration of Mg
  24. what is cause of transport tetany?
    low Mg due to stress - catecholemines move Mg into cells; worsened by low Mg diet
  25. what is cause of milk tetany?
    low Mg because milk low in Mg already, growing calf outgrows the Mg supply by 4-6wks
  26. what is cause of winter tetany?
    low Mg in late gestation when inadequate crops available (eating mostly corn stalks/straw)
  27. what is cause of wheat pasture tetany?
    • cereal forage so naturally low in Mg
    • (concurrently hypoCa so resembles milk fever)
  28. how is hypoMg reliably diagnosed postmortem?
    • low Mg in vitreous humor for 24-48hrs
    • low Mg in CSF
    • (serum levels not reliable)
  29. 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)
  30. 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
  31. what is main function of K?
    maintenance of resting membrane potential
  32. 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
  33. what are clinical signs seen w/HypoK?
    • muscle fasciculations and profound flaccidity
    • recumbent, unable to hold up head
    • cardiac arrhythmias, atrial fibrillation, Vtach
  34. what clinical pathology is consistent with hypoK syndrome?
    • hypoK (<2)
    • hypoP
    • mild elevation in CPK
  35. 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
  36. how is hypoK treated?
    • *IV + oral* K (IV alone not effective)
    • do not excede 0.5mEq/kg/hr IV
Card Set
FA Q4, Endocrine II
FA Q4, Endocrine II