SA Med, Q2, VI

Card Set Information

SA Med, Q2, VI
2012-10-29 09:56:29
SA Med Q2 VI

SA Med, Q2, VI
Show Answers:

  1. Which treatment of CRF is overall most important?
    dietary phosphorus restriction
  2. What is goal of treating uremia?
    • make animal feel better
    • reduce oral lesions
    • prevent/slow further loss of renal function
  3. What are some reversible causes of CRF signs that you should look for and treat?
    • pyelonephritis
    • obstruction (neoplasia/urolith)
    • hyperCa
  4. What feature of CRF leaves the patient more prone to UTI, so culture/sensitivity testing should be checked?
    low specific gravity = more prone to infection
  5. Initial conservative treatment for CRF?
    • dietary restriction of phosphorus and protein (and sodium)
    • phosphorus binders
    • H2 receptor blockers (famotadine)
    • encourage water/energy intake
  6. What secondary disease needs to be tested/treated?
    renal secondary hyperparathyroidism, hypertension, anemia
  7. When are special renal diets helpful?
    before the animal is obviously sick; can hopefully increase interval to uremic crisis
  8. what is possible complication of too much protein restriction/
    cachexia (catabolize own tissues)
  9. How does CRF effect the GI system? what are treatment options to help/
    • uremia stimulates gastrin production (severity of gastrinemia correlates w/severity of disease) --> anorexia, GI bleeding, vomiting
    • -proton pump inhibitors (omeprazole) or H2 blockers (famotidine)
  10. what is important about timing for giving phosphorous binders? what is cheapest, most common binder given?
    • give with meal
    • aluminum salts (aluminum hydroxide)
  11. what is a phosphate binder that has no taste aversion and will NOT cause hypercalcemia?
    epakitin (shellfish exoskeleton)
  12. which phosphate binder is less effective than aluminum and needs to be carefully monitored in patients also receiving calcitriol for hyperPTH?
    calcium carbonate (can cause hyperCa)
  13. What food additive is a phosphate binder and has anti-oxidant effects but is only off label in US?
  14. what phosphate binder does not contain any Ca or Al but is expensive?
    sevelamer HCl
  15. what are some positive effects of CRF patients treated w/EPO?
    • resolved anemia
    • wt gain, improved appetite
    • improved hair coat
    • improved alertness/activity
  16. When is it time to give EPO/
    • PCV<20%
    • (frequent dose at first then reduce to once or twice weekly to reach target of 30-40%)
  17. what is most important adverse effect of EPO?
    • antibody formation
    • (can also see vomit, seizure, hypertension, uveitis, hypersensitivity reaction)
  18. what is the name of the engineered version of EPO which will not cause Ab formation?
  19. Why would you give a CRFpatient calcitriol (vit. D)?
    • promote Ca absorption and treats renal 2ndary hyperPTH
    • (reduces PTH secretion by binding calcitriol receptors on parathyroid gland)
  20. What mineral value needs to be monitored in addition to phosphorus when giving calcitriol?
    calcium (can become elevated, esp. if also giving P-binders)
  21. when do you decide to treat hypertension?
    • BP > 160mmHg consistently (maybe even lower if CRF)
    • or high BP + fundic lesions
  22. will diuretics benefit a CRF patient?
    no, harmful because can exacerbate dehydration (esp. loops diuretics like furosemide)
  23. What is the most important drug to give to a CRF patient? what is a good drug to add with it?
    • enalapril (ACE inhibitor w/modest BP effect but other potentially beneficial effects on kidney)
    • amlodipine (Ca blocker) also helpful for reducing BP
  24. Are SQ fluids helpful in management of CRF patient at home?
    yes, best to manage as outpatient whenever possible
  25. What is most common form of CRF?
    idiopathic (so not well understood and variable survival times)
  26. what are some findings that give poorest prognosis?
    • severe intractable anemia (can't keep giving infusions)
    • inability to maintain fluid balance/progressive azotemia
    • advanced osteodystrophy (w/young familial)
    • progressive wt loss
    • severe end stage lesions on biopsy