CattleII1- Lameness

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  1. Why do we care about lameness? (3)
    animal welfare concerns (pain), decreased production, economic losses (increased culling, decreased preg)
  2. Sole ulcers mainly contributes to ____________; digital dermatitis mainly contributes to ____________; foot rot mainly contributes to ____________.
    milk loss; treatment cost; decreased fertility
  3. Causes of lameness. (6)
    hoof diseases, fractures, hip luxations, joint infections, tendon/ligament disorders, muscle trauma
  4. What is the primary concept to localizing lameness?
    they spend less time on the lame leg (down on sound, short-strided)
  5. What is very suggestive of dorsal hip luxation?
    greater trochanter in line with tuber coxae and tuber ischii- greater trochanter should be ventral, forming a triangle
  6. What is very suggestive of ventral hip luxation?
    greater trochanter disappears- rectal palpation to try and feel femoral head in obturator foramen
  7. How does a cow stand if lame on the medial claw(s)?
    • unilateral- leg further under body
    • bilateral- crossed legs
  8. How does a cow stand if lame on the lateral claw(s)?
    leg(s) placed more laterally than normal (put weight on medial claw)
  9. What are the 3 most common pathologies of the stifle joint?
    patellar luxation, collateral ligament rupture, CCL ligament rupture
  10. You can flex the stifle and extend the hock simultaneously...what's wrong?
    peroneus tertius rupture
  11. You can flex the hock with the stifle straight/extended....what's wrong?
    gastroc rupture
  12. What is the 90% rule?
    • 90% of bovine lameness is below the fetlock.
    • 90% is in the rear leg.
    • 90% is in the lateral claw.
  13. What foot diseases may make the cow non-weightbearing lame, but are usually negative with hoof testers? Why?
    foot rot, digital dermatitis (hairy heel wart), interdigital hyperplasia (corn-usually not lame unless huge); soft tissues of interdigital space--> hurts to bear weight, but hard parts of hoof are unaffected
  14. What are the 2 agents most commonly associated with foot rot?
    Dichelobacter nodosus, Fusobacterium necrophorum
  15. Describe the pathogenesis of foot rot?
    maceration from water/urine/feces--> skin gets soft/friable--> mechanical lesions develop in skin--> anaerobic environment for bacteria
  16. What are clinical signs of foot rot? (6)
    pain/lameness, foul odor, swelling, erythemia of soft tissues, exudate, necrosis
  17. What is the treatment of foot rot? (3)
    Pen G, local disinfection (oxytet, erythromycin), animals in clean/dry environment
  18. Describe prevention of foot rot. (3)
    separate infected animals, clean/dry environment, copper or zinc sulfate footbaths
  19. What is the etiology of hairy heel wart?
    spirochete- Treponema
  20. What are the 2 presentations for hairy heel wart?
    erosive/reactive condition; proliferative wart-like lesions
  21. What is the treatment for hairy heel wart?
    topical oxytetracycline
  22. What are prevention measures for hairy heel wart? (3)
    dry environment, segregate infected cows, proper hygiene
  23. What causes corns?
    result of chronic irritation in interdigital region due to buildup of slurry dried on hooves
  24. What are preventative measures for corns?
    prevent buildup of slurry from drying on feet
  25. Describe the pathogenesis of laminitis.
    disturbance of microvascular circulation of the corium--> degeneration and inflammatory changes at the dermal-epidermal junction
  26. What are sequelae of laminitis? (4)
    impaired horn production, sole ulcers, white line disease, claw deformation
  27. What are potential causes of laminitis? (4)
    carb overload and lactic acidosis, excess protein, endotoxemia, mechanical factors
  28. Where do Rusterholz ulcers most commonly occur?
    plantar process of distal phalanx- point of maximal pressure; lateral hind claw
  29. Describe the pathogenesis of sole ulcers.
    [soft diseases soles] laminitis, heel erosions, most environment--> flat soles, long toes--> pressure concentration at plantar process of P3--> ischemic necrosis of corium--> granulation tissue
  30. What is the treatment for sole ulcers? (2)
    pare out lesion, block on opposite toe
  31. What is the pathogenesis of white line disease?
    wet conditions/claw deformities/laminitis soften white line further--> penetration of debris--> abscess formation and disintegration of white line--> ulceration
  32. How do you treat white line disease?
    remove dead tissue, provide drainage, balance claws; +/- check for involvement of deeper structures, claw amputation, facilitated ankylosis
  33. Describe prevention of white line disease.
    proper hygiene, claw trimming, foot baths
Card Set:
CattleII1- Lameness
2016-01-26 12:50:31
vetmed cattleII1

vetmed cattleII1
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