MS- Equine Muscle and Spinal Diseases.txt

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Mawad
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300791
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MS- Equine Muscle and Spinal Diseases.txt
Updated:
2015-04-14 16:41:49
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vetmed equine muscle spinal
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vetmed, equine muscle and spinal diseases
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  1. Clinical signs of rhabdomyolysis include... (7)
    muscle stiffness/soreness, firm muscles, painful to palpation, tachypnea, tachycardia, sweating, hyperthermia
  2. Blood work associated with rhabdomyolysis shows elevated __(4)__ and low __(3)__; eventually there is ________.
    CK, AST, K+, Phosphate; Na, Cl, Ca; azotemia
  3. If both Ck and AST are markedly increased...
    recent or active muscle necrosis
  4. If CK is persistently increased...
    ongoing muscle damage
  5. If AST is increased with decreasing or normal CK,...
    myonecrosis has ceased.
  6. Sporadic rhabdomyolysis is associated with ___________.
    exhaustive exercise
  7. Treatment of sporadic rhabdomyolysis includes... (5)
    fluid therapy, analgesics, stall restriction, muscle relaxants, gradual resumption of exercise
  8. HYPP is ______________.
    hyperkalemic periodic paralysis
  9. HYPP is ____________, meaning that horses with the same genotype have varying levels of severity of disease.
    incompletely penetrant
  10. _____________ are most likely to be affected by HYPP.
    heavily muscled quarterhorses and other stock breeds
  11. With HYPP, there is a defect in the __________, which should be __________ but are not; this causes persistent _________ and ineffective ___________.
    sodium channels; voltage inactivated; depolarization; repolarization
  12. Describe treatment of an acute attack associated with HYPP. (5)
    dextrose, karosyrup, calcium, bicarb, insulin
  13. Describe the preventative treatment of HYPP (to prevent further attacks). (2)
    acetazolamide, hydrochlorthiazide- diuretics to cause increased excretion of potassium
  14. When feeding horses with HYPP, the goal is to ____________; feeding should be ________, and ________ should be avoided.
    minimize dietary potassium (<1.1%); frequent; fasting
  15. PSSM is ____________.
    PolySaccharide Storage Myopathy
  16. Describe the treatment of PSSM. (5)
    fluid therapy, Flunixin meglumine (analgesic), Furosemide (diuretic), hand-walking [treat the myopathy and resulting nephropathy]
  17. PSSM is a ___________ disease of __________.
    glycogen-storage; skeletal muscle
  18. _____________ are most likely to be affected by Type I PSSM.
    Quarter horses and other stock breeds (genetic)
  19. Clinical signs of Type I PSSM include... (4)
    repeated episodes of rhabdomyolysis, muscle atrophy, stiffness/weakness, abnormal elevations in muscle enzymes post exercise
  20. Muscle biopsy from a horse with PSSM shows...
    accumulation of abnormal glycogen in muscles (PAS +, amylase resistant)
  21. __________ is important to managing PSSM; also, diet should contain... (3)
    Exercise (daily); reduced starches and sugars (<10% of ration) and increased fat.
  22. Wobblers is aka _______________; it is a ___________ disease characterized by ________________ resulting in ________________.
    cervicovertebral malformation (CVM)/ cervicovertebral stenotic myelopathy (CSM); developmental; stenosis of the spinal canal spinal cord compression
  23. Wobblers is characterized by... (3)
    ataxia, weakness, and spasticity
  24. What are the 2 clinical manifestations of Wobblers?
    Cervicovertebral instability (CVI), Cervicovertebral Static Stenosis/ Cervicovertebral Malformation (CSS/CVM)
  25. What is the difference b/w CVI and CSS/CVM?
    CVI- dynamic, intermittent compression; CSS/CVM- static, continuous compression
  26. CVI compression occurs during ___________; CSS/CVM compression occurs during ___________.
    neck flexion; all the time
  27. Clinical signs of Wobblers syndrome. (8)
    symmetric ataxia, paresis, spasticity, toe dragging, circumduction of rear legs, lateralization of trunk, hypermetria, and pacing
  28. Clinical signs of Wobblers are worse in _________ because...
    rear legs; spinal tracts to rear legs are more superficial than in the cervical spinal cord
  29. How can OCD contribute to Wobblers?
    OCD lesions at articular facets of cervical vertebrae, leading to instability and degenerative joint disease
  30. The cause of Wobblers has ____________ and ___________ components.
    environmental; genetic
  31. _____________ and ______________ are first tracts to be affected with Wobblers.
    Dorsal (conscious); dorsolateral (unconscious) ascending
  32. Histologically, with Wobblers there is ____________ and ____________ at the compression site.
    wallerian degeneration; fibrosis
  33. Describe the course of impulses from the brain to effectors and lesions at each component.
    • upper motor neuron (motor cortex, brain) --> lower motor neuron (efferent: gray matter of spinal cord) --> effector (muscle, glands)
    • damage in UMN --> spasms
    • damage in LMN --> paralysis
  34. How can you make diagnosis of Wobblers? (4)
    neuro exam, CSF analysis, radiographs w/ narrowing of cervical spinal canal, minimal sagittal diameter
  35. The minimal sagittal diameter is a ratio of the _____________ to the ______________ at its ____________ aspect; _________ is normal.
    spinal canal diameter; vertebral body diameter; cranial; >50%
  36. How do you treat Wobblers? (6)
    Confinement, glucocorticoids, DMSO, NSAIDs, articular facet injections, SOMETIMES surgery (to stabilize cervical vertebrae and decompress spinal cord)
  37. Temporohyoid osteoarthropathy occurs in ________ horses when a ____________ results in _____________ of the tympanic bulla, which spread to the proximal stylohyoid bone, causing _________ of the joint.
    adult; middle ear infection; chronic inflammation; fusion
  38. With temporohyoid osteoarthropathy, the lesion can ultimately affect the _____________, leading to damage of __(2)__.
    internal auditory meatus; cranial nerves VII (facial) and VIII (vestibular)
  39. Clinical signs of temporohyoid osteroarthropathy that are associated with damage to CN VII. (5)
    facial/muzzle deviation, droopy ear, eyelid dysfunction, decreased lacrimation that leads to corneal ulcers, dysphagia
  40. Clinical signs of temporohyoid osteoarthropathy that are associated with damage to CN VIII. (3)
    head tilt, nystagmus, ataxia
  41. How can you make a diagnosis of temporohyoid osteoarthropathy? (5)
    clinical findings, radiography, endoscopy,tomography, CSF analysis
  42. How do you treat temporohyoid osteoarthropathy? (4)
    broad-spectrum antibiotic, NSAIDs, surgery, treat keratitis to prevent loss of eye
  43. Describe the surgical treatment of temporohyoid osteoarthropathy.
    ceratohyoidectomy to remove temporal bone pressure
  44. Equine motor neuron disease affects _____________; equine degenerative myeloencephalopathy affects __________.
    grey matter; white matter
  45. Both equie motor neuron disease and equine degenerative myeloencephalopathy are associated with ____________.
    vitamin E deficiency
  46. hat are the clinical signs of equine degenerative myeloencephalopathy? (4)
    symmetric ataxia, spasticity, proprioceptive deficit, NO cranial nerve deficits or muscle atrophy
  47. Describe the clinical signs of equine motor neuron disease. (3)
    muscle tremors (fasciculations), muscle wasting, NO ataxia

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