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VMS 3010 > Approach to common muscle diseases in horses > Flashcards

Approach to common muscle diseases in horses Flashcards

1
Q

What two things cause sporadic exertional rhabdomylolysis?

A
  • Overexertion
  • Exhaustion
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2
Q

How does overexertion cause sporadic exertional rhabdomylolysis?

A
  • Increase in work intensity without foundation of training
  • Can affect any horse
    Common in polo ponies early in the season
  • Aetiology unknown
  • History of respiratory infection
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3
Q

How does exhaustion cause sporadic exertional rhabdomylolysis?

A

Racehorses/endurance horses, hot and humid climate
* Weakness, ataxia, tachypnoea, sweating… (collapse)
* May be hyperthermic
* Myoglobinuria and elevated CK, but muscles may palpate normal

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4
Q

What is recurrent exertional rhabdomylolysis?

A

Also known as Monday morning disease, Azoturia and Setfast
* Syndrome rather than a disease as aetiology and pathogenesis still
unknown
* Female > males
* Nervous/anxious horses
* High prevalence in racing Thoroughbreds (4.9-6.7% of TBs affected)
* Also occurs in Standardbreds and Arabians
* Historically affects horses on high grain diets

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5
Q

What are the clinical signs of recurrent exertional rhabdomylolysis?

A

Stiff, painful muscles (large muscle groups- gluteals, triceps)
* Myoglobinuria
* Usually present on day following a rest day

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6
Q

How might you diagnose RER?

A

History and signalment (Trainer often recognises the signs)
* Elevated muscle enzymes
* Muscle biopsy of semimembranosus- often to rule out other
myopathies as no specific changes associated with RER

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7
Q

What is the gold-standard diagnosis for RER?

A

in vitro contracture studies
on intercostal muscle (not commercially available)

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8
Q

What are the two ways you can manage RER?

A
  • Exercise
  • Dantrolene
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9
Q

What is dantrolene?

A

RYR1 antagonist → inhibits calcium release from sarcoplasmic reticulum
2-4mg/kg orally
Short half-life. Given 1-2 hours before exercise.
Detection time 48hrs (BHA)

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10
Q

What is the clinical presentation for PSSM?

A

Recurrent episodes
* Muscle pain, weakness, tremors or fasciculations
* Shifting lameness
* Sweating
* Myoglobinuria
* Reluctance to move or in extreme cases recumbency

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11
Q

How might you diagnose PSSM?

A

Marked elevation of muscle enzymes (CK and AST)
* Myoglobinuria in more severe cases
* Muscle biopsy of semimembranosus
* reveals abnormal polysaccharide in myofibres
* Genotyping for PSSM1

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12
Q

How does PSSM1 occur?

A

Associated with a single dominant missense mutation in
the equine muscle glycogen synthase gene (GYS1).
* Glycogen synthase catalyses the formation of 1-4
glycosidic bonds in the glycogen molecule
* The ratio between GS and glycogen branching enzyme
should result in normal branched glycogen formation
* The mutant enzyme is unable to be switched off thereby
altering the GS:GBE and making abnormally
polysaccharide
* Pathogenesis not fully understood

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13
Q

What is PSSM 2?

A

Still a disease of abnormal glycogen
storage.
* Pathogenesis unknown
* Likely to be a group of conditions:
MFM?, MIM?
Abnormal polysaccharide on muscle
biopsy , but absence of GYS1 mutation

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14
Q

What are the dietary changes needed for PSSM 1 management?

A
  1. Limit glycogen synthesis (reduce insulin activity)
  2. Promote breakdown of glycogen
  • Low starch, high fat
  • Provide 1.5-2% BWT as roughage
  • < 10% Digestible energy as non-structural carbohydrates
  • > 13 % fat
  • Vegetable oil up to 1ml/kg/day
  • Supplemental Vitamin E
  • Commercial diets
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15
Q

How might you treat rhabdomylolysis?

A
  1. Minimise continued muscle damage
  2. Analgesia
  3. Correct fluid deficit
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16
Q

What are four ways you can minimise continued muscle damage?

A
  1. Rest- deep bed
  2. Anti-inflammatories (e.g NSAIDS)
  3. Acepromazine
  4. Antioxidants
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17
Q

What does post-anaesthetic myopathy look like?

A
  • Localised rather than general myopathy
  • Hard, Hot, swollen muscles
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18
Q

What causes compartment syndrome?

A

inappropriate positioning

19
Q

How would you treat compartment syndrome?

A

Symptomatic and supportive treatment

20
Q

What are the risk factors for atypical myopathy?

A
  • Autumn and spring
  • Wet and windy weather
  • Presence of Sycamore trees (UK)
  • Access to pasture
21
Q

What are the clinical signs of atypical myopathy?

A
  • Weakness: Horses struggle to walk and stand. May be found recumbent.
  • Muscle tremors and painful, firm muscles may be appreciated on palpation
  • Myoglobinuria
  • Tachycardia, tachypnoea, congested mucous membranes
  • Signs of severe colic but normal appetite
  • Distended bladder on rectal palpation
22
Q

How might you diagnose atypical myopathy?

A
  • Elevated muscle enzymes (CK>10,000iu/L)
  • Myoglobinuria and acidic urine
  • Submit plasma for acylcarnitine profile/serum for hypoglycin A and conjugated MCPA
    Confirmation takes 48-72h via RVC Neuromuscular Lab
23
Q

What does atypical myopathy look like on post-mortem?

A

necrosis and lipid accumulation in deep postural muscles, necrosis of respiratory and cardiac muscle

24
Q

What causes hypoglycin A toxicity?

A

Seeds and seedlings of acer trees

25
Q

What is the pathogenesis of hypoglycin A toxicity?

A
  • Ingested toxin from sycamore tree seeds
  • Toxic metabolite
  • Binds to FAD to inhibit acyl-coA dehydrogenase
  • Beta-oxidation of long chain fatty acids are blocked
  • Type-1 muscle fibres are the worst affected
26
Q

What is the prognosis for atypical myopathy?

A
  • Guarded (potentially 84% mortality)
  • If horse survives the first few days of treatment it may be better
27
Q

What clinical signs may decrease the prognosis for atypical myopathy?

A

hypoxia, dyspnoea, tachypnoea, sweating, hypothermia, bladder distension, tachycardia, CK >100 000 IU/litre and recumbency

28
Q

How might you be able to prevent atypical myopathy?

A

Avoid sycamore trees
* Provide supplementary forage in the autumn.
* Clear fallen sycamore leaves and seeds from grazing area (especially in stormy weather).
* Fence off areas where sycamore leaves/seeds have fallen.
* Bring horses in at night.
* Check neighbouring areas for high-risk plants/seeds.
* Test for the prevalence of HGA in your own horse’s pastures.

29
Q

How would a horse with a metabolic myopathy present?

A

Horses present with signs of AM but do not have HGA or MCPA detected on blood tests

30
Q

What is HYPP?

A

Gene mutation alters voltage-dependent skeletal muscle sodium
channel
Membrane potential close to firing
Some sodium channels fail to inactivate = ↑ sodium in, ↓ potassium
out

31
Q

What are the clinical signs of HYPP?

A

May have daily fasciculations and weakness, may be asymptomatic
May begin with third eyelid prolapse → sweating/fasciculations
Overt cramping
Severe attacks may cause swaying, dog sitting, recumbency
Even paralysis of upper respiratory muscles → respiratory tract
obstruction
Episodes 15-60min long
Fasting, anaesthesia and stress may precipitate signs.

32
Q

What is malignant hypothermia?

A

RYR1 (ryanodine receptor) gene mutation
↓ activation and ↑ threshold of receptor → dramatic increase in
intracellular calcium → contraction → muscle heat and necrosis

33
Q

What are the clinical signs of malignant hypothermia?

A
  • Muscle rigidity
  • Abnormally high body temperature
  • Tachycardia, tachypnoea
34
Q

What is nutritional myodegeneration also known as?

A

White muscle disease

35
Q

What two nutrients may cause nutritional myodegeneration?

A
  • Selenium
  • Vitamin E
36
Q

What are the main forms of nutritional myodegeneration?

A
  • Cardiac
  • Skeletal muscle
37
Q

How might you diagnose nutritional myodegeneration?

A

Clinicopathologic abnormalities
* CK/AST elevation
* Myoglobinuria
* Electrolyte derangements
Low selenium (whole blood), low GSH-Px, low α-tocopherol (vit E) (plasma)
Clinical signs
Gross pathology
* Pale, oedematous muscle, calcification
* Hypercontracted muscle fibres on histology

38
Q

How might you treat nutritional myodegeneration?

A

Selenium injections IM (irritant, can dilute before injection)
* Oral α-tocopherol supplementation
* Supportive nursing

39
Q

What is the prognosis for nutitional myodegeneration?

A
  • Cardiorespiratory disease → poor prognosis
  • Skeletal muscle disease → better prognosis
40
Q

What are the clinical signs of vitamin E-Deficient Myopathy?

A
  • Weakness, toe-dragging
  • Muscle atrophy
  • trembling and muscle fasciculations
  • Weight shifting
41
Q

How would you diagnose vitamin E-Deficient myopathy?

A

SCDM biopsy: Presence of myopathic not
neuropathic change in sacrocaudalis dorsalis
medialis (SCDM) biopsy
* May have normal serum α-tocopherol

42
Q

How would you treat Vitamin-E deficient myopathy?

A

Oral α-tocopherol supplementation
* Not powders, needs to be bioavailable

43
Q
A

VMS 3010 (79 decks)

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