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SP2 Musculoskeletal > Lecture 39 5/1/25 > Flashcards

Lecture 39 5/1/25 Flashcards

1
Q

What are the roles of K+ and Ca2+ in muscle contraction?

A

-K+ is important for the action potentials
-Ca+ is involved in binding troponin for muscle contraction

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2
Q

What are the possible responses of the muscle to injury?

A

-rhabdomyolysis
-atrophy
-hypertrophy
-changes in muscle tone

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3
Q

What aspects of signalment and history are important to assessing muscle injury?

A

-breed
-age
-gender
-exercise
-nutrition
-genetics
-previous episodes

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4
Q

What should be assessed on PE in horses with muscle injury?

A

-muscle symmetry and development
-palpation
-gait analysis looking for lameness, weakness, and stiffness

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5
Q

What are the primary plasma/serum enzyme activities used to assess muscle injury?

A

-creatine kinase
-aspartate aminotransferase (AST)
-lactate dehydrogenase (LDH)
-troponin

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6
Q

What are the characteristics of creatine kinase?

A

-catalyzes transfer of phosphate groups to creatine
-primarily originates from skeletal muscle
-can come from smooth muscle, brain, and photoreceptor cells
-rapid peak and decay
-increases with acute or ongoing muscle damage

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7
Q

What are the characteristics of AST?

A

-functions in amino acid breakdown
-primarily originates from skeletal muscle and hepatocytes
-can be produced by RBCs, intestine, and kidneys
-slower to rise and longer half-life than CK

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8
Q

What are the characteristics of CK exercise testing?

A

-2 minutes @ a walk and 13-20 minutes @ a trot
-measure CK pre-exercise and 2 to 4 hours post-exercise
-CK should not be greater than 2x baseline
-CK should return to baseline by 24 hours post-exercise

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9
Q

Which findings on UA are used to assess muscle injury?

A

-myoglobinuria
-specific gravity
-casts
-proteinuria

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10
Q

What are the characteristics of muscle fiber type?

A

-all horses have both types
-amount of each muscle fiber type varies with breed, individual, and anatomic location
-type 2 fibers are fast twitch
-type 1 fibers are slow twitch

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11
Q

Which other diagnostic tests can be used in muscle injury cases?

A

-muscle biopsy
-genetic testing
-ultrasonography
-electromyography
-thermography
-scintigraphy

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12
Q

What is exertional rhabdomyolysis?

A

-syndrome of muscle pain and cramping typically associated with exercise
-breakdown of muscle cells leads to leakage of intracellular content
-not a specific dz; no single cause or cure

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13
Q

What are the possible causes of exertional rhabdomyolysis?

A

-overexertion, which leads to sporadic dz
-underlying disorder, which leads to chronic or recurrent dz

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14
Q

What are the possible contributing factors to exertional rhabdomyolysis?

A

-sudden change in exercise pattern
-performing beyond conditioning level
-genetics
-electrolyte imbalances
-metabolic abnormalities
-dietary factors
-infections
-trauma
-surgery/anesthesia
-hormonal

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15
Q

What are the causes of chronic rhabdomyolysis?

A

-polysaccharide storage myopathy; type 1 or 2
-myofibrillar myopathy
-recurrent exertional rhabdomyolysis
-myosin heavy chain myopathy
-vitamin E abnormalities

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16
Q

What are the characteristics of exertional rhabdomyolysis pathophysiologic changes?

A

-generally shared regardless of inciting cause
-acute episodes share signs and treatment

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17
Q

What are the clinical signs of exertional rhabdomyolysis?

A

-subclinical to severe
-poor performance
-stiff gait/reluctant to move
-firm, painful muscles
-sweating
-increased heart rate and resp rate
-muscle tremors
-colic and/or lameness

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18
Q

What are the emergency recommendations for acute episodes of exertional rhabdomyolysis?

A

-stop exercise; do not force exercise
-blanket in cool weather
-call veterinarian
-provide fluids +/- electrolytes
-only hay to eat

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19
Q

What are the goals of exertional rhabdomyolysis treatment?

A

-limit further muscle damage
-minimize inflammation
-restore fluid and electrolyte balance
-provide adequate supportive care

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20
Q

What are the steps to limiting further muscle damage in exertional rhabdomyolysis?

A

-stop exercise
-anti-inflammatory medications (hydrate before NSAIDs)
-increase blood flow to muscles (IV fluids, ace)
-muscle relaxants

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21
Q

What are the characteristics of fluid and electrolyte balance in exertional rhabdomyolysis?

A

-fluid diuresis to restore volume
-use furosemide or dopamine to promote urination if not urinating after volume restoration
-monitor acid/base and electrolyte status; treat appropriately

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22
Q

What are the supportive care steps for exertional rhabdomyolysis?

A

-sedatives to decrease anxiety
-warm, comfortable stall
-nutritious palatable food and water with easy access

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23
Q

What are the characteristics of polysaccharide storage myopathy type 1?

A

-point mutation in a gene that results in unregulated glycogen synthesis
-accounts for >90% cases of type 1
-second mutation (malignant hyperthermia) present in some cases and make signs worse

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24
Q

What are the characteristics of PSSM type 2?

A

-more than one disorder; PSSM2-QH and PSSM2-MFM
-gene not yet identified for either disorder

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25
Which breeds are affected by PSSM type 1?
-quarter horses -draft horses -warmbloods -morgans
26
Which breeds are rarely affected by PSSM type 1?
-thoroughbreds -standardbreds -arabians
27
What are the clinical signs of PSSM?
-chronic rhabdomyolysis stiffness and gait asymmetry -muscle wasting -weight loss -weakness -exercise intolerance
28
What are the characteristics of PSSM in draft breeds?
-very common -similar to "shivers" -no confirmation of a relationship between the two conditions
29
What is the pathogenesis of PSSM type 1?
-autosomal dominant mutation -glycogen storage disorder -abnormal accumulation of normal glycogen -abnormal polysaccharide; less branching, resistant to amylase
30
What are the samples used for genetic testing for PSSM type 1?
-hair -blood
31
What are the characteristic of muscle biopsy for PSSM diagnosis?
-can use semimembranosus or semitendinosus muscles -want type 2 muscle fibers -currently required for PSSM type 2 dx
32
What are the muscle biopsy findings in PSSM type 1?
-increased amount of glycogen -structurally abnormal glycogen
33
What are the muscle biopsy findings in PSSM type 2?
-abnormal aggregates -amount and structure may vary with type of PPSM2
34
What is the treatment for PSSM?
-treat acute episodes with general rhabdomyolysis treatment -return to exercise as soon as horse is moving without profound stiffness -consistent daily exercise -diet that limits carbs, increases fat, and balances vitamins and minerals
35
What is the prognosis for PSSM?
-guarded to good with diet and exercise modifications -most will improve to some degree -severely effected horses may not respond to treatment
36
What is the pathogenesis of myofibrillar myopathy?
disruption of the alignment of the myofibrils
37
What is the signalment of myofibrillar myopathy?
-most common in arabians and warmbloods -arabians present with intermittent episodes, elevations in muscle enzymes, and mild clinical signs -warmbloods experience performance decline and gait abnormality but have normal enzymes
38
How is myofibrillar myopathy diagnosed?
-biopsy -NO validated genetic test
39
What is the treatment for myofibrillar myopathy?
-consistent exercise to strengthen core -diet high in quality protein, cysteine, and antioxidants
40
What are the characteristics of myosin-heavy chain myopathy?
-muscle disease or quarter horses and related breeds -autosomal co-dominant mutation with variable penetrance -two distinct clinical presentations are immune-mediated myositis and non-exertional rhabdomyolysis
41
What is the prognosis for myosin-heavy chain myopathy?
-majority of patients improve by 50% or more within 4 weeks -65% meet performance expectations after treatment
42
What are the characteristics of recurrent exertional rhabdomyolysis?
-mostly seen in thoroughbreds -complex disorder affected by modifier genes and environmental factors -excess release of Ca leads to excessive contraction
43
What is the typical signalment for recurrent exertional rhabdomyolysis?
-young -mostly female -nervous and stressed animals -high level of fitness -underlying lameness -winter months -high grain diets
44
How is recurrent exertional rhabdomyolysis diagnosed?
-signalment -history -clinical signs -CK management -biopsy
45
What are the management steps for recurrent exertional rhabdomylosis?
-minimize stress -regular exercise -treat lameness -avoid stall rest -diet limiting carbs and increasing fat
46
What is the prognosis for RER?
good to guarded
47
What are the common nutritional myopathies in horses?
-nutritional myodegeneration/nutritional muscular dystrophy/white muscle dz -vitamin E myopathy
48
What are the PE findings in nutritional myopathies?
-unable to open mouth due -PE otherwise normal -no pain on palpation -neuro exam normal -rads normal -blood work normal -endoscopic exam normal
49
What are the characteristics of masseter biopsy findings?
-chronic, severe muscle degeneration -consistent with white muscle disease
50
What is nutritional myodegeneration?
non-inflammatory degenerative disease of skeletal and/or cardiac muscle caused by selenium deficiency
51
What are the functions of selenium?
-component of several selenoproteins -glutathione peroxidases -synergistic with vitamin E
52
What is the acute/cardiac presentation of nutritional myodegeneration?
-usually very young foals -recumbent and unable to rise -tachypnea -dyspnea -variable temp -often fatal
53
What is the subacute/skeletal presentation of nutritional myodegeneration?
-profound weakness -stiff, spastic gait -tense, painful muscles -dysphagia/poor suckle reflex -tachycardia -arrhythmias -systolic murmurs -bright and alert or depressed
54
What are the consequences of dysphagia in nutritional myodegeneration?
-masseter myopathy +/- tongue -weight loss -masseter atrophy -limited range of jaw motion
55
How is nutritional myodegeneration diagnosed?
-increased muscle enzymes possible -myoglobinuria -decreased selenium levels -vitamin E conc.; variable -response to therapy
56
What is the treatment for nutritional myodegeneration?
-vitamin E/selenium supplementation; injections or oral -restrict exercise -nutritional support -NSAIDs -supportive care
57
How is nutritional myodegeneration prevented?
adequate dietary selenium and vitamin E via oral supplementation or injections
58
What are the characteristics of hyperkalemic periodic paralysis/HYPP?
-genetic dz affecting quarter horses and related breeds -characterized by episodic muscle fasciculations and weakness associated with hyperkalemia -may be severe and cause recumbency and death
59
What is the genetic basis for HYPP?
single amino acid substitution in the gene coding the muscle membrane voltage-gated Na channel
60
What is the pathogenesis of HYPP?
-Na channels fail to inactivate when potassium is high -excessive inward flux of Na and outward flux of K leads to persistent depolarization -resting membrane potential is always closer to firing
61
What is the presentation of HYPP?
-severity is highly variable -horses may be several years old before showing signs -episodes may be precipitated by stress
62
What is the treatment for HYPP?
-dextrose -sodium bicarbonate -calcium gluconate
63
How is HYPP prevented?
-avoid high potassium feeds -acetazolamide (diuretic) -regular exercise -avoid rapid feed changes -minimize stress -do not use affected animals for breeding

SP2 Musculoskeletal (43 decks)

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