Muscle Flashcards

1
Q

Enzyme activities to assess muscle damage

A
Creatine kinase (CK)
Aspartate aminotransferase (AST)
Lactate dehydrogenase (LDH)
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2
Q

What is Serum CK a sensitive indicator for?

A

myonecrosis in both skeletal and heart muscle

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3
Q

When does Serum CK activity increase?

A

Increased within hours of a muscle insult and peaks within 4-6 hours after injury

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4
Q

When can CK elevate?

A

training
transport
strenuous exercise

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5
Q

What enzyme has high activity in skeletal and cardiac muscle as well as Liver, RBCs, and other tissues?

A

AST

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6
Q

When is the peak time for AST levels after an insult?

A

24 hours

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7
Q

What do elevations in CK and AST reflect?

A

recent or active myonecrosis

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8
Q

What do elevations of CK reflect?

A

myonecrosis is likely going on

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9
Q

What do elevated AST and decreasing or normal CK levels indicate?

A

Myonecrosis not continuing

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10
Q

Elevations in LDH specify what?

A

rhabdomyolysis
myocardial necrosis
hepatic necrosis

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11
Q

What tests assess concurrent renal disease?

A
Urine specific gravity 
White blood cell count 
Protein content 
Red Blood cell count 
Evaluation of cast formation
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12
Q

What does a positive Hemastix test in the absence of hemolysis or RBCs in urine indicate?

A

Myoglobinuria

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13
Q

Exercise Challenge test

A

15 mins of slow trot with CK activity sampled before and 4-6 hours after

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14
Q

What do elevations of greater than 5-fold CK indicate?

A

exertional rhabdomyolysis

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15
Q

Electomyography

A

to detect spontaneous or evoked potentials of neurogenic or myogenic

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16
Q

What do horses with abnormalities show on electromyography?

A

Spontaneous electrical activity
Fibrillation potentials: spontaneous firing of muscle fibers
Positive sharp waves
Myotonic discharges: bursts of complex high-frequency potentials
Complex repetitive discharges

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17
Q

What are EMG and NCVs used to classify?

A

classify the disease Neuropathic or Myopathic

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18
Q

Use of Nuclear Scintigraphy

A

ID some forms of muscle damage

area of deep muscle damage

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19
Q

How does Nuclear Scintigraphy work?

A

Technetium 99 m methylene diphosphonate is taken up in inflamed and damaged muscle

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20
Q

How is muscle fiber disruption seen on Ultrasonography?

A

hypoechoic area with loss of the normal fiber striation

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21
Q

How do es a defect in muscle/hematoma appear on ultrasonography?

A

Hypoechoic

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22
Q

How does increased connective tissue or loss of muscle appear on ultrasonography?

A

Hypoechoic

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23
Q

How does mineralization or gas pockets appear on ultrasonography?

A

Hyperechoic shadowing artifacts

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24
Q

“Sweeney”

A

suprascapular nerve is damaged and muscle over the scapula are atrophied

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25
Q

How long does it take for denervation to result in 50% muscle mass loss?

A

2 - 3 week period

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26
Q

What are the causes of Atrophy?

A

Denervation
Disuse
Malnutrition and cachexia
Immune-mediated myositis

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27
Q

HYPP

A

Hyperkalemic Periodic Paralysis

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28
Q

What causes HYPP?

A

inherited defect in the skeletal muscle sodium channel

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29
Q

What type of trait is HYPP?

A

Autosomal dominant

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30
Q

What does HYPP cause?

A

Abnormal skeletal muscle membrane excitability leads to episodes of myotonia, muscle contraction, and paralysis

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31
Q

What can trigger an episode of HYPP?

A

Ingestion of diets high in potassium, alfalfa hay, molasses
Electrolyte supplements
Sudden dietary changes and fasting
Anesthesia, heavy sedation or trailer rides

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32
Q

What are the clinical signs of an episode of HYPP?

A

Myotonia
prolapse of the third eyelid
Sweating
muscle fasciculations in the flanks, neck, and shoulders and then become generalized
Respiratory distress due to paralysis of the upper respiratory muscles
dysphagia

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33
Q

What are the clinical pathological signs seen in horses with HYPP?

A

Hyperkalemia
Hemoconcentration
Mild hyponatremia

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34
Q

How do you control HYPP?

A

Decreasing dietary potassium and increasing renal losses of potassium
Avoid high potassium feeds
Regular exercise
Balanced minerals
Commercially available complete feeds with a guaranteed Potassium content

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35
Q

What drugs are used to control horses with HYPP?

A

Acetazolamide

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36
Q

Acetazolamide

A

stabilizes blood glucose and potassium by stimulating insulin secretion

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37
Q

Muscle Cramping

A

painful condition that arises from hyperactivity of motor units cause by repetitive firing of the peripheral and/or central nervous system

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38
Q

What is the cause of Muscle cramping?

A

Dehydration
Electrolyte abnormalities
Disturbances in thermoregulatory and local circulatory function

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39
Q

What deficiency is common in horses?

A

Sodium

40
Q

What deficiencies can result in muscle stiffness, weakness, and occasional elevation in CK?

A

sodium or potassium

41
Q

What is a common muscle condition seen in endurance horses?

A

Muscle cramping

42
Q

What are the common electrolyte abnormalities of exhaustion?

A

hypochloremic metabolic alkalosis with hypokalemia, hypomagnesemia and low serum ionized calcium

43
Q

What can be seen with muscle cramping in horses?

A

Synchronous diaphragmatic flutter

44
Q

What is the treatment for muscle cramping?

A

Signs abate with rest or light exercise
oral or intravenous polyionic fluids
Cooling horses down with water and fans
Supplement with sodium chloride and potassium chloride

45
Q

What are the two types of Rhabdomyolysis?

A

Non-exertional

exertional

46
Q

Clostridial Myonecrosis

A

Disease characterized by a rapid clinical sourse, fever, systemic toxemia, and high mortality

47
Q

Clinical signs of Clostridial Myonecrosis

A
Crepitus
Malodorous serosanguinous fluid
Tremors 
Ataxia
Dyspnea
recumbence
coma
death within 12-24 hours
48
Q

What is the cause of Clostridial Myonecrosis?

A

Recent injection

49
Q

What is a site of invasion for Clostridium in foals?

A

Umbilicus

50
Q

What is the treatment for Clostridial myonecrosis?

A

Antibiotic therapy
Aggressive surgical debridement
supportive care

51
Q

What is the drug of choice for treatment for Clostridial myonecrosis?

A

Penicillin

52
Q

Clinical signs of Rhabdomyolysis associated with Streptococcus

A

Stiff gait

rapidly to markedly firm, swollen painful epaxial and gluteal muscles

53
Q

What are the two causes of Rhabdomyolysis/ Streptococcus equi?

A
  1. Toxic Shock

2. Bacteremia

54
Q

What is the treatment for Rhabdomyolysis/ Streptococcus equi?

A

Flushing infected guttural pouches and draining abscessed lymph nodes
NSAIDs
CRI of lidocaine, detomidine, or ketamine

55
Q

What are the clinical signs of Immune-mediated polymyositis?

A

Rapid onset of muscle atrophy of the back and croup muscles
accompanied with stiffness
Generalized weakness

56
Q

What do you see on biopsy of Immune mediated Polymyositis?

A

lymphocyte vasculitis
angular atrophy
fiber necrosis with macrophage infiltration
regeneration

57
Q

What is the treatment for Immune Mediated Polymyositis?

A

Corticosteroids

58
Q

What viruses are associated with myopathy?

A

Equine Influenza A2

EHV1

59
Q

What muscles are affected by virus associated myopathy?

A

Skeletal muscles and cardiac muscles

60
Q

Seasonal Pasture Myopathy and Atypical Myopathy

A

a highly fatal acquired lipid storage myopathy of pastured horses kept on wooded pastures for more than 12 hours a day without additional feed

61
Q

What are the clinical signs of Seasonal Pasture Myopathy and Atypical Myopathy?

A
Acute muscular weakness
Sweating 
fasciculations 
stiffness
tachycardia
tachypnea
recumbence
myoglobinuria
62
Q

What are the clinical pathological signs of Seasonal Pasture Myopathy and Atypical Myopathy?

A

increase in CK and AST activity
hyperglycemia
lactic acidemia

63
Q

How do you diagnose Seasonal Pasture Myopathy and Atypical Myopathy?

A

Identified deficiency in multiple acetyl coA dehydrogenase
Isolation of the conjugated toxic metabolite methylenecyclopropyl acetic acid in blood or urine
Extensive necrosis in deep postural, respiratory muscles and myocardium

64
Q

What is responsible for causing Seasonal Pasture Myopathy and Atypical Myopathy

A

Seeds of Acer species trees such as the box elder containing toxic amino acid hypoglycin A

65
Q

What is the paathophysiology of the Seed of Acer species tree?

A

Hypoglycin A is metabolized in the liver to MCPA
MCPA irreversibly binds to multiple enzymes that are essential for metabolism fatty acids and branched chain amino acids
Accumulation of fat esters can damage muscle cell membranes, and an energy deficiency also arises from an inability to metabolize fat

66
Q

What is the treatment and control of Seasonal Pasture Myopathy and Atypical Myopathy

A

Early aggressive supportive care

Avoid pasture with Acer species trees

67
Q

What are the two forms of Postanesthetic Myoneuropathy

A

Localized myopathy-neuropathy

Generalized myopathy

68
Q

Localized myopathy-neuropathy

A

occurs in muscles that are in contact with a hard surface or with compromised arterial blood supply

69
Q

What is the cause of Postanesthetic Myoneuropathy?

A

Duration of anesthesia, ischemia, and hypoperfusion as a result of prolonged immobility, muscle compression, systemic hypotension, and hypoxia

70
Q

What is the treatment for Localized myopathy-neuropathy?

A

Supportive care

Anti-inflammatory drugs

71
Q

How do you control localized myopathy-neuropathy?

A

Goo padding and proper placement of limbs and body to reduce pressure
Maintaining anesthesia at the lightest plane possible and adequate arterial blood pressure

72
Q

What are the clinical signs of Generalized Anesthetic Reactions?

A
Anxiety
hyperthermia
tachycardia
tachypnea
profuse sweating
myoglobinuria
73
Q

What are the aims of treatment for myopathy-neuropathy?

A

Relief of pain
Correction of fluid and electrolyte abnormalities
Attempts to prevent ongoing necrosis
High-quality nursing care

74
Q

What is used to release calcium from the sarcoplasmic reticulum helping to break the cycle of muscle damage from myopathy-neuropathy?

A

Dantrolene

75
Q

What myopathy is common in jumpers, dressage, harness horses and thoroughbreds?

A

Exertional myopathies of the lumbar and gluteal muscles

76
Q

What myopathy is common in Quarter horses?

A

Strain semitendinosus and semimembranosus muscles

77
Q

What is caused by chronic exertional myopathies?

A

fibrotic myopathy

78
Q

What is a clinical sign of strain the semitendinosus and semimembranosus muscles?

A

Stride has a short anterior phase with a characteristic hoof-slapping gait
No pain

79
Q

How do you treat strain of semitendinosus and semimembranosus muscles?

A

Surgical procedures fro correction of fibrotic myopathy

excision or transection of the fibrotic part of the muscle

80
Q

What is the most common muscle disorder of horses?

A

Sporadic Exertional Rhabdomyolysis

81
Q

What are the clinical signs of Sporadic Exertional Rhabdomyolysis?

A

Stiff gait
excessive sweating
high respiratory rate during or after exercise with firm painful muscles after 15-30 minutes of light exercise
Myoglobinuria

82
Q

How do you diagnose Sporadic Exertional Rhabdomyolysis?

A

abnormally elevated serum CK and AST

Myoglobinuria

83
Q

What causes Sporadic Exertional Rhabdomyolysis?

A

Level of exercise
Signs of muscle stiffness and gait changes
Severity of elevations of serum CK activity

84
Q

What dietary imbalance exacerbates Sporadic Exertional Rhabdomyolysis?

A

selenium and vitamin E

85
Q

How do you treat Sporadic Exertional Rhabdomyolysis?

A
Anti-inflammatories
Sedative or tranquilizer
Fluid therapy 
Muscle relaxants
Nutrition
86
Q

What can severe rhabdomyolysis lead to?

A

Renal damage due to combined nephrotoxic effects of myoglobinuria, dehydration, and NSAIDs

87
Q

How do you treat Sporadic Exertional Rhabdomyolysis?

A

Stall rest
Resume training gradually
Avoid excessive calorie intake and ensure proper nutritional balance

88
Q

What triggers Recurrent Exertional Rhabdomyolysis?

A

Exercise

89
Q

What are the clinical pathological findings of Recurrent Exertional Rhabdomyolysis??

A

Rise in serum CK and myoglobin

Rise in Cortisol concentrations

90
Q

How do you diagnose Recurrent Exertional Rhabdomyolysis?

A

Biopsy

91
Q

What type of diet should horses be on to manage Recurrent Exertional Rhabdomyolysis?

A

Low-starch High-fat concentrates

92
Q

What is discouraged for horses with Recurrent Exertional Rhabdomyolysis predisporsition?

A

Days off training in a stall

93
Q

What medications are used to help control Recurrent Exertional Rhabdomyolysis?

A
Acepromazine
Reserpine
fluphenazine
Dantrium sodium
Oral Dantrolene
Phenytoin
94
Q

Polysaccharide Storage Myopathy

A

horses have 2-fold higher glycogen concentration than normal horses and abnormal granular amylase-resistant inclusion in histiologic sections because of a malfunction in glycogen synthase enzyme due to a single base-pair mutation in GYS1

95
Q

What is the common trigger for Type 1 Polysaccharide Storage Myopathy?

A

Exercise

96
Q

How do you diagnose Type 1 Polysaccharide Storage Myopathy?

A

Elevated serum CK and AST
Exercise test produce a minimum of a three fold elevation in CK activity 4-6 hours after exercise
Muscle Biopsy