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Muscle disorders Flashcards

1
Q

<p>Spastic paresis is seen in what age calves? And manifests as:</p>

A

<p>Calves: 2 months-7 months<br></br>— decreased ability to flex the hock because of continuous tension on the gastrocnemius & straight angle to hock & stifle</p>

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2
Q

<p>What is a similar condition to spastic paresis in calves seen in horses?</p>

A

<p>Shivers</p>

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3
Q

<p>Shivers is seen in horses of what breed/size typically</p>

A

<p>Draft breeds, warmbloods and warmblood crosses older than 1 yr of age<br></br><br></br>**usually taller than 16.3 hands</p>

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4
Q

<p>Define myotonia</p>

A

<p>Prolonged contraction of mm contraction</p>

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5
Q

<p>Clinical signs of shivers:</p>

A

<p>Primarily affects hindlimbs<br></br>-periodic, involuntary spaspsm of muscles in the pevlic reigon, pelvic limbs and tail<br></br> **exacerbated by backing and up or picking up hind libs<br></br> ** tailhead usually elevates concurrently/trembles<br></br>-hindlimb is suddenly raised, semi-flexed and abducted with hoof held in air for several seconds or minutes</p>

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6
Q

<p>Myotonic muscle disorders share the feature of what?</p>

A

<p>Delayed relaxation of muscle after mechanical stimulation or voluntary contraction<br></br><br></br>**abnormal muscle membrane excitability</p>

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7
Q

<p>Appearance of myotonia congenita in horses</p>

A

<p>Mild to moderate pelvic limb stiffness<br></br> **bilateral bulging of thick and rump muscles<br></br>Pronounced when exercise begins & diminishes as exercise continues</p>

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8
Q

<p>Is there progression of myotonia congenita in horses?</p>

A

<p>Not beyond 6 to 12 months of age</p>

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9
Q

<p>In goats what is the inheritance of myotonia congenita?</p>

A

<p>Autosomal dominant mutation in skeletal muscle chloride channel (CLCN1) that is incoplete penetrance</p>

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10
Q

<p>Myotonia dystrophica is separate from myotonia congenita in horses. What are the differences?</p>

A

<p>Severe clinical signs of myotnoia that progress to amarke dmm atrophy & involve a variety of organ systems<br></br><br></br>—> Quarterhorses, Appaloosa, Italian-bred foals</p>

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11
Q

<p>What is the definitive diagnosis of myotonia in horses?</p>

A

<p>Based on electromyographic examination</p>

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12
Q

<p>Examination of muscle biopsies from foals with myotonia congenita show:</p>

A

<p>Normal or demonstrate extremely variable muscle fiber dimensions up to twice those of normal age matched controls<br></br> +/- Type 1 fiber hypertrophy or hypotrophy</p>

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13
Q

<p>Changes in muscle biopsy seen with myotonic dystrophy</p>

A

<p>Ringed fibers<br></br>Alterations in shape & position of myonuclei, sarcoplasmic masses & inc in ednomysial & perimysial connective tissue<br></br>Fiber type grouping & atrophy of both type 1 & type II muscle fibers may be present</p>

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14
Q

<p>What are the treatment recommendations of myotonia?</p>

A

<p>No treatment</p>

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15
Q

<p>Myotonia prognosis</p>

A

<p>Variable & dependent on clinical signs<br></br> **regression of C/S unknown <br></br> ** euthanasia often warranted</p>

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16
Q

<p>Is myotonia congenital?</p>

A

<p>Unknown<br></br>**warn owners of possibility of this disease is heritable</p>

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17
Q

<p>Equine hyperkalemic periodic paralysis (HYPP) is caused by:</p>

A

<p>Inherited defect in the skeletal mm sodium channel</p>

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18
Q

<p>Equine HYPP manifests as</p>

A

<p>Abnormal skeletal mm membrane excitability leading to episodes of myotonia or sustained mm contraction and paralysis</p>

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19
Q

<p>How is HYPP inherited in horses?</p>

A

<p>Autosomal dominant trait in Quarterhorses, American Paint Horses, Appaloosas & QH horse crossbreeds</p>

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20
Q

<p>In HYPP, intermittent clinical signs start at what age?</p>

A

<p>2 to 3 years of age with no apparent abnormalities between episodes</p>

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21
Q

<p>What are examples of diets high in potassium (>1.1%)?</p>

A

<p>Alfalfa hay<br></br>Molasses<br></br>Electrolyte ysupplements<br></br>Kelp-based supplements<br></br><br></br>**sudden dietary changes</p>

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22
Q

<p>What can precipitate clinical signs of HYPP?</p>

A

<p>**unpredictable<br></br><br></br>Fasting<br></br>Anesthesia or heavy sedation<br></br>Trailer rides<br></br>Stress<br></br>Exposure to cold<br></br>Fasting<br></br>Pregnancy<br></br>Concurrent dz<br></br>Rest following exercise</p>

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23
Q

<p>Clinical episodes of HYPP start as</p>

A

<p>— brief period of myotonia<br></br>Prolapse of third eyelid<br></br>Sweating & muscular fasciculations<br></br><br></br>**muscular weakness is a common characteristic of HYPP</p>

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24
Q

<p>Clinical signs of severe HYPP attacks</p>

A

<p>Apparent weakness with swaying<br></br>Staggering<br></br>Dog sitting <br></br>Recumbency w/in a few minutes<br></br>INC HR and RR</p>

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25
Q

<p>How long do HYPP episodes last?</p>

A

<p>15 to 60 minutes</p>

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26
Q

<p>Respiratory distress can result in HYPP episodes due to:</p>

A

<p>Paralysis of upper respiratory muscles <br></br> ** may require tracehostomy</p>

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27
Q

<p>What is the concern for horses homozygous for HYPP?</p>

A

<p>Dysphagia/respiratory distress</p>

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28
Q

<p>However horses with HYPP may be normal between attacks, does electromyography show any abnormalities?</p>

A

<p>Yes<br></br>* abnormal fibirllation potentials<br></br>Complex repetitive discharges with occasional myotonic potentials & trains of doublets between episodes</p>

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29
Q

<p>What is the exact mutation that leads to HYPP horses?</p>

A

<p>Point mutation that causes a phenylalanine/leucine substitution in voltage- dependent skeletal muscle sodium channel alpha subunit</p>

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30
Q

<p>The result of the mutation in HYPP causes:</p>

A

<p>Resting membrane potential is closer to firing than in normal horses<br></br>- subpopulation of sodium channels inactivate when serum potassium concentrations are increased<br></br> —> excessive inward flux of sodium and outward flux of potassium ensues<br></br> —> results in persistent depolarization of muscle cells and temporary weakness</p>

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31
Q

<p>Does serum concentration of potassium increase in HYPP episodes?</p>

A

<p>6 to 9 mEq/L increase during episode<br></br> ** serum potassium concentration return to normal following abatement of C/S</p>

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32
Q

<p>What are differentials for hyperkalemia?</p>

A

<p>Delay before sample centrifugation<br></br>Hemolysis<br></br>Acidosis<br></br>Renal failure<br></br>Severe rhabdomyolysis<br></br>High-intensity exercise</p>

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33
Q

<p>Treatment options for HYPP episodes</p>

A

<p>Feeding grain/corn syrup to stimualte insulin-mediated movement of potassium across cell membranes<br></br>Epinephrine 0.006 mg/kg/500 kg IM<br></br>Acetazolamide: 3 mg/kg PO every 8 to 12 hours<br></br><br></br>**most recover from episodes of paralysis and appear normal by time a veterinarian arrives</p>

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34
Q

<p>In severe cases of HYPP intravenous treatment with what medications can be used to enhance intracellular movement of potassium?</p>

A

<p>Calcium gluconate: 0.2-0.4 ml/kg of 23% solution in 1 L of 5% dextrose or combinated with sodium bicarbonate (1 to 2 mEq/kg)</p>

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35
Q

<p>How does calcium gluconate assist in treatment of HYPP?</p>

A

<p>Increase in extracellular calcium concentration raises muscle membrane threshold potential— decreasing membrane hyperexcitability</p>

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36
Q

<p>For horses with recurrent episodes of muscle fasciculations with HYPP?</p>

A

<p>Acetazolamide: 2-3 mg/kg PO every 8 to 12 hours<br></br><br></br>Hydrochlorothiazide: 0.5 to 1 mg/kg PO, every 12 hours</p>

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37
Q

<p>Chronic fibrotic myopathy stride</p>

A

<p>Short anterior phase with characteristic hoof-slapping gait</p>

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38
Q

<p>Clinical signs of exertional rhabdomyolysis</p>

A

<p>Develop a stiff, stilted gait, with excessive sweating & high respiratory rate during or after exercise<br></br>- seen 15 to 30 minutes after light exercise<br></br>-firm, painful muscles (back and hind limb mm)<br></br>-myoglobinuria</p>

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39
Q

<p>Sporadic exertional rhabdomyolysis is seen in what population of horses?</p>

A

<p>Any age, breed or sex involved in a wide variety of athletic disciplines</p>

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40
Q

<p>Diagnosis of sporadic exertional rhabdomyolysis</p>

A

<p>History<br></br>C/S<br></br>Elevations of serum muscle enzymes</p>

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41
Q

<p>What are causes of sporadic exertional rhabdomyolysis?</p>

A

<p>Overexertion<br></br>Exhaustion<br></br>Dietary imbalances</p>

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42
Q

<p>What are clinical signs of heat exhaustion?</p>

A

<p>Weakness<br></br>Ataxia<br></br>Rapid breathing<br></br>Muscle fasciculations<br></br>Sweating<br></br>Severe cases of collapse<br></br>Body temp: 105 to 108<br></br>INC Ck activity<br></br>Myoglobinuria</p>

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43
Q

<p>Sporadic forms of exertional rhabdomyolysis due to</p>

A

<p>an extrinsic event or recurring extrinsic events that induce muscle damage with exercise</p>

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44
Q

<p>Causes of sporadic exertional rhabdomyolysis include</p>

A

<p>focal or generalized trauma to muscle<br></br>exercise performed beyond any training adaptation or performed to the point of exhaustion<br></br>dietary imbalances that affect muscle fasciculation</p>

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45
Q

<p>Resolution of sporadic exertional rhabdomyolysis occurs after:</p>

A

<p>-period of rest<br></br>-provision of balanced diet<br></br>-gradual introduction of a training program matched with performance demands</p>

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46
Q

<p>dietary imbalances that can trigger exertional rhabdomyolysis episdoes</p>

A

<p>high nonstructural carbohydrates (NSC) & low forage content<br></br>diets deficient in electrolytes<br></br>+/- exacerbation inadequate selenium/vit E</p>

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47
Q

<p>Horses competing in hot, humid weather what electrolytes require higher concentrations?</p>

A

<p>sodium chloride<br></br> -30 to 50 g/day combined with 15 to 25 g of "lite" salt containing KCL<br></br> -ideal Ca:Phos ratio of 2:1</p>

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48
Q

<p>Reason for administration of dantrium sodium in exertional rhabdoymyolysis?</p>

A

<p>in severely affected horses may decrease muscle contracture sand possible prevent furthe rmuscle necrosis</p>

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49
Q

<p>Overdoing dantrium sodium can lead to?</p>

A

<p>muscle weakness</p>

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50
Q

<p>What are causes of chronic exertional myopathies in horses?</p>

A

<p>Polysaccharide storage myopathy T1<br></br>Polysaccharide storage myopathy T2<br></br>Malignant hyperthermia<br></br>Recurrent exertional rhabdomyolysis<br></br>Idiopathic exertional rhabdomyolysis</p>

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51
Q

<p>Mutation in what gene has shown to be highly associated with the presence of amylase resistant polysaccharide in skeletal muscle from Quarter Horses with PSSM?</p>

A

<p>GYS1 gene <br></br> **glycogen synthetase gene</p>

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52
Q

<p>Do all horses with PSSM have gene mutations in GYS1 gene?</p>

A

<p>No-- <br></br>PSSM type 1- GYS1 gene mutation<br></br>PSSM type 2-- unknown origin</p>

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53
Q

<p>what is the gene mutation at GYS1?</p>

A

<p>single base pair mutation in GYS1 gene resulting in arginine to histidine substitution at codon 309</p>

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54
Q

<p>GYS1 gene mutation in PSSM type 1 horses leads to what functional abnormality?</p>

A

<p>Gain in function in glycogen synthase enzyme= higher than normal activity at basal states & when active by insulin & glucose 6-phosphate <br></br>-->a deficit in energy metabolism</p>

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55
Q

<p>The highest prevalence of PSSM1 appears in what breeds?</p>

A

<p>draft horses derived from Continental European drafts <br></br>-->north american belgians, percherons, trekpaards</p>

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56
Q

<p>what are the prevalence estimates for PSSM1 in quarter horses?</p>

A

<p>6 to 10% Quarterhorses</p>

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57
Q

<p>what is the prevalence of PSSM1 in light horse breeds (arabians, Standardbreds, thoroughbreds)?</p>

A

<p>very low to nonexistent</p>

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58
Q

<p>What are risk factors for the development of clinical signs with PSSM1?</p>

A

<p>exercise (<20 minutes especially)<br></br>Diets high in NSCs<br></br>+/- seasonal incidence<br></br>systemic illness</p>

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59
Q

<p>What is a supportive diagnostic for subclinical exertional rhabdomyolysis is present?</p>

A

<p>lunge for max of 15 minutes-- a minimum of 3-fold increase in CK activity 4 hours after exercise</p>

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60
Q

<p>What are distinctive features of PSSM1 on muscle biopsy?</p>

A

<p>-numerous subsarcolemmal vacuoles<br></br><br></br>-dense crystalline periodic acid-SCHIFF (PAS) positive, amylase resistant inclusions</p>

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61
Q

<p>When can false-positives for PSSM1 occur on muscle biopsy?</p>

A

<p>small muscle biopsies<br></br>horses <1 yr of age</p>

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62
Q

<p>What is the gold standard diagnosis for PSSM1?</p>

A

<p>genetic testing for GSY1 mutation-- whole blood or hair root samples</p>

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63
Q

<p>What age range do clinical signs of PSSM1 appear?</p>

A

<p>at 5 years of age (range 1-14 yrs)</p>

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64
Q

<p>In an acute episode of exertional rhabdomyolysis associated with PSSm1, elevations of CK are greater than?</p>

A

<p>35,00 U/L CK<br></br>**myoglobinuria present</p>

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65
Q

<p>What other gene mutation can cause severe clinical signs of exertional rhabdomyolysis with GSY1 mutation?</p>

A

<p>RYR1 mutation for malignant hyperthermia<br></br>**small number of Quarterhorses and paints</p>

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66
Q

<p>Are draft horses with PSSM clinical?</p>

A

<p>No-- asymptompatic</p>

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67
Q

<p>what is the average age that drafts are diagnosed with PSSM?</p>

A

<p>8 years old</p>

68
Q

<p>What are the median serum CK and AST activities in draft horses from which biopsies were sent to the Equine Neuromuscular DIagnostic laboratory:</p>

A

<p>Ck: 459 U/L<br></br>AST: 537 U/L</p>

69
Q

<p>In theory, why does feeding high nonstructural carbohydrate diets to PSSM horses lead to the development of muscle pain?</p>

A

<p>Nutrient switches do not fully activate enzymes such as pyruvate dehydrogenase during exercise, limiting adequate acetyl-CoA for oxidative metabolism, thus<br></br><br></br>**do not generate enough Acetyl-CoA to from either carbohydrate or or fat metabolism to fuel muscle contraction during submaximal exercise</p>

70
Q

<p>What is the prevalence of PSSM2?</p>

A

<p>approximately 28% of cases of PSSM diagnosed by muscle biopsy in Quarterhorses (that do not have GYS1 mutation)</p>

71
Q

<p>What is the prevalence of cases of PSSM that are warm bloods that have PSSM2?</p>

A

<p>Approximately 80%</p>

72
Q

<p>What abnormality is seen in PSSM2 on muscle biopsy?</p>

A

<p>increase in normal beta glycogen particles</p>

73
Q

<p>Acute cases of PSSM2 resemble</p>

A

<p>exertional rhabdomyolysis in QH, Thghbd, Stdbreds & Arabians<br></br><br></br>intermittent exertional rhabdomyolysis in warmbloods</p>

74
Q

<p>Chronic signs of PSSM2</p>

A

<p>**related to poor performance: undiagnosed gait abnormality, sore mm & drop in energy level & willingness to perform after 5 to 10 minutes of exercise</p>

75
Q

<p>Do chronic cases of PSSM2 have marked elevated CK/AST values?</p>

A

<p>No--average warmblood: CK: 323 U/L, AST: 331 U/L)</p>

76
Q

<p>What is diagnostic for PSSM2 on muscle biopsy?</p>

A

<p>abnormal amount of amylase-sensitive glycogen= subjective<br></br>specificity= low<br></br>false-positive results likely occur</p>

77
Q

<p>What percentage of horses diagnosed with PSSM1/PSSM2 show notable clinical improvement and return to acceptable levels of performance?</p>

A

<p>70%<br></br>**when adhere to diet and exercise regimen**</p>

78
Q

<p>How much stall confinement should horses with PSSM have?</p>

A

<p>less than 48 hours after an episode of rhabdomyolysis, then increase turnout in pastures increasing in size gradually</p>

79
Q

<p>The beneficial response to low-starch, fat supplemented diets only occur when in conjunction with??</p>

A

<p>a regular incremental exercise program</p>

80
Q

<p>What are important principles to follow when starting exercise programs in PSSM horses?</p>

A

<p>1. provide adequate time for adaptation to a new diet before commencing exercise<br></br>2. recognize that the duration of exercise, not its intensity is of primary importance<br></br>3. ensure the program is gradually introduced and consistently performed<br></br>4. minimize any days without some form of exercise</p>

81
Q

<p>When instituting an exercise program, is it beneficial to recheck serum CK levels in PSSM horses?</p>

A

<p>No, not unless overt episode of rhabdomyolysis<br></br><br></br>** common to have subclinical elevations in CK activity when exercise is reintroduced and return to normal levels requiring 4 to 6 weeks of gradual exercise</p>

82
Q

<p>What is the basis for diet change of lowering daily starch and sugar intake & increasing dietary fiber content in diets of PSSM horses?</p>

A

<p>-Will decrease glucose load<br></br>-Increase availability of non-esterified fatty acid for muscle metabolism<br></br>-lower serum insulin concentration</p>

83
Q

<p>Selecting hay with what percent of NSC for PSSM horses and why?</p>

A

<p>12% or less (+/- room for fat in diet)<br></br>--> because insulin stimulates the already overactive enzyme glycogen synthase in muscle of PSSM1 horses</p>

84
Q

<p>What form of fat in diet is best for PSSM horses?</p>

A

<p>long chain fat diets</p>

85
Q

<p>What are examples of acceptable fat supplementation in horses with PSSM?</p>

A

<p>rice bran<br></br>animal based fat (tallow, lard, fish oil)<br></br>Vegetable oils</p>

86
Q

<p>NSC goal for low starch, high fat concentrate feeds for horses with PSSM?</p>

A

<p>calories supplied byNSC no more than 10-15% of daily DE <br></br>calories supplied by fat comprise 12-15% daily DE</p>

87
Q

<p>Myofibrillar myopathy clinical signs</p>

A

<p>exercise intolerance or intermittent exertional rhabdomyolysis<br></br><br></br>-lack of stamina, unwillingnes to go forward, inability to collect, abnomral canter transitions, inability to sustain a normal canter, unresolved lamness, stiffness, mm pain</p>

88
Q

<p>Myofibrillar myopathy breed predilection?</p>

A

<p>warm blood horses (6-8 years age)</p>

89
Q

<p>Myofibrillar myopathy on muscle biopsy?</p>

A

<p>cytoplasmic aggregates of cytoskeletal protein desmin scattered muscle fibers<br></br><br></br>(**desmin aligns sarcomeres at Z-dsic & tether them to cell membrane**)</p>

90
Q

<p>Myofibrillar myopathy horses management recommendations</p>

A

<p>**similar to PSSM2<br></br>** no information to suggesting limiting NSC or addition of fat is necessarily beneficial</p>

91
Q

<p>Define recurrent exertional rhabdomyolysis (RER)</p>

A

<p>subset of exertional rhabdomyolysis is believed to be due to an abnormality in regulation of muscle contraction and relaxation</p>

92
Q

<p>Recurrent exertional rhabdomyolysis usually occurs in what phases of exercise?</p>

A

<p>When the horse is held back to a paced speed (ie: racetrack, ER commonly occurs when RER horses are held back to paced gallop)</p>

93
Q

<p>What is believed to be the pathogenesis of recurrent exertional rhabdomyolysis?</p>

A

<p>intrinsic abnormality in intramuscular calcium regulation</p>

94
Q

<p>Risk factors for RER</p>

A

<p>temperament (nervous temperament)<br></br>diet (thghbd fed >2.5 kg grain/day more likely C/S RER)<br></br>rest before exercise</p>

95
Q

<p>Is there a genetic basis for recurrent exertional rhabdomyolysis?</p>

A

<p>There is not one identified</p>

96
Q

<p>What management factors need to be managed in horses with RER?</p>

A

<p>environment<br></br>exercise regimen<br></br>diet</p>

97
Q

<p>Is muscle biopsy diagnostic in RER?</p>

A

<p>No<br></br>-- best to rule out other causes of exertional rhabdomyolysis</p>

98
Q

<p>Environmental management for RER is aimed towards:</p>

A

<p>reducing stressful environments<br></br><br></br>(**ie: providing daily turnout with other horses**)</p>

99
Q

<p>Is rest recommended for horses with RER?</p>

A

<p>No</p>

100
Q

<p>What forage should horses with RER recieve?</p>

A

<p>may or may not be as important to select hay with low NSC like in PSSM horses</p>

101
Q

<p>What is the concentrate recommendation for RER horses?</p>

A

<p>low-starch, high-fat concentrates</p>

102
Q

<p>Are supplements containing sodium bicarbonate, B vitamins, branched-chain amino acids and dimethylglycine, have any benefit for horses with RER?</p>

A

<p>no b/c lactic acidosis is no longer implicated as a cause of rhabdomyolysis</p>

103
Q

<p>Dantrium sodium MOA</p>

A

<p>decreases release of calcium from ryanodine receptor in skeletal mm<br></br>**tx malignant hyperthermia</p>

104
Q

<p>Besides malignant hyperthermia dantrium sodium can be used to treat:</p>

A

<p>RER<br></br>** controlled & field studies have shown a decrease in rhabdomyolysis in RER horses<br></br>**MUST BE WITHDRAWN BEFORE COMPETITION**</p>

105
Q

<p>Phenytoin MOA</p>

A

<p>monoaminoxidase activator<br></br>acts on number of ion channels /win mm and nerves (sodium& calcium)</p>

106
Q

<p>What is an undesirable effect of phenytoin?</p>

A

<p>drowsiness and ataxia at high doses<br></br>**if seen, reduce dose by half</p>

107
Q

<p>Genetic mutation resulting in malignant hyperthermia in Quarter horses and paints</p>

A

<p>autosomal dominant mutation that exists in exon 46 of skeletal mm RYR1 gene on ECA 10</p>

108
Q

<p>What is the prevalence of malignant hyperthermia in Quarter horses and paints?</p>

A

<p>less than 1 % (rare)</p>

109
Q

<p>What are risk factors for malignant hyperthermia episodes?</p>

A

<p>exercise<br></br>anesthesia<br></br>** episodes can be intermittent in nature**</p>

110
Q

<p>Horses with GYS1 mutation and RYR1 mutation show what clinical signs?</p>

A

<p>more severe episodes of exertional rhabdomyolysis<br></br>higher serum CK activity after exercise<br></br>moderated response to diet/exercise regimens for PSSM1</p>

111
Q

<p>Is muscle biopsy beneficial for diagnosing malignant hyperthermia?</p>

A

<p>No</p>

112
Q

<p>How do you diagnose malignant hyperthermia?</p>

A

<p>genetic testing</p>

113
Q

<p>what is the treatment for malignant hyperthermia?</p>

A

<p>malignant hyperthermia episodes are so intermittent that hard to justify premed with dantrolene prior to exercise</p>

114
Q

Define muscle contracture

A

Fixation of myofilaments in a persistently shortened position w/o neural input — usu. assoc with rhabdomyolysis

115
Q

Profound muscle weakness can occur in what disorders?

A

-neuropathies affecting motor neurons: equine motor neuron disease, hypoocalcemia-decreased neural input at motor end plates: botulism-marked muscle atrophy: EMNDRhabdomyolysis of postural muscles-severe electorlyte imbalances (hypokalemia)

116
Q

Definition of muscle atrophy

A

Reduction in muscle size **specifically reduction in mm fiber diameter or cross-sectional area **occurs in response to variety of stimuli

117
Q

Denervation to muscle causes:

A

Removes normal low-level tonic neural stimulus that is necessary to maintain muscle fiber mass

118
Q

Complete denervation of muscle results in more than what percent loss of muscle w/in a 2 to 3 week period

A

50% loss of muscle mass

119
Q

Reasons for muscle atrophy:

A

-denervation-disuse-malnutrition-cachexia-corticosteroid excess-immune-mediated myositis

120
Q

Rapid muscle atrophy is characteristic of what type of myopathy?

A

Immune-mediated myopathies

121
Q

Muscle necrosis is represented by

A

Injury to organelles w/in a muscle fiber or within a segment of that fiber

122
Q

Pathogenesis of rhabdomyolysis and muscle necrosis

A

Generalized rhabdoyolysis — interrupt normal muscle metabolism — cell death results form inability to maintain homeostasis w/in the myofiber

123
Q

Besides rhabdomyolysis, what other muscle disorders may lead to muscle necrosis

A

Lipid storage disordersAntioxidant deficiences

124
Q

Infectious causes of nonexertional myopathies in horses

A

ViralSarcocystis fayeriAnaplasma phagocytophilumStreptococcus equiClostridium sppAbscesses

125
Q

Immune mediated causes of nonexertional myopathies in horses

A

Infarctive purpura hemorrhagicaImmune-mediated myositis

126
Q

Nutritional myopathies of nonexertional myopathies in horses

A

Nutritional myodengerationSelenium deficiency, Vit E deficiencyVit E- deficient myopathy

127
Q

Toxic myopathies of nonexertional myopathies in horses

A

Feed contaminantsIonophoresPlant toxinsRematonesHypoglycin A

128
Q

Examples of traumatic or anesthetic causes of nonexertional myopathies in horses:

A

Focal muscle strainFibrotic myopathyPostanesthetic myopathy

129
Q

Examples of muscle cramping of nonexertional myopathies in horses

A

Electrolyte disturbancesHypocalcemiaSynchronous diaphragmatic flutterEar ticksShivers

130
Q

Examples of myotonia, nonexertional myopathies in horses

A

Myotonia congenitaMyotonia dystrophicaHyperkaelmic periodic paralysis

131
Q

Examples of Genetic, nonexertional myopathies in horses

A

Glycogenic branching enzyme deficiencyPolysaccharide storage myopathy type 1Polysaccharide storage myopathy type 2Malignant hyperthermia

132
Q

Classification of Exertional Myopathies in horses

A
  1. Focal muscle strain2. Sproadic exertional rhabdomyolysis dietary imbalances Vit E, selenium, electrolytes exercise in excess of training exhaustion3. Chronic exertional rhabdomyolysis PSSM type.1 & type 2 Malignant hyperthermia recurrent exertional rhabdomyolysis idiopathic exertional rhabdomyolysis
133
Q

Classification of myopathies in food animals

A
  1. Infectious clostridium sarcocystis2. Nutritional selenium, vit E hypokalemia3. Toxic feed additives, ionophores plants Gossypol, cassia, white snakeroot chemical4. Traumatic muscle crush syndrome5. Genetic caprine myotonia Bovine pseudomyotonia porcine malignant hyperthermia bovine and ovine myophophorylase deficiency porcine (RN (-)) glycogen storage disease
134
Q

Mitochondrial myopathy case report in arabian filly cause

A

deficiency of complex I (first step in mitochondrial respiratory chain)

135
Q

What were the biochemical assay changes with mitochondrial myopathy?

A

increased lactic acidosis with light exercise**no changes in CK

136
Q

What clinical signs of mitochondrial myopathy were reported in case report of arabian filly?

A

progressive signs of muscle atrophymarked exercise intolerance

137
Q

Define glycogen branching enzyme deficiency

A

glycogen storage disorder causing abortion, seizures and mm weakness in QH-related breeds

138
Q

What is the genetic mutation resulting in GBED?

A

nonsense mutation in exon 1 of the GBE1 gene at codon 102 (introduces a premature stop codon)

139
Q

What is the prevalence of carriers for GBED?

A

9% of Quarterhorses

140
Q

What percentage of horses show a higher prevalence of GBED?

A

pleasure horses (26%)

141
Q

Glycogen branching enzyme deficiency clinical signs in foals:

A

hypothermiaweaknessflexural deformities of all limbsventilatory failurerecurrent hypoglycemia & collapse

142
Q

What is the confirmatory diagnostic in GBED foals?

A

genetic mutation in tissue samples or by identifying typical PAS-positive inclusions in muscle or cardiac samples

143
Q

Are there gross abnormalities in GBED foals at necropsy?

A

No

144
Q

What is the muscle disease identified in charolais cattle?

A

deficiency in the enzyme Myophosphorylase (McArdle’s disease)

145
Q

C/S with phosphorylase deficiency in charolais cattle?

A

exercise intolerance and collapse (when forced to exercise)

146
Q

When should phosphorylase deficiency be considered as a differential?

A

In white muscle disease animals with normal vit E/ selenium deficiency?

147
Q

What other spp see a phosphorylase deficiency than charolais cattle?

A

Sheep in Australia

148
Q

Clinical signs of pseudomyotonia in cattle?

A

exercise induced muscle stiffness with normal response to percussion**delayed mm relaxation

149
Q

Pseudomyotonia in cattle has been identified in waht breeds?

A

chianinadutch improved red & white crossbreed heifer

150
Q

What is the genetic disorder in Hampshire pigs that reduces meat quality in pigs by increasing glycogen content of muscle?

A

porcine (RN-) glycogen storage disease

151
Q

Muscle cramps arise from

A

Hyperactivity of motor units caused by repetitive firing of the peripheral and/or central nervous system

152
Q

Muscle cramps can be induced by:

A

-Forceful contraction of a shortened muscle -changes in electrolyte composition of extracellular fluid-ear tick infestations in horses

153
Q

Define muscle contracture

A

Painful muscle spasms that represent a stage of muscle contracture unaccompanied by depolarization of the muscle membraneoccur with malignant hyperthermia

154
Q

What are the most common dietary electrolyte deficiencies that cause muscle stiffness, weakness and occasional elevations in mm CK?

A

SodiumPotassium

155
Q

Why is supplementation of the equine diet with sodium necessary?

A

Because forage & grain diets are low in sodium and chloride & high in potassium

156
Q

define muscle stiffness

A

generalized restriction in freedom of movement in a limb, the neck or back
**manifested by limited range of motion by a joint, reduced length of stride or decreased flexibility during bending or turning

157
Q

define plaiting

A

adduction of the lame limb directly in front of or lateral to the opposite limb
–forelimb: commonly assoc with conformational abnormal
hindlimbs– commonly assoc with lameness

158
Q

Nerve block: palmar (plant) digital nerve block

nerves affected:
Structures desensitized

A

nerves affected: palmar (plantar) digital

structures desensitized: heel bulbs, frog, bars, navicular bone and bursa, palmar regions of the third phalanx, distal interphalangeal joint, sole and soft tissues

159
Q

Nerve block: abaxial sesamoid

nerves affected:
Structures desensitized

A

nerves affected: palmar (plantar)

structures desensitized: coronary band, interphalangeal joints, lamellar and solar corium

160
Q

Nerve block: low palmar

nerves affected:
Structures desensitized

A

nerves affected: palmar, palmar metacarpal

structures desensitized: skin of meidal and lateral pastern, metacarpophalangeal joint, proximal sesamoids, flexor tendons, tendon sheath

161
Q

Nerve block: high palmar

nerves affected:
Structures desensitized

A

nerves affected: palmar, palmar metacarpal

structures desensitized: skin and deep structures of palmar cannon region (flexor tendons, suspensory ligament except origin, interosseous ligaments of splint bones)

162
Q

overflexion of the hock means
overextension of the hock means

A

overflexion: gastrocnemius rupture
overextension: peroneus tertius

163
Q

define muscle spasms

A

sudden, transient and involuntary contractions of a single muscle or group of muscles, attended by pain or loss of function

164
Q

define cramp

A

painful, tonic, spasmodic muscular contraction

165
Q

define myoglonus

A

a disturbance of neuromuscular activity characterized by abrupt, brief, rapid, jerky, arrhythmic, asynergic, involuntary contractions involving portions of muscles, entire muscles or groups of muscles, regardless of their functional association
**disappears in sleep

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