Muscle disorders Flashcards
<p>Spastic paresis is seen in what age calves? And manifests as:</p>
<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>
<p>What is a similar condition to spastic paresis in calves seen in horses?</p>
<p>Shivers</p>
<p>Shivers is seen in horses of what breed/size typically</p>
<p>Draft breeds, warmbloods and warmblood crosses older than 1 yr of age<br></br><br></br>**usually taller than 16.3 hands</p>
<p>Define myotonia</p>
<p>Prolonged contraction of mm contraction</p>
<p>Clinical signs of shivers:</p>
<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>
<p>Myotonic muscle disorders share the feature of what?</p>
<p>Delayed relaxation of muscle after mechanical stimulation or voluntary contraction<br></br><br></br>**abnormal muscle membrane excitability</p>
<p>Appearance of myotonia congenita in horses</p>
<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>
<p>Is there progression of myotonia congenita in horses?</p>
<p>Not beyond 6 to 12 months of age</p>
<p>In goats what is the inheritance of myotonia congenita?</p>
<p>Autosomal dominant mutation in skeletal muscle chloride channel (CLCN1) that is incoplete penetrance</p>
<p>Myotonia dystrophica is separate from myotonia congenita in horses. What are the differences?</p>
<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>
<p>What is the definitive diagnosis of myotonia in horses?</p>
<p>Based on electromyographic examination</p>
<p>Examination of muscle biopsies from foals with myotonia congenita show:</p>
<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>
<p>Changes in muscle biopsy seen with myotonic dystrophy</p>
<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>
<p>What are the treatment recommendations of myotonia?</p>
<p>No treatment</p>
<p>Myotonia prognosis</p>
<p>Variable & dependent on clinical signs<br></br> **regression of C/S unknown <br></br> ** euthanasia often warranted</p>
<p>Is myotonia congenital?</p>
<p>Unknown<br></br>**warn owners of possibility of this disease is heritable</p>
<p>Equine hyperkalemic periodic paralysis (HYPP) is caused by:</p>
<p>Inherited defect in the skeletal mm sodium channel</p>
<p>Equine HYPP manifests as</p>
<p>Abnormal skeletal mm membrane excitability leading to episodes of myotonia or sustained mm contraction and paralysis</p>
<p>How is HYPP inherited in horses?</p>
<p>Autosomal dominant trait in Quarterhorses, American Paint Horses, Appaloosas & QH horse crossbreeds</p>
<p>In HYPP, intermittent clinical signs start at what age?</p>
<p>2 to 3 years of age with no apparent abnormalities between episodes</p>
<p>What are examples of diets high in potassium (>1.1%)?</p>
<p>Alfalfa hay<br></br>Molasses<br></br>Electrolyte ysupplements<br></br>Kelp-based supplements<br></br><br></br>**sudden dietary changes</p>
<p>What can precipitate clinical signs of HYPP?</p>
<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>
<p>Clinical episodes of HYPP start as</p>
<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>
<p>Clinical signs of severe HYPP attacks</p>
<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>
<p>How long do HYPP episodes last?</p>
<p>15 to 60 minutes</p>
<p>Respiratory distress can result in HYPP episodes due to:</p>
<p>Paralysis of upper respiratory muscles <br></br> ** may require tracehostomy</p>
<p>What is the concern for horses homozygous for HYPP?</p>
<p>Dysphagia/respiratory distress</p>
<p>However horses with HYPP may be normal between attacks, does electromyography show any abnormalities?</p>
<p>Yes<br></br>* abnormal fibirllation potentials<br></br>Complex repetitive discharges with occasional myotonic potentials & trains of doublets between episodes</p>
<p>What is the exact mutation that leads to HYPP horses?</p>
<p>Point mutation that causes a phenylalanine/leucine substitution in voltage- dependent skeletal muscle sodium channel alpha subunit</p>
<p>The result of the mutation in HYPP causes:</p>
<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>
<p>Does serum concentration of potassium increase in HYPP episodes?</p>
<p>6 to 9 mEq/L increase during episode<br></br> ** serum potassium concentration return to normal following abatement of C/S</p>
<p>What are differentials for hyperkalemia?</p>
<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>
<p>Treatment options for HYPP episodes</p>
<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>
<p>In severe cases of HYPP intravenous treatment with what medications can be used to enhance intracellular movement of potassium?</p>
<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>
<p>How does calcium gluconate assist in treatment of HYPP?</p>
<p>Increase in extracellular calcium concentration raises muscle membrane threshold potential— decreasing membrane hyperexcitability</p>
<p>For horses with recurrent episodes of muscle fasciculations with HYPP?</p>
<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>
<p>Chronic fibrotic myopathy stride</p>
<p>Short anterior phase with characteristic hoof-slapping gait</p>
<p>Clinical signs of exertional rhabdomyolysis</p>
<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>
<p>Sporadic exertional rhabdomyolysis is seen in what population of horses?</p>
<p>Any age, breed or sex involved in a wide variety of athletic disciplines</p>
<p>Diagnosis of sporadic exertional rhabdomyolysis</p>
<p>History<br></br>C/S<br></br>Elevations of serum muscle enzymes</p>
<p>What are causes of sporadic exertional rhabdomyolysis?</p>
<p>Overexertion<br></br>Exhaustion<br></br>Dietary imbalances</p>
<p>What are clinical signs of heat exhaustion?</p>
<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>
<p>Sporadic forms of exertional rhabdomyolysis due to</p>
<p>an extrinsic event or recurring extrinsic events that induce muscle damage with exercise</p>
<p>Causes of sporadic exertional rhabdomyolysis include</p>
<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>
<p>Resolution of sporadic exertional rhabdomyolysis occurs after:</p>
<p>-period of rest<br></br>-provision of balanced diet<br></br>-gradual introduction of a training program matched with performance demands</p>
<p>dietary imbalances that can trigger exertional rhabdomyolysis episdoes</p>
<p>high nonstructural carbohydrates (NSC) & low forage content<br></br>diets deficient in electrolytes<br></br>+/- exacerbation inadequate selenium/vit E</p>
<p>Horses competing in hot, humid weather what electrolytes require higher concentrations?</p>
<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>
<p>Reason for administration of dantrium sodium in exertional rhabdoymyolysis?</p>
<p>in severely affected horses may decrease muscle contracture sand possible prevent furthe rmuscle necrosis</p>
<p>Overdoing dantrium sodium can lead to?</p>
<p>muscle weakness</p>
<p>What are causes of chronic exertional myopathies in horses?</p>
<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>
<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>
<p>GYS1 gene <br></br> **glycogen synthetase gene</p>
<p>Do all horses with PSSM have gene mutations in GYS1 gene?</p>
<p>No-- <br></br>PSSM type 1- GYS1 gene mutation<br></br>PSSM type 2-- unknown origin</p>
<p>what is the gene mutation at GYS1?</p>
<p>single base pair mutation in GYS1 gene resulting in arginine to histidine substitution at codon 309</p>
<p>GYS1 gene mutation in PSSM type 1 horses leads to what functional abnormality?</p>
<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>
<p>The highest prevalence of PSSM1 appears in what breeds?</p>
<p>draft horses derived from Continental European drafts <br></br>-->north american belgians, percherons, trekpaards</p>
<p>what are the prevalence estimates for PSSM1 in quarter horses?</p>
<p>6 to 10% Quarterhorses</p>
<p>what is the prevalence of PSSM1 in light horse breeds (arabians, Standardbreds, thoroughbreds)?</p>
<p>very low to nonexistent</p>
<p>What are risk factors for the development of clinical signs with PSSM1?</p>
<p>exercise (<20 minutes especially)<br></br>Diets high in NSCs<br></br>+/- seasonal incidence<br></br>systemic illness</p>
<p>What is a supportive diagnostic for subclinical exertional rhabdomyolysis is present?</p>
<p>lunge for max of 15 minutes-- a minimum of 3-fold increase in CK activity 4 hours after exercise</p>
<p>What are distinctive features of PSSM1 on muscle biopsy?</p>
<p>-numerous subsarcolemmal vacuoles<br></br><br></br>-dense crystalline periodic acid-SCHIFF (PAS) positive, amylase resistant inclusions</p>
<p>When can false-positives for PSSM1 occur on muscle biopsy?</p>
<p>small muscle biopsies<br></br>horses <1 yr of age</p>
<p>What is the gold standard diagnosis for PSSM1?</p>
<p>genetic testing for GSY1 mutation-- whole blood or hair root samples</p>
<p>What age range do clinical signs of PSSM1 appear?</p>
<p>at 5 years of age (range 1-14 yrs)</p>
<p>In an acute episode of exertional rhabdomyolysis associated with PSSm1, elevations of CK are greater than?</p>
<p>35,00 U/L CK<br></br>**myoglobinuria present</p>
<p>What other gene mutation can cause severe clinical signs of exertional rhabdomyolysis with GSY1 mutation?</p>
<p>RYR1 mutation for malignant hyperthermia<br></br>**small number of Quarterhorses and paints</p>
<p>Are draft horses with PSSM clinical?</p>
<p>No-- asymptompatic</p>
<p>what is the average age that drafts are diagnosed with PSSM?</p>
<p>8 years old</p>
<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>
<p>Ck: 459 U/L<br></br>AST: 537 U/L</p>
<p>In theory, why does feeding high nonstructural carbohydrate diets to PSSM horses lead to the development of muscle pain?</p>
<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>
<p>What is the prevalence of PSSM2?</p>
<p>approximately 28% of cases of PSSM diagnosed by muscle biopsy in Quarterhorses (that do not have GYS1 mutation)</p>
<p>What is the prevalence of cases of PSSM that are warm bloods that have PSSM2?</p>
<p>Approximately 80%</p>
<p>What abnormality is seen in PSSM2 on muscle biopsy?</p>
<p>increase in normal beta glycogen particles</p>
<p>Acute cases of PSSM2 resemble</p>
<p>exertional rhabdomyolysis in QH, Thghbd, Stdbreds & Arabians<br></br><br></br>intermittent exertional rhabdomyolysis in warmbloods</p>
<p>Chronic signs of PSSM2</p>
<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>
<p>Do chronic cases of PSSM2 have marked elevated CK/AST values?</p>
<p>No--average warmblood: CK: 323 U/L, AST: 331 U/L)</p>
<p>What is diagnostic for PSSM2 on muscle biopsy?</p>
<p>abnormal amount of amylase-sensitive glycogen= subjective<br></br>specificity= low<br></br>false-positive results likely occur</p>
<p>What percentage of horses diagnosed with PSSM1/PSSM2 show notable clinical improvement and return to acceptable levels of performance?</p>
<p>70%<br></br>**when adhere to diet and exercise regimen**</p>
<p>How much stall confinement should horses with PSSM have?</p>
<p>less than 48 hours after an episode of rhabdomyolysis, then increase turnout in pastures increasing in size gradually</p>
<p>The beneficial response to low-starch, fat supplemented diets only occur when in conjunction with??</p>
<p>a regular incremental exercise program</p>
<p>What are important principles to follow when starting exercise programs in PSSM horses?</p>
<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>
<p>When instituting an exercise program, is it beneficial to recheck serum CK levels in PSSM horses?</p>
<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>
<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>
<p>-Will decrease glucose load<br></br>-Increase availability of non-esterified fatty acid for muscle metabolism<br></br>-lower serum insulin concentration</p>
<p>Selecting hay with what percent of NSC for PSSM horses and why?</p>
<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>
<p>What form of fat in diet is best for PSSM horses?</p>
<p>long chain fat diets</p>
<p>What are examples of acceptable fat supplementation in horses with PSSM?</p>
<p>rice bran<br></br>animal based fat (tallow, lard, fish oil)<br></br>Vegetable oils</p>
<p>NSC goal for low starch, high fat concentrate feeds for horses with PSSM?</p>
<p>calories supplied byNSC no more than 10-15% of daily DE <br></br>calories supplied by fat comprise 12-15% daily DE</p>
<p>Myofibrillar myopathy clinical signs</p>
<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>
<p>Myofibrillar myopathy breed predilection?</p>
<p>warm blood horses (6-8 years age)</p>
<p>Myofibrillar myopathy on muscle biopsy?</p>
<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>
<p>Myofibrillar myopathy horses management recommendations</p>
<p>**similar to PSSM2<br></br>** no information to suggesting limiting NSC or addition of fat is necessarily beneficial</p>
<p>Define recurrent exertional rhabdomyolysis (RER)</p>
<p>subset of exertional rhabdomyolysis is believed to be due to an abnormality in regulation of muscle contraction and relaxation</p>
<p>Recurrent exertional rhabdomyolysis usually occurs in what phases of exercise?</p>
<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>
<p>What is believed to be the pathogenesis of recurrent exertional rhabdomyolysis?</p>
<p>intrinsic abnormality in intramuscular calcium regulation</p>
<p>Risk factors for RER</p>
<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>
<p>Is there a genetic basis for recurrent exertional rhabdomyolysis?</p>
<p>There is not one identified</p>
<p>What management factors need to be managed in horses with RER?</p>
<p>environment<br></br>exercise regimen<br></br>diet</p>
<p>Is muscle biopsy diagnostic in RER?</p>
<p>No<br></br>-- best to rule out other causes of exertional rhabdomyolysis</p>
<p>Environmental management for RER is aimed towards:</p>
<p>reducing stressful environments<br></br><br></br>(**ie: providing daily turnout with other horses**)</p>
<p>Is rest recommended for horses with RER?</p>
<p>No</p>
<p>What forage should horses with RER recieve?</p>
<p>may or may not be as important to select hay with low NSC like in PSSM horses</p>
<p>What is the concentrate recommendation for RER horses?</p>
<p>low-starch, high-fat concentrates</p>
<p>Are supplements containing sodium bicarbonate, B vitamins, branched-chain amino acids and dimethylglycine, have any benefit for horses with RER?</p>
<p>no b/c lactic acidosis is no longer implicated as a cause of rhabdomyolysis</p>
<p>Dantrium sodium MOA</p>
<p>decreases release of calcium from ryanodine receptor in skeletal mm<br></br>**tx malignant hyperthermia</p>
<p>Besides malignant hyperthermia dantrium sodium can be used to treat:</p>
<p>RER<br></br>** controlled & field studies have shown a decrease in rhabdomyolysis in RER horses<br></br>**MUST BE WITHDRAWN BEFORE COMPETITION**</p>
<p>Phenytoin MOA</p>
<p>monoaminoxidase activator<br></br>acts on number of ion channels /win mm and nerves (sodium& calcium)</p>
<p>What is an undesirable effect of phenytoin?</p>
<p>drowsiness and ataxia at high doses<br></br>**if seen, reduce dose by half</p>
<p>Genetic mutation resulting in malignant hyperthermia in Quarter horses and paints</p>
<p>autosomal dominant mutation that exists in exon 46 of skeletal mm RYR1 gene on ECA 10</p>
<p>What is the prevalence of malignant hyperthermia in Quarter horses and paints?</p>
<p>less than 1 % (rare)</p>
<p>What are risk factors for malignant hyperthermia episodes?</p>
<p>exercise<br></br>anesthesia<br></br>** episodes can be intermittent in nature**</p>
<p>Horses with GYS1 mutation and RYR1 mutation show what clinical signs?</p>
<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>
<p>Is muscle biopsy beneficial for diagnosing malignant hyperthermia?</p>
<p>No</p>
<p>How do you diagnose malignant hyperthermia?</p>
<p>genetic testing</p>
<p>what is the treatment for malignant hyperthermia?</p>
<p>malignant hyperthermia episodes are so intermittent that hard to justify premed with dantrolene prior to exercise</p>
Define muscle contracture
Fixation of myofilaments in a persistently shortened position w/o neural input — usu. assoc with rhabdomyolysis
Profound muscle weakness can occur in what disorders?
-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)
Definition of muscle atrophy
Reduction in muscle size **specifically reduction in mm fiber diameter or cross-sectional area **occurs in response to variety of stimuli
Denervation to muscle causes:
Removes normal low-level tonic neural stimulus that is necessary to maintain muscle fiber mass
Complete denervation of muscle results in more than what percent loss of muscle w/in a 2 to 3 week period
50% loss of muscle mass
Reasons for muscle atrophy:
-denervation-disuse-malnutrition-cachexia-corticosteroid excess-immune-mediated myositis
Rapid muscle atrophy is characteristic of what type of myopathy?
Immune-mediated myopathies
Muscle necrosis is represented by
Injury to organelles w/in a muscle fiber or within a segment of that fiber
Pathogenesis of rhabdomyolysis and muscle necrosis
Generalized rhabdoyolysis — interrupt normal muscle metabolism — cell death results form inability to maintain homeostasis w/in the myofiber
Besides rhabdomyolysis, what other muscle disorders may lead to muscle necrosis
Lipid storage disordersAntioxidant deficiences
Infectious causes of nonexertional myopathies in horses
ViralSarcocystis fayeriAnaplasma phagocytophilumStreptococcus equiClostridium sppAbscesses
Immune mediated causes of nonexertional myopathies in horses
Infarctive purpura hemorrhagicaImmune-mediated myositis
Nutritional myopathies of nonexertional myopathies in horses
Nutritional myodengerationSelenium deficiency, Vit E deficiencyVit E- deficient myopathy
Toxic myopathies of nonexertional myopathies in horses
Feed contaminantsIonophoresPlant toxinsRematonesHypoglycin A
Examples of traumatic or anesthetic causes of nonexertional myopathies in horses:
Focal muscle strainFibrotic myopathyPostanesthetic myopathy
Examples of muscle cramping of nonexertional myopathies in horses
Electrolyte disturbancesHypocalcemiaSynchronous diaphragmatic flutterEar ticksShivers
Examples of myotonia, nonexertional myopathies in horses
Myotonia congenitaMyotonia dystrophicaHyperkaelmic periodic paralysis
Examples of Genetic, nonexertional myopathies in horses
Glycogenic branching enzyme deficiencyPolysaccharide storage myopathy type 1Polysaccharide storage myopathy type 2Malignant hyperthermia
Classification of Exertional Myopathies in horses
- 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
Classification of myopathies in food animals
- 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
Mitochondrial myopathy case report in arabian filly cause
deficiency of complex I (first step in mitochondrial respiratory chain)
What were the biochemical assay changes with mitochondrial myopathy?
increased lactic acidosis with light exercise**no changes in CK
What clinical signs of mitochondrial myopathy were reported in case report of arabian filly?
progressive signs of muscle atrophymarked exercise intolerance
Define glycogen branching enzyme deficiency
glycogen storage disorder causing abortion, seizures and mm weakness in QH-related breeds
What is the genetic mutation resulting in GBED?
nonsense mutation in exon 1 of the GBE1 gene at codon 102 (introduces a premature stop codon)
What is the prevalence of carriers for GBED?
9% of Quarterhorses
What percentage of horses show a higher prevalence of GBED?
pleasure horses (26%)
Glycogen branching enzyme deficiency clinical signs in foals:
hypothermiaweaknessflexural deformities of all limbsventilatory failurerecurrent hypoglycemia & collapse
What is the confirmatory diagnostic in GBED foals?
genetic mutation in tissue samples or by identifying typical PAS-positive inclusions in muscle or cardiac samples
Are there gross abnormalities in GBED foals at necropsy?
No
What is the muscle disease identified in charolais cattle?
deficiency in the enzyme Myophosphorylase (McArdle’s disease)
C/S with phosphorylase deficiency in charolais cattle?
exercise intolerance and collapse (when forced to exercise)
When should phosphorylase deficiency be considered as a differential?
In white muscle disease animals with normal vit E/ selenium deficiency?
What other spp see a phosphorylase deficiency than charolais cattle?
Sheep in Australia
Clinical signs of pseudomyotonia in cattle?
exercise induced muscle stiffness with normal response to percussion**delayed mm relaxation
Pseudomyotonia in cattle has been identified in waht breeds?
chianinadutch improved red & white crossbreed heifer
What is the genetic disorder in Hampshire pigs that reduces meat quality in pigs by increasing glycogen content of muscle?
porcine (RN-) glycogen storage disease
Muscle cramps arise from
Hyperactivity of motor units caused by repetitive firing of the peripheral and/or central nervous system
Muscle cramps can be induced by:
-Forceful contraction of a shortened muscle -changes in electrolyte composition of extracellular fluid-ear tick infestations in horses
Define muscle contracture
Painful muscle spasms that represent a stage of muscle contracture unaccompanied by depolarization of the muscle membraneoccur with malignant hyperthermia
What are the most common dietary electrolyte deficiencies that cause muscle stiffness, weakness and occasional elevations in mm CK?
SodiumPotassium
Why is supplementation of the equine diet with sodium necessary?
Because forage & grain diets are low in sodium and chloride & high in potassium
define muscle stiffness
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
define plaiting
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
Nerve block: palmar (plant) digital nerve block
nerves affected:
Structures desensitized
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
Nerve block: abaxial sesamoid
nerves affected:
Structures desensitized
nerves affected: palmar (plantar)
structures desensitized: coronary band, interphalangeal joints, lamellar and solar corium
Nerve block: low palmar
nerves affected:
Structures desensitized
nerves affected: palmar, palmar metacarpal
structures desensitized: skin of meidal and lateral pastern, metacarpophalangeal joint, proximal sesamoids, flexor tendons, tendon sheath
Nerve block: high palmar
nerves affected:
Structures desensitized
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)
overflexion of the hock means
overextension of the hock means
overflexion: gastrocnemius rupture
overextension: peroneus tertius
define muscle spasms
sudden, transient and involuntary contractions of a single muscle or group of muscles, attended by pain or loss of function
define cramp
painful, tonic, spasmodic muscular contraction
define myoglonus
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
