LA Muscle Disease Flashcards

Question

What are the trigger factors for sporadic ER?

Answer 1

**Overexertion** * Exercise beyond level of training * Muscle stiffness, mild increases in CK * Mild pathological change on light microscopy **Heat exhaustion** * The exhausted horse **Dietary imbalance** * High non-structural carbohydrate feeding * Often associated with day of rest (Monday morning disease) –Vitamin E / Selenium deficiencies = severe muscle problems * Electrolyte imbalance

Answer 2

* Hypovolemia –less oxygen to the muscle= lactic acid = damage * Hyperthermia * Low muscle pH (high-speed exercise) * Depleted glycogen (long slow exercise). Glycogen is the main muscle energy store. Once it runs out --\> horse stops or the muscle hasn’t got enough energy and muscle will die * Impair membrane pump function –Electrolyte imbalances –Deficiency in ATP –Na + /K + , Ca 2+ /Mg 2+ , Ca 2+ /ATPase * Increased sarcoplasmic Ca 2+ –disruption of cell * Ileus, cardiac dysrhythmias * Synchronous Diaphragmatic Flutter (Thumps)

Answer 3

**Treatment :** * rapid cooling * rehydration * NSAIDs (ensuring dehydration is corrected or being corrected first in case of renal damage) * correction of electrolyte imbalances **Prevention :** * training, heat acclimation * free access to water and food * high roughage diet * veterinary checks throughout ride

Answer 4

Underlying muscle defect * Recurrent exertional rhabdomyolysis * Thoroughbred * Autosomal dominant * Polysaccharide storage myopathy * Quarter horse, draft horse

Answer 5

**Abnormal intracellular calcium regulation** * Thoroughbred, standardbred, ?Arabs * Prevalence of 5-9% in racing TBs Prevalence affected by level of exercise * More frequent when fit * When training rather than racing

Answer 6

**Risk factors** * Mares (unrelated to stage of oestrus cycle) * Temperament (nervous) * Diet (high grain diet) * Other MSK disorders (lameness)

Answer 7

* Inherited autosomal dominant trait * Abnormal regulation of muscle contraction * May be similar to MH

Answer 8

Clinical signs and diagnosis Can present as a subclinical disease * Exercise test can be useful for diagnosis History of repeated episodes of ER with raised CK, AST Biopsy * Increase in mature muscle fibres with centrally displaced nuclei * No amylase resistant polysaccharide

Answer 9

**Type 1:** Quarter Horses –Confirmed GYS1 mutation –Won’t see this very much in this country **Type 2:** ~Warmbloods, Drafts –Histopath evidence of disease without GYS1 mutation –Have to muscle biopsy

Answer 10

TYPE 1 : confirmed mutation of GYS1 gene which causes : * Abnormal glycogen branching in muscle cell with increase glycogen storage (1.8-fold) via enhanced sensitivity to insulin * Reduced ability to utilise such glycogen * Being glycogen main muscle source of energy result is exercise intolerance, muscle atrophy/weakness * Muscle necrosis due to abnormal energy metabolism * Exact mechanism unclear AND different between QH and other breeds TYPE2 : * unknown mutation but same histopathologic features

Answer 11

Onset of clinical signs * 5 years * Onset 20 mins after onset of exercise * Worse after period of rest

Answer 12

Persistently INCREASED activities of CK * Three fold increase in CK after exercise test Muscle Biopsy –Semimembranosus * Amylase resistant inclusion Blood test * Genetic test for GYS-1 mutation * Excellent sensitivity for QH * Poor sensitivity in WB, Draft which may have a different mutation

Answer 13

**REST** * Depends on disease, but essential in early stages **Analgesia** * NSAIDS –Flunixin, carprofen, meloxicam * Opioids –Pethidine(morphine –NO VPL) * Other –Lidocaineinfusion (No VPL) * Detomidine, ACP -anxiolytic and may improve perfusion **Other** * Dimethylsulphoxide–DMSO –cell membrane stabilising, free radical scavenging * Vitamin E (effective anti-oxidant) * Corticosteroids –VERY CONTROVERSIAL AND NOT PERSONALLY RECOMMENDED –

Answer 14

Fluid therapy is essential in cases of ER Myoglobin is reno-toxic * Exertion may have led to fluid deficits Mildly affected horses * Fluid and electrolytes by nasogastric tube * 22.5g NaCl, 22.5g LoSalt (NaCl and KCl) per 6l Severely affected (and exhausted horse) * Intravenous fluid therapy * Fluid type is not important although specific abnormalities may require management

Answer 15

Box rest and then pasture turn out CK and AST should be within normal range * CK should be \<200% normal * Reassess 3 days after recommencement of exercise PREMATURE EXERCISE WILL RESULT IN FURTHER MUSCLE DAMAGE

Answer 16

Limited stall confinement * PSSM –pasture rest as soon as possible * No more than 48 hours stabled * Very gradual return to exercise * Steady/Regular low level of exercise * Once in full exercise NO days off RER * Limited time off * Once in full exercise no days off (increases CK)

Answer 17

Environment * Reduce stress, turnout with others Exercise * Avoid days off * Prolonged warm up, rest periods during exercise (interval training) Diet Drugs

Answer 18

**Carbohydrates** level of carbohydrate relative to exercise and weight \<20% of diet should be non structural carbohydrate **Oil** 10% as source of energy **Fibre** amount and type -1% BWT minimum(ideally 2%) **Protein** not excessive protein **Vitamins and minerals** Calcium, magnesium and phosphorus Salts -Na, K, Cal Vitamin E and selenium * storage and handling may be important

Answer 19

**Sedation prior to exercise (Acepromazine)** * temporary benefit **Dantrolene(Dantrium)** * inhibits Ca release from SR * 800mg/day 1 hour pre exercise (NOT IN FOOD) * On day of return to exercise * Reduced affect of exercise on CK rises and ERS * Prevents episodes * Used mostly in the racing industry Phenytoin * affects ion channels and increases the threshold for Ca release from the SR

Answer 20

Sudden onset myoglobinuria * Horses at pasture (poor quality) * Sudden onset exertion Stiffness, myoglobinuria * Spring or autumn

Answer 21

Recently shown to be plant toxin HyperglycinA * Box Elder Tree (USA) * Sycamore Tree (UK/EU)

Answer 22

**Supportive therapy** * IVFT * Glucose, insulin * Carnitine and Vitamin C may be of benefit * No matter what you do the horse will probably die * such a massive breakdown the kidneys are full of myoglobin

Answer 23

* Hoovering-up/picking up sycamore seeds * Fencing off areas where sycamore seeds have fallen from trees * Supplying extra forage (hay or haylage) especially where pasture is poor * Reducing stocking density so there is plenty of palatable grazing for every horse * Turning out horses for only short periods rather than extended periods of the day (ideally \<6 hrs)

Answer 24

* Disease of Pigs (and horses) * Autosomal dominant mutation of Ryanodine Receptor (RYR) * Results in increases [Ca 2+] within cell * Heat from Ca 2+ /ATP ase * Depletion of ATP **Treatment** * Ryanodine receptor antagonist * Dantrolene

Answer 25

* Prolonged recumbency following anaesthesia * Low BP, excessive pressure, poor positioning * Dd neuropathy and myelopathy * High CK/pain * Tries to get up and just struggles

Answer 26

Sporadic disease * Related to restricted pasture access * Poor quality hay Type 1 fibre pathology * so they will look very weak when they stand! * Pull the tail and they fall * When they walk and move they are fine. * Muscles of posture * Oxidative damage * Muscle fasciculation, weight loss * Weak on standing, tremors but then trot them up and they are fine

Answer 27

Clostridial myonecrosis * Affects all large animals affecting different muscle groups with different organisms * Black leg, malignant oedema, gangrene * Rapidy progressive with high mortality * Pyrexia, depression PAIN, lameness DEATH

Answer 28

**Clostridial myonecrosis** Bacteria are ubiquitous in soil * Spores maintain survival Locate within muscle activated by trauma * Anaerobic environment * Necrotisingmyositis * Horse –injection site/ puncture wound –espirritant drugs * Cattle–blunt trauma –High stocking densities in high plane of nutrition * Sheep –Shearing / dipping

Answer 29

Treatment * Debridement and fasciotomy * Antibiotics –High dose penicillin q2h * Metronidazole in horses NO IN FOOD ANIMALS * Avoid IM injections * General supportive management

Answer 30

Prevention * Vaccination –From 3-4 months q 6m * Removal of all dead bodies

Answer 31

Swelling and autolysis * Rancid odour Blood stained fluid at orifices * Mouth, eye, vulva etc. Swell and crepitus -gassy Haemorrhagic dark muscles when you cut them * Cl. perfringens –horse * Cl. sordelli –cattle

Answer 32

S equi var equi (“ strangles ”) * Rare complication * Immune mediated myositis 4 weeks post inf * Tx corticosteroids Parasites * Sarcocyctosis * No clinically significant but important VPH implications –see VPH for more details of parasitic muscle diseases

Answer 33

Peracute to subacute myo degeneration Cardiac and skeletal muscle * Selenium and or vitamin E * Young rapidly growing LA (\<1yr) * Often Se deficient dams * In utero form Dx: Low Selenium and GSHPx Histopathology: inflammatory myositis

Answer 34

Nutritional Muscle Disease

Answer 35

**Cardiac form** * Sudden onset * Death * Depression, respiratory distress * Rhythm disturbances * Remaining cardiac damage **Skeletal form** * Slower onset * Weakness and stiffness * Recumbency * Muscle pain * Can affect respiratory muscles

Answer 36

EMND * Narrow-Base stance –stands like an elephant on a ball * Disease from VitE deficiency and subsequent oxidative muscle damage

Answer 37

Laboratory findings CK and AST * Occasional changes CSF * Inflammatory changes Pigment Retinopathy Vitamin E * \<1ug/ml very low (so we supplement) OGAT * (decrease glucose absorption) Muscle biopsy * Sacrocaudalisdorsalis medialis

Answer 38

* Vitamin E supplementation * Hydro soluble forms of VitE (e.g. Nano-E) better absorbed * Supplement selenium too but DO NOT EXCEED 3mg/kg Selenium * Selenium toxicosis * Prognosis POOR

Answer 39

**Viral myopathy** * Equine influenza * Foot and mouth disease, MCF, BVD, Bluetongue * Skeletal or cardiac **Toxic myopathy** * Gossypol (cotton seed) in pigs * Ionophores * Abxin poultry so may eat these if they get into the bar. Cardiotoxictoo = death * Organophosphate * Trematone containing plants * Cassia spp and white snake root –V rare

Answer 40

Delayed relaxation of skeletal muscle * In goats * Chloride channel * In horses * not chloride related * Stiff gait * Atrophy weakness * Horses –Quarter horses (proximal limbs) * Goats –Fainting goat * Diagnosis –EMG * Treatment –drugs used in humans (phenytoin)

Answer 41

* Genetic disease * Point mutation * Normal between episodes * Sodium channels * Voltage gated * Remain open when triggered * Do not inactivate * Precipitated by increased serum [Potassium] * Hyper excitable then unexcitable

Answer 42

Trigger factors **High K + intake** * Alfalfa, molasses etc **Increased mobilisation** * Fasting * Stress * Anaesthesia * Vigorous exercise

Answer 43

**Mild:** * Pronounced muscle development (thus selected for breeding) * Prolapse of third eyelid * Muscle fasciculations and weakness * Onset 2-3 years **Severe** * Muscle weakness, * Recumbency, dog sitting * Dysphagia, Pharyngeal collapse, Laryngeal Paralysis Can be fatal Normal after episode

Answer 44

Serum biochemistry * Normal CK activities * Increased K + during episodes EMG (between episodes) * Abnormal fibrillation potentials * Complex repetitive discharges * Myotonic potentials DNA testing

Answer 45

**Acute** * Calcium borogluconate (IV) * (0.2-0.4ml/kg of 20% solution in 1 litre saline) * Raises membrane threshold potential * Glucose (IV) * 6ml/kg as a 5% solution * Stimulates insulin secretion * Tracheostomy **Chronic** * Acetazolamide (3mg/kg BED PO) * Carbonic anhydrase inhibitor * Renal loss of potassium * Diet

Answer 46

* Muscle disease is important for production and performance * Important clinical conditions * SIMILAR diagnostic and therapeutic option * Definitive diagnosis often based on histopathological appearance * Although often a clinical diagnosis based on serum biochemistry

Answer 47

Fibrotic myopathy is the classic “mechanical lameness” of the hind limb. The gait change is caused by a mechanical limitation on movement of the hind limb and is not necessarily caused by pain. Injury and scarring of the hamstring muscles in the upper hindquarter of the horse causes a classic change in gait with shortening of the front phase of the stride, loss of the stretchability of the normal muscle, and slapping of the foot to the ground. The injury can result from a single traumatic injury to these muscles (hyperextension injury) but can also can result from repetitive strain, seen most commonly in Western performance horses, especially reiners, cutters and rope horses. In some cases, scarring can occur from repeated IM injections into the hamstring muscles. “Goose-stepping” is the name given to horses that move their hind limb in this characteristic way – the hoof is raised, then brought rearward and slapped to the ground. Fibrotic myopathy is very different from “stringhalt” as are the causes. Importantly, other lameness conditions can cause similar but rarely this classic gait.

Answer 48

* Vascular obstruction of the hindlimbs * Progressive exercise intolerance and hind-leg lameness

Answer 49

Stringhalt is a gait abnormality characterized by exaggerated upward flexion of the hindlimb that occurs at every stride at walk. The gait abnormality usually lessens at trot and is not evident at canter. It may occur unilaterally or bilaterally. All degrees of hyperflexion are seen, from mild, spasmodic lifting and grounding of the foot, to extreme cases in which the foot is drawn sharply up until it touches the belly and is then struck violently on the ground. In severe cases, there is atrophy of the lateral thigh muscles. In Australian stringhalt and lathyrism, the condition may be progressive and the gait abnormality may become so severe that euthanasia is warranted. Mild stringhalt may be intermittent. The signs are most obvious when the horse is sharply turned or backed. In some cases, the condition is seen only on the first few steps after moving the horse. The signs are often less intense or even absent during warmer weather. Although it is regarded as unsoundness, stringhalt may not materially hinder the horse’s ability to work, except in severe cases when the constant concussion gives rise to secondary complications. However, the condition may make the horse unsuitable for some equestrian disciplines (eg, dressage). The etiology is unknown, but lesions of a peripheral neuropathy have been identified in the sciatic, peroneal, and tibial nerves. Severe forms of the condition have been attributed to lathyrism (sweet pea poisoning) in the USA and possibly to flat weed intoxication in Australia. Diagnosis is based on clinical signs but can be confirmed by electromyography.

LA Muscle Disease Flashcards

(75 cards)