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Equine II > Myopathies > Flashcards

Myopathies Flashcards

1
Q

Energy sources for contraction

A

Phosphocreatinine (quickly exhausted)

Carbohydrate - glycolysis and glycogenolysis (efficient source if aerobic, inefficient if anaerobic)

Fatty acid oxidation (preferred source for sustained exercise)

Myokinase reaction (only used when all other stores depleted)

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2
Q

Subdivitions of myopathies

A

Acute muscle injuries

Exertional rhabdomyolysis

Other myopathies

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3
Q

Most common nutritional myopathies

A

Selenium/Vit E deficiency (white muscle disease)

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4
Q

Clinical signs associated with muscle disease

A

Pain, heat, and/or swelling on palpation of muscle

Muscular cramping

Abnormal limb position e.g. muscle tears

Gait abnormalities

Weakness

Fatigue/poor performance

Muscle fasciculation

Muscle atrophy

Sweating

Myoglobinuria

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5
Q

Diagnosis of muscle disease

A

Serum muscle enzyme activity
- creatinine kinase (CK)
- Aspartate transferase (AST)

Urinalysis
- myoglobinuria

Specific blood tests

Muscle biopsies

U/S

Nuclear scintigraphy

Electromyography

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6
Q

Serum muscle enzyme activity (in muscle disease)

A

Increased because of defect in integrity of myofibre membrane and sarcolemma

Creatine kinase (CK)
○ Found in muscle and brain
○ Serum levels are muscle specific

Aspartate transferase (AST)
○ Amino acid metabolism enzyme
○ Not muscle specific
○ Also found in hepatocytes

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7
Q

Post-exercise muscle enzyme activity

A

Some physiological increase in CK and AST will occur after exercise, especially strenuous exercise.

Test looks to detect exaggerated responses to non-strenuous exercise
§ Sub-maximal test

Measure CK and AST before and 4 hours after 15-20 minutes of sub-optimal exercise
§ No more than 200-300% increase in CK
□ Subclinical exertional myopathy
§ No more than 50% increase in AST

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8
Q

Myoglobinuria

A

Myoglobin released into serum from damaged muscle cells

Filtered by kidney -> Presence of myoglobin pigment in urine

Pigment is nephrotoxic

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9
Q

Vitamin E/ Selenium assays for myopathy

A

Keep samples for Vit E analysis in the dark, and on ice

Selenium = component of GSH-Px which can also be measured

GSH-Px destroys hydrogen peroxide/lipoperoxides that are generated by muscle

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10
Q

ELectrolyte tests in myopathies

A

Hypochloraemic metabolic alkalosis

Serum electrolytes and fractional excretion of urinary electrolytes

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11
Q

Muscle biopsies

A

Commonly performed

Consider which diseases you’re aiming to rule in/out in order to sample relevant muscle
- Postural vs locomotor

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12
Q

Postural muscles

A

Mainly type I fibres

DDx: EMND, nutritional myodegeneration

Location: sacrodorsalis medialis

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13
Q

Locomotor muscle

A

Mainly type IIa/IIx fibres

DDx: RER, PSSM

Location: semimembranosus

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14
Q

Exertional myopathies

A

Sporadic exertional myopathy

Recurrent exertional rhabdomyolysis (RER)

Polysaccharide storage myopathy (PSSM)

Equine myofibrillar myopathy (MFM)

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15
Q

Non-exertional myopathies

A

Atypical myopathy

Hyperkalaemic periodic paralysis (HYPP)

Post-anaesthetic myopathy

Malignant hyperthermia

Nutritional myodegeneration (White Muscle Disease)

Vitamin E-deficient myopathy (adults)

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16
Q

Sporadic exertional myopathy - causes

A

‘Tying up’

Increase in work intensity without appropriate training

Exhaustion and overexertion
○ Pyrexic?
○ Electrolytes?

Racehorses/endurance horses
○ Hot and humid climate

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17
Q

Sporadic exertional myopathy- clinical signs

A

Weakness, ataxia, tachypnoea, sweating… (collapse)

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18
Q

Sporadic exertional myopathy- diagnosis

A

Myoglobinuria and increased CK, but muscles may palpate normal

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19
Q

Sporadic exertional myopathy- overexertion

A

Increase in work intensity without foundation of training

Can affect any horse

Common in polo ponies early in the season

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20
Q

Sporadic exertional myopathy- exhaustion

A

Racehorses/endurance horses, hot and humid climate

Weakness, ataxia, tachypnea, sweating… (collapse)

May be pyrexic

Myoglobinuria and elevated CK, but muscles may palpate normal.

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21
Q

Recurrent exertional rhabdomyolysis (RER) - Incidence

A

‘Tying up’, ‘Monday morning disease’, ‘Azoturia’

Common (4.9-6.7% Thoroughbreds)

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22
Q

Recurrent exertional rhabdomyolysis (RER) - signalment

A

Excitable/nervous horses

Female > Male

Historically draught animals fed high grain diets

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23
Q

Recurrent exertional rhabdomyolysis (RER) - clinical signs

A

Stiff, firm, painful muscles
§ Large muscle groups (gluteals, triceps)

Myoglobinuria (absence does not rule out RER)

Stiff gait, reluctance to move

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24
Q

Recurrent exertional rhabdomyolysis (RER) - cause

A

Likely to be autosomal dominant inherited trait
○ Yet to be fully elucidated…
○ We’ve probably selected for it alongside other desired characteristics,
Standardbreds with RER run faster than those without RER for example

Often the day following a rest day

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25
Q

Recurrent exertional rhabdomyolysis (RER) -diagnosis

A

History and signalment
○ Soon after onset of exercise, or shortly after cessation of exercise

Marked CK and AST elevation

Muscle biopsy
○ Often performed to rule out other myopathies
○ Chronic, non-specific changes

In vitro contracture studies
○ Gold standard, use intercostal muscle
○ Not performed in clinical practice really

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26
Q

Recurrent exertional rhabdomyolysis (RER) - diet

A

Low starch

Use fat for extra calories diet
○ E.g. RE-LEVE by Saracen
○ Competition animals: meet high calorie requirement

Access to a salt block

Vitamin E +/- selenium

27
Q

Recurrent exertional rhabdomyolysis (RER) - exercise

A

Don’t exercise beyond scope of training

Avoid rest days

Minimise stress

Appropriate training

When in recovery period from myopathy, put in small pen so can walk around more than in a stable - loosening of stiffness and improvements to circulation. Rather than box rest.

28
Q

Recurrent exertional rhabdomyolysis (RER) - treatment

A

Diet and exercise important

Dantrolene
* RYR1 antagonist -> inhibits calcium release from sarcoplasmic reticulum
* Detection time 48hrs (BHA) - not helpful from a competing point of view

29
Q

Polysaccharide storage myopathy (PSSM) -signalment

A

Heritable: Quarter horses, Connemara, Warmbloods…

30
Q

Polysaccharide storage myopathy (PSSM) - cause

A

Commonly triggered by exercise (can be less than 20min)

31
Q

Polysaccharide storage myopathy (PSSM) - what is it?

A

Accumulate polysaccharide (abnormal glycogen) in the myofibre

Energy source is locked away in muscle cells

32
Q

Polysaccharide storage myopathy (PSSM) - clinical signs

A

Recurrent episodes

may be mild (stretching out, ‘lazy’, may look like shifting lameness)

to severe (sweating, reluctance to move, recumbency)

33
Q

Polysaccharide storage myopathy (PSSM) - PSSM 1

A

GYS1 gene mutation (autosomal dominant)

Increases glycogen synthase activity

Glycogenolysis doesn’t work as well -> less glucose -> less energy

Can see abnormal granules sitting in the cell

Myokinase reaction used for energy - inefficient

34
Q

Polysaccharide storage myopathy (PSSM) - PSSM 2

A

a disease of abnormal polysaccharide storage

-But we don’t know why/mechanism…

Likely to be a group of conditions

Altered staining on a biopsy for glycogen, but absence of GYS1 mutation

35
Q

Polysaccharide storage myopathy (PSSM) - diagnosis

A

May have persistently elevated muscle enzymes
○ Exercise test to challenge if muscle enzymes not elevated
○ Threefold increase in CK 4hrs after exercise

Biopsy semimembranosus muscle
○ Increased skeletal muscle glycogen

Gold standard – test for GYS1 mutation on hair roots/blood

36
Q

Polysaccharide storage myopathy (PSSM) - Management (diet)

A

Limit glycogen synthesis (reduce insulin activity)

Promote breakdown of glycogen

Low starch, high fat

Provide 1.5-2% BWT as roughage

< 10% Digestible energy as non structural carbohydrates

> 13 % fat

Vegetable oil up to 1ml/kg/day

Supplemental Vitamin E +/- selenium

Commercial diets

Lose weight if overweight

37
Q

Polysaccharide storage myopathy (PSSM) - management (exercise)

A

Maintain regular work/turn out routine

Avoid days off

Minimise stress

Minimise changes in management

Don’t exercise beyond scope of training

Prognosis fair if managed correctly

38
Q

Equine myofibrillar myopathy (MFM) - signalment

A

disease in Arabians and warmblood horses

39
Q

Equine myofibrillar myopathy (MFM) - histology

A

there is a disruption of the orderly alignment of myofibrils and aggregates of desmin (cytoskeletal protein) are identified using special stains

40
Q

Equine myofibrillar myopathy (MFM) - clinical signs

A

Clinical signs are predominantly those consistent with an exertional rhabdomyolysis in Arabians and non-specific poor performance in warmblood horses

May not have increased CK/AST

41
Q

Equine myofibrillar myopathy (MFM) - management

A

Recent advice is that horses seem to do best if ridden work is kept to 30-45min, and a long/low lunging warm up for 10-15min is incorporated prior to ridden exercise

42
Q

Atypical myopathy - cause

A

Acute, severe rhabdomyolysis, affects horses at pasture caused by hypoglycin A toxicity

Seeds and seedlings of some Acer trees

UK: Sycamore (Acer pseudoplatanas)

43
Q

Atypical myopathy - mechanism

A

Hypoglycin A forms toxic metabolite (MCPA), which binds to FAD.

MCPA deficiency, because they can’t use FAD as a cofactor.

This means that mitochondrial aerobic metabolism is impaired.

This deprives muscle of an energy source.

Type 1 muscle fibres are worst affected, so clinical signs are consistent with postural muscle disease.

44
Q

Atypical myopathy - risk factors

A

Autumn and spring

Wet and windy weather

Presence of Sycamore trees (UK)

Access to pasture

Often poor body condition, young, or not being fed supplementary feed when on pasture

May be mistaken for cases of colic, severe laminitis, botulism

(neurological exam normal in AM)

Intrinsic horse factors?

Variable concentrations in different parts of the plant (even if from the same tree)?

Likely multiple factors

45
Q

Atypical myopathy - clinical signs

A

Weakness, reluctance to move, may be found recumbent

Painful, firm muscles may be appreciated on palpation

Myoglobinuria

Tachycardia, tachypnoea, congested mucous membranes

Distended bladder on rectal palpation

46
Q

Atypical myopathy - diagnosis

A

High muscle enzymes on serology

Myoglobinuria

Submit plasma for acylcarnitine/serum for hypoglycin A and conjugated MCPA

Confirmation takes 48-72h via RVC Neuromuscular Lab

You cannot wait this long before implementing treatment

Postmortem: samples of masseter/intercostal muscle

47
Q

Atypical myopathy - treatment

A

Start treatment before definitive diagnosis if suspected

Require intensive supportive care and nursing

Fluid therapy (monitor renal function)

Add glucose (5% glucose to provide alternative energy source)

Analgesia

Vitamin E and selenium, riboflavin, oral carnitine

48
Q

Atypical myopathy - prognosis

A

Very hard to predict – survival rates are improving

↓ prognosis: hypoxia, dyspnoea, tachypnoea, hypothermia, bladder distension, absence of intestinal sounds, remaining recumbent

↑ vitamin and anti-oxidant administration (advised for all cases, including subclinical
ones that are diagnosed alongside index clinical case)

49
Q

Hyperkalaemic periodic paralysis (HYPP) - signalment

A

QH, Paint, Appaloosa

50
Q

Hyperkalaemic periodic paralysis (HYPP) - cause

A

Gene mutation alters voltage-dependent skeletal muscle sodium channel = persistent depolarisation of muscle cells

51
Q

Hyperkalaemic periodic paralysis (HYPP) - clinical signs

A

variable (muscle spasms and trembling)

52
Q

Hyperkalaemic periodic paralysis (HYPP) - diagosis

A

Genetic testing (commercially available)

Hyperkalaemia and suggestive clinical signs, no/little change in CK

53
Q

Post-anaesthetic myopathy

A

Localised rather than generalised myopathy

Hard, hot, swollen muscles
○ Gluteals, epaxial muscles, triceps

Onset may be delayed

Compartment syndrome
○ ↑ pressure within muscle -> ischaemia -> muscle swelling ->↑ pressure

Careful consideration RE positioning on table
○ Dorsal recumbency: symmetrical
○ Lateral recumbency: extend lower forelimb forwards/hindlimb back

Monitor and maintain blood pressure under anaesthesia

Symptomatic and supportive treatment

54
Q

Malignant hyperthermia

A

QH/paints (and pigs!)

RYR1 (ryanodine receptor) gene mutation
○ Dramatic increase in intracellular calcium -> contraction -> muscle heat and necrosis

Exercise or anaesthesia induced
○ Worth screening before anaesthetising these breeds?
○ Pre-treat with dantrolene
○ Marked hyperthermia and acidosis

55
Q

Nutritional myodegeneration (White Muscle Disease) - pathophysiology

A

Effects of a deficiency in Vitamin E and Selenium result in the destruction of cell membranes and proteins leading to a loss of cellular integrity.

The precise interrelationships among selenium/Vit E, other metabolic factors and triggering mechanisms in NMD are not fully understood because some deficient animals do NOT have disease.

Selenium appears to be the most important in foals however, and deficiencies in this nutrient are more likely to lead to NMD than vitamin E.

56
Q

Nutritional myodegeneration (White Muscle Disease) - Clinical signs

A

Cardiac form and skeletal form

Dyspnoea, weakness, stiffness, trembling, recumbency, sudden death, irregular tachydysrhythmia

Aspiration pneumonia common secondary to tongue necrosis

Tongue, gastrocnemius, semimembranosus/tendinosus, biceps femoris, lumbar, gluteals, neck affected

57
Q

Nutritional myodegeneration (White Muscle Disease) - diagnosis

A

Clinicopathologic abnormalities
○ CK/AST elevation
○ Myoglobinuria
○ Electrolyte derangements

Low selenium (whole blood), GSH-Px, α-tocopherol (vit E) (plasma)

Gross pathology
○ Pale, oedematous muscle, calcification
○ Hypercontracted muscle fibres

58
Q

Nutritional myodegeneration (White Muscle Disease) - treatment

A

Cardiorespiratory disease -> poor prognosis

Skeletal muscle disease -> better prognosis
○ usually see improvement quickly

Selenium injections IM
○ irritant, can dilute before injection

Oral α-tocopherol supplementation

Supportive nursing

59
Q

Vitamin E-deficient myopathy (adults)

A

Disease in its own right? Precursor to EMND?

Presence of myopathic not neuropathic change in SCDM biopsy

60
Q

Vitamin E-deficient myopathy (adults) - clinical signs

A

Weakness, narrow-base stance

Animals with disease of postural muscles often look better when you
get them walking. May look worse when asked to stand still, weight
shift and look uncomfortable.

Muscle atrophy

Trembling and muscle fasciculations

Weight shifting

61
Q

Vitamin E-deficient myopathy (adults) - diagnosis

A

SCDM biopsy

May have normal serum α-tocopherol

62
Q

Vitamin E-deficient myopathy (adults) - treatment

A

Oral α-tocopherol supplementation

Not powders, needs to be v bioavailable

Is diet deficient, or can horse not absorb it? Re-test.

As with EMND could be because diet is deficient, often stabled animals.

Might consider glucose absorption test if suspect primary
absorption issue.

63
Q

General principles of treatment for myopathy

A

Minimise continued muscle damage
- rest
- NSAIDs
- ACP
- Antioxidants

Analgesia

Correct fluid deficit/diurese

64
Q

Analgesia for myopathy

A

NSAIDs

Opioids
○ Buprenorphine/butorphanol licensed for horses
○ Methadone more potent but use on cascade
○ Morphine commonly used, not licensed in any veterinary spp.

Paracetamol
○ Use as an adjunct, not sole analgesic

Lidocaine infusion
○ Logistics require hospitalisation

Ketamine infusion
○ Requires hospitalisation (scheduled drug and logistics require hospitalisation)

Equine II (28 decks)

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