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Equine > Equine muscle disease > Flashcards

Equine muscle disease Flashcards

1
Q

What is headshaking in horses + signs

A

Uncontrollable, repeatable, persistent OR intermittent, vertical OR horizonal movement of the head

Often very subtle at rest but get worse during exercise

[other signs: avoiding airflow onto face, muscle fasciculations/grimacing, lip smacking)

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2
Q

What is the seasonality of headshaking

A

Most common in spring/summer or spring to autumn
Tend to get remission in winter

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3
Q

What other diseases can mimic headshaking signs

A

Nuchal crest avulsion fracture
Allergic rhinitis
Guttural pouch disease
Temperohyoid osteopathy
Otitis
Ocular disease
Pemphigus
Mites around nares

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4
Q

What is the pathology of idiopathic headshaking

A

Functional trigeminal nerve compromise
[there are studies showing lower activation threshold of trigeminal]

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5
Q

Roberts grading of headshaking

A

1 = signs only whilst exercising and can be ridden
2 = signs only at exercise but unsafe to ride
3 = signs at rest and exercise

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6
Q

What nerve block can be used to help diagnose headshaking

A

Maxillary nerve block BUT not specific as anything could be causing pain in this region e.g dental disease

+ possible complications

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7
Q

What is a cheap and easy possible treatment of headshaking

A

Nose nets/face masks
UNclear how
Seems to work better in younger horses

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8
Q

Pharmaceutical control of headshaking

A

All expensive, not good and many can’t be used in competition
- Cyproheptadine anti-histamine/anti-serotonergic; over 50% improve on this but very expensive and can’t compete

  • Carbamezepone to reduce neuron excitability
  • Gabapendint
  • Dexamethasone; unclear how this could help….
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9
Q

What is the best way to treat idiopathic headhsaking

A

Percutaneous electrical nerve therapy
Up to 80% get back to normal level of ridden activity

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10
Q

How does percutaneous electrical nerve therapy work for idiopathic headshaking

A

Sedate heavily with ACP, then detomidine drip + morphine
Place needle through skin and use U/S to check it is just superficial to the nerve
Complete circuit using clipped patch on other side and do electrical therapy

Short withdrawel from competition (2-3days)

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11
Q

How could surgery be done for idiopathic head shaking

A

Using titanium coils to compress the infraorbital nerve
Can give 50% reduction in sign severity but can make it worse

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12
Q

Three broad categories of muscle disease in horses

A

Acute muscle injurt
Exertional rhabdomyolysis
Other pyopathies

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13
Q

What two specific muscle enzymes can we measure in serum and what are their peaks like with damage

A

Creatinine kinease; from skeletal/cardiac muscle so quite muscle specific –> rapid peak in 4-6hrs; cleared in days

Aspartate transferase = less specific, also liver, RBCs; slower peak 12-24hrs and cleared in 2-3 weeks

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14
Q

What counts as a subclinical exertional myopathy

A

Where there is a more than 200-300% increase in CK levels after gentle exercise

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15
Q

How do we measure post-exercise muscle enzymes activity

A

Test CK before and then 4hrs after a 15-20 min gentle exercise; normal to see some increase in CK but only 2-3X increase

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16
Q

What are we looking for in urinalysis in myopathy cases

A

Myoglobinuria; red/brown colour
Need lab analysis to differentiate it from haemaglobinuria

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17
Q

What must we remember with transporting vitamin E assays

A

Keep on ice in the dark

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18
Q

What may be used to differentiate orthopaedic from neuromuscular atrophy causes

A

Electromyography; have abnormal EMG in atrophy/weakness

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19
Q

What are type 1 fibre vs type 2 fibre muscle types

A

Postural muscles are mainly type 1 fibres
Locomotor muscles are mostly type 2 fibres

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20
Q

What are type 1 muscle fibres

A

Slow contracting fibres; associated with need for fatty acid oxidation for contraction

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21
Q

What are ddx for muscle disorders affecting postural muscles

A

Equine motor neurone disease
Nutritional myodegeneration

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22
Q

What are ddx for locomotor muscle disease

A

Recurrent exertional rhabdomyolysis
PSSM

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23
Q

What is sporadic exertional myopathy

A

Related to increase in work intensity without proper training + exhaustion/overheating
-> Therefore assocaited with racehorses/endurance in hot and humid climates

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24
Q

Signs of sporadic exertional myopathy and tests

A

Weakness, ataxia, tachypnoea, sweating, muscles may palpate normally
See myoglobinuria + increased CK

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25
Q

What is recurrent exertional rhabdomyolysis

A

= where we get stiff, firm, painful muscles the day after a rest day
Common in thoroughbreds, esp excitable fillies; likely to be autosomal dominant inheritance

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26
Q

What do we see with tests/biopsy of recurrent exertional rhabdomyolysis

A

Myoglobinuria, marked elevation in CK and AST
Biopsy used to rule other things out; just see chronic non-specific changes assocaited with muscle regeneration

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27
Q

MAnagement/medication for recurrent exertional rhabdomyolysis

A

Low starch/sugar diet, access to salt block, vit E
Do not exercise above training scope, avoid rest days, minimise stress

Can use dantrolene a RYR1 antagonist to inhibit calcium release from SR

28
Q

What is the recommendation on when to return horses with recurrent exertional rhabdomyolysis to work

A

Recommentation = when CK <3000U/L
But suggested to wait until within reference range <400 to avoid re-triggering it

29
Q

Which breeds do we see polysaccharide storage myopathy in

A

Quarter horses
Connemara
Warmbloods

(see PSSM2 esp in these breeds)

30
Q

What is the pathogenesis of PSSM

A

Due to accumulation of polysacchardie in the myofibril
Get recurrent episodes often triggered by exercise that can range from mild shifting lameness/laziness to recumbency

31
Q

How can we diagnose PSSM

A

Biopsy of muscle; see polysacchardie accumulation in myofibril

32
Q

Differentiating PSSM1 and PSSM2

A

PSSM1 = due to GYS1 gene mutation which increases glycogen synthase; abnormal glycogen shape and less effective glycogenolysis

PSSM2 = no GYS1 mutation but altered glycogen staining on biopsy still

33
Q

What do we expect to happen to CK values after exercise in PSSM case

A

Increase at least 3X

34
Q

Management of PSSM horse

A

Low starch, high fat diet; veg oil making up to 1ml/kg/day
Supplement vit E/se
Lose weight if needed

Minimise stress/change
Keep regular work rhythm as many days as possible but do not exercise beyond training scope

NOT truly reversible but can we well managed

35
Q

Which horses do we seee equine myofibrillar myopathy

A

Arabs and warmbloods (some of these may actually be PSSM2 cases)

36
Q

What do we see on a biopsy with equine myofibrillar myopathy

A

Disorganised myofibrilas and abnormal desmin accumularion

37
Q

What signs do we see with equine myofibrillar myopathy

A

Variable
In arabs stiffness, reluctance to move (like exertional rhabdo)
In warmbloods assocaited with poor performance

38
Q

Which breeds do we see HYPP in

A

Quarterhorse, painthorse, appaloose

39
Q

What is HYPP and how can we diagnose

A

hyperkalaemic periodic paralysis= where there is a gene mutation that laters the voltage gated Na+ channels in skeletal muscles cells causing persistent depolarisation
Variable clinical signs, can see tremors

Diagnosis = genetic tests + hyperkalaemia

40
Q

What is post-anaesthetic myopathy

A

Where there is a localised area of hot, hard swollen muscles
Related to compartment syndrome of increase pressure, ischaemia, swelling etc

Must be careful with the positioning of horses during GA + maintain blood pressure

41
Q

How can we reduce risk of post-anaesthetic myopathy

A

If in dorsal ensure animal is symmetrical
If in lateral, extend the lower forelimb forward/lower hindlimb back
Maintain good blood pressure during GA

42
Q

Which breeds do we get malignant hyperthermia in

A

Quarterhorses
Painthorses

43
Q

What is malignant hyperthermia

A

Where there is a mutation in RYR1 gene causing dramatic increase in intracellular calcium, get contraction, heat in muscles and necrosis

So animal shows marked hyperthermia and acidosis

44
Q

If we pre-screen a horse as having RYR1 gene mutation what might we bre-treat them with before GA

A

Dantrolene

45
Q

What is white muscle disease

A

Nutritional myodegeneration; affects cardiac and skeletal muscles

Usually foals/youngstock where dam has had selenium/vitE deficiency

46
Q

Clinical signs of white muscle disease

A

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

 Affects: tongue, gastrocnemius, semimembranosus/tendinosus, biceps femoris, lumbar, gluteals, cardiac muscle

47
Q

Diagnosis of white muscle disease

A

 Increase in CK/AST
 Myoglobinuria
 Electrolyte derangements
 Low selenium on whole blood, vit E on plasma
 Pale oedematous muscle, calcification, hypercontracted fibres

48
Q

Does cardioresp or skeletal white muscle disease give a better prognosis

A

Skeletal

49
Q

Treatment of white muscle disease

A

 Selenium injections IM (NB = irritant so may dilute before injection)
 Oral alpha-tocopherol (vit E) supplementation
 Supportive nursing

50
Q

What is alpha-tocopherol

A

Vit E

51
Q

General treatment principles for myopathies

A

Rest; do not exercise in acute phase
NSAIDs
Antioxidants
Analgesia from start
Correct fluid deficit and protect kidneys by staying in isothenuric range

52
Q

Why do we want to stay in isothenuric range in myopathy case

A

To avoid pigment nephropathy from myoglobin

53
Q

Why do we need to be more careful with NSAID use in myopathies

A

Bceause kidneys already exposed to nephrotoxic myoglobin

54
Q

What is atypical myopathy

A

Disease of muscle degeneration due to failure of energy production due to an acquired deficiency in acyl-coA dehydrogenase

55
Q

What toxin can cause atypical myopathy

A

Hypoglycin A from sycamore seedlings
–> COnverted to MPCA-CoA which causes irreversible inactivation of dehydrogenases

56
Q

What is the key with managing an atypical myopathy case

A

Buying the animal time to produce new dehydrogenases
+ provide B vits and carnitine as building blocks for this

57
Q

What muscles are affected by atypical myopathy

A

Type 1 muscle cells; postural muscles
Cardiac muscle

58
Q

Clinical signs of atypical myopathy

A

Weakness, stiffness, recumbency, trembling, sweating
Pigmenturia
Dysphagia
Tachycardia
tachypnoea/dyspnoea

59
Q

What is the key way to differentiate atypical myopathy from colic

A

Pigmenturia present in atypical myopathy

60
Q

WHat is it causing pigmenturia in atypical myopathy

A

Myoglobin

61
Q

How can we confirm atypical myopathy and what must we consider in terms of how in house machine can cope with this

A

Measure CK and AST: expect extremely high CK levels in >100,000s
NB: in house machines can struggle with these high numbers so diluting them is a good idea

NB: can get false negatives early in disease process

62
Q

Why might we see dependent oedema and obstruction of URT in atypical myopathy cases

A

Due to low head carried from preferential affectation of muscles holding up the head in some cases
This leads to dependent oedema, oes obstruction etc

63
Q

WHat are the key things to do when managing an atypical myopathy case

A

Pain relief
Fluid therapy; to replace losses + protect kidneys from myoglobin impact (can do oral and IV)
Oxygen supplementation
Nutritional support; these horses rely on carbohydrate metabolism; can do high fibre, can do parenteral nutrition with lipid part taken out
Anti-odixants and vitamins

64
Q

What anti-oxidants/vitamins do we give with atypical myopathy

A

Vit E to prevent lipid peroxidation
Carnitine to bind the toxin hypoglyvin A
Vit B2 to give building blocks to make new acyl dehydrogenase enzymes

65
Q

What metabolism process is compromised in atypical myopathy

A

Fatty acid beta-oxidation
Hence why type 1 muscles affected more

66
Q

Is CK relevant in prognosis for atypical myopathy

A

NO because not a linear relatioship with muscle damage

67
Q

What other causes of trigeminal nerve dysfunction should we rule out before getting diagnosis of idiopathic headhsaking

A
  • Fungal disease
  • Intranasal mass
  • Dental disease
  • Headhsaking after surgery causing nerve damage

Equine (18 decks)

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