Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSK2 > Large animal muscle disease > Flashcards

Large animal muscle disease Flashcards

1
Q

List muscle diseases causing muscle pain/cramping

A
  • Equine rhabdomyolysis syndrome (sporadic or chronic)
  • Atypical myoglobinuria
  • Malignant hyperthermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List the muscle diseases causing muscle weakness in horses

A
  • Muscle atrophy (disuse, neurogenic, cachexia)

- Equine motor neurone disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List the muscle diseases causing collapse in horses

A
  • Myotonia

- Hyperkalaemic periodic paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List muscle disease in horses other than those causing weakness, collapse, or muscle pain/cramping

A
  • Fibrotic myopahty
  • Muscle rupture
  • Aorto-iliac thrombosis
  • Spastic paralysis
  • Stringhalt
  • PPID
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List the possible clinical signs of muscle disease in large animals

A
  • Muscle atrophy
  • Muscle stiffness/pain
  • Myoglobinuria
  • Recumbency/collapse
  • Hyperthermia
  • Exercise intolerance
  • Abnormal contraction
  • Non-specific signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the differentials for myoglobinuria in the horse?

A
  • Muscle disease
  • Haematuria
  • Haemoglobinuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain why hyperthermia may occur with muscle disease

A
  • Inflammation leading to pyrexia

- May also increase heart production from contracting muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What aspects of the history are particularly relevant for investigation of muscle disease in horses

A
  • Temperament, diet
  • Occurrence: acute, recurrent, chronic
  • Progression of signs
  • Other diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which parameters may be raised on biochemistry, indicating muscle disease in a large animal?

A
  • Creatine kinase
  • Aspartate aminotransferase (AST)
  • Lactate dehydrogenase 5 (skeletal muscle isoenzyme)
  • +/- urea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain the interpretation of creatine kinase in an animal with suspected muscle disease

A
  • Can be cardiac or skeletal, where there are clinical signs of muscle disease can decide whether MSK
  • Short half life, good for identification of acute conditions or ongoing pathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain the interpretation of AST in an animal with suspected muscle disease

A
  • Produced in skeletal muscle, bone, liver
  • If both CK and AST are elevated can be fairly certain is due to muscle pathology
  • If CK normal but AST high, may be due to longer half life (7-8days vs 2hrs) of AST but need to rule liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain the interpretation of myoglobinuria in an animal with suspected muscle disease

A
  • Suggestive of significant disease
  • Is toxic to renal tubules
  • In all cases need to administer fluids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why might urea be elevated in muscle disease?

A

Concurrent renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline the exercise test used where muscle disease is suspected

A
  • Used to determine chronic recurrent pathology
  • Biochemistry following 15mins mild exercise e.g. trot lung
  • Normal: CK<200% increase between 2-6 hours, and AST <50% increase at 24 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which parameters are assessed in the diagnosis of muscle disease on urinalysis?

A
  • Myoglobinuria (urine dipstick)

- Fraction excretion of electrolyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain the significance of fractional excretion of electrolytes in muscle disease in the horse

A
  • May increase with recurrent rhabdomyolysis due to myoglobinuria causing damage to the renal tubules
  • Generally more indicative of intracellular ions than serum measurement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where are muscle biopsy samples taken from in the horse for the investigation of the different muscle disease in the horse?

A
  • RER, PSSM: semitendinosus
  • EMND: sacrodorsalis caudalis medialis
  • RER: gluteal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Outline the assessment of muscle biopsies for the diagnosis of muscle diseases

A
  • Confirmation of disease by assessing degeneration, necrosis and regeneration vs lysis or oedema
  • Identify underlying mechanisms
  • Estimate % of fibres affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What advise should be given to a horse owner following a muscle biopsy?

A
  • Likely to be uncomfortable, esp. gluteal biopsy

- Box rest will reduce use of this muscle and thus reduce discomfort perceived by the horse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

List the diagnostic tools used in the diagnosis of equine muscle disease

A
  • Physical examination and palpation
  • Blood biochemistry
  • Urinalysis
  • Exercise test
  • Muscle biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is equine rhabdomyolysis syndrome also known as?

A

Tying up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is equine rhabdomyolysis syndrome usually precipitated by?

A

Exercising beyond their level of fitness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the different presentations of equine rhabdomyolysis syndrome?

A
  • Sporadic: exertional rhabdomyolysis (exhausted horse syndrome)
  • Chronic: Recurrent equine rhabdomyolysis (RER), Polysaccharide storage myopathy (PSSM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Outline the clinical signs of equine rhabdomyolysis syndrome and when might these occur?

A
  • May occur before, during or after exercise
  • Exercise intolerance
  • Stiff gait
  • Reluctance to move
  • Recumbency
  • Muscle pain, hard muscles
  • Myoglobinuria
  • Pain - sweating, tachycardia, tachypnoea
  • Hyperthermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the potential consequences of myoglobinuria in thehorse?

A
  • Pre-renal azotaemia: often hypovolvaemic (dehydration from intense exercise)
  • Renal azotaemia: pigmenturia, damage to kidney, can be life threatening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

When does recurrent/chronic equine rhabdomyolysis syndrome commonly occur?

A
  • Before, during or after only light exercise

- Agitation prior to exercising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the pathology that occurs with equine rhabdomyolysis syndrome

A

Lysis of muscle fibres esp type II (fast twitch) fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

List the trigger factors for sporadic exertional rhabdomyolysis in the horse

A
  • Overexertion
  • Heat exhaustion
  • Dietary imbalance (high non-structural carb feeding, vit E/selenium deficiency)
  • Electrolyte imbalance
  • Viral, immune mediated (rare - viral myositis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the signalment for sporadic exertional rhabdomyolysis in the horse

A
  • No underlying muscle defect

- Any age, breed, sex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Outline the problems related to sporadic exertional rhabdomyolysis in the horse

A
  • Hypovolaemia
  • Hyperthermia
  • Low muscle pH (high speed exercise)
  • Depleted glycogen (endurance exercise)
  • Impaired membrane pump function leading to electrolyte imbalances and ATP deficiency
  • Increased sarcoplasmic Ca2+
  • Ileus, cardiac dysrhyhmias
  • Synchronous diaphragmatic flutter (thumps)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Explain why thumps may develop as a result of sporadic exertional rhabdomyolysis in the horse

A

Most commonly a sign of dehydration and electrolyte depletion among horses performing in endurance races

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Outline the treatment of sporadic exertional rhabdomyolysis/exhausted horse syndrom

A
  • Rapid cooling
  • REhydration with isotonic solution via NG tube or IV
  • NSAIDs (once dehdration corrected)
  • Correciton of electrolyte imbalances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How can exhausted horse syndrome be prevented?

A
  • Training, heat acclimation
  • Free access to water and food
  • High roughage diet
  • Veterinary check throughout ride (esp. for endurance races)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Outline the signalment for recurrent exertional rhabdomyolysis in the horse

A
  • Mares predisposed
  • TB
  • Nervous temperament
  • High grain diet
  • Other concurrent MSK disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When do episodes of recurrent exertional rhabdomyolysis in the horse generally occur?

A
  • When the animal is fit

- Episodes when training, not racing

36
Q

Outline the pathogenesis of recurrent exertional rhabdomyolysis in the horse

A
  • Underlying muscle condition
  • Autosomal dominant gene
  • Abnormal regulation of muscle contraction
37
Q

Outline the clinical signs of recurrent exertional rhabdomyolysis in the horse

A
  • Predisposition for typing up, repeat episodes

- Can be subclinical

38
Q

Outline the diagnosis of recurrent exertional rhabdomyolysis in the horse

A
  • Raised CK and AST post exercise
  • Gluteal/semitendinosus muscle biopsy demonstrating increase in mature muscle fibres with centrally displaced nuclei, no amylase resistant polysaccharide
39
Q

Outline type I polysacchardide storage myopathy in the horse

A
  • Quarter horses
  • GYS1 mutation
  • Abnormal enzyme function results in inappropriate storage of glycogen in muscle cells so there is little energy available
40
Q

Outline type II polysaccharide storage myopathy in the horse

A
  • Warmbloods, Draft horses

- Histopath evidence of disease without GYS1 mutation

41
Q

Outline the pathogenesis of type I PSSM in the horse

A
  • GYS1 mutation
  • Causes abnormal glycogen branching in muscle cells with increased glycogen storage, enhanced sensitivity to insulin
  • Reduced ability to use that glycogen
  • Leads to muscle necrosis due to abnormal energy metabolism
  • Leads to exercise intolerance, muscle atrophy/weakness
42
Q

Describe the clinical signs of PSSM in the horse

A
  • Onset at 5yo
  • Onset of exercise intolerance 20 ins after start exercise
  • Worse after period of rest
  • Variable severity
  • HL more affected than FL
43
Q

Outline the diagnosis of PSSM in the horse

A
  • Persistently increased CK, 3x increase after exercise
  • Semimembranosus muscle biopsy shows amylase resistant inclusion
  • Blood test for GYS1 mutation
44
Q

Outline the generic treatment for all forms of equine rhabdomyolysis

A
  • Rest essential
  • Analgesia: NSAIDs (care - high risk of azotaemia, hypovolaemia), opioids (pethidine), detomidine/ACP, lidocaine infusion (no VPL)
  • DMSO, vit E, dantrolene suggested, little evidence
  • Fluid therapy and electrolytes via NG tube (isotonic soln) if mildly affected, IV if severely affected
45
Q

Outline the management of a case with exercise induced sporadic equine rhabdomyolysis

A
  • Box rest then pasture turnout

- Reassess CK and AST 3 days after starting exercise, should be normal if sporadic

46
Q

Outline the management of chronic exerise induced equine rhabdomyolysis

A
  • PSSM: pasture rest asap, no more than 48hours stabled, gradual return to exercise, once in exercise no days off
  • RER: limited rest, once in full exercise no days off
  • Reduce stress, turnout with others
  • Prolonged warmup and rest periods during training (interval training)
  • Diet
  • Medical management
47
Q

Outline the dietary management of a case of chronic exercise induce equine rhabdomyolysis syndrome

A
  • <20% of diet should be structural cardbohydrates
  • Oil 10% of energy
  • No excessive protein
  • 1% BWT minimum fibre, ideally 2%
  • Supplementation of Ca, Mg, Phos, Na, K, Vit E and selenium
48
Q

Which drugs may be used in the managment of chronic exercise induced equine rhabdomyolysis syndrome?

A
  • Sedation prior to exercise e.g. ACP (CARE)
  • Dantrolene (800mg/day 1hr pre exercise not in food, reduces effect of exercise on CK rises)
  • Phenytoin (affects ion channels and increases threshold for Ca release from SR)
49
Q

Justify the use of sedatives in the management of equine rhabdomyolysos

A
  • Anxiolytic
  • May improve muscle perfusion
  • Reduce use/contraction of muscles
  • In chronic cases may be used prior to exercise with care
50
Q

Describe the clinical signs of atypical myopathy/seasonal pasture myopathy in the horse

A
  • Sudden onset myoglobinura

- Severe stiffness (recumbent, not moving)

51
Q

What causes atypical myopathy/seasonal pasture myopathy in the horse?

A
  • Plat toxin hyperglycin A, found in sycamore tree seeds in the UK (Box Elder in USA)
  • Sudden onset exertion
52
Q

Outline the pathogenesis of atypical myopathy/seasonal pasture myopathy in the horse

A
  • Plant toxin
  • Results in severe myoglobinuria
  • Muscle fibre structure disruption and degeneration of fibres
53
Q

Outline the management of atypical myopathy/seasonal pasture myopathy

A
  • Supportive therapy - v high rates IVFT
  • Glucose, insulin, carnitine and vit C
  • Very high mortality - regardless of treatment likely to be fatal
54
Q

Discuss the prevention of atypical myopathy in the horse

A
  • Prevention of access to sycamore seeds e.g. hoovering/picking up sycamore seeds, fencing off areas, reducing stocking density in pastures, short turnout periods (<6hrs)
  • Supply extra forage where pasture is poor
55
Q

In which species does malignant hyperthermia occur?

A

Pigs and horses

56
Q

Outline the pathogenesis of malignant hyperthermia

A
  • Autosomal dominant mutation of ryanodine receptor (RYR)
  • Results in increased [Ca2+] within the cell
  • Heat from Ca2+/ATPase
  • Depletion of ATP
57
Q

Outline the treatment of malignant hyperthermia

A

Ryanodine receptor antagonist e.g. dantrolene

58
Q

Briefly describe post anaesthetic myopathy in the horse (appearance, key ddx, causes)

A
  • Prolonged recumbency following anaesthesia, muscles may be swollen, v firm, v sore
  • DDx: neuropathy, myelopathy (in these limbs will be paralysed, in PAM are just too weak to stand on limbs), spinal cord malacia
  • Causes: heavy horses, reduced perfusion of muscles, prolonged surgery, low BP, poor positioning
59
Q

Describe the typical presentation for equine motor neurone disease

A
  • Elephant stance
  • Weak when standing, normal during movement
  • Muscle fasciculation, weight loss
60
Q

Explain the development of equine motor neurone disease

A
  • Related to restricted pasture access, poor quality hay without balancers esp. vit E deficiency
  • Selenium deficiency
  • Oxidative daamge to type 1 fibres
61
Q

Describe the typical laboratory findings for EMND

A
  • CK and AST occasionally change
  • CSF inflammatory
  • Pigment retinopathy (line)
  • Vit E <1ug/ml
  • Muscle biopsy of tail head muscle (sacrocaudalis dorsalis medialis)
62
Q

Outline the treatment of EMDN and the prognosis

A
  • Vit E supplementation (hydrosoluble forms), up to 3mg/kg selenium supplementation
  • Poor prognosis
63
Q

Briefly outline the various presentations of nutritional muscle disease in large animals

A
  • Peracute to subacute myodegeneration
  • Very acute: sudden muscle necrosis
  • Cardiac and skeletal muscle forms
64
Q

Briefly describe cardiac and skeletal nutritional muscle disease in horses (cause, signalment, diagnosis)

A
  • Selenium or vit E
  • Often young, rapidly growing LA (<1yr), often Se deficient dams, also in utero form
  • Dx: blood sample showing low Se and GSHPx
  • Histopath showing inflammatory myositis
65
Q

Describe the clinical presentation of cardiac nutritional myodegeneration in the horse

A
  • Sudden onset
  • Death
  • Depression, resp. distress
  • Rhythm disturbances
66
Q

Describe the clinical presentation of skeletal myodegeneration

A
  • Slower onset vs cardiac
  • Weakness and stiffness
  • Recumbency
  • Muscle pain
  • Can affect resp. muscles e.g. diaphragm and therefore affect resp.
67
Q

Give alternative names for clostridial myonecrosis in the large animal

A
  • Black leg
  • Malignant oedema
  • Gangrene
68
Q

Describe the presentation of clostrial myonecrosis in large animals

A
  • Rapidly progressive, high mortality
  • Pyrexia
  • Depression
  • Pain
  • Lameness
69
Q

Describe the common causes of clostrial myonecrosis in horses, cattle and sheep

A
  • Horse: injection site/puncture wounds
  • Cattle: blunt trauma
  • Sheep: shearing/dipping
70
Q

Outline the treatment of clostridal myonecrosis in large animals

A
  • Debridement and fasciotomy (introduce oxygen)
  • Antibiotics: high dose penicillin q2h IV, metronidazole for non-food animals only
  • Generally supportive management
71
Q

Outline the prevention of clostridial myonecrosis in large animals

A
  • Vaccination from 3-4 months q6m (BUT may cause more outbreaks -IM injection may facilitate introduction of bacteria into anaerobic environment)
  • Remove all dead bodies
72
Q

Describe the pathology that occurs with clostridial myonecrosis in large animals

A
  • Swelling and autolysis of site (rancid odour)
  • Blood stained fluid at orifices
  • Swelling and crepitus (gas in tissues) of muscles
  • Haemorrhagic dark muscles
73
Q

Give examples of infectious agents that may cause muscle disease in large animals

A
  • Clostridia
  • S equi var equi (rare complication)
  • Parasites e.g. sarcocystis
  • Viral myopathy: equine flu, FMDV, MCF, BVD, bluetongue
74
Q

Give examples of toxicities that may cause muscle disease in large animals

A
  • Gossypol (cotton seed) in pigs
  • Ionophores
  • Organophosphates
  • Trematone containing plants
  • Cassia spp. and white snake root
75
Q

Outline strangles as a cause of muscle disease in large animals (cause and Tx)

A
  • Rare complication
  • Immune mediate myositis 4 weeks post infection
  • Tx corticosteroids (infection usually already cleared)
76
Q

What is the importance of sarcocyctosis in large animal muscle disease?

A

Not clinically significant but important VPH implications

77
Q

What is myotonia in goats and horses?

A
  • Delayed relaxation of skeletal muscle

- In goats related to chloride channel, but not in horses

78
Q

Describe the presentation, diagnosis and treatment of myotonia in goats and horses

A
  • Atrophy weakness
  • Horses: quarter horse, proximal limbs
  • Goats: fainting goats
  • Diagnosis: EMG (specialist)
  • Tx: phenytoin (human drug)
79
Q

Briefly outline the pathophysiology of hyperkalaemic periodic paralysis in horses

A
  • Genetic disease, point mutation
  • Normal between episodes, high potassium between episodes
  • Caused by voltage gated sodium channels - remain open when triggered and do not inactivate
  • Initially hyperexcitable then unexcitable
80
Q

Describe the appearance of a horse with hyperkalaemic periodic paralysis (HYPP)

A

Muscle hypertrophy, esp. quarters, neck and shoulders

81
Q

Outline the trigger factors for an episode in a horse with HYPP

A
  • High K+ intake (alfalfa, molasses)

- Increased mobilisation (fasting, stress, anaesthesia, vigorous exercise)

82
Q

Describe the clinical signs in a horse with mild HYPP

A
  • Pronounced muscle development
  • Prolapse of third eyelid
  • Muscle fasciculations and weakness
  • Onset at 2-3yo
  • Normal after episodes
83
Q

Describe the clinical signs in a horse with severe HYPP

A
  • Muscle weakness
  • Recumbency, dog sitting
  • Dysphagia, pharyngeal collapse, laryngeal paralysis
  • Can be fatal
  • Normal after episode
84
Q

Outline the diagnosis of HYPP in the horse

A
  • Serum biochem: normal CK, increased K+ during episodes, normal before and after episodes
  • EMG between episodes shows abnormal fibrillation potentials. complex repetitive discahrges, myotonic potentials
  • DNA testing
85
Q

Describe the treatment of acute hyperkalaemic periodic paralysis in the horse

A
  • Calcium borogluconate IV (0.2-0.4ml/kg of 20% soln in 1L saline, raises membrane threshold potential)
  • Glucose IV (6ml/kg as 5% soln, stimulates insulin secretion)
  • Tracheostomy
86
Q

Describe the ongoing treatment of hyperkalaemic periodic paralysis in the horse

A
  • Acetazolamide (3mg/kg BID PO)
  • Carbonic anhydrase inhibitor (increase renal loss of potassium)
  • Dietary management to reduce potassium (can control episodes completely)

MSK2 (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions