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Equine Exam 3/Final > Mighty Muscles Man > Flashcards

Mighty Muscles Man Flashcards

1
Q

Muscle response to injury: Rhabdomyolysis

A

Muscle breakdown

CK is high

Muscle pain

Myoglobinuria

It is seen from a lot of multiple causes

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2
Q

Muscle response to injury: Atrophy

A

Decreased muscle fiber diameter

Focal - neurogenic

Generalized (IMM, PSSM1)

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3
Q

Muscle response to injury: Hypertrophy

A

Increased muscle fiber diameter

Training

Genetics

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4
Q

What must be evaluated in skeletal muscle conditions on the physical exam?

A
  1. Look for atrophy vs hypertrophy
  2. Muscle fasciculados
  3. Weight shifting
  4. Muscle tone - pain
  5. Symmetry
  6. Lameness

Make sure you ask the owner what the use or role of the horse is

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5
Q

What is exertional rhabdomyolysis?

A

Also known as “tying up”
- It is a syndrome with multiple causes
- May be sporadic vs recurrent
- Subclinical to clinical
- Different management

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6
Q

What are some clinical signs of exertional rhabdomyolysis?

A

Pain - potential to be down

Muscle stiffness

Reluctance to move

Myoglobinuria - BAD for kidneys

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7
Q

What is seen on blood work and urinalysis for exertional rhabdomyolysis?

A

BW
1. High CK (up fast and down fast)
2. High AST (Up slow and down slow)
3. +/- Azotemia
4. Hyperkalemia

UA
- Myoglobin

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8
Q

How do you diagnose exertional rhabdomyolysis with an exercise challenge test?

A

Can be used for past exert. Rhab. (ER)

  1. Run a baseline CK
  2. Trot for 15 minutes
    - Stop if stiff
  3. Check CK 4-6 hours after
  4. If CK > 800 U/L then diagnostics for ER
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9
Q

How do you diagnose exertional rhabdomyolysis with a genetic test?

A
  1. Type 1 polysaccharide storage myopathy
  2. Malignant hyperthermia
  3. Glycogen branching enzyme deficiency
  4. Hyperkalemic periodic paralysis
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10
Q

How do you diagnose exertional rhabdomyolysis with a muscle biopsy?

A

Help identify the cause

Has specific pattern damage

Use an experienced equine pathologist

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11
Q

How do you diagnose exertional rhabdomyolysis with Vitamin E and Se levels?

A

Needed for normal function but rarely cause ER. The limitation is Serum.

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12
Q

How do you treat exertional rhabdomyolysis?

A

Mild: Rest for 2-3 days and can move normal

Severe: Decreased muscle mass which may recover in 3-4 months

IV fluids + dextrose: Don’t forget the kidneys (myoglobin)

Condition the horse

Analgesia like torb and ketamine

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13
Q

What are some commonalities seen in recurrent exertional rhabdomyolysis?

A

Common in thoroughbreds
- Young
- Fillies
- Nervous
- Eating > 10 lbs grain/day
- Possible genetic component
- > gallop training =

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14
Q

How do you diagnose recurrent exertional rhabdomyolysis?

A

Signalment

Clinical signs

Exercise test
- Run a basal CK
- Have exercise (trot) then 4 hours later run another

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15
Q

How do you manage recurrent exertional rhabdomyolysis?

A

A. Get the nervous ones out to train first
B. Keep calm
C. Decrease the amount of grains and give a fat diet
D. Turn-out
E. Decrease stall rest

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16
Q

What medication is available for recurrent exertional rhabdomyolysis?

A

Dantrolene (ryanodine antagonist)
- muscle relaxant
- 1 hour pre-exercise
- 48h withdrawal period

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17
Q

What is polysaccharide storage myopathy?
- PSSM1

A

An autosomal dominant mutation in the GYS1 gene leading to elevated glycogen synthase activity.

> 1.5 x glycogen storage in muscle and glycogen is resistant to amylase

If there is no mutation, it is PSSM2

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18
Q

What breeds are affected by polysaccharide storage myopathy (PSSM1)?

A

Mostly quarterhorses
> halter QH
< racing QH

Rare in breeds like:
Arabians, thoroughbreds, or Standardbreds

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19
Q

What are some clinical signs of polysaccharide storage myopathy (PSSM1)?

A

Can range from asymptomatic to severe
1. Exertional rhabdomyolysis
- 15-20 minutes after light exercise
- after resting
2. Stop, stretch, or back pain

High NSC in the diet

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20
Q

How can you test for polysaccharide storage myopathy (PSSM1)?

A
  1. Genetic testing for the GYS1 gene
    - Hair (20-30 w/roots)
    - Blood
  2. High CK, even at rest
  3. CK 3x post exercise
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21
Q

What is amylase resistant polysaccharide mutation (PSSM2)?

A

No mutation! - Glycogen is still there not being degraded by amylase

Older horses?

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22
Q

What will be seen with quarter horses for a PSSM2 mutation?

A

More in the barrel racer, reining, and cutting

Chronic exertional rhabdomyolysis

High CK - AST

Will keep tying up

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23
Q

What will be seen with warmbloods with a PSSM2 mutation?

A

Sore muscles, lameness, and topline atrophy

NORMAL CK post exercise

24
Q

How do you diagnose PSSM2?

A

Muscle biopsy
- Use Semitendinosus or semimembranosus
- Use an equine pathologist but it is subjective
- False +

Do not use the genetic “test”

25
How do you manage polysaccharide storage myopathy (both PSSM 1 + 2)
- Get moving once they are not painful - Gradual return to work - Avoid rest: about 10 min/day - Turn out - Minimize stress - Prolonged warm-up (PSSM2) - Diet - Grazing muzzle - Hay should be low in NSC (<12%) - Fast for 6 hours pre-exercise - Commercial diets - Fat and are easy keepers
26
What is the prognosis for PSSM 1 + 2?
Improve with management PSSM1 is always susceptible Challenging
27
What is myofibrillar myopathy?
It is an abnormal accumulation of Desmin in the muscle - Desmin holds the myofibrils aligned at the z-disc - Increase in Desmin causes sarcomere myofibrils to not be aligned well Not know if PSSM2 plays a role but signs can overlap and some have amylase resistant aggregates
28
What breeds are seen to have myofibrillar myopathy (MFM)?
Arabians and warmbloods
29
What signs are seen in Arabians with myofibrillar myopathy (MFM)?
- A decline in performance 8-10 years old - Intermittent tying-up - CK and AST increase but not too high - +/- dark urine
30
What signs are seen in warmbloods with myofibrillar myopathy (MFM)?
Signs are vague which make things challenging - Poor performance as they age - Tying-up is rare - No increase in CK-AST - Not going forward, hindlimb lameness, not collecting - Rule out lameness, saddle, pelvis, other issues
31
How do you diagnose myofibrillar myopathy (MFM)?
Muscle biopsy - Semitendinosus is easier but can be the semimembranosus or middle gluteal - Special stain - Positive with abnormal aggregates of Desmin - Have an equine pathologist read There are many false + as they look like PSSM2 DO NOT use the genetic test
32
How do you manage myofibrillar myopathy (MFM)?
Core strength Consistent exercise - Prolonged warm-up - Low intensity - 3 days on and 2 off - Variable by individual Diet - Good high quality protein (20%) - Mineral - vitamin balancer - MFM pellet (muscle atrophy) - Coenzyme Q10: antioxidant - Vitamin E if low
33
What is myosin-heavy chain myopathy - MHCM?
A mutation in the MYH1 gene - Myosin in type 2x muscle fibers (the myosin is abnormal) - Fastest contracting muscle fibers - Co-dominant trait: 1 copy is enough - 2 copies is more severe
34
What breeds are affected by myosin-heavy chain myopathy - MHCM?
QH, paints, and appaloosas
35
What is immune mediated myositis (IMM)?
Where the immune system will attack the abnormal 2x fibers Triggers could be strep equi, vaccination, or other
36
What signs are seen with immune mediated myositis (IMM)?
Muscle loss on the topline - rump: 1-3 days Lethargy Anorexia Stiffness Myoglobinuria
37
How is immune mediated myositis managed?
Diet with high quality protein Steroids to immediately treat! Target vaccination for only what is needed - Use a single antigen - 4 to 6 week interval as you do not want to trigger it again
38
What is the prognosis of immune mediated myositis?
Heterozygous - 20% atrophy - Resolve with steroids or longer without - Muscle will come back in 2-3 months Homozygous - More severe - Less likely to recover - Reoccur
39
What is nonexertional rhabdomyolysis?
More severe sequelae of myosin-heavy chain myopathy - Different differential diagnosis to immune mediated myositis - M protein is similar to 2x myosin - Anaplasma phagocytophila - Not all heterozygous develop signs Limit vaccinations like IMM Prognosis is poor if down or if severe atrophy
40
What is glycogen branching enzyme deficiency (GBED)?
Present in QH and other related breeds Defect in the branching enzyme; abnormal glycogen = no fuel - Glycogen is the muscle energy and it’s being folded wrong Signs include - Late term abortion - Stillbirth - Weak foals: —Can have seizures and cause to go down —Sudden death —Euthanized by 3-4 months even with treatment —Low WBC and high CK/AST/GGT Test is a genetic test with hair
41
What is hyperkalemic periodic paralysis (HYPP)?
Inherited autosomal dominant mutation in the Na+ channel Mostly seen in QH (from IMPRESSIVE) Heterozygous are less affected Homozygous are more severe
42
What is actually happening in cases of HYPP?
Failure of Na+ gated channels to close when there is high K+ Muscle contraction causes paralysis because they cannot repolarize Depolarization inactivates voltage gated Na+ channels
43
What are the some clinical signs or HYPP?
Can be subtle to severe: 1. Muscle tremors or twitching 2. Prolapsed 3rd eyelid 3. Sweating from anxiousness 4. Severe muscle cramping 5. High HR, RR 6. Arrhythmias 7. Weakness 8. Paralysis 9 Collapse Usually appear by 2-3 years or younger if homozygous
44
What does bloodwork look like for HYPP horses?
1. Hyperkalemia: 6-9 mEq/L to equal arrhythmias - K will be normal if mild form 2. Hemoconcentration 3. Mild hyponatremia 4. Normal acid base
45
What can trigger an HYPP episode?
1. Feeds high in K 2. Stress - EXERCISE is not a trigger, it is the stress leading up to it 3. Anesthesia 4. Transportation
46
How do you diagnose HYPP?
Genetic testing of hair with roots
47
How do you treat MILD HYPP?
1. Feed grain or corn syrup 2. Insulin release to cause K to move into the cell 3. Light exercise 4. Spontaneous recovery
48
How do you treat SEVERE HYPP?
1. Ca gluconate IV + dextrose: slow 2. Move K into the cell with dextrose IV or NaHCO3 if needed 3. Tracheostomy
49
How do you manage HYPP?
1. Reduce K in the diet 2. Test the hay 3. Do not give molasses 4. No electrolytes (supplements) - there are lots of K 5. Grass okay because it has a decreased K content 6. Regular exercise 7. Avoid stress
50
What is white muscle disease?
A free-radical mediated myopathy caused by areas of low selenium Can be peracute to subacute and affect - Skeletal and cardiac muscle - Tongue in foals - Heart in adults
51
What clinical signs are seen with white muscle disease?
Progressive weakness and poor performance Inability to nurse Severe myopathy - Masseteric atrophy - Dyspnea - Dysphagia Sudden death - there is a high mortality
52
How do you confirm cardiac myopathy?
Measure the cardiac troponin
53
How do you treat and diagnose white muscle disease?
Supplement selenium (organic is better) Selenium IM to foals Do not give injectable Se to adults Serum gluthatione - peroxidase -Serum Se: A normal does not rule it out
54
What is clostridium myonecrosis?
An emergency that is severe and fatal Fast necrosis of the muscle caused by clostridium spp. Go into SIRS
55
What are the clinical signs of clostridium myonecrosis?
Deteriorate very fast - about 48 hours Swelling: painful and warm Fever Crepitus may be seen Tachycardia and tachypnea Inflammatory leukogram Lethargic
56
How do you diagnose clostridium myonecrosis?
History of any injectable (do not give flunixin IM) Trauma Clinical signs + a history Cytology: G+ rod Culture will take time but possible
57
How do you treat clostridium myonecrosis?
Support the SIRS Penicillin 2x the dose and metronidazole Surgical fenestration - debridement: it needs air so cut it! Establish some drainage Will look worse before it gets better Communicate with the client what’s going on

Equine Exam 3/Final (5 decks)

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