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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
Q

How do you manage polysaccharide storage myopathy (both PSSM 1 + 2)

A
  • 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
Q

What is the prognosis for PSSM 1 + 2?

A

Improve with management

PSSM1 is always susceptible

Challenging

27
Q

What is myofibrillar myopathy?

A

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
Q

What breeds are seen to have myofibrillar myopathy (MFM)?

A

Arabians and warmbloods

29
Q

What signs are seen in Arabians with myofibrillar myopathy (MFM)?

A
  • A decline in performance 8-10 years old
  • Intermittent tying-up
  • CK and AST increase but not too high
  • +/- dark urine
30
Q

What signs are seen in warmbloods with myofibrillar myopathy (MFM)?

A

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
Q

How do you diagnose myofibrillar myopathy (MFM)?

A

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
Q

How do you manage myofibrillar myopathy (MFM)?

A

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
Q

What is myosin-heavy chain myopathy - MHCM?

A

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
Q

What breeds are affected by myosin-heavy chain myopathy - MHCM?

A

QH, paints, and appaloosas

35
Q

What is immune mediated myositis (IMM)?

A

Where the immune system will attack the abnormal 2x fibers

Triggers could be strep equi, vaccination, or other

36
Q

What signs are seen with immune mediated myositis (IMM)?

A

Muscle loss on the topline - rump: 1-3 days

Lethargy

Anorexia

Stiffness

Myoglobinuria

37
Q

How is immune mediated myositis managed?

A

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
Q

What is the prognosis of immune mediated myositis?

A

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
Q

What is nonexertional rhabdomyolysis?

A

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
Q

What is glycogen branching enzyme deficiency (GBED)?

A

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
Q

What is hyperkalemic periodic paralysis (HYPP)?

A

Inherited autosomal dominant mutation in the Na+ channel

Mostly seen in QH (from IMPRESSIVE)

Heterozygous are less affected

Homozygous are more severe

42
Q

What is actually happening in cases of HYPP?

A

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
Q

What are the some clinical signs or HYPP?

A

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
Q

What does bloodwork look like for HYPP horses?

A
  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
Q

What can trigger an HYPP episode?

A
  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
Q

How do you diagnose HYPP?

A

Genetic testing of hair with roots

47
Q

How do you treat MILD HYPP?

A
  1. Feed grain or corn syrup
  2. Insulin release to cause K to move into the cell
  3. Light exercise
  4. Spontaneous recovery
48
Q

How do you treat SEVERE HYPP?

A
  1. Ca gluconate IV + dextrose: slow
  2. Move K into the cell with dextrose IV or NaHCO3 if needed
  3. Tracheostomy
49
Q

How do you manage HYPP?

A
  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
Q

What is white muscle disease?

A

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
Q

What clinical signs are seen with white muscle disease?

A

Progressive weakness and poor performance

Inability to nurse

Severe myopathy
- Masseteric atrophy
- Dyspnea
- Dysphagia

Sudden death - there is a high mortality

52
Q

How do you confirm cardiac myopathy?

A

Measure the cardiac troponin

53
Q

How do you treat and diagnose white muscle disease?

A

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
Q

What is clostridium myonecrosis?

A

An emergency that is severe and fatal

Fast necrosis of the muscle caused by clostridium spp.

Go into SIRS

55
Q

What are the clinical signs of clostridium myonecrosis?

A

Deteriorate very fast - about 48 hours

Swelling: painful and warm

Fever

Crepitus may be seen

Tachycardia and tachypnea

Inflammatory leukogram

Lethargic

56
Q

How do you diagnose clostridium myonecrosis?

A

History of any injectable (do not give flunixin IM)

Trauma

Clinical signs + a history

Cytology: G+ rod

Culture will take time but possible

57
Q

How do you treat clostridium myonecrosis?

A

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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