Test 2 - Muscle Diseases Flashcards

1
Q

_______ has remarkable sensitivity as indicator of myonecrosis in skeletal and heart muscle.
Increases within hours of a muscle insult and peaks within 4-6 hrs after injury.

A

Creatinine Kinase has remarkable sensitivity as indicator of myonecrosis in skeletal and heart muscle.
Increases within hours of a muscle insult and peaks within 4-6 hrs after injury.

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2
Q

TRUE/FALSE

Creatinine Kinase is a great marker at all times.

A

FALSE

  • Limited evaluation accompanying training, transport, strenuous exercise.
  • Recumbent or colicky animals may also have slightly elevated CK activity
  • Rhabdomyolysis usually results in substantial elevations in the activity of enzyme (1000-100,000)
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3
Q

TRUE/FALSE

Elevations in Aspartate Aminotransferase are not specific for myonecrosis.

A

TRUE

AST also has high activity in skeletal & cardiac muscle (also liver, RBCs, & other tissues).

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4
Q

What tissues does AST have high activity in?

A

high activity in skeletal & cardiac muscle (also liver, RBCs, & other tissues).

Elevations may result from hemolysis, muscle, liver, or other organ damage.

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5
Q

Describe the relationship of CK and AST in regards to myonecrosis.

Describe the peak hours and half life.

A

• AST activity rises more slowly in response to myonecrosis than does CK.
• Peaking 24 hours after the insult and the T1/2 life of AST is much longer than CK
• Comparing Serial Activities:
• Elevations in CK & AST reflect relatively recent or active myonecrosis
• CK remains persistently elevated, myonecrosis is likely ongoing
• Elevated AST activities accompanied by decreasing or normal CK activities indicate that myonecrosis is not continuing.

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6
Q

When can elevations in Lactate Dehydrogenase be seen?

A

Elevations are not specific to skeletal muscle. May occur with rhabdomyolysis,
myocardial necrosis, and/or hepatic necrosis. RBCs lysis can also liberate AST and LDH.

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7
Q

What is the importance of a U/A when assessing muscle disease?

A

U/A is particularly important with myoglobin, elevations in creatinine or persistent electrolyte imbalances.

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8
Q

A positive Hemastix test (ortho-toluidine) in the absence of hemolysis or RBCs in urine is highly suggestive of ____________.

A

A positive Hemastix test (ortho-toluidine) in the absence of hemolysis or RBCs in urine is highly suggestive of myoglobinuria

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9
Q

What is the purpose of the exercise challenge test?

A

To investigate disease processes that are precipitated by exercise, not currently showing CS

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10
Q

Describe the Exercise challenge test.

A
  • Goal is to induce subclinical elevations in serum CK activity → ↑ CK is more likely to occur if slow trotting is performed rather than strenuous exercise.
  • 15 minutes @ constant slow trot → if any signs of muscle tone changes develop, exercise should be concluded
  • Should be taken before and 4-6 hrs after exercise → CK-blood samples taken immediately after exercise do not reflect the amount of exercise induced muscle damage.
  • In healthy horses 15-30 minutes of light exercise → rarely causes >3x ↑ in CK activity
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11
Q

CK elevations greater than _______ from the exercise challenge test are indicative of exertional rhabdomyolysis.

A

CK elevations greater than 5x from the exercise challenge test are indicative of exertional rhabdomyolysis.

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12
Q

When using nuclear scintigraphy in the diagnosis of muscle disease, _______is taken up by inflamed & damaged muscle.

A

When using nuclear scintigraphy in the diagnosis of muscle disease, Technetium 99M methylene diphosphonate (MDP) is taken up by inflamed & damaged muscle.

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13
Q

Describe the following muscle abnormalities as appearing hyper or hypoechoic on U/S:

• Acute injury: muscle fiber disruption is seen as relatively _______ areas with loss of
the NL fiber striation
• Torn muscle: ________ margin. Tears in muscle fascia may be identified
• Defect in muscle/hematoma is _______. progressively more echogenic as the
muscle repairs
• ↑ CT or loss of muscle cell mass shows ________
• Mineralization or gas pockets shows ______ shadowing artifacts

A

• Acute injury: muscle fiber disruption is seen as relatively hypo echoic areas with loss of
the NL fiber striation
• Torn muscle: Hyperechoic margin. Tears in muscle fascia may be identified
• Defect in muscle/hematoma is hypoechoic. progressively more echogenic as the
muscle repairs
• ↑ CT or loss of muscle cell mass shows hyperechoic
• Mineralization or gas pockets shows hyper echoic shadowing artifacts

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14
Q

TRUE/FALSE:

Fixation in formalin is acceptable for all muscle disorders

A

FALSE

Formalin fixation results in artifacts, which can impact proper interpretation of pathology. May want to send it in saline.

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15
Q

Describe the procedure for muscle biopsy.

A
  • Enough muscle should be obtained to form square inch sample (minimum)
  • Samples don’t tolerate shipping well
  • Care must be exercise to infiltrate only the SQ tissues with anesthetic agent
  • 2 parallel incisions inch apart should be made longitudinal to muscle fibers w/ scalpel
  • Muscle should only be handled in one corner using forceps & avoid crushing
  • Routine histopath samples can be placed in formalin
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16
Q

Caffein and Halothane are used to diagnoes ________.

A

Caffein and Halothane are used to diagnose Recurrent Exertional Rhabdomyolysis & susceptibility to Malignant Hyperthermia.

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17
Q

________ is caused by inherited defect in skeletal muscle sodium channel.

A

Hyperkalemic Periodic Paralysis

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18
Q

What horse breeds are affected by Hyperkalemic Periodic Paralysis?

A

Quarter Horses,
American Paint Horses, Appaloosas & Quarter Horse Cross bred animals worldwide

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19
Q

TRUE/FALSE

Foals born in 2007 and later testing heterozygus affected for HYPP (H/h) are not eligible for registration with the AQHA.

A

FALSE.

They must be homozygous (H/H)

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20
Q

ingestion of diets high in _________, alfalfa hay, molasses can trigger epidose of HYPP.

What are some other causes.

A

Potassium

Stress can precipitate CS → the onset of signs is often unpredictable without a definable cause
• Other possible precipitating factors:
• Cold weather
• Pregnancy or concurrent disease
• Rest following exercise

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21
Q

TRUE/FALSE

Serum CK shows no change or only modest ↑ during episodic fasciculations and weakness of HYPP

A

TRUE

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22
Q

What are some respiratory tract abrnomalities that may be seen with HYPP?

A
  • Respiratory distress due paralysis of the upper respiratory muscles
  • Dysphagia
  • Pharyngeal collapse & Edema
  • DDSP
  • Laryngeal paralysis
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23
Q

What are the relevant clinical pathological findings of HYPP?

A
  • Hyperkalemia (6-9 mEq/L)
  • Hemoconcentration
  • Mild hyponatremia during clinical manifestations of the disease with normal acid-base balance
  • Potassium concentration returns to normal following the abatement of CS
  • Some horses may have normal serum potassium concentrations during minor episodes of muscle fasciculations
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24
Q

How is HYPP Diagnosed?

A

Demonstration of the base-pair sequence substitution in the abnormal segment of the DNA
encoding for the alpha subunit of the sodium channel - muscle biopsy
• Mane or tail hair should be sent to a licensed laboratory

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25
Q

How is HYPP Controlled?

List Diet, exercise and medical control.

A

• ↓ dietary potassium and ↑ renal losses of potassium are the 1° tests
• Avoid high potassium feeds such as alfalfa, soybean meal, sugar molasses, beet molasses
• High water content of pasture grass contains lesser amounts of K+
• Regular exercise and/or frequent access to a large paddock also beneficial
• Diets higher in K+ should gradually be adjusted over a period of 2 weeks.
• Vit E, selenium, salt and balanced minerals
• Commercially available complete feeds with guaranteed K+ content
• For horses with recurrent episodes
Acetazolamide (2-3 mg/kg orally, every 8-12 hrs) → stabilizes blood glucose & K+ by stimulating insulin secretion
Hydrochlorothiazide (0.5 - 1 mg/kg orally q12 hrs)
• Effects are different mechanisms - both ↑ renal K+ excretion
• Meds may be restricted in competitions

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26
Q

What is the prognosis for horses with HYPP?

A
  • In most HYPP is a manageable disorder → recurrent bouts may occur and several can be fatal
  • Owners should be strongly discouraged from breeding these animals → dominant trait, breeding an affected horse to a normal horse results in a 50% chance of producing a foal with HYPP
  • Owners of affected horses should advise vets of HYPP status → before anesthesia or procedures during heavy sedation.
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27
Q

_______ is a painful condition that arises from hyperactivity of motor units. it is Caused by repetitive firing of the peripheral and/or CNS. The origin in most cases is intramuscular portion of the motor nerve terminals.

A

Muscle Cramping

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28
Q

Muscle cramping may result from diets that are deficient in Na or K. Because of this, ______ may also be seen with it.

A

Muscle cramping may result from diets that are deficient in Na or K. Because of this, Synchronous diaphragmatic flutter (thumps) may also be seen with it.

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29
Q

What are the main causes of muscle cramping?

A
  • Dehydration
  • Electrolyte abnormlaities from dietary deficiencies (Na, K, Cl)
  • Exhaustion in Endurance Horses (hot weather and high humidity, extreme sweat loss high in Na, K, Cl)
30
Q

What electrolyte abnormalities are usually associated with muscle cramping?

A

Hypochloremic metabolic alkalosis

Hypokalemia

Hypomagnesium

Low serum Ionized Calcium

31
Q

TRUE/FALSE

Muscle cramping does not produce changes in CK, AST or present with myoglobinuria.

A

TRUE

32
Q

How is muscle cramping treated?

A

Mild: Self-limiting

Severe: PO/IV polyionic fluids, cooling (water, fans)

HCO3- is CONTRAINDICATED

Supplement NaCl and KCl in feed

33
Q

________ is the tick associated with ear tick muscle cramps.

A

Otobius megnini

34
Q

What muscle groups are affected by ear tick muscle cramps?

A

Intermittent cramping of pectoral, triceps, abdominal, or semitendinosus/membranosus

35
Q

TRUE/FALSE

Both dietary and ear tick muscle cramps do not produce elevations in CK

A

FALSE.

Dietary does not. Ear ticks does.

36
Q

How is ear tick muscle cramps treated?

A
  • Local treatment using pyrethrins resulting in recovery within 12-36 hrs
  • Acepromazine may be helpful to relieve painful cramping (prolapsed penis. He will not give)
37
Q

A horse that has recently received an IM injection presents with tremors, ataxia, dyspnea an recumbence. The initial area is swollen, hot and discolored with malordorous serosanguineous discharge coming from the wound.

What do you suspect? What is the prognosis?

A

Clostridial Myonecrosis

Death can occur within 12-24 hours if left untreated. Good with treatment?

38
Q

Clostridial myonecrosis is associated with injections of ______.

A

Flunixin meglumine

39
Q

How is clostridial myonecrosis diagnosed?

A

Smear is usually diagnostic (matchstick organism)

May also take aspirates, use fluorescent antibody testing or anaerobic bacterial culture.

40
Q

What is the treatment for clostridial myonecrosis?

A

Penicillin is the drug of choice -CRI double dose

Oral metronidazole, gentamicin

41
Q

______ is associated with submandibular lymphadenopathy & guttural pouch epyema.
• Horses develop a stiff gait, which progresses rapidly to markedly firm, swollen, painful epaxial and gluteal muscles.

A

Streptococcus equi

42
Q

What are the two etiologies that have been proposed for the myopathy associated with Streptococcus equi?

A

• 1. Toxic Shock-like reaction arising from profound non-specific T cell stimulation by streptococca super
antigens with release of high levels of inflammatory cytokines
• 2. Bacteriemia w/ local multiplication and production of exotoxins or proteases with skeletal muscle

43
Q

Pain management is a big concern with Streptococcus equi. What is the current protocol?

A

• CRI of lidocaine, detomidine, ketamine, may help control anxiety & pain

44
Q

Immune-Mediated Polymyositis has been recently reported in the ______.
• 1/3 of horses with IMM seem to have been exposed to _________.

A

Immune-Mediated Polymyositis has been recently reported in the Quarter horse.
• 1/3 of horses with IMM seem to have been exposed to S. equi or respiratory disease.

45
Q

Immune-mediated polymyositis may be associated with what two viruses?

A

Herpes and influenza

46
Q

A muscle biopsy of epaxial / gluteal muscles with _________ shows lymphocyte vasculitis, angular atrophy, fiber necrosis with macrophage infiltration & regeneration

A

• Immune-Mediated Polymyositis

47
Q

• Immune-Mediated Polymyositis is treated with _______.

A

Corticosteroids

48
Q

_______ is a highly fatal acquired lipid storage myopathy of pastured horses in europe and central and northeastern parts of N. America.

A

Seasonal Pasture Myopathy & Atypical Myopathy

49
Q

Seasonal Pasture Myopathy & Atypical Myopathy is associated with what tree and toxin?

A

Acer species (e.g. boxer elder - Acer negundo)

Toxin = hypoglycin A

50
Q

Seasonal Pasture Myopathy & Atypical Myopathy results in hypoglycin A liver metbolization into MCPA (methylenecyclopropylacetic acid).

• MCPA irreversibly binds to multiple enzymes that are essential for metabolism of fatty acids and
branched chain amino acids
• Accumulation of fat esters can damage muscle cell membranes and energy deficiency also arises from an ___________.

A

easonal Pasture Myopathy & Atypical Myopathy results in hypoglycin A liver metbolization into MCPA (methylenecyclopropylacetic acid).

• MCPA irreversibly binds to multiple enzymes that are essential for metabolism of fatty acids and
branched chain amino acids
• Accumulation of fat esters can damage muscle cell membranes and energy deficiency also arises from an inability to metabolize fat

51
Q

TRUE/FALSE

Post-anesthetic myoneuropahy is associated with radial nerve paralysis.

A

FALSE.

It is not. It ocurs from muscle that are in contact with hard surface or compromised arterial blood supply.

52
Q

What are the two tpe of post-anesthetic myoneuropathy?

A

Localized and generalized (similar to malignant hyperthermia).

53
Q

What is the only medical treatment for post-anesthetic myoneuropathy? (all other treatments are supportive)

A

Dantrolene sodium (decreases Ca release from SR)

54
Q

A horse with a history of anesthesia presents with anxiety, hyperthermia, tachycardia, tachypnea, myoglobinuria. These are all signs of what disease?

A

Post-anesthetic Myoneuropathy

55
Q

__________ is the most common muscle disorder in horses.

A

Sporadic Exertional Rhabdomyolysis is the most common muscle disorder in horses.

56
Q

_________ is a classic sign of sporadic exertional rhabdomyolysis. Other signs include colic or recumbence after 15-30 min of exercise.

A

Myoglobinuria

57
Q

A horse presents with Stiff gait, excessive sweating and a high respiratory rate during or after exercise with firm painful muscles. How would you confirm your suspicion of sporadic exertional rhabdomyolysis?

A

The presence of myoglobinuria

History & Clinical Signs

Confirmation → abNL ↑ of CK and/or AST. Severity reflected by variable elevations of serum CK activity

58
Q

What are the dietary imbalances associated with sporadic exertional rhabdomyolysis?

A

Dietary imbalances: triggered by diets w/ high nonstructural carbohydrate (NSC) content and low forage content.
Diets deficient in electrolytes. May exacerbated by inadequate selenium and vitamin

59
Q

How would you treat sporadic exertional rhabdomyolysis?

A
  • Anti-inflammatories, sedative/tranquilizer, fluid therapy, muscle relaxants, nutrition
  • Severe cases my lead to renal damage d/t to combined effects of NSAIDs and myoglobin.
  • Monitor Creat to assess extent of renal damage. If ↑ continually, give fluid therapy.
  • Horses should be stall rested for a few days on a hay diet, following ER episode
  • Gradually to small paddock turnout in a quiet area → continue monitoring until enzyme concentrations are normal
  • Resume training Gradually
  • Avoid excessive calories intake and ensure proper balance of vitamins and minerals
60
Q

What are the risk factors for recurrent exertional rhabdomyolysis?

A

Nervous Temperment, high cortisol before exercise, thoroughbred, females, young.

Diets with high carbohydrates.

A few days of rest before exercise.

61
Q

What medications may be used with RER?

A

Acepromazine

Reserpine & fluphenazine

Dantrium sodium

Phenytoin

62
Q

What are non-medical management techniques for RER?

A

• Prevention of RER is complex and multiple factors need to be changed to ↓ episodes
• Envornment, exercise regimen, diet
• Medication may be necessary at times to prevent further episodes
• Environment and stressful situations can be monitored
• Tranquilizers
• Diet: An appropriate caloric intake and adequate vitamins and minerals are the core elements of managing RER • Management of RER horses was significantly improved by using a Low-Starch,
Concentrates diet.
• Exercise: Days off training in a stall are discouraged • Post exercise CK activity is higher following 2 days of rest, • Compared to values taken when performing consecutive days of the same amount of submaximal exercise

63
Q

What is the pathogensis of polysaccharide storage myopathy?

A

• Unable to generate sufficient Acetyl-Coa from either carbohydrate or fat metabolism to fuel muscle
contraction during sub maximal exercise.

64
Q

Polysaccharide storage myopathy is associated with the _____ gene mutation.

A

GYS1

65
Q

PSSM1 is associated with ______, while PSSM2 is associated with ______.

(Horse breeds)

A

Draft horses

Quarter horses

66
Q

A draft horse presents tucking up of the abdomen, muscle stiffness, sweating, and firm muscle
contractures. Signs have been goign on for an hour.

Lab work shows mMarkedly elevated serum CK activity >35,000 U/L and myoglobinuria.

What do you suspect?

A

Acute PSSM1

67
Q

A horse presents with low-grade reluctance to exercise, poor performance, stopping and
stretching out as if to urinate and unwillingness toward exercise. Chronic back pain, fasciculations
or pain on palpation of lumbar muscles. • Serum CK activities are elevated even when the horse is at rest. What do you suspect?

A

Chronic PSSM 1

68
Q

PSSM2 is diagnosed by _______ in Quarter Horses.

A

PSSM2 is diagnosed by muscle biopsy in Quarter Horses.

69
Q

Muscle glycogen concentrations in PSSM1 are ______ (<, > ,= ) PSSM2.

A

Muscle glycogen concentrations in PSSM1 > PSSM2.

70
Q

_______ is a common complaint in Quarter Horses with PSSM2.

A

Muscle atrophy is a common complaint in Quarter Horses with PSSM2

71
Q

How is PSSM managed?

A

• Rest
• Stall rest <48 hours after an episode of rhabdomyolysis
• Provide turnout in paddocks of gradually increasing size.
• Hand walking more than 5 to 10 minutes at a time (may trigger another episode of rhabdomyolysis)
• Exercise and diet
• The beneficial response to low-starch, fat-supplemented diets in conjunction with a regular
incremental exercise program
• Many horses with PSSM are easy keepers and May be overweight at the time of diagnosis
• At least 70% of horses show notable improvement in clinical signs and many return to acceptable
levels of performance

72
Q

What are the components of Racetrack Tying up?

A

Sweet feed: High fiber high fat diet with significant amount of protein. Some alfalfa with free choice hay

Furosemide: electrolytes, fluids with vitamins before races or after breezing

Stress: Mg IV, acupuncture

Gastric Ulcers: gastrogard, omeprazole

Other: rubola vaaccine, azoture treatment