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CFT I > Exam 1 - Generalized Neuromuscular Disease > Flashcards

Exam 1 - Generalized Neuromuscular Disease Flashcards

1
Q

what is a differential for acute disease of the muscle in generalized neuromuscular disease?

A

polymyositis

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2
Q

what are differentials for acute disease of the neuromuscular junction in generalized neuromuscular disease?

A

tick paralysis

botulism

myasthenia gravis

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3
Q

what are differentials for acute disease of the nerves in generalized neuromuscular disease?

A

acute idiopathic polyradiculoneuritis - coonhound paralysis

infectious causes

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4
Q

what is a differential for acute disease of alpha motor neurons in generalized neuromuscular disease?

A

myelitis - especially rabies

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5
Q

what neuromuscular diseases may present acutely non-ambulatory tetraplegic & will mimic a high cervical fracture or severe brain injury prior to the neuro exam?

A

tick paralysis, botulism, myasthenia gravis, acute idiopathic polyradiculoneuritis, & myelitis (rabies)

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6
Q

what should be in the standard diagnostic work-up for neuromuscular disease?

A

history of prescription drugs

CBC/chem with creatine kinase

met check - chest rads to r/o megaesophagus, thymoma, & aspiration pneumonia & abdominal ultrasound/rads

endocrine testing - thyroid & hyperadrenocorticism

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7
Q

what makes up a lower motor neuron unit?

A

cell body (CNS), axon (PNS - ventral root, nerve), muscle, & neuromuscular junction

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8
Q

how do patients with acute idiopathic polymyositis present clinically?

A

weakness, stilted gait, atrophy, inability to open jaw, megaesophagus, & dysphonia

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9
Q

what lab abnormalities may be seen with acute idiopathic polymyositis?

A

creatine kinase is typically very high

inflammatory leukogram is possible

negative paired infectious disease titers

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10
Q

how is acute idiopathic polymyositis diagnosed?

A

muscle biopsy is supportive

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11
Q

how is acute idiopathic polymyositis treated?

A

immunosuppression - corticosteroids are the 1st line
azathioprine as a 2nd line or adjunct treatment

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12
Q

how is acute idiopathic polymyositis monitored?

A

serial CKs to monitor remission

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13
Q

what are some causes of infectious polymyositis?

A

neospora - dog

toxoplasma - dog & cat

hepatozoon - dog

FIV - cat

sarcocytis - dog

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14
Q

in a patient with suspected infectious polymyositis, what do you expect the nature of their history to be?

A

chronic problem

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15
Q

tick paralysis effects what part of the neuromuscular system?

A

pre-synaptic neuron

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16
Q

what is the typical onset of tick paralysis?

A

3-7 days

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17
Q

T/F: the absence of ticks on a dog rules out tick paralysis

A

false

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18
Q

how is tick paralysis treated?

A

pull the ticks, treat with acaricides, & shave long thick coats

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19
Q

what diagnostics should be done for a suspected tick paralysis case?

A

bloodwork & CSF tap - usually normal

thoracic radiographs

patient gets better upon removal of ticks

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20
Q

what is the agent that causes botulism?

A

clostridium botulinum

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21
Q

what is the pathogenesis of botulism?

A

blocks the release of ACh at the presynaptic membrane of the neuromuscular junction

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22
Q

how is botulism diagnosed?

A

usually based on history & clinical signs

bloodwork & CSF are typically normal

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23
Q

how is botulism treated?

A

supportive care

recovery can take weeks

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24
Q

what is the most common type of myasthenia gravis in dogs?

A

acquired form

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25
Q

what is the pathogenesis of acquired myasthenia gravis?

A

autoantibodies are directed against the acetylcholine receptors at the neuromuscular junction

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26
Q

what are the clinical signs of acquired myasthenia gravis in dogs?

A

muscular weakness & excessive fatiguability - ocular, facial, oropharyngeal, esophageal, & limb musculature

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27
Q

what is the pathogenesis of congenital myasthenia gravis?

A

animal is born with too few acetylcholine receptors

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28
Q

in working up a suspected myasthenia gravis dog, what is the first step?

A

take radiographs

use to use tensilon but not much anymore

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29
Q

in working up a suspected myasthenia gravis dog, what is the second step?

A

determining if it is congenital or acquired

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30
Q

how is congenital myasthenia gravis diagnosed?

A

intercostal muscle biopsy

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31
Q

how is acquired myasthenia gravis diagnosed?

A

acetylcholine receptor antibody test

met screen

thyroid problems (thymoma)

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32
Q

this condition often occurs secondary to what neuromuscular disease?

A

myasthenia gravis

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33
Q

how is myasthenia gravis in dogs treated?

A

anti-acetylcholinesterase meds probably for life

bailey chair feedings - avoid problems with megaesophagus/aspiration pneumonia

serial AChR Ab titers to monitor

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34
Q

T/F: 50-60% of dogs diagnosed with myasthenia gravis die within 1 year of the diagnosis

A

true

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35
Q

what kind of disease is idiopathic acute polyradiculoneuritis?

A

acquired demyelinating disease

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36
Q

what does idiopathic acute polyradiculoneuritis affect?

A

spinal nerve roots

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37
Q

what is the typical presentation of a dog with idiopathic acute polyradiculoneuritis?

A

rapid (12-24 hour) onset of ascending flaccid paralysis

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38
Q

how is idiopathic acute polyradiculoneuritis diagnosed?

A

history of exposure - bloodwork & CK are often normal, CSF often has elevated protein

EMG, NCV, & muscle/nerve biopsy

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39
Q

how is idiopathic acute polyradiculoneuritis treated?

A

supportive care

40
Q

what bacteria causes idiopathic acute polyradiculoneuritis

A

campylobacter

41
Q

what is the pathogenesis of rabies?

A

virus enters body through saliva/CSF/CNS tissue of infected animal & migrates up the nerves to the spinal cord & then travels to the brain & then down from cranial nerves

viruses arrives in saliva - animal is now infectious

42
Q

what are the infectious materials that can spread rabies?

A

saliva, CNS tissue, & CSF

43
Q

what is the latency period of rabies?

A

2-26 weeks

44
Q

between dogs & cats, which are more likely to be affected by rabies?

A

dogs more so than cats

45
Q

T/F: once clinical signs of rabies begin, death occurs within 7-10 days

46
Q

what may be the first clinical sign seen with rabies?

A

ascending lower motor neuron paresis

47
Q

what disease is an important consideration in a patient presenting with acute, progressive, neurological signs?

48
Q

what are some general clinical signs of rabies?

A

altered mentation, CN paresis, multifocal/diffuse neurological signs

49
Q

what is the typical history of an animal infected with rabies?

A

outdoor, unvaccinated animal presenting with progressive disease

50
Q

what would you expect your results to be in evaluating CSF in a rabies patient?

A

lymphocytic pleocytosis

51
Q

what is the gold standard for rabies diagnoses?

A

IFA virus detection in the brain - negri bodies may be seen in later parts of the disease

52
Q

what is this? what disease is it common in?

A

negri body - rabies

53
Q

T/F: titers are diagnostic for diagnosing rabies

54
Q

how can rabies be diagnosed in humans?

A

skin biopsies

55
Q

how do you make a definitive diagnosis of rabies?

A

necropsy of the animal to look at the brain

56
Q

what is the recommended treatment for rabies?

A

euthanasia

57
Q

why not freeze or shoot a rabies suspect?

A

need the brain intact for samples

58
Q

if a vaccinated animal is bitten by a rabies suspect, what should happen?

A

quarantined for 45 days and boostered

59
Q

if a rabies vaccinated animal bites a person, what should be done? what if they are unvaccinated?

A

observed for 10 days for signs of rabies

60
Q

what should you do if a wild animal bites a person? why?

A

euthanize!

any animal that has bitten people & has neurological signs compatible with rabies

61
Q

if an animal that is unvaccinated is bitten by an animal known to have rabies, what should you do?

A

vaccinate & quarantined for 6 months or euthanized

62
Q

what are some less common differentials for acute neuromuscular disease?

A

coral snake envenomation

blue green algal intoxications

black widow spider envenomation

rare toxicities - lasalocid & other ionophores

63
Q

an animal presents with acute flaccid non-ambulatory tetraparesis, on physical exam/neuro exam, you find that the animal has a weak gag reflex and signs of regurgitation, what are the two diagnostics you’ll pursue next?

A

thoracic rads & arterial blood gas

64
Q

an animal presents with acute flaccid non-ambulatory tetraparesis, on physical exam, its respirations are showing weak chest inspiratory expansion, open-mouth breathing, & labored respirations, what two diagnostics will you pursue next?

A

thoracic rads & arterial blood gas

65
Q

why would you pursue thoracic rads & arterial blood gas in an animal presenting with acute flaccid non-ambulatory tetraparesis with labored breathing & regurgitation/weak gag reflexes?

A

looking for megaesophagus/aspiration pneumonia & to see if the animal is ventilating well

66
Q

an animal presents with acute flaccid non-ambulatory tetraparesis has a PaCO2 > 45mmHg, what should you consider?

A

mechanical ventilation

67
Q

an animal presents with acute flaccid non-ambulatory tetraparesis has a PaCO2 < 45mmHg, what should you consider?

A

monitor their breathing pattern & blood gases every 4-6 hours & provide O2 supplementation

68
Q

an animal presents with acute flaccid non-ambulatory tetraparesis has megaesophagus & aspiration pneumonia, what are your next steps?

A

avoid oral feeding - consider an NG or G tube

check AChAb titers

provide O2 supplementation

69
Q

what are the 8 main categories of chronic generalized LMN disease for differentials?

A
  1. endocrine
  2. infectious
  3. non-infectious inflammatory
  4. paraneoplastic
  5. metabolic
  6. degenerative
  7. drug-related
  8. idiopathic
70
Q

what chemo drugs may cause neuromuscular problems?

A

cisplatin & vincristine

71
Q

T/F: certain antibiotics cause neuromuscular junction blocking effects

72
Q

what 5 antibiotic classes can cause neuromuscular junction blocking effects?

A
  1. aminoglycosides - gentamycin
  2. lincomycin - precursor to clindamycin
  3. penicillamine
  4. polymixins
  5. tetracyclines
73
Q

what cancer is most frequently identified in causing polyneuropathy?

A

insulinomas

74
Q

other than insulinomas, what cancer can cause polyneuropathy?

75
Q

what cancer causes myopathy in boxers?

76
Q

what tumor can cause an associated myopathy?

77
Q

T/F: myasthenia gravis can occur secondary to neoplasia and affect the neuromuscular junction

A

true - common with thymomas

78
Q

what is myotonia?

A

disturbance in muscle relaxation after voluntary contraction or percussion

79
Q

congenital myotonia typically affects what animals?

A

young dogs

80
Q

acquired myotonia can be caused by what drug?

A

glucocorticoids

81
Q

what causes congenital myotonia?

A

malformation in the chloride channels which can cause constant contraction of voluntary muscles

82
Q

what is the typical presentation of a dog with congenital myotonia?

A

sudden onset stiffness with intact consciousness

83
Q

what is the typical presentation of acquired myotonia?

A

stiff, stilted gait

84
Q

what breed is associated with hypokalemic myopathy?

A

burmese cats

85
Q

what is the pathogenesis of hypokalemic myopathy?

A

hyperpolarization of the sarcolemma resting membrane prevents muscle contraction

86
Q

T/F: hypokalemic myopathy may be associated with renal disease, diet, and hyperthyroidism in cats

87
Q

what disease has this typical presentation

A

hypokalemic myopathy

88
Q

what is the pathogenesis of hyperkalemia causing neuromuscular problems?

A

membrane depolarization - leads to weakness, bradycardia, & atrial standstill

89
Q

what are 2 examples of metabolic diseases that have hyperkalemia?

A

post-renal disease & addisons

90
Q

what is the pathogenesis of hypocalcemia causing neuromuscular problems?

A

calcium interacts with sodium channels to reduce excitability & threshold - depolarization leads to weakness, tetany, tremors, tachycardia, hyperthermia, & seizures

91
Q

what is the pathogenesis of hypomagnesemia causing neuromuscular problems?

A

Mg is a part of an ATP molecule, so low Mg causes weakness, tremors, seizures, cardiac arrhythmias secondary to energy depletion (similar to grass staggers)

92
Q

what is the most common lab abnormality in critically ill patients?

A

hypomagnesemia

93
Q

what electrolyte abnormality may be common in brachycephalic dogs?

A

hypomagnesemia

94
Q

what diagnostic test may I use to rule in polymyositis?

A

creatine kinase

95
Q

if i’m concerned about disease affecting the neuromuscular junction, what diagnostics and history questions would be helpful?

A

tick search/tick treatment - treat regardless

myasthenia gravis titers & chest rads

carrion or garbage eater - botulism

96
Q

how can hypoglycemia cause LMN disease signs?

A

ATP depletion - weakness and seizures as a result

97
Q

what are your top 6 differentials for neuromuscular disease?

A
  1. rabies
  2. coonhound paralysis
  3. tick paralysis
  4. myasthenia gravis
  5. myositis
  6. botulism

CFT I (30 decks)

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