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Diseases and Diagnosis > Block 2 #4 > Flashcards

Block 2 #4 Flashcards

1
Q

What is an example of a spinal reflex?

A

patellar reflex

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2
Q

What happens to spinal reflexes when LMN are involved?

A

Reduced or absent

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3
Q

What does it mean if a patient is positive on a crossed extensor?

A

UMN involvement

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4
Q

How is the neurological exam ordered?

A

Least offensive to most offensive

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5
Q

What is an important finding that owners may not bring up in diffuse LMN diseases?

A

Voice change

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6
Q

What lesion will cause LMN disease to both upper and lower limbs?

A

NONE!

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7
Q

What is an elephant on a beach ball posture from?

A

diffuse LMN disease

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8
Q

Do diffuse LMN patients have ataxia?

A

No
This is a CNS thing to have

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9
Q

What are 4 common diffuse LMN diseases?

A

Acute canine polyradiculoneuritis (coonhound paralysis)
Botulism
Tick paralysis
Myasthenia gravis

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10
Q

Do animals with diffuse LMN disease have patella reflex?

A

No

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11
Q

What is the mechanism of acute canine polyradiculoneuritis?

A

Immune-mediated

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12
Q

What is a time an animal can develop acute canine polyradiculoneuritis?

A

After rabies vaccine

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13
Q

What is the pathogenesis of ACP?

A

Production of autoantibodies against axons and myelin

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14
Q

What nerve roots are most affected?

A

Ventral - motor

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15
Q

Which anatomic nerve roots are most affected?

A

Lumbar and sacral (rear end)

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16
Q

What is a common symptom of ACP?

A

Change in bark (dysphonia)

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17
Q

What causes botulism?

A

Ingestion of neurotoxins of clostridium botulinum

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18
Q

Where do the neurotoxins come from?

A

Toxins in flesh (carrion) or spoiled food

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19
Q

Where do toxins enter the nervous system?

A

At the nerve endings

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20
Q

What is the molecular pathogenesis of botulism

A

Cleaves snap-25, VAMP, and syntaxin and prevent Act release from presynaptic terminal

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21
Q

What type of muscles are affected by botulism?

A

Smooth and striated muscles (all? lol)

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22
Q

What is the different between ACP and botulism on physical exam?

A

Megaesophagus common in botulism and not in ACP

Cranial nerves are affected in botulism but not in ACP

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23
Q

Compare progression of botulism to ACP

A

Botulism is 1-3 week recovery, much shorter

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24
Q

What is tick paralysis caused from?

A

tick paralysis

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25
Q

What is the pathogenesis of tick paralysis?

A

toxin interferes with function of Ca in the release of Ach

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26
Q

How long after tick attachment does it occur?

A

5-9 days

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27
Q

What is the difference between tick paralysis and the others?

A

Very rapid and death will occur if not removed fast enough

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28
Q

What is the most common diffuse LMN cause?

A

Myasthenia gravis

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29
Q

What are the 2 forms of myasthenia gravis?

A

Congenital vs acquired

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30
Q

What is the most common form of myasthenia gravis?

A

Acquired

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31
Q

What is the pathogenesis of myasthenia gravis?

A

Auto-antibody mediated destruction of Act receptors at the neuromuscular junction.

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32
Q

What are the 3 types of acquired myasthenia gravis?

A

Generalized (most common in vetted)
Focal
Fulminating (worse)

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33
Q

Where is the focal form limited to?

A

Esophagus

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34
Q

What is a differentiating thing about myasthenia gravis from the other diseases we’ve discussed?

A

Spinal reflexes are normally ok

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35
Q

What is the pathophysiology of myasenthia gravis?

A

Binding of autoantibodies to post-synaptic Ach receptor > compliment-mediated destruction of AchR

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36
Q

What is a very common symptom of dogs with myasthenia gravis?

A

Megaesophagus

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37
Q

How do you diagnose myasthenia gravis?

A

AchR autoantibody test

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38
Q

How is the congenital MG different?

A

No auto-immune component, just a defect in AchR

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39
Q

Why is swelling such a large problem in the brain?

A

Increases inter cranial pressure which reduces blood flow

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40
Q

What are the 4 mechanisms of edema in the brain?

A

Vasogenic
cytotoxic
intramyelinic
transependymal

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41
Q

What is vasogenic edema?

A

Leaky blood vessels

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42
Q

What is cytotoxic edema?

A

Rapid return to normal plasma osmolality where astrocytes cannot unload osmoses fast enough

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43
Q

What is the edema cycle?

A

A positive feedback loop between cytotoxic edema and vasogenic edema resulting in death

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44
Q

What is intramyelinic edema?

A

Splitting of myelin sheaths with fluid accumulation

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45
Q

What is transependymal edema?

A

Blockage of CSF flow, a slow loss of tissue

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46
Q

What is polioencephaloamalacia charactertized?

A

A morphological diagnoses

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47
Q

Where do ruminants need thiamine?

A

Cerebrocortical grey matter

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48
Q

When do ruminant get polio?

A

Ruminants can synthesize their own thiamine but when on high concentrate diets, this will lower rumen pH

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49
Q

How would a fat cat get thiamine polio?

A

Cats that go off food due to hepatic lipidosis (cats get thiamine in food)

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50
Q

What is chronic salt toxicity (bad name)

A

A morphological diagnosis of polio

Dehydrated animals are then given lots of fluid which changes the osmolality of the brain causing cytotoxic osmolality

51
Q

What toxin-related polio can occur?

A

Large amounts of new feed stuffs are given

52
Q

What are pigs especially susceptible to?

A

E coli

53
Q

What are lambs especially susceptible to?

A

C. perfringens

54
Q

What type of edema does salt toxicity trigger?

A

Cytotoxic

55
Q

What type of edema does lead poisoning, endotoxins, and thiamine deficiency trigger?

A

Vasogenic edema

56
Q

How does lead affect horses?

A

Much more sensitive than ruminants
Schwann cells, primary demyelination in PNS

57
Q

What is infarction?

A

Tissue necrosis due to loss of blood flow

58
Q

What is a septic emboli?

A

Embolism caused by bacteria that can get lodged in the brain
Thrombotic meningoencephalitis

59
Q

What is the backup of blood supply to the grey matter of the spinal chord?

A

There isnt one!
It is an “end artery”

60
Q

What happens if the end artery has an infarct?

A

malacia

61
Q

What is pan necrosis?

A

Stoppage of all nutrient to the spot

62
Q

What happens with a slow growing tumor?

A

Selective necrosis that doesn’t trigger the edema cycle

63
Q

Is there hemorrhage with a concussion?

A

NO!

64
Q

What is a concussion?

A

Transient stretching of white matter tracts in the brainstem

65
Q

What is another word for contusion?

A

Bruising

66
Q

What is avulsion?

A

Stretching of vessels resulting in tearing

67
Q

What may a hematoma trigger?

A

Edema cycle due to increased pressure

68
Q

What is delayed onset arteriospasm?

A

constricting of vessels but may lead to an infarct

69
Q

What are the factors mediating potency of arterioles?

A

Endothelial relaxation factor
Prostacyclin

70
Q

What does subarachnoid hemorrhage release?

A

Oxyhemoglobin

71
Q

What does the oxyhemoglobin cause an accumulation of?

A

Diacylglycerol
Endothelin-1

72
Q

What can blood migrate through?

A

White matter

73
Q

What is the migration of blood through white matter called?

A

Ascending-descending myelomalacia

74
Q

What does ischemia mean?

A

Inadequate blood supply to a tissue

75
Q

Where does the end artery for grey matter branch from?

A

Ventral spinal artery

76
Q

What is the worst consequence of disc herniation?

A

Hemorrhage into the subarachnoid space causing ascending-descending myelomalacia

77
Q

What is Wallerian degeneration?

A

An insult that happens cranial to an axon causing the axons caudal to die

78
Q

What are the 3 organizations of the CNS?

A

Motor system
Sensory system
Vestibular system

79
Q

Where are sensory neurons located?

A

Ganglia of the dorsal nerve root

80
Q

What CN is the vestibulocochlear?

A

VIII

81
Q

What is wobblers characterized by?

A

Stenosis of the spinal canal

82
Q

What are the 2 manifestations of wobblers?

A

Cervicovertebral instability (CVI)
Cervicovertebral static stenosis (CSS)

83
Q

What is another term for wobblers

A

Cervicovertebral stenotic myelopathy (CVSM)

84
Q

What is cervicovertebral instability?

A

Dynamic, intermittent compression

85
Q

What is cervicovertebral static stenosis?

A

Static, continuous compression

86
Q

Why are clinical symptoms worse in the read for cervicovertebral stenotic myelopathy?

A

Spinal tracts to the rear are more superficial

87
Q

When does wobblers arise?

A

Usually earlier in life

88
Q

What are the causes of wobblers?

A

Environmental and genetic

89
Q

What is the best diagnostic for wobblers?

A

Minimal sagittal diameter (MSD)

90
Q

What is minimal sagittal diameter?

A

Ratio of spinal diameter to vertebral body diameter

91
Q

What MSD would be wobbler positive?

A

<50%

92
Q

What is the symmetry of EPM?

A

asymmetric disease!

93
Q

What is the definitive host of EPM?

A

Opossum

94
Q

What parts of the body does EPM affect?

A

Spinal cord, brain stem, and cerebrum

95
Q

What is another term for Equine herpes virus?

A

Myeloencephalopathy

96
Q

What does EHV cause?

A

Abortion in mares and neonatal disease

97
Q

Does all EHV cause myeloencephalopathy?

A

No!

98
Q

What is the relevant factor in EDM?

A

Vitamin E deficiency

99
Q

What is EMND?

A

Equine motor neuron disease

100
Q

What does EMND originate from?

A

Neurodegenerative oxidative stress

101
Q

Is there ataxia with EMND?

A

NO!

102
Q

Is CVM or CVI more common in young animals?

A

CVI

103
Q

What type of horses are predisposed to wobblers?

A

Horses growing fast!

104
Q

What protozoa causes EPM?

A

Sarcocystis neurona

105
Q

What is the respiratory presentation of EHV?

A

Rhinopneumonitis

106
Q

What is the neurological manifestation of EHV?

A

EHM (myeloencephalotpathy)

107
Q

What is a defining clinical sign of EHV?

A

Urinary incontenence
Rear limb lameness

108
Q

What is a positive diagnostic of EHV?

A

Xanthochromic CSF

109
Q

What does xanthochromic CSF mean?

A

Increased protein (yellow)

110
Q

What does EMND (equine motor neuron disease) affect?

A

Gray matter

111
Q

What does EDM (equine degenerative myelopathy) affect?

A

White matter

112
Q

Does EMND or EDM have muscle atrophy?

A

EMND
EDM does not!

113
Q

What is a distinct sign of EMND?

A

No ataxia

114
Q

Is there ataxia in EDM? Muscle atrophy?

A

No muscle atrophy! Yes ataxia

115
Q

What is the most common cause of lameness is perfomance horses?

A

Navicular disease (palmar heel pain)

116
Q

Where does navicular disease normally impact?

A

Bilateral forelimb

117
Q

What is laminitis?

A

Inflammation of hoof lamina (velcro of hoof)

118
Q

What are causes of laminitis?

A

Hormones (Cushings)
Sepsis
Supporting limb laminates

119
Q

What is a type I P3 fracture?

A

Non-articular, palmar process

120
Q

What is a type II P3 fracture?

A

Articular, palmar process

121
Q

What is a type III P3 fracture?

A

Sagital, articular

122
Q

What is a type IV P3 fracture?

A

Extensor process

123
Q
A

Diseases and Diagnosis (23 decks)

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