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LAM II - VA > Neuro - 5 Q's > Flashcards

Neuro - 5 Q's Flashcards

1
Q

what to differentiate when evaluating neuro dz

A

central from peripheral

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2
Q

what to avoid with misdiagnosis

A

rabid animal

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3
Q

how to localize

A

evaluate central nervous signs

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4
Q

what to associate neurological signs with

A

clinical scenarios

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5
Q

four types of cerebral lesions

A

vestibular
frontal lobe
brain stem
cortex

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6
Q

vestibular signs

A

circling and head tilt

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7
Q

frontal lobe signs

A

propulsive movement

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8
Q

brainstem signs

A

disturbed sensorium
blind
seizures

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9
Q

cortex signs

A

consciousness

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10
Q

what is the occipital lobe responsible for

A

visual reception and interpretation

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11
Q

what is the basal ganglia and what does it do

A

processing link

initiates and directs voluntary movement

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12
Q

cerebellar signs

A

spastic ataxia
dysmetria
tremors

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13
Q

brain stem controls what

A

neurological function necessary for survival

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14
Q

what are the functions of the brain stem

A 
breathing 
digestion 
heart rate 
blood pressure 
awake and alert
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15
Q

where do most cranial nerves arise from

A

brain stem

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16
Q

brain stem cranial nerves are pathways for what

A

pathway for all neuro tracks to the highest parts of the brain

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17
Q

two types of defecits with a brain stem lesion

A

gait

cranial nerve

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18
Q

three parts of the brain stem

A

midbrain
pons
medulla oblongata

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19
Q

type of abnormalities seen with spinal cord lesion

A

bilateral gait abnormalities

normal mentation

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20
Q

what does Upper Motor Neuron initiate, maintain, and control

A

initiates voluntary motor activity
maintains muscle tone and posture - anti gravity
controls muscular activity assoc. with visceral fxn

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21
Q

what is the efferent neuron of the PNS

A

LMN

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22
Q

what does LMN connect

A

CNS with muscle

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23
Q

where is the function of the CNS manifested

A

through the LMN

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24
Q

what controls spinal reflexes

A

LMN

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25
Q

spasticity, stiffness, hypertonia

A

UMN

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26
Q

loss of inhibition of myotactic reflexes

A

UMN

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27
Q

spinal reflexes in tact and/or exaggerated

A

UMN

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28
Q

loss of voluntary motor function - paresis or paralysis

A

UMN

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29
Q

hypotonia, hyporeflexia

A

LMN

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30
Q

muscle weakness - paresis or paralysis

A

LMN

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31
Q

loss of spinal reflexes

A

LMN

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32
Q

muscle atrophy

A

LMN

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33
Q

loss of motor innervation

A

LMN

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34
Q

2 causes of hydrocephalus

A

blue tongue

akabane

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35
Q

what does vitamin A deficiency interfere with

A

absorption of CSF at arachnoid villi

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36
Q

what happens when CSF pressure elevates from vitamin A deficiency

A

results in blindness first, followed by seizures

papillidema at the optic chiasm

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37
Q

what is an autosomal recessive trait of herefords and shorthorns

A

cerebellar abiotrophy

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38
Q

BVD in relation to cerebellar abiotrophy

A

can cause it between 100-200 days gestation

folial degeneration
cavitation of cerebellum

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39
Q

45-day-old holstein fresian female with cerebellar abiotrophy

A

recumbent and blind

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40
Q

45-day-old holstein fresian female with cerebellar abiotrophy and BVD-MD positive, what to do

A

virus neutralization

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41
Q

another time you can see BVD

A

in utero

21-day-old holstein on the slide

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42
Q

BVD brain lesions

A

ocular lesions seen in both spontaneous and experimental studies of BVD

retinal atrophy
micro-opthalmia
find out rest of the CS, covered with pic on slide

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43
Q

3 reasons for malformed vertebral canal

A

myelin disorder of charolais
neuraxial edema of herefords
hereditary hypomyelinogenesis of jerseys

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44
Q

myelin disorder of charolais etiology

A

probable familial etiology

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45
Q

what is neuraxial edema of herefords

A

autosomal recessive of polled breed

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46
Q

what do we see with hereditary hypomyelinogenesis of jerseys

A

spastic dysmetric gait if they can walk

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47
Q

what is the organism for tetanus

A

clostridium tetani

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48
Q

is c. tetani gram neg or gram positive

A

positive

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49
Q

c. tetani aerobic or anaerobic?

A

anaerobic

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50
Q

what does c. tetani form

A

spore forming rod

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51
Q

how long does c. tetani remain viable

A

years

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52
Q

what does c. tetani produce and release

A

toxins - neurotoxin and tetanolysin

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53
Q

what is TeNT

A

neurotoxin

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54
Q

what does TeNT cause

A

signs called tetanospasmin

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55
Q

what type of effect does tetanolysin have

A

tissue necrotizing effect
decreased tissue oxygenation
facilitates bacterial proliferation

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56
Q

what does TeNT bind to and what happens

A

binds to nerve cell
taken up by endocytosis
moves retrograde up the axon

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57
Q

what kind of interneurons is TeNT internalized into

A

ones that regulate motor neuron activity

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58
Q

what does TeNT inhibit

A

action of inhibitory neurons

prevents release of glycine and GABA

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59
Q

what are the inhibitory neurons

A

glycine and GABA

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60
Q

how does neurotoxin bind

A

irreversibly

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61
Q

recovery after neurotoxin

A

only with the growth of new nerve terminals - can be days to weeks

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62
Q

how is tetanus acquired

A

wound infection - tail docking, castration, puncture wounds, retained placenta

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63
Q

CS of tetanus

A 
stiff gait
mild bloat 
difficulty rising 
'pump-handle' tail 
loss of rumenation
erect ears pulled back to poll - sardonic grin 
prolapsed third eyelid - spasm of retractor oculi mm.. 
spasm of masseter mm. - lock jaw 
loss of swallowing 
spastic paralysis
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64
Q

death via tetanus

A

respiratory paralysis

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65
Q

diagnosing tetanus

A

CS - muscle spasms and hyperesthesia

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66
Q

treating tetanus

A 
elimination of infection 
neutralization of free TeNT
relief of muscle spasms 
provision of good nursing care - need time for toxin to decay
prevention
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67
Q

how to eliminate infection of tetanus

A

wound debridement

gram pos spectrum abx - PPG 24,000IU/kg BID 2-3d

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68
Q

how to neutralize free TeNT

A

can only do this before uptake into nerve

tetanus antitoxin - 1500-100,000U per animal per day for 3-5 days

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69
Q

how to relieve muscle spasms with tetanus

A

tranquilization - acepromazine

muscle relaxation - diazepam

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70
Q

components of good nursing care when treating tetanus

A

minimize stimulation from environment
quiet, dark, well-padded stall, cotton in ears
keep sternal to prevent bloating
rumen fistula

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71
Q

prevention of tetanus

A

routine vaccine with tetanus toxoid
booster pregnant ewes/does in late gestation to protect lambs and kids
tetanus antitoxin when docking and castrating

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72
Q

what is the routine tetanus toxoid usually combined with

A

other clostridium bacterins - C and D

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73
Q

dose of tetanus antitoxin when docking and castrating

A

150-200 IU per animal

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74
Q

when to start the tetanus vaccine and how often to give

A

start around 6 weeks of age - decline of maternal antibodies
give at least twice at 2-4 week intervals
booster at 8-10 weeks

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75
Q

how long is the duration of protection from the tetanus vx

A

unknown but the vx is inexpensive and it works

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76
Q

where to get botulism

A

decaying vegetation, carrion

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77
Q

what happens with botulism

A

exotoxin blocks Ach release, causes flaccid paralysis

see inability to eat, limberneck

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78
Q

what usually happens with botulism

A

usually affects multiple animals in the heard

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79
Q

how quickly after the first signs of botulism have cows died

A

80 were dead within 8 hours of first CS

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80
Q

what did the TMR of botulism herd have

A

rotten oat hay and a dead cat

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81
Q

what did the botulism cat carcass have

A

type C botulinum toxin in the carcass

no botulinum toxin was found in the milk or sera

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82
Q

prevention of botulism

A

no vaccine in the US

treatment via antitoxin - not commercially available

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83
Q

what type of dz is tick paralysis

A

ascending LMN

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84
Q

what does tick saliva contain

A

neurotoxin

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85
Q

how quickly do tick paralysis signs progress

A

24 hours

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86
Q

treatment for tick paralysis

A

remove tick

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87
Q

prognosis for tick paralysis

A

fair if dx quickly

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88
Q

two ticks that can cause paralysis

A

ixodes holycyclus

dermacentor spp.

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89
Q

three phases of rabies

A

prodromal
furious
paralytic

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90
Q

when is infection of the limbic system in rabies

A

furious stage

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91
Q

when is infection of the neocortex in rabies

A

paralytic stage

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92
Q

should you vx all livestock for rabies

A

no, not recommended

vx valuable animals is suggested

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93
Q

what is the rabies vx

A

Imrab 3 - Merial

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94
Q

what organism causes listeriosis

A

listeria monocytogenes

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95
Q

describe L. monocytogenes organism

A 
small 
gram positive 
non-spore forming 
diphtheritic 
rod bacteria
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96
Q

where to find listeria monocytogenes

A

spread in feces of many mammals, birds, and fish

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97
Q

how long can L. monocytogenes survive in the environment

A

months to years

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98
Q

is listeriosis zoonotic

A

yes

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99
Q

what are the serotypes of listeriosis and what do they cause

A

1/2a and 4b

encephalitic listeriosis

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100
Q

which animals is listeriosis more common in

A

more common in sheep than in cattle

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101
Q

sources of contamination for listeriosis

A

silage
fecal contamination
chronic intramammary infection
poultry litter used for bedding

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102
Q

what ph of silage inhibits growth for listeriosis

A

ph less than 5.5

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103
Q

other infectious dz of the brain from listeriosis

A

generalized disease with abnormal behavior

circling, dysphagia

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104
Q

do carrier animals of listeriosis exist

A

yes, small gram positive rod

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105
Q

pathogenesis of listeriosis, commonly associated with what

A

environmental and nutritional stress

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106
Q

what does listeriosis require for entry

A

wound

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107
Q

common types of wounds that obtain listeriosis

A

rough browse/hay

erupting teeth

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108
Q

ages of patients seen with listeriosis

A

1 month or older

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109
Q

hallmark sign of listeriosis

A

multiple unilateral cranial nerve defecits

circling, head tilt, facial paralysis
anorexia, dysphagia

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110
Q

when do we see fever with listeriosis

A

early

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111
Q

what is silage eye from listeriosis

A

uveitis
conjunctivitis
keratitis

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112
Q

what are the late signs of listeriosis

A

recumbent
opisthotonos
paddling

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113
Q

pathogenesis / path of listeriosis

A

rootlet trigeminal -> intra-axonal migration -> brainstem

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114
Q

what type of movement does listeriosis have and what does this accomplish

A

cell to cell movement

evades phagocytosis

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115
Q

treatment of listeriosis

A

difficult

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116
Q

listeria monocytogenes bacteria found where

A

decaying organic matter
found on many areas of the farm
must have a ph above 5.5 for proliferation

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117
Q

listeria bacteria binds to the cell via what

A

surface proteins

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118
Q

after listeria bacteria binds to the surface proteins, how does it enter the cytoplasm

A

via hemolysin - listeriolysin O

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119
Q

after listeria enters via listeriolysin O (hemolysin), what happens

A

multiplies, presses on internal surface cell membrane

forms listeriopods that invaginate into adjacent cell

120
Q

gross lesions with listeriosis

A

absent or minimal

121
Q

CSF with listeriosis

A

turbid

122
Q

medulla oblongata with listeriosis

A

softened

123
Q

fetus with listeriosis

A

autolyzed

124
Q

what type of transmission of listeria is possible

A

venereal

125
Q

how do humans become contaminated with listeria

A

via processed foods - soft cheeses, deli cold cuts, sliced cheese, ice cream

126
Q

how many organisms can be infective with listeria

A

less than 1000

127
Q

how to treat listeria

A

penicillin 44,000U/kg BID for 7 days

reduce to 22,000U/kg for 14 days

OTC 10mg/kg BID

128
Q

what do we see on chemistry with listeriosis

A

stress leukogram

evidence of dehydration

129
Q

what do we see in CSF with listeriosis

A

increased protein - more than 20mg/dL

high number of mononuclear cells - more than 10/uL

130
Q

do we see limb paralysis with listeriosis

A

not usually

131
Q

definitive diagnosis for listeriosis

A

post mortem
multi-focal to coalescing areas of necrosis
severe infiltration of macrophages/neutrophils
axonal swelling and degeneration

lesions most severe in pons and medulla

132
Q

where are the lesions most severe with listeriosis

A

pons and medulla

culture?

133
Q

usual outcome of treatment for listeriosis

A

unrewarding

134
Q

when does mortality approach 100% with listeria

A

if recumbent

135
Q

when is the best chance at successful treatment for listeriosis

A

at the onset of signs

136
Q

what is supportive treatment for listeriosis

A

NSAIDs
fluids
vitamins

137
Q

what antibiotics used for listeria

A

penicillin - 22,000-44,000IU/kg IV q6 or IM q12

or

tetracycline - 10mg/kg IV q 12

138
Q

success rate for treatment of listeria

A

0-62%

139
Q

what is TEME

A

thromboembolic meningoencephalitis

140
Q

main component in TEME

A

histophilus somni

141
Q

is H. somni gram pos or neg

A

negative

142
Q

does H. somni form spores

A

no

143
Q

what type of bacteria is H. somni

A

non spore forming coccobacillus

144
Q

what does TEME cause

A 
pneumonia 
arthritis 
UTI 
abortion 
myocarditis 
neurologic disease
145
Q

in which animals does TEME have a very high case fatality rate

A

feedlot cattle

146
Q

signs and death when it comes to TEME

A

signs develop rapidly

death within 36 hours

147
Q

TEME commensal bacteria in many mammals is where

A

URT and urogenital tract

148
Q

TEME is an obligate microbe of what

A

mucosal surfaces

149
Q

when does TEME dissemination occur

A

as a result of other pathogen or compromised host immune system

150
Q

where does TEME migrate and what does it cause

A

through unprotected epithelial cells to meet brain epithelial cells and cause cytoskeletal rearrangement

151
Q

what does TEME’s migration and rearrangement result in

A

drastic influx of albumin
reduced transendothelial electrical resistance

end result is increased paracellular permeability of vascular endothelial cells - neuro signs

152
Q

death from TEME’s pathogenesis

A

subsequent endothelial cell apoptosis

153
Q

if multiple animals are affected with TEME, what is the only sign that may be noticed

A

sudden death

154
Q

what do we initially see with TEME

A

ataxia and weakness

155
Q

as TEME progresses, what might we see

A 
lateral recumbency 
profound depression 
opisthotonos 
convulsions 
closed or partially closed eyelids
156
Q

what is sleeper syndrome

A

closed or partially closed eyelids - sometimes seen with TEME

157
Q

TEME diagnosis

A

history and physical exam
CBC is nonspecific
cellular changes on CSF are reflective of a bacterial infection with hemorrhage

158
Q

how do we confirm TEME

A

necropsy

159
Q

when to attempt treatment of TEME

A

only attempt early in the disease

160
Q

what antibiotics for TEME

A

gram negative spectrum

161
Q

what do we do with down animals suffering from TEME

A

euthanize

treatment is unrewarding

162
Q

how to prevent TEME

A

vaccine

163
Q

H. somni - wyoming calves with disease syndrome

A

lethargy, fever, death

november-january each year

164
Q

what is the appreciable source of death loss with H. somni

A

focal myocarditis

165
Q

gross lesions detected with h. somni

A

in affected hearts

166
Q

what types of deaths do we see with acute, subacute, and chronic fatal forms of h. somni

A

single deaths over time rather than heavy death loss in a short period

167
Q

when are h. somni cardiac lesions missed

A

when hearts are not opened

specifically when cranial and caudal papillary muscles of the left ventricular myocardium are not incised

168
Q

what is most often the cause of brain and pituitary abscesses

A

trueperella pyogenes

169
Q

brain abscesses in cattle

A

relatively rare

170
Q

lesions with t. pyogenes brain & pituitary abscesses

A

asymmetric

171
Q

signs of brain & pituitary abscesses

A 
vision loss in contralateral eye 
depression 
mania 
head pressing 
circling with head tilt toward lesion
172
Q

treatment of brain & pituitary abscess

A

difficult with grave prognosis

173
Q

origin of pituitary abscess

A

hematogenous - rete mirabile, cavernous sinus
dehorning complication
head butting

174
Q

rete mirabile

A

mesh of capillary beds covering the pituitary

175
Q

cavernous sinus

A

valveless venous system that bathes pituitary

176
Q

signs of pituitary abscess

A 
blindness 
pupillary dysfunction 
nystagmus 
dysphagia 
facial paralysis 
circling 
head tilt
177
Q

polioencephalomalacia

A

swelling and softening of gray matter

178
Q

what dysfunction contributes to polio

A

Na-K-ATP pump

179
Q

what promotes water into the cell

A

intracellular Na

180
Q

what is the cofactor in neuronal ATP production

A

thiamine

181
Q

what do we need for thiamine production

A

rumen microbes

182
Q

what do non-ruminants rely on for thiamine production

A

diet

183
Q

where do thiaminases come from in regards to polio

A

bacterial and plant

184
Q

what are sulfur and sulfates metabolized to with polio

A

toxic sulfide ions

185
Q

what do grain diets promote with polio

A

h2s gas - absorbed or inhaled post eructation

186
Q

what does sulfur (S) interfere with

A

oxidative processes of mitochondria leading to depletion of ATP

187
Q

why does h2s like the brain

A

because of the high lipid content

188
Q

where is h2s found

A 
drinking water 
molasses 
forage 
urine acidifiers 
mineral supplements 
some plants - Brassica
189
Q

how quickly do polio signs develop

A

rapidly

190
Q

what are the signs of polio

A 
central blindness 
ataxia 
proprioceptive deficits 
head pressing 
hyperexcitability - occasionally
191
Q

what do these polio signs lead to

A 
recumbency 
opisthotonus 
seizures 
coma 
death
192
Q

what ages are affected by polio

A

all ages, most common in growing animals

193
Q

what type of strabismus do we see with polio

A

dorsomedial

194
Q

what is the polio diagnosis based on

A

clinical signs and response to treatment

bloodwork and CSF are unrewarding

195
Q

what other test must we do in the face of polio

A

test food and water for h2s

196
Q

how many ppm of h2s in water, diet, and rumen gas to indicate toxic levels

A

> 1000ppm in water
4000ppm in diet
1000ppm in rumen gas

197
Q

thiamine for polio treatment

A

10mg/kg q6hrs IV or IM until improvement

then q12 hrs for 48 hours

198
Q

dexmethasone tx for polio

A

1-2mg/kg q 24h ?

199
Q

when treating polio, what should we increase and add to the diet

A

increase forage and add glucogenic precursors

200
Q

what is nervous ketosis

A

multifactorial metabolic derangement

functional metabolic encephalopathy

201
Q

what do we frequently see with nervous ketosis and what is less common

A

frequently see anorexia and milk drop

less commonly see wandering, head pressing, and compulsive licking

202
Q

what type of necrosis is transpiring in nervous ketosis and what does that result in

A

diffuse cerebrocortical neuronal necrosis
this causes bilateral blindness with in tact pupillary function

also see cerebellar purkinje cell necrosis

203
Q

what type of nystagmus with nervous ketosis

A

vertical

204
Q

main isolate of otitis media/interna

A

mycoplasma bovis

205
Q

what is meningitis usually associated with

A

gram negative septicemia in calves

chronic sinusitis

206
Q

what type of problem is lead toxicosis

A

worldwide problem

207
Q

where is lead toxicosis most common and why

A

pastured cattle in US

because it’s highly palatable to some animals

208
Q

sources of lead

A 
grease 
oil 
old paint 
lead-headed nails 
batteries*
linoleum 
smelter discharges
209
Q

what does the form of lead affect

A

absorption

210
Q

what type of leads are poorly absorbed

A

metallic/sulfide forms

211
Q

what type of leads are readily absorbed

A

lead salts - acetate, phosphate, carbonate, hydroxide

212
Q

what do lead salts bind to

A

erythrocytes, tissues, bone

213
Q

how long does lead remain in the system

A

long time

214
Q

what do the signs of lead toxicosis resemble

A

polio

215
Q

what signs do we see with lead toxicosis

A 
sudden death 
central blindness 
tremors 
chewing fits 
seizures 
bellowing 
occasional aggression
216
Q

diagnosis of lead toxicosis

A

basophilic stippling

normocytic normochromic anemia

217
Q

blood lead measurement

A

heparanized blood - no chelation

218
Q

treatment and prognosis of lead toxicosis

A

usually die before treatment or in spite of treatment

219
Q

what to do immediately with lead tox

A

remove from source

220
Q

what to provide with lead tox

A

intermittent CaEDTA to chelate from bone
66-110mg/kg/d divided into several doses
for 3-5 days then stop 2-3 days

221
Q

what to provide early in the disease with lead tox

A

thiamine 10mg/kg q6h

or 25mg/kg q12 along with the CaEDTA

222
Q

two types of spinal cord diseases

A

congenital or inherited

223
Q

types of acquired spinal cord diseases

A

infectious
traumatic
metabolic/nutritional
toxic or neoplastic

224
Q

signs of spinal cord disease

A

vary with location of the lesion

225
Q

lesion to c1-c5

A

UMN to front limbs and hind limbs

226
Q

lesion to c6-t2

A

LMN to front

UMN to hind

227
Q

t3-L3

A

UMN to hind

228
Q

lesion to sacral intumesence

A

LMN to hind limbs, anus, bladder

229
Q

lesion to coccygeal nerves

A

LMN to tail and spinal area

230
Q

what is sway back considered

A

enzootic ataxia

231
Q

what type of deficiency leads to sway back

A

copper deficiency during prenatal/perinatal period

232
Q

what type of does or ewes birth sway backs

A

cu deficient does and ewes

233
Q

what type of myelin degeneration with sway back

A

bilateral symmetrical myelin degredation in dorsolateral spinal cord tracts
+/- cavitations in cerebral white matter

234
Q

what is myelin degeneration secondary to

A

oxidative degeneration

235
Q

clinical signs of sway back

A

rear limb ataxia
muscle atrophy
paresis
tetraparesis seen at birth

236
Q

when do we usually see signs of sway back

A

usually at birth but may take up to 3 months

237
Q

signs of sway back in neonates

A

static

238
Q

signs of sway back in older animals

A

progressive paresis

239
Q

definitive dx of sway back

A

necropsy

240
Q

where do we measure cu when dealing with sway back

A

in the body tissue
plasma copper status - blood copper will increase with stress
also assess dietary copper

241
Q

what is irreversible in regards to sway back

A

hypomyelinogenesis and demyelination

242
Q

how to prevent more cases of sway back

A

supplement copper

243
Q

copper to molybdenum ratio

A

6:1

244
Q

progressive ataxia is a recessive defect in what animals

A

pure/mixed breed charolais calves 6-36 months

245
Q

what type of paresis seen with progressive ataxia

A

posterior paresis and recumbency by 2 years

246
Q

major lesion with progressive ataxia

A

eosinophilic plaques on white matter in the brain/spinal cord
stiff neck, dragging rear toes, stumbling, proprioceptive deficits

247
Q

when do these signs in progressive ataxia worsen

A

with exercise

248
Q

what happens with urinating with progressive ataxia

A

difficulty maintaining posture during urination, we see pulsatile micturition

249
Q

what is weaver syndrome

A

progressive degenerative myeloencephalopathy

weaving gait

250
Q

common to see weaver syndrome in what animals

A

inherited in brown swiss calves and angler cattle

251
Q

what do we see in animals with weaver syndrome

A 
paraparesis 
ataxia 
dysmetria of pelvic limbs 
insidious progression 
muscle wasting over hind quarters
252
Q

onset of weaver syndrome

A

5-12 months

recumbent by 2 years

253
Q

lesions in weaver syndrome

A

white matter of spinal cord

axonal swelling, degeneration, vacuolation

254
Q

ways to get organophosphate toxicity

A

ingestion
inhalation
percutanous

255
Q

what are the substances in OP tox

A

OP based insecticides or anthelmintics

256
Q

what happens in OP tox

A

bind with acetylcholinesterase – increased Ach

257
Q

what two categories of effects from OP toc

A

muscarinic

nicotinic

258
Q

which effects are sympathetic NS

A

nicotinic

259
Q

which effects are parasympathetic

A

muscarinic

260
Q

what are the muscarinic effects of OP tox

A 
dyspnea 
hypersalivation
diarrhea 
bradycardia 
pupillary constriction
261
Q

what are the nicotinic effects of OP tox

A

muscle tremors
tetany
recumbency
opisthotonus

262
Q

what does the treatment of OP tox depend on

A

route and severity of intoxication

263
Q

what to use in cattle and sheep with OP tox to reduce muscarinic signs

A

atropine 0.25mg/kg IM

264
Q

what else to administer in OP tox

A

oral activated charcoal

oximes (2-pyridine aldoxime methiodide)

265
Q

what are the oximes for in OP tox treatment

A

to break the bond of OP and ACHase within the first 24 hours

266
Q

what can cervical fractures look similar to

A

meningitis

267
Q

characteristics of cervical fractures

A

painful, may refuse to lower head to eat
pain on palpation, may be recumbent
resist passive flexion
BAR

268
Q

what might we see in a c1-c4 lesion in regards to cervical fracture

A

may refuse to lift head

269
Q

which animals most commonly have vertebral osteomyelitis/spinal abscess

A

calves
lambs
fawns

270
Q

what is present with vertebral osteomyelitis/spinal abscess

A

bacteremia with localization in vertebral veins
pulmonary/umbilical infections (tail docking)
clinical signs vary with location of lesion

271
Q

what are the two common organisms present with vertebral osteomyelitis/spinal abscess

A

trueperella pyogenes

fusobacterium necrophorum

272
Q

how to diagnose vertebral osteomyelitis/spinal abscess

A

acute signs after pathologic fracture, vertebral collapse and/or spinal cord compression

273
Q

what other dx for vertebral osteo/spinal abscess

A 
malaise 
fever
stiffness 
proprioceptive deficits 
paresis and/or recumbency 
history and CS
274
Q

what imaging for vertebral osteo/spinal abscess

A

plain rads - look for proliferation, lysis, sclerosis, and soft tissue swelling (2-8 weeks after onset of signs)

275
Q

organisms in epidural abscess

A

trueperella (archanobacter) pyogenes

cornyebacteria spp.

276
Q

treatment for epidural abscess

A

surgical curettage, drainage, lavage

long-term abx

277
Q

how to prevent epidural abscess

A

adequate colostrum

278
Q

what is often associated with poor prognosis in epidural abscesses

A

subsequent meningitis

279
Q

what are two broad causes for spinal cord fracture

A

trauma

osteodystrophy

280
Q

what types of trauma can cause spinal cord fractures

A

squeeze chutes
other animals
AL and atlantoaxial joints in pygmy goats from restraint
TL fractures from extraction during dystocia
LS fractures in adult cattle from slipping on cement floors

281
Q

in which animals do we commonly see spinal cord fractures

A

3-6 month old ruminants due to nutritional deficiencies - vitamin D, calcium, copper

282
Q

CS with degenerative myeloencephalopathy

A

pelvic limb paresis and ataxia
recumbency
usually remain BAR
non-responsive to therapy

283
Q

where have we seen degenerative myeloencephalopathy

A

reports in two non-related adult llamas

284
Q

degenerative myeloencephalopathy - lesions in where

A

spinal cord white matter
marked axonal degeneration
loss of axons and myelin, and status spongiosus

285
Q

hepatic encephalopathy is usually related to what

A

liver disease of some type

history of abnormal behavior - poor doers

286
Q

where is hypoderma bovis found

A

NW united states and canada

287
Q

life cycle / events of hypoderma bovis

A

deposit eggs on legs
hatch and burrow into skin
1st instar larvae migrate subcutaneously to spinal canal
dormancy for 2-3 months in epidural fat thru winter

288
Q

what is spinal hypodermosis

A

neurologic signs associated with death of larvae near spinal cord when treated with OPs and ivermectins

289
Q

what is released by the hypoderma larvae when they die

A

toxins released

severe host inflammatory reaction

290
Q

what do we see with spinal hypodermosis

A

rear limb paresis and ataxia, recumbency
signs can resolve within a week of onset
in severe cases - prolonged recumbency, euthanasia

291
Q

treatment of spinal hypodermosis

A

NSAIDs:
flunixin meglumine 1.1mg/kg BID or
dexmethasone 0.1-0.25mg/kg

want to deworm with ivermectins before larvae reach spinal cord - varies with geographical location

292
Q

in north america, when do hypoderma flies appear and when do the larvae end up near the spinal cord

A

flies appear in may and the larvae are near spinal cord in november

293
Q

when to deworm for hypodermosis

A

august/september in warmer climates

october in colder areas

294
Q

what are the peripheral nerves of the pelvic limb

A 
saphenous nerve
common peroneal nerve 
cutaneous branches of the pudendal nerve 
tibial nerve
cranial clunial nerves 
middle clunial nerves 
lateral cutaneous femoral nerve 
caudal cutaneous femoral nerve 
caudal coccygeal nerves
295
Q

what types of nerve damage with pictures on the slides can we often see

A 
sciatic 
femoral 
tibial 
peroneal 
obturator 
radial nerve paralysis
296
Q

what will we see with radial nerve paralysis

A

dropped elbow will support weight if foot is placed

LAM II - VA (6 decks)

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