Passler Exam 2 Flashcards

(66 cards)

1
Q

5 components of the neurologic exam?

A
mentation
gait analysis
postural reactions
cranial nerves
spinal reflexes
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2
Q

Layers to penetrate for CSF tap?

A

skin–>lumbosacral fascia–>interarcuate ligament–>dura mater–>arachnoid meningeal layer

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3
Q

What does turbidity of CSF indicate?

A

increased white cell number

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4
Q

Two potential causes for foam in CSF?

A

increased protein

improper sample handling

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5
Q

What does protein in CSF indicate? Sources of protein?

A

BBB is not intact;

blood (albumin) and immunoglobulins

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6
Q

When should you preform the cell count on CSF

A

less than 2 hours after collection

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7
Q

What does each cell type indicate in the CSF

1) neutrophils
2) lymphocytes
3) macrophages
4) eosinophils

A

1) bacterial meningitis
2) viral meningoencephalitis; listeriosis
3) trauma; PEM
4) parasite migration

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8
Q

Most common cause of symmetric cerebral signs?

A

Metabolic abnormalities

dehydration, acid/base abnormalities, electrolyte disturbances

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9
Q

4 causes of PEM; which is most common

A

salt toxicity
lead poisoning
thiamine deficiency (most common)
sulfur toxicity

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10
Q

What is PEM

A

Polioencephalomalacia

softening of grey matter of the brain

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11
Q

Pathophysiology of thiamine deficiency

A

Thiamine is required for cerebral glucose metabolism; without it, no glucose is available–>disrupts membrane pumps (Na/K)–>Na builds up in cell, water follows–>neuronal edema

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12
Q

Most common cause of thiamine deficiency?

A

Rumen acidosis/disruption

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13
Q

Describe sulfur toxicity

A

excess sulfur leads to creation of H2S–>inhibits cytochrome C (no oxidative respiration)–>can’t make ATP–>cell swells

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14
Q

How does lead toxicity cause PEM

A

replaces Ca in enzymatic processes (i.e. ones that supply energy to the brain)

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15
Q

Two causes of salt toxicity

A

water restriction

salt poisoning

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16
Q

how does salt toxicity lead to PEM

A

neurons sense water loss and retain electrolytes–>rapid intake of water–>influx into neurons
*longer the deprivation, the more severe the edema

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17
Q

Basophilic stippling is diagnostic for which cause of PEM

A

lead toxicity

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18
Q

Tx for PEM?

A

Thiamine (neuroprotectant)

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19
Q

What does rabies cause in the brain

A

nonsuppurative encephalomyelitis

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20
Q

How long until rabies causes death

A

1 week

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21
Q

Considered the “gold standard” for diagnosing rabies

A

Fluorescent antibody test (FA)

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22
Q

What diagnostic tool should you NOT use with rabies

A

CSF Tap

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23
Q

T/F: Rabies is a core vaccine

A

False

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24
Q

Cause of BSE? (describe changes)

A

infections protein (Prion); changes normal PrPc to PrPSc

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25
How does BSE spread?
ingestino of BSE contaminated food (meat and bone meal)
26
T/F: the altered PrPSc protein elicits an immune response
False
27
Does BSE have a short or long incubation period? Impact of stress on clinical signs?
Long incubation period (4-5 years); stress enhances clinical signs
28
BSE can only be diagnosed _____ ____
post-mortem
29
Most common cause/reason of bacterial meningitis?
failure of passive transfer (neonates); E. coli and other gram negatives
30
What is hypopyon? Associated with what disease?
pus in anterior chamber of eye; | associated with bacterial meningitis
31
CSF findings in an animal with meningitis?
neutrophils, no glucose, increased protein
32
Unique test for meningitis
Pandy test (detect globulins)
33
Two strains of herpes virus? Usual areas of disease?
BoHV-1 (resp. and repro) | BoHV-5 (neurologic)
34
how does BoHV travel to the CNS
via trigeminal and olfactory nerves
35
T/F: the BoHV-1 vaccine can offer cross protection against BoHV-5
True
36
T/F: The BoHV vaccine prevents infection
False (prevents disease)
37
Hallmark sign of this disease is severe pruritis
Pseudorabies (Mad itch)
38
How can you differentiate pseudorabies from rabies
death is more rapid (6-48hrs)
39
Causative agent of pseudorabies?
Suid herpesvirus 1
40
Clinical signs of nervous coccidiosis
inducible seizures, snapping of eyelids; can have periods of normalcy
41
T/F: finding cocidia in the fecal can confirm nervous coccidiosis
False
42
Causative agent of TEME
Histophilus somni
43
TEME is usually seen in what type of cattle
Older feedlot cattle
44
H. somni is normally found in which organ?
Lungs
45
Risk factors for urea toxicity
lack of adaptation of feed high rumen pH lack of fermentable carbs
46
Unique Tx for urea toxicity?
infuse cold water and 5% vinegar into rumen
47
When dose infection with BVDV begin? When do CNS lesions become present?
in utero; CNS lesions around 120 days
48
Usually CNS abnormality caused by BVDV
cerebellar hypoplasia
49
Main clinical signs of BVDV
abnormal gait/ataxia with normal mentation and absent menace
50
Causative agent for grass staggers
Claviceps spp.
51
Clinical signs of grass staggers worsen with
excitement
52
CNN deficits are assoc. with disease in which area of the brain
brainstem
53
Causative agent of listeriosis
Listeria monocytogenes
54
CNN commonly affected by listeriosis
V and VII
55
Will listeriosis show an inflammatory leukogram?
NO
56
How is listeriosis usually diagnosed
response to treatment
57
Causative agent of otitis media in dairy calves
Mycoplasma bovis
58
Disease associated with infection by BLV
spinal lymphosarcoma
59
Clincal signs of spinal lymphosarcoma
hindlimb paresis progressing to paralysis
60
This inherited disease affects the inhibitory interneurons of the spinal cord and usually presents in the first 6-8 months of life
spastic paresis
61
This genetic disease is mainly seen in older dairy breeds
inherited periodic spasticity
62
Causative agent of tetanus
Clostridium tetani
63
Two many causes of tetanus infections
severe metritis post-calving | castration via rubber bands
64
Sawhorse stance is a typical sign of which disease
tetanus
65
Two tetanus toxins
Tetanolysin | Tetanospasmin
66
Physiology of tetanospasmin?
travels to spinal cord and affects renshaw cells (inhibitory interneurons) and inhibits GABA release