Neuro path: study guide (farina) Flashcards
(57 cards)
1
Q
Function of oligodendrocytes
A
Form myelin in the CNS
2
Q
Function of astrocytes
A
They form the BBB
3
Q
Function of microglia
A
- Phagocytic cells of the CNS
- They have a small nuclei and little cytoplasm
4
Q
What is central chromatolysis
A
- Response of the nervous sytem to injury - neuronal change
- Cells swollen with central clearing due to dispersio of Nissl substance
- Nucleus is peripherally displace
5
Q
What is neuronophagia
A
Phagocytes (microglia) gather around necrotic nucle and phagocytose it to remove debris
6
Q
histologic characterisctics of neuronal degeneration
A
- Empty, dilated axon sheaths
- Gitter cells in digestive chambers
- Vacuolization of axons
- Spheroids
7
Q
Spheroid
A
- Focal axonal swellings filled wtih degenerative organelles
8
Q
Type of necrosis typically seen in CNS, and characteristics of this type of necrosis
A
- Liquifactive necrosis
- Seen with ischemic injury to CNS like infarcts
- Cells digested by liquefaction and all cell outlines are absent
9
Q
Astrocytosis
A
Increase in number and size of astrocytes in response to injury
10
Q
Gemistiocytic astrocytes
A
- Plump, reactive astrocytes with eosinophilic (red) cytosplasm
11
Q
Appearance of Alzheimers type II astrocytes
What disease process are these typically seen in
A
- Swollen with large nuclei and chromatin clearing
- Occurs with hyperammonemia
- often due to hepatic encephalopathy
12
Q
Hydroencephalus
A
Abnormal accumulation of fluid in crania cavity
13
Q
Types of hydroencephalus
A
- Internal: fluid in ventricles
- External: fluid in arachnoid space
- Communicating: fluid in ventricles and arachnoid space
14
Q
Breed commonly affected by hydroencephalus
A
Brachycephalic breeds
15
Q
Microencephaly
A
Abnormally small brain
16
Q
Hydranencephaly
A
- Near complete or complete absence of cerebral hemispheres, leaving fluid filled sacs formed by minges filled with CSF
17
Q
Porencephaly
A
- Cystic cavitation of the brain, usually involving cerebral white matter
18
Q
Lissencephaly
A
lack of normal gyri and sulci on brain
19
Q
anencephaly
A
absence of brain
20
Q
Prosencephalic hypoplasia
A
- absence of cerebral hemisphere but has brainstem
21
Q
Cranium bifidum/spina bifida
A
- defect in dorsal midline through which meninges and brain can extrude
- Meningocele: herniation of meninges
- Meningoencephalocele: herniation of meninges and brain
22
Q
Most common brain malformation seen with BVD
A
cerebellar hypoplasia
23
Q
What is the underlying cause of storage disease
A
- Defects in lysosomal enzymes within the catabolism stage
24
Q
What happens to cells that accumulate substrate in lysosomal storage diseases?
A
- Tissues that accumulate substrate first are those that are most active, they cannot clear material so their normal cellular functions get disrupted and the cell will eventually die
25
How are storage diseases inherited?
When do they present with neuro signs?
* Autosomal recessive
* Present early in life with neuro signs
* Progressive and fatal dsease
26
How are the storage diseases named
* Named according to class of molecule whose degeneration is defective
27
What cells in the CNS are most sensitive to ischemia?
* Neurons and oligodentocytes
* Grey matter is more sensitive than white matter
28
Causes of polioencephalomalacia?
Where are the lesions located?
* Causes
* high sulfur intake
* deficiency of thiamine
* disturbance of thiamine metabolism
* Lesions
* laminar softening of grey matter in cerebral cortex
29
Cause of leukoencephalomalacia?
Where are the lesions located?
* Cause
* consumption of moldy corn for \> 1 month
* causes a mycotoxicosis due to fumonisin
* Lesions
* cerebral white matter necrosis
30
Lesions of indirect salt poisoning?
What are the causes
* Cause
* high salt diet with restricted water access
* occurs in swine
* Lesions
* cerebral edema
* laminar cortical necrosis
* eosinophilic meningoencephalitis
31
Ways in which bacterial infections get into CNS
* Heatongenous
* Direct invasion
* through the cribiform plate
* through the middle ear
32
In what species do we see listeriosis?
What is the causative agent?
* Ruminants who eat a lot of silage
* Listeria monocytogenes
33
What are the characteristic lesions of listeriosis?
Where are they located?
* Lesions
* micro abscesses in the brainstem
* Often in focus of microgliosis
34
Pathogenesis of the encephalitis of listeriosis?
* Bacteria spread up the motor and sensory branches of the trigeminal nerve
35
What is the causative agent of thrombotic meningoencephalitis?
What species does it affect?
* Histophilus somni
* Affects cattle and sheep, especially young feedlot cattle
36
Pathogenesis of development of CNS lesions of thrombotic meningoencephalitis?
What are the lesions?
* Pathogenesis
* Septicemia leads to cerebral vasculitis with hemorrhage, necrosis, and thrombosis
* Gross lesions
* multifocal hemorrhage and necrosis
* Histologic lesions
* vasculitis, thrombosis, infarction, neutrophilic meningoencephalitis
37
General histologic features of viral infections
* Non-suppurative meningoencephalitis
* +/- myelitis
* Perivascular cuffing
* Gliosis: infiltration of glial cells
* +/- viral inclusions
* +/- neuronal degeneration/necrosis
38
Principal reservoirs for rabies in the US
* Skunks
* Raccoons
* Foxes
* Bats
39
What tissues is the rabies virus trophic for?
* CNS
* Salivary gland
40
Pathogenesis of rabies from inoculation to spread to CNS
* Virus inoculated into wound from bite - virus replicates in muscle cells near inoculation site - spreads to sensory paravertebral ganglia - virus travels along peripheral nerves to CNS
41
What do lesions in rabies look like?
* Non-suppurative encephalomyelitis
* ganglioneuritis
* parotid adenitis
* amount of inflammation and neuronal degeration varies
* Negri bodies (cytoplasmic inclusions) present most often in hippocampus in carnivores and Purkinje cells in herbivores
42
What is the cause of pseudorabies
Porcine herpes virus 1
43
Species affected by pseudorabies disease
can affect all common domestic species
44
CS pseudorabies in pigs
* Young
* prostration
* convlusions
* twitching
* high mortality rate
* Sows
* SMEDI
45
CS of seudorabies in other species
* Intense pruritis
* fever
* neuro signs (high mortality)
46
CS of caprine arthritis encephalitis virus
* Goat:
* kids 2-4 months
* Hind Limb ataxia
* paresis
* paralysis
* death
* Adults
* mastitis
* pneumonia
* arthritis
47
CS of Visna-Maedi virus
* Sheep \> 2 yrs old
* Hind limb ataxia
* lip trembling
* Hind limb paresis
* death due to secondary infection and starving
* Adults
* mastitis
* pneumonia
* arthritis
48
Lesions associated with caprine arthritis encephalitis virus
* Non suppurative leukoencephalomyelitis
* demyelination
49
Species typically affected by Cryptococcus neoformans
* Cats
* Dogs
* Horses
50
How do Visna-Maedi viruses get to the brain
* Starts in nasal or sinus infection, enters through direct invasion through cribiform plate
51
What are the histologic lesions of the cryptococcus
* Thick, non-staining mucopolysaccharide capsule, makes it look like soap bubbles on tissue sections
52
Infectious agent of equine protozoal myelopathy
* Sarcocystic neurona
53
Why are organisms not usually seen in most cases of EPM
Most animals have been treated for EPM before they were euthanized
54
Cause of transmissible spongiform encephalopathies
* Prions
* Normal is PrPC and changed into abnormal form PrPSc
55
How do animals typically acquire TSEs
* Horizontal transmission
* Due to consumption of infected feed material
56
What are the lesions of TSE
* Intracytoplasmic neuronal vacuolation
* astrocytosis
57
Difference between static and dynamic stenosis in wobblers
* Dynamic
* compression of spinal cord only when horse bends or extends neck
* usually occurs in young animals
* C3-C4 and C4-C5 usually affected
* Static
* Occurs regardless of position of neck
* usually older animals
* C5-C6 and C6-C7 usually affected
