Central Nervous (awesome) Sauce Flashcards

1
Q

In all cases of CNS disease, what do we need to do?

A

Remove the spinal cord! Even though clinical signs may be referable ONLY to the brain

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2
Q

In small animals, how can we expose the spinal cord?

A

Dorsal laminectomy with bone rongeurs; Then remove by holding dura mater w/forceps and sectioning spinal roots as close to intervertebral foramina as possible (so basic…)

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3
Q

On PM examination of the nervous system, what do we need to do with the brain and spinal cord before sectioning and submitting for histopath?

A

Immerse in formalin and fix for 5-7 days!

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4
Q

What 2 protoplasmic properties are highly developed in neurons?

A

Irritability: generation of an impulse Conductivity: ability to transmit such an impulse from one location to another

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5
Q

What are neuroglia and how can they be classified?

A

Maintenance (support, protection, cleanup) cells of the neuronal microenvironment MACROglia: astrocytes and oligodendrocytes MICROglia: gitter cells (globular/swollen after phagocytosis of debris from injury) *immunosurveillance/regulation, repair*

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6
Q

Gliosis, perivascular cuffing (like that seen in Distemper on histo) indicates migration of inflammatory cells from where to where? Why?

A

From parenchyma–>vasculature Glial cells are phagocytic, so they’re responding to neuropil injury

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7
Q

Astrocytes in the nervous system are analogous to what cell type?

A

Fibroblasts! They also proliferate/repair in response to injury

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8
Q

Main distinction between Wallerian-type degeneration and Neuronal cell injury leading to axonal degeneration? (The 2 types of Degeneration that look awfully similar…)

A

Wallerian axons can potentially regenerate, depending on the damage; Whereas neuronal cell injury leading to axonal degeneration could be a result of an etiological agent TARGETING the neuron and the neuron will eventually die

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9
Q

Term given to large fluid filled cavities in the brain (Not just ^CSF in ventricles, but also ^CSF in parenchyma*)

A

Hydranencephaly

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10
Q

Term given for small fluid filled cavities in the brain

A

Porencephaly

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11
Q

What viruses can lead to hydranencephaly/porencephaly?

A

Akabane Bluetongue Rift Valley Wesselsbron Pestiviruses

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12
Q

Cerebellar hypoplasia may be the result of in utero OR peri-natal viral infection of ________ in kittens and _______ in calves.

A

Feline Panleukopenia (aka Feline Parvovirus; Parvoviridae–>protoparvovirus) BVD (Flavi–>Pestivirus)

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13
Q

How do we distinguish Spina Bifida from Spina Bifida Occulta?

A

SB: defective closure of bony encasement of spinal cord - visually apparent SBO: can’t see this from the outside- need palpation

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14
Q

Ingestion of locoweeds cause what?

A

Acquired form of mannosidosis The locoweeds contain potent inhibitors of alpha-mannosidase (which breaks down CHOs)

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15
Q

Name the 3 traumatic injuries discussed in lecture in order of increasing severity…. GO!

A

Concussion
Contusion
Laceration

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16
Q

What are 2 sources of sulfur toxicity that can result in polioencephalomalacia?

A

1) high sulfate concentrations in drinking water 2) ingestion of sulfate accumulating plants

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17
Q

Thiamine deficiency is an important cause of what encephalopathy?

A

Polioencephalomalacia (Areas of softening in the grey matter that represent necrosis)

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18
Q

Salt poisoning or water deprivation can lead to what encephalopathy?

A

Polioencephalomalacia

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19
Q

Sheep with thiamine-responsive PEM may display what clinical sign?

A

Opisthotonus (“star-gazing”) And signs similar to those of CEREBELLAR DZ!

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20
Q

Feline Ischemic Encephalopathy (FIE) resulting in cerebral infarction is usually a result of what parasitic migration?

A

Cuterebra via nasal passages thru piriform plate

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21
Q

What term do we use to describe the breakdown/lysis of cytoplasmic Nissl bodies?

A
  • *Chromatolysis**
  • indicates neuronal cell injury*
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22
Q

What’s the most suitable description for neurons that demonstrate cytoplasmic eosinophilia (red/pink cytoplasm), nuclear pyknosis (darkly-stained nucleus), or karyolysis?

A

Energy-deprivation change
may be result of ischemia, hypoglycemia, etc..

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23
Q

What are we looking at?

A

Satellitosis

24
Q

What is this?

A

Neuronophagia
“neuronophagic nodules”
undergoing necrosis and being invaded by phagocytic cells

25
Q

Hepatic Encephalopathy in a Steer:
What do we call this?
what does the morphology represent, especially on the boundary of grey/white matter?

A

Status Spongiosus;
Myelin!

26
Q

Rut-roh
Cerebellum of this dog is indicating what?
what do the vacuolations suggest?

A

Distemper :(
Family: Paramyxoviridae
Genus: Morbillivirus

vacuoles suggest demyelination and perivascular cuffing

27
Q

What do we call this?
What cell is reacting?

A

Astrogliosis

Reactive (gemistocytic) astrocytes;
homogenous, eosinophilic - nuclei become eccentric

28
Q
  • *Cerebellar white matter from K9 w/Distemper**
  • What cardinal tings are supporting this diagnosis?*
A

Perivascular cuffing,
Eosinophilic intracytoplasmic inclusion bodies within neuroglia,
and status spongiosus

29
Q

A variant of this disease is indicated with contaminated BSE meat.

Describe the abnormalities…

A

Creutzfeldt-Jakob Dz (CJD)

vacuolation, increased cellularity (GLIOSIS), and spongiform change

30
Q

What do we call these “foamy macrophages” seen in this lamb with Focal Symmetric Encephalomalacia (FSE)?

A

Glitter cells
aka Activated Microglial Cells

“git ‘er done!”

31
Q

This congenital microencephaly in a newborn donkey is the result of what…

A

Prosencephalic Hypoplasia

32
Q

Microencephaly in a newborn donkey, resulting from prosencephalic hypoplasia, is pictured.
If we saw this lesion in a calf, what would we suspect the etiological agent to be?
What about if we saw this in piglets?

A

Calf: in utero infection w/ BVD
Piglet: in utero infection w/ Classical Swine Fever

(remember: both of these are Pestiviruses belonging to the family Flaviviridae**)

33
Q

Cerebral edema can result in gyral herniation. What happened here?

A

Parahippocampal gyri herniated under the tentorium cerebelli

34
Q

Main lesion we would see in polioencephalomalacia?

A

Neuronal cerebral cortical necrosis

*note: in this case, we do NOT fix; we section the brain FRESH and look for the lesions: areas of palor in grey matter (may be subtle)

35
Q

What diagnostic tool can we use for detecting SPECIFICALLY thiamine-responsive PEM?

A

Wood’s Lamp

36
Q

Because hypernatremia is chemotactic for neurons, what may accompany polioencephalomalacia in pigs (or poultry) suffering from salt poisoning?

A

perivascular and meningeal eosinophilic infiltration

37
Q

Thiamine deficiency can also occur in carnivores, resulting in polioencephalomalacia, but how is it different in these animals compared to herbivores?

A

Lesions tend to be bilaterally symmetrical and specific to grey matter of the brain stem (as opposed to cerebral cortex in herbies)

*Chastek Paralysis*

ALSO: has more to do with diet…
diets containing fish as primary ingredient=high in thiaminase;
diets based entirely in cooked meat=thiamine deficient
(cats may demonstrate VENTROflexion)

38
Q

This transverse section of brain stem thru the pons demonstrates what?

A

necrosis of the caudal colliculi seen in B1-deficiency among carnivores
*this has been in the NAVLE*

39
Q

This was a case of alkaloid toxicity in a steer. We know that Severe Liver Dz can lead to neurological signs… but HOW?

A

toxins in the blood (ammonia) –> hyperammonemia –> microcavitation in the white matter –> myelin edema –> splitting of myelin sheath (esp at interface of white/grey matter) –> head pressing, mentation abnormalities, circling…

40
Q

Lambs with good BCS may demonstrate this type of lesion. What would the MDx be and what is it associated with?

A
  • *Focal Symmetrical Encephalomalacia**
  • throughout brain stem and basal nuclei*

associated with the epsilon toxin produced by C.perfringens (type D)

41
Q

Ingestion of moldy feed (corn) contaminated with the fungus, Fusarium verticillioides (F.moniliforme/F.proliferatum) can result in this lesion.
MDx?
what is the lesion actually associated with?

A

Equine Leukoencephalomalacia
It’s actually associated with the mycotoxin: Fumonisin B1

42
Q

Also known as “Chewing Dz of Horses,” muscles of prehension, mastication, and deglutition are characteristically dysfunctional as a result of the Repin toxin from ingesting Centaurea Solstitialis (Yellow Star Thistle/Russian Knapweed).
What is the MDx and what is the damage incurred?

A

Nigropallidal Encephalomalacia
MDx: bilaterally symmetric foci of liquefactive necrosis within the midbrain (substantia nigra and nucleus pallidus)
oxidative damage to dopaminergic neurons bc glutathione is depleted
*usu die from starvation, dehydration, or aspiration pneumonia*

43
Q

Nigropallidal Encephalomalacia
the lesions pictured here are specifically where?

A

globus pallidus (part of the basal nuclei)

44
Q

Pig: meningoencephalitis, ependymitis, and ventriculitis (the abscesses around the ventricles)

Et?

A

E.coli

45
Q

This important etiological agent of feedlot cattle is also indicated in myocarditis and fibrinopneumonia
What is it?
How do we describe this nastiness?

A

Histophilus somni
fibrino-suppurative, hemorrhagic, and necrotizing meningoencephalitis (TEME)
is NOT bilaterally symmetric
NOR does it discriminate between grey and white matter

focal areas of hemorrhage seem to follow blood vessels

46
Q

Focal areas of suppurative inflammation like this are HIGHLY indicative of what etiological agent?

How do we confirm the diagnosis?

A

Listeria monocytogenes

these nasty beezies (not to be confused with Ashley Judd) are gram positive, so we gram stain

47
Q

Typically, when we think of bacterial infections, we think of neutrophilic infiltrate and when we think of viral infections, we think of lymphoplasmacytic infiltrate…
This is an exception.
MDx?
Et?

Predilection site(s)?

A

Polioencephalomyelitis
EEEV (Togaviridae–>alphavirus)
brain stem/grey *matter

perivascular cuffing, degeneration on histo*

48
Q

Dz in horses characterized by ataxia, paresis, paralysis (esp of bladder);
vasculitis leads to thrombosis and infarction

MDx?
Et?

A

Hemorrhagic and ischemic myeloencephalitis
EHV-1 (same agent that causes respiratory dz)

49
Q

Bovine necrotizing meningoencephalitis is caused by _______;
whereas Bovine meningoencephalomyelitis is cause by ________.

A

BHV-5;
BHV-1 (IBR)

*usually affecting young cattle, 5-18 mo*

50
Q

Eosinophilic intracytoplasmic inclusions bodies of this pathogen have a strong attraction to the urinary tract epithelium seen here

A

K9 Distemper Virus

51
Q

K9 Distemper can also result in these lesions when they attack enamelblasts.
What is this lesion found in survivors?

A

enamel hypoplasia

52
Q

Thrombosis in a venule:
this is pretty characteristic of H.somni in association with thrombotic meningoencephalitis (TME).
what is this MDx exactly?

A

Fibrinonecrotizing vasculitis and thrombosis
remember, it likes the venules

53
Q

What is this cerebellar histo slide from a dog with distemper exhibiting?

A

Demyelination

54
Q

Whats a good MDx for this piece of cerebellum from a Distemper dog?

A

Lymphocytic meningoencephalitis
primarily affects glia (astrocytes)
and white matter (esp oligodendrocytes)

55
Q

Serositis, fluid accumulation in the abdominal cavity, and varying degrees of pyogranulomatous inflammation are associated with which form of FIP?

A

Effusive (wet)

56
Q

Leptomeningitis, chorioependymitis, focal encephalomyelitis, and ophthalmitis are associated with which for of FIP?

A

Non-effusive form

57
Q

On histology, what cells might we see in the manifestation of the dry form of FIP?

A

mix of neutrophils, lymphocytes, plasma cells, and histiocytes