Spr 16- Nervous Pathology- Farina Flashcards by Jess Martini

Oligodendrocyte function

A glial cell that forms myelin around axons in CNS

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Astrocyte function

Cell processes form the blood brain barrier

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Microglia function

Phagocytic cells

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Gitter cells

derived from microglia - after they have phagocytosed infectious material

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What is central chromatolysis

Degenerative change, swelling of neurons with central clearing from Nissl substance dispersion, peripheral displacement of the nucleus

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What is neuronophagia

In necrosis (eosinophilic cytoplasm), microglia gather around a necrotic neuron and phagocytose to remove debris

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Histo characteristics of axonal degeneration

Wallerian degeneration - degeneration of the axon segment distal to the damage - dilation, empty, gitter cells in a digestion chamber - caterpillar cross section

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What is a spheroid

focal axon swellings filled degenerative organelles

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What kind of necrosis is typical in CNS, describe

Liquefactive - ischemic injury, cell outlines are absent and grossly looks like jelly

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What is astrocytosis

Increase in size and number of astrocytes in respnse to injury because they are responsible for repair

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What are gemistocytic cells

Astrocytes that are plump, reactive and filled with eosinophilic cytoplasm (bigger cell, bigger nucleus)

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What do Alzheimer II cells look like

Swollen astrocytes with large nuclei with clearing around the nucleus - tend to flank neurons

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What disease process are Alz II cells seen in

hyperammonemia

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What is hydrocephalus

Accumulation of fluid in the cranial cavity

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Internal hydrocephauls

Excess fluid in ventricles

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External hydrocephalus

Excess fluid in arachnoid space

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Communicating hydrocephalus

Fluid in both ventricles and arachnoid

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Breeds predisposed to hydrocephalus

Brachycephalic, chihuahuas

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Microencephaly

Small brain- cerebrum

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Hydranencephaly

Little or no cerebral hemisphere - leaves fluid filled sacs (meninges filled with CSF)

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Porencephaly

Cystic cavitation (from in utero infarcts) involving cerebral white matter

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Lissencephaly

Absence of gyri and sulci (rodents, rabbits, some primates, non mammals, lhasa apsos)

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Prosencephalic hypoplasia

No cerebral hemispheres but brainstem preserved - stems from dysraphia

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Cranium bifidum

dysraphia defect in dorsal midline where meninges (+/- brain) can herniate

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Spina bifida

Dysraphia defect in vertebral arch(es) leading to herniation of meninges +/- spinal cord (missing dorsal lamina that covers cord)

Meningocele

herniation of meninges in cranium bifidum or spina bifida

Meningoencephalocele

Herniation of meninges and brain in cranium bifidum

Herniation of spinal cord and meninges in spina bifida

meningomyelocele

Most common brain malformation with BVD

Cerebellar hypoplasia (also with feline panleuk, hog cholera, parvovirus)

Underlying cause of storage diseases

Lysosomal enzyme defects - defective catabolism

What happens to cells that accumulate substrate in storage diseases

Cells will swell and can necrose, interferes with cell function

How are storage diseases inherited

Autosomal recessive

When do storage diseases present

Early, rapidly progressive and fatal

How are storage diseases named

According to molecule whose degradation is defective

Which CNS cells are most prone to ischemia

Neurons and oligodendroglia (highest metabolic rate)

What matter is more sensitive than which to ischemia

Grey more sensitive than white

Causes of polioencephalomalacia

high sulfur intake, thiamine deficiency or thiamine metabolism disturbance

Where are polioencephalomalacia lesions

Softening of grey matter of cerebral cortex

Leukoencephalomalacia causes

Moldy corn intake for over a month- fumonisin from fusarium

Leukoencephalomalacia lesion location

Cerebral white matter necrosis

Lesions of indirect salt poisoning

Cerebral edema, laminar cortical necrosis, eosinophilic meningoencephalitis

Cause of indirect salt poisoning

Hihg salt diet and sudden restricted water intake - swine

Ways bacterial infections get to CNS

septicemia, septic emboli from endocarditis, direct invasion, hematogenous spread

Direct invasion routes of bacterial infection

Cribiform plate or middle ear

Listeriosis common species

Ruminants

Listeriosis causative agent

listeria monocytogenes in heavy feeding of silage

Listeriosis characteristic lesions and locations

brainstem (medulla and pons) - microabscess (often in a focus of microgliosis)

Pathogenesis of encephalitis

Bacteria spread up the motor and sensory branches of trigeminal nerve

thrombotic meningoencephalitis species (infectious TME)

Cattle and sheep (young cattle in feed lots)

Causative agent of thrombotic meningoencephalitis (infectious TME)

hisophilus somni

Pathogenesis of development of CNS lesions of thrombotic meningoencephalitis (infectious TME)

Septicemia leads to cerebral vasculitis with hemorrhage, necrosis and thrombosis

thrombotic meningoencephalitis (infectious TME) lesions

Mulitfocal hemorrhage and necrosis grossly, vasculitis, thombosis, infarction, netropphilic meningoencephalitis

Histo features of viral infection

Non-suppurative meningoencephalities, peri-vascular cuffing, gliosis, +/- viral inclusions and neuronal degeneration/necrosis

Cause of pseudorabies

Porcine herpesvirus 1

Species affected by pseudorabies

All common domestic species

CS of pseudorabies

Pigs- mild fever, no pruritis; non-pigs- intense pruritis, high mortality, fever, neuro signs; young pigs- mortality, convulsions, treamor/twitching, abortion, mummified fetus

CS of CAE

Caprine arthritis encephalitis virus - hind limb ataxia to paresis or paralysis, can be fatal

When is neuro disease observed with CAE or visna maedi

2-4 months, >2 years respectively

Lesions of CAE/visna maedi

CAE- non-supp encephalo VM: non-supp meningoenceph both in white matter, both have demyelination

Species affected by cryptococcus neoformans

cats, dogs horses

How does crypto get to the brain

Nasal or sinus infection through cribiform or hematogenously through pulmonary infection

Crypto histo lesions

Grey, gelatinous foci in brain and meninges

Cause of equine protozoal myelitis

Sarcocystis neurona

Why arent equine protozoal myelitis organisms not seen

ponazuril deowrming usually gets them before patho

Causes of TSEs

Abnormal isoform (PrP-sc) of normal prion protein (PrP-c)

How do animals acquire TSEs

Horizontal trasmission from consumption of infected feed

Lesions of TSEs

intracytoplasmic neuronal vacuolation, astrocytosis

Static vs dynamic stenosis in wobbler syndrome

Static- No matter what position the head or neck are in, the lesion is compressive. Dynamic- The spinal cord will only be compressed during flexion.

Spr 16- Nervous Pathology- Farina Flashcards

(68 cards)