Pathology II > Test 2- Neuro > Flashcards

Test 2- Neuro Flashcards

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1
Q

Ectodermal Origin

A

Ectodermal Origin (sensitive to hypoxia)

  • Neurons
  • Astrocytes
  • Oligodendrocytes
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2
Q

Mesodermal Origin

A

Mesodermal Origin (not as sensitive to hypoxia)

  • Microglia
  • Vascular endothelium
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3
Q

nuclei

A

Arranged in nuclei

– CNS

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4
Q

ganglia

A

• Arranged in ganglia

– PNS

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5
Q
A

Neuron with nissl substance

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6
Q
A

Chromatolysis in a neuron

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7
Q

Chromatolysis

A
  • Swelling of cell body and dissolution of nissl granules with margination of nucleus
  • Degenerative change (reversible)
  • Non-specific cause (eg injuries to axons, overstimulation/deficiencies)
  • Seen in EMN, dysautonomias, copper def,
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8
Q
A

Acidophilia

Ischemic change, permanent

Cell death

Cell is shrunken, acidophilic, angular

Nucleus pyknotic-absent

Depending on cause may be regional

Occurs in trauma, hypoglycaemia, thiamine deficiency

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9
Q
A

Cytoplasmic vacuolation

• Lipid

Intracytoplasmic oedema

Lysosomal storage (accumulation of products) eg GM1 gangliosidosis

Transmissible Spongiform Encephalopathies (TSE eg BSE)

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10
Q
A

Rabies inclusions (in cytoplasm)

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11
Q
A

Herpes inclusion body (in nucleus)

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12
Q

Neuronophagia

A

Neuronophagia “eating neurons”

  • Phagocytosis of neurons by microglia/monocytes
  • Hallmark in some viral infections
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13
Q

oligodendrocytes

A

sythesized myelin in the CNS

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14
Q

Schwann cells

A

synthesize myelin in the PNS

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15
Q

gliosis

A

Proliferation of astrocytes

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16
Q

gemistocytes

A

Swelling of astrocytes

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17
Q

Gitter Cell

A

Following brain trauma microglial cells will replicate and activate to clear up debris

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18
Q

Myelophages

A

Microglial cells, when they mop up myelin are called myelophages

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19
Q

Ependymal Cells

A
  • Ciliated cubodial cells lining neural canal, ventricles, choroid plexus
  • Formation of CSF
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20
Q
A

Cerbellar coning

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21
Q
A

Vasculitis (inflammation of a blood vessel)

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22
Q
A

Area of malacia(softening) within a portion of brain

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23
Q

Encephalo

A

involving brain

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24
Q
A

GM1 Gangliosidosis of
Friesian Calves

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25
Parasitic cysts in various portions of brain
26
Coenuris cerebalis
Common in sheep T. Multiceps (dog faeces)- ingestion by sheep- migration to CNS Acute Gid: 3-4 weeks following ingestion, multiple parasites & malacia Chronic Gid: 6 months PI, cysts large, compression, oedema, hydrocephalus, bone softening. – Cerebrum most common location
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Toxoplasmosis * Sheep: abortion, multifocal encephalitis in foetus * Dogs: rare, as complication of CDV immunosuppression * Cats: rare
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Typical cotyledon necrosis seen in toxoplasmosis abortions
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Neospora Caninum
* Dog is definitive host, excretes oocysts in faeces * Similar to T gondii • Vertical (transplacental) transmission – Myositis/ meningoencephalomyelitis – Hindlimb paralysis - CAN CAUSE ABORTIONS IN CATTLE!
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Neospora caninum Myelitis / Myositis Seen in spinal cord in this case leading to paralysis
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Equine protozoal encephalomyelitis
Most common disease in horses with multifocal or asymmetric neurologic deficits. Sudden or gradual onset of pelvic limb paresis and ataxia Caused by infection with Sarcocystis neurona
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In the horse the organism replicates in the CNS rather than in muscle. Asymmetry of clinical signs help to differentiate this disease from wobbler syndrome and herpesvirus myeloencephalitis (usually symmetric or mildly asymmetric).
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Halicephalobus gingivalis (H. deletrix) and Strongylus vulgaris larvae migration are the most common cause of verminous encephalomyelitis in the horse Cerebrospinal nematodiasis, horse,
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Cat, Cryptoccocus neoformans (cryptococcal meningo- encephalitis) Viscous mucoid exudate–mucopolysaccharide capsule of the yeasts
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Swayback
• Newborn or young lambs Copper deficiency during periods of myelination Deficiency can be primary or secondary (competing with sulfates) • Forms – Congenital – Delayed – Acute delayed
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Congenital Swayback From birth, blind, unable to suckle Cavitation/gelatinous subcortical white matter Hydranencephaly/hydrocephalus See wallerian degeneration of spinal cord Bilateral, symmetrical in dorsolateral and ventromedial columns
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Congenital Swayback / Lamb Marked loss of white matter making ventricles look big
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Delayed swayback
• At 1-2 months show ataxia No gross brain lesions Chromatolysis of neurons in red nucleus and brainstem nuclei Spinal cord lesions similar to congenital form
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Pathogenesis of Swayback
* Not sure * Cu needed for myelin stability, for cytochrome oxidase and superoxide dismutase * Accumulation of toxic superoxides Large neurons rich in cytochrome oxidase Get neuronal damage (mitochondrial) Axonal degeneration then secondary demyelination Loss of support for myelin * Congenital form observed when Cu deficiency occurs during 100-120 days of gestation * Period of marked myelination in cerebrum and cord * Mild winters * Less hand feeding * Soil intakes (rich in molybdenum/sulphates) • Admin Cu injections to ewes mid- pregnancy
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Cerebrocortical Necrosis
• Laminar cortical necrosis, polioencephalomalacia • Young ruminants (cattle/sheep) – Cattle 4-6 mts, june-august – Sheep, no age or seasonal predisposition * Sudden onset 5-10days after change in pasture/management * Blindness, opisthotonus (star-gazing), nystagmus, convulsion, death
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CCN Gross Pathology * Brain swelling & herniation in acute cases * Reduction in brain size and narrowing of gyri in chronic cases * Affected areas yellow-tan coloured with autofluorescence under UV light
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Since the lesions of CCN are hard to see what do you do?
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CCN aetiology
Thiamine deficiency Animals respond to thiamine within hours Thiamine critical for carbohydrate metabolism Low in young ruminants (ruminal microbes) Diet changes lead to proliferation of thiaminase producing bacteria (Cl sporogenes)
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Thiamine deficiency
Thiamine deficiency is also reported in cats, dogs and farmed wild carnivores (mink and foxes). Diets containing fish as the primary ingredient contain high levels of thiaminase (destroys thiamine). Diets based entirely in cooked meat are thiamine deficient and also produce the disease
45
Hound Ataxia
* Ireland, UK * Foxhounds, Beagles, Harriers * Packs fed on paunches (rumen/intestines) • No access to carase meats * Ataxia * No pain * Sluggish reflexes • No gross lesions Degenerative myelopathy Myelin vacuolation of descending motor tracts Axons preserved Disappeared when carcase diet restored Suggested methionine deficiency
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Salt Poisoning
* Common in pigs, occasional in ruminants * Direct- excessive salt in diet & restricted water (rare, no swill feeding) * Indirect- water supply restricted (frozen pipes, or relative if animals have diarrhoea) * Acute onset convulsions, opisthotonus, blindness, recumbency, paddling * High mortality * Gross lesions – brain swelling (congestion/oedema)
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Histo of salt poisioning
Histopathology Oedema/laminar necrosis of cerebral cortex Eosinophils in perivascular spaces (first 48 hours)- pathognomonic in pigs Neuronal changes (degeneration- death)
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Laminar Necrosis in salt poisoning
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Salt Posioning Pathogenesis
* High intracellular Na, reduced ATP for Na/K pump --- intracellular oedema * Increased vascular permeability ---- extracellular oedema * Neurons synthesize small mol. Wt proteins, chemotactic for eosinophils * Return water slowly or else get excessive oedema
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Lead Poisoning
* Occurs in all species, but mainly cattle/calves * Batteries, old paint, fishing weights, contaminated feeds * Confirm with kidney lead * Acute, subacute, chronic disease Acute most common Convulsions, bellowing, blindness, hyperaesthesia PNS damage also eg oesophageal impaction, laryngeal paralysis
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Lead poisoning- gross pathology and histo
• Gross pathology – Cerebral oedema, congestion with brain swelling • Histopathology – Endothelial cell degeneration with astrocytic swelling – Vasogenic oedema – Neuronal ischemia & necrosis (laminar)
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Focal Symmetrical Encephalomalacia
* Lambs (calves) * Associated with Cl perfringens type D enterotoxaemia • Acute onset head pressing, paralysis, death * Short course * Gross pathology – Brain swelling, bilateral symmetrical areas of malacia in midbrain, thalmus, hippocampus, frontal cerebral cortex, cerebellum
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Focal Symmetrical Encephalomalacia
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Focal symmetrical Encephalomacia HISTO
Histopathology – Oedema, sometimes haemorrhage (perivascular), white and grey matter malacia, swelling of endothelial cells
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Oedema Disease
Rapidly growing weaner pigs • Haemolytic E Coli endotoxaemia • Sudden changes in feeding systems • Acute onset, convulsions, pigs die with 24 hours Brain oedema Fibrinoid Necrosis of small blood vessels Oedema Encephalomalacia (cerebrospinal angiopathy)
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fribrinoid necrosis
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MOULDY CORN TOXICITY
Ingestion of moldy feed, specially corn and corn by-products - contaminated by the fungus Fusarium verticillioides (F. moniliforme ) and/ or F. proliferatum (Fumonisin B1)
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Leukoencephalomalacia in horse with mouldy corn toxicity
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Bilaterally symetric foci of liquefactive necrosis within the substantia nigra, Horse, UCDavis. Affected horses exhibit idle drowsiness and are unable to grasp food or drink water. Purposeless chewing motions are apparent. Horses die of starvation, dehydration or aspiration pneumonia
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Hepatic Encephalopathy
• Acute/chronic liver disease * Cattle- ragworth poisoning * Dogs- porto-systemic shunts • Sheep- copper posioning
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Some dramatic neurological disorders do not produce extensive neuropathology Examples....
Some dramatic neurological disorders do not produce extensive neuropathology * Strychnine * Metaldehyde • Tetanus * Botulism
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Dysautonomias
Dysautonomias • Degenerative changes in autonomic ganglia – Key-Gaskell Syndrome in cats – Grass sickness in horses – Chromatolysis, vacuolar degeneration in sympathetic and parasympathetic ganglia
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Key-Gaskell Syndrome Pupillary dilation Megaoesophagus, constipation Anorexia, dehydration • Few survive Was more common in early 1990s UK mainly
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Grass Sickness
Acute, subacute, chronic Dyphagia, bowel stasis Distended abdomen, constipation Mortality almost 100% Ileal biopsy (enteric ganglia) for antemortem diagnosis
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Equine Motor Neuron Disease
Progressive weakness, muscle atrophy, weight loss USA, UK & Ireland Sporadic Both sexes, all ages (outbreaks in Brazil) • No gross lesions • Degeneration and loss of motor neurons in ventral horns of spinal cord • Some degenration of neurons in brain nuclei
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CNS neoplasia
* Primary CNS tumours rarely metastasise outside CNS * Extracranial tumours can metastasis to CNS • Mammary carcinomas, lymphosarcoma * Grow expansile, cause compression, hydrocephalus * Prognosis poor * Glial more common than neuronal • Most solid, firm, greyish * Haemorrhagic if rapidly growing
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Most common CNS tumors
Astrocytoma \* Oligodendroglioma\* Meningioma\* Pituitary\*
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Medullablastoma * Undifferentiated cells of cerebellum * Cells of external granular layer * Rare in animals (children more common)
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Astrocytoma • Most common
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Oligodendroglioma
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Choroid Plexus Tumour
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Meningioma
* Frontal, retrobulbar areas * Most common in cats * Histologically benign (shell-out)
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Meningioma Dog
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Meningioma Cat
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Pituitary Tumours • Chromophobe adenoma Diabetes insipidus (pressure on pars nervosa, interference with ADH transport to nervosa) Hyperadrenocorticism (ACTH producing chromophobes • Dogs/horses
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Pituitary Tumours (equine)
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Canine, metastatic mammary tumour
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Metastatic Hemangiosarcoma
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Osteochondroma: tumor of calverium compressing on brain
Pathology II
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