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Pathology II > Test 2- Neuro > Flashcards

Test 2- Neuro Flashcards

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
Q
A

Parasitic cysts in various portions of brain

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26
Q

Coenuris cerebalis

A

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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27
Q
A

Toxoplasmosis

  • Sheep: abortion, multifocal encephalitis in foetus
  • Dogs: rare, as complication of CDV immunosuppression
  • Cats: rare
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28
Q
A

Typical cotyledon necrosis seen in toxoplasmosis abortions

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29
Q

Neospora Caninum

A
  • 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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30
Q
A

Neospora caninum Myelitis / Myositis

Seen in spinal cord in this case leading to paralysis

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31
Q

Equine protozoal encephalomyelitis

A

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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32
Q
A

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).

33
Q
A

Halicephalobus gingivalis (H. deletrix) and Strongylus vulgaris larvae migration are the most common cause of verminous encephalomyelitis in the horse

Cerebrospinal nematodiasis, horse,

34
Q
A

Cat, Cryptoccocus neoformans (cryptococcal meningo- encephalitis)
Viscous mucoid exudate–mucopolysaccharide capsule of the yeasts

35
Q

Swayback

A

• Newborn or young lambs

Copper deficiency during periods of myelination

Deficiency can be primary or secondary (competing with sulfates)

• Forms
– Congenital

– Delayed
– Acute delayed

36
Q
A

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

37
Q
A

Congenital Swayback / Lamb
Marked loss of white matter making ventricles look big

38
Q

Delayed swayback

A

• 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

39
Q

Pathogenesis of Swayback

A
  • 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

40
Q

Cerebrocortical Necrosis

A

• 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
41
Q
A

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
42
Q

Since the lesions of CCN are hard to see what do you do?

A
43
Q

CCN aetiology

A

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)

44
Q

Thiamine deficiency

A

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
Q

Hound Ataxia

A
  • 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

46
Q

Salt Poisoning

A
  • 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)
47
Q

Histo of salt poisioning

A

Histopathology

Oedema/laminar necrosis of cerebral cortex

Eosinophils in perivascular spaces (first 48 hours)- pathognomonic in pigs

Neuronal changes (degeneration- death)

48
Q
A

Laminar Necrosis in salt poisoning

49
Q

Salt Posioning Pathogenesis

A
  • 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
50
Q

Lead Poisoning

A
  • 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

51
Q

Lead poisoning- gross pathology and histo

A

• Gross pathology

– Cerebral oedema, congestion with brain swelling

• Histopathology

– Endothelial cell degeneration with astrocytic swelling

– Vasogenic oedema
– Neuronal ischemia & necrosis (laminar)

52
Q

Focal Symmetrical Encephalomalacia

A
  • 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

53
Q
A

Focal Symmetrical Encephalomalacia

54
Q

Focal symmetrical Encephalomacia HISTO

A

Histopathology

– Oedema, sometimes haemorrhage (perivascular), white and grey matter malacia, swelling of endothelial cells

55
Q

Oedema Disease

A

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)

56
Q
A

fribrinoid necrosis

57
Q

MOULDY CORN TOXICITY

A

Ingestion of moldy feed, specially corn and corn by-products - contaminated by the fungus Fusarium verticillioides (F. moniliforme ) and/ or F. proliferatum (Fumonisin B1)

58
Q
A

Leukoencephalomalacia in horse with mouldy corn toxicity

59
Q
A

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

60
Q

Hepatic Encephalopathy

A

• Acute/chronic liver disease

  • Cattle- ragworth poisoning
  • Dogs- porto-systemic shunts

• Sheep- copper posioning

61
Q

Some dramatic neurological disorders do not produce extensive neuropathology

Examples….

A

Some dramatic neurological disorders do not produce extensive neuropathology

  • Strychnine
  • Metaldehyde • Tetanus
  • Botulism
62
Q

Dysautonomias

A

Dysautonomias
• Degenerative changes in autonomic ganglia

– Key-Gaskell Syndrome in cats – Grass sickness in horses

– Chromatolysis, vacuolar degeneration in sympathetic and parasympathetic ganglia

63
Q
A

Key-Gaskell Syndrome

Pupillary dilation

Megaoesophagus, constipation

Anorexia, dehydration •

Few survive

Was more common in early 1990s

UK mainly

64
Q

Grass Sickness

A

Acute, subacute, chronic

Dyphagia, bowel stasis

Distended abdomen, constipation

Mortality almost 100%

Ileal biopsy (enteric ganglia) for antemortem diagnosis

65
Q

Equine Motor Neuron Disease

A

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

66
Q

CNS neoplasia

A
  • 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
67
Q

Most common CNS tumors

A

Astrocytoma *

Oligodendroglioma*

Meningioma*

Pituitary*

68
Q
A

Medullablastoma

  • Undifferentiated cells of cerebellum
  • Cells of external granular layer
  • Rare in animals (children more common)
69
Q
A

Astrocytoma

• Most common

70
Q
A

Oligodendroglioma

71
Q
A

Choroid Plexus Tumour

72
Q

Meningioma

A
  • Frontal, retrobulbar areas
  • Most common in cats
  • Histologically benign (shell-out)
73
Q
A

Meningioma Dog

74
Q
A

Meningioma Cat

75
Q
A

Pituitary Tumours

• Chromophobe adenoma

Diabetes insipidus (pressure on pars nervosa, interference with ADH transport to nervosa)

Hyperadrenocorticism (ACTH producing chromophobes

• Dogs/horses

76
Q
A

Pituitary Tumours (equine)

77
Q
A

Canine, metastatic mammary tumour

78
Q
A

Metastatic Hemangiosarcoma

79
Q
A

Osteochondroma: tumor of calverium compressing on brain

Pathology II (20 decks)

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