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Year 3 > CNS Pathology > Flashcards

CNS Pathology Flashcards

1
Q

Swayback is caused by a deficiency in what?

Which animals are affected?

A

Copper

Lambs

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2
Q

What are the two types of invertebral disc herniation?

A

Hansen type 1: extrusion of degenerated disc material

Hansen type 2: protrusion without rupture of the annulus fibrosus

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3
Q

What does the notochord becomes in most tetrapods?

A

The nucleus pulposus of the intervertebral disc

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4
Q

What does the rhombencephalon become?

A

Cerebellum

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5
Q

What lines the 4 ventricles of the brain?

A

Ependyma

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6
Q

What is cerebrospinal fluid?

A

Blood ultra infiltrate produced by choroid plexuses

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7
Q

Where is CSF produced?

Where is it drained?

A

Produced continuously within ventricles, drained by dorsal saggital sinus

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8
Q

How is the neural tube formed?

A

Lateral margins of the neural plays fold and bend inward

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9
Q

What is neurulation?

A

Formation and closure of the neural tube

It drives the sagittal closure of overlying structures (skin, ectoderm, muscle etc)

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10
Q

What is the posterior fossa made of?

A

Cerebellum and brainstem

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11
Q

What are the 5 divisions of the brain?

A 
Telencephalon (cerebrum)
Diencephalon 
Metencephalon (cerebellum and pons)
Mesencephalon (midbrain)
Myelencephalon (medulla oblongata)
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12
Q

What is the principle cell type in nervous tissue?

A

Neurons

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13
Q

What makes neurons basophilic?

A

RER (ie lysosomes)

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14
Q

What is the function of astrocytes?

A

Creation and maintenance of the integrity of the BBB
Uptake and recycling of neurotransmitters
Maintenance of extracellular pH and osmotic pressure (via uptake of K+)
Supporting migration of neurons during neuronogenesis

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15
Q

What is the function of oligodendrocytes?

A

Production of myelin within the CNS

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16
Q

Give the 3 layers of meninges surrounding the CNS

A

Dura mater: closest to bone, thicker, rich in collagen
Arachnoid: fine trabecules gently surrounding and supporting the vasculature
Pia mater: thin layer in contact with neuroparenchyma (eg brain)

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17
Q

What is the neuropil?

A

Dense mesh of dendrites and axons inter-connecting

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18
Q

How does calcium deficiency affect neurons?

A

Red hypoxic neurons

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19
Q

What happens to neurons during chromatolysis?

A

Nissl bodies disintigrate, nucleus migrates to periphery, increase in cell body and nuclear size

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20
Q

How do neurons react to damage?

A 
'Red dead neurons' (hypoxic)
Chromatolysis 
Apoptosis
Intracytoplasmic accumulation 
Vacuolation (BSE)
Intranuclear and intracytoplasmic inclusions
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21
Q

How do astrocytes react to damage?

A

Astrogliosis (increase in number)
Astrocytosis (increase in cell volume)
Cell swelling
Scar tissue formation

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22
Q

How do oligodendrocytes react to damage?

A

Damage to oligodendrocytes alters cell membrane and causes:

  • Impaired or defective myelin formation (primary demyelination)
  • Myelin destruction and phagocytosis (secondary demyelination)
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23
Q

What are microglia?

A

Macrophage-like cells in the CNS
Active immune surveillance
When resting: ramified morphology (long branching processes and a small cellular body)
They are then activated: activated non-phagocytic: rod shaped. Activated phagocytic: ameboid shape

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24
Q

What are gitter cells?

A

The eventual result of microglial cell’s phagocytosis of infectious material or cellular debris. After engulfing a certain amount of material, microglia are unable to phagocytose any further materials -> granular corpuscle, named for its ‘grainy’ appearance.
By looking at tissues stained to reveal gitter cells, pathologists can see post-infection areas that have healed

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25
Q

What is meant by infarction?

A

Obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue

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26
Q

Why are neurons so susceptible to damage?

A

Lack of proliferating activity
High metabolic demands
Low capacity of ‘metabolic adaptation’
Majority of neurons extend their processes far from the cell body (perikarion)

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27
Q

Microglia make up what % of the cells in the CNS?

A

12%

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28
Q

What makes the CNS susceptible to ischaemia?

A

High metabolic request (one third of total glucose)
Impossibility for local storage
Ischaemia starts after 60% decrease in blood flow
A few minuets of hypoxia -> neuronal cell death (red neurons)

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29
Q

Give some causes of ischaemia in the CNS

A

Blockage
Reduced 02 content in erythrocytes - hypoxia
Reduced flow of normally oxygenated blood

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30
Q

What would be seen histologically when looking at acute and chronic brain infarction?

A

Acute: pale area with red neurons and spheroids, surrounded by hyperaemia and astrocytosis

Chronic: area of liquefactive necrosis and astrogliosis surrounded by glial scar formation

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31
Q

What is siderocalcinosis?

A

Deposition of iron salts with calcium in tissues, principally blood vessels (mineralisation)

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32
Q

How do infectious agents reach the brain?

A

Local accumulation of bacteria within vessels and consequent suppuration
Retrograde axonal transport (eg rabies, listeria monocytogenes)
‘Trojan horse’ mechanism (eg toxoplasma)
Direct infection of endothelial cells (eg classical swine fever)
Deposition of immune complexes (eg FIP)

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33
Q

What is polioencephalitis?

A

Inflammation of grey matter of the brain

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34
Q

What is myelitis?

A

Inflammation of spinal cord

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35
Q

What is polioencephalomyelitis?

A

Inflammation of grey matter of brain and spinal cord

36
Q

What is leukoencephalitis?

A

Inflammation of white matter of brain

37
Q

What is leukoencephalomyelitis?

A

Inflammation of white matter of brain and spinal cord

38
Q

What is meningoencephalitis?

A

Inflammation of leptomeninges and brain

39
Q

What is pachimeningitis?

A

Inflammation of the dura mater

40
Q

What is choroiditis?

A

Inflammation of the choroid plexuses

41
Q

What is a perivascular cuff?

A

Accumulation of extravasated inflammatory cells within the perivascular space

42
Q

Histologically, are viral infections suppurative?

A

No

43
Q

Describe rabies virus

A

RNA virus, family Rhabdoviridae, genus Lyssavirus
Inflammation pattern: mild, non-suppurative polioencephalomyelitis (inflammation of grey matter of brain and spinal cord)
Inoculum site -> muscle -> axons -> CNS
Presence of inclusion bodies (Negri’s bodies) in cytoplasm of pyramidal neurons of hippocampus (carnivores) and purkinje cells of cerebellum (ruminants)

44
Q

Describe pseudorabies

A

DNA virus, suid herpes virus 1, pseudorabies virus (PRV)
Nuclear inclusion bodies
Inflammatory pattern: non-suppurative meningo-polioencephalomyelitis (inflammation of grey matter of brain and spinal cord) with glial nodules and neuronal necrosis with neuronophagia (phagocytosis of nerve cells)
Pigs, dogs
Horses resistant
Pruritus causes violent scratching and automutilation of head
Occasional intranuclear eosinophilic inclusion bodies

45
Q

What are glial cells?

A

Surround neurons and provide support for and insulation between them
Types include astrocytes, oligodendrocytes, Schwann cells, microglia

46
Q

What is satellitosis?

A

Histology: accumulation of neuroglial cells around a damaged neuron

47
Q

Pigs of what age are affected by swine polioencephalomyelitis?

A

Piglets within 10 weeks of age

48
Q

Describe canine distemper virus

A

Family Paramixoviridae
Inflammatory pattern: demyelinating leukoencephalitis (inflammation of white matter of brain); primary- defective myelin
Histology: Acute: pale demyelinated areas (gliosis and macrophages)
Chronic: non-suppurative inflammation with evident cavitation

49
Q

What is louping ill transmitted by?

A

Ticks (Ixodes ricinus)

50
Q

What causes malignant catarrhal fever?

A

Ovine herpes virus 2, caprine herpes virus 2

51
Q

Which species get louping ill?

A

Sheep, pigs, horses

52
Q

Describe herpetic encephalomyelitis

A

Horses
Equine herpes virus type 1
Petechial or ecchymotic haemorrhages in white and grey matter of spine
Inflammatory pattern: vasculitis with thrombosis, suppurative myelitis and haemorrhages

53
Q

Describe the general inflammatory pattern of bacterial infections

A

Suppuration (due to recruitment of neutrophils), tissue lysis, gliotic reaction

54
Q

Describe the general inflammatory pattern of viral infections

A

Non-suppurative with frequent formation of neuronophagic nodules

55
Q

Describe listeriosis

A

Listeria monocytogenes, gram +
Retrograde transport along axons and trans-synaptic spreading
Oral cavity -> cranial nerves-> brainstem
Inflammatory pattern: Multifocal to coalescing micro abscesses
Can be more marked on one side
Small leukomalacic areas
Cows, sheep, pigs

56
Q

What are the intermediate hosts of toxoplasma?

What is the definitive host?

A

All warm-blooded animals

Definitive: cats

57
Q

What are the intermediate hosts of neospora?

What is the definitive host?

A

Intermediate: primarily Cattle, also deer
Definitive: dogs

58
Q

Describe the inflammatory pattern for toxoplasmosis in young and adult animals

A

Young: non-suppurative polioencephalitis with gliosis
Adult: necrotising and granulomatous encephalitis

59
Q

What causes cerebral coeneurosis in sheep?
What is a characteristic symptom?
What is seen in the brain?

A

Infection by the metacestode larval stage (coeneurus) of Taenia multiceps; migrates around body but frequently within brain
Characteristic symptom: walking in circles
Single or multiple (rare) soft fluid-filled cysts in brain

60
Q

What is the difference between a gyrus and a sulcus?

A 
Sulcus= depression
Gyrus= fold
61
Q

What is spina bifida?

A

Failure of development of the vertebral arch of the lumbar spine

62
Q

What is hydrocephalus?

A

Increase in volume of CSF in ventricles of brain -> increased intracranial pressure

63
Q

Corticocerebral necrosis is thought to be caused by what?

A

Sulfur intoxication or thiamin deficiency (imbalance between thiamin-producing and thiamin-destroying ruminal bacteria)
Small animals: hypoglycaemia, organic mercury poisoning

64
Q

Describe a brain affected by corticocerebral necrosis

A

Swollen brain due to oedema and laminar necrosis (red hypoxic neurons)
Cavitation of the affected cortex, gitter cell proliferation, glial scar formation

65
Q

What is thiamin?

A

Vitamin b1

66
Q

How can you identify a lamb with swayback?

A

Blind and ataxic -> severe incoordination -> immobility -> death
Hollowed back
Neurological symptoms present at birth

67
Q

The presence of which cell type indicates hepatic encephalopathy?

A 
Alzheimer type II astrocytes 
Astrocytes' ammonia-removing capacity is overwhelmed by increased blood ammonia due to hepatic dysfunction 
Astrocytes swell (cytotoxic oedema)
68
Q

Describe the two types of tumours found in the CNS

A

Primary: arising from CNS cell types (eg astrocytoma), single masses, rarely metastasising
Secondary or metastatic: colonising the CNS from distant areas of primary growth (eg melanoma), often multifocal distribution

69
Q

Describe an astrocytoma

A

Some dog breeds (brachycephalic) have higher incidence
Generally arise in white matter of cerebral hemispheres
On cut surface, appear firmer than normal parenchyma, whitishand poorly to undemarcated
Increasing malignancy (cell atypia, infiltration, mitoses) -> neoangiogenesis (red colour) -> necrosis (malacia)

70
Q

Describe an oligodendroglioma

A

Brachycephalic breeds more susceptible
Frontal, temporal, parietal cortex
Pronounced neoangiogenesis and intra-tumoral haemorrhages
Grossly: well circumscribed, sharply demarcated, gelatinous
Areas of necrosis, haemorrhage and cystic degeneration are associated with increased malignancy
Histo: honeycomb appearance, small nuclei surrounded by empty halo

71
Q

What is a Psammoma body?

A

Round collection of calcium, seen histologically and associated with meningiomas and other tumours

72
Q

Describe a meningioma

A

Tumour arising from meninges
Grossly: lobulated, often granular, white to tan with a broad based attachment to the meninges
Histologically: consists of uniform spindloid cells with elongated oval nuclei, cells are arranged in whorls often centred around mineralised Psammoma bodies

73
Q

What is considered a causative condition of motor neuron diseases?

A

Vitamin E and selenium deficiency

74
Q

What is the main and most common hallmark of motor neurone diseases?

A

Neuronal chromatolysis

75
Q

What are Purkinje cells?

A

Large neurons in the cerebellum, constitute the sole output of all motor coordination in Cerebellar cortex

76
Q

What are storage disorders?

A

Specific enzymatic defects result in intracytoplasmic storage of non-degradable catabolites that accumulate in neurons -> impair cell functions -> degeneration -> premature death

77
Q

Small amounts of lipofucsin pigment in neurons are usual and are associated with what?

A

Age-related changes of the brain

78
Q

Give the clinical signs of scrapie in sheep

A 
Pruritus, ataxia, paralysis, emaciation 
Histology: 
-Neuronal vacuolation
-Neuropil vacuolation
-Astrogliosis 
-No inflammation
79
Q

Give the clinical signs of BSE

A 
Aggression, nervousness, hypermetria, ataxia 
Histology: 
-Neuronal vacuolation
-Neuropil vacuolation
-Astrogliosis 
-No inflammation
80
Q

What is the myenteric plexus?

A

Major nerve supply to the GI tract, controls GI tract motility

81
Q

What is Wallerian degeneration?

A

Process that results when a nerve fibre is cut or crushed, and part of the axon is separated from the neuronal cell body distal to the injury. Influx of macrophages. Disintegration of the axon.
Not the consequence of focal trauma (ischaemia)
Causes enervation atrophy of effector organ (eg muscle) and chromatolysis of neurons (degeneration)

82
Q

Describe ileo-aortic thromboembolism

A

Thrombosis of distal abdominal aorta at junction with internal and external iliac arteries -> acute ischaemic infarction of peroneal and tibial nerves and muscles
Associated with valvular endocarditis
Sudden paraparesis or paraplegia with painful hard muscle and no femoral pulse
Cats

83
Q

Horses with cauda equina neuritis develop paralysis where?

A

Sphincter and tail

84
Q

What is neuropraxia?

A

Occurs after trauma
Nerve is structurally intact but transmission of impulses is impaired
Full recovery will follow

85
Q

What is axonotmesis?

A

Axon is structurally damaged and interrupted (trauma)
Basal lamina is intact
Axon can regenerate but time depends on distance to effector organ

86
Q

What are dysautonomias?

A

Neuronal degeneration followed by reactive gliosis/satellitosis
Eg equine grass sickness

Year 3 (28 decks)

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