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Pathology 3 > Neuro 2 - degeneration > Flashcards

Neuro 2 - degeneration Flashcards

1
Q

when does brain atrophy occur

A
  • aging

- chronic disease (metabolic, nutritional, ischemia, inherited, inflammatory, idiopathic)

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2
Q

neuronal injuries or response

A
  • cytoplasmic vacuolation
  • cytoplasmic inclusion
  • reaction of neuronal cell body to axonal damage
  • neuroaxonal dystrophy
  • cell death (necrosis v apoptosis)
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3
Q

selective neuronal necrosis

A
  • due to high metabolic rate, only specialized neurons are affected
  • minimal or no gross changes
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4
Q

pan-necrosis

A
  • malacic disease (malacia = softening)
  • general insults may affect all tissue elements (neurons, glia, vessels)
  • selective vulnerability (general insults may directly or indirectly destroy neurons and supporting cells/tissue in specific areas of the brain) –> focal or regional malacia
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5
Q

global brain insult that gives rise to focal lesions in brain regions

A

selective vulnerability

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6
Q

causes of neuronal degeneration (7)

A
  • hypoxia/ischemia
  • inflammatory mediators
  • bacterial toxins
  • heavy metals
  • nutritional deficiency (thiamine, copper, vit E)
  • reduced ATP generation
  • excitotoxicity
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7
Q

reduced ATP generation and neuronal degeneration

A
  • hypoglycemia
  • interference with cytochrome oxidase (cyanide poisoning - plants)
  • inhibition of oxygen intake (CO poisoning)
  • inhibition of kreb’s cycle (fluoroacetate poisoning)
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8
Q

excitotoxicity and neuronal degeneration

A
  • unique form of neuronal cell death
  • neurons stimulate themselves to death
  • typically due to excess glutamate
  • intracellular rise in Ca
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9
Q

consequences of degenerative disease (3)

A
  • increased ICP
  • necrosis or apoptosis of nerve tissue
  • brain atrophy (if animal survives –> chronic)
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10
Q

gross features of degenerative disease (4)

A
  • brain swelling
  • flattening of gyri
  • herniation
  • asymmetry
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11
Q

origin of degenerative disease in the nervous system (4)

A
  • nutritional disease
  • metabolic disease
  • toxic disease
  • hereditary/familiar/idiopathic (less emphasis)
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12
Q

nutritional causes of degenerative disease (3)

A
  • Cu deficiency
  • thiamine deficiency
  • vitamin E deficiency
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13
Q

what does copper deficiency cause

A

swaysback and enzootic ataxia of lamb and goats (degenerative disease)

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14
Q

what does thiamine deficiency cause

A

-polioencephalomalacia (cortex necrosis)
-chastek’s paralysis
(degenerative disease)

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15
Q

what does vitamin E deficiency cause

A

equine degenerative myeloencephalopathy (degenerative disease)

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16
Q

metabolic causes of degenerative disease (3)

A
  • hypoglycemia
  • aminoacidopathies (bovine)
  • hepatic encephalopathy (very important disease)
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17
Q

heavy metals and degenerative disease

A

arsenic, lead**, mercury

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18
Q

organic/inorganic compounds and degenerative disease

A
  • organophosphates
  • cyanide, nitrate/nitrite, fluroacetate, CO
  • sodium chloride
  • selenium**
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19
Q

toxic plants and degenerative disease

A
  • plant induced storage diseases

- centaurea solstitalis, c repens

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20
Q

microbial toxins and degenerative disease

A
  • focal symmetric encephalomalacia
  • tetanus, botulism
  • tremogenic toxins
  • leukoencephalomalacia (moldy corn poisoning)
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21
Q

2 categories of hereditary/familiar/idiopathic degenerative disease

A
  • storage diseases (inherited v acquired)

- multisystem neuronal degenerations

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22
Q

5 multisystem neuronal degenerations

A
  • primary cerebellar degeneration
  • mitochondrial encephalopathy
  • motor neuron disease
  • neuroaxonal dystrophy
  • degenerative leukomyelopathy
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23
Q

what is hypoglycemia

A

primary energy failure in which highly susceptible cell populations are first affected (selective neuronal necrosis) by delayed onset degeneration and necrosis

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24
Q

what neurons are most susceptible to hypoglycemia

A

neurons in superficial cerebral cortex and hippocampus (selective neuronal vulnerability)

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25
Q

changes seen in hypoglycemia

A
  • first morphologic evidence is mitochondrial swelling

- light microscopic changes characterized by hypereosinophilia of neurons

26
Q

causes of hypoglycemia

A
  • insulinoma

- piglets in first week of life (incapable of gluconeogenesis)

27
Q

2 types of bovine aminoacidopathies

A
  • maple syrup urine disease

- citrullinemia

28
Q

maple syrup urine disease

A
  • bovine aminoacidopathy
  • inherited defect of chain ketoacid dehydrogenase complex enzyme
  • accumulation of ketoacids and abnormal metabolites
  • marked status spongiosus
29
Q

citrullinemia

A
  • bovine aminoacidopathy
  • inborn error of metabolism of urea cycle
  • accumulation of citrulline and ammonia in fluids and abnormal metabolites (hyperammonemia)
  • brain edema (cytotoxic edema)
30
Q

what is hepatoencephalopathy

A

-CNS disease caused by insufficient processing of portal blood by liver –> caused by portal-caval shunt or extreme hepatic malfunction

31
Q

mechamisms of cerebral malfunction in hepatoencephalopathy

A
  • inhibition of energy metabolism (loss of kreb’s cycle intermediates)
  • direct toxic effects of increased blood ammonia (vasogenic and cytotoxic edema)
  • exposure to neurotransmitters (glutamine, GABA) and false neurotransmitters
32
Q

structural changes in hepatoencephalopathy

A
  • small animals: indistinguishable from normal aging (sometimes primary demyelination that follows prolonged edema)
  • herbivores: more subtle changes (astrocyte hypertrophy and hyperplasia)
33
Q

what is equine degenerative myeloencephalopathy

A
  • neuroaxonal dystrophy affecting proprioceptive system neurons manifesting as spinal cord disease
  • functional defect involves axoplasmic transport
34
Q

what causes equine degenerative myeloencephalopathy

A
  • acquired: vitamin E deficiency (standardbreds, zebra)

- heritable: morgans, rottweilers

35
Q

anatomic changes in equine degenerative myeloencephalopathy

A
  • axonal spheroids affecting distal axon segment
  • spheroids contain neurofilament tangles, membranous whorls, lysosomal bodies
  • proprioceptive nuclei of brainstem, brain stem nuclei (level of obex)
  • myelin degeneration secondary to axonal degeneration
36
Q

what is a spheroid

A

degenerating axon (swollen)

37
Q

what is thiamine (b1) deficiency

A
  • thiamine is cofactor in oxidative energy pathways
  • deficiency results in degenerative and necrotic changes in tissues that have high demand for the vitamin and is associated with decreased high-energy phosphate levels
38
Q

what tissues are most susceptible to thiamine deficiency

A

CNS tissue

39
Q

changes seen in thiamine deficiency

A
  • vascular damage, neuronal necrosis progressing to malacia
  • changes differ in distribution between species
  • decreased CNS tissue content, decreased thiamine-dependent serum enzymes, occurrence of characteristic lesions
40
Q

5 suggested mechanisms for polioencephalomalacia

A
  • decreased ruminal production of thiamine by rumenal microflora
  • feeder cattle (decreased rumen pH)
  • animals consuming thiaminase
  • decreased thiamine absorption
  • excessive sulfide intake
41
Q

neuronal lesions in polioencephalomalacia

A

neuronal lesions predominate early (edema of neuropil, prominent small vessels, neuronal necrosis, cerebral swelling +/- herniation, flattening of gyri, pallor, petechia)

42
Q

classical lesion of polioencephalomalacia

A
  • laminar necrosis (malacia)
  • associated with brain swelling, gitter cells begin to accumulate, deep lamina may be involved
  • evident grossly as thin line following sulci and gyri - line autofluoresces under UV light (woods lamp)
43
Q

what happens if animal with polioencephalomalacia survives for several days

A

separation of lamina may occur

44
Q

histological features of cortical necrosis

A

central chromatolysis –> becomes irreversible –> gone

45
Q

what is chastek’s paralysis

A
  • carnivores require dietary thiamine (ruminants synthesize their own)
  • dietary requirements are readily met unless the animal is consuming a foodstuff high in thiaminase (ex: raw fish)
46
Q

histological changes in chastek’s paralysis

A
  • edema and vascular dilation
  • occurs following 2-4wks deficiency)
  • hemorrhage, neuronal degeneration, necrosis, malacia (lower part of brain)
47
Q

what is chronic salt intoxication

A

-cascade of pathologic changes follow a sudden imbalance between brain osmolality (astrocyte regulated) and plasma osmolality (kidney regulated) in which the brain becomes hyperosmolar relative to plasma

48
Q

result of chronic salt intoxication

A
  • CNS edema, brain swelling –> impedes circulation –> cerebrocortical laminar edema, neuronal necrosis, malacia
  • pigs, ruminants
  • pigs: eosinophilic infiltrates in meninges and around cerebral vessels may be seen in early stages
49
Q

what is focal symmetrical encephalomalacia

A
  • enteric overgrowth of specific pathogenic bacterial species results in the absorption and systemic dissemination of toxins that induce widespread vascular damage
  • in the brain, this vasogenic edema, complimented by a cytotoxic component, causes symmetric malacia
50
Q

microbes and toxins in focal symmetrical encephalomalacia

A
  • clostridium perfringens D (epsilon toxin) –> pulpy kidney

- e coli (shiga toxin 2e) –> edema disease of swine

51
Q

sequence of events in focal symmetrical encephalomalacia

A
  • organisms overgrow in intestinal lumen and produce toxins
  • systemic dissemination of bacterial toxin results in degeneration of small arterioles (focal hemorrhage and malacia of gray matter, basal ganglia/internal capsule, thalamus, substantia nigra)
52
Q

lead poisoning

A
  • discarded batteries and lead-based paints are potential sources
  • occurs especially in young animals
  • calves particularly susceptible
53
Q

mercury poisoning

A
  • occurs when seed grain treated with alkylmercury compounds is consumed
  • swine, cattle most frequently affected
54
Q

moldy corn poisoning

A
  • widespread multifocal cerebral white matter malacia (leukoencephalomalacia) develops acutely following the prolonged ingestion of fumonisi B1 (fusarium fungus)
  • horses particularly sensitive
  • malacia secondary to pronounced vasogenic edema
  • vascular damage results in hemorrhage (periphery of malacic foci)
55
Q

lysosomal storage diseases are specific lysosomal hydrolase deficiencies characterized by intralysosomal accumulation of what (5)

A
  • sphingolipids
  • glycolipids
  • oligosaccharides
  • mucopolysaccharides
  • autofluorescent lipopogments (neuronal ceroid lipofuscinoses)
56
Q

acquired lysosomal storage diseases

A
  • plant poisoning

- amphophilic drogue

57
Q

a-mannosidosis

A
  • naturally acquired storage disease in grazing livestock
  • induced by alkaloid swainsonine
  • locoweed species (astragalus, ocytropis, swainsona)
58
Q

mechanism of action of swainsonine

A

inhibition of the lysosomal a-mannosidase and golgi a-mannosidase II

59
Q

histo of storage disease

A

acquired sphingolipids: lamellar membrane-bound concentric bodies

60
Q

what are transmissible spongiform encephalopathies

A
  • accumulation, typically in CNS, of aberrant isoform of the host encoded normal prion protein (PrPc), designated PrPres, suggested to be infectious by itself and resistant to proteolysis
  • vacuolization of gray matter
61
Q

examples of TSEs

A
  • scrapie
  • transmissible mink encephalopathy
  • CWD
  • bovine spongiform encephalopathy
62
Q

scrapie genetic sensitivity resistance

A
  • codon polymorphism confers resistance or sensitivity to scrapie
  • resistant sheep did not develop disease but are asymptomatic carriers

Pathology 3 (11 decks)

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