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004 - path (test III) > Neuro02-01 > Flashcards

Neuro02-01 Flashcards

1
Q

(1)

A
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2
Q

(2)

(Neural Injuries or response)

A
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3
Q

(3)

(Classification by degree of cell death)

(selective neuronal necrosis)

  1. why does this occur?
  2. gross changes?

(Pan-necrosis (Malacic disease))

  1. general insults may affect what?
  2. Selective vulnerability

general insults may directly or indirectly destroy neurons and supporting cell or tissue (vessels, glia) in specific areas of the brain

focal or regional malacia

A
  1. due to high metabolic rate
  2. none/minimal
  3. all tissue elements (neurons, glia, vessels)
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4
Q

(4)

(Causes of Neuronal Degeneration)

(Hotel By RHINE)

1-7. what are they?

(+look at extra details)

A
  1. hypoxia/ischemia
  2. bacterial toxins
  3. reduced ATP generation
  4. heavy metals
  5. inflammatory mediators
  6. nutritional deficiency: Thiamine, copper, Vit E
  7. excitotoxicity
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5
Q

(5)

(Consequences of Degenerative disease)

1-3. what three?

A

1 increased intracranial pressure

  1. Necrosis or apoptosis of nerve tissue
  2. brain atrophy
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6
Q

(6)

(Gross features of degenerative disease)

1-4. what four?

A
  1. brain swelling
  2. flattening of gyri
  3. herniation
  4. asymmetry
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7
Q

(7)

(Origin of degenerative disease of the nervous system)

1-4. what four?

(Neutral Milk Hotel Tour)

A
  1. nutritional disease
  2. metabolic disease
  3. hereditary (familiar and idiopathic degenerative disease)
  4. toxic disease
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8
Q

(8)

(Nutritional Causes of Degenerative disease)

  1. copper deficiency

what in lamb and goats?

  1. Thiamine def

what two?

  1. Vit E deficiency

in what?

A
  1. swaysback and enzootic ataxia
  2. polioencephalomacia

Chastek’s paralysis

  1. equiine degenerative myeloencephalopathy
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9
Q

(9)

(Metabolic causes of degenerative disease)

1-3. what three?

A
  1. hypoglycemia
  2. aminiaciopathies (Bovine)

3 hepatic encephalopathy

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10
Q

(10)

(Toxic causes of degenrative disease)

(heavy metals)

  1. which ones?

(organic and inorganic compounds)

  1. like what? (look at pic for answer)

(toxic plants)

3 like what?

(microbial toxins)

  1. like what
A
  1. arsenic, lead, mercury
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11
Q

(11)

(Hereditary, familiar and idiopathic degenerative disease)

(storage diseases)

  1. inherited or acquired?

(Multisystem neuronal degenerations)

  1. like what?
A
  1. either…
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12
Q

(12)

A

C

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13
Q

(13)

(Hypoglycemia)

  1. A primary energy failure in which what occurs?
  2. Neurons where are most susceptible?
  3. the first morph evidence of neuronal degeneartion = ?
  4. Light microscopic changes are characterized by what?
  5. what are two causes?
A
  1. highly susceptible cell populations are affected (selective neuronal necrosis) by a delayed onset of degeneration and necrosis
  2. superficial cerebral cortex and hippocampus (selective neuronal vulnerability)

3 mitochondrial swelling

  1. hypereosinophilia of neurons (difficult to distinguish from autolysis)
  2. insulinoemia

piglets in first week of life (incapable of gluconeogenesis)

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14
Q

(14)

(Aminoacidopathies (Bovine))

(Maple syrup urine disease)

  1. inheritied defect of what?
  2. accumulation of what?
  3. marked what?

(Citrullinemia)

  1. inborn error of metabolism of what?
  2. accumulation of what in fluids?
  3. brain edema (cytotoxic edema)
A
  1. chain ketoacid dehydrogenase complex enzyme
  2. ketoacids and abnormal metabolites
  3. status spongiosus
  4. urea cycle
  5. citrullin and ammonia (and abnormal metabolites (hyperamonemia)
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15
Q

(15)

(Hepatoencephalopathy)

  1. CNS disease caused by what?

may be caused by what?

  1. Mechanisms of cerebral malfunction include:

inhibition of what?

direct toxic effect of what?

exposure to what?

  1. Structural changes ard mild and insignificant

small animals - may look like what?

herbivores - look how?

A
  1. insufficient processing of portal blood by liver

portal-caval shunt, extreme hepatic malfunction

  1. energy metabolism (loss of Kreb’s cycle intermediates)

increased blood ammonia (vasogenic or cytotoxic edema)

NT (glutamine, GABA) and false NT (tyramine, octamine, b-phenylethanolomine)

  1. normal aging (may be primary demyelination if prolonged edema)

more subtle - astrocyte hypertrophy and hyperplasia

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16
Q

(16)

(Equine Degenerative Myeloencephalopathy)

  1. a neuroaxonal dystrophy affecting what?

manifesting as what?

  1. functional defect involvens what?
  2. In some instances, there is acquired/heritable predisposition

like what?

  1. anatomic changes

spheroids affecting what?

spheroids contain what?

distribution: where in brainstem?

A
  1. proprioceptive system neurons

spinal cord disease

  1. axoplasmic transport
  2. vit E deficiency

heriatble (morgans, rottweilers)

  1. distal axon segment

neurofilament tangles, membranous whorls, and lysosomal bodies

proprioceptive nuclei of the brainstem, (accessory cuneate, cuneatre, gracilus)

17
Q

(17)

(Thiamine (Vitamin B1) Deficiency)

  1. thiamine is a cofactor in what?
  2. Deficiency results in degenerative and necrotic changes in tissues that have a high demand for the vitamin and is associated with decreased what?
  3. what tissue is most susc?
  4. Changes are characterized by what?
  5. changes differ in distribution with species
  6. deficiency may be documented by what trhee things?
A
  1. oxidative energy pathways
  2. high‐energy phosphate levels
  3. CNS
  4. vascular damage and neuronal damage progressing to malacia
  5. decreased CNS tissue content

decreased thiamine-dependent serum enzymes (eg pyruvate kinase)

occurrence of charactersitc lesions

18
Q

(18)

(polioencephalomalacia - Ruminants)

1-5. what are the five suggested mechanisms?

A
  1. decreased ruminal production of thiamine by microflora
  2. feeder cattle (decreased rumen pH)
  3. animals consuming thiaminase (coccidosatic amprolium, horsetail, brackenfern)
  4. decrased thiamine absorption
  5. excessive sulfide intake (important w/o concurrent thiamine deficiency)

(mostc ases of polioencephalomalacia in feedlot cattle occur 15‐30 days following introduction of a high sulfur diet.)

19
Q

(19)

(Polioencephalomalacia - Ruminants)

  1. neuronal lesions predominate early

edema of what?

evident grossly as what?

  1. classical lesion is characterized by what?

associated with brain swelling, gitter cells will begin to accumulate, deep lamina may eventually be involved

evident grossly as what?

  1. if animal survives several day - separation of what may occur?
A

1 neuropil, prominent small vesses, neuronal necrosis

cerebral swelling +- herniation, flattening of gyri, pallor, petehcia

  1. “laminar necrosis malacia”

thin line following sulci and gyri (in fixes/unfixed will fluoresce)

  1. lamina
20
Q

(20)

(Chastek’s Paralysis)

  1. Carnivores need dietary thiamine (ruminants make themeselves) - this is easy to meet unless what?

then just read this…

A
  1. diet is high in thiamininases (raw fish)

004 - path (test III) (13 decks)

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