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Neuro_week3 > Toxic/metab/nutirtional diseases > Flashcards

Toxic/metab/nutirtional diseases Flashcards

1
Q

acute alcohol intoxication in large quantity cause death by

finding in brain

A

central cardiorespiratory paralysis

massive cerebral edema, flattening of gyri, obliteration of sulci

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2
Q

chronically effect of alcohol on cerebral hemispheres

A

hemispheres shrink via diffuse loss of white matter (atrophy) and meningeal fibrosis

some neurons lost from frontal cortex with cell body shrink, retract dendrites, incr lipofuscin

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3
Q

chronically effect of alcohol on cerebellum

A

degeneration of superior vermis

folial crests are more affected than deeper structures (and lose purkinje, granule) with incr astrocytes

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4
Q

clinical presentation of alcoholic cerebellar degeneration

A

1) truncal instab
2) leg ataxia
3) wide based gait

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5
Q

how does cirrhotic liver affect brain

A

liver can’t process toxins –> heepatic encephalopathy likely due to ammonia

change proportion of excit/inhib NT or make false NT

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6
Q

hepatic cirrhosis characterized by what symptoms

A

1) confusion, forgetfulness
2) asterixis
3) stupor, coma

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7
Q

define hepatic encpehalopahty and mechanism of ammonia intox

A

fulminant liver failure due to high ICP from high blood ammonia from GI hemorrhage and severe cirrhosis (above 200)

ammonia from protein catabolism and urease-containing bacteria

ammonia not convert to urea (portal HTN) –> ammonia enter BBB and taken up by astrocytes

astrocyte’s glutamine synthetase for detox overwhelmed

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8
Q

histology of astrocytes in hepatic encephalopathy

A

alzheimer type 2 cells
astrocytes with
1) swollen nuclei
2) little cytoplasm

in deep cortex, globus pallidus, dentate nucelus of cerebellum

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9
Q

wernicke’s encephalopathy and korsakoff psychosis due to

assoc with

histo changes

A

thiamine b1 deficiency

assoc with

1) chronic etoh
2) poor food intake
3) absorb problem (G tube and hyperemesis )
4) malutilization and incr excretion

edema, necrosis, demyelination, neuron loss, gliosis

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10
Q

wernicke’s encephalopathy and korsakoff psychosis precipitated by

A

sudden glucose intake without thiamine

B1 needed for transketolase fxn and cofactor for glucose metab

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11
Q

triad of wernicke’s encephalopathy

A

1) ataxia
2) nystagmus
3) confusion

reversible if treat with thiamine

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12
Q

korsakoff syndrome

A

1) memory loss
2) confabulation = create false memories to fill gaps

irreversible

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13
Q

what structure involved in wernicke’s and korsakoff

A

mamillary bodies but also

1) wall of 3rd ventricle
2) periaquductal
3) inferior colliculi and thalamus
4) floor of 4th ventricle

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14
Q

acute stage of wernicke’s and korsakoff histologically

A

macro and microscopic petechial hemorrhage

prominant and dilated capillaries

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15
Q

imaging of wernicke’s and korsakoff

A

disrupt BBB from cytotoxic edema causing astrocyte swelling –> gives off NO –> change glutamate –> more free radicals

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16
Q

subacute vs acute wernicke’s and korsakoff

A

subacute

1) myelin lost
2) microglia and macrophage influx
3) fibrous gliosis

chronic

1) loss neurons
2) hemosiderin
3) mamillary atrophy

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17
Q

treatment of wernicke’s and korsakoff

A

IV thiamine

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18
Q

describe central pontine myelinolysis

A

symm demyelination affects pons usu from rapid correction of hyponatremia

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19
Q

symptoms of central pontine myelinolysis

A

triangular regions of demyelination with spared axons and neurons

quadriparesis
pseudobulbar palsy
pseudocoma

20
Q

sites of vulnerability in central pontine myelinolysis

A

ventral pons

extrapontine sites

21
Q

treatment of central pontine myelinolysis

A

slow treatment of hyponatremia

22
Q

colbalamin deficiency
occurs due to

importance of colbalimin

A

decr intake (strict vegan or GI cancer), pernicious anemia (most common) and immune mediated atrophic gastritis

cobalimin impt for methionine synthase for myelination

23
Q

colbalamin deficiency can cause

A

megaloblastic anemia

24
Q

colbalamin deficiency
early signs

later sign

A

paresthesias and ataxia (loss of DC/ML from swelling of myelin) and lower limb paresthesia

spastic paraparesia
ataxia
lower limb/trunk sensory defect

treatable dementia from patchy white matter dmg, psychoses
incontinence
orthostatic hypotension

25
Q

colbalamin deficiency
affects where

mechanism of myelin loss

A

ascending (sensory) and descending tracts (motor in the cord white matter esp lower cervical and thoracic (subacute combined degeneration)

1) initial = spongy vacuolization of white matter
2) myelin break down
3) macrophage influx and axon degenerate

26
Q

colbalamin deficiency

treat with

A

IV B12 supplementation

27
Q

Wilson’s disease
genetics

presents age

A

AR (chorm 13) disorder of copper metabolism

present in children or young adult

28
Q

Wilson’s disease

differnece btwn child and adult

A

child = copper accum in liver –> jaundice

adult = copper accum in CNS esp lentiform nucleus –> basal ganglia degeneration (

29
Q

Wilson’s disease

degeneration of basal ganglia causes

A

movement disorders

  • flap tremor, spasticity
  • dysarthria
  • limb incoordination
  • gait problems, involuntary movement
  • dystonia
30
Q

Wilson’s disease
most commonly affects where in brain

cells on histo

A

putamen

globus pallidus

31
Q

Wilson’s disease

cells on histo

A

alzheimer type 2 just like hepatic encephalopathy (swollen nuclei, small cyto)
damaged neurons via free radicals by copper or oxid of membrane lipids
astrocytosis

32
Q

treatment of wilson’s disease

A

chelating agents (pencillamine or trientine)

fatal if not treat

33
Q

what part of brain is affected by methanol toxicity

A

hemorrhagic necrosis in putamen

34
Q

fetal alcohol syndrome

features

A

poor motor skills
learning difficulties
mental retardation

indistinct philtrum
thin upper lip
small head, eyes, nose

35
Q

brain disease related to liver cirrhosis may or may not be

A

related to alcohol abuse

36
Q

treatment of hepatic encephalopathy

A

antibitoics to decr normal flora of gut

add lactuolose to acidify colon contents

37
Q

hepatic encephalpathy

affects what part of brain

A

globus pallidus causing confusion and asterixis

38
Q

chronic acquired non-wilsonian hepatocerebral degeneration = chronic hepatic encephalopathy

A

irrev neuro damage with chronic liver failure

destruction of neurons in deep cortex and putamen

39
Q

effects of protein-caloric malnutrition

kawshiorkor

A

protein deficiency with edema due to
low protein
ascites
hepatomegaly with hepatic statosis

40
Q

effects of protein-caloric malnutrition

caloric deficiency yields

A

marasmus with extreme cachexia and growth failure

–> apathy, lack of activity; effect glial formation, branching

41
Q

effects of protein-caloric malnutrition

reversibility

A

reversible if proper nutrition restored

42
Q

mechanism of B12 injury to nervous system

A

incorporation of abnormal fatty acids into bio membranes –> myelin instability

and NO inactiates methionine synthetase –> spinal path similar to subacute combined degeneration

43
Q

subacute combined degeneration
early

late symptoms

A

early = sensory,
lower limb paresthesia, loss of vibration/proprioception/fine touch

late = spastic paralysis, ataxia, lower limb and trunk sensory defects

44
Q

vitamin E deficiency seen when?

A 
intestinal malabsorption
cystic fibrosis
celiac disease
abetaliprproteinemia
congenital biliary atresia
45
Q

vitamin E deficiency

clinical features

A 
acanthocytosis
sensory periphery neuropathy
ataxia
retinopathy
myopathy 
cardiomyopathy
46
Q

vitamin E deficiency pathology

A

loss of dorsal root nerve cell bodies and dengeerate axons so DCML and spinocerebellar tracts affected

axonal spheroids in lower medulla

47
Q

toxic leukoencephalopathy due to __

A

external beam irradiation and chemo for tumor

white matter damage

Neuro_week3 (23 decks)

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