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TOX 4000 Medical Toxicology > Neurotoxicology > Flashcards

Neurotoxicology Flashcards

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USMLE® Step 1 flashcards
1
Q

what part of the body is CNS

A

brain, spinal cord

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2
Q

what part of the body is PNS

A

nerves, ganglia

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3
Q

what part of the body is ENS

A

digestive tract

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4
Q

what does brain step and midbrain control

A

blood pressure and respiration, visual and auditory systems

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5
Q

what does cerebellum do

A

posture and coordination of movement

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6
Q

what does diencephalon do

A

Thalamus: relays infomation to and from cortex
Hypothalamus: hormone secretion and autonomic nervous system

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7
Q

what does the cerebral hemispheres do

A

Cerebral cortex: perception, cognition, memory
Hippocampus: learning and memory
Basal Ganglia: assists cortex with motor function

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8
Q

what is BBB made of

A

endothelial cells and astrocytes

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9
Q

what chemicals is the nervous system vulnerable to

A

lipophilic chemicals

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10
Q

why is neuron loss permaneny

A

neurons do not divide

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11
Q

what is neuronopathy

A

damage to the cell body

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12
Q

examples of chemicals that lead to neuronopathy

A

methylmercury, MPTP

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13
Q

what is axonopathy

A

damage to neuronal axons and dendrites

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14
Q

what is proximal axonopathy

A

alterations in cell body and adjacent axon

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15
Q

what is distal axonopathy

A

alteration in terminal axon

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16
Q

examples of chemicals that lead to axonopathy

A

acrylamide

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17
Q

what is myelinopathy

A

damage to myelin sheaths

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18
Q

what is affected in central myelinopathies

A

oligodendrocytes in CNS

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19
Q

what is affected in distal myelinopathies

A

Schwann cells in PSN

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20
Q

what is indirect neurotoxicity

A

toxins in blood or damage to CNS vessel

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21
Q

example of chemical that leads to indirect neurotoxicity

A

carbon monoxide

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22
Q

example of chemical that leads to myelinopathy

A

lead

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23
Q

what is synaptic and neuromuscular toxicity

A

alterations in neurochemistry

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24
Q

examples of chemicals that lead to synaptic and neuromuscular toxicity

A

tetrodotoxin, botulinum toxin, organophosphates, bungarotoxin

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25
Q

describe methylmurcury neuronopathy

A
  • environmental exposure
  • bioaccumulates
  • lipophilic (enters CNS easily)
  • brain regions/neurons affected
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26
Q

methyl mercury toxicity is not correlated with?

A

cellular accumulation

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27
Q

how does methyl mercury bind

A

covalently binds -SH groups

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28
Q

what are the changes observed with methylmercyry toxicty

A
  • glycolysis
  • neurotransmitter release/reuptake
  • mitochondrial respiration
  • oxidative stress
  • protein and nucleic acid synthesis
29
Q

what does increased oxidative stress lead tp

A
  • impaired GSH antioxidant system

- generation of reactive oxygen species

30
Q

altered membrane potential involves what molecules

A

Na/K

31
Q

ATPase contains how many SH groups

A

2

32
Q

what is the role of Na/K/ATPase

A
  • maintains neuronal cell potential
33
Q

what is Na/K/ATPase inhibited by

A

MeHg (methylmurcury

34
Q

What does methyl mercury do regarding cell potential

A

leads to increased NA concentration in the cell

which leads to increase n calcium and subsequent neurotransmitter release

35
Q

what is the selective neuronopathy of methyl mercury neurotoxicity in adults

A

cerebellum and visual cortex affected

- cerebellar granule cells particularly vulnerable but with increased exposure other neurone also die

36
Q

describe how the cortex if affected with methyl mercury neuronopathy in adults

A

peripheral vision disturbance and blindness

37
Q

describe how the cerebellum is affected with methyl mercury neuronopathy in adults

A

ataxia, general incoordination, loss of sensation

38
Q

describe how basal ganglia are affected with methyl mercury neuronopathy in adults

A

tremors, chorea, intellecutual impairment

39
Q

describe how a fetus in utero is affected by methyl mercury neurotoxicity

A
  • delayed growth/development
  • impaired movement
  • intellectual disability
  • cerebral palsy
40
Q

what is MPTP

A

a contaminant of synthetic heroin

41
Q

how is MPTP transported

A

transported into neurons via dopamine transporter

42
Q

where does MPTP metabolize

A

in astrocytes

43
Q

effects of an acute high dose fo MPTP

A

loss of single population of neurons= imbalance of pathway

= paralysis, akinesia

44
Q

effect of lower dose of MPTP

A

delayed development of parkinsonism

45
Q

what is the primary site of toxicity of axonopathies

A

the axon

46
Q

what is the role of an axon

A

communicate with neurons and tissues; electrical impulses, transport of molecules to and from cell body

47
Q

explain how fast transport of axons goes

A

bi-directional movement of membrane associated materials

48
Q

explain slow axonal transport

A

primarily anterograde transport of cytoskeletal proteins

49
Q

what is 2,5-hexanedione

A

neurotoxic metabolite of n-butyl-ketone and n-hexane

50
Q

what are the symptoms of 2,5-hexanedione toxicity

A

swelling and neurofilament accumulation in distal axon

51
Q

accumulation of neurofilaments in distal axon is a symptom of what

A

2,5-hexanedione toxicity

52
Q

how does 2,5-hexanedione cause neurofilament accumulation in distal axon

A

there is no change in neurofilament synthesis but transport is accelerated which leads to accumulation within the distal axon

53
Q

what is acrylamide

A

polymer used industrially and in laboratories

54
Q

what is the main symptom of acrylamide toxicity

A

distal axon degeneration

- with prolonged exposure, dying back of axon occurs

55
Q

explain the mechanism of action of acrylamide toxicity

A
  • binds SH group on tubulin= microtubule disassembly

- minor swelling and neurofilament accumulation in distal axon

56
Q

can a single dose of acrylamide affect you

A

can affect retrograde axonal transport without producing structural changes

57
Q

what does acrylamide inhibit

A
  • kinesin

- fast transport proteins

58
Q

what is the main symptom of lead toxicity in adults

A

myelinopathy

- peripheral motor axons predominantly affected

59
Q

how does lead toxicity

A

mimics ca2+ and interferes with Schwann cell Ca2+ transport

- accumulates in and damages mitochondria, depletes GSH (glutathione)

60
Q

what happens initially with lead toxicity in adults

A

segmental demyelination

61
Q

what happens eventually with lead toxicity in adults

A

wallerian axonal degredation

62
Q

what are the symptoms of lead toxicity in children

A

cognitive decline

  • impaired learning and memory
  • tremors, ataxia, blindness, seizures
63
Q

what if children are acutely exposed to a massive dose of lead

A

cerebral edema due to damage of microvascular endothelial cells

64
Q

how does tetrodotoxin work

A

reversibly binds Na+ channel and prevents conduction of nerve impulse

65
Q

what are the initial symptoms of tetrodotoxin

A

tingling around mouth, dizziness

66
Q

what are the later symptoms of tetrodotoxin

A

ataxia, convulsions, respiratory paralysis, death

67
Q

where does the botulinum toxin come from

A

bacteria

68
Q

how does botulinum toxin work

A

irreversibly binds to SNARE proteins in peripheral cholinergic synapses and then decreases ACh release

69
Q

what are the symptoms of botulinum toxin

A

progressive limb paralysis, difficulty swallowing, respiratory paralysis and death

TOX 4000 Medical Toxicology (6 decks)

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