Toxic Disorders of the Nervous System

Card Set Information

Author:
jknell
ID:
195354
Filename:
Toxic Disorders of the Nervous System
Updated:
2013-01-25 22:09:25
Tags:
MBB II
Folders:

Description:
MBB II
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user jknell on FreezingBlue Flashcards. What would you like to do?


  1. Toxin access to nervous system
    • -primarily hematogenous
    • -occasionally deposited locally through trauma
  2. Toxin time course
    • -varies
    • -usually subacute
    • -highly dependent on amount of toxin and rate of exposure
    • -single relatively time-limited exposure
    • -multiple intermittent exposures
    • -ongoing, long lasting exposure
  3. Alcohol
    • Affects nervous system many ways:
    • -acute intoxication
    • -toxicity from chronic exposure
    • -toxicity from nutritional deficits
    • -withdrawal
  4. Alcohol: Acute intoxication
    • 30mg/dL: mild euphoria
    • 200mg/dL: confusion, mental slowing
    • 400mg/dL: life threatening sedation and dysautonomia

    Patients may become habituated (tolerance)

    • Pathophysiology:
    • -enhances GABAA inhibitory signaling
    • -inhibits NMDA receptor
    • -potentiates seratonin currents (reward)
    • -dissolves in the lipid membrane and changes rigidity of the membrane
  5. Alcohol Metabolism
    • -90% oxidation
    • -<10% excreted in urine, perspiration, breath
    • -alcohol dehydrogenase in liver

  6. Alcohol: Toxicity from chronic exposure
    • 1. Alcoholic Dementia
    • -controversial
    • -at risk for disorders that cause cognitive dysfunction
    • -most believe long term heavy use can cause mild dementia with frontal dysfunction
    • -brain atrophy

    • 2. Cerebellar Degeneration
    • -atrophy of anterior and superior vermis
    • -may actually be due to nutrition deficit
    • -tx: thiamine

    • 3. Alcoholic Myopathy
    • -acute: during binge drinking (severe muscle pain and tenderness, elevated CK)
    • -chronic: painless proximal weakness of lower > upper extremeties

    • 4. Depression
    • -mood swings
    • -can resemble major depressive episode
  7. Alcohol Withdrawal
    • -full syndrome is know as Delirium Tremens
    • 1. Tremor: typically first sign of withdrawal
    • 2. Hallucinations: animate objects, unpleasant
    • 3. Seizures: 1-2 days, generalized tonic clonic, almost always self limited
    • 4. Delirium Tremens: autonomic instability (changes in BP, HR, temp etc), life threatening

    • Treatment:
    • -benzos
  8. Opiates
    • -overdose intoxication
    • -withdrawal
  9. Opiates: Overdose intoxication
    • Presentation:
    • -acute onset
    • -decreased LOC
    • -shallow respirations
    • -slowed respiratory rate
    • -pinpoint pupils
    • -bradycardia
    • -hypothermia

    ***some ppl are more susceptible to overdose: children, adults with myxedema, chronic liver disease, pneumonia

    ***opiate OD should be suspected in anyone with decreased LOC or hypoventilation of unknown etiology!!!

    • Treatment:
    • -Naloxone (due to very short half life may need multiple doses)
    • -gastric lavage in oral OD
  10. Opiates: Withdrawal
    • -high dosages of opiates have a very high rate of withdrawal sx
    • -withdrawal is miserable, but won't kill you

    • Presentation:
    • 1. 8-16 hours: sweating, yawning, piloerection, tearing
    • 2. 36 hours: severe restlessness, hot and cold flashes, N/V, diarrhea
    • 3. 72 hours: peak, decline over the next two weeks

    • Treatment = Symptomatic
    • -autonomic overactivity: alpha agonist
    • -abdominal pain: loperamide
    • -NSAIDs: analgesics
    • -anxiety: benzos
    • **oral methadone: controversial
  11. Stimulants
    • -amphetamines
    • -cocaine
  12. Amphetamines
    • -Rx: disorders of sleep and attention
    • -illicit

    • -energy and mental acuity at low doses
    • -ecstasy at high doses

    -common in San Diego

    -very high risk for addiction
  13. Amphetamine: Overdose
    • Presentation:
    • -restlessness
    • -agitation
    • -hallucinations
    • -paranoia
    • -psychosis
    • -increased sympathetic function:
    •      -hypertension
    •      -cerebral infarct (vasospasm)
    •      -intracerebral hematoma

    • Treatment:
    • -support through abstinence
  14. Amphetamine: Withdrawal
    • Presentation:
    • -fatigue
    • -depression
    • -sleepiness
    • -problems concentrating
    • -intense hunger

    • Treatment:
    • -support through abstinence
  15. Cocaine
    • -snorted, smoked, injected
    • -applied topically as a local anesthetic (ENT, ophtho)

    Crack: heat stable, can be smoked

    • Intoxication:
    • -cognitive effects
    • -emotional effects
    • -tachycardia
    • -hypertension
    • -vasoconstriction leading to infarct
    • -seizures
    • -hyperpyrexia

    • Pathophysiology:
    • -blocks reuptake of central DA and peripheral NE
  16. Cocaine: Withdrawal
    • -fatigue
    • -depression
    • -sleepiness
    • -problems concentrating
    • -intense hunger
  17. Sedative and Hypnotics
    • -Barbituates
    • -Benzos
    • -Non-benzo hypnotics
  18. Barbituates
    • Presentation:
    • 100-300mg:
    • -drowsy or asleep
    • -mildly incoordinated
    • -mentally slow

    • 5-10x:
    • -stupor
    • -depressed deep tendon reflexes
    • -slow, full respirations

    • 10-20x:
    • -comatose
    • -slow, shallow respirations
    • -flaccid
    • -decreased or absent reflexes

    • Pathophysiology:
    • -enhance inhibitory GABAA transmission
    • ***strongly potentiated by alcohol or other CNS depressant
  19. Benzodiazepines
    • Clinical Role:
    • -anxiolytics
    • -anticonvulsants
    • -anti-tremor
    • -anti-spasticity
    • -anesthetics

    different types of benzos differ in potency and half life but are very similar
  20. Benzos: Overdose
    -it is harder to OD on benzos

    • Presentation:
    • -unsteadiness of gait
    • -drowsiness
    • -depressed consciousness at high doses
    • -rarely depressed respiration or cardiac dysfunction

    • Treatment:
    • -flumazenil (benzo antagonist)
  21. Benzos: Withdrawal
    • Presentation:
    • -anxiety
    • -jitteriness
    • -insomnia
    • -seizures (rare)

    -seen within d3-7 of abstinence

    • Treatment:
    • -slow taper off benzos
    • -start benzo with longer half life
  22. Non-Benzodiazepine Hypnotics
    -Zolpidem

    -acts at GABAA site

    • Clinical Uses:
    • -decrease sleep latency
    • -increase sleep duration
    • -w/o anxiolytic, anticonvulsant, or anti-spasticity properties of benzos

    • Intoxication:
    • -idiosyncratic effects (may occur suddenly)
    • -sonambulism
    • -amnestic episodes

    -little evidence for dependence or addiction
  23. MDMA
    -synthetic amphetamine

    • Intoxication:
    • -euphoria
    • -hypersexuality
    • -hallucinogen-like feeling

    • Pathophysiology:
    • -increased serotonin release in the CNS
    • -followed by interference with serotonin synthesis

    • Overdose:
    • -seizures
    • -cerebral hemorrhage
    • -psychotic behaviour
  24. Marijuana
    • Intoxication:
    • -transient drowsiness
    • -euphoria
    • -perceptual distortions
    • -mild-moderate psychomotor retardation
    • -hallucination with higher doses
    • -even higher doses may cause severe depression and stupor
    • -death is extremely rare

    • Pathophysiology:
    • -THC interacts with cannabinoid receptors of endogenous system

    • Chronic Use:
    • **NOT clear if there is chronic dependence or withdrawal syndrome
    • -some deficits in short term memory and attention even with abstinence
    • -no clear pathologic changes

    • Clinical Use:
    • -meaningful antiemetic and appetite stimulant
    • -role in anti-spasticity or neuropathic pain not supported
  25. Hallucinogens
    • -LSD
    • -mescaline
    • -PCP

    • Intoxication:
    • -vivid hallucinations
    • -distortions of visual perceptions
    • -unusual dreams
    • -depersonalization
    • -dizziness, nausea, paresthesias, blurry vision, sympathomimetic effects
  26. Botulinum Toxin
    • Presentation:
    • -rapid subacute onset diffuse weakness
    • -First: anorexia, nausea, vomiting
    • -Later: severe constipation
    • -First Neuro: blurred vision and diplopia
    • -Later Neuro: failure of pupil reactivity, diffuse motor weakness, paralysis, respiratory failure

    • Pathophysiology:
    • -canned food, honey
    • -G+ rod, anaerobic, creates spores in soil
    • -produces toxins
    • -toxin binds gangliosides on motor neurons and enters cell
    • -once inside cell it blocks the ability of Ach vesicles to fuse with PM

    • Rule out:
    • -Myasthenia Gravis: prominent eye findings
    • -Guillain Barre:prominent weakness worsening over days, descending weakness, somatosensation is normal, CSF is normal

    • Treatment:
    • -advanced life support
    • -trivalent antiserum
    • -tx infected wounds (PCN, metronidazole)

    • Prognosis:
    • -good recovery (weeks to months)
  27. Botulinum Toxin: Clinical Uses
    • -dystonia/spasticity
    • -cosmetic use
    • -refractory migraines

    ***chronic use may lead to development of neutralizing antibodies (can switch to a different type)
  28. Malignant Hyperthermia
    • -rare adverse effect of general anesthesia (1/50,000)
    • -usually with inhalation agent

    • Presentation:
    • -paradoxical stiffening of jaw muscles (given succinylcholine)
    • -diffuse muscle stiffness
    • -rise in body temp
    • -frank rhabdomyolysis
    • -acidemia
    • -elevated CK
    • -myoglobinuria
    • -death

    • Pathophysiology:
    • -increase in SKM intracellular Ca leading to sustained muscle contraction and hyperthermia
    • -genetic abnormality in RyR1

    • Treatment:
    • -cease anesthetic
    • -Dantrolene (CCB)
  29. Pseudotumor Cerebri Causes
    • -idiopathic intracranial hypertension
    • -secondary pseudotumor cerebri
  30. Pseudotumor Cerebri: Idiopathic Intracranial Hypertension
    • Epidemiology:
    • -overweight adolescent girls
    • -short stature
    • -menstrual irregularties

    • Presentation (over months):
    • -increased ICP w/o localizing signs
    • -HA (worse when supine, progressive)
    • -visual obscurations
    • - sometimes mild double vision
    • -papilledema
    • -abducens nerve palsy
    • -NO: hydrocephalus, mass lesion

    • Diagnosis:
    • -fundoscopic exam
    • -test visual acuity and fields
    • -venography
    • -LP
    • -long term serial visual testing

    • Treatment:
    • -weight reduction
    • -acetazolamide (reduces CSF production)
    • -CSF shunting
    • -optic nerve sheath fenestration (effective up to 1 year)
  31. Pseudotumor Cerebri: Secondary Pseudotumor Cerebri
    • Causes:
    • 1. otherwise asymptomatic occlusion of cerebral dural venous sinuses, this causes cerebral venous hypertension leading to a decreased outflow of CSF
    • 2. meningeal diseases
    • 3. hypervitaminosis A
    • 4. tetracycline

    • Diagnosis:
    • -fundoscopic exam
    • -test visual acuity and fields
    • -venography
    • -LP
    • -longer term serial visual testing

    • Treatment:
    • -tx underlying lesions
    • -anticoagulants
    • -immunosuppresives
    • -antimicrobials
  32. Chronic Fatigue Syndrome
    • Epidemiology:
    • -more common in women than men
    • -3rd to 5th decades of life

    • Presentation:
    • -persistent and disabling fatigue for at least 6 months, with 6 of the following:
    • -recurrent somatic or neuropsych sx
    • -low grade fever
    • -cervical or axillary lymphadenopathy
    • -myalgias
    • -migrating arthralgias
    • -sore throat
    • -forgetfulness
    • -HAs
    • -difficulty concentrating/thinking
    • -irritability
    • -sleep disturbances

    • Causes:
    • -associated with depression and anxiety
    • -maybe after non-specific viral illness
    • -often no clear cause

    • Treatment:
    • -education
    • -CBT
    • -antidepressants
  33. Lead Poisoning
    • Epidemiology:
    • -more common in children

    • Presentation:
    • -In kids --> encephalopathy: lowered intelligence, decreased attention, hyperactivity
    • -In adults --> motor polyneuropathy, bilateral "wrist drop"

    • Pathology:
    • -cerebral edema
    • -necrosis of cortical neurons
    • -astrocytic proliferation
    • -demyelination of cerebral and cerebellar hemispheres
    • -axonal degeneration

    • Pathophysiology:
    • -lead competes with calcium
  34. Arsenic Poisoning
    • Epidemiology:
    • -in adults due to intoxication with herbicides, insecticides or rodenticides
    • -may be fatal

    • Presentation:
    • -low dose: subacute onset sensorimotor polyneuropathy
    • -high dose: acute encephalopathy, multi-organ failure, death

    • Pathology:
    • -multiple punctate hemorrhages in the white matter
    • -capillary necrosis
    • -sensorimotor polyneuropathy

    • Pathophysiology:
    • -may interfere with ox phos
  35. Carbon Monoxide Poisoning
    • Epidemiology:
    • -victims of fires
    • -suicide attempts
    • -faulty ventilation

    • Presentation:
    • -amnesia
    • -ataxia
    • -UMN dysfunction
    • -additional cognitive dysfunction
    • -parkinsonism

    • Pathophysiology:
    • -same effects as anoxic ischemia
    • -also binds globus pallidus (iron rich)
    • -CO binds to Hbg --> global ischemia
    • -selectively vulnerable: hippocampus, purkinje cells, outer layers of cerebral cortex, GP
  36. Organophosphate Poisoning
    • Epidemiology:
    • -pesticides

    • Presentation:
    • -HA
    • -vomiting
    • -sweating
    • -abdominal cramping
    • -salivation
    • -wheezing
    • -miosis
    • -weakness
    • -fasciculations
    • -high dose: cardiovascular collapse
    • -late effects (d-wks): distal symmetrical motor > somatosensory polyneuropathy, UMN findings

    • Pathophysiology:
    • -acute anticholinesterase activity
  37. MPTP
    • Pathophysiology:
    • -metabolized to a toxic metabolite which binds melanin in DA neurons of substantia nigra leading to their death

    • Presentation:
    • -Parkinsonism (acute, bilateral)
  38. Inhalants
    • -NO, hydrocarbons
    • -propellants and solvents in household products

    • Presentation:
    • -euphoria
    • -irritability
    • -aggression
    • -depressed mood
    • -bizarre thoughts
    • -Chronic exposure: distal polyneuropathy

    ***can be an occupational hazard for OR staff
  39. Plant and Animal Neurotoxins
    • -black widows
    • -snake venom
    • -scorpion venom
    • -jimson weed
    • -ciguatera
    • -fish and shellfish toxins

    • Pathophysiology:
    • -toxins affect peripheral nerve function and neuromuscular transmission
    • -Dinoflagellates block axonal transmission by impairing Na channels
  40. Tetanus Toxin
    • -C. tetani exotoxin
    • -spores can live in soil for decades

    • Presentation:
    • -sustained muscle contractions
    • -lockjaw (masseter particularly susceptible)

    • Pathophysiology:
    • -toxin carried to CNS by retrograde axonal transport
    • -toxin prevents exocytosis of GABA vesicles
    • -loss of inhibitory neurons in reflex arcs causes neuronal hyperexcitability

    • Treatment:
    • -DPT vaccine
  41. Ionizing Radiation
    • Pathophysiology:
    • -damage to DNA
    • -more rapid delivery, larger volume and greater rapidity of cell division in the affected area --> greater injury

    • Pathology:
    • -late response: recurrent and de novo tumor formation
    • -demyelination and necrosis (secondary to vascular injury)
  42. Non-Ionizing Radiation
    -UV, visible light, infrared, microwave, radiofrequency emissions

    • Presentation:
    • -burns and cataracts
    • -unclear if specific nervous system injury can result
  43. Hypothermia
    1. Direct injury of superficial structures with crystallization of intra and extracellular water

    2. peripheral vasoconstriction --> vascular sludging --> local ischemia

    Can lead to significant CNS depression
  44. Hyperthermia
    • Causes:
    • -cessation of sweating
    • -marked peripheral vasodilation
    • -venous pooling
    • -systemic shock

    • Multiorgan system failure (> 42C)
    • Injury due to lack of perfusion
  45. Agent Orange
    • Epidemiology:
    • -increased incidence of disorders in Vietnam vets

    • Presentation:
    • -polyneuropathy
    • -Parkinson's Disease
    • -cancers of brain and nervous system (eye)
    • -neuropsychiatric disorders
    • -etc!!!
  46. Gulf War Syndrome
    "medically unexplained multi-symptom illness reported by Gulf War veterans"

    • Presentation:
    • -chronic fatigue
    • -HAs
    • -joint pain
    • -indigestion
    • -insomnia
    • -dizziness
    • -respiratory disorders
    • -memory problems

    No pathology or pathophysiology

    • Causal relationship with:
    • -PTSD

    • Significant Association with:
    • -psychiatric disorders
    • -GI sx
    • -multisystem illness
    • -chronic fatigue syndrome

What would you like to do?

Home > Flashcards > Print Preview