Intoxications and Infections of the CNS Flashcards

1
Q

Where does the tetanus toxin come from?

A

Tetanus is an exotoxin produced from Clostridium tetani

It is either produced anaerobically in dirty wounds or from a non-sterile needle or drug abusers

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2
Q

How does the tetanus toxin produce an effect?

A

After hours to weeks, the exotoxin binds to interneurons of the CNS, preventing release of inhibitory glycine and GABA —> motor disinhibition

(generalized seizures, painful spasms etc)

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3
Q

How is a tetanus diagnosis made?

A

Clinically

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4
Q

How is tetanus treated?

A

ICU care, neuromuscular blockade, sedation, anticonvulscents, tetanus immune globulins and antibiotics

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5
Q

Where does the botulism toxin come from?

A

Exotoxin of clostridium botulinum- produced anaerobically in improperly canned or prepared food.

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6
Q

How does the botulinum toxin produce an effect?

A

The botulinum exotoxin binds to presynaptic nerve terminals preventing the release of ACh

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7
Q

Administration of what aids in the release of ACh from the pre-synaptic cleft?

A

Guanidine

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8
Q

How is botulism diagnosed?

A

Clinical picture, EMG tests, bioassay

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9
Q

How does lead poisoning manifest in adults?

A

Peripheral neuropathy

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10
Q

How does lead poisoning manifest in children?

A

Encephalopathy, abdominal pain

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11
Q

How does organic solvent toxicity manifest in patients?

A

Encephalopathy or peripheral neuropathy

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12
Q

What are symptoms associated with CO poisoning?

A

Early: headache, vomiting, blurred vision
Later: coma, seizures, or cardiopulmonary arrest

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13
Q

Survivors of CO poisoning may have what lasting effects?

A

Amnesia and parkinsonianism

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14
Q

What drugs cause stroke syndromes in atypical patients?

A

Cocaine (most common), amphetamines, PCP, and LSD

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15
Q

What are the neurological symptoms caused by acute alcohol intoxication?

A

social disinhibition, impaired consciousness, cerebellar dysfunction
secondary head trauma
very high levels may lead to coma, death

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16
Q

What are the neurologic symptoms caused by alcohol withdrawal?

A

early, hypersympathetic stage (tremulous, sweaty, tachycardic);
limited number of convulsive seizures 12 hrs-3 days after drinking stopped;
later stage of delirium tremens, 3-4 days after drinking stopped, with fluctuating motor and autonomic activity, confusion, hallucinations

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17
Q

How do we treat alcohol withdrawal?

A

treat with benzodiazepines for sedation and seizure control, provide hydration and metabolic support, thiamine

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18
Q

What is acute Wernicke Encephalopathy?

A

nystagmus, ophthalmoplegia, gait ataxia, confusion…acute phase of Wernicke-Korsakoff syndrome

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19
Q

How is wernike encephalopathy corrected?

A

thiamine supplimentation

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20
Q

What is korsakoff psychosis?

A

Korsakoff psychosis (amnesia, confabulation) is the chronic phase of Wernicke-Korsakoff syndrome.

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21
Q

Where does alcoholic cerebellar degeneration occur?

A

Anterior superior cerebellar vermis

22
Q

What are the symptoms of alcoholic cerebellar degeneration?

A

gait ataxia and dysmetria of the lower limbs (inability to judge distance/scale –> discoordination)

23
Q

Define meningitis

A

Inflammation of the leptomeninges due to blood, foreign material, or infection within the subarachnoid space.

24
Q

What agents cause acute meningitis vs chronic meningitis?

A

Acute: bacterial, viral
Chronic: unusual organisms

25
How are the CSF white counts and glucose affected by typical bacterial meningitis?
White count; increased neutrophils | Glucose: decreased
26
How should the patient be treated if bacterial meningitis is suspected?
1) Look for primary source of infection 2) Give broad spectrum antibiotics 3) Narrow antibiotics once culprit is identified 4) Observe for complications +/- DEX to minimize risk of complications
27
Name 4 complications of bacterial meningitis
1) Hydrocephalus (from pus obstructive CSF pathway) 2) Secondary inflammation and edema of cortex (meningoencephalitis) 3) Infarction from thrombosis of inflamed superficial vessels 4) Deafness (monitor hearing in children)
28
who is most susceptible to chronic meningitis?
Elderly, malnourished, and immunosuppressed patients
29
What are the symptoms of chronic meningitis?
subtle symptoms of mild headache, confusion, no obvious meningeal signs
30
What usually causes encephalitis?
Viral infection
31
How do you usually acquire viral encephalitis?
Viral transmission by seasonal arthropods (ticks, mosquitoes), inhalation or reactivation (herpes simplex)
32
What are the symptoms of encephalitis?
High fever and headache (like with meningitis) | Seizures, focal neurologic deficits, changes in behavior and consciousness (more specific for encephalitis)
33
Which strain of herpes causes herpes encephalitis?
HSV-1 (cause of oral herpes)
34
The herpes virus has a predilection for which lobes of the brain? How does this correlate to neurologic symptoms?
Frontal and temporal | * aphasia, behavioral changes and memory impairment
35
What is the treatment for herpes encephalitis?
acyclovir: reduces mortality from 40-70% to 20%
36
What are the symptoms of west nile virus?
Encephalitis --> fever, headache, rash | Weakness from affected peripheral nerves or anterior horn cells
37
Which cells are targeted by the polio virus?
motor neurons in the brain stem, spinal cord
38
Survivors of polio suffer from what long term effects?
Asymmetrical atrophy and weakness in one limb
39
What are shingles?
Reactivation of chicken pox (varicella zoster), which lies latent in the dorsal root ganglia Causes a vesicular rash in 1 or 2 dermatomes
40
HIV destroys which WBCs?
T4 helper lymphocytes
41
HOw is the nervous system affected by HIV?
Direct viral invasion (dementia, meningitis) Indirect damage from cell lysis, inflammation Complications of an immunodeficient state
42
How is AIDS dementia diagnosed?
Clinical diagnosis of exclusion MRI shows nonspecific atrophy or white matter alterations
43
Progressive Multifocal Leukoencephalopathy (PML) is an opportunistic infection in immunodeficient patients caused by what virus?
papovavirus
44
What cells of the CNS are infected by the papovavirus in PML? What is the outcome?
Oligodendrocytes Leads to patchy demyelination in the CNS and focal deficits. It is untreatable
45
What is the causative agent in prion disease?
Infectious protein
46
What is the most common prion disease?
Creutzfeldt-Jakob Dementia (CJD)
47
How is prion disease transferred?
human graft tissue or neurosurgical instruments Other prion diseases are hereditary in nature
48
How do prions cause disease?
Infectious proteins induce conformational changes in normal proteins --> neuronal death WITHOUT inflammation
49
What is the timing of Creutzfeldt-Jakob Disease?
Rapidly progressive, untreatable, fatal in weeks to months
50
What are the symptoms of Creutzfeldt-Jakob Disease?
Dementia with prominent myoclonus | Often corticospinal, extra-pyramidal, cerebellar or LMN signs