Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurology Clerkship > Intoxications and Infections of the Nervous System > Flashcards

Intoxications and Infections of the Nervous System Flashcards

1
Q

MOA tetanus toxin?

A

Tetanospasmin binds to cortical, brain stem, and spinal interneurons, preventing the release of inhibitory glycine and GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Presentation of tetanus?

A

Motor neuron disinhibition begins days to 2 weeks after exposure

Severe, prolonged, painful muscle spasms - may be local or diffuse; trismus (lockjaw), risus sardonicus (grimacing smile), opisthotonus (arching back)

Generalized convulsive seizures

Impaired swallowing or breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Management of tetanus?

A

ICU care with mechanical ventilation, sedation, pharmacologic neuromuscular blockade, anticonvulsants

Human tetanus IG (neutralize toxin)
ABX for wound infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MOA botulism?

A

Exotoxin binds to presynaptic nerve terminals and prevents the release of ACh from LMNs and parasympathetic nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Presentation of botulism?

A

Paralysis of skeletal muscle, bowel, bladder, salivary glands within 12-48 hours of ingestion

Ptosis, diplopia, pupillary paralysis -> dysphagia, facial and limb weakness, possible respiratory paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DDx of botulism?

A

MG
Brain stem infarction
GBS variant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Dx botulism?

A

MRI and EMG may help exclude other causes of paralysis

Toxin may be detected by bioassay in food samples or fecal testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Manage botulism?

A

ICU monitoring
Antitoxin
Guanidine - facilitates ACh release form motor nerve endings and may improve clinical strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Presentation of lead poisoning in adults?

A

Peripheral neuropathy, often with prominent focal neuropathies like wrist drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Presentation of lead poisoning in children?

A

Encephalopathy and abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rx lead poisoning?

A

Chelating agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Presentation of CO poisoning?

A

Headache, vomiting, blurry vision, can progress to coma, seizures, and CP arrest

Survivors may have residual memory or cognitive deficits; some may shown signs of parkinsonism (basal ganglia is sensitive to CO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Rx CO poisoning?

A

Inhalation of 100% O2

Hyperbaric chamber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes Wernicke-Korsakoff syndrome?

A

Deficiency of thiamine (B1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Presentation of Wernicke’s encephalopathy?

A

Nystagmus, ophthalmoplegia, gait ataxia, and confusion; may resolve within hours to days of thiamine administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Presentation of Korsakoff’s psychosis?

A

Chronic memory deficit or amnestic memory with frequent confabulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cause and presentation of alcoholic cerebellar degeneration?

A

Lesion in the anterior-superior vermis

Ataxic gait and dysmetria of the lower limbs

18
Q

What causes central pontine myelinosis?

A

Demyelination of the CST and corticobulbar tacts in the pons, often due to overly rapid correction of severe hyponatremia

19
Q

Presentation of meningitis?

A

Evolves over hours to days with symptoms that may be severe including fever, headache, stiff neck, malaise, lethargy, N/V

Bacterial - serious, may be fatal
Viral - usually milder, resolves spontaneously

On exam - lethargy to coma, nuchal rigidity, Kernig or Brudzinski signs

20
Q

Petechial rash in the setting of meningitis suggests what cause?

A

Meningococcal (N. meningitidis)

21
Q

Management of meningitis?

A

Cx blood, CSF, other infected material
Start broad spectrum ABX immediately - initial coverage typically consists of ceftriaxone (or other newer generation cephalosporin) + vancomycin; add ampicillin if Liseria is a concern (elderly or neonates)

In adults, IV dexamethasone (0.15 mg/kg) reduces neurological complications and lower mortality

LP as soon as possible

22
Q

Sequelae of meningitis?

A

Hydrocephalus if pus develops and obstructs CSF pathways

Meningoencephalitis if pus accumulates over the cortical subarachnoid space

Infarction of brain or spinal cord if local vessels become inflamed and thrombose

Deafness (young children)

23
Q

Suspected organisms causing bacterial meningitis in neonates (0-4 weeks old)

A

GBS

E. coli

24
Q

Suspected organisms causing bacterial meningitis in children (<15 y/o)

A

N. meningitidis

S. pneumoniae

25
Q

Suspected organisms causing bacterial meningitis in adults (>15 y/o)

A

S. pneumoniae
N. meningitidis
E. coli

26
Q

Reasons to delay an LP?

A

Thrombocytopenia
Clotting factor deficiency
Infection along the skin of the back
Concern for elevated ICP (unconscious, papilledema) or intracranial mass with edema (new onset seizure, focal neuro deficit, history of stroke, cerebral mass lesion or infection, immunocompromised)

27
Q

Typical CSF profile of bacterial meningitis?

A

> 500-1000 WBCs, PMN predominance
High protein
Low glucose
Gram stain/culture

28
Q

Typical CSF profile of viral, tuberuculous, fungal, syphilitic meningitis?

A

All: <500 WBCs, lymphocytic predominance
Protein high in all, except viral which can be normal or high
Glucose normal in viral, low in TB/fungal, and normal to low in syphilis

29
Q

Normal CSF profile?

A

No WBCs
<45 mg/dL protein
>50% blood glucose

30
Q

Presentation of chronic meningitis?

A

More subtle symptoms over weeks or months
Typically infect elderly, malnourished, immunocompromised
Confusion, low grade fever, mild headache, may not have obvious nuchal rigidity

31
Q

Typical causes of chronic meningitis?

A

TB, fungus, syphilis, some parasites

32
Q

Presentation of encephalitis?

A

Symptoms evolve over hours to days
Involve fever and headache with signs and symptoms of brain involvement, such as seizures, focal deficits, behavioral changes, impaired consciousness

33
Q

Work-up of encephalitis?

A

CSF (lymphocytic pleocytosis, normal or slightly decreased glucose)
Antibody titers for suspected viruses (CSF and serum), especially HSV-1
MRI

34
Q

Herpes simplex encephalitis is important to recognize since it is non-epidemic, non-seasonal, and carries a high mortality rate when not treated. What causes it, what parts of the brain does it tend to affect, how does it present, and how should it be treated?

A

HSV-1
Inferior frontal and medial temporal lobes (often bilaterally and asymmetrically)
Aphasia, behavioral changes, memory deficits
IV acyclovir

35
Q

Unique presentation of WNV encephalitis?

A

Significant weakness -> affects peripheral nerves (like GBS) or anterior horn cells (like polio)

36
Q

Presentation of polio?

A

Acute febrile illness, with a preferential viral invasion and destruction of anterior horn cells and brain stem motor nuclei

LMN signs, often asymmetric

Chronic joint or back pain, fatigue, imbalance

37
Q

Presentation and Rx of shingles?

A

Eruption of a vesicular rash with severe neuralgic pain along one or two adjacent dermatomes on the torso or limb; acyclovir or other anti-viral

38
Q

Describe nervous system manifestations of HIV/AIDS.

A

Early: acute, aseptic meningitis, myopathy or inflammatory polyneuropathy

Late: chronic, painful sensory neuropathy, cognitive changes, HIV dementia, myelopathy akin to subacute combined degeneration

Primary cerebral lymphoma

Opportunistic infections: cerebral toxoplasmosis, cryptococcal meningitis, CMV retinitis or encephalitis, PML (reactivation of JC virus)

39
Q

Presentation of abscesses?

A

Fever, headache
Seizures and focal signs
Brain edema with mass effect, increased ICP
Abscess may rupture -> meningitis

40
Q

Dx abscess?

A

CT or MRI with and without contrast

41
Q

Presentation of CJD?

A

Very rapidly progressive dementia with cerebellar, CST, LMN, or EPS signs and symptoms; myoclonus is usually present

42
Q

Dx CJD?

A

Brain biopsy with spongiform changes (cytoplasmic vacuoles in neurons and astrocytes, neuronal loss without inflammation)

Periodic sharp wave discharge on EEG

Neurology Clerkship (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions