Intoxications and Infections of the Nervous System Flashcards

1
Q

Tetanus (demented monkeys)

A
  • prevent release of inhibitory GABA
  • prolonged painful muscle spasms
  • localized vs generalized (diffuse mu spasms and generalized convulsive seizures from cortical disinhibition)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

painful muscle spasms of tetanus

A
  • clenching lockjaw (trismus)
  • grimacing smile (risus sardonicus)
  • arching back (opisthotonus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Botulism (robots)

A
  • improperly canned or contaminated food or in wound infections
  • prevent release of ACh from LMN and parasympathetic nerves=paralysis of skeletal muscle, bowel, bladder, and salivary glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Guanidine

A

oral drug helps facilitate ACh release from motor nerve endings

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

Environmental toxins

A
  • lead poisoning: adults-peripheral neuropathy + focal neuropathy (wrist drop); kids-encephalopathy and abdo pain
  • organic solvent/glues and adhesives: peripheral neuropathy +/or encephalopathy
  • CO-HA, v, blurry vision…coma, sz, cardiopulm arrest. survivors: memory and cognition deficits, parkinsonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what should a stroke syndrome in a young, otherwise healthy, pt make you think of?

A

drug induced vasoconstriction or HTN leading to ischemic infarction or brain hemorrhage. **cocaine

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

Alcohol withdrawal

A
  1. hypersympathetic stage-tremulousness, sweating, tachy, jitters
  2. 12hr-3d after last drink: cluster of generalized tonic-clonic seizures (d/t diffuse toxic effect on the brain)
  3. 3-4d after last drink: DTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what provides sedation and seizure control for DTs

A

benzos

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

Wernicke-Korsakoff syndrome

A
  • B1 (thiamine) deficiency in pts with malnutrition or malabsorption
  • acute phase: W’s encephalopathy=nystagmus, ophthalmoplegia, gait ataxia, and confusion (resolve in hours to days of thiamine administration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Korsakoff’s psychosis

A
  • 2/2 persistent, severe, or recurrent thiamine deficiency

- chronic memory deficit or amnestic syndrome leading to confabulation

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

pathology of Korsakoff

A

-tiny petechial hemorrhages and gliosis around 3rd and 4th ventricles and connecting aqueduct, involving mammilary bodies, fornix, and dorsomedial thalamus

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

alcoholic cerebellar degeneration

A

-involves anterior-superior vermis=ataxic gait and dysmetria of the lower limbs

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

central pontine myelinolysis

A
  • 2/2 overly rapid correction of severe hyponatremia

- get demyelination of the corticospinal and corticobulbar tracts in the pons

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

where can meningitis come from

A

-can directly spread form an infection in an area near (ex otitis or sinusitis) or f/m infectious organisms spread through the bloodstream from a remote infection (PNA)

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

acute meningitis

A
  • fever, HA, stiff neck, malaise, lethargy, n/v

- acute bacterial meningitis can be fatal!!

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

what causes neck stiffness/nuchal rigidity?

A
  • meningeal irritation or inflammation

- can cause signs of Kernig or Brudsinski

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

what is initial Abx coverage for meningitis

A

ceftriaxone and vancomycin (add Ampicillin to cover for Listeria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

role of iv dexamethasone (0.15mg/kg)

A
  • reduces neuro complications
  • lowers mortality
  • give just before/with initial abx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When substantial amt of purulent exudate or pus develops from bacterial meningitis what can it cause

A

hydrocephalus by obstructing CSF pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

meningoencephalitis

A

when pus accumulates over the cortical subarachnoid space and leads to inflammation and edema of the cortex itself…can also get infraction of underlying brain or SC when local superficial blood vessels become inflamed and thrombose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what should young kids recovering from meningitis be observed for

A

subsequent deafness which may impede their ability to learn to talk

22
Q

LP

A

-perform asap in meningitis management

23
Q

reasons to delay an LP

A
  • thrombocytopenia
  • deficient clotting factors
  • infection along skin of the back
  • elevated ICP
  • intracranial mass with edema (new onset sz, focal neuro deficit, h/o stroke, IC)
24
Q

what is the most typical profile for bacterial meningitis

A

PMN WBCs and low CSF glucose

25
Q

encephalitis primary site of infection and indllmation

A

THE BRAIN

26
Q

modes of infection by the causative virus of the encephalitis

A
  • arthropods (ticks, mosquitoes)
  • ingestion (polio virus)
  • inoculation (Rabies from animal bites)
  • inhalation
  • reactivation (Herpes simplex)
27
Q

encephalitis microscopically

A

neuronal destruction by proliferating microglia, perivascular lymphocytes, and viral inclusions within neurons and glia

28
Q

are antiviral drugs useful in encephalitis

A

only herpes simpex wherein acyclovir is used

29
Q

HSE

A
  • 2/2 HSV1

- involves inferior frontal and medial temporal lobes, often b/l an asymmetric

30
Q

whatre s/s highly suggestive of HSE

A
  • aphasia
  • behavioral changes
  • memory deficits
31
Q

polio

A
  • viral invasion and destruction of anterior horn cells and BS motor nuclei
  • asymmetrical LMN signs
  • postpolio muscular atrophy in contra stronger limb
32
Q

Zoster or shingles

A
  • eruption of a vesicular rash with severe neuralgic pain along 1 or 2 adjacent dermatomes on torso or limb
  • admin acyclovir
  • sequelae: post-herpetic neuralgia
33
Q

HIV1

A

destroys T4 helper lymphocytes

34
Q

later sequelae of AIDS

A

-chronic painful sensory neuropathy along with cognitive changes, HIV dementia and myelopathy

35
Q

AIDS and primary cerebral lymphoma

A

-PCL is a rare immune system tumor arising within the brain and most often occurs in AIDS pts

36
Q

common opportunistic infections in AIDS

A
  • cerebral toxo (protozoal parasite)
  • cryptococcal meningitis (fungal)
  • CMV retinitis or encephalitis
37
Q

PML

A
  • progressive multifocal leukoencephalopathy
  • most cases occur in AIDS pts
  • involves reactivation of latent JC virus (polyomavirus)–goes on to infect oligodendrocytes=patchy demyelination of CNS white matter=focal neuro deficits
38
Q

What is an abscess?

A
  • a localized encapsulated infection within or outside (epidural or subdural) the brain or spinal cord
  • usually bacterial, but may be fungal or parasitic in IC pts
  • may be solitary or numerous
39
Q

How does an abscess develop

A

-f/m adjacent infection
OR
-through bloodstream from a distant infection

40
Q

cerebral abscess may cause…

A
  • seizures and focal neurological signs dependent on its location
  • may create brain edema with mass effect and increased ICP
  • may rupture into ventricular system or subarachnoid space and produce meningitis
41
Q

how is the diagnosis of abscess confirmed

A

-CT or MRI brain scan with and without contrast

42
Q

Prion dz

A

-prions=infectious proteins that can cause transmissible spongiform encephalopathies in human and animals

43
Q

Creutzfeldt-Jakob dementia

A
  • most common prion dz, sporadic
  • v. rapidly progressive dementia with cerebellar, corticospinal, LMN or EPS s/s
  • myoclonus is usually present
44
Q

EEG of CJD

A

periodic sharp wave discharges

45
Q

diagnostic brain bx of CJD

A
  • spongiform changes which are cytoplasmic vacuoles in neurons and astrocytes
  • neuronal loss sans inflammation
46
Q

mad cow dz

A

bovine spongiform encephalopathy thats an epidemic prion dz in cattle

47
Q

HSV encephalitis

A
  • affects mostly temporal lobe and may present acutely (<1wk duration) with focal neurological findings
  • csf: lymphocytic pleocytosis, inc erythrocytes, elevated protein
  • standard for diagnosis: HSV PCR analysis
48
Q

Creutzfeldt-Jakob dz probably diagnosis

A
  • rapidly progressive dementia
  • two out of 4:
  • –myoclonus
  • –akinetic mutism
  • –cerebellar or visual disturbances
  • –pyramidal/extrapyramidal dysfunction (hypokinesia)
  • periodic sharp wave complexes on EEG and.or positive 14-3-3 CSF assay
49
Q

CJD definitive diagnosis (need 2/4 features) and

A

-brain biopsy (gold standard) or demonstrated PRNP gene mutations

50
Q

autonomic dysfunction

A
  • postural hypotension
  • abnormal sweating
  • disturbance of bowel or bladder control
  • abnormal salivation or lacrimation
  • impotence
  • gastroparesis