Exam 1: Acute Neuro Flashcards

(45 cards)

1
Q

Time from O2 deprivation to neuronal death:

A

6 min

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2
Q

Why are neurons so sensitive to hypoxic states?

A

Store very little glycogen and are dependent on it for ATP production

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3
Q

Two mechanisms that cause brain cell death:

A

Anaerobic metabolism

Deterioration of ion gradients

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4
Q

By what two pathways do brain injuries lead to increased ICP?

A

Invasion, which leads to focal deficits and cerebral edema

Compression, which leads to cerebral edema

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5
Q

Signs of increased ICP:

A
Diminished cognitive function
Headache
Vomiting
Seizure
Papilledema
Unsteady gait
Loss of sphincter control
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6
Q

Define secondary injury:

A

Progressive damage resulting from body’s physiologic response to insult

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7
Q

How does anaerobic metabolism lead to brain cell death?

A

When pyruvate is converted to lactate, H+ ions build up and lead to cellular acidosis and decreased membrane integrity

Lack of energy leads to shutdown of ion pumps; K+ leaves cell; Na+, Cl-, Ca2+ enter cell in order to equilibrate intra/extracellular concentrations

Water follows ions; cellular edema

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8
Q

What is glutamate’s role in brain injury?

A

Glutamate binds to NMDA receptor and allows for Ca2+ influx

Impaired membrane integrity leads to excessive glutamate release, and decreased energy leads to decreased glutamate removal

Glutamate now excites nearby neurons as well, which also allow Ca2+ influx

Ca2+ influx is not regulated and leads to cell injury/death

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9
Q

What are EAAs’ role in brain injury?

A

Activate NMDA receptors, which in turn produce NO

Increases production of ROS/free radicals which damage cellular components

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10
Q

What type of injury does reperfusion cause? How?

A

Secondary

O2 reentering cells can produce reactive oxygen species (free radicals)

Lipid peroxidation produces free radicals

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11
Q

What controls local cerebral blood flow?

A

Autoregulation/myogenic reflex

Metabolic vasodilation triggered by increased H+ / CO2, decreased O2 - byproducts of cell work

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12
Q

Is local CBF regulated more by vasoconstriction or vasodilation?

A

Vasoconstriction

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13
Q

How does impaired vasoconstriction lead to brain injury?

A

Hyperperfusion can lead to edema

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14
Q

How are compliance and ICP related?

A

Compliance drops dramatically at high ICPs

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15
Q

Normal ICP:

A

0-15mmHg

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16
Q

Causes of increased ICP:

A

Space-occupying lesions
Vasogenic/cytotoxic edema
CSF obstruction/production in excess

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17
Q

Four types of herniation

A

Subfalcine
Central (bad news bears)
Transtentorial
Tonsillar

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18
Q

CPP should be kept above:

A

60mmHg

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19
Q

Focus of treatment for brain compression/herniation:

A

Removal of lesion/CSF

Manage cerebral oxygenation

20
Q

Most sensitive indication of altered brain function:

21
Q

What part of the brain regulates consciousness?

A

Reticular activating system

22
Q

Complete loss of consciousness called:

23
Q

CN involved in pupil reflex:

24
Q

CN involved in eye movement:

25
Tests for oculovestibular reflex:
Doll's eyes | Cold calorics
26
Reflexes that indicate brain function:
Pupillary Oculovestibular Corneal
27
Three types of TBI primary injury:
Focal Polar Diffuse
28
Concussion vs. contusion:
Concussion: alteration/LOC but no CT evidence of damage Contusion: damage seen on CT or MRI
29
Each type of hematoma typically involves which type of vessel:
Epidural: arteries Subdural: bridging veins Subarachnoid: bridging veins?
30
S/s of epidural hematoma:
Brief period of AMS, then lucid interval, then rapid decline
31
Three types of subdural hematoma:
Acute (within 24 hrs) Subacute (s/s of inc ICP 2-10 days later) Chronic (rebleeding)
32
SAH usually happen due to:
Aneurysm or AVM rupture
33
S/s of SAH:
``` Meningeal irritation Hydrocephalus Headache Vasospasm Ischemia ```
34
Treatment for ischemic stroke:
ASA | CEA or angioplasty for 70%+ occlusion
35
Hemorrhagic stroke occurs secondary to:
Severe, chronic hypertension
36
Most hemorrhagic strokes occur in:
Basal ganglia or thalamus
37
Sequelae of stroke motor deficits:
Initially flaccid/paralysis | Recover of function occurs with onset of spasticity
38
Motor and sensory aphasias:
Broca: motor | Wernicke's: sensory
39
Risk factors for aneurysm rupture:
Hypertension ETOH Recreational drug use
40
Most common bacterial meningitis pathogen:
Strep pneumoniae
41
Pathway of damage from bacterial meningitis:
Bacterial toxins trigger apoptosis, which damages the blood brain barrier and increases vascular permeability. This leads to edema and increased ICP, decreased perfusion, hypoxia, and neuron necrosis.
42
How can meningitis cause infarcts?
Vasculitis and clotting
43
How can meningitis cause hydrocephalus?
Accumulation of inflammatory exudate leads to obstructive hydrocephalus
44
LP signs of meningitis:
Bacteria and neutrophils Elevated protein Decreased glucose
45
Layers of a brain abscess:
Infected core (neutrophils, tissue debris) Granulation tissue Perifocal edema