Exam 1: Acute Neuro Flashcards
Time from O2 deprivation to neuronal death:
6 min
Why are neurons so sensitive to hypoxic states?
Store very little glycogen and are dependent on it for ATP production
Two mechanisms that cause brain cell death:
Anaerobic metabolism
Deterioration of ion gradients
By what two pathways do brain injuries lead to increased ICP?
Invasion, which leads to focal deficits and cerebral edema
Compression, which leads to cerebral edema
Signs of increased ICP:
Diminished cognitive function Headache Vomiting Seizure Papilledema Unsteady gait Loss of sphincter control
Define secondary injury:
Progressive damage resulting from body’s physiologic response to insult
How does anaerobic metabolism lead to brain cell death?
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
What is glutamate’s role in brain injury?
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
What are EAAs’ role in brain injury?
Activate NMDA receptors, which in turn produce NO
Increases production of ROS/free radicals which damage cellular components
What type of injury does reperfusion cause? How?
Secondary
O2 reentering cells can produce reactive oxygen species (free radicals)
Lipid peroxidation produces free radicals
What controls local cerebral blood flow?
Autoregulation/myogenic reflex
Metabolic vasodilation triggered by increased H+ / CO2, decreased O2 - byproducts of cell work
Is local CBF regulated more by vasoconstriction or vasodilation?
Vasoconstriction
How does impaired vasoconstriction lead to brain injury?
Hyperperfusion can lead to edema
How are compliance and ICP related?
Compliance drops dramatically at high ICPs
Normal ICP:
0-15mmHg
Causes of increased ICP:
Space-occupying lesions
Vasogenic/cytotoxic edema
CSF obstruction/production in excess
Four types of herniation
Subfalcine
Central (bad news bears)
Transtentorial
Tonsillar
CPP should be kept above:
60mmHg
Focus of treatment for brain compression/herniation:
Removal of lesion/CSF
Manage cerebral oxygenation
Most sensitive indication of altered brain function:
Changed LOC
What part of the brain regulates consciousness?
Reticular activating system
Complete loss of consciousness called:
Coma
CN involved in pupil reflex:
II and III
CN involved in eye movement:
III, IV, VI
Tests for oculovestibular reflex:
Doll’s eyes
Cold calorics
Reflexes that indicate brain function:
Pupillary
Oculovestibular
Corneal
Three types of TBI primary injury:
Focal
Polar
Diffuse
Concussion vs. contusion:
Concussion: alteration/LOC but no CT evidence of damage
Contusion: damage seen on CT or MRI
Each type of hematoma typically involves which type of vessel:
Epidural: arteries
Subdural: bridging veins
Subarachnoid: bridging veins?
S/s of epidural hematoma:
Brief period of AMS, then lucid interval, then rapid decline
Three types of subdural hematoma:
Acute (within 24 hrs)
Subacute (s/s of inc ICP 2-10 days later)
Chronic (rebleeding)
SAH usually happen due to:
Aneurysm or AVM rupture
S/s of SAH:
Meningeal irritation Hydrocephalus Headache Vasospasm Ischemia
Treatment for ischemic stroke:
ASA
CEA or angioplasty for 70%+ occlusion
Hemorrhagic stroke occurs secondary to:
Severe, chronic hypertension
Most hemorrhagic strokes occur in:
Basal ganglia or thalamus
Sequelae of stroke motor deficits:
Initially flaccid/paralysis
Recover of function occurs with onset of spasticity
Motor and sensory aphasias:
Broca: motor
Wernicke’s: sensory
Risk factors for aneurysm rupture:
Hypertension
ETOH
Recreational drug use
Most common bacterial meningitis pathogen:
Strep pneumoniae
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.
How can meningitis cause infarcts?
Vasculitis and clotting
How can meningitis cause hydrocephalus?
Accumulation of inflammatory exudate leads to obstructive hydrocephalus
LP signs of meningitis:
Bacteria and neutrophils
Elevated protein
Decreased glucose
Layers of a brain abscess:
Infected core (neutrophils, tissue debris)
Granulation tissue
Perifocal edema
