Exam 1: Acute Neuro

Question 1

Time from O2 deprivation to neuronal death:

Answer 1

6 min

Question 2

Why are neurons so sensitive to hypoxic states?

Answer 2

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

Question 3

Two mechanisms that cause brain cell death:

Answer 3

Anaerobic metabolism

Deterioration of ion gradients

Question 4

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

Answer 4

Invasion, which leads to focal deficits and cerebral edema

Compression, which leads to cerebral edema

Question 5

Signs of increased ICP:

Answer 5

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

Question 6

Define secondary injury:

Answer 6

Progressive damage resulting from body’s physiologic response to insult

Question 7

How does anaerobic metabolism lead to brain cell death?

Answer 7

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

Question 8

What is glutamate’s role in brain injury?

Answer 8

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

Question 9

What are EAAs’ role in brain injury?

Answer 9

Activate NMDA receptors, which in turn produce NO

Increases production of ROS/free radicals which damage cellular components

Question 10

What type of injury does reperfusion cause? How?

Answer 10

Secondary

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

Lipid peroxidation produces free radicals

Question 11

What controls local cerebral blood flow?

Answer 11

Autoregulation/myogenic reflex

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

Question 12

Is local CBF regulated more by vasoconstriction or vasodilation?

Answer 12

Vasoconstriction

Question 13

How does impaired vasoconstriction lead to brain injury?

Answer 13

Hyperperfusion can lead to edema

Question 14

How are compliance and ICP related?

Answer 14

Compliance drops dramatically at high ICPs

Question 15

Normal ICP:

Answer 15

0-15mmHg

Question 16

Causes of increased ICP:

Answer 16

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

Question 17

Four types of herniation

Answer 17

Subfalcine
Central (bad news bears)
Transtentorial
Tonsillar

Question 18

CPP should be kept above:

Answer 18

60mmHg

Question 19

Focus of treatment for brain compression/herniation:

Answer 19

Removal of lesion/CSF

Manage cerebral oxygenation

Question 20

Most sensitive indication of altered brain function:

Answer 20

Changed LOC

Question 21

What part of the brain regulates consciousness?

Answer 21

Reticular activating system

Question 22

Complete loss of consciousness called:

Answer 22

Coma

Question 23

CN involved in pupil reflex:

Answer 23

II and III

Question 24

CN involved in eye movement:

Answer 24

III, IV, VI

Question 25

Tests for oculovestibular reflex:

Answer 25

Doll’s eyes

Cold calorics

Question 26

Reflexes that indicate brain function:

Answer 26

Pupillary
Oculovestibular
Corneal

Question 27

Three types of TBI primary injury:

Answer 27

Focal
Polar
Diffuse

Question 28

Concussion vs. contusion:

Answer 28

Concussion: alteration/LOC but no CT evidence of damage
Contusion: damage seen on CT or MRI

Question 29

Each type of hematoma typically involves which type of vessel:

Answer 29

Epidural: arteries
Subdural: bridging veins
Subarachnoid: bridging veins?

Question 30

S/s of epidural hematoma:

Answer 30

Brief period of AMS, then lucid interval, then rapid decline

Question 31

Three types of subdural hematoma:

Answer 31

Acute (within 24 hrs)
Subacute (s/s of inc ICP 2-10 days later)
Chronic (rebleeding)

Question 32

SAH usually happen due to:

Answer 32

Aneurysm or AVM rupture

Question 33

S/s of SAH:

Answer 33

Meningeal irritation
Hydrocephalus
Headache
Vasospasm
Ischemia

Question 34

Treatment for ischemic stroke:

Answer 34

ASA

CEA or angioplasty for 70%+ occlusion

Question 35

Hemorrhagic stroke occurs secondary to:

Answer 35

Severe, chronic hypertension

Question 36

Most hemorrhagic strokes occur in:

Answer 36

Basal ganglia or thalamus

Question 37

Sequelae of stroke motor deficits:

Answer 37

Initially flaccid/paralysis

Recover of function occurs with onset of spasticity

Question 38

Motor and sensory aphasias:

Answer 38

Broca: motor

Wernicke’s: sensory

Question 39

Risk factors for aneurysm rupture:

Answer 39

Hypertension
ETOH
Recreational drug use

Question 40

Most common bacterial meningitis pathogen:

Answer 40

Strep pneumoniae

Question 41

Pathway of damage from bacterial meningitis:

Answer 41

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.

Question 42

How can meningitis cause infarcts?

Answer 42

Vasculitis and clotting

Question 43

How can meningitis cause hydrocephalus?

Answer 43

Accumulation of inflammatory exudate leads to obstructive hydrocephalus

Question 44

LP signs of meningitis:

Answer 44

Bacteria and neutrophils
Elevated protein
Decreased glucose

Question 45

Layers of a brain abscess:

Answer 45

Infected core (neutrophils, tissue debris)
Granulation tissue
Perifocal edema