Exam 1: Acute Neuro Flashcards Preview

ARCHIVED: Pathophysiology > Exam 1: Acute Neuro > Flashcards

Flashcards in Exam 1: Acute Neuro Deck (45):
1

Time from O2 deprivation to neuronal death:

6 min

2

Why are neurons so sensitive to hypoxic states?

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

3

Two mechanisms that cause brain cell death:

Anaerobic metabolism
Deterioration of ion gradients

4

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

5

Signs of increased ICP:

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

6

Define secondary injury:

Progressive damage resulting from body's physiologic response to insult

7

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

8

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

9

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

10

What type of injury does reperfusion cause? How?

Secondary

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

Lipid peroxidation produces free radicals

11

What controls local cerebral blood flow?

Autoregulation/myogenic reflex

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

12

Is local CBF regulated more by vasoconstriction or vasodilation?

Vasoconstriction

13

How does impaired vasoconstriction lead to brain injury?

Hyperperfusion can lead to edema

14

How are compliance and ICP related?

Compliance drops dramatically at high ICPs

15

Normal ICP:

0-15mmHg

16

Causes of increased ICP:

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

17

Four types of herniation

Subfalcine
Central (bad news bears)
Transtentorial
Tonsillar

18

CPP should be kept above:

60mmHg

19

Focus of treatment for brain compression/herniation:

Removal of lesion/CSF
Manage cerebral oxygenation

20

Most sensitive indication of altered brain function:

Changed LOC

21

What part of the brain regulates consciousness?

Reticular activating system

22

Complete loss of consciousness called:

Coma

23

CN involved in pupil reflex:

II and III

24

CN involved in eye movement:

III, IV, VI

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