Neurology Flashcards
Intracerebral Bleed Incidence Associated with
HTN, anticoagulation therapy or coagulopathy, drug and alcohol abuse, neoplasia, amyloid angiopathy, infection
aneurysm etiologies
trauma, inflammation, atherosclerosis, congenital, peak age 35-50
ischemic stroke risk factors
increasing age, underlying atherosclerotic disease, hx TIA’s, associated with CV disease
patients at risk for stroke anesthetic implications
control DM, HTN, coagulation therapy
SAH risk factors
HTN, DM, CAD
oligodendrocytes
form myelin around CNS axons (schwann cell in PNS)
astrocytes
help regulate composition of ISF in CNS, provide glucose to and remove ammonia from neurons
-repair after neuronal injury and maintain metabolic environment
microglia cells
specialized macrophages that phagocytize neuronal cells
CSF emptying
from saggital sinus to superior jugular vein to SVC
CSF pathway
made in ependymal cells in lateral and 3rd ventricle, then goes to 4th ventricles, then foramen of magendie, then cerebellar versus spinal pathway
which artery carries 80% of blood to the brain
MCA
susceptibility to aneurysm formation
structural abnormalities, genetics, atherosclerosis, HTN, coarctation of aorta, connective tissue DO’s
where are most AVM’s
75% supratentorial
3rd leading cause of death in US
ischemic stroke
thrombus formations associated with these risk factors
atherosclerosis, hyper coagulation, sickle cell disease, polycythemia vera, decreased BF
TBI: extradural hematoma
usually arterial source of bleeding, can lead to herniation because bleed is compressing veins
TBI: subdural hematoma
usually torn bridging vein or venous sinus, increased ICP compresses tear, can lead to herniation
TBI: intracerebral bleed
small blood vessel trauma- shearing or penetration. increased ICP and brain compression, brain edema. dont have effect on CSF movement like the others
what can predispose to seizures
hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation, sleep phases
tonic phase of seizures
muscle contraction/increased muscle tone. occurs when neuronal excitation spreads to subcortical, thalamic, and brainstem areas
clonic phase
alternating muscle contraction and relaxation. this is essentially periodic interruption of tonic phase. occurs when inhibitory neurons (in cortex, thalamus, and basal ganglia) begin to inhibit neuronal (cortical) excitation
seizure risk factors
genetic-idiopathic
genetic predisposition for disorder associated with DiGeorge syndrome- hypoparathyroidism and hypocalcemia
tumor, trauma, infection, fever
sah, stroke damage
metabolic origin (fever, uremia, hypoxemia, hyperglycemia, hyponatramia, hypocalcemia)
hypoxia, hyperventilation (resp alkalosis)
drugs or alcohol OD or withdrawal
fatigue or stress
excessive sensory stimuli
cytotoxic edema
ischemia induced neuronal ion influx that facilitates cell swelling. no net increase in fluid, brain ISF goes to ICF
vasogenic edema
ischemia- damages endothelial cells, BBB breakdown in 2-3 days, BBB breach means plasma protein moves into ISF