Family history of

hypertriglyceridemia
Increased intake of
fatty and fried foods
Smoking Alcohol
Increased risk of
hypertriglyceridemia
Hypertriglyceridemia
Impairment of
vasodilatory
function
Increased Peripheral
vascular resistance
Devt of Fatty
streaks in intima
Endothelial damage
to blood vessels
Atherosclerosis
Hyper-aggregation
of platelets
Risk for excessive
clot formation
Increased CO levels
Thromboembolism
Plaque/Atheroma
formation
CEREBRAL
HYPOPERFUSION
Hgb combine more
readily with CO than O2
Inflitration of
endothelium
Inflammatory response
to injury to vascular
epithelium
Possible rupture of
plaque
Thrombus formation
Obstruction to blood
flow
Further narrowing of
blood vessels
Smooth muscle
proliferation
Foam cell formation

Transient Ischemic
Attack of right
hemisphere
Further energy
depletion
Failure of
mitochondria
Influx of calcium
Release of
excitatory
neurotransmitter
glutamate
Failure production
of adenosine
triphosphatase
Production of
oxygen free radicals
and other reactive
oxygen species
Anaerobic
metabolism by
mitochondria
Generates large
amounts of lactic
acid
Cerebral Ischemia
(Initiation of ischemic
cascade)
Tissue hypoxia and cellular
starvation
CEREBRAL
HYPOPERFUSION
Failure of energy
dependent process
(ion pumping)
Metabolic Acidosis
Activates enzymes that digest
cell proteins, lipids and
nuclear material
Hgb combine more
readily with CO than O2
Shortness of breath
Respiratory
compensation

Structural integrity loss of brain tissue
and blood vessels
Brain sustains an irreversible
cerebral damage
Transient Ischemic
Attack of right
hemisphere
Break down of collagen, hyaluronic acid
and other elements of connective tissue
Release of metalloprotrease
(zinc and calcium-dependent enzymes)
motor weaknesses (dragging
of left leg when walking)
ataxic gait; Unable to keep
balance when standing
Slurred speech; facial
asymmetry
Asymmetrical movement of
sternocleidomastoids; left lags
Impaired perfusion and
function
Vascular Congestion