ARTERIOSCLEROSIS & ATHEROSCLEROSIS

TYPES OF PATHOPHYSIOLOGY ( ATHEROSCLEROSIS)

ARTERIOSCLEROSIS ATHEROSCLEROTIC LESIONS MODIFIABLE RISK FACTORS NON MODIFIABLE RISK FACTORS
-

Nicotine
most disease of the arteries
• use o
Age
common )
; fig,ty( contributing tohyperlipidemia
- .

⑨
gender
"
of the arteries
" '
FATTY STREAKS 2 FIBROUS PLAQUES
-

hardening DM (
• Familial predisposition 1 genetics
thickened composed of : speeds atherosclerotic process )
o
small arteries and arterioles -

yellow & smooth

-
.

Obesity
-

smooth muscle cell

°
o

protrude slightly in the lumen Stress

plasma components
- °
.

"S of
artery .
lipids
-

sedentary lifestyle
ATHEROSCLEROSIS
-

composed of : -
white to white yellow
- .
Elevated C-reactive protein
acclimation of lipids
o -
protrude in various degrees o
Hyper homocysteinemia

)
- :

'
elongated smooth muscles in the arterial lumen
r# lipids " "ed "

jithaegruoemas
"

fgoruonupdiinnctyuediargtenrfianstsgfallo.ge
-

Eimcaicivm -
found predominantly in :

Em blood components .abdominal aor ta 1

ianicarbohydrate
-
not clear if this predisposes a o
coronary arteries prolonged hemodynamic forces
Eni fibrous tissue person to formation of fibrous o
popliteal arteries shearing stress & turbulent flow , irradiation ,

-
large and medium sized arteries -

plaques or if reversible o internal carotid arteries

n
(chemical exposure or chronic hyperlipidemia )
generalized disease of the arteries clinical symptom
g
lesions I
Not usually cause progressive
- -
-

if it ) extremities ( t) elsewhere in the body reduction of of nutrients and

supply
- -_ .

oxygen
RISK FACTORS I

NICOTINE
C- REACTIVE PROTEIN
HYPERHOMOCYSTEIMIA
Vascular endothelial injury
( ( RP) (ischemic necrosis dlt deficient blood flow )

tobacco of the most sensitive marker of CV inflammation ft ) correlated c- the risk of PAD CAD I
products :
-
one
1
- - .

, ,

important risk factors (

systematically & locally) cerebrovascular disease
aggregation of platelets and monocytes
.

T
-
t blood flow to the extremities -
slight TCRPWIS damage risk of in vasculature -

Homocysteine = protein that promotes

+ heart rated blood pressure 4> espifl accompanied by :
coagulation by T Factor V and X1 activity : at the site of injury
isms vasoconstriction)
onager hypercholesterolemia depressing protein C. activation & flipprotein
-
-

triskcaoggfregaf.it?ntofpfa7eYe7s,ation l
ofemale obesity o
(a) in fibrin DT thrombin formation D
- -

and
-

carbon monoxide ctoxin produced by tobacco) oHPN of blood glucose Irl thrombosis smooth muscle cells
migrate proliferate
readily c- hemoglobin smoking (t ) family hx of CVD Folate
therapy NCEPguidelines : folic acid 1
-

LD combines more o o =

than Oz -
b.
depriving tissues c- 02 -
H) association bet PADI hemostatic supplements of 0.5 -1010mg daily reserved
and elastic fibers to form
matrix of
collagen
.

for pts who have hx of atherosclerosis

-
amt tobacco . used a extent of disease or
inflammatory markers fibrinogen
and D dimer
1
-

ATHEROSCLEROSIS
PREVENTION

INTERMITTENT PRIMARY GOAL

DIET MODIFICATION ( TX HYPERLIPIDEMIA) COLLATERAL CIRCULATION
CLAUDICATION
fat diet # atherosclerosis 100mg 1dL DIRECT RESULTS
generalized atherosclerosis high LDL <
- -

of
-

of arterial lumen
-

symptom LDL a>

omg 1dL
recommended for pts of ATHEROSCLEROSIS
-
gradual narrowing
-
marker of occult CAD
-
measure serum cholesterol and to begin c- DM , smokers HPN , stimulates this circulation
diet modification atherosclerosis arrowing ( stenosis ) of lumen
.

on
-
AHA : reduce amt fat ingested -
-
arises from preexisting vessels that enlarge to
saturated fats
° Obstruction by thrombosis reroute blood flow around a
hemodynamically
vlcholesterol
'
aneurysm significantstenosis or occlusion .

• ulceration -
allows continued perfusion to the tissues but :
•
rupture
often inadequate -17 ischemia
SECONDARY GOAL STATINS HYPERTENSION Cdlttmetabolic demand)
( TXHYPERLIMDEMIAI INDIRECT RESULTS OF
accelerate the rate at Wtc
may ATHEROSCLEROSIS
-

Cholesterol lvlsc
200mg 1dL HMG-CoA reductase inhibitors
- -

atherosclerotic lesions form in high

-

1st line tx reduce incidence of major MOST COMMON LOCATIONS

triglyceride lvlsctsomgldl
"
-

malnutrition
- -

pressure vessels can lead to

- o
CV events
.

subsequent fibrosis of TO DEVELOP

organs
o
- at or vast at in a
cerebrovascular accident
r Suva statin ( CVA , brain attack , stroke)
• Proximal lower extremity
simvastatin a ischemic renal disease
distal abdominal aorta
ten
• CAD common iliac arteries
PAD
CLINICAL MANIFESTATION
⑧ severe Im orifice of superficial femoral & profunda femoris
↳ HPN major risk factor for the arteries
-

depend on the organ or tissue affected

development of PAD superficial
Im femoral
artery
°
Coronary atherosclerosis t
o
angina twofold risk development of
* Atherosclerosis can
develop anywhere @ the body
* Vulnerable : arteries branch into smaller vessels
a acute Ml claudication
.
cerebrovascular disease
°
Atherosclerosis of aorta
•
aneurysm
°
atherosclerosis lesion of extremities