This document defines atherosclerosis and its causes and risk factors. It discusses how atherosclerosis is initiated by inflammation in artery walls in response to LDL particles. As LDL particles accumulate in arteries, they can become oxidized, attracting macrophages. If macrophages cannot process the oxidized LDL, foam cells form, which can rupture and further narrow arteries. Risk factors include older age, male sex, diabetes, high LDL and low HDL cholesterol levels, smoking, and genetic factors. Diagnosis involves medical tests, and treatment includes medications, surgery, lifestyle changes, and managing underlying conditions like high blood pressure and cholesterol.
4. Arteriosclerosis ( general term )
• (Arterio) "artery"
(sclerosis) "hardening“
• Def: Hardening and thickening of the walls of the arteries
1) fatty deposits on the inner lining of arteries
(atherosclerosis)
2) calcification of the wall of the arteries
3) thickening of the muscular wall of the arteries from
chronically elevated blood pressure (hypertension).
5. Atherosclerosis
• specific form of arteriosclerosis
• due to formation of multiple atheromatous plaques
within the arteries
6. • accumulation of degenerative material in the tunica
intima of artery walls & forms a swelling in it
• The material consists of
i. (mostly) macrophage cells,
or debris, containing cholesterol and fatty acids
ii. calcium
iii. variable amount of fibrous connective tissue.
• The accumulated material forms a swelling in the artery
wall, which may lead to narrowing it & blood flow
Underlying areas of
at the outer base of older or more
advanced lesions.
7.
8. • Initiated by inflammatory processes in the endothelial
cells of the vessel wall in response to LDL particles
• small dense LDL (sdLDL) particles are more prone to
pass between the endothelial cells
• LDL particles and their content are susceptible to
oxidation by free radicals
• the risk is higher If LDL particles are in the wall of BVs
than in the bloodstream.
9. • Once inside the vessel wall, LDL particles can become
more prone to oxidation.
• Endothelial cells respond by attracting monocyte white
blood cells,
causing them to leave the blood stream,
penetrate into the arterial walls
and transform into macrophages.
• If HDL removal of fats from the macrophages does not
continue , the macrophages' ingestion of oxidized LDL
particles can produce an
10. • The immune system's specialized white blood cells
(macrophages and T-lymphocytes) absorb the oxidized
LDL, forming
• If these foam cells are not able to process the oxidized
LDL and recruit HDL particles to remove the fats,
they grow and eventually rupture,
leaving behind cellular membrane remnants, oxidized
materials, and fats (including cholesterol) in the artery
wall.
• This attracts more white blood cells, resulting in
formation of & blockage of the artery
11.
12. • These can be divided into various categories:
congenital or acquired
modifiable or not
classical or non-classical.
• Advanced age
• Male sex
• Genetic abnormalities, e.g. familial hypercholesterolemia
13. 1. Diabetes incidence of coronary artery disease
2. Dyslipoproteinemia
(presence of abnormal concentrations of lipoproteins)
High serum concentration of LDL
“ bad if elevated concentrations and small ”
Low serum concentration of functioning HDL
“ protective if large and high enough "
3. An LDL:HDL ratio greater than 3:1
4. Tobacco smoking
( risk by 200% after several years)
14. • Cholesterol is a waxy substance that's found in all of
your cells
it is an essential structural component of cell membranes
to maintain membrane structural integrity
within cells, it serves as a precursor for the biosynthesis
of steroid hormones, bile acids, and vitamin D.
• It's carried through your bloodstream attached to
proteins called lipoproteins.
15. Types of cholesterol
good cholesterol
( HDL )
bad cholesterol
( LDL )
act as cholesterol scavengerscarry cholesterol to different organs and
tissues
• Pick up excess cholesterol in blood
and take it back to liver to be broken
down
• The higher HDL level,
the less LDL in blood.
• if your body has more cholesterol than
it needs,
• the excess keeps circulating in blood &
enter blood vessel walls
• Then form plaques
& narrow the vessels to the point of
blocking blood flow
16. • LDL concentrations and HDL concentrations
• strongly associated with cardiovascular disease
because these causes atherosclerosis
• Abnormally low levels of cholesterol
• Causes : depression, cancer, and cerebral hemorrhage
• known as Familial alpha-lipoprotein deficiency or
Hypoalphalipoproteinemia is a rare inherited disorder
• characterized by : HDL and ApoA-I
• Treatment : elusive problem due to
1. variability of manifestation from patient to patient
2. low numbers of identified patients
17.
18.
19. Doctor may suspects atherosclerosis in these cases :
• weakened pulse
• Aneurysm
(abnormal bulging of an artery
due to weakness)
• slow wound healing
which indicates restricted blood flow
• Abnormal heart sounds
which indicates that an artery is blocked
21. A) Medications
• cholesterol-lowering medications,
including statins and fibric acid derivatives
• antiplatelet drugs and anticoagulants,
such as aspirin,
to prevent blood from clotting and clogging the arteries
• beta blockers or calcium channel blockers
to lower blood pressure
• diuretics (water pills)
to help lower blood pressure
• angiotensin converting enzyme (ACE) inhibitors,
which help prevent narrowing of the arteries
22. B) Surgery
• bypass surgery:
a vessel from elsewhere in the body, or a synthetic tube,
is used for diverting blood around a blocked or narrowed
artery
• thrombolytic therapy:
dissolves a blood clot by injecting a drug into the
affected artery
• angioplasty:
a thin, flexible tube called a catheter and balloon are
used to expand an artery
23. •
hypertension, high cholesterol, and diabetes
How to Increase HDLHow to Decrease LDL
Exercise
for 30 to 60 minutes per
day
six days per week
Increase aerobic exercise
Cessation of smokingHealthy diet
(Decrease saturated fat intake)
Weight reductionIncrease dietary fiber
24. omega-3 fatty acids
(Eicosapentaenoic acids)
Form more TXA3
than TXA2
*TXA3 is less
effective in
platelets
aggregation
Form more PGI3
than PGI2
*PGI3 is more
effective in
platelets anti-
aggregation
T.G.
Cholesterol
VLDL
LDL
HDL