Arteriosclerosis.pdf

Arteriosclerosis

2. Ms. HafsaAyyub
University Institute of Radiological sciences & Medical Imaging
University of Lahore

3. To understand the structure of Arteries
What is Arteriosclerosis?
What is Atherosclerosis and its
pathogenesis?

4. Structure of
Arteries
Arteriosclerosis
definition
Morphological
Patterns
Risk Factors
Atherosclerosis
Definition
Risk Factors
Signs and
symptoms
Pathogenesis
Diagnosis
Treatment
Medication

6. Three coats from inside out
1.Tunica intima-extracellular tissue
matrix and smooth muscle cells
2.Tunica media-Elastic tissue and
muscles
3.Tunica adventitia-nerve fibers, vasa-
vasorum

7. Hardeningofarteries
Groupofdisordersasassociatedwith
itthatarerelatedtothehardening
andthickenofarteries
Healthyarteriesareflexibleand
elastic,butovertime,thewallsin
arteriescanharden,acondition
commonlycalledhardeningofthe
arteries

8. Atherosclerosis is a specific type
of arteriosclerosis
These terms sometimes use
interchangeably

10. 1.Atherosclerosis-formation of fibrofatty
plague-involves medium and large vessels
2.Monckeberg’smedial calcificsclerosis-
Calcification in the media of muscular
arteries
-In elderly aging change
-No abnormality
3.Arteriolosclerosis-small vessel sclerosis
4.Artherosclerosis

11. Etiology is unknown
Age
Male gender
-More in men than in premenopausal
women (protecting agent: estrogen)

12. Family History
-males-before 45 years
-Females-after 50 years
-Genetic derangement in lipoprotein
metabolism
Diabetes Mellitus

13. Hypertension
Cigarette smoking
Obesity
Lifestyle (lack ofexercise, alcoholism,
diet)
Oral contraceptives
Gout
Infections
Inc. levels of Coagulating factors

14. Ms. Mahjabeen
University Institute of Radiological sciences
& Medical Imaging
University of Lahore

15.  Arteriosclerosisinwhich
anarterywallthickensasaresult
ofinvasionandaccumulation
ofwhitebloodcells(foamcells)
andproliferationofintimal-
smooth-muscle cellcreating
an atheromatous (fibrofatty)
plaque.

16. The plaque is divided into three
distinct components:
Theatheromawhich is the nodular
accumulation of a soft, flaky, yellowish
material at the center of large plaques,
composed of macrophages nearest
thelumenof the artery
Underlying areas of cholesterol
crystals
Calcification at the outer base of older
or more advancedlesions.

17. 1:Diabetesorimpaired glucose
tolerance.
2:Dyslipoproteinemia(unhealthy
patterns of serum proteins carrying
fats &cholesterol).
3:Tobacco smoking increases risk by
200% after severalpack years
.
4: Elevated serumC-reactive
proteinconcentration.

18. 5:Vitamin B
6deficiency.
6:Dietaryiodine
deficiencyandhypothyroidism,
which causeelevated serum
cholesterol.
7:Advanced age and Malesex.
8:Obesity.

19. Atherosclerosis is asymptomatic
for decades because the arteries
enlarge at all plaque locations,
thus there is no effect on blood
flow.

20. Even mostplaque rupturesdo not
produce symptoms until enough
narrowing or closure of an artery,
due to clots, occurs. Signs and
symptoms only occur after severe
narrowing or closure impedes
blood flow to different organs
enough to induce symptoms.

21. Marked narrowingin the coronary
arteries, which are responsible for
bringing oxygenated blood to the
heart, can produce symptoms such as
the chest pain of angina and shortness
of breath, sweating, nausea, dizziness
or light-headedness, breathlessness
or palpitations.Abnormal heart
rhythms called arrhythmias (the heart
is either beating too slow or too fast)
are another consequence of ischemia.

22. Onerecenthypothesissuggeststhat,
forunknown reasons,leukocytes,
suchasmonocytesorbasophils,begin
toattacktheendotheliumoftheartery
lumen incardiacmuscle.The
ensuing inflammation leadsto
formationofatheromatousplaquesin
thearterialtunicaintima,aregionof
thevesselwalllocatedbetween
theendotheliumandthetunicamedia.

23. The bulk of these lesions is made of
excess fat,collagen, andelastin. At
first, as the plaques grow, onlywall
thickeningoccurs without any
narrowing.Stenosisis a late event,
which may never occur and is often
the result of repeated plaque rupture
and healing responses, not just the
atherosclerotic process by itself.

25. 1.Angiography.
2.Stress testing.
3.Coronary calcium scoring by CT,
carotid IMT (intimal media thickness).
4.Intravascular ultrasound(IVUS).
5.HbA1c
6.Lipid profile
7.ECG

28. Lifestyle changes:
Reducingriskfactorsthatleadto
atherosclerosiswillsloworstopthe
process. That means a
healthy diet, exercise, and
nosmoking.Thesechangeswon't
removeblockages,butthey’reproven
tolowertheriskofheartattacksand
strokes.

29. Medication:
Taking drugs forhigh
cholesterolandhigh blood
pressurewill slow and may even
halt atherosclerosis. They could
also lower your risk of heart
attack andstroke.

30. Angiographyandstenting:
Usingathintubeinsertedintoan
arteryinthelegorarm,doctorscan
gettodiseasedarteries.Blockagesare
visible on a live X-ray
screen.Angioplasty(catheterswith
balloontips)andstentingcanoften
openupablockedartery.Stenting
helpstoreducesymptoms,althoughit
doesnotpreventfutureheartattacks.

31. Bypass surgery:Surgeons "harvest" a
healthy blood vessel (often from the
leg or chest). They use the healthy
vessel to go around a blocked
segment.
These procedures can have
complications. They’re usually saved
for people with significant symptoms
or limitations caused by
atherosclerosis.

34. •Short text book of pathology by
Mohammad InamDanish.
•General pathology by Firdaus.
•Pathology-Wikipidea

35. We understand the structure of
Arteries and their composition.
We have learnt that What is
Arteriosclerosis and its morphological
patterans?
Know about Atherosclerosis and its
pathogenesis?