This document discusses arteriosclerosis and atherosclerosis. It defines arteriosclerosis as the hardening and thickening of arteries. Atherosclerosis is a specific type of arteriosclerosis where plaque builds up in the arteries due to an inflammatory response. The document outlines the structure of arteries, risk factors for atherosclerosis such as smoking and diabetes, symptoms of atherosclerosis like chest pain, and treatments including lifestyle changes, medication, surgery, and stenting.

2. Ms. Hafsa Ayyub
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.  Hardening of arteries
 Group of disorders as associated with
it that are related to the hardening
and thicken of arteries
 Healthy arteries are flexible and
elastic, but over time, the walls in
arteries can harden, a condition
commonly called hardening of the
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’s medial calcific sclerosis-
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 of exercise, 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.  Arteriosclerosis in which
an artery wall thickens as a result
of invasion and accumulation
of white blood cells (foam cells)
and proliferation of intimal-
smooth-muscle cell creating
an atheromatous (fibrofatty)
plaque.

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

17. 1:Diabetes or impaired glucose
tolerance.
2:Dyslipoproteinemia (unhealthy
patterns of serum proteins carrying
fats & cholesterol).
3:Tobacco smoking increases risk by
200% after several pack years.
4: Elevated serum C-reactive
protein concentration.

18. 5:Vitamin B6 deficiency.
6:Dietary iodine
deficiency and hypothyroidism,
which cause elevated serum
cholesterol.
7: Advanced age and Male sex.
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 most plaque ruptures do 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 narrowing in 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.  One recent hypothesis suggests that,
for unknown reasons, leukocytes,
such as monocytes or basophils, begin
to attack the endothelium of the artery
lumen in cardiac muscle. The
ensuing inflammation leads to
formation of atheromatous plaques in
the arterial tunica intima, a region of
the vessel wall located between
the endothelium and the tunica media.

23.  The bulk of these lesions is made of
excess fat, collagen, and elastin. At
first, as the plaques grow, only wall
thickening occurs without any
narrowing. Stenosis is 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:
Reducing risk factors that lead to
atherosclerosis will slow or stop the
process. That means a
healthy diet, exercise, and
no smoking. These changes won't
remove blockages, but they’re proven
to lower the risk of heart attacks and
strokes.

29.  Medication:
Taking drugs for high
cholesterol and high blood
pressure will slow and may even
halt atherosclerosis. They could
also lower your risk of heart
attack and stroke.

30.  Angiography and stenting:
Using a thin tube inserted into an
artery in the leg or arm, doctors can
get to diseased arteries. Blockages are
visible on a live X-ray
screen. Angioplasty (catheters with
balloon tips) and stenting can often
open up a blocked artery. Stenting
helps to reduce symptoms, although it
does not prevent future heart attacks.

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 Inam Danish.
• 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?