TOPIC FOR UNDERGRADUATE PATHOLOGY STUDENTS.PPT SOLELY FROM ROBBIN s PATHOLOGY BOOK

1. ATHEROSCLEROSIS
&ANEURYSMS
Dr.MEGALA,MD,DNB.
PATHOLOGY

2. OBJECTIVES
To Learn About Epidemiology,risk
Factors,pathogenesis,morphology And Clinical
Consequences Of Atherosclerosis.
Aneurysms and Dissections.

3. Atherosclerosis underlies the
pathogenesis of coronary,cerebral and
peripheral vascular disease, and causes
more morbidity and mortality (roughly
half of all deaths) in the Western world
than any other disorder

4. Epidemiology
Dramatic increase during the last 50 years
In USpeaked and is now declining
In UK & other countries
- continue to increase

5. Major Risk Factors for Atherosclerosis
NONMODIFIABLE MODIFIABLE
Genetic abnormalities Hyperlipidemia
Family history Cigarette smoking
Increasing age Hypertension
Male gender Diabetes

6. Additional risk factors
Inflammation
Hyperhomocystenemia
Metabolic syndrome
Lipoprotein a [Lp(a)]
Factors affecting hemostasis
“type A” personality
and obesity

7. PATHOGENESIS

9. Endothelial Injury.
 Hemodynamic Disturbances
 Hypercholesterolemia

10. Inflammation
• inflammation is triggered by the accumulation of
cholesterol crystals and free fatty acids in
macrophages and other cells.
• cytosolic innate immune receptors
• The net result of macrophage and T cell
activation is the local production of cytokines and
chemokines.
• Activated macrophages produce reactive oxygen
species
• elaborate growth factors that drive smooth
muscle cell proliferation

11. Infection
• herpesvirus, cytomegalovirus,
• and Chlamydophila pneumoniae

12. Smooth Muscle Proliferation and
Matrix Synthesis
• Intimal smooth muscle cell proliferation and
extracellular matrix deposition convert a fatty
streak into a mature atheroma and contribute to
the progressive growth of atherosclerotic lesions
• PDGF, fibroblast growth factor, and transforming
growth factor-α.
• In constrast, activated inflammatory cells in
atheromas may increase the breakdown of
extracellular matrix components, resulting in
unstable plaques

13. Pathogenesis of Atherosclerosis
 Endothelial injury and dysfunction.
 Accumulation of lipoproteins
 Monocyte adhesion , migration and transformation into
macrophages and foam cells
 Platelet adhesion
 Factor release
 Smooth muscle cell proliferation, extracellular matrix
production and recruitment of T cells.
 Lipid accumulation both extra cellularly and within cells.

14. STRUCTURE OF
ATHEROSCLEROTIC PLAQUE

15. MORPHOLOGY
• Fatty streaks: Fatty streaks are composed of lipid-
filled foamy macrophages. Beginning as multiple
minute flat yellow spots,they eventually coalesce into
elongated streaks 1 cm long or longer.
• Aortas of infants & adolescents.
• The observation that coronary fatty streaks begin to
form in adolescence, at the same anatomic sites that
later tend to develop plaques, suggests a temporal
evolution of these lesions.

16. Fatty streaks

17. Atherosclerotic Plaque
Three principal components:
 smooth muscle cells, macrophages, and T
cells;
 extracellular matrix, including collagen,
elastic fibers, and proteoglycans; and
intracellular and extracellular lipids

18. Atherosclerotic Plaque

19. PATHOLOGIC CHANGES OF
ATHEROSCLEROTIC PLAQUES
• Rupture, ulceration, or erosion.
• Hemorrhage into a plaque.
• Atheroembolism
• Aneurysm formation

20. Consequences of Atherosclerotic Disease
• Myocardial infarction (heart attack)
• cerebral infarction (stroke)
• aortic aneurysms and
• peripheral vascular disease (gangrene of the
legs)

22. CLINICOPATHOLOGIC MANIFESTATION
• Atherosclerotic Stenosis
• Acute Plaque Change
• Thrombosis.
• Vasoconstriction.

23. Aneurysms and Dissection
• localized abnormal dilation of a blood vessel
or the heart that may be congenital or acquired
• Site::
- Aorta
- Heart
- Cerebral vessels

24. CLASSIFICATION
• TRUE
• FALSE
• SACCULAR
• FUSIFORM

26. ETIOLOGY
• Atherosclerosis
• Cystic Medial Degeneration
• Congenital Defects
• Infection - Eg. Mycotic

27. ABDOMINAL AORTIC ANEURYSM
• Cause - Atherosclerosis
• Location - Below Renal arteries & above
Bifurcation of Aorta, Common Iliac, Arch,
Thoracic Aorta also.
• Shape - Saccular , cylindroid / fusiform
• Size - 15 cm diameter
- 25 cm length
• Mural thrombus common

29. PATHOGENESIS
• Atherosclerosis
• Familial, Genetic:(Marfan’s syndrome)
• Men aged > 50 years are more
susceptible

30. Three AAA variants
• Inflammatory AAA
• Immunoglobulin G4 (IgG4)-related disease.
• Mycotic AAA

31. COMPLICATIONS
Depend on Location & Size
• Rupture
• Occlusion of a branch
• Embolism from atheroma / thrombus
• Impingement on adjacent structures

32. RUPTURE OF ANEURYSM
• Directly related to the Size of the lesion
• < 4 cms : 0 % risk
• 4 - 4.9 cms: 1%
• 5 – 5.9 cms:11 %
• > 6 cms:: 25% risk.
• Aneurysms expand @ 0.2- 0.3 cm / Year
• Surgical bypass with prosthetic grafts.

33. SYPHILITIC AORTITIS & ANEURYSM
• Seen as a complication of Tertiary Syphilis
• Venereal (Sexually transmitted) infection.
• Caused by a Spirocheate:: T. palladium.
• Complications are Less seen now a days.

34. SYPHILITIC AORTITIS & ANEURYSM
• Pathogenesis:: Obliterative Endarteritis of
vasavasorum in Tunica Adventia  Ischaemic
destruction of Elastic tissue & Muscle of Tunica
media  Stellate scars in Media Contraction
of scars
• TREE BARKING OF TUNICA INTIMA.
• Superimposed Atherosclerosis develops

35. PATHOGENESIS
• Destruction of Media Loss of Elastic
support Dilation of Aorta
• Involvement of Aortic ring  AR, LVH,
Cor Bovinum
• Arch & Thoracic Aorta aneurysms are common

37. COURSE OF SYPHILITIC ANEURYSM
• Encroachment on Mediastinal Structures
• Respiratory difficulties
• Compression on Esophagus
• Cough due to Rec. Laryngeal nerve pressure
• Erosion of ribs & Vertebral bodies
• Cardiac disease:: AR, LVH, MI
• Rupture

38. AORTIC DISSECTION
• Dissection of blood between & along the
Laminar planes of Aorta, forming blood filled
channels within the wall.
• Seen in 2 groups of patients
- Hypertensive Men ; 40 -60
- Marfan’s Syndrome

40. MORPHOLOGY
• 90 % located within 10 cm of aortic valve
• Next common site:: Descending Thoracic aorta
• Begin with Intimal tear. Propagates between
middle & outer third of media
- Proximally
- Distally
• Double Barreled Aorta

41. MICROSCOPICALLY
• cystic medial degeneration

43. CLINICAL COURSE OF DISSECTING
ANEURYSM
• Type A Lesions are Potentially Damaging &
Dangerous.
• Sudden onset of Chest Pain:: Confused to that
of MI
• Death is by Rupture of Dissection into:
Pericardial / Pleural / Peritoneal cavity.
• Retrograde dissection causes: Cardiac
Tamponade