special pathology

2. ANEURYSMS
 DR.ABDUL AZIZ SHAIKH
 MBBS,M.PHIL(Histopathology)
LUMHS JAMSHORO

3. LEARNING OBJECTIVES OF ANEURYSMS
DEFINATION
TRUE & FALSE
ANEURYSM
CLASSIFICATION
PATHOGENESIS
ABDOMINAL
AORTIC
ANEURYSMS
THORASIC
AORTIC
ANEURYSMS
AORTIC
DISSECTION

4. ANEURYSMS
 An aneurysm is a localized abnormal dilation of
a blood vessel or the heart.
 congenital or acquired.
 When an aneurysm involves an attenuated but
intact arterial wall or thinned ventricular wall of
the heart, it is called a “true” aneurysm.
cont

5.  Examples: Atherosclerotic, syphilitic, and congenital
vascular aneurysms, as well as ventricular aneurysms
that follow transmural myocardial infarctions
 In contrast, a false aneurysm (also called pseudo-
aneurysm) is a defect in the vascular wall leading to an
extravascular hematoma
Examples: include a ventricular rupture after myocardial
infarction

6. Aneurysms
 Aneurysms are classified by macroscopic shape
and size
 Saccular aneurysms: are spherical outpouchings
involving only a portion of the vessel wall.
 Fusiform aneurysms are diffuse, circumferential
dilations of a long vascular segment
 can involve extensive portions of the aortic arch,
abdominal aorta, or even the illiacs.

9. Pathogenesis of Aneurysms
 To maintain their structural and functional
integrity, arterial walls constby synthesizing,
degrading, and repairing damage to their
extracellular matrix constituents.
 Aneurysms can occur when the structure or
function of the connective tissue within the
vascular wall is compromised.

10. PATHOGENESIS
1. Intrinsic quality of vascular wall connective tissue is
poor eg Marfan syndrome, Loeys Dietz syndrome,
Ehlers-Danlos syndrome.
2. The balance of collagen degradation and synthesis is
altered by inflammation and associated proteases.
 atherosclerotic plaque or in vasculitis
3.The vascular wall is weakened through loss of smooth
muscle cells or the synthesis of non collagenous or non
elastic extracellular matrix. cont

11.  Systemic hypertension can also cause significant
narrowing of arterioles of the vasa vasorum (e.g.in the
aorta), which causes outer medial ischemia.
 Medial ischemia may lead to “degenerative changes”
of the aorta, whereby smooth muscle cell loss—or
change in synthetic phenotype—leads to scarring
(and loss of elastic fibers), inadequate extracellular
matrix synthesis, and production of increasing
amounts of amorphous ground substance
(glycosaminoglycan).

12. Cystic medial degeneration.
Aortic media from a patient with
Marfan syndrome, showing
elastin fragmentation and areas
devoid of elastin that resemble
cystic spaces but are actually
filled with proteoglycans
(asterisks).
Normal media for comparison,
showing the regular layered pattern of
elastic tissue.

13. Continued
 Two most important disorders that predispose to
aortic aneurysm are atherosclerosis and
hypertension.
 Hypertension is the most common etiology
associated with ascending aortic aneurysms.
 Other factors include trauma, vasculitis ,
congenital
 defects (e.g. berry aneurysms typically in the
circle of Willis; and infections (mycotic
aneurysms)

14. ABDOMINAL AORTIC ANEURYSM(AAA)
 Aneurysms occurring as a consequence of atherosclerosis
 form most commonly in the abdominal aorta and common
 iliac arteries.
 More frequently in men and in smokers, rarely
developing before age 50
 Usually positioned below the renal arteries and above bifurcation of
the aorta.
 Can be saccular or fusiform and upto 15cm in diameter.
 Two AAA variants:
a) Inflammatory AAAs
b) Mycotic AAAs

15. Continued
Clinical consequences of AAA include
a) Rupture into the peritoneal cavity or retroperitoneal
tissue with massive and fatal hemorrhage.
b) Obstruction of a branch vessel resulting in ischemic
injury.
c) Embolism from the atheroma or mural thrombosis.
d) Impingment on adjacent structure.
e) Presentation as abdominal mass.

16. THORACIC AORTIC ANEURYSMS
 Most commonly due to hypertension.
 Signs and Symptoms are:
1) Encroachment on mediastinal structures.
2) Respiratory difficulties.
3) Difficulty in swallowing
4) Persistent cough
5) Cardiac diseases
6) Pain
7) Rupture

17. AORTIC DISSECTION
 An arterial dissection arises when blood enters the arterial wall
itself.
 Aortic dissection occurs when blood splays apart the laminar
planes of the media to form a blood filled with in the aortic wall.
 This can be catastrophic if the dissection rupture through
adventitia and haemorrhages into adjacent spaces
 Aortic dissection may or may not be associated with aortic
dilatation.
 It occur principally only in two groups.

18. Continued
 1-men aged 40 to 60, with antecedent
hypertension.
 2-Younger patients with systemic or localized
abnormalities of connective tissue affecting the
aorta.
 It can be iatrogenic ( complicating arterial
cannulation during diagnostic catheterization or
cardiopulmonary by pass).
 Rarely associated with pregnancy.

19. PATHOGENESIS
 Hypertension is major risk factor. It leads to
degenerative changes in aortic media with variable
loss of medial smooth muscle cells ,due to
mechanical or ischemic injury
 Inherited or acquired connective tissues disorder eg
Marfan syndrome,Ehlers-Danlos syndrome,vitamin C
deficiency,copper metabolic defects.

20. MORPHOLOGY
 The most frequent histological lesion is cystic medial
degeneration.
 Aortic dissection usually intiates with an intimal tear.
 Sometimes dissecting haematoma spreads along laminar
planes of the aorta.

21. CLINICAL FEATURES
 These depend on the region affected.Two types
 Most common (dangerous) proximal lesions (called type A
dissections) involving either both the ascending and descending
aorta.
 Distal lesions not involving the ascending part and usually
beginning distal to subclavian artery (called type B)
 The symptoms are sudden onset of excruciating pain in the
anterior chest, radiating to the back and confused with myocardial
infarction.

22. Continued
 Common cause of death is rupture of dissection
into the pericardial,pleural,or peritoneal
cavities.
 Common clinical manifestations include cardiac
tamponade, aortic insufficiency and myocardial
infarction and obstruction of various arteries.
 Rapid diagnosis and antihypertensive therapy
with surgical intervention can save patient life.

23. THE KEY PROCESSES IN THE DEVELOPMENT
OF ATHEROSCLEROSIS ARE:
A Intimal thickening and lipid accumulation
B Migration of smooth muscle cells and lipid accumulation
C Intimal thickening and chronic endothelial injury
D Adhesion of blood monocytes and platelets
E Adhesion of platelets and chronic endothelial injury

24. ANS
A Intimal thickening and lipid
accumulation