aneurysm pathology pptx from.robbins sss

Pathology

1. ANEURYSMS

2. ANEURYSM
Definition
Classification
Pathogenesis
Complication

3. Definition-
Aneurysm is a localized abnormal permanent
dilation of a blood vessel or heart that may be
congenital or acquired

4. Definition

5. Classification
Origin
Location
Gross appearance
Composition of vessel wall
Etiology

6. CLASSIFICATION
Depending upon location
-Arterialand venous, with arterial being more
common.
-Capillaries
-Theheart, including coronary artery aneurysms,
ventricular aneurysms, aneurysm of sinus of
Valsalva, and aneurysms following cardiac surgery.
-The aorta, namely aortic aneurysms including
thoracic aortic aneurysms and abdominal aortic
aneurysms

7. Classification
-Thebrain, including cerebral aneurysms, berry
aneurysms
-The legs, including the popliteal arteries
-The kidney, including renal artery aneurysm

8. Classification
1.Saccularhaving large spherical outpouching.
2.Fusiform having slow spindle-shaped dilatation.
3.Cylindrical with a continuous parallel dilatation.
4.Serpentine or varicose which has tortuous dilatation of
the vessel.
5.Racemoseor circoidhaving mass of
intercommunicating small arteries and veins.
Depending upon shape :

10. Discrete outpouching of blood vessel
Ranging from 5-20 cms in diameter
Often contain thrombus

12. Circumferential dilation of blood vessels
20 cms in diameter
Most commonly involved Aortic arch ,
Abdominal aorta , iliac arteries

13. Composition of wall
True Aneurysm
False Aneurysm
Arterial dissection

14. Classification
Depending upon composition of the wall

15. Classification
Depending upon composition of the wall
Trauma to vessel wall

16. Classification

17. Composition of the wall of
aneurysm
True Aneurysm-all layers
False Aneurysm-traumatic rupture or
perforating injury
Arterial dissection-intimal defect

18. Classification
Depending upon pathogenic mechanisms
-Atherosclerotic aneurysms are the most
common type
-Syphilitic (luteic) aneurysms found in the
tertiary stage of the syphilis
-Dissecting aneurysms(Dissecting hematoma)
in which the blood enters the separated or
dissected wall of the vessel

19. Classification
-Mycotic aneurysms resulting from weakening
of the arterial wall by microbial infection.
-Berry aneurysms which are small dilatations
especially affecting the circle of Willis in the
base of the brain.

20. Pathology
Predisposing factors
Atherosclerosis especially in aortic aneurysms
Hypertension especially in ascending aortic
aneurysms
Trauma
Vasculitis
Congenital defects
Fibromuscular dysplasia
Berry aneurysms typically in the circle of
willis

21. Infections -
–Syphilic aneurysms
–Mycotic aneurysms
–From embolization of a septic embolus
-complication of infective endocarditis
–As an extension of an adjacent
suppurative process
–By circulating organisms directly
infecting the arterial wall.

22. Pathogenesis -Occur when structureor function
of the connective tissue within the vascular wall
is compromised.
Poorintrinsic quality of the vascular wall
connective tissue.
Imbalancein vascular wall collagen
degradationand synthesiscaused by
inflammationand associated proteases.
Weakeningof vascular walldue to
lossof smooth muscle cells
synthesisof non-collagenous/non-elastic
extracellular matrix.

23. Poorintrinsic quality of the vascular wall
connective tissue
–defective synthesis of fibrillin leads to
aberrant TGF-β activity and weakening of
elastic tissue in the aorta, this may result in
progressive dilation in Marfan syndrome.
–mutations in TGF-β receptors lead to
defective synthesis of elastin and collagens I
and II in Loeys-Dietz syndrome.

24. –Weak vessel walls due to defective type III
collagen synthesis are also a hallmark of
the vascular forms of Ehlers-Danlos
syndrome.
–altered collagen cross-linkingassociated
with Vitamin C deficiency (scurvy)

25. Imbalance in vascular wall collagen degradation
& synthesis
Increased matrix metalloprotease (MMP)
expression, especially by macrophages in
atherosclerotic plaque or in vasculitis degrade
virtually all components of the extracellular
matrix in the arterial wall (collagens, elastin,
proteoglycans, laminin, fibronectin).
Decreased expression of tissue inhibitors of
metalloproteases (TIMPs)

26. Weakening of vascular wall
Ischemia of the inner media occurs when there
is atherosclerotic thickening of the intima.
Systemic hypertension causes significant
narrowing of arterioles of the vasa vasorum.
Medial ischemia may lead to “degenerative
changes” of the aorta.
Smooth muscle cell loss/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).

27. Pathology

28. ABDOMINAL AORTIC ANEURYSMS
Most common form of aortic aneurysms.
Common in men, smokers
More commonly seen in males over the age of
50 years.
Most common sites abdominal aorta, thoracic
aorta, iliac arteries and other large systemic
arteries.

29. Pathogenesis

30. ATHEROSCLEROTIC ANEURYSMS

31. External view, gross photograph
of a large aortic aneurysm that ruptured
Opened view, with location of rupture tract
indicated by a probe. The wall of the aneurysm is
exceedingly thin, with lumen filled by large uantity
of layered but largely unorganized thrombus

32. Atherosclerotic AAA
-Atherosclerotic plague –intima-necrosis ,
weakness and thinning of arterial wall
-Excessive degradation of ECM by MMP

33. Inflammatory AAA
Periaortic fibrosis
C reactive protein
Lymphoplasmacytic infiltrate

34. Immunoglobulin IgG4 related disease
Mycotic Abdominal Aortic aneurysm-
salmonella gastroenteritis

35. Morphology
Site-below the renal arteries ,above the
bifurcation of aorta
Saccular/fusiform
15-25cms
Intimal surface-atherosclerosis
Lumen-thrombus

36. COMPLICATIONS :
1. Rupture
-Most serious and fatal complication.
-Depends upon the size and duration of the
aneurysm and the blood pressure.
-Rupture of abdominal aneurysm may occur
either into the peritoneum or into the
retroperitoneum resulting in sudden and
massive bleeding.
-A ruptured aneurysm is more likely to get
infected.

37. 2. Compression
-The atherosclerotic aneurysm may press upon some
adjacent structures such as compression of ureter and
erosion on the vertebral bodies.
3. Arterial occlusion
-Atherosclerotic aneurysms of the abdominal aorta may
occlude the inferior mesenteric artery, or there may be
development of occlusive thrombosis.
-Thromboembolism is rather common in abdominal
aneurysms.

38. Thoracic aortic aneurysm
•HT
•Symptoms-respiratory failure , difficulty in
swallowing, cough

39. SYPHILITIC ANEURYSM

40. Obliterativeendarteritis:
•Luminal narrowing and
obliteration, scarring of the
vessel wall, and a dense
surrounding rim of
lymphocytes and plasma
cells that may extend into
the media
•The aorta loses its elastic
recoil with destruction of
the media and becomes
dilated, producing an
aneurysm.
•Valvularinsufficiency and
massive volume overload
lead to hypertrophy of the
left ventricle.
•The greatly enlarged hearts
are sometimes called "cor
bovinum" (cow's heart).

42. Syphilitic Aneurysm

43. COMPLICATIONS
1.Rupture
-Causes massive and fatal haemorrhageinto
the pleural cavity, pericardial sac, trachea and
oesophagus.
2.Compression
•The aneurysm may press on the adjacent
tissues and cause symptoms :
on trachea causing dyspnoea,
on oesophaguscausing dysphagia,
on recurrent laryngeal nerve leading to
hoarseness

44. 3.Cardiac dysfunction
-When the aortic root and valve are involved,
syphilitic aneurysm produces aortic
incompetence and cardiac failure.
-Narrowing of the coronary ostia may further
aggravate cardiac disease

45. Berry Aneurysm of cerebral
arteries

47. MYCOTIC ANEURYSM
Aneurysm that is secondary to weakening of
vessel wall due to infection
Staphylococcus aureus
S. epidermis, Salmonella, Streptococcus
pneumonia
Fungal arterial infections
Candida , Cryptococcus , Aspergillus
Immunosupression (Diabets Mellitus)

49. Femoral Artery most common site of mycotic
aneurysm
Abdominal Aorta-second most common site
Intracranial arteries
Coronary arteries

50. Dissecting aneurysm of the aorta
(Aortic dissection)
•Refers to a dissecting haematoma in which the
blood enters the separated (dissected) wall of
the vessel and spreads for varying distance
longitudinally.
•The most common site is the aorta and is an
acute catastrophic aortic disease.
•Men,50-70 yrs
•In women, dissecting aneurysms may occur
during pregnancy.

51. Dissecting aneurysm of the aorta
(Aortic dissection)
The aortic wall has split (dissected) at the level of the media producing an outer false
lumen running parallel to the central true lumen which is narrowed.

52. Dissecting aneurysm of the aorta
(Aortic dissection)
PATHOGENESIS
1.Hypertension in about 90% cases of
dissecting aneurysm.
2.40-60 yrs
3.Marfan’s syndrome.
4.Iatrogenic trauma during cardiac
catheterization or coronary bypass surgery
5.Pregnancy, for some unknown reasons

53. •Ascending aorta
•Transverse/oblique
•Tunica media
•Extension

54. Dissecting aneurysm of the aorta (Aortic dissection)
CLASSIFICATION

55. Dissecting aneurysm of the aorta (Aortic dissection)
HISTOLOGY
i.Focal separation of the
fibromuscularand elastic
tissue of the media.
ii.Numerous cystic spaces in
the media containing
basophilic ground
substance.
iii.Fragmentation of the
elastic tissue.
iv.Increased fibrosis of the

56. COMPLICATIONS
Rupture
-Haemorrhageoccurs into the pericardium; less
frequently it may rupture into thoracic cavity,
abdominal cavity or retroperitoneum.
•Cardiac disease
-cardiac tamponade.

57. 3.Ischemia
-Obstruction of the branches of aorta by
dissection results in ischaemiaof the tissue
supplied.
-There may be renal infarction, cerebral
ischaemiaand infarction of the spinal cord.

58. Arteriosclerosis
•Small arteries and arterioles
•Cause ischemic injury
•Arterial wall thickening and loss of elasticity

59. Variants
•Hyaline arteriosclerosis
•Hyperplastic arteriosclerosis

60. Hyaline Arteriosclerosis
•Arterioles with benign HT
•Thickening of wall by hyaline material

61. Hyperplastic Arteriosclerosis
•Onion skin laminated thickening of arteriolar
walls
•Necrotizing arteriolitis

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