True aneurysm: dilation of wall of artery cz artery lose its elasticity, bmot bel nos, byeftah

False aneurysm: rupture of wall but CT is intact--> pulsating hematoma or arteriovenous fistula [blood
by2t3 3ade w fi pulse]

Dissection: tear in media or between media and adventitia [we see blood btwn these layers]

Saccular aneurysm: 1 part of arteriole dilates (intracranial)

Fusiform aneurysm: 2 parts of arteriole dilate (abdominal aorta/iliac)

Causes:
Hypertension/atherosclerosis are considered risk factors for aneurysm formation
They alter the formation of ECM--> abnormal formation/degradation of ECM.
Pathogenesis:
o Abnormal collagen formation (defective type 3) --> low quality of tissue--> dilation "Ehler's
disease"
o During inflammation, inc TGF-B secretion--> dec ECM secretion--> dilation "Marfans" in
ascending aorta [mmkn ykun fi aneurysm]
o Inflammatory components associated with factors affecting collagen (proteases)--> no
balance in secretion/degradation of collagen
o Loss of smooth muscle cells [SMCs] --> no CT formation--> weak wall--> dilation
o Atherosclerotic plaque thickens wall--> increasing diffusion distance--> ischemia of media-->
aneurysm
o Systemic hypertension--> narrowing of arterioles of vasovasorum--> ischemia of media

Microscopically: Medial degeneration [degeneration of elastic fibers inside media]

AORTIC ANEURYSM:
Causes:
 Atherosclerosis, hypertension
 Smoking- old age- trauma
[atherosclerosis in abdominal aorta]
[hypertension in ascending aorta and aortic arch]
Abdominal aneurysm:
 Atherosclerosis
 More frequent in men and smokers (abdominal aneurysm)
 more than 5.5 cm and up to 25 cm in length, can be saccular/fusiform
 Contains poorly organized mural thrombus (caused by coagulation of blood in dilated part)
 Mass itself doesn’t cause symptoms but they appear due to consequences
Variants:
Inflammatory: giant and inflammatory cells caused by aneurysm in young people

Mycotic: fungi from embolization/ extension from another organ/ circulating organism infects arterial
wall--> inflammation--> aneurysm

Suppuration further destroys media--> rapid dilatation and rupture

Clinical features:
Asymptomatic, during abdominal exam: pulsating mass (if it was big enough)
Other manifestations: more severe
 Rupture of aneurysm into peritoneal cavity or retroperitoneal tissue with massive fatal
hemorrhage
 Thrombosis in aneurysm truh w t3ml obstruction [tsaker iliac] of a branch downstream tissue
ischemic injury (iliac- renal): cause leg gangrene
 Embolism from mural thrombus
 Impingement on adjacent structure (compression of ureter/ erosion of vertebrae=waja3 daher)

Treatment:
Open surgical repair: in surgery, clip ends of aneurysm and sew new graft to abdominal aorta: Invasive
surgical repair
Endovascular approach: insert catheter through femoral artery to reach abdominal aorta--> open stent
[Insert 2 stents to cover both iliac to prevent spread of aneurysm]

Thoracic aortic aneurysm:

Ascending, descending, arch
Associated with hypertension
Symptoms:
 Chest pain from erosion to bone of thoracic cage
 MI from compression of coronary artery
 Difficulty swallowing
 Hoarseness from irritation of recurrent laryngeal nerves
 Respiratory complications from compression of bronchi
Treatment: same as above

AORTIC DISSECTION:
HYPERTENSION MOST COMMON CAUSE
 Formation of blood in media due to tear
 Disastrous if dissection ruptures--> hemorrhage to adjacent space
 Can extend from ascending to descending (stays inside wall)
 Occurs in 2 groups:
Antecedent hypertension: 40-60 yrs
Syndromic disease affecting aorta: young pts like in Marfan
Or can be caused by pregnancy and iatrogenic (injury of intima during medical procedure)
-trigger is unknown in most cases-
 Blood flow dissects through media--> progression of blood in arterial path
 Disruption of penetrating vessels of vasavasorum--> intramural hematoma without tear
 Traumatic chest injury: car accident: heart bumped to chest--> intimal tear--> aortic
dissection
 Morphology: sudden extravasation of blood inside media with NO inflammation
 Most spontaneous area of aortic dissection: 10 cm from aortic arch--> heart--> aortic valve
1st to be damaged--> dilation of its annulus--> nonfunctional
 Clinical features: most serious complications occur with dissections between aortic valve
and distal arch
 STANFORD'S: from aortic valve to:
 Type A: most common, involves ascending and descending aorta or ascending
aorta alone [dissection of asc aorta may extend and involve carotid arteries
which lead to stroke, coronary arteries which lead to acute MI, and proximal
part of asc aorta leads to cardiac tamponade]
 Types B: dissections begin distal to subclavian

 DeBakey:
 Type I: aortic valve till abdominal aorta
 Type II: aortic valve till ascending aorta
 Type III: distal subclavian till descending aorta
 Clinical features:
 Usually after some accident
 Sudden onset of pain in anterior chest that will move back reflects
between scapula and then downward
 Disrupt aortic valve annulus--> nonfunctional
 Cardiac tamponade and aortic insufficiency due to blood accumulation filling
pericardium
 Treatment:
 Pressure reducing therapy limits evolving dissection: strong antihypertensives
then to OR for surgery
 Surgery and replace with graft