ANEURISMA KULIAH 1
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Transcript of ANEURISMA KULIAH 1
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Dr.Gunawan Tohir SpB, M
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Figure 19.1a
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Aneurysm: localized dilation of thevessels or the heart
May occur at any site, most important is
aorta and ventricles.
True aneurysm is bounded by vessel wall
False aneurysm: extravascular hematoma
with communication to vascular space(Pulsating hematoma)
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Most aneurysms are caused bydegenerative disease affecting the vessel(atherosclerosis)
Structural weakness & Haemodynamicforces Damage to, and loss of intima
Reduction in the elastin and collagen contentof the media
Collagen; tensile strength, adventitia
Elastin; recoil capacity, media
Risk factors smoking, hypertension, hypercholesterolaemia
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Laplaces low
(Tension varies directly with radius when pressure
is constant)
For every increase in the radius there is a large
increase in tension, leading to further
enlargement of the aneurysm
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Congenital Marfans syndrome, Berry aneurysms
Post-stenotic Coarctation of the aorta, Cervical rib, Popliteal
artery entrapment syndrome
Traumatic Gunshot, stab wounds, arterial punctures
Inflammatory Takayasos disease, Behcets disease
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Mycotic
Bacterial endocarditis, syphilis
Pregnancy associated
Splenic, cerebral, aortic, renal, iliac & coronary
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False Due to traumatic
breach in the wall The sac made up
from thecompressedsurrounding tissue
True Dilatation involving
all layers of thewall
Fusiform Spindle-shaped
involving wholecircumference
Saccular Small segment of
wall ballooning dueto localized
weakness
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>90% affecting abdominal aorta
Infra-renal segment in ~95%
Male : Female ratio 4:1
More common in western countries
5% over 50s, 15% over 80s
Associated with iliac aneurysms in 30%
Associated with popliteal aneurysms in
10%
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Asymptomatic in 75%
Incidentally discovered during clinical exam.or
radiographic investigation
Pain Central abdominal radiating to the back
Chronic due to stretching the vessel wall or
compression/erosion of surrounding structures
Acute pain due to rupture
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Rupture
Risk of rupture correlate with aneurysm size
Retroperitoneal, back pain, stable
Intraperitoneal, abdo/back/falnk pain, shock 5-year rupture rate 0% in AAA 5cm
Risk of rupture can be predicted by
High diastolic BP, COAD
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Fistulation, rare Gut, IVC, left renal vein
Thrombosis, rare Acute lower limb ischaemia
Distal embolism Acute ischaemia to small distal areas (trash foot)
Distal obliteration Claudication, rest pain, gangrene
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MEKANISME YANG DIDUGA
1.DEGRADASI PROTEOLITIK DARI JAR IKAT
2.INFLAMASI DAN RESPONS IMUN
3.STRESS BIOKIMIA DARI DINDING 4.MOLEKULER GENETIK
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