Peripheral Vascular And Aortic Diseases Pathology Flashcards
Internal elastic lamina
Thin layer of the tunica intima in arteries that is composed of elastin and has holes in them
- allows for better diffusion of substances (oxygen) from blood to get into the artery deeper or out completely
External elastic lamina
A external layer that surrounds the tunica media of arteries
Vasa vasorum
Blood vessels for the blood vessel itself
Varicose veins
Abnormally dialated tortuous veins that are caused by weakened vessel walls w/ increased intraluminal pressures
- almost always include the superifical veins of the leg
- renders venous valves incompetent since the veins are dilated so much
Rates include 1/5 men and 1/3 women
- obesity increases this risk
- genetics does play a part in premature varicose veins
Why does women usually have high rates of varicose veins?
Chronic increased venous pressure always found in pregnancy
What is the most disabling symptom of varicose veins?
Persistent edema and secondary ischemic skin issues such as stasis dermatitis and ulcerations
- redness/heat/ scaly skin around the ankle
- note: it is very rare to get an embolism in superficial varicose veins (more likely in deep)*
Thrombophlebitis/ phlebothrombosis
Moving thrombosis that are accompanied by inflammation
-90% of these are caused by DVTs
Risk factors:
- most important risk factor for DVT in legs is prolonged immobilization*
- CHF
- pregnancy
- oral contraceptive
- being male
- age over 50 yrs
- inherited coagulation defects
- cancer (procoagulation factors are high)
Migratory thrombophlebitis (Trousseau syndrome)
Thromboses in different vascular beds at different times due to the systemic Hypercoagulability state that cancer puts the body into
Sings and symptoms of thrombophlebitis/ phlebothrombosis
Edema
Cyanosis of face and distal extremities
Superifical vein dilation
Heat/tenderness/redness/swelling
Bilateral swelling
(+)Homan sign = dorsiflexion of the swollen foot elicits pain
- Note: that DVTs are wide spectrum for symptoms and sometimes can be asymptomatic*
Lymphangitis
Acute inflammation caused by bacterial seeding of the lymphatic vessels
- often appear red and painful and in streak shaped (often outlining the pattern of lymph drainage
- presents with enlargement of the sentinel lymph node associated with the streak
- can lead to bacteremia/sepsis if not controlled*
Primary lymphedema
Occurs due to congenital defects
- examples: familial Milroy disease
Results in agenesis or hypoplastic lymphatic
Secondary (obstructive) lymphedema
Stems from physical blockage of the lymphatics
Examples:
- tumors
- surgical procedures gone wrong
- postradiation fibrosis
- filariasis
- post-inflammatory scarring
What physiologic effect does all edema do to the body?
Increases the hydrostatic pressure in the lymphatics distal to the obstruction
- leads to edema
Peau d’orange
Bryant induration appearance of overlying skin of chronic edema
- caused by deposition of ECM and fibrosis
Monckeberg medial sclerosis
Arteriosclerosis that produces calcium deposits around the internal elastic lamina layer
- do not encroach on vessel lumen and are not clinically significant (usually)
- common in people older than 50
True aneurysms
Include saccular and fusiform variations
- saccular often include thrombi
Involve all 3 layers of the artery and can be caused by atherosclerosis or congenital causes
Pathogenesis of aneurysms
Occur due to alteration in SM cells or ECM. These alterations effect the strucutral integrity of the arterial media
Factors include:
- inadequate CT synthesis
- excessive CT degradation
- loss of SMCs or changes in synthesis of SMCs
Inadequately abnormal CT synthesis
A possible way for aneurysms and dissections to occur
- caused by TGF-B receptor mutations which results in defective elastin and collagen synthesis since TGF-B is the prime mover in CT synthesis
marfan syndrome is a examples of this, which causes increased TGF-B production due to defective synthesis of fibrillin. This causes a decrease in elasticity of the artery and makes it proved to rupture
Excessive CT degradation
A way for aneurysms or dissections to occur
Example is increasing MMP (matrix metalloproteases) expression by macrophages in atherosclerotic plaques which contributes to aneurysms in arteries
- MMPs degrade ECM properties
Cystic medial degeneration
Histologically changes to vessels caused by ischemia
Results in
- SMC loss
- fibrosis
- inadequate ECM synthesis
- accumulation of proteoglycans
Two most important predisposing conditions for aortic aneurysms
Atherosclerosis
- more associated with AAAs and Stanford type B dissections
HTN
- more associated with Ascending aortic aneurysms/ TAAs and Stanford type A dissections
AAA’s
Most cases develop from ECM degradation by MMPs and proteoglycans. Also thins the arterial wall
Typically occur between renal arteries and can be saccular or fusiform
- also typically has clots in it
Occur more frequently in men and smokers
- also usually occur after 50 yrs of age
Most common cause is extensive atherosclerosis (not the only factor though)
AAA clinical consequences
Obstruction of vessels branching off of it
Embolism production
Impingement of adjacent structures
Can appear like a palpable tumor if big enough (usually about to rupture at this point
Rupturing of the AAA (results in fatal internal hemorrhage)
Size risks associated with AAAs
3-4 cm = AAA but has near 0% chance of rupture
4-5 cm = AAA w/ 1% chance of rupture
5-6 cm = AAA w/ 11% chance of rupture
6+ cm = AAA w/ 25% chance of rupture
- must use surgery if the aneurysm is 5cm+*
TAAs
Most commonly associated with HTN
- also are associated with bicuspid aortic valve stenosis/regurgitation and Marfan syndrome
Aortic dissection
Occurs when blood AP lays apart the tunica intima and media
- if untreated also breaks through adventitia
- also blocks vasa vasorum so can lead to necrosis
2 age groups are most likely to get these:
1) men 40-60yrs old (90%)
2) <21 yrs old with genetic abnormalities (10%)
* HTN is the major risk factor for aortic dissection*
Where is the most common part of origin of initial intima tear in aortic dissections
Ascending aorta (within 10 cm of aortic valve)
- usually transverse or oblique
- usually lies within the middle-outer tunica media
Clinical symptoms of aortic dissection
- Hallmark symptom*
- excruciating tearing/stabbing pain beginning in the anterior chest and radiating to the back between the scapulae
(If un treated, the pain will radiate further down overtime)
Most common cause of death for aortic dissections
Rupture and internal hemorrhaging into the pericardial/ peritoneal or pleural cavities
Difference in treatment between type A and type B aortic dissections
Type A =
- intensive anti-hypertensive therapy
- surgical repair of the intima
- mortality rate = 70% w/ hemorrhage, 40-60% w/out
- more serious
Type B =
- less intensive anti-hypertensive therapy
- surgical repair of intima
- mortality rate = 25%
- less serious
Physiology of the main three layers of blood vessels
1) tunica intima:
- thin subendothelial layer of loose connective tissue w/ sparse smooth muscle fibers
2) tunica media:
- helically arranged smooth muscle cells W/ variable amounts of elastic/reticular fibers and proteoglycans.
3) tunica adventitia:
- connective tissue consisting of type 1 collagen and elastic fibers.
Chylous ascites
Rupture of dilated lymphatics that typically follow obstruction of the lymph vessels. Causes lymph from the ruptured vessels to pool in potential spaces.
- named for the space the lymph occupies (chylothroax, chylopericardium, etc.)
Two variants of arteriosclerosis
Hyaline and hyperplastic
- affects small arteries and arterioles and often caused by downstream ischemic injury
What are the most common sites for fusiform aneurysms when they occur?
Aortic arch
Abdominal aorta
Iliac arteries
Two types of clinical arteriolosclerosis
Hyperplastic and hyaline
