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Cardiology > Peripheral Vascular And Aortic Diseases Pathology > Flashcards

Peripheral Vascular And Aortic Diseases Pathology Flashcards

1
Q

Internal elastic lamina

A

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

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2
Q

External elastic lamina

A

A external layer that surrounds the tunica media of arteries

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3
Q

Vasa vasorum

A

Blood vessels for the blood vessel itself

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4
Q

Varicose veins

A

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
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5
Q

Why does women usually have high rates of varicose veins?

A

Chronic increased venous pressure always found in pregnancy

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6
Q

What is the most disabling symptom of varicose veins?

A

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)*
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7
Q

Thrombophlebitis/ phlebothrombosis

A

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)
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8
Q

Migratory thrombophlebitis (Trousseau syndrome)

A

Thromboses in different vascular beds at different times due to the systemic Hypercoagulability state that cancer puts the body into

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9
Q

Sings and symptoms of thrombophlebitis/ phlebothrombosis

A

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*
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10
Q

Lymphangitis

A

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*
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11
Q

Primary lymphedema

A

Occurs due to congenital defects
- examples: familial Milroy disease

Results in agenesis or hypoplastic lymphatic

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12
Q

Secondary (obstructive) lymphedema

A

Stems from physical blockage of the lymphatics

Examples:

  • tumors
  • surgical procedures gone wrong
  • postradiation fibrosis
  • filariasis
  • post-inflammatory scarring
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13
Q

What physiologic effect does all edema do to the body?

A

Increases the hydrostatic pressure in the lymphatics distal to the obstruction
- leads to edema

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14
Q

Peau d’orange

A

Bryant induration appearance of overlying skin of chronic edema
- caused by deposition of ECM and fibrosis

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15
Q

Monckeberg medial sclerosis

A

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
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16
Q

True aneurysms

A

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

17
Q

Pathogenesis of aneurysms

A

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
18
Q

Inadequately abnormal CT synthesis

A

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

19
Q

Excessive CT degradation

A

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

20
Q

Cystic medial degeneration

A

Histologically changes to vessels caused by ischemia

Results in

  • SMC loss
  • fibrosis
  • inadequate ECM synthesis
  • accumulation of proteoglycans
21
Q

Two most important predisposing conditions for aortic aneurysms

A

Atherosclerosis
- more associated with AAAs and Stanford type B dissections

HTN
- more associated with Ascending aortic aneurysms/ TAAs and Stanford type A dissections

22
Q

AAA’s

A

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)

23
Q

AAA clinical consequences

A

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)

24
Q

Size risks associated with AAAs

A

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+*
25
Q

TAAs

A

Most commonly associated with HTN

- also are associated with bicuspid aortic valve stenosis/regurgitation and Marfan syndrome

26
Q

Aortic dissection

A

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*

27
Q

Where is the most common part of origin of initial intima tear in aortic dissections

A

Ascending aorta (within 10 cm of aortic valve)

  • usually transverse or oblique
  • usually lies within the middle-outer tunica media
28
Q

Clinical symptoms of aortic dissection

A
  • 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)

29
Q

Most common cause of death for aortic dissections

A

Rupture and internal hemorrhaging into the pericardial/ peritoneal or pleural cavities

30
Q

Difference in treatment between type A and type B aortic dissections

A

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
31
Q

Physiology of the main three layers of blood vessels

A

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.

32
Q

Chylous ascites

A

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.)

33
Q

Two variants of arteriosclerosis

A

Hyaline and hyperplastic

- affects small arteries and arterioles and often caused by downstream ischemic injury

34
Q

What are the most common sites for fusiform aneurysms when they occur?

A

Aortic arch

Abdominal aorta

Iliac arteries

35
Q

Two types of clinical arteriolosclerosis

A

Hyperplastic and hyaline

Cardiology (46 decks)

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