Vascular Heart Disease Flashcards

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1
Q

Describe the intimal response to vascular injury

A

Intimal thickening

  1. recruitment of smooth muscle cells to the intima (smooth muscle cells are normally only found in the media)
  2. smooth muscle cells mitosis
  3. elaboration of extracellular matrix

the thicker intima may make it more difficult for O2 and nutrients to diffuse therefore it is more prone to ischemic injury

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2
Q

Arteriosclerosis

A

Hardening of the arteries” (arterial wall thickening and loss of elasticity)

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3
Q

3 types of arteriosclerosis

A

Atherosclerosis
Monckeberg’s medial calcific sclerosis
Arteriosclerosis - hypertension induced

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4
Q

Atherosclerosis modifiable risk factors

A
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes mellitus
“Inflammation” (increased C peptide)
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5
Q

Atherosclerosis non-modifiable risk factors

A

Genetic abnormalities
Family history
Increasing age
Male gender

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6
Q

“Response to injury” hypothesis:

A

Atherosclerosis is a chronic inflammatory response of the arterial wall to endothelial injury.

Lesion progression involves interaction of lipoproteins, monocyte-derived macrophages, T lymphocytes and the cellular constituents

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7
Q

Atheroma morphology

A

forms inbetween the subendothelium and internal elastic lamina (intima process)
eccentric

fibrous cap
necrotic center

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8
Q

what are the components of the fibrous cap of an atheroma

A

smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization

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9
Q

what are the components of the center of an atheroma

A

cell debris, cholesterol crystals, foam cells, calcium

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10
Q

how is the media affected by an atheroma

A

the media begins to shrink and nearly dissapear in some areas due to lack of nutrients (cannot diffuse)

this thinning makes the media very weak, less elastic, and more vulnerable to becoming an aneurysm

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11
Q

what are possible faits of a plaque

A
Rupture/ulceration/erosion (rupture of a cap leads to thrombus formation)
Emboli
 Hemorrhage
Weakening of media – aneurysm formation
Calcification, growth, lumen occlusion
Thrombosis
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12
Q

what happens when the fibrous cap ruptures

A

platelets become exposed to the necrotic debris and basement membrane causing activation and formation of a thrombus- which further occludes the vessel and may lead to infarct and necrosis of the down stream organ

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13
Q

what do cholesterol deposits look like histologically

A

they fall out of the samples and look like open (white) spaces

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14
Q

Atherosclerosis- Complications

A

myocardial ischemia- angina, infarcts, sudden death

cerebral ischemia- stroke, TIA

Peripheral vascular Dz- claudication, gangrene

aneurysms- rupture

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15
Q

Monckeberg’s Medial 
Calcific Sclerosis

A

Calcifium deposits
In the MEDIA
Medium sized muscular arteries
NONobstructive

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16
Q

what are the 2 types of Hypertension Induced Arteriosclerosis

A

Hyaline arteriolosclerosis

Hyperplastic arteriolosclerosis

17
Q

Hyaline arteriolosclerosis

A

Arterioles

Hemodynamic stress- due to long term hypertension which causes fenestrations and plasma proteins are able to leak into wall of the vessel

Plasma protein leakage
Homogeneous pink hyaline thickening (histologically)
Lumenal narrowing

18
Q

Hyperplastic arteriolosclerosis

A
  • Severe acute blood pressure elevation (200s)
  • Onion skin concentric thickening
  • Smooth muscle cells with thickened, reduplicated membranes
  • Progressive lumenal narrowing
19
Q

what is an aneurysm

A

Localized abnormal dilatation of a blood vessel

20
Q

what is a false aneurysm

A

looks like the wall is pouching out but there was an injury to the wall of the blood vessel and now blood from the lumen is getting caught by the extravascular / external part of the blood vessel

21
Q

what leads to aneurysms

A

Poor intrinsic quality of vascular wall connective tissue
• Marfan Syndrome (defective synthesis fibrillin; loss of elastic tissue)
• Ehlers Danlos (defective type III collagen)

Weakened vascular wall through loss of smooth muscle cells or inappropriate synthesis of extracellular matrix
• Ischemia (Atherosclerosis,HTN, syphillis)
• Histology - Cystic medial degeneration

Altered balance of collagen degradation and synthesis
• Local inflammatory infiltrates
• Destructive proteolytic enzymes (Matrix metalloproteinases)

22
Q

Cystic Medial Degeneration

A

*elastin fragmentation
loss of smooth muscle cells
leading to areas resembling “cystic” spaces
weakens the blood vessel

the media normally has a very regular pattern of elastin with smooth muscle in between.

23
Q

causes of aneurysms

A
Atherosclerosis
HTN
Congenital defects
Inflammation
Infections
Vasculitis
Trauma
24
Q

Abdominal Aortic Aneurysm etiology/pathogenesis

A
  • End result of a multifactorial process leading to the destruction of aortic wall connective tissue
  • Matrix metalloproteinasis play a key role
25
Q

affects of atherosclerosos in AAA

A

Compresses media
Compromises nutrient and waste diffusion from vascular lumen into arterial wall
Media undergoes degeneration and necrosis
Arterial wall weakness and thinning

26
Q

pts at higher risk for AAA

A

men, who smoke, over 50 y/o

27
Q

Complications of an AAA

A

Compression/Obstruction/Embolism

Rupture

28
Q

when should you screen for an AAA

A

screen every man who has ever smoked at least once in their life

29
Q

syphilis’ affect on the aorta

A

in tertiary syphilis - lots of chronic inflammatory cells and cytokines secreted. Vaso vasorum is injured and the wall is weakened

intima becomes wrinkly like tree bark
can lead to aortic regurgitation

30
Q

Aortic Dissection

A

Blood splays apart laminar planes of the media to form a blood filled channel within the aortic wall

the intima tears and blood can enter the wall (not limited to luminal blood flow)

31
Q

causes of aortic dissections

A

HTN
Pressure related mechanical or ischemic injury
Medial hypertrophy of vasovasorum
Degenerative changes of media, loss of smooth muscle cells

Connective tissue disorders
Abnormal vascular extracellular matrix

Bicuspid aortic valves

32
Q

type A dissections

A

involve the ascending/proximal aorta (may or may not involve the descending aorta also)

33
Q

type B dissections

A

do not involve the proximal aorta

34
Q

how does an aortic dissection present

A

Sudden onset ripping chest pain radiating to back

stabbing feeling and sometimes can be felt ripping downward

35
Q

treatment of an aortic dissection

A

Medical tx – Blood pressure control (can decrease propagation)

Surgical tx (type A need to be repaired immediately but type B may or may not need surgery)