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PATHO I > Atherosclerosis and Aneurysms > Flashcards

Atherosclerosis and Aneurysms Flashcards

1
Q

T/F: Atherosclerosis can begin in childhood with the development of fatty streaks advancing with age

A

True

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2
Q

What is the typical cause of death due to atherosclerosis?

A

Ischemic heart disease (IHD)

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3
Q

What are (2) major predictors of atherosclerosis?

A
  • HTN
  • Hypercholesterolemia
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4
Q

Describe what atherosclerosis is.

A
  • Lesions of the vascular intima called atheromas
  • Atheromas impinge on vascular lumen (stenosis) and can suddenly rupture leading to occlusion

Occlusion –> ischemia + hypoxia

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5
Q

Weakening of the tunica media due to atherosclerosis can lead to what disorder?

A

Aneurysm

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6
Q

What is the pathogenesis of atherosclerosis?

A
  • Chronic stress on endothelium leads to endothelial injury and dysfunction
  • Leads to upregulation of ICAM-1 and VCAM-1
  • Invasion of monocytes and lymphocytes through disrupted endothelial barrier
  • Platelets adhere to endothelial (vessel) wall and release mediators
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7
Q

Plaque deposition along the arterial walls leads to what type of blood flow?

A

TURBULENT

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8
Q

How is the fibrous cap created during atherosclerosis?

A
  • Platelets, macrophages, endothelial cells, and smooth muscle cells release growth factors
  • Smooth muscle cells synthesize ECM including collagen that creates the fibrous cap

This is done to stabilize plaque

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9
Q

How are fatty streaks formed during atherosclerosis?

A
  • Macrophages ingest oxidized LDL cholesterol and transform into foam cells
  • Foam cells accumulate and turn into fatty streaks (early atherosclerotic lesions)
  • Foam cells release cellular proteases and inflammatory cytokines
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10
Q

What is the basic structure of an atheromatous plaque?

A
  • Fibrous cap: macrophages (foam cells), smooth muscle cells, and collagen & eastin
  • Necrotic center: cholesterol crystals, foam cells, cell debris (garbage)
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11
Q

How do macrophages disrupt the integrity of the fibrous cap of an atheroma?

A
  • Macrophages secrete matrix metalloproteinases leading to weakning of the fibrous cap
  • This is due to breakdown of ECM via MMPs
  • Minor stress leads to fibrous cap rupture (leading to thrombus
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12
Q

What is the molecule that antagonizes (balances) the activity of MMP?

A

Tissue inhibitor of MMP (Matrix metalloproteases)

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13
Q

Dysfunctional endothelial cells express adhesion molecules that stimulate what?

A

Leukocyte adhesion

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14
Q

Macrophages that take up oxidized LDL release what chemicals?

A

Inflammatory mediators

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15
Q

CRP is a strong independent risk factor for?

A
  • MI
  • Stroke
  • PAD
  • Sudden cardiac death

Even in apparently healthy individuals

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16
Q

Role of inflammation in atherosclerosis: INF-γ

A

Activation of macrophages, endothelial cells, and smooth muscle cells

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17
Q

Role of inflammation in atherosclerosis: IL-1

A

Recruitment and activation of macrophages & T-cells

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18
Q

Role of inflammation in atherosclerosis: ROS

A

LDL oxidation (macrophages ingest oxidized LDL)

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19
Q

Role of inflammation in atherosclerosis: MMPs

A

Breakdown of Extracellular matrix (ECM)

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20
Q

Role of inflammation in atherosclerosis: Platelets, macrophages, endothelial cells, and smooth muscle cells

A
  • Secrete growth factors TGF, FGF, PDGF
  • Leads to smooth muscle cell proliferation
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21
Q

What is a proven drug that treats the inflammatory response seen in atherosclerosis? What is its MOA?

A
  • Canakinumab
  • Targets IL-1
22
Q

Compare a Stable plaque versus an Unstable plaque.

A

Stable Plaque
* Small lipid core w/ a thick fibrous cap
* Little inflammation w/o intraplaque hemorrhaging or rupture
* Reduction in blood flow during exertion

Unstable Plaque
* Large lipid core w/ a thin fibrous cap
* High inflammation w/ intraplaque hemorrhaging and rupture
* MMP –> degradation of collagen & fibrous components –> exposing of thrombogenic core –> thrombus formation and vessel occlusion

23
Q

What is an extrinsic factor on plaques that can lead to instability?

A

HTN (increased BP)

24
Q

What are the most commonly involved vessels in atherosclerosis?

A
  • Abdominal Aorta
  • Coronary Artery
  • Popliteal Artery
  • Internal Carotids
  • Circle of Willis

Abundant Corona Pops In Circles

25
Q

When does the risk of MI increase 5x?

A

Between 40-60 yo

Accumulation of vascular injury

26
Q

T/F: Estrogen therapy in post-menapausal women has been shown to decrease cardiovascular risk

A

False, it has not shown any benefit

27
Q

What age group appears to be protected from cardiovascular disease when age-matched with the other population?

A

Females

28
Q

What is the cigarette/day evaluated to increase cardiovascular mortality significantly?

A

10 cigarettes/day
* Males: 20%
* Females: 30%

29
Q

What are the (5) factors of metabolic syndrome?

A
  • HTN
  • Waistline (M: 40”; F: 35”)
  • Low HDL (M: < 40 mg/dL; F: 50 mg/dL)
  • High Tg > 150 mg/dL
  • FBG > 100 mg/dL
30
Q

What is a rare inborn error of metabolism that results in elevated levels of circulating homocysteine and is associated with premature vascular disease?

A

Hyperhomocysteinemia

31
Q

What is a hematoma?

A

Abnormal collection of blood outside of a vessel

32
Q

What are aneurysms?

A

Abnormal dilations of arteries defined as a ≥50% increase in arterial diameter compared to normal

33
Q

Compare a true aneurysm versus a false aneurysm.

A

True aneurysm
* Involves all 3 layers of artery (intima, media, adventitia)

False aneurysm
* Bulging pulsatile mass
* Local hematoma

34
Q

The infrarenal aorta relies on what to acquire nutrients?

A

Nutrient diffusion from abdominal aorta
* has a poorly developed vaso vasorum (vessels dedicated to it)

35
Q

What is the pathogenesis of aneurysms due to atherosclerosis?

A
  • Atherosclerosis leads to thickening of intima
  • Increases distance that O2 and nutrients diffuse to reach the tunica media
  • Activates macrophages leading to MMP secretion and ECM degradation
36
Q

What is the pathogenesis of aneurysms due to systemic HTN?

A
  • Systemic HTN leads to hyaline arteriosclerosis resulting in lumenal stenosis leading to decreased supply of O2 and nutrient delivery to the tunica media
  • Increased shear stress leading to endothelial injury and atherosclerosis
37
Q

What is the pathogenesis of aneurysms due to tertiary syphilis?

A
  • Tertiary syphilis leads to inflammation of vasa vasorum of the thoracic aorta leading to tunica media ischemia
  • Leads to smooth muscle cell, elastic fiber, and ECM loss
38
Q

What is the pathogenesis of aneurysms due to infections?

A
  • Microorganisms seed vessel wall
  • Suppuration and inflammation that leads to tunica media destruction causing rapid dilation and rupture of the vessel wall
39
Q

What is the pathogenesis of aneurysms due to Marfan Syndrome?

A
  • Inability to sequester endogenously produced TGF-β
  • Fragmentation of elastic lamina and fibrosis
  • Abnormal TGF-β siganling leads to defective elastin and collagen synthesis
  • Diminished ECM contents and aneurysmal dilation
40
Q

What is the pathogenesis of aneurysms due to Ehlers-Danlos Syndrome?

A

Defective Type III collagen leading to thin skin, arterial rupture and easy bruising

41
Q

Where is Type I Collagen found?

A

One BITE
* Bones
* Eyes
* Teeth
* Ears

42
Q

Where is Type II Collagen found?

A

CarTWOlage = Type II collagen

Cartilage

43
Q

Where is Type III collagen found?

A

Three = Reticulin fibers
* vessels, uterus, granulation tissue

44
Q

Where is Type IV Collagen found?

A

Four = Floor
* Basement membrane
* Lens

45
Q

When does the USPSTF recommend screening for abdominal aortic aneurysm (AAA)?

1-time screening

A

Males 65-75 yo who have smoked

46
Q

Where do abdominal aortic aneurysms typically occur?

A

Between renal arteries and the aortic bifurcation
* Decreased collagen content

47
Q

What type of inflammation characterizes abdominal aortic aneurysms?

A

Transmural inflammation

Degradation of elastin & collagen by MMP & loss of smooth muscle

48
Q

What is the sizing standard of thoracic aortic aneurysms?

A

≥3 cm

49
Q

What are some common risk factors for thoracic aortic aneurysms?

A
  • HTN, smoking, age
  • Tertiary syphilis
  • Bicuspid aortic valve
  • Connective tissue disease (e.g., Marfans; Ehlers-Danlos)
50
Q

What occurs in cystic medial degeneration?

A

Accumulation of mucopolysaccharides in the tunica media of vessels leading to a loss of muscle and elastic fibers

Non-inflammatory

51
Q

How can a thoracic aortic aneurysm present?

A
  • Respiratory or feeding difficulties due to airway or esophageal compression
  • Persistent cough from irritation of the recurrent laryngeal nerves
52
Q

How may an abdominal aortic aneurysm present?

A

During PE as a palpable, puslatile, non-tender abdominal mass

PATHO I (8 decks)

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