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Cardiovascular 2 > Vascular Injury, Arteriosclerosis, Hypertension, Aneurysm, Dissection > Flashcards

Vascular Injury, Arteriosclerosis, Hypertension, Aneurysm, Dissection Flashcards

1
Q

Structures of vascular intima

A

Endothelium + internal elastic lamina

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2
Q

Structures of vascular media

A

Smooth muscle + elastic fibers

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3
Q

See autosomal dominant polycystic kidney disease…

Think ____

A

Berry aneurysms (circle of willis)

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4
Q

3 types of congenital anomalies in vascular walls

A
  • Berry aneurysms
  • AV fistulas
  • Fibromuscular dysplasia
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5
Q

Berry aneurysms can lead to…

A

Fatal subarachnoid hemorrhage

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6
Q

Large AV fistulas can lead to…

A

High-output heart failure via L–>R shunt (increased venous return)

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7
Q

Most common cause of AV fistula

A

Developmental defect

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8
Q

Focal thickening of intima and media of medium to large muscular arteries, causing stenosis

A

Fibromuscular dysplasia

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9
Q

Young woman + renal artery stenosis

A

Fibromuscular dysplasia

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10
Q

Stimuli that can induce endothelial cell damage/activation

A
  • Turbulent flow
  • Hypertension
  • Complement, cytokines
  • Bacterial or lipid products, glycation products (DM)
  • Viruses
  • Hypoxia, acidosis
  • Tobacco smoke
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11
Q

An ACTIVATED endothelial cell does what?

A

Expresses… (thrombogenic state)

  • Adhesion molecules (inflammatory cells)
  • Pro- and anti-coagulants
  • Vasoactive and growth factors, cytokines
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12
Q

How does DM cause endothelial cell activation?

A

Glycation end-products activate endothelial cells

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13
Q

Endothelial activation vs. endothelial dysfunction

A

Activation = short-term stimulus that can be removed
Dysfunction = result of CHRONIC stimulus
- Coagulation, inflammation, smooth muscle stimulation

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14
Q

Chronic vascular injury (via any stimulus) leads to what stereotypical response? What is it?

A

INTIMAL THICKENING

  • Smooth muscle cells migrate to intima, proliferate and elaborate extracellular matrix
  • Blood flow is thus potentially affected
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15
Q

People w/ hypertention are at risk for what 5 things?

A
  • Atherosclerosis
  • Heart disease
  • Stroke
  • Renal disease
  • Aortic dissection
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16
Q

Risk factors for essential HTN (5)

A
  • High Na+ intake
  • Obesity
  • Stress
  • Smoking
  • Physical inactivity
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17
Q

2 components of blood pressure

A

Cardiac output, peripheral resistance

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18
Q

Components that affect cardiac output (5)

A
  • Sodium
  • Aldosterone
  • ANP
  • Heart rate
  • Contractility
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19
Q

Components that affect peripheral resistance (many)

A
  • Adrenergics
  • Angiotensin 2
  • PGs/LTs/Tx
  • Vasodilator substances (NO, kinins)
  • Autoregulation
  • pH
  • Hypoxia
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20
Q

MAIN regulator of blood pressure

A

RAAS system, ANP

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21
Q

Pathologic things that increase blood volume

A
  • Excess sodium intake
  • Renal failure
  • Hyperaldosteronism
  • Increased sodium reabsorption (Bartter, etc.)
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22
Q

Pathologic things that increase peripheral resistance

A
  • Increased sympathetics (pheochromocytoma)

- Increased RAAS baseline

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23
Q

Main vascular change in chronic HTN or DM

What is it?

A

Hyaline arteriolosclerosis

- Increased SM matrix –> damaged endothelium –> proteins leak into vessel wall –> vessel narrowing

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24
Q

Main vascular change in malignant HTN or DM

A

Hyperplastic arteriolosclerosis

- SM concentric hyperplasia (“onion skin”) –> vessel narrowing

25
Q

Constitutional risk factors for atherosclerosis (3)

A
  • Family history
  • Age (> 60)
  • Gender (male, post-menopause female)
26
Q

Modifiable risk factors for atherosclerosis (4)

A
  • Hyperlipidemia (high LDL, low HDL)
  • Hypertension
  • Smoking
  • DM
27
Q

Describe why high LDL and low HDL are risk factors for atherosclerosis

A

LDL takes cholesterol to vessel walls (periphery) to be stored, while HDL brings it back to be broken down

  • More LDL = more deposition
  • Less HDL = less breakdown
28
Q

How to increase HDL w/o drugs? (2)

A
  • Moderate alcohol, exercise
29
Q

How are obesity and smoking risk factors for atherosclerosis?

A

Both cause chronic immune system activation, causing vascular inflammation and endothelial damage

30
Q

Metabolic syndrome

A

Central obesity, HTN, Type-2 DM

31
Q

5 steps of atherosclerotic plaque formation

A
  1. Chronic endothelial injury (see risk factors above)
  2. Endothelial dysfunction (permeability, immune migration)
  3. Macrophage activation, SM recruitment to intima
  4. Macrophages and SM cells engulf lipids (FATTY STREAK)
  5. SM proliferation, collagen/matrix deposition, necrosis
32
Q

Contents of the necrotic core in atherosclerosis (5)

A

Foam cells, inflammatory cells, dead cells, lipids, cholesterol ester crystals

33
Q

Purpose of the fibrous cap on a plaque

A

Attempt to contain and heal the process

34
Q

The location of an atherosclerotic plaque tends to be related to what?

A

Places of TURBULANCE

35
Q

5 most common locations of atherosclerosis

A
  • Posterior abdominal aorta
  • Coronary arteries
  • Popliteal arteries
  • Internal carotid arteries
  • Circle of Willis
36
Q

Where are fatty streaks often found?

A

At ostia of vessels branching from aorta

37
Q

What is a foam cell?

A

Endothelial cell stuffed w/ cholesterol trying to metabolize it, making it CLEAR and FOAMY

38
Q

Potential consequences of atherosclerotic plaques (6)

A
  • Rupture/ulceration
  • Thrombosis –> occlusion
  • Hemorrhage (into plaque or body cavity)
  • Embolism
  • Aneurysm of vessel wall
  • Stenosis of arterial lumen
39
Q

Describe the gradual lumen stenosis from a plaque

A
  • Plaques grow over time due to injury/healing cycle
  • Eventually CRITICAL STENOSIS (70%) causes ischemia downstream
  • Get chronic ischemia of end-organs
40
Q

Organs/structures prone to ischemia from atherosclerosis

A

Myocardium, bowel, brain, extremities

41
Q

Causes of plaque rupture (3)

A
  • Increased inflammation in plaque –> weakens fibrous cap
  • Changes in blood pressure (want to keep it level)
  • Vasoconstriction
42
Q

Vulnerable vs. stable plaque

A 
Vulnerable = thin cap, likely to rupture
Stable = thick cap, unlikely to rupture
43
Q

True vs. False aneurysm

A 
True = thinned wall, ALL wall layers in tact
False = defective wall, hematoma under connective tissue
44
Q

Aneurysm vs. Dissection

A 
A = Dilation of blood vessel due to weak/broken wall
D = Splitting of muscle layer via escape/movement of blood
45
Q

Marfan syndrome

A

Defective fibrillin –> defective vascular connective tissue

46
Q

2 ways atherosclerosis can cause aneurysm

A
  • Degrade vascular wall via inflammation

- Weaken vascular wall (media) via ischemia

47
Q

See abdominal aortic aneurysm…

Think?

A

ATHEROSCLEROSIS –> vessel wall weakening

48
Q

See ascending thoracic aortic aneurysm…

Think?

A

HYPERTENTION –> outer media ischemia (vaso vasorum)

49
Q

No matter the cause, ALL aneurysms result in what w/in them?

What is it?

A

Cystic medial degeneration (disrupted and disorganized elastin and increased proteoglycans)

50
Q

Severe chest pain that radiates to back between the scapulae

A

Aortic dissection - CLASSIC PRESENTATION

51
Q

2 risk categories for aortic dissection

A
  • HYPERTENSIVE males, 40-60 (MOST COMMON)

- Marfan syndrome

52
Q

Most common location of aortic dissection

A

Ascending aorta

53
Q

See intramural hematoma…

Think?

A

Aortic dissection

54
Q

Type A (DeBakey 1) aortic dissection

A

Involves ascending aorta AND descending aorta

55
Q

Type A (DeBakey 2) aortic dissection

A

Involves ascending aorta ONLY

56
Q

Type B (DeBakey 3) aortic dissection

A

Involves descending aorta ONLY

57
Q

Most common cause of death w/ aortic dissection

A

Rupture

58
Q

Common complication of aortic dissection besides rupture

A

Occlusion of arterial branches (renal arteries, etc.)

59
Q

Treatment of aortic dissection

A

Anti-HTN therapy + surgery to repair the intimal tear

Cardiovascular 2 (20 decks)

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