Vascular Injury, Arteriosclerosis, Hypertension, Aneurysm, Dissection Flashcards Preview

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

Flashcards in Vascular Injury, Arteriosclerosis, Hypertension, Aneurysm, Dissection Deck (59):
1

Structures of vascular intima

Endothelium + internal elastic lamina

2

Structures of vascular media

Smooth muscle + elastic fibers

3

See autosomal dominant polycystic kidney disease...

Think ____

Berry aneurysms (circle of willis)

4

3 types of congenital anomalies in vascular walls

- Berry aneurysms
- AV fistulas
- Fibromuscular dysplasia

5

Berry aneurysms can lead to...

Fatal subarachnoid hemorrhage

6

Large AV fistulas can lead to...

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

7

Most common cause of AV fistula

Developmental defect

8

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

Fibromuscular dysplasia

9

Young woman + renal artery stenosis

Fibromuscular dysplasia

10

Stimuli that can induce endothelial cell damage/activation

- Turbulent flow
- Hypertension
- Complement, cytokines
- Bacterial or lipid products, glycation products (DM)
- Viruses
- Hypoxia, acidosis
- Tobacco smoke

11

An ACTIVATED endothelial cell does what?

Expresses... (thrombogenic state)
- Adhesion molecules (inflammatory cells)
- Pro- and anti-coagulants
- Vasoactive and growth factors, cytokines

12

How does DM cause endothelial cell activation?

Glycation end-products activate endothelial cells

13

Endothelial activation vs. endothelial dysfunction

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

14

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

INTIMAL THICKENING
- Smooth muscle cells migrate to intima, proliferate and elaborate extracellular matrix
- Blood flow is thus potentially affected

15

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

- Atherosclerosis
- Heart disease
- Stroke
- Renal disease
- Aortic dissection

16

Risk factors for essential HTN (5)

- High Na+ intake
- Obesity
- Stress
- Smoking
- Physical inactivity

17

2 components of blood pressure

Cardiac output, peripheral resistance

18

Components that affect cardiac output (5)

- Sodium
- Aldosterone
- ANP
- Heart rate
- Contractility

19

Components that affect peripheral resistance (many)

- Adrenergics
- Angiotensin 2
- PGs/LTs/Tx
- Vasodilator substances (NO, kinins)
- Autoregulation
- pH
- Hypoxia

20

MAIN regulator of blood pressure

RAAS system, ANP

21

Pathologic things that increase blood volume

- Excess sodium intake
- Renal failure
- Hyperaldosteronism
- Increased sodium reabsorption (Bartter, etc.)

22

Pathologic things that increase peripheral resistance

- Increased sympathetics (pheochromocytoma)
- Increased RAAS baseline

23

Main vascular change in chronic HTN or DM

What is it?

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

24

Main vascular change in malignant HTN or DM

Hyperplastic arteriolosclerosis
- SM concentric hyperplasia ("onion skin") --> vessel narrowing

25

Constitutional risk factors for atherosclerosis (3)

- Family history
- Age (> 60)
- Gender (male, post-menopause female)

26

Modifiable risk factors for atherosclerosis (4)

- Hyperlipidemia (high LDL, low HDL)
- Hypertension
- Smoking
- DM

27

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

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

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

- Moderate alcohol, exercise

29

How are obesity and smoking risk factors for atherosclerosis?

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

30

Metabolic syndrome

Central obesity, HTN, Type-2 DM

31

5 steps of atherosclerotic plaque formation

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

Contents of the necrotic core in atherosclerosis (5)

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

33

Purpose of the fibrous cap on a plaque

Attempt to contain and heal the process

34

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

Places of TURBULANCE

35

5 most common locations of atherosclerosis

- Posterior abdominal aorta
- Coronary arteries
- Popliteal arteries
- Internal carotid arteries
- Circle of Willis

36

Where are fatty streaks often found?

At ostia of vessels branching from aorta

37

What is a foam cell?

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

38

Potential consequences of atherosclerotic plaques (6)

- Rupture/ulceration
- Thrombosis --> occlusion
- Hemorrhage (into plaque or body cavity)
- Embolism
- Aneurysm of vessel wall
- Stenosis of arterial lumen

39

Describe the gradual lumen stenosis from a plaque

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

40

Organs/structures prone to ischemia from atherosclerosis

Myocardium, bowel, brain, extremities

41

Causes of plaque rupture (3)

- Increased inflammation in plaque --> weakens fibrous cap
- Changes in blood pressure (want to keep it level)
- Vasoconstriction

42

Vulnerable vs. stable plaque

Vulnerable = thin cap, likely to rupture
Stable = thick cap, unlikely to rupture

43

True vs. False aneurysm

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

44

Aneurysm vs. Dissection

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

45

Marfan syndrome

Defective fibrillin --> defective vascular connective tissue

46

2 ways atherosclerosis can cause aneurysm

- Degrade vascular wall via inflammation
- Weaken vascular wall (media) via ischemia

47

See abdominal aortic aneurysm...

Think?

ATHEROSCLEROSIS --> vessel wall weakening

48

See ascending thoracic aortic aneurysm...

Think?

HYPERTENTION --> outer media ischemia (vaso vasorum)

49

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

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

50

Severe chest pain that radiates to back between the scapulae

Aortic dissection - CLASSIC PRESENTATION

51

2 risk categories for aortic dissection

- HYPERTENSIVE males, 40-60 (MOST COMMON)
- Marfan syndrome

52

Most common location of aortic dissection

Ascending aorta

53

See intramural hematoma...

Think?

Aortic dissection

54

Type A (DeBakey 1) aortic dissection

Involves ascending aorta AND descending aorta

55

Type A (DeBakey 2) aortic dissection

Involves ascending aorta ONLY

56

Type B (DeBakey 3) aortic dissection

Involves descending aorta ONLY

57

Most common cause of death w/ aortic dissection

Rupture

58

Common complication of aortic dissection besides rupture

Occlusion of arterial branches (renal arteries, etc.)

59

Treatment of aortic dissection

Anti-HTN therapy + surgery to repair the intimal tear