Vascular Disease 1- Leah (6)- Arteriosclerosis* Flashcards Preview

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Flashcards in Vascular Disease 1- Leah (6)- Arteriosclerosis* Deck (53):
1

List the three layers of an arterial wall.
What are they comprised of?

1) intima, made up of endothelium (blood/ tissue barrier)
2)Media, made up of Muscle "M"
3) Adventitia, made up of CT, nerves, vasa vasorum
*adventitia is outermost*

2

Describe the function of the vasa vasorum:

Supplies blood to the outer 1/2 --> 2/3 of a vessel

3

List the four types of arteries:

1. elastic
2. muscular
3. small arteries (less than 2mm diameter)
4. arterioles

4

Describe elastic artery properties.
Which arteries are classified as elastic?

-Large arteries that actively expand and contract (recoil) at systole and diastole
-Elastic, hence rich in elastic tissue
-Aorta and its large braches are elastic

5

Describe muscular arteries.
Which arteries are classified as muscular?

-rich in smooth muscle
1. smaller aortic branches (carotids)
2. coronary
3. renal vessels

6

Function of arterioles:

-maintain TPR
-transition blood from pulsatile --> steady state as enters capillary bed
-reduce pressure and velocity of blood

7

Describe makeup of capillaries: wall, diameter, xs surface area?

-made up of intima/ endothelial cells only
(lacks adventitia and media)

-diameter of a single RBC
(smallest individual vessel types)

-largest overall cross sectional area of all vessel tpyes

8

Preferred site of inflammation in vasculature?

post capillary venules

9

Describe structure of veins: lumen? wall thickness? special features?

-large lumens
-thin walls
-have valves to direct flow (loss of valves = venous insufficiency/ varicose veins)

10

Describe structure of wall (1) and function of lymphatic vessels (3):

- Thin walled, endothelium lined
- Fxn: drain interstitial fluid
-disseminate disease*
-play a role in edema*

11

Normal function of endothelial cells in vessels (5):

-prevent thrombosis (maintain blood/ tissue interface)
-metabolize hormones
-regulate immune/ inflammatory processes
-modulate resistance
-affect growth of other cells (mostly SMCs)

**Most "biochemically" active vascular cells**

12

Normal function of SMCs in vessels (3):

***VASCULAR REPAIR:
-synthesize ECM/ CT***
-migration/ proliferation
-contraction/ dilation

**Most "physically" active vascular cells.

13

How might tight endothelial junctions be loosened in the vasculature (2)?
What is the result?

-HTN or HISTAMINE most commonly loosen tight junctions.
-Result: EDEMA--> loss of leukocytes, proteins, and/or electrolytes

14

Basic definition of activation and dysfunction of endothelial cells:

Gaining some inducible property
(activation - good property; dysfunction- bad property)
*Not easy to distinguish the two processes, not testable

15

Describe abilities that an endothelial cell may gain during activation (4)

-production of adhesive molecule
-cytokines
-coagulants/ anticoagulants
-vasoactivators etc.

16

Describe abilities that an endothelial cell may gain during dysfunction:

adhesive/ thrombogenic properties

17

List three disease processes that involve endothelial cell dysfunction:

1) Hypertension
2) Thrombus
3) Atherosclerosis

18

Describe three events that may lead to vascular smooth muscle injury:

1. mechanical (angioplasty)
2. immunologic (i.e. transplant arteriosclerosis)
3. multifactoral (atherosclerosis)

19

"neointimal formation" may be used to describe?

"new intima" --> intimal thickening; a response to injury

20

Result of intimal thickening:

some stenosis and occlusion, but less so than atherosclerosis

21

What are three steps of intimal thickening after injury is induced?

1) recruitment of SM--> intima either from adjacent tissue or circulating precursors
2) SMC mitosis and proliferation
3) SMC elaborate intimal ECM; create new CT

22

Compare and contrast SMCs in normal vasculature vs during intimal thickening

-During intimal thickening, SMCs are in a *PROLIFERATIVE* state, located in the intima
-In a normal vessel, SMCs are in a *CONTRACTILE* state, located in the media

23

Define arteriOsclerosis.
What are three types?

"Hardening of the arteries"- blanket term that includes:
1- atherosclerosis
2- arteriOLOsclerosis
3- Monckeberg medial sclerosis

24

Arteriolosclerosis effects what vessels?
What are the causes of arteriolosclerosis?

-small arteries and aterioles (usually renal)
-caused by HTN and DM

25

What are two types of arteriOLOsclerosis?
What are their causes?

-HYALINE
(mild chronic HTN, DM)

-HYPERPLASTIC thickening/ onion skinning
(malignant hypertension)

26

Monckeberg medial stenosis:
What is it and in what population is it observed?

- benign ring calcifications found in muscular arteries
- media layer
- elderly population
- may be palpable or visible on Xray (pipestem appearance)
- Does NOT lead to occlusion of vessels

*Common benign finding on mammogram*

27

Cause of 50% deaths in the western world?

atherosclerosis

28

Atherosclerosis effects what types of arteries?
Arteriolosclerosis?

Who gets atherosclerosis?

-Atherosclerosis = elastic and muscular
-ArteriOLOsclerosis = aterioles and small arteries

*Old men + post menopausal women, esp w. genetic risk*

29

Function of LDL and HDL

LDL (bad): transports cholesterol to tissue
HDL (good): transports cholesterol out of tissue and into the liver for biliary excretion

30

Dietary way to reduce LDL

Omega-3-FAs, statins

31

Surpising way to
1)lower
2)increase
HDL:

-EtOH may INCREASE GOOD FAT/HDL!! (Yay beer!)
-Statins may decrease HDL

32

By how much does smoking increase the risk of Ischemic HD? HTN? DM?

smoking 1 ppd- doubles IHD risk
HTN- increasesd IHD risk by 60%
DM- doubles risk of MI (induces hypercholesterolemia)

33

How is inflammation related to atherosclerosis?

-Along with cholesterol, it leads to plaque formation
(^MMP-->Destabilize plaque--> rupture--> ^ disease)
-CRP* (acute phase reactant) levels are indicative of MI, stroke, and PVD risk

34

How is hyperhomocystinuria related to atherosclerosis (3)?

-assc with CAD, PVD, stroke like inflammation

35

How is metabolic syndrome (prediabetes/ biscuit poisoning) related to atherosclerosis (3)?

Induces:
-HTN
-dislipidemia
-proinflammatory state

36

Major hypothesis for the pathogenesis of atherosclerosis:

"response to injury hypothesis"

(Chronic inflammatory and healing response of arterial wall to endothelial injury)

37

Three general steps of plaque formation:

HTN, hypercholesteremia, or hyperglycemia-->

1. ENDO INJURY-->

2. VASCULAR PERMEABILITY + LEUKOCYTE ADHESION-->

3. FAT ACCUMULATION + THROMBOSIS

38

6 detailed steps of plaque formation

1) VASCULAR PERM--> lipoproteins enter vessel intima

2) MONOCYTES enter intima and subendothelium

3) MONOCYTES convert to MQs --> FOAM CELLS

4) PLATELETS stick to endothelium + recruit SMC

5) SMCs proliferate + produce ECM

6) LIPIDS (cholesterol/ esters) continue to accumulate in ECM and within cells

39

Where are plaques most commonly observed?

ostia of branching vessels due to turbulence

40

What are fatty streaks?

-earliest atherosclerotic plaques
-seen as early as age 1yoa and always by 10yoa
-composed of only foam cells in the intima of vessels

41

three
layers of a mature plaque:

-intima (thickened)
-fibrous cap
-necrotic center/ lipid core
**media uneffected by disease process**

42

What does a plaque contain (cells, fat, ECM)?

-Cells: SMCs, MQs, T cells = chronic inflammation
-Fat: cholesterol and cholesterol esters
-ECM: fibrin, proteoglycans, CT

43

What is the fibrous cap of a plaque made up of (3)?

SMCs, collagen, inflammatory cells

44

Top five sites for atherosclerotic plaque

#1: abdominal aorta
2-coronaries
3-popliteal
4-internal carotids
5-circle of willis

45

Four plaque "change" types:

1. acute (which consists of three subtypes)
2. massive calcification/patchy (loss of elasticity)
3. aneurysm (plaque weakens wall)
4. atheroembolism (possible infarct)

46

What are the three acute changes assc with plaque formation?

1. RUPTURE/ fissure
(releases plaque contents --> thrombosis)
2. EROSION/ ulceration
(exposes plaque BM --> thrombosis)
3. HEMORRHAGE into plaque (expands volume)

47

What makes plaque hemorrhage possible?

neovascularization at plaque shoulders

48

Describe CRITICAL stenosis and 4 consequences:

-small artery occlusion--> O2 demand>>>O2 supply--> INTERMITTENT PROCESSES:
-angina (AT LEAST 70% occlusion)
-claudication
-chronic ischemic disease
-bowel ischemia

49

What is the most common cause of MI

thrombosis caused by plaque rupture or erosion

50

How does vasoconstriction contribute to ischemic injury?

- may be a response to ruptured plaques
- can cause a partial occlusion-->complete occlusion

51

Describe vulnerable plaques that are likely to undergo acute changes:
What makes them so vulnerable?
Do they typically cause critical stenosis?
Why are they clinically important?

-THIN fibrous cap + THICK necrotic center*--> ^MMPs + Inflammation--> ^ Likelihood rupture

-Usually DO NOT cause critical stenosis--> ASYMPTOMATIC until rupture--> unexpected EMERGENCY

**common cause unexpected/sudden cardiac death is rupture of previously non-critical plaque**

52

4 Important modifiable risk factors for atherosclerosis:

1. Hyperlipidemia
2. HTN
3. Cigarette smoking
4. DM

53

Two types of cells that can become "foamy":

SMC, MQs