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DT3- EXAM 1 > Vascular Disease 1- Leah (6)- Arteriosclerosis* > Flashcards

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

1
Q

List the three layers of an arterial wall.

What are they comprised of?

A

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*

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2
Q

Describe the function of the vasa vasorum:

A

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

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3
Q

List the four types of arteries:

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

Describe elastic artery properties.

Which arteries are classified as elastic?

A
  • 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
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5
Q

Describe muscular arteries.

Which arteries are classified as muscular?

A
  • rich in smooth muscle
    1. smaller aortic branches (carotids)
    2. coronary
    3. renal vessels
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6
Q

Function of arterioles:

A
  • maintain TPR
  • transition blood from pulsatile –> steady state as enters capillary bed
  • reduce pressure and velocity of blood
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7
Q

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

A

-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

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8
Q

Preferred site of inflammation in vasculature?

A

post capillary venules

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9
Q

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

A
  • large lumens
  • thin walls
  • have valves to direct flow (loss of valves = venous insufficiency/ varicose veins)
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10
Q

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

A
  • Thin walled, endothelium lined
  • Fxn: drain interstitial fluid
  • disseminate disease*
  • play a role in edema*
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11
Q

Normal function of endothelial cells in vessels (5):

A
  • 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

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12
Q

Normal function of SMCs in vessels (3):

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

**Most “physically” active vascular cells.

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13
Q

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

A
  • HTN or HISTAMINE most commonly loosen tight junctions.

- Result: EDEMA–> loss of leukocytes, proteins, and/or electrolytes

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14
Q

Basic definition of activation and dysfunction of endothelial cells:

A

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

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15
Q

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

A
  • production of adhesive molecule
  • cytokines
  • coagulants/ anticoagulants
  • vasoactivators etc.
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16
Q

Describe abilities that an endothelial cell may gain during dysfunction:

A

adhesive/ thrombogenic properties

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17
Q

List three disease processes that involve endothelial cell dysfunction:

A

1) Hypertension
2) Thrombus
3) Atherosclerosis

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18
Q

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

A
  1. mechanical (angioplasty)
  2. immunologic (i.e. transplant arteriosclerosis)
  3. multifactoral (atherosclerosis)
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19
Q

“neointimal formation” may be used to describe?

A

“new intima” –> intimal thickening; a response to injury

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20
Q

Result of intimal thickening:

A

some stenosis and occlusion, but less so than atherosclerosis

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21
Q

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

A

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

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22
Q

Compare and contrast SMCs in normal vasculature vs during intimal thickening

A
  • 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
Q

Define arteriOsclerosis.

What are three types?

A

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

24
Q

Arteriolosclerosis effects what vessels?

What are the causes of arteriolosclerosis?

A
  • small arteries and aterioles (usually renal)

- caused by HTN and DM

25
Q

What are two types of arteriOLOsclerosis?

What are their causes?

A

-HYALINE
(mild chronic HTN, DM)

-HYPERPLASTIC thickening/ onion skinning
(malignant hypertension)

26
Q

Monckeberg medial stenosis:

What is it and in what population is it observed?

A
  • 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
Q

Cause of 50% deaths in the western world?

A

atherosclerosis

28
Q

Atherosclerosis effects what types of arteries?
Arteriolosclerosis?

Who gets atherosclerosis?

A
  • Atherosclerosis = elastic and muscular
  • ArteriOLOsclerosis = aterioles and small arteries

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

29
Q

Function of LDL and HDL

A

LDL (bad): transports cholesterol to tissue

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

30
Q

Dietary way to reduce LDL

A

Omega-3-FAs, statins

31
Q

Surpising way to
1)lower
2)increase
HDL:

A
  • EtOH may INCREASE GOOD FAT/HDL!! (Yay beer!)

- Statins may decrease HDL

32
Q

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

A

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

33
Q

How is inflammation related to atherosclerosis?

A

-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
Q

How is hyperhomocystinuria related to atherosclerosis (3)?

A

-assc with CAD, PVD, stroke like inflammation

35
Q

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

A

Induces:

  • HTN
  • dislipidemia
  • proinflammatory state
36
Q

Major hypothesis for the pathogenesis of atherosclerosis:

A

“response to injury hypothesis”

Chronic inflammatory and healing response of arterial wall to endothelial injury

37
Q

Three general steps of plaque formation:

A

HTN, hypercholesteremia, or hyperglycemia–>

  1. ENDO INJURY–>
  2. VASCULAR PERMEABILITY + LEUKOCYTE ADHESION–>
  3. FAT ACCUMULATION + THROMBOSIS
38
Q

6 detailed steps of plaque formation

A

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
Q

Where are plaques most commonly observed?

A

ostia of branching vessels due to turbulence

40
Q

What are fatty streaks?

A
  • earliest atherosclerotic plaques
  • seen as early as age 1yoa and always by 10yoa
  • composed of only foam cells in the intima of vessels
41
Q

three

layers of a mature plaque:

A
  • intima (thickened)
  • fibrous cap
  • necrotic center/ lipid core
  • *media uneffected by disease process**
42
Q

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

A
  • Cells: SMCs, MQs, T cells = chronic inflammation
  • Fat: cholesterol and cholesterol esters
  • ECM: fibrin, proteoglycans, CT
43
Q

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

A

SMCs, collagen, inflammatory cells

44
Q

Top five sites for atherosclerotic plaque

A 
#1: abdominal aorta
2-coronaries
3-popliteal
4-internal carotids 
5-circle of willis
45
Q

Four plaque “change” types:

A
  1. acute (which consists of three subtypes)
  2. massive calcification/patchy (loss of elasticity)
  3. aneurysm (plaque weakens wall)
  4. atheroembolism (possible infarct)
46
Q

What are the three acute changes assc with plaque formation?

A
  1. RUPTURE/ fissure
    (releases plaque contents –> thrombosis)
  2. EROSION/ ulceration
    (exposes plaque BM –> thrombosis)
  3. HEMORRHAGE into plaque (expands volume)
47
Q

What makes plaque hemorrhage possible?

A

neovascularization at plaque shoulders

48
Q

Describe CRITICAL stenosis and 4 consequences:

A
  • small artery occlusion–> O2 demand»>O2 supply–> INTERMITTENT PROCESSES:
  • angina (AT LEAST 70% occlusion)
  • claudication
  • chronic ischemic disease
  • bowel ischemia
49
Q

What is the most common cause of MI

A

thrombosis caused by plaque rupture or erosion

50
Q

How does vasoconstriction contribute to ischemic injury?

A
  • may be a response to ruptured plaques

- can cause a partial occlusion–>complete occlusion

51
Q

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?

A
  • 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
Q

4 Important modifiable risk factors for atherosclerosis:

A
  1. Hyperlipidemia
  2. HTN
  3. Cigarette smoking
  4. DM
53
Q

Two types of cells that can become “foamy”:

A

SMC, MQs

DT3- EXAM 1 (26 decks)

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