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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
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

DT3- EXAM 1 (26 decks)

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