Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular > Endothelium, Plaque Rupture, and Vascular Injury > Flashcards

Endothelium, Plaque Rupture, and Vascular Injury Flashcards

1
Q

Normal endothelium is ______, ______, and ______.

A

anti-inflammatory, anti-thrombotic, and vasodilatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

While there are different mechanisms of ischemia depending on the vascular bed, all of them involve ______.

A

Endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is endothelium?

A

A tissue consisting of a single layer of cells that lines the blood and lymph vessels, heart, and some other cavities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Is endothelium the same between arteries, capillaries, veins, and lymphatics?

A

No, there are differences.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 layers of normal artery wall?

A

Tunica intima, tunica media, tunica adventitia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is in normal tunica intima?

A

Endothelium and thin layer of connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is in normal tunica media?

A

Smooth muscle cells and connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is normal tunica adventitia?

A

Loose connective tissue. Gives structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in pathologic tunica media?

A

There is dysfunctional smooth muscle and excess connective tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does artery composition depend on level of artery?

A

Large arteries - more elastin (more recoil) Smaller arteries - more collagen Arterioles - more smooth muscle (because arterioles control vascular resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are 5 characteristics of normal endothelial cells?

A
  1. Impermeable to large molecules 2. Anti-inflammatory 3. Resist leukocyte adhesion 4. Promote vasodilation 5. Resist thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 5 characteristics of abnormal/activated endothelial cells?

A
  1. Increased permeability 2. Increased inflammatory cytokines 3. Increased leukocyte adhesion molecules 4. Decreased vasodilatory molecules 5. Decreased antithrombotic molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are 3 characteristics of normal smooth muscle cells?

A
  1. Normal contractile function 2. Maintain extracellular matrix 3. Contained in medial layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are 3 characteristics of abnormal/activated smooth muscle cells?

A
  1. Increased inflammatory cytokines 2. Increased extracellular matrix synthesis 3. Increased migration and proliferation into subintima (behaves like cancer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What was the first gas to be discovered as a signaling molecule in the body?

A

NO (nitric oxide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is nitric oxide made and what enzyme makes it?

A

Endothelial cell, nitric oxide synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the does nitric oxide synthase convert into NO?

A

L-arginine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the cofactors used for converting L-Arginine into NO?

A

BH4, NADPH, Calmodulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does eNOS stand for?

A

Endothelial nitric oxide synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where is eNOS expressed?

A

Luminal side of endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are 5 stimuli that eNOS responds to?

A
  1. Acetylcholine 2. Serotonin 3. Thrombin 4. Bradykinin 5. Shear Stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Once NO is made in endothelium, where can it diffuse to?

A

Diffuses into smooth muscle in tunica media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does NO do in the vascular smooth muscle cell?

A

cGMP-mediated vasodilation GTP -> cGMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In disease states with decreased NO and presence of oxidative stress, what can happen via cascade and activation of genes?

A

In these states, signaling cascades can trigger inflammatory genes to be expressed which up regulates mRNA for creation of inflammatory proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Some of the up-regulated inflammatory proteins from decreased NO and presence of oxidative stress allow for circulating monocytes to attach. What are these 3 proteins?

A

Selectins, cell adhesion molecules, and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are selectins?

A

Selectins are proteins on the luminal side of endothelial cells that allow attachment of circulating monocytes (margination) so that they can enter the vessel wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are foam cells?

A

They are macrophages that have engulfed LDL lipoproteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do monocytes trigger formation of atherosclerotic plaque once entering the sub-endothelial space?

A
  1. Monocytes enter sub endothelial space and turn into macrophages 2. Macrophages engulf LDL and turn into foam cells 3. Foam cells are active in secreting cytokines which changes the phenotype of smooth muscle cells which causes them to start acting malignant, trigger apoptosis, trigger fibrosis, and trigger ongoing inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Foam cells actively secrete cytokines. What 4 things are triggered?

A
  1. Smooth muscle activation/migration/malignancy 2. Apoptosis 3. Fibrosis 4. Ongoing inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 3 general stages of atherosclerotic plaque progression?

A
  1. Fatty streak 2. Plaque progression 3. Plaque disruption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the fatty streak stage of atherosclerotic plaque? (4 things)

A

Endothelial dysfunction, lipoprotein entry and modification, leukocyte recruitment, foam cell formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the plaque progression stage of atherosclerotic plaque? (2 things)

A

Smooth muscle cell migration, altered matrix synthesis and degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the plaque disruption stage of atherosclerotic plaque? (2 things)

A

Disrupted plaque integrity, thrombus formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

T lymphocytes can trigger foam cells to create Matrix Metalloproteinase. What does MMP do?

A

MMP degrades the fibrous cap in atherosclerotic plaque which makes the plaques unstable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Activated (abnormal) smooth muscle cells can express ____ and ____ which form the fibrous cap.

A

Collagen and elastin. These make the ECM that forms the fibrous cap.

36
Q

What is the danger of plaque rupture?

A

The lipid core of plaques is composed of highly thrombotic components. When plaques rupture, clot formations happen.

37
Q

What are 5 characteristics of a stable plaque?

A
  1. Rich in fibrous tissue 2. Calcified 3. Less lipid content 4. Less inflammation 5. Less apoptosis
38
Q

____ plaques are less likely than ____ plaques to rupture and cause thrombotic events.

A

Stable, vulnerable

39
Q

What are 5 characteristics of vulnerable plaques?

A
  1. Less fibrous tissue 2. Less calcified 3. More lipid content (more LDL, foam cells) 4. More inflammation 5. More apoptosis
40
Q

What are two different outcomes of a ruptured plaque? both with serious consequences

A
  1. Acute MI 2. Healed rupture causes severely narrowed lumen and fibrous tunica intima
41
Q

How does normal endothelium regulate thrombosis? Name 3 examples and what they do

A

The endothelium regulates thrombosis through surface molecules and secreted molecules. These include: Heparin sulfate (expressed on endothelium surface) which inhibits thrombin. NO (secreted by endothelium) which inhibits platelet activation Prostacyclin (secreted by endothelium) which inhibits platelet activation

42
Q

The degree of _____ dysfunction is further progressed by _____ (unique to patients).

A

endothelial dysfunction, risk factors

43
Q

What are 5 different mechanisms of ischemia?

A
  1. Narrowing of vessel by fibrous plaque 2. Plaque ulceration or rupture 3. Intraplaque hemorrhage 4. Peripheral emboli 5. Weakening of vessel wall
44
Q

What is the mechanism of ischemia for Embolic Stroke?

A

Peripheral emboli

45
Q

What is the mechanism of ischemia for Thrombotic Stroke?

A

Plaque ulceration or rupture, intraplaque hemorrhage

46
Q

What is the mechanism of ischemia for Myocardial Ischemia?

A

Narrowing of vessel by fibrous plaque

47
Q

What is the mechanism of ischemia for Unstable Angina?

A

Plaque ulceration or rupture, intraplaque hemorrhage

48
Q

What is the mechanism of ischemia for Myocardial Infarction?

A

Plaque ulceration or rupture, intraplaque hemorrhage

49
Q

What is the mechanism of ischemia for Atheroembolic Renal Disease?

A

Peripheral emboli

50
Q

What is the mechanism of ischemia for Renal Artery Stenosis?

A

Narrowing of vessel by fibrous plaque

51
Q

What is the mechanism of ischemia for Aneurysms?

A

Weakening of vessel wall

52
Q

What is the mechanism of ischemia for Limb Claudication?

A

Narrowing of vessel by fibrous plaque

53
Q

What is the mechanism of ischemia for Limb Ischemia?

A

Narrowing of vessel by fibrous plaque, peripheral emboli

54
Q

What is the mechanism of ischemia for Raynaud’s Phenomenon?

A

Vasospasm in the presence of cold

55
Q

What is a common site of atheroembolization for stroke events?

A

Carotid bifurcation lesion The source lesion does not need to be obstructive. Bits can break off and travel to cause stroke

56
Q

What artery can be blocked by embolus (typically from carotid bifurcation lesion) to cause temporary or permanent blindness in one eye?

A

Ophthalmic artery

57
Q

What is a common site of thromboembolization for stroke events?

A

Left atrial appendage (setting of atrial fibrillation)

58
Q

Why is it important to recognize the difference between thromboembolization and atheroembolization?

A

The treatment is different. For thromboembolization (e.g. left atrial appendage thromboembolization from atrial fibrillation), you can use anti-coagulants. For atheroembolization, you need to treat the atherosclerosis.

59
Q

While _____ and _____ are both manifestations of CAD, vascular pathology is different.

A

Myocardial infarction, chronic stable angina

60
Q

What is the vascular pathology of myocardial infarction? and why is this a dangerous killer?

A

Ruptured plaque, in-situ thrombosis, not necessarily obstructive prior to rupture. This is particularly dangerous because patients can have plaques that are asymptomatic but when they rupture it causes MI and possibly leading to death.

61
Q

What is the vascular pathology of angina?

A

Stable, obstructive plaques (>70% diameter reduction). Fixed obstruction leads to lack of O2 delivery which results in angina.

62
Q

Are myocardial infarctions all of the same severity?

A

NO

63
Q

What is the flow of events of a Myocardial Infarction that can be stabilized and treated?

A

Plaque rupture -> non-occlusive thrombosis -> some flow but intermittent occlusion or embolization -> stabilize with anticoagulation/vasodilators

64
Q

What is the flow of events for a Myocardial Infarction that cannot be stabilized?

A

Plaque rupture -> occlusive thrombus -> no flow -> clinical emergency -> recanalize

65
Q

What is a sequela(e)?

A

A sequela is a pathological condition resulting from a disease, injury, therapy, or other trauma

66
Q

What is the most benign outcome of a coronary thrombus from ruptured coronary plaque? What kind of patients are more likely to have these benign events?

A

The most benign outcome is when the thrombus is small and non-flowlimiting. In these cases, there are no ECG changes and the case is resolved with healing and plaque enlargement. The plaque enlargment results in a more severe stenosis of the site.

Patients that are more likely to have these benign events probably have their risk factors well managed (not smoking, treating hypertension, controls diabetes, aspirin to limit thrombosis, etc)

67
Q

What 2 diagnosis can you arrive at with a partially occlusive thrombus? What finding allows you to differentiate between the 2 diagnosis?

A

Partially occlusive thrombus causes unstable angina or non-ST-segment elevation MI. On ECG, these BOTH have ST segment depression and/or T wave inversion.

Unstable angina shows negative for serum biomarkers (troponin).

Non-ST-segment elevation MI shows positive for serum biomarkers (troponin).

68
Q

TRUE or FALSE: Partially occlusive thrombus events (unstable angina or non-st-segment elevation MI) are not urgent.

A

FALSE! These are urgent events. You typically aim to do angiogram and revascularization within 24 hours.

69
Q

What is the most severe outcome of ruptured coronary plaque causing coronary thrombus? How is it diagnosed?

A

Occlusive thrombus causing ST-segment elevation MI.

Manifests as unrelenting chest discomfort. On ECG, ST elevation occurs and Q waves appear later. Positive serum biomarkers (troponin)

70
Q

What is the proper response to an ST-segment elevation MI?

A

These are emergencies! You need to try to get the artery unobstructed within 90 minutes. Typically done with angioplasty (mechanical) or thrombolytic (pharmaceutical).

71
Q

_____ and _____ are manifestations of peripheral arterial disease but their underlying endothelial pathology differs.

A

Claudication, acute limb ischemia

72
Q

What is the vascular pathology of claudication?

A

Similar/same as angina.

Obstructive, stable plaque. (>70% diameter reduction)

73
Q

What is the vascular pathology of acute limb ischemia?

A

Acute event obstructs blood flow without prior development of collaterals. Could be atheroembolization or thromboembolization. Rarely in-situ thrombosis.

74
Q

Are stable or unstable plaques more biologically active?

A

Unstable

75
Q

What kind of plaque (stable or unstable) cause angina and claudication (exertional ischemia)?

A

Stable plaques

76
Q

What kind of plaques are less likely to cause thrombotic and embolic events?

A

Stable plaques

77
Q

What kind of plaque (stable or unstable) causes MI and stroke?

A

Unstable

78
Q

TRUE or FALSE: Venous thrombosis and arterial thrombosis have different vascular pathology.

A

TRUE

79
Q

What are two issues caused by venous thromboembolic disease?

A

Deep Venous Thrombosis, Pulmonary Embolism

80
Q

What 6 factors are characteristic of venous thrombosis (in comparison to arterial thrombosis)?

A
  1. Fibrin rich
  2. More RBC
  3. Areas of Stasis
  4. Genetic predisposition
  5. Environmental predisposition (plane for 20 hours, or just had knee surgery and immobile in bed)
  6. Treated with anticoagulation
81
Q

What 5 factors are characteristic of arterial thrombosis (in contrast to venous thrombosis)?

A
  1. Platelet rich
  2. Plaque rupture
  3. Areas of high flow
  4. Atherosclerosis, trauma, Anti Phospholipid Antibody Syndrome (acquired)
  5. Focus more on antiplatelet therapy
82
Q

What’s the difference between Primary and Secondary Raynaud’s Phenomenon?

A

Primary is more common in younger people and is not associated with other disorder/disease/tissue loss.

83
Q

What are vasospastic disorders?

A

These are disorders where endothelium is dysfunctional but not necessarily with thrombosis or atherosclerosis.

84
Q

What is an example of a vasospastic disorder?

A

Raynaud’s Phenomenon

85
Q

What is Raynaud’s Phenomenon?

A

It is a disorder where there is excessively decreased blood flow to fingers, toes, and occasionally other areas during times of high stress or cold temperature.

Cardiovascular (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions