Endothelium Flashcards

1
Q

Components of intima, media and adventitia

A

intima: endothelium + thin layer of CT. Media: vascular smooth muscle and Ct. Adventitia: loose CT

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2
Q

Compare large arteries, small arteries and arterioles (composition)

A

Large arteries – more elastin. Smaller arteries – more collagen. Arterioles – more smooth muscle
Large arteries – more elastin. Smaller arteries – more collagen. Arterioles – more smooth muscle

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3
Q

Compare normal vs activated endothelial cell functions

A

Normal: impermeable, anti-inflammatory, resists leukocyte adhesion, promotes vasodilation, resists thrombosis. Activated: increased permeability, increased inflammatory cytokines, increased leukocyte adhesion molecules, increased vasodilatory molecules, increased antithrombotic molecules

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4
Q

Where is NO produced and what does it do

A

NO synthase is expressed on luminal side of endothelium and makes NO from Arginine. NO diffuses to smooth muscle cells inmedia and causes cGMP mediated vasodilation. Decreased NO causes inflammatory state

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5
Q

Inflammatory molecules in vasculature

A

selectins (bind to leukocytes), Cell adhesion molecules, cytokines

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6
Q

Steps in formation of atherosclerotic plaque

A

LDL crosses the vascular endothelium > LDL is oxidized > cytokines are released > Monocytes differentiate into macrophages and cross the vascular endothelium > macrophages take up LDL (become foam cells > smooth muscle cells are activated and migrate to foam cell > apoptosis, fibrosis and ongoing inflammation occur

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7
Q

Stable vs vulnerable plaques

A

stable plaque: Rich in fibrous tissue, Calcified, Less lipid content, Less inflammation, Less apoptosis. Unstable plaque: Less fibrous tissue, Less calcified, More lipid content, More inflammation, More apoptosis

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8
Q

What can happen when a plaque ruptures?

A

Thrombus formation can occur, and the rupture will either heal with a narrowed lumen or acute MI occurs

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9
Q

Where does regulation of thrombosis occur?

A

endothelium- molecules are expressed on the surface or secreted by endothelial cells (ie. Heparan/ thrombin, NO/platelet activation, prostacyclin)

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10
Q

Risk factors for coronary atherosclerosis

A

HTN, hyperlipidemia, smoking, diabetes, age

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11
Q

For each of the following events, what is the mechanism of ischemia? Stroke, MI, angina, claudication, acute limb ischemia, pulmonary embolism, Raynauds phenomenon

A

Stroke: Atheroembolism. MI:thromboembolism, ruptured plaque. Angina: stable obstructive lesion. Claudication: Trauma, in situ thrombosis. Acute limb ischemia: stable obstructive plaque. Pulmonary embolism: vasospasm. Raynauds phenomenon: vasospasm

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12
Q

Stroke: common mechanism, location,

A

Atheroembolization from carotid bifurcation lesion (Source lesion does not need to be obstructive ). Ophthalmic artery is common location. Also, Thromboembolization from left atrial appendage in setting of atrial fibrillation
Atheroembolization from carotid bifurcation lesion (Source lesion does not need to be obstructive ). Ophthalmic artery is common location. Also, Thromboembolization from left atrial appendage in setting of atrial fibrillation

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13
Q

Explain different severities of MI’s

A

Less severe: Plaque rupture > non-occlusive thrombosis > some flow but intermittent occlusion or embolization > stabilize with anticoagulation / vasodilators
More severe: Plaque rupture > occlusive thrombus > no flow > clinical emergency > recanalize
Less severe: Plaque rupture > non-occlusive thrombosis > some flow but intermittent occlusion or embolization > stabilize with anticoagulation / vasodilators
More severe: Plaque rupture > occlusive thrombus > no flow > clinical emergency > recanalize

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14
Q

Explain what causes ST segment depression vs elevation

A

Partially occlusive thrombus and/or transient ischemia can cause ST segment depression and/or T wave inversion. Totally occlusive thrombus with prolonged ischemia can cause ST elevation with Q waves later

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15
Q

Manifestations of peripheral arterial disease and underlying pathologies

A

Claudication and acute limb ischemia are PAD. Claudication: obstructive (>70% diameter reduction), stable plaque. Acute limb ischemia: acute event obstructs blood flow without prior development of collaterals. could be atheroembolization or thromboembolization. rarely in-situ thrombosis

Claudication and acute limb ischemia are PAD. Claudication: obstructive (>70% diameter reduction), stable plaque. Acute limb ischemia: acute event obstructs blood flow without prior development of collaterals. could be atheroembolization or thromboembolization. rarely in-situ thrombosis

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16
Q

Compare stable and unstable plaques in regards to symptoms

A

stable: causes angina and claudication if obstructive, but less likely to cause thrombotic and embolic events. Unstable: causes MI and stroke, more likely via thrombotic and embolic mechanisms

17
Q

Venous vs arterial thrombosis

A

Venous: fibrin rich, RBCs, areas of stasis, genetic predisposition, environmental predisposition, treated with anticoag therapy. Arterial: platelet rich, plaque rupture, areas of high flow, atherosclerosis, trauma, antiplatelet therapy.

18
Q

What are some vasospastic disorders

A

Raynauds, Pernio, erythromyalgia, acrocyanosis