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Cardiovascular System > Endothelium Function and Pathology (Brodsky) > Flashcards

Endothelium Function and Pathology (Brodsky) Flashcards

1
Q

Most relevant endothelium functions

A

Blood vessel diameter (blood pressure / supply), Coagulation

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2
Q

What is the most relevant endothelium pathology?

A

Atherosclerosis

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3
Q

What local factors affect arteriolar constriction locally?

A

Decreased local temperature, autoregulation

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4
Q

Local local factors affecting arteriolar dilatation

A

Increased CO2 and decreased O2, Increased K+, adenosine, lactate, etc., Decreased local pH, Increased local temperature.

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5
Q

Hormones affecting constriction of arterioles

A

Adrenaline (except in skeletal muscle and liver), Noradrenaline, AVP, Angiotensine II, Circulating Na+-K+ ATPase inhibitor, Neuropeptide Y

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6
Q

Hormones affecting dilatation of arterioles

A

Epinephrine in skeletal muscle and liver, CGRP, Substance P, histamine, ANP, VIP.

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7
Q

What neural factors affect arteriolar constriction?

A

Increased discharge of sympathetic neurons.

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8
Q

What neural factors affect arteriolar dilation?

A

Decrease discharge of sympathetic neurons, Activation of sympathetic cholinergic vasodilator nerves to skeletal muscle.

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9
Q

What endothelial products affect arteriolar constriction?

A

Endothelin-1, Locally released platelet serotonin, Thromboxane A2.

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10
Q

What endothelial products affect arteriolar dilation?

A

NO, Kinins, Prostacyclin

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11
Q

What is the use of serotonin?

A

Brain and blood vessels. Vasoconstriction. Related to depression and migraine headaches.

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12
Q

What are signaling molecules?

A

Signaling molecules derived from different 20-carbon essential fatty acids.

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13
Q

What is the most important 20-carbon essential fatty acid that forms eicosanoids

A

Arachidonic acid

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14
Q

Functions of Eicosinoids

A

Functions: Regulation of blood pressure, Coagulation, Inflammation, Fever, Immune system modulation, Control of reproductive processes, Regulation of sleep/wake cycle.

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15
Q

What are the classical eicosanoids synthesized by?

A

Cyclooxygenase (COX1/2) or Lipoxygenases (LOX)

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16
Q

What are the 2 classes of eicosanoids?

A

Prostanoids (from COX) and leukotriens (from LOX)

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17
Q

What are the prostanoids?

A

Prostaglandings (PG), Prostacyclins (PGI2), Thromboxanes (TX)

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18
Q

Formation of Eicosanoids: pathway through LOX or COX

A
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19
Q
A
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20
Q

Where are prostacylcins produced?

A

Endothelial cells

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21
Q

Where is Thromboxane A2 produced?

A

In platelets

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22
Q

From what are Prostacyclins and Thromboxane A2 produced?

A

Arachidonic acid via Cyclooxygenase pathway

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23
Q

What is the actino of thromboxane A2?

A

Promotes platelet aggregation and vasoconstriction

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24
Q

What is the response to prostacyclin?

A

Inhibition of platelet aggregation and vasodilation. Vascular relaxation, blocks platelet reactivity, stimulates cytokine production.

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25
Q

What is the effect of aspirin on Thromboxane A2 and Prostacyclin

A

Shifts balance between them towards prostacyclin. Produces irreversible inhibition of COX reducing productino of both but endothelial cells can recover while platelets cannot

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26
Q

How is NO synthesized?

A

From arginine in a reaction catalyzed by NO synthase (NOS)

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27
Q

What are the 3 isoforms of NOS?

A

NOS1-nervous system, NOS2-macrophages and other immune cells, NOS3-endothelial cells

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28
Q

What is the effect of NO on blood vessels

A

Diffuses through endothelium (intima to media) to smooth muscle, activates soluble guanylyl cyclase producing cGMP, mediates relaxation of vascular smooth muscle-vasodilation. Inhibits platelet reactivity.

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29
Q

What inactivates NO?

A

Hemoglobin

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30
Q

What common pharmaceutical use does NO have?

A

Viagra and cialis

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31
Q

What are the 3 factors that lead to Ca2+ release (and thus NOS activation)?

A
  1. Acetylcholine, 2. Bradykinins, 3. Sheer stress
32
Q

Where is Endothelin 2 produced?

A

Kidney and intestine

33
Q

Where is endothelin 3 produced

A

In brain

34
Q

What are the actions of endothelin-1

A

Vasoconstrictor, mostly paracrine.

35
Q

What stimulates endothelin secretion?

A

Angiotensin II, catecholamines, shear stress.

36
Q

What inhibits Endothelin secretion?

A

NO, ANP, PGE2, prostacyclin

37
Q

Where is Endothelin 2 produced?

A

Kidney and intestine

38
Q

Where is endothelin 3 produced?

A

Brain

39
Q

What are the actions of endothelin-1?

A

Potent vasoconstrictor, paracrine.

40
Q

What stimulates endothelin-1?

A

Angiotensin II, catecholamines, shear stress

41
Q

What inhibits endothelin-1?

A

NO, ANP, PGE2, prostacyclin

42
Q

Which thromboregulators modulate platelet activation and blood vessel contractility?

A

NO, PGI2 (prostacyclin), ET

43
Q

What are the thromboregulators involved in inflammation?

A

CD99, Selectins, JAMs and CAMs.

44
Q

What are the 3 actions of different molecules associated with the endothelial cell?

A

Contractility, Inflammation and Coagulation

45
Q

What is percentage of people dying of arteriosclerosis in western world?

A

40% (leading cause of death in western world)

46
Q

What is the mechanism of arteriosclerosis?

A

Too much lipid/lipoproteins–>enter intima–>lipid/lipoprotein modification–>attract monocytes/leukocytes through inflammation to intima–>macrophages eat fat through scavenger receptors–>differentiate into foam cells–>hardening, migration of smooth muscle cells into intima–>production of matrix of atheroma–>erosion of atheroma–>thrombus formation

47
Q

Definition of arteriosclerosis

A

Hardening of arteries caused by the deposition of fatty material in the arterial wall.

48
Q

What is the “Fatty Streak” in atherosclerosis?

A

The initial lesion of atherosclerosis, arising from focal increase in content of lipoproteins within regions of intima.

49
Q

How does hypercholesterolemia affect atherosclerosis?

A

Promotes accumulation of LDL particles.

50
Q

What is the fate of the fatty streak?

A

Lipoprotein particles in the extracellular space of the intima undergo oxidative modifications. Modified HDL particles function poorly as cholesterol acceptors which impairs reverse cholesterol transport. Modified LDL have pro-inflammatory properties. Lipoprotien partricles need to be oxidized and modified in order to cause problems.

51
Q

What is atheroma?

A

Accumulation and swelling in artery walls that is made up of (mostly) macrophage cells, or debris, that contain lipids (cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue.

52
Q

How is the migration of leukocytes directed?

A

Chemoattractant factors including modified lipoprotein particles themselves and chemoattractant cytokines are produced by endothelia cells in response to modified lipoproteins.

53
Q

How do modified lipoproteins recruit monocytes to migrate into intima?

A

Upregulate expression of adhesion molecules and chemoattractant cytokines.

54
Q

What inflammatory cells are found in the atheroma?

A

Monocyte derived macrophages and lymphocytes.

55
Q

How do laminar shear forces affect leukocyte adhesion molecules?

A

Suppress expression. Atherosclerotic sites often have disturbed flow.

56
Q

How are foam cell formed?

A

Leukocytes in the fatty streak can divide and exhibit augmented expression of receptors for modified lipoproteins (scavenger receptors). These mononuclear phagocytes ingest lipids and become foam cells represented by cytoplasm filled with lipid droplets.

57
Q

Picture of monocyte adherence and differentiation into foam cell

A
58
Q

Formation of lesions and endothelial dysfunction in the first 4 decades

A
59
Q

Formation of complex atheroma

A

Smooth muscles move from tunica media into intima, The smooth muscle cell synthesizes the bulk of the extracellular matrix of the complex athrosclerotic lesion.

This supports transformation of the fatty streak into a more fibrous smooth muscle cell and extracellular matrix-rich lesion.

60
Q

In which direction does atheroma grow?

A

Outward, increasing diameter of vessel but preserves caliber of lumen. Compensatory enlargement.

61
Q

What is the response of coronary arteriography to atheromas?

A

Tend to underestimate the degree due to compensatory enlargement.

62
Q

What is the response of a normal artery wall to thrombosis?

A

Fibrinolytic/antithrombotic mechanisms resist thrombosis and lyse clots in situ. When overwhelmed leads to arterial occlusion.

63
Q

When do microvessels form?

A

Connect to artery vasa vasorum ass atherosclerotic lesions advance.

64
Q

What are the adverse effects of microvessels?

A

May furnish foci for intraplaque hemorrhage, Such a vascular leak can provoke thrombosis in situ and contribute to plaque complications.

65
Q

How does calcification occur?

A

Proteins usually found in bone also localize in atherosclerotic lesion.

Mineralization of the atherosclerotic plaque recapitulates many aspects of bone formation.

66
Q

Picture of factors contributing to vulnerable vs stable plaques

A
67
Q

How does stenosis affect the vessels in an atheroma?

A

Form later in the plaque. Many such plaques cause stable syndromes (e.g. demand-induced angina pectoris, intermittent claudication in the extremities). Limits flow. Even total vascular occlusion by an atheroma does not invariably lead to infarction because collateral vessels are formed during chronic hypoxic state.

68
Q

What sort of atheromas do not produce a flow-limiting stenosis?

A

Acute or unstable atherosclerotic syndroems.

69
Q

How do acute or unstable atheromas appear on arteriography?

A

Minimal luminal irregularities, low traditional significance.

70
Q

What is the consequence in MI for thrombi from nonocclusive stenosis?

A

Why MI is an initial manifestation of coronary artery disease (CAD) in patients who report no prior history of angina pectoris, a syndrome usually caused by flow-limiting stenoses.

71
Q

What is angina usually caused by?

A

Flow limiting stenosis

72
Q

What portion of CAD patients suffer an MI as the first manifestation?

A

At least 1/3.

73
Q

What usually produces the thrombus that causes episodes of unstable angina pectoris or the occlusive and relatively persistent thrombus that causes acute MI?

A

Superficial erosion of endothelium or plaque.

74
Q

How do inflammatory cells affect the plaque?

A

Secrete mediators that thin and weaken the fibrous cap that overlies the lipid‐rich core.

75
Q

What is the mechanism of the consequences of rupture of the plaque’s fibrous cap?

A

Contact between coagulation factors in the blood and highly thrombogenic tissue factor expressed by macrophage foam cells in the plaque’s lipid-rich core.

76
Q

What are the plaques most likely to cause fatal thrombosis?

A

Tend to have thin fibrous caps, relatively large lipid cores, and a high content of macrophages.

Cardiovascular System (28 decks)

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