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What are the Three cell types of blood vessels
- Endothelial cells (ECs)
- Smooth muscle cells (SMCs)
- Extracellular matrix (ECM)
What are the Three Concentric layers of blood vessels
What are the components of the intima?
- Single layer of ECs
- Underlaying dense elastic membrane (internal elastic lamina) consisting of ECM
What are the components of the Media
- Layers of SMCs and connective ECM
- The outer limit of the media is defined by the external elastic lamina consisting of ECM
What are the components of the Adventitia
- Connective tissue
- Nerve Fibers
- Vasa vasorum
How do cells of the media layer receive nutrients and oxygen and get rid of wastes and carbon dioxide?
Cells of this layer receive nutrients and oxygen from pores in internal elastic lamina (fenestrations) and from small arterioles that originate from outside the vessel and reside in the adventitia (vasa vasorum)
What is the function of Arteries?
carry oxygenated, nutrient-rich blood to tissues
What is the function of Capillaries?
responsible for diffusion exchange of nutrients, oxygen, and waste between blood and tissues
What is the function of Veins?
Carry deoxygenated blood to lungs
What is the function of Large (elastic) arteries
- Include the aorta and its large branches (innominate, subclavian, common carotid, and iliac)
- The elastic, fiber rich media layer of these vessels expands during systole and recoils during diastole. This propels blood through the peripheral vasculature
- These vessels can be affected by atherosclerosis
What is the function of Medium sized (muscular) arteries?
- Include other brances of the aorta, such as the coronary and renal arteries
- Rich in SMCs and regulates blood flow and blood pressure by vasoconstriction and vasodilation
- These vessels can be affected by atherosclerosis
What is the function of Small arteries and arterioles
- Lie within organs and tissues
- The media layer of these vessels is rich in SMCs and regulates blood flow and blood pressure by vasoconstriction and vasodilation
- The arterioles are principal points for regulating blood pressure and velocity and for changing pulsatile flow and steady flow
What are the characteristics of capillaries?
- They are approximately the diameter of a RBC (7-8micrometers)
- They consist of an endothelial cell lining but no media layer
- Their thin walls and slow blood flow make them ideal for diffusion exchange between blood and tissues
In comparison to arteries, veins have _____ diameters, _____lumen, ______ walls
larger, larger, thinner
Veins are predisposed to:
- Irregular dilation (varicose veins) varices
- Compression restricted blood flow
- Penetration by tumors tumor metastatsis
- Damage by inflammatory processes thrombophlebitis
Hypertensive vascular disease is a risk factor for what diseases?
- Coronary heart disease
- Cerebrovascular accidents
- Cardiac hypertrophy and subsequent heart failure
- Aortic dissection
- Renal failure
What are the mechanisms by which blood pressure is regulated?
- Blood volume (Na homeostasis)/cardiac output
- Peripheral resistance (vasodilation/constriction of arterioles)
- Kidneys (regulate bp in two ways)
How does Renin production by the kidneys regulate blood pressure?
Renin converts angiotensin to angiotensin 1. ACE then converst ANG1 to ANG2. ANG2 is responsible for vasoconstriction and aldosterone secretion (signals NA reabsorption)
How does Glomerular filtration rate control blood pressure?
controls the amount of Na reabsorbed
What are the mechanisms by which blood pressure is dysregulated in hypertensive vascular disease?
- Genetic factors possibly due to combinations of mutations or polymorphisms that cooperate to result in HTN
- Reduced renal Na secretion causes increased blood volume needed to maintain Na homeostasis
- Vasoconstrictive influences
- Stress (vasoconstrictive factors; epinephrine)
- Smoking (vasoconstrictive; nicotine)
- Obesity (increase in capillary bed size)
- Excessive salt consumption (increase blood volume)
What is the definition of atherosclerosis?
Atherosclerosis is characterized by fibrofatty deposits or plaques that protrude into or obstruct the vascular lumina. It contributes to approximately half of all deaths in the western world.
Atherosclerosis is a risk factor for what diseases?
- Myocardial infarction (heart attack)
- Cerebral infarction (stroke)
- Aortic aneurisms
- Peripheral vascular disease (gangrene of the legs)
- Ischemic injury
How does Hyperlipidemia cause ec injury
directly impairs EC function through increased production of Oxygen Free Radicals
What are the risk factors for atherosclerosis?
- Familial (genetic) predisposition (hyperlipidemia)
- Hyperlipidemia/ hypercholesterolemia (lifestyle)
- Cigarette smoking
How does Hypertension cause ec injury
physical injury to EC
How does Smoking cause EC injury
circulating constituents of smoke cause EC damage
How do Toxins, viruses, immune reactions cause EC injury
how do Hemodynamic factors cause ec injury
disruptions of laminar flow contribute to monocyte and platelet adhesion to endothelial cells
What are the mechanisms of chronic endothelial cell injury?
Chronic endothelial injury �!endothelial dysfunction; monocyte adhesion and migration �! macrophage activation; smooth muscle recruitment �! Macrophage and smooth muscle cells engulf lipid �! smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
How does endothelial cell dysfunction resulting from endothelial cell injury contribute to atherosclerosis?
- Increased vascular permeability
- Leukocyte and monocyte adhesion, emigration (into the lamina), and transformation into macrophages causing swelling of intima
- Insudation (integration and invasion) of liproproteins into the vessel wall and the intima and subsequent oxidation of these lipids
- 1. Stimulates monocyte accumulation in intima (chemoattractant)
- 2. Is cytotixic to ECs and can induce EC dysfunction
- Platelet adhesion and activation
- Activation of platelets and macrophages and release of factos that promote SMC emigration
What are the events that occur during the pathogenesis of atherosclerosis?
- EC injury and dysfunction
- SMC emigrate from media to intima- this is accompanied by SMC proliferation and SMC synthesis and secretion of ECM components, resulting in accumulation of collagen and proteoglycans in intima and intima swelling
- Oxidized lipids accumulate within macrophages and SMCs
- oThis stimulates the release of growth factors and cytokines by macrophages and SMCs
- oThis is cytotoxic to SMCs- causing inflammation as body attempts to clear dying SMCs