L9: structure of BV 1 Flashcards
3 layers in BV
tunica intima
tunica media
tunica adventitia
elastic arteries examples, and function
Elastic arteries ( or conducting arteries) are the aorta and
pulmonary arteries which occur just downstream of the ventricles. Their function is to store blood during ventricular ejection
(systole), then recoil during ventricular filling (diastole) in order
to squeeze blood steadily outwards into the arterial tree
elastic arteries: structural characteristics
-intima layer thicker than in muscular arteries( up to 20% of the vessel wall)
and contains longitudinal elastin fibres in the subendothelial connective tissue.
An IEL is
present but is indistinguishable from the elastic laminae of the
media alongside
The media comprises many lamellar units (50-60 in the
aorta). All of these run mainly in a circular
orientation around the vessel.
The adventitia contains the usual collagen and elastic
fibres, small blood vessels (vasa vasorum) and autonomic nerves
internal elastic lamina is part of what layer?
intima
lamellar unit is made up of…
Each unit is made up of an elastic lamina, smooth muscle and collagen fibres
what class of arteries are affected by artherosclerosis?
muscular arteries
muscular arteries structure
Tunica Intima; the innermost coat.
1) Endothelium
2) Basement membrane of endothelium
3) Subendothelial connective tissue
4) A distinctive Internal Elastic Lamina IEL,
smooth in life but with longitudinal folds
after death.
Tunica Media; the middle (and thickest) coat.
Smooth muscle fibres to control the diameter
of the vessel, elastin fibres to give resiliency,
and collagen fibres to limit expansion and
prevent rupture. The outer margin sometimes
includes an External Elastic Lamina EEL
which is never as prominent as the IEL.
Tunica Adventitia; the outermost coat.
Usually only collagen and elastin fibres. Vasa
vasorum to service the outer layers of the
vessel wall.
berry aneurism
A berry aneurysm, also known as a saccular aneurysm or a cerebral aneurysm, is a type of abnormal bulging or outpouching of a blood vessel in the brain. It is called a “berry” aneurysm because it typically appears as a small round sac, resembling a berry, that is attached to the side of a blood vessel.
Berry aneurysms usually develop at the points where the blood vessels branch or bifurcate. They are most commonly found in the circle of Willis, which is a circular network of arteries at the base of the brain that supplies blood to the brain and surrounding structures.
-bleeding into the media layer
dissecting aneurism
A dissecting aneurysm, also known as aortic dissection, is a serious and potentially life-threatening condition involving a tear in the layers of the aorta, the largest artery in the body. It occurs when blood enters the tear and creates a false channel within the wall of the aorta.
Aortic dissection typically begins with a tear in the innermost layer of the aortic wall (intima), allowing blood to flow into the middle layer (media) and separate the layers of the arterial wall. This separation creates a false lumen or channel that can extend along the length of the aorta. The dissection can occur in different segments of the aorta, such as the ascending aorta, aortic arch, or descending aorta.
intima damage> blood leaks into the media layer & slips between fenestrated elastin sheets
effects of hypertension on arteries
increased smooth m.
duplication of IEL
increased tunica intima(TI) thickness
decreased lumen size
extra:
Hypertension, or high blood pressure, can have significant effects on arteries throughout the body. Over time, the constant force of elevated blood pressure against the arterial walls can cause structural and functional changes, leading to several adverse effects:
Arterial Stiffness: Chronic hypertension can result in the thickening and stiffening of arterial walls. The excessive pressure can cause the smooth muscle cells within the arterial walls to hypertrophy (increase in size) and the elastic fibers to become less elastic. This increased arterial stiffness impairs the ability of the arteries to expand and contract, affecting their normal function.
Endothelial Dysfunction: The endothelium, which is the innermost layer of the arterial walls, plays a vital role in regulating vascular function. Hypertension can lead to endothelial dysfunction, which is characterized by a reduced production of nitric oxide, increased production of vasoconstrictors, and increased inflammation. Endothelial dysfunction contributes to impaired vasodilation, increased vascular tone, and an imbalance in the regulation of blood flow and pressure.
Atherosclerosis: Hypertension is a significant risk factor for the development of atherosclerosis, a condition characterized by the build-up of fatty plaques within the arterial walls. The elevated blood pressure damages the endothelium, creating sites where lipids, cholesterol, and other substances accumulate, leading to the formation of atherosclerotic plaques. These plaques can narrow and stiffen the arteries, reducing blood flow and increasing the risk of complications, such as heart attacks and strokes.
Arterial Remodeling: In response to hypertension, arteries may undergo remodeling to adapt to the increased pressure. This can result in inward thickening of the arterial walls (medial hypertrophy) and outward expansion of the artery (arterial dilatation). These structural changes further contribute to increased arterial stiffness and can adversely affect blood flow dynamics.
Increased Risk of Aneurysm and Dissection: Prolonged hypertension can weaken arterial walls, increasing the risk of developing aneurysms (abnormal bulging or ballooning of arteries) or arterial dissections (tears in the arterial walls). These complications can lead to life-threatening situations if the weakened artery ruptures or blood flow is blocked.
Target Organ Damage: Persistent hypertension places excessive strain on various organs, leading to target organ damage. This includes effects on the heart (such as left ventricular hypertrophy, heart failure), brain (increased risk of stroke), kidneys (nephrosclerosis, impaired renal function), and peripheral arteries (peripheral arterial disease).
It’s important to manage hypertension effectively through lifestyle modifications (such as a healthy diet, regular exercise, weight management, and stress reduction) and, if necessary, medications prescribed by a healthcare professional. Controlling blood pressure helps reduce the risk of arterial damage and associated complications, supporting overall cardiovascular health. Regular monitoring, adherence to treatment plans, and routine medical check-ups are essential for individuals with hypertension.
steps of atherosclerosis development
Endothelial Dysfunction: The process of atherosclerosis starts with endothelial dysfunction, which can be caused by various factors, including high blood pressure, smoking, high cholesterol levels, inflammation, and oxidative stress. Endothelial dysfunction impairs the normal function of the endothelium, including its ability to regulate vascular tone, inflammation, and the formation of blood clots.
Lipid Accumulation: The dysfunctional endothelium allows low-density lipoprotein (LDL) cholesterol particles to infiltrate the arterial wall. LDL cholesterol can become trapped within the intima (the middle layer of the arterial wall) and undergo modification, such as oxidation or chemical alteration, making it more likely to be taken up by immune cells.
Inflammatory Response: The presence of modified LDL cholesterol triggers an inflammatory response within the arterial wall. Immune cells, particularly monocytes, migrate into the arterial wall and transform into macrophages. Macrophages engulf the modified LDL cholesterol, forming foam cells. This accumulation of foam cells contributes to the formation of fatty streaks within the arterial wall.
Foam Cell Formation and Fatty Streaks: Foam cells, which consist of lipid-filled macrophages, accumulate in the intima layer. As foam cells accumulate, they form fatty streaks, which are the earliest visible signs of atherosclerosis. Fatty streaks may not cause significant narrowing of the artery, but they are considered precursors to more advanced plaques.
Smooth Muscle Cell Proliferation and Migration: In response to inflammatory signals and the presence of foam cells, smooth muscle cells within the arterial wall begin to proliferate and migrate from the media layer to the intima layer. These smooth muscle cells contribute to the growth and development of atherosclerotic plaques.
Formation of Fibrous Cap: The proliferating smooth muscle cells secrete extracellular matrix proteins, such as collagen, which accumulate and form a fibrous cap over the fatty streak. The fibrous cap provides structural stability to the plaque.
Plaque Maturation: The atherosclerotic plaque continues to evolve, with additional lipid accumulation, inflammation, and smooth muscle cell proliferation. The plaque may also undergo calcification, where calcium deposits accumulate within the plaque, further contributing to its stability.
Plaque Rupture or Erosion: Atherosclerotic plaques can become unstable and prone to rupture or erosion. Plaque rupture exposes the highly thrombogenic (clot-promoting) substances within the plaque to the blood, leading to the formation of a blood clot or thrombus at the site. The clot can partially or completely block the artery, leading to reduced blood flow or complete occlusion.
which vessels have the thickest musclular coat in their media relative to their size?
arterioles
arterioles structure
