Atherosclerosis, Hypertension, and other diseases of blood vessels Flashcards
Artery
Constructed of 3 types of cells:
1. Endothelial Cells
Form inner layer of blood vessels
Maintain homeostasis of flow and do not allow clots to form.
Secrete substances that control vascular tone.
2. Smoother muscle cells
Relax and contract to control vascular tone.
Contraction, flow slows.
Relaxation, greater amounts of flow.
Fibrous tissue which forms the matrix of the blood vessel is produced by smooth muscle cells.
3. Connective Tissue
vessel matrix, binds everything together.
Structure of blood vessels
Intima: Thin portion of the inner lining of vessel
predominantly endothelial cells on innermost later, which sit on a basement membrane of collagen and fibrous material.
Media: Comprised of mainly smooth muscle cells which provide vascular tone of artery; concentric layers allow artery to absorb pulsatile force from heart.
Smooth muscles cells in this layer are what change the tone and caliber of blood vessel.
Also has fibrous cells
Adventitia: outermost structure of blood vessel; acts as protective coat and composed mainly of fibrous tissue. Nerve endings interact with vessels at this layer. The blood supply to nourish cells in vessel wall are found here and called vasa vasorum.
Circulatory Vessels
Large Arteries: Elastic; have fairly substantial muscularis layer to control flow and absorb pulsatility.
Arterioles: endothelial lining and a thin layer of smooth muscle cells.
Capillaries: single layer of endothelial tissue; semipermeable membrane; usually leak and excess fluid carried away via lymph.
System is now low flow, low pressure
Venules
Veins: no direct pulsatility or force, so blood is propelled by movement of structures around veins; have one way valves; more stiff, have less capability of generating large amounts of vascular tone.
Atherosclerosis
Earliest form of abnormal placement of lipoproteins on intimal surface of membrane=fatty streaks.
Lipoproteins accumulate and bind to other structures such as proteoglycans on intimal surface of vessel.
Presence of lipoproteins allows WBC to begin to adhere to vessel and congregate.
More inflammatory molecules produced, allowing WBC to penetrate outer intimal layer into intimal itself.
WBC begin to evolve into macrophages that are able to take up lipoproteins as foam cells=beginning of plaque!
Tend to form a branch points
Foam cells-once entrenched in artery, can replicate and take up more lipid.
As plaque initially forms, it grows outward, with greater progression it begins to form inward, compromising size of lumen.
As they progress, they form microcirculation and produce calcium, causing calcification.
Coronary Artery Disease
Atherosclerotic plaques build up and gradually reduce the totally capacity of blood flow through artery.
Exertional angina=chest pain, may be first manifestation of disease; may remain asymptomatic until caliber decreases enough to significantly restrict flow.
Exercise increases demand and blood flow is inadequate down the diseased artery to provide enough nutrients and O2 to maintain muscle performance; pain occurs as consequence.
Plaque may progress and become unstable; associated with waxing and waning platelet aggregation and thrombus formation on top of ruptured plaque.
Myocardial Infarction
Artery may totally occlude due to the ruptured plaque.
Atherosclerotic Carotid Artery Disease
Plaques build up slowly and become unstable; if flow becomes severely compromised, stroke-like symptoms may occur, if these symptoms lack only a short period of time, they are called transient ischemic attacks (stroke like symptoms coming and going over minutes and hours.
This could also be due to a ruptured plaque that ejects debris downstream into brain arteries.
Total occlusion of carotid is sometimes silent if there is alternate flow from other sources or may cause severe stroke with permanent brain death of region.
Hypertension, smoking, diabetes, and hypercholesterolemia are most prominent risk factors.
Peripheral artery disease
Plaques build slowly with no symptoms; progression occurs to what is termed intermittent claudication; here, plaques become severe enough to reduce blood flow to certain muscle groups.
Acute onset of pain and weakness can occur in muscle group (cramp or ache); person stops exercising and pain goes away.
Ischemic dysfunction of the muscle, when blood flow catches back up to replace oxygen debt the pain goes away.
Severe occlusion or total occlusion can cause critical limb ischemia; can cause constant pain, ulceration, and break down of skin, gangrene which can result in death of portions of a limb.
Diabetes, smoking, and increased cholesterol are most prominent risk factors.
Aneurysms
Areas of focal enlargement of an artery to a diameter of at least 50% above normal size; not generally caused by atherosclerotic plaque.
May be due to focal inflammation of artery or abnormal connective tissue in artery or abnormal collagen formation causing weakening of wall.
Tend to expand gradually.
Aortic dissection
Tear of the intimal layer of the artery.
Associated abnormalities may be necrosis of the medial layer with the generation associated with this.
Inciting event not well understood, but acute deterioration in performance of an artery may cause ripping of the intima to occur and it may rapidly move upstream or downstream in artery.
Patients with aneurysms, inflammatory disease, and inherited diseases of collagen likely to have dissection.
Vasculitis
Local inflammation of the artery which can cause deterioration of the vessel, bleeding, and compromise of the lumen.
Diseases associated with abnormal antigen and antibody formation may infiltrate wall of artery and cause inflammatory deterioration.
Anti-inflammatory meds might improve.
Telangelectasias
Localized dilations of small veins of skin
Discoloration due to reflux of blood in the vein and poor flow
Varicose Veins
Dysfunction of larger superficial veins
Become dilated, tortuous, elongated, and enlarged.
Venous function deteriorates, resulting in poor blood flow, swelling, and sometimes clot formation within the vein.
Chronic venous insufficiency
Disease of the larger veins and sometimes deeper veins associated with poor flow and reflux.
Failure of venous valves, resulting of stasis, edema, deterioration of skin, ulceration of skin due to ISF in lower extremity outside vessel.
Venous Thrombosis
Stasis, endothelial injury to artery or vein, presence of alterations in blood clotting system increase risk of clot forming in vein. Stasis or poor blood flow occurs in situations of reduced activity.
Poor flow also associated with heart failure because of poor cardiac output.
Also associated promoted with inherited conditions and acquired changes in patient scubas pregnancy, malignancy, certain drugs.
