Chap 18 Disordes of Bld Flow & BP Flashcards
*Atherosclerosis
a progressive disease characterized by the formation of fibrofatty plaques in the intima of large and medium-sized vessels, including aorta, coronary arteries, and cerebral vessels, that protrude into and can eventually obstruct blood flow.
Atheros- paste
sclerosis- hardening
The major risk factors for atherosclerosis are?
Hypercholesterolemia and inflammation
*Hyperlipidemia
involves abnormally elevated levels of any or all lipids and/or lipoproteins in the blood
-cholesterol & triglycerides (dietary lipids) are insoluable in plasma as encapsulated by lipoproteins
*Name different types of lipoproteins:
Chylomicrons
VLDL-very low density lipo=
55-65% triglycerides
10% cholesterol
5-10% protein
LDL- low density lipo
10% triglyceride
50% cholesterol
25% protein
IDL- intermediate density lipo
HDL- high density lipo (good one)
5% triglyceride
20% cholesterol
50% protein
lipoproteins are named based on their?
protein content, which is measured by their density. Fats are less dense than protein
Possible causes of hyperlipidemia
Lipid blood levels raised by:
- nutrition
- genetics
- comorbid conditions
- meds
2 areas of lipoprotein synthesis
liver and small intestine
*Risk factors of atherosclerosis
nonmodifiable:
potentially modifiable:
additional nontraditional:
Nonmodifiable
- hypercholesteremia
- increasing age
- gender, male
- family hx
- premature coronary artery disease that cannot be changed
Potentially modifiable
- smoking
- obesity
- HTN
- Hyperlipidemia
- DM
Additional nontraditional
- inflammation marked by elevated C-reactive protein
- increased lipoprotein
*Sites of atherosclerosis: arteries
these form at branches!!
1- Adb aorta and iliac arteries
2-Proximal coronary arteries
3-Thoracic aorta, femoral ad popliteal arteries
4-interna carotid arteries
5- Vertebral, basilar and middle cerebral arteries
Describe the types of lesions that can occur from atherosclerosis
1- the fatty streak
2-the fibrous atheromatous plaque
3- complicated lesions
*The fatty streak
the complicated lesion. Thin, flat, yellow intimal discolorations that progressively enlarge by becoming thicker and slightly elevated as they grow in length.
- in childrens 1st year of life.
- found in all ages/geographic areas/race/lifestyle/ect.
*Fibrous atheromatous plaque
accumulation of lipids, smooth muscle cells and scar tissue. Eventually may occlude artery and may predispose to thrombus (!!!most important complication!!!)
*The complicated lesion
-most advanced atherosclerotic lesions may contain hemorrhage, ulceration and scar tissue deposits.
The development of atherosclerotic lesions is a progressive process involving:
1- Endothelial cell injury
2- Migration of inflammatory cells
3- Lipid accumulation and smooth muscle cell proliferation
4- Plaque structure
Endothelial Cell Injury
The vascular endothelium is single layer cell-to-cell protection of subendothelial layer that separates blood cells and other blood components.
- agents that are the cause the endothelial injury cause adhesion of monocytes and platelets.
Migration of inflammatory cells
Early in develop athero lesions, endo cells begin to express selective adhesion molecules that bind monocytes and other inflam cells that initiate atherosclerotic lesions.
-after monocytes adhere endothelium, they migrate between the endo cells to localize in the intima, transform into macrophages, and angulf lipoproteins> largely LDL.
Lipid accumulation and smooth muscle cell proliferation
Although The adhesion of monocytes to remove LDL protects, it is also the contribution of athero.
- the activated macrophages release toxic O2 species that oxidize LDL
- the oxidized LDL is then ingested by macrophages through scavenger receptor, resulting in formation of foam cells, which are the primary component of athero lesions
- activated macrophages also produce growth factors that contribute to the migration and proliferation of smooth muscle cells (SMC) and the elaboration of the extracellular matrix (ECM).
Plaque structure
Athero plaque consists of aggregation of SMCs, macrophages, and other leukocytes, ECM-with collagen and elastic fibers, intra and extra cellular lipids.
- Fibrous cap consists of SMCs and dense ECM.
- beneath SMCs, and around cap consists of macrophages, and lymphocytes.
- Below that is central core of lipid laden foam cells and fatty debris.
- Rupture , ulceration or erosion of cap may lead to hemorrhage into the plaque or thrombotic occlusion of the vessel lumen.
*LDL is the main carrier of ________ but leaves some behind for uptake in arterial wall
cholesterol
*HDL also carry _________ but remove it from tissues and take to ______ for disposal.
cholesterol
Liver
*Lipid blood levels raised by
Nutrition
- -High-calorie diet increases production of VLDL & it’s conversion to LDL
- -Genetics
- -Comorbid conditions/diseases
- -Medication
*Tobacco Use
Increases blood lipid levels Damages endothelium Enhances thrombosis formation Increases blood viscosity Increases circulating catecholamines
*Arteriosclerosis
hardening of walls of artery
*Arteriolosclerosis
sclerosis and thickening of the walls of arterioles
*Atherosclerosis
a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls
*What happens during atherosclerosis?
Inflam is key factor to athero.
- wht bld cells LDL accumulates in the arterial wall, it undergoes chemical changes and signals to endothelial cells to latch onto wht bld cells circulating in the bld. These immune cells penetrate into the intima and trigger an inflame response, devouring LDLs, to become fat-laden “foam cells” and
- form a fatty streak, the earliest stage of atherosclerotic plaque.
- the plaque continues to grow and forms a fibrous cap. Substances released by foam cells can eventually destabilize the cap, allowing it to rupture, causing a blood clot which can block bld flow and trigger a heart attack.
*Stable plaques
- thick fibrous caps
- partially blocks vessels
- doesn’t tens to form clots/thrombus
*Unstable plaques
- thin fibrous caps
- may completely block arery
- may break free
*Peripheral Artery Disease:
and risk factors:
Atherosclerosis distal to the aortic arch Risk Factors: Male >60 years old Smokers Diabetes Mellitus
*Peripheral Artery Disease:
manifestations:
- Intermittent claudication (pain with walking). stops when you stop moving
- Thinning of skin & SC tissues of the lower leg
- Gradual atrophy of muscles
- Decreases blood supply, leads to:
- –weak absent pulses
- –cool extremities
- –brittle toenails, hair loss (men and women no hair on legs)
- – pallor
- – dependent rubor- when blood pools in the legs and arteries cant move the blood
