Let's Talk Medically

hellooo guys..!!

it's been a week since my last post..!!so i wanna try something new here and which is why i wanna share some medical facts that i used to learn in my classes..!!as a starter, let me share with you about ATHEROSCLEROSIS..!!

does anyone familiar with that term..??

i know i know, let me explain in a simple but informative sentences..!!

let's start our medical class, shall we..!!? :P

Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a condition in which an artery wall thickens as the result of a build-up of fatty materials such as cholesterol. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low-density lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL), (see apoA-1 Milano). It is commonly referred to as a hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries.

The atheromatous plaque is divided into three distinct components:

1. The atheroma ("lump of gruel," from ἀθήρα, athera, gruel in Greek), which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery
2. Underlying areas of cholesterol crystals
3. Calcification at the outer base of older/more advanced lesions.

The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: arteriosclerosis, arteriolosclerosis, and atherosclerosis. Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (from the Greek arteria, meaning artery, and sclerosis, meaning hardening); arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries); atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque. The term atherogenic is used for substances or processes that cause atherosclerosis.

Atherosclerosis, though typically asymptomatic for decades, eventually produces two main problems: First, the atheromatous plaques, though long compensated for by artery enlargement (see IMT), eventually lead to plaque ruptures and clots inside the artery lumen over the ruptures. The clots heal and usually shrink but leave behind stenosis (narrowing) of the artery (both locally and in smaller downstream branches), or worse, complete closure, and, therefore, an insufficient blood supply to the tissues and organ it feeds. Second, if the compensating artery enlargement process is excessive, then a netaneurysm results.

These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures (seevulnerable plaque), causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately 5 minutes. This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of acoronary artery, causing myocardial infarction (a heart attack). Even worse is the same process in an artery to the brain, commonly called stroke. Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs, typically due to a combination of both stenosis and aneurysmal segments narrowed with clots. Since atherosclerosis is a body-wide process, similar events occur also in the arteries to the brain, intestines, kidneys, legs, etc. Many infarctions involve only very small amounts of tissue and are termed clinically silent, because the person having the infarction does not notice the problem, does not seek medical help or when they do, physicians do not recognize what has happened.

Causes

Atherosclerosis develops from low-density lipoprotein molecules (LDL) becoming oxidized (ldl-ox) by free radicals, particularly reactive oxygen species (ROS). When oxidized LDL comes in contact with an artery wall, a series of reactions occur to repair the damage to the artery wall caused by oxidized LDL. The LDL molecule is globular shaped with a hollow core to carry cholesterol throughout the body. Cholesterol can move in the bloodstream only by being transported by lipoproteins.

The body's immune system responds to the damage to the artery wall caused by oxidized LDL by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL forming specialized foam cells. These white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle.

Eventually, the artery becomes inflamed. The cholesterol plaque causes the muscle cells to enlarge and form a hard cover over the affected area. This hard cover is what causes a narrowing of the artery, reduces the blood flow and increases blood pressure.

Some researchers believe that atherosclerosis may be caused by an infection of the vascular smooth muscle cells; chickens, for example, develop atherosclerosis when infected with the Marek's disease herpesvirus. Herpesvirus infection of arterial smooth muscle cells has been shown to cause cholesteryl ester (CE) accumulation.Cholesteryl ester accumulation is associated with atherosclerosis.

Also, cytomegalovirus (CMV) infection is associated with cardiovascular diseases.

Signs And Symptoms

Atherosclerosis typically begins in early adolescence, and is usually found in most major arteries, yet is asymptomatic and not detected by most diagnostic methods during life. Atheroma in arm, or more often in leg arteries, which produces decreased blood flow is called peripheral artery occlusive disease (PAOD).

According to United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of onset of the symptom).

Most artery flow disrupting events occur at locations with less than 50% lumen narrowing (~20% stenosis is average). The illustration above, like most illustrations of arterial disease, overemphasizes lumen narrowing, as opposed to compensatory external diameter enlargement (at least within smaller arteries, e.g., heart arteries) typical of the atherosclerosis process as it progresses (see Glagov^]the ASTEROID trial,^] and the IVUS photographs on page 8, as examples for a more accurate understanding). The relative geometry error within the illustration is common to many older illustrations, an error slowly being more commonly recognized within the last decade.

Cardiac stress testing, traditionally the most commonly performed non-invasive testing method for blood flow limitations, in general, detects only lumen narrowing of ~75% or greater, although some physicians claim that nuclear stress methods can detect as little as 50%.

Treatment

·         Lifestyle changes (diet, smoking, physical activity)

·         Drug treatment of diagnosed risk factors

·         Antiplatelet drugs

·         Possibly statins, ACE inhibitors, β-blockers

Diet: Several changes are beneficial:

·         Less saturated fat

·         No trans fats

·         More fruits and vegetables

·         More fiber

·         Moderate (if any) alcohol

Substantial decreases in saturated fat and simple carbohydrate intake and increases in fruit, vegetable, and fiber intake are recommended. These dietary changes are a prerequisite for lipid control and weight reduction and are essential for all patients. Calorie intake should be limited to keep weight within the normal range.

Small decreases in fat intake do not appear to lessen or stabilize atherosclerosis. Effective change requires limiting fat intake to 20 g/day, consisting of 6 to 10 g of polyunsaturated fat with ω-6 (linoleic acid) and ω-3 (eicosapentaenoic acid, docosahexaenoic acid) fatty acids in equal proportion, ≤ 2 g of saturated fat, and the rest as monounsaturated fat. Trans fatty acids, which are highly atherogenic, should be avoided.

Increasing carbohydrates to compensate for decreasing saturated fats in the diet increases plasma triglyceride levels and reduces HDL levels. Thus, any caloric deficiency should be made up with proteins and unsaturated fats rather than simple carbohydrates. Excessive sugar intake should be avoided, although sugar intake has not been directly related to cardiovascular risk. Instead, consumption of complex carbohydrates (eg, vegetables, whole grains) is encouraged.

Fruits and vegetables (5 daily servings) seem to decrease risk of coronary atherosclerosis, but whether this effect is due to phytochemicals or to a proportional decrease in saturated fat intake and increase in fiber and vitamin intake is unclear. Phytochemicals called flavonoids (in red and purple grapes, red wine, black teas, and dark beers) appear especially protective; high concentrations in red wine may help explain why incidence of coronary atherosclerosis in the French is relatively low, even though they use more tobacco and consume more fat than Americans do. But no clinical data indicate that eating flavonoid-rich foods or using supplements instead of foods prevents atherosclerosis.

Increased fiber intake decreases total cholesterol and may have a beneficial effect on glucose and insulin levels. Daily intake of at least 5 to 10 g of soluble fiber (eg, oat bran, beans, soy products, psyllium) is recommended; this amount decreases LDL by about 5%. Insoluble fiber (eg, cellulose, lignin) does not appear to affect cholesterol but may confer additional health benefits (eg, reduced risk of colon cancer, possibly by stimulating bowel movement or reducing contact time with dietary carcinogens). However, excessive fiber interferes with the absorption of certain minerals and vitamins. In general, foods rich in phytochemicals and vitamins are also rich in fiber.

Alcohol increases HDL and has poorly defined antithrombotic, antioxidant, and anti-inflammatory properties. These effects appear to be the same for wine, beer, and hard liquor, and occur at moderate levels of consumption; about 30 mL (1 oz) 5 to 6 times/wk protects against coronary atherosclerosis. However, at higher doses, alcohol can cause significant health problems. Thus, the relationship between alcohol and total mortality rate is J-shaped; mortality rate is lowest for men who consume < 14 drinks/wk and women who consume < 9 drinks/wk.

There is little evidence that dietary supplementation with vitamins, phytochemicals, and trace minerals reduces risk of atherosclerosis. The one exception is fish oil supplements. Although alternative medicines and health foods are becoming more popular, and some may have minor effects on blood pressure or cholesterol, these treatments are not always proven safe or effective and may have negative interaction with proven drugs. Levels of coenzyme Q10, which is necessary for the basic functioning of cells, tend to decrease with age and may be low in patients with certain heart and other chronic diseases; thus, coenzyme Q10 supplementation has been used or recommended, but its therapeutic benefit remains controversial.

Physical activity: Regular physical activity (eg, 30 to 45 min of walking, running, swimming, or cycling 3 to 5 times/wk) reduces incidence of some risk factors (hypertension, dyslipidemia, diabetes), CAD (eg, MI), and death attributable to atherosclerosis in patients with and without previous ischemic events. Whether the association is causal or merely indicates that healthier people are more likely to exercise regularly is unclear. Optimal intensity, duration, frequency, and type of exercise have not been established, but most evidence suggests an inverse linear relationship between aerobic physical activity and risk. Walking regularly increases the distance patients with peripheral vascular disease can walk without pain.

An exercise program that involves aerobic exercise has a clear role in preventing atherosclerosis and promoting weight loss. Before starting a new exercise program, the elderly and people who have risk factors for atherosclerosis or who have had recent ischemic events should probably be evaluated by a physician; evaluation includes history, physical examination, and assessment of risk factor control.

Antiplatelet drugs: Oral antiplatelet drugs are essential because most complications result from plaque fissure or rupture with platelet activation and thrombosis. The following are used:

•       aspirin
•       clopidogrel
•       ACE inhibitors 
•       angiotensin II receptor blockers
•       statins 
•       thiazolidinediones

so, to simplify those turn off sentences, atherosclerosis is the most serious form of arteriosclerosis

because it causes coronary artery disease and also cerebrovascular disease. in order to prevent this

from happening, please please please, change your lifestyle coz PREVENTION IS THE BEST

METHOD THAN CURE THE DISEASE..!! :P