motoged
Elite Nomad
Posts: 6481
Registered: 7-31-2006
Location: Kamloops, BC
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Mood: Gettin' Better
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Coco Update
Nomads,
The following is an update on Coco....
http://forums.bajanomad.com/viewthread.php?tid=39055&page=1#pid421210
Don't believe everything you think....
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Ken Cooke
Elite Nomad
Posts: 8964
Registered: 2-9-2004
Location: Riverside, CA
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Mood: Pole Line Road postponed due to injury
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Thanks for the update, Ged. Diabetes is a terrible disease.
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boe4fun
Super Nomad
Posts: 1040
Registered: 1-22-2006
Location: Margaritaville
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Mood: Circling the drain........
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Hi Ken, Actually what I found out when we met with Coco on our last trip down to La Paz (and cast/measured him for his prostheses) is that his
amputations were the result of Atherosclerosis. He said he was not diabetic. I'll be seeing him this fall to follow up on how he's doing. Paul Boe
Two dirt roads diverged in Baja and I, I took the one less graveled by......
Soy ignorante, apático y ambivalente. No lo sé y no me importa, ni modo.
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Ken Cooke
Elite Nomad
Posts: 8964
Registered: 2-9-2004
Location: Riverside, CA
Member Is Offline
Mood: Pole Line Road postponed due to injury
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These rumors that run around on the Internet. Thanks for clearing that up for me.
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David K
Honored Nomad
Posts: 65293
Registered: 8-30-2002
Location: San Diego County
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Mood: Have Baja Fever
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From Wikipedia
| Quote: | Originally posted by boe4fun
Hi Ken, Actually what I found out when we met with Coco on our last trip down to La Paz (and cast/measured him for his prostheses) is that his
amputations were the result of Atherosclerosis. He said he was not diabetic. I'll be seeing him this fall to follow up on how he's doing. Paul Boe
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Atherosclerosis is the 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. It is 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 (especially small particle) 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.[1]
The atheromatous plaque is divided into three distinct components:
The atheroma ("lump of wax", from Athera, wax 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
Underlying areas of cholesterol crystals
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
Arterio, 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. Therefore, atherosclerosis is a form of
arteriosclerosis.
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 net aneurysm results.
These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures (see
vulnerable 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 a coronary 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.
Yet, 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 oxygen free radicals
(ROS). Blood in arteries contains plenty of oxygen and is where atherosclerosis develops. Blood in veins contains little oxygen[citation needed] where
atherosclerosis rarely develops. 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 to generate brain
tissues, vitamin D, and so on. Cholesterol does not dissolve in water. Blood is 70% water. Cholesterol can move in the bloodstream only by being
transported by LDL.
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. Unfortunately, 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.[2] Herpesvirus infection of arterial smooth muscle cells has been shown to cause
cholesteryl ester (CE) accumulation.[3] Cholesteryl ester accumulation is associated with atherosclerosis.
[edit] 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. The stage immediately prior to actual atherosclerosis is known as subclinical atherosclerosis. The majority of the
process leading to subclinical atherosclerosis can happen without our knowing it, especially given the large variety of risk factors.[4] Autopsies of
healthy young men who died during the Korean and Vietnam Wars showed evidence of the disease.[5][6] It most commonly becomes seriously symptomatic
when interfering with the coronary circulation supplying the heart or cerebral circulation supplying the brain, and is considered the most important
underlying cause of strokes, heart attacks, various heart diseases including congestive heart failure, and most cardiovascular diseases, in general.
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 reader might reflect that
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[7] and the
ASTEROID trial,[8] 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%.
[Edited on 6-5-2009 by David K]
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