How can an aneurysm lead to a blood clot which would cause an infarction???
A patient suffers from severe leg pain while golfing. And pees discolored urine. He was misdiagnosed with muscle trauma when in reality he had a blocked artery in his leg caused by a popliteal artery aneurysm. By the time the blockage was diagnosed, a great deal of muscle tissue had already died and the patient eventually gets an infarction. My question is, how does a Popliteal Artery Aneurysm lead to a blood clot???
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Haha, I know exactly where you're getting this from!! House, right?? (sorry, I just LOVE that show)
Anyways, blood clotting is a big risk with aneurysms. Clots can break off and travel through the bloodstream until they get stuck. Normally, treatment is given quickly, and amputation or invasive measures like that are not required. But if it is not diagnosed soon enough, muscle tissue dies, and the limb may have to be amputated.
If you want a more in-depth explanation, here's a good article: http://www.evtoday.com/AAA/2003%20Files/Popliteal%20Artery%20Aneurysms.html (
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I want to define anterior infarction?
An infarction is a blockage of blood circulation to a localized area or organ of the body resulting in tissue death. A myocardial infarction, or heart attack, is usually caused by a blockage in one of the coronary arteries that supply blood to the heart muscle. The coronary arteries 'wrap around' the heart from top to bottom, front (or anterior) to back (or posterior). Thus an anterior infarction is one that occurs in the anterior part of one or both coronary arteries. (
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can anterior bridging ossification (if too close)perforate the left side neck carotid artery;patricia?
never. (
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A patient has an 80% blockage of his left anterior descending coronary artery. Describe what occurs in terms?
If your asking what happens because of that blockage.....
A blockage/partial blockage of any coronary artery results in ischemia to the myocardium. These will cause localized death of the myocardium resulting in a myocardial infarction. So you're looking at the setup for a heart attack here. (
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Do you know of Cerebral Vascular Accident (CVA) and Middle Cerebral Artery (MCA)?
What is Cerebral Vascular Accident (CVA)?
What is Middle Cerebral Artery (MCA)?
Is CVA and MCA is related?
How do they connected?
It is all about Nursing process assignment...
Need to know all about it in Nursing ways....
Please explain details with website or any references....
I need this information to do my case study of Nursing course...
Very important one....
Doctor diagnosis this patient with...
1. Left MCA infarct
2. Hypertension emergency with organ damage retinohemorragic
3. Uncontrolled DM secondary to not complaint to meds
Help please....
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A CVA is an artery in the brain which has grow. The surroundings of this cel became thinner. The risk is that the braincell can collapse. It's a very vital organ and normally the damage is that braincells and arteries can be damaged. This can paralyze parts of the body. When there's a CVA on the left side it's possible you cannot speak: Afasie.
It's important the patient has enough rest. The revalidationperiod can take 6-12 months. It's important to exercise every day. (
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what is a anterior infarction?
Anterior infarction means a heart attack of the front part of the heart. It is usually do to a blocked artery (almost always the left anterior descending or LAD artery) that supplies blood mostly the left ventricle which is the main chamber that pumps blood through the body.
Heart attacks can be anterior (front), posterior (back), inferior (bottom), right sided, or lateral (left). It can also be a combinations of these. The location of the clot determines where the heart attack happens. The size and location of the clot in the artery determines how "big" the heart attack is. Bigger clots in bigger arteries causes more heart muscle to die, leaving a scar that is not capable on contracting and pumping blood like it used to.
Hope that helps. (
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what is anterior mayocardiac infarction?
Shrek_tn is wrong - "Anterior" means the front part of the heart; "posterior" refers to the rear (think about it).
Basically, it is a heart attack in the left side of the heart, so affects the side that pumps blood to the lungs to be oxygenated. The main issue here is that there may not be enough blood going to the lungs to pick up oxygen for the rest of the body.
The correct term is "Anterior Myocardial Infarction" (
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What will a partial obstruction in a coronary artery likely cause?
a. pulmonary embolus
b. hypertension
c. angina attack
d. myocardial infarction
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c.
Can we do all of your homework for you? (
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How will I know if the artery begins to close again?
I've had a myocardial infarction on whom PTCA+STENT was done 2 1/2 years back.
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To understand your question you must understand what a myocardial infarction is.
This term refers to the death of a certain segment of the heart muscle (myocardium), usually the result of a focal complete blockage in one of the main coronary arteries or a branch thereof.
The main cause of myocardial infarction is atherosclerosis in the coronary arteries. This event results in impaired contractility of the heart muscle within seconds, and is initially restricted to the affected segment.
The myocardial ischemia or infarction begins in the endocardium (the inner lining of the heart) and spreads to the epicardium (the outer lining of the heart). Irreversible heart damage will occur if the blockage is complete for at least 15-20 minutes. Irreversible damage occurs maximally in the area at risk, and when the occlusion is maintained for 4-6 hours. Most of the damage occurs in the first 2-3 hours. Restoration of flow within the first 4-5 hours is associated with salvage of the heart muscle, but the salvage is greater if flow is restored in the first 1-2 hours. A major determinant of death and illness is the size of the infarct. Increasing the oxygen supply to the involved site of blockage by coronary reperfusio is more effective in salvaging the myocardium than decreasing oxygen demand.
The onset of acute Q-wave myocardial infarction occurs commonly in the morning hours shortly after arising, when there is increasing adrenergic activity, as well as increased blood fibrinogen levels and increased platelet (blood cell) adhesiveness. Non Q wave infarction does not show this circadian rhythm.
The traditional concept that myocardial infarctions can be classified as transmural or nontransmural on the basis of the presence or absence of Q waves is misleading, since autopsy studies have demonstrated convincingly that pathologic Q waves may be associated with nontransmural infarction and may be absent with transmural infarction. These misnomers have been replaced by the terms Q-wave infarction and nonQ-wave infarction for transmural and nontransmural infarction, respectively.
The evolution of a non-Q-wave infarction is charcterized by a lack of development of an abnormal Q wave and by the appearance of reversible ST-T-wave changes with ST depression that usually returns to normal over a few days, but occasionally is permanent. Differentiation between these two types of infarctions has become entrenched, since there are major differences in their pathogenesis, clinical manifestations, treatment, and prognosis. The initiating events in the pathogenesis of Q-wave and non-Q-wave infarction are thought to be identical, namely, coronary occlusion induced by thrombus superimposed on a plaque together with vasoconstriction.
There is considerable evidence, however, to indicate that in non-Q-wave infarction, early spontaneus reperfusion occurs, the mechanism of which remains uncertain. In contrast, in Q-wave infarction, the coronary occlusion is sustained at least for a long enough period to result in extensive necrosis.
One explanation for early spontaneous reperfusion is the lack of sustained vasoconstriction, which may contribute to ocusion. The evidence supporting the existence of early spontaneous reperfusion in non-Q-wave infarction is as follows:
1. Coronary angiographic studies performed in the early hours after onset show that only 20-30% of patients have complete coronary occlusion of the infarct-related vessels;but for Q-wave infarction it is about 80 to 90%.
2. Infarct size is routinely much less than observed with Q wave infarction, which is consistent with salvage by early reperfusion.
3. Peak plasma CK levels are reached on an average of 12 to 13 h after onset of symptoms, indicating early washout of the enzyme, as opposed to about 27 h after Q-wave infarction.
4. Reperfusion-induced contraction necrosis is extremely common, as it is in patients who undergo early reperfusion induced by thrombolytic therapy.
5. Acute mortality rates are around 2 to 3 percent, compared with 10 percent for Q-wave infarction.
6. The complications are minimal compared with those after a Q-wave infarction.
7. Finally, the long-term prognosis is characterized by recurrent episodes of reinfarction, so that after about 2 years, survival is the same as that after Q-wave infarction.
Quite often with the initial heart attack over half of the patients have significant obstructive atherosclerosis in only one vessel. However, in a recent study two fifths of the patients with acute myocardial infarction had angiographic evidence of multiple complex coronary plaques, which were associated with a less favorable in-hospital course. The presence of these plaques with complex morphologic features is the angiographic hallmark of unstable coronary syndromes and correlates with pathologic plaque and thrombus
I'm not a Doctor... I'm just a Corpsman... (
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what is anterior myocardial infarction?
I had the very same thing in 2001. It is a heart attack in the front lower part of the heart. It may or may not have caused damage to the heart. Usually there is always some damage with a heart attack, mine did not show up for a few years later and now the right side of my heart is larger than the left and I have a valve that leaks that is not supposed to. Right now, it's nothing life threatening but my cardiologist keeps a check on it every 6 months with tests and such. Sometimes in lower part of the heart where you had your heart attack will cause the heart tissue to die, it does not repair itself so if you have symptoms of another heart attack get to a hospital immediately. (
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