Having An Adverse Cardiovascular Event Biology Essay

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By using the cardiovascular risk chart, the patients absolute risk of having an adverse cardiovascular event within the next 5 years is 15~20%.

B: what is the Crystalline material is cholesterol salt. It is formed when macrophages consume huge amounts of lipids, so dies by necrosis and causes the contents of the cytoplasm to spill out. The spilled out contents have a very high concentrated and as a result crystallizes.

The Empty spaces are called cholesterol clefts.

In the vicinity of the empty spaces, large cells with round or oval nuclei and extensive cytoplasm may be found. What are these cells? Foam cells.

What are these cell loaded with? Foam cells are loaded with cholesterol, oxidised lipoprotein, other fats and cells that have died during being up taken by macrophages.

C: What linked set of pathologies are most likely to have caused the chest pain in your patient? Chest pain (angina) is a characteristic symptom of myocardial infarction (MI), which is the death of cardio myocyte in the heart caused by insufficient blood supply through the coronary artery. Relating back to this patient as he is gardening, the insufficient blood supply to his heart doesn't meet the requirement to continue this exercise. So the patient needs to breath with increased difficulty and therefore feels shortness of breath. Endothelial cell injury or turbulence promotes thrombosis. Cells become hypoxic and the Ph of the tissue decreases. The injury (or activation) to endothelial cells turns on haemostasis and so aggregation of platelets and promotes the coagulation cascade. The narrowing of vessels and an increase in blood flow this leads to turbulence, causing atherosclerotic plugs to become torn and are visible to blood with the pro-thrombosis substances within the plug. Hence platelets are triggered and the coagulation cascade takes place. Therefore thrombus is created, leading to ischemia and necrosis infarction and so, angina.

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D: What are the factors that promote thrombosis? Endothelial injury, abnormal blood flow and hypercoagulability (the factors from Virchow's triad)

Summarizes what you see:

red bands (lines of Zahn) were easily seen, which are densely packed of red blood cells and over time entrapped into the thrombus. However the paler areas do not contain many red blood cells. These red patches or bands show that the thrombus is new, as the thrombus ages, these patches have a tendency to disappear. Also, the thrombus nearly fills up the lumen of the coronary artery.

What five things can happen to a thrombus?

Recanalisation (small blood vessels can grow into the thrombus)

dissolution (the fibrinolytic system breakdown thrombi) or resolution(thrombus is removed entirely)

embolisation (parts of thrombi break off and flow into the circulation)

Organisation of thrombus (fibrous scar)

propagation (thrombus grows bigger)

What pathological changes, at the cellular and molecular level, are likely to have caused these abnormal ECG and serum protein test results?

The inverted T-wave shows that the heart dies by necrosis. So the raised protein levels shows that the heart muscle died by necrosis and allows the cytoplasm contents to spill out into the blood. This leads to infarction of cardiomyocytes of the heart due to thrombus developed on top of the atherosclerotic plug therefore blocking the coronary artery (not enough blood supply -hypoxia).

What do you think has happened?

There has been a thrombus embolised from inside the patient's heart (this type of thrombus is called a mural thrombus).Since a big part of the patients heart muscle is dead, that part of the heart can no longer contribute ,thus creates turbulence. All three parts of 'Virchow's triad' have been turned on. So the left ventricle in the heart has a thrombus. The first thrombus is on the heart plaque and the second thrombus is inside the chamber of ventricle. The patient becomes unconscious because of infarction in some parts of his brain thus this leads to stroke. The abdominal pain and bloody diarrhoea is caused by infarction of the gut. All this is due to the embolism where it breaks off from thrombi and is passed down to the smaller blood vessels in the brain and the gut. So there is blockage of the vessels, blood cannot flow through and this lead to an infarction.

What has caused the heart failure?

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The heart muscle dies so the heart cannot pump blood from that part. There is turbulence (part of the heart is dead or altered rhythm of heart) ,there is a alteration in the electrical activity of the heart and blood respond to this kind of major injury via stimulating the coagulation cascade.

What does it mean when the patient's hospital notes describe this heart failure as low output failure?

This means the heart fails to maintain normal cardiac output (volume of blood pumped out of the heart per beat) to meet the body's demands.

What organs will be most affected by this type of heart failure?

The lungs

How do each of these drugs and lifestyle changes alter the cellular and molecular processes occurring within the blood vessel walls to reduce the risk of further cardiovascular events?

Aspirin -inhibits cyclozxygenase enzymes which inhibit thrombxanase (involved in activation of platelets and indirectly the coagulation cascade), so this reduces further thrombus form.

A 'beta blocker' drug - block the effects of adrenaline in B-1 adrenergic receptor in heart; this decreases cardiac output (working load) of the heart.

An 'Angiotension Converting Enzyme Inhibitor' (=ACE inhibitor) drug - act on the rennin angiotensin aldosterone system.

A 'statin' drug - reduces LDL cholesterol in the blood, therefore reduces atherosclerotic plugs.

Stops smoking - less endothelial injury and fewer effects on haemostasis and less effects on coagulation, thus reduces thrombus form.

Improve his diet and loose weight - altered lipids

Regular exercise - Many effects including allows new collateral vessels to bypass the coronary artery.