The four functions of endothelial cells including containment of the blood vessels, selective permeable to fluids, gases, ions and proteins into tissue, control the activation of haemostasis (control the activation of platelets and coagulation cascade) and control of blood pressure (release NO regulates smooth muscle cells to contract or relax.
Cells within larger artery walls receive oxygen and nutrients through vasa vasorum (small blood vessels located in tunica externa).
Internal elastic lamina (IEL) are not continuous as they are broken in places, the tunica intima layer is no longer single layer cell thick (as in the healthy vessels) and contains macrophages and smooth muscle cells (from tunica media).
If the theory from some scientist is correct, this change of appearance of coronary artery may be the predisposing factor to later cardio vascular disease (e.g. atherosclerosis).
We are still not certain, as this significance of change is still under research. Some people believe that these lesions may regress and may not develop atherosclerosis in their later age; others think that this is a strong predisposing factor to atherosclerosis at later age.
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The pathological changes I have observed in the following structures:
The lumen has decreases its diameter.
The tunica intima becomes thickened, forms 2 layers and is irregular.
The internal elastic lamina is quite separate to the lumen, duplicated, incomplete and broken down.
Risk factors may affect the patient's arteries, and the risk factors contribute to arthrosclerosis.
Three of the main positive risk factors (factors that'll increase the risk of atherosclerosis) present in the patient are cigarette smoking, hyperlipidaemia (ratio of cholesterol to HDL is 6.5) and hypertension (blood pressure: 160/95). In addition, he has other minor positive risk factors such as being moderately obese (high concentration of lipids in blood), male (as in pre-menopausal females may be protected by oestrogens), low birth weight and family history (may have some genes involved). All these factors tend to cause damage in endothelial cell layers of arteries, so artery walls become more permeable to lipids or chemicals and attract leucocytes, in turn leads to inflammation of the vessel. Thus, atherosclerosis plug is formed and may activate thrombosis, leading to narrowing of the artery and perhaps blockage.
Using this chart, write down the patients' absolute risk of having an adverse cardiovascular event within the next 5 years:
By using the chart, the patient's absolute risk of having an adverse cardiovascular event within the next 5 years is 15~20%.
The Crystalline material is cholesterol salt. This is formed when macrophages ingest huge amount of lipids thus died by necrosis and causes cytoplasm content to spill out. The spilled out contents have very high concentrated thus crystallizes.
The Empty spaces are cholesterol clefts.
The large cells with round or oval blue stained nuclei with extensive cytoplasm are foam cells.
Foam cells are loaded with oxdised lipoprotein, cholesterol, other fats and cells that have died when taken up by macrophages.
What linked set of pathologies are most likely to have caused the chest pain in your patient?
Chest pain (angina) is a classical symptom of myocardial infarction (MI), which is the death of cardio myocyte in heart due to inadequate blood supply through the coronary artery. Applying to this patient as he is gardening the inadequate of blood supply to his heart doesn't meet the requirement to maintain this exercise. Endothelial cell injury (or activation) or turbulence (abnormal blood flow) promotes thrombosis. The injury or activation to endothelial cells turns on haemostasis thus aggregation of platelets and promotes coagulation cascade. As there's narrowing of vessels, increase in blood flow thus turbulence, causing atherosclerotic plugs becomes torn and are exposed to blood with the pro-thrombosis substances inside the plug. Hence platelets are activated and coagulation cascade is turned on. Thus thrombus is formed, leading to ischemia and necrosis infarction thus angina.
What are the factors that promote thrombosis?
Factors are summarized via 'Virchow's triad' involving endothelial injury, abnormal blood flow and hypercoagulability.
Summarizes what you see:
We can see red bands (lines of Zahn), which are laid down of red blood cells over time entrapped into the thrombus. Whereas the paler areas, which doesn't have many red blood cells. These red patches or bands indicate that the thrombus is fresh, so as the thrombus age, these patches tend to disappear.
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In addition, 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), propagation (this usually happens in stagnant blood at a distance to an occluded vein, down the blood, towards the heart), stenosis (narrowing of blood vessels) or occlusion (blocking) of vessel and embolisation (parts of thrombi breaks off and flow into the circulation).
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 indicates that the heart die by necrosis. In addition, both tropnin-1 and the MB isotype of creatine kinase, are specific enzyme in heart. Thus the raised serum levels of these enzymes indicate that the heart muscle died by necrosis and allow its cytoplasm content to be released into the blood. Altogether, these lead to infarction of cardiomycytes of the heart due to thrombus formed on top of the atherosclerotic plug thus blocks the coronary artery.
What do you think has happened?
The patient becomes unconscious due to infarction in some parts of his brain thus leads to stroke. The abdominal pain and bloody diarrhea is due to infarction of gut.
All this is due to embolism where it breaks off from thrombi and passed down to the smaller blood vessels in the brain and gut. Hence block the vessels, blood cannot flow through and lead to infarction.
The patient developed mild heart failure…
What has caused the heart failure?
Thrombus, it is activated by the change in lining of blood vessels (necrosis on endothelium of heart), turbulence (part of the heart is dead or altered rhythm of heart) and lastly 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 pump out of the heart per beat) to meet body demands.
The heart failure affected predominantly the left side of your patient's heart..
What organs will be most affected by this type of heart failure?
Aspirin -inhibits cyclozxygenase enzymes and in turn inhibits thrombxanase (involved in activation of platelets and also indirectly the coagulation cascade), thus reduces further thrombus form.
A 'beta blocker' drug - block the effects of adrenaline in B-1 adrenergic receptor in heart, thus reduces cardiac output (working load) of the heart.
An 'Angiotension Converting Enzyme Inhibitor' (=ACE inhibitor) drug - act on the rennin angiotensin aldosterone system but inhibiting ACE. This actively doesn't activate angiotensin-2 that will in turn increase the cardiac output (i.e. the work load) of heart.
A 'statin' drug - reduces LDL cholesterol in the blood, thus reduces atherosclerotic plugs.
Stops smoking - less endothelial injury, thus reduces atherosclerotic plug. And less effects on coagulation, thus reduces thrombus form.
Improve his diet and loose weight - altered and collateral vessels
Regular exercise - Many effects including allows new collateral vessels to by pass the coronary artery.