Kana plaque mepasuka, yo lenda sala nde menga kukuma ngolo mpi kukanga nzila sambu menga yina kele ti oxygène mingi ve kukuma na misuni ya ntima.
Kukonda ya oxygène yai ke salaka nde baselile ya misuni ya ntima kufwa, ebuna yo ke nataka maladi ya ntima.
Mutindu maladi yango kenyokula ntima ketadila kiteso ya kisika yina misisa ya nene ya menga kekotaka mpi ntangu yina meluta banda na ntangu yina maladi yango kubwilaka muntu tii na ntangu ya bo mesadila nkisi.
Bimangu ya maladi ya ntima lenda vanda mpasi na ntulu, mpema mpasi, kubela, ntu mpasi, mpi mpasi na maboko, na nkingu, na luketo to na mukongo.
Mbala mingi, lusansu ya maladi ya ntima kelombaka kuvutula menga na misisa ya ntima nswalu mutindu yo lenda salama, yo vanda na nsadisa ya bankisi to na nsadisa ya bametode bonso angioplastie mpi stenting to operasio ya bypass ya misisa ya ntima.
Yo kele mfunu na kuzaba nde maladi ya ntima ke vandaka mpasi mpi yo ke vandaka ti mambu mingi, mu mbandu kimvwama, luzingu mpi mambu ya ke vandaka na nzyunga.
Bantu yina ke waka mpasi mingi na ntima kele bantu yina ke vandaka ti tansio ya ngolo, ba cholestérol mingi, ke nwaka makaya, ke vandaka ti diabete, ke vandaka nene, ke salaka ve bisalu ya ngolo mpi bantu ya dibuta na bo ke belaka maladi ya ntima.
Kuzaba mambu yai lenda sadisa na kufyotuna kigonsa ya maladi ya ntima.
Scott J: Pathophysiology and biochemistry of cardiovascular disease. Curr Opin Genet Dev. 2004, 14 (3): 271-9.
Liu Chung Ming C, Sesperez K, Ben-Sefer E, Arpon D, McGrath K, McClements L, Gentile C: Considerations to Model Heart Disease in Women with Preeclampsia and Cardiovascular Disease. Cells. 2021, 10 (4): .
Hansen J, Victor RG: Direct measurement of sympathetic activity: new insights into disordered blood pressure regulation in chronic renal failure. Curr Opin Nephrol Hypertens. 1994, 3 (6): 636-43.
LaMacchia JC, Roth MB: Aquaporins-2 and -4 regulate glycogen metabolism and survival during hyposmotic-anoxic stress in Caenorhabditis elegans. Am J Physiol Cell Physiol. 2015, 309 (2): C92-6.
Tham YK, Bernardo BC, Ooi JY, Weeks KL, McMullen JR: Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets. Arch Toxicol. 2015, 89 (9): 1401-38.
Lonn E: The clinical relevance of pharmacological blood pressure lowering mechanisms. Can J Cardiol. 2004, 20 Suppl B (): 83B-88B.
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What is pathophysiology of heart attack?
The pathophysiology of a heart attack, also known as myocardial infarction, involves the disruption of blood flow to a part of the heart muscle, leading to the death of heart cells.
This typically occurs due to the obstruction of a coronary artery by a blood clot, which is often the result of atherosclerosis, a condition where plaque builds up in the arteries.
The plaque is made up of cholesterol, fatty substances, cellular waste products, calcium, and fibrin.
When a plaque ruptures, it can cause a blood clot to form, which can block the artery and prevent oxygen-rich blood from reaching the heart muscle.
This lack of oxygen causes the heart muscle cells to die, leading to a heart attack.
The extent of the damage depends on the size of the area supplied by the blocked artery and the time between the attack and treatment.
Symptoms of a heart attack can include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and pain in the arms, neck, jaw, or back.
Treatment for a heart attack usually involves restoring blood flow to the heart muscle as quickly as possible, either through medication or procedures such as angioplasty and stenting or coronary artery bypass surgery.
It is important to note that the pathophysiology of a heart attack is complex and involves multiple factors, including genetic, lifestyle, and environmental factors.
Risk factors for heart attack include high blood pressure, high cholesterol, smoking, diabetes, obesity, lack of physical activity, and a family history of heart disease.
Managing these risk factors can help reduce the likelihood of experiencing a heart attack.
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