Ihi i bhangesa o muthu ku kala ni muxima ua toloka?
O uhaxi ua muxima, a uixana ué infarto do miocárdio, u fidisa o manhinga ku bokona mu mukutu ua muthu, ni ku bhangesa o ji célula ja muxima kufua.
O uhaxi iú u bhita mukonda dia manhinga a mu di bhongolola mu phuna, o manhinga a mu di bhongolola ué mukonda dia ku kala ni ixete iavulu mu phuna.
O ifuba íii iala ni ima iavulu, kála o manhinga a makota, iangu, ni ima ia mukuá dingi.
Kioso o manhinga kia di muanga, a tena ku bhangesa o manhinga ku di lunga, kiki ki fidisa o manhinga ku bhixila ku muxima.
O manhinga a fidisa o ji célula ja muxima ku kalakala kiambote, kiki ki bhangesa o muthu ku kala ni uhaxi ua thulu.
O uhaxi iú u bhinga ku u saka ni lusolo.
O uhaxi iú u tena ku kala ni ndolo ku muxima, ku kala ni kikote ku muxima, ku kamba o ku bhuima, ku divua kia iibha, ku kala ni ndolo ku maku, ku xingu, ku mazu mba ku dikunda.
O ukexilu ua ku saka o uhaxi ua muxima, o ku bhangesa o manhinga ku bokona ni lusolo mu phuna ia muxima, bhu kaxi ka milongo, mba ku bhanga pelasá.
O uhaxi iú ua bhonzo kiavulu, u bhangesa o muthu ku kala ni uhaxi ua thulu.
O uhaxi ua thulu ni ua izavu, u bhangesa o muthu ku kala ni muxima ua toloka.
O ku langa o ima íii, i tena ku kuatekesa o muthu ku kala ni muxima ua tululuka.
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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