Para munthu wasuzgika na nthenda ya mtima, ndopa zikunjilira mu mtima yayi, ndipo maselo gha mtima ghakufwa.
Kanandi ivi vikuchitika chifukwa chakuti nthenda ya atherosclerosis yikupangiska kuti ndopa zinandi zikwane mu misipa.
Vinthu ivi ni cholesterol, mafuta, calcium, na fibrin.
Para ndopa zaleka kukhazikika, ndopa zikunjira mu misipa ndipo zikutondeka kufika ku mtima.
Para munthu walije mphepo iyi, maselo gha mtima ghakumara ndipo wakuŵa na nthenda ya mtima.
Para ndopa zaleka kwenda, munthu wangalwara matenda ghakupambanapambana.
Vimanyikwiro vya nthenda ya mtima ni vyakuŵinya mu chifuŵa, kutondeka kuthuta, kusuzgika maghanoghano, kupwetekeka mu mawoko, mu singo, mu matama, panji mu msana.
Kuti munthu waleke kulwara na nthenda iyi, kanandi pakukhumbikwira kuti ndopa ziweleremo luŵiro mu mtima.
Ntchakuzirwa kumanya kuti nthenda ya mtima njakusuzga chomene ndipo yikupangika na vinthu vinandi, nga majini, umoyo, na malo.
Vinyake ivyo vingapangiska kuti munthu wasuzgike na nthenda iyi ni kuthamanga kwa ndopa, kuŵa na cholesterol yinandi, kukhweŵa hona, nthenda ya shuga, kunenepa chomene, kutondeka kuchita maseŵero ghakukhozga thupi, kweniso usange mu banja linu muli nthenda ya mtima.
Para mungacita vinthu mwamahara na vinthu ivi, mungacepeskako suzgo la mtima.
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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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