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What happens when myocardial cells are injured?

What happens when myocardial cells are injured?

Myocardial injury and inflammation lead to the disruption of cellular membranes and the release of myosin heavy chain. Necrosis is a nonregulated process that results in cell membrane disruption and the loss and release of intracellular content into the extracellular environment.

What is adaptation in cell injury?

When cells are injured, one of two patterns will generally result: reversible cell injury leading to adaptation of the cells and tissue, or irreversible cell injury leading to cell death and tissue damage. When cells adapt to injury, their adaptive changes can be atrophy, hypertrophy, hyperplasia, or metaplasia.

What happens to the cells during myocardial infarction?

During myocardial infarction, cardiac myocytes in the ischemic zone die by both apoptosis and necrosis. Surprising, the magnitudes of each form of cell death remain unclear.

What causes myocardial injury?

Myocardial ischemia occurs when blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques (atherosclerosis). If the plaques rupture, you can have a heart attack (myocardial infarction).

What causes myocardial damage?

Acute myocardial infarction, also known as a heart attack, is a life-threatening condition that occurs when blood flow to the heart muscle is abruptly cut off, causing tissue damage. This is usually the result of a blockage in one or more of the coronary arteries.

What are basic principles of cell injury and adaptation?

Under physiological stresses or pathological stimuli (“injury”), cells can undergo adaptation to achieve a new steady state that would be compatible with their viability in the new environment. If the injury is too severe (“irreversible injury”), the affected cells die.

What are the types of cell adaptation?

Overview: The four basic types of cellular adaptation to be discussed in this section are hyperplasia, hypertrophy, atrophy, and metaplasia.

What type of cell injury is myocardial infarction?

Myocardial injury or myocardial necrosis refers to the cell death of cardiomyocytes and is defined by an elevation of cardiac troponin values. It is not only considered a prerequisite for the diagnosis of myocardial infarction but also an entity in itself and can arise from non-ischemic or non-cardiac conditions.

What are the main causes of myocardial infarction?

Myocardial infarction (MI) usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply to a portion of the myocardium.

What are the 4 mechanisms of cellular adaptation?

What is cellular adaptation to injury?

Cellular Adaptation to Injury • Cellular adaptations can be induced and/or regulated at any of a number of regulatory steps including receptor binding, signal transduction, gene transcription or protein synthesis • The most common morphologically apparent adaptive changes are

What is the relationship between adapted cell injury and hypertension?

The relationship among adapted, reversible and irreversible cell injury can be seen in heart muscle. Myocardial fibers when subjected to increasing load, as in case of hypertension, the cell adapts and undergoes hypertrophy i.e. an increase in size and heart sufficiently pumps against the increased load structure.

What is the cellular adaptation of hypertrophy?

The cellular adaptation depicted here is hyper- trophy, the type of reversible injury is ischemia, and the irreversible injury is ischemic coagulative necrosis. In the example of myocardial hypertrophy (lower left), the left ventricular wall is thicker than 2cm (normal, 1–1.5cm).

How does myocardium adapt to myocardial load?

Myocardium subjected to persistent increased load, as in hypertension or with a stenotic valve, adapts by undergoing hypertrophy—an increase in the size of the individual cells and ultimately the entire heart—to generate the required higher contractile force.

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