Liquefactive necrosis and gangrenous necrosis
Coagulative necrosis and liquefactive necrosis.
Traumatic fat necrosis
Enzymatic fat necrosis
Coagulative necrosis and calcifications
A defect in physiologic apoptosis and developmental involution
A defect in pathologic apoptosis and developmental involution
A defect in physiologic apoptosis and organogenesis
A defect in pathologic apoptosis and cell death induced by cytotoxic T cells
Preservation of cardiac tissue structure without nuclei
Rupture of cardiac cell membranes
Amorphous appearance of cardiac tissue
Mitochondrial swelling associated with reversible injury.
Nuclear lysis associated with irreversible injury.
Increase in intracellular calcium associated with irreversible injury.
Damage of cell membranes associated with irreversible injury.
Physiologic apoptosis and developmental involution.
Pathologic apoptosis and developmental involution
Physiologic apoptosis and hormonal dependent involution
Pathologic apoptosis and hormonal dependent involution
Influx of Na+ and Ca++ resulting in liquefactive necrosis
Influx of K+ and Ca++ resulting in coagulative necrosis
Efflux of K+ and Ca++ resulting in liquefactive necrosis
Efflux of Na+ and Ca++ resulting in coagulative necrosis
Coagulative necrosis of myocardium
Increased serum creatinine kinase myocardiaI band (CK-MB) fraction
Left ventricle hypertrophy
Neutrophils infiltrating the myocardium
Barrett's esophagitis, which is an irreversible metaplastic adaptive response
Barrett's esophagitis which is an irreversible dysplastic adaptive response
Barrett's esophagitis which is a reversi ble hyperplastic adaptive response
Barrett's esophagitis which is a reversible metaplastic adaptive response
Acute purulent pneumonitis
Parasitic migration tracts
Swelling of the mitochondria
Disruption of protein synthesis
Heterophagy by Iysosomes
Damage to the cell membrane
Karryorhexis of the nucleus