Acid poisoning typically leads to which type of necrosis?

Acid poisoning typically leads to coagulative necrosis. This type of necrosis is characterized by the preservation of tissue architecture while the cellular details become obscured. In cases of acid exposure, particularly with strong acids like sulfuric or hydrochloric acid, the cellular proteins denature and coagulate, leading to the characteristic changes associated with coagulative necrosis.

This process is most often observed in solid organs such as the kidneys and heart, where damage from acids can disrupt cellular function while still allowing the overall structure of the tissue to be more or less conserved initially. Over time, if the tissue remains damaged, additional processes may induce further necrosis or inflammation, but the initial response to acid exposure tends to produce coagulative necrosis due to protein denaturation and cellular integrity being initially maintained.

In contrast, other types of necrosis involve different mechanisms or pathological processes, such as liquefactive necrosis, which typically occurs due to bacterial infections and results in the transformation of tissue into a liquid viscous mass; caseous necrosis, often seen in tuberculosis infections, is characterized by a cheese-like appearance of necrotic tissue; and fat necrosis, which is typically associated with pancreatic damage or trauma to fat tissue, not directly related to acid poisoning