Introduction to Pathology and Cell Injury

The study of the underlying causes of diseases, such as infections, trauma, or genetic abnormalities.

The mechanisms by which diseases develop and progress, focusing on how these causes disrupt normal cellular function.

Structural and functional abnormalities in cells and tissues that result from disease processes, such as swelling or abnormal formations.

The ability of cells to adapt to mild, transient stressors by undergoing changes like organelle swelling, membrane blebbing, and lipid accumulation.

The point where cell damage becomes permanent and irreversible, leading to either uncontrolled cell death (necrosis) or programmed cell death (apoptosis).

Mitochondria are the powerhouses of the cell responsible for producing ATP. When mitochondria get damaged, they produce less ATP, leading to energy depletion in the cell.

Damaged mitochondria produce harmful molecules called reactive oxygen species (ROS) that can damage cellular components.

A form of cell death where the cell swells and bursts, releasing its contents into the surrounding environment.

Damage-associated molecular patterns are molecules released from dying cells that signal the immune system about cellular damage. These molecules trigger an inflammatory response.

When cells die, ATP, usually confined within mitochondria, leaks out into the surrounding area.

Uric acid and UTP are released when DNA breaks down during cell death.

The release of DAMPs activates immune cells, like macrophages, prompting them to generate pro-inflammatory cytokines, which initiate an inflammatory response to clear dead cells and repair damaged tissue.

The process where an infarcted (dead) area of kidney tissue is replaced by fibrous scar tissue.

A clear boundary between healthy kidney tissue and the infarcted area, representing the abrupt cessation of blood supply.

Preserved tissue structure despite cell death, a characteristic feature of coagulative necrosis in kidney infarcts.

Neutrophils, white blood cells, arrive at the infarct site to initiate the inflammatory response, clearing dead cell debris.

A kidney infarct caused by a blockage in an end artery, completely cutting off blood supply.

The glomerulus and tubules remain visible in an early-stage kidney infarct, indicating structural integrity despite cell death.

The absence of cell nuclei in an early-stage infarct, signifying cell death due to nuclear dissolution.

The lack of neutrophils in an early-stage infarct, indicating the inflammatory response has not yet begun.

A kidney infarct where the affected area lacks erythrocytes (red blood cells), leading to a pale appearance.

Fatty acids, released during the breakdown of fat tissue, react with calcium ions to form insoluble salts. This reaction is specific to fat necrosis and creates a chalky white appearance.

The death or destruction of fat tissue, often caused by the release of digestive enzymes in conditions like pancreatitis.

Inflammation of the pancreas caused by the activation of digestive enzymes within the organ itself.

The process by which digestive enzymes, like lipases, break down triglycerides into fatty acids.

A common cause of pancreatitis caused by the accumulation of gallstones in the bile duct, blocking the flow of digestive enzymes.

The premature activation of digestive enzymes within the pancreas, leading to autodigestion of the organ.

The process by which injured acinar cells release digestive enzymes, causing local tissue damage.

The obstruction of the pancreatic duct, leading to interstitial edema, impaired blood flow, and activation of digestive enzymes.

The process by which inactive digestive enzymes (proenzymes) are prematurely activated within the lysosomes, leading to acinar cell death.

A key factor in pancreatitis, where the pancreas becomes inflamed and swollen due to tissue damage, leading to a cascade of detrimental events.

Latent tuberculosis (TB) infection can reactivate in individuals with weakened immune systems, such as those with COVID-19, RSV, or HIV. This reactivation leads to active TB disease, causing widespread tissue damage and potentially fatal consequences.

Caseous necrosis is a type of cell death, characterized by a soft, white, and cheese-like appearance of the necrotic tissue. It is often seen in chronic granulomatous diseases, like tuberculosis.

In caseous necrosis, the necrotic tissue lacks any recognizable tissue architecture. This makes it distinct from coagulative necrosis, where the tissue structure is preserved.

Caseous necrosis is caused by bacterial infections, primarily Mycobacterium tuberculosis, rather than ischemia or infarction.

Caseous necrosis is characterized by the presence of a granuloma, which is a cluster of inflammatory cells, including macrophages and lymphocytes, surrounding the necrotic core. This shows the immune system's attempt to contain the infection.

Fibrinoid necrosis is characterized by the presence of bright pink, amorphous material in the vessel walls on histology. This material resembles fibrin.

Fibrinoid necrosis was initially thought to be composed primarily of fibrin, but now it is understood to also contain proteins and collagen, contributing to its fibrin-like appearance.

Fibrinoid necrosis is triggered by immune complex deposition in blood vessels. This activates the immune response, leading to fibrin leakage and accumulation of plasma proteins within the vessel wall.

Fibrinoid necrosis is commonly found in immune-mediated vascular damage, such as vasculitis and autoimmune diseases like systemic lupus erythematosus (SLE).

Fibrinoid necrosis can also occur due to non-immune causes, such as severe hypertension or mechanical stress on vessel walls.