Pathophysiology focuses on understanding how diseases alter normal function. It highlights the mechanisms behind disease development and progression.

Inflammation is the body's initial protective mechanism to remove harmful stimuli and begin healing. Its classic signs include redness, heat, swelling, and pain.

Cellular adaptation involves changes that enable cells to cope with stressful conditions. These modifications can be reversible if the stress is removed.

Hyperplasia involves a greater number of cells rather than an increase in cell size. It is often a response to a stimulus and can be reversible.

Necrosis is an uncontrolled process of cell death that results in cell rupture and inflammation. It is usually pathological and contrasts with apoptosis.

Histamine is released by mast cells and increases blood vessel permeability, causing vasodilation. It is an early mediator in the acute inflammatory response.

Apoptosis is a carefully regulated process of removing damaged or unnecessary cells. It prevents harmful inflammation and helps maintain tissue homeostasis.

Ischemia restricts oxygen and nutrient delivery, which causes cellular injury or death. This lack of perfusion is a central mechanism in many pathophysiological conditions.

Acute inflammation is marked by the rapid recruitment of neutrophils to the site of injury. These cells are the primary responders in the early stages of inflammation.

Free radicals are highly reactive molecules that damage cellular components through oxidation. Their uncontrolled activity can lead to significant cellular dysfunction.

Metaplasia can sometimes progress to dysplasia when cellular changes become abnormal and disorganized. This progression indicates an increased risk for malignant transformation.

Cytokines are key signaling proteins that modulate inflammation and orchestrate the immune response. They enable communication between immune cells during an inflammatory reaction.

Oxidative stress occurs when free radicals exceed the capacity of antioxidant defenses, leading to damage of lipids, proteins, and DNA. This imbalance is a key mechanism in many pathological states.

Apoptosis is a programmed and orderly cell death that typically avoids provoking an inflammatory response. In contrast, necrosis is uncontrolled and often leads to inflammation.

Rheumatoid arthritis is characterized by an autoimmune response that causes chronic inflammation and joint damage. This distinguishes it from degenerative conditions such as osteoarthritis.

Reperfusion injury happens when the restoration of blood flow leads to a burst of reactive oxygen species. The consequent inflammatory response can exacerbate the damage originally caused by ischemia.

Chronic inflammation can lead to ongoing tissue injury and the excessive deposition of extracellular matrix, resulting in fibrosis. This scar formation can impair the normal function of the affected tissue.

Cellular senescence stops cells from dividing and often leads to the secretion of pro-inflammatory cytokines. This senescence-associated secretory phenotype contributes to tissue dysfunction and age-related pathologies.

Tumor Necrosis Factor (TNF) is a cytokine that plays a key role in regulating both apoptosis and the inflammatory response. Its dual functions make it critical in many pathophysiological processes.

Fibroblasts are essential for tissue repair, but in chronic inflammation, their overactivity leads to excessive collagen deposition. This results in fibrosis, which compromises tissue structure and function.