TEP Patologia key terms

The branch of medicine that studies the causes, mechanisms, and structural and functional changes produced by disease in cells, tissues, and organs.

The study of the causes of disease, including intrinsic genetic factors and extrinsic agents such as infections, chemicals, physical forces, and immune reactions.

The sequence of cellular and molecular events through which an etiologic agent produces structural and functional abnormalities, from the initial trigger to the clinical manifestation.

Cellular damage that can be repaired if the harmful stimulus is removed, typically showing swelling, fatty change, and mild organelle alterations without loss of the plasma membrane.

Damage beyond the cell's capacity for repair, marked by membrane integrity loss, mitochondrial failure, and enzyme leakage, culminating in cell death by necrosis or apoptosis.

Cell death in living tissue accompanied by inflammation, resulting from severe injury, with loss of membrane integrity, enzymatic digestion, and leakage of intracellular contents.

Programmed cell death driven by regulated intracellular signaling, producing cell shrinkage, chromatin condensation, and membrane-bound bodies cleared without significant inflammation.

A pattern of necrosis in which tissue architecture is preserved as a ghost outline for days, typically caused by ischemia in organs other than the brain.

A pattern of necrosis in which dead tissue is rapidly digested into a viscous liquid mass, classically seen in brain infarcts and in abscesses rich in neutrophils.

A form of necrosis with a friable, cheese-like appearance and loss of tissue architecture, characteristically found in tuberculosis and some fungal infections.

Fat tissue necrosis caused by released lipases that split triglycerides into fatty acids, which bind calcium to form chalky white deposits, as in acute pancreatitis.

Inadequate blood supply to a tissue or organ caused by arterial obstruction, vasoconstriction, or reduced perfusion, leading to oxygen and nutrient deprivation.

A state of reduced oxygen availability to cells, which impairs oxidative phosphorylation and ATP production, triggering anaerobic metabolism and cell injury.

An area of ischemic necrosis produced by occlusion of the arterial supply or venous drainage of a tissue, commonly in the heart, brain, or kidney.

Highly reactive chemical species with unpaired electrons that damage lipids, proteins, and DNA, contributing to cell injury, aging, and many disease processes.

An imbalance in which reactive oxygen species exceed the capacity of antioxidant defenses, causing oxidative damage to cellular macromolecules and promoting disease.

A rapid, short-lived response to injury or infection characterized by vasodilation, increased vascular permeability, and neutrophil recruitment to the affected tissue.

A prolonged inflammatory response in which mononuclear cells, especially macrophages and lymphocytes, predominate, often with tissue destruction and attempts at repair.

An inflammatory fluid rich in protein and cells that escapes from vessels due to increased permeability, distinguishing it from a protein-poor transudate.

A protein-poor, low-cell fluid that accumulates due to increased hydrostatic pressure or reduced oncotic pressure rather than inflammation, as in heart failure.

Endogenous molecules such as histamine, prostaglandins, leukotrienes, cytokines, and complement fragments that initiate, amplify, and regulate the inflammatory response.

A compact aggregate of activated macrophages, often with multinucleated giant cells and a rim of lymphocytes, formed in chronic inflammation to contain persistent agents.

The process of restoring tissue structure after injury, occurring by regeneration of surviving cells or by scar formation with fibrous connective tissue.

Excessive deposition of collagen and extracellular matrix replacing normal tissue after injury or chronic inflammation, which may impair organ function.

Newly formed vascularized repair tissue composed of proliferating capillaries, fibroblasts, and inflammatory cells that fills wounds before scar maturation.

An increase in the number of cells in a tissue or organ in response to a stimulus, which may be physiologic or pathologic and usually remains controlled.

An increase in the size of individual cells resulting in enlargement of the affected organ, commonly seen in cardiac and skeletal muscle under increased workload.

A reduction in the size of a cell, tissue, or organ due to decreased workload, loss of innervation or blood supply, malnutrition, or aging.

A reversible change in which one differentiated cell type is replaced by another better adapted to stress, such as squamous metaplasia of the bronchial epithelium.

Disordered growth with altered cell size, shape, and organization, often reflecting genetic damage and considered a precursor of malignancy when severe.

An abnormal mass of tissue whose growth exceeds and is uncoordinated with that of normal tissue, persisting after removal of the initiating stimulus.

A tumor that remains localized, grows slowly, is usually well circumscribed, and does not invade adjacent tissues or spread to distant sites.

A cancer that invades surrounding tissues, is capable of metastasis, and typically shows anaplasia, high mitotic activity, and uncontrolled growth.

The spread of tumor cells from a primary site to distant organs through lymphatic channels, blood vessels, or body cavities, forming secondary tumor deposits.

Severe dysplasia affecting the full thickness of an epithelium but confined by the basement membrane, without invasion into underlying tissue.

Abnormal accumulation of fluid in interstitial tissue spaces or body cavities, resulting from altered hydrostatic or oncotic pressures, lymphatic obstruction, or inflammation.

Increased blood volume within a tissue due to arteriolar dilation, producing redness and warmth, as seen in acute inflammation or exercise.

Passive accumulation of blood in a tissue caused by impaired venous return, leading to cyanosis and potentially chronic organ damage.

Formation of a solid blood clot within an intact vessel or heart chamber during life, favored by endothelial injury, abnormal flow, and hypercoagulability.

A solid mass formed from blood constituents inside the vascular system during life, which may partially or completely obstruct the vessel lumen.

The passage of a detached solid, liquid, or gaseous mass through the bloodstream until it lodges in a vessel too small to permit further travel.