Pathophysiology: Inflammation and Chemical Mediators

Comprehensive vocabulary flashcards covering the definition, signs, types, processes, and chemical mediators of inflammation as described in the pathophysiology lecture notes.

Inflammation

A protective vascular and cellular response of living tissues to injury, infection, or irritation that aims to eliminate the harmful stimulus and initiate healing.

Rubor

A classical sign of inflammation referring to redness caused by increased blood flow.

Calor

A classical sign of inflammation referring to heat caused by vasodilation and increased circulation.

Tumor

A classical sign of inflammation referring to swelling due to the accumulation of fluid in tissues.

Dolor

A classical sign of inflammation referring to pain caused by the stimulation of nerve endings.

Functio Laesa

A classical sign of inflammation referring to the loss of function due to pain and tissue damage.

Acute Inflammation

A rapid and short-term response to tissue injury or infection usually lasting from a few hours to a few days, characterized by neutrophils and exudation of plasma proteins.

Chronic Inflammation

A prolonged inflammatory response lasting weeks, months, or years, characterized by the presence of macrophages, lymphocytes, tissue destruction, and fibrosis.

Chemical Mediators

Biologically active substances that initiate, regulate, and control inflammatory reactions, produced by plasma proteins or cells like mast cells and neutrophils.

Chemotaxis

The migration of white blood cells toward the site of injury following chemical signals.

Phagocytosis

The process where neutrophils and macrophages engulf and destroy bacteria and damaged cells.

Histamine

A mediator sourced from mast cells, basophils, and platelets that causes vasodilation and increases vascular permeability during acute inflammation.

Serotonin

A mediator sourced from platelets and enterochromaffin cells that causes vascular changes and participates in platelet aggregation.

Prostaglandins

Mediators produced from arachidonic acid by Cyclooxygenase ($COX$) enzymes that cause vasodilation and are important mediators of pain and fever.

Leukotrienes

Mediators produced from arachidonic acid through the Lipoxygenase pathway that cause bronchoconstriction and attract neutrophils.

Cytokines

Proteins such as tumor necrosis factor ($TNF$) and interleukins ($IL-1$, $IL-6$) that coordinate inflammatory and immune responses.

Chemokines

Substances that attract white blood cells to the site of injury and regulate leukocyte migration.

Nitric Oxide ($NO$)

A substance produced by endothelial cells and macrophages that causes vasodilation, reduces platelet aggregation, and kills microorganisms.

Reactive Oxygen Species ($ROS$)

Produced by neutrophils and macrophages to destroy microorganisms, though excessive amounts may damage normal tissues.

Complement System

A system of plasma proteins activated during infection that performs opsonization of microbes, cell lysis via the Membrane Attack Complex ($MAC$), and attraction of neutrophils.

Bradykinin

The main mediator of the kinin system responsible for vasodilation, increased vascular permeability, and pain production.

$$NSAIDs$$

Non-steroidal anti-inflammatory drugs, such as aspirin and ibuprofen, that inhibit cyclooxygenase enzymes and reduce prostaglandin synthesis.

Corticosteroids

Drugs like prednisolone that suppress immune responses and cytokine production.

Angiogenesis

The formation of new blood vessels, listed as a vascular change characteristic of chronic inflammation.

Exudation

The process of plasma proteins and fluid leaking into tissues, a feature of acute inflammation leading to swelling.