Pathophysiology Module 1: Cellular Adaptation, Injury, and Death

Vocabulary practice cards reviewing fundamental pathophysiological framework definitions, cellular adaptation types, and cellular injury mechanisms.

Pathophysiology

The study of the abnormal functioning of diseased organs and how it applies to medical treatment and patient care.

Etiology

The study of causes or reasons for phenomena, identifying causal factors that act in concert to provoke a particular disease or injury.

Idiopathic Etiology

A disease or condition classification indicating that the underlying cause is unknown.

Iatrogenic Etiology

A disease or condition classification indicating that the cause results directly from medical treatment.

Intrinsic Etiology

A classification of disease etiology where the causal factors originate or come from within the body.

Extrinsic Etiology

A classification of disease etiology where the causal factors originate or come from an outside force.

Pathogenesis

The development or evolution of a disease, tracing progression from the initial stimulus to the ultimate expression of clinical manifestations.

Signs vs. Symptoms

Signs are objective or observed manifestations of disease, whereas symptoms are subjective feelings of abnormality expressed by the patient.

Homeostasis

Meaning 'similar standing,' it is the process that allows the body to maintain a stable internal cellular environment within a range while adjusting to changing external conditions.

Compensation

The body's adaptive effort to return to homeostasis, which can produce pathology if prolonged.

Atrophy

A cellular adaptation involving a decrease in cell size due to decreased protein synthesis or increased protein catabolism, caused by reduced workload, blood supply, nutrition, or stimulation.

Hypertrophy

A cellular adaptation involving an increase in cell size, which can be physiologic (work demand/hormones) or pathologic (chronic hemodynamic overload like HTN).

Hyperplasia

A cellular adaptation characterized by an increase in cell number caused by an increased rate of cellular division.

Metaplasia

The reversible replacement of one mature cell type by another less mature cell type that is better suited to tolerate persistent injurious stimulation.

Dysplasia

A disorganized appearance of cells due to abnormal variations in size, shape, and arrangement, which acts as a preneoplastic lesion with significant potential to transform into cancer.

Hypoxia

The most common cause of cellular injury, defined by a reduced amount of oxygen in tissues, loss of hemoglobin, or decreased red blood cell production.

Ischemia

A reduced blood supply to tissues, most commonly caused by progressive arterial narrowing (arteriosclerosis) or thrombosis; it is the most common cause of hypoxia.

Reperfusion Injury

The paradoxical exacerbation of cellular dysfunction and death that occurs following the restoration of blood flow to previously ischemic tissues.

Mitochondrial Permeability Transition Pore (MPTP)

A large conductance pore on the mitochondrial membrane that opens during calcium overload and oxidative stress, causing massive escape of ATP and triggering apoptosis.

Free Radical

Any molecular species capable of independent existence that contains a single unpaired electron in an outer orbit, leading to damaging oxidation of lipids, proteins, and nucleic acids.

Pathogenicity

Also referred to as virulence, it is the disease-producing potential of a microorganism via invasion, destruction, toxin production, or hypersensitivity reactions.

Immunologic Complement Injury

An immune response mechanism associated with rapid leakage of potassium ($\text{K}^+$) out of the cell and rapid influx of water, causing severe cellular damage.

Necrosis

A common type of cell death characterized by severe cell swelling and breakdown of intracellular organelles following irreversible injury.

Apoptosis

A form of programmed cell death involving cellular self-destruction to eliminate unwanted or damaged cell populations.

Human Exposure Pathways

The primary body entry routes (Skin, Lung, GI tract) through which environmental chemicals absorb into the bloodstream for distribution, metabolism, storage, toxicity, or excretion.