Pathophysiology: Cellular Biology, Adaptation, Injury, and Immunity

Vocabulary flashcards detailing cellular structure, transport mechanisms, cellular adaptations, accumulation pathologies, cellular injury/death, acute inflammation, plasma protein cascades, immune system cells, and hypersensitivities based on lecture notes.

Plasma Membrane

A semipermeable structure that keeps intracellular and extracellular fluid separate and controls the movement of substances into and out of the cell.

Homeostasis

The state of equilibrium in which cells self-regulate to counteract changes in the environment and maintain normal function.

Negative Feedback

A homeostatic mechanism where the body responds to a stimulus in the opposite direction to resist change and return to an ideal value or normal state.

Positive Feedback

A feedback mechanism where the body responds to a stimulus in the same direction to augment the stimulus, moving away from homeostasis (e.g., labor during birth with oxytocin).

Passive Transport

Cell membrane transport that requires no energy ($\text{ATP}$) and moves solutes downhill along a concentration gradient (e.g., simple diffusion, carrier-mediated facilitated diffusion, channel-mediated facilitated diffusion, and osmosis).

Active Transport

Cell membrane transport that requires oxygen and energy ($\text{ATP}$) to move solutes uphill against a concentration gradient, such as the $\text{Na}^+/\text{K}^+$ pump.

Phagocytosis

A form of endocytosis referred to as cell eating, primarily carried out by specialized immune cells such as macrophages and neutrophils.

Pinocytosis

A form of endocytosis referred to as cell drinking, involving the cellular uptake of extracellular fluid and dissolved solutes.

Cellular Atrophy

A decrease in cell size and functional components caused by disuse, denervation, lack of endocrine stimulation, decreased nutrition, ischemia, or aging.

Cellular Hypertrophy

A compensatory increase in cell size in response to increased workload or stress, which can be physiologic (temporary/reversible) or pathologic (usually irreversible d/t disease).

Cellular Hyperplasia

An increase in the number of cells resulting from an increased rate of cell division, occurring only in cell types capable of DNA synthesis and division.

Cellular Metaplasia

The reversible replacement of one normal mature cell type by another normal cell type that is better able to tolerate ongoing environmental stress.

Cellular Dysplasia

Abnormal changes in cell size, shape, organization, and appearance (atypical hyperplasia) that are not true adaptations but are strongly associated with cancer development.

Steatosis

An intracellular accumulation of fats or triglycerides within parenchymal cells, commonly exemplified by fatty liver.

Gierke Disease

A genetic defect characterized by a lack of enzymes needed to convert glycogen to glucose, leading to glycogen accumulation in the liver and kidneys.

Gout

An intracellular accumulation of uric acid crystals caused by an enzymatic deficiency in breaking down purines or an overproduction of purines.

Russell Bodies

Excessive accumulations of protein observed in plasma B-lymphocyte tumors.

Hypoxia

A lack of sufficient oxygen, which represents the single most common cause of cellular injury.

Necrosis

Unregulated cell death resulting from acute injury, characterized by cellular swelling (oncosis), breakdown of the plasma membrane, leakage of intracellular contents, and adjacent inflammation.

Apoptosis

Programmed, regulated cellular suicide characterized by chromatin condensation, membrane blebbing, cellular fragmentation, and phagocytosis without inducing inflammation.

Coagulative Necrosis

A pattern of cell death usually caused by hypoxia from ischemia, where acidosis denatures cellular proteins, resulting in a firm, opaque appearance (infarct) in organs such as the heart.

Caseous Necrosis

A form of necrosis where dead cells persist without full enzymatic digestion, resulting in a soft, cheesy appearance and walled-off calcified tissue, characteristic of tuberculosis.

Fat Necrosis

Necrotic breakdown of adipose tissue where released free fatty acids combine with calcium, magnesium, and sodium ions to form chalky-white soaps.

Innate Immunity

The first line of immune defense comprising natural surface barriers and a rapid, non-specific inflammatory response that functions without immunological memory.

Adaptive Immunity

The secondary immune defense system mediated by T and B lymphocytes that provides specific long-term protection and immunological memory upon repeat exposure.

Mast Cells

Sentinel inflammatory cells located near blood vessels and skin surfaces that initiate inflammation by releasing histamine through degranulation and synthesizing lipid mediators.

Neutrophils

Short-lived phagocytic white blood cells making up approximately $55\%$ of total leukocytes that serve as the primary first responders at sites of acute inflammation.

Complement System

A plasma protein cascade activated by classical, lectin, or alternative pathways that generates opsonins ($\text{C3b}$), anaphylatoxins ($\text{C3a, C5a}$), and membrane attack complexes ($\text{C5b--C9}$).

Bradykinin

The primary vasoactive peptide generated by the kinin system that induces vasodilation, smooth muscle contraction, increased vascular permeability, and direct stimulation of pain nerve endings.

Dendritic Cells

Antigen-presenting cells residing in peripheral tissues that engulf pathogens and present processed antigens to T cells in secondary lymphoid organs, linking innate and adaptive immunity.

Natural Killer Cells

Nonspecific lymphocytes that recognize and eliminate virus-infected cells and tumor cells using toxins and cytokines to trigger target-cell apoptosis.

T Regulatory Cells

A specialized subset of T lymphocytes that suppress immune responses to maintain self-tolerance and cellular homeostasis.

T Cytotoxic Cells

Specific T lymphocytes that destroy virus-infected and cancerous target cells by releasing cell-membrane-disrupting enzymes or directly inducing apoptosis.

Type IV Hypersensitivity

A delayed ($24\text{--}72\text{ hours}$) cell-mediated hypersensitivity reaction driven by sensitized T cells, responsible for contact dermatitis (poison ivy), organ transplant rejection, and positive tuberculin skin tests.