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A complete set of vocabulary practice flashcards covering core pathology topics including cell death, adaptations, inflammation mechanisms, granulomatous conditions, and wound healing from lecture notes.
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Apoptosis
A genetically programmed, energy-dependent, and regulated form of cell death in which cells die in a controlled manner without causing an inflammatory reaction or damage to surrounding tissues.
Caspases
A family of cysteine proteases present as inactive procaspases that mediate apoptosis when activated into initiator or executioner forms.
Apoptosome
A protein complex formed during the intrinsic apoptotic pathway when cytochrome c binds to Apaf-1 and procaspase-9, leading to activation of initiator caspase-9.
Dysregulated Apoptosis
An imbalance in programmed cell death resulting in either defective apoptosis (leading to cell survival in cancer or autoimmune disease) or excessive apoptosis (leading to cell loss in neurodegenerative or ischemic injury).
Necrosis
Localized death of cells or tissues in a living body due to irreversible injury, followed by enzymatic degradation of dead tissue and accompanied by an inflammatory response.
Coagulative Necrosis
The most common pattern of necrosis, usually caused by sudden loss of blood supply (ischemia), characterized by preservation of basic tissue architecture for several days.
Liquefactive Necrosis
A type of necrosis caused by rapid enzymatic digestion of dead cells to form a soft, liquid mass, commonly seen in ischemic brain injury and purulent bacterial or fungal infections.
Caseous Necrosis
A crumbly, cheese-like form of cell death combining features of coagulative and liquefactive necrosis, classically found in the center of tuberculous lesions.
Fat Necrosis
Focal tissue destruction involving adipose tissue due to trauma or pancreatic lipase release, resulting in chalky white deposits through calcium saponification.
Fibrinoid Necrosis
A special pattern of vascular injury characterized by bright eosinophilic fibrin-like deposits in blood vessel walls caused by immune-mediated vasculitis or severe hypertension.
Pyknosis
A nuclear alteration during cell death characterized by nuclear shrinkage and increased basophilia.
Karyorrhexis
A nuclear change in cell death where the pyknotic nucleus undergoes fragmentation into small granular pieces.
Karyolysis
The complete dissolution and fading of a cell nucleus during necrosis due to enzymatic degradation by deoxyribonucleases.
Reversible Cell Injury
Cellular changes occurring when an injurious stimulus is mild or brief, allowing the cell to recover normal structural and functional state upon removal of the stress.
Irreversible Cell Injury
Permanent structural and functional damage caused by persistent hypoxia or injury, resulting in loss of membrane integrity and inevitable cell death.
Hyperplasia
An adaptive increase in the total number of cells in an organ or tissue.
Hypertrophy
An adaptive increase in individual cell size resulting in an enlarged organ without an increase in overall cell number.
Atrophy
An adaptive decrease in cell size and/or cell number, leading to reduced mass of a tissue or organ.
Metaplasia
A reversible cellular adaptation in which one adult mature cell type (epithelial or mesenchymal) is replaced by another adult mature cell type.
Dysplasia
Disordered cellular development characterized by cytologic atypia, cellular and nuclear pleomorphism, loss of polarity, and increased abnormal mitoses.
Barrett's Esophagus
A premalignant condition where chronic gastroesophageal reflux disease (GERD) causes normal esophageal stratified squamous epithelium to be replaced by intestinal-type columnar epithelium with goblet cells.
Gangrene
Tissue necrosis—most commonly ischemic coagulative necrosis—associated with superadded putrefactive bacterial infection and tissue decomposition.
Gas Gangrene
A variant of wet gangrene caused by anaerobic Clostridium perfringens bacteria, characterized by tissue swelling, foul odor, and crepitus due to accumulation of CO2​ gas bubbles.
Dystrophic Calcification
Deposition of calcium phosphate salts in necrotic or degenerated tissues occurring in the presence of normal calcium metabolism and normal serum calcium levels.
Metastatic Calcification
Deposition of calcium salts in normal intact tissues resulting from metabolic disorders causing hypercalcemia.
Free Radicals
Highly reactive chemical species containing a single unpaired electron in an outer orbit that induce cytotoxicity through lipid peroxidation, protein oxidation, and DNA breakage.
Lipofuscin
A yellowish-brown, granular intracellular lipid-protein pigment derived from membrane peroxidation, commonly accumulating in atrophied or aging cells as a wear-and-tear marker.
Steatosis
The abnormal intracellular accumulation of neutral fat (triglycerides) within parenchymal cells, most frequently observed in the liver.
Autophagy
A catabolic lysosomal survival mechanism in which a cell degrades its own cytoplasmic components and organelles to survive stress and starvation.
Necroptosis
A programmed, caspase-independent form of necrotic cell death mediated by RIPK1, RIPK3, and MLKL proteins that triggers an inflammatory response.
Lipoxins
Anti-inflammatory lipid mediators derived from arachidonic acid via the lipoxygenase pathway that inhibit leukocyte recruitment and promote resolution of inflammation.
Acute Inflammation
An immediate, short-duration response (<2Â weeks) to injury characterized by vascular dilation, fluid exudation, and predominantly neutrophilic cell infiltration.
Transudate vs Exudate
Transudate is non-inflammatory extravascular fluid low in protein (<3Â g/dL) caused by hydrostatic or oncotic pressure imbalance; exudate is inflammatory fluid high in protein (>3Â g/dL) and leukocytes caused by increased vascular permeability.
Diapedesis
The movement of leukocytes squeezing between endothelial cells of post-capillary venules to enter interstitial tissues, mediated primarily by PECAM-1 (CD31).
Chemotaxis
The oriented, directional movement of leukocytes along a chemical concentration gradient toward an inflammatory stimulus or site of injury.
Opsonization
The coating of microorganisms or foreign particles with specific proteins (opsonins such as IgG or C3b) to enhance phagocyte recognition and attachment.
Arachidonic Acid Metabolites
Lipid mediators (eicosanoids) synthesized via cyclooxygenase or lipoxygenase pathways that regulate vascular tone, permeability, leukocyte chemotaxis, and pain.
Granuloma
A localized collection of activated macrophages (epithelioid cells) surrounded by a peripheral rim of lymphocytes, formed during specific patterns of chronic inflammation.
Langhans Giant Cells
Multinucleated giant cells formed by fused epithelioid cells with nuclei arranged peripherally in a horseshoe pattern, classic for tuberculous granulomas.
Foreign Body Giant Cell vs Tumor Giant Cell
Foreign body giant cells contain uniform nuclei scattered throughout abundant cytoplasm; tumor giant cells originate from neoplastic cells with pleomorphic, hyperchromatic nuclei arranged haphazardly.
Ghon Complex
The classic primary pulmonary tuberculosis lesion consisting of a parenchymal lung focus (Ghon focus) combined with caseating involvement of draining hilar lymph nodes.
Miliary Tuberculosis
A disseminated form of tuberculosis resulting from hematogenous spread of Mycobacterium tuberculosis, characterized by tiny (1–2 mm) caseating nodules across multiple organs.
Lepromatous vs Tuberculoid Leprosy
Lepromatous leprosy (LL) is marked by suppressed cell-mediated immunity, symmetrical lesions, and abundant lepra bacilli; tuberculoid leprosy (TT) features strong cell-mediated immunity, sparse lesions, and very few bacilli.
Granulation Tissue
Specialized, vascularized connective tissue containing proliferating new capillaries (angiogenesis), active fibroblasts, and inflammatory cells formed during wound repair.
Angiogenesis
The formation of new blood vessels from pre-existing capillaries during tissue repair, regulated primarily by growth factors such as VEGF and FGF.
Healing by Primary Intention
Healing of clean, uninfected surgical wounds with well-approximated edges, minimal tissue loss, scanty granulation tissue, and a thin linear scar.
Healing by Secondary Intention
Healing in large tissue defects with unapposed margins, characterized by intense inflammation, extensive granulation tissue, prominent wound contraction by myofibroblasts, and substantial scarring.
Fracture Callus
Reproductive tissue at a bone fracture site that evolves from an uncalcified soft fibrocartilaginous procallus into a calcified hard osseous callus prior to bone remodeling.