Increase in cell size resulting in increase in tissue/organ size. No increase in cell number.
Decreased cell development or decreased number of cells. Leads to decrease in tissue/organ size.
Increase in cell number. Leads to increase in tissue/organ size.
Reduced size of organ/tissue due to reduced cell number and reduced cell size.
Reversible replacement of one differentiated cell type with another differentiated cell type.
Always pathologic result of lysozymal enzymes leaking into the cytoplasm causing cell death via organelle digestion and protein degradation. Cell contents leak into environment.
Controlled form of cell death, pathologic and normal. Characterized by nuclear dissolution, fragmentation of cell, without complete loss of membrane integrity and rapid removal of the cellular debris
Reduction of blood flow to a tissue. Often causes hypoxia.
Deficiency of oxygen in tissue. Often a result of poor blood flow (ischemia), Cardiac failure, respiratory failure, decreased SpO2 (anemia, toxins...), Blood loss.
Most common pattern of necrosis. Proteins denature, but cell and tissue framework remain intact. Characteristic of hypoxic death (except brain).
Mitochondrial permeability transition pore
High conductance channel in mito membrane. When open, mito membrane potential is lost, leading ot failure of ox phosph and eventual depletion of ATP causing cell necrosis. Cyclophillin D is a major part of the pore, and target of immunosuppressants.
ROS: Reactive Oxygen Species
Oxygen radical causing cell injury and death. Broken down by superoxide dismustase into H2O2 which is broken down into H2O by catalase.
Ischemia Reperfusion Injury
Return of blood/O2 to ischemic tissue. Causes increased injury due to ROS from return of oxygen. Increased adhesion molecules increase PMNs, IgM deposited --> complement activation.
Intrinsic Pathway of Apoptosis
Major Pathway and mito pathway of apoptosis. Stressed cells activate BH3 Proteins. BH3s activate BAX and BAK, opening mito pore.
Extrinsic pathway of apoptosis
Initiated when plasma membrane death receptors engage a variety of targets. Death receptors: TNF family employing intracellular death domain, Fas/FasL, and caspase activation.
Dystrophic - coagulative, liquefactive, caseous type and in foci of enzymatic necrosis of fat.
Metastatic - Hypercalcemia in any normal tissue affects tissue w alkaline compartments secreting acid.
Short repeated (TTTAAAGG) DNA sequences at the ends of chromosomes. Ensure complete replication of chromosomes and protect ends from degradation.
Local response to cellular injury marked by capillary dilatation, leukocytic infiltration, redness, heat, pain, swelling, loss of function. Serves as a mechanism for eliminating noxious agents and damaged tissue
Rapid host response that serves to deliver leukocytes and plasma proteins (like antibodies) to sites of infection or tissue injury.
Inflammation of prolonged duration (weeks or months) in which inflammation, tissue injury, and attempts at repair COEXIST in varying states.
extravascular fluid that has high protein concentration, contains cellular debris, and has high specific gravity
fluid with low protein (most albumin), little or no cellular material, and low specific gravity
abnormal increase in interstitial fluid
Diapedesis! K-N-O-W Forever.
Locomotion oriented along a chemical gradient.
when cells recognize and attach, engulf and fuse, then degrade
endothelial cells are induced by TNF and IL-1 to express adhesion molecules, synthesize chemical mediators; produce enzymes asstd with matrix remodeling; increase in the surface thrombogenicity. Become sticky and leaky.
Localized collection of inflammatory tissue tissue caused by suppuration buried in an organ.
Pus. Fluid from nfx. Rich in: PMNs, cellular debris and microbes.
Focus of chronic inflammation consisting of aggregations of macrophages transformed into epithelial like lining (giant cells) and TH1 Tcells.
Acute Phase Proteins
Plasma proteins mostly made in liver. Concentration increases as inflammatory response. Up regulated by IL6 IL1 and TNF.
Leukocytosis and Leukopenia
Cytosis: High lymphocyte count,, usually from inflammation. Stimulated by CSFs TNF and IL1.
Penia - Decrease in WBCs
Proliferation of cells to replace lost cells in tissue. Liver is the best example.
Most often done through some regeneration and scar formation via deposition of collagen.
Less specialized tissue develops into a more specialized tissue.
Embryonic Stem Cell
Pluripotent stem cells contained in inner cell mass of blastocysts in early embryonic development.
Adult (somatic) Stem Cell
Cells present in tissues that continuously divide such as bone marrow, the skin, and lining of GI tract; divide slowly and can give rise to amplifying cells—lose capacity of self-perpetuation and give rise to progenitor cells
Induced Pluripotent Stem Cell
Reprogrammed fibroblast cells; done so by the transduction of 4 genes encoding TFs; able to generate cells from endodermal, mesdermal, and ectodermal origin; these TFs act to prevent differentiation
Receptor Mediated Signal Transduction
Binding of ligand to receptor causes extracellular signals to be transduced into the cell resulting in gene expression change -Intrinsic tyrosine kinase - Receptors lacking tyrosine kinase activity
G-protein linked- steroid hormone receptor
Extracellular Matrix (ECM)
outside of cells; regulates the growth, proliferation, movement, and differentiation of cells living within it
Focal Adhesion Complex
Formed when ligands bind to integrins and the receptors cluster; composed of talin, vinculin, and paxillin; function as activated receptors, triggering signal transduction pathways including the MAP kinase, PKC, and PI3K.
Blood vessel formation in adults; involves branching and extension of adjacent pre-existing vessels but can also occur by recruitment of endothelial progenitor cells (EPCs) from the bone marrow.
Healing by Primary Union
healing of a clean, uninfected surgical incision approximated by surgical sutures
Healing by secondary Union
Healing for large defects in the skin with extensive loss of tissue and cells. More intense inflammatory rxn, formation of granulation tissue, and extensive collagen deposition leading formation of a scar which generally contracts
Hallmark of tissue repair. Made of fibroblasts and vascular endothelial cells; first 24-72 hours of injury; histologically presence of new small blood vessel and the proliferation of fibroblasts
Excessive formation of the components of the repair process; collagen accumulation that leads to a scar BEYOND the boundaries of the original wound that does not regress.
Excessive deposition of collagen and other ECM component in a tissue; CHRONIC
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