Path Terms

Medicine Smd 535 with Koles at Wright State University

About this deck

By: Anonymous
Textbook:

Robbins & Cotran Pathologic Basis of Disease: With STUDENT CONSULT Online Access (Robbins Pathology)
Created: 2011-08-15
Size: 50 flashcards
Views: 16

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Etiology

Cause of a disease

Pathogenesis

Mechanisms of disease development

Morphologic Changes

Gross or microscopic

Hypertrophy

Increase in cell size resulting in increase in tissue/organ size. No increase in cell number.

Hypoplasia

Decreased cell development or decreased number of cells. Leads to decrease in tissue/organ size.

Hyperplasia

Increase in cell number. Leads to increase in tissue/organ size.

Atrophy

Reduced size of organ/tissue due to reduced cell number and reduced cell size.

Metaplasia

Reversible replacement of one differentiated cell type with another differentiated cell type.

Necrosis

Always pathologic result of lysozymal enzymes leaking into the cytoplasm causing cell death via organelle digestion and protein degradation. Cell contents leak into environment.

Apoptosis

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

Ischemia

Reduction of blood flow to a tissue. Often causes hypoxia.

Hypoxia

Deficiency of oxygen in tissue. Often a result of poor blood flow (ischemia), Cardiac failure, respiratory failure, decreased SpO2 (anemia, toxins...), Blood loss.

Coagulative Necrosis

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.

Calcification

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.

Telomere

Short repeated (TTTAAAGG) DNA sequences at the ends of chromosomes. Ensure complete replication of chromosomes and protect ends from degradation.

Inflammation

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

Acute Inflammation

Rapid host response that serves to deliver leukocytes and plasma proteins (like antibodies) to sites of infection or tissue injury.

Chronic Inflammation

Inflammation of prolonged duration (weeks or months) in which inflammation, tissue injury, and attempts at repair COEXIST in varying states.

Exudate

extravascular fluid that has high protein concentration, contains cellular debris, and has high specific gravity

Transudate

fluid with low protein (most albumin), little or no cellular material, and low specific gravity

Edema

abnormal increase in interstitial fluid

Transmigration

Diapedesis! K-N-O-W Forever.

Chemotaxis

Locomotion oriented along a chemical gradient.

Phagocytosis

when cells recognize and attach, engulf and fuse, then degrade

Endothelial activation

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.

Abscess

Localized collection of inflammatory tissue tissue caused by suppuration buried in an organ.

Purulent Exudate.

Pus. Fluid from nfx. Rich in: PMNs, cellular debris and microbes.

Granuloma

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

Regeneration

Proliferation of cells to replace lost cells in tissue. Liver is the best example.

Repair

Most often done through some regeneration and scar formation via deposition of collagen.

Differentiation

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.

Angiogenesis (neovascularization)

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

Granulation Tissue

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

Keloid

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.

Fibrosis

Excessive deposition of collagen and other ECM component in a tissue; CHRONIC

About this deck

By: Anonymous
Textbook:

Robbins & Cotran Pathologic Basis of Disease: With STUDENT CONSULT Online Access (Robbins Pathology)
Created: 2011-08-15
Size: 50 flashcards
Views: 16

About StudyBlue

“Simply amazing. The flash cards are smooth, there are many different types of studying tools, and there is a great search engine. I praise you on the awesomeness.”
Dennis