Term
| Focal/pocket of pus filled that may be caused by deep seeding of pyogenic organs (purulent exudate) into a tissue or by 2nd infections of necrotic foci. Extensive neutrophil infiltration occurs. Can be filled with trans exudate or exudate. Hard to treat with antibodies. Leads to scarring. |
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Definition
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Term
| C3a and C5a (Stimulate the release of histamine from mast cells during inflammation) |
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Definition
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Term
| Tumor cells that lack of differentiation Common feature includes: cellular and nuclear pleomorphism; nuclear hyperchromasia and pleomorphism; increased nuclear to cytoplasmic ratio; increased number of mitosis; loss of orientation of cells; formation of tumor giant cells |
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Definition
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Term
| Formation of new blood vessels. It occurs 48 to 72 hours after injury and can last for days. It is regulated by macrophages and fibroblasts. A hole is made in the vessel (proteolytic degradation) and endothelial cells migrate out. They mature and differentiate and begin remodeling by forming a basement membrane. The new vessels are leaky and not as strong. All of the steps in angiogenesis are regulated by FGF-basic (bFGF) and VEGF |
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Definition
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Term
| Inhibits the activity of thrombin (which promotes clotting) and other serum proteases. “Prevent random clots”. A deficiency will cause hyper coagulability |
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Definition
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Term
| Cell death by activation of internal suicide program. Little disruption of surrounding tissues. Eliminates unwanted host cells. Cause by endogenous stimulation. |
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Definition
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Term
| Shrinking of cells in size with a secondary decrease in organ size |
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Definition
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Term
| one of the mechanisms of action of soluble chemical mediators (polypeptide growth factors among most important) ; of, relating to, or being a substance that acts on surface receptors of the same cell that produced it |
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Definition
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Term
| Manifested in heterozygous females. For example: one parent usually affected, new mutations can occur with the parents and siblings unaffected. Both males and females are affected and can transmit the condition. Reduced penetrance and variable expressivity. Each child has 50% chance if only 1 parent is affected. Age onset may be delayed. Two major non-enzymes proteins are affected: (1) those involved in regulation of metabolic pathways and membrane receptors and transport proteins (2) key structural proteins • A Mendelian disorder. |
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Definition
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Term
| Largest group of Mendelian disorders. Both alleles in a giving locus are mutated. Parents usually not affected. Each parent must have 1 mutant gene. Siblings may show disorder 25% of the time. Consanguious marriage increases the chance. Expression of defect is more uniform than autosomal dominant disorders. Complete penetrance is common. Early in life onset. New mutation rarely clinically detected. Enzyme proteins frequently affected. 50% reduction in enzyme mutation can usually be compensate for. |
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Definition
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Term
| Anaphylatoxin, induces the degranulation of mast cells and basophils. Increase vascular permeability and vasodilation. Released during IgE reaction |
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Definition
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Term
| Opsonins that help phagocytosis of material. The Fc portion of the Ig reacts to this |
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Definition
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Term
| Anaphylatoxin, induces the degranulation of mast cells and basophils. Activates lipoxygenase pathway of arachidonic acid metabolism, a potent chemotactic factor for neutrophils, monocytes eosinophils and basophils. Increase vascular permiability and vasodilation. |
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Definition
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Term
| helps to initiate the activation of the Membrane Attack Complex (the "anchoring" point) |
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Definition
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Term
| Membrane attach complex. Initiated by C5 |
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Definition
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Term
| Progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anemia. Can appear before tumor is clinically evident. Reduced food intake alone is not enough to explain findings. Clinical Sign and Symptoms: anorexia, decreased fat, decreased muscle. Pathophysiology: TNF (decrease appetite; inhibits the activity of lipoprotein lipase); IL-1; IFN-gamma. |
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Definition
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Term
| Deposit of calcium in dead, dying or damaged tissues. Serum calcium levels are normal |
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Definition
| calcification, dystrophic |
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Term
| Deposit of calcium in normal tissue. Serum calcium levels are high—hypercalcemia. |
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Definition
| calcification, metastatic |
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Term
| Most common element in body, provides energy |
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Definition
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Term
| Result of reprogramming of these cells is metaplasia, usually brought about by the action of cytokines, growth factors, and extracellular matrix components |
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Definition
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Term
| Active movement of cells along a chemical gradient generated by a chemoattractant. |
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Definition
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Term
| Fibrillar collagen, found in skin, bone, tendons. Has high tensile strength |
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Definition
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Term
| Fibrillar collagen, found in blood vessels, skin, uterus, thin and pliable |
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Definition
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Term
| Non fibrillar collagen, found in basement membranes |
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Definition
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Term
| A passive process. Impaired outflow of venous blood or lymph which results in edema. Venous stasis, barely moving. Affected tissues have a blue-red color (cyanosis). Morphology: distended venules, sinusoids, microscopic hemorrhages, hemosiderin laden marcophages. |
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Definition
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Term
| Control the entry and progression of cells thru cell cycle. They change in levels and activities. They work by complexing with and activating cyclin dependent kinase, which phosphorylates things in the cell. They’re responsible for DNA replication, depolymerization of nuclear lamina and formation of mitotic spindle. |
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Definition
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Term
| Modulate the function of other cell types. Polypeptide factors produced by activated macrophages, lymphocytes and others. Regulates leukocyte adhesion, chemotaxis, leukocyte activation, lymphocyte function and systemic effects (fever, no appetite) Examples: IL-1 and TNF, which are important in the inflammatory response and induce endothelial activation. |
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Definition
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Term
| Subcutaneous edema, has to do with gravity and position of body. Example: happened with CHF; elderly patient on bed rest will have presacral dependent edema (same place you’d get bed sores) |
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Definition
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Term
| Abnormal accumulation of fluid within the interstitial spaces of body cavities can be inflammatory or non-inflammatory. Found and seen throughout the entire body/system. |
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Definition
| edema, generalized, systemic |
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Term
| Seen with congestive heart failure. Increased hydrostatic pressure, causes pleural effusion which is a collection of fluid in the pleural cavity. |
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Definition
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Term
| Aka Systemic Thromboembolism. Emboli traveling through the arterial circulation. Origin: 80% intracardiac mural thrombi, aortic aneurysms, thrombi on ulcerated atherosclerotic plaques and vegetations. Sites: lower extremities, brain, ect… |
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Definition
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Term
| Tend to lodge primarily in one vascular bed (for example the lungs) Causes pulmonary thromboembolism. In >95% originate in the deep veins of the leg. 20-25 per 100,000 hospitalized patients have this condition. Accounts for 200,000 deaths a year. Saddle embolus = occludes the main pulmonary artery. Branches into the left and right pulmonary arteries. |
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Definition
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Term
| Air enters the circulation. Causes: obstetric procedures, chest wall injury, iatrogenic (doctor caused), decompressions sickness. Generally in excess of 100cc is required to have clinical effect. Bubbles cause physical obstruction. |
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Definition
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Term
| Grave but uncommon complication of labor and delivery. Mortality >80%. Sudden severe dyspnea, cyanosis and hypotensive shock. May have seizures and even coma. If patient survives initial crisis = pulmonary edema, diffuse alveolar damage and DIC (disseminated intravascular coagulation) |
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Definition
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Term
| Microscopic fate globules found in circulation after fractures of long bones. Occur in 90% of patients with severe skeletal injuries but only 10% have findings. “Syndrome” begins 1-3 days following injury. Sudden onset of dyspnea, tachypnea and tachycardia. Neurologic symptoms: irritability, restlessness à insomnia. May have diffuse petechial rash, thrombocytopenia. In full blown form, it’s fatal in 10% of cases. |
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Definition
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Term
| Most common form of increased vascular permeability. A reversible process elicited by histamine, bradykinin, leukotrienes and other chemo-mediators. Usually short lived and fast. Takes place in venules (immediate transient response) |
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Definition
| endothelial cell, contraction (with gap formation) |
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Term
| Causes vascular leakage. Seen after toxins, burns chemicals. Fast and maybe long lived (hours to days); immediate sustained response. |
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Definition
| endothelial cell, direct injury (necrosis and detachment) |
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Term
| Causes mitosis for a variety of epithelial cells and fibroblasts in vitro. Causes hepatic cell division in vivo. Is widely distributed. TGF alpha uses same receptor and similar activities. |
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Definition
| epidermal growth factor (EGF) |
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Term
| An example of a selection on endothelial cells |
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Definition
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Term
| It is a family of peptides and has an affinity for heparin and basement membranes. It has two forms which both stimulate growth: Basic FGF (bFGF) found in many tissues and organs. It can induce all steps necessary for angiogenesis. It is made by activated macrophages and other cells. Acidic FGF (aFGF): it is confined to neural tissues. |
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Definition
| fibroblast growth factor, basic (FGF-basic) |
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Term
| Single unpaired electrons in a outer orbital. Highly reactive, unstable and can initiate autocatalytic reactions which produce more free radicals. Cause cell damage and aging. |
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Definition
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Term
| Specialized tissue type, hallmark of healing, has a granular pink appearance. Histological features: angiogenesis, proliferation of fibroblasts and edema. Granulation is found at the end of inflammation response and at the beginning of repair. |
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Definition
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Term
| Pulmonary thromboembolism |
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Definition
| heart failure, left-sided |
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Term
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Definition
| heart failure, right sided |
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Term
| A hemoglobin-derived granular pigment that accumulates in tissues when there is a local or systemic excess of iron. It is golden-brown in color. |
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Definition
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Term
| A vasoactive amine. Found in mast cells, basophils and platelets. Causes dilation of arterioles. Increase vascular permeability, causes endothelial cell contraction and widening of inter endothelial cell junctions (gap formations) Also released in response to anaphylatoxins |
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Definition
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Term
| Decreased in normal capillaries at venule end. Increased in normal capillaries, higher at arteriole end. In acute inflammation, increased overall. Extravasated fluid from all ends during acute inflammation. Increased both localized and generalized/systemic edema. Localized = venous obstruction à thrombosis, external compression (fetal P), inactivity of lower extremity. Generalize = CHF, constrictive pericarditis, cirrhosis à back up of portal system = ascites. |
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Definition
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Term
| Altered state of blood requiring less than normal clot-promoting activities to produce thrombosis. Causes: primary (usually genetic) = mutations on factor V, anti-thrombin III defect, protein C or S deficiency, defects in fibrinolysis; secondary = immobilization, MI, tissue damage, cancer, lupus anticoagulation, late pregnancy and following delivery, oral contraceptives. 1 of 3 factors of Vichow’s triad (hypercoagulability, endothelial cell damage, and venous stasis) |
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Definition
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Term
| Active process. Increased blood flow in local areas. Arteriolar dilation. Produces redness in the affected tissue. Often associated with edema. Example: blushing. |
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Definition
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Term
| Increase in the number of cells leading to an increase in size of organ or tissue. Hormonal or compensatory. Also see increase in function. Not in heart or skeletal muscle. Pathologic or physiologic. Seen in breasts (lactation) and prostate |
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Definition
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Term
| Increase in size of cell with secondary increase in organ size. Also see increase in function. Pathologic or physiologic. |
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Definition
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Term
| Responsible for opsonization. Very important for recognition and attachment of leukocytes to micro-organisms. IgG is responsible for triggering the activation of the complement cascade which is responsible for putting C3b on targeted particle. |
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Definition
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Term
| Immediate and early response to injury. 3 major components: alteration in vascular caliber, structural changes in microvascular, emigration of leukocytes (WBCs) which accumulate at site of injury. Relatively short duration, lots of neutrophils, exudation of fluid and proteins, lots of platelets (histamine and GFs). Neutrophil is number 1 cell. |
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Definition
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Term
| Prolonged duration. Tissue destruction, repair, active inflammation involving mononuclear cells à monocytes, macrophages, and lymphocytes. May follow acute inflammation, primary response, persistent infections, prolonged exposure to toxins, or autoimmune. Macrophage is number 1 cell. |
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Definition
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Term
| Cytokines produced by macrophages and mediate innate immunity. Initiate nonspecific proinflammatory responses, such as the activation of endothelium and mononuclear inflammatory cells and induction of acute-phase reactant synthesis by the liver. Macrophages are the major source. |
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Definition
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Term
| Excessive repair product. Dense bands of irregular collage in the dermis. Hypertrophic scar. Protrudes beyond margins of initial injury. |
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Definition
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Term
| Most abundant glycoprotein in the basement membrane; Mediates cell attachment to connective tissue substances; Binds to the integrin receptor family |
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Definition
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Term
| Decrease in number of all white blood cells can be caused by some infections such as AIDS and cancer; it can be caused by malnutrition, typhoid fever, viral infections and rickettsia. Systemic affect of inflammation |
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Definition
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Term
| Increase in number of all white blood cells caused by the release of mediators from macrophages and other cells. Systemic affect of inflammation. |
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Definition
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Term
| Potent chemotactic agent and causes aggregation of neutrophils. Metabolite of the lipoxygenase pathway causes edema and increased attachment. It is a chemotactic factor for phagocytic cells. It stimulates the adherence and aggregation of phagocytic cells, especially PMN’s |
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Definition
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Term
| Formed by thrombi in heart or aorta. Grossly apparent laminations produced by pale layers of platelets and fibrin that alternate with dark layers containing red blood cells. Imply a thrombosis at site of blood flow. |
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Definition
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Term
| An example of selectin on leukocytes. |
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Definition
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Term
| Once activated, release cytokines (IL-1 and TNF). Come from monocyte (blood) à macrophage (tissue). Activated macrophage: tissue injury, fibrosis, produces products to control inflammation and repair. Primary cell in chronic inflammation. |
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Definition
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Term
| Endogenous, brown/black pigment formed by melanocytes. Non-heme pigment, not based on hemoglobin. It is an intracellular accumulation found in dermis. Gives eyes, hair, skin color. |
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Definition
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Term
| Degrades collagen and other extracellular matrix components during tissue remodeling. Depends on Zinc for activity. |
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Definition
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Term
| Reversible change in which one adult cell type is replaced by another adult cell type. It is usually caused by persistent injury. Result of reprogramming cells. Example: replace ciliated pseudostratified columnar epithelial cells with stratified squamous epithelial as a result of smoking |
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Definition
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Term
| change in the genetic material (DNA) inside the cell |
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Definition
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Term
| Lymphocytes capable of destroying tumor cells without prior sensitization. After activation with IL-2, can lyse a wide range of human tumors. Can also participate in antibody-dependent cellular cytotoxicity. |
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Definition
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Term
| Number of patients with a disease misclassified by a test. |
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Definition
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Term
| Number of patients without the disease correctly classified by a test. |
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Definition
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Term
| Recognition and attachment of WBCs to most micro-organism is facilitated by the generic serum proteins. Most important opsonins are immunoglobulins (IgG-Fc portion), C3b fragment of complement cascade and collectins |
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Definition
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Term
| Osteolysis by either primary bone cancer or metastasis will result hypercalcemia that is not a paraneoplastic syndrome |
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Definition
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Term
| one of the mechanisms of action of soluble chemical mediators (polypeptide growth factors among most important) ; of or relating to a hormone or to a secretion released by (endocrine) cells into the adjacent cells or surrounding tissue rather than into the bloodstream |
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Definition
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Term
| Symptoms not readily explained by either the local or distant spread of the tumor, or by the elaboration of hormones indigenous to the tissue from which the tumor arose. May represent the earliest manifestation of a malignancy; in affected patient, may represent clinical problems and may even be lethal; may mimic metastatic disease, confounding treatment; occurs in ~10-15% of patients with malignancy. |
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Definition
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Term
| Percentage of individuals with an autosomal dominant gene who express the gene trait (some individuals who inherit the gene are phenotypically normal = don’t express the trait.) |
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Definition
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Term
| Taking in and destroying material. Three steps: recognition/ attachment, engulfment, and killing/degradation |
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Definition
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Term
| the number of patients without a disease misclassified by a test |
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Definition
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Term
| number of diseased patients correctly classified by a test |
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Definition
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Term
| Excessive formation of granulation tissue. It prevents scab formation and bleeds easily. All of the tissue has to be removed so that normal healing can occur. Exuberant granulation. Protrudes above surface of skin blocking re-epithelialization. Painful, has to be removed. |
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Definition
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Term
| Shrinkage of nucleus and increased basophilia. DNA condenses into solid, shrunken mass. Part of irreversible cell injury |
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Definition
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Term
| Set of values of a measured quantity obtained from a group of individuals deemed “healthy”. +/- 2 standard deviations from the mean. Encompasses 95% of normal individuals. |
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Definition
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Term
| Replacement of dead cells by cells of the same type |
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Definition
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Term
| Replace dead cells with connective tissue à results in scar. Occurs in heart |
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Definition
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Term
| Probability a lab test is positive in the presence of a disease. Rules out false negatives. Increase sensitivity so don’t get false positives |
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Definition
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Term
| Low cardiac output. Results from myocardial pump failure. Causes: MI, ventricular rupture, arrhythmia (intrinsic damage), cardiac tamponade, and pulmonary embolism |
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Definition
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Term
| Results from loss of blood or plasma volume caused by hemorrhage, fluid loss (vomiting, diarrhea), severe burns, or trauma |
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Definition
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Term
| Probability a lab test is negative in the absence of a disease. Rules out false positives. Increase specificity so don’t get false negatives. |
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Definition
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Term
| Associated with paraneoplastic syndromes regarding ectopic hormone production. It is the most common endocrinopathy; 50% of patients with this have lung cancer; excessive production of ACTH (adrenocorticotrophic hormone) or ACTH-like peptide by tumor. Small cell lung cancer |
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Definition
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Term
| Usually occlusive. May embolize. Common sites: coronary, cerebral, and femoral artery. Usually fill vessel. Usually associated with atherosclerotic plaque |
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Definition
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Term
| Usually occlusive. May embolize. If in deep veins of legs à clinically significant. Can embolize to lungs |
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Definition
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Term
| Cytokine. Fever, no appetite. Important in inflammation process. Endothelial activation. Induce fibroblast proliferation. Chemotactic for fibroblasts. Stimulate collagen synthesis and collagenases (control amount of collagen put down) |
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Definition
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Term
| Has similar activities and use the same receptor as epidermal growth factor which cause mitogenic for a variety of epithelial cells and fibroblasts in vitro and widely distributed. |
|
Definition
| transforming growth factor-alpha (TGF-a) |
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Term
| Belong to family of homologous polypeptides. Produced in an inactive form which must be proteolytically cleaved to become functional. Conflicting roles. Low concentration = promotes growth and induces synthesis and secretion of PDFG. High concentration = inhibits growth and expression of PDGF receptor. Stimulates fibroblast chemotaxis and production of collagen and fibronectin; inhibits collagen degradation. Signals via cell surface receptors with serine/thyrine kinase activity. Inhibits cell cycle progression in S phase. |
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Definition
| transforming growth factor-beta (TGF-b) |
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Term
| Minimal tissue loss; narrow defect. Clean à no significant bacterial contamination. Example: surgery, cut shaving, ect. |
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Definition
| wound healing, first intention |
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Term
| Large tissue defect. More intense inflammation reaction; large amounts of granulation tissue. Wound contraction. Example: ulcer on foot |
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Definition
| wound healing, second intention |
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Term
| A submicroscopic infectious agent that is unable to grow or reproduce outside a host cell. It is non-cellular but consisting of a core of DNA or RNA surrounded by a protein coat. |
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Definition
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Term
| Sex linked. Less common than autosomal disorders. Males get more often because only have on X chromosome. For females to get, have to have it on both Xs; transmitted by heterozygous female carrier. An affected male transmits to daughters only. Sons of heterozygous women have 1 chance in 2 of receiving mutant gent. Example: hemophilia, muscular dystrophy. |
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Definition
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Term
| Associated with pulmonary embolism. Sudden death, right heart failure, or cardiovascular collapse occurs when __% or more of the pulmonary circulation is obstructed |
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Definition
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Term
| Fat embolism occurs in __% of individuals with severe skeletal injuries, but only 10% have clinical findings |
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Definition
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Term
| __% of patients with Cushing Syndrome have lung cancer; venous thrombosis is asymptomatic in __% of those affected; in Autosomal Dominant disorders each child has __% chance of getting the disorder if 1 parent has it |
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Definition
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Term
| greater than __% of pulmonary embolisms arise from deep veins of the leg |
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Definition
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