Term
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Definition
| A structural or functional change within the body judged to be abnormal via clinical manifestation of the abnormal structure and function. |
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Term
| Describe the difference between physiology and pathology. |
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Definition
| Physiology is the science of understanding how the various organs of thebody operate to bring about a healthy individual. pathology is the study of disease so we can understand its nature and enable us to alter the course of disease for patient survival. |
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Term
| What brings about abnormality? |
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Definition
| The breakdown of organs/tissues bc of damage to structures within the tissues and the consequent loss of functional that occur as a result. |
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Term
| How do you know there are abnormalities in structure and function? |
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Definition
| Signs, symptoms, and diagnostic tests |
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Term
| What role does diagnosis play in pathology? |
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Definition
| In determining or selection of line of treatment, indicating the likelihood of a favorable or unfavorable outcome, and if it is useful to future patients. |
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Term
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Definition
| It is aimed at fixing the structure in the body that has lost its function through attempts at lessending the destructive effects of the causative agents and providing a conducive environment for repair to take place. |
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Term
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Definition
| Expected or predicted course and outcome of the treatment. |
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Term
| Describe the causes of disease. |
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Definition
| Certain (stimuli) stressors to cells. Loss of such physiological roles results in disease. |
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Term
| What are the sources of stress that cause disease? |
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Definition
| Hypoxia, Environmental Agents, Microbiologic Agents, Genetic Defects, Immune Disorders, Neoplasia, Aging Process. |
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Term
| Describe parts of the cell that are susceptible to damage? |
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Definition
| Cell membrane, mitochondria, DNA, ribosomes. |
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Term
| Describe the physiological consequence of cell membrane damage. |
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Definition
| Cell membrane damage-> disturbance in transport of materials (inorganic and organic) across the cell membrane -> Excess of internal calcium -> (I) activation of proteases -> disrupion of internal membranes and cytoskeletal proteins, (II) endonucleases -> nuclear chromatin damage |
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Term
| Describe the physiological consequence of mitochondria damage. |
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Definition
| Mitochondria damage -> loss of ability to synthesize ATP |
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Term
| Describe the physiological consequence of DNA damage. |
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Definition
| DNA damage -> mutation in genes -> defective proteins |
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Term
| Describe the physiological consequence of Ribosomes damage. |
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Definition
| Ribosomes detachment from ER -> reduction in protein synthesis |
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Term
| Describe the morphological changes in cells that are reversible caused by non lethal injury. |
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Definition
| Swelling of the whole cell, accumulation of fats in the cytoplasm, plasma membrane alterations, mitochondrial changes, ER, Nuclear alterations, lysosomes. |
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Term
| What are the 2 morphological changes that are observed in tissues following irreversible cell death? |
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Definition
| Increase Ca 2+ influx and Increase leakage of enzymes (CK, LDH) |
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Term
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Definition
| The sequence of morphological changes in a tissue that follow pathological death of some of its cells in lethal injury. |
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Term
| ID the various types of necrosis. |
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Definition
| Coagulative necrosis, Liquifactive necrosis, caseous necrosis, and enzymic fat necrosis |
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Term
| What is the fat of necrotic cells in living patients? |
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Definition
| Enzymatic digestion and fragmentation with leukocyte phagocytosis of the particulate debris by leukocytes -> disappearance of their debris. 2)Dystrophic calcification |
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Term
| Define and describe phagocytosis? |
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Definition
| The process of engulfing and ingestion of particles by the cell or a phagocyte (e.g. macrophage) to form a phagosome (or food vacuole), which in turn fuse with lysosome and become phagolysosome where the engulfed material is eventually digested or degraded and either released extracellularly via exocytosis, or released intracellularly to undergo further processing. |
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Term
| Define and describe dystrophic calcification. |
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Definition
| if necrotic cells aren't promptly destroyed and reabsorbed, they tent to attract calcium salts and other minerals and to become calcified. |
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Term
| Describe pathological cell death (apoptosis). |
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Definition
| Its a natural (physiologic) process used to eliminated unwanted body cells thus avoiding over accumulation of cells. Normally stimulus is internal and varis (physiologic). |
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Term
| Describe examples of situations in the body under which apoptosis occurs. |
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Definition
| During embryogenesis, homeostatic mechanism to maintain cell population in a tissue (ie. return of uterus to normal size after childbirth), death of immune cells, death of cells deranged by disease or noxious agents, death of aging cells, induced pathologically by external injurious stimuli (ie. viruses) |
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Term
| How does metaplasia arise? |
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Definition
| A reprogramming of stem cells that are known to exist in most epithelia and undifferentiated mesenchymal cells present in connective tissue. |
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Term
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Definition
| A complex reaction of vascularized tissues to injurious agents that serves to destroy, dilute or wall off the injurious agent, and sets into motion a series of events that try to heal and reconstitute the damaged tissue. |
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Term
| What are the differences between the two types of inflammatory responses? |
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Definition
| Acute inflammation-reactions are sudden and intense, short duration. Chronic inflammation- longer duration associated with presence of lymphocytes and macrophages, proliferation of BV, and tissue necrosis. |
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Term
| Describe the processes that occur in the two major events in acute inflammation. |
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Definition
| exudation of fluid and plasma protein-> edema and emigation of leukocytes (predominantly neutrophils) |
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Term
| Describe the various changes that take place in the blood vessels in inflammation (vascular events). |
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Definition
| Presence of lymphocytes and macrophages, proliferation of BV, and tissue necrosis. |
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Term
| What are the cardinal signs of inflammation? |
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Definition
| Heat, redness, edema, and pain |
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Term
| What are the benefits of acute inflammatory reactions? |
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Definition
| contain and isolate injury; destroy, kill, wall off invading microorganism; inactivate toxins secreted by microorganisms; act to rid of necrotic tissue; achieve healing and repair; inflammation is a protective response |
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Term
| What parts of vascularized tissue are involved in inflammation? |
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Definition
| Plasma, circulating blood cells, bloof vessels, cellular/extracellular constituents of connective tissue. |
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Term
| For cellular events in acute inflammation what types of cells play a role in the process? |
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Definition
| Leukocytes, neutrophils, monocytes/macrophages |
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Term
| List the steps involved in how blood cells leave the blood vessel into the interstitium in the cellular event of the inflammatory process? |
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Definition
| 1. Leukocytes rest on the capilly wall (margination) and roll along the walls (rolling) 2. Leukocytes arrest and adhere to the endothelium of the walls of the capillary (adhesion) |
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Term
| Which are the stps at which selectins and integrins act in acute inflammation? |
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Definition
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Term
| define the term diapedesis. |
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Definition
| Part of the swelling due to the injury. The transmigration through endothelium |
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Term
| Describe how the cells are attracted to the site of the injury after they enter the interstitium in acute inflammation. |
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Definition
| by special chemicals called chemotactic agents to become involved in chemotaxis |
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Term
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Definition
| the movement of these leukocytes to the location of the injury under the direction of chemicals. |
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Term
| What substances act as chemoattractants? |
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Definition
| The chemotactic agents which are bacterial products, complement fragments, arachidonic acid metabolites and certain cytokines. |
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Term
| What is the function of chemotaxis? |
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Definition
| To migrate leukocytes in the interstitium to the injury site |
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Term
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Definition
| Removes foreign cells, inflammatory cells and necrotic debris. |
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Term
| Describe the steps involved in phagocytosis of acute inflammation. |
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Definition
| 1. Recognition and attachment of the particle to be ingested by the leukocyte. 2. Engulfment 3. Killing or degradation of the ingested material |
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Term
| What cells are involved in phagocytosis? |
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Definition
| Neutrophils and macrophages are responsible for eliminating the injurious agents so constitute two of the major benefits derived from the accumulation of leukocytes at the inflammatory focus. |
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Term
| How are the cells activated to become phagocytic? |
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Definition
| Dead cells by neutrophils and macrophages are initiated by recognition of mannose receptors and scavenger receptors of leukocyte surface. Particles have to be coated with opsonins to be recognized. Once opsonization has taken place phagocytic leukocyte can now recognize the microbe |
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Term
| What are opsonins? and give two examples |
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Definition
| Special proteins that have to coat the particles to be recognized by the phagocytes. IgG antibodies and C3B breakdown product of complement |
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Term
| How is Acute Inflammation Terminated? |
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Definition
| 1. Reduced action of hte mediatory that occur from degradation 2. Stop signals: as inflammation develops the process also triggers a variety of stop signals that serve to actively terminate the reaction. |
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Term
| What is the fate of leukocytes after phagocytosis? |
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Definition
| Neutrophils rapidly undergo apoptic cell death and are either ingested by macrophages or are cleared by lymphatics. |
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Term
| What are the possible outcomes of acute inflammatory reactions? |
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Definition
| Resolution, Fibrosis, Chronic Inflammation |
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Term
| What is a leukocyte induced injury? |
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Definition
| If the events in inflammation are exacerbated or remain for a long period and become harmful. Ex reactions to insect bites, chronic diseases, RA, Artherosclerosis, |
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Term
| Define chronic inflammation. |
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Definition
| inflammation of prolonged duration in which active inflammation, tissue destruction, and attempts at healing are proceeding simultaneously. |
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Term
| What is chronic inflammation caused by? |
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Definition
| 1. Persistent infections (syphilis) 2. Prolonged exposure to potentially toxis agents (silicosis, atherosclerosis) 3. autoimmunity (RA and lupus) |
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Term
| Describe the process of chronic inflammations |
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Definition
| An influx of lymphocytes; macrophages remain or increase in #. Tissue destruction beyond the capacity of the site to regenerate; a repair reaction that is associated with vascular proliferation New BV grow int othe site increasing vascularity and fibrosis (scarring) |
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Term
| What are the possible outcomes of chronic inflammation? |
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Definition
| Resolution to a scar or remain as a persistent chronic inflammation |
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Term
| What cells play a role in chronic inflammation? |
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Definition
| Lymphocytes- T and B; mononuclear phagocytic cells(macrophages -tissue monocytes, and eosinophils); plasma cells- transformed lymphocyte B cells |
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Term
| What role does each of the chronic inflammatory cells play? |
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Definition
| Macrophages- central figure figure in chronic inflamm. Tissue destruction, neovascularization, CT accumulation, remodeling; Lymphocytes T and B represent the immune system at the site. Antibody manufacturing plants; Eosinophils- allergic reactions. Parasitic infections, common in immunological reactions. |
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Term
| What is granulomatous inflammation? |
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Definition
| distinctive pattern of chronic inflammatory reaction characterized by focal accumulations of activated macrophages which develop an epithelial like appearance called granulomas. |
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Term
| What is granulomatous inflammation caused by? |
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Definition
| Immune reactions to infectious and non-infectious conditions which result in the formation of granulomas. |
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Term
| What are the two granulomas? |
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Definition
| 1. Foreign body granulomas- associated with drug abuse, sutures or other fibers large enough to preclude phagocytosis by a single macrophage 2. Immune granulomas- caused by insoluble particles capable of inducing a cell-mediated immune response.Macrophage engults foreign material. |
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Term
| What are examples of diseases with granulomatous inflammation? |
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Definition
| Tuberculosis, leprosy, syphilis, cat scratch disease. |
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Term
| name the morphologic patterns of chronic inflammation and example. |
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Definition
1. Serous Inflammation- skin burn
2. Fibrinous inflammation- acute fibrinous pericarditis
3. Suppurative or purulent inflammation- staph
4. Ulcer- duodenal ulcer |
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Term
| What are the systemic effects of inflammation? |
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Definition
| Acute Phase responses or systemic inflammatory response |
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Term
| What brings about the acute phase response or SIRS? |
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Definition
| reactions to cytokines produced in response to bacterial products such as LPS and by other inflammatory stimuli. |
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Term
| What are the clinical and pathological changes associated with the acute phase response? |
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Definition
| Fever, Leukocytosis and increase pulse and BP |
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Term
| What condition causes change in leukocytes? |
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Definition
1. Neutrophilia- bacterial
2. Lymphocytosis- measles, mumps, and mono
Eosinophilia- asthma, hay fever, parasitic infestations
4. Leukopenia- typhoid fever, infections caused by viruses. |
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Term
| What is the role of hte lymphatic system in inflammation? |
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Definition
| To filter and police the extravascular fluids |
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Term
| Are the lymphatics fail proof? |
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Definition
| No they maybe become secondarily inflamed (lymphangitis) or hte draining lymph nodes may become secondarily inflamed (lymphadenitis) |
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Term
| What causes the nodeal enlargement in inflammation of the lymphatic system? |
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Definition
| hyperplasia of the lymphoid follicles and by hyperplasia of the phagocytic cells lining the sinuses of the lymph nodes. |
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Term
| What happens in severe infections of the lymphatic system? |
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Definition
| Sometimes spreads the infection but in severe infections the organisms gain access to the vascular circulation inducing a bacteremia. Endocarditis, eningitis, renal abscesses, and septic arthritis may develop |
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Term
| Identify the types of repair. |
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Definition
| regeneration of parenchymal cells or fibrous replacement |
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Term
| When does cellregeneration and fibrous repair begin? |
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Definition
| Immediately after injury. within 24 hours dead parenchymal cells are being replaced by regeneration or fibrosis depending on the inherent regenerative capacity of the injured tissue. |
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Term
| What types of tissues have cells that can be regnerated? |
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Definition
| Parenchymal cells; Labile or continuously dividing cells- lost on daily basis, oral cavity, vagina, cervix.; Quiescent stable cells- Does not divide continuously but will divide. Parenchymal cells of hte liver cells, pancreas, vascular endothelium and fibroblast. |
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Term
| What types of tissues have cells that can't regenerate? |
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Definition
| non-dividing (permanent) cell. Nerve cells, cardiac myocytes mainly and skeletal muscle. |
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Term
| How does fibrous tissue infiltrate and replace dead tissue? |
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Definition
1. Migration of healthy cells into damaged area.
2. Proliferation of migrated cells
3. Reintegration of new cells w/old
4. Deposition of ECM
5. Differentiation of proliferation tissue. (Migrate, Proliferate and differentiate. |
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Term
| What is involved in cellular proliferation? |
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Definition
| Cell surface receptors, signal transduction enzymes, and transcription facts. |
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Term
| What are the general characteristics of cellular division? |
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Definition
| Quiescent cells in physiologic state called Go. Biochemical factors produced in local microenvironment of cell stimulate the cell to go from quiescent stage to dividing stage, from Go-> G1-> S -> G2-> M |
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Term
| What does ECM consist of? |
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Definition
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Term
| What are the three stages of fibrous repair? |
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Definition
| Angiogenesis, Fibrosis, Maturation. |
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Term
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Definition
| Formation of new blood vessels |
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Term
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Definition
| Migration and proliferation of fibroblasts that synthesize and deposit extracellular matrix proteins |
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Term
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Definition
| maturation and organization of fibrous tissue, and formation of scar tissue |
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Term
| What are the four steps of angioneogenesis? |
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Definition
| Degradation, Migration, Proliferation, Organization |
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Term
| What is the hallmark of healing? |
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Definition
| Formation of granulation tissue |
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Term
| What are the two steps of fibrosis? |
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Definition
1. Emigration and proliferation of fibroblasts
2. Deposition of ECM |
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Term
| Describe the maturation process. |
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Definition
| Synthesis and activation of metalloproteinases then the inhibition of the activity of metalloproteinases |
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Term
| Describe systemic factors that influence wound healing. |
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Definition
| Circulatory status, Nutrition and metabolic status, and Hormones |
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Term
| Describe local factors that are obstacles to normal repair. |
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Definition
| Infection, Foreign bodies, Size location and type of wound and mechanical factors. |
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Term
| Therma injuries, diabetes, malignancy, sepsis, immunodeficiencies are defects of what? |
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Definition
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Term
| Hemodialysis, diabetes are defects of what? |
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Definition
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Term
| Leukemia, anemia, sepsis, diabetes and malnutrition are defects in what (2)? |
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Definition
| Phagocytosis and microbiocidal activity |
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