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146 Cards in this Set
- Front
- Back
acute inflammation
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*the classic response to any type of injury
*the immediate and early response to an injurious agent. |
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5 things that occur at the injured site of acute inflammation
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1. swelling
2. redness 3. pain 4. heat 5. loss of function |
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left shift
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immature white blood cells.
neutrafils on a blood smear mean an infection is going on 10-12k normal wbc count |
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erysipleas
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involves the skin and lymphatic portions. blood cultures will be negative until treated if not treated then it will enter the blood stream.
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leukocyte, extraversion, phagocytosis
3 step process in inflammation |
1. margination, rolling and adhesion
2. trasmigration across endothelium, 3. migration toward chemotactic stimulus |
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acute inflammation may have one of the four outcomes
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1. complete resoultion
2. abscess formation 3. fibrosis 4. chronic inflammation |
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steps involved in phagocytosis
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1. recognition and attatchment to particle
2. engulfment with phagocytoic vacule 3. killing of degradation of the ingested material. |
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neutrophil
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*1st line of defense. first thing to go and meet the pathogen.
* most numerous wbc in the circulating blood, 60 to 70% of the wbc count. |
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the steps and response of the neutrophil to injury and infection
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1. margination-rolling-adhesion
2. transmigration across the edothelium 3. migration toward chemotactic stimulus. |
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histamine
chemical mediator |
Dialation of the arterioloes
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serotonin
chemical mediator |
diliation of arterioloes
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Complement components; C3a, C5a, C4a
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Produced by the liver
C3a helps ingulf bacteria. All increase vascular permeability and cause vasodilation by stimulating the release of histamine from mast cells. |
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complement components; C5a
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chemotactic for neturophils, increases leukocyte adhesion.
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complement components; C3b, C3bi
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act as opsoninis that favor phagocytosis
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bradykinin
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produced by the liver
increases vascular permeability, smooth muscle contraction dilation of blood vessels, participates in pain sensation. |
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leukotrienes
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vasoconstriction, bronchospasm, increased vascular permeability
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prostaglandins
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vasodialation, potentiate edema
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thromboxane
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vasoconstriction, platelet aggregation
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prostacyclin
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vasodilation, inhibits platelet aggregation
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exudate
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an inflammatory extravascular fluid that has high protein concentraion, much cellular debris, and a specific gravity > 1.020
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transudate
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a fluid with low protein content and a specific gravity of < 1.012
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purulent exudate (pus)
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exudate right in leukocytes and parenchymal cell debris
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edema
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denoates an excess of fluid in the interstitial or serous cavities.
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cytokines
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proteins produced by many cell types that alter or modulate the function of other cell types
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cytokines produced by mononuclear phagocytes are often called...
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monkines
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cytokines produced by lymphocytes are often called..
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lymphokines
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interleukins (IL)
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represent a broad family of cytokines that act primarily on leukocytes
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chemokines
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cytokines that share the ability to stimulate leukocyte movement (chemokinesis) and directed movement (chemotaxis)
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Summary of the acute inflammatory response
patterns of inflammation |
*increased blood flow to the injured area
*slowing of blood flow at area of injury * Increased vascular permability *leukocyte migration to area *phagocytosis of offending agent *potential tissue damage *resortoration of tissue structure and function. |
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serous
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blister from being bitten from a fire ant
occurs at the dermal/epidermal function |
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fibrinous
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huge gaps between cells.
forms around the heart or around the pericardial sac |
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outcomes of acute inflammation
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1. complete resolution
2. abscess formation 3. progression to chronic inflammation 4. Healing by connective tissue replacment (fibrosis) |
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complete resolution
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neutralization and spontaneous decay of the chemical mediators, with subsequent return of normal vascular permeability, cessation of leukocytic infiltration; death of neutrophils, and finallay removal of edema fluid and protein, leukocytes, forgein agents and necrotic debris from the site.
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absess formation
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occurs with pyogenic organisms, cellular debris, protein aceous material, low pH (very acidic)
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healing by connective tissue replacement (fibrosis)
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occurs after siginificant tissue destruction in tissues that do not regenerate, or when there is abundant fibrin exudation. Also occurs in tissues or serous cavities whent eh fibrinous exudate cannot be adequately absorbed.
regeneration, scarring |
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progression to chronic inflammation
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occurs when the acute inflammatory response cannot be resolved, owing to the persistence of the injurious agent or to some interference with the normal process of healing.
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chronic inflammation
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inflammation of prolonged duration (weeks, months, years) in which active inflammation, tissue destruction, and attemps to repair are proceeding simultaneously.
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chronic inflammation can arise under the following conditions
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1. persistent infection
2. prolonged exposure to potentially toxic agents 3. autoimmunity |
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persistant infection
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a ganulomous reaction pattern is usually seen
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prolonged exposure to potentially toxic agents
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agents are non-degradable inanimate material
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autoimmunity
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autoimmue diseases that produce autoantigens that evoke a self-perpetuating immune response
Cells and activites involved= mononuclear cell infilitrate, tissue distruction, and connective tissue replacement |
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lymphocytes
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are mobilized in non-immune mediated inflammatory reactions. lymphocytes of varying types use adhesion molecules and are influenced by chemokines to migrate to inflammatory sites. cytokines from activated macrophages, in turn activate lymphocytes, which themselves also produce inflammatory mediators.
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mast cells
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widely distributed in connective tissues. . possess receptors for igE antibody. degranulation occurs when antigen binds to IgE molecule that is attatched to mast cell. histamine is released and an anaphylactic reaction occurs.
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eosinophils
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have granules that contain major basic protein, a very toxic and injurious agen to parasites and cells.
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granulomatous inflammation
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a distinctive pattern of chronic inflammatory reaction in whcih the predominant cell type is the activated macrophage with a modified epithelioid appearance. epithelioid cells fuse to form gian cells.
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granuloma
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this is a focal area of granulomatous inflammation. it consists of micrscopic aggregation of macrphages that are transformed into epithelium-like cells (giant cells) surrounded by a collar of lymphocytes and plasma cells.
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giant cell
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a lot of macrophages that are fused together
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2 types of giant cells
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1. langerhans type
2. foreign body type |
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foreign body type
giant cell |
nuclei are scattered all over the cytoplasm
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langerhans type
giant cell |
looks like a horseshoe and the nuclei are lined up around the edge. can be found in the immunineffective process.
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2 types of granulomas
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1. foreign body granuloma
2. immune granuloma |
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foreign body granuloma
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incited by inert material (eg. suture material)
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immune granuloma
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incited by insoluble immogenic material
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fever
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fever is a systematic manifestation of inflammation.
mediators cause fever. fever is one of the most prominent systemic effects of inflammation. fever depends on humoral signals from the body. |
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the major forms of wound healing
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1. healing by first intention (wounds with opposed edges) by surgical scars
2. healing by second intention (wounds with seperate edges) the edges are too far apart to bring together. |
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steps involved for healing by first intention
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1. within 24 hrs fibrin clot forms, neutrophils appear at the margins of the incision, mitotic activity begins in the basal layer. epithelial cells from the edges migrate and frow along cut margins.
2. in 3-7 days, epithelial cells fuse at midline beneath the surface scab, neutrophils replaced by macrophages, granulation tissue invades incision space. 3. day 5, incision space is filled with granulation tissue. collagen fibrils begin to bridge the incision. epidermis recovers normal thickness and architecture. |
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healing by second intention
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the same steps that are in the first intention healing are also involved in the second intention healing but with extensive loss of cells and tissue, surface wounds that create large defects, which must be filled.
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secondary healing differs from primary healing in the following aspects
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*if involves muscles: thick scars will be left. the scars are thick because the muscles can not rejuvinate themselves.
1. inflammatory reaction is more intense. more fibrin is present, more necrotic debris and exudate must be removed. 2. much larger amounts of granulation tissues are formed 3. wound contraction also involved in myofibrils. |
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2 types of immunity
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1. natural immunity (innate)
2. acquired immunity (adaptive) |
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natural immunity (innate)
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natural protective mechanisms
-epidermis (mechanical layer) -ciliary movement of bronchial epithelium (physical forces) - lysozyme (a potent bactericidal agent found in tears) |
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acquired immunity (adaptive)
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ability of the immune system to recognize and mount a defense against foreign material, bacterial or viral invaders. this response requires;
-antigen/antibody reaction that is amplified - the body must distinguish self from non-self |
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2 types of cell mediated immunity
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1. humoral response
2. cellular immunity |
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humoral response
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effective in finding extracellular infections (bacteria)
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cellular immunity
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fights viral infections. combats intracellular infections
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Cell mediated immunity (CMI) intracellular microbes
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T helper cells-secrete cytokines
cytotoxic T cells-destroys altered self cells. |
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natural killer cell
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1st line of defense
lyse cell invaders no sensization antibody dependent cell cytotoxicity |
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dendritic cell
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antigen presenting cell
widely distributed. Contains class 1 and class 2 |
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T Lymphocytes
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cellular immunity is mediated by thymus-derived (T) lymphocytes. Each T cell is genetically programmed to recognized a specific cell-bound antigen by means of an antigen specific T cell receptor (TCR)
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T helper cells
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CD4+ and CD3
T cells are the gate keeper of the immune system. goes to antigen-presenting cell |
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T cytotoxic cells
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CD8+ and CD3
destroys infected cells, that have been infected by a virus. releases cytokines-which cause the cell the burst and destroy these cells go to infected target cell. |
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B lymphocytes
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become antibodies.
b cells become plasma cells that secrete antibody when stimulated by antigen and cytokines. immunoglobulins are the mediators of humoral immunity. Immunoglobulin M (IgM) constitues the antigen-binding component of B cells. Surface antibody attatched to the membrane. |
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effector cells
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basophils,
eosinophils NK cell (natural killer) mast cell |
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eosinophils
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account for 2-3% of circulating wbc. these cells apear 2-3 days after the neurtophils.
interact with basophils and are prominant in allergic reactions. also participate in the inflammatory response to parasitic infections, and are present in chronic inflammations. |
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basophils
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account for less than 1% of wbc.
most prominant in allergic reactions mediated by IgE. |
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macrophages
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macrophages are derived from blood monocytes. appear at the sight of inflammation 3-4 days after the onset of infection or tissue destruction. typically present in chronic inflammation.
capable of phagocytosis, and are active in bacterial killing. secrete mediators of inflammation (cytokines) that act locally on other cells and the body as a whole. *Antigen presening cell Ag* *this cell is required to process and present antigen to immunocompetent T cells. Other antigen presenting cells include langerhan cells, and follicular dendritic cells. |
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Plasma cells
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make and secrete antibodies: IgG, IgM, IgE, IgA, & IgD
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types of lymphocytes
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t lymphocyte
b lymphocyte macrophage |
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order of appearance in antibody infection
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1. IgM is the primary response. first antibody present after an infection
2. IgG is part of the secondary response. *if the person has had the virus before than IgG will be the first to respond* |
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IgG
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secreted by plasma cells.
abundant, crosses placenta and facilitates phagocytosis. |
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IgM
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primary response in infection or an immunization.
composed of five units that are held together by a J-chain |
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IgA
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2 units held together by a J-Chain, found in mucosal secretions (found in any open area, ie nose)
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IgE
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mediates allergic and parasitic reactions
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IgD
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found only on B cells.
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antibodies (IgM, IgG, IgA, IgE, IgD)
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contain a C-terminal end that can attatch to other immune cells and an N terminal endthat binds antigen.
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antibody production
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T cell activation of B cells to become antibody secreting plasma cells is required for most antigens (T cell dependent antigens)
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Class 1 (MHC- major histocompatability complex) antigens
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Class I antigens are expressed on all nucleated cells and platelets.
found on all somatic cells, but not on macrophage or T Cells. Class I molecules bind to those peptides derived from viral antigens assembled within the cell. This process proteolytic digestion of protein (ex. viral) transport to ER. Viral protein is association with class I molecules and transported to the cell surface for recognition by cytotoxic T cells. |
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Class II (MHC) antigens
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Class II antigens are expressed on specific immune cells not on somatic cells.
Class II molecules present exogenous antigens (ex. extracellular microbes) with class II molecules assembled in the ER. This MHC peptide complex is transported to the surface where it can be recognized by T helper cells. |
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major histocompatability complex (MHC)
also known as HLA markers |
the principle function of the cell surface histocompatability molecues is to bind peptide fragments of foreign proteins for presentation to appropriate antigen specific T cells.
*very important to fight viral infections* |
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primary lymphoid organ
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thymus
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-once in the cell, viruses are invisible to the immune system.
-cells of the immune system are derived from stem cells. -macrophage/dendritic cells can engulf many things. -CD8+ T cells recognize foreign antigens (AGs) associated with MHC 1. -mediators affect B cells |
important info.
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Asthma
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extrinsic and intrinsic mast cell activation. mast cell activation has granuales.
with asthma Ige membrane binding is required. and there is mast cell degranulation. . -Ige membrane binding will clear whatever antigen is present. |
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antigen-antibody reactions
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antigens contain sites where antibodies can bind. these sites are known as epitopes . more than one antibody can bind to their surface.
-when an immunoglobulins bound to an antigen this is known as antigen-antibody complex. |
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Type I hypersensitivity
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2 types: 1. systemic 2. local.
type 1 is a rapidly developing immunologic reaction occuring within minutes after the combination of an antigen with antibody bound to mast cells or basophils in individuals previosuly sensitized to the antigen. Ex. asthma, hay fever, anaphylactic shock) |
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hyper-responsive (type 1 hypersensitivity)
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over response to immune encounters/particular antigens. (location dependent)
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systemic
type 1 hypersensitivity |
takes place by antigen injected directly into the bloodstream. ex. the patient is extremely allergic to penacillin and it is given to them in an IV drip.
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local
type 1 hypersensitivity |
this is the second type of type 1 hypersensitivity.
local has 2 well defined phases 1. initial response 2. late phase. |
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initial response
local-type 1 hypersensitivity |
this is characterized by vasodilation, vascular leakage and depending on the location smooth muscle spasm, and/or grandular secreations. these changes begin 5-30 minutes after exposureto an allergen and subside in about 30 minutes.
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late phase
local-type 1 hypersensitivity |
begins 2-8 hours later without further exposure and may last several days. this phase is characterized by more intense infilitration of tissues with eosinophils, neutrophils, basophils, monocytes, and CD4+ T cells. the tissue destruction in the form of mucosal epithelial damage also occurs in this phase.
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Type II hypersensitivity
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mediated antibodies (IgE or IgM) directed towards antigens present on the surface of cells or other tissue components.
there are 4 types of type II reactions 1. direct lysis 2. opsonization 3.antibody-dependent cell-mediated cytotoxicity 4. antibody mediated cellular dysfunction |
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complement dependent reactions characteristics
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erthrblastis fiabois
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direct lysis
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antibodies against cell antibodies.
antibody (IgM or IgG) reacts with an antibody present on the surface of the cell, causing the activation of complement membrane attack sequence that drills holes through the lipid bilayer. |
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antibody -dependent cell mediated cytotoxicity
type II hypersensitivity |
this form of antibody mediated cell injury requires cooperation from leukocytes. nonsensitized cells that have Fc receptors kill target cells, coated with low concentration of IgG antibody. cell lysis proceeds without phagocytosis.
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antibody-mediated cellular dysfunction
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antibodies that are directed against cell surface receptors impair or dysregulate function without causing cell injury or inflammation.
ex. graves disease-stimulatory hyperthyrodism. |
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Example of type 2 hypersensitivity
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Rh system. Mother is rH- and the Rh is not compatible with the child Rh+ and the antibodies attack the childs circulation
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Type III Hypersensitivity
Antigen/Antibody mediated Complex |
This is also known as immune complex mediated. it is induced by antigen-antibody complexes that produce tissue damage as a result of their capacity to activate the complement system. the toxic reaction is initiated when antigen combines with antibody, whether within the circulation (deposited in cells and tissues and the area lining bloodvessels.)
ex. systemic immune complex disease (SICD) |
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the pathogenesis of systematic immune complex disease can be resolved into three phases
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1. formation of antigen-antibody complexes in circulation
2. deposition of complexes in various tissues 3. an inflammatory reaction is initiated at dispersed sites throughout the body |
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type IV hypersensitivity (cell mediated)
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cell-mediated hypersensitivity is initiated by specifically sensitized CD4+ T lymphocytes and involves direct cell cytoxicity mediated by CD8+ T cells.
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autoimmune disease
criteria |
-prescense of an autoimmune reaction
-not secendary to tissue damage. a breakdown of control mechanisms that regulate self-recognition |
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systemic lupus erythematosus
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this is the failure of the immune system to recognize itself. there is the production of antibodies against self-antigens. T & B Cell activiation.
this is an example of an autoimmune disease. -There is a malfunction of suppressor T cell function and uncontrolled B lymphocyte proliferation of clones that secrete antobodies. *T Cells turn against and attack!* |
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Central tolerance
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deletion of self-reactive T and B cells
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peripheral tolerance
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activation induced cell death
T cell mediated suppression. |
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Anti-dsDNA= anti-double stranded DNA. This is an antibody
Anti-SM= histone proteins. this is an antibody Both of these antibodies are used to diagnose lupus |
imp. info
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4 of the 11 criteria that is needed for lupus diagnosis
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autoantibody directed injury:
1. kidneys 2. joints 3. serosal surface 4. skin 5. red blood cells 6. malar rash 7. discoid rash 8. photosensitivity 9. oral ulcers 10. arthritis |
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M protein
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antigen. as an amino acid sequence that is similar to AA sequence that is found in heart tissue.
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Lab abnormalities
Lupus |
-Lupus prolongs PTT (partial thromboplastin time)- time it takes for blood to clot. The average time is 36 sec. Patients with lupus have prolonged PTT. This happens because lupus patients have antibodies that do not allow the blood to clot.
lupus anticoagulant is a secondary antiphospholipid antibody syndrome. Prolonged PTT can only be found out in a test tube, and no other way. The blood inside lupus patient's bodies does clot, but once outside the body it will not clot. Lupus patients are actually at an increased risk for forming blood clots. |
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Lab abnormalities
Lupus False/Positive test for syphilis |
this occurs only with lupus patients.
there are antibodies to cardiolipin antigen which are used in the test, which does not allow an accurate reading for syphillis in lupus patients. |
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Severe combine immunodeficiency
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-defect in lymphoid stem cell in which there is no further differentiation to pre-B or pre-T cell lines. humoral as well as cell mediated immunity is hindered. There are severe life threatening infections that are possible.
-Death usually occurs in infancy unless the patient is placed in strict isolation. *this is an autosomal recessive disease. it stios at stem cell stage. It stops bc cells are deficient of ADA (adenosine deaminase deoxyadenosine) **Stops at lymphoid cells on the graph** |
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pathogenisis
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recurrent severe infections.
a wide range of pathogens. |
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Isolated IgA deficiency
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-this is the most common immunodeficiency disease
-IgA is the major immunoglobulin in mucosal secretions in the respiratory and gastrointestional tract. -Block in terminal differentiation of IgA-secreting B cells to plasma cells. -reccurent sinopulonary infections and diarrhea in patients. These patients are very susceptible to respiratory, gastrointestional, and urogenitis. |
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Thymic hypoplasia: DiGeorge Syndrome
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this person has:
No T helper Cells No T Cytotoxic Cells No T suppressor Cells the thymus does not develop properly there is a loss of T cell immunity and the person is susceptible to fungal and viral infections. |
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Brutan disease
X Linked agammaglobulnemia |
This person has no mature B cells.
Stops at pre- B cell stage -Failure of B Cell differentiation, absense of B & K, antibody deficient, and manifestations occur after 6 months. This person can develop extracellular pathogens: -H. Influenzae -S. pneumoniae -S. aureus -enterovirus infections |
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Common variable immunodeficiency
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-Block in B cell maturation
-Block in Plasma cell differentation -hypogammaglbulinemia -T Cell aberrant signal - M& F - common in childhood and adolscents These people are more susceptible to H. Influenzae. |
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AIDS
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AIDS is a retroviral disease that is caused by the human immondeficiency virus (HIV) and is characterized by profound immunosuppression leading to opportunistic infections, secondary neoplasms, and neurologic manifestations.
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AIDS
Sexual transmission |
Sexual transmission is the predominant mode of infection worldwide.
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Mother to infant transmission
vertical transmission |
This is the major cause of pediatric AIDS
Three routes are involved: 1. in utero by transplacental spread (accounts for most cases) 2. intrapartum- during delivery 3. via ingestion of HIV contaminated breast milk. |
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AIDS immunity
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people who are immune to AIDS to not have a chemokine receptor
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AIDS dementia
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this is caused by mediators of inflammation. cytokines and mediators.
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AIDS etiology
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The viral envelope is studded by viral glycoproteins, g[120 and gp41
AIDS attacks CD4+ cells |
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AIDS
immunopathogenesis |
Entry of HIV into host cells involves an intricate process between viral glycoproteins (gp120 and gp41) and host cell CD4 receptor, and chemokine receptors (CXCR4 and CCR-5)
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3 Phases of HIV infection
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1. Acute phase
2. chronic phase 3. crisis phase |
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Acute Phase of HIV infection
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-this begins 3-6 weeks after infection.
-sore throat, myalgias, fever, rash, aseptic menigitis -high level virus production -CD4+ T cell reduction -Virus specific immune response develops -CD4+ T cell numbers return to normal levels -Viremia abates, viral replication continues in specific cells. -Flu-like symptoms |
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Qualitative and quantitative loss in T cells
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apoptosis- self destruct
T Cell fusion-the cells come together and are useless. The T cells are very important because they regulate and protect the immune system. |
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Chronic Phase
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continued HIV replication lasting several years.
Lymphadenopathy develops Minor opportunistic infections such as thrush CD4+ cell decline viral replication continues |
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Crisis Phase
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fatigue, weightloss, diarrhea, and fever
catastrophic breakdwon of host defenses Marked viremia Fever that lasts more than one month CD4+ cell count reduced below 500cells/ul serious opportunistic infections, secondary neoplasms neurological infections. immune related: opportunistic infections, secondary neoplasms-AIDS dementia |
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Enzyme Linked immunosorbent Assay (ELISA)
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-initial screening
-antigen/antibody assay -99% sensitive -repeated if positive -p24 is readily detectable |
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Western Blot
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-Confirmatory Test
-2 bands from either gag and or env region must be present for a positive test. p24, p41 g120 or g160. if this test comes out negative, then repeat it. |
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kaposi syndrom and lymophoma are common in people with aids
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imp. info
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tumor
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the proliferation of neoplastic cells that form a mass in a tissue or organ
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nomenclature
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begin tumors end with a suffix; -oma.
sarcoma denoates malignant tumors of mesenchyme or connective tissue origin. Carcinoma denotes malignant tumors of epithelial tissue. Sarcoma and carcinoma are malignant The prefix adeno- when used denoates tumors composed of ducts or glands. |
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benign tumors
MACROscopic features |
-benign tumors are sharply demarcated and are often encapsulated.
-growth is by expansion and compression of adjacent normal tissue -sharp borders are distinct between tumor and normal tissue. |
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benign tumors
MICROscopic tumors |
-benign tumors are composed of cells that resembe the tissue from which they have arisen.
-these tumors show a high degree of differentiation- the cells look almost normal. |
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benign tumors
cellular features |
-benign tumors are composed of a uniform cell population in which all cells have the same features
- these features include, reguarly shaped nuclei and the nucleus accounts only for a small part of the total cell volume. chromatin is distributed evenly in the nucleus. -benign tumors never metastasize |
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Malignant tumors
MACROscopic features |
-lack a capsule and invade adjacent tissue by infiltration
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Malignant tumors
MICROscopic features |
-these cells show anaplasia and acquire new characteristics not inherent to the tissue of their origin.
-malignant cells are undifferentiated. |
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Malignant tumors
Cellular features |
-malignant cells show marked pleomorphism (different sizes and shapes). the nuclei are of different shapes and sizes, the nuclei are hyperchromatic, nucleoli are prominant and nucleus accounts for most of the cells volume. increased nuclear to cytoplasm ratio; high N/C ratio.
-increased cellular division. chromosal abnormalities are present - malignant tumors can metastasize |
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Biology of tumors
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-the acquisition of new atypical features by malignant cells is known as anaplasia. anaplastic cells are larger than normal cells and show nuclear irregularity.
-tumor cells often regress and assume fetal features. ex. Liver cancer cells secrete alpha fetal protein, a major secretory product of fetal liver cells, not are not synthesized by normal liver cells. -colon cancer cells produce carcinoembryonic antigen, a glycoprotien normally found only on embryonic intestinal cells. |