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TEST #2- Immunity
Patho
| Question | Answer |
|---|---|
| What are 4 risk factors of the immune system? | nutritional factors, chronic diseases, age, and immunosuppression |
| What are 3 different types of organisms that may hurt the immune system? | Our normal flora, bacteria, and viruses |
| What are 3 components of the immune system? | Central Lymphoid Tissue, Peripheral Lymphoid Tissue, and Immune Cells |
| What are 4 Body Defenses of the Immune System? | Barriers, phagocytes, natural killer cells, and blood born cells |
| the system that includes all the lymph vessels that collect tissue fluid and return it to the blood, the lymph nodes and nodules, the spleen, and the thymus | Lymphatic system |
| a white blood cell responsible for much of the body’s immune protection. Less than 1% are present in the circulating blood; the rest lie in the lymph nodes, spleen, and the other lymphoid organs, where they can maximize contact with foreign antigens | Lymphocyte |
| white blood cells (neutrophils and macrophages) with the ability to ingest and destroy microorganisms, cell debris, and other particles in the blood or tissues | Phagocyte |
| a large granular lymphocyte that bonds to cells and lyses them by releasing cytotoxins. Unlike other lymphocytes, these cells do not have B cell or T cell surface markers, and they can be activated without previous antigen exposure | Natural Killer Cells |
| Which defense approach cannot distinguish between pathogens? | nonspecific |
| What are the 2 lines of defense for the nonspecific defense approach? | Skin and mucous membrane, chemical signals, antimicrobial substances, phagocytes, and natural killers |
| 1st line of defense and distingushes self from nonself | nonspecific defense approach |
| develops over time and distingushes self from nonself and between pathogens | Specific defense approach |
| can distingush between pathogens | Specific defense approach |
| Which dense approach includes lymphocytes? | Specific defense approach |
| a lymphocyte that matures in the bone marrow and then migrates to lymphoid tissues, where a foreign antigen stimulates it to produce antibodies. They are antigen specific and respond to only one foreign protein. The spleen and lymph nodes contain many o | B Cell |
| effector cells that directly lyse organisms, are an important defense against viruses; most produce gamma interferon, one of the strongest stimulators of macrophage activity | CD8 T cells |
| serve primarily as regulators, secreting cytokines that stimulate the activities of other white blood cells | CD4 T cells |
| a lymphoid cell from the bone marrow that migrates to the thymus gland, where it develops into a mature differentiated lymphocyte that circulates between blood and lymph, serving as one of the primary cells of the immune response | T Cell |
| Is the primary site for T-lymphocyte differentation | thymus |
| T lymphocytes multiply here, and B lymphocytes proliferate and manufacture antigen-specific antibodies here | lymph nodes |
| filters antigens from the blood | spleen |
| composed of lymphocytes and follicles, form sheaths around arterial vessels and collects in larger nodules containing germinal centers | white pulp |
| destroys old red blood cells | red pulp |
| contains the red and white pulp | spleen |
| located near the respiratory and urogenital tracts and acts as a gate keeper into the body | mucosa |
| a protein or olisaccaride marker in the surface of cells that identifies the cell as self or nonself; it identifies the type of cell, stimulates the production of antibodies by B lymphocytes that will neutralize or destroy the cell if necessary | antigen |
| distinct proteins produced by WBC. They provide signals to regulate immunological aspects of cell growth and function during both inflammation and specific immune response | cytokine |
| a group of protein markers on the surface of a WBC. These markers are used to classify immune cell types. Mature T and B cells have surface molecules | Cluster of Differentation |
| identify cytotoxic T cells, which are essential to the defense against viral infections | Markers for CD8 |
| are found on all T helper cells, macrophages, and some B cells. They are “booster cells” and help make things work better | Markers for CD4 |
| Key players in the process of differentiating b/t self and non-self | Major Histocompatibility Complex |
| a group of genes on chromosome 6 that code for the antigens that determine tissue and blood compatibility | Major Histocompatibility Complex |
| immature macrophages that contain the foreign substance until the troops arrive; they are activated by antigens to engulf and digest the substance | monocytes |
| essential in the acquired immune response and helps with memory | dendrite celld |
| What are 3 lymphoid organs? | thymus, lymph nodes, and the spleen |
| result of an antigen | antibody |
| a foreign cell/object in body | antigen |
| a diverse group of plasma proteins (antibody class of proteins), that are one of the primary mechanisms for protection against disease | Immunoglobulin |
| it prevents pathogenic bacteria and viruses from invading the body through the mucosa of the GI, pulmonary, and genourinary tracts. Found in breast milk, respiratory and intestinal mucin, saliva, and tears | IgA |
| is present on the surface of B lymphocytes and acts as an antigen receptor; supervisor of other B cells | IgD |
| plays a role in allergic reactions; 50% of allergen patients have > IgE levels; is important in the formation of reagin, which is found in the blood of individuals with atopic hypersensitivity | IgE |
| in human serum; helps in producing immunity in the infant before birth, most abundant | IgG |
| formed in almost every immune response during the early stage or reaction; controls A, B, O blood antibody responses; 1st immunoglobulin produced after birth | IgM |
| once activated, they can produce 1000s of antibodies/sec | B Cells |
| develop specific antibodes as they mature and they respond quickly | B Cells |
| activate T and B cells | T Cells |
| controls viral ifections and rejects foreign tissue grafts | T Cells |
| functions in teh delayed hypersensitivity reaction | T Cells |
| are proteins that are produced in all phases of the immune response | cytokines |
| a type of cytokine that enables communication among leukocytes and other cells active in inflammation or the specific immune response | Interleukin |
| a cytokine released by almost all nucleated cells that activates the growth and function of neutrophils, lymphocytes, and macrophages | Interleukin 1 |
| are involved in fever production and other systemic effects of inflammation | Interleukin 1 and Tumor Necrosis Factor |
| a cytokine released primarily by activated CD4 helper T lymphocytes; it is a major mediator of T cell proliferation, promotes production of other cytokines, enhances natural killer cell function, and is a cofactor for immunoglobulin secretion | Interleukin 2 |
| any group of glycoproteins with antiviral activity | Interferon |
| (alpha and beta) enable invaded cells to produce class I major histocompatibility complex surface antigens, > their ability to be recognized and killed by T lymphocytes; they inhibit virus production within infected cells | Type 1 interferon |
| helps regulate the immune response and some hematopoietic functions; kill tumor cells | Tumor Necrosis Factor |
| initiates blood cell production; the blood forming tissue and organs of the body; it included bone marrow, spleen, and lymphatic tissue | Hematopoietic Colony Stimulation Factors |
| immunity resulting from the development within the body of antibodies or sensitized T lymphocytes that neutralize or destroy the infective agent (can result from invading organism or vaccine); long lasting and takes a few days to become effective | Active Immunity |
| immunity acquired by the introduction of preformed antibodies into an unprotected individual. This can occur though intravenous infusion of immune globulin or, in utero, from antibodies passed from mother to baby through placenta or breast feeding | Passive Immunity |
| the protective activities of antibodies against infection or re-infection by common organisms; B lymphocytes with receptors to a specific antigen react when they encounter that antigen by producing plasma cells and memory cells | Humoral Immunity |
| protects against viruses, intracellular bacteria and cancer cells; T cells and macrophages are the key player | Cell-Mediated Immune Response |
| produces an inflammatory response; lyses foreign cells; > phagocytosis; tissue trama | Complement System Immune Response |
| What are the 5 regulations of the immune response? | 1. it is self-regulated 2. an inadequate response may lead to immunodeficiency 3. an excess response may lead to an allergic reaction or autoimmune disorders 4. it is self-limiting 5. it may gain tolerance |
| When is the immune system developed? | 5-6 weeks into fetal development |
| What immunoglobulin does the mother transfer to the new born? | IgG |
| What immunoglobulin does the infant produce a few months after birth? | IgM |
| What immunoglobulin is first detected after birth? | IgA |
| vascular reaction that results in a delivery of fluid, dissolved substances, and cells from the blood into interstitial space | inflammation |
| dilatation (expanding) of blood vessels, small arteries, and arterioles | Vasodilation |
| an > in the diameter of blood vessels, which > blood flow and lowers blood | Vasodilation |
| an immediate inflammatory response, that is nonspecific and short lived. What is its purpose and S/S? | Acute Inflammatory Repsonse. Purpose: remove the agent and limit tissue damage. S/S: redness, edema, warmth, pain, and fever |
| swelling | edema |
| occurs imediatly, erythema and warmth results; fluid shift and pain occurs | Acute vascular inflammatory response |
| redness | erthema |
| stage of acute inflammatory response when the leukocytes move in | cellular stage |
| 3 types of Granulocytes | neutrophils, eosinophils, basophils |
| granular WBC, are essential to the nonspecific immune response to inflammation; general reactor | Basophils |
| granular WBC, contribute to the destruction of parasites and to allergic reactions by releasing chemical mediators such as histamine | Esoinophils |
| granular WBC, most common, are responsible for much of the body’s protection against infection. They play the primary role in inflammation and are first to arrive | Neutophils |
| most abundant WBC | (acute) mononuclear phagocytes |
| longer living phagocytes | (acute) mononuclear phagocytes |
| destroys the causative agent and aids in signaling processes. also resolves the inflammatory processes | (acute) mononuclear phagocytes |
| Describe the 4 steps to teh cellular inflammatory response | 1. pavementing: cells become more periable (get ready) 2. emigration: things shift to inflammed area (getting lined up) 3. chemotaxis: cells cross boarder and jump over 4. phagocytosis: phagocytes engulf and destroy (clean up) |
| 5 inflammatory mediators (triggers) | histamine, plasma proteases, prostaglandins, leukotrienes, platelets |
| a round or oval disk found in the blood of vertebrates; they are fragments of megakaryocytes, large cells found in bone marrow; they contribute to chemical blood clotting and to other aspects of hemostasis | Platelets |
| any of a group of arachidonic acid metabolites that functions as a chemical mediator of inflammation; they are extremely powerful bronchconstrictors and vasodilators and mediate the adverse vascular and bronchial effects of systematic anaphylaxis | Leukotrienes |
| any large group of biologically active, carbon-20, unsaturated fatty acids; they are autacoids, which are local short-range hormones that are formed rapidly, act in the immediate area, and then decay or are destroyed by enzymes | Prostaglandins |
| class of enzymes that breakdown or hydrolyze the peptide bonds that join amino acids in a protein. The protein is broken down into basic building blocks | Proteases |
| a substance produced from the amino acid histidine, which causes dilation of blood vessels, > secretion of acid by the stomach, smooth muscle constriction, and mucus production, tissue swelling, and itching | Histamine |
| may last weeks to years and may be related to recurrent or progressive acute infections ot low grade fever | chronic inflammation |
| infiltration of macrophages and lymphocytes instead of neutrophils...and fibroblasts instead of exudate...also > risk of scarring | chronic inflammation |
| any cell from which connective tissue is developed; it produces collagen, elastin, and reticular protein fibers | fibroblast |
| drainage, fluid released from body | exudate |
| what are some potential sources for chronic inflammation? (5) | foreign substances, viruses, bacteria, fungi, and large parasites |
| what are the 2 patterns of chronic inflammation? | nonspecific and granulomatous inflammation |
| repeatative chronic build up | grangranulomatous inflammation |
| What are some exudate side effects of local manifestation of inflammation? (6) | serous (clear), serosanganous (clear w/ little blood), hemorrhagic (straight blood), fibrinous (scabbing causing scarring), membranous, purulent or suppurative (yellowish drainage) |
| clear fluid drainage, usually plasma | serous |
| clear fluid with a little blood causing a little pink tint | serosanganous |
| straight blood drainage | hemorragic |
| yucky, yellow/greenish drainage | purulent/supporative |
| result of local manifestations of inflammation (3) | exudates, abesses, ulceration |
| a localized collection of pus in any body part that results from invasion of a pyogenic bacterium or other pathogen | abscess |
| a supportive or nonhealing lesion on a surface such as skin, cornea, or mucous membrane | ulceration |
| something breaking down tissue because of lack of blood supply | pressure ulcer |
| new cell growth | granulation |
| results of an acute systematic manifestion of inflammation (6) | changes in concentration of plasma proteins, > ESR, fever, > # of leukocytes, skeletal muscle catabolism, - N balance |
| the rate it takes to spin blood down and separate the plasma | ESR-Erythrocyte Sedimentation Rate |
| WBC response to systematic manifestation of inflammation (4) | Leukocytosis, bands, > neutrophils with bacterial infection, < neutrophils in parasitic allergic reactions, or overwhelming infections |
| inflammation in the lymph nodes (occurs in almost any infection) | lymphadenitis |
| > in WBC | leukocytosis |
| an increase | cytosis |
| the replacement of injured tissue with cells of the same type and left with no evidence of injury | regeneration |
| a cell that is always mitotically activate | Labile Cells |
| close wound (stiches) | Primary intention to repair connective tissue |
| leave wound open | Secondary intention to repair connective tissue |
| why would secondary intention of tissue repair be used? | because it needs to be watched for infection...preventing a warm, moist place for bacterial growth |
| the okay stage fro redness and swelling | inflammatory stage to repair connective tissue |
| what are the two results of the proliferation stage of the repair of connective tissue? | Fibroblast's role and granulation tissue forms |
| what is the result of the remodeling phase of the repair of connective tissue? | the infection/wound getting back to normal, although it will probably never gain full function....or Keloid (thick raised scar) |
| who is at a higher risk for keloids? | darker skined people |
| what are the 3 factors that effect wound healing? | malnutrition, blood flow, and impaired inflammatory and immune responses |
| what are 4 complication of wound healing? | wound contamination, dehiscence, foreign bodies, evisceration |
| wound pops open and viseral organs pop out | evisceration |
| wound pops open | dehiscence |
| inflated immune response to a foreign substance...an overreaction usually an allergy | hypersensitivity |
| abnormal response to an allergen | allergy |
| substance, foreign protein or cell, capable of causing alteration in sensitiviy | allergens |
| how do allergens enter body? (4) | inhalation, ingestion, injection, skin contact |
| wound pops open (commonly an abdominal wound) | Dehiscence |
| wound pops open and visceral organs come out….result of dehiscence | Evisceration |
| a rash | Uticaris |
| swelling in the face | Angioedema |
| life threatening | Anaphylaxis |
| fast pulse | Tachycardia |
| blood in urine | Hematuria |
| flu-like symptoms as a result of antibiotic, foods, drugs, etc | Serum Sickness |
| what immunoglobulin deals with Type I Hypersensitivity? | IgE |
| What are different types of immediate responses to Type I hypersensitivity? (4) | allergic asthma, allergic rhinitis, allergic conjuncivitis, and hives |
| What denotes a rapid Type I hypersensitivity reaction? | anaphylaxis reaction (life threatening) |
| causes vasodilataion, > vascular permeability, vascular congestoin, and edema | histamines |
| they activate the T cells, monocytes, esoinophils, neutriphils producing contraction of smooth muscle causing bronchuolar constriction and edema | leukotrienes and cytokinies |
| usually results from injected allergies such as dye and bees | Type I: systemic anaphlactic reactions |
| allergic rhinitis and food allergies normally is the cause of this type of hypersensitivity | Type I: localized atopic disorders |
| what immunoglobulin does Type II hypersensitivity react with? | IgG and IgM |
| what hypersensitivity deals with transfusions? | Type II |
| a hemolytic disease of the newborn marked by anemia, jaundice, enlargement of the liver and spleen, and generalized edema | erythroblastosis fetalis |
| self distruction of one's blood | autoimmune hemolytic anema |
| What immunoglobulins react with type III hypersensitivity? | IgG or IgM |
| what is type III hypersensitivity called? | immune complex-mediated hypersensitivity reaction |
| what is type IV hypersensitivity also called? | delayed hypersensitivity reaction |
| what are the 3 manifestations of the latex allergy? | allergic contact dermatitis, immediate hypersensitivity (type I), anaphlaxis |
| donor and recipient are related or unrelated, but share similar HLA types | allogenic |
| donor and recipient are identicial twins | syngenic |
| donor and recipient are the same person | autologous |
| most successful type of transplant? | autologous |
| the recipient's immune system attempts to eliminate the donor cells | host vs. graft |
| major players in host vs. graft | T Cells |
| immediate or 2-3 days after transplant & d/t preformed antibodies & sensitized T cells to antigens in the donor organ; common in pt w/ previous transplants | Hyperacute |
| most common; treatable; occurs b/t 4 days & 3 months after transplant; Cell-mediated & results in transplant cell destruction | Acute |
| occurs 4 months to years after transplant; It is likely the result of antibody-mediated immune response; Antibodies and complements deposit in transplanted tissue vessel walls resulting in decreased blood flow and ischemia | Chronic |
| Occurs when immunocompetent fatal cells recognize host tissue as foreign and mount a cell-mediated immune response | graft vs. host |
| What are the 3 basic requirements for development of a graft vs. host transplantation? | 1. donor marrow must have a functional cellular immune component 2. recipient's tissue must bear antigens foriegn to the donor tissue 3. recipent's immunity must be compromised to the point that it cannot destroy the transplanted cells |
| the immune system losses the ability to recognize self and the defenses are directed at the host cell | autoimune disorders |
| autoimmune disorders are more common in ___ | females |
| what plays a role in autoimmune disorders? (3) | genetics, sex (females more common), abnormal stressers |
| mechanisms that trigger these type of immune disorders are not clear | autoimmune |
| autoimmune disorders proposed mechanisms in the failure of self-tolerance- includes disorders of regulatory or surveillance and remission | failure of T cell-mediated suppression |
| autoimmune disorders proposed mechanisms in the failure of self-tolerance- anergy involves the prolonged or irreverible inactivation of t cells under certain conditions and normally not expressed costimulatory molecules become activated | breakdown in T cell Anergy |
| autoimmune disorders proposed mechanisms in the failure of self-tolerance- problems with either the antigen structure, TCR recognition antigen, or MHC antigen presentation | MHC antigen complex receptor interactions |
| autoimmune disorders proposed mechanisms in the failure of self-tolerance- when any self-antigen is isolated during development and then introduced later | release of sequestered antigens |
| autoimmune disorders proposed mechanisms in the failure of self-tolerance- A foreign antigen so closely resembles a self-antigen that antibodies produced against the foreign reacts with the host | molecular mimicry |
| autoimmune disorders propsed mechanisms in the failure of self-tolerance-Short circuits in the normal sequence of events in an immune response leading to inappropriate activation of CD4 cells | superantigens |
| examples of autoimmune disorders involving superantigens that lead to an inappropriate activation of CD4 cells | Staph, strep exotoxins |
| examples of autoimmune disorders involving superantigens that are directly linked to the MCH II molecules | Toxic shock and Kawasaki's disease |
| autoimmune disorders propsed mechanisms in the failure of self-tolerance- Directly linked to the MCH II molecules causing a massive release of cytokines and uncontrolled proliferation of T cells | superantigens |
| what 3 things (criteria) can lead a DX to be an autoimmune disorder? | 1. evidence of an immune response 2. findings not r/t another condition 3. no other identifiable cause (rule out everything else) |
Created by:
TayBay15
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