Immunity flashcards

Card Set Information

Author:
sashatom
ID:
40701
Filename:
Immunity flashcards
Updated:
2010-10-13 14:59:46
Tags:
immunity autoimmunity HIV allergies rheumatoid arthritis
Folders:

Description:
NURS 501 lecture on immunity
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user sashatom on FreezingBlue Flashcards. What would you like to do?


  1. What is the immune response?
    A collective and coordinated response of cells of the immune system
  2. What are the 3 functions of immunity?
    • Protect host from invasion of anything foreign
    • Distinguish self from non-self
    • Mediate healing
  3. Which cell of innate immunity Are phagocytic cells?
    Monocytes, macrophages and dendritic cells
  4. Which cell of innate immunity Are antigen presenting cells (APC)?
    Monocytes, macrophages and dendritic cells
  5. Are very important in Agn binding and non-specific phagocytosis?
    Neutrophils
  6. Are also known as polymorphonuclear leukocytes?
    Neutrophils
  7. Which cell of innate immunity Fight parasites?
    Eosinophils
  8. Which cell of innate immunity Are very important in inflammatory response?
    • Neutrophils
    • Eosinophils
  9. Which cell of innate immunity release potent mediators during allergic responses?
    Basophils
  10. Which cell of innate immunity have binding sites for IgE Abys?
    Basophils
  11. Which cell of innate immunity releases histamine but is found in tissues?
    Mast Cells
  12. Which cell of innate immunity can bind with Aby coated target cells?
    Natural Killer Cells
  13. Which cell of innate immunity is involved in antibody dependent cell-mediated cytotoxicity?
    Natural killer cells
  14. Which cell of innate immunity can attack virus-infected cells or cancer cells without help or activation first?
    Natural killer cells
  15. Which cell of innate immunity can recognize Agn without MHC resitrictions?
    Natural killer cells
  16. Which cell of innate immunity are regulated by cytokines, prostaglandins and thromboxane and release toxins?
    Natural killer cells
  17. What happens when APCs are activated?
    They secrete cytokines
  18. What are the two major components of adaptive immunity?
    • Cell-mediated
    • Aby-mediated
  19. Which type of immunity is specific and acquired?
    Adaptive Immunity
  20. Which type of immunity is the first line of defense?
    Innate Immunity
  21. What are cytokines made by?
    • T-cells
    • Macrophages
  22. What is lymphokine?
    Special cytokine released by lymphocyte
  23. What are released by immune cells and act on other immune cells?
    Cytokines
  24. What part of the inflammatory response are cytokines important?
    Early on
  25. What stimulates the acute phase protein production by the liver?
    Cytokines
  26. What is the action of cytokines in adaptive immunity?
    Activate immune cells to proliferate and differentiate into effector and memory cells.
  27. What is triggered when first line of defense’s integrity has been breached?
    Inflammation
  28. What are the three steps of the vascular phase of acute inflammation?
    • Rapid vasoconstriction of small vessels
    • Rapid vasodilation of arterioles and venules
    • Increased capillary permeability
  29. How long does an immediate sustained response last and what occurs as a result?
    Several days and can cause vessel damage
  30. What is the delayed hemodynamic response?
    Increased capillary response 4-24 hours after an injury
  31. What allows leukocytes to migrate to the local area during the cellular phase of inflammation?
    • Release of cytokines by innate immunity cells
    • Increased capillary permeability
  32. Which inflammatory mediater causes dilation and increased capillary permeability?
    Histamine
  33. What is released from mast cells in response to binding of IgE Abys?
    Histamine
  34. What are the two pathways that can metabolize arachidonic acid?
    • Cyclooxygenase pathway
    • Lipoxygenase pathway
  35. What does the cyclooxygenase pathway metabolism of arachidonic acid produce?
    • Inflammation (prostoglandins)
    • Platelet aggregation (TXA2)
  36. What inhibits the first enzyme in the cyclooxygenase pathway?
    Non-steroidals (aspirin)
  37. What does the lipoxygenase pathway metabolism of arachidonic acid pathway produce?
    • Leukotrienes
    • Anaphylaxis
  38. What do newer anti-asthma drugs (Singulair) target?
    Lipoxygenase pathway of arachidonic acid metabolism
  39. What three actions does platelet activating factor produce?
    • Platelet aggregation
    • Neutrophil activation
    • Eosinophil chemotaxis
  40. What is the primary mediator of the innate and adaptive humoral immune response?
    Complement System
  41. What are the three pathways that activate the complement system?
    • Classical Pathway
    • Alternate Pathway
    • Lectin Pathway
  42. What is the main activity of the Classical Pathway of complement activation?
    • IgG or IgM binds to invading org.
    • Bind complement to circulations Agn-Aby complex
  43. What is the main activity of the Alternate Pathway of complement activation?
    Interactions between complement and polysaccharides on microbes
  44. What is the main activity of the Lectin Pathway of complement activation?
    Binding proteins interacting with cell surface proteins in bacteria and yeast
  45. Where do the three pathways of activating the complement system converge?
    C3
  46. What does the membrane attack complex do?
    Creates a hole in the target cell membrane causing lysis
  47. What four things result from the activation of C3?
    • Inflammation
    • Opsonization
    • Chemotaxis
    • Membrane attack complex
  48. What is opsonization?
    Increased phagocytosis as a result of complement-binding
  49. What does anaphylatoxin induce?
    Histamine release in mast cells and basophils
  50. What is the result of histamine release?
    • Contraction of smooth muscle
    • Increased muscle permeability
    • Edema
  51. What causes chronic inflammation?
    Moderate to low-grade persistent irritants
  52. What are two patterns of chronic inflammation?
    • Non-specific diffuse accumulation of cells of the inflammatory response that leads to fibroblast proliferation and scar tissue
    • Granulomatous lesion (local)
  53. What is exravascular influx of fluid with a high concentration of proteins, salts, cells and cell debris?
    exudation
  54. What does exudation do?
    • Dilutes injurous chemicals
    • Brings complement, Abys and chemotaxic substances
    • Pull water out of plasma and promotes containment of pathogens
  55. What is fibrinous exudate?
    Contains large amounts of fibrinogen
  56. What type of exudate contains necrotic debris in fibrinous matrix on mucus membrane surface?
    Membranous exudate
  57. Why does autocrine and paracrine signaling predominate in inflammation?
    Inflammatory mediators have very short half lives
  58. When do systemic signs of inflammation appear?
    When inflammation is large/robust enough
  59. What are signs of systemic inflammation?
    • Increase in plasma proteins
    • Increase erythrocyte sedimentation rate
    • Fever
    • Leukocytosis
    • Muscle wasting (negative nitrogen balance)
    • Lymphadenitis
  60. What is lymphadenitis?
    Regional swelling of lymph nodes, painful upon palpation
  61. What is the focus of treatment for inflammation?
    Prevent synthesis and release of pro-inflammatory mediators
  62. Which anti-inflammatory drugs inhibit cyclooxgenase?
    NSAIDs
  63. What is cyclooxygenase?
    An enzyme that converts arachidonic acid to prostaglandins and thromboxane
  64. Which anit-inflammatory drugs work in several ways, mostly to impair immune cell proliferation or cytokine release?
    Steroids
  65. What is responsible for the adverse effects of NSAIDs?
    Inhibition of COX-1
  66. Which COX inhibition impairs the GI mucosal barrier, impairs renal function and prevents platelet aggregation?
    COX-1
  67. Which COX is predominantly in immune cells?
    COX-2
  68. Which COX inhibition results in the therapeutically desireable effects of NSAIDs?
    COX-2
  69. What is the result of inhibiting COX-2?
    • Suppression of inflammation
    • Alleviation of pain
    • Reduction of fever
  70. Why should NSAIDs be avoided in mid- to late-pregnancy?
    • May cause premature closure of ductus arteriosus
    • Might cause prolonged bleeding following delivery because of their effect on platelets
  71. What is an irreversible inhibitor of both COX-1 and COX-2?
    Aspirin
  72. What is aspirin metabolized into and how long does it take?
    Salicylic acid, about 20 minutes
  73. What inhibits both COXs reversibly and has a longer half-life than aspirin?
    Salicylic Acid
  74. What are the uses of Aspirin?
    • Anti-inflammatory
    • Anti-pyretic
    • Analgesic
    • Dysmenorrheal
    • Suppression of platelet aggregation
  75. How is aspirin used to suppress platelet aggregation?
    81-mg enteric coated tablet, 1/day
  76. What adverse effects are common to all aspirin formulations?
    • Salicylism
    • Reye’s syndrome
    • Poisoning
  77. What are the symptoms of salicylism?
    • Tinnitus
    • Headache
    • Dizziness
    • Possibly rheumatoid arthritis and respiratory alkalosis
  78. What are five aspirin formulations?
    • Plain aspirin tablet
    • Buffered aspirin
    • Enteric coated aspirin
    • Time released
    • Rectal suppositories
  79. What are adverse effects of nonspecific COX inhibitors?
    Interaction with warfarin, increased bleeding
  80. What are adverse effects of specific COX-2 inhibitors?
    Increased risk of heart attacks
  81. What are the major functional cells of the adaptive immune response?
    • B-cell lymphocytes
    • t-cell lymphocytes
  82. What are two types of t-cell lymphocytes?
    • T-helper cells
    • Cytotoxic T Cells
  83. Under what circumstances can a hapten become immunologically active?
    When it is bound to a carrier protein
  84. What is the Major Histocompatibility Complex (MHC)?
    • Differentiates between self and non-self
    • Differentiates individuals within same species
  85. Which cells recognize MHC complexed with antigen?
    • Cytotoxic T Cells
    • T Helper Cells
  86. Which MHC are found primarily on Agn presenting cells?
    MHC II
  87. Which MHC are found on most all nucleated cells of the body?
    MHC-I
  88. Where do lymphocytes stem cells reside?
    Bone marrow
  89. Which lymphocytes migrate through lymphoid tissue?
    B cells
  90. Which lymphocytes undergo a genetic rearrangement that results in a unique receptor and type of effector Aby?
    B lymphocytes
  91. What do B lymphocytes differentiate into with the help of T helper cells?
    • Plasma Cells
    • Memory Cells
  92. What occurs during the primary immune response?
    • Agn is introduced into body
    • Agn is processed
    • MHC-Agn complex is ID by T helper cell
    • Activated T helper cells release cytokines
    • Cytokines trigger B cells to make plasma and memory cells
    • Plasma cells release Aby
  93. What occurs during secondary immune response?
    Memory cells ID Agn and respond quickly
  94. Which Aby is found primarily on a cell membrane of B lymphocytes and acts an antigen receptor?
    IgD
  95. Which Aby is involved in inflammation, allergic responses and combating parasitic infections?
    IgE
  96. Where do T-cells undergo genetic modification to form a unique T-cell Agn receptor?
    Peripheral lymphoid organs
  97. What is a T-cell receptor with a CD4+ protein called?
    T-helper cell
  98. What is a T-cell receptor with a CD8+ protein called?
    Cytotoxic T-cell
  99. Which T cell is the regulatory master switch of the immune system?
    Helper T cell
  100. Which T-cell is an effector cell?
    Cytotoxic T-cell
  101. What activates T-helper cells?
    Agn recognition and cytokines
  102. Why are secondary lympoid organs important?
    Support lymphocytes
  103. What are three secondary lymphoid organs?
    • Lymph nodes
    • Spleen
    • MALT (Mucosa-Associated Lymphoid Tissue)
  104. When are adult levels of Igs reached?
    Between 1-2 years
  105. Which Ig can transform into other Igs after Agn stimulus?
    IgM
  106. What kind of immunodeficiency is a primary disorder and causes a delay in the maturation of B cells in children?
    Transient Hypogammaglobulinemia of Infancy
  107. What are children who have Transient Hypogammaglobulinemia more prone to?
    Upper respiratory and middle ear infections
  108. What is the source of primary immunodeficiency?
    Defective congenital or inherited genes
  109. What are three rare primary immunodeficiencies?
    • X linked agammaglobulinemia-Bruton’s (no Abys)
    • DiGeorge Syndrom (lack of thymus)
    • Severe combined immunodeficiency syndrome (no T/B cells)
  110. What is the source of secondary immunodeficiency and when do they occur?
    • Later in life…
    • Selective loss of Igs through GI or GU tract
    • Chronic/recurrent infections
    • Neoplasia
    • Iatrogenic causes
    • Stress/aging
    • Drug abuse, maternal alcoholism
  111. What are the four types of hypersensitivity disorders?
    • Type I: IgE mediated
    • Type II: Aby-mediated
    • Type III: Immune Complex Allergic Disease
    • Type IV: T-cell mediated
  112. Which hypersensitivity disorder is short-term, causes itchy skin and can cause anaphylaxis and is triggered by binding of Agn to mast cell or basophil with attached IgE?
    Type I: IgE-mediate
  113. What is released during the primary phase of Type I: IgE-mediated hypersensitivity?
    • Histamine
    • Compliment is activated
    • Ach causes bronchoconstriction and vasodilaion of small vessels
    • Chemotaxis
    • Kinis are activated
  114. What is released during secondary phase of Type 1: IgE mediated hypersensitivity?
    • Leukotrienes
    • Cytokines
    • Platelet activating factor
    • prostaglandins
  115. What are two types of IgE-mediated disorders?
    • Atopic
    • Non-atopic
  116. Which IgE-mediated disorder is local-anaphylaxis?
    Atopic
  117. What are common allergens for non-atopic IgE mediated disorders?
    Nuts, shellfish, penicillin, insect stings
  118. What kind of receptor does an antihistamine block?
    H1
  119. What else do most first generation H1 blockers also block that have sedating effects?
    Muscarinic receptors
  120. What are some examples of Type II-Aby mediated disorders?
    • ABO antigens in blood transfusion reactions
    • Rh Antigens of fetus
    • Drug Reactions
    • Autoimmune hemolytic anemia
    • Graft rejections, parasites
  121. Which hypersensitiviy involves antibody cytotoxicity?
    Type II-Aby-mediated
  122. What is Type III-Immune Complex allergic disease triggered by?
    Formulation of insoluble Agn-Aby complexes in blood circulation or extravascular sites that lead to precipitate formation and complement activation
  123. What type of injuries are caused by Type III-Immune Complex Allergic Disease?
    • Change in blood flow
    • Vacular permeability
    • Inflammatory response
  124. What can localized reactions of Immune Complex disorders lead to?
    • Vasculitis
    • Immune Complex Pneumonitis
  125. Which hypersensitivity has a delayed response, is triggerd by specifically sensitized T-lymphocytes and not antibodies and are not tissue specific?
    Type IV T-Cell mediated
  126. What are three types of Type IV T-cell mediated hypersensitivity?
    • Contact dermatitis
    • Response to the Tuberculin test
    • Granulomatous inflammation with large, insoluble Agns
  127. What is Host Versus Graft Disease?
    A cell-mediated response where recipient attacks donor cells
  128. What three responses occur when T-helper cells activate the production of antibodies and targe graft vasculature?
    • Complement-mediated toxicity (Type II)
    • Agn-Aby complexes (Type III)
    • Antibody-mediated cytolysis (Type II)
  129. What immune disease may be T cell-mediated or Agn-Aby complexes, more common in females and elderly, tissue or system specific.
    Autoimmunity
  130. What is Rheumatoid Factor an antibody against?
    IgG
  131. What are rheumatoid nodules?
    bumps that form under the skin close to the joints
  132. What are three major systemic manifestations of RA?
    • Vasculaitis
    • Pleuritis
    • Pericarditis
  133. What signs are used to diagnose RA?
    • Morning stiffness for > 1 horu
    • Swelling of >3 joints for >6 weeks
    • Symmetric joint swelling
    • Rheumatoid nodules
    • Presence of serum RF Aby
  134. What medications are used to treat RA?
    • NSAIDs
    • Disease Modifying Anti-Rheumatic Drugs
    • Immunosuppressants
    • Corticosteroids
    • Combo therapy
  135. What are two actions of disease modifying anti-rheumatic drugs?
    • Reduced number of immune cells
    • Block cytokines
  136. What are primary causes of OA?
    Idiopathic, no identified risk factors
  137. What are secondary causes of OA?
    • Joint stress
    • Congenital abnormalities
    • Joint instability
    • Trauma
  138. What are some signs and symptoms of OA?
    • Sudden/insidious
    • Mild synovitis
    • Hip, knee, lumbar an cervical region
    • Joint enlargment
    • Hard joint
  139. What are the main differences between RA and OA?
    • No or very little synovitis
    • No systemic signs and symptoms
    • Normal synovial fluid (no pannus)
    • Affects cartilage and subchondral bone only
    • Not always symmetric
    • Not always polyarticular
    • Hardness around joint
  140. What are some causes of secondary immunodeficiency?
    • Nutrition
    • Chemotherapy
    • Burns
    • Stress
    • AIDS
  141. Two big risk factors for patients infected with HIV?
    • Opportunistic infections
    • Neoplastic complications
  142. What are the components of the HIV viral genome?
    • Two short strands of RNA
    • Three major genes that encode reverse transcriptase, protease and integrase
  143. What are the components of the outer lipid envelop of the HIV viron?
    GP 120 Antigen, which binds to CD4 of T-helper cell
  144. What is used to classify HIV infection?
    CD4 cell count
  145. Which classification of HIV infection is characterized by a positive test for HIV Aby’s but only produces mild disease or is asymptomatic?
    Primary Infection
  146. Which classification of HIV infection may last 10 years and is concentrated in the lymph nodes, is asymptomatic and not very well detected in blood?
    Latent Period
  147. What happens to CD4 cell count during latent period HIV infection?
    Falls gradually
  148. What is clinically apparent HIV disease characterized by?
    • Persistent generalized lymphadenopathy
    • Fatigue, weight loss, night sweats
    • Diarrhea
    • Fungal infections
    • CD4 count < 500 cells
  149. What is full blown AIDS characterized by?
    • CD4 count < 200 cells
    • Opportunistic infections
    • Neoplastic malignancies
    • Wasting Syndrome
  150. What are patients with HIV disases most likely to die from?
    Neoplastic complications and opportunistic infections
  151. How is HIV diagnosed?
    • HIV aby test
    • Western Blot
    • CD4 count
    • Symptoms

What would you like to do?

Home > Flashcards > Print Preview