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IHO Week 3 - WLB > Hypersensitivity Reactions - Nelson > Flashcards

Hypersensitivity Reactions - Nelson Flashcards

1
Q

Define innate immunity.

A

Pre-existing defense mechanisms present to prior infection that have evolved to recognize microbial pathogens and protect the individual against infection.

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2
Q

Define adaptive immunity.

A

Reactive immune mechanisms that are stimulated by (adapt to) microbes and other foreign antigens, and are capable of recognizing microbial and nonmicrobial substances.

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3
Q

What are the key components of innate immunity?

A
  • Epithelial barriers
  • Phagocytic cells (neutrophils, monocytes/macrophages)
  • Eosinophils, basophils, mast cells
  • Dendritic cells
  • Natural killer cells
  • Innate lymphoid cells
  • Plasma proteins
    • complement system
    • c-reactive protein
    • lung surfactant
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4
Q

What are the two types of adaptive immunity?

A
  • Humoral immunity
    • protects against extracellular microbes and toxins
  • Cell-mediated (cellular) immunity
    • protects against against intracellular microbes, tumor cells
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5
Q

What is the function of T-lymphocytes?

A
  • recognize a specific cell-bound antigen by means of an antigen specific T-cell receptor
    • monoclonal (neoplastic) proliferations will have the same TCR gene rearrangement
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6
Q

What is the function of CD4+ T-cells?

A
  • Helper T lymphocyte (via cytokine release)
    • activate macrophages (IFN-gamma)
    • induce inflammation
    • activate (proliferation & differentiation) of T and B lymphocytes (IL-4)
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7
Q

What is the function of CD8+ T-cells?

A
  • Cytotoxic T lymphocyte
    • kill infected cell
      • release perforin, granzymes, and granulysin
      • activate caspace cascade
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8
Q

What is the function of regulatory T lymphocytes?

A
  • suppression of immune response
    • release IL-10 & TGF-beta
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9
Q

What is the function of B-lymphocytes?

A
  • Recognize antigens
    • proliferate and differentiate into antibody-secreting plasma cells
    • neutralize microbes and toxins
    • opsonize microbes
    • phagocytose opsonized microbes
    • antibody-depended cytotoxicity
    • lysis of microbes via complement system
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10
Q

What is the function of Natural Killer Cells?

A
  • Kill cells missing self markers of MHC Class I
    • Cytolytic granule-mediated cell apoptosis
    • Antibody-dependent cell-mediated cytotoxicity
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11
Q

What are the functions of Dendritic Cells?

A
  • Capture microbial antigens from epithelia and tissues and transport the antigens to lymph nodes
    • Present antigen to T-cell
    • Activate T-cells (secrete IL-2)
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12
Q

What are Generative Lymphoid Organs (primary or central)?

A

Sites where T and B lymphocytes mature and become competent to respond to antigens:

  • Thymus - for T lymphocytes
  • Bone marrow - for B lymphocytes
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13
Q

What are Peripheral Lymphoid Organs (secondary)?

A

Sites where the adaptive immune response is initiated:

  • lymph nodes
  • spleen
  • mucosal and cutaneous lymphoid tissues
    • GI tract
    • respiratory tract
    • skin
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14
Q

What happens to the follicles in lymph nodes when B lymphocytes respond to an antigen?

A
  • Follicle develops a germinal center
  • Becomes hyperplastic = Reactive Follicular Hyperplasia
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15
Q

What is the physiologic function of Major Histocompatibility Complexes (MHC)?

A
  • Display peptide fragments of proteins for recognition by antigen specific T cells
    • MHC Class I: display antigens that are recognized by CD8+ T-lymphocytes and NK cells
    • MHC Class II: display antigens that are recognized by CD4+ T lymphocytes
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16
Q

Where are the genes for Major Histocompatibility Complexes located in humans?

A
  • Chromosome 6 = Human Leukocyte Antigen (HLA) Complex
    • MHC Class I: coded by HLA-A, HLA-B, and HLA-C genes
    • MHC Class II: coded by HLA-DP, HLA-DQ, and HLA-DR genes
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17
Q

What are the two uses of HLA testing?

A
  • Can be used to determine disease risk
    • e.g. 90% of patients with ankylosing spondylitis are positive for HLAB27
  • Used in transplantation workup
    • close matches of HLA-A, HLA-B, HLA-C, and HLA-D in both the donor and graft recipient increase the chance of graft survival
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18
Q

What is a hypersensitivity reaction?

A
  • excessive, injurious pathologic immune reaction to the repeat exposure of an antigen
    • exogenous (environmental)
    • endogenous (self-antigens, autoimmune diseases)
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19
Q

What do hypersensitivity reactions usually result from?

A

Imbalance between the effector mechanisms of immune responses and the control mechanisms that serve to normally limit such responses.

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20
Q

What happens in Type I Hypersensitivity reactions (allergic reactions)?

A
  • Mast cell degranulation
    • ​due to repeat exposure to the antigen (allergen)
  • Mediated by IgE antibody-dependent activation of mast cells
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21
Q

Define atopy.

A

Predisposition to develop immediate hypersensitivity reactions.

(susceptibility to immediate hypersensitivity reactions is genetically termined)

22
Q

What is the difference between the immediate phase reaction and late phase reaction in Type I Hypersensitivity reactions?

A
  • immediate reaction:
    • eosinophils secrete major basic protein and eosinophil cationic protein (toxic to epithelial cells)
    • vasodilation
    • congestion
    • angioedema
  • Late phase reaction:
    • amplifying and sustaining the inflammatory response via release mediators from activated mast cells
    • inflammatory infiltrate rich in eosinophils, neutrophils, and T-cells
23
Q

What is a localized allergic reaction?

A

only affects particular body systems

  • respiratory system
  • intestinal mucosa
  • skin
24
Q

What are some common examples of localized allergic reactions?

A
  • Allergic rhinitis
  • Sinusitis
  • Bronchial asthma
  • Food allergies
  • Urticaria
25
Q

What are three common features in systemic anaphylaxis?

A
  • laryngeal edema
  • bronchospasm
  • decreased BP
26
Q

What is the mechanism behind systemic anaphylaxis?

A
  • Massive mast cell activation and degranulation releasing:
    • ​Histamine
    • Proteases
    • Chemotactic factors
  • ​Results in vasodilation, vascular leakage, and smooth muscle spasm
27
Q

What are the clinical findings in systemic anaphylaxis?

A
  • Acute onset of illness (minutes-hours)
  • Involvement of the skin, mucosal tissue, or both
    • hives, pruritus, flushing, angioedema
  • Respiratory compromise
    • dyspnea, wheeze, stridor
  • Reduced BP
  • GI symptoms (abdominal pain, vomiting)
28
Q

What are some of the common inciting agents in fatal systemic anaphylaxis?

A
  • Death due to:
    • asphyxiation (deficient oxygen supply to body due to abnormal breathing)
    • acute respiratory failure (bronchial restriction/obstruction)
    • cardiovascular collapse
29
Q

What is a Type II Hypersensitivity Reaction? Mechanism of injury?

A
  • Antibodies react with normal or altered cell surface antigens, or with antigens in the extracellular matrix
    • autoantibodies
    • drugs
30
Q

What is Goodpasture’s syndrome?

A
  • Make antibodies to glomerular basement membrane components
    • linear pattern of deposition
31
Q

What is a Type III Hypersensitivity Reaction? Mechanism of injury?

A
  • Deposition of antigen-antibody complexes that form in the serum
    • circulating immune complexes are deposited in vessel walls
      • exogenous
      • endogenous
32
Q

Why are the clinical manifestations of Type III Hypersensitivity Reactions diverse?

A
33
Q

What is a Type IV Hypersensitivity Reaction? Mechanism of injury?

A
  • Inflammation resulting from cytokines produced by CD4+ T lymphocytes and cell killing by CD8+ T lymphocytes
  • Mechanisms:
    • CD4+ T cell-mediated inflammation
      • recruits/activates macrophages and neutrophils
    • CD8+ T cell-mediated cytotoxicity
      • kill antigen-expressing target cells
34
Q

What are the mechanisms of injury in Type II Hypersensitivity Reactions?

A
  • Opsonization and phagocytosis
  • Complement- and Fc receptor-mediated inflammation
  • Antibody-mediated cellular dysfunction
35
Q

What is the mechanism of injury in Type III Hypersensitivity Reactions?

A
  • Immune complex formation
  • Immune complex deposition
  • Immune complex-mediated inflammation and tissue injury
    • e.g. fibrinoid necrosis
36
Q

Low levels of what are used to monitor disease in systemic immune complex-mediated diseases (type III hypersensitivities)?

A

C3

(low levels indicate active disease)

37
Q

How do granulomas form?

A
  • Strong activation of T lymphocytes
  • Recruitment of monocytes from the blood to become activated macrophages in the tissue
    • chronic inflammation consisting of a microscopic aggregation of macrophages
    • macrophages transform into epithelial-like cells (histiocytes)
    • histiocytes fuse to form multi-nucleated giant cells
38
Q

What are the three types of granulomas?

A
  1. Foreign body granulomas
  2. Caseating granulomas
  3. Non-caseating granulomas
39
Q

What do foreign body granulomas look like?

A
  • See foreign material within histiocytes/giant cells
  • called “foreign body giant cell reaction”
40
Q

What are caseating granulomas?

A
  • Granulomas that induce cell-mediated immune response with central necrosis
    • usually associated with infection
      • e.g. mycobacterial, fungal infections
41
Q

What are non-caseating granulomas?

A
  • Granulomas that induce cell-mediated immune response without central necrosis
    • e.g. Sarcoidosis, Crohn’s disease
42
Q

How can light-chain expression be used to determine if a B-lymphocyte proliferation is clonal?

A
  • Monoclonal (neoplastic) proliferations typically produce/express only one type of immunoglobulin
  • Immunoglobulin light chain expressed by a neoplastic, monoclonal B lymphocyte population will be of either kappa or lambda type
    • LIGHT CHAIN RESTRICTION
43
Q

How does flow cytometry detect the presence of a monoclonal population?

A
  • Detects light chain restriction
  • Quantifies cells in a stream of fluid
    • fluorescent labeled antibodies can bind to specific antigens on the cells
    • electronic detection device records the cell types & percentage of each
  • Can be performed on fresh/unfixed tissue, blood, or body fluids
44
Q

How does serum protein electrophoresis detect the presence of a monoclonal population?

A
  • Quantifies the fraction of certain proteins in serum using an electrical field to separate the proteins in the serum into groups of similar size, shape & charge
  • measures specific proteins in the blood to help identify some diseases
    • Albumin
    • Alpha 1, Alpha 2
    • Beta
    • Gamma
45
Q

How does immunofixation electrophoresis detect the presence of a monoclonal population?

A
  • allows the detection of monoclonal antibodies representative of diseases
    • deposit the serum on a gel
    • apply electric current that allows the separation of proteins according to their size and charge, antibodies specific for each type of immunoglobulin were laid upon the gel
46
Q

How does kappa and lambda in situ hybridization detect the presence of a monoclonal population?

A
  • Dark-staining areas indicate Kappa
  • Light-staining areas indicate Lambda
  • If only light staining = kappa light chain restriction
  • If only dark staining = lambda light chain restriction
47
Q

What is the benefit of doing T-cell receptor gene rearrangement studies and B-cell immunoglobulin gene rearrangement studies?

A
  • Help distinguish a B lymphocyte reactive proliferation from a monoclonal (neoplastic proliferation when light chain restriction is difficult to detect
48
Q

What are the five pillars of cancer treatment?

A
  1. Surgery
  2. Chemotherapy
  3. Radiation
  4. Molecular targeted therapy
  5. Immunotherapy
49
Q

What are some examples of Type II Hypersensitivity diseases?

A
  • Autoimmune hemolytic anemia
  • Pemphigus vulgaris (antibody-mediated destruction of epidermal cadherin)
  • Myasthenia Gravis (antibody-mediated destruction of acetylcholine receptor)
  • Graves disease (antibody-mediated stimulation of TSH receptors)
  • Insulin-resistant diabetes (antibody inhibits binding of insulin)
  • Pernicious anemia (antibodies neutralize intrinsic factor of gastric parietal cells –> decreased absorption of vitamin B12)
50
Q

What are some examples of Immune Complex-Mediated Disease (Type III Hypersensitivity)?

A
  • Systemic Lupus Erythematous
  • Poststreptococcal glomerulonephritis
  • Reactive arthritis
  • Serum sicknus
51
Q

What are some examples of T Cell-Mediated Diseases (Type IV Hypersensivitiy)?

A
  • Rheumatoid arthritis
  • Multiple Sclerosis (myelin destruction by activated macrophages due to TH1 & TH17))
  • Type 1 Diabetes
  • Inflammatory Bowel Disease
  • Psoriasis (inflammation by TH17 cytokines)
  • Contact sensitivity

IHO Week 3 - WLB (10 decks)

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