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General Pathology > Immunopathology: Hypersensitivity > Flashcards

Immunopathology: Hypersensitivity Flashcards

1
Q

What is Immunopathology

A
  • Disease characterized by abnormal or inappropriate immune responses
  • Reactions involve coordinated and integrated contribution from both immune and inflammatory responses
  • Major conditions include:
    • hypersensitivity reactions
    • Immunodeficiency
    • autoimmunity
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2
Q

Wht are Hypersensitivity reactions?

A
  • Most immune responses to antigens are advantageousto the host
  • Some immune responses can cause host injury (hypersensitivity reactions)
  • Host injury due to hypersensitivity reactions occurs by several main mechanisms
    • Type I
    • Type II
    • Type III
    • Type IV
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3
Q

What is Type I hypersensitivity reaction?

A
  • An immediate response characterized by prominent vasoactive events and the release of inflammatory mediators
  • Key features:
    • Antigens that induce IgE production
    • IgE-mediated mast cell degranulation
    • Vascular leakage and eosinophil infiltration
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4
Q

What is the mechanism of Type I hypersensitivity reactions?

A
  1. Prior exposure to an antigen stimulates production of antigen-specific IgE
  2. IgE binds to Fc receptors of mast cells and basophils
  3. Subsequent antigen exposure results ini crosslinking of IgE and cell degranulation
  4. Vasoactive mediators are releaed into the surrounding tissues
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5
Q

What are the local manifestations of Type I hypersensitivity reactions to ingested allergens?

A
  • Ingested allergens (food alergies)
    • Gastrointestinal sign range from milkd, to severe with bloody diarrhea and vomiting
    • ~1/2 of food allergies have skin manifestations
      • erythema, pruritis, urticaria
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6
Q

What are the local manifestations of Type I hypersensitivity reactions to inhaled allergens?

A
  • Inhaled allergens (respiratory allergies)
    • Responses to most inhaled allergens are manifested in the skin
      • Atopic dermatitis:
        • lesions range from acute erythema to chronic hyperpigmentation and pyodermas
        • Pruritis is a major feature
    • Responses to some are manifested in teh respiratory tract
      • Nasolacrimal urticaria (hay fever)
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7
Q

What are the local manifestations of Type I hypersensitivity reactions to cutaneous allergens?

A
  • Cutaneous allergens (skin allergies)
    • Most ingested or inhled allergens result in skin responses
      • atopic dermatitis
    • Locally applied allergens can also result in hypersensitvity dermatitis
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8
Q

What are the systemic manifestations of Type I hypersensitivity reactions?

A
  • Anaphylaxis:
    • Signs and lesions are usually typical of shock
    • Include:
      • Respiratory distress and pulmonary failure
      • Gastrointestinal dysfunciton and liver failure
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9
Q

What are Type II Hypersensitivity reactions?

A
  • Cytotoxicity induced by reactions against cell membrane antigens
  • Key features:
    • Antigens that induce IgG or IgM production against cell membrane antigens
    • Antibody-mediated activation of complement or leukocytesz results in cell damage
  • End result is membrane damage and cell injur
  • 2 different mechanisms damage cells:
    • Complement-mediated
    • Leukocyte-mediated
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10
Q

What is the Cmplement-mediated mechanism of Type II hypersensitivity?

A
  1. Antibody binds a cell membrane or basement membrane ntigen
  2. Classical complement cascade is activated
  3. Formation of the terminal membrane attack sequence and cell lysis
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11
Q

What is the leukocyte-mediated mechanism of Type II hypersensitivity?

A
  1. Antibody binds a cell membrane or basement membrane antigen
  2. Leukocytes bind ia their Fc receptors
  3. Leukocyte products damage he membrane
    • Lysosomal enzymes
    • Oxygen free radicals
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12
Q

What are the manifestation of Type II hypersentitivities against erythrocytes?

A
  • Common targets are circulating cells, epidermis and basement membranes
  • Reactions against erythrocytes:
    • Transfusion reactions
    • Neonatal isoerythrolysis
    • Autoimmune hemolytic anemia
    • Drug-induced hemolysis
    • Infectious agents
  • The notable clinical sign in most cases is hemolytic anemia
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13
Q

What are the pathologic features of reaction against erythrocytes?

A
  • Icterus
  • Splenomegaly
  • Hemosiderosis of various tissues
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14
Q

What are the manifestations of Type II hypersensitivity against Leukocytes?

A
  • Reactions against Leukocyctes
    • Neonatoal leukopenia
    • Agranulocytosis (acquired leukopenia)
  • There may be increased susceptibility to infection
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15
Q

What are the manifestations of Type II hypersensitivity against platelets?

A
  • Reactions against platelets
    • Drugs
    • Infectious agents
    • Autoimmunity
  • Thrombocytopenia is the major finding
  • Pathologic findings are predominately multiple petechial to ecchymotic hemorrhages
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16
Q

What are the manifestations of Type II hypersensitivity reactions against basement membranes?

A
  • Reactions against basement membranes
    • Antibodies are directed against basement membrane components
      • Glomerular and epidermal basement membranes are common targets
    • Injury can be mediated by complement or leukocytes
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17
Q

What are Type III Hypersensitivity Reactions?

A
  • Tissue damage induced by inflammatory responses to immune complexes
  • Key Features:
    • Appropriate immune complexes
      • formed in slight antigen excess
    • Complement and leukocyte-induced tissue injury
    • Reactions can occur to localized or circulating immune complexes
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18
Q

What are the mechanisms of Type III hypersensitivity reactions?

A
  • 2 different pathways of injury are described, based on the location of the immue complex
    • Localized hypersensitivity (Artus reaction)
    • Systemic Hypersensitivity (Serum sickness)
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19
Q

What is the Arthus reaction?

A
  • Interstitial antigen and intravascular antibody meet and precipitate within vessel walls
  • Complement and leukocytes mediate vessel damage
  • There is vascular necrosis, hemorrhage, thrombosis and local tissue damage
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20
Q

What is Serum Sickness?

A
  • Soluble, circulating immune complexes can be deposited within vessels of mutiple tssues
  • Complement and leukocyte induce vessel and tissue damage
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21
Q

What are the manifestations of Type III hypersentivity reactions?

A
  • Vasculitis
    • Some degree occurs with all Type III reactions
  • Commonly affected tissues include:
    • Kidney
    • Lungs
    • Joints
    • Eyes
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22
Q

How are Kidneys affected by Type III hypersensitivity reactions?

A
  • Immune complexes can be formed in many diseases, and can be deposited near glomerular basement membranes
  • Complement and leukocyte-mediated damage cause glomerulonephritis
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23
Q

How are lungss affected by Type III hypersensitivity reactions?

A
  • Deposition of immune complexes near alveolar and endothelial basement membranes
  • Complement and leukocyte-mediated damage cause alveolitis
24
Q

How are joints affected by Type III hypersensitivity reactions?

A
  • Immune complexes can be deposited in synovial membranes
  • Complement and leukocyte-mediated damage cause synovitis and arthritis
25
Q

How are eyes affected by Type III hypersensitivity reactions?

A
  • Immune complexes can be deposited in the uvea
    • this is common as a sequella to canine adenovirus-1 infection
  • Complement and leukocyte-mediated damage cause anterior uveitis and corneal edema
26
Q

What are Type IV hypresensitivity reactions?

A
  • A delayed hypersensitivity reaction medited by antibody-independent immune responses
  • Key Features:
    • Persisten antgen
    • T-lymphocyte proliferation and production of lymphokines
    • Macrophage proliferation and activation
  • 2 pathways of damage are described:
    • One for tissue
    • One for cells
27
Q

What is the mechanism of delayed Type IV hypersensitivity?

A
  • Antigen persistence stimulates lymphocyte and macrophage infiltration to the site
    • Vasodiltion and increased vascular permeability are minor parts of the typical response
  • T-lymphocytes and macrophges proliferate locally and produce cytokines that mediate removal of the antigen and associated tissue damage
28
Q

What is the mechanism of cell-mediated cytotoxicity?

A
  • Certain cell-associated antigens cause the generation of cytotoxic T-lyphocytes
    • Often these are virus infected cells and tumor cells
  • Natural killer cells recongized abnormal membrane antigens
  • Cytotoxic T-lymphocytes and natural killer cells bind to and destroy the abnormal cells
29
Q

What are Tuberculin reaction of Type IV hypersensitivity reactions?

A
  • Intradermal injection of antigen in a sensitized animal causes local swelling and macrophage infiltration
  • This is used for diagnostic testing to a variety of agents
    • Mycobacterium sp.
30
Q

What is Granulomatous hypersensitivity?

Type IV hypersensitivity

A
  • This is a combination of delayed hypersensitivity and granulomatous inflammation
    • antigen persistence is a characteristic of both
  • Lymphocytes and macrophages are prominent at the site
  • Common causes include:
    • Systemic fungal infections
    • Mycobacterial infections
31
Q

What is Contact hypersensitivity?

Type IV hypersensitivity

A
  • Dermal contact with certain antigens induces a cell-mediated delayed hypersensitivity
  • Cellular infiltrate is largely lymphocytic
  • Common causes:
    • Plants (poison ivy)
    • Flea collars
    • Wood preservatives and waxes
    • Paints, dyes, fabric chemicals
32
Q

What is Autoimmunity?

A
  • Immune responses directed against self
  • The immune mechanisms that mediate autoimmunity are the same that mediate reactions against exogenous antigens
    • The only difference is the source of the antigen
33
Q

What are the mechanisms of Autoimmunity?

A
  • Several general theories have been made about the origin of autoreactive immunity
    • Release of sequestered antigens
    • Alteration of self antigens
    • Alteration of immune reactivity
34
Q

What is the Release of sequestered antigens autoimmunity mechanism?

A
  • Some substances in the body are not normally exposed to the immune system
  • Includes:
    • Myelin
    • Lens
    • Sperm
35
Q

What is the alteration of self antigens autoimmunity mechanism?

A
  • Sel antigens may be modified so that they are no longer recognized as self
    • Viral alteration of cell membrane features
    • Chemical alteration of cell membranes
36
Q

What is the alteration of immune reactivity autoimmunity mechanism?

A
  • There is a loss of tolerane to self antigens
  • Autoreactive B- and T-lymphocytes are normally present, but non-functional
    • Changes may occur that allow functions of these cells to be manifested
37
Q

What are the predisposing factors of Autoimmunity?

A
  • Genetic predisposition:
    • certain conditions have definite inherited patterns of breed or familial occurrence
  • Gender predisposition:
    • More common in females
      • over 75% of cases os systemic lupus erythematosis are diagnosed in females
    • Comparative levels of estrogen and testosterone can influence autoimmunity
38
Q

What are the manifestations of Autoimmunity?

A
  • Autoimmune thyroiditis
  • Periodic ophthalmia
  • Autoimmune skin disease
  • Autoimmune hemolytic anemia
  • Autoimmune thrombocytopenia
  • Myasthenia gravis
  • systemic lupus erythematosis
39
Q

What is Autoimmune thyroiditis?

A
  • Antibodies are produced against thyroid epithelium or thyroglobulin
  • A common cause of hypothyroidism in dogs
40
Q

What is periodic ophthalmia?

A
  • Anti-leptospiral antibodies that are cross reactive with corneal self antigens cause anterior uveitis and vision deficiencies
41
Q

What is Autoimmune skin disease?

A
  • Antibodies are produced to various components of the epidermis
  • A variety of different syndromes exist
    • Pemphigus vulgaris
    • Pemphigus foliaceous
42
Q

What is autoimmune hemolytic anemia?

A
  • Antibodies against erythrocytes result in complement or leukocyte-mediated hemolysis
43
Q

What is Autoimmune thrombocytopenia?

A
  • Anti-platelet antibodies destroy platelets and predispose to hemorrhage
44
Q

What is myasthenia gravis?

A
  • antibodies are produced against acetylcholine receptors of neuromuscular junctions causing weakness and muscle atrophy
45
Q

What is systemic lupus erythematosis?

A
  • Autoantibodies are directed against a variety of tissues most likely due to a loss of immunoregulation
  • Antibodies are commonly formed against nucleic acids, erythrocytes, platelets, muscle, skin, lymphocytes
46
Q

What is immunodeficiency?

A
  • Immunological defects thatlead to depression of certain immune functions and increase susceptibility to infectious disease
  • Any component ofthe immune system can be affected?
47
Q

What are the mechaisms of immunodeficiency?

A
  • Inherited defects
    • gnetic abnormalities result in the failure of proper development of the immune system
  • Acquired defects
    • expsure to certain infectious agents or chemicals, or nutritional deficiencies
48
Q

What is Combined Immunodeficiency (CID)

A
  • Manifestation of Immunodeficiency
  • SOme inherited defects involve multiple immune cells
    • CID is most common in Arab foals, but similar syndromes are reported in dogs, mice and other species
    • Functional B- and T-lymphocytes are absent or decreased
    • Affected animals usually die before 6 months of age due to infectious disease
49
Q

What is selective immunodeficiency?

A
  • Manifestation of immunodeficiency
  • Certain geneti defects involve specific immune cells
    • B-lymphocytes
      • IgM deficiency in Arabs and Doberman pinschers
      • IgG deficiencyin dogs and cattle
    • T-lymphocytes
      • Trait A-46 in Friesian cattle
50
Q

What is viral-induced immunodeficiency?

A
  • Immunodeficiency manifestation
  • A large number of viruses can alter immune functions
    • Some viruses destroy lymphoid cell and tissues
    • Some viruses cause lymphocyte dysfunction
51
Q

What Viruses that destroy lymphoid cells and tissues?

A
  • canine parvovirus
  • Canine distemper virus
  • Feline panleukopenia virus
  • Bovine virus diarrhea virus
52
Q

What viruses cause lyphocyte dysfunction?

A
  • Feline leukemia virus
  • Feline immunodeficiency virus
  • Bovine leukosis virus
  • Equine infectious anemia virus
  • Mareks disease virus
53
Q

What is chemical-induced immunodeficiency?

A
  • Immunodeficiency manifestation
  • Various chemicals reportedly induce immunosuppresion
  • Include:
    • Halogenated biphenyls
    • Certain Heavy metals
    • Mycotoxins
54
Q

What is nutrition-induced immunodeficiency?

A
  • Immunodeficiency manifestation
  • Severe malnutrition or starvation will depress immune function
  • Deficiencies of certain vitamins or minerals can suppress immune responses
    • Zinc, magnesium
    • Vitamins A and B
55
Q

What is Failure of passive transfer?

A
  • Immunodeficiency manifestation
  • Colostral antibodies are not obtained by the newborn
  • Neonates not receiving colostrum are predisposed to infections early in life

General Pathology (34 decks)

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