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Immunopathology Flashcards

1
Q

Immunopathology

A

Disease where the response to foreign or self antigens is abnormal or inappropriate

  • hypersensitivity rxns
  • autoimmunity
  • immunodeficiency
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2
Q

Hypersensitivity

A

Inappropriate or exaggerated response to certain antigens

  • 1: immediate
  • 2: cytotoxic
  • 3: immune complex
  • 4: delayed
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3
Q

Type 1 hypersensitivity

A

Develops rapidly (within minutes) following exposure to an antigen binding to IgE

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4
Q

Type 1 mechanism

A

Prior exposure to an antigen stimulates production of IgE –> specific IgE binds to Fc receptor of mast cells/basophils –> subsequent exposure to antigen causes binding and crosslinking of IgE on surface of mast cells –> degranulation occurs with release of mediators into surrounding tissue
*mediators: vasodilation, increased vascular permeability, bronchial smooth muscle constriction

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5
Q

What antigens are involved with type 1?

A
  • pollen
  • parasite
  • insect venom proteins
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6
Q

Factors that determine a type 1 hypersensitivity

A
  • genetic component
  • dose/route of exposure
  • antigen processing –> if IL-4 predominates then Th2 lymphocytes will induce B cells to produce IgE
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7
Q

Anaphylactoid reactions

A

Others substances that can activate mast cells (not by the IgE receptor)
- cytokines, complement, drugs, physical stimuli (heat, cold, trauma)

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8
Q

Type 1 hypersensitivity results in ________

A

Anaphylaxis or anaphylactic shock (systemic)

- drop in bp, bronchoconstriction, laryngeal edema, pulmonary congestion

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9
Q

Signs of shock

A
  • cattle/sheep: respiratory distress, pulmonary hypertension, lung is shock organ with severe pulmonary edema
  • horse: diarrhea and coli, lung and intestine are shock organs = bronchoconstriction with edema and edematous/hemorrhagic entercolitis
  • dog: abdominal pain with vomiting, muscle weakness and collapse, portal hypertension and systemic hypotenesion, liver is shock organ
  • cat: lung is shock organ
  • pig: lung and intestine is shock organ
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10
Q

Type 1 hypersensitivity usually has ______ lesions

A

Localized

  • restricted to specific tissue (commonly epithelial)
  • ex: mites, chemicals, flea allergy dermatitis
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11
Q

Allergic dermatitis

A

Route of exposure may be inhalation, ingestion, or percutaneous absorption

  • most inhaled or ingested antigens result in dermatitis
  • acute inflammatory rxn, often perivascular
  • red raised areas, often around muzzle, periocular area, conjunctiva, interdigital areas
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12
Q

Atopic dermatitis

A

Genetic predisposition

- production of IgE antibodies after exposure to common environmental allergens

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13
Q

Angioedema

A

Swelling of skin and mucous membranes

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14
Q

Type 2 hypersensitivity - cytotoxic

A

Cell destruction mediated by presence of antibodies directed against cell surface antigens
- antibodies are endogenous (directed against self antigens) or exogenous (directed against foreign antigens)

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15
Q

Type 2 mechanisms

A
  • complement mediated cytotoxicity (MAC –> cell lysis)
  • leukocyte mediated cytotoxicity (cell mediated, opsonization by antibody –> phagocytosis)
  • antibody against cell surface receptor (altered cell function –> may function as agonist or antagonist
  • results in decrease or loss of population of cells*
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16
Q

Rxns against erythrocytes - transfusion rxn

A

When an animal receives blood from an incompatible donor

  • acute hemolytic anemia
  • splenomegaly and hemosiderosis of various tissues
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17
Q

Rxns against erythrocytes - hemolytic disease of newborn

A

Neonatal isoerythrolysis

  • mother develops antibodies against fetal erythrocytes
  • leakage of fetal erythrocytes across placenta, antibodies to fetal RBCs are concentrated in the colostrum
  • absorption of colostrum results in acute hemolytic crisis in the newborn
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18
Q

Autoimmune hemolytic anemia

A

Autoantibodies are made to self-antigens on erythrocytes

- hemolytic anemia occurs due to complement mediated erythrocyte destruction

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19
Q

Drug induced hemolysis

A

Certain drugs can alter erythrocyte membranes

- immunoglobulin binding and complement activation

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20
Q

Infectious diseases (type 2)

A

Certain viral, bacterial, protozoal antigens can adhere to erythrocytes and initiate hypersensitivity
- ex: anaplasmosis, EIA

21
Q

Neonatal leukopenia

A

Antibodies produced against fetal leukocyte antigens that cross placenta during gestation
- neutropenia

22
Q

Thrombocytopenia (immune mediated)

A

Anti-platelet antibodies are formed

  • antibody formation may be autoimmune or caused by drug-induced membrane alteration
  • chemical: petechiae and purpuric hemorrhage
23
Q

Myasthenia gravis

A

Antibodies block acetylcholine receptors causing muscle weakness and paralysis

  • autoimmune
  • no gross or microscopic lesions
24
Q

Type 3 hypersensitvity

A

Antigen-antibody complexes that form in circulation or in tissues become stuck or lodged in tissue

  • develop from antibody response to endogenous or exogenous antigens
  • Fc segment activates complement and leukocytes = damage to cell and tissue
25
Size of immune complex
- determines pathogenicity - immune complexes formed during antibody excess are insoluble and phagocytosed - immune complexes formed with a large excess of antigen are usually too small to be trapped in tissue - complexes formed with slight antigen excess are most pathogenic
26
Predilection sites for immune complexes
- kidney and glomeruli - eye - skin
27
Localized type 3 hypersensitivity
Localized area of tissue necrosis from acute necrotizing vasculitis (Arthus rxn) - antigen-antibody complexes formed at site of injection and within blood vessel - complement and neutrophil mediated damage to vessel occurs - tissue damage dependent of quantity of complexes formed - vascular necrosis, increased vascular permeability, hemorrhage, thrombosis, local tissue necrosis
28
Systemic type 3 hypersensitivity
Deposition of soluble, intravascular immune complexes within multiple organs - antibodies form complexes with intravascular antigens - immune complexes are deposited within blood vessel of many tissues (kidney, joints, cardiovascular) - complement and neutrophil-mediated damage to tissue - macrophages produce pro-inflammatory cytokines - *result of persistent infections, autoimmune disease or inhalation to foreign antigens
29
Local or systemic immune complexes result in ______ and ______
Tissue damage; inflammation
30
Vasculitis
Occurs to a degree in all type 3 rxns - immune complex within the vessel wall - induces damage to adjacent tissue (ischemia) - systemic viral diseases, systemic lupus erythematosus, food hypersensitivity, drug rxn - vessel wall thickened by eosinophilic material (fibrin)
31
Systemic lupus
Presence of autoantibodies against DNA, nucleoproteins, cell surface antigens, etc - glomerulonephritis, arthritis, vasculitis
32
Pupura hemorrhagica
Occurs in horses following infection with streptococcus equi | - swelling and hemorrhage, skin may slough, affects all organs
33
Type 3 - renal immune complexes
Deposition of soluble immune complexes in the glomerulus = glomerulonephritis - damage to filtration structure - component of many diseases with constant antigenic stimulation - viral: EIA, feline leukemia, FIP - bacterial: pyometra, endocarditis - parasitic: heartworm
34
Type 3 - respiratory complexes
Hypersensitivity penumonitis - immune complex formation involving a variety of inhaled antigens - diffuse alvelitis following inhalation of antigens by a sensitized animal - type 1 sensitivity contributes - inhalation of fungal spores in cattle
35
Type 3 - ocular complexes
Viral antigen-antibody complexes in the eye, causes anterior uveitis and damage to corneal endothelium (corneal edema) - inflammation secondary to infection or vaccination with canine adenovirus type 1
36
Type 4 hypersensitivity
Delayed hypersensitivity mediated by specific T cells following exposure to antigen - chronic and antibody independent - cell mediated hypersensitivity - result of interaction of T cells and specific antigen to which they have been sensitized - rxn to persistent antigens
37
Delayed hypersensitivity
Persistent antigen stimulates the infiltration of lymphocytes and macrophages to the site - macrophages and lymphocytes coordinate to remove the inciting antigen
38
Direct cytotoxicity
Certain cell associated antigens result in the generation of cytotoxic T cells - targets are virus infected cells and tumor cells
39
Tuberculin rxn
Local swelling of macrophage infiltration following intradermal injection of antigen in sensitized animal - following intradermal injection of tuberculin, a sensitized host will develop a localized type 4 rxn with 24-72 hrs - antigen taken up by dendritic cell and presented to antigen-specific CD4 cell, activated to produce and secrete cytokines that attract other inflammatory cells - used to diagnostic testing
40
Granulomatous hypersensitivity
Persistent antigen that results in granulomatous and lymphocytic inflammation - macrophages, giant cells, lymphocytes, necrosis and fibrosis - bacteria, fungi, and certain parasites
41
Contact dermatitis
Antigen too small to elicit immune response by itself - antigens are complexed with larger proteins - processing and presentation by APCs - in a sensitized host repeat exposure = effector phase response = epidermal vesicle formation with mononuclear cell infiltration - causes: poison ivy, flea collars, paints, dyes
42
Autoimmunity
Production of antibody and T cells that are reactive to self antigens - many autoimmune diseases are type 2 or 3
43
Mechanisms of autoimmunity
- release of sequestered antigens (substances not normally exposed to immune system) - alteration of self antigens (normal proteins are altered, chemicals can alter cell surfaces) - alteration of immune reactivity (loss of tolerance to self antigens, self reactive B and T cells are present in normal animals, but are non functional)
44
Susceptibility
- genetic: species and breed (systemic lupus erythematosus common in collies and shelties) - gender: more frequent in females
45
Autoimmunity is a _______ hypersensitivity
Type 2
46
Autoimmune skin disease
Antibodies directed against epidermal antigens activate complement then neutrophil-mediated skin damage
47
Pemphigus foliaceious
Autoantibodies against adhesion molecules on keratinocytes
48
Pemphigus vulgaris
Autoantibodies against antigens in or near the epidermal-dermal junction - severe and rare
49
Bullous pemphigoid
Autoantibodies against basement membrane antigens | - vesicles then ulceration

Pathology (19 decks)

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