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Pathology > Exam 3: Hypersensitivity > Flashcards

Exam 3: Hypersensitivity Flashcards

1
Q

What is immunopathology?

A

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

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2
Q

What are example of immunopathology?

A

Hypersensitivity reactions
Autoimmunity
Immunodeficiency

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3
Q

What is hypersensitivity?

A

An inappropriate or exaggerated response to certain antigens

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4
Q

What is a type I hypersensitivity?

A

Immediate hypersensitivity

Develops rapidly following exposure to an antigen binding to IgE

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5
Q

What is a type II hypersensitivity?

A

Cytotoxic hypersensitivity

Cell destruction mediated by the presence of antibodies directed against cell surface antigens

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6
Q

What is a type III hypersensitivity?

A

Immune complex hypersensitivity
Antigen-antibody complexes (immune complexes), which form in circulation or in tissues, become “stuck” or lodged in tissue

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7
Q

What is a type IV hypersensitivity?

A

Delayed hypersensitivity
A delayed hypersensitivity mediated by specific T-lymphocytes following exposure to antigen
Chronic and antibody independent

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8
Q

What is the mechanism of type I hypersensitivity?

A

Prior exposure to an antigen stimulates the production of antigen specific IgE
Specific IgE binds to the Fc receptors of mast cells and basophils
Subsequent exposure to antigen causes binding and crosslinking of IgE on the surface of mast cells and basophils
Degranulation occurs with the release of mediators into surrounding tissues

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9
Q

What are the mediators of type I hypersensitivity?

A

Vasodilation
Increased vascular permeability
Bronchial smooth muscle contraction

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10
Q

What are the antigens frequently involved in type I hypersensitivities?

A

Pollen
Parasite antigens
Insect venom proteins

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11
Q

What are the factors that determine a type I 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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12
Q

What are anaphylactoid reactions?

A

When other substances (such as cytokines, complement, drugs, physical stimuli) activate mast cells

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13
Q

What are the systemic effects of type I hypersensitivities?

A

Anaphylaxis or anyphylactic shock

Drop in blood pressure, bronchoconstriction, laryngeal edema, pulmonary congestion

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14
Q

What are causes of type I hypersensitivities?

A

Venmous insect bites
Certain foods
Drugs/vaccines

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15
Q

What are the signs of type I hypersensitivities in cattle/sheep?

A

Respiratory distress
Systemic hypotension with pulmonary hypertension
Lung is the shock organ with sever pulmonary edema

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16
Q

What are the signs of type I hypersensitivities in horses?

A

Diarrhea and colic

Lung and intestine are shock organ

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17
Q

What are the signs of type I hypersensitivities in dogs?

A

Abdominal pain with vomiting, defecation, muscle weakness, and collapse
Portal hypertension and systemic hypotension
The liver is the shock orgsn

18
Q

What are the signs of type I hypersensitivities in cats?

A

Shock organ: lung

19
Q

What are the signs of type I hypersensitivities in pigs?

A

Shock organ: lung and intestine

20
Q

Describe localized type I hypersensitivities

A

The clinical signs and pathology are restricted to a specific tissue, commonly epithelial surfaces

21
Q

What are examples of type I hypersensitivities?

A

Insect bites
Mites
Chemical substance
Flea allergy dermatitis

22
Q

What are the mechanisms of type II hypersensitivities?

A
  1. Complement mediated cytotoxicity
    - –MAC –> cell lysis
  2. Leukocyte mediated cytotoxicity (cell mediated)
    - –Opsonization by antibody –> phagocytosis
  3. Antibody against cell surface receptor
    - –Altered cell function- may function as agonist or antagonist
23
Q

What are examples of type II hypersensitivities?

A

Reactions against erythrocytes
Reactions against leukocytes and platelets
Reactions against cell receptors

24
Q

What can type III hypersensitivities develop from?

A

Antibody response to endogenous or exogenous antigens–> immune complexes deposited in a wide variety of tissue

25
Q

Why is the size of the immune complex relevant in type III hypersensitivities?

A

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
Q

What are the predilection sites of type III hypersensitivities?

A

Kidney (glomerulus)
Eye
Skin
Joints

27
Q

What is local type III hypersensitivity?

A

Localized area of tissue necrosis from acute necrotizing vsculitis

28
Q

What is the mechanism of local type III hypersensitivities?

A

Antigen-antibody complexes formed at the site of injection and within blood vessel
Complement and neutrophil-mediated damage to the vessel occurs
Tissue damage dependent of quantity of complexes formed
Vascular necrosis, increased vascular permeability, hemorrhage, thrombosis, and local tissue necrosis

29
Q

What is systemic type III hypersensitivities?

A

Deposition of soluble, intravascular immune complexes within multiple organs

30
Q

What is the mechanism of systemic type III hypersensitivities?

A

Antibodies form complexes with intravascular antigens
Immune complexes are deposited within blood vessels of many tissues
Complement and neutrophil-mediated damage to tissue
Macrophages also recruited and produce pro-inflammatory cytokines

31
Q

What are systemic type III hypersensitivities the result of?

A

Persistent infections, autoimmune disease or inhalation to foreign antigen

32
Q

What are examples of type III hypersensitivities?

A 
Vasculitis
Purpura hemorrhagica
Renal immune complexes
Respiratory (hypersensitivity pneumonitis)
Ocular
33
Q

What are type IV hypersensitivities the result of?

A

T lymphocytes and the specific antigen to which they have been sensitized
Reaction to persistent antigens: viruses, fungi, protozoa, parasites, certain bacteria, certain chemicals

34
Q

What is a delayed hypersensitivity?

A

Persistent antigen stimulates the infiltration of lymphocytes and macrophages to the site
Macrophages and lymphocytes coordinate to remove the inciting antigen

35
Q

What is direct cytotoxicity?

A

Certain cell antigens result in the generation of cytotoxic T-lymphocytes
Targets are virus infected cells and tumor cells

36
Q

What are examples of type IV hypersensitivities?

A

Tuberculin reaction
Granulomatous hypersensitivity
Contact dermatitis

37
Q

What is autoimmunity?

A

Production of antibody and T cells that are reactive to self antigens

38
Q

Which hypersensitivities are many autoimmune disease?

A

Type II or III

39
Q

What are the mechanisms of autoimmunity?

A

Release of sequestered antigens
—substances not normal exposed to immune system
Alteration of self antigenically
—Normal proteins are altered antigenically
—-certain microorganisms or chemical substances 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

40
Q

What can make an individual susceptible to autoimmunity?

A

Genetics
—Species and breed predilections
Gender
—generally more frequent in females

41
Q

What is an example of autoimmunity that is a type II hypersensitivity?

A

Autoimmune skin disease

Pathology (16 decks)

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