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Inflammation and Hypersensitivity Flashcards

1
Q

The process by which the body attempts to destroy or contain a noxious agent and repair damage

A

Inflammation

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2
Q

What are the four phases of immune-mediated inflammatory responses?

A
  1. ) Stimulation
  2. ) Release of inflammatory mediators and chemotactic agents
  3. ) Invasion of tissue
  4. ) Removal of cell debris and secretion of growth factors
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3
Q

Which can act locally or systemically, and the response of local or distant target organs to them

A

Inflammatory mediators

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4
Q

Attract immune cells to the area and modify endothelium to allow their adhesion and extravasion

A

Chemotactic agents

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5
Q

The invasion of tissue is by activated immune cells which defend against infection and can also

A

Damage tissue

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6
Q

Stimulate cell migration and proliferation, with tissue repair and formation of new blood vessels

A

Growth factors

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7
Q

In acute local inflammation, inflammatory mediators produce which 4 things?

A
  1. ) Heat and redness
  2. ) Edema
  3. ) Pain
  4. ) Loss of function
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8
Q

The heat and redness is from

A

Dilation of small blood vessels

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9
Q

From endothelial retraction and increase in permeability of post-capillary venules

-causes fluid to leak from blood to tissue

A

Edema

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10
Q

Cytokines with systemic effects are chiefly produced by

A

Monocytes

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11
Q

Shape the systemic response of the body to infection, and produce many signs and symptoms by which illness is recognized

A

TNF-a, IL-1, and IL-6

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12
Q

Overproduction of inflammatory cytokines can produce the

A

Systemic Inflammatory Response Syndrome [SIRS]

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13
Q

Leads to loss of blood volume, and vasodilation, with decreased blood pressure and tissue perfusion, can lead to organ dysfunction, shock, and death

A

Increased Vascular Permeability

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14
Q

Severe shock produced by systemic infection is called

A

Septic shock

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15
Q

Bacterial components such as LPS activate the

A

Blood clotting cascade

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16
Q

Inflammatory cytokines act on endothelium to promote

A

Blood clotting

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17
Q

Multiplication of bacteria in the bloodstream [septicemia] can lead to

A

Disseminated Intravascular Coagulation [DIC]

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18
Q

Exhaustion of clotting factors by DIC can lead to simultaneous

A

Multiple hemorrhages

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19
Q

In chronic inflammation, persistent reactions to a stimulus that cannot be removed results in formation of a

A

Granuloma

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20
Q

A lesion with a necrotic core surrounded by macrophages and lymphocytes

A

Granuloma

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21
Q

On a longer time scale the granuloma becomes surrounded by fibrous tissue, to wall off the lesion. Eventually the wall of the lesion may

A

Calcify

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22
Q

Immune responses which damage the body

A

Hypersensitivity reactions

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23
Q

The immune system may over-react to an innocuous antigen [allergy]. The antigen is the

A

Allergen

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24
Q

A genetically-determined state of abnormal responsiveness is called

A

Atopy

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25
Q

An atopic person is not allergic until exposure to an allergen generates an

-may require months or years of exposure

A

Immune response

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26
Q

Classified by the mechanism that causes damage

A

Hypersensitivity reactions

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27
Q

Immediate hypersensitivity because the early phase happens so rapidly

A

Type I

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28
Q

Delayed or tuberculin-type hypersensitivity, because a classic stimulus is tuberculin, an extract of cultures of the bacterium which causes TB

A

Type IV

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29
Q

In responses of types I-III The antigen-specific component is

A

Immunoglobin

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30
Q

In responses of types I-III The antigen-specific component is immunoglobulin, and hypersensitivity can be transferred to an unsensitized individual with

A

Serum

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31
Q

Type IV antigen sensitivity is conferred by

-antibodies play no significant role

A

T cells

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32
Q

There are several subtypes of Type IV reactions: (1) granulomatous reactions, where the major cells are

A

TH and monocyte macrophages

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33
Q

There are several subtypes of Type IV reactions: (2) cytotoxic reactions, in which the important cells are

A

TH and CTL

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34
Q

Hypersensitivity reactions are used diagnostically. Small, localized, skin reactions are induced as tests of

A

Immune system competence, prior exposure, and allergic hypersensitivity

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35
Q

Anaphylactic hypersensitivity based on IgE and mast cells

A

Type I reactions

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36
Q

Opposite of prophylaxis; deleterious effects of exposure to antigen, as opposed to the beneficial effect of immunization

A

Anaphylaxis

37
Q

The basis of a type I reaction is the

A

Synthesis of IgE and antigen-stimulated degranulation of mast cells

38
Q

Binds tightly and specifically to Fc receptors [FCR] on mast cells

39
Q

Cross-linking of cell-bound IgE by polyvalent antigen causes release of

A

Mast cell granule contents

40
Q

Microbial polysaccharides or immune complexes containing IgG/IgM also stimulate mast cells via activation of

A

Complement

41
Q

This occurs directly by alternate pathway, or by classical pathway in the presence of

42
Q

Peptides generated by Complement activation bind to mast-cell receptors, again cause

A

Degranulation

43
Q

Stimulated mast cells release

A

Inflammatory Mediators

44
Q

Made prior to simulation, stored in mast cell granules, released on degranulation

A

Pre-formed mediators

45
Q

Causes airway smooth muscle contraction, dilation of small blood vessels, increased permeability of post-capillary venules, and secretion of mucus by the nasal mucosa

46
Q

Acts by binding to several types of G-protein coupled receptors on target cells

47
Q

Occupy these receptors but do not activate the target cells, i.e. they are receptor antagonists

A

Antihistamines

48
Q

Contraction of bronchial smooth muscle in response to mast cell products is one basis of

A

Allergic asthma

49
Q

Synthesized and released after mast cell stimulation

A

Lipid mediators

50
Q

Derived from C20 cell-membrane lipids

A

Prostaglandins and Leukotrienes

51
Q

Before the identity of mast-cell prostaglandins/leukotrienes was known they were referred to as the

A

Slow-Reacting Substance of Anaphylaxis [SRS-A]

52
Q

Defends us against tissue parasites

A

IgE/Mast cell system

53
Q

Stimulated mast cells release the protein

A

Esosinophil Chemotactic Factor A (ECFA)

54
Q

A chemoattractant for eosinophils

55
Q

Type II reactions are classified as

A

Cytotoxic hypersensitivity

56
Q

Antibody binds to specific antigen on cell surface, causing destruction by Complement or phagocytosis in

A

Cytotoxic hypersensitivity (Type II reaction)

57
Q

The antibodies responsible for type II reactions are mostly

A

IgG or IgM

58
Q

Bound IgG antibody facilitates

A

Phagocytosis (opsonization)

59
Q

Bound IgG antibody facilitates phagocytosis (opsonization) because phagocytes have membrane receptors

A

FCRy for its Fc region

60
Q

Transfusion of mismatched blood is an example of a

A

Type II reaction

61
Q

Fetal hemolytic disease arising from Rh incompatibility between mother and fetus is an example of a

A

Type II reaction

62
Q

What are two other examples of type II reactions?

A

Hyperacute rejection of organ transplant and some drug allergies

63
Q

Binds to red cell proteins, acts as a hapten, and stimulate formation of antibodies that then lyse drug-coated red cells

A

Penicillin

64
Q

Type II reactions are classified as

A

Immune complex diseases

65
Q

In a type II reaction, the reaction of antigen with antibody [especially in antigen excess] forms soluble

A

Immune complexes

66
Q

These complexes can cause

A

Arthritis, glomeronephritis, and vasculitis

67
Q

What are four examples of type III reactions?

A
  1. ) Pulmonary reactions
  2. ) Arthus reaction
  3. ) Autoimmune diseases
  4. ) Serum sickness
68
Q

Pulmonary reactions to inhaled antigens is the basis of many occupationally-related disease, such as Farmer’s lung. The antigens responsible are often

69
Q

Arises from reaction to fungal spores in moldy hay

A

Farmer’s lung

70
Q

Experimental administration of soluble antigen to an immune subject results in a skin lesion redness, and swelling

-takes 3-8 hours to develop].

A

Arthus reaction

71
Q

Rheumatoid Arthritis is an example of a

A

Type III reaction

72
Q

In RA, the antigen is

73
Q

Autoantibodies are made to many cell components including DNA, RNA, nucleoproteins in

A

Systemic Lupus erythematosis

74
Q

Caused by repeated administration of non-human serum, for example injection of equine antiserum for snakebite in a person who had received horse serum before

A

Serum sickness

75
Q

Type IV reactions are called

A

Cell mediated

76
Q

Antigen specificity for type IV reactions is provided by

A

CD4+ TH cells

77
Q

Antigen specificity is provided by CD4+ TH cells, on stimulation they release cytokines/chemokines, infiltration of the site by

A

Macrophages and CTL

78
Q

Classic Type IV skin reactions are characterized by

A

Induration and erythema

79
Q

Hardness, from cell infiltration

A

Induration

80
Q

Require 48-72 hours to develop

A

Class IV skin reactions

81
Q

Skin response to a panel of common antigens is used diagnostically to assess competence of

A

Cell-mediated immunity

82
Q

Class IV skin reactions are often called

A

Tuberculin-type reactions

83
Q

Form at sites infected by microbes that survive/multiply inside cells

A

Granulomatas

84
Q

Granulomas form at sites infected by microbes that survive/multiply inside cells. The classic cause is

A

Mycobacterium tuberculosis

85
Q

Follows exposure to poison ivy or chemicals such as chromate salts or metals

A

Contact hypersensitivity dermatitis

86
Q

Allergens bind to cell surface proteins, act as haptens, and stimulate

A

Cell-mediated immunity

87
Q

Like tuberculin reactions, they develop in 2-3 days

A

Contact hypersensitivity dermatitis

88
Q

Acute rejection of organ transplants. Requires weeks/months and involves both

A

CD4+ and CD8+ cells

89
Q

Takes months or years and the mechanism is obscure; possibly fibrosis in response to cytokine release

A

Chronic rejection

Immunity (33 decks)

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