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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
An atopic person is not allergic until exposure to an allergen generates an -may require months or years of exposure
Immune response
26
Classified by the mechanism that causes damage
Hypersensitivity reactions
27
Immediate hypersensitivity because the early phase happens so rapidly
Type I
28
Delayed or tuberculin-type hypersensitivity, because a classic stimulus is tuberculin, an extract of cultures of the bacterium which causes TB
Type IV
29
In responses of types I-III The antigen-specific component is
Immunoglobin
30
In responses of types I-III The antigen-specific component is immunoglobulin, and hypersensitivity can be transferred to an unsensitized individual with
Serum
31
Type IV antigen sensitivity is conferred by -antibodies play no significant role
T cells
32
There are several subtypes of Type IV reactions: (1) granulomatous reactions, where the major cells are
TH and monocyte macrophages
33
There are several subtypes of Type IV reactions: (2) cytotoxic reactions, in which the important cells are
TH and CTL
34
Hypersensitivity reactions are used diagnostically. Small, localized, skin reactions are induced as tests of
Immune system competence, prior exposure, and allergic hypersensitivity
35
Anaphylactic hypersensitivity based on IgE and mast cells
Type I reactions
36
Opposite of prophylaxis; deleterious effects of exposure to antigen, as opposed to the beneficial effect of immunization
Anaphylaxis
37
The basis of a type I reaction is the
Synthesis of IgE and antigen-stimulated degranulation of mast cells
38
Binds tightly and specifically to Fc receptors [FCR] on mast cells
IgE
39
Cross-linking of cell-bound IgE by polyvalent antigen causes release of
Mast cell granule contents
40
Microbial polysaccharides or immune complexes containing IgG/IgM also stimulate mast cells via activation of
Complement
41
This occurs directly by alternate pathway, or by classical pathway in the presence of
IgG/IgM
42
Peptides generated by Complement activation bind to mast-cell receptors, again cause
Degranulation
43
Stimulated mast cells release
Inflammatory Mediators
44
Made prior to simulation, stored in mast cell granules, released on degranulation
Pre-formed mediators
45
Causes airway smooth muscle contraction, dilation of small blood vessels, increased permeability of post-capillary venules, and secretion of mucus by the nasal mucosa
Histamine
46
Acts by binding to several types of G-protein coupled receptors on target cells
Histamine
47
Occupy these receptors but do not activate the target cells, i.e. they are receptor antagonists
Antihistamines
48
Contraction of bronchial smooth muscle in response to mast cell products is one basis of
Allergic asthma
49
Synthesized and released after mast cell stimulation
Lipid mediators
50
Derived from C20 cell-membrane lipids
Prostaglandins and Leukotrienes
51
Before the identity of mast-cell prostaglandins/leukotrienes was known they were referred to as the
Slow-Reacting Substance of Anaphylaxis [SRS-A]
52
Defends us against tissue parasites
IgE/Mast cell system
53
Stimulated mast cells release the protein
Esosinophil Chemotactic Factor A (ECFA)
54
A chemoattractant for eosinophils
ECFA
55
Type II reactions are classified as
Cytotoxic hypersensitivity
56
Antibody binds to specific antigen on cell surface, causing destruction by Complement or phagocytosis in
Cytotoxic hypersensitivity (Type II reaction)
57
The antibodies responsible for type II reactions are mostly
IgG or IgM
58
Bound IgG antibody facilitates
Phagocytosis (opsonization)
59
Bound IgG antibody facilitates phagocytosis (opsonization) because phagocytes have membrane receptors
FCRy for its Fc region
60
Transfusion of mismatched blood is an example of a
Type II reaction
61
Fetal hemolytic disease arising from Rh incompatibility between mother and fetus is an example of a
Type II reaction
62
What are two other examples of type II reactions?
Hyperacute rejection of organ transplant and some drug allergies
63
Binds to red cell proteins, acts as a hapten, and stimulate formation of antibodies that then lyse drug-coated red cells
Penicillin
64
Type II reactions are classified as
Immune complex diseases
65
In a type II reaction, the reaction of antigen with antibody [especially in antigen excess] forms soluble
Immune complexes
66
These complexes can cause
Arthritis, glomeronephritis, and vasculitis
67
What are four examples of type III reactions?
1. ) Pulmonary reactions 2. ) Arthus reaction 3. ) Autoimmune diseases 4. ) Serum sickness
68
Pulmonary reactions to inhaled antigens is the basis of many occupationally-related disease, such as Farmer's lung. The antigens responsible are often
Fungal
69
Arises from reaction to fungal spores in moldy hay
Farmer's lung
70
Experimental administration of soluble antigen to an immune subject results in a skin lesion redness, and swelling -takes 3-8 hours to develop].
Arthus reaction
71
Rheumatoid Arthritis is an example of a
Type III reaction
72
In RA, the antigen is
IgG
73
Autoantibodies are made to many cell components including DNA, RNA, nucleoproteins in
Systemic Lupus erythematosis
74
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
Serum sickness
75
Type IV reactions are called
Cell mediated
76
Antigen specificity for type IV reactions is provided by
CD4+ TH cells
77
Antigen specificity is provided by CD4+ TH cells, on stimulation they release cytokines/chemokines, infiltration of the site by
Macrophages and CTL
78
Classic Type IV skin reactions are characterized by
Induration and erythema
79
Hardness, from cell infiltration
Induration
80
Require 48-72 hours to develop
Class IV skin reactions
81
Skin response to a panel of common antigens is used diagnostically to assess competence of
Cell-mediated immunity
82
Class IV skin reactions are often called
Tuberculin-type reactions
83
Form at sites infected by microbes that survive/multiply inside cells
Granulomatas
84
Granulomas form at sites infected by microbes that survive/multiply inside cells. The classic cause is
Mycobacterium tuberculosis
85
Follows exposure to poison ivy or chemicals such as chromate salts or metals
Contact hypersensitivity dermatitis
86
Allergens bind to cell surface proteins, act as haptens, and stimulate
Cell-mediated immunity
87
Like tuberculin reactions, they develop in 2-3 days
Contact hypersensitivity dermatitis
88
Acute rejection of organ transplants. Requires weeks/months and involves both
CD4+ and CD8+ cells
89
Takes months or years and the mechanism is obscure; possibly fibrosis in response to cytokine release
Chronic rejection

Immunity (33 decks)

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