Immunity Flashcards

1
Q

What is the purpose of the acute inflammatory response?

A

1) Neutralize and destroy harmful agent
2) Localize injury
3) Allow healing

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2
Q

What are the cardinal signs of inflammation?

A

1) heat
2) redness
3) swelling
4) pain
5) +/- loss of function

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3
Q

What factors determine the intensity and extent of the inflammatory response?

A

1) the severity of the injury
2) the reactive capability of the host

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4
Q

What are the five causes of inflammation?

A

1) surgery or physical trauma - mechanical injury
2) UV/radiation
3) chemicals
4) microbes/bugs
5) ischemia

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5
Q

What are the 3 events of the inflammatory process?

A

1) release of chemical mediators
2) vascular response
3) cellular response

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6
Q

What are the key properties of the acute inflammatory response?

A
  • non-specific
  • no memory is created
  • short duration (8-10 days)
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7
Q

What are the five chemical mediators involved in AIR?

A

1) histamine
2) leukotriene
3) prostaglandin
4) bradykinin
5) platelet activating factor

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8
Q

What is inflammation?

A

A homeostatic process that is activated by cellular injury - regardless of the mechanism of injury.

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9
Q

What are the properties of histamine?

A
  • 1st and most abundant mediator released *
    Derived from mast cells (connective tissue - skin, respiratory, GI)
    Involved in allergic reactions
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10
Q

What are the effects of histamine?

A

Vasodilation
Endothelial cell retraction = increased CMP

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11
Q

How are prostaglandins produced?

A

Produced via cellular injury:
Injured cells release arachadonic acid — processed via cyclo-oxygenase pathway — results in prostaglandins

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12
Q

What are the effects of prostaglandins?

A

Vasodilation
Increased CMP
Chemotaxis
Pain

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13
Q

How are leukotrienes produced?

A

Produced via cellular injury;
Arachadonic acid is processed via lipo-oxygenase pathway— results in leukotriene production

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14
Q

What are the effects of leukotrienes?

A

Chemotaxis
Increased CMP
Neutrophil aggregation

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15
Q

What are the properties of bradykinin?

A

Plasma protein produced via the kinin cascade - injured cells release clotting factors (Hageman factor)

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16
Q

What are the effects of bradykinin?

A

Vasodilation
Endothelial cell retraction = increased CMP
Chemotaxis
Pain

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17
Q

Which five cells release platelet activating factor?

A

Mast cells
Neutrophils
Monocytes
Endothelial cells
Platelets

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18
Q

What are the effects of platelet activating factor?

A

Increased CMP
Platelet activation
Leukocyte adhesion to endothelium (allows them to stick to area of cellular injury)

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19
Q

What are the five steps of the vascular response (AIR)?

A

1) vasoconstriction
2) vasodilation
3) increased increased capillary membrane permeability
4) platelet adhesion
5) slowed circulation

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20
Q

Explain the vasoconstriction step in the vascular response (AIR)

A

Occurs briefly and immediately after injury – is a mechanism to prevent bloodloss

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21
Q

Explain the vasodilation step in the vascular response (AIR)

A

Occurs due to release of chemical mediators - histamine, prostaglandin, bradykinin
Purpose: to increase blood flow to the site of injury
Increased blood flow increases hydrostatic pressure = results in fluid being pushed out of the vasculature (swelling)

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22
Q

Explain the step of increased capillary membrane permeability in the vascular response (AIR).

A

Occurs due to the release of chemical mediators that cause endothelial cell retraction - histamine and bradykinin
Purpose: dilute toxins if present and shift plasma fluid out of the vasculature into the interstitial space
Result: increased blood viscosity, WBC emigration to site of injury
edema, pain, +/- loss of function

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23
Q

Explain the platelet adhesion step of the vascular response (AIR).

A

Platelets move to site of injury and stick to exposed collagen of vasculature - coagulation occurs
Purpose: clot formation to localize injury and prevent spread of pathogen
Also prevents widespread/systemic inflammatory response

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24
Q

Explain the slowed circulation step of the vascular response (AIR).

A

Fluid shift caused by vasodilation and increased CMP = increased blood viscosity which slows blood flow
Purpose: allows WBCs to marginate and get to site of injury to start cellular response

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25
Q

What are the four steps of the cellular response (AIR)?

A

1) margination & pavementing
2) emigration of WBCs via diapedesis
3) chemotaxis
4) phagocytosis

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26
Q

Explain the step of margination and pavementing in the cellular response (AIR).

A

Pavementing: the cobblestone appearance from neutrophils and monocytes migrating along the vessel wall
Facilitated by selectin

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27
Q

What is selectin?

A

An adhesion protein presented by endothelial cells to facilitate margination

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28
Q

How is pavementing different from the normal physiological relationship between blood cells and the endothelium?

A

Endothelial cells normally produce nitric oxide to repel blood cells away from vessel walls
**response in inhibited during AIR

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29
Q

Explain the emigration of WBCs during the cellular response of AIR.

A

Neutrophils and monocytes pass through the capillary wall (made possible by endothelial cell retraction) to get to the site of injury

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30
Q

What is diapedesis?

A

Process of the WBC leaving the vasculature – WBC sticks its foot our through the gaps in the capillary wall from endothelial cell retraction

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31
Q

What is integrin?

A

An adhesion molecule on the WBCs surface - it binds to selectin on endothelial cells
Helps to catch the WBCs so they can leave the vasculature

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32
Q

Explain the step of chemotaxis in the cellular response of AIR.

A

Chemotaxis: the process of WBCs being drawn to the site of injury
Occurs due to release of chemical mediators - prostaglandin, bradykinin, leukotriene

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33
Q

Explain the step of phagocytosis in the cellular response of AIR.

A

The 4-step process of phagocytes (neutrophils and monocytes) ingesting and destroying antigens/microorganisms/debris

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34
Q

What are the four steps of phagocytosis?

A

RAID
Recognition
Attachment
Ingestion
Digestion

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35
Q

Explain the recognition step of phagocytosis.

A

Phagocyte must recognize the pathogen/antigen as foreign
Accomplished through:
(PAMP) pathogen associated molecular patterns
(PRR) pathogen recognition receptors
or antibodies

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36
Q

Explain the attachment step of phagocytosis.

A

Phagocyte attaches to surface of pathogen via opsonization or binding sites

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37
Q

What is opsonization?

A

The process of covering an antigen with opsonins (immunoglobulins and complement C3b) to make it more susceptible for phagocyte ingestion because they provide more binding sites for attachment
** increases effectiveness of phagocytosis **

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38
Q

What is an opsonin?

A

A normally inactive protein in the bloodstream that is activated with the activation of the complement system

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39
Q

Explain the ingestion step of phagocytosis.

A

The cell membrane of the phagocyte extends projections (pseudopods) that wrap around the bacteria, then meet and fuse to encapsulate the bacteria in a phagosome

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40
Q

Explain the digestion step of phagocytosis.

A

The phagosome fuses with lysosomes creating a digestive vacuole called a phagolysosome
Lysosomes destroy the antigen
Antigen is broken down into small protein fragments and spit out via exocytosis

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41
Q

What is the phagocyte called after phagocytosis has occurred?

A

An antigen presenting cell
Displays some of the protein fragments on the cell surface (MHC 2) so that B cells and T cells can recognize it and begin building immunity to that antigen

42
Q

What is the purpose of the complement system?

A

To complement/enhance the immune system in localizing and destroying foreign agents

43
Q

How is the complement system activated?

A

Complement proteins normally circulate in the blood in inactive form
Activated via one of two pathways:
Classic pathway - requires an antibody-antigen complex
Alternative pathway - bacterial endotoxins

44
Q

What is the classic pathway?

A

Requires an antibody-antigen complex
Usually occurs during a second exposure to an antigen as the immune system has had the opportunity to create antibodies

45
Q

What is the alternative pathway?

A

Triggered by endotoxins, cell wall fragments, etc.

46
Q

What are the three ways the complement system enhances the inflammatory response?

A

1) chemotaxis and mast cell degranulation
2) Opsonization
3) membrane attack complex (MAC)

47
Q

What is the complement protein most important in opsonization?

A

C3b

48
Q

What are the complement proteins most important in MAC?

A

C6 through C9

49
Q

Explain the process of membrane attack complex (MAC)?

A

Complement proteins C6-C9 form ring-like structure, punches holes in bacterial cell membrane, allows sodium and water to rush into the cell
Results in lysis of the cell

50
Q

What is self-tolerance?

A

The ability of the immune system to differentiate between self and non-self.

51
Q

What are the key cells in adaptive/specific immunity?

A

Lymphocytes – T cells and B cells

52
Q

What two properties distinguish immunity from non-specific defenses?

A

Specificity: the ability to create immunity for specific antigens
Memory: ability to remember an antigen and mount a faster and more intense response in subsequent exposures

53
Q

What is a major histocompatability complex (MHC)?

A

A molecule on the cell’s surface that is used to display self or foreign antigens
Can be classified into two groups, MHC1 and MHC2
Can also be called Human Leukocyte Antigens (HLA)

54
Q

What are the function and properties of MHC 1?

A

Function: presents self-antigen
Involved in cell-mediated immunity – T-cytotoxic cells (CD8) look for cells that are supposed to but are no longer displaying self-antigen

55
Q

What are the function and properties of MHC 2?

A

Function: presents foreign antigen (APC)
Involved in humoral immunity – T-helper cells (CD4) look for APCs displaying non-self antigens

56
Q

What are the three types of T-cells involved in adaptive immunity?

A

T-helper cells (CD4)
T-cytotoxic cells (CD8)
T-suppressor cells

57
Q

What are the two kinds of lymphocytes involved in adaptive immunity?

A

T Cells and B Cells

58
Q

What are the two kinds of immune responses involved in adaptive immunity?

A

Humoral and cell-mediated

59
Q

Where do T-cells mature and differentiate?

A

Thymus gland

60
Q

Where do B-cells mature?

A

Bone marrow

61
Q

What is the role of T-cells in adaptive immunity?

A

T-helper and T-suppressor cells are regulatory cells – they regulate the activities of other cells
T-cytotoxic cells are effector cells – they have a direct effect (cell death) on cells

62
Q

What is the role of B-cells in adaptive immunity?

A

Produce antibodies (via plasma cells) and memory cells

63
Q

What is an antigen?

A

Any foreign substance that can elicit an immune response when introduced to the body

64
Q

What is immunogenicity?

A

The ability to provoke an immune response
Influenced by 3 factors – foreign, size and complexity, quantity

65
Q

What are the three factors that influence the immunogenicity of an antigen?

A

1) how foreign the antigen is
2) the size and complexity of the antigen
3) the quantity of the antigen

66
Q

What is reactivity?

A

The ability of an antigen to react specifically with produced antibodies.

67
Q

What is an antigenic determinant?

A

** also called and epitope **
The specific binding area on an antigen that determines the type of antibody created
The variation in epitopes determines the complexity of an antigen, and the complexity of the antibodies created for that antigen.

68
Q

What is a hapten?

A

A small molecule that cannot elicit an immune response without coupling with a protein carrier

69
Q

What is an antibody?

A

A protein produced by the body (plasma/B cells) in response to an antigen that should only combine specifically with that antigen
** also called an immunoglobulin **

70
Q

Describe the basic structure of an antibody.

A

All have the same basic structure – is Y-shaped that’s formed by two identical light chains and two identical heavy chains

71
Q

Describe the variable region of the antibody.

A

The tips of the heavy and light chains that form the antigen binding site = FAB - antigen binding fragment
Is different for each kind of antibody

72
Q

What is the constant fragment?

A

The stem of the antibody that determines which class it belongs to = determines the characteristics

73
Q

What is the purpose of the hinge?

A

Gives flexibility to the antibody so it can attach to antigens a distance apart

74
Q

What are the five main classes of antibodies?

A

IgG
IgM
IgE
IgA
IgD

75
Q

Which is the smallest and most abundant antibody class?

A

IgG
makes up 75-80% of Ig concentration

76
Q

Which class has the largest antibody?

A

IgM
[M for massive]
Why it’s only found intravascularly - it’s too large to escape

77
Q

Which class of antibodies is associated with allergic reactions and parasitic infections?

A

IgE
why it has a variable concentration amount

78
Q

What class of antibodies is found in secretions?

A

IgA
[nurses scream AAAAAA when they see secretions]

79
Q

What is the physiological role of IgG?

A

Phagocytosis
Complement system
Neutralize toxins

80
Q

What is the physiological role of IgM?

A

Is the initial response to an antigen
[they’re so big so they tons of binding sites]

81
Q

What is the physiological role of IgA?

A

Provides localized protection of mucous membranes

82
Q

Which two classes of antibodies can be transferred to offspring?

A

IgG - transfers via placenta
IgA - transfers via colostrum

83
Q

What makes the structure of IgA different from the other antibody classes?

A

Contains a secretory piece
Has two basic units - dimer

84
Q

Which classes of antibodies are monomers?

A

IgG, IgE, IgD

85
Q

How many basic units does the antibody class IgM have?

A

five - pentameter

86
Q

What is the function of IgD?

A

Unknown - theory is that it’s involved in the maturation and differentiation of B cells
Only makes up <1% of total Ig concentration

87
Q

What are the four main functions of antibodies?

A

1) Agglutination
2) Neutralization
3) Opsonization
4) Complement system activation via classic pathway

88
Q

Explain agglutination of antibodies and describe the two ways it benefits the immune response?

A

Allows antibodies to stick together – when they’re clumped together:
- more recognizable to macrophages
- allow for phagocytosis of large clumps of antigens

89
Q

What is neutralization?

A

Antibodies attach to viruses and toxins to prevent the spread of toxins
Prevents damage to surrounding tissues

90
Q

What is humoral immunity?

A

The immune response used against bacteria and free viruses

91
Q

What is the main cell type in humoral immunity?

A

B cells

92
Q

What is the goal of humoral immunity?

A

Antibody production

93
Q

What is a T-independent antigen?

A

An antigen that is capable of stimulating B cells without the help of T-helper cells

94
Q

What is a T-dependent antigen?

A

Antigens that require T-helper cells to activate B cells

95
Q

What are the classifications of humoral immunity?

A

Active and Passive Immunity

96
Q

What is active humoral immunity?

A

Immunity that results from active production of antibodies
Is long-lasting

97
Q

What are the two subtypes of active humoral immunity?

A

Natural active immunity - person contracts disease
Acquired active immunity - person receives vaccine

98
Q

What is passive humoral immunity?

A

The transfer of a specific antibody from a donor to a host – does not involve the host’s immune response
Is short-lived because memory isn’t created from the exposure

99
Q

What are the two subtypes of passive humoral immunity?

A

Natural passive immunity - transfer of antibodies from mom to newborn/fetus
Artificial passive immunity - transfer of antibodies from immune person to susceptible person

100
Q

What is the cell-mediated response?

A

Immunity against foreign cells - involves T-cytotoxic cells
No antibodies are produced