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Pathophysiology Exam 1 > Inflammation and Immunity > Flashcards

Inflammation and Immunity Flashcards

1
Q

Body’s Three Lines of Defense

A

First: physical barriers, epithelial cells, mucous membranes
Second: non-specific, innate inflammation
Third: specific (takes time), T cells, antibodies, adaptive immune system response

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2
Q

Innate Immune Response

A

the physical, chemical, molecular and cellular defenses that are in place before infection, non-specific, automatic and rapid response to cell injury

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3
Q

Adaptive Immune Response

A

second major immune defense.

specific but takes a few days to mount a full response

long-term protection from the memory cells

antibody and T cell mediated

activated by antigen, co-stimulators and cytokines (helper T cells, B cells)

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4
Q

When does an innate immune response occur?

A

rapidly, once there are harmful microbial agents within the body that the innate immune system is able to recognize and react to

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5
Q

What is the purpose of the inflammatory response?

A

a complex, nonspecific response to tissue injury, intended to

  1. minimize the effects of injury or infection
  2. remove the damaged tisue
  3. generate new tissue
  4. facilitate healing
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6
Q

What happens in the Vascular Stage of Inflammation

A
  • Vasodilation (opening of the capillary beds)
  • Erethema
  • Warmth in the area
  • Increased permeability in the vasculature
  • Outpouring of exudate into the extravascular spaces
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7
Q

What are the Three Patterns of Responses with the Vascular Stage of Inflammation

A
  1. Immediate Transient Response
  2. Immediate Sustained Response
  3. Delayed Response
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8
Q

What is the Immediate Transient Response

A

occurs with minor injury and develops rapidly after injury, usually reversible and of short duration

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9
Q

What is the Immediate Sustained Response

A

occurs with more serious types of injuries and continues for several days

affects all levels of the microcirculation and is due to direct damage of the endothelium (burns or the product of bacterial infections)

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10
Q

What is the Delayed Response

A

increased permeability begins after a 2-12 hour delay and lasts several hours or even days

Involves venules as well as capillaries and is due to radiation injuries (sunburn)

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11
Q

Cellular Stage of Inflammation

A

marked by changes in the endothelial cells lining the vasculature and movement of phagocytic leukocytes into the area of injury or infection

Mast cells and Macrophages are responding

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12
Q

Sequence of the Cellular Response to Inflammation

A
  1. Leukocyte margination and adhesion
  2. Leukocyte transmigration
  3. Leukocyte chemotaxis
  4. Leukocyte activation and phagocytosis
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13
Q

What is Chemotaxis

A

a dynamic and energy directed process of cell mitigation

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14
Q

What is Margination

A

the process of leukocyte accumulation and adhesion

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15
Q

What is Phagocytosis

A

involves neutrophils, monocytes and tissue macrophages that become activated to engage and degrade the bacteria and cellular debris (engulf)

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16
Q

What is exudate and what are the different types?

A

protein-rich fluid that is leaked into the extravascular spaces during the vascular stage of inflammation

  1. serous (clear)
  2. fibrinous
  3. purulent (pus, cyst/abscess)
  4. hemorrhagic or sanguineous (blood)
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17
Q

How does the body mount a systemic inflammatory response?

A

Occurs with severe bacterial infection (sepsis)

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18
Q

What happens during a systemic inflammatory response?

A

uncontrolled inflammatory response with the production and release of enormous quantities of inflammatory cytokines and development the systemic inflammatory response syndrome

fever and lethargy will occur

decrease in total WBC (leukopenia) may occur during overwhelming infections or impaired ability to produce WBC

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19
Q

Systemic Inflammatory Response

A

Tumor Necrosis Factor and Interleukin 1

hypothalamus controls temperature, which increases during a systemic inflammatory response

anorexia, myalgia and fatigue occur

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20
Q

Stages of the Systemic Inflammatory Response

A

First Stage: Prodromal- HA, fatigue, malaise, aches
Second Stage: Chill- shaking, rigors, piloerection
Third Stage: Flush- warm and red
Fourth Stage: Defervescence- sweating

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21
Q

What are the Cytokines?

A

Interleukins
Tumor Necrosis Factor
Interferons

all pleotropic and redundant (work on more than one cell and do the same thing)
low molecular weight proteins
brief, self limiting, mediate cell reactions

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22
Q

Interleukins

A

call lymphocytes and WBCs into action

causes fever (systemic inflammatory response)

activates other cells

increases the production of WBCs

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23
Q

Tumor Necrosis Factor

A

induces fever

stimulates proteins needed during inflammation

responds to gram negative bacteria

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24
Q

Interferons

A

interferes with viral binding and replication

inhibits cancer proliferation

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25
Mast Cells
the most important activator in the inflammatory response release of granules stimulates inflammatory response (histamine) Stimulates cytokine and chemokine synthesis by other inflammatory cells such as monocytes and macrophages
26
Histamine
a biochemical mediator that releases vasoactive amines causes vasodilation and increased vascular permeability
27
Leukotrienes
Increases vascular permeability increases smooth muscle contraction bronchoconstriciton causes neutrophil and eosinophil chemotaxis act later/last to insure a longer response than histamine
28
Prostaglandins (Eicosanoids)
increase vascular permeability vasodilation bronchoconstriction induce pain cause neutrophil chemotaxis
29
Coagulation (Clotting) System
Platelet Activating Factor (PAF) Fibrin
30
Platelet Activating Factor (PAF)
includes platelet aggregation, clotting and stimulates leukocyte aggregation and migration, endothelial cells and vascular permeability
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Fibrin
insoluble, polymerized protein forms meshwork at the injured or inflamed site
32
Chemokine
a mast cell secretion they attract a specific type of WBC to the inflammation site (neutrophils/eosinophils)
33
Neutrophils
first responders phagocytic (engulf bacteria) short lifespan (24-48 hours)
34
Macrophages
phagocytic (engulf and kill invading bacteria) antigen-presenting cells (adaptive immunity) secretion of cytokines and co-stimulators to cause inflammation and innate and adaptive immune response activate T cells, B cells and innate immune cells
35
Dendritic Cells
Phagocytic under epithelial tissues in most organs antigen-presenting cells activate helper T cells and B cells
36
Acute Inflammation
vasodilation capillary permeability occurs hours to days from onset CRP binds to pathogen (opsonin) marking it for phagocytosis SAA (increased HDL to macrophages) fibrinogen (increased erythrocyte sedimentation rate (ESR)) Increased HR, anorexia, somnolence, malaise
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Chronic Inflammation
develops if the acute inflammatory response is inadequate can persist for weeks or months dense infiltration of lymphocytes and macrophages
38
Abscess
localized (chronic) inflammation with purulent exudate, necrotic core with pus, surrounded by neutrophils fibroblasts wall off
39
Granuloma
Chronic Inflammation 2-3mm lesions surrounded by macrophages, resembling epithelial cells cells clump in a mass and surround pathogen membrane o connective tissue encapsulates and isolates (infection is localized)
40
Antigen Presenting Cells
Macrophages and phagocytes they present antigens to T cells to activate the active immunity the bridge between inflammatory and active immune system produce cytokines
41
Humoral Immunity
mediated by secreted molecules the principal defense against extracellular microbes and toxins
42
Cell-Mediated Immunity
is mediated by specific T lymphocytes defends against intracellular microbes such as viruses.
43
Helper T Cells
linchpin of adaptive immune system the conductors that cause everything else to be activated (B cells) activated by antigens secrete cytokines only recognize specific antigen peptide fragments bound to MHC molecule help B lymphocytes produce antibodies help phagocytic cells destroy ingested pathogens
44
Major Histocompatibility Complex (MHC 1)
MHC 1 and 2 are involved in self-recognition and cell-to-cell communication MHC 1 are expressed on all nucleated cells and platelets display epitopes on infected cells recognized by the CD8+ cytotoxic T cells which destroy the infected cells by secreting perforin
45
Major Histocompatibility Complex (MHC 2)
molecules expressed mainly on dendritic cells, macrophages and B lymphocytes protein molecules on cell membrane that mark cells as “self” processes antigen and presents epitopes for Helper T cell recognition on cell surface
46
Epitope
small peptide fragments recognized by the immune system
47
Antigenic Determinant
epitope area of antigen recognized by the immune system
48
Antigen-Binding Site
paratope matching portion on the antibody
49
How to antibodies function?
Opsonization Neutralization Agglutination Complement Proteins
50
Opsonization
the coating of particles (microbes) to mark them for more efficient identification by phagocytes (to engulf)
51
Neutralization
blocks viral binding sites coats bacteria, enhances phagocytosis
52
Agglutination
(Direct) formation of clumps of cells or inert particles by specific antibodies to surface antigenic components (Passive Hemagglutination) antigenic components absorbed or chemically coupled to RBCs or (passive agglutination) inert particles
53
Complement Proteins
Opsonins tag pathogen surface, alert the phagocytes to engulf them. Chemokines signaled to migrate, form membrane, attack complexes which cause pores in the pathogen Pathogen lyses and dies
54
Antibody (Humoral) Primary Response
when antigen is first introduced to the body latent period before antibody can be detected in the serum latent period involves processing antigen by the antigen-presenting cells and it's recognition by CD4+ helper T cells After recognition, T cells become activated and produce cytokines to further stimulate and direct the immune system
55
Antibody secondary (Memory) Response
occurs on second or subsequent exposure to antigen during primary response a fraction of the activated B cells do not differentiate into plasma cells they form a pool of memory B cells the rise in antibodies occurs sooner and reaches a higher level because of the available memory cells
56
Different Types of Antibodies
``` IgM (10%) IgG (75-80%) IgA IgD IgE ```
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IgM
Primary Response effective in agglutination can't cross the placenta initiate complement proteins
58
IgG
``` Most common form complement activation crosses blood vessels crosses the placenta passive immunity to fetus ```
59
IgA
secreted from mucus membranes and breast milk (colostrum) | prevents attachment of bacterial to epithelial surface
60
IgD
B cell activation | can't cross placenta
61
IgE
histamine reactions and allergies parasite infections on basophils and mast cells
62
Complement System
activation of this system is highly regulated, involving the sequential breakdown of complement proteins to generate a cascade of cleavage products capable of proteolytic enzyme activity amplification b/c each enzyme molecule activated by one step can generate multiple activated enzyme molecules activation is inhibited by proteins that are present on normal host cells it's actions are limited to microbes and other antigens that lack inhibitory proteins group of proteins that are activated by microbes and promote inflammation and destruction of microbes
63
Recognition of Microbes by Complement Occurs in Three ways
1. Classical Pathway: adaptive immune pathway, recognizes antibodies bound to surface of a microbe or other structure 2. Lectin pathway: innate pathway that uses plasma protein called the mannose-binding ligand, binds to mannose residue on microbial glycoproteins or glycolipids 3. Alternative Pathway: innate pathway which recognizes certain microbial molecules
64
Basophils
granulocytes that account for less than 1% of WBC Prominent in allergic reactions Release histamine and vasoactive agents
65
Eosinophils
2-3% WBC important in allergic reaction, parasitic infections, chronic inflammation
66
Natural Killer Cells
Do not have T cell or B cell receptors innate immune response primary defense against tumor cells, abnormal body cells, cells infected with pathogens
67
Complement System
plasma proteins that are biologically active fragments that recruit phagocytes, activate mast cells and destroy pathogens utilized in both innate and humoral (antibody) response Activation of C3 and C5 proteins, by pathogens or antibody-antigen complexes * Opsonins (C3b) * Chemokine (C3a, C5a) * C5b-C9 membrane attack complexes
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Bradykinin
dilution of blood vessels induces pain causes smooth muscle contraction increases vascular permeability
69
Local Symptoms of Inflammation (Five Cardinal Signs)
1. Rubor (redness) blood flow to the area 2. Tumor (swelling) capillary permeability 3. Calor (heat) blood flow to the area 4. Dolor (pain) stretching of nerves by swelling 5. Loss of Function
70
Systemic Changes
fever leukocytosis increase in circulating plasma proteins
71
Lymphocyte Classes
T Cells: mature in the thymus B Cells: mature in bone marrow, plasma cells and memory cells Memory Cells: B and T cells, remember specific antigens Natural Killer Cells: innate Response
72
T Lymphocytes
CD4 (effector): control system responses and components * helper T cells activate B cells, cytotoxic T cells * Regulatory T-turn off system CD8 (effector): interact directly with intercellular target (virus, cancer)
73
Humoral Immunity B Lymphocytes
Memory cells: display antibody on surface, remain in body for subsequent infection Plasma Cells (effector): secrete antibody extracellularly into bloodstream
74
Cells of Inflammation
* Granulocytes: * neutrophils * eosinophils * basophils * mast cells Agranulocytes * macrophages * dendritic cells Lymphocytes * natural killer cells

Pathophysiology Exam 1 (7 decks)

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