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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
Q

Mast Cells

A

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

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26
Q

Histamine

A

a biochemical mediator that releases vasoactive amines

causes vasodilation and increased vascular permeability

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27
Q

Leukotrienes

A

Increases vascular permeability

increases smooth muscle contraction

bronchoconstriciton

causes neutrophil and eosinophil chemotaxis

act later/last to insure a longer response than histamine

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28
Q

Prostaglandins (Eicosanoids)

A

increase vascular permeability

vasodilation

bronchoconstriction

induce pain

cause neutrophil chemotaxis

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29
Q

Coagulation (Clotting) System

A

Platelet Activating Factor (PAF)

Fibrin

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30
Q

Platelet Activating Factor (PAF)

A

includes platelet aggregation, clotting and stimulates leukocyte aggregation and migration, endothelial cells and vascular permeability

31
Q

Fibrin

A

insoluble, polymerized protein

forms meshwork at the injured or inflamed site

32
Q

Chemokine

A

a mast cell secretion

they attract a specific type of WBC to the inflammation site (neutrophils/eosinophils)

33
Q

Neutrophils

A

first responders

phagocytic (engulf bacteria)

short lifespan (24-48 hours)

34
Q

Macrophages

A

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
Q

Dendritic Cells

A

Phagocytic

under epithelial tissues in most organs

antigen-presenting cells

activate helper T cells and B cells

36
Q

Acute Inflammation

A

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

37
Q

Chronic Inflammation

A

develops if the acute inflammatory response is inadequate

can persist for weeks or months

dense infiltration of lymphocytes and macrophages

38
Q

Abscess

A

localized (chronic) inflammation with purulent exudate, necrotic core with pus, surrounded by neutrophils

fibroblasts wall off

39
Q

Granuloma

A

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
Q

Antigen Presenting Cells

A

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
Q

Humoral Immunity

A

mediated by secreted molecules

the principal defense against extracellular microbes and toxins

42
Q

Cell-Mediated Immunity

A

is mediated by specific T lymphocytes

defends against intracellular microbes such as viruses.

43
Q

Helper T Cells

A

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
Q

Major Histocompatibility Complex (MHC 1)

A

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
Q

Major Histocompatibility Complex (MHC 2)

A

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
Q

Epitope

A

small peptide fragments recognized by the immune system

47
Q

Antigenic Determinant

A

epitope

area of antigen recognized by the immune system

48
Q

Antigen-Binding Site

A

paratope

matching portion on the antibody

49
Q

How to antibodies function?

A

Opsonization
Neutralization
Agglutination
Complement Proteins

50
Q

Opsonization

A

the coating of particles (microbes) to mark them for more efficient identification by phagocytes (to engulf)

51
Q

Neutralization

A

blocks viral binding sites

coats bacteria, enhances phagocytosis

52
Q

Agglutination

A

(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
Q

Complement Proteins

A

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
Q

Antibody (Humoral) Primary Response

A

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
Q

Antibody secondary (Memory) Response

A

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
Q

Different Types of Antibodies

A 
IgM (10%) 
IgG (75-80%) 
IgA 
IgD
IgE
57
Q

IgM

A

Primary Response
effective in agglutination
can’t cross the placenta
initiate complement proteins

58
Q

IgG

A 
Most common form
complement activation
crosses blood vessels
crosses the placenta 
passive immunity to fetus
59
Q

IgA

A

secreted from mucus membranes and breast milk (colostrum)

prevents attachment of bacterial to epithelial surface

60
Q

IgD

A

B cell activation

can’t cross placenta

61
Q

IgE

A

histamine reactions and allergies
parasite infections
on basophils and mast cells

62
Q

Complement System

A

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
Q

Recognition of Microbes by Complement Occurs in Three ways

A
  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
Q

Basophils

A

granulocytes that account for less than 1% of WBC

Prominent in allergic reactions

Release histamine and vasoactive agents

65
Q

Eosinophils

A

2-3% WBC

important in allergic reaction, parasitic infections, chronic inflammation

66
Q

Natural Killer Cells

A

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
Q

Complement System

A

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
68
Q

Bradykinin

A

dilution of blood vessels

induces pain

causes smooth muscle contraction

increases vascular permeability

69
Q

Local Symptoms of Inflammation (Five Cardinal Signs)

A
  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
Q

Systemic Changes

A

fever

leukocytosis

increase in circulating plasma proteins

71
Q

Lymphocyte Classes

A

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
Q

T Lymphocytes

A

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
Q

Humoral Immunity B Lymphocytes

A

Memory cells: display antibody on surface, remain in body for subsequent infection

Plasma Cells (effector): secrete antibody extracellularly into bloodstream

74
Q

Cells of Inflammation

A
  • Granulocytes:
    • neutrophils
    • eosinophils
    • basophils
    • mast cells

Agranulocytes

* macrophages
* dendritic cells

Lymphocytes
* natural killer cells

Pathophysiology Exam 1 (7 decks)

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