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PATHOPHYSIOLOGY > Inflammation > Flashcards

Inflammation Flashcards

1
Q

innate immune system

A

the unchanging immune system we’re born with. It has the same response every time it’s activated (non-specific)

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2
Q

adaptive immune system

A

the immune system we continually develop as we are exposed to different pathogens over our lifetime. It has memory and is unique to each person

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3
Q

3 lines of defense against pathogens

A
  1. Innate immune system - natural barriers
  2. Inflammation
  3. Immune system - adaptive immunity
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4
Q

natural barriers

A

our first line of defense that includes skin and mucous membranes. They can be mechanical or chemical barriers

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5
Q

mechanical barriers

A

cilia, sloughing, mucous, etc.

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6
Q

chemical barriers

A

acidic pH of stomach or vagina, saliva

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7
Q

humoral immunity

A

an immune response derived from body fluids such as the plasma. Inflammation uses the complement system and the immune system uses antibodies through B cells to tag the pathogen

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8
Q

cellular immunity

A

an immune response that occurs between cells. Inflammation recruits neutrophils and macrophages and lymphocytes (T and B cells) are recruited in the immune response involving an intracellular or processed antigen. Does not involve antibodies

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9
Q

inflammation

A

the protective response of vascularized tissue that involves eliminating the initial cause of injury, removing damaged tissue, and building new tissue

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10
Q

goals of inflammation

A
  1. movement of blood and cellular components to site of injury
  2. delivery of nutrients and blood cells to get rid of the offender
  3. injurious agents are diluted, confined, and eliminated
  4. stimulate and assist the immune system
  5. promote healing and generate new tissue
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11
Q

how goals of inflammation are accomplished

A
  1. Increased metabolic rate to increase production of cellular items needed for battle
  2. Vasodilation to speed up delivery of cellular components to site of injury
  3. Increased vascular permeability to allow leukocytes (namely neutrophils), proteins, and nutrients into affected tissue
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12
Q

causes of inflammation

A
  • Microbes
  • Immune reactions between antigen and antibody
  • Trauma
  • Burns
  • Physical/chemical agents
  • Tissue necrosis
  • Temperature extremes
  • Oxygen deprivation
  • Nutrient deprivation
  • Genetic/immune defects
  • Ionizing radiation
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13
Q

Characteristics of acute inflammation:

A
  • Response to injury/insult that occurs early and quick (mins to hours)
  • Triggered by variety of stimuli
  • Doesn’t last very long, self limiting
  • Non-specific (ex. response for cutting finger/stubbing toe is exactly the same)
  • 2 phases (vascular and cellular)
  • Results in either healing or chronic inflammation
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14
Q

What cells are involved in inflammation? 7

A
  • Endothelial cells
  • Platelets
  • Neutrophils
  • Monocytes/macrophages
  • Eosinophils
  • Basophils
  • Mast cells
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15
Q

Function of endothelial cells?

A
  • Line blood vessel walls, tight space under normal conditions, limits movement
  • Produce antiplatelet/antithrombotic agents to prevent clots
  • Regulate leukocyte extravasation through use of adhesion molecules
  • Regulate immune cell proliferation
  • Participate in repair process
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16
Q

What are platelets also known as?

A

Thrombocytes

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17
Q

Function of platelets?

A
  • Primary role = hemostasis
  • Activated then produce inflammatory mediators leads to increased vascular permeability, chemotaxis, adhesive and proteolytic properties of the endothelium
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18
Q

Function of neutrophils?

A
  • Chief phagocytic leukocytes

- Have lysosomal enzymes, called upon to destory invaders and remove debris

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19
Q

What are bands?

A

Immature neutrophils

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20
Q

What does it mean when the band count is elevated on a CBC?

A

Bone marrow is overworked

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21
Q

Function of monocytes/macrophages?

A
  • Leukocytes derived from bone marrow
  • Larger and fewer lysosomes than neutrophils
  • Stimulate growth of granulocytes and monocytes in the bone marrow and substances that promote wound healing
  • Replace neutrophils as they die off
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22
Q

When do macrophages appear?

A

Later than neutrophils (24-48 hours post injury)

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23
Q

What are macrophages associated with?

A

chronic inflammation

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24
Q

What do macrophages produce?

A

Potent vasoactive mediators

  • Prostaglandins
  • Leukotrienes
  • Platelet activating fcator
  • Inflammatory cytokines
  • Growth factor
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25
Q

How long are macrophages lifespan?

A

3-4x longer than neutrophils

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26
Q

What happens to neutrophils when they die?

A
  • Become exudate (pus)

- Release chemotactic factor to attract macrophages to injury

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27
Q

When do neutrophils appear?

A
  • Early in inflammatory process (90 mins to 6-12 hrs post injury) cells attracted to site because of chemotactic factors
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28
Q

What causes an increased demand for neutrophils?

A
  • Severe inflammation, bone marrow cannot keep up and releases bands
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29
Q

Function of eosinophils?

A
  • Prominent in allergic response and hypersensitivity disorders
  • Good at tackling parasitic infections
  • Circulate in blood until needed,
  • migrate to tissue where they modulate release of inflammatory mediators
  • degrade vasoactive molecules,
  • controlling vascular effects of histamine and serotonin
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30
Q

What are eosinophils?

A

Granulocytes with many lysosomes

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31
Q

What do eosinophils do?

A
  • Circulate in blood until needed,
  • migrate to tissue where they modulate release of inflammatory mediators
  • degrade vasoactive molecules,
  • controlling vascular effects of histamine and serotonin
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32
Q

Function of basophils?

A
  • Produce lipid mediators and cytokines to induce inflammatory response
  • Important in allergic and hypersensitivity reactions
  • Trigger histamine and vasoactive agent release
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33
Q

Function of mast cells?

A
  • Mast cell degranulation
  • Activate the 3 plasma protein systems
  • Release of cell derived mediators
  • Important in response to hypersensitivity and allergic reactions
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34
Q

Where are mast cells located?

A

Connective tissue, close to blood vessel, prevalent along mucosa of lung, GI tract and dermis of skin

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35
Q

What do mast cells produce?

A

Lipid mediators and cytokines which induce inflammation

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36
Q

What is within neutrophils cytoplasm??

A

Pre-formed granules

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37
Q

What are the contents of these granules?

A
  • Histamine
  • Serotonin
  • Chemotactic factors
  • Enzymes
  • Proteoglycans
  • Proteases
  • Cytokines
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38
Q

What are the three plasma protein systems

A
  • Complement system
  • Clotting system/coagulation cascade
  • Kinin system
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39
Q

What do complement fragments cause?

A

Vasodilation, increase vascular permeability and enhance activity of phagocytes

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40
Q

What do C3 and C5 do?

A

Formation of opsonins, chemotactic factors and anaphylatoxins

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41
Q

C3b?

A

used in the opsonization and tagging

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42
Q

C5a?

A

Chemotactic and anaphylatoxic factors

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43
Q

C2b?

A

Increase vasodilation/permeability (smooth muscle relaxation)

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44
Q

C4a?

A

Anaphylatoxin inducing cell degranulation with histamine release

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45
Q

What is the endpoint of the complement cascade?

A

Formation of membrane attack complex (MAC) composed of C5-C9, creates holes in membranes of pathogens, allows water in and causes cells to explode

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46
Q

What are the three ways to activate the complement cascade?

A
  1. Classical pathway - activated by antibodies, immune system can take advantage of this for the destruction of bacteria
  2. Lectin pathway - activated by bacterial carbohydrates, no antibody required
  3. Alternative pathway - activated by gram negative bacteria, fungal cell wall polysacchardies (endotoxins) no antibody required
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47
Q

Which of the pathways requires an antibody to be activated?

A

The classical pathway

48
Q

Which of the pathways does not require an antibody to be activated?

A
  • Lectin pathway

- Alternative pathway

49
Q

What are the major effects of complement?

A
  • Opsonization
  • Mast cell degranulation
  • Leukocyte chemotaxis
  • Cell lysis
50
Q

How is the clotting system activated?

A

Substances released during tissue destruction and infection, two pathways (intrinsic and extrinsic)

51
Q

What is the goal of the clotting system?

A

Produce a fibrous clot, fibrous mesh network that traps offending agent and prevents the spread of infection, keeps it at the site of inflammatory activity, prevents bleeding and promotes healing

52
Q

What is inflammation enhanced by?

A

By products of fragments that are produced during the clotting cascade

53
Q

What are the byproducts and how do they enhance inflammation?

A
  • Fibrin production, fibrinogen releases fibrinopeptides, this acts as a chemotactic for neutrophils, increases vascular permeability, enhances effect of bradykinin
  • Plasmin works with complement to activate C3a and C5a causing the release of histamine
54
Q

What does the kinin system do?

A

Works closely with the clotting system

55
Q

What is the kinin system activated by?

A

Factor XII (XIIA) like the clotting cascade

56
Q

What is the end result of the kinin cascade?

A

Production of bradykinin causes vasodilation, increased vascular permeability, smooth muscle contraction, enhances leukocyte chemotaxis, stimulates pain receptors

57
Q

What are bradykinin effects similar to?

A

Histamine, the effects are shorter, appears to be of greater importance during latter phases of inflammation

58
Q

What components of the plasma protein systems does Hageman factor activate?

A
  • Clotting cascade through factor XI (Hageman factor)
  • Fibrinolytic system through conversion of plasminogen
  • Kinin system by prekallekrein activator
  • C1 and complement cascade
59
Q

Where are plasma derived mediators formed?

A

In the liver

60
Q

What are the major sources of cell derived mediators? 9

A
  • Platelets
  • Neutrophils
  • Macrophages
  • Monocytes
  • Mast cells
  • Endothelial cells
  • Smooth muscle
  • Fibroblasts
  • Most epithelial cells
61
Q

Why are mediators of inflammation important?

A

Without some method of control over the plasma protein systems we would be in a constant state of inflammation which would be very uncomfortable

62
Q

Where is histamine found?

A

Well perfused connective tissue, circulating platelets, basophils and within mast cells granules

63
Q

What does histamine cause?

A

Vasodilation, increased vascular permeability, increased adherence of leukocytes to endothelium

64
Q

What are the negative consequences of histamine?

A

Smooth muscle constriction of bronchioles (makes breathing difficult during acute inflammatory reaction), antihistamines will antagonize effects of acute inflammatory response

65
Q

What is serotonin released by?

A

Mast cells, basophils and platelets

66
Q

What does serotonin do?

A

Causes smooth muscle contraction, small vessel dilation, increased vascular permeability

67
Q

What are lyosomal enzymes?

A

Membrane enclosed sacs containing powerful enzymes

68
Q

What is the function of lysosomal enzymes?

A

Fuse with phagocytes to destroy foreign invaders

69
Q

What are arachidonic metabolites?

A

Fatty acids in phospholipids in the cell membrane

70
Q

Where are arachidonic metabolites released from? What do they do when released?

A
  • Released from mast cells

- Initiate complex reactions which cause production of other inflammatory mediators (prostaglandins and leukotrienes)

71
Q

What is the function of prostaglandins?

A
  • Induce inflammation and enhance effects of histamine and other mediators
  • Promote vasodilation/bronchoconstriction/increase neutrophil chemotaxis, cause pain through action on nerves and fever
72
Q

How can you counteract the effects of prostaglandin synthesis?

A

Use of ASA and NSAID’s

73
Q

What is thromboxane A2 produced by?

A

Platelets at the site of the injury

74
Q

What is the effects of thromboxane A2?

A
  • Promote platelet aggregation
  • Promote bronchoconstriction
  • Promote vasoconstriction
75
Q

When are leukotrienes synthesized?

A

While histamine is working

76
Q

What are the effects of leukotrienes?

A

Increase vascular permeability, smoothing muscle contraction, constrict pulmonary airways (mediation of asthma and anaphylaxis), affect adhesion properties of endothelial cells, extravasation and chemotaxis of neutrophils, eosinophils and monocytes

77
Q

What do leukotrienes help to do?

A

Prolong the inflammatory response

78
Q

Where is platelet aggregating factor generated from?

A

Lipids stored in cell membrane

79
Q

What effect does platelet aggregating factor have?

A

Induces platelet aggregation, activates neutrophils and acts as a chemoattractant for eosinophils

80
Q

What are cytokines/chemokines activated by?

A

Macrophages and lymphocytes, endothelium, epithelium, connective tissue

81
Q

What effect do cytokines and chemokines have?

A

Modulate inflammatory response by travelling and binding to and affecting the functions of those target cells

82
Q

What effect does nitric oxide have?

A
  • Causes smooth muscle relaxation,
  • antagonizes platelet adhesion, aggregation
  • degranulation
  • Regulates recruitment of leukocytes
83
Q

What occurs where there is blocked nitric oxide production?

A

Promotes leukocyte rolling and adhesion to capillary venules

84
Q

What occurs with delivery of nitric oxide?

A

Reduces leukocyte recruitment, reduces cellular phase of inflammation

85
Q

What occurs with impaired nitric oxide production?

A

Inflammatory changes associated with atherosclerosis, some microbial properties

86
Q

When are oxygen free radicals released?

A

Released by leukocytes after exposure to microbes, cytokines and immune complexes or during phagocytic process

87
Q

What do low levels of oxygen free radicals cause?

A

Increased expression of cytokines and adhesion molecules

88
Q

What do high levels of oxygen free radicals cause?

A

Damage to endothelium and increased vascular permeability

89
Q

Describe vascular phase of inflammation

A
  • Brief arteriolar vasoconstriction
  • Profound vasodilaton
  • Increased vessel size encourages blood to go to the area
  • Blood velocity slows, increases hydrostatic pressure
90
Q

Describe cellular phase of inflammation

A
  • Biochemical mediators retract endothelial cells, causes increased vascular permeability
  • Large proteins leave vessel, move into extra-vascular space taking fluid with them
  • Blood = more viscous, slows down velocity
  • Leukocytes stick to endothelium then migrate out to the site of injury
91
Q

What are the three major changes that happen to microcirculation during vascular response of inflammation?

A
  1. Brief vasoconstriction and then vasodilation
    - Increased capillary permeability
    - Movement of leukocytes into tissues
92
Q

What do the changes to microcirculation cause? (think changes in the body)

A
  • Heat
  • Redness
  • Edema
  • Pain
  • Loss of function
93
Q

How do leukocytes emigrate?

A
  • During inflammation certain molecules become sticky and adhere to endothelial wall
  • Leukocytes recruited to site of injury and linger there because of slowed blood flow
  • Line up along endothelial wall and adhere to it
  • Chemotaxis, then leukocytes encouraged to move into tissue where the injury occurred
94
Q

What is migration?

A

Leukocytes move along the endothelial wall

95
Q

What is adhesion?

A

Leukocytes stick to the endothelium with the help of adhesion molecules

96
Q

What is transmigration?

A

Leukocytes move to the site of injury (chemotactic factors)

97
Q

What is chemotaxis?

A

Response involving cell orientation or cell movement that is either toward (positive chemotaxis) or away from (negative chemotaxis) a chemical stimulus

98
Q

How does chemotaxis work?

A
  • Directed cell migration, leukocytes leave capillary, move in response to chemical gradient caused by chemokines, bacterial and cellular debris, and protein fragments from the complement system
99
Q

Phagocytosis process review

A
  1. Margination (leukocytes move, adhere to endothelium, move along periphery of blood vessels)
  2. Pseudopod formation (plasma membrane of phagocyte extends finger like projections)
  3. Diapedesis (leukocytes move through wide gaps in endothelium into the tissue)
  4. Migration (phagocytes move toward target)
  5. Opsonization
  6. Engulfment (phagocytes surround and encircle target, from intracellular phagocytic vacuole or phagosome)
  7. Fusion with lysosome (forms phagolysosome, works on destruction and digestion of target)
  8. Destruction (target dies, phagocyte dies becomes exudate and products exit via the lymphatics)
100
Q

How do we avoid toxicity?

A

Alpha-1 antitrypsin (plasma protein from liver) released and inhibits destructive effects

101
Q

How is heat caused?

A
  • Vasodilation -

- Increased blood flow to the site of the injury

102
Q

How is redness caused?

A
  • Vasodilation

- Increased blood flow to the site of the injury

103
Q

How is edema caused?

A
  • Vasodilation
  • Increased blood flow to the site of the injury
  • Increased capillary permeability
  • Leakage of proteins and cells out of the endothelial wall (taking water with it)
  • Increased fluid in tissues
104
Q

How is pain caused?

A
  • Increased fluid in tissues

- Prostaglandins act on nerve endings to cause pain

105
Q

How is pus formed?

A
  • Neutrophils die off

- Contents become exudate

106
Q

How is a clot formed?

A
  • Initiation of clot cascade

- Thrombus sequesters invaders to site of injury

107
Q

How does loss of function occur?

A

Due to edema and pain

108
Q

When can inflammation be considered chronic?

A

When it lasts 2 weeks or longer

109
Q

How is granulamatous inflammation characterized?

A

Inflitration of lymphocytes and macrophages, body isolates site and walls it off

110
Q

What is a granuloma encapsulated by?

A

Fibrous deposits

111
Q

How does inflammation interact with atherosclerosis?

A
  • Elevated cholesterol causes monocytes to become sticky and attach to endothelium
  • Macrophages consume foam LDLs and turn them into foam cells
  • Phagocytes release cytokines which interact with local tissue cells in pro or anti-inflammatory way
  • Subendothelium ecposed to blood components, platelets adhere and aggregate at the site of injury, smooth muscle poliferates and then endothelium pouches out and makes lumen smaller
  • Lipids accumulate beneath endothelial layer, hard lipid core formed
  • Enzymes eat at the fibrous cap
  • Plaque unstable, can rupture
  • Thrombus formed b/c rupture encourages thrmbus to form, platelets adhere
  • Occlusion of vessel
  • Myocardial infarction
112
Q

Function of Opsonins

A

Coat bacteria and tag them for destruction

113
Q

Chemotactic factors do what?

A

Draw other inflammatory mediators to site of injury

114
Q

Anaphylatoxins function

A

Rapid degranulation of mast cells

115
Q

What is the most potent anaphylatoxins?

A

C3a

116
Q

Bradykinin Function

A
  • causes vasodilation
  • smooth muscle contraction
  • enhances chemotaxis
  • pain receptors
  • increase vascular permeability

PATHOPHYSIOLOGY (9 decks)

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