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FPP Weeks 1 & 2 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Beneficial goals of inflammation

A

Destroying/containing harmful agent

Preparation for healing/repair

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2
Q

Four cardinal signs of inflammation

A 
Calor (heat)
Rubor (redness)
Tumor (swelling)
Dolo (pain)
*Functio lasea (loss of function)*
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3
Q

Acute Inflammation Features: Onset, Cellular infiltrate, tissue injury, fibrosis, local and systemic signs

A

Onset: Fast, minute or hours
Cells: Mainly neutrophils
Tissue injury: Usually mild and self-limited
Local and systemic signs: Prominent

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4
Q

Chronic Inflammation Features: Onset, Cellular infiltrate, tissue injury, fibrosis, local and systemic signs

A

Onset: Slow, days
Cells: Monocytes/macrophages and lymphocytes
Tissue: Often severe and progressive
Local and systemic signs: Less prominent; may be subtle

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5
Q

Acute Inflammation Stimuli

A

Infections and microbial toxins (bacteria, viruses, fungi, parasites)
Physical trauma
Physical and chemical agents (burns, frostbite, irradiation, environmental chemicals)
Tissue necrosis (any kind(
Foreign bodies (splinters, dirt, sutures, crystal deposits)
Immune (hypersensitivity)

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6
Q

Initiation - Stimulus recognition cells

A

Epithelial cells
Dendritic cells
Phagocytes

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7
Q

Initiation - Receptors

A

Toll-like receptors

Inflammasome

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8
Q

Where are TLRs located?

A

Located in plasma membrane

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9
Q

What do TLRs recognize?

A

Bacteria, viruses, and other pathogens

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10
Q

What do TLRs do when activated?

A

Release of cytokines (TNF)

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11
Q

What/where is the inflammasome?

A

Cytoplasmic complex

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12
Q

What does the inflammasome recognize?

A

Dead cells (uric acid, ATP, crystals, some microbial products)

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13
Q

What does the inflammasome do upon activation?

A

Activation of caspase-1, activating IL-1, triggering leukocyte recruitment

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14
Q

Vascular changes - Vessel caliber and flow

A

Vasodilatation induced by chemical mediators such as histamine and NO
Leads to stasis and margination of leukocytes

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15
Q

Vascular changes - Permeability changes

A

Endothelial cell contraction (histamine, bradykinin, etc.) and endothelial cell injury - directly injured by burns, microbes, neutrophils resulting in increased vascular permeability and subsequent edema

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16
Q

Vascular changes - Lymphatic vessel response

A

Increased flow allows drainage of edema fluid and cellular debris
Occasionally lymphangitis/lymphadenitis occurs (secondary infection/inflammation of lymphatic vessels/lymph nodes)

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17
Q

Role of histamine mediation

A

Mast cell release

Vasodilation and increased vascular permeability

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18
Q

Role of nitric oxide mediation

A

Endothelial cell response to injury

Vasodilation

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19
Q

Bradykinin

A

Kinin system activation from endothelial injury

Vasodilation, increased permeability, and pain

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20
Q

Transudate

A

Hypocellular & low protein content

Non-inflammatory extravascular fluid, low specific gravity: <1.012

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21
Q

Exudate

A

Cellular and protein rich

Inflammatory extravascular fluid; high specific gravity: >1.020

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22
Q

Pus

A

Purulent exudate rich in leukocytes

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23
Q

Margination

A

Leukocyte accumulation at periphery of vessels

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24
Q

Rolling

A

Weak & transient adhesions to endothelium

Uses selectins

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25
Adhesion
Firm adhesion to endothelium | Uses integrins
26
Transmigration
Movement through endothelium to interstitium Diapedis (movement of leukocytes through vessel wall) Cells squeeze between endothelial cells
27
Chemotaxis
Movement towards injury site in the interstitium
28
Where is selectin found?
Endothelial (E-), Platelet (P-), Leukocyte (L-)
29
What on the leukocyte binds to selectin?
Sialyl-Lewis glycoprotein
30
What causes presentation of selectins?
Mediators (histamine, thrombin)
31
What kind of attachment does selectin do?
Loose attachment
32
Where is integrin found?
Leukocytes
33
How are integrins activated?
Chemokine expression on endothelial cells activate integrins
34
What kind of attachment does integrin do?
Stable attachment of leukocytes to endothelium
35
What drives transmigration?
CD31 (PECAM1) on leukocytes & endothelial cells
36
What are some chemotactic factors?
Chemokines, complement, leukotrienes
37
When are leukocytes activated?
After recruitment to site of injury
38
What do leukocytes do? (4 things)
Phagocytosis Intracellular destruction Release of substances that destroy tissue & microbes Increase mediator production
39
How are microbes recognized by leukocytes?
1) Specific surface receptors | 2) Opsonins (IgG, Complement, Lectins)
40
Steps of phagocytosis
1. Recognition and attachment 2,. Engulfment by phagocyte membrane around microbe 3. Phagosome fusion with lysosome 4. Oxidative burst 5. Secretion of enzymes into extracellular space to degrade microbes & dead tissue
41
Principal mediators of vasodilation
*Histamine *Nitric oxide Prostaglandins
42
Principal mediators increased vascular permeability
*Histamine *Bradykinin C3a, C5a Leukotrienes C4, D4, E4 Platelet activating factor Substance P
43
Principal mediators chemotaxis, leukocyte recruitment and activation
*IL-1, TNF *Bacterial products Chemokines C3a, C5a Leukotriene B4
44
Fever
IL-1, TNF, PGE2
45
Pain
*Bradykinin | Prostaglandins
46
Tissue damage
*ROS *Nitric oxide Lysosomal enzymes of leukocytes
47
What are the most common causes of leukocyte defects? (Specifically production, adhesion/taxis, phagocytosis/microbicidal)
Overall it is acquired causes not genetic Production: Bone marrow suppression Adhesion: Sepsis, diabetes, dialysis, malignancy Phagocytosis & microbicidal activity: Sepsis, diabetes, anemia, malnutrition
48
Possible outcomes of acute inflammation
Resolution Chronic inflammation Scarring or fibrosis
49
Serous inflammation
Mildest form of acute inflammation | Outpouring of thin fluid (protein-poor) from plasma or serosal cavity linings
50
Fibrinous inflammation
Occurs secondary to more severe injury | Larger vascular leaks, passage of fibrinogen, conversion to fibrin
51
Where does fibrinous inflammation affect?
Linings: Meninges, pericardium, pleura, peritoneum
52
Suppurative (purulent) inflammation
When large numbers of neutrophils are present, with necrotic cells, edema fluid and bacteria to form pus
53
What kind of bacteria are more likely to produce suppurative inflammation?
Pyogenic bacteria
54
Abscess
Central area of necrotic tissue surrounded by preserved neutrophils, vessels, fibroblasts
55
Ulcer
Sloughing of surface of an organ or tissue covering necrotic inflammatory tissue
56
Duration of chronic inflammation
Weeks to months to years | Active inflammation, tissue injury & healing occur at same time
57
Causes of chronic inflammation
Persistent infections Prolonged toxic exposure Immune-mediated inflammatory diseases (autoimmunity)
58
What happens to macrophages during chronic inflammation?
They persist Constant stimulation by dead cells, microbes, activated T cell cytokines (IFN-gamma) Resuls in continued tissue injury
59
What other cells are involved in chronic inflammation?
Lymphocytes Plasma cells Eosinophils Mast cells
60
What do lymphocytes do in chronic inflammation?
T&B migrate to site Respond to chemokines Interact with macrophages
61
What do plasma cells do in chronic inflammation?
Immunoglobulin production against persistent antigens
62
What do eosinophils do in chronic inflammation?
Release major basic protein which is toxic to parasites & epithelium
63
What do mast cells do in chronic inflammation?
Activated by IgE for environmental antigens Release histamine and arachidonic acid metabolites Central in allergic & anaphylactic reactions
64
Granulomatous inflammation (Morphology, Stimulus, Causes)
Morphology: Distinctive pattern of chronic inflammation with prominent macrophages with an epithelioid appearance. Formation of multinucleated giant cells due to IFN-gamma with a collar of lymphocytes and plasma cells Stimulus: Develop in response to specific infections, inert foreign bodies, autoimmunity Causes: Can be caused by infectious and non-infectious causes
65
What is the name for the systemic effects of inflammation?
Acute phase reaction or systemic inflammatory response syndrome (SIRS)
66
What are the major clinical changes due to SIRS?
Fever Elevated plasma levels of acute-phase proteins Leukocytosis
67
What is fever in response to?
Pyrogens (general term) Exogenous: LPS from bacteria Endogenous: IL-1, TNF release from leukocytes
68
What is the process of temperature change?
Prostaglandine (PGE2) release | Stimulates hypothalamus to increase temperature set point
69
What stimulates elevation of acute-phase proteins?
IL-6
70
What acute-phase proteins are formed?
C-reactive protein, Fibrinogen, Serum amyloid A protein
71
What actions do acute-phase proteins do?
Bind to microbe wall aiding in elimination | Fibrinogen binds to erythrocytes causing stacks (rouleaux) that sediment more rapidly than normal
72
What stimulates leukocytosis?
TNF & IL-1
73
Leukocytosis
WBC count increases typically 15,000-20,000 | Accelerated release of cells from bone marrow
74
What is the leukemoid reaction?
Extreme leukocytosis (>20,000)
75
Specific types of leukocytosis and underlying causes
Neutrophilia - Bacterial infection Lymphocytosis - Viral infections Eosinophilia - Allergies, asthma, parasitic Leukopenia - Typhoid, rickettsiae, some protozoans

FPP Weeks 1 & 2 (18 decks)

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