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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
Q

Adhesion

A

Firm adhesion to endothelium

Uses integrins

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26
Q

Transmigration

A

Movement through endothelium to interstitium
Diapedis (movement of leukocytes through vessel wall)
Cells squeeze between endothelial cells

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27
Q

Chemotaxis

A

Movement towards injury site in the interstitium

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28
Q

Where is selectin found?

A

Endothelial (E-), Platelet (P-), Leukocyte (L-)

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29
Q

What on the leukocyte binds to selectin?

A

Sialyl-Lewis glycoprotein

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30
Q

What causes presentation of selectins?

A

Mediators (histamine, thrombin)

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31
Q

What kind of attachment does selectin do?

A

Loose attachment

32
Q

Where is integrin found?

A

Leukocytes

33
Q

How are integrins activated?

A

Chemokine expression on endothelial cells activate integrins

34
Q

What kind of attachment does integrin do?

A

Stable attachment of leukocytes to endothelium

35
Q

What drives transmigration?

A

CD31 (PECAM1) on leukocytes & endothelial cells

36
Q

What are some chemotactic factors?

A

Chemokines, complement, leukotrienes

37
Q

When are leukocytes activated?

A

After recruitment to site of injury

38
Q

What do leukocytes do? (4 things)

A

Phagocytosis
Intracellular destruction
Release of substances that destroy tissue & microbes
Increase mediator production

39
Q

How are microbes recognized by leukocytes?

A

1) Specific surface receptors

2) Opsonins (IgG, Complement, Lectins)

40
Q

Steps of phagocytosis

A
  1. Recognition and attachment
    2,. Engulfment by phagocyte membrane around microbe
  2. Phagosome fusion with lysosome
  3. Oxidative burst
  4. Secretion of enzymes into extracellular space to degrade microbes & dead tissue
41
Q

Principal mediators of vasodilation

A

*Histamine
*Nitric oxide
Prostaglandins

42
Q

Principal mediators increased vascular permeability

A

*Histamine
*Bradykinin
C3a, C5a
Leukotrienes C4, D4, E4
Platelet activating factor
Substance P

43
Q

Principal mediators chemotaxis, leukocyte recruitment and activation

A

*IL-1, TNF
*Bacterial products
Chemokines
C3a, C5a
Leukotriene B4

44
Q

Fever

A

IL-1, TNF, PGE2

45
Q

Pain

A

*Bradykinin

Prostaglandins

46
Q

Tissue damage

A

*ROS
*Nitric oxide
Lysosomal enzymes of leukocytes

47
Q

What are the most common causes of leukocyte defects? (Specifically production, adhesion/taxis, phagocytosis/microbicidal)

A

Overall it is acquired causes not genetic
Production: Bone marrow suppression
Adhesion: Sepsis, diabetes, dialysis, malignancy
Phagocytosis & microbicidal activity: Sepsis, diabetes, anemia, malnutrition

48
Q

Possible outcomes of acute inflammation

A

Resolution
Chronic inflammation
Scarring or fibrosis

49
Q

Serous inflammation

A

Mildest form of acute inflammation

Outpouring of thin fluid (protein-poor) from plasma or serosal cavity linings

50
Q

Fibrinous inflammation

A

Occurs secondary to more severe injury

Larger vascular leaks, passage of fibrinogen, conversion to fibrin

51
Q

Where does fibrinous inflammation affect?

A

Linings: Meninges, pericardium, pleura, peritoneum

52
Q

Suppurative (purulent) inflammation

A

When large numbers of neutrophils are present, with necrotic cells, edema fluid and bacteria to form pus

53
Q

What kind of bacteria are more likely to produce suppurative inflammation?

A

Pyogenic bacteria

54
Q

Abscess

A

Central area of necrotic tissue surrounded by preserved neutrophils, vessels, fibroblasts

55
Q

Ulcer

A

Sloughing of surface of an organ or tissue covering necrotic inflammatory tissue

56
Q

Duration of chronic inflammation

A

Weeks to months to years

Active inflammation, tissue injury & healing occur at same time

57
Q

Causes of chronic inflammation

A

Persistent infections
Prolonged toxic exposure
Immune-mediated inflammatory diseases (autoimmunity)

58
Q

What happens to macrophages during chronic inflammation?

A

They persist
Constant stimulation by dead cells, microbes, activated T cell cytokines (IFN-gamma)
Resuls in continued tissue injury

59
Q

What other cells are involved in chronic inflammation?

A

Lymphocytes
Plasma cells
Eosinophils
Mast cells

60
Q

What do lymphocytes do in chronic inflammation?

A

T&B migrate to site
Respond to chemokines
Interact with macrophages

61
Q

What do plasma cells do in chronic inflammation?

A

Immunoglobulin production against persistent antigens

62
Q

What do eosinophils do in chronic inflammation?

A

Release major basic protein which is toxic to parasites & epithelium

63
Q

What do mast cells do in chronic inflammation?

A

Activated by IgE for environmental antigens
Release histamine and arachidonic acid metabolites
Central in allergic & anaphylactic reactions

64
Q

Granulomatous inflammation (Morphology, Stimulus, Causes)

A

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
Q

What is the name for the systemic effects of inflammation?

A

Acute phase reaction or systemic inflammatory response syndrome (SIRS)

66
Q

What are the major clinical changes due to SIRS?

A

Fever
Elevated plasma levels of acute-phase proteins
Leukocytosis

67
Q

What is fever in response to?

A

Pyrogens (general term)
Exogenous: LPS from bacteria
Endogenous: IL-1, TNF release from leukocytes

68
Q

What is the process of temperature change?

A

Prostaglandine (PGE2) release

Stimulates hypothalamus to increase temperature set point

69
Q

What stimulates elevation of acute-phase proteins?

A

IL-6

70
Q

What acute-phase proteins are formed?

A

C-reactive protein, Fibrinogen, Serum amyloid A protein

71
Q

What actions do acute-phase proteins do?

A

Bind to microbe wall aiding in elimination

Fibrinogen binds to erythrocytes causing stacks (rouleaux) that sediment more rapidly than normal

72
Q

What stimulates leukocytosis?

A

TNF & IL-1

73
Q

Leukocytosis

A

WBC count increases typically 15,000-20,000

Accelerated release of cells from bone marrow

74
Q

What is the leukemoid reaction?

A

Extreme leukocytosis (>20,000)

75
Q

Specific types of leukocytosis and underlying causes

A

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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