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IHP 1001 > Ch.2 Acute inflammation > Flashcards

Ch.2 Acute inflammation Flashcards

1
Q

To stimulate and permit inflammatory cells as well as plasma proteins (complement) and fluid to migrate out of blood vessels and into the target interstitial space.

A

Inflammation

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2
Q

Inflammation helps rid host cell of the ____ cause of cell injury (microbes & toxins) and the _______ of injury (necrotic cells & tissues) + initate _____ of tissues

A

Rid of initial cause and consequences, initiate repair

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3
Q

What are he two phases of inflammation?

A

Acute (start) and chronic inflammation

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4
Q

rapid response to infections and tissue damage

A

Acute inflammation

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5
Q

Presence of edema & neutrophils in tissue=

A

Acute inflammation

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6
Q

leakage of fluid and plasma proteins into the interstitial or serous cavities. Exudate or transudate

A

edema

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7
Q

If there is failure to clear the stimulus inflammation progresses to a protracted phase called ____ inflammation

A

Chronic

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8
Q

longer duration and is associated with continuing tissue destruction and fibrosis (the deposition of connective tissue).

A

Chronic inflammation

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9
Q

Acute or chronic?

mainly neutrophils

A

Accute

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10
Q

Acute or chronic?

monocytes / macrophaes & lymphocytes

A

Chronic

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11
Q

Acute or chronic?

Mild & self limited tissue injury

A

Acute

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12
Q

Acute or chronic?

May be significant injury

A

Chronic

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13
Q

Acute or chronic?

no fibrosis

A

Accute

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14
Q

Acute or chronic?

May be severe/progressive fibrosis

A

Chronic

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15
Q

Acute or chronic?

Requires gene activation

A

chronic, slow.

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16
Q

What are the 5 external manifestations of inflammation?

A

Heat, redness, swelling, pain, & loss of function.

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17
Q

5 Steps of inflammatory run

A
  1. Recognition
  2. Recruitment
  3. Removal
  4. Regulation
  5. Repair
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18
Q

Acute or chronic?

Glomerulunphritis, vasculitis (antibodies & complement, neutrophils)

A

Acute

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19
Q

Acute or chronic?

Septic shock (cytokienes)

A

Acute

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20
Q

When cytokines overwhelm the buffering system of body, HYPOTENSION .

A

Septic shock

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21
Q

Acute or chronic?

Rheumatoid Arthritis (lymphocytes, macro, antibodies)

A

chronic

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22
Q

Acute or chronic?

Asthma (IgE, eosinophils)

A

Chronic

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23
Q

Acute or chronic?

Pulmonary fibrosis (Mac, fibroblasts)

A

Chronic

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24
Q

Acute or chronic?

Acute respiratory distress syndrome (neutrophils)

A

Acute

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25
Q

Inadequate inflammation is manifested how?

A

Increased susceptibility to infections

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26
Q

-Reduced production of leukocytes
-Immunosuprrsive ages
-Malnutrition

Are all what?

A

Things that impair inflammation

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27
Q

Are local and systemic signs of acute inflammation low or high? and why?

A

High b.c presence of signal still there

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28
Q

Are local and systemic signs of chronic inflammation low or high? and why?

A

Low/variable because signal strength change over time, so its harder to detect,

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29
Q

-Infection (microbe)
-tissue necrosis (molecules released trigger)
-foreign bodies(sutures, tissue implants)
-Immune reactions (hypersensitivities)

are all what?

A

Causes of inflamation

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30
Q

The first step is : ____ of microbs and nectrotic cells by cellular receptors and circulating proteins.

A

Recognition

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31
Q

Most important resident cells who function is to detect the presence of foreign invader, ingest & destroy

Then illicit inflammatory response by recruiting cells & proteins from blood to complete elimination process

A

macrophages & dendritic cells

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32
Q

Step?

Injury or infection

Releases chemoattractant agent molecules (chemotaxis) that alert immune cell in vicinity of the need of inflammatory cells

A

Step Zero.

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33
Q

Activation of ___ leads to production of cytokines that trigger inflamation

A

Toll-like receptors

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34
Q

Macrophages have _____ on their (1) surface, in the (2) extracellular space; in endosomes, into which microbes are ingested; and ion (3) cytosol

A

TLRs

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35
Q

recruit and activate a multiprotein complex (the inflammasome) which generates the biologically active cytokine interleukin-1 (IL-1).

A

NOD like receptors (NLRs)

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36
Q

Causes redness (erythema) and warmth in acute

A

Vasodilation

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37
Q

What is the most important chemical mediator in vasodilatation?

A

Histamine

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38
Q

Follow vasodilatation

outpouring of protein-rich fluid into the extravascular tissues

A

increased permeability of the microvasculature

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39
Q

escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities

A

Exudation

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40
Q

Extravascular fluid that is high in protein and contains cellular debris

A

Exudate

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41
Q

What does the presence of exudate imply?

A

That there is increased permeability in small blood vessels typically during inflammatory rxn.

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42
Q

a fluid with low protein content (most of which is albumin), little or no cellular material, and low specific gravity.

A

Transudate

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43
Q

What is produced as a result of osmotic or hydrostatic pressure imbalances across vessel wall?

not associated with vas. permeability or inflamation

A

Trasudate

44
Q

A purulent inflammatory exudate, rich in leukocytes (neutrophils) debris of dead cells, microbs

A

Pus

45
Q

Contraction of endothelial cells, creating inter0endothelial opening

is the primary mechanism to what?

A

Increased vascular permeability

46
Q

Histamine, bradykinin, leukotrienes + others all elicit what?

rapid after exposure, short lived.

A

Increase vascular permeability

47
Q

What does increased vascular permeability result in?

A

-slower blood flow
-Higher viscosity of blood b/c more RBCs
-Localized redness of tissues

48
Q

Normal condition= blood has laminar flow, red cells incenter, leukocytes towards vessel walls.

Stasis (early inflammation) -> increase caliper of vessels, blod flow slows, leukocytes are larger than red cells, slow down more.

Leukocytes assume a peripheral position along endothelial surfacem

A

Step 1, Margination

49
Q

When endothelial cells are activated by cytokines/other mediators produced locally, they express adhesion molecules to which _____ attach loosely

What step?

A

Leukocytes

Step 2: rolling

50
Q

receptors expressed on leukocytes and endothelium that have an extracellular domain that binds carbohydrates

A

Selectins

51
Q

Edothelial cells express two selectins, ___ - and ___-selectins, as well as the ligand for L-selectin, whereas leukocytes express L-selectin

A

E and P selectin
They are expressed in low amount but unregulated after stimulation by cytokines

52
Q

If endothelium area has not received signal for activation (cytokines) then ____ and ____ are not there or expressed in low amounts

A

E and P selectin

53
Q

binding of _____ is largely restricted to endothelium at sites of infection or tissue injury (where the mediators are produced)

A

Leukocytes

54
Q

Found primarily in intracellular membrane-bound vesicles called Weibel-Palade bodies

BUT

Following exposure to mediations (histamines), traffics to cell surface.

A

P-selectin

55
Q

___ and ___ _induced after stimulation by the cytokines IL-1 and tumor necrosis factor (TNF) from tissue macrophages .

Mediate initial weak leukocyte binding to endothelium

Not normally expressed on normal endothelium

__ is stimulated on the leukocyte

A

E-selecting and P-selectin endothelium ‘
L-selectin on leukocyte

56
Q

_____ mediated interaction have low affinity, easily shut off by flowing blood so, there’s a bind & detach process until proper adhesion can occur

Leukocyte (sialyl lewis X) bind selecting, handshake !

A

Selectin- mediated interactions

57
Q

What does this show ?

A

Multistep process of leukocyte migration through vessels

58
Q

Mediate firm adhesion of leukocytes to endothelium.

leukocyte surface protein family

A

Integrins

59
Q

transmembrane two-chain glycoproteins that mediate the adhesion of leukocytes to endothelium and of various cells to the extracellular matrix

A

Integrins

60
Q

What activates intengrin to switch to high affinity form for leukocytes?

A

Chemokies

61
Q

chemoattractant cytokines that are secreted by many cells at sites of inflammation, bind to endothelial cell proteoglycans

A

Chemokines

62
Q

Cytokines that activate endothelial cells to increase their expression of ligands for integrins.

A

TNF and IL-1

63
Q

C5a and LTB4 do what to integrins?

They mediate firm adhesion of leukocyte to endothelium following weak connection btwn leukocyte and selectins

A

Up-regulate them to become high affinity

64
Q

What is the result of impaired leukocyte adhesion and defective inflammation.

A

result in recurrent bacterial infections

65
Q

-Delayed separation of umbilical cord
-High # of circulating neutrophils
-Recurrent bacterial infection, can’t form pus

All results of what? Autosomal recessive

A

Leukocyte adhesion disorder (LAD) that affects their adhesion to endothelial surface.

66
Q

extravasation of leukocytes following adhesion

A

Transmigration (diapedesis)

67
Q

Cellular adhesion molecule expressed on leukocytes, mediate the binding event needed for leukocyte to traverse the endothelium.

A

PECAM-1 (CD31)

68
Q

locomotion along a chemical gradient produced by chemotactic agents that started the process.

A

chemotaxis

69
Q

Bacterial product Peptides, cytokines, C5a from complement, and leukotrienes are all what?

A

chemoattractants

70
Q

What is produced in response to infections and tissue damage and during immunologic reactions,

bind G-protien leukocyte receptors

A

Chemoattractants

71
Q

neutrophils predominate in the inflammatory infiltrate during the first 6 to 24 hours and are replaced by monocytes in 24 to 48 hours

(left red= neutrophils) (right red= macrophages)

A

Acute inflammation

72
Q

What causes cellular infiltrate:

dominated by continuously recruited neutrophils for several days

A

Pseudomonas bacteria

73
Q

What causes cellular infiltrate:

lymphocytes may be the first cells to arrive

A

Viral infections

74
Q

What causes cellular infiltrate:

dominated by activated lymphocytes, macrophages, and plasma cells (reflecting the immune response

A

Hypersensitivities

75
Q

What causes cellular infiltrate:

eosinophils may be the main cell type.

A

Allergic reactions or certain parasites

76
Q

Blocking of what cytokine?

is extremely useful therapeutics for chronic inflammatory diseases such as rheumatoid arthritis

A

TNF

77
Q

the ingestion of particulate material by cells.

A

Phagocytosis

78
Q

Neutrophils (short lived) & macrophages (long-lived, slower response) are what ?

A

Phagocytes

79
Q

antibodies (IgG), the C3b cleavage product of complement, and certain plasma lectins which

all coat microbs and allow for more efficient phagocytosis

A

Opsonins

80
Q

Membrane bound vesicle that inject micron and fuses with lysosome=

Psuedopodes extend from leukocytes to form these

Merging with lysosome=

A

phagosome

Phagolysosome

81
Q

Problem in protien trafficking (autosome recessive) which affects formation of phagolysososme

Clinical features similar to LAD, more pyrogenic infection (pus forming), BUT (neutropina, death of neutrophils)

A

Chediak-Higashi Syndrome

82
Q

Inter medullary death of neutrophils, low count in blood.

A

Neutropina

83
Q

Killing of microbes and destruction of ingested materials are accomplished by

A

Reactive oxidative species (ROS) & nitrogen species (RNS)

84
Q

What method of killing I most effective mechanism for killing microbes?

A

O2 Dependent killing (done by Neutrophils)

85
Q

Neutrophil or macrophage?

1-2 days, rapid short lived, O2 killing, prominent secretion of lysosomal enzymes

A

Neutrophil

86
Q

Neutrophil or macrophage?

Days/weeks, slow, dependent on gene transcription activation of cytokine genes.

A

Macrophages

87
Q

What 3 things do neutrophils and macrophages share in common?

A

-Phagocytois
-Migrate through blood vessels
-Chemotaxis

88
Q

O2 converted into O2- by NDAPH oxidase

this processes is called what?

A

Oxidative Burst

89
Q

What does an oxidative burst do?

A

Supply electron to an NADPH oxidase in the phagosomal membrane

90
Q

Once a neutrophil is activated what enzyme is rapidly assembled in the membrane of the phagylosome to bind in O2 dependent killing?

A

NADPH oxidase

91
Q

Following oxidative burst, O2- Is converted into H2O2 via what enzyme?

A

Superoxide Dismutase (SOD)

92
Q

H2O2 is finally converted to HOCL (bleach) by what enzyme in O2 dependent killing?

A

Myleperoxidase MPO

93
Q

A potent antimicrobial agent that destroys microbes by halogenation or via oxidation of proteins and lipids

A

HOCL

94
Q

What inflammatory cell up regulates NOS in order for it to participate in microbial Killing?

A

Macrophages

95
Q

1 of the 2 types of granules in Neutrophils
contain lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and alkaline phosphatase.

A

Specific (secondary) granule

96
Q

1 of the 2 types of granules in Neutrophils
contain myeloperoxidase, bactericidal factors (such as defensins), acid hydrolases, and a variety of neutral proteases (elastase, cathepsin G, nonspecific collagenases, proteinase 3).

A

Azurophil (primary) granule

97
Q

Macrophages contain _____ filled with
acid hydrolases, collagenase, elastase, and phospholipase, all of which can destroy ingested materials and cell debris

A

Lysozymes

98
Q

activated neutrophils liberate chromatin components, including histones, which form fibrillar networks called

A

neutrophil extracellular traps (NETs)

99
Q

NETs in blood during sepsis Is a consequence of what?

A

Widespread neutrophil activation

100
Q

Disease characterized by by poor O2 dependent killing pathway
due to NADPH oxidase defect.

A

Chronic Granulomatous Disease (CDG) (X-linked or AR)

101
Q

CDG leads to recurrent infection and granuloma formation with what kind of organism?

A

Catalase (+) organisms

ex. Staph Aureus , Serratia Marcessens, Aspergillus

102
Q

____ definceny results in defective conversion of H2O2 to HOCL

A

MPO

103
Q

MPO definceny causes increase risk of what kind of infections, with no symptoms?

A

Candida

104
Q

Less effective killing, uses 2nd enzymes housed in leukocyte 2nd granules ex. lysozyme in macrophages & eosinophils

A

O2 INdependent killing

105
Q

What is the final step once all infection has been cleared in acute inflammation?

A

Neutrophils undergo apoptosis within 24hr of dissipation of initial inflammatory signal.

106
Q
A

IHP 1001 (18 decks)

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