Acute Inflammation

Question 1

What are the cardinal features of inflammation?

Answer 1

rubor, calor, tumor, dolor

loss of function

Question 2

What is acute inflammation?

Answer 2

the reaction of vascularized tissue to injury

Question 3

What are the factors interacting in acute inflammation?

Answer 3

pathogen/injury
host inflammatory cells
complement/coagulation cascades
chemokines/cytokines

Question 4

Acute inflammation is an immediate tissue reaction characterized by the accumulation of what?

Answer 4

fluid, plasma proteins, innate immune cells

Question 5

What is the intensity of an acute inflammatory response determine by?

Answer 5

the stimulus, the duration of the stimulus, the genetics of the host, and medical interventions

Question 6

What are 4 causes of inflammation?

Answer 6

infections, necrosis, foreign bodies, immune reactions

Question 7

What does the innate immune system recognize, and how do they respond?

Answer 7

DAMPS/PAMPS activate TLRs/other recognition factors, forming the inflammasome

Question 8

What is the inflammasome?

Answer 8

A multi-protein complex characterized by activation of CASPASE 1

Question 9

What sets inflammatory cytokines into action?

Answer 9

cleavage of IL-1 to its active form (IL-1beta)

Question 10

What is the vasculature regulated by?

Answer 10

cytokines, chemokines, other inflammatory mediators

Question 11

What does NO do?

Answer 11

mediates vasodilation which increases blood flow and increases vascular permeability

Question 12

What do changes in the endothelium allow

Answer 12

cytokine/chemokine induced endothelial changes allow innate cells access to the inflammatory site

Question 13

describe the sequence of events of a leukocyte homing to a tissue

Answer 13

marginate to the outer parts of a vessel

rolling adhesion

tight binding

diapedesis

migration

Question 14

What are the interactions between a leukocyte and vessel endothelium?

Answer 14

E and P selectins on epithelium interact with SL-X glycoproteins on the leukocyte (rolling)

CXCL8R (IL-8 receptor) on leukocyte interacts with CXCL8R (IL-8), and LFA-1 on leukocyte interacts with ICAM-1 on epithelium (tight binding)

Question 15

How do PMNs move from a blood vessel to a point of injury?

Answer 15

chemotaxis due to bacterial peptides, complement proteins (esp. C5a), and the pro-inflammatory cytokine tetrad

Question 16

How does a leukoocyte move to the site of inflammation?

Answer 16

chemoattractants activate membrane receptors that activates the cytoskeleton (esp. actin)

Question 17

What is the second phase in an inflammatory response?

Answer 17

monocyte/macrophage recruitment, secretion of cytokine/chemokines

Question 18

What is the third phase of an inflammatory response?

Answer 18

inhibition of further neutrophil activation

Question 19

What inhibits continual neutrophil activation?

Answer 19

apoptotic neutrophils

Question 20

What are the distinction of the nomenclature of monocytes?

Answer 20

monocytes are in the blood, when it enters a cavity it becomes a macrophage, when it’s in a tissue it’s a histiocyte

Question 21

What is the sequence of cellular traffic in inflammation?

Answer 21

Edema, neutrophils, monocytes/macrophages

Question 22

What is the signature cell of acute inflammation?

Answer 22

neutrophils

Question 23

What is the most numerous leukocyte in circulation?

Answer 23

neutrophils

Question 24

What is the half life of neutrophils in blood vs tissue?

Answer 24

~12’ in blood, 1-2” at inflammatory site

Question 25

What is a left shift/bandemia?

Answer 25

immature neutrophils are in the blood (marrow responds to infection by pushing out mature and slightly immature PMNs)

Question 26

What are the 5 functions of neutrophils at the site of injury?

Answer 26

phagocytosis

recognition/attachment: Antibody & C3b coating bind the pathogen to FcR and C3bR

engulfment/degranulation: Formation of the phagolysosome

killing/degradation: Oxidative burst that generates killing molecules

NETS: Chromatin spray to the outside of the cell to trap bacteria and fungi

Question 27

How does the oxidative burst work?

Answer 27

activation of NADPH generated H2O2

lysosomal enzymes donate MPO (myeloperoxidase)

MPO + halide - HOCl

Question 28

What cytokines is phase IV characterized by?

Answer 28

TGF-beta and IL-10

Question 29

What is phase IV of an inflammatory reaction?

Answer 29

scavenging of apoptotic neutrophils promotes macrophage growth factors and repair

Question 30

What is the control of acute inflammation highly dependent on?

Answer 30

macrophages

Question 31

No TLR or phagocytic receptor activation leads to what?

Answer 31

Decreased pro-inflammatory mediator synthesis and release -

Macrophages sense this as they clean up dying neutrophils

Question 32

What is serous inflammation?

Answer 32

Least severe

Protein poor fluid from capillary to a space: peritoneal, pericardial or pleural.

Known clinically as a transudate

Question 33

What is fibrinous inflammation?

Answer 33

intermediate severity

Fluid with larger molecules dominated by fibrinogen which converts to fibrin and potential scarring

Question 34

What is suppurative/abscess inflammation?

Answer 34

most severe

Protein rich fluid with inflammatory cell, alive and dead necrotic debris.

Known clinically when in a body space as an exudate

Question 35

What is ulcerative inflammation?

Answer 35

underlying inflammation that causes excavation of a mucosal or skin surface