Local Inflammation

Question 0

chronic inflammation

Answer 0

inflammation of prolonged duration (weeks to yrs)

Question 1

acute inflammation

Answer 1

immediate & early response to cell injury (min to few days)

Question 2

sentinel cells

Answer 2

resident tissue cells on epithelial surfaces

Question 3

function of sentinel cells

Answer 3

1. recognize PAMPs/DAMPs via cellular receptors

2. Release signaling molec. that recruit & activate other cells (effector cells)

Question 4

Types of Sentinel cells

Answer 4

1. Epithelial cells
2. Mast cells
3. Macrophages
4. Dendritic Cells

Question 5

Mast Cells

Answer 5

tissue cells w/ specialized granules that store some key inflammatory mediators

Question 6

Dendritic cells

Answer 6

• tissue cells w/ long, slender branching cytoplasmic processes.
• specialized to capture antigens, present them to T-cells, & initiate adaptive immune response.
• recognize pathogens
• release inflammatory mediators

Question 7

Chemical mediators of acute inflammation

Answer 7

1. Complement C3a & C5
2. histamine
3. prostaglandin E2
4. leukotriene B4
5. Il-1, TNF-a
6. chemokines
7. bacterial peptides

Question 8

Complement

Answer 8

Function: activate mast cells
Origin: Plasma
Source: Plasma

Question 9

C3a + C5

Answer 9

Function: activate mast cells, chemotaxis
Origin: Tissue fluids
Source: Tissue fluids

Question 10

histamine

Answer 10

Function: vasodilation, increase vascular permeability
Origin: Pre-formed
Source: mast cells
Inhibited by: antihistamines, glucocorticoids

Question 11

prostaglandin E2

Answer 11

Function: enhances vasodilation
Origin: Cellular Synthesis
Source: mast cells, macrophages, other cells
Inhibited by: NSAIDs, glucocorticoids

Question 12

leukotriene B4

Answer 12

Function: chemotaxis
Origin: cellular synthesis
Source: mast cells, macrophages, other cells
Inhibited by: NSAIDs (some), glucocorticoids

Question 13

IL-1, TNF-a

Answer 13

Function: induce endothelial adhesion molecules
Origin: cellular synthesis
Source: Mast cells, macrophages, other cells
Inhibited by: glucocorticoids

Question 14

chemokines

Answer 14

Function: chemotaxis
Origin: cellular synthesis
Source: many cells
Inhibited by: glucocorticoids

Question 15

bacterial peptides

Answer 15

Function: chemotaxis
Origin: bacterial
Source: bacteria

Question 16

Microvascular Events of Inflammation

Answer 16

1. Vasodilation
2. Endothelium leaky to plasma & plasma proteins
3. Diapedesis (leukocytes exit from venules)
4. Neutrophils emigrate initially b/c of lg #s
5. Monocytes & lymphocytes emigrate

Question 17

How do you tell how long inflammation has been present?

Answer 17

the types of cells present in the tissue

Question 18

Vasodilation

Answer 18

Consequence: redness
Functional role: ^ blood flow to infection site
Mechanism: relaxation of pre-capillary sphincter in arterioles

Question 19

Chemical Mediators of Vasodilation

Answer 19

histamine, serotonin, prostaglandin E2

Question 20

Increased Vascular Permeability

Answer 20

Consequence: Swelling
Functional Role: recruitment of antimicrobial plasma proteins
Mechanism: several mechansims, including gaps b/n endothelial cells

Question 21

Chemical mediators of increased vascular permeability

Answer 21

histamine

Question 22

Leukocyte Emigration

Answer 22

Consequence: Pus formation
Functional Role: recruit phagocytes
Mechanism: (1) adhesion to endothelium. (2) diapedesis. (3) chemotaxis

Question 23

Chemical mediators of Leukocyte Emigration

Answer 23

Adhesion: histamine, serotonin, IL-1, TNF-a

Chemotaxis: chemokines, C5a, leukotriene B4, bacterial peptides

Question 24

Inflammatory cytokines that act locally & distant

Answer 24

IL-1, TNF-a, IL-6, G-CSF

Question 25

CNS effects of acute inflammation

Answer 25

fever, lethargy/somnolence, appetite loss, induction of glucocorticoid synthesis by adrenal cortex

Question 26

Acute-Phase proteins

Answer 26

• proteins whose [plasma] ^ during acute inflammation

- made by hepatocytes

Question 27

functions of Acute-Phase proteins

Answer 27

1. Amplify host defenses
2. PAMP recognition –> opsonization &/or complement activation
3. Microbial killing (C3 & C4)
4. Regulate host defenses (limit inflammation location)
5. assist in tissue repair (fibrinogen)

Question 28

Leukocytosis

Answer 28

elevated WBC count

caused by G-CSF

Question 29

When would Systemic inflammatory responses most likely occur?

Answer 29

• infections of certain organs (uterus)
• severe local infections w/ certain pathogens
• bacteria/fungi in bloodstream
• severe traumatic tissue damage, even in absence of infection

Question 30

Systemic Inflammatory Response Syndrome (SIRS)

Answer 30

clinical manifestation of systemic response to injury

Question 31

Spesis

Answer 31

SIRS in association w/ bacterial, viral, protozoal, or fungal infection

(SIRS + infection)

Question 32

Severe Sepsis

Answer 32

sepsis + evidence of organ dysfunction, hypoperfusion, or hypotension

Question 33

Septic Shock

Answer 33

sepsis + hypotension despite adequate fluid resuscitation

Question 34

Multiple Organ Dysfunction Syndrome (MODS)

Answer 34

altered organ function in acutely ill patient

Question 35

Things involved in sepsis

Answer 35

cells (leukocytes, mast cell lymphocytes)
cytokines & chemokines
plasma enzyme systems (complement, coagulation, contact activation)
acute-phase proteins
organs

Question 36

TNF-a

Answer 36

-its serum concentrations positively correlate w/ death in certain types of sepsis. (ie. parvo)

Question 37

IL-1

Answer 37

synergizes w/ TNF-a in early sepsis.

could correlate w/ death at certain [serum]