2.1 Acute inflammation, part 1

Question 1

What are the cells that are present in tissue during acute and chronic inflammation respectively?

Answer 1

Acute = PMNs
Chronic = Lymphocytes

Question 2

What are the two primary hallmarks of acute inflammation?

Answer 2

Edema and PMNs

Question 3

What are the two major causes of acute inflammation?

Answer 3

Infection and tissue necrosis

Question 4

What are the cells of the immune system that have TLRs? What is the role of TLRs?

Answer 4

• Macrophages and dendritic cells

- Recognize PAMPs

Question 5

What is the TLR that is on macrophages, and has the ability to recognize LPS?

Answer 5

CD14

Question 6

Where is LPS on gram negative bacteria?

Answer 6

Outer membrane

Question 7

What is the transcription factor that is upregulated with TLR activation? What does this do?

Answer 7

• NF-kappa B

- Leads to the production of multiple immune mediators

Question 8

True or false: TLRs are not present on lymphocytes, and therefore do have a role in chronic inflammation

Answer 8

False–they are on lymphocytes, and they do play a role in chronic inflammation

Question 9

Where is Arachidonic acid released from? What is the enzyme that mediates this?

Answer 9

Released from the phospholipid cell membrane by phospholipase A2

Question 10

What are the two pathways that arachidonic acid can gown down? What are the enzymes that mediate each pathway?

Answer 10

• COX for prostaglandins

- 5-Lipoxygenase for leukotrienes

Question 11

What are the prostaglandins that are mediate vasodilation, and increased vascular permeability?

Answer 11

PGI2
PGD2
PGE2

(“Help 2 DIE-ilate”)

Question 12

Which PG, in addition to mediating increased vascular permeability, mediates fever and pain?

Answer 12

PGE2

Question 13

Where do PG mediate vasodilation and increased vascular permeability respectively?

Answer 13

Vasodilation at the arterioles

Increased vascular permeability in the postcapillary venules

Question 14

What is the function of LTB4?

Answer 14

Attracts and activates PMNs

Question 15

What are the leukotrienes that mediate vasoconstriction, bronchospasm, and increased vascular permeability?

Answer 15

LTC4
LTD4
LTE4

Question 16

Which leukotriene activates PMNs?

Answer 16

LTB4

Question 17

What are the four primary PMN chemoattractants?

Answer 17

• LTB4
• C5a
• IL-8
• Bacterial products

Question 18

What are the function of LTC4, LTD4, and LTE4?

Answer 18

Smooth muscle contraction (bronchoconstriction, vasoconstriction)

Question 19

What is the function of the pericyte in endothelial cells?

Answer 19

Contraction of the vessels, to open up spaces between endothelial cells during edema

Question 20

Where are mast cells found?

Answer 20

Widely distributed throughout the CT of the body

Question 21

What are the three main mechanisms of activating mast cells?

Answer 21

• Tissue trauma
• Complement (C3a + C5a)
• Cross linking of surface IgE by antigen

Question 22

What is the immediate response of mast cell activation?

Answer 22

Release of preformed histamine causes vasodilation of arterioles and increased vascular permeability

Question 23

What are the components of the delayed response of mast cell activation?

Answer 23

Production of arachidonic acid metabolites (leukotrienes)

Question 24

How is complement normally found in the blood?

Answer 24

Inactive precursors in the blood

Question 25

DAF inactivates which complement components?

Answer 25

C4b and C3b

Question 26

What initiates the classical complement pathway?

Answer 26

C1 binds to IgG or IgM

Question 27

What initiates the alternative pathway?

Answer 27

C3 directly binds and activates complement

Question 28

What activates the lectin pathway?

Answer 28

Mannose binding lectin binds mannose on microorganisms, and activates complement

Question 29

Where do all three of the complement pathways converge? What does this do?

Answer 29

C3 convertase, to generate C3a and C3b

Question 30

What is the most common complement deficiency?

Answer 30

C2

Question 31

What is the defect in paroxysmal hemoglobinuria?

Answer 31

-Loss of CD55 (DAF) d/t loss of GP anchor)

Question 32

How is C5 convertase activated? What does this do?

Answer 32

From C3b

C5 convertase produces C5a and C5B to help produce the MAC

Question 33

What is the major function of C5a?

Answer 33

Chemotactic factor for PMNs

Question 34

What is the major function of C3b?

Answer 34

Opsonin for phagocytosis

Question 35

What is the function of the MAC?

Answer 35

Lyses microbes by creating holes in the cell membrane

Question 36

Which complement if associated with GMN?

Answer 36

C3

Question 37

What is Hageman factor? What activates it?

Answer 37

Inactive proinflammatory protein produced in the liver, that is activated upon exposure to subendothelial or tissue collagen

Question 38

Why does gram - Sepsis lead to DIC?

Answer 38

Gram negative bacteria can activate Hageman factor

Question 39

What is the function of Hageman factor?

Answer 39

• Activates the coagulation and fibrinolytic systems
• Activates the complement system
• Activates Kinin system

Question 40

What is the Kinin system that is activated by Hageman factor?

Answer 40

Hageman cleaves HMWK to bradykinin, which mediates vasodilation, pain, and increased vascular permeability

Question 41

What are the two major inflammatory cytokines that mediate pain? MOA?

Answer 41

PGE2
Bradykinin

Sensitive sensory nerve endings

Question 42

What are the key mediators of Rubor and calor? (3)

Answer 42

Histamine
PGs
Bradykinin

Question 43

What are the two major mediators of swelling?

Answer 43

Histamine

Tissue damage

Question 44

Where does leakage of fluid occur with edema?

Answer 44

Post capillary venule

Question 45

What are the cells that release IL-1 and TNF to cause fever?

Answer 45

Macrophages

Question 46

What is the MOA of IL-1 and TNF to produce fever?

Answer 46

Increased COX activity in the perivascular cells of the hypothalamus produces PGE2 to increase set point of hypothalamus