2-Acute/Chronic inflammation

Question 1

main cells of acute inflammation

Answer 1

neutrophils

Question 2

main cells of chronic inflammation

Answer 2

lymphocytes and macrophages

Question 3

acute inflammation

Answer 3

early response to tissue damage

• vasodilation
• vascular leakage and edema
• leukocyte emigration (PMNs)

Question 4

acute inflammation: vasodilation

Answer 4

• accounts for warmth and redness (rubor, calor)
• opens microvascular beds
• increased intravascular pressure causes an early transudate into interstitium-tumor

Question 5

transudate

Answer 5

protein-poor filtrate of plasma

Question 6

vascular leakage

Answer 6

• transudate gives way to exudate (protein rich)
• increases interstitial osmotic pressure
• edema

Question 7

transmigration

Answer 7

• (diapedesis)
• occurs after firm adhesion via CD31
• collagenases
• intergrins
• early in inflammatory response mostly PMNs, later monocytes and lymphocytes

Question 8

Chemotaxis

Answer 8

• Leukocytes follow chemical gradient to site of injury

- bacterial products, complement components (C5a), cytokines (eg IL-8),

Question 9

pseudopods

Answer 9

• extended by leukocytes

- they express integrins that bind ECM during chemotaxis

Question 10

Once at the site of injury, leukocytes:

Answer 10

• recognize and attach
• engulf (form phagocytic vacuole)
• kill (degrade)

Question 11

How do leukocytes recognize and bind?

Answer 11

corresponding receptors on leukocytes (FcR, CR1, 2, 3) bind to immunoglobulins from opsonized serum complement (C3b, and Fc portion of IgG)

Question 12

Phagolysosome

Answer 12

after engulfment which forms vacuole, the vacuole fuses with lysosomal granule membrane

Question 13

degranulation

Answer 13

granules discharge within phagolysosome and extracellularly

Question 14

Oxidative burst

Answer 14

• increased oxygen constumptoin
• glycogenolysis (glycogen breakdown)
• increased glucose oxidation
• formation of superoxide ion

Question 15

how is an oxidant/antimicrobial agent (“bleach”) made?

Answer 15

MPO (axurophilic granules) converts hydrogen peroxide to HOCl- which is the “bleach”

Question 16

premature degranulation causes:

Answer 16

leukocyte-induced tissue injury (destructive enzymes enter extracellular space)

Question 17

causes of leukocyte-induced tissue injury

destructive enzymes enter extracellular space when:

Answer 17

• premature degranulation
• frustrated phagocytosis (large, flat)
• membranolytic substances (urate crystals)
• persistent leukocyte activation (RA, emphysema)

Question 18

Defects of leukocyte adhesion:

Answer 18

1. LFA-1 and Mac-1 (integrins) subunit defects=”leukocyte adhesion deficiency” or LAD-1
   - these patients have recurrent bacterial infections with impaired wound healing
2. absence of sialyl-Lewis X, and defect in E- and P- selectin sugar epitopes (LAD-2)
   - more mild than LAD-1 but still have recurrent bact infections

Question 19

defects of leukocyte chemotaxis/phagocytosis:

Answer 19

• microtubule assembly defect leads to impaired locomotion and lysosomal degranulation
• neutropenia, defective neutrophil degranulation, delayed microbial killing, recurrent bacterial infections

Question 20

defects of leukocute funciton: defects of microbicidal activity:

Answer 20

• deficiency of NADPH oxidase that generates superoxide, therefore no oxygen-dependent killing mechanism (Chronic Granulomatous disease)
• recurrent bacterial infections

Question 21

serotonin:

Answer 21

vasodilatory effects similar to those of histamine; platelet dense-body granules;
-release triggered by platelet aggregation

Question 22

what causes dolor (pain)

Answer 22

the kinin system which creates bradykinin

Question 23

the kinin system creates brady kinin, which:

Answer 23

• vascular permeability
• arteriolar dilation
• smooth muscle contraction (eg bronchial)
• causes pain
• rapidly inactived by kininases

Question 24

Mediators or inflammation:

Answer 24

1. arachidonic acid metabolites
2. leukotrienes
3. cytokines
4. Nitric Oxide

Question 25

arachidonic acid (cell membrane phospholipid) metabolites:

Answer 25

- prostaglandins and thromboxane - produced by cyclooxygenase pathway - causes vasodilation=tumor (swelling) - COX-1, COX-2 blocked by aspirin and NSAIDS

Question 26

leukotrienes:

Answer 26

- via lipoxygenase pathway - chemotaxins - vasoCONSTRICTORS - cause increased vascular permeability and bronchospasm

Question 27

Nitric Oxide is produced by:

Answer 27

endothelial cells and macrophages

Question 28

nitric oxide causes:

Answer 28

- vascular smooth muscle RELAXATION and VASODILATION - kills microbes in activated macrophages - counteracts platelet adhesion, aggregation, and degranulation

Question 29

possible outcomes of acute inflammation:

Answer 29

1. complete resolution 2. scarring (fibrosis) 3. abscess formation 4. progress to chronic inflammation

Question 30

which cells produce antibodies?

Answer 30

-Plasma cells, which come from B cells

Question 31

eosinophils

Answer 31

- parasitic infection or | - allergic (IgE-mediated) sites

Question 32

Granulomatous inflammation

Answer 32

- chronic inflammation - macrophage is the major player - Granuloma is focal area of inflammation

Question 33

granuloma

Answer 33

- "cement encasing" - made up of macrophages, lymphocytes and plasma cells - occurs with foreign material that cannot be destroyed, so it is surrounded and kept in check

Question 34

systemic effects of inflammation:

Answer 34

1. fever -IL-1, 6, TNF -anorexia muscle protein degradation -hypotension 2. Leukocytosis -elevated wbc

Question 35

neutrophilia

Answer 35

bacterial infection

Question 36

eosinophilia

Answer 36

parasitic infection

Question 37

lymphocytosis

Answer 37

viral infection