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General Pathology > 2-Acute/Chronic inflammation > Flashcards

2-Acute/Chronic inflammation Flashcards

1
Q

main cells of acute inflammation

A

neutrophils

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2
Q

main cells of chronic inflammation

A

lymphocytes and macrophages

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3
Q

acute inflammation

A

early response to tissue damage

  • vasodilation
  • vascular leakage and edema
  • leukocyte emigration (PMNs)
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4
Q

acute inflammation: vasodilation

A
  • accounts for warmth and redness (rubor, calor)
  • opens microvascular beds
  • increased intravascular pressure causes an early transudate into interstitium-tumor
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5
Q

transudate

A

protein-poor filtrate of plasma

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6
Q

vascular leakage

A
  • transudate gives way to exudate (protein rich)
  • increases interstitial osmotic pressure
  • edema
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7
Q

transmigration

A
  • (diapedesis)
  • occurs after firm adhesion via CD31
  • collagenases
  • intergrins
  • early in inflammatory response mostly PMNs, later monocytes and lymphocytes
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8
Q

Chemotaxis

A
  • Leukocytes follow chemical gradient to site of injury

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

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9
Q

pseudopods

A
  • extended by leukocytes

- they express integrins that bind ECM during chemotaxis

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10
Q

Once at the site of injury, leukocytes:

A
  • recognize and attach
  • engulf (form phagocytic vacuole)
  • kill (degrade)
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11
Q

How do leukocytes recognize and bind?

A

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

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12
Q

Phagolysosome

A

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

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13
Q

degranulation

A

granules discharge within phagolysosome and extracellularly

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14
Q

Oxidative burst

A
  • increased oxygen constumptoin
  • glycogenolysis (glycogen breakdown)
  • increased glucose oxidation
  • formation of superoxide ion
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15
Q

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

A

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

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16
Q

premature degranulation causes:

A

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

17
Q

causes of leukocyte-induced tissue injury

destructive enzymes enter extracellular space when:

A
  • premature degranulation
  • frustrated phagocytosis (large, flat)
  • membranolytic substances (urate crystals)
  • persistent leukocyte activation (RA, emphysema)
18
Q

Defects of leukocyte adhesion:

A
  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
19
Q

defects of leukocyte chemotaxis/phagocytosis:

A
  • microtubule assembly defect leads to impaired locomotion and lysosomal degranulation
  • neutropenia, defective neutrophil degranulation, delayed microbial killing, recurrent bacterial infections
20
Q

defects of leukocute funciton: defects of microbicidal activity:

A
  • deficiency of NADPH oxidase that generates superoxide, therefore no oxygen-dependent killing mechanism (Chronic Granulomatous disease)
  • recurrent bacterial infections
21
Q

serotonin:

A

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

22
Q

what causes dolor (pain)

A

the kinin system which creates bradykinin

23
Q

the kinin system creates brady kinin, which:

A
  • vascular permeability
  • arteriolar dilation
  • smooth muscle contraction (eg bronchial)
  • causes pain
  • rapidly inactived by kininases
24
Q

Mediators or inflammation:

A
  1. arachidonic acid metabolites
  2. leukotrienes
  3. cytokines
  4. Nitric Oxide
25
Q

arachidonic acid (cell membrane phospholipid) metabolites:

A
  • prostaglandins and thromboxane
  • produced by cyclooxygenase pathway
  • causes vasodilation=tumor (swelling)
  • COX-1, COX-2 blocked by aspirin and NSAIDS
26
Q

leukotrienes:

A
  • via lipoxygenase pathway
  • chemotaxins
  • vasoCONSTRICTORS
  • cause increased vascular permeability and bronchospasm
27
Q

Nitric Oxide is produced by:

A

endothelial cells and macrophages

28
Q

nitric oxide causes:

A
  • vascular smooth muscle RELAXATION and VASODILATION
  • kills microbes in activated macrophages
  • counteracts platelet adhesion, aggregation, and degranulation
29
Q

possible outcomes of acute inflammation:

A
  1. complete resolution
  2. scarring (fibrosis)
  3. abscess formation
  4. progress to chronic inflammation
30
Q

which cells produce antibodies?

A

-Plasma cells, which come from B cells

31
Q

eosinophils

A
  • parasitic infection or

- allergic (IgE-mediated) sites

32
Q

Granulomatous inflammation

A
  • chronic inflammation
  • macrophage is the major player
  • Granuloma is focal area of inflammation
33
Q

granuloma

A
  • “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
34
Q

systemic effects of inflammation:

A
  1. fever
    -IL-1, 6, TNF
    -anorexia
    muscle protein degradation
    -hypotension
  2. Leukocytosis
    -elevated wbc
35
Q

neutrophilia

A

bacterial infection

36
Q

eosinophilia

A

parasitic infection

37
Q

lymphocytosis

A

viral infection

General Pathology (9 decks)

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