Park Lec 1 Flashcards

1
Q

what are the characteristics of acute inflammation

A
  1. Rapid in onset and short duration
    –> Minutes to days
  2. Accumulation of fluid and plasma proteins
    –> Exudation
  3. Accumulation of neutrophils
  4. Tumor necrosis factor (TNF), interleukin-1 (IL-1), chemokines
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2
Q

what are the characteristics of chronic inflammation

A
  1. Insidious and of longer duration (months to years)
  2. Tissue destruction by inflammatory cells
  3. Vascular proliferation and fibrosis
    –> Scarring
  4. Influx of lymphocytes and macrophages
  5. Interferon- y (IFN-y) by T cells and interleukin-I2 (IL-I2) by macrophages
    –> Synergistic stimulation
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3
Q

what are some characteristics of inflammation

A
  • Occurs upon infections or noxious stimuli
    –> Injuries, burns, foreign bodies, etc.
  • Eliminates harmful agents and necrotic cells
    –> Microbes and toxins
  • Initiates the healing process
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4
Q

inflammation can cause injury but what are the different types of responses

A
  1. Too strong response
    –> Severe infection
  2. Prolonged response
    –> Persistent or recurrent infection
  3. Inappropriate response
    –> Self-antigens in autoimmune diseases
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5
Q

what are some pharmacologic approaches of inflammation

A
  1. Glucocorticoids
  2. NSAIDs
  3. Antihistamines
  4. Leukotriene antagonists
  5. Biologics targeting cytokine signaling
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6
Q

what are the characteristics

A
  1. Heat
    – calor
  2. Redness
    – rubor
  3. Swelling
    – tumor
  4. Pain
    – dolor
  5. Loss of function
    – Functio laesa
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7
Q

what are the events occurring during the acute inflammation response

A
  1. Phagocytosis in tissues recognize offending agents and liberate chemical mediators of inflammation
  2. Chemical mediators widen blood vessels (vasodilation) and increase their permeability in the vicinity
  3. Plasma and circulating leukocytes diffuse to the location of the offending agents
    –> Leukocyte recruitment
  4. Activated leukocytes remove the offending agents
    –> Phagocytosis
  5. Leukocytes produce signaling molecules that suppress inflammation
    – Lipoxins
  6. The damaged tissue is repaired
    – Cell proliferation
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8
Q

what are some vascular stages responses

A
  1. vasodilation
  2. increased lipophilicty
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9
Q

whaat are some stages of cellular acute inflammation

A
  1. Leukocyte recruitment
  2. phagocytosis
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10
Q

what results in vasodilation

A
  1. Decrease in fluid velocity
  2. Increased viscosity
    –> Due to fluid loss to tissues
  3. Increased leukocytes settling along the inner surface of the blood vessels
    –> margination
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11
Q

what results in increased lipophilicty

A
  1. Gaps due to endothelial contraction
    –> Most common mechanism
    –> Histamines, leukotrienes, bradykinin
  2. Increase fluid life through endothelial cells
    –> transcytosis
  3. Direct endothelial traumatic injury
  4. Leukocyte dependent endothelial cell damage/death due to release of toxic mediators by leukocytes
  5. Leakage from new blood vessels that form at the site of injury
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12
Q

what changes can result from vascular changes

A
  1. Transudate
    –> Small holes
    –> Plasma with little proteins
    –> No cells
  2. Exudate
    –> Bigger holes
    –> Protein rich fluid with numerous cells
  3. Edema
    –> Accumulation of fluid and swelling at site of inflammation
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13
Q

what are the secret of events in leukocyte recruitment

A
  1. Margination
  2. Loose attachment and rolling
    –> Selectins
  3. Adhesion
    –> Integrins
  4. Transmigration
  5. Chemotaxis
    –> Bacterial products
    —–> LPS
    –> Chemokines
    –> Complement system
    —–> C5a
    –> Leukotriene B4 (LTB4)
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14
Q

what is involved in the recognition of phagocytosis

A

direct and indirect

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15
Q

what is the engulfment of phagocytosis

A
  • Receptor-mediated endocytosis
  • Pseudopods extend around foreign body and form a phagosome
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16
Q

what is the intracellular killing of phagocytosis

A
  1. Fusion of the phagosome with a lysosome (phagolysosome)
  2. Lysosomal degradation
    –> Digestive enzymes and defensins
  3. Release of toxic nitrogen and oxygen compounds (oxidative burst)
    –> H2O2, hydrochloric radical, NO
17
Q

what is involved in direct recognition

A
  • microbes by pattern recognition receptors
    –> Toll-like receptors — LPS, flagellin, etc.
    –> Mannose receptors
18
Q

what is involved in indirect recognition

A
  • Opsonins: IgG, C3b, and collectins (carb-binding lectins)
  • Coat of foreign body and dead cells
    –> Opsonization
  • Specific receptors recognize opsonins
    –> Fc receptor; C3b receptor