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Pathology > Unit II: Inflammation key points/overview > Flashcards

Unit II: Inflammation key points/overview Flashcards

1
Q

3 initiators of inflammation

A
  1. tissue damage
  2. bacteria
  3. activation of local mast cells or tissue macrophages
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2
Q

What can initiate histamine release from mast cells?

A

Direct injury, cold innervation, cross linking of IgE

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3
Q

Margination

A

Margination

  • cells/proteins fall out of axial flow due to hemostasis
  • Stasis due to: increased blood delivery to capillaries, but efflux remains the same
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4
Q

Endothelial activation occurs in…..

A

POST CAPILLARY VENULES==> vasodilation, increased local blood flow, increased vascular permeability

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5
Q

Transudate

A

passage of FLUID due to increased hydrostatic pressure across endothelial tight junctions

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6
Q

Exudate

A

passage of fluid, protein, and cells due to increased vascular permeability

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7
Q

wheal (from “wheal and flare”)

  • what is it?
  • pathophysio
A
  • raised pale area around the injured skin
  • caused by edema at dermal/epidermal border (causing them to seaparate)==> paleness and swelling
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8
Q

Flare

  • what is it
  • what causes it/pathophysio (x2–injury vs ice)
A
  • bothcy red area around the “wheal”
  • ice: local release of histamine from mast cells that covers area greater than ice contact
  • axonal reflex= peripheral nerve stimulation opens up arterioles around the injured area
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9
Q

increased vascular permeability:

  1. Immediate transient
  2. augment immediate transient response
  3. delayed prolonged
  4. immediate sustained leakage
A
  1. histamine- acts within minutes but reversed within an hour
  2. cell derived plasma proteins augment histamine response
  3. inflammatory cell mediators
  4. physical disruption of vessel wall
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10
Q

Cellular phase=

Order of cells after injury

A

Cellular phase= passage of cells from vasculature to extracellular phase, and activation of local cells.

  1. Immediately: platelets (activated when exposed to ECM)
  2. 24hrs: Neutrophils- venous stasis and mediators help them into tissue
  3. 24-48 hrs: monocytes==> macrophages; tissue macrophages
  4. 72 hrs: Lymphocytes
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11
Q

diapedesis

A

movement of cells through the vascular wall

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12
Q

Neutrophil extravasation

A
  1. margination- fall out of axial flow
  2. weak adhesion (selectins)
  3. strong adhesion= ICAM and LFA-1
    • e-selectin and ICAM (on endothelium) enhanced by inflammatory mediators
    • LFA-1 (integrin) on neutrophils expressed when activated by local inflammatory mediators
  4. diapedesis toward chemotactic signal
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13
Q

Weibel-Palade bodies

A

make p-selectin and von willebrand factor

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14
Q

After 24 hours, inflammation is mediated by…..

A

tissue macrophages and monocytes- they dictate continuation or resolution (healing and regeneration) of immune response

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15
Q

two cells important for resolution of immune response

A

Macrophages and neutrophils= phagocytosis of harmful debris

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16
Q

2 mechanisms neutrophils kill with

A
  1. enzyme release from membrane bound granules into phagolysosomes
  2. ROS in azurophilic granules
17
Q

Most effective method of killing in macrophages

A

making hyperchlorus acid from myeloperoxidase and chloride

18
Q

chronic granulomatous disease- what is it, diagnosis?

A

inability to make ROS, nitroblue tetrazolium or neutrophil oxidative burst assay

19
Q

Chronic inflammation is always accompanied by _____. Why?

A

FIBROSIS

chronically activated macrophages==> more activation of macrophages==> chronic stimulation of fibroblasts

20
Q
  1. Selectins bind to ______, 3 examples.
  2. integrins bind to____. 2 examples
A
  1. Selectins bind to carbs–P (platelet and endothelium), E (endothelial), L (leukocyte)
  2. integrins bind to immunoglobin like molecules (Ig family)
    • LFA-1 (PMN) to ICAM (endothelial cell)
    • VLA-4 (monocyte) to VCAM (endothelial cell)
21
Q

6 Benefits of inflammation

A
  1. dilution of harmful influence
  2. localization of injury
  3. destruction of bacteria/etc
  4. delivery of plasma protiens and cirulating cells
  5. clearing of debris
  6. intiation of healing
22
Q
  1. Seconds to minutes=
  2. Amplification of above mediators=
A
  1. histamine, serotonin
  2. serum proteins= hageman factor (XII), complement, coagulation facotrs, kinins
23
Q

Minutes to hours after inflammation begins-

  1. process, mediators and morphology
  2. process, mediators and morphology
A
  1. Process: reflex vasoconstriction followed by vasodilation
    • Mediators: Axonal reflex, histamin PGs
    • Morphology: Vascular congestion, vasodilation
  2. Process: increased vascular permeability
    • Mediators: Histamin, C3a, C5a, kinins Pgs
    • Morphology: edema
24
Q

Hours to Days from inflammation

A

Process: activation and migration of cells

  • Mediators: leukotrienes, prostaglandins, cytokines
  • Morphology: emigration of neutrophils, monocytes, lymphocytes
25
Q

Days- process, mediators, morphology

A
  • Process: phagocytosis and cytokine production
  • mediators: PGs, cytokines,
  • Morphology: Cell adaptation, necrosis, infiltrate
26
Q

Days to weeks

Process, mediators, morphology

A
  • Process: clearing of debris, cell proliferation- regeneration, scarring, immune response)
  • Mediators: cytokines, growth factors
  • Morphology: Angiogenesis, fibroblast proliferation, collagen synthesis, epithelial proliferation
27
Q

fluid movement through cells

A

via increased pinocytosis

28
Q

Immediate transient permeability changes (15-30 mins)

  1. where do they occur
  2. mediators
  3. blocked by?
A

Formation of endothelial gaps in venules

  1. post-capillary venules
  2. histamine, bradykinin, leukotrienes, substance P
  3. antihistamies
29
Q

delayed prolonged leakage (hours to days)

2 causes- mediators?

A

cytoskeletal reorganization

  1. mediators: PGs, cytokines
  2. leukocyte–mediated endothelial injury
30
Q

Immediate sustained permeability changes

Cause?

A

DIRECT damage to endothelial cells–affects all levels of vasculature

31
Q

Factors that slow the inflammatory process

A

acute phase proteins, TGF-B

32
Q

4 causes of chronic inflammation

A
  1. persistent injury
  2. persistent infection
  3. inability to neutralize toxin
  4. persistence of immune response
33
Q

E-selectin is stimulated by ___(1)____. Time course (2)?

A
  1. IL-1
  2. peaks at 4 hrs, reversed by 24 hrs
34
Q

inhibition of neutrophil rolling on endothelium

A

antibodies to L-lectin

35
Q
A

Pathology (7 decks)

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