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General Pathology VDMP832 > Acute Inflammation Purpose and Process > Flashcards

Acute Inflammation Purpose and Process Flashcards

1
Q

Inflammation

A
  • The host response to injury
    • vascular and cellular events
  • It is complex and integrated response involving the microvasculature, blood elements, and local ECM
  • Overlaps with other host responses
    • hemostasis and immunity
  • Essential for life, but can have adverse consequences
  • can last for hours or years
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2
Q

Inflammation:

Causes

A
  • Microorganisms
  • Chemicals
  • Trauma
  • Thermal or Radiation injury
  • Foreign Bodies
  • Immune Reactions
  • Necrosis
  • Neoplastic/altered cells
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3
Q

Inflammation:

Purpose

A
  • To isolate, dilute, neutralize, confine and remove the offending agents
  • To clear the area of debris
  • To initiate healing and repair
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4
Q

Inflammation:

Outcomes

A
  • Elimination of the agent and return to normal
  • Stalemate: Ongoing inflammation
  • Death of the host
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5
Q

What do you see

A

Lung, dark red, dry,

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6
Q

What do you see

A

Larynx and Abomasum, swelling

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7
Q

Cardinal Signs of Inflammation

A

Rubor (redness)

Tumor (swelling)

Calor (heat)

Dolor (Pain)

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8
Q

5th sign of Inflammation

A
  • Function Laesa (Loss of Function)
  • Added by Rudolf Virchow about 1860
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9
Q

Inflammation:

Learn about it by investigating

A

Vascular changes

Cellular Events

Chemical mediators

Duration

Acute vs. chronic

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10
Q

Inflammation:

Vascular Events descovery

A
  • The pattern of vascular change associated with acute inflammation was originally described in 1867 by Julius Cohnheim
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11
Q

Inflammation:

Review of the Microcirculation

A
  • Blood flow is not constant through the microcirculation
    • Flow is usually determined based on physiologic needs
    • It also changes following injury
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12
Q

Inflammation:

Vascular Events

A
  • Sequential series of vascular events in response to inflammation are:
  1. Transient arteriolar vasoconstriction
  2. Arteriolar vasodilation
  3. Capillary congestion
  4. Increased vascular permeability
  5. Slowing of blood flow
  6. Redistribution of blood cell elements
  7. Blood flow stasis
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13
Q

Transient Arteriolar Vasoconstriction

A
  • Caused by the direct effect of the inciting stimulus on arteriolar smooth muscle
    • regulated by the release of local mediators
  • This does not occur with all stimuli
  • Vasoconstriction lasts several seconds, up to 5 minutes
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14
Q

Arteriolar Vasodilation

A
  • A wave of vasodilation starting at the arteriole progressing to the venule causes hyperemia
    • mediators of vasodilation
      • Histamine
      • Bradykinin
      • Prostacycline
      • Prostaglandin D2
      • Leukotriene B4
      • Nitric Oxide
      • Local Neurogenic substances
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15
Q

Increased Vascular Permeability

A
  • Endothelial junctions become leaky resulting in fluid and molecule loss to the interstitium
    • Mediators include:
      • Immediate stranseint response:
        • histamine, bradykinin, Leukotrienes B4C4D4E4, Platelet activating facotr, C3a and C5a, Substance P
      • Delayed sustained response:
        • TNF, IL-1, Gamma-IFN
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16
Q

Increased Vascular Permeability:

Edema Factor

A
  • This was one of our mechanisms for edema
    • increased intravascular hydrostatic pressure, and increased extravascular osmotic pressure also contribute to fluid loss
  • Fluid that moves into the extravascular space contains proteins involved in inflammation and helps to dilute the inciting stimulus
    • Fluid changes in character form a transudate to an exudate
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17
Q

Slowing of Blood Flow

A
  • Due to large vascular diameter resulting in slower flow and increased numbers of bood cells
  • Increased blood viscosity due to plasma loss
  • Increased Adhesiveness or erythrocytes
18
Q

Redistribution of blood cell elements

A
  • Laminar flow is disrupted due to vasodilation and congestion
    • Erythorcytes become ventrally located
    • Leukocytes move to the periphery along the endothelaial surface
      • THis relocation is essential to begin the cellular changes associated with inflammation
19
Q

Inflammation:

Cellular Events

A
  • Critical Event in inflammation is the movement of cells from the blood vessel to the site of injury
  • Major steps include:
    • Margination and adhesion of endothelium
    • Emigration
    • Chemotaxis
    • Accumulation
20
Q

Margination and adhesion to endothelium:

A
  • A vascular event that moves leukocytes to the periphery to the vessels; adjacent to the endothelium
  • Initially, leukocytes transiently adhere (roll) along the endothelial surface
    • mediated by endothelial E- and P-selectins
    • Mediated by leukocyte L-selectin
  • Later, leukocytes firmly adhere to endothelium
    • Endothelial Receptors:
      • Intercellulr Adhesion Molecule -1 (ICAM-1)
      • Vascular Cell Adhesion Molecule-1 (VCAM-1)
    • Leukocyte receptors:
      • B-2 integrins
        • Increased expression on activated leukocytes
21
Q

Leukocytes adhesion molecules

A

B-2 integrins include:

Mac-1, LFA-1, P150,95 and adB2

All of these share a B-subunit CD18

22
Q

Emigration

A
  • The movement of leukocytes form the endothelial surface into the extravascular space
    • facilitated by the enlarged gaps between endothelial cells
    • Leukocyte-endothelial interactions occur within the inter-endothelial junction
    • Active mobility of leukocytes enable them to exert pseidopods into inter-endothelial junctions to pull themselves throug the extravascular space
23
Q

Emigration:

Order

A
  1. Neutorphils emigrate first
    1. Initial emigration can occur within 30-40 minutes of the stimulus and predoinate for 6-24 hours
  2. Monocytes emigrate next
    1. predominate by 24-48 hours
  3. Lymphocytes are sluggish
    1. Don’t emigrate until later
24
Q

Chemotaxis

A
  • the directed movement of leukocytes to the site of an inflammatory stimulus
    • occurs in response to a concentration gradient of a chemkcal attraction
      • activated complement components
      • Bacterial products
      • Arachidonic Acid metabolites
      • Kinins
      • Collagen and fibrin breakdown products
      • Leukocyte production
      • Chemotaxis
25
Q

Chemotaxis:

Mechanisms

A
  • Chemotactic factors interact with specific leukocyte membrane receptors
  • Membrane phospholipase C is activated and results in localized release of Ca2+ in the cytoplasm
  • Fluxes in Ca2+ concentrations result in localized assembly and disassembly of microtubules and microfilaments
  • Leukocytes B1 integrins bind to ECM components to pull themselves in the direction of the sitmulus
26
Q

Accumulation::

A
  • Neutrophils are the first cell to accumulate at the site of the stimulus
    • first to emigrate, most motile, are short-lived in the tissues
  • Macrophages become more numerouse after 24-48 hours
    • Emigrage later, but emigration is more sustainded
    • Long lived and can replicate locally
  • Lymohocytes may accumulate later in response to persistent immunologic stimuli
27
Q

What has been accomplished

A

Leukocytes have moved out of the blood vessels at the site of injury

Leukocytes have migrated through the ECM to the location of the inflammatory stimulus

28
Q

Inflammation:

Cellular Events:

Phagocytosis

A
  • This is the uptake and degredation of particular material by leukocytes
    • Neutrophils and macrophages are the most important phagocytes in inflammation
  • Purpose:
    • Destroy and remove the inflammation stimulus
    • Clean up debris to stimulate the healling process
29
Q

Phagocytosis

A
  • The process can be divided inot stages
    • Opsonization
    • Attachment
    • Ingestion
    • Killing and degradation
30
Q

Opsonization

A
  • This is the coating of foreign material by factors that enhance phagocytosis
  • Major Opsonins
    • C3b
    • IgG
    • Collectins
31
Q

Attachment

A
  • The phagocyte attaches to the foreign material
    • Phagocytes readily attach the opsonized material
      • phagocytes have specific membrane receptors for C3b and the Fc protion of IgG
    • Phagocytes can attach to unopsonized material, but much less efficiently
32
Q

Ingestion

A
  • Cell membrane pseudopods extend around the material to internalize it into an intra-cytoplasmic vacuole
    • caled a phagosome
  • Ingestion is an active process similar to that which occurs with chemotaxis
    • Ca2+ fluxes regulate cytoskeletal changes
33
Q

Killing and Degradation

A
  • A lysosome fuses to a phagosome to form a phagolysosome
    • Lysosomal enzymes are relaeased itnot he phagolysosome
    • If the material is a microorganism, it must first be killed
      • Oxygen-independent killing mechanisms
      • Oxygen-dependent killing mechanisms
        *
34
Q

Oxgen-Independent Killing

A
  • Mediators are the contents of lysosomes
    • acid hydrolases
    • Bactericidal permiability increased protien
    • Major basic protein
    • Lysozomes
    • Lactoferrin
    • Defensins
    • Cathepsin G
35
Q

Oxygen-dependent Killing

A
  • Increased oxygen uptake results in the production of a variety of oxygen metabolites
    • Are highly reactive and potent killing agents
      • Two Killing pathways
        • Myeloperoxidase-indepent pathways
        • Myeloperoxidase-dependent pathway
36
Q

Myeloperoxidase-Independent Pathways

A
  • Killing mediated by the direct oxidative effects of oxygen metabolites
    • Superoxide anion
    • Hydrogen peroxide
    • Hydroxyl radical
  • Formation of NADPH oxidase during the respiratory burst initiates the process
37
Q

Myeloperoxidase-dependent Pathways

A
  • H2O2 + Cl = HOCl
    • hypochlorous acid: bleach
  • Considered the most potent killing mechanisms
    • Pathway is present in neutrophils, but plays an insignificant role in macrophages
38
Q

Digestion of the material

A
  • Following killing, degradation
    • Acid hydrolases and other proteolytic enzymes liquify the debris
    • Unliquefied debris persists as a residual body
  • Following phagocytosis, neutrophils undergo apoptosis and are removed
  • Macrophages persist and continue to function at the site until no longer needed
39
Q

Phagocytosis:

What can go wrong?

A
  • Some organisms survive within the phagolysosome
  • some organisms are virulent to phagocytes
  • timing errors in phagosomes-lysosome fusion may occur
  • Large or indigestible substances can’t be internalized
  • Reactive metabolites damage the cell
40
Q

Cellular Events:

What can go wrong

A
  • Decreased circulating leukocytes
  • Defective adhesion to endothelium
  • Defective movement
  • Defective phagocytosis
  • Defective intracellular Killing

The result is a decreased host response to the inflammatory stimulus

General Pathology VDMP832 (26 decks)

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