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Mechanism of Human Disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define inflammation. What are the components?

A

def: reaction of vascularized tissue to neutralize and remove injurious/infected tissue

components:

  • pathogen/injury
  • host cells
  • complement and coagulation
  • chemokines and cytokines
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2
Q

What are the characteristics of acute inflammation?

A
  • short clinical duration
  • immediate reaction
  • accumulation of fluid, plasma proteins, and leukocytes (PMNs)
  • sudden onset
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3
Q

What are the characteristics of chronic inflammation?

A
  • long clinical duration
  • accumulation of lymphocytes and macrophages
  • proliferation of blood vessels
  • formation of connective tissue at site
  • slow onset
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4
Q

List the factors that determine intensity of inflammation.

A
  • duration of stimulus
  • type of injury
  • genetics of host
  • local factors (blood supply)
  • medical interventions (drug interactions)
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5
Q

What are clinical signs of acute inflammation?

A
  • rubor (redness)
  • calor (heat)
  • tumor (swelling)
  • dolor (pain

systemic: fever, leukocytosis, malaise, chills

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6
Q

What are the overall vascular changes that occur during acute inflammation? What are the localized and systemic symptoms of these events?

A
  • vasodilation: nitric oxide => increased flow and permeability => erythema, warmth
  • leakage of fluid, plasma proteins, complement proteins, and innate immune molecules => edema
  • leukocyte (neutrophil) emigration and accumulation in tissue (recruited by cytokines)

localized symptoms = swelling and warmth
systemic symptoms = increase in CO, decrease in TPR

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7
Q

Recall formation of an inflammasome.

A
  1. DAMPs/PAMPs activate TLRs on macrophages and monocytes
  2. activation of CASPASE-1
  3. activation of IL-1, -6, -8, and TNF-a
  4. formation of an inflammasome
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8
Q

What are the steps to leukocyte movement?

A
  1. marginalization
  2. rolling adhesion
  3. stable adhesion
  4. diapedesis
  5. transmigration
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9
Q

What is required for leukocyte adhesion?

A
  1. cytokines upregulate endothelial marginalization factors

2. upregulation of adhesion proteins on endothelial barrier via inflammatory cytokines

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10
Q

Define pseudopods.

A
  • extensions of neutrophils and other leukocytes through the endothelial barrier before the entire cell transmigrates
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11
Q

Define diapedesis.

A

movement of neutrophils through the membrane via pseudopods

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12
Q

Define chemotaxis.

A

unidirectional movement of leukocytes along a chemical gradient composed of:

  • bacterial peptides
  • complement components (esp. C5a)
  • arachnidonic metabolites
  • inflammatory tetrad (IL-1, -6, -8, TNF-a)

gradient components trigger PMN changes in cytoskeleton makeup to allow it to move along the gradient

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13
Q

Describe the steps of leukocyte phagocytosis.

A
  1. Recognition and Attachment - opsonins on the surface of the injured cell/infection will bind to complementary surface proteins on macrophages/lymphocytes
  2. Engulfment into a phagosome via pseudopod extension around the microbe; requires actin, myosin, energy, and intracellular calcium
  3. Granulation within the phagolysosome via toxic enzymes
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14
Q

List enzymes/methods used for degradation and killing by neutrophil degranulation.

A
  • Myeloperoxidase (MPO) in conjunction with halides (ex: HOCl)
  • lysosomal enzymes
  • ROS (NADPH oxidase converts oxygen to a superoxide => H2O2 => free radical)
  • NETS (neutrophil extracellular traps): neutrophils release granules and chromatin to trap bacteria and fungi
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15
Q

Define monocytes vs macrophages.

A
  • monocytes are circulating leukocytes with MHCII antigen presenting capabilities
  • tissue macrophages are monocytes that have exited the blood and entered the tissue. They take on regional phenotypic modifications to adjust to the area.
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16
Q

Describe the mechanism by which acute inflammation is controlled.

A
  1. stimulus is destroyed/neutralized => decreased PAMP/DAMP
  2. decreased TLR stimulation => decreased inflammatory mediator production (IL-1, -6, -8, TNF-a) by activated macrophages
  3. neutrophilic granule release prevents more neutrophils from entering the site; instead they recruit monocytes
  4. decreased TLR stimulation => conversion of M1 macrophages to M2 => production of IL-10 and TGF-b => antiinflammatory milieu sets the stage for cleanup and repair
17
Q

What are the outcomes of acute inflammation?

A
  • resolution and repair

- chronic inflammation

18
Q

List the 4 classifications of acute inflammation in order of severity.

A
  • serous
  • fibrinous
  • supperative/abscess
  • ulcerative (special category)
19
Q

Characterize serous acute inflammation.

A
  • protein poor transudate from blood vessels into peripleural space (ex: pericardial, peritoneal, between epidermis and dermis (blister)
20
Q

Characterize fibrinous acute inflammation.

A
  • fluid with larger molecules (mostly fibrinogen) from blood vessels into extracellular space
  • fibrinogen converts to fibrin => scaffold for scar formation
21
Q

Characterize abscess/supperative acute inflammation.

A
  • collection of protein-rich fluid, containing inflammatory cells and debris ==> pus
  • if walled off by fibroblasts => abscess
22
Q

Define abscess.

A

collection of inflammatory cells, debris (pus) surrounded by fibroblasts

23
Q

Characterize ulcerative acute inflammation.

A
  • underlying inflammation causes excavation of skin or mucos to form indentations (ulcers) in the mucosal linings or surface
24
Q

What kind of tissue can undergo acute inflammation?

A

VASCULAR

25
Q

Define PAMPs vs DAMPs.

A

PAMPs = Pathogen-Associated Molecular Patterns

  • microbes
  • viruses

DAMPs = Damage-Associated Molecular Patterns
- ROS

26
Q

How does smoking affect acute inflammation control?

A
  • turns off PMN prevention signal
  • neutrophil recruitment and release continue
  • chronic inflammation b/c monocytes aren’t recruited
27
Q

Define proliferative pool vs maturation pool of PMNs.

A

Once PAMPs/DAMPs are activated, activated macrophages stimulate PMNs in both pools.

  • proliferative = bone marrow activation of PMNs by cytokines and growth factors
  • maturation = circulating monocytes
28
Q

What is the characteristic immune cell of acute inflammation?

A
  • neutrophils

- most numerous innate immune cell in circulation

29
Q

Define bandemia.

A
  • stimulation of proliferative pool causes release of not-fully-matured PMNs into circulation
  • circulating PMNs undergo a “left shift” to a less mature level overall during inflammation

Mechanism of Human Disease (18 decks)

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