Acute inflammation Flashcards

1
Q

Define acute inflammation

A

Reaction of vascularized tissue to injury

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2
Q

Inappropriate inflammatory response with no foreign substances to remove is the basis of . . .

A

Autoimmune inflammation

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3
Q

What four things are involved in the formation and clearing of acute inflammation?

A
  1. Pathogen/injury
  2. Host inflammatory cells
  3. Complement and coagulation cascades
  4. Chemokines and cytokines
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4
Q

Three things involved in immediate tissue reaction

A
  1. Fluid
  2. Plasma proteins
  3. Innate immune cells
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5
Q

Intensity of immune response dictated by these four things

A
  1. Stimulus
  2. Duration of the stimulus
  3. Genetics of the host local factors
  4. Medical interventions
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6
Q

Four causes of inflammation

A
  1. Infections
  2. Tissue necrosis
  3. Foreign bodies
  4. Immune reactions
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7
Q

Recognition by the innate immune system

A

DAMPs/PAMPs activate TLRs and other recognition receptors on monocytes

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8
Q

Inflammasome

A

Multi-protein complex characterized by activation of caspase 1; cleaves IL-1 to active form that sets the inflammatory cytokines in action

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9
Q

Nitric oxide in the inflammatory response

A

Mediates vasodilation that increases flow and vascular permeability

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10
Q

Three main events of inflammation

A
  1. Vascular dilation and increased blood flow (erythema and warmth)
  2. Extravasation of plasma fluid and proteins (edema)
  3. Leukocyte (mainly neutrophil) emigration and accumulation
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11
Q

Movement of the leukocytes into the extravascular space

A

TNF alpha and IL-1 beta signal for the leukocytes to move out of laminar flow and roll along vascular wall until they attach and move through the cell space through diapedesis

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12
Q

Chemotaxis

A

Unidirectional movement along a chemical gradient used by

  • Bacterial peptides
  • Complement proteins, especially C5a
  • Proinflammatory cytokine tetrad
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13
Q

How does chemotaxis work?

A

Chemoattractants activate membrane receptors on the innate cells that then activate cytoskeleton, particularly actin, changes that move the cell along the gradient

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14
Q

Three phases of leukocyte activity in inflammation

A
  1. Moving out of the blood vessel using diapedesis
  2. Releasing acute inflammatory mediators; immediately undergoing checkpoint mechanism to stop acute inflammation
  3. Degranulation and quick cleanup moderated by the monocyte/macrophage system
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15
Q

Where are extra neutrophils derived during acute inflammation?

A

More blood can be dumped out from the spleen, which has more neutrophils in it (cannot actually produce more neutrophils)

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16
Q

What do neutrophils look like histologically?

A

They have a lot of different lopes to each nucleus, but has ONLY ONE nucleus

17
Q

What do macrophages look like morphologically?

A

Have one single, solid, round nucleus

18
Q

Describe the name changes of monocytes.

A

In the cavity: macrophage

Into a tissue: histocyte

19
Q

Which cells are present at the site of inflammation first, neutrophils or macrophages?

A

Neutrophils and THEN macrophages

20
Q

Rheologic

A

Increased delivery of cells per unit time increases the chance that a leukocyte can respond to a signal

21
Q

Most numerous leukocyte in circulation

A

Neutrophils (“PMNs”)

22
Q

Half lives of neutrophils

A

12 hours in the blood, 1-2 minutes at the site of inflammation

23
Q

Left shift

A

Bone marrow pushes immature neutrophils out earlier to deal with acute inflammation

24
Q

Five features of neutrophils at the site of injury

A

-Phagocytosis
-recognition/attachment of complement
-engulfment/degranulation
killing/degradation by oxidative burst
-NETS

25
Q

Phagolysosome

A

Part of membrane breaks off to form a bubble with the pathogen in it, which then fuses with the lysosome inside the cell and kills the pathogen

26
Q

What is the most important ROS, and how is it formed?

A

Myeloperoxidase (MPO) combines with a halide and forms HOCl, which is the most important ROS

27
Q

What is a NET?

A

Neutrophil extracellular trap: sacrifices its nucleus by casting its chromatin laden with killer granules out of the cell as a net to trap bacteria and fungi

28
Q

Half life of monocytes

A

Circulate for 16 hours (largest leukocyte in the blood)

29
Q

Interleukins involved in “cleanup” of the inflammatory response

A

IL-10 and TGF-beta; establish the correct milieu for appropriate healing and wound repair

30
Q

Control of acute inflammation

A
  • Controlled mostly by macrophages

- Also by decreased activation of TLRs

31
Q

Least severe form of acute inflammation

A

Serous - protein-poor transudate from capillary to a space: peritoneal, pericardial, or pleural

32
Q

Intermediate morphology of acute inflammation

A

Fibrinous - fluid with larger molecules dominated by fibrinogen which converts to fibrin and potential scarring

33
Q

Severe morphology of acute inflammation

A

Suppurative/abscess - protein-rich fluid with inflammatory cell, alive and dead necrotic debris

34
Q

Example of serous inflammation

A

Blister

35
Q

Example of fibrinous inflammation

A

Pericarditis; deposits fibrin on the pericardium

36
Q

Example of suppurative inflammation

A

Bacterial abscesses in the lung in bronchopneumonia

37
Q

Ulcerative inflammation

A

Underlying inflammation causes excavation of a mucosal or skin surface