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POD Exam III > Inflammation (1 and 2) > Flashcards

Inflammation (1 and 2) Flashcards

1
Q

Actue Inflammation (4):

A
  • Onset: Fast, minutes or hours.
  • Infiltrate: Mainly neutrophils.
  • Tissue injury, fibrosis: Mild and self limited.
  • Local and systemic signs: Prominent.
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2
Q

Chronic inflammation (4):

A
  • Onset: slow, days.
  • Infiltrate: monocytes/macrophages and lymphocytes.
  • Tissue injury, fibrosis: severe and progressive.
  • Local and systemic signs: less prominent, subtle.
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3
Q

Clinical features of inflammation (5):

A
  • Rubor/redness.
  • Calor/warmth.
  • Tumor/swelling.
  • Dolor/pain.
  • Functio laesa/loss of function.
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4
Q

Leukocyte emigration to extravascular tissues (3):

A
  1. Margination and rolling.
  2. Activation and adhesion.
  3. Transmigration.
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5
Q

Transudate:

A

Fluid with low protein content.

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6
Q

Exudate:

A

Extravascular fluid that has a high protein concentration and contains cellular debris.

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7
Q

Pus:

A

Purulent exudate, exudate rich in leukocytes, the debris of dead cells and in some cases microbes.

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8
Q

Most common mechanism of vascular leakage:

A

Retraction of endothelial cells.

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9
Q

Leukocyte rolling:

A

Mediated by selectins.

  • L, E, P
  • Low affinity interactions, easily disrupted by blood flow.
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10
Q

Leukocyte adhesion:

A

Mediated by integrins.

  • Slow down the leukocytes, bind more firmly.
  • Causes leukocytes to stop rolling.
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11
Q

Leukocyte transmigration:

A

Mediated by CD31/PECAM-1

- Chemokines stimulate cells to migrate through interendothelial spaces toward the chemical concentration gradient.

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12
Q

Chemotaxins (5):

A
  • N-formylmethionine.
  • IL-8.
  • C5a.
  • TNF-alpha.
  • LTB4.
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13
Q

Major opsonins (3):

A
  • Mannose binding lectin.
  • IgG.
  • C3b.
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14
Q

Phagocytosis steps (3):

A
  1. Recognition and opsonization.
  2. Engulfment with subsequent formation of a phagosome.
  3. Killing or degradation of the ingested material.
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15
Q

ROS are produced by:

A
  • NADPH oxidase.

- Oxidizes NADPH and in the process reduces oxygen to superoxide anion.

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16
Q

Hypochlorite created by:

A

Conversion of H2O2 with Cl- by MPO.

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17
Q

iNOS (3):

A
  • Inducible NO synthase.
  • Involved in microbial killing.
  • Induced when macrophages or neutrophils are activated.
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18
Q

Chediak-Higashi disease (6):

A
  • Autosomal recessive.
  • Infants and children.
  • Neutropenia with recurrent infections.
  • Oculocutaneous albinism.
  • Aberrant granules in neutrophils and other WBCs - giant lysosomes.
  • Melanocytes - “giant” melanosomes.
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19
Q

Chronic granulomatous disease of infancy (4):

A
  • X-linked recessive.
  • Infants and children.
  • Recurrent infections, especially by catalase-producing microorganisms.
  • Basic defect is of NADPH oxidase.
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20
Q

Serous inflammation (3):

A
  • Contains low MW proteins, especially albumin.
  • Clear yellow fluid.
  • No cells.
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21
Q

Fibrinous inflammation (3):

A
  • Contains larger proteins, especially fibrin.
  • Often coats a surface.
  • No cells.
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22
Q

Ulcer:

A
  • Local defect of the surface of an organ or tissue that is produced by necrosis of cells and sloughing of necrotic and inflammatory tissue.
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23
Q

Purulent inflammation

A
  • Exudate contains neutrophils in addition to proteins.
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24
Q

Eosinophilic inflammation:

A

Eosinophil is prominent or predominant in exudate.

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25
Q

Hemorrhagic inflammation:

A

RBCs leak into the surrounding tissue due to damage to endothelial cells and vessel walls.

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26
Q

Cellulitis:

A

Diffuse area of acute inflammation composed of edema fluid, bacteria and neutrophils spread through tissue.

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27
Q

Abscess:

A

A focus of acute inflammation composed of pyogenic exudate and necrotic tissue.

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28
Q

Histamine sources (3):

A
  • Mast cells.
  • Basophils.
  • Platelets.
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29
Q

Histamine actions (3):

A
  • Vasodilation.
  • Increased vascular permeability.
  • Endothelial activation.
30
Q

Serotonin (2):

A
  • Platelets.

- Vasoconstriction.

31
Q

Prostaglandin sources (2):

A
  • Mast cells.

- Leukocytes.

32
Q

Prostaglandin actions (3):

A
  • Vasodilation.
  • Pain.
  • Fever.
33
Q

Leukotriene sources (2):

A
  • Mast cells.

- Leukocytes.

34
Q

Leukotriene actions (3):

A
  • Increased vascular permeability.
  • Chemotaxis.
  • Leukocyte adhesion and activation.
35
Q

Platelet-activating factor sources (2):

A
  • Mast cells.

- Leukocytes.

36
Q

Platelet-activating factor actions (6):

A
  • Vasodilation.
  • Increased vascular permeability.
  • Leukocyte adhesion.
  • Chemotaxis.
  • Degranulation.
  • Oxidative burst.
37
Q

ROS (2):

A
  • Source: leukocytes.

- Action: killing of microbes, tissue damage.

38
Q

Nitrous oxide sources (2):

A
  • Endothelium.

- Macrophages.

39
Q

NO actions (2):

A
  • Vascular smooth muscle relaxation.

- Killing of microbes.

40
Q

Chemokine sources (2):

A
  • Leukocytes.

- Activated macrophages.

41
Q

Chemokine actions (2):

A
  • Chemotaxis.

- Leukocyte activation.

42
Q

Kinin actions (4):

A
  • Increased vascular permeability.
  • Smooth muscle contraction.
  • Vasodilation.
  • Pain.
43
Q

Preformed mediators (3):

A
  • Histamine.
  • Serotonin.
  • Lysosomal enzymes.
44
Q

Histamine (4):

A
  • Causes dilation of arterioles.
  • Increases permeability of venules.
  • Principal mediator of the immediate transient phase of increased vascular permeability.
  • Contraction of some smooth muscles.
45
Q

Converts phospholipids to arachidonic acid:

A

Phospholipase.

46
Q

Converts arachidonic acid to prostaglandins:

A

Cycloxygenase (COX-1 and COX-2).

47
Q

Inhibits creation of prostaglandins:

A

COX-1 and COX-2 inhibitors.

- Aspirin, NSAIDs, indomethacin.

48
Q

Converts arachidonic acid to leukotrienes:

A

5-Lipoxygenase.

49
Q

Prostaglandins (4):

A
  • Involved in the pathogenesis of pain and fever in inflammation.
  • Generated by COX-1 and COX-2.
  • COX-1 constitutively expressed.
  • COX-2 induced by inflammatory stimuli.
50
Q

Plasma derived chemical mediators (2):

A
  • Factor XII (Hageman factor) activation.

- Complement activation.

51
Q

C3a/C5a (3):

A
  • Increase vascular permeability.
  • Induce mast cell histamine release.
  • C5a: chemotaxin.
52
Q

Hageman factor activated by (4):

A
  • Negatively charged surfaces.
  • Bacterial LPS.
  • Sodium urate crystals.
  • Enzymes.
53
Q

Bradykinin actions (4):

A
  • Vasodilation.
  • Increase vascular permeability.
  • Bronchial smooth muscle contraction.
  • Pain.
54
Q

Activates the alternative pathway of macrophages:

A

IL-13 and IL-4.

55
Q

Activates the classical pathway of macrophages:

A

IFN-gamma and microbes.

56
Q

Acute phase proteins:

A

Plasma proteins synthesized in the liver, plasma concentration may increase as part of the inflammatory response.

57
Q

ESR (3):

A

Erythrocyte sedimentation rate:

  • Rate at which RBCs “settle” to the bottom of the tube.
  • Determined by the amount of fibrinogen.
  • Increased non-specifically in pts undergoing an inflammatory response.
58
Q

C-reactive protein:

A

Non-specifically elevated in pts who are undergoing an inflammatory response.

59
Q

Cytokines involved in acute inflammation (5):

A
  • TNF
  • IL-1
  • IL-6
  • Chemokines
  • IL-17
60
Q

Cytokines involved in chronic inflammation (3):

A
  • IL-12
  • IFN-gamma
  • IL-17
61
Q

TNF actions (2):

A
  • Stimulates expression of endothelial adhesion molecules.

- Stimulates secretion of other cytokines.

62
Q

IL-1 actions (2):

A
  • Similar to TNF.

- Fever.

63
Q

IL-17 action:

A
  • Recruitment of neutrophils and monocytes.
64
Q

IL-12 action:

A

Increased production of IFN-gamma.

65
Q

IFN-gamma action:

A

Activation of macrophages.

66
Q

Principal mediators or vasodilation (2):

A
  • Histamine.

- Prostaglandins.

67
Q

Principal mediators of increased vascular permeability (4):

A
  • Histamine.
  • Serotonin.
  • C3a/C5a
  • Leukotrienes.
68
Q

Principal mediators of chemotaxis, recruitment and activation (5):

A
  • TNF
  • IL-1
  • Chemokines
  • C3a/C5a
  • Leukotriene B4
69
Q

Principal mediators of fever (3):

A
  • TNF
  • IL-1
  • Prostaglandins
70
Q

Principal mediators of pain (2):

A
  • Prostaglandins

- Bradykinin

71
Q

Principal mediators of tissue damage (2):

A
  • Lysosomal enzymes.

- ROS.

POD Exam III (13 decks)

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