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PATHO LEC PRELIMS > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

is the local response of living mammalian tissues to injury from any agent which could be microbial, immunological, physical or chemical agents.

A

inflammation

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2
Q

2 types of inflammation

A

Acute
Chronic

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3
Q

[which type of inflammation]

  • due to early response by the body
  • short duration
A

acute inflammation

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4
Q

[which type of inflammation]

  • occurs after delay
  • it is for longer duration
  • Characterized by response by chronic inflammatory cells.
A

Chronic inflammation

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5
Q

Features of Acute inflammation

onset:
cellular infiltrate:
tissue injury, fibrosis:
local and systemic signs:

A

onset: fast
cellular infiltrate: many neutrophils
tissue injury, fibrosis: mild. self-limited
local and systemic signs: prominent

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6
Q

Features of Chronic inflammation

onset:
cellular infiltrate:
tissue injury, fibrosis:
local and systemic signs:

A

onset: slow
cellular infiltrate: monocytes/macrophages & lymphocytes
tissue injury, fibrosis: severe and progressive
local and systemic signs: less prominent, subtle

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7
Q

trigger stimuli for acute inflammation

A

infections
trauma
tissue necrosis
foreign bodies
immune (hypersensitivity reactions)

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8
Q

Acute Inflammation Acute inflammation has 5 cardinal signs:

A

redness (rubor)
heat (calor)
swelling (tumor)
pain (dolor)
loss of function

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9
Q

Mechanism of Inflammation

A
  1. vasodilation
  2. exudation - edema
  3. emigration of cells
  4. chemotaxis
  5. phagocytosis
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10
Q

Symptoms of:

increased blood flow

A

heat

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11
Q

Symptoms of:

  • vasodilation
  • increased blood flow
A

redness

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12
Q

Symptoms of:

extravasation of fluid (permeability)

A

swelling

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13
Q

Symptoms of:

  • release of soluble chemical mediators
  • cellular influx (chemotaxis)
A

pain

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14
Q

The two main events of the acute inflammation are:

A

Vascular events

Cellular events

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15
Q

vascular events (7)

A

Initial transient vasoconstriction of arterioles.

Persistent progressive vasodilatation.

Elevation of the local hydrostatic pressure.

Increase in vascular permeability.

Transudation of fluid into the extracellular space.

Slowing or stasis of microcirculation.

Leucocytic margination.

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16
Q

Increased permeability of vessels due to widened intercellular junctions and contraction of endothelial cells (Histamine, VEGF, Bradykinin)

A

VASODILATION

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17
Q

Increased intravascular pressure causes an early ___ into interstitium.

A

transudate
(protein-poor filtrate of plasma)

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18
Q

Causes of increased vascular permeability

A

Endothelial cell contraction → intercellular gaps in postcapillary venules

Endothelial injury
- Direct
- Leukocyte induced

Increased transcytosis of fluid

Leakage from new blood vessels

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19
Q

Immediate sustained response - Occurs immediately and lasts until vessel repaired.

A

Direct Endothelial Injury

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20
Q

Results of severe injuries (burns) or infections.

A

Direct Endothelial Injury

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21
Q

Direct Endothelial Injury results in ___ by causing endothelial cell necrosis and detachment.

A

vascular leakage

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22
Q

may also be damaged as a consequence of leukocyte accumulation along the vessel wall.

A

Endothelial cells

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23
Q

Activated leukocytes release many toxic mediators that may cause ___

A

endothelial injury or detachment

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24
Q

Cellular Events

A
  1. Leukocyte recruitment to site of injury
  2. Leukocyte Activation at the site of injury
  3. Phagocytosis of particles
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25
Q

Sequence of events in the recruitment of leukocytes from the vascular lumen to the extravascular space.

A

Extravasation

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26
Q

Process of engulfment of solid particulate material by the leukocytes (neutrophils and monocytes)

A

Phagocytosis of particles

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27
Q

leukocytes assume peripheral portion of lumen

A

MARGINATION

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28
Q

leukocytes tumble slowly along the endothelium and adhere transiently, detach and bind again.

A

ROLLING AND ADHESION

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29
Q

Transmigration of leukocytes across the endothelium.

A

DIAPEDESIS

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30
Q

leukocyte migration towards the site of injury (locomotion oriented along a chemical gradient)

A

CHEMOTAXIS

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31
Q

Major role of:

P-selectin

A

Rolling

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32
Q

Major role of:

E-selectin

A

Rolling and Adhesion

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33
Q

Major role of:

ICAM-1 (Integrin – β1)

A

Adhesion, Arrest & Transmigration

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34
Q

Major role of:

VCAM-1 (Integrin – β2)

A

Adhesion

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35
Q

Major role of:

PECAM-1 (CD-31)

A

Diapedesis

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36
Q

Chemical Mediators of Inflammation:

Cell derived (Preformed)

A

Histamine
Serotonin
Lysosomal enzymes

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37
Q

Chemical Mediators of Inflammation:

Cell derived (Newly synthesized)

A

Prostaglandins
Leukotrienes
Platelet activating factor
Nitric Oxide
Cytokines

38
Q

Chemical Mediators of Inflammation:

Plasma protein derived

A

Complement proteins
Kinins
Proteases activated during coagulation
Factor XII

39
Q

Chemical Mediators of Inflammation:

Vasodilation

A

Prostaglandins
Nitric oxide
Histamine

40
Q

Chemical Mediators of Inflammation:

↑ Vascular permeability

A

Vasoactive amines
C3a, C5a
Bradykinin
Leukotrienes
PAF
Substance P
VEGF

41
Q

Chemical Mediators of Inflammation:

Chemotaxis, Leukocyte activation

A

C5a
LTB4
Chemokines
IL-8
TNF
Bacterial products

42
Q

Chemical Mediators of Inflammation:

Pain

A

Prostaglandins esp PGE2
Bradykinin
Substance P

43
Q

Chemical Mediators of Inflammation:

Tissue damage

A

Neutrophils and macrophage lysosomal enzymes
O2 metabolites
Nitric oxide

44
Q

Both exogenous and endogenous substances can be chemotactic for ___

A

leukocytes

(Chemoattractants)

45
Q

___ predominate in the inflammatory infiltrate during the first 6 -24 hrs

A

Neutrophils

46
Q

Neutrophils are replaced by ___ in 24-48 hrs.

47
Q

Chemoattractants

A

Bacterial products, peptides with N-formylmethionine termini.

Cytokines, especially those of the chemokine family, IL-8.

Components of the complement system, particularly C5a.

Products of the lipoxygenase pathway of arachidonic acid (AA) metabolism, particularly leukotriene B4 (LTB4)

48
Q

defined as the process of engulfment of solid particulate material by the cells (cell- eating).

A

Phagocytosis

49
Q

The cells performing Phagocytosis are called ___

A

phagocytes

50
Q

Degranulation and the oxidative burst destroy the engulfed particle

A

Phagocytosis

51
Q

2 main types of phagocytic cells

A

Polymorphonuclear neutrophils (PMNs)
macrophages

52
Q

Neutrophils and macrophages upon reaching the tissue spaces produce several proteolytic enzymes:

A

Lysozyme
Protease
Collagenase
Elastase
Lipase
Proteinase
Gelatinase
Acid hydrolases

*These enzymes degrade collagen and extracellular matrix.

53
Q

Phagocytosis of the microbe by polymorphs and macrophages involves the following 3 steps:

A
  1. Recognition and attachment – Opsonisation
  2. Engulfment – Phagolysosome formation
  3. Killing and degradation
54
Q

Killing and degradation

O2 dependent by:

A

O2 free radicals
Lysosomal granules

55
Q

Killing and degradation

O2 independent by:

A

Lysozymal hydrolases
Lacoferrin
Major Basic Proteins
Defensins
Nitric Oxide

57
Q

polymorphs after phagocytosis undergo

A

apoptotic cell death

58
Q

most potent bactericidal system of neutrophils

A

Hydrogen peroxide-MPO-Halide system

59
Q

Causes vasodilatation and venular endothelial cell contraction, Junctional widening

60
Q

Released by mast cells, basophils, platelets in response to injury (trauma, heat), immune reactions (IgE-mast cell)

61
Q

Vasodilatory effects similar to those of histamine

62
Q

Platelet dense - body granules; Release triggered by platelet aggregation

63
Q

Prostaglandins and leukotrienes are derived from arachidonic acid metabolism through:

A

Cyclo-oxygenase and lipoxygenase pathway

64
Q

Arachidonic acid metabolism Cyclooxygenase pathway produces:

A

Thromboxane
Prostacycline
Prostaglandin

65
Q

Aggregates platelets & causes vasoconstriction

A

Thromboxane

66
Q

Inhibit platelets aggregation and dilates blood vessels.

A

Prostacycline

67
Q

Increases vasodilation and increases vascular permeability.

A

Prostaglandin

68
Q

chemical mediators (plasma derived)

A

complement
kinins
coagulation factors

69
Q

Chemical Mediators (cell derived)

A

mast cell -histamine
prostaglandins

70
Q

specific mediators:

A

histamine
serotonin

71
Q

Leads to formation of bradykinin from cleavage of precursor (HMWK

A

Kinin system

72
Q

Components C1-C9 present in inactive form
- Activated via classic (C1) or alternative (C3) pathways to generate MAC (C5 – C9) that punch holes in microbe membranes

A

complement system

73
Q

Polypeptide products of many cell types but mainly lymphocytes and macrophages that act on same cell autocrine, as a message to other cells paracrine effect or systemically endocrine effect .

74
Q

Increase endothelial cell adhesion molecule expression and activation and aggregation of PMNs.

75
Q

important cytokines in inflammation.

A

L-1
TNF-α and -β
IFN-γ

76
Q
  • short-acting soluble free-radical gas. - - Produced by endothelial cells, macrophages, causes:
    - Vascular smooth muscle relaxation and vasodilatation
    - Kills microbes in activated macrophages
A

nitric oxide

77
Q

Leak from PMNs and macrophages after demise, attempts at phagocytosis.

A

lysosomal components

78
Q

Increased vascular permeability

A

Histamine
Prostaglandin
Leukotrienes
Serotonin
Bradykinin
PAF (Platelet Activating Factor)
NO (Nitric Oxide)

79
Q

FACTORS DETERMINING VARIATION IN INFLAMMATORY RESPONSE

A

1) Factors involving the organisms
-type of injury
-virulence
-dose

2) Factors involving the host
-general health of host
-immune state of host
-leukopenia
-local host factors

80
Q

Accumulation of excessive clear watery fluid with a variable protein content.

A

serous inflammation

81
Q

serous inflammation occurs in:

A

skin
peritoneal, pleural and pericardial cavities

82
Q

resulting from a burn or viral infection is a good example of the accumulation of a serous effusion either within or immediately beneath the epidermis of the skin

A

skin blister

83
Q

Large amounts of fibrinogen pass the vessel wall, and fibrins are formed in the fluid exudate of extracellular spaces.

A

Fibrinous inflammation

84
Q

fibrin is deposited on the pericardium.

A

Fibrinous pericarditis

85
Q

The formation of purulent exudates or pus.

A

Suppurative (purulent) inflammation

86
Q

Pus is made up of:

A

neutrophils
necrotic cells
edema fluid

87
Q

a localized collection of purulent inflammation accompanied by liquefactive necrosis.

88
Q

FATE OF ACUTE INFLAMMATION

A

resolution
repair
suppuration
chronic inflammation

89
Q

Complete return to normal tissue following acute inflammation.

A

Resolution

90
Q

Healing by regeneration in case of superficial tissue loss
Healing by fibrosis in case of extensive tissue loss

91
Q

Persisting or recurrent acute inflammation leads to ___

A

chronic inflammation

92
Q

EXAMPLES OF ACUTE INFLAMMATION

A

Acute appendicitis
Acute meningitis
Lobar pneumonia
Acute pyelonephritis

PATHO LEC PRELIMS (4 decks)

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