pathology of inflammation Flashcards

1
Q

Symptoms of inflammation: tumor

A

inflammatory tissue swelling

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2
Q

Symptoms of inflammation: rubor

A

inflammatory hyperemic erythema

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3
Q

Symptoms of inflammation: calor

A

inflammatory heat in the tissue

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4
Q

Symptoms of inflammation: dolor

A

pain in the inflamed area

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5
Q

Symptoms of inflammation: Functio laesa

A

functional impairment of the inflamed organ or tissue

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6
Q

Local inflammation

A

is limited to a circumscribed area

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7
Q

Generalized infection

A

the pathogen spreads diffusely throughout the entire body

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8
Q

Metastatic inflammation

A

the transmission of the inflammatory pathogens into other tissues, where the pathogen can trigger a septico-pyemia (septic metastases)

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9
Q

Cells involved in the process of inflammation

A
  • T helper CD4+ cells for humoral immune response
  • T cytotoxic CD8+ cells for cellular immune response
  • B cells which transform into plasma cells, that produce antibodies
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10
Q

What types of cells have granules containing heparin and histamine?

A

Mast cells and basophils.

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11
Q

What additional effect do the substances in the granules of mast cells and basophils have aside from increasing permeability?

A

they cause platelet aggregation

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12
Q

Neutrophils are phagocytic cells, which generate:

A

lysozyme - unspecific germicide
NO synthase - produces nitrous oxide (a bactericide)
the NADPH oxidase system - uses myeloperoxidase to produce oxygen metabolites, a bactericides

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13
Q

Endothelial cells: pro inflammatory cells that generate:

A

selectins – cause adhesion of lymphocytes and granulocytes
factor VIII activator – activates the complement and kinin cascade → increases permeability

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14
Q

Thrombocytes: pro-inflammatory cells that generate

A

inflammation mediators and PDGF

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15
Q

Inflammation Mediators
definition

A

Chemical substances that trigger certain processes in an inflammatory reaction

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16
Q

inflammation mediators Effects:

A

vasodilatation, increased vascular permeability and chemotaxis.

17
Q

Cell-Derived Mediators

A
  • Histamine (produced by mast cells)
  • Serotonin (produced by entero-chromaffin cells)
  • Neutrophilic proteases (produced by PMN)
    Interleukins (IL-1, TNF-α)
  • Chemokines (produced by macrophages and lymphocytes): link up with CXC-R & CC-R mediated by G-proteins
  • Arachidonic acid derivatives (from cell membranes):
    Lipo-oxygenase breaks it down into leukotrienes
    Cyclo-oxygenase breaks it down into prostaglandins
  • Platelet activating factor produced by thrombocytes
18
Q

Plasma-Derived Mediators

A
  • Kinin system (activated by necrosis)
  • Complement system (from serum)
  • C-reactive protein (from hepatocytes)
19
Q

Exudative Inflammatory Reaction definition

A

Response pattern of acute inflammation, characterized by exudation of blood components and emigration of blood cells.

20
Q

Exudative Inflammatory Reaction - Biologic purpose:

A
  • Increased perfusion due to hyperemia → rapid removal of the noxious agent from the site.
    Exudation of blood serum → rapid dilution of the noxious agent.
  • Elimination of pathogens by phagocytosis → rapid destruction of the noxious agent.
  • Rapid containment of the noxious agent.
21
Q

Exudative Inflammatory Reaction - Pathogenetic elements:

A
  • Changes in microcirculation
  • Increases in permeability
  • Leukocyte transmigration
22
Q

Changes in Microcirculation - First phase

A

A transient arteriolar vasoconstriction lasting a few seconds to a few minutes.

23
Q

Changes in Microcirculation - second phase

A

Inflammation mediators lead to vasodilatation of the arterioles, capillaries, and post-capillary venules.
This causes exudation of blood serum that leads to inflammatory tissue swelling with stimulation of the nociceptive nerves (pain nerves)
Result: erythema, swelling, and pain in the inflamed area

24
Q

Changes in Microcirculation - third phase

A

It is brought about by vasodilatation of the capillaries and arterioles and is accompanied by vasoconstriction of the venules.
The circulation slows, filtration pressure elevates, and vascular permeability increases in the inflamed area
The area damaged by the noxious agent is sealed off, paving the way for the “strike force” of leukocytes

25
Q

The biologic purpose of exudation:

A
  • Contaminants are diluted by the protein-rich exudate
  • Contaminants are neutralized by antibodies
  • Contaminants are fixed and damage is controlled
26
Q

Leukocytes migration
Biologic purpose

A

The leucocytes travel into the inflamed regions, exiting the blood via the vascular wall, and defend the infected tissue

27
Q

Leukocyte Margination
Normal Travel:
Activation:

A

Normal Travel: Granulocytes move in the center of the blood vessel.
Activation: Mediators (like histamine, PAF, TNF-a, IL-1, and C5a) cause the endothelium to express adhesion molecules (P-selectin, then E- and L-selectin), making granulocytes roll along the vessel wall.

28
Q

Leukocyte Adhesion

A

Stable Adhesion: TNF-a and IL-1 stimulate the endothelium to produce sticky molecules (ICAM-1).
Firm Attachment: Granulocytes firmly stick to the endothelium and become activated.

29
Q

Leukocyte Diapedesis

A

Attraction: Granulocytes move towards the inflamed area, attracted by chemical signals.
Migration: Granulocytes bind to endothelial molecules (ICAM-1, PECAM-1), create gaps in the endothelium, and migrate through these gaps to reach the inflammation site.

30
Q

In humans, TLR have 2 roles:

A

the recognition of endotoxins in association with CD14 from PMN (e.g.: TLR4 recognizes S lipopolysaccharide)
the recognition of lipoarabinoman from BK wall (e.g.: TLR2)

31
Q
A