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Medical Pathology - Robin's Basic Pathology > Lecture 04 - Inflammation > Flashcards

Lecture 04 - Inflammation Flashcards

1
Q

Inflammation - General Characteristics

A

reaction of a vascular system to a destructive factor

good unless becomes chronic or excessive

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2
Q

Inflammation - Inducers

A
  1. infection
  2. cell death
  3. tumor
  4. chemical/physical injury
  5. foreign objects
  6. immunologic injury
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3
Q

Chronic Inflammation Characteristics

A
  1. slow
  2. lymphocytes, macrophages
  3. often sever and progressive tissue injury
  4. subtle local and systemic signs
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4
Q

Acute Inflammation Characteristics

A
  1. fast
  2. neutrophils
  3. mild, self-limited tissue injury
  4. prominent local and systemic injury
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5
Q

Inflammation Effective Factors

A
  1. WBCs
  2. Plasma proteins
  3. Endothelium
  4. intercellular matrix elements
  5. CT cells: mast cells, fibroblasts, macrophages
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6
Q

Inflammation Process

A
  1. recognition
  2. recruitment
  3. removal
  4. resolution
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7
Q
  1. Recognition
A

recognition of destructive agent from self cells by TLRs
- Extracellular domain: a head full of lucine aa.
- Intracellular domain: Toll Interleukin I Receptor (TIR)
- Transmembrane domain
elements
PAMPs

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8
Q

PAMPs

A
  • liposacharides: g- bacteria
  • peptidoglicans: g+ bacteria
  • viral nucleic acids
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9
Q

TLRs

A 
TLR1,2: bacterial parasites
TLR2,6: g+ bacteria and fungi
TLR4: g- bacteria
TLR5: flagellated bacteria
TLR3: viral dsRNA
TLR7,8: viral ssRNA
TLR9: bacterial DNA 
PRP --> connection to PAMP
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10
Q

Inflammazon

A 
like TLR
activated by:
Ca
Free radicals
Urate
Cholesterol
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11
Q
  1. Recruitment
A 
WBCs migration:
Phase 1: vascular changes (hemodynamic)
- vessels dilation
- increased vascular permeability
Phase 2: cellular migration
- transuade --> exudate
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12
Q

Transudate

A

fluid with low protein, in 1.012 gravity, as a result of imbalance between osmotic and hydrostatic pressures

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13
Q

Exudate

A

inflammatory extravascular fluid with high protein, cellular debris, in 1.020 gravity

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14
Q

Vascular Permeability Change Mechanisms

A
  1. contraction of endothelium cells –> histamine, bradykinin, leukotriene –> 15-20 mins
  2. damage to endothelium cells –> pyogens, chemicals, buned flesh, … –> immediate and long
  3. increased transcytosis –> VEGF –> increased phagocytosis/macrocytosis and pinocytosis –> mostly in venules
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15
Q

Inflammatory Responses

A
  1. immediate and short
    - histamine
  2. immediate and prolonged
    - direct endothelial injury
  3. delayed and prolonged
    - UV injury
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16
Q

WBCs Migration Mechanisms

A
  1. migration
  2. rolling
  3. adhesion
  4. transmigration
17
Q
  1. Migration
A

As a result of increased viscosity of cells in plasma

18
Q
  1. Rolling
A

Receptor-ligand bonds
ligand:
- Endothelial selectin: on endothelium
- Leukocytal selectin: on WBCs
- Placketal selectin: on plackets and endothelium
receptor:
GlyCam-1 on endothelial cells on Sialyl Lewis X

19
Q
  1. Adhesion
A

immunoglobulins: ICAM-1, VCAM-1 on endothelial cells
integrin: LFA-1, VLA-1
- surface by IL-1, TNF, complement system

20
Q

Weibel-Palade

A

intracellular P-selectin –> under inflammatory mediators (histamine, thrombin, complement system) surfaces

21
Q
  1. Transmigration
A

CD31 (PECAM-1) –> mucin-like glycoprotein
chemotaxis:
1. exogen elements–> bacterial cell wall (N-formil-methionine)
2. endogen elements –> chemokines, LTs

22
Q
  1. Removal
A
  1. recognition –> opsonization –> IgG (FcR), C3D (CR1-3)
  2. Engulfment –> phagosome
  3. phagolysosome –> 1. O2 dependent: NADPH oxydase then MPO for HOCL- 2. BPI + acid hydrolase (azurophilic granules), MBP (eosinophil’ specific granules)
23
Q
  1. Resolution
A

the debris is destroyed

24
Q

Inflammation Damage

A
  1. frustrated phagocytosis: micro organism attached to a surface
    - glumeronephritis
  2. membranolytic substance –> urate mono sodium
  3. persistent leukocyte activation: in case of resistant ag
  4. premature degranulation
25
Q

Genetic Inflammatory Defects

A
  1. leukocyte adhesion deficiency I: no beta integrin peptide
  2. leukocyte adhesion deficiency II:no sialyl-lewis X
  3. chronic granulomatosis: no membranous NADPH oxydase (X-linked) or no cytoplasmic NADPH oxydase (autosomal)
  4. Chediac-Hidashi syndrome: cant make any phagolysosome
26
Q

Chemotaxis Defects

A

burned
diabetes
immunodeficiency
sepsis

27
Q

Adhesion Defects

A

sweet diabetes

chronic hemodialysis

28
Q

Bactericidal Defects

A 
leukemia
anemia
diabetes
malnutrition
newborns

Medical Pathology - Robin's Basic Pathology (9 decks)

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