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Chapter 2.5- Pathology Of Inflammation Flashcards

1
Q

What are the four cardinal signs of inflammation?

A
  1. Rubor
  2. Rubmor
  3. Calor
  4. Dolor
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2
Q

What cells are primarily associated with acute inflammation?

A

Neutrophils

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3
Q

What are the components of acute inflammation?

A
  1. Alterations in vascular caliber (vasodilation)
  2. Structural changes in microvasculature (edema)
  3. Emigration of leukocytes from microcirculation
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4
Q

What can stimulate inflammation?

A

Infections
Tissue necrosis
Foreign bodies
Immune reactions

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5
Q

What is the function of toll-like receptors?

A

Recognize ligands on Bacteria

Binding triggers the production of inflammatory mediators

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6
Q

What elicits inflammation?

A

Molecules realized from
necrotic cells

Hypoxia (HIF-1alpha)

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7
Q

What changes do blood vessels undergo in response to inflammation?

A
  1. Increased hydrostatic pressure (decreased colloid)
  2. Increased permeability- exudation (high protein concentration to interstitium)
  3. Pus
  4. Vasodilation
  5. Stasis- fluid loss and increased vessel diameter
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8
Q

What is vasodilation induced by?

A

Histamine

NO

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9
Q

What increases vessel permeability?

A

Endothelial contraction

Endothelial injury

Transcytosis

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10
Q

What are the two kinds of lymphatic inflammation?

A

Lymphangitis- channels

Lymphadenitis- nodes

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11
Q

What are the phases of leukocyte extravasation?

A
  1. Margination- vasoconstriction
  2. Rolling- via selectins
  3. Adhesion- via integrins
  4. Migration- across vessel wall (PECAM-1)
  5. Chemotaxis- migration to injury
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12
Q

What molecules mediate rolling and adhesion?

A

Rolling- L, E and P selectins, TNF and IL-1

Adhesion- integrins, TNF, IL-1 and V and I-CAM-1

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13
Q

How does diapedesis occur?

A

Chemokines stimulate leukocyte migration

Cells pierce the BM (collagenases)

Migration along the chemotactic gradient

Adherence to ECM (integrins and CD44)

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14
Q

What molecules are involved with diapedesis?

A

PECAM-1 and CD31

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15
Q

What are the two types of genetic deficiencies in adhesion molecules?

A

Type I- defect in LFA-1 and Mac-1 integrins

Type II- absence of ligand for E and P selectins

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16
Q

What is chemotaxis?

A

Morphological changes that move leukocytes along a chemical gradient

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17
Q

How does chemotaxis occur?

A

Chemokines bind to GPCRs and induce actin polymerization and myosin localization

Filopodia extend

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18
Q

What receptors due leukocytes express to recognize external stimuli?

A
  1. TLRs- microbial products
  2. GPCRs- recognize components of bacterial cell walls
  3. Opsonin- proteins coating microbes
  4. Cytokine- bind those produced in response to microbes (INF-gamma)
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19
Q

What are the characteristics of mediators?

A

Active

One mediator can stimulate the release of others

Vary in range of targets

Short lived

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20
Q

What are types of cell derived mediators and their characteristics?

A
  1. Histamine- mast cells, released upon degranulation, vasodilation and increased permeability, allergic reactions and anaphylaxis
  2. Serotonin- plts, vasodilation and increases vessel permeability
  3. Prostaglandins- mast cells, macrophages, endothelial cells, pain and fever, vascular reaction
  4. Leukotrienes- mast cells and leukocytes, chemoattractants, vasoconstriction and increased permeability, bronchospasm (asthma)
  5. PAF- leukocytes and mast cells, vasodilation and increased permeability, leukocyte adhesion, chemotaxis, oxidative burst
  6. ROS- leukocytes, smooth muscle relaxation, microbicidal
  7. Chemokines- leukocytes and activated macrophages, chemotaxis, leukocyte activation
  8. Cytokines- activated macrophages, endothelial activation, chemical mediator synthesis, IL-1 production, fever, pain
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21
Q

What are the two forms of vascular reaction induced by prostaglandins and which are they produced by?

A

Prostacyclin- vasodilation, plt aggregation inhibition

Thromboxane- vasoconstriction, plt aggregation promotion

22
Q

What is the function of complement?

A

Innate and adaptive immunity for pathogen defence

Proteins are involved with increasing vascular permeability, chemotaxis, opsonization

23
Q

What are the different complement pathways?

A
  1. Classical- Ab binding
  2. Alternative- surface molecules
  3. Lectin- plasma mannose binding lectin binds microbes and activates the pathway directly
24
Q

What is common among all the complement pathways?

A

C3 convertase is produced

C3b attaches and forms MAC

25
Which complement proteins stimulate histamine release?
C3a, C5a, C4a
26
What complement proteins act as opsonins?
C3b and iC3b
27
What are the phases of phagocytosis?
1. Recognition and attachment 2. Engulfment (phagocytosis vacuole) 3. Killing and degradation (respiratory burst)
28
What are neutrophil extracellular traps?
Viscous meshwork of nuclear chromatin that can trap microbes Antimicrobial peptides and enzymes
29
How is inflammation terminated?
Stimulus removed Mediators and neutrophils have short half lives Stop signals
30
What kinda of stop signals terminate inflammation?
Switch in amino acid metabolite produced Liberation of anti-inflammatory cytokines Production of anti-inflammatory mediators Neural impulses can inhibit TNF production
31
How can leukocytes injure normal cells?
ROS NOS Enzymes
32
What types of inflammation are seen in acute?
Serous- thin fluid Fibrinous- fibrin is formed and deposited, scarring Suppurative- large amounts of pus from pyogenic bacteria (abscesses=localized collections) Ulcer- sloughing of necrotic tissue (inflammation and necrosis on surface)
33
What are the outcomes of acute inflammation?
Complete resolution Healing/fibrosis Chronic inflammation
34
What can cause excessive inflammation?
Allergies Autoimmune disorders Atherosclerosis Alzheimer’s disease
35
How do leukocyte induced injuries occur?
When materials that can’t be easily ingested are encountered granular contents are released Cells may rupture Enzymes may be released into the extracellular space
36
What are the inherited defects in leukocyte function?
1. Adhesion- defects of integrin and selectin ligands 2. Phagolysosome function (Chediak-Higashi)- defect of phagosome and lysosome fusion, defective degranulation, giant granules 3. Microbicidal activity (granulomatous disease)- defects in phagocyte oxidase
37
What is the most common cause of acquired defects in leukocyte function?
Marrow suppression
38
What are causes of chronic inflammation?
Persistent infections Immune mediated inflammatory diseases Prolonged exposure to toxic agents
39
What cell type predominates in chronic inflammation?
Mononuclear cells Macrophages specifically
40
What is associated with chronic inflammation?
Angiogenesis Fibrosis
41
What activates macrophages?
Microbial products Cytokines (T lymphs and NK cells) Mediators
42
What cells are responsible for most tissue damage in chronic inflammation?
Macrophages
43
How do lymphs participate in chronic inflammation?
Cells migrate (adhesion molecules and chemokines) Activated by Ags displayed by macrophages Produce cytokines that recruit monocytes
44
What cells are associated with lymphoid organogenesis?
Plasma cells
45
What types of inflammatory reactions do eosinophils mediate?
Parasitic infections IgE
46
What do eosinophil granules contain?
Major basic protein
47
What inflammatory reactions do mast cells mediate?
Hypersensitivity (allergies) IgE
48
What do mast cell granules contain?
Histamine Prostaglandins
49
What is granulomatous inflammation?
Pattern of chronic inflammation Microscopic aggregation of macrophages surrounded by lymphs Attempt to contain a difficult to remove agent
50
What types of granulomatous reactions are there?
1. Foreign body- objects big enough to avoid engulfment | 2. Immune- agents capable of inducing a cell mediated response
51
What is the prototype of the granulomatous reaction?
Tuberculosis
52
What is a naked granuloma?
No surrounding lymphs

Pathology (25 decks)

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