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Pathology > Chapter 2.5- Pathology Of Inflammation > Flashcards

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
Q

Which complement proteins stimulate histamine release?

A

C3a, C5a, C4a

26
Q

What complement proteins act as opsonins?

A

C3b and iC3b

27
Q

What are the phases of phagocytosis?

A
  1. Recognition and attachment
  2. Engulfment (phagocytosis vacuole)
  3. Killing and degradation (respiratory burst)
28
Q

What are neutrophil extracellular traps?

A

Viscous meshwork of nuclear chromatin that can trap microbes

Antimicrobial peptides and enzymes

29
Q

How is inflammation terminated?

A

Stimulus removed

Mediators and neutrophils have short half lives

Stop signals

30
Q

What kinda of stop signals terminate inflammation?

A

Switch in amino acid metabolite produced

Liberation of anti-inflammatory cytokines

Production of anti-inflammatory mediators

Neural impulses can inhibit TNF production

31
Q

How can leukocytes injure normal cells?

A

ROS

NOS

Enzymes

32
Q

What types of inflammation are seen in acute?

A

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
Q

What are the outcomes of acute inflammation?

A

Complete resolution

Healing/fibrosis

Chronic inflammation

34
Q

What can cause excessive inflammation?

A

Allergies

Autoimmune disorders

Atherosclerosis

Alzheimer’s disease

35
Q

How do leukocyte induced injuries occur?

A

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
Q

What are the inherited defects in leukocyte function?

A
  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
Q

What is the most common cause of acquired defects in leukocyte function?

A

Marrow suppression

38
Q

What are causes of chronic inflammation?

A

Persistent infections

Immune mediated inflammatory diseases

Prolonged exposure to toxic agents

39
Q

What cell type predominates in chronic inflammation?

A

Mononuclear cells

Macrophages specifically

40
Q

What is associated with chronic inflammation?

A

Angiogenesis

Fibrosis

41
Q

What activates macrophages?

A

Microbial products

Cytokines (T lymphs and NK cells)

Mediators

42
Q

What cells are responsible for most tissue damage in chronic inflammation?

A

Macrophages

43
Q

How do lymphs participate in chronic inflammation?

A

Cells migrate (adhesion molecules and chemokines)

Activated by Ags displayed by macrophages

Produce cytokines that recruit monocytes

44
Q

What cells are associated with lymphoid organogenesis?

A

Plasma cells

45
Q

What types of inflammatory reactions do eosinophils mediate?

A

Parasitic infections

IgE

46
Q

What do eosinophil granules contain?

A

Major basic protein

47
Q

What inflammatory reactions do mast cells mediate?

A

Hypersensitivity (allergies)

IgE

48
Q

What do mast cell granules contain?

A

Histamine

Prostaglandins

49
Q

What is granulomatous inflammation?

A

Pattern of chronic inflammation

Microscopic aggregation of macrophages surrounded by lymphs

Attempt to contain a difficult to remove agent

50
Q

What types of granulomatous reactions are there?

A
  1. Foreign body- objects big enough to avoid engulfment

2. Immune- agents capable of inducing a cell mediated response

51
Q

What is the prototype of the granulomatous reaction?

A

Tuberculosis

52
Q

What is a naked granuloma?

A

No surrounding lymphs

Pathology (25 decks)

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