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Pathology - Exam 1 > Overview of Inflammation > Flashcards

Overview of Inflammation Flashcards

1
Q

What are the major signs of inflammation?

A

Calor (heat)
Rubor (redness)
Tumor (swelling)
Dolor (pain)

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2
Q

Acute inflammtion

A

Lasts from hours to days

Characterized by exudation and neutrophil infiltration

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3
Q

Chronic inflammtion

A

Lasts days to years
Characterized by mononuclear inflammatory cell infiltration (lymphocytes, macrophages, plasma cells) with vascular proliferation and fibrosis in later stages

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4
Q

Fever stemming from inflammation is mediated by what?

A

IL-1
TNF
PGE2

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5
Q

Vasodilation of acute inflammation

A

Begins in the precapillary arterioles and results in engorgement of capillary beds
Accounts for the redness and localized heat of inflammation

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6
Q

What mediates the vascular changes associated with Acute inflammation

A

NO (endothelial derived) that induces vascular smooth muscle relaxation
Mast cell release of histamine
Prostaglandins

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7
Q

What maintains vasodilation associated with acute inflammation?

A

Prostaglandins (PGI2, PGD2, PGE3, PGF2)

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8
Q

What are the major vascular changes associated with acute inflammation?

A

Vasodilation

Increased vascular permeability

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9
Q

What two things can cause increased vascular permeability?

A

May be due to inflammatory mediators
OR
Direct injury to endothelial cells

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10
Q

Accumulation of fluid in the extravascular tissue leads to what?

A

Swelling (edema)

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11
Q

Transudate

A

Low protein content

Low specific gravity (

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12
Q

What are the two types of Transudate?

A

Inflammatory

Non-inflammatory

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13
Q

Inflammatory Transudate

A

Early endothelial contraction

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14
Q

Non-inflammatory Transudate

A

Intact endothelium

Some fluid can still escape - due to increased hydrostatic pressure and/or decreased serum oncotic pressure

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15
Q

Exudate

A

Indicative of tissue and endothelial cell damage
High protein content and specific gravity (>1.012)
Often contains inflammatory cells

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16
Q

What are the different types of exudate

A

Fibrinous exudate
Purulent exudate
Sanguineous

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17
Q

Fibrinous exudate

A

High protein (fibrin) content
Few cells
Cloudy

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18
Q

Purulent exudate

A

Pus
Contains cells (neutrophils)
Opaque

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19
Q

Sanguineous exudate

A

Pink to red fluid due to blood

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20
Q

Endothelial cell contraction

A

Forms intercellular gaps (mainly in postcapillary venules) due to reversible contraciton
This occurs rapidly and lasts for 15-30 min

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21
Q

What mediates endothelial cell contraction?

A

Early = Histamine and Bradykinin
Later = Leukotrines and PAF
C3a and C5a induce vasoactive amine release that leads to edema

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22
Q

Endothelial cell retraction

A

Delayed - takes 4-6 hrs to develop and lasts 24+ hours

Occurs due to the restructuring of cytoskeletal proteins

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23
Q

What mediates endothelial cell retraction?

A

IL-1
TNA
IFN-y

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24
Q

Direct venule endothelial injury

A

Can be immediate or delayed

May occur from neutrophilic release of ROS and lysozomal enzymes from inflammation, or injurious agent

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25
Q

What are some factors that activate endothelial cells?

A

Infectious agents
Hypoxia
Inflammatory mediators

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26
Q

Activated endothelial cells are characterized by what?

A

Produce PGI2 and NO (vasodilation)
Contraction/retraction
Increase expression of adhesion molecules
Increased synthesis of inflammatory mediators

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27
Q

What is the sequence of leukocyte events?

A 
Margination
Rolling
Adhesion
Emigration or transmigration
Chemotaxis
28
Q

Margination

A

Mechanical process due to slowing of blood flow
RBCs flow in the middle of the vessel at a slightly faster rate
Neutrophils are closer to the cell wall moving slower

29
Q

Leukocyte rolling

A

Selectins mediate a weak, transient, sticking that slows the cells forward progression

30
Q

What mediates leukocyte adhesion

A

Integrins - ICAM and VCAM on endothelial cells

31
Q

What mediates leukocyte transmigration through vessel walls?

A

PECAM-1

32
Q

Chemotaxis

A

A non-random movement of leukocytes to the site of injury along a concentration gradient of chemotactic factors
Chemotactic factors bind to cell surface receptors
These factors also stimulate leukocyte activation

33
Q

What are some chemotactic factors?

A 
C5a
LTB4
PAF
Cytokines
Bacterial lipids and peptides
FDP
34
Q

What factors activate leukocytes during an inflammatory response?

A 
Bacterial products
Cellular debris
Ab-Ag complexes
Chemokines
Cytokines
Chemotactic factors
35
Q

Activation of leukocytes is characterized by what?

A

Production of Leukotrines and Prostaglandins from Arachadonic Acid
Degranulation and release of Lysozomal enzymes
Production of ROS
Synthesis and secretion of cytokines
Altered expression of cell adhesion molecules

36
Q

Phagocytosis steps

A

1) Attachment mediated by opsonins on targets and specific leukocyte receptors
2) Engulfment into a phagocytic vacuole
3) Lysozomal degranulation by fusion with the phagosome
4) Oxidative burst releasing ROS

37
Q

What are some additional mechanisms of intracellular killing by Leukocytes?

A

Lysozyme
Major basic protein
Defensin
Bactericidal permeability-increasing protein

38
Q

What are the major cells involved in Acute Inflammation?

A

Neutrophils

Monocytes (Macrophages/Histocytes)

39
Q

Neutrophils

A

Morphologic hallmark of acute inflammation
Begin to accumulate within 6-24 hours
Infiltrate tissue in response to tissue necrosis, bacterial, and some fungal infections
Undergo apoptosis after phagocytosis and digestion
Release ROS and lysozomal enzymes

40
Q

Monocytes

A

Emigrate within 48 hours and replace PMNs
Called histocytes, or macrophages after they enter the tissue
Half-life is months in tissue as compared to one day for circulating phagocytes

41
Q

What are some of the functions of activated Monocytes

A

Phagocytize and digest cellular debris and organisms

Take up and metabolize antigens and present membrane=bound antigen to immunocompetent T-cells

42
Q

What are the different types of Inflammatory patterns?

A

Cellulitis
Abscess
Ulcer

43
Q

What are some other Inflammatory cells?

A

Lymphocytes - immune function
Eosinophils - allergic reactions and parasites
Mast Cells - histamine

44
Q

Cellulitis

A

Diffuse, permeative infiltration of neutrophils with edema into the tissues
Firm, ‘woody’ feel

45
Q

Abscess

A

Localized area of liquefactive necrosis or PMNs

46
Q

Ulcer

A

Erosion of an epithelial surface, exposing underlying connective tissue

47
Q

How does acute inflammation differ from chronic inflammation?

A

Acute inflammation takes 10-14 days, Chronic occurs from months-years
Acute inflammation is innate, wheras chronic inflammation relies upon specific, adaptive immune system
Both may be reversible or fatal

48
Q

What are some potential causes for chronic inflammation?

A

Persistent infections
Prolonged exposure to a toxic agent
Immune-mediated inflammatory response

49
Q

Non-specific chronic inflammation

A

Often associated with tissue repair (granulation tissue/fibrosis)
The cellular infiltrate may contain macrophages, lymphocytes, plasma cells and/or eosinophils
A few neutrophils may also be present

50
Q

Degranulomatous Chronic Inflammation

A

Linked to the delayed-type IV hypersensitivity immune reaction

51
Q

Histamine Source and function

A 
Source = Mast cells
Function = Vasodilation and increase vascular permeability
52
Q

Bradykinin Source and function

A 
Source = Plasma protein
Function = Increase vascular permeability, pain
53
Q

NO Source and function

A 
Source = Endothelial cells
Function = Vasodilation, tissue damage
54
Q

Prostaglandins Source and function

A 
Source = Membrane phospholipids
Function = Vasodilation, pain, fever, potentiate other mediators
55
Q

PAF Source and funciton

A 
Source = Leukocytes, endothelial cells
Function = Increase vascular permeability, chemotactic
56
Q

Cytokines source and function

A 
Source = Macrophages, endothelial cells
Function = Endothelial cell and leukocyte activation, fever
57
Q

Leukotrines C, D, E source and function

A 
Source = Membrane phospholipids
Function = Increase vascular permeability, vasoconstriction, bronchoconstriction
58
Q

C5a and C3a source and funciton

A 
Source = Plasma protein
Funciton = Chemotaxis (C5a), Phagocytosis (C3b), Increase vascular permeability (both)
59
Q

What are the different types of wound healing?

A

Labile
Stable
Permanent

60
Q

What does Labile mean and what tissues do it?

A

Continuously dividing

Hematopoeitic cells and surface epithelium

61
Q

What does stable mean (for wound healing), and what tissues do it?

A 
Some replicative activity
Parenchymal cells (liver), smooth muscle cells, fibroblasts
62
Q

What does Permanent mean (for wound healing) and what tissues fall in this category?

A

Non-proliferative - replaced by scar tissue

Neurons and cardiac muscle

63
Q

Healing by Primary Intention

A
  1. Blood clot (minutes)
  2. Neutrophils (within 24 hours)
  3. Early proliferation/migration of epithelial cells (24-48 hrs)
  4. Macrophages replace neutrophils; early granulation tissues (day 3)
  5. Peak neurovasculature (day 5)
  6. Progressive collagen deposition (2nd week)
  7. Increased wound strength during next 4 months
64
Q

Healing by Second Intention

A

More inflammation and granulation tissue

Wound contraction due to fibroblasts

65
Q

What is the effect of GF on wound healing?

A 
Epithelial proliferation
Monocyte chemotaxis
Fibroblast proliferation
Angiogenesis
Collagen synthesis
66
Q

What factors affect wound healing?

A 
Infection (this is the primary cause of delayed healing)
Nutrition
Steroids
Mechanical factors
Poor tissue perfusion

Pathology - Exam 1 (9 decks)

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