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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Non-specific immune response that occurs in response to any type of bodily injury.

A

Inflammation

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2
Q

3 Roles of Inflammation. How does it accomplish this?

A
  1. Eliminates the initial cause of cell injury
  2. Removes damaged tissue
  3. Generates new tissue
    Diluting, destroying, neutralizing the harmful agent. Followed by events to heal tissue
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3
Q

Causes of Inflammation (6)

A
  1. Immune Response to Pathogenic Microorganism
  2. Trauma (sprains/strains)
  3. Surgery
  4. Caustics (burning, corrosives), Chemical (poisons)
  5. Temperature Extremes (burning)
  6. Ischemic Tissue Damage
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4
Q

Cardinal Signs of Inflammation

A
  1. Swelling
  2. Heat
  3. Altered Function
  4. Redness
  5. Pain
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5
Q

Rubor

A

Redness

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6
Q

Calor

A

Heat

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7
Q

Tumor

A

Swelling

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8
Q

Dolor

A

Pain

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9
Q

Types of Inflammation

A
  1. Acute

2. Chronic

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10
Q

Mechanisms of Acute Inflammation

A
  1. Recognition of Occurred Injury
  2. Inflammatory Response
  3. Elimination of the Cause
  4. Inhibition of the Inflammatory Response
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11
Q

After recognition of the occurred injury, the Acute Inflammatory response has three stages:

A
  1. Vascular
  2. Cellular
  3. Mediators
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12
Q

Vascular change after recognition of occurred injury (Acute Inflammation)

A

Immediate Vascular Changes:

  • Vasodilation
  • Increase Capillary Permeability
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13
Q

Cellular change after recognition of occurred injury (Acute Inflammation)

A

-Influx of Inflammatory Cells (WBCs)

neutrophils, monocytes, macrophages

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14
Q

The study of the forces involved in circulating the blood around the body

A

Hemodynamic

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15
Q

Hemodynamic changes begin… (Acute Inflammation)

A

with inflammation almost immediately post injury

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16
Q

Sequence of the Vascular Stage of Acute Inflammation. (SHARP)

A
  • Momentary constriction of small BVs in area
  • Rapid vasodilation of arterioles and venules that supply area
  • Increase capillary blood flow Heat, Redness
  • Vascular permeability
  • Outpour of protein-rich fluid into extracellular space Swelling, Pain, Altered Function
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17
Q

What happens when the fluid moves out of the vessels? Why is this important? (Acute Inflammation)

A

-Stagnant Flow
-Clotting of blood occurs
Aids in localizing the spread of infectious microorganism

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18
Q

Immediate Transient Response Occurs

A

(Vascular Change)

With Minor Injury

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19
Q

Immediate Sustained Response Occurs

A

(Vascular Change)

  • With more serious injury
  • Continues for several days
  • Damages vessels in the area
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20
Q

Delayed Hemodynamic Response Occurs

A
  • 4-24hrs after injury

- Increase in capillary permeability (sunburn)

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21
Q

What is the cellular stage of acute inflammation marked by?

A

Movement of phagocytic WBCs into the area of injury

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22
Q

2 Types of Leukocytes in Acute Inflammation

A
  1. Granulocytes (neutrophils, eosinophils, basophils)

2. Monocytes (largest o/WBCs)

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23
Q

Sequenced events of Cellular Response in Acute Inflammation

A
  1. Margination/Adhesion of WBCs to endothelial lining of capillaries
  2. Emigration of WBCs into interstitial space
  3. Chemotaxis–WBCs to site of damage
  4. Adherence–Phagocytes to pathogen
  5. Phagocytosis–WBCs engulf and degrade bacteris
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24
Q

3 Stages of Phagocytosis

A
  1. Recognition and adherence
  2. Engulfment
  3. Intracellular Killing
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25
Q

Signs and Symptoms are produced by ____

A

Chemical Mediators

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26
Q

Chemical Mediators originate from either:

A
  1. Plasma

2. From Cells

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27
Q

Mediators Example + Function

A

Vasoactive/Smooth mm constricting properties:
(Histamine, Prostaglandins, Leukotrienes)
Chemotatic Factors:
(Cytokines) –can damage the surrounding tissue

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28
Q

When does an acute inflammation become chronic?

A

When healing begins to occur at same time as active inflammation

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29
Q

When will a Chronic Inflammation begin?

A
  • Recurrent/progressive acute inflammatory response

- Low grade responses that failed to evoke acute response

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30
Q

2 Patterns of Chronic Inflammation

A
  1. Granulomatous Formation

2. Non-Specific Chronic Inflammation

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31
Q

Small lesion, which has a mass of macrophages surrounded by lymphocytes

A

Granulomatous Formation

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32
Q

Granulomatous Formation Associations

A 
Foreign Bodies (splinters, sutures, silica, asbestos)
-Poorly Digested, not controlled by other inflammatory processes
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33
Q

Diffuse accumulation of macrophages and lymphocytes at the site of the injury.

A

Non-Specific Chronic Inflammation

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34
Q

In a Non-Specific Chronic Inflammation, what replaces the normal CT?

A

Subsequent Scar Formation–Made from fibroblast proliferation

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35
Q

Manifestations of Inflammation can be:

A

Local or Systemic

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36
Q

Manifestations range from swelling, abscess, or ulcerations

A

Local Manifestation

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37
Q

A mass of cells and fluid that has seeped out of blood vessels or an organ

A

Exudates

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38
Q

Watery fluids low in protein, results from plasma entering inflammatory site (ex. Blister)

A

Serous Exudates

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39
Q

Occurs when there is severe tissue injury that causes damage to BVs. Or significant leakage of RBCs from capillaries

A

Hemorrhagic Exudates

40
Q

Develops of mucous membrane surfaces, composed of necrotic cells enmeshed in fibropurulent (pussy) exudates (Tonsilitis)

A

Membraneous or Pseudomembranous Exudates

41
Q

Contains pus: Degraded WBCs, protein, tisssue debris (found in abscess, pockets of pus-leukocytes, necrotic tissue, bacteria and edema)

A

Purulent of Suppurative Exudates

42
Q

Large amounts of fibrinogen, form a thick and sticky meshwork

A

Fibrinous Exudates

43
Q

Usually for more severe injuries. Resolves by scar formation

A

Fibrinous Exudates

44
Q

Localized area of inflammation containing purulent exudates

A

Abscess

45
Q

Site of inflammation where an epithelial surface has become necrotic and eroded

A

Ulceration

46
Q

Mediators are released into the circulation

A

Systemic Manifestations

47
Q

Systemic Manifestations Include… (5)

A
  1. Acute Phase Response
  2. Alteration in WBC count
  3. Fever
  4. Lymphandenitis (itis of lymph nodes)
  5. Sepsis and Septic Shock
48
Q

Infection in the blood

A

Sepsis

49
Q

Clinically:

  • Redness, Heat
  • Sharp pain
  • Swelling
  • Loss of Function
A

Acute Inflammation

50
Q

Clinically:

  • Pale, Cool
  • Pain Dulled
  • Swelling not marked
  • Loss of Function
A

Chronic Inflammation

51
Q

Microscopically:

  • PMN’s, platelets
  • Exudates
  • Hyperplasia of local epithelium
A

Acute Inflammation

52
Q

Microscopically:

  • Macrophages, Lymphocytes
  • Proliferation of Fibroblasts (scars)
A

Chronic Inflammation

53
Q

Overlaps with the inflammatory process

A

Tissue Repair and Wound Healing

54
Q

Tissue Repair and Wound Healing Occurs in 3 ways:

A
  1. Resolution
  2. Regeneration
  3. Replacement
55
Q

Process that occurs when there is minimal tissue damage

A

Resolution

56
Q

Process that occurs when there is damaged tissue that is capable of mitosis

A

Regeneration

57
Q

Process that occurs when there is extensive tissue damage or cells are incapable of mitosis

A

Replacement

58
Q

Injured cells are replaced by CT which leaves a permanent scar

A

Fibrous Tissue Repair

59
Q

Resolution, Regeneration, and Replacement occur by similar mechanism called ___

A

Proliferation (cell migration), Differentiation, Interaction with ECM

60
Q

2 Structure Types that make up organs and structures

A
  1. Parenchymal Tissue

2. Stromal Tissue

61
Q

Contains functional cells of an organ or body part

A

Parenchymal Tissue

62
Q

Parenchymal Tissue is divided into 3 types

A
  1. Labile
  2. Stable
  3. Permanent
63
Q

Division of Parenchymal Tissue is divided according to ___

A

Their ability to undergo regeneration

64
Q

Consists of supporting CT, BVs, ECM, and Nerve fibres

A

Stromal Tissue

65
Q

Tissue Regeneration Points (3)

A
  1. Only cells that undergo mitosis
  2. Mild/Moderate injury
  3. Damage to parenchymal cells
66
Q

How is there little or no evidence of previous injury with regeneration?

A

Replaces injured tissue with cells of the same type

67
Q

Capacity of regeneration varies with ___ and ____

A

Tissue and Cell type

68
Q

Body cells are divided into 3 types according to their ability to undergo regeneration

A
  1. Labile
  2. Stable
  3. Permanent/ Fixed
69
Q

Continue to divide and replicate through life, replacing cells that are continually being destroyed (surface epitelial, columnar epithelium, RBCs)

A

Labile Cells

70
Q

Are those that normally stop dividing when growth ceases.
-Capable of undergoing regeneration with added stimulus
(Parenchymal cells of liver and kidneys, smooth muscle cells, vascular endothelial cells)

A

Stable Cells

71
Q

Cannot undergo mitotic division. Replaced by fibrous scar tissue (nerve cells, skeletal/cardiac mm cells)

A

Permanent/Fixed Cells

72
Q

This type of repair occurs with severe or persistent injury

A

Replacement/Fibrous Tissue Repair

73
Q

Replacement/Fibrous Tissue Repair occurs when there is damage to both ___ and ____

A

Parenchymal Cells and ECM

74
Q

Replacement/Fibrous Tissue Repair replaces CT with ____

A

generation granulation tissue and formation of scar tissue

75
Q

Glistening red, moist CT

A

Granulation

76
Q

What is the “pre-tissue” of Replacement/Fibrous Tissue Repair

A

Granulation

77
Q

New cells of Granulation Tissue

A
  • Capillaries
  • Proliferating fibroblasts
  • Residual inflammatory cells
78
Q

New Developements of Granulation Tissue

A
  1. Angiogenesis
  2. Fibrogenesis
  3. Involution to scar tissue formation
79
Q

Growth of new capillaries, new BVs from pre-existing BVs. Minute red granules show at the surface of wound

A

Angiogenesis

80
Q

Activated fibroblasts secrete ____, which contributes to ____.

A

ECM components (fibronectin, collagen), formation of scar tissue

81
Q

Formation built on the granulation tissue framework of new vessels and loose ECM

A

Scar Tissue

82
Q

Process of Scar Tissue occurs in 2 phases

A
  1. Emigration and proliferation of fibroblasts into injury site
  2. Deposition of ECM by these cells
83
Q

As healing progresses, what increases/decreases?

A

Increases: Synthesis and deposition of collagen
Decreases: Proliferating fibroblasts and new BVs

84
Q

Highly vascular granulation tissue is replaced by ___

A

Pale, largely avascular scar tissue

85
Q

Process of repair of injured tissue

A

Wound Healing

86
Q

Primary objective of wound healing

A

To fill the gap created by tissue destruction and to restore functional continuity of the injured part

87
Q

Sutured, surgical incision

  • Healing at faster rate
  • No loss of tissue
A

Primary/First Intention

88
Q

Larger wounds (burns, surface wounds)

  • Healing at slower rate
  • Greater tissue loss
  • Scar tissue formation
A

Secondary/Second Intention

89
Q

Phases of Wound Healing

A
  1. Inflammatory Phase
  2. Proliferation Phase
  3. Maturation/Remodelling Phase
90
Q

Begins at time of injury. Lasts 3-4 days

A

Inflammatory Phase

91
Q

Begins 2-3 days after injury. Lasts 2-3 weeks

-Primary focus to build new tissue to fill wound space

A

Proliferation Phase

92
Q

Proliferation Phase is characterized by:

A
  1. Angiogenesis
  2. Collagen Synthesis
  3. Granulation Tissue Formation
  4. Epithelialisation
  5. Wound Contracture
93
Q

Begins 3 weeks after injury. Lasts 6 months or longer

  • Collagen is remodelled and realigned along tension lines
  • Cells that are no longer needed are removed by apoptosis
A

Maturation/Remodelling Phase

94
Q

Causes of Impaired Wound Healing (10)

A
  1. Desiccation (cells are dehydrated then die)
  2. Malnutrition
  3. Maceration
  4. Necrosis
  5. Impaired Blood Flow (O2 delivery)
  6. Impaired Inflammatory/Immune Responses
  7. Infection or Abnormal Bacteria Presence
  8. Wound Separation
  9. Foreign Bodies
  10. Age
95
Q

Abnormality in healing by scar tissue. Tumor like mass caused by excessive production of collagen

A

Keloid Formation

Pathology (7 decks)

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