Inflammation Flashcards

(95 cards)

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
Signs and Symptoms are produced by ____
Chemical Mediators
26
Chemical Mediators originate from either:
1. Plasma | 2. From Cells
27
Mediators Example + Function
Vasoactive/Smooth mm constricting properties: (Histamine, Prostaglandins, Leukotrienes) Chemotatic Factors: (Cytokines) --can damage the surrounding tissue
28
When does an acute inflammation become chronic?
When healing begins to occur at same time as active inflammation
29
When will a Chronic Inflammation begin?
- Recurrent/progressive acute inflammatory response | - Low grade responses that failed to evoke acute response
30
2 Patterns of Chronic Inflammation
1. Granulomatous Formation | 2. Non-Specific Chronic Inflammation
31
Small lesion, which has a mass of macrophages surrounded by lymphocytes
Granulomatous Formation
32
Granulomatous Formation Associations
``` Foreign Bodies (splinters, sutures, silica, asbestos) -Poorly Digested, not controlled by other inflammatory processes ```
33
Diffuse accumulation of macrophages and lymphocytes at the site of the injury.
Non-Specific Chronic Inflammation
34
In a Non-Specific Chronic Inflammation, what replaces the normal CT?
Subsequent Scar Formation--Made from fibroblast proliferation
35
Manifestations of Inflammation can be:
Local or Systemic
36
Manifestations range from swelling, abscess, or ulcerations
Local Manifestation
37
A mass of cells and fluid that has seeped out of blood vessels or an organ
Exudates
38
Watery fluids low in protein, results from plasma entering inflammatory site (ex. Blister)
Serous Exudates
39
Occurs when there is severe tissue injury that causes damage to BVs. Or significant leakage of RBCs from capillaries
Hemorrhagic Exudates
40
Develops of mucous membrane surfaces, composed of necrotic cells enmeshed in fibropurulent (pussy) exudates (Tonsilitis)
Membraneous or Pseudomembranous Exudates
41
Contains pus: Degraded WBCs, protein, tisssue debris (found in abscess, pockets of pus-leukocytes, necrotic tissue, bacteria and edema)
Purulent of Suppurative Exudates
42
Large amounts of fibrinogen, form a thick and sticky meshwork
Fibrinous Exudates
43
Usually for more severe injuries. Resolves by scar formation
Fibrinous Exudates
44
Localized area of inflammation containing purulent exudates
Abscess
45
Site of inflammation where an epithelial surface has become necrotic and eroded
Ulceration
46
Mediators are released into the circulation
Systemic Manifestations
47
Systemic Manifestations Include... (5)
1. Acute Phase Response 2. Alteration in WBC count 3. Fever 4. Lymphandenitis (itis of lymph nodes) 5. Sepsis and Septic Shock
48
Infection in the blood
Sepsis
49
Clinically: - Redness, Heat - Sharp pain - Swelling - Loss of Function
Acute Inflammation
50
Clinically: - Pale, Cool - Pain Dulled - Swelling not marked - Loss of Function
Chronic Inflammation
51
Microscopically: - PMN's, platelets - Exudates - Hyperplasia of local epithelium
Acute Inflammation
52
Microscopically: - Macrophages, Lymphocytes - Proliferation of Fibroblasts (scars)
Chronic Inflammation
53
Overlaps with the inflammatory process
Tissue Repair and Wound Healing
54
Tissue Repair and Wound Healing Occurs in 3 ways:
1. Resolution 2. Regeneration 3. Replacement
55
Process that occurs when there is minimal tissue damage
Resolution
56
Process that occurs when there is damaged tissue that is capable of mitosis
Regeneration
57
Process that occurs when there is extensive tissue damage or cells are incapable of mitosis
Replacement
58
Injured cells are replaced by CT which leaves a permanent scar
Fibrous Tissue Repair
59
Resolution, Regeneration, and Replacement occur by similar mechanism called ___
Proliferation (cell migration), Differentiation, Interaction with ECM
60
2 Structure Types that make up organs and structures
1. Parenchymal Tissue | 2. Stromal Tissue
61
Contains functional cells of an organ or body part
Parenchymal Tissue
62
Parenchymal Tissue is divided into 3 types
1. Labile 2. Stable 3. Permanent
63
Division of Parenchymal Tissue is divided according to ___
Their ability to undergo regeneration
64
Consists of supporting CT, BVs, ECM, and Nerve fibres
Stromal Tissue
65
Tissue Regeneration Points (3)
1. Only cells that undergo mitosis 2. Mild/Moderate injury 3. Damage to parenchymal cells
66
How is there little or no evidence of previous injury with regeneration?
Replaces injured tissue with cells of the same type
67
Capacity of regeneration varies with ___ and ____
Tissue and Cell type
68
Body cells are divided into 3 types according to their ability to undergo regeneration
1. Labile 2. Stable 3. Permanent/ Fixed
69
Continue to divide and replicate through life, replacing cells that are continually being destroyed (surface epitelial, columnar epithelium, RBCs)
Labile Cells
70
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)
Stable Cells
71
Cannot undergo mitotic division. Replaced by fibrous scar tissue (nerve cells, skeletal/cardiac mm cells)
Permanent/Fixed Cells
72
This type of repair occurs with severe or persistent injury
Replacement/Fibrous Tissue Repair
73
Replacement/Fibrous Tissue Repair occurs when there is damage to both ___ and ____
Parenchymal Cells and ECM
74
Replacement/Fibrous Tissue Repair replaces CT with ____
generation granulation tissue and formation of scar tissue
75
Glistening red, moist CT
Granulation
76
What is the "pre-tissue" of Replacement/Fibrous Tissue Repair
Granulation
77
New cells of Granulation Tissue
- Capillaries - Proliferating fibroblasts - Residual inflammatory cells
78
New Developements of Granulation Tissue
1. Angiogenesis 2. Fibrogenesis 3. Involution to scar tissue formation
79
Growth of new capillaries, new BVs from pre-existing BVs. Minute red granules show at the surface of wound
Angiogenesis
80
Activated fibroblasts secrete ____, which contributes to ____.
ECM components (fibronectin, collagen), formation of scar tissue
81
Formation built on the granulation tissue framework of new vessels and loose ECM
Scar Tissue
82
Process of Scar Tissue occurs in 2 phases
1. Emigration and proliferation of fibroblasts into injury site 2. Deposition of ECM by these cells
83
As healing progresses, what increases/decreases?
Increases: Synthesis and deposition of collagen Decreases: Proliferating fibroblasts and new BVs
84
Highly vascular granulation tissue is replaced by ___
Pale, largely avascular scar tissue
85
Process of repair of injured tissue
Wound Healing
86
Primary objective of wound healing
To fill the gap created by tissue destruction and to restore functional continuity of the injured part
87
Sutured, surgical incision - Healing at faster rate - No loss of tissue
Primary/First Intention
88
Larger wounds (burns, surface wounds) - Healing at slower rate - Greater tissue loss - Scar tissue formation
Secondary/Second Intention
89
Phases of Wound Healing
1. Inflammatory Phase 2. Proliferation Phase 3. Maturation/Remodelling Phase
90
Begins at time of injury. Lasts 3-4 days
Inflammatory Phase
91
Begins 2-3 days after injury. Lasts 2-3 weeks | -Primary focus to build new tissue to fill wound space
Proliferation Phase
92
Proliferation Phase is characterized by:
1. Angiogenesis 2. Collagen Synthesis 3. Granulation Tissue Formation 4. Epithelialisation 5. Wound Contracture
93
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
Maturation/Remodelling Phase
94
Causes of Impaired Wound Healing (10)
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
Abnormality in healing by scar tissue. Tumor like mass caused by excessive production of collagen
Keloid Formation