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2420 Pathology > Module 4 Inflammation & Repair > Flashcards

Module 4 Inflammation & Repair Flashcards

1
Q

Inflammation Purpose

A
  • Destroy/limit spread of injurious agent
  • Repair/replace damaged tissue
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2
Q

Inflammation Response Components

A
  • Blood vessels
  • Leukocytes (WBC)
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3
Q

R’s of Response

A
  • Recognition
  • Recruitment
  • Removal
  • Regulation
  • Resolution
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4
Q

Recognition

A
  • Offending agent identified
  • By host cells & molecules
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5
Q

Recruitment

A
  • Leukocytes & plasma proteins
  • From circulation
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6
Q

Removal

A
  • Agent destroyed & elimination
  • By activated leukocytes & proteins
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7
Q

Regulation

A
  • Reaction controlled & terminated
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8
Q

Resolution

A
  • Repair damaged tissue
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9
Q

Response Coordination

A
  • Macrophages recognize microbes & damaged cells
  • Liberate mediators
  • Trigger vascular & cellular reactions
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10
Q

Inflammation Principles

A
  • Dynamic process
  • Protective response (can be harmful)
  • Non-specific reaction
  • Modified by host & injurious/etiologic factors
  • Injury in non-lethal
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11
Q

Blood Vessels in Response

A
  • Dilations & opening of capillary beds
  • Increased permeability
  • Blood vessel lining alteration (endothelial)
  • Endothelial cell contraction
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12
Q

Increased Permeability

A
  • Protein rich fluid flows out into tissue
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13
Q

Endothelial Cell Contraction

A
  • Response to histamine
  • Leukocytes pass through
  • Interendothelial spaces
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14
Q

Leukocytes

A
  • Able to ingest microbes, dead cells, foreign material
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15
Q

Vascular Events

A
  • Take place in arteries, capillaries, venules
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16
Q

Cellular Events

A
  • WBCs/leukocytes
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17
Q

Chemical Events

A
  • Release mediators
  • Cause changes in cells & vessels
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18
Q

Vascular Reactions of Acute Inflammation

A
  • Changes to blood flow
  • Permeability of vessels
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19
Q

Purpose of Vascular Reactions

A
  • Maximize leukocytes plasma protein movement
  • Out of circulation to injury site
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20
Q

Vascular Events of Capillary Bed

A
  • Transient vasoconstriction of arterioles
  • Vasodilation of vessels (chemically mediated)
  • Increase vascular permeability
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21
Q

Vasodilation of Vessels

A
  • Opening of precapillary sphincters of arterioles
  • Opening of new capillary beds
  • Opening of arterial venous shunts
  • Increase blood flow to affected area
  • Visible redness (rubor)
  • Heat (calor)
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22
Q

Increased Vascular Permeability

A
  • Outpouring of fluids & proteins from vessels
  • Escape of plasma/plasma proteins & WBC from vessel
  • Edema & tissue swelling
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23
Q

Inducing Increased Vascular Permeability

A
  • Histamine
  • Kinins
  • Produce gaps in endothelial cells
  • Increase fluid passage through endothelium
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24
Q

Local Hemoconcentration

A
  • Increased blood viscosity
  • Packing of RBC
  • Slowing blood flow
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25
Cellular Events of Leukocytes
- Engulf, degrade bacteria, immune complexes, cell debris - Release lysosomal enzymes - Release chemical mediators - Release toxic radicals
26
Margination
- Viscous blood from stagnation of blood flow - WBCs pushed into periphery of vessels
27
Adhesion of Leukocytes
- To endothelium at inflammation site - Promoted by cell adhesion molecules
28
Transmigration/Diapedesis
- Leukocytes through vessel wall - Squeeze between widened endothelial cell gaps - Penetrate basement membrane
29
Movement Towards Offending Agent
- Neutrophils (PMNs) attract to area of injury - 1st type of leukocyte at inflamed area - Later replaced by macrophages
30
Chemotaxis
- Attraction of cells (WBC) to site of injury - By release factors from injured cells - Movement along chemical gradient
31
Phagocytosis
- Inflammatory cells phagocytose invading agent/organism - Process of ingestion of foreign components - By neutrophils & macrophages
32
Phagocytosis Actions
- Recognition & attachment to neutrophil/macrophage - Engulfment of micro-organisms by phagocytic cells - Killing/degradation
33
Chemical Mediator Characteristics
- Produced locally or circulating - Few targets or widespread activity - Tightly regulated function - Potential harmful effects
34
Cell-Derived Vasoactive Mediators
- Produced locally by cells - At injury site
35
Plasma Derived Vasoactive Mediators
- Circulating within plasma
36
Histamine
- Cell-derived mediator - Early phases of acute inflammation - Released from mast cells
37
Histamine Functions
- Vasodilation of arterioles - Increased vascular permeability in venules
38
Prostaglandins & Leukotrienes
- Cell-derived mediator - Increase vascular permeability
39
Platelet Activating Factor Functions
- Vasodilation - Increase vascular permeability - Produces aggregation of platelets at injury site
40
Plasma Protease Systems
- 3 interrelated systems - Series of inactive enzymes (proenzymes) - Activation of first proenzyme - Initiates cascade of enzyme activation
41
Kinin System
- Release bradykinin
42
Kinin System Functions
- Increase vascular permeability - Contraction of smooth muscle - Vasodilation - Produces pain
43
Complement System
- Non-specific self defense mechanism
44
Complement System Activation
- Antigen-antibody complexes - By-products released by bacteria - By components of other plasma protein systems
45
Clotting (Coagulation) System
- Forms fibrinous exudate (meshwork) at inflamed site - Fibrin mesh - Trap foreign components
46
Clotting (Coagulation) System Function
- Prevent spread of infection & inflammation - Keep foreign components at site of phagocytic activity - Forms clot to stop bleed - Framework for repair/healing
47
Cardinal Signs of Inflammation
- Redness (rubor) - Swelling/tumor - Heat (calor) - Pain (dolar) - Loss of function (functio laesa)
48
Pus Contents
- Neutrophils - Liquefied debris of dead cells - Edema fluid
49
Inflammation Side Effects
- Fever - Leukocytosis - Malaise - Anorexia - Sleepiness
50
Fever
- Release of factors from RBC/pyrogens - Act on temp regulating centre in hypothalamus - Prostaglandins mediator
51
Leukocytosis
- Increase in WBC count - Bone marrow increases production
52
Acute Leukocytosis
- Increase in neutrophils
53
Chronic Leukocytosis
- Lymphocytosis (lymphocyte increase)
54
Allergy Leukocytosis
- Eosinophilia
55
Harmful Consequences of Inflammation
- Misdirected (autoimmune) - Exaggerated (against harmless agents) - Uncontrolled (anaphylaxis)
56
Acute Inflammation
- Sudden onset - 1+ cardinal signs - Hours to days - Neutrophils
57
Acute Morphology
- Vascular & exudative changes - Vasodilation - Increase vascular permeability - Inflammatory exudate
58
Chronic Inflammation
- Agent persists - Weeks to months - Increase in macrophages, lymphocytes, plasma, eosinophils
59
Chronic Morphology
- Proliferation of connective tissue/vessels - More fibroblasts, vessels, angiogenesis
60
Angiogenesis
- Formation of new blood vessels
61
Common Sites of Acute Inflammation
- Skin - Mouth - GI around gut - Lung
62
Purulent/Suppurative Inflammation
- Pus producing pyogenic bacteria - Liquefactive tissue necrosis
63
Abscess Occurrence
- Pus localized to cavity - Caused by tissue destruction - Walled off - No blood vessels
64
Pus Collection
- Localized - Cardinal signs of tumor
65
Skin Abscess Treatment
- Incision & drainage - Cleanout infected contents
66
Deep Abscess Treatment
- Organs effected - Surgical approach
67
Fibrinous Inflammation
- Increased vascular permeability - Large fibrinogen molecules pass through inter endothelial spaces - Resulting in fibrin deposits
68
Fibrinous Exudates
- Occur in spaces - Pleural, pericardial, meninges
69
Fibrous Pericarditis
- Exaggerated immune response - Cardiac surgery - Stringy fibrous exudate
70
Serous Inflammation
- Exudation of cell poor fluid
71
Effusion
- Serous inflammation in pleura/pericardium
72
Ascites
- Serous inflammation in peritoneum
73
Bulla/Blister
- Serous inflammation in skin
74
Ulcer
- Local defect on mucosal surfaces - Create breach/hole in mucosa
75
Acute Inflammation Outcomes
- Complete resolution - Healing by connective tissue replacement (scarring/fibrosis) - Progression to chronic inflammation
76
Causes of Chronic Inflammation
- Persistent infection/injury - Hypersensitivity - Chronic exposure to toxins
77
Macrophages
- Dominant cell type
78
Lymphocytes
- Adaptive immunity - Activated by microbes & environmental antigens - Release cytokines (amplify response) - T, B, NK cells
79
Eosinophils
- Allergic reactions & parasitic infections - Granules contain toxic protein - Tissue damage in allergic reactions
80
Plasma Cells
- Differentiated B cell type - Create antibodies/immunoglobulins
81
Granulomas
- Activated macrophages surrounded by T lymphocytes - Macrophages accumulated in cytoplasm (epithelioid histiocytes) - Macrophages fuse to form giant multinucleate cells (langhan) - Containment of foreign body
82
Granuloma Causes
- Mycobacterial - Fungal - Bacteria
83
Restoration to Structural/Function Integrity
- Removal of exudate - Removal of cellular & tissue debris - Replacement of lost cells/tissue
84
Regeneration
- Replacing tissue/cells lost in inflammation - Identical/very similar
85
Repair
- Replacement by cells/tissues - Same or different often simpler type
86
Labile Cells
- Continue to proliferate throughout life - Follow cell cycle
87
Stable Cells
- Low level of replication - Divide in response to stimuli - G0 but recruited to G1
88
Permanent Cells
- No division postnatal life - Exited cell cycle
89
Repair Process
- Angiogenesis (form new vessels) - Fibrosis (proliferation of fibroblasts & EMC deposits - Maturation/organization of scar, collage, ECM
90
Repair Functionality
- Never regain initial strength (70-80%) - Original tensile strength at 3 months
91
Crust Formation
- Quick wound closure - Infection barrier - Stops blood leakage - After hemorrhage wound covered by coagulated blood
92
Removal of Dead Debris
- Removed by sloughing (falling off) - Inflammatory response initiates repair - Small debris removed by liquefaction & phagocytosis
93
Replacement of Lost Cells
- Cell migration - Cell proliferation (division)
94
Skin Wound Healing Cells
- Fibroblasts - Endothelium (after angiogenesis) - Epithelium (migrates in sheets) - Direction of fibers determines tissue tension
95
Granulation Tissue
- New tissue - Proliferating cellular & extracellular components - Replace lost tissue
96
Pink Granules
- Newly formed capillaries - Fibroblasts elaborating connective tissue (extracellular) - Macrophages
97
Granulation Tissue Characteristics
- Bleeds if touched - Insensitive to pain (no nerves) - Resistant to infections
98
Adhesions
- Fibrosis & fibrous connections of serosal surfaces - Form in injury repair/inflammation of serosal surfaces
99
Keloid
- Post-traumatic repair - Connective tissue proliferation in dermis - Beyond necessary amount
100
Keloid Lesions
- Red - Raised - Firm - Sharp & irregular outline - Smooth & shiny surface - Prominent scar
101
Superficial Primary Repair
- Epidermis only (dermis intact) - No bleeding - Regeneration of epithelium - Epithelial cells migrate across wound
102
Deep Primary Repair
- Involves dermis - Few capillaries injured - Some bleeding - Fibroblasts & endothelial cells migrate
103
Secondary Repair
- Considerable tissue loss - Edges unable to be approximated - Granulation tissue to scar
104
Rate of Wound Closure
- Latent period (size of wound unchanged) - Period of contraction (granulation tissue shrinkage) - Epidermization
105
Cicatrization
- Scar formation
106
Transudate
- Fluid contains little/no protein cells Changes in hydrostatic/osmotic pressure in vessels
107
Affecting Factors of Local Healing Rate
- Decreased blood supply - Denervation - Local infection - Foreign bodies - Necrotic tissue - Mechanical stress - Hematoma - Increased wound size - Tissue type
108
Affecting Factors of Systemic Healing Rate
- Decreased blood supply - Age - Anemia - Malignancy - Malnutrition - Obesity - Diabetes - Infection - Organ failure
109
Promoting Healing
- Protect wound - Irrigation - Immobilize - Avoid manipulation - Drain pus & exudate - Antibiotics - Debridement - Control bleeding/remove clotted blood - Preserve blood supply (no tight dressing) - Suture material if necessary - Elevate - Thermal modification - Optimal nutrition

2420 Pathology (13 decks)

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