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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
Q

Cellular Events of Leukocytes

A
  • Engulf, degrade bacteria, immune complexes, cell debris
  • Release lysosomal enzymes
  • Release chemical mediators
  • Release toxic radicals
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26
Q

Margination

A
  • Viscous blood from stagnation of blood flow
  • WBCs pushed into periphery of vessels
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27
Q

Adhesion of Leukocytes

A
  • To endothelium at inflammation site
  • Promoted by cell adhesion molecules
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28
Q

Transmigration/Diapedesis

A
  • Leukocytes through vessel wall
  • Squeeze between widened endothelial cell gaps
  • Penetrate basement membrane
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29
Q

Movement Towards Offending Agent

A
  • Neutrophils (PMNs) attract to area of injury
  • 1st type of leukocyte at inflamed area
  • Later replaced by macrophages
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30
Q

Chemotaxis

A
  • Attraction of cells (WBC) to site of injury
  • By release factors from injured cells
  • Movement along chemical gradient
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31
Q

Phagocytosis

A
  • Inflammatory cells phagocytose invading agent/organism
  • Process of ingestion of foreign components
  • By neutrophils & macrophages
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32
Q

Phagocytosis Actions

A
  • Recognition & attachment to neutrophil/macrophage
  • Engulfment of micro-organisms by phagocytic cells
  • Killing/degradation
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33
Q

Chemical Mediator Characteristics

A
  • Produced locally or circulating
  • Few targets or widespread activity
  • Tightly regulated function
  • Potential harmful effects
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34
Q

Cell-Derived Vasoactive Mediators

A
  • Produced locally by cells
  • At injury site
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35
Q

Plasma Derived Vasoactive Mediators

A
  • Circulating within plasma
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36
Q

Histamine

A
  • Cell-derived mediator
  • Early phases of acute inflammation
  • Released from mast cells
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37
Q

Histamine Functions

A
  • Vasodilation of arterioles
  • Increased vascular permeability in venules
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38
Q

Prostaglandins & Leukotrienes

A
  • Cell-derived mediator
  • Increase vascular permeability
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39
Q

Platelet Activating Factor Functions

A
  • Vasodilation
  • Increase vascular permeability
  • Produces aggregation of platelets at injury site
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40
Q

Plasma Protease Systems

A
  • 3 interrelated systems
  • Series of inactive enzymes (proenzymes)
  • Activation of first proenzyme
  • Initiates cascade of enzyme activation
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41
Q

Kinin System

A
  • Release bradykinin
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42
Q

Kinin System Functions

A
  • Increase vascular permeability
  • Contraction of smooth muscle
  • Vasodilation
  • Produces pain
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43
Q

Complement System

A
  • Non-specific self defense mechanism
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44
Q

Complement System Activation

A
  • Antigen-antibody complexes
  • By-products released by bacteria
  • By components of other plasma protein systems
45
Q

Clotting (Coagulation) System

A
  • Forms fibrinous exudate (meshwork) at inflamed site
  • Fibrin mesh
  • Trap foreign components
46
Q

Clotting (Coagulation) System Function

A
  • Prevent spread of infection & inflammation
  • Keep foreign components at site of phagocytic activity
  • Forms clot to stop bleed
  • Framework for repair/healing
47
Q

Cardinal Signs of Inflammation

A
  • Redness (rubor)
  • Swelling/tumor
  • Heat (calor)
  • Pain (dolar)
  • Loss of function (functio laesa)
48
Q

Pus Contents

A
  • Neutrophils
  • Liquefied debris of dead cells
  • Edema fluid
49
Q

Inflammation Side Effects

A
  • Fever
  • Leukocytosis
  • Malaise
  • Anorexia
  • Sleepiness
50
Q

Fever

A
  • Release of factors from RBC/pyrogens
  • Act on temp regulating centre in hypothalamus
  • Prostaglandins mediator
51
Q

Leukocytosis

A
  • Increase in WBC count
  • Bone marrow increases production
52
Q

Acute Leukocytosis

A
  • Increase in neutrophils
53
Q

Chronic Leukocytosis

A
  • Lymphocytosis (lymphocyte increase)
54
Q

Allergy Leukocytosis

A
  • Eosinophilia
55
Q

Harmful Consequences of Inflammation

A
  • Misdirected (autoimmune)
  • Exaggerated (against harmless agents)
  • Uncontrolled (anaphylaxis)
56
Q

Acute Inflammation

A
  • Sudden onset
  • 1+ cardinal signs
  • Hours to days
  • Neutrophils
57
Q

Acute Morphology

A
  • Vascular & exudative changes
  • Vasodilation
  • Increase vascular permeability
  • Inflammatory exudate
58
Q

Chronic Inflammation

A
  • Agent persists
  • Weeks to months
  • Increase in macrophages, lymphocytes, plasma, eosinophils
59
Q

Chronic Morphology

A
  • Proliferation of connective tissue/vessels
  • More fibroblasts, vessels, angiogenesis
60
Q

Angiogenesis

A
  • Formation of new blood vessels
61
Q

Common Sites of Acute Inflammation

A
  • Skin
  • Mouth
  • GI around gut
  • Lung
62
Q

Purulent/Suppurative Inflammation

A
  • Pus producing pyogenic bacteria
  • Liquefactive tissue necrosis
63
Q

Abscess Occurrence

A
  • Pus localized to cavity
  • Caused by tissue destruction
  • Walled off
  • No blood vessels
64
Q

Pus Collection

A
  • Localized
  • Cardinal signs of tumor
65
Q

Skin Abscess Treatment

A
  • Incision & drainage
  • Cleanout infected contents
66
Q

Deep Abscess Treatment

A
  • Organs effected
  • Surgical approach
67
Q

Fibrinous Inflammation

A
  • Increased vascular permeability
  • Large fibrinogen molecules pass through inter endothelial spaces
  • Resulting in fibrin deposits
68
Q

Fibrinous Exudates

A
  • Occur in spaces
  • Pleural, pericardial, meninges
69
Q

Fibrous Pericarditis

A
  • Exaggerated immune response
  • Cardiac surgery
  • Stringy fibrous exudate
70
Q

Serous Inflammation

A
  • Exudation of cell poor fluid
71
Q

Effusion

A
  • Serous inflammation in pleura/pericardium
72
Q

Ascites

A
  • Serous inflammation in peritoneum
73
Q

Bulla/Blister

A
  • Serous inflammation in skin
74
Q

Ulcer

A
  • Local defect on mucosal surfaces
  • Create breach/hole in mucosa
75
Q

Acute Inflammation Outcomes

A
  • Complete resolution
  • Healing by connective tissue replacement (scarring/fibrosis)
  • Progression to chronic inflammation
76
Q

Causes of Chronic Inflammation

A
  • Persistent infection/injury
  • Hypersensitivity
  • Chronic exposure to toxins
77
Q

Macrophages

A
  • Dominant cell type
78
Q

Lymphocytes

A
  • Adaptive immunity
  • Activated by microbes & environmental antigens
  • Release cytokines (amplify response)
  • T, B, NK cells
79
Q

Eosinophils

A
  • Allergic reactions & parasitic infections
  • Granules contain toxic protein
  • Tissue damage in allergic reactions
80
Q

Plasma Cells

A
  • Differentiated B cell type
  • Create antibodies/immunoglobulins
81
Q

Granulomas

A
  • 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
Q

Granuloma Causes

A
  • Mycobacterial
  • Fungal
  • Bacteria
83
Q

Restoration to Structural/Function Integrity

A
  • Removal of exudate
  • Removal of cellular & tissue debris
  • Replacement of lost cells/tissue
84
Q

Regeneration

A
  • Replacing tissue/cells lost in inflammation
  • Identical/very similar
85
Q

Repair

A
  • Replacement by cells/tissues
  • Same or different often simpler type
86
Q

Labile Cells

A
  • Continue to proliferate throughout life
  • Follow cell cycle
87
Q

Stable Cells

A
  • Low level of replication
  • Divide in response to stimuli
  • G0 but recruited to G1
88
Q

Permanent Cells

A
  • No division postnatal life
  • Exited cell cycle
89
Q

Repair Process

A
  • Angiogenesis (form new vessels)
  • Fibrosis (proliferation of fibroblasts & EMC deposits
  • Maturation/organization of scar, collage, ECM
90
Q

Repair Functionality

A
  • Never regain initial strength (70-80%)
  • Original tensile strength at 3 months
91
Q

Crust Formation

A
  • Quick wound closure
  • Infection barrier
  • Stops blood leakage
  • After hemorrhage wound covered by coagulated blood
92
Q

Removal of Dead Debris

A
  • Removed by sloughing (falling off)
  • Inflammatory response initiates repair
  • Small debris removed by liquefaction & phagocytosis
93
Q

Replacement of Lost Cells

A
  • Cell migration
  • Cell proliferation (division)
94
Q

Skin Wound Healing Cells

A
  • Fibroblasts
  • Endothelium (after angiogenesis)
  • Epithelium (migrates in sheets)
  • Direction of fibers determines tissue tension
95
Q

Granulation Tissue

A
  • New tissue
  • Proliferating cellular & extracellular components
  • Replace lost tissue
96
Q

Pink Granules

A
  • Newly formed capillaries
  • Fibroblasts elaborating connective tissue (extracellular)
  • Macrophages
97
Q

Granulation Tissue Characteristics

A
  • Bleeds if touched
  • Insensitive to pain (no nerves)
  • Resistant to infections
98
Q

Adhesions

A
  • Fibrosis & fibrous connections of serosal surfaces
  • Form in injury repair/inflammation of serosal surfaces
99
Q

Keloid

A
  • Post-traumatic repair
  • Connective tissue proliferation in dermis
  • Beyond necessary amount
100
Q

Keloid Lesions

A
  • Red
  • Raised
  • Firm
  • Sharp & irregular outline
  • Smooth & shiny surface
  • Prominent scar
101
Q

Superficial Primary Repair

A
  • Epidermis only (dermis intact)
  • No bleeding
  • Regeneration of epithelium
  • Epithelial cells migrate across wound
102
Q

Deep Primary Repair

A
  • Involves dermis
  • Few capillaries injured
  • Some bleeding
  • Fibroblasts & endothelial cells migrate
103
Q

Secondary Repair

A
  • Considerable tissue loss
  • Edges unable to be approximated
  • Granulation tissue to scar
104
Q

Rate of Wound Closure

A
  • Latent period (size of wound unchanged)
  • Period of contraction (granulation tissue shrinkage)
  • Epidermization
105
Q

Cicatrization

A
  • Scar formation
106
Q

Transudate

A
  • Fluid contains little/no protein cells
    Changes in hydrostatic/osmotic pressure in vessels
107
Q

Affecting Factors of Local Healing Rate

A
  • Decreased blood supply
  • Denervation
  • Local infection
  • Foreign bodies
  • Necrotic tissue
  • Mechanical stress
  • Hematoma
  • Increased wound size
  • Tissue type
108
Q

Affecting Factors of Systemic Healing Rate

A
  • Decreased blood supply
  • Age
  • Anemia
  • Malignancy
  • Malnutrition
  • Obesity
  • Diabetes
  • Infection
  • Organ failure
109
Q

Promoting Healing

A
  • 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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