Inflammation and Repair Flashcards
(122 cards)
1
Q
complex reaction in the vascularized connective tissue characterized by reaction of blood vessels leading to the accumulation of fluid and leukocytes in extravascular tissues
A
inflammation
2
Q
- it is fundamentally a protective response
- it serves to destroy, dilute or wall off the injurious agent
- closely intertwined with the process of repair or healing so that injured tissues is replaced by regeneration of parenchymal cells or filling of the defect with fibroblastic tissue (scarring), or most commonly, by a combination of both processes
A
inflammation
3
Q
- plasma and circulating cells
- blood vessels and connective tissue cells
- extracellular matrix
A
Vascularized connective tissue
4
Q
neutrophils, monocytes, eosinophils, lymphocytes, basophils, platelets
A
plasma and circulating cells
5
Q
mast cells, fibroblast, macrophages
A
blood vessels and connective tissue cells
6
Q
structural fibrous proteins (collagen and elastin), adhesive glycoproteins (fibronectin, laminin, nonfibrillar collagen), basement membrane
A
extracellular matrix
7
Q
2 forms of inflammation
A
acute & chronic inflammation
8
Q
exudation of fluid and plasma proteins and emigration of leukocytes predominantly neutrophils
A
acute inflammation
9
Q
predominant cell infiltrates are lymphocytes, macrophages, plasma cells with proliferation of blood vessel and connective tissue
A
chronic inflammation
10
Q
Cardinal signs of acute inflammation:
A
rubor (redness)
tumor (swelling)
calor (heat)
functio laesa (loss of function)
dolor (pain)
11
Q
the escape of fluids, proteins and blood cells from the vascular system into interstitial tissue or body cavities
A
exudation
12
Q
– inflammatory extravascular fluid that has a high protein content, much cellular debris and specific gravity of above 1.020
- it implies significant alteration in the normal permeability of small blood vessels in the area of injury
A
exudate
13
Q
– fluid with low protein content (most is albumin) and a specific gravity of less than 1.012
- it is essentially an ultrafiltrate of blood plasma and results from hydrostatic imbalance across vascular endothelium; vascular permeability is normal
A
transudate
14
Q
– denotes an excess of fluids in the interstitial or serous cavities, it can either be an exudate or transudate
A
edema
15
Q
– a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris
A
pus
16
Q
3 Major Components of Acute Inflammation
A
- Vascular changes
- Structural changes in microvasculature
- Cellular events
17
Q
- changes in vascular caliber and flow
- transient vasoconstriction followed by vasodilatation resulting to increased blood flow
A
vascular changes
18
Q
- increased permeability of microvasculature = slowing of circulation
A
structural changes in microvasculature
19
Q
Structural changes in microvasculature
A
- stasis of blood flow
- margination
- rolling
- adhesion
- pavementing
- diapedesis
- chemotaxis
20
Q
small blood vessels packed with red blood cells
A
stasis of blood flow
21
Q
As stasis occurs, peripheral orientation of leukocytes, principally neutrophils along the vascular endothelium
A
margination
22
Q
– individual and then rows of leukocytes tumble slowly along the endothelium
A
rolling
23
Q
adherence of leukocytes in the endothelium
A
adhesion
24
Q
endothelium can be virtually lined by white blood cells
A
pavementing
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transmigration across the endothelium
diapedesis
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migration in interstitial tissue towards an inflammatory stimulus
chemotaxis
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Steps in leukocytes extravasation
- Extravasation
- Increased vascular permeability (vascular leakage)
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journey of leukocytes from lumen to interstitial tissue
extravasation
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- in the lumen
- diapedesis
- chemotaxis
Extravasation
30
Extravasation
stasis, margination, rolling, adhesion, pavementing
in the lumen
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Extravasation
migration to chemotactic stimulus or towards the site of injury
chemotaxis
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Extravasation
the hallmark of acute inflammation; mainly due to injury of endothelium
increased vascular permeability (vascular leakage)
33
Steps in Phagocytosis
1. Recognition and attachment of foreign substance to phagocytic cells
2. Invagination of cell membrane carrying the foreign agent, detachment of phagocytic vacuole or phagosome from the cell membrane and internalization to the cytoplasm
3. In the cytoplasm fusion of the phagosome and lysosomal granules forming the phagolysosome rupture of lysosome and empty their enzymes to the vacuole initiating the killing and digestion of foreign substance
4. Extrusion of digestive debris from the phagocyte
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Chemical Mediators of Inflammation from cell
- histamine
- serotonin
- lysosomal granules
- prostaglandins
- leukotrienes
- platelet activating factor
- cytokines
- nitric oxide
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Chemical Mediators of Inflammation from plasma
- complement activation
- bradykinin
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Major Cellular source
Mast cells, basophils, platelets
histamine
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Major Cellular source
Platelets, mast cells
serotonin
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Major Cellular source
Neutrophils, macrophages
lysosomal granules
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Major Cellular source
All leukocytes, platelets, endothelial cells
prostaglandins
40
Major Cellular source
All leukocytes
leukotrienes
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Major Cellular source
All leukocytes, endothelial cells
platelet activating factor
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Major Cellular source
Macrophages, endothelial cells
cytokines & nitric oxide
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Major Cellular source
C3a, C4a, C5a
complement activation
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cause dilation of arterioles and increase in vascular permeability
histamine
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action similar to histamine
serotonin
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anaphylatoxins, induce the release of histamine therefore can increase vascular permeability
C3a,C4a,C5a
47
more potent to produce increase vascular permeability
C5a
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has no permeability effect but is a chemotactic agent
C5b67 complex
49
increase vascular permeability; responsible for pain
bradykinin
50
Arachidonic Acid Metabolites
- prostaglandins
- leukotrienes
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vasodilatation
prostaglandins
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vasoconstriction, bronchospasm, increase in vascular permeability
leukotrienes
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increase vascular permeability
Platelet activating factor (PAF)
54
Interleukin – l (IL-1) and Tumor necrosis factor (TNF) induce acute phase reaction like fever, increase in sleeping time, decrease in appetite
cytokines
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- synthesized by endothelium and macrophages
- vasodilatation and increase in vascular permeability
nitric oxide
56
Outcome of Acute Inflammation
mediators injury -> acute inflammation -> resolution / abscess formation / healing
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Outcome of Acute Inflammation with Chronic inflammation
mediators injury -> mediators -> chronic inflammation -> regeneration / scarring
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Outcome of Acute Inflammation with Acute to Chronic
mediators injury -> acute inflamation -> chronic inflammation -> regeneration / scarring
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prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at healing are proceeding simultaneously
chronic inflammation
60
Chronic inflammation arises under the following settings
1. persistent infections
2. prolonged exposure to potentially toxic agents like silica and asbestos inhalation
3. autoimmune disease
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Chronic inflammation
tuberculosis, syphilis, certain fungal infections
persistent infections
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Chronic inflammation
systemic lupus erythematosus, rheumatoid arthritis
autoimmune diesease
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autoimmune disease characterized by:
1. infiltration with mononuclear cells like macrophages, plasma cells and lymphocytes
2. tissue destruction
3. attempts at repair by connective tissue replacement by fibroblast to produce fibrosis
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- principal cells in chronic inflammation
- originate from bone narrow as monoblast, migrate to the blood as monocytes, then after a few days migrate to the tissues
- main function is phagocytosis
macrophages
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persistent tissue destruction with damage to both parenchymal cells and stromal framework
hallmark of chronic inflammation
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4 components of repair by connective tissue fibrosis
1. formation of new blood vessels (angiogenesis or neovascularization)
2. migration and proliferation of fibroblast
3. deposition of extracellular matrix
4. maturation and organization of fibrous tissue
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- hallmark of healing
granulation tissue
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granulation tissue microscopic features
proliferation of new small blood vessels and fibroblasts
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distinct pattern of chronic inflammatory reaction in which the predominant cell type is an activated macrophage with modified epithelial-like appearance known as epithelioid cells
granulomatous inflammation
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a focal area of granulomatous inflammation consisting of a microscopic aggregation of epithelioid cells surrounded by a collar of mononuclear cells principally lymphocytes and occasional plasma cells
granuloma
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Epithelioid cells fuse forming multinucleated giant cells
langhans
foreign body
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type with peripherally arranged nuclei
langhans
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type with haphazardly arranged nuclei
foreign body
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Examples of granulomatous infection
- tuberculosis
- leprosy
- syphilis
- cat scatch disease
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Mycobacterium tuberculosis
tuberculosis
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– Mycobacterium leprae
leprosy
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Treponema pallidum
syphilis
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Gram negative bacillus
cat scratch disease
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Morphologic Patterns in Acute and Chronic Inflammation
- serous inflammation
- fibrinous inflammation
- suppurative/purulent inflammation
- ulcers
80
- outpouring of thin fluid derived either from blood serum or secretions of mesothelial cells resulting to effusion
- Ex. Skin burn blister, pleural or pericardial effusion
serous inflammation
81
- fibrin pass through vascular barrier producing fibrinous exudate
- characteristic of inflammation of body cavities
fibrinous inflammation
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- purulent exudate
- seen in abscesses
suppurative/purulent inflammation
83
a local defect or excavation of the surface of an organ or tissue that is produced by sloughing of inflammatory necrotic tissue
ulcers
84
1. inflammation necrosis of mucosa of mouth, stomach, intestine or genitourinary tract
2. subcutaneous inflammation of lower extremity in older individuals with circulatory disturbance such as in diabetic ulcer
ulcers
85
Wound Healing 2 forms:
- primary union or healing by first intension
- secondary union or healing by second intention
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- healing of a clean, uninfected surgical wound in which adjacent surfaces are closely apposed by surgical sutures
primary union or healing by first intension
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Primary Union or healing by first intension
- neutophilic infiltration, acute inflammatory reaction
- epithelial cells at edges undergo mitosis and begin to migrate across the wound
day 1
88
Primary Union or healing by first intension
- neutrophils replaced by macrophages
- granulation tissue and deposition of collagen fibers
- epithelial cell proliferation continues thickening the epidermal covering layer
day 3
89
Primary Union or healing by first intension
- collagen fibers are more abundant
- epidermis achieves normal thickness
day 5
90
Primary Union or healing by first intension
- sutures commonly removed
- wound approximates 10% of tensile strength of normal skin
day 7
91
Primary Union or healing by first intension
- continued accumulation of collagen and proliferation of fibroblasts
- disappearance of leukocyte infiltrate, edema, increased vascularity
- blanching begins
day 15
92
Primary Union or healing by first intension
- scar now comprises a cellular connective tissue devoid of inflammatory infiltrate, covered now by intact epidermis; 50% of tensile strength of normal skin
day 30
93
- large tissue defect that must be filled with regenerating parenchmal cells and abundant granulation tissue
- occur in infarction, inflammatory ulceration, abscesses, surface wounds with large defects
secondary union or healing by second intention
94
secondary union or healing by second intention differs from primary healing:
a. inflammatory reaction more intense
b. much larger amounts of granulation tissue are formed
c. wound contraction
95
- most important proteins providing extracellular framework
- product of fibroblasts
- 14 types
collagen
96
Systemic host factors influencing healing
- nutrition
- steroids hinder formation of granulation tissue
- ischemia to tissues
- metabolic status
97
proteins , vitamin C
nutrition
98
Local Host factors influencing healing
- Infection
- Foreign materials
- Exposure to radiation
- Mechanical factors
- Size of wound, location and type of the wound
99
Pathological Aspects of Repair
A . Deficient Scar Formation
B. Excessive Formation of the Repair Components
C. Formation of Contractures
100
Deficient Scar Formation
- wound dehiscence
- ulceration
101
Inadequate formation of granulation tissue can lead to two types of complications
Deficient Scar Formation
102
Deficient Scar Formation
Rupture of a wound is more common after abdominal surgery & is due to increased abdominal pressure
wound dehiscence
103
Deficient Scar Formation
Wounds can ulcerate because of inadequate vascularization during healing
ulceration
104
Excessive formation of the components of the repair process can complicate healing
- hypertrophic scar
- keloid
- exuberant granulation (proud flesh)
- incisional scars or traumatic injuries
105
Excessive formation of the components of the repair process can complicate healing
– raised tumorous scar due to deposition of excessive amount of collagen, it generally develops after thermal or traumatic injury that involves the deep layers of the dermis.
hypertrophic scar
106
Excessive formation of the components of the repair process can complicate healing
-if the scar tissue grows beyond the boundaries of the original wound and does not regress
- formation appears to be an individual predisposition and for unknown reasons is somewhat more common in African – Americans
keloid
107
Excessive formation of the components of the repair process can complicate healing
- formation of excessive amounts of granulation tissue which protudes above the level of the surrounding skin and blocks re-epithelialization
- must be removed by cautery or surgical excision to permit restoration of the continuity of the epithelium
exuberant granulation (proud flesh)
108
Excessive formation of the components of the repair process can complicate healing
- may be followed by exuberant proliferation of fibroblasts or other connective tissue elements that may in fact recur after excision
- desmoids or aggressive fibromatosis – lie in the interface between benign proliferations and malignant (low grade) tumors
incisional scars or traumatic injuries
109
in the size of the wound is an important part of the normal healing process
contraction
110
- an exaggeration of contraction is called a ___, and results in deformities of wound and the surrounding tissues.
- partic prone to develop on the palms, the soles, and the anterior aspect of the thorax.
- commonly seen after severe burns and may compromise the movement of joints.
Contracture
111
Types of Cells According to their Mitotic Activity
- static cell populations (permanent)
- stable cell population
- renewing cell population (labile)
112
- no longer divide (postmitotic cells), - e.g. CNS, skeletal & cardiac muscle
static cell populations (permanent)
113
- divide episodically & at slow rates; stimulated by injury;
- e.g. periosteal & perichondrial cells, smooth muscle cells & endothelial cells, fibroblasts
stable cell population
114
- display regular mitotic activity;
- e.g. blood cells, epithelial cells
renewing cell populations (labile)
115
The cell of the body are divided into three groups on the basis of their proliferative capacity and their relationship to the cell cycle:
- continuously dividing cells (labile cells)
- quiescent (stable cells)
- non-dividing (permanent cells)
116
- Go around the cell cycle from one mitosis to the next.
- These cells continue to proliferate throughout life, replacing cells that are continuously being destroyed.
- Tissues that contain labile cells include
- surface epithelia such as stratified squamous surface of the skin, oral cavity, vagina, and cervix
continuously dividing cells (labile cells)
117
- the lining mucosa of all the excretory ducts of the glands of the body, such as salivary glands, pancreas and biliary tract
- columnar epithelium of the GIT and uterus
- transitional epithelium of the urinary tract
- cells of the bone marrow and hematopoietic tissues
continuously dividing cells (labile cells)
118
- Are neither cycling nor dying and can be induced to re-enter the cycle by an appropriate stimulus.
- Normally demonstrate a low level of replication, however this cells can undergo rapid division in response to stimuli and are thus capable of reconstituting the tissue of origin.
quiescent (stable cells)
119
Quiescent (Stable Cells)
of virtually all the glandular organs of the body such as liver, kidneys, pancreas
parenchymal cells
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Quiescent (Stable Cells)
fibroblasts and smooth muscle cells and vascular endothelial cells
mesenchymal cells
121
- Have left the cell cycle and are destined to die without dividing again.
- Cannot undergo mitotic division in post natal life.
non-dividing (permanent cells)
122
Cannot undergo mitotic division in post natal life
Nerve cells,
skeletal muscle cells and
cardiac muscle cells
