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Pathology > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

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

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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

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3
Q
  • plasma and circulating cells
  • blood vessels and connective tissue cells
  • extracellular matrix
A

Vascularized connective tissue

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4
Q

neutrophils, monocytes, eosinophils, lymphocytes, basophils, platelets

A

plasma and circulating cells

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5
Q

mast cells, fibroblast, macrophages

A

blood vessels and connective tissue cells

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6
Q

structural fibrous proteins (collagen and elastin), adhesive glycoproteins (fibronectin, laminin, nonfibrillar collagen), basement membrane

A

extracellular matrix

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7
Q

2 forms of inflammation

A

acute & chronic inflammation

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8
Q

exudation of fluid and plasma proteins and emigration of leukocytes predominantly neutrophils

A

acute inflammation

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9
Q

predominant cell infiltrates are lymphocytes, macrophages, plasma cells with proliferation of blood vessel and connective tissue

A

chronic inflammation

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10
Q

Cardinal signs of acute inflammation:

A

rubor (redness)
tumor (swelling)
calor (heat)
functio laesa (loss of function)
dolor (pain)

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11
Q

the escape of fluids, proteins and blood cells from the vascular system into interstitial tissue or body cavities

A

exudation

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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

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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

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14
Q

– denotes an excess of fluids in the interstitial or serous cavities, it can either be an exudate or transudate

A

edema

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15
Q

– a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris

A

pus

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16
Q

3 Major Components of Acute Inflammation

A
  1. Vascular changes
  2. Structural changes in microvasculature
  3. Cellular events
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17
Q
  • changes in vascular caliber and flow
  • transient vasoconstriction followed by vasodilatation resulting to increased blood flow
A

vascular changes

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18
Q
  • increased permeability of microvasculature = slowing of circulation
A

structural changes in microvasculature

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19
Q

Structural changes in microvasculature

A
  • stasis of blood flow
  • margination
  • rolling
  • adhesion
  • pavementing
  • diapedesis
  • chemotaxis
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20
Q

small blood vessels packed with red blood cells

A

stasis of blood flow

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21
Q

As stasis occurs, peripheral orientation of leukocytes, principally neutrophils along the vascular endothelium

A

margination

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22
Q

– individual and then rows of leukocytes tumble slowly along the endothelium

A

rolling

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23
Q

adherence of leukocytes in the endothelium

A

adhesion

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24
Q

endothelium can be virtually lined by white blood cells

A

pavementing

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25
Q

transmigration across the endothelium

A

diapedesis

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26
Q

migration in interstitial tissue towards an inflammatory stimulus

A

chemotaxis

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27
Q

Steps in leukocytes extravasation

A
  • Extravasation
  • Increased vascular permeability (vascular leakage)
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28
Q

journey of leukocytes from lumen to interstitial tissue

A

extravasation

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29
Q
  • in the lumen
  • diapedesis
  • chemotaxis
A

Extravasation

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30
Q

Extravasation
stasis, margination, rolling, adhesion, pavementing

A

in the lumen

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31
Q

Extravasation
migration to chemotactic stimulus or towards the site of injury

A

chemotaxis

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32
Q

Extravasation
the hallmark of acute inflammation; mainly due to injury of endothelium

A

increased vascular permeability (vascular leakage)

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33
Q

Steps in Phagocytosis

A
  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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34
Q

Chemical Mediators of Inflammation from cell

A
  • histamine
  • serotonin
  • lysosomal granules
  • prostaglandins
  • leukotrienes
  • platelet activating factor
  • cytokines
  • nitric oxide
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35
Q

Chemical Mediators of Inflammation from plasma

A
  • complement activation
  • bradykinin
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36
Q

Major Cellular source
Mast cells, basophils, platelets

A

histamine

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37
Q

Major Cellular source
Platelets, mast cells

A

serotonin

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38
Q

Major Cellular source
Neutrophils, macrophages

A

lysosomal granules

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39
Q

Major Cellular source
All leukocytes, platelets, endothelial cells

A

prostaglandins

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40
Q

Major Cellular source
All leukocytes

A

leukotrienes

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41
Q

Major Cellular source
All leukocytes, endothelial cells

A

platelet activating factor

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42
Q

Major Cellular source
Macrophages, endothelial cells

A

cytokines & nitric oxide

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43
Q

Major Cellular source
C3a, C4a, C5a

A

complement activation

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44
Q

cause dilation of arterioles and increase in vascular permeability

A

histamine

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45
Q

action similar to histamine

A

serotonin

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46
Q

anaphylatoxins, induce the release of histamine therefore can increase vascular permeability

A

C3a,C4a,C5a

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47
Q

more potent to produce increase vascular permeability

A

C5a

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48
Q

has no permeability effect but is a chemotactic agent

A

C5b67 complex

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49
Q

increase vascular permeability; responsible for pain

A

bradykinin

50
Q

Arachidonic Acid Metabolites

A
  • prostaglandins
  • leukotrienes
51
Q

vasodilatation

A

prostaglandins

52
Q

vasoconstriction, bronchospasm, increase in vascular permeability

A

leukotrienes

53
Q

increase vascular permeability

A

Platelet activating factor (PAF)

54
Q

Interleukin – l (IL-1) and Tumor necrosis factor (TNF) induce acute phase reaction like fever, increase in sleeping time, decrease in appetite

A

cytokines

55
Q
  • synthesized by endothelium and macrophages
  • vasodilatation and increase in vascular permeability
A

nitric oxide

56
Q

Outcome of Acute Inflammation

A

mediators injury -> acute inflammation -> resolution / abscess formation / healing

57
Q

Outcome of Acute Inflammation with Chronic inflammation

A

mediators injury -> mediators -> chronic inflammation -> regeneration / scarring

58
Q

Outcome of Acute Inflammation with Acute to Chronic

A

mediators injury -> acute inflamation -> chronic inflammation -> regeneration / scarring

59
Q

prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at healing are proceeding simultaneously

A

chronic inflammation

60
Q

Chronic inflammation arises under the following settings

A
  1. persistent infections
  2. prolonged exposure to potentially toxic agents like silica and asbestos inhalation
  3. autoimmune disease
61
Q

Chronic inflammation
tuberculosis, syphilis, certain fungal infections

A

persistent infections

62
Q

Chronic inflammation
systemic lupus erythematosus, rheumatoid arthritis

A

autoimmune diesease

63
Q

autoimmune disease characterized by:

A
  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
64
Q
  • 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
A

macrophages

65
Q

persistent tissue destruction with damage to both parenchymal cells and stromal framework

A

hallmark of chronic inflammation

66
Q

4 components of repair by connective tissue fibrosis

A
  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
67
Q
  • hallmark of healing
A

granulation tissue

68
Q

granulation tissue microscopic features

A

proliferation of new small blood vessels and fibroblasts

69
Q

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

A

granulomatous inflammation

70
Q

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

A

granuloma

71
Q

Epithelioid cells fuse forming multinucleated giant cells

A

langhans
foreign body

72
Q

type with peripherally arranged nuclei

A

langhans

73
Q

type with haphazardly arranged nuclei

A

foreign body

74
Q

Examples of granulomatous infection

A
  • tuberculosis
  • leprosy
  • syphilis
  • cat scatch disease
75
Q

Mycobacterium tuberculosis

A

tuberculosis

76
Q

– Mycobacterium leprae

A

leprosy

77
Q

Treponema pallidum

A

syphilis

78
Q

Gram negative bacillus

A

cat scratch disease

79
Q

Morphologic Patterns in Acute and Chronic Inflammation

A
  • serous inflammation
  • fibrinous inflammation
  • suppurative/purulent inflammation
  • ulcers
80
Q
  • 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
A

serous inflammation

81
Q
  • fibrin pass through vascular barrier producing fibrinous exudate
  • characteristic of inflammation of body cavities
A

fibrinous inflammation

82
Q
  • purulent exudate
  • seen in abscesses
A

suppurative/purulent inflammation

83
Q

a local defect or excavation of the surface of an organ or tissue that is produced by sloughing of inflammatory necrotic tissue

A

ulcers

84
Q
  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
A

ulcers

85
Q

Wound Healing2 forms:

A
  • primary union or healing by first intension
  • secondary union or healing by second intention
86
Q
  • healing of a clean, uninfected surgical wound in which adjacent surfaces are closely apposed by surgical sutures
A

primary union or healing by first intension

87
Q

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

A

day 1

88
Q

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

A

day 3

89
Q

Primary Union or healing by first intension
- collagen fibers are more abundant
- epidermis achieves normal thickness

A

day 5

90
Q

Primary Union or healing by first intension
- sutures commonly removed
- wound approximates 10% of tensile strength of normal skin

A

day 7

91
Q

Primary Union or healing by first intension
- continued accumulation of collagen and proliferation of fibroblasts
- disappearance of leukocyte infiltrate, edema, increased vascularity
- blanching begins

A

day 15

92
Q

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

A

day 30

93
Q
  • 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
A

secondary union or healing by second intention

94
Q

secondary union or healing by second intention differs from primary healing:

A

a. inflammatory reaction more intense
b. much larger amounts of granulation tissue are formed
c. wound contraction

95
Q
  • most important proteins providing extracellular framework
  • product of fibroblasts
  • 14 types
A

collagen

96
Q

Systemic host factors influencing healing

A
  • nutrition
  • steroids hinder formation of granulation tissue
  • ischemia to tissues
  • metabolic status
97
Q

proteins , vitamin C

A

nutrition

98
Q

Local Host factors influencing healing

A
  • Infection
  • Foreign materials
  • Exposure to radiation
  • Mechanical factors
  • Size of wound, location and type of the wound
99
Q

Pathological Aspects of Repair

A

A . Deficient Scar Formation

B. Excessive Formation of the Repair Components

C. Formation of Contractures

100
Q

Deficient Scar Formation

A
  • wound dehiscence
  • ulceration
101
Q

Inadequate formation of granulation tissue can lead to two types of complications

A

Deficient Scar Formation

102
Q

Deficient Scar Formation
Rupture of a wound is more common after abdominal surgery & is due to increased abdominal pressure

A

wound dehiscence

103
Q

Deficient Scar Formation
Wounds can ulcerate because of inadequate vascularization during healing

A

ulceration

104
Q

Excessive formation of the components of the repair process can complicate healing

A
  • hypertrophic scar
  • keloid
  • exuberant granulation (proud flesh)
  • incisional scars or traumatic injuries
105
Q

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.

A

hypertrophic scar

106
Q

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

A

keloid

107
Q

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

A

exuberant granulation (proud flesh)

108
Q

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

A

incisional scars or traumatic injuries

109
Q

in the size of the wound is an important part of the normal healing process

A

contraction

110
Q
  • 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.
A

Contracture

111
Q

Types of Cells According to their Mitotic Activity

A
  • static cell populations (permanent)
  • stable cell population
  • renewing cell population (labile)
112
Q
  • no longer divide (postmitotic cells), - e.g. CNS, skeletal & cardiac muscle
A

static cell populations (permanent)

113
Q
  • divide episodically & at slow rates; stimulated by injury;
  • e.g. periosteal & perichondrial cells, smooth muscle cells & endothelial cells, fibroblasts
A

stable cell population

114
Q
  • display regular mitotic activity;
  • e.g. blood cells, epithelial cells
A

renewing cell populations (labile)

115
Q

The cell of the body are divided into three groups on the basis of their proliferative capacity and their relationship to the cell cycle:

A
  • continuously dividing cells (labile cells)
  • quiescent (stable cells)
  • non-dividing (permanent cells)
116
Q
  • 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
A

continuously dividing cells (labile cells)

117
Q
  • 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
A

continuously dividing cells (labile cells)

118
Q
  • 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.
A

quiescent (stable cells)

119
Q

Quiescent (Stable Cells)
of virtually all the glandular organs of the body such as liver, kidneys, pancreas

A

parenchymal cells

120
Q

Quiescent (Stable Cells)
fibroblasts and smooth muscle cells and vascular endothelial cells

A

mesenchymal cells

121
Q
  • Have left the cell cycle and are destined to die without dividing again.
  • Cannot undergo mitotic division in post natal life.
A

non-dividing (permanent cells)

122
Q

Cannot undergo mitotic division in post natal life

A

Nerve cells,
skeletal muscle cells and
cardiac muscle cells

Pathology (3 decks)

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