inflammation and tissue healing and repair Flashcards
1
Q
Inflammation is a protective response involving
A
- host cells
- blood vessels
- proteins and
- other mediatiator
2
Q
mission of inflammation
A
to eliminate the initial cause of cell injury
3
Q
inflammation protective mission by
A
- Diluting
- destroying
- Neutralizing
4
Q
what is inflammare
A
to set on fire
5
Q
rubor et tumor cum calore et dolore
A
redness and swelling with heat and pain
6
Q
who added the 5th sign
A
Rudolf virchow
7
Q
what is the 5th cardinal sign
A
functio laesa or loss of function
8
Q
who said inflammation is not a disease but just a response
A
John Hunter
9
Q
Who discovered the process of phagocytosis
A
Elie Metchinkoff
10
Q
Exogenous causes
A
Physical agents
Chemical agents
Biological agents
11
Q
Endogenous causes
A
Circulation disorders
Enzymes activation
Metabolic products deposals
12
Q
Target of cell injury
A
- function
- biochemical reaction
13
Q
Changes in inflammation
A
- Tissue damage
- Cellular –vascular response
- Metabolic changes
- Tissue repair
14
Q
onset of acute
onset of chronic
A
fast: mins or hours
slow: days
15
Q
tissue injury of acute
tissue injury of chronic
A
acute - mild and self-limited
chronic - severe and progressive
16
Q
why is it prominent in acute inflammatory?
A
because the 5 cardinal signs are seen in acute inflammation,
17
Q
an immediate and early response to an injurious agent
A
acute inflammation
18
Q
characteristics of AI
A
- presence of exudates fluids and plasma proteins
- emigration of neutrophilic leukocytes to the site of injury
19
Q
external manifestation of AI
A
- rubor
- calor
- tumor
- dolor
20
Q
due to dilation of small blood
vessels within damaged tissue
A
rubor or redness
21
Q
example of rubor
A
cellulitis
22
Q
results from increased blood flow due to regional vascular dilation
A
calor or heat
23
Q
example of calor
A
hyperemia
24
Q
due to accumulation of fluid in the
extravascular space
A
tumor or swelling.
25
results from the stretching & destruction of tissues due to inflammatory edema
dolor or pain
26
inflamed area is inhibited by pain
loss of function
27
chemicals or mediator of AI that contributes to vasodilation
- bradykinins
- prostaglandins
- serotonin
28
2 events of AI
- vascular response / vascular changes
- cellular response / cellular changes
29
what are the vascular response/vascular changes?
- there will be increase in the blood flow
- to bring cells and proteins to the site of injury
- by vasodilation and increased vascular permeability
30
what are the cellular response/cellular changes?
- recruitment of leukocytes
- activation of leukocytes leading to the process of destruction of invaders and production of mediators
31
Stages of Vascular response
1. Vascular dilation and increased blood flow
2. extravasation and deposition
of plasma fluid and proteins
3. leukocyte emigration and
accumulation in the site of injury
32
Mechanism of vascular response
* Vasoconstriction
* Vasodilatation of arterioles and
venules
* Stasis of blood blood flow
33
immediate due to neurogenic/ chemical stimuli
vasoconstriction
34
Stages/mechanism of cellular
response
- margination
- diapedesis
- chemotaxis
- phagocytosis
35
peripheral positioning of white cells along the endothelialcells
Margination
36
rows of leukocytes tumble slowly along the endothelium
rolling
37
endothelium can be lined by white cells the binding of leukocytes with endothelial cells is facilitated by cell adhesion molecules
pavementing
38
mediator of margination
- selectins
- immunoglobulins
- integrins
39
The movement of leukocytes
by extending pseudopodia
through the vascular wall
diapedesis
40
unidirectional attraction of leukocytes from vascular channels
towards the site of inflammation within the tissue space
guided by chemical gradients.
chemotaxis
41
important chemotactic factors for neutrophils
- C5a complement system
- leukotriene B4
- cytokines (IL-8)
42
the process of engulfment and
internalization by specialized cells of particulate material
phagocytosis
43
Leukocyte recruitment is a multi-step process consisting of
- loose attachment to and rolling on endothelium (mediated by selectins);
- firm attachment to endothelium (mediated by integrins)
- migration through interendothelial spaces.
44
Steps of the inflammatory response (5Rs)
* Recognition of the injurious agent
* Recruitment of leukocytes
* Removal of the agent
* Regulation (control) of the response
* Resolution (repair)
45
Defects in Leukocyte Function
could be acquired or inherited
46
Defects in Leukocyte Function
lead to increased susceptibility to infections, which may be recurrent
and life-threatening
47
Acquired diseases
- diabetes
- sepsis
- anemia
- malignancy
- malnutrition
48
Genetic diseases
- chronic granulomatous
- X-linked
- autosomal recessive
49
Major role of P-selectin
rolling
50
major role of e-selectin
rolling and adhesion
51
three steps in Phagocytosis
1. recognition and attachment of the
particle to the ingesting leukocyte
2. engulfment, with subsequent
formation of a phagocytic vacuole
3. killing and degradation of the
ingested material
52
The outcome of acute inflammation
* Elimination of the noxious stimulus
* Decline of the reaction
* Repair of the damaged tissue,
* Persistent injury resulting in chronic inflammation
53
Outcomes of acute
inflammation:
1. Resolution
2. Fibrosis or healing by scarring
3. chronic inflammation
54
Morphological Feature of AI
* Serous inflammation
* Fibrinous inflammation
* Suppurative (purulent) inflammation
55
characterized by the outpouring of a watery, relatively
protein-poor fluid that, depending on the site of injury
Serous inflammation
56
Fluid in a serous cavity is called
effusion
57
resulting in greater vascular permeability allows large molecules to pass the endothelial barrier
fibrinous inflammation
58
fibrinous exudate is characteristics of inflammation in the lining of body cavities
meninges
pericardium
pleura
59
manifested by the presence of large amounts of purulent exudate
Suppurative (purulent) inflammation
60
focal collections of pus that may be caused by seeding of
pyogenic organisms into a tissue
Abscesses
61
secondary infections of necrotic foci
Abscesses
62
local defect, or excavation, of the surface of an organ or tissue
that is produced by necrosis of cells and sloughing (shedding) of
inflammatory necrotic tissue
ulcer
63
chemical mediator and regulation of inflammation
- cell derived
- plasma protein derived
64
preformed mediator in cell derived
- histamine
- serotonin
65
location or sources of histamine
- mast cells
- basophils
- platelets
66
inflammation of prolonged duration
chronic inflammation
67
chronic inflammation is characterized by
◦ Infiltration with mononuclear cells
◦ macrophages,
◦ lymphocytes,
◦ plasma cells
◦ Tissue destruction,
◦ Repair
68
2 repairs of chronic inflammation
- angiogenesis
- fibrosis
69
the dominant cells of chronic inflammation
Macrophages
70
Chronic Inflammatory Cells
macrophage
plasma cell
eosinophils
mast cells
71
cells in the liver
kupffer cells
72
cells in the spleen and lymph nodes
histiocytes
73
cells in central nervous system
microglial cells
74
cells in lungs
alveolar macrophages
75
Classification of chronic inflammation
Nonspecific chronic
inflammation and Specific inflammation
(granulomatous inflammation)
76
This involves a diffuse
accumulation of
macrophages and
lymphocytes at site of
injury that is usually
productive with new
fibrous tissue
formations
Nonspecific chronic
inflammation:
77
characterized by the presence of
granuloma
Specific inflammation
78
distinctive pattern of chronic
inflammation characterized by
aggregates of activated
macrophages that assume an
epithelioid appearance
Granulomatous inflammation
79
Two types of giant cells:
Foreign body-type giant cells
Langhans giant cells
80
which have irregularly scattered nuclei in
presence of indigestible materials
Foreign body-type giant cells
81
the nuclei are arranged peripherally in a
horse –shoe pattern
Langhans giant cells
82
Langhans giant cells typically seen in
tuberculosis, and sarcoidosis
83
Types of granulomas
Foreign body granuloma
Immune granulomas
84
Major causes of granulomatious inflammation
Bacterial, fungal, helminthic, protozoal, chlamydia
85
SYSTEMIC EFFECTS OF
INFLAMMATIONS
* a. Fever
* b. Endocrine & metabolic responses
* c. Autonomic responses
* d. Behavioral responses
* e. Leukocytosis
* f. Leukopenia
* g. Weight loss
86
restoration of tissue architecture and function after an injury
Tissue repair
87
Tissue repair occurs in 2 ways
– Regeneration of injured tissue
– Replacement by connective tissue
88
factors involve in tissue repair
- cell proliferation
- interaction between cells and extracellular matrix
89
Mechanisms regulating cell
populations/cellular proliferation
- Cell numbers can be altered by increased or decreased rates of stem cell input and cell death due to apoptosis
- Changes in the rates of
proliferation or differentiation
90
Processes in the proliferation of cells
1. DNA replication
2. Mitosis
91
Cellular Proliferation
* divided into three groups:
* . Continuously dividing (labile) tissues
* * Stable tissues
* * Permanent tissues
92
what is Continuously dividing (labile) tissues
* Cells are continuously proliferating
* * Can easily regenerate after injury
* * Contain a pool of stem cells
93
example of labile tissues or Continuously dividing tissuea
bone marrow, skin, epithelium
94
what is Stable tissues
Cells have limited ability to proliferate
* Limited ability to regenerate
* Can proliferate if injured
95
examples of Stable tissues
liver, kidney, pancreas
96
what is Permanent tissues
Cells can’t proliferate
* Can’t regenerate
* injury always leads to scar
97
Example of Permanent tissues
neurons, cardiac muscle
98
Three phases in granulation -
tissue
Phase of inflammation
Phase of demolition
Ingrowth of granulation tissue
99
a mechanical
reduction in the size of the defect.
Wound contraction
100
Sources of Growth Factors:
* 1. Platelets, activated (TGF)
* 2. Damaged epithelial cells, (EGF)
* 3. Circulating serum growth factors,
* 4. Macrophages, (angiogenic factor)
* 5. Lymphocytes recruited to the area of injury
101
have the capacity to stimulate cell division and proliferation
Growth factors
102
main phases of cutaneous wound
healing
Inflammation
* Formation of granulation tissue
* ECM remodeling
103
Two forms of eCM
interstitial matrix and basement membrane
104
Functions of ECM
- provides mechanical support to tissues
- acts as a substrate for cell growth
105
2 types of Wound Healing
regeneration
repair by scarring
106
Two patterns of wound healing
Healing by first intention
Healing by second intention
107
process of granulation tissue in 3-5 days
* new blood vessels (angiogenesis)
* fibroblasts
108
By 24 hours
* clot forms
* * neutrophils come in
* * epithelium begins to regenerate
109
By 3-5 days
* macrophages come in
* * granulation tissue is formed
* * collagen begins to bridge incision
* * epithelium increases in thickness
110
Weeks later
* granulation tissue gone
* * collagen is remodeled
* * epidermis full, mature
* * eventually, scar forms
111
Factors that influence wound healing
Local Factors
Systemic Factors
112
local factors of wound healing
> Type, size, and location of the wound
* > Vascular supply
* > Infection
Ø Movement
Ø Ionizing radiation
113
systemic factors of wound healing
Circulatory status
Infection
Metabolic status
Nutritional deficiencies
114
Complications of Wound Healing
* Infection
* Deficient Scar Formation
- Wound Dehiscence
- Ulceration
* Excessive Scar Formation
- Keloid Formation
- Hypertrophic Scar
