inflammation
TRANSCRIPT
![Page 1: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/1.jpg)
1
INFLAMMATION
![Page 2: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/2.jpg)
Topic OutcomesAt the end of this lecture, students are able to :1.Describe orally the signs of inflammation2.Describe and differentiate in written between
acute and chronic inflammation3.Explain the morphological of types of
inflammation4.Describe in written the mechanism of healing
and repairing
![Page 3: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/3.jpg)
CONTENTS
2.1: Definitions & Concepts Of Inflammation
2.2: Stages Of Inflammation
2.3: Mediators Of Inflammation
2.4: Morphologic Pattern Of Acute & Chronic
Inflammation
2.5: Repair Or Healing
3
![Page 4: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/4.jpg)
2.1: Definitions & Concepts Of Inflammation
• The local response of living mammalian tissues to injury due to any agent.
• Body defense reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cells and tissues.
4
![Page 5: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/5.jpg)
• Causes of inflammation;
i. Physical agent e.g. mechanical trauma, radiation etc.
ii. Chemical agent e.g. simple chemical poisons, organic poisons
iii. Infective agents e.g. bacteria, viruses, parasites, their toxins
iv. Immunological agents e.g. Ag-Ab reaction, cell mediated
5
![Page 6: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/6.jpg)
• Involves 2 basic processes (overlapping):
• Have protective role against injurious agents
• Cause considerable harm to the bodyeg; anaphylaxis, atherosclerosis etc
6
Inflammatory response
healing
![Page 7: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/7.jpg)
Signs of Inflammation
• The famous 4 cardinal signs of inflammation:(i) rubor (redness)(ii) tumor (swelling)(iii) calor (heat)(iv) dolor (pain)
Added latest – functio laesa (loss of function)
7
![Page 8: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/8.jpg)
Heat Redness Swelling Pain Loss Of Func.
8
![Page 9: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/9.jpg)
2.2: Stages Of Inflammation
INFLAMMATION
ACUTE INFLAMMATION
CHRONIC INFLAMMATION
9
![Page 10: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/10.jpg)
• Acute inflammation– Short duration & represents the early body
reaction and usually followed by repair– The main features :
(a) Accumulation of fluid & plasma at the affected site
(b) Intravascular activation of platelets(c) Polymorphonuclear neutrophils as
inflammatory cells
10
![Page 11: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/11.jpg)
• Chronic Inflammation- longer duration and occurs either :
(a) after the causative agent of acuteinflammation persists for a long
time(b) Stimulus that induces chronic
inflammation from the beginning- main features :
presence of chronic inflammatory cells (lymphocytes, plasma cells and
macrophages)
![Page 12: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/12.jpg)
I) ACUTE INFLAMMATION
• The changes can be conveniently described under:(i) Vascular events(ii) Cellular events
13
Infected toenail showing the characteristic redness and swelling associated with acute inflammation
![Page 13: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/13.jpg)
(i) VASCULAR EVENTS• Alteration in the microvasculature (arterioles,
capillaries & venules)• Earliest response to tissue injury• Alterations includes:
(a) haemodynamic changes(b) changes in vascular permeability
14
![Page 14: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/14.jpg)
(a) Haemodynamic Changes
• Earliest features of inflammatory response result from changes in the vascular flow and calibre of small blood vessels in the injured tissue
15
![Page 15: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/15.jpg)
The sequence of these changes:
16
Transient vasoconstriction
Persistent progressive vasodilatation
Local hydrostatic pressure
Slowing or stasis
Leucocytic margination
![Page 16: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/16.jpg)
• Lewis Triple Response/ red line response;
(Eg: form stroking with a blunt point)
i. Red line : Appears a few second; Capillary & venules
dilatation
ii. Flare : Bright reddish appearance/flush
surrounding the red line; Anteriolar dilation
iii. Wheal : Swelling or oedema of the surrounding skin
occurring due to transudation of fluid into the extravascular space
17
![Page 17: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/17.jpg)
18
Triple response
![Page 18: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/18.jpg)
(b) Altered vascular permeability• Vascular changes begin quickly after the
injury but may develop at variables rates, depending on the nature & severity of the original injury.
• The interchange of fluid between the vascular & extra vascular space results from balance of fluid into the vascular space or out into the tissues;
i. Hydrostatic pressure
ii. Oncotic pressure - protein
iii. Osmotic pressure
iv. Lymph flow
19
![Page 19: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/19.jpg)
Fluid interchange between blood and extracellular fluid (ECF). (HP = Hydrostatic
pressure, OP = Osmotic pressure)
20
NO OEDEMA OEDEMA
![Page 20: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/20.jpg)
Edema
21
![Page 21: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/21.jpg)
• MECHANISMS OF INCREASED VASCULAR PERMEABILITY
(i) Endothelial cell contraction(ii) Endothelial cell retraction(iii) Direct injury to endothelial cells(iv) Endothelial injury mediated by leucocytes(v) Neovascularisation
23
![Page 22: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/22.jpg)
a) Contraction of endothelial cells
• Microvasculature : venules• Response type :
Immediate transient (15-30 min)• Pathogenesis :
Histamine, bradykinin, other chemical mediators
• Examples : Mild thermal injury
24
![Page 23: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/23.jpg)
b) Retraction of endothelial cells
• Microvasculature : venules• Response type :
somewhat delayed (in 4 – 6 hrs)prolonged (for 24 hrs or more)
• Pathogenesis :Interleukin-1(IL-1)Tumor Necrosis Factor (TNF)
• Examples : In vitro experimental work only25
![Page 24: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/24.jpg)
c) Direct injury to endothelial cells• Microvasculature : Arteriols, venules,
capillaries• Response type :
Immediate sustained leakage (immediate after injury prolonged (hrs to days)Delayed sustained leakage (delayed (2-12hrs) prolonged (hrs-days))
26
![Page 25: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/25.jpg)
• Pathogenesis :cell necrosis and detachment
• Examples : Moderate to severe burns, severe bacterial infection, radiation injury
27
![Page 26: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/26.jpg)
d) Endothelial injury mediated by leucocytes
• Microvasculature : venules, capillaries• Response type :
delayed, prolonged• Pathogenesis :
Leucocyte activation• Examples : pulmonary venules and capillaries
28
![Page 27: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/27.jpg)
e) Neovascularisation
• Microvasculature : All levels• Response type :
Any type• Pathogenesis :
Angiogenesis, vascular endothelial growth factor (VEGF)
• Examples : Healing, tumors
29
![Page 28: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/28.jpg)
ii) CELLULAR EVENTS • Cellular events; cells of the acute
inflammatory response are the neutrophils, monocytes & macrophages.
Polymorphonuclear neutrophils (PMNs)(within 24 hrs; Life long 24-48 hrs)
MonocytesMacrophages
(24-48 hrs; Survive much longer)30
![Page 29: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/29.jpg)
• The movements of neutrophils out of the vessels & their role in combat can be divided into 5 steps;
i. Margination = ?
ii. Adhesion = ?
iii. Emigration/ diapedesis=?
iv. Chemotaxis = ?
v. Phagocytosis & degranulation=?
31
![Page 30: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/30.jpg)
• Concentrates the leucocytes adjacent to endothelial wall- Margination
• Adherence of inflammatory cell to the endothelium/ vascular basement membrane- Adhesion
• Neutrophil lodged between endothelial cell and basement membrane and escape out into the extravascular space- Diapedesis
• Chemotactic factor mediated transmigration of leucocytes to reach the interstitial tissue- Chemotaxis
• The process of engulfment of solid particulate material bt the cell (cell eating)- Phagocytosis 32
![Page 31: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/31.jpg)
THE INFLAMMATION PROCESS
33
![Page 32: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/32.jpg)
34
![Page 33: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/33.jpg)
Neutrophil Margination
35
![Page 34: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/34.jpg)
FATE OF ACUTE INFLAMMATION• Acute inflammation generally has one of
FOUR (4) outcomes;
i. Resolution – complete return to normal/ tissue changes are slight and cellular changes are reversible eg; resolution in lobar pneumonia
ii. Healing by scarrimg– tissue destruction is extensive, no tissue regeneration; healing by fibrosis
36
![Page 35: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/35.jpg)
iii) Suppuration – the progression process of severe necrosis cause by pyogenic bacteria; neutrophilic infiltration; form an abcess; abcess – organised by dense fibrous tissue and get calcified
iv) Progression to chronic inflammation may follow acute inflammation, although signs of chronic inflammation may be present atthe onset of injury; healing proceed side by side.
37
![Page 36: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/36.jpg)
An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of necrotic tissue surround central areas of pus
38
![Page 37: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/37.jpg)
II) CHRONIC INFLAMMATION
• Chronic inflammation; prolonged process in which tissue destruction and inflammation occur at the same time.
39
![Page 38: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/38.jpg)
• Caused one of the following 3 ways:i) Chronic inflammation following acute inflammation – the tissue destruction is extensive, or bacteria survive & persist in small numbers at the site of acute inflammation ii) Recurrent attacks of acute inflammation – repeated bouts of acute inflammation eg; repeated acute infection of gallbladder chronic cholecystitisiii) Starting de novo – infection with organisms of low pathogenecity (chronic from the beginning)
40
![Page 39: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/39.jpg)
• General features of Chronic inflammation:
i. Infiltration with mononuclear cells
Infiltrated by mononuclear inflammatory cells : phagocytes & lymphoid cells
phagocytes : circulating monocytes, tissue macrophages, epithelioid cells,
multinucleated giants cells
ii. Tissue destruction
Central feature of lesions
iii. Proliferative changes
Result of necrosis, proliferation of small vessels and fibroblasts; healing by fibrosis and collagen 41
![Page 40: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/40.jpg)
Systemic effects of chronic inflammation
Associated with following systemic features:1. Fever – mild fever, loss of weight and
weakness2. Anemia – varying degree of anemia3. Leucocytosis - general 4. ESR – elevated in all cases5. Amyloidosis – long term cases of chronic
suppurative inflammation (secondary systemic (AA) amyloidosis
42
![Page 41: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/41.jpg)
Types of chronic inflammation
NON-SPECIFIC• Formation of granulation
tissue and healing by fibrosis
• Eg; Chronic osteomyelitis, Chronic ulcer
SPECIFIC• Injurious agent causes a
characteristic histologic tissue response
• Eg; tuberculosis, leprosy, syphilis
43
![Page 42: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/42.jpg)
Types of chronic inflammation (based on histological classification)
CHRONIC NON-SPECIFIC INFLAMMATION
• Characterised by:(a) non-specific inflammatory cell infiltration eg; chronic osteomyelitis, lung abcess(b) Infiltration by polymorphs and abcess formation Eg; Actinomycosis
CHRONIC GRANULOMATOUS INFLAMMATION
• Formation of granulomas• Eg; tuberculosis, leprosy,
syphilis, sarcoidosis
44
![Page 43: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/43.jpg)
Granulomatous Inflammation
• Granulomatous inflammation; mechanism whereby the body deals with certain “indigestible” bacteria, fungi, or foreign particles.
• Examples;
i. Bacteria e.g. Tuberculosis, Leprosy
ii. Parasitic e.g. Schistosomiasis
iii. Fungal e.g. Blastomycosis, Histoplasma capsulatum
iv. Inorganic metals or dusts e.g. Silicosis
v. Foreign body e.g. Vascular graft
vi. Unknown e.g. Sarcoidosis
45
![Page 44: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/44.jpg)
46
INJURY(e.g; by M. tuberculosis,
talc
Failure to digest agent
Weak acute inflammatory response
Persistence of injurious agent
T cell-mediated immune response
Poorly digestible agent
• Activation of CD+4 T cells (release of lymphokines IL-1, IL-2. growth
factors IFN-ˠ and IFN-ɑ)
• Monocyte chemotactic factor
![Page 45: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/45.jpg)
47
Accumulation of tissue macrophages (Increased recruitment from circulation, local
proliferation)
Macrophages activated by IFN-ˠ
Transformed to epithelioid cells, giant cells
GRANULOMA
![Page 46: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/46.jpg)
Granuloma tissue
48
![Page 47: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/47.jpg)
• Examples of disorders associated with inflammation include;
i. Asthma
ii. Autoimmune diseases
iii. Hypersensitivities
iv. Pelvic inflammatory disease
v. Rheumatoid arthritis
vi. Transplant rejection
49
![Page 48: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/48.jpg)
2.3: Mediators Of Inflammation• What are mediators?
i. May be circulating in the plasma or may be produced
locally by cells at the site of inflammation.
ii. Induce their effects by binding to specific reactors on
target cells.
iii. May stimulate target cells to release secondary effector
molecules.
iv. May act on only one or a very few targets.
v. Function is generally tightly regulated.
50
![Page 49: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/49.jpg)
• 2 types of chemical mediators of Acute inflammation;
i. Plasma-derived mediators e.g. kinin system,
coagulation & fibrinolytic system, complement
system.
ii. Cell-derived mediators e.g. vasoactive amines,
cytokines, platelet activating factor, growth factor.
51
![Page 50: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/50.jpg)
• Chronic inflammatory cells & mediators;
i. Macrophages
ii. T & B-lymphocytes
iii. Eosinophils
iv. Mast cells
52
![Page 51: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/51.jpg)
• Inflammatory cells release mediators such as;
i. Cytokines-
(IL-8, interferon-neutrophil)
ii. Vasoactive amines-
(histamine, serotinin- mast cell, basophil, platelet)
iii. Prostanoids-
(arachidonic acid metabolics)
iv. Reactive oxygen intermediates-
(released from activated neutrophil) 53
![Page 52: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/52.jpg)
• If the mediators in the inflammatory response are successful;
i. Invading & infectious agents will be removed.
ii. Damaged tissues will be disposed of.
iii. New tissue will be induced to form.
iv. New blood supply to the area will be established.
54
![Page 53: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/53.jpg)
Chronic inflammation cells
55
![Page 54: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/54.jpg)
Chronic Inflammation – Lung Abscess56
![Page 55: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/55.jpg)
2.4: Morphologic Patterns Of Acute & Chronic Inflammation
• Serous inflammation; excessive clear watery fluid with a variable protein content but no fibrin e.g. pleural effusion associated with tuberculosis.
57
![Page 56: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/56.jpg)
Serous Inflammation - effusion58
![Page 57: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/57.jpg)
Serous Inflammation - effusion59
![Page 58: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/58.jpg)
• Fibrinous inflammation; the formation of fibrin is striking e.g. in acute pleurisy.
60
![Page 59: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/59.jpg)
Fibrinous Inflammation61
![Page 60: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/60.jpg)
• Purulent (Suppurative) inflammation; production of pus is the main characteristic e.g. abscess & acute apendicitis.
62
![Page 61: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/61.jpg)
Purulent Inflammation - PUS
63
![Page 62: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/62.jpg)
Purulent Inflammation - PUS64
![Page 63: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/63.jpg)
• Ulceration; complication of many disease process
• Divided into 2 groups;
i. Simple ulcer
ii. Malignant (cancerous) ulcer
65
![Page 64: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/64.jpg)
A skin ulcer resulting from infection with Corynebacterium diphtheriae
66
![Page 65: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/65.jpg)
Mouth Apthus Ulcer
67
![Page 66: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/66.jpg)
Gastric Ulcer
68
![Page 67: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/67.jpg)
2.5: Repair Or Healing
• The processes that take place during & after the injury are;
i. Removal of dead & foreign material.
ii. Regeneration of injured tissue from cells
of the same type.
iii. Replacement of damage tissue by new
connective tissue.69
![Page 68: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/68.jpg)
• Cells can be divided into 3 major groups;
i. Labile (continuous dividing) e.g. epithelial & blood cells.
ii. Stable (low level of replication; decrease or lose their ability to proliferate after adolescence) e.g. fibroblast, smooth muscle cells, bone & cartilage cells
iii. Permanent (never divide) e.g. nerve cells, cardiac myocytes.
70
![Page 69: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/69.jpg)
HEALING
• 2 processes:(i) Granulation tissue formation(ii) Contraction of wounds
71
![Page 70: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/70.jpg)
(i) Granulation tissue formation
• 3 phases :(a) PHASE OF INFLAMMATION
trauma, blood clots (site of injury)acute response :exudation of plasma,
neutrophils, monocytes (24 hours)
72
![Page 71: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/71.jpg)
(b) PHASE OF CLEARANCE- proteolytic enzymes from neutrophils- Autolytic enzymes from dead tissue
cells- Phagocytic activity : macrophages(function : clear of the necrotic tissue,
debris & RBCs)
73
![Page 72: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/72.jpg)
(c) PHASE OF INGROWTH OF GRANULATION2 main processes:i. Angiogenesis (neovascularisation) formation of new blood vesselsii. Fibrogenesis formation of fibrocytes and mitotic
division by fibroblasts; myofibroblasts In 6th days, more collagen is formed
74
![Page 73: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/73.jpg)
ii) Contraction of wounds
• Start after 2 -3 days; completed: 14th day• Wound reduced 80% of its original size• Contraction occur: rapid healing process• Factors under mechanism of wound
contraction: (a) dehydration(b) contraction of collagen(c) myofibroblasts
75
![Page 74: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/74.jpg)
WOUND HEALING
1. Healing by first intention (Primary union)characteristics:- clean & uninfected- surgical incised- without much loss of cells & tissue- edges of wound – surgical sutures
76
![Page 75: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/75.jpg)
2. Healing by second intention (Secondary union)Characteristics:- Large tissue defect- extensive loss of cells & tissues- not approximated by surgical sutures but left open
77
![Page 76: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/76.jpg)
• 5 stages of healing (primary Union);
i. Initial Haemorrhage
ii. Acute Inflammation response
iii. Epithelial changes
iv. Organization
v. Suture tracks
78
![Page 77: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/77.jpg)
• 6 stages of healing (secondary Union);
i. Initial Hemorrhage
ii. Inflammation phase
iii. Epithelial changes
iv. Granulation tissue
v. Wound contraction
vi. Presence of infection79
![Page 78: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/78.jpg)
• Repair; regeneration of injured tissue by parenchymal cells of the same type.
• Replacement by connective tissue occur when repair by parenchymal regeneration alone cannot be accomplished.
• Involves production of Granulation tissue.
• Replacement of parenchymal cells with proliferating fibroblasts & vascular endothelial cells.
80
![Page 79: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/79.jpg)
Scars present on the skin, evidence of fibrosis & healing of a wound
81
![Page 80: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/80.jpg)
Granulation tissue
82
![Page 81: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/81.jpg)
Healing Skin wound
83
![Page 82: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/82.jpg)
Healing - Skin scar84
![Page 83: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/83.jpg)
• Factors affecting healing;
i. Systemic e.g. age, nutrition, immune
status.
ii. Local e.g. infection, blood supply,
mobility, foreign body.
85
![Page 84: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/84.jpg)
"Each time you are honest and conduct yourself with honesty, a
success force will drive you toward greater success. Each time you lie, even with a little
white lie, there are strong forces pushing you toward failure."
86
![Page 85: inflammation](https://reader036.vdocument.in/reader036/viewer/2022070315/5550859fb4c905a85c8b493f/html5/thumbnails/85.jpg)
THANK YOU
FOR YOUR ATTENTION
87