1
Topic OutcomesAt the end of this lecture, students are able to :1.Describe orally the signs of inflammation2.Describe and ...
CONTENTS2.1: Definitions & Concepts Of Inflammation2.2: Stages Of Inflammation2.3: Mediators Of Inflammation2.4: Morpholog...
2.1: Definitions & Concepts Of             Inflammation• The local response of living mammalian  tissues to injury due to ...
• Causes of inflammation;  i. Physical agent e.g. mechanical trauma, radiation  etc.  ii. Chemical agent e.g. simple chemi...
• Involves 2 basic  processes (overlapping):   Inflammatory              • Have protective role     response              ...
Signs of Inflammation• The famous 4 cardinal signs of inflammation:  (i) rubor (redness)  (ii) tumor (swelling)  (iii) cal...
Heat   Redness Swelling Pain Loss Of Func.                                             8
2.2: Stages Of Inflammation         INFLAMMATION     ACUTE          CHRONIC INFLAMMATION    INFLAMMATION                  ...
• Acute inflammation  – Short duration & represents the early body    reaction and usually followed by repair  – The main ...
• Chronic Inflammation  - longer duration and occurs either :     (a) after the causative agent of acute           inflamm...
I) ACUTE INFLAMMATION• The changes can be conveniently described  under:  (i) Vascular events  (ii) Cellular events     In...
(i) VASCULAR EVENTS• Alteration in the microvasculature  (arterioles, capillaries & venules)• Earliest response to tissue ...
(a) Haemodynamic Changes• Earliest features of inflammatory response  result from changes in the vascular flow and  calibr...
The sequence of these changes:         Transient vasoconstriction     Persistent progressive vasodilatation         Local ...
• Lewis Triple Response/ red line response; (Eg: form stroking with a blunt point) i. Red line   : Appears a few second;  ...
Triple response                  18
(b) Altered vascular permeability• Vascular changes begin quickly after the injury  but may develop at variables rates, de...
Fluid interchange between blood and extracellular fluid (ECF). (HP = Hydrostatic     pressure, OP = Osmotic pressure)NOOED...
Edema        21
• MECHANISMS OF INCREASED VASCULAR  PERMEABILITY(i) Endothelial cell contraction(ii) Endothelial cell retraction(iii) Dire...
a) Contraction of endothelial cells• Microvasculature : venules• Response type :  Immediate transient (15-30 min)• Pathoge...
b) Retraction of endothelial cells• Microvasculature : venules• Response type :  somewhat delayed (in 4 – 6 hrs)  prolonge...
c) Direct injury to endothelial cells• Microvasculature : Arteriols, venules,  capillaries• Response type :  Immediate sus...
• Pathogenesis :  cell necrosis and detachment• Examples : Moderate to severe burns, severe  bacterial infection, radiatio...
d) Endothelial injury mediated byleucocytes• Microvasculature : venules, capillaries• Response type :  delayed, prolonged•...
e) Neovascularisation• Microvasculature : All levels• Response type :  Any type• Pathogenesis :  Angiogenesis, vascular en...
ii) CELLULAR EVENTS• Cellular events; cells of the acute inflammatory  response are the neutrophils, monocytes &  macropha...
• The movements of neutrophils out of the vessels  & their role in combat can be divided into 5  steps;  i. Margination = ...
• Concentrates the leucocytes adjacent to endothelial  wall- Margination• Adherence of inflammatory cell to the endotheliu...
THE INFLAMMATION PROCESS                           33
34
Neutrophil Margination                         35
FATE OF ACUTE INFLAMMATION• Acute inflammation generally has one of FOUR  (4) outcomes;  i. Resolution – complete return t...
iii) Suppuration – the progression process of   severe necrosis cause by pyogenic bacteria;   neutrophilic infiltration; f...
An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of                   ...
II) CHRONIC INFLAMMATION• Chronic inflammation;  prolonged process in which tissue  destruction and inflammation occur  at...
• Caused one of the following 3 ways:  i) Chronic inflammation following acute       inflammation – the tissue destruction...
• General features of Chronic inflammation:  i.   Infiltration with mononuclear cells       Infiltrated by mononuclear inf...
Systemic effects of chronic             inflammationAssociated with following systemic features:1. Fever – mild fever, los...
Types of chronic inflammation        NON-SPECIFIC                      SPECIFIC• Formation of granulation     • Injurious ...
Types of chronic inflammation (based     on histological classification)    CHRONIC NON-SPECIFIC           CHRONIC GRANULO...
Granulomatous Inflammation• Granulomatous inflammation; mechanism whereby the  body deals with certain “indigestible” bact...
INJURY                     (e.g; by M. tuberculosis, talc                          Failure to digest agent                ...
Accumulation of tissue macrophages(Increased recruitment from circulation, local proliferation)               Macrophages ...
Granuloma tissue                   48
• Examples of disorders associated with inflammation  include;  i. Asthma  ii. Autoimmune diseases  iii. Hypersensitivitie...
2.3: Mediators Of Inflammation• What are mediators?  i. May be circulating in the plasma or may be produced     locally by...
• 2 types of chemical mediators of Acute inflammation;  i. Plasma-derived mediators e.g. kinin system,    coagulation & fi...
• Chronic inflammatory cells & mediators; i. Macrophages ii. T & B-lymphocytes iii. Eosinophils iv. Mast cells            ...
• Inflammatory cells release mediators such as;  i. Cytokines-(IL-8, interferon-neutrophil)  ii. Vasoactive amines-(histam...
• If the mediators in the inflammatory response are  successful;  i. Invading & infectious agents will be removed.  ii. Da...
Chronic inflammation cells                             55
Chronic Inflammation – Lung Abscess                                      56
2.4: Morphologic Patterns Of Acute & Chronic                Inflammation• Serous inflammation; excessive clear watery  flu...
Serous Inflammation - effusion                                 58
Serous Inflammation - effusion                                 59
• Fibrinous inflammation; the formation of  fibrin is striking e.g. in acute pleurisy.                                    ...
Fibrinous Inflammation                         61
• Purulent (Suppurative) inflammation;  production of pus is the main characteristic  e.g. abscess & acute apendicitis.   ...
Purulent Inflammation - PUS                              63
Purulent Inflammation - PUS                              64
• Ulceration; complication of many disease  process• Divided into 2 groups; i. Simple ulcer ii. Malignant (cancerous) ulce...
A skin ulcer resulting from infection with Corynebacterium                         diphtheriae                            ...
Mouth Apthus Ulcer                     67
Gastric Ulcer                68
2.5: Repair Or Healing• The processes that take place during & after  the injury are;  i. Removal of dead & foreign materi...
• Cells can be divided into 3 major groups;  i. Labile (continuous dividing) e.g. epithelial &       blood cells.  ii. Sta...
HEALING• 2 processes:  (i) Granulation tissue formation  (ii) Contraction of wounds                                     71
(i) Granulation tissue formation• 3 phases :  (a) PHASE OF INFLAMMATION      trauma, blood clots (site of injury)      acu...
(b)   PHASE OF CLEARANCE      - proteolytic enzymes from neutrophils      - Autolytic enzymes from dead tissue  cells     ...
(c)   PHASE OF INGROWTH OF GRANULATION      2 main processes:      i. Angiogenesis (neovascularisation)         formation ...
ii) Contraction of wounds•   Start after 2 -3 days; completed: 14th day•   Wound reduced 80% of its original size•   Contr...
WOUND HEALING1. Healing by first intention (Primary union)   characteristics:   - clean & uninfected   - surgical incised ...
2. Healing by second intention (Secondary   union)   Characteristics:   - Large tissue defect   - extensive loss of cells ...
• 5 stages of healing (primary Union); i. Initial Haemorrhage ii. Acute Inflammation response iii. Epithelial changes iv. ...
• 6 stages of healing (secondary Union); i. Initial Hemorrhage ii. Inflammation phase iii. Epithelial changes iv. Granulat...
• Repair; regeneration of injured tissue by  parenchymal cells of the same type.• Replacement by connective tissue occur w...
Scars present on the skin, evidence of fibrosis &              healing of a wound                                         ...
Granulation tissue                     82
Healing Skin wound                     83
Healing - Skin scar                      84
• Factors affecting healing; i. Systemic e.g. age, nutrition, immune   status. ii. Local e.g. infection, blood supply,   m...
"Each time you are honest and conductyourself with honesty, a success force will  drive you toward greater success. Each  ...
THANK YOUFOR YOUR ATTENTION                     87
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inflammation

  1. 1. 1
  2. 2. 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
  3. 3. CONTENTS2.1: Definitions & Concepts Of Inflammation2.2: Stages Of Inflammation2.3: Mediators Of Inflammation2.4: Morphologic Pattern Of Acute & Chronic Inflammation2.5: Repair Or Healing 3
  4. 4. 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
  5. 5. • 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
  6. 6. • Involves 2 basic processes (overlapping): Inflammatory • Have protective role response against injurious agents • Cause considerable harm to the body healing eg; anaphylaxis, atherosclerosis etc 6
  7. 7. 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
  8. 8. Heat Redness Swelling Pain Loss Of Func. 8
  9. 9. 2.2: Stages Of Inflammation INFLAMMATION ACUTE CHRONIC INFLAMMATION INFLAMMATION 9
  10. 10. • 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
  11. 11. • Chronic Inflammation - longer duration and occurs either : (a) after the causative agent of acute inflammation 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)
  12. 12. I) ACUTE INFLAMMATION• The changes can be conveniently described under: (i) Vascular events (ii) Cellular events Infected toenail showing the characteristic redness and swelling associated with acute inflammation 13
  13. 13. (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
  14. 14. (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
  15. 15. The sequence of these changes: Transient vasoconstriction Persistent progressive vasodilatation Local hydrostatic pressure Slowing or stasis Leucocytic margination 16
  16. 16. • 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
  17. 17. Triple response 18
  18. 18. (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
  19. 19. Fluid interchange between blood and extracellular fluid (ECF). (HP = Hydrostatic pressure, OP = Osmotic pressure)NOOEDEMA OEDEMA 20
  20. 20. Edema 21
  21. 21. • 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
  22. 22. 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
  23. 23. 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 only 25
  24. 24. 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
  25. 25. • Pathogenesis : cell necrosis and detachment• Examples : Moderate to severe burns, severe bacterial infection, radiation injury 27
  26. 26. d) Endothelial injury mediated byleucocytes• Microvasculature : venules, capillaries• Response type : delayed, prolonged• Pathogenesis : Leucocyte activation• Examples : pulmonary venules and capillaries 28
  27. 27. e) Neovascularisation• Microvasculature : All levels• Response type : Any type• Pathogenesis : Angiogenesis, vascular endothelial growth factor (VEGF)• Examples : Healing, tumors 29
  28. 28. 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) Monocytes Macrophages (24-48 hrs; Survive much longer) 30
  29. 29. • 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
  30. 30. • 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
  31. 31. THE INFLAMMATION PROCESS 33
  32. 32. 34
  33. 33. Neutrophil Margination 35
  34. 34. 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
  35. 35. 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 calcifiediv) Progression to chronic inflammation may follow acute inflammation, although signs of chronic inflammation may be present at the onset of injury; healing proceed side by side. 37
  36. 36. An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of necrotic tissue surround central areas of pus 38
  37. 37. II) CHRONIC INFLAMMATION• Chronic inflammation; prolonged process in which tissue destruction and inflammation occur at the same time. 39
  38. 38. • 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 cholecystitis iii) Starting de novo – infection with organisms of low pathogenecity (chronic from the beginning) 40
  39. 39. • 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
  40. 40. Systemic effects of chronic inflammationAssociated with following systemic features:1. Fever – mild fever, loss of weight and weakness2. Anemia – varying degree of anemia3. Leucocytosis - general4. ESR – elevated in all cases5. Amyloidosis – long term cases of chronic suppurative inflammation (secondary systemic (AA) amyloidosis 42
  41. 41. Types of chronic inflammation NON-SPECIFIC SPECIFIC• Formation of granulation • Injurious agent causes a tissue and healing by characteristic histologic fibrosis tissue response• Eg; Chronic osteomyelitis, • Eg; Chronic ulcer tuberculosis, leprosy, syphili s 43
  42. 42. Types of chronic inflammation (based on histological classification) CHRONIC NON-SPECIFIC CHRONIC GRANULOMATOUS INFLAMMATION INFLAMMATION• Characterised by: • Formation of granulomas (a) non-specific • Eg; inflammatory cell tuberculosis, leprosy, syphili infiltration eg; chronic s, sarcoidosis osteomyelitis, lung abcess (b) Infiltration by polymorphs and abcess formation Eg; Actinomycosis 44
  43. 43. 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
  44. 44. INJURY (e.g; by M. tuberculosis, talc Failure to digest agent Weak acute inflammatory response Persistence of injurious agentT 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 46
  45. 45. Accumulation of tissue macrophages(Increased recruitment from circulation, local proliferation) Macrophages activated by IFN-ˠ Transformed to epithelioid cells, giant cells GRANULOMA 47
  46. 46. Granuloma tissue 48
  47. 47. • 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
  48. 48. 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
  49. 49. • 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
  50. 50. • Chronic inflammatory cells & mediators; i. Macrophages ii. T & B-lymphocytes iii. Eosinophils iv. Mast cells 52
  51. 51. • 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
  52. 52. • 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
  53. 53. Chronic inflammation cells 55
  54. 54. Chronic Inflammation – Lung Abscess 56
  55. 55. 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
  56. 56. Serous Inflammation - effusion 58
  57. 57. Serous Inflammation - effusion 59
  58. 58. • Fibrinous inflammation; the formation of fibrin is striking e.g. in acute pleurisy. 60
  59. 59. Fibrinous Inflammation 61
  60. 60. • Purulent (Suppurative) inflammation; production of pus is the main characteristic e.g. abscess & acute apendicitis. 62
  61. 61. Purulent Inflammation - PUS 63
  62. 62. Purulent Inflammation - PUS 64
  63. 63. • Ulceration; complication of many disease process• Divided into 2 groups; i. Simple ulcer ii. Malignant (cancerous) ulcer 65
  64. 64. A skin ulcer resulting from infection with Corynebacterium diphtheriae 66
  65. 65. Mouth Apthus Ulcer 67
  66. 66. Gastric Ulcer 68
  67. 67. 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
  68. 68. • 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
  69. 69. HEALING• 2 processes: (i) Granulation tissue formation (ii) Contraction of wounds 71
  70. 70. (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
  71. 71. (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
  72. 72. (c) PHASE OF INGROWTH OF GRANULATION 2 main processes: i. Angiogenesis (neovascularisation) formation of new blood vessels ii. Fibrogenesis formation of fibrocytes and mitotic division by fibroblasts; myofibroblasts In 6th days, more collagen is formed 74
  73. 73. 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
  74. 74. WOUND HEALING1. Healing by first intention (Primary union) characteristics: - clean & uninfected - surgical incised - without much loss of cells & tissue - edges of wound – surgical sutures 76
  75. 75. 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
  76. 76. • 5 stages of healing (primary Union); i. Initial Haemorrhage ii. Acute Inflammation response iii. Epithelial changes iv. Organization v. Suture tracks 78
  77. 77. • 6 stages of healing (secondary Union); i. Initial Hemorrhage ii. Inflammation phase iii. Epithelial changes iv. Granulation tissue v. Wound contraction vi. Presence of infection 79
  78. 78. • 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
  79. 79. Scars present on the skin, evidence of fibrosis & healing of a wound 81
  80. 80. Granulation tissue 82
  81. 81. Healing Skin wound 83
  82. 82. Healing - Skin scar 84
  83. 83. • Factors affecting healing; i. Systemic e.g. age, nutrition, immune status. ii. Local e.g. infection, blood supply, mobility, foreign body. 85
  84. 84. "Each time you are honest and conductyourself 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
  85. 85. THANK YOUFOR YOUR ATTENTION 87

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