General pathology lecture 5 inflammation & repair

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  • 1. INFLAMMATION AND REPAIR Lecture 5
  • 2. INFLAMMATORY CELLS
  • 3. SIGNS OF INFLAMMATION• RUBOR- REDNESS DUE TO INCREASED BLOOD BLOW AND VASODILATION• CALOR- OR HEAT DUE TO INCREASE BLOOD FLOW TO THE PERIPHERY• TUMOR- SWELLING FROM INFLAMMATORY EDEMA• DOLOR-PAIN FROM SWELLING AND PRESENCE OF INFLAMMATORY MEDIATORS• FUNCTIO LAESA-LOSS OF FUNCTION DUE TO MAIN AND STRUCTURAL NECROSIS
  • 4. Question• Pain associated with acute inflammation is thought to be caused by A. pressure effects of exudate fluid B. histamine C. serotonin D. kinins E. all of the above
  • 5. Acute Inflammation • What is it? – Series of reactions of vascularized tissue to injury • What is its purpose? – Defend against foreign substances (infection) – Dispose of dead / dying tissue – Immobilize injured area – Compartmentalize area
  • 6. Acute Inflammation• Events in Acute Inflammation – Neurologic events – Hemodynamic events – Cellular events• Events Overlap and are related• Events are the same regardless of cause of inflammation – Magnitude of events depends on: • severity of injury • immune status • temperature
  • 7. Acute Inflammation – Neurologic events• Initial Vasoconstriction – Transatory & reflexive – usually lasts up to 30 seconds• Gradual Vasodilation – Relaxation of reflexive spasm – Causes “bleeding” to start
  • 8. Acute Inflammation – Hemodynamic Events• Vasodilation – From relaxation of reflex & chemical mediators• Slowing of bloodflow – Relationship of flow to diameter• Margination of Leukocytes – ???? Nobel prize for Medicine• Hemostasis• Permeability Changes
  • 9. Acute Inflammation – Hemodynamic Events• Permeability Changes – Mostly from inflammatory chemicals – Occurs in capillaries & small venules – Junctions between epithelial cells loosen – Fluid leaks (transudate exudate) – Leads to hemoconcentration – Makes margination easier
  • 10. ACUTE INFLAMMATION
  • 11. Events in Acute Inflammation• The order of the events in acute inflammation are 1. vascular dilatation 2. increased vascular permeability 3. local hemoconcentration and slowing of blood 4. margination of white blood cells 5. emigration of leukocytes
  • 12. Acute Inflammation – Cellular Events• Circulating Leukocytes – Marginated cells emmigrate from vasculature (diapedesis) – smaller first, larger later – Basophils – release anti-coagulants – Neutrophils – vicious phagocytes • Release many chemical mediators – chemotaxis • Primary job is to phagocytize bacteria • Magnifies inflammation above required level in musculoskeletal injury – Monocytes Macrophages • Arrive ~ 5h post-injury • Remove dead tissue debris (clean up the mess)
  • 13. Acute Inflammation – Chemical events• Over 180 different chemicals involved in acute inflammation• Sources = damaged cells, inflammatory cells, platelets, plasma, etc.• Histamine – 1st chemical, strong vasodilator & increases permeability• Bradykinins – increases permeability & pain (especially with prostaglandins)• Prostaglandins – made from released phospholipids (arachadonic acid cascade) – Target of NSAIDS & steroidal anti-inflammatories
  • 14. Acute Inflammation – big picture• First few seconds • After the first hour? – Immediate vasoconstriction – Hemoconcentration• First Hour from edema – Ischemia – Gradual vasodilation – Growing interaction of – Hemostasis begins chemical mediators – Mast Cell degranulation – Emmigration of larger – Margination of WBC’s WBC’s – Large scale neutrophil – Complement System response begins
  • 15. Question• Of the following events that are part of the acute inflammatory response, which would occur THIRD in correct sequence? A. vascular dilatation B. local hemoconcentration and slowing of blood C. margination of WBC’s D. emigration of WBC’s E. increased vascular permeability
  • 16. TYPES OF INFLAMMATION BASED ON SITE AFFECTED• ABSCESS• ULCER• CELLULITIS or PHLEGMON• PSEUDOMEMBRANOUS INFLAMMATION
  • 17. Chronic Inflammation• Immunologists define as period when macrophages predominate• Clinicians define as recurrent inflammation prior to completion of repair or resolution• Cellular Aspects – Leukocytes during early post-acute phase • CD8+ (T- killer) & CD4+ (delayed hypersensitivity)
  • 18. CHRONIC OSTEOMYELITIS- BRODIE’S ABSCESS
  • 19. Chronic Inflammation• Easy to re-start inflammation – Clinically, must control activity level & protect injury site• Leads to hypertrophic scarring – Additional infiltration of fibroblasts – Abundance of stimulating chemicals
  • 20. Question• The features, monocytes, giant cells, fibroblasts and lymphocytes, are characteristics of A. acute inflammation B. granulation tissue C. wound healing D. chronic inflammation E. suppuration
  • 21. ABSCESS-HEART
  • 22. Question Which of the following inflammation commonlyis characterized by collections of dead and dyingpolymorphs, dead and dying bacteria, andnecrosis of tissue, all of which form a turbid orthick fluid in tissues? A. catarrhal inflammation B. phlegmonous inflammation C. cellulitis D. abscess formation E. granulomatous inflammation
  • 23. ULCER-GASTRIC MUCOSA
  • 24. PEPTIC ULCER
  • 25. CELLULITIS
  • 26. PSEUDOMEMBRANOUSINFLAMMATION - DIPTHERIA
  • 27. TYPES OF INFLAMMATION BASED ON THE NATURE OF EXUDATES• SEROUS INFLAMMATION• MUCOUS INFLAMMATION• FIBRINOUS INFLAMMATION• CATARRHAL INFLAMMATION• HEMORRHAGIC INFLAMMATION• PURULENT OR SUPPURATIVE
  • 28. FIBRINOUS INFLAMMATION- PERICARDIUM
  • 29. HEMMORRHAGIC INFLAMMATION-RIGHT
  • 30. GRANULOMATOUS INFLAMMATION• Granulomatous inflammation occurs after the acute-phase response and consists of epithelioid and giant cells.• Two types of granuloma: 1. Foreign Body granuloma-formed in response to indigestible materials 2. Allergic granuloma-formed in delayed hypersensitivity reactions
  • 31. QuestionWhich of the following findings is aninvariably histologic feature ofgranulomatous inflammation? A. caseous necrosis B. multinucleated giant cells C. positive acid-fast staining of causative organism D. surrounding cuff of lymphocytes E. epithelioid cells
  • 32. GRANULOMATOUS INFLAMMATION-LUNGS THYROIDITIS WITH GRANULOMA
  • 33. GRANULOMATOUS INFLAMMATION WITH SPHERULES
  • 34. LANGHAN’S GIANT CELLS FOREIGN BODY GIANT CELL- IN SUTURE LINE
  • 35. SYNCYTHIAL GIANT CELLS
  • 36. REED-STERNBERG GIANT CELL
  • 37. TOUTON GIANT CELLWARTHIN-FINKELDEY GIANT CELL
  • 38. PRIMARY SKIN LESIONS
  • 39. PRIMARY SKIN LESIONS MACULE• MACULE IS A CIRCUMSCRIBED FLAT AREA LESS THAN 1 CM OF DISCOLORATION WITHOUT ELEVATION OR DEPRESSION OF SURFACE RELATIVE TO SURROUNDING SKIN
  • 40. MACULE
  • 41. PAPULE• PAPULE IS A CIRCUMSCRIBED, ELEVATED, SOLID LESION LESS THAN 1 CM IN DIAMETER, SUCH AS THE LESIONS OF LICHEN PLANUS AND NONPUSTULAR ACNE
  • 42. PAPULE
  • 43. PATCH AND BULLA• PATCH IS A CIRCUMSCRIBED AREA OF DISCOLORATION, GREATER THAN 1CM WHICH IS NEITHER ELEVATED OR DEPRESSED RELATIVE TO THE SURROUNDING SKIN• BULLAE ARE RAISED, CIRCUMSCRIBED LESION GREATER THAN 0.5 CM THAT CONTAIN SEROUS FLUID
  • 44. PATCH and BULLAE
  • 45. PLAQUE AND PUSTULE• PLAQUE IS A WELL-CIRCUMCRIBED, ELEVATED, SUPERFICIAL, SOLID LESION, GREATER THAN 1 CM IN DIAMETER• PUSTULE IS A SMALL (1CM IN DIAMETER) CIRCUMSCRIBED SUPERFICIAL ELEVATION OF THE SKIN THAT IS FILLED WITH PURULENT MATERIAL
  • 46. PLAQUE and PUSTULE
  • 47. TUMOR and VESICLE• TUMOR – is a solid, firm lesion about 1 cm in diameter that can be above, level with or beneath the skin surface. It is also called a mass.• VESICLE – is a small , superficial elevation of the skin, less than 0.5 cm, that contains serous fluid.
  • 48. TUMOR and VESICLE
  • 49. WHEAL OR PLAQUES ARE TRANSIENT,CIRCUMSCRIBED, ELEVATEDPAPULES OFTEN WITHERYTHEMATOUS BORDERS AND PALE CENTERS
  • 50. REPAIR, REGENERATION AND FIBROSIS• Cell types and regenerative ability: 1. Labile cells- cells with short life span that constantly proliferate. Excellent regeneration. (Ex. skin, gut, hemopoietic cells) 2. Stable cells-normally with little proliferation but remain capable of more raid cell division following injury. Good regeneration. (Ex. liver, renal PCT) 3. Permanent cell- are not capable of proliferation. No regeneration. Healed by scarring (Ex. Brain, heart)
  • 51. Tissue Repair• Fibroplasia – fibrous repair – Formulation of Granulation tissue • Capillary budding results from mitogens – PDGF most important, hypoxia contributes • Forms meshlike framework for scar development – Infiltration of fibroblasts – Collagen laid down in random pattern • Structure can be manipulated!!!!! – Scar tissues excessive if inflammation re-initiated
  • 52. Tissue Repair• Maturation & Remodeling – Initial scar formation takes weeks – Scar matures • Longest part of inflammation (over 1 yr) • Re-absorb temporary vasculature – Scar shrinks (contraction) & changes color – Scar remodels • Collagen fibers re-align with stress (SAID) • Less tensile strength than tissue it replaces
  • 53. GRANULATION TISSUE IN HEALED SCAR
  • 54. SURGICAL WOUNDS• HEALING BY PRIMARY INTENTION – is letting a surgical wound heal without a big scar, where the wound hasneatly apposed edges• HEALING BY SECONDARY INTENTION- is letting a surgical wound heal and leave a big scar, called granulation tissue that is formed from the bottom up, with the edges not neatly apposed.
  • 55. GRANULATION TISSUE IN MYOCARDIAL INFARCT
  • 56. KELOIDS