The document discusses various aspects of inflammation and repair. It describes the signs of acute inflammation as redness, heat, swelling, pain, and loss of function. It then covers the events in acute inflammation, including neurologic events like vasoconstriction and vasodilation, hemodynamic events such as increased permeability and slowing of blood flow, and cellular events like margination and emigration of leukocytes. Chronic inflammation and types of inflammation based on location and exudates are also summarized. The document concludes by discussing repair through granulation tissue formation, remodeling and fibrosis.

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

22. ABSCESS-HEART

23. Question
Which of the following inflammation commonly
is characterized by collections of dead and dying
polymorphs, dead and dying bacteria, and
necrosis of tissue, all of which form a turbid or
thick fluid in tissues?
A. catarrhal inflammation
B. phlegmonous inflammation
C. cellulitis
D. abscess formation
E. granulomatous inflammation

24. ULCER-GASTRIC MUCOSA

25. PEPTIC ULCER

26. CELLULITIS

27. PSEUDOMEMBRANOUS
INFLAMMATION - DIPTHERIA

29. TYPES OF INFLAMMATION BASED
ON THE NATURE OF EXUDATES
• SEROUS INFLAMMATION
• MUCOUS INFLAMMATION
• FIBRINOUS INFLAMMATION
• CATARRHAL INFLAMMATION
• HEMORRHAGIC INFLAMMATION
• PURULENT OR SUPPURATIVE

30. FIBRINOUS INFLAMMATION-
PERICARDIUM

31. HEMMORRHAGIC INFLAMMATION-RIGHT

32. 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

33. Question
Which of the following findings is an
invariably histologic feature of
granulomatous inflammation?
A. caseous necrosis
B. multinucleated giant cells
C. positive acid-fast staining of causative
organism
D. surrounding cuff of lymphocytes
E. epithelioid cells

34. GRANULOMATOUS INFLAMMATION-LUNGS
THYROIDITIS WITH GRANULOMA

35. GRANULOMATOUS INFLAMMATION
WITH SPHERULES

36. LANGHAN’S GIANT CELLS FOREIGN BODY GIANT CELL- IN
SUTURE LINE

37. SYNCYTHIAL GIANT CELLS

38. REED-STERNBERG GIANT CELL

39. TOUTON GIANT CELL
WARTHIN-FINKELDEY GIANT CELL

40. PRIMARY SKIN LESIONS

41. 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

42. MACULE

43. PAPULE
• PAPULE IS A CIRCUMSCRIBED,
ELEVATED, SOLID LESION LESS THAN
1 CM IN DIAMETER, SUCH AS THE
LESIONS OF LICHEN PLANUS AND
NONPUSTULAR ACNE

44. PAPULE

45. 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

46. PATCH and BULLAE

47. 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

48. PLAQUE and PUSTULE

49. 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.

50. TUMOR and VESICLE

51. WHEAL OR
PLAQUES ARE
TRANSIENT,
CIRCUMSCRIBED,
ELEVATED
PAPULES OFTEN
WITH
ERYTHEMATOUS
BORDERS AND
PALE CENTERS

52. 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)

53. 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

54. 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

55. GRANULATION TISSUE
IN HEALED SCAR

56. 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.

57. GRANULATION TISSUE IN
MYOCARDIAL INFARCT

58. KELOIDS