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.
3. SIGNS OF INFLAMMATION
โข RUBOR- REDNESS DUE TO INCREASED
BLOOD BLOW AND VASODILATION
โข CALOR- OR HEAT DUE TO INCREASE
BLOOD FLOW TO THE PERIPHERY
โข TUMOR- SWELLING FROM INFLAMMATORY
EDEMA
โข DOLOR-PAIN FROM SWELLING AND
PRESENCE OF INFLAMMATORY
MEDIATORS
โข FUNCTIO LAESA-LOSS OF FUNCTION DUE
TO MAIN
AND STRUCTURAL NECROSIS
4. Question
โข 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
โข What is it?
โ Series of reactions of
vascularized tissue to injury
โข What is its purpose?
โ Defend against foreign
substances (infection)
โ Dispose of dead / dying
tissue
โ Immobilize injured area
โ Compartmentalize area
6. Acute Inflammation
โข Events in Acute Inflammation
โ Neurologic events
โ Hemodynamic events
โ Cellular events
โข Events Overlap and are related
โข Events are the same regardless of cause of
inflammation
โ Magnitude of events depends on:
โข severity of injury
โข immune status
โข temperature
7. Acute Inflammation โ Neurologic events
โข Initial Vasoconstriction
โ Transatory & reflexive
โ usually lasts up to 30 seconds
โข Gradual Vasodilation
โ Relaxation of reflexive spasm
โ Causes โbleedingโ to start
8. Acute Inflammation โ Hemodynamic
Events
โข Vasodilation
โ From relaxation of reflex & chemical mediators
โข Slowing of bloodflow
โ Relationship of flow to diameter
โข Margination of Leukocytes
โ ???? Nobel prize for Medicine
โข Hemostasis
โข Permeability Changes
9. Acute Inflammation โ Hemodynamic
Events
โข Permeability Changes
โ Mostly from inflammatory chemicals
โ Occurs in capillaries & small venules
โ Junctions between epithelial cells loosen
โ Fluid leaks (transudate exudate)
โ Leads to hemoconcentration
โ Makes margination easier
11. Events in Acute Inflammation
โข 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 โ Cellular Events
โข Circulating Leukocytes
โ Marginated cells emmigrate from vasculature
(diapedesis) โ smaller first, larger later
โ Basophils โ release anti-coagulants
โ Neutrophils โ vicious phagocytes
โข Release many chemical mediators โ chemotaxis
โข Primary job is to phagocytize bacteria
โข Magnifies inflammation above required level in musculoskeletal
injury
โ Monocytes Macrophages
โข Arrive ~ 5h post-injury
โข Remove dead tissue debris (clean up the mess)
13. Acute Inflammation โ Chemical events
โข Over 180 different chemicals involved in acute
inflammation
โข Sources = damaged cells, inflammatory cells, platelets,
plasma, etc.
โข Histamine โ 1st chemical, strong vasodilator & increases
permeability
โข Bradykinins โ increases permeability & pain (especially
with prostaglandins)
โข Prostaglandins โ made from released phospholipids
(arachadonic acid cascade)
โ Target of NSAIDS & steroidal anti-inflammatories
14. Acute Inflammation โ big picture
โข First few seconds โข After the first hour?
โ Immediate vasoconstriction โ Hemoconcentration
โข First Hour from edema
โ Ischemia
โ Gradual vasodilation
โ Growing interaction of
โ Hemostasis begins
chemical mediators
โ Mast Cell degranulation
โ Emmigration of larger
โ Margination of WBCโs WBCโs
โ Large scale neutrophil โ Complement System
response begins
15. Question
โข 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 WBCโs
D. emigration of WBCโs
E. increased vascular permeability
16. TYPES OF INFLAMMATION
BASED ON SITE AFFECTED
โข ABSCESS
โข ULCER
โข CELLULITIS or PHLEGMON
โข PSEUDOMEMBRANOUS
INFLAMMATION
17. Chronic Inflammation
โข Immunologists define as period when
macrophages predominate
โข Clinicians define as recurrent inflammation
prior to completion of repair or resolution
โข Cellular Aspects
โ Leukocytes during early post-acute phase
โข CD8+ (T- killer) & CD4+ (delayed
hypersensitivity)
19. Chronic Inflammation
โข Easy to re-start inflammation
โ Clinically, must control activity level & protect
injury site
โข Leads to hypertrophic scarring
โ Additional infiltration of fibroblasts
โ Abundance of stimulating chemicals
20. Question
โข 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
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
29. TYPES OF INFLAMMATION BASED
ON THE NATURE OF EXUDATES
โข SEROUS INFLAMMATION
โข MUCOUS INFLAMMATION
โข FIBRINOUS INFLAMMATION
โข CATARRHAL INFLAMMATION
โข HEMORRHAGIC INFLAMMATION
โข PURULENT OR SUPPURATIVE
32. GRANULOMATOUS
INFLAMMATION
โข Granulomatous inflammation occurs after
the acute-phase response and consists of
epithelioid and giant cells.
โข 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
41. PRIMARY SKIN LESIONS
MACULE
โข MACULE IS A CIRCUMSCRIBED FLAT
AREA LESS THAN 1 CM OF
DISCOLORATION WITHOUT
ELEVATION OR DEPRESSION OF
SURFACE RELATIVE TO
SURROUNDING SKIN
45. PATCH AND BULLA
โข PATCH IS A CIRCUMSCRIBED AREA OF
DISCOLORATION, GREATER THAN 1CM
WHICH IS NEITHER ELEVATED OR
DEPRESSED RELATIVE TO THE
SURROUNDING SKIN
โข BULLAE ARE RAISED, CIRCUMSCRIBED
LESION GREATER THAN 0.5 CM THAT
CONTAIN SEROUS FLUID
47. PLAQUE AND PUSTULE
โข PLAQUE IS A WELL-CIRCUMCRIBED,
ELEVATED, SUPERFICIAL, SOLID LESION,
GREATER THAN 1 CM IN DIAMETER
โข PUSTULE IS A SMALL (1CM IN DIAMETER)
CIRCUMSCRIBED SUPERFICIAL ELEVATION
OF THE SKIN THAT IS FILLED WITH
PURULENT MATERIAL
49. TUMOR and VESICLE
โข TUMOR โ 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.
โข VESICLE โ is a small , superficial
elevation of the skin, less than 0.5 cm,
that contains serous fluid.
51. WHEAL OR
PLAQUES ARE
TRANSIENT,
CIRCUMSCRIBED,
ELEVATED
PAPULES OFTEN
WITH
ERYTHEMATOUS
BORDERS AND
PALE CENTERS
52. REPAIR, REGENERATION
AND FIBROSIS
โข 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
โข Fibroplasia โ fibrous repair
โ Formulation of Granulation tissue
โข Capillary budding results from mitogens
โ PDGF most important, hypoxia contributes
โข Forms meshlike framework for scar development
โ Infiltration of fibroblasts
โ Collagen laid down in random pattern
โข Structure can be manipulated!!!!!
โ Scar tissues excessive if inflammation re-initiated
54. Tissue Repair
โข Maturation & Remodeling
โ Initial scar formation takes weeks
โ Scar matures
โข Longest part of inflammation (over 1 yr)
โข Re-absorb temporary vasculature
โ Scar shrinks (contraction) & changes color
โ Scar remodels
โข Collagen fibers re-align with stress (SAID)
โข Less tensile strength than tissue it replaces
56. SURGICAL WOUNDS
โข HEALING BY PRIMARY INTENTION โ is
letting a surgical wound heal without a big
scar, where the wound hasneatly apposed
edges
โข 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.