Chapter 5

Inflammation and Healing

(Revised/Reviewed)
 Review of Body Defenses
 First line of defense (block entry of bacteria)
 Nonspecific
 Mechanical barrier
 Unbroken skin and mucous membranes
 Secretions such as tears and gastric juices
(enzymes and chemicals) inactivate/destroy
 Second line of defense
 Nonspecific processes
 Phagocytosis (destruction of pathogens) –engulf
and destroy
 Inflammation – sequence of events – limit impact
of injury

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 Review of Body Defenses
(Cont.)
 Third line of defense
 Specific defense
 Production of specific antibodies or cell-mediated
immunity

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Defense Mechanisms in the Body

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 Physiology of Inflammation
 Inflammatory response
 A protective defense mechanism and important basic
concept in pathophysiology
 Disorders are named using the ending –itis.
 Allergic reaction, insect bite
 Signs and symptoms serve as warning for a
problem:
 Problem may be hidden within the body.
 It is not the same as infection. (no microbe)
 Infection, however, is one cause of inflammation.

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 Causes of Inflammation
 Direct physical damage –
 cut, sprain
 Caustic chemicals - acid, drain cleaner
 Ischemia or infarction
 Allergic reactions
 Extremes of heat or cold
 Foreign bodies - splinter, glass
 Infection

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 Definition/Steps of Inflammation
INJURY (capillaries and tissue cells)
Release of bradykinin from injured cells
(stimulates pain receptors)
Pain causes release of histamine.
Bradykinin and histamine cause
capillary dilation.
Break in skin allows bacteria to enter tissue
Neutrophils phagocytize bacteria.
Macrophages (mature monocytes) leave the
bloodstream and phagocytose microbes.

Bradykinin – peptide that helps control inflammation

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 Acute Inflammation
 Process of inflammation is the same, regardless of cause.
 Timing varies with specific cause (immediate or delayed) –
sunburn (delayed)
 Chemical mediators (released) affect blood
vessels and nerves in the damaged area:
 Vasodilation
 Hyperemia (excess of blood in the vessels)
 Increase in capillary permeability
 Leukocytes are attracted by chemotaxis
 Chemotaxis – damaged cells release chemicals
 Diapedesis – cells destroy foreign material, cell
debris (phagocytosis)

Chemotaxis – movement of a motile cell

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Chemical Mediators in the
Inflammatory Response

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 Local Effects of Inflammation
 Redness and warmth
 Caused by increased blood flow to damaged area
 Swelling (edema)
 Shift of protein and fluid into the interstitial space
 Pain
 Increased pressure of fluid on nerves; release of chemical
mediators (e.g., bradykinins)
 Loss of function
 May develop if cells lack nutrients; edema may interfere with
movement.

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 Exudate
 Serous
 Watery, consists primarily of fluid, some proteins, and white blood
cells
 Fibrinous
 Thick, sticky, high cell and fibrin content
 Purulent
 Thick, yellow-green, contains more leukocytes, cell debris, and
microorganisms (bacterial infection) “pus”
 Abscess – pocket of purulent/pus in solid tissue

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 Systemic Effects of Inflammation
 Mild fever (pyrexia)
 Common if inflammation
is extensive
 Release of pyrogens-
fever producing
substances
 Impact of high fever
destroys pathogens
 Malaise
 Feeling unwell
 Fatigue
 Headache
 Anorexia
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 Changes in the Blood
with Inflammation
 Increased WBC –
leukocytosis
 Differential count –
(neutrophils, lymphocytes,
eosinophils, monocytes, basophils)
 Elevated Serum C-
reactive protein
 Elevated erythrocyte
sedimentation rate
(ESR)
 Helps identify viral from
bacterial etiology
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 Potential Complications of
Inflammation
 Local – inflammation in lungs – reduce expansion,
decrease oxygen diffusion – joints – decreased ROM
 Infection
 Microorganisms can more easily penetrate
edematous tissues. (damaged tissue)
 Some microbes resist phagocytosis.
 The inflammatory exudate also provides an
excellent medium for microorganisms.
 Skeletal muscle spasm
 May be initiated by inflammation
 Protective response to pain
 Bones/joints out of normal alignment

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 Chronic Inflammation
 Follows acute episode of inflammation
 Less swelling and exudate
 Presence of more lymphocytes,
macrophages, and fibroblasts
 Continued tissue destruction
 More fibrous scar tissue
 Granuloma may develop around foreign
object (small mass of cells with a necrotic center)

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 Potential Complications
 Deep ulcers may result from severe or
prolonged inflammation
 Caused by cell necrosis and lack of cell
regeneration that causes erosion of the tissue
• Can lead to complications such as perforation of viscera
• Extensive scar tissue formation

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 Treatment of Inflammation

 Acetylsalicylic acid (ASA)

 Aspirin (pain, inflammation, fever – irritation of GI, bleeding and ulcers)
 Acetaminophen
 Tylenol (fever, pain, not inflammation)
 Nonsteroidal anti-inflammatory drugs (NSAIDs)
 Ibuprofen (inflammation, pain, fever – celecoxib (celebrex)
 Glucocorticoids
 Corticosteroids (anti inflammatory)

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 Anti-Inflammatory Effects of
Glucocorticoids (short term)
 Decreased capillary permeability (stabilize
vascular system)
 Reduced number of leukocytes and mast
cells
 Reduces immune response

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 Adverse Effects of
Glucocorticoids (long term, high dose)
 Atrophy of lymphoid tissue; reduced hemopoiesis
 Increased risk of infection
 Catabolic effects
 Increased tissue breakdown; decreased protein
synthesis
 Delayed healing
 Delayed growth in children
 Retention of sodium and water because of
aldosterone-like affect in the kidney (HTN,
edema) HTN and edema

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“RICE” Therapy for Injuries (first aid)
 Rest
 Ice
 Compression - stockings
 Elevation - improve blood flow

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 Types of Healing
 Resolution
 Minimal tissue damage – return to normal short
period (sun burn)
 Regeneration
 Damaged tissue replaced with cells that are
functional (mitosis) – replicate (not all cells can do
this) – heart, liver
 Replacement
 Functional tissue replaced by scar tissue (fibrous)
 Loss of function

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 The Healing Process
 Healing of incised wound by first intention

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 The Healing Process (Cont.)
 Healing by second intention

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 Scar Formation
 Loss of function
 Result of loss of normal cells and specialized
structures – lack of
• Hair follicles
• Nerves
• Receptors
 Contractures and obstructions
 Scar tissue is nonelastic. Shrinks over time
 Can restrict range of movement
 Adhesions
 Bands of scar tissue joining two surfaces that are
normally separated (intestine) – distort and twist

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 Scar Formation

 Hypertrophic scar tissue

 Overgrowth of fibrous tissue
• Leads to hard ridges of scar tissue or
keloid formation
 Ulceration
 Blood supply may be impaired around
scar
• Results in further tissue breakdown
and ulceration at future time

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 Burns
 Thermal—caused by flames or hot fluids
 Chemical
 Radiation
 Electricity
 Light
 Friction

 Cause an acute inflammatory response

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 Classification of Burns
 Superficial partial-
thickness (first-degree)
burns
 Involve epidermis and part
of dermis
 Little, if any, blister
formation (sun burn, scald)
 Deep partial-thickness
(second-degree) burns
 Epidermis and part of
dermis
 Blister formation – red and
edematous, pain
 Become infected, scars
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 Full-thickness (third- and
fourth-degree) burns
 Destruction of all skin
layers and often
underlying tissues
 Charring – hard and dry
on the surface
 Shrinking and tightening =
pressure
 Treatment – escharotomy
– cutting through the crust
– relieve pressure and
allow circulation

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Classification of Burn Injury
by Depth

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 Effects of Burn Injury
 local and systemic  Respiratory problems:
 Dehydration and edema inhalation of toxic
 no bleeding fumes
 Shock (massive fluid  Need high levels of
shift into tissues = oxygen
edema)
 Damage to mucosal
 Decreased circulating lining of trachea and
bronchi
blood volume – low  Inflammation –
BP, hypovolemic obstruction
shock  Wheezing, coughing
 Sputum – black
 Pneumonia
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 Continued
 Very painful throughout  Infection – microbes in
treatment process hair follicles and in
 Body movements, tissues
grafts
 Staphylococcus
 Pain medications are aureus
 Drug resistance
required  Culture necessary for
treatment
 Need for increased
dietary protein and
carbohydrates
 Feel chilled
 Anemia
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Assessment of Burn Area Using
the Rule of Nines

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 Healing of Burns
 Immediate covering of a clean wound is
needed to prevent infection.
 Healing is a prolonged process.
 Scar tissue develops, even with skin grafting.
 Physiotherapy and occupational therapy may
be necessary.
 Surgery may be necessary to release
restrictive scar tissue.
 Biosynthetic skin substitutes – severe burns
 May have living human cells
 Strong and elastic - rapid healing

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 References
 Vanmeter, K & Hubert, R (2014) Gould’s
Pathophysiology for the Health professions
(5th Ed) Elsevier

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