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Transcript
Review of Inflammation
and Fever
1
Inflammation
A non-specific response to injury or necrosis
that occurs in a vascularized tissue.
Signs: Redness, heat ,swelling, pain, and
loss of function
2
Stages of Inflammation
n
n
n
Vascular stage
Cellular stage
Tissue repair
3
4
5
Response at site of injury:
blood vessels briefly constrict, then
dilate
Edema:
due to increased pressure in vessels
blood vessels become permeable
plasma forced into tissues =
transudate, watery
Exudates - small proteins and cells
move out of blood vessles because of
increased permeability
6
7
Functions of transudates and exudates:
•
dilute toxins from dead cells
•
pain – limits use; prevents additional
injury
•
carry blood cells and proteins to site
(antibodies and complement)
•
carry toxins and wastes from site (mostly
through lymphatic system)
8
Cellular Stage
n
n
Marked by movement of white blood cells
(leukocytes) to the area of injury.
When fluid is lost from blood, blood
becomes more viscous.
10
Release of chemical mediators and cytokines
cause the leukocytes to increase production of
adhesion molecules.
Leukocytes –neutrophils, macrophages –
phagocytic cells, leave the capillaries
and enter tissues by transmigration or
emigration.
11
12
n
Biochemicals released by leukocytes and tissue
cells serve as signals to coordinate all body
defenses.
n
“calling molecules”
n
Movement of leukocytes – chemotaxis
n
Neutrophils then macrophages
n
Steps of phagocytosis:
– Adherence plus opsonization (marked for digestion)
– Engulfment
– Intracellular killing
n
die - form pus
13
14
n
Other mediators:
–Prostaglandins
–Platelet-activating factor
–Cytokines, signaling molecules
–Nitric oxide
15
Systemic manifestations of
inflammation
n
Release of cytokines in Acute-phase response:
–
–
–
–
n
Affects hypothalamus and may cause fever
Affects bone marrow, ↑ neutrophil production
Affects the CNS causing lethargy
Affects liver to produce more fibinogen and Creactive protein, which increases the ESR
(erythrocyte sedimentation rate, to measure
inflammation)
Lymphadenitis
– inflammation of a lymph node
16
Excessive inflammation
n
n
n
Prolonged pain
Swelling impairs function
Therapies:
– Temperature
n Cold - 10 on 10 off (or alternate heat and cold)
– Elevation and pressure
– Drug therapy
n
Antihistamines, nonsteroidal anti-inflammatory
agents, corticosteroids
17
Chronic Inflammation
n
May last for weeks, months or years
– Recurrent acute inflammation or low-grade
responses
n
Characteristics:
– Infiltration by macrophages and lymphocytes
– Proliferation of fibroblasts instead of exudates
– Cause may be foreign matter, viruses, bacteria,
fungi or larger parasites
18
Excessive inflammation
n
n
n
n
Pain is intense or prolonged and swelling
impairs function of organ
Cold – 10 minutes only
Drugs – steroids
Elevation – decreases blood flow
19
Resolution or Tissue Repair
Inflammatory phase
n Proliferative phase
n Remodeling phase
n
20
Resolution and repair:
resolution – restoration of normal tissue
structure and function.
repair – replacement of destroyed tissue
with scar tissue.
Débridement, suturing
Vessel dilation and permeability are reversed
Leukocyte migration ends
Exudate is drained away – lymphatics
21
Repair – scar formation
Processes
fill the wound
cover the wound
shrink the wound
22
Fever (pyrexia)
n
n
Called “hallmark of infection”
Many infections are called fevers:
– Typhoid fever, rheumatic fever, etc.
23
Normal thermoregulation
Body temperature is maintained within ± 1oF
Varies over the course of the day
Cells constantly produce heat by metabolism
Mechanisms to lose heat:
dilation of surface blood vessels
sweating
Body temperature is set and controlled by the
hypothalamus
24
With infection (or some toxins) :
some bacteria release biochemicals into
blood stream – exogenous pyrogens (esp.
lipopolysaccharides of Gram-negative
bacteria) – these signal white blood cells
(monocytes/macrophages) to produce their
own biochemicals – endogenous pyrogens
(interleukins or interferons) – induce synthesis
of prostaglandins – cause hypothalmus to
raise its set point.
25
n
n
n
Many non-infectious disorders can also
produce fever
NON-SPECIFIC
Patterns of fever:
–
–
–
–
n
Intermittent fever
Remittent fever
Sustained or continuous fever
Recurrent or relapsing fever
Heart rate increases with fever
26
n
Hypothalamus :
– releases TSH to increase production of T3 &
T4
– releases ACTH which increases release of
glucocorticoids
– Causes increase of release of epinephrine
– Decreases production of ADH
27
Prostaglandins inhibited by non-steroidal antiinflammatory drugs (aspirin, tylenol, motrin
etc.)
(although overdose of aspirin raises body
temp.)
28
Benefits of fever
Increased temperature kills microorganisms
and adversely affects their growth and
reproduction
29
Causes lysosomal breakdown and
autodestruction of cells, preventing viral
replication in infected cells
Increased leukocyte motility
Facilitates the immune response – activation
of T cells
Enhances phagocytosis
Production of interferon increased
30
But fever is bad when:
too high – impairs neurological and/
respiratory functions
increased work load of heart in patients
with heart disease or stroke
damage to hypothalamus can cause
temp. to become dangerously
high
Can cause complications in pregnancy
Fever over 106oF requires emergency
care
31
n
n
n
Infants under 3 months of age have difficulty
regulating temperature
Young children can develop very high fevers,
sometimes seizure can be induced
Body temperature is lowered in the elderly, so
fevers are not as high
32