Unit 2 Part 3 Flashcards
COMPLEX response to injurious
agents
inflammation
COMPLEX response to injurious
agents
inflammation
leads as to the healing and reconstitution of the damaged tissue
(repair)
inflammation
Aims of inflammation
- Eliminate the initial cause of cell injury
- Remove necrotic cells and tissue
- Initiate the process of repair
INFLAMMATION is part of a broader
protective response OR
innate immunity
Components of the inflammatory
process
white blood cells and
plasma proteins
Inflammation is terminated when
offending agent is eliminated
secreted mediators are broken down
inflammation is potentially harmful process if
Components are capable of destroying microbes
-injure
no foreign substances to fight leads to
autoimmunity
inflammatory process is tightly regulated by
immune system
causes of inflammation
bacteria
viral
protozoal
fungal
immunological
chemical, toxins
tumor
radiation
5 ancient cardinal signs of inflammatory
tumor-swelling
rubor-redness
calor-warmth
dolor-pain
functio laesa-loss of function
systemic manifestations of inflammation
fever
chills
myalgia
discomfort
Increased blood flow due to vascular dilatation gives
redness and heat
rubor and calor
Increased vascular permeability gives edema causing
tissue swelling
tumor
Certain chemical mediators stimulate sensory nerve
endings giving
pain
dolor
Pain and swelling result in loss of
function
functio laesa
features of acute inflammation
fast mins or hrs, neutrophil infiltrate, mild and self-limited, prominent
features of chronic inflammation
slow days, monocytes infiltrate, severe and progressive, less prominent and subtle
rapid response to an injurious agent
deliver mediators of host defense-leukocytes and plasma proteins
acute inflammation
stimuli for acute inflamation
infection
necrosis
foreign bodies
immune reactions
Events of Acute Inflammation
VASCULAR:
hemodynamic/ Vasoactive changes
increased vascular permeability
CELLULAR
leukocyte recruitment
changes in vascular flow and caliber
earliest manifestation
hemodynamic/vasoactive changes
hemodynamic events
- vasoconstrict
- vasodilation
Increased Vascular Permeability events
- Elevation of the local hydrostatic pressure
- Increased permeability of the microvasculature
- Leakage of proteinaceous fluid
- Stasis
- Margination of circulating leukocytes and endothelial activation
general term for swelling
edema
maintain a “colloid osmotic pressure”
Plasma proteins
(e.g. heart failure)
and/or colloid pressure (decresased protein synthesis/retention)
pushes out more fluid (transudate) into tissue bed
Dysregulation of hydrostatic pressure
causes endothelial cells to separate
inflammation
excess of fluid in the interstitial or serous cavities
edema
<1.012 gravity
low protein content
ultrafiltrate of blood plasma
Transudate
> 1.020 gravity high protein concentration,
alteration in the normal permeability of small blood vessels
Exudate
recruited from the blood
into the extravascular tissue
leukocytes
predominate in the
inflammatory infiltrate during the first 6 to
24 hours.
neutrophils
more numerous in the blood
respond more rapidly to chemokines
may attach more firmly to the adhesion molecules
short-lived, they die by apoptosis and disappear
within 24 to 48 hours.
neutrophils
leukocyte recruitment events
margination
rolling
activation
adhesion
transmigration
chemotaxis
phagocytosis
killing
leukocyte accumulation at the periphery of vessels.
Fluid leaves the vessel (exudate)
Leukocytes are pushed out of the
central axial column
Margination
◼ Leukocytes tumble on the endothelial
surface, transiently sticking along the way.
◼ This weak and transient adhesion
◼ Enables leukocytes to slow down and travel
along the endothelial surface
Rolling
Integrin — by chemokines
Chemotaxis
Activation
chemotactic cytokines which
support firm adhesion to endothelial cell
Chemokines
movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.
Chemotaxis
Proteins that function mechanically, by attaching the cell cytoskeleton to the extracellular matrix (ECM), and biochemically, by sensing whether adhesion has occurred
Integrins
mediated by selectin
family expressed on leukocyte cell
surfaces interacting with their ligands on
endothelial cell
Adhesion
selectin family
◼ E selectin (endothelium)
◼ P selectin (platelets, endothelium)
◼ L selectin (leukocytes)
leukocytes migrate through the
vessel wall primarily by squeezing
between cells at intercellular junctions
(diapedesis)
Transmigration
leukocytes migrate toward sites of infection or injury
locomotion oriented along a chemical gradient
Chemotaxis
process of coating a particle
Coated microbes are recognized by
receptors on phagocytes
Leukocyte Activation
(opsonization)
◼ The process of engulfment of solid
particulate material by cells
◼ responsible for eliminating the injurious
agent
Phagocytosis
3 interrelated steps of phagocytosis
Recognition and Attachment
Engulfment
Killing of Degradation
◼ Involves the particle
to be ingested by
the leukocyte
◼ Foreign objects
coated with
opsonins IgG and
C3b which attach to
receptors on
polymorph surface
Recognition and
Attachment
- Cell membrane fuses around an object
- this gives rise to ‘regurgitation during feeding’ and enzymatic damage to surrounding tissue
Engulfment
-H2O2, hypohalous acid (HOC1) produced by myeloperoxidase and superoxides kill bacteria.
-After phagocytosis, neutrophils undergo apoptosis and are ingested by macrophages
Killing of Degradation
Outcome of Acute Inflammation
◼ Complete resolution
◼ Tissue destruction and persistent acute inflammation
◼ Healing by connective tissue replacement
◼ Chronic Inflammation
Morphologic patterns of Acute Inflammation (7)
Serous
Catarrhal
Fibrinous
Hemorrhagic
Suppurative
Gangrenous
Pseudomembranous
◼ Accumulation of excessive clear watery fluid
◼ Blister arising from a burn or viral infection
Serous Inflammation
◼ Large amounts of fibrinogen pass the vessel wall and fibrins are formed
◼ Fibrinous pericarditis
Fibrinous Inflammation
◼ Local defect or excavation of the surface of an organ or tissue
◼ Most commonly encountered in the oral mucosa, subcutaneous tissue
Ulcerative Inflammation
Laboratory Manifestations in Acute Inflammation
◼ Leukocytosis
◼ Elevated serum active phase proteins
◼ Increased ESR
◼ Hypercoagulability
Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair proceed simultaneously
Chronic Inflammation
Causes of Chronic
Inflammation
-Persistent injury of infection
-Prolonged exposure to potentially toxic
agents
-Autoimmune disease
—self-perpetuating
immune reaction that results in tissue
damage and inflammation
auto immune disease
Morphologic features inflammation
Infiltration
Tissue destruction
Healing
◼ A special form of chronic inflammation
◼ Characterized by focal activation of
activated macrophages
Granulomatous inflammation
focal aggregation of
epithelioid macrophages surrounded by
a collar of mononuclear leukocytes
Granuloma
