Clinical Correlates-Inflammation Flashcards
(33 cards)
Inflammation-define
Body’s attempt at self protection
Inflammation is the body’s attempt at self-protection;
the aim being to remove harmful stimuli, including
damaged cells, irritants, or pathogens - and begin the
healing process.
Causes of Inflammation (3)
Physical, Biological, Chemical
Physical, Biological, Chemical-examples of each cause of inflammation
Physical
-temp, injury, foreign bodies
Biological
-infection, hyperinsensitivity, stress
Chemical
-toxins and alcohol
Inflammation = infection?
NO
infection causes
inflammation
Infection is the ____ and inflammtion is the
reason, inflammation is body’s response
Inducers/infection –> tissue damage –>
Sensors which release mediators to the target tissue
Inducers can be one of two classes
Exogenous
- PAMP, virus
- Allegens, toxin,
Endogenous
- Stress signal
- Products of ECM breakdown
What triggers the production of numerous inflammatory mediators
inducers of inflammation
Alters the functional states of tissues and organs
Mediators
Inflammatory mediators are classified into seven groups
according to their biochemical properties:
- Vasoactive amines
- Vasoactive peptides
- Complement components
- Lipid mediators
- Cytokines
- Chemokines
- Proteolytic enzymes
Vasoactive amines function/effect
increased vascular permability,
vasodilatation, vasoconstriction
Vasoactive peptides effect
Vasodilation and pain
Lipid mediators effect
fever
Proteolytic enzymes effect
tissue degradation, leukocyte migration
Cardinal signs of inflammation (5)
Heat Redness Swelling Pain Loss of Function
Key steps of inflammatory process (~4)
Pathogens invade and release toxins/enzymes –> tissue injury and cell death which causes inflammation and immune cell recruitment (host response) –> Phagocytosis/killed/removed –> side effect (5 signs)
Systemic effects of inflammation (6)
then there are two others which could be results
★ Acute-phase proteins (e.g. CRP) ★ Fever ★ Increased blood pressure ★ Malaise ★ Loss of appetite ★ Somnolence ★ Leukocytosis
Also shock and sepsis
If pathogens are not killed/persist
chronic
biggest problem with chronic inflammation
continued cell damage with some evidence of healing
Outcomes of inflammation (4)
★ Resolution (Regeneration)
Cells Removed-Complete restoration/regeneration of the inflamed tissue back to a normal status.
★ Fibrosis (Repair)
Tissue destruction cannot be regenerated by the body. Fibrous scar
composed primarily of collagen.
★ Abscess Formation
Defensive reaction of the tissue to prevent the spread of infectious
materials to other parts of the body.
★ Chronic inflammation
If the injurious agent persists, then chronic inflammation will ensure.
Initial gingavitis
- plaque?
- vasculature?
- Immune cells?
- Tissue description?
- Clinical change?
★ Accumulation of plaque biofilm in sulcus
★ Slight increase in vascular permeability
★ Migration of PMNs towards biofilm (across
connective tissue, junctional epithelium, and
into the sulcus)
★ Firm, pink tissue
★ No bleeding upon probing
★ No change in clinical presentation as
compared to health
Clinical presentation of initial gingivitis?
None- appears as health
Early gingivits
- plaque? migration?
- vasculature?
- Immune cells?
- Tissue description
- Color?
- Tissue destruction?
- Clinical change?
★ Biofilm more mature; increased pathogenicity
★ Some pathogens migrate into connective tissue
★ Increased vascular permeability and vasodilation
★ Release of inflammatory mediators by epithelial
cells
★ Cytokines, LPS, and PGE2 and antibodies present
★ Continued migration of PMNs
★ Collagen destruction and proliferation of epithelium
★ Gingival margin changes from pink to red
★ Early sings of edema
★ Bleeding upon probing is likely
★ May not be a distinct clinical entity, but clinical
changes are beginning to manifest