Clinical Correlates-Inflammation Flashcards

1
Q

Inflammation-define

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of Inflammation (3)

A

Physical, Biological, Chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Physical, Biological, Chemical-examples of each cause of inflammation

A

Physical
-temp, injury, foreign bodies

Biological
-infection, hyperinsensitivity, stress

Chemical
-toxins and alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Inflammation = infection?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

infection causes

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Infection is the ____ and inflammtion is the

A

reason, inflammation is body’s response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Inducers/infection –> tissue damage –>

A

Sensors which release mediators to the target tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Inducers can be one of two classes

A

Exogenous

  • PAMP, virus
  • Allegens, toxin,

Endogenous

  • Stress signal
  • Products of ECM breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What triggers the production of numerous inflammatory mediators

A

inducers of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alters the functional states of tissues and organs

A

Mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Inflammatory mediators are classified into seven groups

according to their biochemical properties:

A
  1. Vasoactive amines
  2. Vasoactive peptides
  3. Complement components
  4. Lipid mediators
  5. Cytokines
  6. Chemokines
  7. Proteolytic enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Vasoactive amines function/effect

A

increased vascular permability,

vasodilatation, vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Vasoactive peptides effect

A

Vasodilation and pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lipid mediators effect

A

fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Proteolytic enzymes effect

A

tissue degradation, leukocyte migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cardinal signs of inflammation (5)

A
Heat
Redness
Swelling
Pain
Loss of Function
17
Q

Key steps of inflammatory process (~4)

A

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)

18
Q

Systemic effects of inflammation (6)

then there are two others which could be results

A
★ Acute-phase proteins (e.g. CRP)
★ Fever
★ Increased blood pressure
★ Malaise
★ Loss of appetite
★ Somnolence
★ Leukocytosis

Also shock and sepsis

19
Q

If pathogens are not killed/persist

A

chronic

20
Q

biggest problem with chronic inflammation

A

continued cell damage with some evidence of healing

21
Q

Outcomes of inflammation (4)

A

★ 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.

22
Q

Initial gingavitis

  • plaque?
  • vasculature?
  • Immune cells?
  • Tissue description?
  • Clinical change?
A

★ 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

23
Q

Clinical presentation of initial gingivitis?

A

None- appears as health

24
Q

Early gingivits

  • plaque? migration?
  • vasculature?
  • Immune cells?
  • Tissue description
  • Color?
  • Tissue destruction?
  • Clinical change?
A

★ 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

25
Q

Clinical appearance of early gingavitis

A

★ Bleeding upon probing is likely
★ May not be a distinct clinical entity, but clinical

**Also maybe pain

26
Q

collagen depleted in initial gingivitis? Early?

A

In early, yeah

27
Q

Clinical signs of health to inflammed

Color
Size and shape
Position
Consistency/Texture
BOP?
A
Color
-pink to red
Size/shape
-flat thin/knife --> rolled margins
Position
-normal vs hyperplasia
Consistency & texture
-firm/stippled vs smooth glassy and soft
BOP
28
Q

BEST clinical sign of gingivitis

A

BOP

29
Q

Key for long term success

A

maintenance

30
Q

Lack of space of mucosa during 3rd molar eruption causes inflammation of mucosa called

A

pericoronitis

31
Q

Apthous stomatitis

A

swelling of the oral mucosa such as an ulcer or canker sore

32
Q

Contact stomatitis

A

Tongue inflammation

33
Q

To remove inflammation, you must do what

A

remove the cause