Path Chapter 3

Front 1

What are the 5 cardinal points of inflammation:

Back 1

1. Rubor: redness
2. Calor:heat
3. Dolor: pain
4. Tumor: swelling
5. Functio Laesa: (loss of function)

Hint 1

1. Rubor: redness --> Hyperemia
2. Calor:heat--> Hyperemia
3. Dolor: pain --> Edema
4. Tumor: swelling --> Edema and chem. mediator
5. Loss of function --> Edema

Front 2

Acute Inflammation:

Back 2

Acute Inflammation:
- limited in area and duration
- characterized by Cardinal Signs of Inflammation

Front 3

Chronic Inflammation:

Back 3

Chronic Inflammation:
- may be result of acute inflammation
- characterized by long duration
- or repeated injury

Front 4

When does repair process begin?

Back 4

Almost at the same time when the inflammatory process is activated

Front 5

Inflammation:

Back 5

Inflammation:
-non-specific response to tissue damage --> injury

Hint 5

Inflammation:
-localized vs. systemic
-acute vs. chronic

Front 6

What are the cell involved in acute inflammation response?

Back 6

- short-term
- neutrophils

Front 7

What are the cell involved in chronic inflammation response?

Back 7

- long-term
-->Mononuclear cells:
- lymphocytes
- plasma cells
- histiocytes

Front 8

Definition of Inflammation:

Back 8

Definition of Inflammation:
"A coordinated series of events that is designed to neutralize, destroy, isolate and remove injurious agent from tissue, clean out necrotic debris, and initiate tissue repair."

Front 9

What are the 3 phases of Inflammation:

Back 9

1. Initiation
2. Amplification
3. Termination

Front 10

What is required to resolve inflammation:

Back 10

to resolve inflammation, the stimuli must be removed!

Front 11

What are the two possible outcomes of inflammation?

Back 11

What are the two possible outcomes of inflammation?
Resolution or Chronic

Front 12

Define Abscess:

Back 12

Abscess:
Localized accumulation of puss

Front 13

Define Cellulitis:

Back 13

Cellulitis:
a diffuse infection/ inflammation of soft tissue

Front 14

What are the 3 phases of acute inflammation?

Back 14

What are the 3 phases of acute inflammation?
1. Initiation
2. Amplification
3. Termination

Front 15

Acute inflammation:
1. Initiation

Back 15

Acute inflammation:
1. Initiation
- comprises changes to small vessels (microcirculation) in the area of injury
- loss of fluid from the blood
- movement of white blood cells to injured area

1. VASOCONSTRICTION:
- constriction of the microcirculation (arterioles, capillaries, and venues) --> serves to control bleeding
- chemical mediators are released to start infl. process
2. VASODILATION:
-> is the increase in diameter so that more blood (hyperemia) & nutrients can be brought
3. PERMEABLE
-> blood vessel become permeable --> forming gaps between the cells
PLASMA FLUID & WHITE BLOOD CELLS
--> travel out of the vessel and to injury to clear the area -> of dead and injured cells and foreign bodies
----> the skin becomes red, warm and swollen
Swelling/ EDEMA is caused by the plasma fluid flowing out of the now more permeable vessels--> fluid called EXUDATE
-------continues next slide ---------

Hint 15

Initiation:
4. VASCULAR STASIS
- slowing down blood flow through affected vessels
- blood becomes thicker and viscous
- allows more nutrient to be removed from blood and brought to affected tissue --> but slows removal of waste products

Slower blood flow causes --> RED BLOOD CELLS to move towards center of the blood vessels ---> while WHITE BLOOD CELLS (LEUKOCYTES/ PMNs) move to the lining/ ENDOTHELIUM --> called MARGINATION (4a) --> they bounce against the endothelium --> called ROLLING and stick to the endothilium called ADHESION/ PAVEMENTING (4b) and squeeze through the gaps between the cells of vessels called TRANSMIGRATION/ EMIGRATION (4c) --> PMN leave blood vessel and migrate to the injured area --> CHEMOTAXIS (5) --> PMNs remove and destroy foreign substances

Front 16

Acute inflammation:
2. Amplification

Back 16

Acute inflammation:
2. Amplification
- action of chem. substances --> direct different white blood cells
- increased response
- quickly neutralize the stimuli
- clean up debris

Hint 16

Amplification
- begins when the first PMNs gather at the injury
- some pathogens are resistant and difficult to remove
OPSONIZATION (6) --> allows PMNs to destroy & remove resistant organisms --> those pathogens are prepared by chem. substances called OPSONINS --> found in exudate
OPSONIN --> exmp. IMMUNOGLOBULINS (antibodies) --> forein matter is removed and digested by PMNs --> PHAGOCYTOSIS

Front 17

Acute inflammation:
3. Termination

Back 17

Acute inflammation:
3. Termination
- requires other chem. now to stop the inflammatory process
- if it continues unhindered it will produce more injury than the initial injury

Hint 17

3. Termination
--> foreign material and cellular debris are removed from body by lymphatic system (8)

Front 18

Exudate

Back 18

Exudate
- fluid from blood vessels
- contains chemical mediators and nutrients for white blood cells
- dilute toxic substances
- contains enzymes that neutralize toxic substances --> can cause edema if in large amounts

Hint 18

Padilla:
- dilutes toxind
- entraps and washes away injurious agents
- supports inflammatory cells

Front 19

Forms of Exudates

Back 19

1. Serous
2. Purulent or Suppurative
3. Fibrinous

Hint 19

1. Serous - watery (burns, friction)
2. Purulent or Suppurative (PMN rich)
--> puss, pyogenic
3. Fibrinous --> sticky (immune & fisical)
--> skin (crust or scab)
--> wet mucosa (white coating or pseudomembrane)

Front 20

Vascular Stasis

Back 20

Vascular Stasis
- step in inflam. process
- slowing of blood flow in injured area
- removes nutrient from blood to tissue
- but slows down waste removal

Front 21

Hypermia

Back 21

Hypermia
- more blood

Front 22

Which blood cells are involved in inflammation process?

Back 22

Which blood cells are involved in inflammation process?
White Blood Cells:
leukocytes / PMNs

Front 23

What are PMN?

Back 23

What are PMN?
1.White blood cells
2. Leukocytes
3. Neutrophils

Front 24

What does PMN stands for?

Back 24

What does PMN stands for?
Poly-morpho-nuclear neutrophils

Front 25

What is called leukocytes?

Back 25

What is called leukocytes?
Different name for White blood cells

Front 26

What are the two classes of leukocytes?

Back 26

What are the two classes of leukocytes?
1. Granulocytes
2. Agranulocytes

Front 27

What belong to the class of Granulocytes?

Back 27

1. Polymorphonuclear Neutrophils (PNM)
2. Eosinophils
3. Basophils

Front 28

What are the characteristics of Polymorphonuclear Neutrophils (PNM)?

Back 28

1. Polymorphonuclear Neutrophils (PNM)
--> granulocytes
--> first cell to arrive at acute inflammation
- active in fighting bacterial & fungal infections
- motile phagocytes --> attracted by chemotactic factors

Hint 28

Padilla:
- Bone marrow
- Circulate in blood
- no or few mitochondria
- 2-7 days outside blood
- inflammation shortens their life span
- can function in anaerobic condition
- release chemotactic agents and granule contents upon death

Front 29

What are the characteristics of Eosinophils & Basophils?

Back 29

What are the characteristics of Eosinophils & Basophils?
-->granulocytes
--> important in inflammation related to allergic reactions

Hint 29

in addition --> Eosinophils are active in fighting off parasitic infections like tapeworms

Front 30

Who are the Agranulocytes?

Back 30

1. Lymphocytes (lymphoid Cells)
2. Monolymphocytes = Monocytes = Macrophages

Front 31

What are the characteristics of Agranulocytes?

Back 31

Agranulocytes:
- more active in later stage of acute inflammatory process
- longer-lived (several months, opposed to 6-9 hr.)
- slower in response to chem. mediators

Hint 31

Padilla:
Monocytes
- origin in bone marrow
- circulate in blood
- capable of aerobic metabolism - long lifespan
- become phagocytic
- have chemotactic reseptors
- PMN's and lymphokines (from T lymphocytes)
- become macrophages with vacuoles
- lysosomal digestion, storage or "defecation"

Front 32

What are the characteristics of Monocytes?

Back 32

- circulate with blood until enter "specific" tissue and become fixed
- differentiate into macrophages

Hint 32

many different macrophages monocytes that become fixed in:
=> in liver = Kupffer cell
=> in CT = histiocytes

=> in tuberculosis = Langhans cells
=> in rheumatic fever = Aschoff

Front 33

What are the characteristics of Lymphocytes?

Back 33

What are the characteristics of Lymphocytes?
- found in the lymph system
- important in immune system

Front 34

What are Mast Cells?

Back 34

- NOT leukocytes
- formed in bone marrow
- travels through circulatory system to tissue here it matures
- stay in CT close to vessels
- contain HISTAMINE --> important chem mediator

Hint 34

- have granules in their cytoplasm, like basophils (Granulocytes)
- histamine is released when granules break open

Front 35

What are Prostaglandis?

Back 35

What are Prostaglandis?
- chemical mediator
- synthesized by all leukocytes
- causes vasodilation
- increased vascular permeability
- increased feelings of pain
- cause bronchoconstriction
- smooth muscle contraction
- elevate body temperature

Hint 35

- associated with tissue destruction in periodontal disease

Front 36

What are Cytokines?

Back 36

What are Cytokines?
- produced by macrophages and some lymphocytes

Front 37

What are the Cytokines active in inflammatory process?

Back 37

What are the Cytokines active in inflammatory process?
1. Chemokines
2. Tumor Necrosis Factor (TNF)
3. Interleukin - 1 (IL-1)

Front 38

What are the effects of Tumor Necrosis Factor (TNF) and Interleukin - 1 (IL-1) during inflammatory process?

Back 38

What are the effects of Tumor Necrosis Factor (TNF) and Interleukin - 1 (IL-1) during inflammatory process?
- produce fever
- increase need for sleep
- decrease appetite
- increase leukocyte adherence
- prostaglandis synthesis
- fibroblast production

Hint 38

- associated with tissue destruction in periodontal disease