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Flashcards in Inflammation Deck (64):
1

Define Inflammation

Dynamic Process of tissue injury that involves a series of events
Protective response - required for healing
Nonspecific

2

Inflammation...

DOES NOT EQUAL INFECTION
- infection will have inflammation though

3

Primary Signs and Symptoms

Heat
Swelling
Redness
Pain
Disturbed Function

4

Vascular Changes

- Tissues first response to injury
- Initial phases involve neural mechanisms
- Remaining changes related to plasma and cell derived mediators
- Leads to hyperemia (inc blood flow to the area)

5

Events of Acute Inflammation

- Control by nervous system
1. Vasoconstriction
2. Vasodilation
3. Increased vascular permeability
4. Emigration of leukocytes

6

Vasoconstriction

- Neural Control (ANS)
- Arterioles vasoconstric - sphincter btw arteriole and capillary bed is shut down
- Lasts for seconds

7

Vasodilation

- Move away from ANS and is more nervous system
- Arterioles vasodilate and precapillary sphincter relaxes
- Venous side remains vasoconstricted during this phase
- Capillaries contain more blood

8

Structure of a capillary

Basement membrane and one cell layer - makes it permeable

9

Vasoactive Events

A variety of interdependent events are occurring
Cell and plasma derived substances are activated
- As soon as blood hits the tissue in an injured aream variety of mediators are activated and cause vasoactive events to occur - further vasodilation and permeability of capillary walls

10

Events of Inflammation

- Cells that have been injured release substances that are chemotaxic to inflammatory substances
- Increased blood into area increase the number of leukocytes, platelets, and other substances

11

1. Margination

- Leukocytes move out of the central column and move toward the margins
- Roll along epithelium (inside vascular walls)

12

2. Pavementing

- Cytokines are released by the cells injured
- Activates response within the leukocytes and the endothelial membrane
- Causes adhesion of leukocytes to the endothelial cells

13

3. Emigration

- WBCs move through the epithelial gaps
- Move into the extravascular tissues

14

1st responders

Neutrophils - go out into tissue to clean debris

15

RBCs/Platelets

- Begin to stack, known as Rouleaux of RBC
- Platelets become stickier and and take the stacked RBCs to stick to them
- Leads to more viscosity of blood
- Slows blood flow - blood clots form

16

Primary Mediators of Inflammation

1. Histamine
2. Serotonin
3. Nitric Oxide
4. Kinin System
5. Complement System
6. Clotting System
7. AA metabolites
8. Plate Activating Factors

17

Mast Cell found in...

Found in CT

18

Mast Cell Degranulation Stimulated by...

Direct Injury
Binding of IgE
Complement System
Leukocyte derived proteins
Cytokines (interleukins)

19

Mast Cell Functions When it Degranualtes it...

1. Binds IgE
2. Releases Hieparin (dec speed of clotting, blood thinner)
3. Synthesis and release of:
- Histamine
- Leukotrines and prostoglandins via AA
- Platelet activating facot
- TNF
- Interleukins

20

Platelets (Thrombocytes)

NOT a cell
Fragmented megakaryocytes
Contain cytoplasmic granules
As the aggregate and adhere, the degranulate
Three primary inclusions (dense, alpha, lysosomes)

21

Platelets - Dense Granules Release...

Serotonin, histamine - affect smooth muscle contractility
- Vasocon of vessel walls
- Vasodil of capillary venules
Ca and ADP
- stickiness

22

Platelets - Alpha Granules Contain...

Fibrinogen, coagulation proteins, PDGF

23

Platelets - Lysosomes

Antimicrobial

24

Histamine

Mast cell = primary source
Dilation and increased vascular permeability
Short term

25

Serotonin

Released from platelets
Effects similar to Histamine
Sticks around longer though

26

Nitric Oxide

Three forms (eNOS, iNOS, nNOS)
Short lived
Anti-inflammatory as well as inflammatory
Vasodilator
Decrease platelet adhesiveness
Mediator of macrophage action
Greater role in chronic inflammatory conditions

27

Kinin System

Plasma proteins
Primary = bradykinin

28

Effects of Kinin System

Dilation
Increased venule permeability
Pain (also from swelling on nerves)
Leukocyte chemotaxis

29

AA (Arachidonic Acid) Metabolites

Fatty acid element present in cell membranes

30

AA released...

During the injury of the cell as well as from mast cells

31

End products of AA

Prostoglandins and leukotrines

32

AA - Leukotrienes

Effects similar to histamine
Slower acting, but longer term because of strong chemotaxic effect
Neutrophil and eosinophil chemotaxis

33

AA - Prostaglandins

Strong vasodilator (arterioles)
Slow acting and long effect
Pain producer

34

Clotting System (Coagulation Cascade)

Series of plasma proteins
Activated by diff. substances
Creates a net (made of fibrin) and starts catching things and then clots to form a frame for tissue repair
- Enhances activation of bradykinin and neutrophil chemotaxis

35

Plasma proteins made...

In the liver
- Patients with liver pathology may have an impaired clotting system

36

Complement System

Series of plasma proteins (C1-C10)
Inc vascular permeability
Activation of leukocyte metabolism - WBCs are going to inflamed area so need to replace them and reproduce faster than normal - this system helps with this
Chemotaxis effects
Improves phagocytosis

37

Platelet Activating Factors

Released from mast cells
Increases vascular permeability
Increased leukocyte adhesiveness
Activates platelets

38

Sub P

Pain producer

39

Fever

Sign of inflammation somewhere
Not necessarily an infection
Post trauma is just enough inflammation to produce the feve

40

How long it will take someone to heal depends on...

The type of pathology they have

41

Leukocytes

Produced in bone marrow, less production as get older
Granulocytic will release substances that have some sort of lytic action in the area
Also Agranulocytic

42

Types of Leukocytes

1. Neutrophils
2. Monocytes/Macrophages
3. Lymphocytes
4. Eosinophils
5. Basophils

43

Neutrophils

Granulocytic
Phagocytic
Primary inflammatory

44

Monocytes/Macrophages

Agranulocytic
Phagocytic
Many functions - have receptors, dont produce anything to release though
Macro will increase when becoming more chronic

45

Lymphocytes

Agranulocytic
Not phagocytic
Immune Response (not really inflammation)

46

Eosinophils

Granulocytic
Parasitic infections
Allergies

47

Basophils

Granulocytic
Phagocytic
Release heparin, histamine
Is a hypersensitivity response (bee stings)

48

Results of Inflammation

Edema
Tissue Injury

49

Results of Inflammation - Edema

Transudate = low protein count
Exudate = high protein count

50

Transudate Edema

Low protein count
Implies intact endothelial barrier
The capillary endothelial basement membrane isn't gapping as much as it might so only letting small things through
Ex = cut on finger, congestive heart failure

51

Exudate Edema

High protein count
Occurs as vascular permeability increases
Will generally produce edema in inflammatory reactions

52

Results of Inflammation - Tissue Injury

Because of dec. in O2 available to the tissue
Tissue that needs O2 is far from the arterial bed because of edema
Lysosomal activity - they are secreting lytic things (can get good too though)
Phagocytic cell activity (can also get good thing)

53

Classification of Etiology

Duration
Etiology
Location
Morphology (based on exudate)

54

Acute Inflammation

A few hours or days
No clear cut delineation
Dominated by the presence of PMN - neutrophil count inc.
- Depends on how injured the tissue is and how vigorous the response is

55

Chronic Inflammation

Nobody really knows duration
Characterized by presence of macrophages, lymphocytes, and plasma cells
Proliferation of fibroblasts
Continues to release inflammatory mediators (but not short ones, more of the long ones)
There may be inc. blood vesels and CT in the area - thicker and diff color externally

56

Etiology

Pathogen - Bacterial infec. vs trauma...
Physical agent
Chemical agent
Immune cause

57

Morphologic

Serous or Serosanguineous
Fibrinous
Perulent
Granulomatous

58

Serous Morphology

Occurs in early phases of most infections
Leaking out, clear or pink...
if bloody = hemorrhagic

59

Fibrinous Morphology

Indicative of severe inflammatory response OR a bacterial infection

60

Perulent Morphology

May be caused by pus forming bacteria
Pus = debris associated with phagocytosis of pathogens
Not always an infection - maybe dirty

61

Granulomatous Morphology

Secondary to chronic inflammation
Macrophages and T lymphocytes dominate
Might start to develop thicker tissue that walls itself off (TB)

62

Inflammation _____

is NOT infection

63

Infection ____

will ALWAYS have inflammation

64

For inflammation to occur, you must have____

blood flow to the area