Inflammation Flashcards
1
Q
Define Inflammation
A
Dynamic Process of tissue injury that involves a series of events
Protective response - required for healing
Nonspecific
2
Q
Inflammation…
A
DOES NOT EQUAL INFECTION
- infection will have inflammation though
3
Q
Primary Signs and Symptoms
A
Heat Swelling Redness Pain Disturbed Function
4
Q
Vascular Changes
A
- 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
Q
Events of Acute Inflammation
A
- Control by nervous system
1. Vasoconstriction
2. Vasodilation
3. Increased vascular permeability
4. Emigration of leukocytes
6
Q
Vasoconstriction
A
- Neural Control (ANS)
- Arterioles vasoconstric - sphincter btw arteriole and capillary bed is shut down
- Lasts for seconds
7
Q
Vasodilation
A
- 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
Q
Structure of a capillary
A
Basement membrane and one cell layer - makes it permeable
9
Q
Vasoactive Events
A
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
Q
Events of Inflammation
A
- 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
Q
- Margination
A
- Leukocytes move out of the central column and move toward the margins
- Roll along epithelium (inside vascular walls)
12
Q
- Pavementing
A
- 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
Q
- Emigration
A
- WBCs move through the epithelial gaps
- Move into the extravascular tissues
14
Q
1st responders
A
Neutrophils - go out into tissue to clean debris
15
Q
RBCs/Platelets
A
- 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
Q
Primary Mediators of Inflammation
A
- Histamine
- Serotonin
- Nitric Oxide
- Kinin System
- Complement System
- Clotting System
- AA metabolites
- Plate Activating Factors
17
Q
Mast Cell found in…
A
Found in CT
18
Q
Mast Cell Degranulation Stimulated by…
A
Direct Injury Binding of IgE Complement System Leukocyte derived proteins Cytokines (interleukins)
19
Q
Mast Cell Functions When it Degranualtes it…
A
- Binds IgE
- Releases Hieparin (dec speed of clotting, blood thinner)
- Synthesis and release of:
- Histamine
- Leukotrines and prostoglandins via AA
- Platelet activating facot
- TNF
- Interleukins
20
Q
Platelets (Thrombocytes)
A
NOT a cell
Fragmented megakaryocytes
Contain cytoplasmic granules
As the aggregate and adhere, the degranulate
Three primary inclusions (dense, alpha, lysosomes)
21
Q
Platelets - Dense Granules Release…
A
Serotonin, histamine - affect smooth muscle contractility - Vasocon of vessel walls - Vasodil of capillary venules Ca and ADP - stickiness
22
Q
Platelets - Alpha Granules Contain…
A
Fibrinogen, coagulation proteins, PDGF
23
Q
Platelets - Lysosomes
A
Antimicrobial
24
Q
Histamine
A
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
