Acute Inflammation Flashcards
1
Q
Define ‘inflammation’
A
A reaction to injury or infection involving cells such as neutrophils and macrophages
2
Q
In what two instances is inflammation good
A
- Infection
2. Injury
3
Q
In what two instances is inflammation bad
A
- Autoimmunity
2. Over-reaction to a stimulus
4
Q
In what two ways is inflammation classified as?
A
Acute and Chronic
5
Q
Three characteristics of an acute condition
A
- Sudden Onset
- Short Duration
- Usually resolves
6
Q
Three characteristics of chronic inflammation
A
- Slow onset or sequel to acute
- Long Duration
- May never resolve
7
Q
Name five cells involved in inflammation
A
- Neutrophil Polymorphs
- Macrophages
- Lymphocyte
- Endothelial Cell
- Fibroblasts
8
Q
How long do macrophages survive for
A
Weeks to months
9
Q
Role of macrophages (3)
A
- Ingest bacteria and debris
- Carry debris away
- Present antigen to lymphocyte
10
Q
How long do lymphocytes last
A
Years (almost as long as we can do!)
11
Q
Role of lymphocyte
A
Produce chemicals which attract in other inflammatory cells
Immunological memory
12
Q
What lymphocyte produces antibodies
A
Plasma cells
13
Q
What lymphocyte produces cytokines
A
T-cells
14
Q
Where are endothelial cells found
A
Lining capillary blood vessels in areas of inflammation
15
Q
What happens to endothelial cells in areas of inflammation (3)
A
- Become sticky so inflammatory cells adhere to them
- Become porous to allow inflammatory cells to pass into tissues
- Grow into areas of damage to form new capillary vessels
16
Q
What is produced by fibroblasts and under what condition is this produced
A
Collagen in areas of chronic inflammation and repair
17
Q
Give an example of an acute inflammation
A
Acute Appendicitis
18
Q
What causes acute appendicitis
A
Unknown why it happens
19
Q
Name four things that happen when acute inflammation takes place
A
- Neutrophils appear
- Blood Vessels Dilate
- Inflammation of serosal surface occurs
- Pain felt
20
Q
Give an example of chronic inflammation
A
Tuberculosis
21
Q
At what point during TB does inflammation occur
A
Later on - does not appear initially
22
Q
What four things occur during chronic inflammation
A
- Mycobacteria ingested by macrophages
- Lymphocytes appear
- Macrophages appear
- Fibrosis
( Macrophages often fail to kill kill mycobacteria)
23
Q
When does acute inflammation occur
A
Initial tissue reaction to injury
24
Q
What two things happen during acute inflammation
A
- Vascular component: Dilatation of vessels
2. Exudative component: Vascular leakage of protein-rich fluid
25
How long does acute inflammation last
Few hours to a few days
26
What suffix is given to conditions caused by inflammation
-itis
27
5 causes of acute inflammation
1. Microbial Infections
2. Hypersensitivity reactions
3. Physical Agents
4. Chemicals (acids and alkalis)
5. Tissue necrosis
28
What is the most common cause of inflammation
Microbial infection
29
How are microbial infections caused
1. Bacteria release specific exotoxins which initiate inflammation or endotoxins which are associated to the cell walls
30
What is a hypersensitivity reaction
An excess immune reaction that damages tissues
31
What physical agents cause acute inflammation
UV Lights and ionising radiation
32
How do irritants cause acute inflammation
By tissue damage or directly releasing specific chemical irritants
33
How does tissue necrosis cause acute inflammation
Death of tissues from lack of oxygen or nutrients
34
What factors are indications of acute inflammation
```
Redness
Heat
Swelling (oedema)
Pain (stretching of tissues)
Loss of function
```
35
What are the early stages of acute inflammation
Odema fluid accumulates in extracellular space
36
What is the cellular component of oedema fluid called
Neutrophil polymorph
37
What happens to the microcirculation during acute inflammation
1. Smooth muscle of arteriolar walls form pre capillary sphincters which regulate blood flow through the capillary bed.
2. Flow through some capillaries shut down
38
Where are blood cells located in the capillary
Centre of the lumen (axial flow)
39
Where does plasma flow along the capillaries
The plasmatic zone (outer part of the lumen)
40
Why does axial flow exist
Keeps blood cells away from and adhering to the blood wall
41
What are fenestrations
Areas of the capillaries where the wall gets thinner than the rest of the vessel
42
What happens to vascular permeability during acute inflammation
1. High colloidal osmotic pressure causes fluid to be ejected into extravascular space.
2. Colloidal proteins also pushed into extracellular fluid which increases oncotic pressure at venule end (exudation).
3. Less fluid re-enters capillary at venule end
43
What can be found in fluid exudate
Immunoglobulins
| Coagulation factors
44
What are acutely inflamed organ surfaces covered by
Fibrin
45
Are endothelial cells damaged during inflammation
No
46
Why are endothelial cells not damaged during inflammation
They contain a protein called actin which causes contraction of endothelial cells, opening transient pores when stimulated by inflammatory mediators
47
Example of an inflammatory mediator
Histamine
48
How do chemicals like x-rays contribute to inflammation
By delaying prolonged leakage which CAN damage endothelial cells
49
How does tissue sensitivity impact inflammation
Tissues in different parts of the body respond to inflammatory mediators in different ways (e..g those in the CNS are very insensitive to them)
50
What is the diagnostic histological feature of acute inflammation
Accumulation of neutrophil polymorphs
51
What happens to neutrophils during inflammation
1. Margination of neutrophils
2. Adhesion of neutrophils
3. Neutrophil emigration
4. Diapedesis
52
What is the margination of neutrophils
Cells usually confined to axial flow end app in plasmatic zone near to endothelium due to loss of fluid
53
What is the adhesion of neutrophils
Neutrophils adhere to endothelium which doesn't normally happen
54
Do neutrophils make contact with the endothelial walls normally
Yes, randomly but don't adhere to it
55
Along with neutrophils what other cell adheres to endothelial walls
Leucocytes
56
What is neutrophil emigration
They move through opened pores formed by endothelial cells (the actin contractions in response to inflammatory mediator) through basal lamina into adventitia.
57
What is diapedesis
Red blood cells escape passively through vessels due to hydrostatic pressure.
58
When does diapedesis occur
Major damage to blood vessels
59
What happens to neutrophils in later stages of acute inflammation
Chemotaxis
60
What is chemotaxis
Neutrophil polymorphs are attracted to chemical substances in solution
61
What two substances early in the inflammatory response are released by inflammatory stimulus
Histamine and Thrombin
62
Role of thrombin and histamine in inflammation
Up-regulation of adhesion molecules on surface of endothelial cells
63
What is the result of adhesion molecules increasing on surface of endothelial cells to neutrophils
They have a firm adhesion to the endothelial surface
64
Role of Histamine
1. Vascular dilatation
| 2. transient phase of increased vascular permeability
65
Where are histamines stored
Mast Cells
66
What components stimulate the release of histamine
C3a and C5a
Lysosomal proteins released from neutrophils
Serotonin
Chemokines
67
How many cascade systems are in place in the plasma flow to produce chemical mediators
```
4:
Kinin
Fibrinolytic
Coagulation
Complement
```
68
What factor activates the kinin, fibrinolytic and coagulation systems
Hageman factor (XII)
69
What are the most important cytokines that stimulate inflammation due to injury
1. IL-1
| 2. TNF - alpha
70
When do IL-1 and TNF-alpha have an effect
Following histamine and thrombin's effects
71
What is E-selectin
An adhesion molecule that binds + activates neutrophils
72
Role of IL-8
Chemotaxins for neutrophil polymorphs
73
What is the effect of IL-8 and TNF-alpha on endothelial cells
Cause secretion of MCP-1 which is chemotactic for neutrophil polymorphs
74
What is the role of lymphatics in inflammation
1. Channels become dilated as they drain fluid away from inflamed site.
2. Limits oedema collection in tissues
75
What is the role of neutrophil polymorph
1. Movement
2. Adhesion to microorganisms
3. Phagocytosis
76
How do neutrophil polymorphs cause movement
Contraction of cytoplasmic microtubules bring about amoeboid movement allowing chemotaxis
77
What does the amoeboid movement of neutrophil polymorphs depend on
Calcium ions and intracellular concentrations of cyclic nucleotides
78
define chemotaxis
Movement of a compound in one direction in response to inflammation
79
How are microorganisms opsonised
By immunoglobulins or complement compounds
80
How do neutrophils carry out phagocytosis
Phagocytes become pseudopodia shaped
:
1. Neutrophils produce H2O2 which reacts with myeloperoxidase in cytoplasmic granules
2. Produces microbicidal agent
81
Why are lysosomal products released from neutrophils
1. Damages local tissues by proteolysis
2. Activates coagulation factor XII
3. Attracts leucocytes in the area
82
Role of mast cells in acute inflammation
Metabolise arachidonic acid to inflammatory mediators
83
What are mast cells stimulated by
C3a/C5a complement factors
84
Why is inflammation beneficial (6)
1. Dilution of toxins
2. Entry of antibodies due to increased intravascular permeability
3. Transport of antibiotics
4. Fibrin formation traps microbes facilitating phagocytosis
5. Delivery of nutrients and oxygen
6. Stimulation of immune response by drainage of this fluid into lymphatics allows soluble antigens to reach local lymph nodes
85
What other cells drive at the site of inflammation
Blood macrophages
86
What happens to blood macrophages upon leaving the blood vessels
Transform into macrophages by becoming more metabolically active
87
Role of macrophages
Clearing away tissue debris and damaged cells
88
Three harmful effects of inflammation
1. Digestion of normal tissues (by collagenases and proteases)
2. Swelling in certain areas
3. OTT inflammatory response
89
What happens during resolution of acute inflammation
1. Minimal cell death + tissue damage
2. Occurrence in an organ that has regenerative capacity
3. Rapid destruction of causal agent
4. Rapid removal of fluid + debris
90
What are the three sequence of events that lead to resolution
1. Phagocytosis of bacteria by neutrophils
2. Fibrinolysis
3. Phagocytosis of debris by macrophages
4. Carry debris through lymphatics
5. Disappearance of vascular dilatation
91
What is Suppuration
Formation of Pus (mixture of living, dying and dead neutrophils and bacteria)
92
What must happen in order for suppurating to occur
Causative stimulus must be persistent and always caused by an infective agent (pyogenic bacteria)
93
Describe Suppuration process
1. Puss accumulates in tissue
2. Puss surrounded by pyogenic membrane consisting of sprouting capillaries, neutrophils and fibroblasts
3. Forms an abscess
94
What is problematic about an abscess
Bacteria within abscess are inaccessible to antibodies and antibiotics
95
How does an abscess close up
1. It bursts
2. Cavity collapses
3. Cavity obliterated by organisation and fibrosis
4. Scar formation
96
What happens if pus accumulates inside a hollow viscus
Mucosal layers of the outflow tract are covered by fibrin resulting in an empyema
97
Where is pus from an abscess discharged
Into the sinus tract
98
What is the sinus tract
A layer between the abscess and skin or mucosal surface
99
When does a fistula form
When sinus tract pus connects two mucosal surfaces together
100
What is organisation
Replacement by granulation tissue as part of repair
101
What three circumstances favour this outcome
1. Large amounts of fibrin are formed which can't be removed by fibrinolytic enzymes
2. Large volumes of tissues become necrotic
3. Exudate and debris can't be removed
102
Describe organisation
1. New capillaries grow into the inert material, macrophages migrate into the zone
2. Fibroblasts proliferate under the influence of TGF-beta resulting in fibrosis
103
Where does organisation typically occur
lung parenchyma
104
What is the consequence of fibrin not being easily removed
Capillaries grow into fibrin
105
What stage follows on from suppuration
Organisation
