Acute Inflammation Flashcards
(205 cards)
1
Q
What is acute inflammation?
A
The response of living tissue to injury
2
Q
What is acute inflammation initiated to do?
A
Limit tissue damage
3
Q
What is the purpose of acute inflammation?
A
It is a protective reposponse
4
Q
What are the features of acute inflammation?
A
Innate
Immediate and early
Stereotyped
Short duration
5
Q
What is meant by acute inflammation being innate?
A
You are both with it
6
Q
What is meant by acute inflammation being stereotyped?
A
It is the same every time it happens, and doesn’t get better or worse
7
Q
What is the duration of acute inflammation?
A
Minutes/hours/few days, depending on process
8
Q
What type of reactions occur in acute inflammation?
A
Vascular
Cellular
9
Q
What is the result of vascular and cellular reactions in acute inflammation?
A
Accumulation of fluid exudate
Neutrophils in tissues
10
Q
What is acute inflammation controlled by?
A
A variety of chemical mediators
11
Q
What are the chemical mediators that control acute inflammation derived from?
A
Plasma cells
12
Q
Why is control of acute inflammation very strict?
A
Don’t want it to get out of control
13
Q
When is acute inflammation a good thing?
A
Nearly all the time
14
Q
When is acute inflammation not a good thing?
A
It can lead to local complications and systemic effects
15
Q
What causes acute inflammation?
A
Microbial infections Hypersensitivity reactions Physical agents Chemicals Tissue necrosis
16
Q
What type of microbial infections particularly cause acute inflammation?
A
Bacteria
17
Q
What are pyogenic organisms?
A
Pus forming
18
Q
What are hypersensitivity reactions?
A
Immunological reactions
19
Q
What part of hypersensitivity reactions causes acute inflammation?
A
Acute phase
20
Q
What physical agents cause acute inflammation?
A
Heat
Other forms of energy
21
Q
What are the clinical features of acute inflammation?
A
Rubor (redness) Tumour (swelling) Calor (heat) Dolour (pain) Loss of function
22
Q
Why isn’t loss of function independent from the other clinical features?
A
Because it occurs partly because whatever is inflamed is sore, swollen, hot and red
23
Q
What changes does acute inflammation cause in tissues?
A
Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells
24
Q
What is required for each step of acute inflammation?
A
Inflammatory mediators
25
What happens in the vascular phase of acute inflammation?
Changes in blood flow
26
What are the stages of the vascular phase of acute inflammation?
- Transient vasoconstriction of arterioles
- Vasodilation of arterioles and then capillaries cause increase in blood flow to injured tissue
- Increased permeability of blood vessels
- Concentration of red blood cells in small vessels and the increased viscosity of blood leads to stasis
27
How long does transient vasoconstriction of arterioles take?
A few seconds
28
What is the result of increased blood flow to injured tissue?
Causes heat and redness
29
What does the increased permeability of blood vessels lead to?
Exudation of protein rich fluid from plasma into tissues
| Slowing of circulation
30
Why does increased permeability of blood vessels slow the circulation?
If liquid leaves the blood, left with cells, so slows
31
What does slowing of circulation lead to?
Swelling
32
What is the chemical mediator of the immediate early response of the vascular phase of acute inflammation?
Histamine
33
What kind of molecule is histamine?
Protein
34
Where is histamine released from?
Mast cells, basophils, platelets
35
What is histamine released in response to?
```
Many stimuli, including-
Physical damage
Immunological reactions
C3a
C5a
IL-1
Factors form neutrophils and platelets
```
36
What does histamine cause?
Vascular dilation
Transient increase in vascular permeability
Pain
37
What are the chemical mediators of the persistent response in the vascular phase of acute inflammation?
Many and varied chemical mediators, which are interlinked and of varying importance
38
What is the problem with studying the chemical mediators of the persistent response of the vascular phase of acute inflammation?
They are incompletely understood
39
Give two examples of chemical mediators of the persistent response of the vascular phase of acute inflammation?
Leukotrienes
| Bradykinin
40
What are leukotrienes derived from?
Arachidonic acid
41
What is significant about leukotrienes?
They are the most important chemical mediator
42
What law does fluid loss from vessels follow?
Starling’s Law
43
What is Starling’s Law?
Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure comparing plasma and interstital fluid
44
What is hydrostatic pressure?
The blood pressure- force with which the blood flows
45
What is colloid osmotic pressure?
The protein level between plasma and interstitial fluid
46
What does increased hydrostatic pressure lead to?
Increased fluid flow out of the vessel
47
Why is hydrostatic pressure increased in acute inflammation?
Because of the increased flow
48
What does increased colloid osmotic pressure of the interstitium cause?
An increase in fluid flow out of the vessel
49
Why does in increased colloid osmotic pressure cause an increase in fluid flow out of the vessel?
Because it sucks fluid out to balance the levels
50
What does exudation of fluid cause in inflammation?
Protein levels to increase
51
Why does exudation of fluid occur in acute inflammation?
Arteriolar dilatation
| Increased permeability of vessel walls
52
Why does arteriolar dilatation cause exudation of fluid?
Because it causes an increase in hydrostatic pressure
53
Why does increased permeability of vessel walls cause exudation of fluid?
Because it leads to loss of protein to the interstitium
54
What does net flow of fluid out of vessels lead to?
Oedema
55
What is oedema?
Increase fluid in tissue spaces
56
What can fluid be?
Transudate or exudate
57
What does oedema lead to?
Increased lymphatic drainage
58
Why does oedema lead to increased lymphatic drainage?
Because if fluid gets into tissue space by leaking out of vessels, there has to be a means for it to get away again, and therefore it is drained out of the lymphatic system
59
What is exudate?
Fluid loss in inflammation
60
What is the protein content of exudate?
High
61
What is transudate?
Fluid loss due to hydrostatic pressure imbalance
62
What is the protein content of transudate?
Low- the same as plasma
63
When does transudate formation occur?
When there is cardiac failure or venous outflow obstruction
64
What are the mechanisms of vascular leakage?
```
Endothelial contraction
Cytoskeletal reorganisation
Direct injury
Leukocyte dependent injury
Increased transcytosis
```
65
Why does endothelial contraction cause vascular leakage?
Because it leads to the formation of gaps, which are leaky
66
What is endothelial contraction mediated by?
Histamine
| Leukotrienes
67
Why does cytoskeletal reorganisation lead to vascular leakage?
Leads to formation of gaps
68
What is cytoskeletal reorganisation mediated by?
Cytokines
IL-1
TNF
69
What kinds of direct injury can cause vascular leakage?
Toxic burns
| Chemicals
70
What can cause leukocyte dependent injury?
Toxic oxygen species
| Enzymes from leukocytes
71
What causes transcytosis?
Channels across endothelial cytoplasm, where fluid moves along normally for a lot of physiological systems
72
What mediates an increase in transcytosis in inflammation?
VEGF
73
What is exudate rich in?
Fibrin
74
Where is fibrin an important component?
The acute inflammatory process
75
What is fibrin good at?
Making stuff sticky, and keeping it together
76
What is the purpose of fibrin?
To localise area of inflammation around injured tissue
77
Where is fibrins role in acute inflammation important?
If get inflammation in an organ that has a serosal surface
78
Give 3 examples of organs with serosal surfaces?
Lungs
Appendix
Heart
79
Why is fibrin important if you get inflammation in an organ that has a serosal surface?
Because where there is acute inflammatory infiltrate on a serosal surface, you run the risk that you’ll exudate all of the blood volume into the cavity. Fibrin is good at preventing this.
80
What is a neutrophil leucocyte?
A primary type of white blood cell involved in inflammation
81
What kind of cell is a leucocyte?
A type of granulocyte, also known as a polymorphonuclear leucocyte. This means that they are myeloid cells.
82
What are the characteristics of myeloid cells?
Granular cytoplasm with lots of cells in it
83
What is the predominant purpose of neutrophil leucocytes?
Acute inflammation
84
What are the stages of infiltration of neutrophils?
- Stasis causes neutrophils to line up at the edge of blood vessels
- Neutrophils roll along endothelium, becoming loosely adherent, sticking to it intermittently
- They then stick more avidly
- Followed my emigration of neutrophils along the blood vessel wall
85
Why does stasis occur?
Due to laminar flow
86
Why does laminar flow cause stasis?
Blood cells tend to flow down the middle of the vessel, not the edges, however, when the blood gets static, the blood cells go to the periphery
87
What is the process of neutrophils sticking intermittently to the endothelium called?
Rolling
88
What is the process of more avid neutrophil sticking called?
Adhesion
89
What is responsible for each of the different stages of neutrophil infiltration?
White cells and endothelial ligands have different receptors
90
How do neutrophils escape from vessels?
Relaxation of inter-endothelial cell junctions
Digestion of vascular basement membrane
Movement of white cells
91
Why does the digestion of the vascular basement membrane allow neutrophils to escape from vessels?
It creates gaps, and the cells move into the gaps
92
What happens to the digested vascular basement membrane at the end of inflammation?
It is rebuilt
93
What is chemotaxis?
Movement along concentration gradients of chemoattractants
94
Why is chemotaxis important?
Because it’s how, once a polymorph gets out of a capillary, it knows where to go and what to do, as it needs to get to the bit of tissue thats most injured
95
What can chemotaxis occur due too?
Chemotaxins
| Receptor-ligand binding
96
Give 3 examples of chemotaxins
C5a
LTB4
Bacterial peptides
97
What is C5a?
An activated component of complement
98
Where is lTB4 from?
Cell membranes
99
What are bacterial peptides?
Stuff from outside the body that are very potent chemotaxins
100
Where are the receptors for receptor-ligand binding?
On the surface of white cells
101
What happens in receptor-ligand binding?
Once the receptor has bound to the ligand on a neutrophil, it rearranges the cytoskeleton and produces a pseudopod
102
What are pseudopods important for?
They are how cells move
103
What is the main function of white cells?
Phagocytosis
104
What are the three stages of phagocytosis?
Contact
Recognition
Internalisation
105
What happens once internalisation has happened?
It means all things that sit inside lysosomes and the cytoplasm can do their job
106
What is phagocytosis facilitated by?
Opsonins
107
Give two examples of opsonins?
Fc
| C3b
108
What is Fc?
A fixed component of immunoglobulin
109
What is C3b?
A complement component
110
What changes does phagocytosis involve?
Cytoskeletal
111
What is produced when phagosomes fuse with lysosomes?
Secondary lysosomes
112
What are the two classes of phagocytitic killing mechanisms?
Oxygen dependent
| Oxygen independent
113
What are the oxygen dependent killing mechanisms?
Production of superoxide and hydrogen peroxide
| Hydrogen peroxide-myeloperoxidase-halide system
114
What is produced in the hydrogen peroxide-myeloperoxidase-halide system?
HOCl -
115
What are the oxygen independent killing mechanisms?
Lysosome and hydrolases
Bacterial Permeability Increasing Protein (BPI)
Cationic proteins (defensins)
116
What are the stages of neutrophil chemotaxis and phagocytosis?
#NAME?
117
What are the chemical mediators of acute inflammation?
Proteases
Prostaglandins/leukotrienes
Cytokines/chemokines
118
Where are proteases produced?
Liver
119
Where are proteases found?
Plasma
120
What is the function of proteases in acute inflammation?
Kinins
Complement system
Coagulation system
121
What proteases are involved in the complement system?
C3a, C5
122
Why are proteases important in the complement system?
In producing chemotaxins and opsonins
123
What are prostaglandins/leukotrienes?
Metabolites of arachidonic acid, produced by different enzymatic reactions
124
Where are cytokines/chemokines produced by?
White blood cells
125
Give two examples of cytokines/chemokines?
Interleukins
| TNF α
126
What do the chemical mediators of acute inflammation cause?
Increased blood flow
Vascular permeability
Neutrophil chemotaxis
Phagocytosis
127
What chemical mediators cause increased blood flow?
Histamine
| Prostaglandins
128
What chemical mediators cause vascular permeability?
Histamine
| Leukotrienes
129
What chemical mediators cause neutrophil chemotaxis?
C5a
LTB4
Bacterial peptides
130
What chemical mediators cause phagocytosis?
C3b
131
Why are the immune system and the inflammatory response said to by symbiotic?
They work together, and both as defence mechanisms, but are different
132
What is the hallmark of acute inflammation?
Exudate of fluid
| Infiltrate of inflammatory cells
133
What is the purpose of the exudation of fluid?
Delivers plasma proteins to area of injury
Dilutes toxins
Increases lymphatic drainage
134
What plasma proteins need to be delivered to the site of injury?
Immunoglobulins
Inflammatory mediators
Fibrinogen
135
What is the advantage of the increase in lymphatic drainage in acute inflammation?
Delivers microorganisms to phagocytes and antigens to the immune system
136
What is the purpose of infiltration of cells in acute inflammation?
Removes pathogenic organisms and necrotic debris
137
What is the purpose of vasodilation in acute inflammation?
Increases delivery
| Increases temperature
138
What is the purpose of pain and loss of function in acute inflammation?
Enforces rest
| Reduces chance of further traumatic damage
139
What are the local complications of acute inflammation?
Swelling
Exudate
Loss of fluid
Pain and loss of function
140
What can swelling in acute inflammation lead to?
Blockage of tubes
141
When is swelling causing blockage of tubes likely to be problematic?
If you have acute inflammation in a small tube with a narrow lumen
142
What can a blocked bile duct cause?
Jaundice
143
What problems can exudate cause?
Compression
| Serositis
144
Give an example of when compression can be problematic
Cardiac tamponade
145
What happens in cardiac tamponade?
Fluid splints the heart, stopping it from beating
146
What is serositis?
Inflammation of a serosal surface
147
When my loss of fluid be a problem?
In burns, when plasma can be lost through the skin
148
When can pain and loss of function be particularly problematic?
If prolonged
149
What are the systemic complications of acute inflammation?
Fever
Leukocytosis
Acute phase response
150
Why does acute inflammation cause fever?
‘Endogenous pyrogens’ produced
| Prostaglandins produced
151
Give two examples of endogenous pyrogens
IL-1
| TNF α
152
How can aspirin reduce temperature
It inhibits the production of prostaglandins
153
What is leukocytosis?
An increased number of WBC in blood
154
What do IL-1 and TNF α produce?
Accelerated release from marrow
155
What do macrophages and T lymphocytes produce?
Colony-stimulating factors
156
What do bacterial infections recruit?
Neutrophils
157
What do viral infections recruit?
Lymphocytes
158
What happens when there is severe acute inflammation?
There is a big area of infarcted tissue
159
Give an example of where they will be severe acute inflammation?
Appendicitis
160
What can severe acute inflammation lead to?
Systemic pathological symptoms
161
What systemic pathological systems will severe acute inflammation lead to?
Decreased appetite
Raised pulse rate
Altered sleep patterns
Change in plasma concentrations of acute phase proteins
162
What acute phase protein concentrations are changed when there is severe acute inflammation?
```
C-reaction protein
α-1 antitrypsin
Haptoglobin
Fibrinogen
Serum amyloid A protein
```
163
How can Cr-reaction protein be useful?
Can help tell if a patient has had an infarction
164
What happens if inflammation doesn’t work?
It doesn’t rapidly localise and deal with infection, so can get spread of microrganisms and toxins
165
What is shock?
Clinical syndrome of circulatory failure
166
What kind of shock is inflammatory shock?
Septic shock
167
What can happen after development of acute inflammation?
Complete resolution
Continued acute inflammation with chronic inflammation
Chronic inflammation and fibrous repair
Death
168
What outcome of acute inflammation happens most of the time?
Complete resolution
169
What happens in complete resolution of acute inflammation?
Changes gradually reverse
Vascular changes stop
Exudate drains to lymphatics
Fibrin is degraded by plasmin and other proteases
Neutrophils die, break up and are carried away, or are phagocytosed
170
What happens when vascular changes stop in complete resolution?
Neutrophils no longer marginate
Vessel permeability returns to normal
Vessel calibre returns to normal
171
Can damaged tissue regenerate in acute inflammation?
May be able too
172
When is complete resolution not possible?
If tissue architecture has been destroyed
173
What does continued acute inflammation with chronic inflammation lead to when there is a pus forming microorganism?
Abscess
174
What are the mechanisms of resolution of acute inflammation?
All mediators of acute inflammation have short half lives
May be inactivated by degradation
Inhibitors may bind
May be unstable
May be diluted in exudate
Specific inhibitors of acute inflammatory changes
175
Give an example of a mediator of acute inflammation that is inactivated by degradation
Heparinase
176
Give an example of a mediator of acute inflammation that is stopped by a binding inhibitor
Various anti-proteases
177
Give an example of a mediator of acute inflammation that is unstable
Some arachidonic acid derivatives
178
Give an example of a mediator of acute inflammation that is diluted in the exudate
Fibrin degradation produces
179
Give two examples of specific inhibits of acute inflammatory changes
Lipoxins
| Endothelin
180
What happens in bacterial meningitis?
Bacterial infection in the meninges causes acute inflammation in them
181
What are meninges?
Spaces surrounding the brain
182
What can acute inflammation in meninges cause?
Vascular thrombosis and reduced perfusion
183
What is the outcome of bacterial meningitis?
If recognised and treated quickly, fine.
| If don’t, death
184
What causes death in bacterial meningitis?
Because the acute inflammatory exudate in meningeal space in the hard skull results in a raised intracranial pressure.
185
What can acute inflammation in meninges damage?
Things that cross in the meningeal space- blood vessels, cranial nerve
186
What happens in lobar pneumonia?
Inflammatory exudate and infiltrate into alveolar space
187
What can happen if lobar pneumonia is severe?
Can kill
188
What causes lobar pneumonia?
Streptococcus pneumoniae
189
What are the symptoms of lobar pneumonia?
```
Worsening fever
Prostration
Hypoxaemia
Dry cough
Breathlessness
```
190
What is the outcome of lobar pneumonia if treated?
Can resolve completely
191
What can skin blisters be due to?
Heat
Sunlight
Chemicals
192
What are the predominant features of skin blisters?
Pain
| Profuse exudate
193
What causes the skin blister?
Collection of fluid strips off overlying epithelium
194
Why is the exudate clear in a skin blister?
Because inflammatory cells are relatively flew
195
Why is bacterial infection a problem in burns?
There is no skin, so no protection
196
What is the outcome of skin blisters?
Either resolves or scars
197
What are abscesses?
Solid tissues that occur when inflammatory exudate forces tissue apart, with liquefactive necrosis in the centre
198
When do abscesses occur?
When acute inflammation can’t get out
| When there are pus forming organisms that the body can localise, but not deal with
199
What can abscesses cause?
Pain
Tissue damage
Squash adjacent structures
200
Why do abscesses cause pain?
Because causes high pressure
201
What happens when you get acute inflammation in serous cavities?
Exudate pours into the cavity
202
What can acute inflammation in serous cavities cause?
Ascities
| Pleural or pericardial effusion
203
What can pleural or pericardial effusion cause?
Respiratory or cardiac impairment
204
How is acute inflammation in serous cavities dealt with?
Localised fibrin deposition, which helps localise the inflammation, favouring resolution rather than continuation of inflammation
205
Give 5 disorders of acute inflammation
Hereditary angio-oedema Alpha-1 antitrypsin deficiency Inherited complement deficiencies Defects in neutrophil function Defects in neutrophil numbers
