Lecture 4 Flashcards
1
Q
What is Inflammation?
A
Inflammation is a local response to cellular injury
2
Q
What are characteristics of inflammation?
A
- Capillary dilatation
- Leukocytic infiltration
3
Q
What are symptoms inflammation?
A
- Redness
- Heat
- Pain
4
Q
What is the purpose of inflammation?
A
A mechanism initiating the elimination of noxious agents and of damaged tissue
5
Q
What is acute inflammation?
A
The immediate and early
response to tissue injury
6
Q
Functions of Acute inflammation:
A
Deliver leukocytes to the site of injury to eliminate:
- Invading pathogens/non-pathogens
- Clear necrotic tissue
7
Q
Leukocytes may prolong inflammation and induce tissue damage by releasing:
A
- Enzymes
- Chemical mediators
- Toxic free radicals
8
Q
What are the cardinal signs of Acute Inflammation?
A
- Rubor (redness)
- Tumor (swelling)
- Calor (heat)
- Dolor (pain)
- Functiolaesa (loss of function)
9
Q
First line of defence
A
- Physical barriers and their associated secretions
- Normal microbiota
- Chemical action
10
Q
Physical First Line of Defence
A
- Skin
- Nasal hair
- Eyelashes & eyelids
- Mucous membranes
- Mucociliary Clearance
- Urination
11
Q
Chemical First line of Defence
A
- Low pH
- Antimicrobial molecules (Mucous, lysozyme, pepsin)
12
Q
Second line of defence
A
- Inflammation
- Complement series of enzymes
- Toll like receptors
- NOD proteins
- Fever
- Interferon
- Phagocytosis
13
Q
Third line of defence
A
Specific immune response:
- Cell mediated response
- Antibody mediated response
14
Q
What cells are involved in the acute inflammatory response
A
Leukocytes (WBCs)
15
Q
What are the types of leukocytes?
A
- Neutrophils
- Lymphocytes
- Eosinophils
- Basophils
- Monocytes
16
Q
What does an increase of neutrophils indicate?
A
Bacterial infection
17
Q
What does an increase of lymphocytes indicate?
A
Viral infection
18
Q
What does an increase of eosinophils indicate?
A
Parasite infection
19
Q
What happens to the WBCs in acute inflammation?
A
They increase
20
Q
What is leukocytosis?
A
Increase in WBCs
21
Q
What is Leukopenia?
A
Decrease in WBCs
22
Q
What is vasodilation?
A
Vessels widening
23
Q
What is hyperaemia?
A
Increased blood flow to tissue
24
Q
What is the vascular response to acute inflammation?
A
- Vasodilation (increase blood flow to area, causing redness and warmth)
- Increased blood flow = increased intravascular hydrostatic pressure
- Increased movement of fluid from capillaries into tissue
- Increase vascular permability
25
What mechanisms are involved in increasing vascular
permeability?
1. Endothelial cell contraction via
various chemical mediators
2. Loosening of intercellular
junctions
3. Direct endothelial injury
4. Leukocyte-endothelial injury via enzymes and free radicals
26
The movement of protein-rich exudate from the plasma causes:
- Reduction of intravascular osmotic pressure
- Increase in osmotic pressure of interstitial fluid
27
What is the importance of haemodynamic changes?
- Allow exudation of fluid which dilute toxic and irritating agents
- Control effects of injurious agents
- Blood clotting
28
Leukocytes are leaving the venules and to a lesser extent in capillaries and moving towards the site of injury via some steps:
1. Margination and rolling
2. Adhesion and Emigration
3. Chemotaxis
4. Phagocytosis
29
Leukocytes Margination
The leukocytes marginating to the vessel periphery
30
Leukocytes Rolling
the leukocytes tumble on the endothelial
surface, transiently sticking along the way
31
Leukocytes Adhesion
The leukocytes firmly adhere to areas exposed on endothelial
32
Leukocytes Emigration
leukocytes through the endothelial basement membrane into the extravascular space
33
Leukocytes Chemotaxis
leukocytes move toward the site of injury along a chemical gradient of various inflammatory mediators
34
Leukocytes Phagocytosis
engulfment and killing of the
pathogens by the phagocytes
35
What are inflammatory mediators?
chemical mediators which facilitate the acute
inflammatory process.
36
What are the 3 systems of inflammatory mediators
1. Degranulation of mast cells
2. Activation of plasma systems
3. Release of cellular components
37
Degranulation of mast cells
This allows the release of:
* Histamine
* Serotonin
* Chemotactic factors
* Prostaglandins
* Leukotrienes.
38
Activation of Plasma systems
1. Kinin System
- Produces bradykinin, which causes pain and swelling.
2. Complement System
- a system of enzymes
- results in the death of the antigen
3. Clotting System
- Stops bleeding
- Localises microbes and provides a stroma for repair processes
39
Release of cellular components
Depending on the agent,
this may include:
* Platelets
* Neutrophils
* Lymphocytes and
* Monocytes.
40
Inflammatory exudates present clinically as:
- Serous exudate
- Fibrous exudate
- Membranous exudate
- Purulent exudate
- Haemorrhagic exudate
41
Sequelae of acute inflammation
- Resolution
- Scarring
- Abscess
- Progression to chronic inflammation
- Death
42
What is Inflammation?
Inflammation is a local response to cellular injury marked by capillary dilatation, leukocytic infiltration, redness, heat, and pain.
43
What is the primary function of inflammation?
To eliminate the initial cause of cell injury and the necrotic cells and tissues resulting from such injury.
44
How is inflammation linked to tissue repair?
The inflammatory response is tightly linked to tissue repair processes activated to heal damaged tissue.
45
True or False: Inflammation and Infection are the same.
False.
46
What is acute inflammation?
The immediate and early response to tissue injury characterized by delivery of leukocytes to the site.
47
What are the characteristics of acute inflammation?
Rubor (redness), Tumor (swelling), Calor (heat), Dolor (pain), Functio laesa (loss of function).
48
What is the role of inflammation in the body's defense?
Inflammation is a mechanism to defend against foreign agents and internal stressors.
49
What are the three levels of defense in the body?
1st line: Physical barriers and secretions, Normal microbiota, Chemical action. 2nd line: Inflammation, Complement enzymes, TLR, NOD proteins, Fever, Cytokines, Phagocytosis. 3rd line: Specific immune responses.
50
What are Toll-like receptors (TLR)?
Pattern recognition receptors that allow cells to recognize certain molecules indicating the presence of microbes.
51
What types of leukocytes are involved in inflammation?
Neutrophils, lymphocytes, eosinophils, basophils, and monocytes.
52
Which leukocyte is most commonly associated with bacterial infections?
Neutrophil.
53
Which leukocyte is most commonly associated with viral infections?
Lymphocyte.
54
Which leukocyte is most commonly associated with parasitic infections?
Eosinophil.
55
What is leucocytosis?
An increase in white blood cell count during infection, often rising to 20.0 x 10^9 cells per litre or more.
56
What is leukopenia?
A severe drop in white blood cell levels, occasionally occurring in severe infections.
57
Fill in the blank: The normal white blood cell count in blood is _______.
4.0-11.0 x 10^9 cells per litre.
58
What is the main function of leukocytes in acute inflammation?
To help clear invading infectious or non-infectious agents and degrade necrotic tissue.
59
What can leukocytes release that may prolong inflammation?
Enzymes, chemical mediators, and toxic free radicals.
60
What happens during the earliest phase of inflammation?
Vasodilation and increased blood flow to the tissue occur
## Footnote
This process is facilitated by various chemical mediators.
61
What is hyperaemia?
Increased blood flow to the tissue
## Footnote
It is a key feature of inflammation.
62
What results from increased intravascular hydrostatic pressure?
Increased movement of fluid from the capillaries into the tissues
## Footnote
This movement is due to pressure from water molecules.
63
What is transudate?
An ultrafiltrate of blood plasma that contains little protein
## Footnote
It is the fluid that first moves into the tissues during inflammation.
64
What follows transudation in the inflammatory process?
Increased vascular permeability permits flow of protein-rich fluid called exudate
## Footnote
This fluid eventually contains inflammatory cells.
65
What causes the permeability of blood vessels to increase?
Endothelial cell contraction, loosening of intercellular junctions, direct endothelial injury, leukocyte-endothelial injury
## Footnote
These events are mediated by various chemical signals.
66
What is exudate?
A protein-rich fluid that flows from blood vessels during inflammation
## Footnote
It contains inflammatory cells and is different from transudate.
67
How does the movement of protein-rich exudate affect osmotic pressure?
Reduces intravascular osmotic pressure and increases osmotic pressure of interstitial fluid
## Footnote
More protein in a fluid compartment leads to higher osmotic pressure.
68
What is oedema?
Accumulation of fluid in extravascular tissues, causing swelling
## Footnote
It results from the outflow of water and ions.
69
What are the consequences of tissue swelling during inflammation?
Pain and impaired function result
## Footnote
This occurs due to the release of chemical mediators.
70
What is stasis in the context of inflammation?
Increased blood viscosity and slowed circulation due to vascular leakage
## Footnote
This effect concentrates red blood cells.
71
What are the haemodynamic changes during inflammation?
Allow exudation of fluid, aid in controlling injurious agents, allow blood clotting in small capillaries
## Footnote
These changes help localize the effects of injury.
72
What is the first step in the cellular response of leukocytes to tissue invasion?
Margination of leukocytes
## Footnote
This process involves leukocytes settling out of the central blood column to the vessel periphery.
73
What is the process called where leukocytes crawl between endothelial cells into the extravascular space?
Emigration or diapedesis
## Footnote
This occurs after leukocytes adhere to the exposed areas on endothelial cells.
74
What are the three main steps of phagocytosis?
* Recognition and attachment of the particle
* Engulfment
* Killing and degradation of the ingested material
## Footnote
Each step is crucial for effective phagocytosis.
75
What is chemotaxis?
The movement of leukocytes toward the site of injury along a chemical gradient
## Footnote
Chemotaxis is driven by various inflammatory mediators.
76
What are some chemotactic agents for leukocytes?
* Soluble bacterial products
* Products of activated leukocytes and macrophages (e.g., leukotrienes, interleukins)
* Activated complement components
## Footnote
These agents guide leukocytes to the site of inflammation.
77
True or False: Neutrophils predominate in the first 24 hours of acute inflammation.
True
## Footnote
Neutrophils are followed by monocytes in the following days.
78
What role do opsonins play in phagocytosis?
They facilitate recognition and attachment of particles to leukocytes
## Footnote
Immunoglobulin G (IgG) is a major opsonin.
79
Fill in the blank: The leukocytes move by extending _______ that anchor themselves to the extracellular matrix.
pseudopods
## Footnote
This movement helps leukocytes navigate towards the site of inflammation.
80
What can reduce the numbers of adhesion molecules in the context of leukocyte emigration?
Diabetes Mellitus
## Footnote
This condition can hinder the ability to fight off infections.
81
What is the major benefit of leukocyte accumulation at the site of inflammation?
Phagocytosis
## Footnote
Phagocytosis helps eliminate pathogens and debris.
82
What happens if leukocytes cannot perform phagocytosis due to the size of foreign material?
They may release toxic metabolites and proteases outside the cell
## Footnote
This can lead to tissue damage.
83
What types of materials might lead to tissue damage during inflammation?
* Foreign bodies
* Antigen-antibody complexes
* Endogenous antigens in autoimmune processes
## Footnote
Autoimmune processes can lead to inappropriate inflammation against normal tissues.
84
What is the role of reactive oxygen metabolites in phagocytosis?
They are involved in the killing of bacteria and other microbes
## Footnote
Hydrolytic enzymes also contribute to the degradation process.
85
What is the term for the initial slowing of blood flow that allows leukocytes to marginate?
Vasodilation
## Footnote
Increased vascular permeability also contributes to this process.
86
What are the consequences of leukocyte destruction during inflammation?
They can become a source of tissue-damaging materials
## Footnote
This is especially evident in autoimmune conditions.
87
What are inflammatory mediators?
Chemical mediators that facilitate the acute inflammatory process.
88
What systems are involved in the production of inflammatory mediators?
3 different systems:
* Degranulation of mast cells
* Activation of plasma systems
* Release of cellular components
89
What is released during the degranulation of mast cells?
Histamine, serotonin, chemotactic factors, prostaglandins, and leukotrienes.
90
What are the three activation plasma systems involved in inflammation?
1. The kinin system
2. The complement system
3. The clotting system
91
What role does bradykinin play in inflammation?
Produces pain, increases vascular permeability, contracts smooth muscle.
92
What is the function of the complement system?
Enhances the inflammatory response and results in the death of the antigen.
93
What is the role of the clotting system in inflammation?
Stops bleeding, localizes microbes, and provides a stroma for repair processes.
94
Which cellular components may be released during inflammation?
Platelets, neutrophils, lymphocytes, and monocytes.
95
Fill in the blank: IL stands for _______.
interleukins
96
Fill in the blank: IFN stands for _______.
interferon
97
Fill in the blank: IgG stands for _______.
Immunoglobulin G
98
Fill in the blank: PAF stands for _______.
platelet activating factor
99
Fill in the blank: TNF stands for _______.
tumour necrosis factor
100
True or False: C5a and C3b are complement enzymes.
True
101
Mediators of Inflammation
102
What is serous exudate?
Watery, low protein fluid, largely plasma
## Footnote
Serous exudate is commonly seen in mild inflammation.
103
What characterizes fibrinous exudate?
Contains large amount of plasma proteins, fibrinogen and fibrin
## Footnote
Fibrinous exudate must be removed for healing to occur.
104
Where does membranous exudate develop?
On mucous membranes
## Footnote
Membranous exudate comprises necrotic cells within a fibro-purulent exudate.
105
What is purulent exudate?
Suppurative containing pus rich in protein, leukocytes and cell debris from necrotic leukocytes
## Footnote
Purulent exudate indicates a bacterial infection.
106
What does haemorrhagic exudate contain?
Blood
## Footnote
Haemorrhagic exudate occurs with severe tissue injury.
107
What is the usual outcome of resolution in acute inflammation?
Restoration to histologic and functional normalcy
## Footnote
Resolution involves neutralisation or removal of invading agents.
108
What happens during the repair phase of inflammation?
Regeneration follows to restore normal tissue structure and function
## Footnote
This phase occurs after resolution of inflammation.
109
What is scarring (fibrosis)?
Occurs when inflammation happens in tissues that do not regenerate or after substantial tissue destruction
## Footnote
Scarring involves the ingrowth of connective tissue.
110
What may lead to abscess formation?
Certain bacterial infections such as Staphylococci, Klebsiella, and Pseudomonas
## Footnote
These organisms are considered pyogenic or 'pus forming'.
111
What is an abscess?
A localized collection of pus, sometimes enclosed in a connective tissue capsule
## Footnote
Pus consists of tissue debris, exudate, and leukocytes.
112
What happens if acute inflammation cannot be completely resolved?
Progression to chronic inflammation may occur
## Footnote
Chronic inflammation can lead to ongoing tissue damage.
113
What can inflammatory reactions lead to in severe cases?
Life-threatening anaphylactic responses
## Footnote
This may cause massive swelling of the airways, leading to asphyxiation.
