Immunopathology - Week 4 - Acute Inflammation Flashcards
Define Inflammation
Inflammation is a local response to cellular injury. It is a mechanism initiating the elimination of noxious agents and of damaged tissue.
Explain the role of inflammation in the defence of the body.
Acute inflammation is the immediate and early response to tissue injury.
Functions:
Delivers leukocytes to the site of injury to eliminate:
* Invading pathogens/non-pathogens
* Clear necrotic tissue
What are the Cardinal signs of Acute Inflammation?
- Rubor(redness)
- Tumor(swelling)
- Calor(heat)
- Dolor(pain)
- Functiolaesa (loss of function)
What are the functions of the first line of defence?
Physical barriers and their associated secretions.
- Skin
- Nasal hair
- Mucous membranes
Normal Microbiota
Chemical action
- acidic nature of urine
What is involved in the second line of defence?
- Inflammation
- Phagocytosis
- Fever
- Release of enzymes to enhance inflammatory response.
- Toll Like Receptors (TLR): allow cells to recognise certain molecules and change gene expression.
- NOD proteins
- Interferon and other cytokines
What is involved in the third line of defence?
- Cell mediated response
- Antibody mediated response
Example: Lymphocyte produce Antibodies to destroy Antigens.
Name the type of cells involved in acute inflammation.
Leukocytes (white blood cells)
5 types of Leukocytes:
* Neutrophils - Associated with bacterial infection
* Lymphocytes - associated with viral infection
* Eosinophils - associated with parasite infection
* Basophils
* Monocytes
Describe the early stages of vascular responses that contribute to acute inflammation.
Earliest phase:
- Vasodilation (vessels widening)
- Hyperaemia (increased blood flow)
- Increased blood flow -> increased pressure within the vessels due to water molecules)
-> Results in an increases movement of transudate (blood plasma) from the capillaries into the tissue.
Explain the role of chemical mediators in the inflammatory process.
Facilitate the acute inflammatory process.
3 different systems:
1- Degranulation of mast cells.
Allows the release of:
* Histamine
* Serotonin
* Chemotactic factors
* Prostaglandins
* Leukotrienes
2 - Activation of plasma systems.
1. The kinin system releases bradykinin, which:
* Produces pain
* Increases vascular permeability
* Contracts smooth muscle
2. The complement system:
* results in the death of the antigen (the
foreign agent)
3. The clotting system
* Stops bleeding
3- Release of cellular components.
* Platelets
* Neutrophils
* Lymphocytes and
* Monocytes
Describe the possible consequences of acute inflammation.
Death
* Inflammatory reactions underlie life threatening
anaphylactic
responses to insect bites, some food.
Abscess formation
* Is a localised collection of pus,
sometimes enclosed in a connective tissue capsule.
Progression to chronic inflammation
* May follow acute inflammation, if it cannot be completely resolved.
Scarring (fibrosis) occurs in tissues that do not regenerate.
Explain the pathophysiological basis for the clinical manifestations of acute inflammation.
Describe the cellular responses that contribute to acute inflammation.
Occurs when Leukocytes leave the venules, to a lesser extent in capillaries and move towards the site of injury via some steps: Margination and rolling:
* Margination: the leukocytes marginating to the vessel periphery
* Rolling: the leukocytes tumble on the endothelial surface, transiently sticking along the way.
Adhesion and Emigration:
* Adhesion: the leukocytes firmly adhere to areas
exposed on endothelial
* Emigration: leukocytes through the endothelial
basement membrane into the extravascular space.
Chemotaxis: leukocytes move toward the site of
injury along a chemical gradient of various inflammatory mediators.
Phagocytosis: engulfment and killing of the pathogens by the phagocytes.
Describe the later stages of vascular responses that contribute to acute inflammation.
Increasing vascular permeability, which allows protein-rich fluid called exudate.
The movement of protein-rich exudate from the plasma. Results in outflow of water and ions into the extravascular tissues which causes oedema (swelling).
Vascular leakage causes the blood become more concentrated. This is called Stasis.
