Lecture 6 - Inflammation (TBC) Flashcards
What is acute inflammation?
The process of inflammation through which our body’s tissues initially respond to infection or injury
Why do we have inflammation?
The body needs a way of eliminating injured tissue and infectious agents and repairing tissue damage
What can acute inflammation be in response of?
Infections
Necrosis
Ionising radiation
Extreme cold
Burns
Toxins
Trauma
Ischaemia
What are the local clinical features of acute inflammation?
Redness
Swelling
Heat
Pain
Loss of function
What is redness caused by in acute inflammation?
Vasodilation
What factors are involved with vasodilation in acute inflammation?
Histamine
Prostaglandin
What is swelling caused by in acute inflammation?
Inflammatory exudate resulting from increased vascular permeability
What factors are involved with swelling in acute inflammation?
Histamine
Leukotrienes
What is heat caused by in acute inflammation?
Vasodilation
What is pain caused by in acute inflammation?
Tissue damage
What is loss of function caused by in acute inflammation?
Tissue damage
What is loss of function caused by in acute inflammation?
Tissue damage
What factors are involved with pain in acute inflammation?
Prostaglandin
Bradykinin
What factors are involved with loss of function in acute inflammation?
ROS
NO
Lysosomal enzymes
What are the different patterns of acute inflammation?
Purulent (suppurative) Inflammation
Serous Inflammation
Fibrinous Inflammation
What is purulent (suppurative) inflammation characterized by?
Characterized by production of pus (an inflammatory exudate rich in neutrophils and fluid and liquefied debris of necrotic cells) - primarily cellular
- Pimple
What is purulent (suppurative) inflammation caused by?
Caused by pyogenic (pus-producing) organisms that cause tissue necrosis and liquefaction.
What is an abscess?
Abscess is a localized collection of pus.
What is pus?
an inflammatory exudate rich in neutrophils and fluid and liquefied debris of necrotic cells
What is serous inflammation characterized by?
Characterized by a fluid rich, cell-poor exudate
- a skin blister or a runny nose
Where does serous inflammation occur?
Occurs in peritoneum, pleura, pericardium.
What is fibrinous inflammation characterized by?
Characterized by a fibrinogen-rich exudate
and fibrin deposition
Where can fibrinous inflammation occur?
pericardium and peritoneum
What are the four steps of acute inflammatory response?
- Recognition
- Pattern Recognition Receptors
- Vascular changes - Recruitment
- of leukocytes - Removal of the agent
- killing and degradation
- ROS/NO
- phagocytosis - Resolution
What two types of sentinel cells in tissues are important initiators of acute inflammation?
Macrophages and mast cells
What are macrophages?
- Monocytes differentiate into macrophages in the tissue
- Long-lived in tissue
- Phagocytic
- Produce pro-inflammatory cytokines (esp. IL1b and TNFa) in response to damage/pathogens
What are mast cells?
- Tissue resident cells that can be long lived
- Contain numerous granules
- Release chemical mediators such as histamine, leukotrienes and prostaglandin
- Released chemicals mediate vascular changes, pain
- Mast cells can survive degranulation
What do macrophages produce in acute inflammation?
Produce pro-inflammatory cytokines (esp. IL1b and
TNFa) in response to damage/pathogens
What do mast cells release in acute inflammation?
Release chemical mediators such as histamine,
leukotrienes and prostaglandin
How do macrophages and mast cells recognise antigen for acute inflammation?
Pattern recognition receptors
What do pattern recognition receptor recognise?
PAMPs and DAMPs
What are DAMPs?
Damage-associated molecular patterns
What are PAMPs?
Pathogen-associated molecular patterns
What is released after DAMP recognition?
Chemical mediators such as histamine, leukotrienes and prostaglandin
What is released after PAMP recognition?
Chemical mediators including:
-histamine
-prostaglandin
-leukotrienes
What can acute inflammation can measured by?
- increased temperature
- increased acute phase proteins in serum (e.g. C-reactive protein, fibrinogen – measured by erythrocyte sedimentation rate – ESR)
- increased neutrophils in blood
What do the vascular mediators in acute inflammation mediate?
Vasodilation and vascular permeability
What vascular mediators cause vasodilation?
Prostaglandin and Histamine
What vascular mediators alter vasuclar permeability?
Leukotrienes
Histamine
What are the two main cells in step 2 of acute inflammation? (recruitment of leukocytes)
Neutrophils and monocytes
What are neutrophils?
Large, granular phagocytic cells with a multi-lobed nucleus (polymorphonuclear cells)
What recruits neutrophils in acute inflammation?
Neutrophils are recruited into tissues in response to proinflammatory cytokines e.g. IL-1b and TNFa
What is the life span of neutrophils?
Neutrophils are short-lived
- Half-life 4 – 10 h in circulation, 1 - 2 days in tissue
What are monocytes?
Large phagocytic cells found in the blood which produce pro-inflammatory cytokines (IL-1b, TNFa)
What is the circulation time of monocytes in blood?
Circulation time 20 - 40 hours in
blood
What is diapedesis?
The process of cells in the blood moving through the vessel wall (endothelium) to the tissues
What are the steps in the movement of leukocytes from the blood to affected tissue?
- Cytokine production from tissue macrophage
- Vessels become sticky and leaky
- Margination: Slow flow, high viscosity
- Rolling: Leukocytes attracted
- Adhesion: Leukocyte stick to vessels
6: Diapedesis
7: Chemotaxis: Leukocytes attracted by chemokines (esp IL8)
What is the order for the kinetics of acute inflammation?
- Edema
- Neutrophils
- Monocytes/macrophages
What do macrophages and neutrophils release for the removal of agent in acute inflammation?
Reactive oxygen species (ROS)
Nitric Oxide (NO)
Lysosomal enzymes
