Acute Inflammation Flashcards
(54 cards)
Define inflammation(3)
a defensive reaction (innate immune response) of a macro-organism against injury caused by trauma, toxic chemicals, or an invading pathogen.
- Protective response, but also a potentially harmful process: Components of inflammation that can destroy microbes can also injury bystander normal tissue
- Rapid response to tissue injury; minutes/hours to develop and of relative short duration (hours or days).
Triggers of acute inflammation…
- Infections Bacteria, viruses, parasites, fungi, toxins
- Tissue damage
- Foreign bodies: Splinters, sutures, dirt
What can damage to tissue be due to
o Physical agents: Frost bites, burns, radiation (ionising, UV)
o Chemical agents: Chemical burns, irritants, bites
o Mechanical injury & ischemia: Trauma, tissue crush, reduced blood flow
What is the purpose of acute inflammation?(5)
- Alert the body and initiate appropriate immune response
- Limit spread (of infection and/or injury)
- Protect injured site from becoming infected
- Eliminate dead cells/tissue
- Create the conditions required for healing
Summarise the steps in acute inflammation(5)
- Recognition of injury
- Recruitment of leucocytes
- Removal of injurious agent
- Regulation (closure of inflammatory response)
- Resolution/Repair of affected tissue
Signs of acute inflammation…(5)
- Heat (Latin: Calor) Increased blood flow (hyperaemia) to injured area Swelling
- Increased blood flow and metabolic activity Redness (Rubor)
- (Tumor) Fluid accumulation due to permeability of vessels
- Pain (Dolor) Release of pain mediators; pressure on nerve ends
- Loss of function (Functio laesa) Damage
Systematic changes of acute inflammation
- Fever
- Neutrophilia- GM-CSF (cytokine) stimulation of bone marrow to replenish dead neutrophils
- • Acute phase reactants.
- • Complications. In rare cases causing a sever systemic inflammatory reaction called sepsis or a form of inflammatory response syndrome (SIRS)
What are the molecules that cause fever?
- Endogenous pyrogens (IL-1, TNF-α)- acts on preoptic areas of hypothalamus to raise the temperature
- Exogenous pyrogens (microbial components)
Name some acute phase reactants as part of the systemic changes
- C-reactive protein (CRP), fibrinogen, complement, serum amyloid A protein (SAP)
- Produced in the liver
- Induced by the cytokines IL-6, IL-1, TNF-alpha
- Increased Fibrinogen => stacking of RBCs => faster sedimentation rate (Increased ESR (Erythrocyte Sedimentation Rate)
The components of an acute inflammatory response…
- Vascular: acute changes in local vasculature. Vasodilatation, plasma exudation and oedema
- Cellular: infiltration of inflammatory cells. Cell recruitment, phagocytosis, NETosis
- Humoral: release of inflammatory mediators. Complement, plasma factors, clotting cascade, cytokines and chemokines
- Resolution: Inflammation is controlled and self-limiting. Healing, regeneration and repair of tissue
Summarise what happens in vascular events
- Vasodilation
2. Increased vascular permeability
What happens during vasodilation in vascular events?(3)
– Vasodilation: an increase in vascular diameter
Induce by histamine and serotonin released by injured cells, mast cells and macrophages
• This results in hyperaemia (increase in blood volume to the area) (Redness)
• The increased blood volume heats up the tissues (Heat)
What happens during increased vascular permeability?(3)
- Leading to leakage of fluids into the tissues (Swelling)
- As exudate accumulates, pressure increases. Nerve endings are stimulated by the excess fluid and inflammatory mediators (Pain).
- Endothelial cell activation increasing their expression of adhesion molecules
Why does gaps appear between endothelial?
Gaps occur due to contraction of e.g myosin and shortening of individual endothelial cells
What does loss of proteins like albumin and fibrinogen from the plasma?
the tissue increase the osmotic pressure/gradient, leading to fluid leakage to the area, causing oedema.
• Cell transmigration
What is inflammatory exudate due to?
due to increased vessel permeability
What other substances enter tissues or serous tissues?
Water, salts, small plasma proteins (fibrinogen) inflammatory cells, red blood cells
Why does transudate occur?
fluid leaks due to altered osmotic/hydrostatic pressure; vessel permeability normal
What are the mediators of inflammation?
- Macrophages
- Neutrophils
- Mast cells
- Platelets
• Humoral factors of inflammation…
- Complement
- Plasma factors
- Clotting cascade
- Cytokines
- Chemokines
What are proinflammatory cytokines?
• Activated tissue resident macrophages secrete the inflammatory cytokines
- • Mast cells in the tissue secrete Histamine
• These chemical signals released by activated macrophages and mast cells at the injury site cause endothelial activation, vasodilation and increased vascular permeability
Which factors regulate and repair tissue?
the release of immunoregulatory factors (TGF-)
Summarise the steps in neutrophil recruitments
- Margination & rolling mediated by selectins
- Integrin activation by chemokines
- Firm adhesion to endothelium mediated by integrins and cell adhesion
- Transmigration through endothelium into tissue
Describe transmigration through endothelium into tissue
Neutrophils migrate through interendothelial spaces
Neutrophils pass through vessel wall and enter tissue
Migrate (chemotaxis) through tissue towards inflamed site
Gradient of chemoattractants guides migration in tissues
