Inflammation Flashcards
What is inflammation?
- Response of living tissue to injury/insult, can be physical/chemical/infective/hypersensitive
- Protective reaction: dilute/destroy/isolate/initiate repair
- Potentially harmful - componments can injury bystander normal tissue
Two types of inflammation
Acute and chronic
Signs of infection
Heat/redness/swelling/pain/loss of function
Characteristics of acute inflammation
Fast
Mainly neutrophils
Usually mild and self-limited
Prominent symptoms
Characteristics of chronic inflammation
Slower
Mainly monocytes/macrophage and lymphocytes
Severe and progressive tissue injury
More subtle symptoms
Vascular response of acute inflammation
Vasodilation, leaky capillaries
Cellular response of acute inflammation
Margination, adhesion, emigration and activation of neutrophils
Is the complement cascade activated in acute inflammation?
Yes
How is vasodilation stimulated?
Histamines and NO act on smooth muscle
What is stasis?
Shortened blood flow, hyperviscosity
Characteristics of vasodilation
Increased permeability of vasculature: formation of early transudate (protein-rich filtrate of plasma) gives rise to exudate (protein rich filtrate) into extracellular tissues
Which molecules cause endothelial cell contact to widen intercellular gaps of venues?
Histamines, bradykinins, leukotrienes
Process of vascular leakage
- Histamines, bradykinins, leukotrienes cause endothelial cell contraction that widens intercellular gaps of venules
- Outpouring of exudate into extracellular tissue leads to reduction of intravascular osmotic pressure and increase in extravascular, interstitial osmotic pressure
- Increase of interstitial osmotic pressure leads to edema (water and ions)
How can leukocytes leave vasculature?
Margination and rolling
Activation and adhesion
Transmigration
How is CRP produced?
Interleukins stimulate liver to produce CRP
What impact does TNF have on the heart?
Negative - stops it beating as strongly
Increases risk of thrombosis
Symptoms of systemic infection
Lower blood pressure, change in heart rate, fatigue, depression, fever
What happens to [albumin] in inflammation?
Goes down
Factors impacting would healing
Infection/pressure /nutrition/ age/ immunocompromised/diabetes /BMI
Factors aiding wound healing
Oxygen, maggots, Manuka honey, general good health, antibiotics
Symptoms of acute inflammation
Malaise, fever, pain, rapid pulse
Laboratory investigations for acute inflammation
Increased neutrophils, increased erythrocyte sedimentation rate, increased concentration of acute-phase proteins
CRP begins to rise and peak at 36-50 hours after infection
ESR shows slower rise and return to normal than CRP
Components of chronic inflammation
Lymphocytes, plasma cells, macrophage infiltration
How are cells repaired after chronic inflammation?
Fibrosis and angiogenesis
Through which routes can chronic inflammation occur?
May progress from acute inflammation or repeated episodes of acute inflammation or occur ‘de novo’ if the causative agent produces only a mild acute response
Chemicals stimulating vasodilation
Prostaglandins, NO
Chemicals stimulating increased vascular permeability
Histamines, serotonin, C3a, C5a, bradykinin, leukotrienes (C4, D4, E4), platelet activating factor
Chemicals stimulating chemotaxis and leukocyte activation
C5a, leukotriene B4, bacterial products, chemokines (IL-8)
Chemicals stimulating fever
IL-1, IL-6, TNF, prostaglandins
Chemicals stimulating pain
Prostaglandins, bradykinin
Chemicals stimulating tissue damage
Neutrophil and macrophage lysosomal enzymes, oxygen metaboplites, NO
Where can chemical mediators arise from?
May be derived locally at the site of inflammation or may be derived from circulating inactive precursors that are activated at the inflammation site
When are cell-derived mediators created?
Normally sequestered in intracellular granules, they are rapidly secreted when activated or are synthesised ‘de novo’ in response to stimulus
What are plasma protein-derived mediators?
Complement proteins/kinins which circulate in an inactive form and undegro proteolytic cleavage to acquire biologic activities
