Acute Inflammation Flashcards
(37 cards)
What is acute inflammation?
The response of living tissue to injury, initiated to limit tissue damage - innate, immediate and of short duration.
Vascular and cellular reactions lead to the accumulation of what in tissues? How is it controlled?
Fluid exudate and neutrophils.
Controlled by chemical mediators from cells/plasma.
What are the causes of acute inflammation?
Microbial infections (e.g. Pyogenic/pis-causing organisms), hypersensitivity reactions, physical agents, chemicals and tissue necrosis.
What are the clinical features of acute inflammation?
Rubor, tumor, calor, dolor and loss of function
Which changes lead to rubor and calor?
Transient vasoconstriction of arterioles happen first, then vasodilation of arterioles followed by capillaries, which increases blood flow to an area, making it redder and more hot.
What affect does the increased permeability of blood vessels have?
Exudation of protein-rich fluid into tissues and slowing of circulation - swelling.
Stasis is concentration of RBCs in small vessels and increased blood viscosity.
Which chemical mediators acts immediately/as part of the early response in the 1st half an hour, and what does it do?
Histamine is released from mast cells, basophils and platelets in response to many stimuli including compliment components and factors from neutrophils and platelets. It causes vascular dilation, a transient increase in vascular permeability and pain.
Which chemical mediators are part of the persistent response?
Leukotrienes and bradykinin - many and varied with interlinked and varying importance.
How may oedema arise in acute inflammation?
Starling’s Law - hydrostatic and colloid osmotic pressure balance. Increased blood flow leads to increased hydrostatic pressure in vessels and increased colloid osmotic pressure in interstitium from exudate, so there’s increased fluid flow out of the vessel.
Oedema caused by arteriolar dilation and increased blood vessel permeability.
What are the 2 types of oedema and why is it employed in acute inflammation?
Oedema (increased fluid in interstitium), can be transudate, e.g. From cardiac failure or venous outflow obstruction, where the fluid in the interstitium has the same protein content as the plasma, or exudate, where it has a higher plasma concentration. It’s useful in acute inflammation, as it leads to increased lymphatic drainage, potentially leading pathogens to dendritic cells in lymph nodes.
What are the mechanisms of vascular leakage? Why is it helpful?
Endothelial contractions creating gaps, cytoskeleton reorganisation creating gaps, direct injury, leukocyte dependent injury and increased transcytosis - channels across endothelial cytoplasm.
Used to deliver plasma proteins to the site of injury, e.g. Fibrin, so meshwork can localise, which is important at serous cavities.
What is a neutrophil/polymorph?
The primary type of WBC involved in acute inflammation, a type of granulocyte, with multilobed nuclei. Make up pus.
Outline the steps of neutrophil infiltration.
Margination - stasis causes neutrophils to line up at the edges of blood vessels, along the endothelium.
Rolling - along endothelium, sticking intermittently.
Adhesion - neutrophils then stick more avidly.
Emigration - neutrophils go through blood vessel wall.
Neutrophils escape the vessels by relaxation of interendothelial cell junctions, digestion of vascular basement membrane and movement.
Explain the importance of chemotaxins.
When neutrophils infiltrate the tissue, they move along concentration gradients of chemoattractants.
Chemotaxins: C5a, LTB4, bacterial peptides. Receptor-ligand binding induces rearrangement of cytoskeleton and production of pseudopod.
Neutrophils phagocytise, how?
Contact, recognition, internalisation. Facilitated by opsonins, cytoskeleton changes, phagosome + lysosome = phagolysosome/secondary lysosome. The kill is either oxygen dependent - produces superoxide and hydrogen peroxide, myeloperoxidase-halide system produces HOCl to manage cause of inflammation, or oxygen independent - lysozyme and hydrolases, bactericidial permeability increase protein (BPI) and cationic proteins -‘defensins’.
What is a downside of oxygen dependent killing of pathogens by neutrophils?
Activated neutrophils may release toxic metabolites and enzymes, causing damage to the host tissue.
Name and mention the origins of 4 types of chemical mediators in acute inflammation.
Proteases-plasma proteins produced in liver.
Kinins-complement system, coagulation/fibrinolytic system.
Prostaglandins/Leukotrienes-metabolites of archidonic acid.
Cytokines/chemokines are produced by white blood cells - many and varied including interleukins and tissue necrosis factor alpha.
Some functions of chemical mediators include to increase blood flow, to stimulate vascular permeability, induce neutrophil chemotaxis and phagocytosis, which do which?
Blood flow - histamine and prostaglandins.
Vascular permeability - histamine and leukotrienes.
Neutrophils chemotaxis - C5a, LTB4, bacterial peptides.
Phagocytosis - C3b.
What are the 2 hallmarks of inflammation?
- Exudate of fluid (oedema).
2. Infiltrate of inflammatory cells.
How is injury combated by exudation of fluid?
Delivers plasma proteins to area of injury (immunoglobulins, fibrinogen, inflammatory mediators), dilutes toxins and increases lympathic drainage, so microorganisms are delivered to phagocytes and antigens go to the immune system.
How is injury combated by infiltration of cells?
Removes pathogenic organisms and necrotic debris by phagocytosis.
How is injury combated by vasodilation?
Increased delivery of inflammatory substances by the blood and an increase in temperature.
How is injury combated by pain and loss of function?
Enforces rest, reduces the chance of further traumatic damage.
State 4 local complications of acute inflammation.
- Swelling causing blockage of tubes.
- Exudate - compression e.g. Cardiac tamponade, serositis.
- Loss of fluid e.g. Burns.
- Pain and loss of function are unhelpful if prolonged.
