Flashcards in 0416 - Acute Inflammation - RM Deck (12):
What is Inflammation?
Essential protective part of the non-specific (but not innate) immune response, to limit damage and lay the foundation for repair.Characterised by redness, swelling, heat, pain, and loss of function of the affected area.
What is the difference between acute and chronic inflammation?
Acute – ‘normal’ inflammation. Short time course (up to days). Contains leucocytes (primarily neutrophils), and exudate of fluid and plasma.Chronic – ‘abnormal’ inflammation. Longer time course (weeks-years). Contains lymphocytes and macrophages, and characterised by proliferation of blood vessels, and tissue fibrosis and necrosis.
What are the components of inflammation? (4)
Microvasculature changes (size, blood flow, and ‘leakiness’)Circulating blood cells (Red and White both leave microvasculature)Tissue cells (damaged cells secrete/release inflammatory mediators)Inflammatory mediators (numerous types and roles)
Briefly describe the changes in microvasculature in the initial part of the inflammatory response.
1. Arterioles briefly constrict.2. All vessels vasodilate to increase blood flow.3. Vasodilation leads to permeability of microvasculature – exudate leaks out.4. Blood flow slows down (stasis)5. Leucocytes become ‘marginated’ and migrate into extravascular space.6. The site becomes red, swollen and hot.
What is the difference between exudate and transudate?
Transudate – fluid normally found inside vessels in tissues, very little in ECF. Low protein content.Exudate – Significantly more protein (reflects plasma protein contents) and cell debris, leaks into the ECF.
What are inflammatory mediators? What is their purpose?
Products of blood cells, damaged tissue, and plasma proteins that serve as a signal to attract leukocytes to the site of injury to facilitate phagocytosis of the injurious agent, or otherwise affect the immune response.
What characterises the plasma protein-derived inflammatory mediators?
Complement, coagulation, fibrinolytic and kinin systems.They are all cascade processes – with each step deactivating the previous enzyme. This represents very tight control.
What are the cell and tissue-derived inflammatory mediators?
Cytokines (signalling peptides or glycoproteins) that can be autocrine (act on releasing cell), or paracrine (act on nearby cells). Can be classified by family (interferons, interleukins etc), or Function (proinflammatory, anti-inflammatory).Arachadonic acid metabolites – prostaglandins and leukotrienes – serve to mediate or enhance immune responseHistamine and other amines – case ‘wheal and flare’ tissue response.
What are the cellular contributions to inflammation? (6)
Polymorphs – first to arrive, engulf, kill, and digest microbes.Mast cells – stimulated by complement and release mediators (including histamine).Monocytes/macrophages – Late arrivals, secrete cytokines and chemokines, and engulf microbes and cell debris.Platelets – pro-inflammatory, assist in clottingVascular Endothelium – contract/relax (vasoconstriction/vasodilation), and assist in angiogenesis.Neurons – release compounds including substance P (transmits pain).
What are the systemic sequelae of inflammation?
Increased temperatureIncreased leukocytes (and later lymphocytes)Stimulated synthesis of plasma proteins.
Which cellular membrane components take part in ‘margination’ of white cells?
Selectins, Integrins, and Cytokines