3 Flashcards
What is inflammation?
Inflammation is a non-specific, dynamic, local physiological tissue response to injury, infection, or cell death. It aims to restrict damage, remove the causative agent, allow immune access, and initiate repair.
What are the two main types of inflammation?
Acute Inflammation – Initial, transient response.
Chronic Inflammation – Prolonged, follows acute inflammation if the cause persists.
What are the key aims of the inflammatory response?
Restrict damage or infection to a localized area.
Remove the causative agent and damaged tissue.
Allow immune cells and molecules to access the site.
Initiate tissue repair.
What are the cardinal signs of acute inflammation?
Redness (rubor)
Heat (calor)
Swelling (tumor)
Pain (dolor)
Loss of function (functio laesa)
What are the major cellular players in inflammation?
Neutrophils (acute inflammation)
Macrophages (chronic inflammation)
Mast cells (release histamine)
Lymphocytes and plasma cells (chronic immune responses)
What are the main causes of acute inflammation?
Infection, physical trauma, toxins, ischemia, and immune reactions.
What is oedema?
An accumulation of fluid in tissues due to increased vascular permeability.
Which cell type dominates in the first 24 hours of acute inflammation?
Neutrophils.
What triggers mast cells to release histamine?
Injury, IgE cross-linking, complement components (C3a, C5a), and physical stimuli.
What are the major mediators of acute inflammation?
Histamine – Vasodilation, increased permeability.
Arachidonic acid derivatives (prostaglandins, leukotrienes) – Inflammation regulation.
Platelet-activating factor (PAF) – Leukocyte activation.
Nitric oxide (NO) – Vasodilation, microbial killing.
Cytokines (IL-1, TNF-α, IL-6, CXCL8, IL-12) – Coordinate immune response.
What is the function of IL-1β?
Local effects: Activates vascular endothelium, lymphocytes, tissue destruction, and increases effector cell access.
Systemic effects: Induces fever and IL-6 production.
What is the function of TNF-α?
Local effects: Increases vascular permeability, allowing IgG and complement entry.
Systemic effects: Fever, metabolite mobilization, and shock.
What is the function of IL-6?
Local effects: Activates lymphocytes and increases antibody production.
Systemic effects: Fever and acute-phase protein production.
What is the function of CXCL8 (IL-8)?
Recruits neutrophils, basophils, and T cells to infection sites.
What is the function of IL-12?
Activates NK cells and induces CD4 T-cell differentiation into TH1 cells.
What are the four plasma enzyme cascade systems in acute inflammation?
Complement system.
Coagulation factors.
Kinin system.
Fibrinolytic system.
What are the three main pathways of complement activation?
Classical pathway.
Alternative pathway.
Lectin pathway.
What are C3a and C5a?
Anaphylatoxins that increase vascular permeability and recruit immune cells.
What does bradykinin do?
Increases vascular permeability and mediates pain.
What is plasmin’s role in inflammation?
Breaks down fibrin, affecting vascular permeability and complement activation.
What are the four steps of neutrophil migration?
Margination – Leukocytes move to vessel edges.
Adherence – Leukocytes stick to endothelium.
Emigration – Leukocytes exit blood vessels.
Chemotaxis – Leukocytes migrate to injury sites.
What are selectins?
Adhesion molecules that mediate rolling of leukocytes on endothelium.
What is ICAM, and what does it do?
Intercellular adhesion molecule; helps leukocytes bind firmly to endothelium.
What is the role of sialyl Lewis-X?
Binds to selectins for leukocyte rolling.
What is the function of LFA-1?
Integrin that binds to ICAM for firm leukocyte adhesion.
What are the steps of phagocytosis?
Recognition and attachment.
Internalisation.
Phagosome formation.
Phagolysosome fusion.
Digestion and waste release.
Which cells carry out phagocytosis?
Neutrophils and macrophages.
What causes chronic inflammation?
Persistent infection, autoimmune disease, prolonged exposure to toxins.
What are the primary cells in chronic inflammation?
Macrophages, lymphocytes, plasma cells.
What is a giant cell?
A large, multinucleated cell formed by macrophage fusion.
What do circulating monocytes become?
Macrophages in tissues.
What are the hallmarks of chronic inflammation?
Tissue destruction, persistent immune activation, simultaneous healing attempts.
What is granulomatous inflammation?
A distinct form of chronic inflammation featuring granulomas.
What is a granuloma?
A small cluster of activated macrophages (epithelioid cells) surrounded by lymphocytes.
What is the significance of Langhans giant cells?
They are multinucleated macrophages found in tuberculosis granulomas.
Name diseases caused by chronic inflammation.
Rheumatoid arthritis, inflammatory bowel disease, allergies, silicosis.
How does chronic inflammation cause tissue damage?
By releasing pro-inflammatory cytokines, proteases, and reactive oxygen species.
What is the consequence of prolonged neutrophil activity?
Excessive tissue damage and impaired healing.
What is the role of nitric oxide in inflammation?
Vasodilation, microbial killing, and immune regulation.
What are the effects of platelet-activating factor (PAF)?
Platelet aggregation, leukocyte activation, and increased permeability.
Which mediators increase vascular permeability?
Histamine, kinins (e.g., bradykinin), prostaglandins (PGE2, PGF2, PGD2), fibrin breakdown products (FDPX, Y, D, E), nitric oxide (NO)
What are the primary cellular players in acute inflammation?
Neutrophils are the primary cells in the first 24 hours, recruited due to local chemotaxins like IL-8, C3a, and C5a. Mast cells also play a critical role in early inflammation.
What are the four plasma-derived enzymatic cascade systems involved in acute inflammation?A:
Complement system
Coagulation system
Kinin system
Fibrinolytic system
What adhesion molecules mediate leukocyte adherence to endothelial cells?
Selectins (P-selectin, E-selectin) mediate rolling adhesion; integrins (LFA-1, CR3) mediate tight adhesion by binding to ICAM-1, ICAM-2, and VCAM-1.
hat are the steps of phagocytosis? Which cells can carry it out?
Recognition and attachment (via opsonins like C3b)
Internalisation (formation of a phagosome)
Fusion (phagosome merges with lysosome)
Digestion (destruction of internalized material)
Release (removal of digested products)Cells: Neutrophils and macrophages.
