Inflammation Flashcards
What are the four key responses of inflammation, and why are they important?
How can inflammation both promote healing and cause tissue damage?
What is the difference between an inflammatory stimulus and an inflammatory mediator?
How do the time course and key cellular players differ between acute and chronic inflammation?
What is the primary function of neutrophils in acute inflammation?
What are some common causes of chronic inflammation?
How does the immune response contribute differently to acute and chronic inflammation?
What is the role of mast cells in inflammation, and what mediator do they release?
How do monocytes and macrophages contribute to the inflammatory response?
What is the function of endothelial cells in inflammation?
How do plasma proteins such as complement and clotting factors contribute to the inflammatory response?
What are the roles of cytokines in inflammation?
What are Pattern Recognition Receptors (PRRs), and what do they detect?
How do PAMPs and DAMPs differ in their role in inflammation?
What are Toll-like receptors (TLRs), and what types of structures do they recognize?
How do inflammasomes detect cell damage?
What happens when PRRs detect a pathogen or cell damage?
What are the key vascular changes that occur during inflammation?
How does vasodilation contribute to the cardinal signs of inflammation?
What causes increased vascular permeability, and what effect does this have?
What is stasis, and how does it facilitate leukocyte recruitment?
What are the five steps of leukocyte recruitment, and what molecules are involved in each step?
How do selectins contribute to leukocyte rolling?
What role do integrins play in firm adhesion?
What is diapedesis, and what molecule facilitates it?
What types of molecules guide leukocytes to the site of injury via chemotaxis?
How does vasodilation contribute to heat and redness?
Why does inflammation lead to swelling?
What are the two main causes of pain in inflammation?
Why does inflammation sometimes cause a loss of function?
How do Pattern Recognition Receptors (PRRs), like TLRs and inflammasomes, contribute to the inflammatory response?
What are the main vascular changes that occur during the early stages of inflammation?
Describe the process of leukocyte recruitment during inflammation. What are the key steps involved?
How does margination facilitate leukocyte recruitment to the site of injury?
What role does chemotaxis play in leukocyte migration, and what are the key signals involved in this process?
Explain the process of phagocytosis from the initial recognition of a pathogen to its removal.
What is the function of the phagosome, and how does it differ from the phagolysosome?
How do lysosomal enzymes contribute to the degradation of pathogens inside a phagocyte?
What is the role of actin in the process of phagocytosis?
Describe the process of reactive oxygen species (ROS) generation during respiratory burst and its role in killing pathogens.
How do reactive nitrogen species (RNS), like peroxynitrite, contribute to pathogen killing?
What is the function of lysosomal enzymes in killing and degrading pathogens? Provide examples of specific enzymes involved.
How does phospholipase contribute to the breakdown of microbial cell membranes during the killing process?
Why can the inflammatory response sometimes lead to tissue injury rather than healing?
What are some mechanisms by which leukocytes can cause bystander damage during an inflammatory response?
How can misdirected immune responses, such as in autoimmune diseases, lead to tissue injury?
Explain how the rupture of the phagolysosome can lead to tissue damage, using urate crystals as an example.
What happens during the resolution of inflammation, and why is it important for minimizing tissue damage?
How does chronic inflammation develop, and what role does the persistence of the offending agent play?
What is the relationship between significant tissue destruction and the development of fibrosis or scarring?
What are the cellular events that contribute to tissue repair and scar formation during inflammation?
