Inflammation

Flashcard Set: Inflammation

Card 1 (Front): What is the primary nature of inflammation (local or systemic)?

Card 1 (Back): Inflammation is mostly a local tissue phenomenon, but there are systemic responses to inflammation.

Card 2 (Front): What is the main purpose of the inflammation phase?

Card 2 (Back): To ensure the injurious substance is neutralized or removed, and to set in motion events for tissue reconstitution.

Card 3 (Front): What are the two basic components of inflammation?

Card 3 (Back): Plasma and white blood cells.

Card 4 (Front): Can inflammation always be beneficial?

Card 4 (Back): No, inflammation and repair can be harmful in certain circumstances, acting as a double-edged sword.

Card 5 (Front): What usually initiates the repair process and inflammation?

Card 5 (Back): Injury to cells, including damage and microbial injury.

Card 6 (Front): What are DAMPs and MAMPs? What recognizes them?

Card 6 (Back): Damage associated molecular patterns (DAMP) and microbial associated molecular patterns (MAMP) are released upon injury and microbial invasion. They are recognized by Toll-like receptors (TLR), C-type lectin receptors (CLR), and other receptors on macrophages, dendritic cells, and neutrophils.

Card 7 (Front): What is the result of DAMP/MAMP recognition?

Card 7 (Back): The release of inflammatory cytokines.

Card 8 (Front): What is plasma in the context of inflammation? What is serum?

Card 8 (Back): Plasma is the fluid fraction of blood including proteins, nutrients, and water. Serum is the liquid component after coagulation proteins are removed.

Card 9 (Front): Name the five main types of white blood cells involved in inflammation.

Card 9 (Back): Neutrophils, monocytes, platelets, eosinophils, and lymphocytes.

Card 10 (Front): What is the role of blood vessels, especially the endothelium, in inflammation?

Card 10 (Back): Blood vessels are extremely important, and the endothelium has a major function in the inflammatory reaction.

Card 11 (Front): Name important connective tissue cells and components involved in inflammation.

Card 11 (Back): Fibroblasts, mast cells, resident macrophages, and structural proteins.

Card 12 (Front): What is the typical duration of acute inflammation? What are its dominant components?

Card 12 (Back): Typically lasts minutes to days, dominated by plasma and neutrophils.

Card 13 (Front): What are the three main components of acute inflammation? [See Previous Conversation]

Card 13 (Back): Vascular changes (increased blood flow), increased permeability of the microvasculature (fluid exudation), and cellular changes (leukocyte emigration and accumulation) [See Previous Conversation].

Card 14 (Front): What are the cardinal signs of inflammation and their physiological basis? [See Previous Conversation]

Card 14 (Back): Rubor (redness) and calor (heat) (increased blood flow), tumour (swelling) (fluid exudation), dolor (pain) (nerve stimulation by mediators), and loss of function [See Previous Conversation].

Card 15 (Front): Describe the process of leukocyte emigration.

Card 15 (Back): Involves margination and rolling, adhesion (via selectins and integrins), and transendothelial migration (diapedesis). Chemotaxis then attracts leukocytes to the injury site.

Card 16 (Front): How long does chronic inflammation typically last? What are its dominant cells and a key feature?

Card 16 (Back): Goes on for a long time, dominated by mononuclear cells (macrophages, plasma cells), and characterized by proliferation of mature tissue such as fibrous tissue (fibrosis).

Card 17 (Front): When does chronic inflammation typically occur?

Card 17 (Back): After acute inflammation fails to heal, with repeated acute inflammation, insidious smouldering reactions, immune reactions, and autoimmunity.

Card 18 (Front): What is granulomatous inflammation? What are its key cellular components?

Card 18 (Back): A subtype of chronic inflammation dominated by activated macrophages with lymphocytes and usually multinucleated giant cells.

Card 19 (Front): What is the hallmark of granulomatous inflammation?

Card 19 (Back): The formation of a granuloma.

Card 20 (Front): What type of hypersensitivity reaction is involved in granulomatous inflammation? What are the key lymphocytes?

Card 20 (Back): Type 4 hypersensitivity reaction, involving CD4 or T-helper lymphocytes.

Card 21 (Front): What is the function of these T-helper lymphocytes in granulomatous inflammation? What are the effector cells?

Card 21 (Back): They recognize antigen and release lymphokines that activate macrophages, which are the effector cells.

Card 22 (Front): What are chemical mediators (chemokines) of inflammation? Where do they originate?

Card 22 (Back): Chemicals that orchestrate, control, and resolve inflammation. They originate from plasma or cells.

Card 23 (Front): Give examples of vasoactive amines and their primary effects.

Card 23 (Back): Histamine (from mast cells) is vasodilatory and increases permeability.

Card 24 (Front): Name three types of plasma proteases involved in inflammation.

Card 24 (Back): Complement, kinins, and proteins of the coagulation cascade.

Card 25 (Front): What is the precursor for arachidonic acid metabolites? What enzyme releases it? What are the two main pathways and their products?

Card 25 (Back): Phospholipid in the cell membrane. Released by phospholipase A. Metabolized by cyclooxygenase to form prostaglandins, and by lipoxygenase to form leukotrienes.

Card 26 (Front): What are cytokines? Give examples important in inflammation.

Card 26 (Back): Polypeptide products of cells that modulate other cells. Examples include interleukin (IL) 1 and tumour necrosis factor (TNF).

Card 27 (Front): What are systemic factors that modulate healing?

Card 27 (Back): Age, malnutrition (Vitamin C, zinc, amino acids), haematological abnormalities (neutropenia, haemophilia), diabetes mellitus, corticosteroids, cytotoxic chemotherapy.

Card 28 (Front): What are local factors that modulate healing?

Card 28 (Back): Blood supply, infection, foreign bodies (including implants).

Card 29 (Front): What is the acute phase response? What is its underlying mechanism?

Card 29 (Back): Systemic effects of inflammation. It involves the release of cytokines into the blood.

Card 30 (Front): Name some common manifestations of the acute phase response.

Card 30 (Back): Fever (pyrexia), secretion of acute phase proteins by the liver, increased production of glucocorticoids (cortisol), autonomic nervous reaction (increased heart rate/blood pressure), clinical signs (shivering, malaise, etc.).

Card 31 (Front): What is leukocytosis? Which cytokines drive it?

Card 31 (Back): Increased number of leukocytes in the blood, driven by IL-1 and TNFα.

Card 32 (Front): What conditions are associated with neutrophilia, eosinophilia, and lymphocytosis?

Card 32 (Back): Neutrophilia: infections. Eosinophilia: allergic conditions (asthma, hay fever), parasitic infections. Lymphocytosis: some viral diseases (mononucleosis).

These flashcards cover the key concepts of inflammation from the provided sources. You can expand on these with more specific details as needed for your studying.