You are in browse mode. You must login to use MEMORY

level: Level 1

Questions and Answers List

level questions: Level 1

Question	Answer
Infections	Most common cause of inflammation
Pain	Dolor
Response of a living thing to trauma (inflammation)	Vital Reaction
increased blood in an organ or other body part	Hyperemia
Mediators of inflammation	Humoral Response
Movement of WBC's	Cellular Response
Stacking of RBC's	Rouleaux formation
Neutrophils lining up/adhering to endothelium	Margination
Movement of WBC'S out of blood vessels towards the site of tissue damage	Diapedesis
Neutrophils	polymorphonuclear cells
Cells on the interior surface of blood vessel	Endothelial cells
found in blood and involved in blood clotting	Platelets
Early in inflammatory response, released quickly from platelets and mast cells.	Histamine
Found in numbers of connective tissue. Releases histamine + serotonin	Mast cells
Induces distillation and increased permeability. Chemotatic agents for phagocytes.	Bradykinin
Synthesis of Bradykinin (increased permeability), Plasmin, (fibrinolysis or clot remodeling), Fibrin (formation of a clot) complement system activation.	Hageman Factor
A group of 9 plasma proteins produced by liver, circulating in an inactive form. Stimulate: histamine release, attract neutrophils by chemotaxis, promote phagocytosis and cell lysis.	Complement system
One of the 3 ways complement system can occur. Antibody/antigen complexes in an immune reaction	Classical pathway
One of the 3 ways complement system occurs. Plasma carbohydrate binding protein.	Lectin pathway
The common ending of the 3 pathways of complement system. Destroys cells drilling holes into plasma membrane. Act on leukocytes and endothelial cells.	membrane attack complex
An antibody that attaches to foreign microorganisms making them more susceptible to phagocytosis of bacteria.	Opsonin
Histamine release with increased vessel wall permeability	Anaphylaxis
Derived from phospholipids of the plasma membrane. Becomes active through phospholipase. Metabolized through 2 pathways. Lipoxygenase pathway and cyclooxygenase pathway.	Arachidonic acid
Metabolite of Arachidonic acid. Promote Chemotaxis of neutrophils, vascular permeability, bronchospasm (airway)	Leukotrienes
Platelet aggregation, thrombosis	Thromboxane
Opposes effects of thromboxane	Prostacyclin
Smooth muscle contraction to slow blood flow down (so inflammatory reaction can take place) creates pain, fever.	Prostaglandins
Due to increased permeability of vessel wall. Increased hydrostatic pressure. Fluid leakage into interstitial tissue called Exudate. Leakage of plasma from vessels into interstitial spaces.	Emigration of WBC'S
One of 2 ways an excess of fluid in tissues may occur. Cauces increaed hydrostatic pressure within capillary. Decreased osmotic pressure (decreased protein blood)	Transudate
One of 2 ways an excess of fluid may develop. Fluid and protein leakage. Vasodilation and stasis. increased interendothelial spaces.	Exudate
Present in later stages of inflammation. 2-3% WBC's. Respond after PMN's. Slower reacting. arriving 2-3 days after injury. Phagocytic, Bactericidal. Prominent in allergic reactions such as asthma, hay fever.	Eosinophils
Less than 1% of WBC'S. Prominent in allargic reactions. Precursors of mast cells. Granules containing histamine and heparin (anticoagulant)	Basophils
Secreted by macrophages. A mediator that attracts more platelets.	Cytokines
Present in later stage of inflammation. Derived from monocytes. secrete mediator cytokines. live longer and appear in chronic inflammation.	Macrophages
seen in chronic inflammation. part of immune response.	Lymphocytes
An immediate reaction to injury. Sudden onset, short duration. Typically mediated by neutrophils.	Acute inflammation
Defined by it's duration (lasts a long time) Onset cannot be established. Mediated by macrophages, lymphocytes, plasma cells. Often involves other cell types and tissue components involved with tissue repair (fibroblasts, angioblasts)	Chronic inflammation
Infection in bloodstream	Bacteremia
Toxins in bloodstream	Toxemia
Systemic inflammatory response syndrome	Sepsis
Early stage of most inflammation. Viral infection. Joint swelling in rheumatoid arthritis. Mildest form of inflammation. Lesions heal without permanent consequences.	Serous Inflammation
Exudate rich in fibrin. indicative of severe inflammation, bacterial infections. does not resolve as easily as serous inflammation. Macrophages invade exudate, lyse. Fibrin and thrombi.	Fibrous inflammation
Caused by pus forming bacteria.	Purulent inflammation
Accumulation of pus in organ or tissues. Localized in purulent inflammation.	Abscess
Forms a tract connecting the abscess to the skin, allowing drainage of pus outside the body.	Sinus
An inflammatory tract that connects 2 hollow organs or a hollow organ with the skin.	Fistula
Happens when there is inflammation of body surfaces, stomach or intestines. Involves epithelium but may affect deeper tissues.	Ulceration
Form of ulcerative inflammation but has fibrino-purulent exudation. Includes mucus, cellular debris, fibrin, pus.	Pseudomembranous inflammation
Form when the immune system attempts to wall off substances it percieves as foreign but is unable to eliminate. Consists of lymphocytes, macrophages, multinucleated giant cells.	Granulomatous inflammation
Thermorgulator	Endogenous pyrogens
Non specific symptoms: fatigue, weakness, depression, lack of appetite, exhaustion.	Constitutional symptoms