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145 Cards in this Set
- Front
- Back
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What are the 5 cardinal signs of acute inflammation?
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1. Red (rubor)
2. Swelling (tumor) 3. Warm (calor) 4. Tender (dolor) 5. Loss of fxn (functio laesa) |
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What are characteristics of acute inflammation?
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1. Edema in tusses due to vascular response
2. Influx of neutrophils 3. Influx of monocytes/macrophages **Anytime you see neutrophil influx, think acute inflammation |
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In a parasitic infection, what type of cells would you see?
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See eosinophils instead of neutrophils
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What type of cells are see in mircobacterium/fungi infections?
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This is more of a chronic lesion, so would see more macrophages and fewer of neutrophils
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What is the general sequence of events in acute inflammation?
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Edema -> neutrophils -> macrophages
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What is pavementing?
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Endothelium appears to be lines by white cells
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With injury, where do changes occur?
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in the neutrophil AND in the endothelial cells
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What molecules are responsible for the rolling of neutrophils?
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Selectins are expressed on the sruface of endothelial cells
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How long does it take for an acute inflammatory reaction to occur?
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Within a few minutes to an hour after the insult
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What is the general problem that occurs in Chediak-Higashi syndrome and diabetes mellitus?
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Both of these affect neutrophils so they lose their ability to actively bind, emigrate, and phagocytose and actively participate in the killing of the noxious stimulus
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What happens if you cant make C5?
What happens when you have immunoglobulin deficiency? |
Cant make C5 then you wont have C5a once complement is activated
W/o the the Ab-Ag complex, you wont stimulate the complement cascade, so you wont get the C5a |
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What occurs if you have an increase in C5 inactivators?
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have compounds in blood that inhibit complement 5, which leads to not having C5a which means you cant have chemotaxis
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What are the 3 distinct steps in phagocytosis and degranulation?
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1. Recognition
2. Attachment 3. Engulfment |
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What are some receptors used in recognition/attachment step of phagocytosis?
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mannose receptor, MAC-1 integrin, and the scavenger receptor
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What is the role of inducible nitric oxide synthase?
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Found in macrophages and can bind to free radicals to give you peroxynitrite, which can lead to death/destruction of the material
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What is HOCl?
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bleach
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Where are the majority of chemical mediators synthesized?
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liver
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What substance keeps inflammation in check? How do they work?
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steroids
they inhibit phosphlipases, which are the very first steo in break down phospholipids into arachidonic acid, which can either go to prostaglands or leuketrienes |
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What does the cyclo-oxygenase pathway result in?
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production of prostaglandins
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Name substances that can inhibit the cyclo-oxygenase pathway?
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COX1, COX2, aspirin, indomethacin
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Define transudate.
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fluid is low in protein and has a specific gravity that is less than 1.012
It's an indication of a mild inflammatory rxn |
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What is the purpose of the red-top tube.
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Instead of testing the specific gravity.. one can see if the liquid coagulates. IF it does then its an exudate; if there is no clotting then its a transudate
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Define exudate.
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Fluid composed of plasma proteins that clots -- composed mainly of plasma proteins and clotting factors
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Describe serous exudates.
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blister in thermal burn
Serous = aren't many blood cells because there is no infectious component Usually have bad damage to the blood supply in that area that although its mostly just fluid, serum has high enough protein levels to be considered an exudate |
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Describe fibrinous exudate.
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made up of fibrin--soluble protein within the blood
fibrin comes out of the blood into the tissue or space within the body |
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Describe purulent exudate.
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abcesses are good examples of purulent exudates
WBCs, serum, bacteria, and dead WBCs all mixed together |
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Describe eosinophilic exudate. When is it often seen?
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IgE mediated
asthma and parasitic infections mainly see eosinophils |
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Describe hemorrhagic exudate. What is a common cause?
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rickettsial
Organisms that damage the blood vessels so you get inflammatory cells plus blood due to hemorrhage |
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Describe pseudomembranous exudates.
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There is damage to the whole layer of endothelium. The whole layer dies and because of that damage to the epithelial layer, you get damage to the underlying blood vessels so you get the serum that comes out
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Define edema.
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excess fluid in the interstitial tissue, usuyally serous fluid
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Define ascites.
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edema fluid inside the abdominal cavity
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Define pus.
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purulent exudate which is rich in leukocytes
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What is inflammation?
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the response of vascularized living tissue to injury
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What are the 2 main components of inflammation?
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1. Vascular wall response
2. Inflammatory cell response |
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How are the effects of inflammation mediated and terminated?
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Effects mediated by circulating plasma proteins and by factors produced locally by vessel wall or inflammatory cells
Terminated when offending agent is eliminated and the secreted mediators are removed |
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Give the characteristics of acute inflammation.
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early onset (seconds to mins)
short duration (mins to days) involving fluid exudate (edema) Neutrophil emigration |
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Give the characteristics of chronic inflammation.
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later onset (days)
longer duration (weeks to years) involving lymphocytes and macrophages inducing blood vessel proliferation and scarring |
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What are the 4 classical signs of inflammation (most prominent in acute inflammation)?
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Heat (calor)
Redness (rubor) Pain (dolor) Edema (tumor) Loss of fxn may also be considered a sign |
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Define Edema.
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excess fluid in interstitial tissue or body cavities, may be either an exudate or transudate
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Define exudate.
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An inflammatory extravascular fluid that has a high protein concentration and cellular debris
specific gravity above 1020 |
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Define exudation.
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extravasation of fluid, proteins, and blood cells from vessels into the interstitial tissue or body cavities
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Define Pus
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A purulent inflammatory exudate rich in neutrophils and cell debris
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Define transudate.
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extravascular fluid with low protein content and specific gravity below 1.012
essentially an ultrafiltrate of blood plasma resulting from elevated fluid pressures or diminished osmotic forces in the plasma |
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What are the 3 major components that contribute to causing the clinical signs of acute inflammation?
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1. Alterations in vascular caliber leading to increased blood flow (heat and redness)
2. Structural changes in the microvasculature, permitting plasma proteins and leukocytes to leave the circulation to produce inflammatory exudates (edema) 3. Leukocyte emigration from blood vessels and accumulation at the site of injury (edema and pain) |
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What are the 2 opposing forces that determine NORMAL fluid exchange in vascular beds?
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Hydrostatic pressure - causes fluid to move out of the circulation
Plasma colloid osmotic pressure - causes fluid to move into the capillaries |
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Describe vasodilation and how it affects vascular pressure?
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vasodilation causes increased flow into areas of injury, thereby increasing hydrostatic pressure
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Describe vascular permeability and how it affects vascular pressure?
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Causes exudation of protein rich fluid and decreases plasma osmotic pressure
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With an increase in hydrostatic pressure and a decrease in osmotic pressure, in which direction will fluid flow?
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It will flow out of the vascular beds
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What is stasis?
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It occurs when fluid loss causes concentration of red cells and increased blood viscosity, slowing the blood flow
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What are the different pathways that can cause increased vascular permeability?
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1. Formation of venule intercellular endothelial gaps
2. Direct endothelial injury 3. Delayed prolonged leakage 4. Leukocyte mediated endothelial injury 5. Increased transcytosis 6. Leakage from new blood vessels |
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What and how are venule intercellular endothelial gaps formed?
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Endothelial cells are induced to contract therey opening intercellular gaps.
Contraction is elicited by chemical mediators (histamine) and occurs rapid, is transient, and is reversible. Involves only small venules Can also be caused by cytokines (IL-1/TNF) but will be prolonged (4 to 6 hrs) and protracted (24 hrs or more) |
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How does direct endothelial injury cause increased vascular permeability?
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Severe necrotizing injury causes endothelial cell necrosis and detachment that affects venules, capillaries, and arterioles
Damage usually evokes immediate and sustained endothelial leakage |
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What is delayed prolonged leakage and how does it contribute to an increase in vascular permeability?
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Delayed prolonged leakage beings after a delay of 2 to 12 hours and may last for days.
Venules and capillaries are affected. Causes: thermal injury, x-rays, UV injury |
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What is leukocyte mediated endothelial injury and how does it contribute to an increase in vascular permeability?
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Results from leukocyte aggregation, adhesion, and emigration across the endothelium.
Leukocyte release of reactive oxygen species and proteolytic enzymes cause endothelial injury or detachment |
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What is increased transcytosis?
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Increased transcytosis means that transendothelial channels have formed by the interconnection of vessels from the vesiculovacuolar organelle.
Certain factors (vascular endothelial growth factor) induce vascular leakage by increasing the number of these channels |
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How does leakage from new blood vessels increase the vascular permeability?
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During repair, endothelial proliferation and angiogensis result in leaky vessels. This persists until the endothelium matures and intercellular jxns are formed.
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What is extravasation and what are the steps involved?
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Extravasation - leukocyte delivery to site of injury
1. Margination, rolling, and adhesion of leukocytes to the endothelium 2. Transmigration across the endothelium (aka diapedesis) 3. Migration in interstitial tissues toward a chemotactic stimulus |
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What are the major adhesion molecules involved in leukocyte adhesion and transmigration?
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Selectins (E, P, and L) - bind via lectin domains (sugar binding) to oligosaccharides (ie Sialyl Lewis X) on cell surface glycoproteins
Ig family molecules on endothelial cells - ICAM1 (intracellular adhesion molecule 1) and VCAM1(vascular cell adhesion molecule 1); these bind integrins on leukocytes Integrins on leukocytes bind to members of the Ig family molecules and to the extracellular matrix. The principal integrins that bind to ICAM-1 are the so called beta-2 integrins LFA-1 and Mac-1 (also called CD11a/CD18 and CD11b/CD18); the principal integrin that binds to VCAM-1 is the beta-1 integrin alpha-4::beta-1 (also called VLA4) |
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How do chemoattractants and chemokines affect adhesion and transmigration?
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by modulating the surface expression or avidity of the adhesion molecule
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Name the three mechanisms in which modulating molecules induce leukocyte adhesion in inflammation.
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1. Redistribution of preformed adhesion molecules to the cell surface
2. Induction of adhesion molecules on endothelium. 3. Increased avidity of binding |
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How does redistribution of preformed adhesion molecules to the cell induce leukocyte adhesion in inflammation?
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After histamine exposure, P selectin is rapidly translocated from the endothelial Weibel-Palade body membranes to the cell surface where it can bind leukocytes
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How are adhesion molecules induced to form on the endothelium?
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IL-1 and TNF increase endothelial expression of E-selectin, ICAM-1, and VCAM-1
Activated endothelial cells have increased leukocyte adherence |
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How is avidity increased in order to induce leukocyte adhesion in inflammation?
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Increasing avidity is most important for integrin binding
These integrins are normally present on leukocytes in a low affinity form. They are converted to high affinity binding by a variety of chemokines. Activation causes firm adhesion of the leukocytes to endthelium and is required for subsequent transmigration |
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What are the steps involved in neutrophil adhesion and transmigration in acute inflammation?
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1. Endothelial activation
2. Leukocyte rolling 3. Integrin activation and stable adhesion 4. Transmigration (diapedesis) |
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What interactions occur during transmigration?
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This is mediated by homotypic interactions between PECAM-1/CD31 on leukocytes and endothelial cells
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What type of leukocyte emigrates into a site of injury?
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Depends on the age of the inflammatory response and the original stimulus
Neutrophils predominate during the first 6 to 24 hours, then are replaced by monocytes after 24-48 hours |
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Why neutrophils invade an injured site first?
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Neutrophils are more numerous in the blood than monocytes, they respond more rapidly to chemokines, they respond more rapidly to the particular chemokines, and they attach more firmly to the particular ashesion molecular that are induced on endothelial cells at early points.
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Describe the process of chemotaxis.
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involves binding of chemotactic agents to specific leukocyte surface G protein couple receptors, which triggers phospholipase C, PIP kinase, and protein kinases
IP(3) --> DAG + PIP(2) Causes increase cytosolic calcium and GTPase activities that polymeriza actin and facilitate cell movement. |
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Name 4 things that chemotactic agents activate.
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1. Production of arachidonic acid metabolites
2. Degranulation and secretion of lysosomal enzymes 3. Cytokine secretion 4. Increased adhesion molecule expression and increased integrin avidity |
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What are the three steps involved in phagocytosis?
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1. Recognition and binding
--opsonins enhance phagocytosis efficiency by binding to leukocyte receptors 2. Engulfment by encircling pseudopods 3. Killing and degradation of phagocytosed particles -- accomplished largely by oxygen dependent mechanisms |
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What are 2 major opsonins?
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Ig Fc fragment and the complement fragment C3b
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What does the NADPH oxidase system do?
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converts oxygen to surperoxide anion and eventually producing hydrogen peroxide
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What is the fxn of myeloperoxidase?
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Converts hydrogen peroxide and chloride into bleach (HOCl)
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What is the difference between leukocyte adhesion deficiency type 1 and type 2?
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Type 1 - defective synthesis of beta-2 integrins
Type 2 - is due to a defect in the fucose metabolism causing loss of sialyl Lewis X (ligand for E and P selectin) |
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What is Chediak-Higashi Syndrome?
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Neutrophils have aberrant organellar fusion with defective lysosomal enzyme delivery to phagosomes
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What is granulamtous disease?
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Inherited defects in NADPH oxidase, leading to a defect to a defect in the respiratory burst, hydrogen peroxide production, and the MPO bactericidal mechanism
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What is the most common clinical cause of leukocyte defects?
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neutropenia cause by cancer chemotherapy or by metastatic tumor replacing normal bone marrow
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What are the first mediators in inflammation?
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histamine and serotonin -- they cause vasodilation and increased vascular permeability
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What stimulates mast cell release?
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physical agents, immune reactions involving IgE, complement fragments C3a and C5a, cytokines, and leukocyte derived histamine releasing factor
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What stimulates platelet release?
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contact with collagen, thrombin, adenosine diphosphate, antigen-Ab complexes, and platelet activating factor
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What is the most important step for the biologic functioning of complement?
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activation of the C3
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What activates the classical pathway?
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C3 cleavage by C3 convertase after fixation of C1 to antigen-Ab complexes
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What activates the alternative pathway?
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triggered by microbial surface molecules and complex polysaccarides
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What triggers the lectin pathway?
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Binding to microbial carbs
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What are anaphylatoxins?
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C3a and C5a
stimulate histamine release from mast cells and thereby increase vascular permeability and vasodilation C5a also activates the arachidonate metabolism causing additional inflammatory mediator release |
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How is complement activation regulated?
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cell associated (decay accelerated factor) and circulating (Chloride) regulatory protein
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What does a defect in DAF cause?
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Paroxysmal nocturnal hemoglobinuria - recurrent complement mediated red cell lysis and anemia
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What causes hereditary angioneurotic edema?
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chloride inhibitor deficiency
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What generates bradykinin?
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Plasma protein kininogens are cleaved by specific proteases called kallikreins to generate bradykinin
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What produces clotting factor XIIa?
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surface activation of Hageman factor and kallikrein
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What is the function of XIIa?
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converts plasma prekallikrein into kallikrein
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Describe the clotting system.
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Series of plasma proenzymes that can be activated by Hageman factor, resulting in the activation of thrombin, cleavage of fibrinogen, and generation of fibrin clot
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What is plasmin's function?
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plasmin degrades fibrin, thereby solubilizing the clot
Plasma also cleaves C3 to produce C3 fragments, forming fibrin split products that increase vascular permeability and activating Hageman factor |
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What are eicosanoids?
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lipid short range signaling molecules from membrane derived arachidonic acid
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What does Cyclooxygenase generate? What inhibits this pathway?
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prostaglandins and thromboxanes
Aspirin |
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What does lipoxygenase produce?
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leukotrienes and lipoxins
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What do prostaglandin I2(prostacyclin) and prostaglandin E2 cause?
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vasodilation
E2 also casues an increase in sensitivity to painful stimula and can mediate fever |
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What do the following cause:
thromboxane A2? Leukotrienes C4, D4, and E4? Leukotriene B4? Lipoxins? |
A2 - vasoconstriction
C4, D4, E4 - increase vascular permeability and vasoconstriction B4 - chemotactic agent lipoxins - negative regulators of leukotriene action |
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Which cells produce Platelet Activating Factor?
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mast cells and other leukocytes
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What does PAF cause?
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platelet aggregation and release, bronchoconstriction, vasodilation, increased vascular permeability, increased leukocyte adhesion, and leukocyte chemotaxis
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What are the major cytokines mediating inflammation? Where are they produced?
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TNK\F and IL-1
activated macrophages |
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What do TNF and IL-1 induce?
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endothelial activation, including induction of endothelial adhesion molecules and chemical mediators, enzymes associated with matrix remodeling, and increases in endothelial thrombogenicity
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Describe the acute phase response.
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fever, anorexia, lethargy, neutrophilia, release of corticotropin and corticosteroids, and hemodyname effects of septic shock
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How does TNF-alpha regulate body mass?
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it promotes lipid and protein mobilization and by suppressing appetite.
Sustained TNF production contributes to cachexia, a pathologic state characterized by weight loss and anorexia that accompanies some infections and neoplasias. |
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What are the 4 major classes of chemokines?
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1. CXC - recruit neutrophils - example is IL-8
2. CC - generally recruit monocytes, eosinophils, basophils, and lymphocytes but NOT neutrophils - example eotaxin recruits eosinophils 3. C - specific for lymphocytes 4. CX(3)C - fractalkine |
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Describe the fxn of the different forms of fractalkine.
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cell surface form - promotes firm lymphocyte and monocyte adhesion
soluble form is a chemoattractant for the same cells |
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What is the other name for nitric oxide?
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endothelium derived relaxation factor (EDRF)
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Describe the acute phase response.
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fever, anorexia, lethargy, neutrophilia, release of corticotropin and corticosteroids, and hemodyname effects of septic shock
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How does TNF-alpha regulate body mass?
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it promotes lipid and protein mobilization and by suppressing appetite.
Sustained TNF production contributes to cachexia, a pathologic state characterized by weight loss and anorexia that accompanies some infections and neoplasias. |
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What are the 4 major classes of chemokines?
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1. CXC - recruit neutrophils - example is IL-8
2. CC - generally recruit monocytes, eosinophils, basophils, and lymphocytes but NOT neutrophils - example eotaxin recruits eosinophils 3. C - specific for lymphocytes 4. CX(3)C - fractalkine |
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Describe the fxn of the different forms of fractalkine.
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cell surface form - promotes firm lymphocyte and monocyte adhesion
soluble form is a chemoattractant for the same cells |
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What is the other name for nitric oxide?
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endothelium derived relaxation factor (EDRF)
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What are the functions of NO in its local environment?
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1. Vasodilation
2. inhibit platelet aggregation and adhesion 3. kill certain microbes and tumor cells - via free radical formation |
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What is NO synthesized from?
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arginie, molecular oxygen, NADPH, and other cofactors by nitric oxide synthase (NOS)
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What are the three types of NOS?
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endothelial NOS
cytokine inducible NOS neuronal NOS |
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What are the expression patterns of NOS?
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eNOS and nNOS - constitutively expressed but become active only in the setting of increased cytoplasmic calcium
iNOS - synthesized by macrophages after induction by certain cytokines |
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What are the functions of each type of NOS?
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eNOS - maintaining vascular tone
iNOS - reduce leukocyte recruitment |
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What are the 2 types of granules found in neutrophils?
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1. smaller specific (for secondary) granules
2. larger azurophila (or primary) granules |
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What are the effects of reactive oxygen species?
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1. endothelial cell damage causing increased vascular permeability
2. inaactivation of antiproteases resulting in unopposed protease activity 3. injury to multiple cell types |
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What is the role of neuropeptides?
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play a role in initiating and propagating inflammatory responses
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What is Substance P?
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powerful mediator of vascular permeability, transmits pain signals, regulated blood pressure, and stimulates immune and endocrine cell secretion
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Describe the response to hypoxia.
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hypoxia alone can directly induce inflammatory response
largely mediated by the protein hypoxia induced factor 1 alpha produced by cells deprived of oxygen |
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Describe the response to necrotic cells.
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elicits inflammatory reactions designed to eliminate these cells.
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What are the outcomes of acute inflammation?
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1. Complete resolution with regeneration of native cells and restoration of normalcy
2. Healing by connective tissue replacement (fibrosis) occurs after substantial tissue destruction when inflammation occurs in non-regenerating tissues or in the setting of abundant fibrin exudation -- abcess formatino will be replaced by fibrosis 3. Progression to chronic inflammation |
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Describe serous inflammation.
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reflected by tissue fluid accumulation and indicates a modest increase in vascular permeability
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Describe fibrinous inflammation.
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marked increase in vascular permeability with exudates containing large amounts of fibrinogen
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Describe suppurative or purulent inflammation.
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production of purulent exudates (pus) consisting of leukocytes and necrotic cells
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Define an abcess.
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refers to a localized collection of purulent inflammatory tissue accompanied by lquefactive necrosis
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What are 3 reasons chronic inflammation can occur.
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1. Following an acute inflammation either because the inciting stimulus persists or because normal healing is somehow interrupted
2. From repeated bouts of acute inflammation 3. Most commonly as low grade, smoldering response without prior acute inflammation |
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Describe the characteristics of chronic inflammation.
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1. infiltration with mononuclear inflammatory cells
2. tissue destruction 3. attempts at healing by connective tissue replacement, accomplished by vascular proliferation (angiogenesis), and fibrosis |
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Activated T lymphocytes activate what?
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activate monocytes and macrophages which then activate T and B lymphcyte function
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Eosinophils are recruited in what type of infection? Their granules contain what susbtance?
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parasitic infection
Contain major basic protein - a cationic molecule that is toxic to parasites but also lyses mammalian epithelium |
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What is a granuloma?
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focal accumulations of activated macrophages
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What are epitheloid macrophages?
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macrophages that have been activated and become enlarged and flattened
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In granulomatous inflammation, describe the epitheloid macrophages.
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they are surrounded by a collar of lymphocytes elaborating factors necessary to induce macrophage activation
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What are giant cells?
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activated macrophages that fuse
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What are immune granulomas?
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formed by T cell mediated responses to persistent antigens
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What causes macrophage transformation to epitheloid cells and multinucleate giant cells?
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interferon gamma
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What is the prototypical immune granuloma caused by?
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tuberculosis bascillus
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What is the name for when lymphatics become inflamed? when draining lymph nodes become inflamed?
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lymphangitis
lymphadenitis |
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Systemic changes associated with inflammation are collectively called?
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acute phase response - or in severe cases the systemic inflammatory response syndrome (SIRS)
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What are the clinical and pathologic changes associated with acute phase response?
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1. Fever - 1-4 degrees in response to pyrogens
2. Acute phase proteins - plasma proteins that increase several hundred fold - CRP, fibrinogen, and serum amyloid A (SAA) 3. Leukocytosis 4. Others: increased BP, decr sweating, shivering, chills, anorexia, etc |
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What is the clinical triad associated with septic shock?
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1. disseminated intravascular coagulation
2. hypoglycemia 3. Cardiovascular failure |
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What are pyrogens?
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substances that stimulate prostaglandin synthesis in the hypothalamus
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What is leukocytosis? How does it occur?
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increased white cell number in peripheral blood
occurs by accelerated release of bone marrow cells, typically with increased numbers of immature neutrophils (shift to left) |
