07- NSAIDS Flashcards
analgesic
is any member of the group of drugs used to achieve analgesia, or relief from pain (painkiller)
-accomplished by NSAIDs through reduction of PGE2 and PGI2 induced hyperalgesia and general reduced inflammation (not effective against non-inflammatory pain
anti-platelet
drugs that decrease platelet aggregation and inhibit thrombus formation
-NSAIDs inhibit platelet COX-1 (no COX-2)
antipyretic
are substances that reduce fever
-antipyretics cause the hypothalamus to override an PGE2-induced increase in temperature
gastric effects
histamine activation of H2 receptors in mucosal lining of stomach leads to increased acid production, pepsin, and intrinsic factor
-leads to mucosal erosion and ulceration
arachidonic acid
the substrate for production of lipid mediators of inflammation (prostaglandins produced by cyclooxygenase, or leukotrienes produced by lipoxygenase)
- cyclooxygenase inhibited by NSAIDS
- lipoxygenase inhibited by Zileuton (Zyflo)
cyclooxygenase (COX)
produces prostaglandins which are lipid mediators of inflammation
-inhibited by NSAIDS
dyspepsia
indigestion, upper abdominal pain, bloating, nausea
-common symptom of chronic NSAID use
eicosanoids
prostanoid and leukotriene derivatives of C-20 fatty acids
Fc Domain
area of an antibody protein that does not change
-this area does not bind to antigen (variable region is specific for and binds antigens)
humanized antibody
also know as chimeric antibody
- graft ligand binding domain from animals onto backbone of fully human antibody
- has same function as a fully human antibody with out resistance produced from animal antibodies
leukocytes
cell that circulates in the blood and body fluids and is involved in counteracting foreign substances and disease; a white (blood) cell
-several types including lymphocytes, granulocytes, monocytes, and macrophage
mast cells
a cell filled with basophil granules, found in numbers in connective tissue and releasing histamine and other substances during inflammatory and allergic reactions
-most dense in tissue with higher chance of injury such as mouth, nose, hands/feet, blood vessels, GI mucosa
motion sickness
triggered by histamine activation of H1 receptors in the emetic center of the CNS
phospholipase A2 (PLA2)
hydrolyzes phosphatidylcholine in plasma membrane to release free arachidonic acid (AA)
- eventually leads to production of lipid mediators by AA
- activity inhibited by annexins (aka lipocortins) (annexin expression increased by glucocorticosteroids)
phospholipase C (PLC)
activates signaling pathways that increase Ca+2 mobilization and promote fusion of cytoplasmic vesicles with the plasma membrane and extracellular release of their contents (degranulation)
- stored mediators (e.g., histamine) are released in response to PLC activation
- inhibited by agents such as cromolyn (Intal) and nedocromil (Tilade)
prostaglandin
lipid compounds that play a major role in initiation and mediation of inflammatory response
-formed by cyclooxygenase and can be inhibited by NSAIDs and glucocorticosteroids
prostanoid
synthesized by cyclooxygenase
- short half-lives and lack of stored products make activity synthesis dependent
- membrane permeable and passively released from other cells
- have autocrine and paracrine activity
- can effect blood vessels, smooth muscles, platelet aggregation, pain response, and body temperature