NSAIDs Flashcards
a physiological response to tissue injury and infection
inflammation
other term for inflammation
inflammatory response
T or F: inflammation is not a synonym for infection
True
Mediate response to inflammation
vascular diameter, vascular permeability
increases blood flow to the area of injury, resulting in the heating and reddening of the tissue
vascular diameter (vasodilation)
allows leakage of fluid from the blood vessels into the damaged tissue, resulting in swelling (edema)
vascular permeability
when will NSAIDs be used
when inflammation is CHRONIC
During chronic inflammation - leukocytes arrive at the site of injury to _________ the invading pathogens and release __________
phagocytize; soluble mediators
soluble mediators released during chronic inflamm
cytokines, prostaglandins, leukotrienes
response to tissue injury
Acute inflamm
leading to progressive tissue destruction, as seen in chronic infections, autoimmunity, and certain cancers
Chronic inflamm
T or F: chronic inflamm can lead to autoimmunity and cancers
True
Type of inflamm wherein clotting and kinin systems are activated
Acute
fibrin strands to form clots, limiting the spread of infection into the blood
Clotting systems
Clotting systems - ________ strands to form clots, limiting the spread of infection into the blood
fibrin
Kinin system results in the production of ____________
bradykinin
a peptide that induces vasodilation and enhanced vascular permeability
bradykinin
dominate the landscape during acute inflammation
Non-protein–based soluble factors
represent a diverse family of lipid mediators with fundamental roles in physiology and disease
Eicosanoids
results from continuous exposure to the
offending element.
Chronic inflammation
Due to _____________, autoimmune diseases in which self-antigens continuously activate T cells, and cancers.
pathogen persistence
Hallmark of chronic inflammation
the accumulation and activation of macrophages and lymphocytes and fibroblasts
primary factors of chronic inflammation
Cytokines, chemokines, growth factors, and secreted/released enzymes, and ROS
The treatment of patients with inflammation involves two primary goals:
the relief of symptoms (NSAIDS) and the maintenance of function, slowing or arrest of the tissue-damaging processes is desirable, and
disease-modifying drugs (DMARDs) are necessary.
the most abundant of the eicosanoid precursors
Arachidonic acid (AA) (5,8,11,14-eicosatetraenoic acid)
an essential fatty acid, is converted to linolenic acid, followed by conversion to AA. (omega-6-fatty acid)
Linoleic acid
Major Effects of PG Synthesis Inhibition
- Analgesia
- Antipyresis
- Anti-inflammatory
- Anti-thrombotic
- Closure of Ductus Arteriosus
generates prostanoids for “housekeeping” functions such as gastric epithelial cytoprotection
COX-1
is the major source of prostanoids in inflammation and cancer.
COX-2
All NSAIDs inhibit
PG synthesis
Prostaglandin, prostacyclin (PG1) and thromboxane (TXA2) are produced from _____________
Arachidonic acid
The enzyme responsible for NSAIDs is ______________ also known as cyclooxygenase or COX
prostaglandin synthase
COX in 2 forms:
constitutive COX-1 and inducible COX 2
NSAIDs ADR for CNS
Headaches, tinnitus, dizziness, and rarely aseptic meningitis.
NSAIDs ADR for Cardiovascular
Fluid retention, hypertension, edema, and rarely myocardial infarction and congestive heart failure (CHF).
Gastrointestinal ADR of NSAIDs
Abdominal pain, dyspepsia, nausea, vomiting, and rarely ulcers or bleeding
Hematologic ADR of NSAIDs
Rare thrombocytopenia, neutropenia, or even aplastic anemia.
Hepatic ADR of NSAIDs
Abnormal liver function test results and rare liver failure.