NSAIDs & Non-Opiod Analgesics Flashcards
test 4
NSAIDs =
Nonsteroidal anti-inflammatory drugs
T/F: steroids are anti-inflammatory
T
Why is acute inflammation beneficial?
Gets blood to cells: oxygen nutrients, and WBC to area of injury
What do WBC do?
Help clear out infection
What are the mediators involved in the autocoid group? Which one does NSAIDs target?
Histamine
serotonin
bradykinin
prostaglandins
leukotrienes
Prostaglandins
Which is more problematic: acute or chronic inflammation? Why?
Chronic
-Destruction of cell membrane
-alot more WBC in the area
-release of additonal mediators from WBCs
What are the additional mediators released in chronic inflammation & what do they do?
- Interleukins: cytokines that communicate in between WBC to activate additional WBC to bring more into the area
- GM-CSF (granulocyte–macrophage colony stimulating factors): stimulates growth of granulocytes -> neutrophils, eosinophils, basophils & mast cells; all of WBC are increased by this
- TNF: pro-inflammatory
- Interferons: interfere with viral replication
- PDGF: platelet derive growth factor
** all of these increase WBCs, or get more WBCs to the area**
T/F: chronic inflammation is always a problem
T
Briefly describe the cyclooxygenase pathway
Arachidonic acid converted to prostaglandin by COX
AA =
Arachidonic acid
Briefly describe the lipoxygenase pathway
AA converted to leukotrienes by lipoxygenase
Describe AA
Fatty acid molecule with 20 carbons
What is the precursor to AA? What enzyme is used to convert to AA?
Phospholipids
Phospholipase
What is produced from cyclooxygenase? what do they do?
Prostaglandins (increase inflammation response)
thromboxane A2 (plateletlet aggregation)
prostacyclin (inhibits platelet aggregation)
What is produced from lipoxygenase? what do they do?
Leukotrienes:
LTC4/LTD4/LTE4: inflammation
LTB4: phagocyte attraction (calls in more WBC)
Compare COX 1 & COX2
COX1: Constitutive & deals w/ homeostatic functions
-GI
-Renal
-platelet function
-Macrophage differentiation
COX2: Pain-mediated
-inflammatory response
What are our anti-inflammatory drugs?
NSAIDs
Glucocorticoids
Antirheumatic
What is the original NSAID & prototype?
Aspirin
What do NSAIDs do?
- Suppress S/S of inflammation by inhibiting prostaglandin synthesis
- Antipyetics
- Analgesic
How are NSAIDs metabolized?
Phase 2 in the liver (normal)
Phase 1 (abnormal)
Where are NSAIDs excreted?
Urine & Bile
What are general properties of NSAIDs?
Weak acid
well absorbed
highly metabolized
highly protein bound to albumin
Which mediators causes leaky vessels that can cause HA?
Bradykinin
Histamine
ASA =
aspirin