COX and NSAIDs
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cyclooxygenase inhibitors - therapeutic effects?
- 1 - decreased inflammation
- 2 - decreased pain
- 3 - reduced fever
MSA-4 protects against what?
stroke and MI
when cyclooxygenase is inhibited, it decreases amount of what?
COX @ site of tissue injury?
decreased pain and inflammation
COX @ stomach
protects gastric mucosa
COX @ blood vessels
COX @ brain
COX @ platelets
COX @ uterus?
2 forms of COX?
- COX 1 - found in all tissues
- COX 2 - produced at site of tissue inflammation/injury
inhibition of COX-1
gastric erosion, bleeding, renal impairment. protects against MI and stroke
COX-1 normal effects?
found in all tissues, protects gastic mucosa, supports renal fx, promotes platelets
COX-2 normal effects?
produced at sites of tissue injury. mediates inflammation and sensitizes to painful stimuli. in the brain - mediates fever and contributes to pain perception
inhibition of COX-2?
suppresses inflammation, alleviates pain, reduces fever. increased risk of MI and stroke
difference between NSAIDs and acetaminophen?
- NSAIDS - have anti-inflamm properties
- acetaminophen lack anti-inflamm properties
aspirin (first generation NSAIDs)
inhibits COX-1 and COX-2. treats inflamm disorders
adverse effects of aspirin?
- GI upset
- renal impairment
- salicylism (s/s headache, tinnitus, sweating, dizziness)
- Reye's syndrome (in children - do not give < 2 years)
methotrexate - type of drug & therapeutic use?
- DMARD (disease modifying antirheumatic)
- used for rheumatoid arthritis
methotrexate - given how many times?
once a week via IM
sulfasalazine (Azulfidine)- therapeutic uses?
rheumatoid arthritis, IBD
Hydroxychloroquine (Plaquenil)- onset?
Hydroxychloroquine (Plaquenil)- significant side fx?
- retinal damageneed frequent eye exams
sulfasalazine (Azulfidine)- action?
- slows progression of joint deterioration
Enteracept (Enbrel)- therapeutic use?
- mild to moderate RA
- delays progression of joint damage
Enteracept (Enbrel)- administration? side fx?
- given subQ
- may have local site reaction
- ^ risk of infection
- what type of medication?
Tumor necrosis factor (TNF) blocker
mech of action of TNF blockers?
inhibits TNF (tumor necrosis factor), thus reducing inflammation, as in RA
disease of altered purine metabolism. associated with hyperuricemia
goals of therapy for gout?
- block inflamm process
- increase excretion & decrease production of uric acid
usual meds given for an acute gout attack?
NSAIDS & glucocorticoids
colchicine - therapeutic use?
acute gout attacks
allopurinol - therapeutic use?
- chronic gout
- inhibits uric acid production
probenecid - therapeutic use/ action?
- chronic gout symptoms
- decreases reabsorption of uric acid; thereby promoting excretion
probenecid - long term side fx?
GI effects, renal fx
first gen NSAIDs inhibit what?
COX-1 and COX-2
second gen NSAIDs inhibit what?
causes effects in stomach, kidneys, platelets.
effects on inflammation, pain, fever
difference between inhibition of COX-1 and COX-2?
- COX 1: bleeding, renal impairment, stomach erosion (acts systemically)
- COX 2: reduces inflammation, pain, fever. (acts on CNS and @ sites of tissue injury)
benefits of ASA?
suppression of pain, fever, inflammation. also protects against MI/stroke.
first line treatment/ drug of choice for arthritis?
which drug decreases ASA's protection against MI/stroke?
ibuprofen. (reduces ASA's side effect of blood thinning)
ASA is contraindicated for which children?
<2 years of age, with the flu, with chickenpox
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