Drugs for arthritis and inflammation Flashcards
How do NSAIDs work?
Block Prostaglandins
What are prostaglandins?
pain mediating substances that irritate nociceptors and transmit feeling of pain to brain
What are some important Fx of prostaglandins?
stabilize gastric lining and maintain renal artery vasodilation.
When cell membrane is injured, what is released? and by what?
Arachidonic acid (AA)
by enzyme phospholipase A2
What does AA act on>?
lipoxygenase making leukotrienes
orrrr
Cyclooxygenase making prostaglanding/thromboxane causing vasoconstriction
What does prostaglandin do as opposed to Postacyclin?
vasoconstriction
Vasodilation
both make sticky platelets/ pain production
Cyclooxygenase enzyme (makes prostaglandins)
2 types and purpose?
Cox-1: in platelet/kidney/stomach
Cox-2:in inflammation/infection only.
Cox-3:brain?
MOA of aspirin?
inhibit Cox therefore block prostaglandin (anti-inflammatory) and thromboxane (cardiac protection) synthesis.
low dose aspirin relation to cardiac?
protective bec binds to platelet for life. decreasing release of thromboxane. causing anticoagulation.
Effects of aspirin?
dec pain
inflammation
prevent thrombus/colon cancer
ADR of aspirin?
Gi problems
renal Dsfx
anemia
Bronchospasm
signs of aspirin overdosE?
headache tinnitus confused hyperventilating metabolix acidosis
NSAIDS MOA
reversibly block Cox
same as aspirin but don’t offer cardiac protection
watch for GI problems fr fr.
ADR of NSAIDs
- BP increase
- Cns disturbances.
- affect cells of hypertrophy
- decrease effectiveness of diuretics/Betablockers/and ACE I
Cox-2 Inhibitiors MOA
block action of Cox-2
muscle pain reduction.
to prevent Coz-1 inhibition but not platelet aggregation
ADR of Cox-2 Inhibitors?
increased Cardio events.
Acetaminophen MOA?
tylenol
inhibit Cox enzyme in CNS.
for pain+fever. no t inflammatory./cardio
ADR of acetaminophen?
increase BP
liver toxicity
If patient on aspiring and NSAID what u do?
take aspirin 2 hrs before NSAID so it can bind to platelet for life.
Nsaid related to heart disease?
can elevate BP
reduce effect of anti-hypertensives
Pathology of RA?
increased cytokines IL-6 induce c reactive protein (CRP predictor of cardiovascular risk)
increase chance of MI with RA
Corticosteroids MOA
activate protein that inhibits Phospholipase A2 therefore impairing everything after. (inf/pglds/immune)
Before DMARDS, what is given?
corticosteroids
1x/day
or 4 injections/year
ADR of corticosteroids?
catabolic on tissue OP muscle wasting HTN/glaucoma bushings hormone suppression..
WEAN OFF OF THEN+M> DONT STOP ABRUPTLY
Conventional Synthetic DMARDS MOA
impair DNA synthesis (dec cytokines)
can cause GI/liver/hair loss/ulcer
Targeted Synthetic DMARD MOA?
inhibit enzymes that trigger inflammation.
cause neutropenia/cholesterol
Biologic DMARDS MOA?
lower levels of TNF-a.
lower ability to fight infection.
Non TNF inhibitors?
oencia
prevent action of lymphocytes.. decrease inflammation but is a biologic DMARD so increased risk of infection
Recommendations for RA?
start with traditional DMARD like methotrexate along with prednisone (steroid) and then move on to biologic.
ADR of biologics?
TB
infection
Cancer
Skin rash
injected hyaluronan to help restore normal viscosity of synovial fluid?
Viscosupplementation