OA Flashcards
oa pathophysiology
cartilage degradation
chondrocyte activity to repair damage
more breakdown
bone remodelling and osteophyte formation
synovial inflammation
goals of therapy oa
relieve pain and inflammation
preserve range of motion, joint function
pharmacotherapy choices in oa
- TOP NSAID
- PO NSAID
- PO paracetamol/tramadol
- Intra-articular glucocorticoid injections
risk factors for nsaid-induced GI ulceration/bleeding
> 65 yo
hx of gastric ulcer
use of high dose/chronic nsaid
concurrent gc/antiplatelets/anticoag
high risk: at least 3 risk factors
how to protect against gi toxicity for nsaid
- use coxib
- add PPI
se of nsaids
gi
inhibition of platelet functions (stop 3 days before surgery)
CVS (MI, stroke, vascular death),
renal,
NSAID - induced AKI
ci of nsaids
pregnancy 3rd trimester
HF/IHD/peripheral arterial disease
egfr<15
COPD/asthmatic patients (bronchoconstriction), uncontrolled HTN, PUD/GI bleed
ddi of nsaids
(Increased renal toxicity) ACEi/ARBs, diuretics, aminoglycosides, amphotericin B, radiocontrast material
non pharmaco OA
exercise - strengthening, low impact aerobics (walking, swimming)
weight management
cortisone/lubrication injections
location of OA
weight-bearing joints (hand, knee, hip), asymmetrical polyarthritis
pain characteristics of OA
pain on movement, worse at end of day
s/sx of OA
early morning stiffness <30min
crepitus (clicking of joints)
joint swelling (maybe)
erythema (maybe)
risk factors of OA
age, anatomic factors, joint injury, obesity
men or women more likely
<50 yo: men
>70 yo: women
max dose of celecoxib
400mg/d
ra/oa: which is worse after rest
RA
RA/OA: which is worse at the end of day
OA
ra/oa: which has nocturnal pain
RA
RA/OA: which is relieved with exercise
RA
ra/oa: which has early morning stiffness more than 30 mins
RA
what is considered overdose for panadol
10g per 24 hours (send to ED)
20 tablets is overdose
what risk is increased with more than 5 days of nsaids
peptic ulcers
functions of prostaglandins
- reduce gastric acid secretions
- increase mucosal blood flow
- increase secretion of mucus
- increase secretion of bicarbonate
what does inhibition of pge2 production result in
sodium retention
water retention
peripheral edema
hypertension
what does inhibition of pgi2 production result in
suppression of renin aldosterone secretion
hyperkalemia
acute renal failure
where does pge2 inhibit sodium reabsorption primarily
thick ascending limb
what does nsaid inhibit
pge2 and pgi2
what does aldosterone stimulate
reabsorption of Na+ and excretion of K+
