Friday, August 19, 2011

(¬_¬) rheumatoid arthritis. cause i think this will help me pass my exam.

Rheumatoid Arthritis
40-60's woman are prone to have this. more RA pt get Osteoporosis. shorter life span. 
sometimes happen in children below 16 y.o.
called juvenile rheumatoid arthritis.
[symptom: inflammation of the joint for >6weeks. complication:eye inflammation. pauciarticular, affect 4 joint; polyarticular, affect 5 joint; systemic JRA, affect all body]
an autoimmune disease. unknown cause. happens when immune system consider your joint as foreign substance. so it will send WBC to to attack your joint [knee,ankle,hand and wrist] -synovium will become thicken called pannus as WBC release protein [prostaglandin,cytokines] to that site and cause this symptom:
joint inflammation
joint pain
joint tender to touch
morning stiffness 
decrease in body weight
as the years by, this will destruct your bone, ligament and cartilage.
RF [Rheumatoid Factor] 
ACPA's [Anti-Citrullinated Peptides]
*both AB
Excessice Erythrocyte Sedimentation Rate [ESR]
Radiological Changes [MRI]
Goals of theraphy:
Prevent/Slow Joint deformation
Increase pain/symptom
preserve quality of life
1st Line - NSAID and Corticosteroid
2nd Line - DMARD [Disease Modifying Anti-Rhematoid Drugs]

MOA: inhibit prostaglandin synthesis by blocking COX 1 and COX 2
COX 1 found everywhere in the body
COX 2 found in the site of inflammation
there is 2 types of NSAID which is
Non Selective COX 1 and COX 2 
[mefenamic acid, piroxicam, indomethacin, ibuprofen]
Selective COX 2 Inhibitor
[meloxicam, etoricoxib, diclofenac]
renal impairment 
bleeding problem
stomach irritation
increase HPT
[*as this link to prostaglandin inhibition]
*COX 2 have a safer GI profile than Non Selective
Pharmacokinetic DI
absorption: sucralfate - coated stomach acid, low A
antacid - low A of NSAID
*high stomach PH, more ionised drug, less absorbtion
protein binding: warfarin, digoxin and aspirin [WDA]
NSAID are more protein bound, concentration WDA will increase in blood plasma
metabolism: Fluconazole - enzyme inhibitor
increase NSAID in blood cause no metabolism
Rifampicin - Liver Enzyme Inducer
Warfarin - low metabolize of warfarin, warfarin increase in blood, increase bleeding
excretion: probenecid - increase reabsorbtion of NSAID
Pharmacodynamic DI
increase bleeding: salycylic acid, anticoagulant, antidepressant
nephrotoxicity: aminoglycoside, MTX, cyclosporin
Pro and [Cons]:
reduce pain+inflammation, reduce swelling, increase mobility and quality of life and low cost
[CVS Toxicity, Renal Impairment, GI Toxicity, Hepatic dis(fx) and doesn't affect RA progreesion]

oral, iv, im and intramuscular [methyprednisolone]
1st high dose and need to tapered slowly
*to avoid worsening of RA and SE
S/E: cushion syndrom [buffalo hump, moon face, redness, puffy]
supress immune system, prone to infection
decrease bone mass
muscle wasting 
increase BP
pro: fast onset, reduce inflammation and overactive body system immune, can be inject to IA
cons: lower bone mass, tapering discontinue not successful, S/E, does not affect RA progression.

DMARD [Disease Modifyying Anti-Rheumatoid Drug]
moa: supress body immune/inflammatory system
*pt often get infection cough, sakit tekak etc
*Mohd Hazwan Suka Cari LA PAI MaGgi*
Methotrexate - cause lung damage
Hydrochloroquine - retina damage
Sulfasalazine - sweat, urine, tears orange
intramuscular gold
combination of drug
why combine?
decrease toxicity level
long term use are more favorable
better than using one type of DMARD

ini yang aku hafal, keluar soalan lain. memang hancus la.

*update on the same day, 12:31pm
dem. aku salah 1 soalan. MTX ambik seminggu sekali OK?!
aku tak tahu and tak terbaca.


kak ijan said...

Boleh buat e-reading kalau macam ni Lin. hehe... good info bytheway. Kak Ijan pernah ada kawan kena arthritis at age of 20s. pity her. :(

#ciksuzlin said...

hahaha. ye la kak~mentang2 ada nook baru kan~happy belated bday :]

kesiannya kawan akak tu. :(