📖 Pharmacology
BETA-LACTAM ANTIBIOTICS
PharmacologyCarbapenems: Broadest spectrum of beta-lactam antibiotics.
imipenem with cilastatin
meropenem
ertapenem
Monobactams: Unlike other beta-lactams, there is no fused ring attached to beta-lactam nucleus. Thus, there is less probability of cross-sensitivity reactions.
aztreonam
Beta-lactamase Inhibitors No antimicrobial activity. Their sole purpose is to prevent the inactivation of beta-lactam antibiotics by beta-lactamases, and as such, they are co-administered with beta-lactam antibiotics.
clavulanic acid
tazobactam
sulbactam
Drugs causing FOLATE deficiency
PharmacologyMedications can interfere with folate metabolism, including:
anticonvulsant medications (such as phenytoin, primidone, carbamazepine or valproate)
metformin (sometimes prescribed to control blood sugar in type 2 diabetes)
methotrexate, an anti-cancer drug also used to control inflammation associated with Crohn disease, ulcerative colitis and rheumatoid arthritis.
5-fluorouracil
Hydroxyurea
trimethoprim
sulfasalazine (used to control inflammation associated with Crohn disease, ulcerative colitis and rheumatoid arthritis)
triamterene (a diuretic)
birth control pills
Piroxicam
PharmacologyPiroxicam:
Half‐life of 45 hrs. Once‐daily dosing. Delay onset of action.
High doses inhibits PMN migration, decrease oxygen radical production, inhibits lymphocyte function.
used to relieve the symptoms of arthritis, primary dysmenorrhoea, pyrexia; and as an analgesic,non-selective cyclooxygenase (COX) inhibitor
The risk of adverse side efects is nearly ten times higher than with other NSAIDs. Peptic ulcer (9.5 higher)
Diclofenac
PharmacologyDiclofenac
Short half life (1‐2 hrs), high 1stpass metab., accumulates in synovial fluid after oral admn., reduce inflammation, such as in arthritis or acute injury
Mechanism of action
inhibition of prostaglandin synthesis by inhibition of cyclooxygenase (COX). There is some evidence that diclofenac inhibits the lipooxygenase pathways, thus reducing formation of the
leukotrienes (also pro-inflammatory autacoids). There is also speculation that diclofenac may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain the high potency of diclofenac - it is the most potent NSAID on a molar basis.
Inhibition of COX also decreases prostaglandins in the epithelium of the stomach, making it more sensitive to corrosion by gastric acid. This is also the main side effect of diclofenac and other drugs that are not selective for the COX2-isoenzyme.
