Opioids/NSAIDs

Alfentanil has lower lipid solubility than fentanyl but higher non-ionized fraction so it works really fast. 

All opioids can be retained by the lungs (first-pase uptake) and then redistribute once systemic concentrations fall.

Opioids have context-sensitive halflife because blood concentration is decreased from redistribution at small doses and biotransformation at large doses.

Normeperidine can cause seizures. Norfentanyl is nonactive but used to determine abuse. Codeine is a prodrug that has variable biotransformation depending on CYP enzymes. Pseudocholinesterase deficiency does not affect esmolol or remi. Both meperidine and morphine metabolites are excreted in urine. Alfentanil biotransformation is impaired by erythromycin

Meperidine has atropine-like affects (tachycardia) and causes cardiodepression unlike other opioids. Meperidine, hydromorphone, and morphine evoke histamine release and bronchospasm (benzylisoquinolones). Fentanyl-like opioids induce chest wall rigidity.

APNEIC THRESHOLD - greatest PaCO2 at which a patient remains apneic increases with opioids.

Opioids decrease CMRO2, cerebral q and volume, ICP but less than barbiturates, propofol, or benzos

NSAIDS inhibit COX, which catalyzes the production of prostaglandin H1, a key mediator of inflammation. COX2 is less selective than COX1 purely by size (ie. a bigger molecule fits in COX2 but not COX1). COX1 is widely distributed in the body and COX2 is made for inflammation. COX2 decreases the risk of platelet dysfunction but causes increased thrombosis.