The nursing instructor teaches the students that traditional nonsteroidal anti-inflammatory drugs (nsaids) work by blocking cox-1 and cox-2. the teacher further instructs that by blocking cox-2, which effects will be achieved?

Explanation:

Non-steroid anti-inflammatory drugs (NSAIDs) are the competitive inhibitors of cyclooxygenase (COX -1 and COX -2). COX-2 inhibitors are a class of medicaments that selectively inhibit COX-2 (celecoxib, rofecoxib, meloxicam). COX-2 inhibitors provide anti-inflammatory and analgesic effects.

COX is the enzyme that regulates the bioconversion of arachidonic acid to inflammatory prostaglandins. The COX enzyme catalyzes the initial reactions in the conversion of arachidonic acids to a variety of eicosanoids, prostaglandins and thromboxanes. The pharmacological inhibition of COX may provide a decrease in the symptoms such as inflammation and pain.

COX-2 is primarily induced to produce prostaglandins that mediate inflammation and pain. They further suppress prostaglandin by the COX-2 enzyme. They provide anti-inflammatory and analgesic effects due to the fact that is produced at the site of inflammation.

The anti-inflammatory action of NSAID is due to the inhibition of COX-2. COX-2  levels are increased in expression and inflammation. COX catalyzes the formation of prostaglandins and thromboxanes from arachidonic acid. The arachidonic acid is formed from the cellular phospholipid bilayer by phospholipase A₂.

The side-effects such as gastrointestinal and renal toxicity are due to the COX-1 inhibition.  The most common gastrointestinal side-effects are dyspepsia, peptic ulcer, perforation and bleeding. These complications are due to NSAID-induced impairment of the protective effects of prostaglandins and prostacyclin produced by COX in the gastric mucosa.

The selective COX-2 inhibitors are administered in cancer chemotherapy and neurological diseases (Parkinson’s disease, Alzheimer’s disease), rheumatoid arthritis, osteoarthritis, metastatic bone pain, headache, migraine, postoperative pain, pyrexia, ileus, renal colic, dysmenorrhea.

COX-2 inhibitors are linked to the reduction of gastrointestinal risk. In case of the inflamed or ulcerated gastrointestinal mucosa, COX-2 is produced at the site and cause the secretion of prostaglandins, In this way, prostaglandins regenerate the gastrointestinal mucosa.

COX-2 selective inhibitors may increase sodium and water retention. In this way, the blood pressure is also increased. Thus, they may cause the onset of congestive heart failure. COX-2 selective inhibitors have been noted to reduce the colorectal polyps. COX-2 are involved in many stages of the carcinogenesis. The most important are as xenobiotic reactions, metabolism, cell proliferation, angiogenesis, apoptosis, immune reactions and tumour invasiveness.  

COX-2 activity may be the source of prostaglandin I₂.  In the epithelium I₂ is involved in decreasing platelet aggregation. Thus, its activity causes vasodilatation and prevents the proliferation of vascular smooth muscle cells. Thromboxane A₂ is produced by COX-1 enzyme. It is involved in platelet aggregation, vasoconstriction and smooth muscle proliferation. In the individuals, if COX-2 is inhibited, it may lead to high blood pressure, accelerated atherogenesis and higher thrombotic response due to plaque rupture.

COX-2 inhibition has been noted to improve endothelium-dependent vasodilatation. It reduces chronic inflammation and oxidative stress in individuals with coronary artery disease.

COX-2 plays an important role in the regulation of kidney function (perfusion, water homeostasis and renin secretion).

Induction of COX-2 is involved in ovulation and during the third trimester, increased uterine levels of COX-2 are necessary for the initiation of birth.