Mechanism of non steroid hormone action animation

Traditionally, the analgesic action of nonsteroidal anti-inflammatory drugs (NSAIDs) has been explained on the basis of their inhibition of the enzymes that synthesise prostaglandins. However, it is clear that NSAIDs exert their analgesic effect not only through peripheral inhibition of prostaglandin synthesis but also through a variety of other peripheral and central mechanisms. It is now known that there are 2 structurally distinct forms of the cyclo-oxygenase enzyme (COX-1 and COX-2). COX-1 is a constitutive member of normal cells and COX-2 is induced in inflammatory cells. Inhibition of COX-2 activity represent the most likely mechanism of action for NSAID-mediated analgesia, while the ratio of inhibition of COX-1 to COX-2 by NSAIDs should determine the likelihood of adverse effects. In addition, some NSAIDs inhibit the lipoxygenase pathway, which may itself result in the production of algogenic metabolites. Interference with G-protein-mediated signal transduction by NSAIDs may form the basis of an analgesic mechanism unrelated to inhibition of prostaglandin synthesis. These is increasing evidence that NSAIDs have a central mechanism of action that augments the peripheral mechanism. This effect may be the result of interference with the formation of prostaglandins within the CNS. Alternatively, the central action may be mediated by endogenous opioid peptides or blockade of the release of serotonin (5-hydroxytryptamine; 5-HT). A mechanism involving inhibition of excitatory amino acids of N-methyl-D-aspartate receptor activation has also been proposed.

Most modern steroid enemas are foam based - as the likelihood of someone with colitis being able to retain a water based enema is quite low. These act topically applying the steroid directly to the colon - with only small amounts being absorbed into the bloodstream. This makes side effects less likely. The downside is that they can only reach the descending colon and rectum - so for those with extensive colitis oral steroids may be needed. A combination of Entocort and steroid enemas can provide topical treatment to the majority of the colon - again minimizing side effects. As the two main steroid enemas differ quite greatly I will cover them separately.

Progestogens The discovery that ethinyl substitution leads to oral potency led to the preparation of ethisterone, an orally active derivative of testosterone. In 1951, it was found that removal of the carbon-19 from ethisterone to form norethindrone did not destroy the oral activity and, most importantly, changed the major hormonal effect from that of an androgen to that of a progestogen. Accordingly, the progestational derivatives of testosterone were designated 19-nortestosterones. The androgenic properties of these compounds, however, were not completely eliminated, and minimal anabolic and androgenic activity remains. Examples of this class of progestogens include norethindrone, norethynodrel, ethynodiol diacetate, and some other related compounds not used in the United States. The second group of 19-nor compounds are gonanes, which have an 18-ethyl instead of an 18-methyl group. They include racemic norgestrel, levonorgestrel, and three newer compounds: gestodene, desogestrel (a pro-drug that must be converted to 3-ketodesogestrel to be biologically active) and norgestimate, which is the 17-acetyl-3-oxime derivative of norgestrel, into which it is rapidly metabolized.

Mechanism of non steroid hormone action animation

mechanism of non steroid hormone action animation


mechanism of non steroid hormone action animationmechanism of non steroid hormone action animationmechanism of non steroid hormone action animationmechanism of non steroid hormone action animationmechanism of non steroid hormone action animation