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Pharmacology – NSAIDs & PROSTAGLANDIN ANALOGS (MADE EASY)

Posted on October 30, 2022 By
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NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are painkillers commonly used to treat pain, fever, and inflammation. Prostaglandin analogs are simply mimickers of endogenous prostaglandins, which are hormone-like substances involved in numerous body functions including the dilation and constriction of blood vessels, control of blood pressure, modulation of inflammation, and the contraction and relaxation of smooth muscle. This pharmacology lecture covers topics such as the role of cyclooxygenases (COX-1 & COX-2) in inflammation, thromboxane, prostaglandins; mechanism of action, therapeutic uses and side effects of NSAIDs and various prostaglandin analogs. Drugs mentioned include; Selective COX-1 inhibitors; Ketorolac, Flurbiprofen, Ketoprofen, Indomethacin, low-dose Aspirin; Non-selective COX inhibitors; Naproxen, Ibuprofen, Piroxicam, Diflunisal; Selective COX-2 inhibitors; Meloxicam, Diclofenac, Celecoxib, Etodolac; Prostaglandin E1 analogs; Alprostadil, Lubiprostone, Misoprostol; Prostaglandin F2α analogs; Bimatoprost, Latanoprost, Travoprost; Prostacyclin analogs; Iloprost, and Treprostinil.

Anti-inflammatory drugs known as nsaids as well as pharmacology of prostaglandin inflammatory response so following tissue injury or irritation the cell membrane into arachidonic acid now arachidonic acid is a substrate for abbreviated as 5-lox in this lecture we’re gonna focus just on the which are cox-1 and cox-2 the first one cox-1 isoform is expressed constantly and

Prostaglandins which stimulate normal body functions such as platelet aggregation and maintenance of renal blood flow now on the other hand it is induced at sites of inflammation so unlike cox-1 cox-2-derived discussed the role of cox enzymes in the inflammatory response let’s talk about which simply leads to decreased production of prostaglandins as a result based on their

Selectivity for cox enzymes nsaids can be divided into flurbiprofen ketoprofen indomethacin and low-dose aspirin in the second category we have relatively non-selective cox inhibitors which include include meloxicam diclofenac celecoxib and etodolac now this relative in efficacy and safety of these nsaids so the most common adverse effects of production of prostaglandin-e2 pge2

For short and prostacyclin pgi2 for short regulating normal gastric blood flow this is why inhibition of cox-1 selective for a cox-1 are associated with the highest risk now the second production of thromboxane-a2 txa2 for short as you may remember antiplatelet effect and thus increased risk of bleeding this effect is irreversibly inhibits cox-1 enzyme in platelets moreover

Because antiplatelet effect persist even after aspirin therapy is so again agents with higher selectivity for cox-1 enzyme are also associated of nsaids which results from their actions on the kidney so renal afferent arteriole which is important for maintaining glomerular filtration only minimal effect on renal perfusion however when kidney function becomes production of

Prostaglandins becomes a significant factor in preservation of prostaglandins they also may increase the risk of kidney injury in susceptible discuss results from their actions on aspirin with high cox-1 selectivity can have protective cox-2 selectivity can have the opposite effect in order to understand where this to the heart so under normal conditions we have a balanced

Effect between vasodilation and inhibition of platelet is produced mainly by cox-1 in platelets and it’s responsible for arises when selective inhibition of cox-2 tips the balance in favor of aggregation more likely to occur this in turn leads to increased risk of that we discuss nsaids let’s talk a little bit more about prostaglandins so inflammation they’re also responsible

For many beneficial effects in order to analogs which simply mimic our endogenous prostaglandins now coupled prostaglandin receptor of which there are at least nine known subtypes and expressed receptors so now let’s discuss some of the commonly used example of agents that belong to this group are alprostadil lubiprostone and were designed for different therapeutic purposes

So alprostadil has two main applied into the urethra it acts via direct stimulation of camp of trabecular smooth muscle and dilation of cavernosal alprostadil is used in neonates with congenital heart defects to temporarily a refresher ductus arteriosus is a blood vessel found in babies before vessel typically closes shortly after birth keeping it open in certain babies

Alprostadil relaxes the ductus arteriosus and supports its patency analog that is lubiprostone so lubiprostone is used in the treatment of epithelial cells lining the intestine by stimulating these channels lubiprostone which increase the liquidity of the intestinal contents this secretion also passage of stool now let’s move on to the next prostaglandin-e1 analog that is to

Treat and prevent stomach ulcers particularly in patients binding to the prostaglandin receptor on the gastric parietal cell and causing thus modest inhibition of acid secretion furthermore misoprostol protects the interacting with prostaglandin receptors in the uterus misoprostol causes the uterine contents now let’s move on to prostaglandin-f2alpha analogs and travoprost

These agents are used opthalmically for treatment of open-angle thus lowering intraocular pressure although latanoprost and travoprost throughout the eye bimatoprost is thought to have a different mechanism of effects of bimatoprost is elongation and darkening of the hypotrichosis now let’s move on to the analogs example of agents that belong to this group are iloprost and

They work by increasing production of camp which leads to decreased levels of causing vasodilation this results in significant reduction in pulmonary for watching i hope you enjoyed this video and as always stay tuned for more

Transcribed from video
Pharmacology – NSAIDs & PROSTAGLANDIN ANALOGS (MADE EASY) By Speed Pharmacology

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