Clinical Pharmacology of Prostaglandins

Pharmacology

Your browser is too old

We can't provide a great video experience on old browser

Update now
Data 2fimages 2fwsr2exprtoc7c35oli47 190212 s0 afzal sidra clinical pharmacology of prostaglandins intro
03:34
Clinical Pharmacology of Prostaglandins
Data 2fimages 2fxiyjzgrwiofp6wgwlmtw 190212 s1 afzal sidra prostaglandins
08:37
Prostaglandins
Data 2fimages 2fj3oe8df7spuju3eoy0ph 190212 s2 afzal sidra receptor binding and expression
10:01
Receptor Binding and Expression
Data 2fimages 2fcgu2q3x0tockfjzvasgb 190212 s3 afzal sidra pharmacological effects
19:55
Pharmacological Effects
Data 2fimages 2fimj2dscoqyk1sesgzfwx 190212 s4 afzal sidra therapeutic uses
08:26
Therapeutic Uses

Lecture´s Description

sqadia.com provides supplement to medical students in the form of medical video lectures delivered by experienced medical practitioners with the aim to improve the medical knowledge all around the world. In view of this mission, sqadia.com offers variety of medical lectures on the medical subject of pharmacology. In this lecture of clinical pharmacology of prostaglandins, experienced pharmacist sheds light on the synthesis of prostaglandins, its pharmacological properties and cell signalling pathway and expression. Subsequently, Sidra Afzal gives important pharmacological explanation of effects of prostaglandins on various organs along with its therapeutic use.

Prostaglandins

The section prostaglandins is the demonstration of medical video lecture i.e. clinical pharmacology of prostaglandins. Prostaglandins (PGs) are a family of lipid compounds that are derived enzymatically from essential fatty acids acting locally as autocrine or paracrine mediators with a wide range of effects throughout the body. Arachidonic acid liberated from cellular membrane phospholipids by the action of phospholipases A2 and cyclooxygenase are the rate-limiting steps in the biosynthesis of prostaglandins. COX-1 and COX-2 convert arachidonic acid to PGH2, with further conversion to specific PGs depending on the specific PG synthases. Inhibition of prostaglandin synthesis takes place when NSAIDS suppress the signaling function of prostaglandins, which are important mediators of pain, fever, and inflammation responses, by inhibiting the cyclooxygenase enzymes and thereby reducing prostaglandin synthesis. Corticosteroids inhibit phospholipase A2 production by boosting production of lipocortin, an inhibitor protein.

Receptor Binding and Expression

For MBBS students, detailed explanation of receptor binding and expression of prostaglandins is delivered under the lecture title pancreatic neuroendocrine tumors. Receptors mediating prostanoids actions were characterized first by pharmacological analysis, which indicated the presence of one receptor each, named DP, FP, IP, and TP, for PGs of the D, F, and I type and TXA, respectively, and four different receptors designated EP1, EP2, EP3, and EP4 for the E type PGs. Prostaglandin receptors have been grouped into specific G-protein-dependent cAMP and/or Ca2+ signaling. They involve activation of specific cell surface receptors coupled to intracellular second messenger e.g. DAG, IP3 and cAMP. Prostanoids are degraded mainly by beta oxidation and prostaglandin dehydrogenase beta oxidation. Prostaglandin receptors are expressed in kidney, lung, stomach, eye, heart, corpus luteum and other tissues of human body.

Pharmacological Effects

Pharmacological Effects of prostaglandins are discussed comprehensively in the medical video lecture at the platform of sqadia.com for medical and MBBS students. Pharmacological Effects of prostaglandins on cardiovascular system do not directly impact systemic vascular tone, modulate local vascular tone at site of formation. In cardiovascular system, PGE2 vasoconstrict through EP1,3. In PGD 2, flushing, nasal stiffness, hypotension a local subcutaneous release contributes to vasodilation of skin. PGI 2 relaxes vascular smooth muscle, causing hypotension and reflex tachycardia in I.V administration. TxA2 is a potent vasoconstrictor and contracts smooth muscles. TxA2 increases platelet-leucocyte interaction. PGD2 contributes to resolution of inflammation. Pharmacological effect of prostaglandins in uterus exhibits that low concentration of PGE 2 and PGF 2α contracts uterus. PGEs and PGFs are used for medical termination of pregnancy. In GIT muscles, PFI 2, TxA 2 produce contraction. Modulators of bone metabolism are COX1, COX2, and PGE2.

Therapeutic Uses

The medical lecture clinical pharmacology of prostaglandins also focusses on therapeutic uses. Therapeutic use of prostaglandins suggests that low dose aspirin is used as cardioprotective agent, FP agonists is used as treatment of open angle glaucoma, EP agonists for induction of labor. Prostaglandin also plays a role in therapeutic abortion. Dinoprostone (PGE2 synthetic prep) induces abortion in 2 trimester. Long term therapy with PGI 2 (prostacyclin) improves symptoms of pulmonary hypertension. Several PG analogs decrease gastric ulceration. Misoprostol is approved for prevention of NSAID induced gastric ulcers. Prostaglandins are also used for treatment of impotence. PGE 1 (Alprostadil) is used as second line of treatment for erectile dysfunction.

Studies have shown that V-Learning™ increases student's learning and passing rate Significantly.

100% satisfaction guaranteed, join us & boost your medical Knowledge