What is the mechanism of action of paracetamol?
Paracetamol has a central analgesic effect that is mediated through activation of descending serotonergic pathways. Debate exists about its primary site of action, which may be inhibition of prostaglandin (PG) synthesis or through an active metabolite influencing cannabinoid receptors.
What is the mechanism of action of NSAIDs?
The main mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX). Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins.  The therapeutic effects of NSAIDs are attributed to the lack of these eicosanoids.
How does aspirin work mechanism?
The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.
What is the action of acetylsalicylic acid?
Aspirin, an acetylated salicylate (acetylsalicylic acid), is classified among the nonsteroidal antiinflammatory drugs (NSAIDs). These agents reduce the signs and symptoms of inflammation and exhibit a broad range of pharmacologic activities, including analgesic, antipyretic, and antiplatelet properties.
Why is paracetamol not an NSAID?
Paracetamol (acetaminophen) is generally not considered an NSAID because it has only minor anti-inflammatory activity. Paracetamol treats pain mainly by blocking COX-2 and inhibiting endocannabinoid reuptake almost exclusively within the brain, but not much in the rest of the body.
How do salicylates reduce fever?
Salicylates reduce fever by working on the brain’s hypothalamus region, which regulates body temperature. Salicylates reduce inflammation by inhibiting the activity of enzymes known as cyclooxygenases (COX-1 and COX-2), essential for the biosynthesis of prostaglandin.
What is the mechanism of action of aspirin in preventing clotting?
The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A2 synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall.
What is the role of COX-1?
Because COX-1 is constitutively expressed in microglia, it functions as the primary source of PGs in the early phase of inflammation. LPS and other inflammatory stimuli also activate MMPs, which regulate BBB permeability and, consequently, cause infiltration of peripheral leukocytes into the brain.
How does NAC work in paracetamol overdose?
The antidote for acetaminophen poisoning, NAC, is theorized to work through a number of protective mechanisms. Since NAC is a precursor of glutathione, it increases the concentration of glutathione available for the conjugation of NAPQI.
How paracetamol is different from NSAIDs?
The main difference between the two medications is that ibuprofen reduces inflammation, whereas paracetamol does not. According to Hamish, there’s no advantage in taking ibuprofen or paracetamol brands such as Nurofen or Panadol over the cheaper chemist or supermarket versions.
What is the purpose of salicylates?
Aspirin and other salicylates are most often used to reduce pain, fever, and inflammation. They also are effective in preventing excessive blood clotting, which can cause a heart attack or stroke.
What are three properties of salicylates?
Salicylates are used as food preservatives and antiseptics and have bacteriostatic, fungicidal and keratolytic (skin peeling) properties. Salicylic acid and acetylsalicylic acid have analgesic (pain relieving), anti-inflammatory, and antipyretic (temperature-lowering) effects.
How does aspirin stop platelet aggregation?
Aspirin acts on platelets by acetylating the cyclooxygenase enzyme at position serine 529, resulting in reduced formation of cyclic endoperoxides (prostaglandin G2 and prostaglandin H2) and thromboxane from arachidonic acid.
How aspirin causes vasodilation?
The mechanism whereby aspirin has a unique blood pressure remains elusive. It has been shown that high doses of salicylates, including aspirin and sodium salicylate, dilate blood vessels in vivo, probably through direct effect on vascular smooth muscle.