Analgesics Flashcards
Describe the action of Cox2 inhibitors
G
Describe the action of paracetamol
NOT FULLY UNDERSTOOD-
3 theories- One theory is that paracetamol increases the pain threshold by inhibiting two isoforms of cyclooxygenase, COX-1 and COX-2, which are involved in prostaglandin (PG) synthesis. Prostaglandins are responsible for eliciting pain sensations. Acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, therefore, has no peripheral anti-inflammatory effects. (paracetamol) blocks COX indirectly.
Studies also suggest that acetaminophen selectively blocks a variant type of the COX enzyme that is unique from the known variants COX-1 and COX-2.6 This enzyme has been referred to as COX-3.
The antipyretic actions of acetaminophen are likely attributed to direct action on heat-regulating centers in the brain, resulting in peripheral vasodilation, sweating, and loss of body heat.
The exact mechanism of action of this drug is not fully understood at this time, but future research may contribute to deeper knowledge.24
Describe the action of Ibuprofen
The exact mechanism of action of ibuprofen is unknown. However, ibuprofen is considered an NSAID and thus it is a non-selective inhibitor of cyclooxygenase, which is an enzyme involved in prostaglandin (mediators of pain and fever) and thromboxane (stimulators of blood clotting) synthesis via the arachidonic acid pathway.27
Ibuprofen is a non-selective COX inhibitor and hence, it inhibits the activity of both COX-1 and COX-2. The inhibition of COX-2 activity decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling while the inhibition of COX-1 is thought to cause some of the side effects of ibuprofen including GI ulceration.
Describe the action of morphine
S
What are COX2 inhibitors
F
Describe the action of Aspirin as an analgesic
Acetylsalicylic acid disrupts the production of prostaglandins throughout the body by targeting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) Prostaglandins increase the sensitivity of pain receptors and substances such as histamine and bradykinin.
Describe the action of Aspirin as an anti platelet inhibitor
The inhibition of platelet aggregation by Asprin occurs because of its interference with thromboxane A2 in platelets, caused by COX-1 inhibition. Thromboxane A2 is an important lipid responsible for platelet aggregation, which can lead to clot formation and future risk of heart attack or stroke
Describe the action of fentanyl
Fentanyl, a potent opioid agonist,
Fentanyl produces strong analgesia through its activation of opioid receptors.
Short answer- opioid receptors activated- cAMP reduced, calcium ion influx into cells reduced, nerves inhibited.
Fentanyl binds to opioid receptors, especially the mu opioid receptor, which are coupled to G-proteins. Activation of opioid receptors causes GTP to be exchanged for GDP on the G-proteins which in turn down regulates adenylate cyclase, reducing concentrations of cAMP. Reduced cAMP decreases cAMP dependant influx of calcium ions into the cell. The exchange of GTP for GDP results in hyperpolarization of the cell and inhibition of nerve activity.
What classification of drug is Asprin
non-selective cyclooxygenase (COX) inhibitor
Describe the action of Aspirin as an antipyretic
Acetylsalicylic acid is considered an antipyretic agent because of its ability to interfere with the production of brain prostaglandin E1. Prostaglandin E1 is known to be an extremely powerful fever-inducing agent
What drug class is ibuprofen?
Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid
Describe the action of corticosteroids eg prednisolone- short answer.
Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals.
Mechanism of action for glucocorticoids (eg prednisolone)
The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation.4 Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.4
Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10.4
Problems with high dose long term prednisolone use
High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.
WHat do low dose corticosteroids do vs high dose
Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive.
