anaesthetics Flashcards
what are the three actions of NSAIDs
analgesia, anti-inflammatory, antipyretic
what is the pathway involved in prostaglandin synthesis
Phospholipase A2=>arachidonic acid=>COX=> prostaglandins
What is the purpose of prostaglandin and bradykinin in the injured tissue
reduction of pain threshold (allodynia) for tissue protection
what GPCRs do Prostaglandins act on in C fibres
Gq EP1, increase in calcium, neurotransmitter and so sensitivity, increase in bradykinin,
what is the effect of increase in peripheral pain signaling
upregulation of COX2 in dorsal horn=> increase in PGE2
What is the effect of PEG2 in CNS
Gi EP3=> raised cAMP and Ca=> heat production and reduced loss; Gs EP2 => phosphorylation of glycine receptors => increased pia perception
what are the common sites for COX1
platelets, gastric mucosa and renal vasculature, renal parenchyma
what is the full name of COX
Cyclooxygenase
what molecules are synthesised by COX enzymes
converts arachidonic acid to various eicosanoids=>prostaglandins, prostacyclin and thromboxane.
describe the mechanism behind protective effect of small doses of aspirin
irreversible inhibitor of COX1. Platelet => not replaced => anti-coagulant activity; mucosal cells => replaced and production of prostacyclin maintained
what parts of the brain are responsive to endogenous opioids
thalamus, limbic system, spinal cord, afferent peripheral terminal
What are the types of endogenous opioids
Enkephalins, Endorphins, Dynorphins
what are the 3 types of opioid receptor types and what type of receptor type are they
Mu, Kappa and Delta Gi
what is the intracellular effect of opioids
decreases cAMP and so Ca => reduced neurotransmitter (substance P) mu also positively coupled to K+ channels and Kappa inhibits voltage gated ion channels
what channels mediates most of the therapeutic effect
mu =>hyperpolarisation via opening K and closing Ca voltage gated channels
