Mechonism of Paramedic drugs Flashcards
Adrenaline
sympathomimetic catecholamine that exerts its pharmacologic effects on both alpha and beta-adrenergic receptors using a G protein-linked second messenger system. It is a non-selective agonist.
A1 increases cAMP which increases calcium which increases actin myosin which causes vasoconstriction and decreases vascular permeability.
B1 increases in cAMP which increases in calcium which increases in actin myosin which causes an increase in HR and force
B2 has an increase in cAMP which causes a decrease in calcium which causes a decrease in actin myosin which causes bronchodilation.
Salbutamol
Salbutamol binds to adrenergic B2 receptors on bronchial smooth muscle.It increases cAMP and by doing this it then decreases calcium influx to the bronchial smooth muscle cells which result in dilation. It increases the sympathetic nervous system and is sympathetically selective.
Atropine
works by attaching itself to the cholinergic M2 receptor which then prevents the acetylcholine from attaching, stopping the parasympathetic response and allowing the sympathetic response to take over which blocks calcium going into the cardiac smooth muscle. Results in a positive chronotropic effect.
Ipratropium Bromide
It binds to M3 receptors on the bronchial smooth muscles which blocks acetylcholine effects stopping the parasympathetic response allowing the sympathetic response to take over which then prevents calcium influx assisting in bronchial dilation.
Hydrocortisone
Inhibits phospholipase A2 blocking the late phase mediators such as histamine, CysLT, txA2 and bradykinin
Ondansetron
Ondansetron is a 5HT3 antagonist which interferes with this process at multiple sites (stomach / vagus nerve / vomiting centre)
frusmide
Its mechanism of action is inhibition of the sodium-potassium-2 chloride (Na+-K+-2 Cl−) co-transporter (symporter) located in the thick ascending limb of the loop of Henle in the renal tubule Jackson
Morphine
Reacts with mu, kappa and delta receptors located on neurons
Mu – agonist on pre synaptic membrane
Inhibits calcium signal
Inhibits transmission
Mu – agonist on pre synaptic membrane
Stimulates potassium channels, K+ efflux
Hyperpolarises cell (makes it more negative – harder to reach threshold to trigger action potential)
Reduces transmission of action potential
Reduces pain signalling
Naloxone
Naloxone is an antagonist of mu opioid receptor
On presynaptic membrane
Binding removes inhibition on calcium channel
On postsynaptic membrane
Binding removes stimulation of potassium channels
Naloxone occupies binding sites
Morphine therefore cannot bind
Calcium flux can occur
Neurotransmitters can pass across membrane
Action potential can be generated
Normal neurotransmission – Pain can be felt again – Respiratory depression will be reversed
Paracetamol
Inhibits synthesis of prostaglandin
Modulates inhibitory descending serotonergic pathways
NSAIDS e.g asprin, ibuprofen
Inhibits conversion of arachidonic acid into Prostaglandins thromboxanes, prostacylcins COX inhibitors may be Non-selective (inhibit COX-1 and 2) Aspirin, diclofenac, ibuprofen, naproxen Inhibition of COX analgesia antipyretic antiplatelet action impaired gastric cyto-protection Selective (COX-2) Celecoxib Inhibition of COX-2
Midazolam
Allosterically binds to benzo receptors couple with GABAa
Over stimulates GABA allowing for Cl- channels to remain open longer
Cl- floods into the membrane and causes hyperpolarisation
Lignocaine
Lignocaine is a sodium channel blocker
When administered into a nerve, lignocaine prevents the movement of sodium into local nerve cells
In doing so, lignocaine prevents nerve signalling (action potential) from progressing from the site of injury / pain to the spinal cord
Aprisin
Inhibits cyclooxygenase
prevents synthesis of – Thromboxane (TxA2) and – Prostacyclin (PGI2) and other prostaglandins
GTN
It is a prodrug which converts to nitric oxide. Nitric Oxide then: Increases levels of cGMP Reduces calcium levels Reduces actin/myosin interaction Result it vasodilation
