Paramedic Drugs
Paramedic Drug Revision
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- MOA: Antagonises DA2 receptors in chemotrigger zone. Antagonises 5HT3 receptors in GIT. Agonises 5HT4 peristalis increases gastric motility
- Antagonises 5HT3 receptor. No vomiting reflex.
- loop diuretic. inhibits Na, K and Cl symport, Na, K and Cl not absorbed down concentration gradient. Na excreted and H2O follows -> polyuria
- volume replacement of systemic vasculature. MOA: Frank Sterling law. Increased systemic fluid increases cardiac output
- antihistamine. MOA: 2nd gen. H1 antagonist. Blocks the action of histamine by occupying the H1 receptor. sites.
- Synthetic corticosteroid. MOA: inhibits phosphalyase A2, this blocks late phase mediators.
- sympathomimetic. MOA: binds to B2 receptor -> increase CAMP -> decrease intracellular CA2 -> decreases actin and myosin interaction ->bronchial relax.
- non-selective sympathomimetic agonist. Alpha 1, Beta 1 and Beta 2 increase CAMP which leads to vasoconstriction, forced intropic and bronchodilation
- anticholinergic antagonist. MOA: binds to M2 receptor and antagonises it. Increases rate of SA node and conduction of AV node. Increase HR only.
- anticholinergic antagonist. MOA:binds to M3 receptor in lungs ->blocks parasympathetic response ->decreases actin myosin interaction ->bronchodilation
- chemical defib. INduces K efflux and inhibits Ca2 influx. Allows SA node to take over and stops reentry circuit in AV.
- sodium channel blocker- local anesthetic. Blocks voltage-gated sodium channel on axon of nerve cells, prevents Na influx, disrupts action potential
- anti-coagulant. Binds to anti-thrombin -> clotting cascade is disrupted -> thrombin not activate -> blocks fibrinogen turning into fibrin.
- pro-drug. metabolised in liver, converted to NO. NO increases CAMP. vasodilation. reduces work load of heart by decreasing preload and after load.
- antiplatelet. irreversably antagonises P2Y12 receptor blocking ADP. decreased intracellular CA. prevents degranulation of platelets, shape change.
- non-selective NSAID. non-selectively inhibits COX1&2, this inhibits synthesis of prostaglandins, reduces late phase mediators.
- tissue plasminogen activator. Activates plasminogen -> converts to plasmin -> cleaves fibrin -> fibrin mesh in broken down. works on dissolution phase
- benzodiazepine. Allosterically binds to GABAa via benzodiazepine binding site. D/C membrane potential. I/C GABA binding, gate opening frequency, Cl in
- NMDA receptor agonist. Antagonises NMDA receptors -> glutamate release -> dissociative effects -> slows CNS.
- Non-selective NSAID. Irreversably inhibits platelet aggregation. Non-selectively inhibits COX 1+2 -> prevents synthesis of TxA2 and PGI2
- class 3 anti-arrythmic. Blocks K channels -> inhibits efflux -> interfers with repolarisation -> refractory period extended
- non-selective COX inhibitor. Inhibits COX 1+2 -> D/C PGE2 -> D/C pain potentiation -> has antipyretic effects.
- opioid receptor antagonist. Binds to MU receptors blocking morphine binding by competing for site. I/C Ca in presynaptic neuron -> pain transmission
- opioid agnoist. pre-synaptic neuron. Interacts with mu receptor. inhibits calcium influx and release of neurotransmitters into synapse. pain signal X
- 24. But synthetic, smaller molecule and lipophilic = increased potency and half life.
- dopamine antagonist. Antagonises D1 and D2 receptors. Blocks dopamine transmission in brain -> CNS depression.
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