MOA of Amiodarone
Antidysrhythmic with a broad spectrum of activity. It has predominantly class III activity. It prolongs the action potential duration, reduces automaticity, and prolongs the refractory period of atrial, nodal, and ventricular tissues. The electrophysiological effects result in a reduction in abnormal electrical activity (for example ectopy), a reduction in electrical conduction, a reduction in heart rate, and a stabilisation of the SA and AV nodes. It also causes a small increase in coronary blood flow and a reduction in myocardial oxygen consumption by reducing inotropy (Its slight coronary vasodilation is due to smooth muscle relaxation from calcium channel effects, and the reduced inotropy comes partly from its beta-blocking properties, which lowers oxygen demand)
MOA of Cefazolin
First-generation cephalosporin antibiotic with activity against gram-negative and mainly gram-positive bacteria. It inhibits production of the bacterial cell wall, causing bacteria to die.
MOA of Ceftriaxone
Cephalosporin antibiotic with broad activity against gram-negative and gram-positive bacteria. It inhibits production of the bacterial cell wall, causing bacteria to die.
MOA of Clopidogrel
- Has antiplatelet activity.
- It antagonises the binding of ADP to platelets and impairs platelet function.
- It provides significantly more antiplatelet activity than aspirin.
Clopidogrel puts a padlock on the P2Y₁₂ ADP receptor on platelets. That receptor is normally part of the “activation handshake” platelets use to get sticky. Once blocked, platelets can’t fully activate or recruit their friends, so clot formation slows right down. Because this blockade is irreversible, each affected platelet stays chilled-out for the rest of its lifespan, which is why its antiplatelet effect ends up stronger and more consistent than aspirin’s.
MOA of Droperidol
Blocks dopamine and alpha receptors centrally, resulting in sedation, reduced agitation and a state of mental detachment, and antiemetic action.
MOA of Enoxaparin
Low molecular weight heparin (LMWH) anticoagulant. It potentiates the activity of antithrombin lll (a naturally occurring anticoagulant) causing inhibition of multiple coagulation factors, particularly factor Xa.
MOA of Fentanyl
Opiate analgesic. It is an opiate agonist (or stimulator) that binds to opiate receptors in the brain and spinal cord causing analgesia.
MOA of Heparin
Anticoagulant. It potentiates the activity of antithrombin lll (a naturally occurring anticoagulant) causing inhibition of multiple coagulation factors.
MOA of Hydrocortisone
Corticosteroid with anti-inflammatory and immunosuppressant actions. It inhibits the production of inflammatory mediators, including prostaglandins and leukotrienes, resulting in a reduction in the inflammatory and immune response.
MOA of Ketamine
Has complex actions but is predominantly an N-methyl-d-aspartate (NMDA) receptor antagonist (blocker), resulting in inhibition of excitatory neurotransmitters in the brain. Low doses cause analgesia, larger doses cause amnesia and dissociation, and high doses cause anaesthesia.
MOA of Levetiracetam
Anticonvulsant. It is thought to inhibit seizure activity by blocking some calcium channels and also binding synaptic proteins to modulate neurotransmitter release.
MOA of Lignocaine 1%
Local anaesthetic. It blocks the initiation and transmission of nerve impulses by blocking the movement of sodium ions across the nerve cell membrane.
MOA of Metoprolol Tartrate
Immediate release beta blocker. It antagonises (blocks) beta-1 receptors in the heart, causing a decrease in heart rate, cardiac output, and blood pressure.
MOA of Midazolam
Benzodiazepine. It enhances the activity of gamma-aminobutyric acid (GABA) at GABA receptors within the central nervous system, resulting in anticonvulsant activity, sedation, amnesia, anxiolysis, and muscle relaxation.
MOA of Morphine
Opiate analgesic. It is an opiate agonist that binds to opiate receptors in the brain and spinal cord causing analgesia.
MOA of Naloxone
Opiate receptor antagonist (blocker). By blocking opiate receptors, naloxone reverses the effects of opiates, particularly respiratory depression and sedation.
MOA of Olanzapine
Atypical antipsychotic. It has actions at multiple receptors within the brain causing a reduction in agitation, sedation, anxiolysis, and stabilisation of mood.
MOA of Oxytocin
Synthetic version of the naturally occurring hormone oxytocin which is normally released from the pituitary gland. It stimulates oxytocin receptors on the uterus, causing increased uterine contraction and reducing blood loss from the uterus.
MOA of Tenecteplase
Fibrinolytic that accelerates the breakdown of blood clots. It converts the plasma protein plasminogen into the active enzyme plasmin, which breaks down fibrin within blood clots.
MOA of Ticagrelor
Has antiplatelet activity. It produces reversible inhibition of the ADP receptor on platelets, decreasing platelet aggregation.
MOA of Tranexamic Acid
Antifibrinolytic medicine. It blocks the conversion of plasminogen to plasmin, reducing fibrinolysis (breakdown of blood clots) and bleeding.
