USMLE Step 1
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| Glycosides MOA | MOA: inhibits the Na-K pump & thus as Na levels rise also inhibits the Na-Ca pump also allowing Ca to rise for aiding in increasing CO (used for severe LV systolic dysfx like CHF), derived from the foxglove plant
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| Glycosides ADRs (note enhanced by hypoK, alkalosis, hypoxia & hypothyroidism) | ADRs: therapeutic index low, need regular monitoring serum levels, 1st indications of toxicity change in vision, arrhythmias & AV- due 2 hypokalemia (b careful w/ use of thiazides/loop diuretics), nausea, ab pain, fatigue, confusion, color misperception
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| Digitoxin | MOA: glycoside that inhibits Na/K ATPase also allowing for increase in Na & Ca concs, ADRs: cant be used in those w/ liver probs since relies on liver for metabolism, long duration of action
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| Dobutamine | MOA: beta-1 agonist that activate adenyl cyclase -> cAMP -> protein kinase -> phosphorylate Ca channels that increases Ca; ADRs: less tachy or peripheral side effects than isoproterenol or epi
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| Dopamine | MOA: beta-1 agonist that activate adenyl cyclase -> cAMP -> protein kinase -> phosphorylate Ca channels that increases Ca, enhances renal flow thus used for tx of shock; ADRs: less tachy or peripheral side effects than isoproterenol or epi
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| Inamrinone | MOA: Phosphodiesterase - that prevents the catabolism of cAMP in order to prolong action of protein kinase thus resulting in increase in intracellular Ca, *Note used to be called AMRINONE*; ADRs: thrombocytopenia
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| Milrinone | MOA: Phosphodiesterase - that prevents the catabolism of cAMP in order to prolong action of protein kinase thus resulting in increase in intracellular Ca, doesnt affect platelets
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| Digoxin | MOA: glycoside -Na/K ATPase decrease exchange levels in the Na/Ca thus result in higher levels of Ca, short duration of action; ADRs: low therapeutic index, excreted unchanged in urine
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jerrica_08
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