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Drugs that have been shown to improve long-term survival in patients with heart failure 2/2 left ventricular systolic dysfunction

1. Beta blockers (eg, carvedilol, metoprolol)
2. ACE inhibitors (eg, lisinopril, ramipril)
3. Angiotensin II receptor blockers aka ARBs (eg, valsartan)
4. Aldosterone antagonists (eg, spironolactone, eplerenone)



1. Class III antiarrhythmic agent.
2. Prolongs APD and therefore QT interval by blocking outward potassium currents during phase 3 of AP, prolonging repolarization.
3. Unlike other drugs that cause QT prolongation, AMIODARONE has very little risk of inducing torsades de pointes. Thought to be 2/2 more homogenous effect on ventricular repolarization than other drugs (ie, less QT dispersion).



1. Prolongs AV nodal conduction by augmenting vagal parasympathetic tone
2. Increases cardiac contractility by inhibiting Na+/K+ATPase (increasing intracellular calcium).
3. Decreases APD and can cause QT interval shortening rather than prolongation.
4. Improves symptoms of HF and reduces rate of hospitalization but has not been shown to improved overall survival.



1. Class IC antiarrhythmic
2. Used occasionally for management of SVT in patients with a structurally normal heart.
3. Slows AP conduction velocity by blocking sodium channels (phase 0 of AP).



1. Adenosine receptor antagonist, phosphodiesterase inhibitor and indirect adrenergic agent used sometimes as an alternate therapy for COPD/asthma, with a NARROW therapeutic index.
2. Causes bronchodilation by increasing intracellular cAMP and has mild anti-inflammatory effects.
3. Metabolized by hepatic cytochrome oxidases. Inhibition of these enzymes by concurrent illness or drugs can raise serum concentration and cause theophylline toxicity 2/2 drug's narrow TI (eg, Ciprofloxacin-induced theophylline toxicity).
4. Theophylline toxicity presents as excessive CNS stimulation (eg, tremor, insomnia, seizures), GI disturbances, and CV abnormalities (eg, cardiac arrhythmias, hypotension, tachycardia).


Drugs that inhibit hepatic cytochrome oxidases

Cimetidine, ciprofloxacin, macrolides, verapamil


Biologic response modifiers (BRMs)

Class of treatments including antibiotics, cytokines, and other substances that are intended to restore or induce the immune system's ability to overcome disease.



A monoclonal antibody used in lymphoma immunotherapy that targets the CD20 surface immunoglobulin expressed on B-cells.



Trastuzumab (Herceptin) is a monoclonal antibody used to treat breast cancer that targets HER2-neu receptor expressed by some breast cancers.



A chimeric (human/murine) IgG1 monoclonal antibody against TNF-alpha. Used to treat RA, ankylosing spondylitis and fistulizing Crohn's disease.



Cytokine that regulates activation and differentiation of T-cells to aid in tumor cell destruction. FDA-approved for treatment of renal cell carcinoma and melanoma.


Imatinib mesylate

A small molecule potent inhibitor of the BCR/ABL fusion protein tyrosine kinase expressed in CML (due to the Philadelphia chromosome mutation). Imatinib inhibits the proliferation of BCR/ABL-expressing cells without inducing apoptosis. Imatinib has dramatically changed management of CML.



A chimeric mouse-human monoclonal antibody against the platelet GP IIB/IIIa receptor. It works by blocking the final step in platelet aggregation and is often administered during angioplasty in patients with ACS.



A neprilysin inhibitor, prevents the degradation of ANP by neprilysin, enhancing its beneficial hemodynamic effects in HF patients, ie, natriuresis, vasodilation, and diuresis.


Side effects of loop diuretics (eg, furosemide, torsemide, bumetanide)

1. Inhibit Na/K/2Cl symporters in ascending limb of loop of Henle.
2. Inhibition of similar symporters in inner ear believed to cause ototoxicity (tinnitus, vertigo, hearing impairment, deafness) seen with loop diuretic use.
3. Ototoxicity typically occurs with higher doses, preexisting CKD, rapid IV administration or when used in combination with other ototoxic agents (aminoglycosides, salicylates, cisplatin).
4. Additional side effects include hypokalemia, hypomagnesemia, and hypocalcemia.


Ototoxic drugs

1. Loop diuretics (furosemide, torsemide, bumetanide)
2. Aminoglycosides (gentamicin, tobramycin, amikacin)
3. Salicylates (aspirin)
4. Cisplatin


Digoxin toxicity

Cardiac arrhythmias, hyperkalemia, N/V, confusion


HCTZ side effects

Hypokalemia, hyponatremia, hypomagnesemia, hypercalcemia


ACE inhibitor side effects

Cough (bradykinin), hyperkalemia, angioedema, anaphylactoid reactions



1. Aldosterone antagonist (competitive inhibitor) with mild K-sparing diuretic effects.
2. Blocks detrimental cardiac effects of aldosterone (ie, produced by myocardium in HF, leading to fibrosis and myocardial hypertrophy, resulting in cardiac remodeling that worsens LV dysfunction.)
3. Structurally similar to androgens and acts as androgen receptor antagonist, inhibiting testosterone synthesis.
4. Adverse effects: hyperkalemia, b/l or unilateral gynecomastia, impotence, decreased libido.
5. Eplerenone is a newer, more selective aldosterone antagonist that produces fewer endocrine side effects.



1. Inhibits carbonic anhydrase, enzyme found in high concentrations in proximal renal tubule responsible for catalyzing reactions necessary for HCO3- reabsorption.
2. Inhibition of CA blocks HCO3- reabsorption, resulting in HCO3- and H2O excretion, causing alkaline urine and metabolic acidosis.
3. CA also present in eyes, pancreas, GI tract, CNS, and RBCs.
4. In the eye, inhibition of CA decreases HCO3- secretion and aqueous humor formation, thus relieving intraocular pressure in glaucoma.
5. Adverse effects: somnolence, paresthesias, urine alkalinization.
6. Rare side effects include metabolic acidosis, dehydration, hypokalemia, and hyponatremia.


How do OCPs work to reduce hirsutism in PCOS?

1. Decrease ovarian androgen production by suppressing LH secretion from pituitary through negative feedback.
2. Also increase sex hormone binding globulin (SHBG) synthesis by liver, decreasing free testosterone levels.
3. Androgen receptor antagonists (eg, spironolactone) also effective in suppressing androgen-dependent hair growth.
4. 5-alpha reductase inhibitors (eg, finasteride) decrease peripheral conversion of testosterone to DHT but less effective than spironolactone in treating hirsutism.
5. Both spironolactone and finasteride strongly teratogenic.



Topical ornithine decarboxylase inhibitor used to decrease rate of facial hair growth. Inhibition leads to decreased cell growth and increased apoptosis.



Selective estrogen receptor modulator that prevents negative feedback inhibition on the hypothalamus and pituitary by circulating estrogen, resulting in increased gonadotropin production (FSH and LH) and ovulation.



11-beta-hydroxylase inhibitor. Blocks cortisol synthesis.



Dopamine agonist. Decreases pituitary release of prolactin, useful in patients with infertility due to hyperprolactinemia or in patients with pituitary prolactinoma.



Dopamine agonist. Decreases pituitary release of prolactin, useful in patients with infertility due to hyperprolactinemia or in patients with pituitary prolactinoma.



Relaxes skeletal muscle by reducing the release of Ca++ from the sarcoplasmic reticulum. Used to tx malignant hyperthermia and neuroleptic malignant syndrome.


Nondepolarizing NMJ muscle relaxants

1. Vecuronium, rocuronium, pancuronium, tubocurarine.
2. Competitively inhibit postsynaptic ACh receptors at motor endplate as well as presynaptic ACh receptors, leading to progressively less ACh release at the NMJ.
3. Competitive inhibition of postsynaptic receptors prevents activation of some muscle fibers, decreasing strength of twitch compared to normal muscle twitch.
4. TOF stimulation displays progressive reduction in each of 4 responses (fading pattern) as result of less Ach being released with each subsequent impulse 2/2 the additional effect of presynaptic Ach receptor blockade.



1. Reversible acetylcholinesterase inhibitor.
2. Tx myasthenia gravis
3. Used routinely in anesthesia to reverse nondepolarizing muscle relaxants (rocuronium, vecuronium) at the end of an operation.
3. Tx postoperative or neurogenic ileus and urinary retention.
4. As quaternary amine, does not penetrate CNS like physostigmine does. NEOstigmine = NO CNS.