Penicillin G (IV), Penicillin V (oral)


Mech:  Binds PBP’s, blocks transpeptidase X-linking of cell wall, activates autolytic enzymes


Clinical Use:  Bactericidal for Gram+ cocci, rods, and spirochetes. NOT penicillinase resistant.


Toxicity:  Hypersensitivity reactions, hemolytic anemia




Methicillin, Nafcillin, Dicloxacillin


Mech:  Same as penicillin.  Narrow spectrum; Penicillinase RESISTANT because of bulkier R group.


Clinical Use:  Staph. Aureus


Toxicity:  Hypersensitivity reactions; Methicillin: Interstitial nephritis





Ampicillin, Amoxicillin


Mech:  Same as penicillin. Wider spectrum; penicillinase sensitive. Combine with clavulanic acid (penicillinase inhibitor) to enhance spectrum. AmOxicillin has greater Oral bioavailability than ampicillin.


Clinical Use:  Extended-spectrum penicillin: certain gram+ bacteria and GNR’s (Haemophilus influenza, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enterococci – HELPS kill Enterococci)


Toxicity:  Hypersensitivity; Ampicillin: rash, pseudomembranous colitis

Carbenicillin, Peperacillin, Ticarcillin


Mech:  Same as penicillin. Extended spectrum.


Clinical Use:  Pseudomonas species and GNRs; susceptible to penicillinase; use with clavulanic acid


Toxicity:  Hypersensitivity






Mech: b-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinase. Bactericidal.

Clinical Use: 1st Gen: Gram+ cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae (PEcK). 2nd Gen: Gram+ cocci, H. influenzae, Enterobacter aerogenes, Neisseria species, Proteus, E. coli, Klebsiella, Serratia marcescens (HEN PEcKS). 3rd Gen: Serious gram- infections resistant to other b-lactams; meningitis (most penetrate the BBB). Eg. Ceftazidime for Pseudomonas; ceftriaxone for gonorrhea. 4th Gen: increased activity against Pseudomonas and gram+ orgs.

Toxicity: Hypersensitivity, increases nephrotoxicity of aminoglycosides, disulfuram-like rxn w/ ethanol (in ceph. w/ methylthiotetrazole group)




Mech: Monobactam RESISTANT to b-lactamases. Inhibits cell wall synthesis (binds to PBP3)


Clinical Use: GNRs: Klebsiella, Pseudomonas, and Serratia species. No activity against gram+ or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cant take aminoglycosides


Toxicity: Usually nontoxic; occasional GI upset





Mech: Wide-spectrum, b-lactamase RESISTANT carbapenem. Always given with cilastatin (inhib. of renal dihydropeptidase I) to decrease inactivation in renal tubules. With imipenem “the kill is lastin with cilastatin


Clinical Use: Gram+ cocci, GNRs, and anaerobes. Drug of choice for Enterobacter.

Toxicity: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels. 




Mech: Inhibits cell wall mucopeptide formation. Bactericidal. Resistance occurs with amino acid change of D-ala D-ala to D-ala D-lac.

Clinical Use: Serious gram+ MDR bugs, incl. Staph aureus and C. difficile (pseudomembranous colitis).


Toxicity: Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing – “red man syndrome” (mostly prevented by pre-tx w/ antihistamine and slow infusion). Well tolerated in general: does NOT have many problems.

Protein Synthesis Inhibitors


30S Subunit:  A = Aminoglycosides (streptomycin, gentomycin, tobramycin, amikacin); T = Tetracyclines


50S Subunit:  C = Chloramphenicol, E = Erythromycin, L = Lincomycin, L = cLindamycin


Pneumonic: “Buy AT 30, CELL at 50




Aminoglycosides: Gentamycin, neomycin, amikacin, tobramycin, streptomycin


Mech: Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes.

Clinical Use: Severe GNR infection. Synergistic w/ b-lactam abx. Neomycin for bowel surgery.

Toxicity: Nephrotoxicity (esp. w/ cephalosporins), Ototoxicity (esp. w/ loop diuretics). Teratogenic.



Tetracyclines: tetracycline, doxycycline, demeclocycline, minocycline


Mech: Bacteriostatic, binds to 30S and prevents attachment of aminoacyl-tRNA, limited CNS penetration. Doxycycline is fecally eliminated so ok in renal failure. Do not take w/ mild/antacids because divalent cations inhibit its gut absorption.

Clinical Use: Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi (lyme dz), Rickettsia, tularemia. VACUUM your BedRoom.

Toxicity: GI distress, discolors teeth and inhibits bone growth in kids, Fanconi’s syndrome, photosensitivity.


Macrolides: Erythromycin, azithromycin, clarithromycin


Mech: Inhibits protein synth by blocking translocation; binds the 23S rRNA of the 50S subunit. Bacteriostatic.


Clinical Use: URI’s, pneumonias, STD’s: gram+ cocci (strep in pts allergic to penicillin), Mycoplasma, Legionella, Chlamydia, Neisseria.


Toxicity: GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis, eosinophilia, skin rash






Mech: Inhibits 50S peptidyl transferase. Bacteriostatic.


Clinical Use: Meningitis (H. influenzae, Neisseria meningitides, Strep pneumoniae). Conservative use owning to toxicities.


Toxicity: Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in preemies because they lack liver UDP-glucuronyl transferase).




Mech: Blocks peptide bond formation at 50S subunit. Bacteriostatic.


Clinical Use: Anaerobic infections (B. fagilis, C. perfringens). Treats anaerobes ABOVE the diaphragm.


Toxicity: Pseudomembranous colitis (C. difficile), fever, diarrhea.





Sulfonamides: Sulfamethoxazole (SMX), sulfisoxazole, triple sulfas, sulfadiazine

Mech: PABA antimetabolites inhibit dihydropteroate synthase (nucleotide synth). Bacteriostatic.

Clinical Use: Gram+, Gram-, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

Toxicity: Hypersensitivity, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (eg. Warfarin), Stevens-Johnson Syndrome.





Mech: Inhibits bacterial dihydrofolate recuctase (nucleotide synth). Bacteriostatic.

Clinical Use: Used in combination with sulfonamides (TMP-SMX), causing sequential block of folate synthesis. Combination used for recurrent UTI, Shigella, Salmonella, PCP.

Toxicity: Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid).

Trimethoprim = TMP: Treats Marrow Poorly



Fluoroquinolones: Ciprofloxacin, norfloxacin, ofloxacin, sparfloxacin, mortifloxacin, gatifloxacin, enoxacin (fluoroquinolones), nalidixic acid (quinolone)

Mech: Inhibit DNA gyrase (topoisomerase II). Bactericidal.

Clinical Use: GNRs of urinary and GI origin (incl. Pseudomonas), Neisseria, some gram+ organisms. Anthrax.

Toxicity: GI upset, superinfections, skin rash, HA, dizziness. Contraindicated in pregnant women and children because may damage cartilage. Tendonitis and tendon rupture in adults.






Mech: Forms toxic metabolites in the bacterial cell. Bactericidal.


Clinical: Antiprotazoal. Giardia, Entamoeba, Trichomonas, Garnerella vaginalis, anaerobes (Bacteroides, Clostridium). Used with bismuth and amoxicillin or tetracycline for “triple tx” against H. pylori.

GET on the Metro! 

Anaerobic infection BELOW the diaphragm.


Toxicity: Disulfuram-like reaction with alcohol, HA.


Polymyxins:  Polymyxin B, Polymyxin E


Mech: Bind to cell membrane of bacteria and disrupt their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents.


Clinical: Resistant Gram- infections


Toxicity: Neurotoxicity, ATN




Isoniazid (INH)


Mech: Decreases synthesis of mycolic acids.


Clinical: TB. The only agent used as solo prophylaxis against TB.


Toxicity: Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicity, SLE-like syndrome.  Pyridoxine (vit. B6) can prevent neurotoxicity.

INH Injures Neurons and Hepatocytes.

Different INH half-lives in fast vs. slow acetylators





Mech: Inhibits DNA-dependent RNA polymerase.

Clinical: TB, delays resistance to dapsone when used for leprosy. Always used in combination with drugs except in tx of meningococcal carrier state, and chemoprophylaxis in contacts of children w/ H. influenzae type B.


Toxicity: Minor hepatotoxicity and drug interactions (increased P450)


4 R’s: RNA polym. Inhibitor, Revs up microsomal P450, Red/Orange body fluids, Rapid resistance if used alone.

Anti-TB Drugs


Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid


Cycloserine (second line)


All are hepatotoxic.  INH is used alone for TB prophylaxis.






Amphotericin B


Mech: Binds ergosterol (unique to fungi), forms membrane pores that disrupt homeostasis. Amphotericin “tears” holes in the membrane.


Clinical: Used for wide spectrum of systemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross BBB.


Toxicity: Fever/chills, (shake and bake), hypotension, nephrotoxicity, arrhythmias (amphoterrible)



Mech: Binds to ergosterol, disrupting fungal membranes.


Clinical: “Swish and swallow” for oral candidiasis (thrush).








Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole


Mech: Inhibit fungal steroid (ergosterol) synthesis.


Clinical: Systemic mycoses. Fluconazole for cryptocccal meningitis in AIDS patients and candidal infections of all types. Ketoconazole for Blastomyces, Coccidioides, Histoplasma, C. albicans; hypercortisolism.


Toxicity: Hormone synth inhibition (gynecomastia), liver dysfxn (inhibits P450), fever, chills.





Mech: Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (eg. Nails).


Clinical: Oral tx of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).


Toxicity: Teratogenic, carcinogenic, confusion, HA, increased coumadin metabolism.





Mech: Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes release of dopamine from intact nerve terminals.


Clinical: Prophylaxis for influenza A; Parkinson’s disease.


Toxicity: Ataxia, dizziness, slurred speech.


Amantidine blocks influenza A and rubellA and causes problems with the cerebellA

Rimantidine is a derivative with fewer CNS side effects.



Mech: Inhibits influenza neuraminidase


Clinical: Influenza A and B










Mech: Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.


Clinical: RSV


Toxicity: Hemolytic Anemia







Mech: Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.


Clinical: HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.


Toxicity: Delirium, tremor, nephrotoxicity




Gancyclovir - DHPG (dihydroxy-2-propoxymethyl guanine)


Mech:  Phosphorylation by viral kinase, preferentially inhibits CMV DNA polymerase.


Clinical: CMV, especially in immunocompromised patients.


Toxicity: Pancytopenia, renal toxicity. More toxic to host enzymes than acyclovir.






Mech: Viral DNA polymerase inhibitor that binds to the pyrophosphate binding site of the enzyme. Does not require activation by viral kinase.

Foscarnet = pyroFosphate analog.


Clinical: CMV retinitis in immunocompromised pt when gancyclovir fails.


Toxicity: Nephrotoxicity



HIV Therapy

Protease Inhibitors: Saquinavir, Ritinavir, Indinavir, Nelfinavir, Amprenavir


Mech: Inhibits assembly of new viruses by blocking protease enzyme


Toxicity: GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir)



Part of triple therapy: 2 RT inhibitors + 1 protease inhibitor

Initiated when CD4 counts drop below 500 or high viral load

HIV Therapy

Reverse Transcriptase Inhibitors: Nucleosides:  Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC, stavudine (d4T), lamivudine (3TC), abacavir; Non-Nucleosides:  Nevirapine, delavirdine, efanvirenz


Mech: Preferentially inhibit RT of HIV; prevent incorporation of viral genome into host DNA.

Toxicity: Bone marrow suppression (neutropenia, anemia), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT)

Clinical: Triple therapy, AZT in pregnancy to reduce vertical transmission.



Mech: Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.


Clinical: Chronic hepatitis B and C, Kaposi’s Sarcoma.


Toxicity: Neutropenia







Onchocerciasis (rIVER blindness treated with IVERmectin)












Nematode/roundworm (eg. pinworm, whipworm) infections.










Pyrantel pamoate


Giant roundworm (ascaris), hookworm (Necator/Ancylostoma), pinworm (Enterobius).











Trematode/fluke (eg. schistosomes, Paragonimus, Clonorchis) and cysticercosis.











Cestode/tapeworm (eg. D. latum, Taenia species) infections except cysticercosis.









Pentavalent antimony












Chloroquine, quinine, mefloquine














Latent hypnozoite (liver) forms of malaria (P. vivax, P. ovale)












Giardiasis, amoebic dysentery (E. histolytica), bacterial vaginsitis (Garnerella), Trichomonas











Pneumocystis carinii pneumonia prophylaxis












Chagas’ disease, American trypanosomiasis (Trypanosoma cruzi)












African trypanosomiasis (sleeping sickness)












Mech: direct cholinergic agonist


Clinical: Postoperative and neurogenic ileus and urinary retention. Activates bowel and bladder smooth muscle.







Carbachol, Pilocarpine


Mech: direct cholinergic agonist


Clinical: Glaucoma. Activates ciliary muscle of eye (open angle), pupillary sphincter (narrow angle), opening of trabecular meshwork and increased outflow of aqueous humor


Toxicity: Miosis, cyclospasm






Mech: Anticholinesterases (indirect cholinergic agonist). Increases endogenous ACh.


Clinical: Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of NMJ blockade (postOP)








Mech: Anticholinesterase (indirect cholinergic agonist). Increases endogenous ACh; inreases strength.


Clinical: Myasthenia gravis







Edrophonium (Tensilon)


Mech: Anticholinesterase (indirect cholinergic agonist). Increases endogenous ACh.


Clinical: Diagnosis of myasthenia gravis (extremely short acting)









Mech: Anticholinesterase (indirect cholinergic agonist). Increases endogenous ACh.


Clinical: Glaucoma – causes ciliary muscle contraction, opening of trabecular meshwork and increased outflow of aqueous humor (crosses BBB to CNS); and atropine overdose


Toxicity: Miosis, cyclospasm





Mech: Anticholinesterase (indirect cholinergic agonist). Increases endogenous ACh.


Clinical: Glaucoma - causes ciliary muscle contraction, opening of trabecular meshwork and increased outflow of aqueous humor


Toxicity: Miosis, cyclospasm





What are the symptoms of cholinesterase poisoning?




Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation , Sweating, Salivation, and abdominal cramping







Mech: Muscarinic antagonist.


Clinical: Pupil dilation, reduce acid secretion in acid-peptic disease, reduce urgency in mild cystitis, decrease GI motility, reduce airway secretions, organophosphate poisoning, dangerous arrhythmias.Blocks Salivation, Lacrimation, Urination, Defacation

Toxicity: Increased body temp, rapid pulse, dry mouth, dry flushed skin, disorientation, mydriasis with cycloplegia, and constipation.

Blind as a bat, Red as a beet, Mad as a hatter, Hot as a hare, Dry as a bone



Mech: Ganglionic nicotinic ACh receptor antagonist (blocks only at ganglion, so no NMJ blockade)











Mech: Cholinesterase regenerator


Clinical: regenerates active cholinesterase, chemical antagonist, used to treat organophosphate exposure.









Mech: Muscarinic cholinergic antagonist


Clinical: Prevention of nausea and vomiting a/w motion sickness


Toxicity: dry mouth, drowsiness, blurred vision, disorientation








Mech: Muscarinic antagonist


Clinical: Parkinson’s disease








Homatropine, tropicamide


Mech: Muscarinic antagonist


Clinical: Produce mydriasis and cycloplegia










Mech: Muscarinic antagonist


Clinical: Asthma, COPD










Mech: NMJ ACh receptor depolarizing blocker. Phase I (prolonged depolarization) – no antidote. Block potentiated by cholinesterase inhibit. Phase II (repolarized but blocked) – antidote: cholinesterase inhibitors (neostigmine).


Clinical: muscle paralysis in surgery or mechanical ventilation





Tubocurarine, atracurium, mivacurium, pancuronium, vercuronium, rapacuronium


Mech: NMJ ACh receptor non-depolarizing blocker. To reverse blockade, give cholinesterase inhibitor.


Clinical: Muscle paralysis for surgery or mechanical ventilation








Mech: Prevents the release of Ca++ from the sarcoplasmic reticulum of skeletal muscle.


Clinical: Treatment of malignant hyperthermia, which is caused by the concomitant use of halothane and succinylcholine. Also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).







Mech: Catecholamine sympathomimetic.  Direct agonist at a1,a2, b1, b2 adrenergic receptors.


Clinical: Anaphylaxis, glaucoma (open angle – increased outflow of aqueous humor), asthma, hypotension.


Toxicity: Mydirasis, stinging; do not use in closed-angle glaucoma






Mech: Catecholamine sympathomimetic. Direct agonist at a1,a2, b1 adrenergic receptors.


Clinical: Hypotension (but decreases renal perfusion)









Mech: Catecholamine sympathomimetic. Direct agonist at b1=b2  adrenergic receptors


Clinical: AV block (rare)









Mech: Catecholamine sympathomimetic. Direct agonist at D1=D2>b>a adrenergic receptors.


Clinical: Shock (increases renal perfusion), heart failure.









Mech: Catecholamine sympathomimetic. Direct agonist at b1>b2 adrenergic receptors.


Clinical: Shock, Heart failure









Mech: Indirect sympathomimetic. Stimulates release of stored catecholamines.


Clinical: Narcolepsy, obesity, attention deficit disorder









Mech: Indirect sympathomimetic. Stimulates release of stored catecholamines.


Clinical: Nasal decongestion, urinary incontinence, hypotension









Mech: Sympathomimetic.  a1>a2  adrenergic receptor agonist.


Clinical: Pupil dilator, vasoconstriction, nasal decongestion








Albuterol, terbutaline


Mech: Sympathomimetic. b2>b1 adrenergic receptor agonist.


Clinical: Asthma










Mech: Indirect general sympathomimetic; catecholamine uptake inhibitor


Clinical: Vasoconstriction and anesthesia









Mech: Centrally acting a2 agonist.  Decreases central adrenergic outflow.


Clinical: Hypertension, especially with renal disease (no decrease in blood flow to the kidney)








Mech: Nonselective, irreversible alpha adrenergic blocker


Clinical: Pheochromocytoma


Toxicity:  Orthostatic hypotension, reflex tachycardia








Mech: Nonselective, reversible alpha adrenergic blocker


Clinical: Pheochromocytoma








Prazosin, terazosin, doxazosin


Mech:  a1 selective blocker.


Clinical: Hypertension, urinary retention in BPH


Toxicity: First-dose orthostatic hypotension, dizziness, headache








Mech: a2 selective blocker.


Clinical: Impotence (effectiveness controversial)








b-Blockers: Propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol

Mech: Nonselective (b1=b2 ): propranolol, timolol, pindolol, nadolol, labetolol (also blocks alpha-1receptors)

b1 selective (b1>b2): metoprolol, atenolol, esmolol (short acting)

Clinical: Hypertension (decrease CO and renin secretion), Angina Pectoris (decrease HR, contractility, O2 consumption), MI (beta-blockers decrease mortality), SVT: propranolol/esmolol (decrease AV conduction velocity), CHF (slow progression of chronic failure), Glaucoma: timolol (decrease secretion of aqueous humor)

Toxicity: Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep prob), caution in DM



Mech: Alpha antagonist


Clinical: Glaucoma – decreased aqueous humor synthesis


Toxicity: No pupillary or vision changes






Acetazolamide, dorzolamide, brinzolamide


Mech: Carbonic anhydrase inhibitor.


Clinical: Diuretic. Glaucoma – decrease aqueous humor secretion due to decreased HCO3-


Toxicity: No pupillary or vision changes.







Mech: prostaglandin


Clinical: Increased flow of aqueous humor


Toxicity: Darkens color of urine (browning)






Barbiturates: Phenobarbital, pentobarbital, thiopental, secobarbital


Mech: Facilitate GABAa action by increasing duration of Cl- channel opening, thus decreasing neuron firing.


Clinical: Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)


Toxicity: Dependence, additive CNS depression with EtOH, resp or CV depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cyt. P450)


Benzodiazepines: Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide


Mech: Facilitate GABAa action by increasing frequency of Cl- channel opening. Most have long half lives and active metabolites.

Clinical: Anxiety, spasticity, status epilepticus (diazepam), detoxification (esp. after alcohol withdrawl  DT’s)

Short Acting = Triazolam, Oxazepam, Midazolam (TOM)

Toxicity: Dependence, additive CNS depression w/ EtOH. Less resp depression and coma than barbi’s,

Treat overdose with flumazenil (competitive antagonist at GABA receptor)

Classical Antipsychotics (neuroleptics): Thioridazine, haloperidol, fluphenazine, chlorpromazine

Mech: Most block dopamine D2 receptors (excess dopamine a/w schizophrenia)

Clinical: Schizophrenia, psychosis

Toxicity: Extrapyramidal system: sedation, endocrine, muscarinic, alpha, and histamine receptor blocking effects.

Neuroleptic Malignant Syndrome: rigidity, autonomic instability, hyperpyrexia (tx w/ dantrolene and dopamine agonists)

Tardive Dyskinesia: stereotypic oral-facial movements probably due to dopamine receptor sensitization; results of long-term antipsychotic use

EPS: 4h acute dystonia-4d akinesia-4wk akathisia-4mo TD

Atypical Antipsychotics: Clozapine, olanzapine, risperidone


Mech: Block 5HT2 and dopamine receptors


Clinical: Tx of schizophrenia; +/- symptoms. Olanzapine is also used for OCD, anxiety disorder, and depression.


Toxicity: Fewer EPS and anticholinergic side effects than other antipsychotics. Clozapine may cause agranulocytosis (wkly WBC cts)






Mech: not established. May inhibit phosphoinositol cascade.


Clinical: Mood stabilizer for bipolar affective disorder, blocks relapse and acute manic events.


Toxicity: Tremor, hypothyroidism, polyuria (ADH antagonist causing nephrogenic DI), teratogenesis. Narrow therapeutic window requiring close monitoring of serum levels.



Tricyclic Antidepressants: Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin


Mech: Block reuptake of NE and serotonin

Clinical: Endogenous depression, bedwetting (imipramine), OCD (clomipramine).


Side effects: Sedation, a-blocking, atropine-like effects. Tertiary TCA’s (amitriptyline) have more anticholinergic effects than secondary (nortriptyline). Desipramine is least sedating.

Toxicity: Tri-C’s: Convulsions, Coma, Cardiotoxicity; resp depression, hyperpyrexia; confusion and hallucinations in elderly

SSRI’s: Fluoxetine, sertraline, paroxetine, citalopram


Mech: Serotonin-specific reuptake inhibitors.


Clinical: Endogenous depression. It may take 2-3 wks for SSRI’s to have an effect.


Toxicity: Fewer than TCA’s. CNS stimulation: anxiety, insomnia, tremor, anorexia, nausea, and vomiting; Serotonin Syndrome w/ MAOIs: hyperthermia, muscle rigidity, CV collapse.





Heterocyclics: 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used in major depressive disorders.


Mech: Primarily inhibits serotonin reuptake.


Toxicity: Sedation, nausea, priapism, postural hypotension







Heterocyclics: 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used in major depressive disorders.

Also used for smoking cessation.


Mech: not known.


Toxicity: Stimulant effects (tachycardia, agitation), dry mouth, aggravation of psychosis





Heterocyclics: 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used in major depressive disorders. Also used in GAD.


Mech: Inhibits serotonin and dopamine reuptake.


Toxicity: Stimulant effects (anxiety, agitation, headache, insomnia)






Heterocyclics: 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used in major depressive disorders.


Mech: a2-antagonist (increases release of NE and serotonin) and potent 5HT2 receptor antagonist.


Toxicity: Sedation, increased serum cholesterol, increased appetite.




MAO Inhibitors: Phenelzine, tranylcypromine


Mech: Nonselective MAO inhibition


Clinical: Atypical depressions (w/ psychotic or phobic features), anxiety, hypochondriasis.


Toxicity: Hypertensive crisis w/ tyramine ingestion (cheese or wine) and meperidine; CNS stimulation. Contraindication with SSRIs or beta-agonists.



Selegiline (deprenyl)


Mech: Selectively inhibits MAO-B, thereby increasing the availability of dopamine.


Clinical: adjunctive agent to L-dopa in treatment of Parkinson’s dz.


Toxicity: May enhance adverse effects of L-dopa.





L-Dopa (levodopa)/carbidopa


Mech: Increases level of dopamine in brain. Parkinsonism thought to be due to loss of dopaminergic neurons and excess cholinergic fxn. Unlike dopamine, L-dopa can cross the BBB and is converted by dopa decarboxylase in the CNS to dopamine.

Clinical: Parkinsonism


Toxicity: Nausea. Arrhythmias from peripheral conversion to dopamine. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to increase bioavailability in brain and limit peripheral side effects. Dyskinesias also occur.

Parkinson’s disease drugs


Dopamine agonists: L-dopa/carbidopa, bromocriptine (ergot alk and partial dopamine agonist), amantidine (enhances dopamine release)


MAO inhibitors: Selegiline (selective MAO-B inhibitor)


Antimuscarinic: Benztropine (improves tremor and rigidity, but has little effect on bradykinesia)




Opioid Analgesics: Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan


Mech: Act as agonists at opioid receptors (mu=morphine, kappa=dynorphin, delta=enkephalin) to modulate synaptic transmission

Clinical: Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone)

Toxicity: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression w/ other drugs. Tolerance does not develop to miosis and constipation. Tx toxicity w/ naloxone or naltrexone (opioid receptor antagonists)



Mech: 5HT1D agonist. Half life < 2hrs


Clinical: Acute migraine, cluster headaches


Toxicity: Chest discomfort, mild tingling (contraindicated in pts w/ CAD or Prinzmetal’s angina)







Mech: 5HT3 antagonist. Powerful central-acting anti-emetic.


Clinical: Control vomiting post-OP and in patients undergoing cancer chemotherapy


Toxicity: HA, diarrhea







Mech: Blocks voltage sensitive Na+ channels.  TCA with antiepileptic effects


Clinical: Epilepsy (Simple, complex, GTC, trigeminal neuralgia), Mania.

Contraindicated in absence seizures, MAOI’s, glaucoma


Toxicity: Diplopia, ataxia, induction of P450, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity (always check LFT’s)




Mech: Use-dependent blockade of Na+ channels. Also a class IB antiarrhythmic


Clinical: GTC, simple, complex seizures, status epilepticus


Toxicity: Nystagmus, ataxia, diplopia, lethargy, gingival hyperplasia (chronic use in children), peripheral neuropathy, hirsutism, megaloblastic anemia (decreased Vit. B12), malignant hyperthermia, teratogenic (fetal hydantoin syndrome)




Mech: Ca++ channel blocker


Clinical: Absence seizures


Toxicities: GI, lethargy, HA, urticaria, Steven’s Johnson Syndrome








Mech: Facilitate GABAa action by increasing duration of Cl- channel opening.


Clinical: Epilepsy (GTC), safer in pregnant women and Crigler-Najjar II


Toxicity: Sedation, induction of P450, tolerance, dependence




Valproic Acid


Mech: Blocks Ca++ channels, weak block of Na+ channels. May potentiate GABA


Clinical: Epilepsy (absence, myoclonic, GTC), acute mania


Toxicity: GI, rare, but fatal hepatotoxicity, neural tube defects in fetus (teratogen)






Mech: Blocks voltage sensitive Na+ channels, inhibits excitatory neurotransmission


Clinical: Epilepsy (simple, partial, GTC)


Toxicity: Life threatening rash, Steven’s Johnson syndrome







Mech: Unknown, GABA analog but doesn’t affect GABA-R


Clinical: Adjunct in refractory epilepsy (simple, partial, GTC), neurologic pain and neuropathy


Toxicity: renal excretion, sedation, movement disorders







Mech: blocks voltage sensitive Na+ channels, inhibits excitatory neurotransmission


Clinical: Adjunct in simple and complex seizure management


Toxicity: Sedation, mental dulling, kidney stones, weight loss







Mech: Enhance GABAergic inhibitory neurotransmission


Clinical: Epilepsy (GTC, status epilepticus), anxiety, panic disorders, conscious sedation


Toxicity: sedation, tolerance, dependence






Inhaled anesthetics: halothane(soluble-slow), enflurane (soluble-slow), isoflurane(soluble-slow), sevoflurane(insoluble-fast), methoxyflurane, nitrous oxide(insoluble-fast)


Mech: the lower the solubility in blood, the quicker the anesthetic induction and the quicker the recovery


Effects: Myocardial depression, resp depression, nausea/emesis, increased cerebral flow

Toxicity: Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), malignant hyperthermia



Mech: Barbiturate, high lipid solubility, rapid entry into brain.


Clinical: IV anesthesia.  Induction of anesthesia and short surgical procedures. Effects terminated by redistribution from brain.


Toxicity: Decreased cerebral blood flow







Mech: Benzodiazepine.


Clinical: IV anesthetic. Most common used drug for endoscopy; used adjunctively with gaseous anesthetics and narcotics.


Toxicity: May cause severe post-operative resp depression and amnesia







Mech: Arylcyclohexylamine. PCP analog.


Clinical: Dissociative IV anesthetic, good for hypovolemic patients. 


Toxicity: Cardiovascular stimulant, dissorientation, hallucination, and bad dreams. Increases cerebral blood flow.





Local Anesthetics: Esters: procaine, cocaine, tetracaine; amides: lidocaine, bupivicaine

Mech: Block Na+ channels by binding to specific receptors on inner portion of channel. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind in charged form. 1. In infected (acidic) tissue, anesthetics are charged and cannot penetrate membrane effectively. So more anesthetic is needed. 2. Order of nerve blockade: small diameter fibers>large diameter. Myelinated>unmyelinated. Size predominates over myelination, so small unmyelinated>small myelinated autonomic>large myelinated autonomic. Order of loss: pain>temp>touch>pressure. 3. Given w/ vasoconstrictors (epi) to enhance local action

Clinical: minor surgery, spinal anesthesia

Toxicity: CNS excitation, severe CV (bupivicaine), HTN/arrhythmias (coc)



Mech: Bind Cl site and block Na-Cl cotransporter in the distal tubule


Clinical: Diuretic, hypertension, edema


Toxicity: hypokalemia, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia







Mech: Sulfonamide loop diuretic. Inhibits Na-K-2Cl cotransporter in the thick ascending limb of the loop of henle. Abolishes the hypertonicity of the medulla, preventing concentration of urine. Increases Ca++ excretion.


Clinical: Edematous states (CHF, cirrhosis, nephrotic syndrome, pulm. edema), HTN, hypercalcemia.


Toxicity: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), interstitial Nephritis, Gout  OH DANG



Mech: Increased cGMP causes smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction


Clinical; Severe HTN, CHF


Toxicity: Compensatory tachycardia, fluid retention, lupus-like syndrome, angina, salt retention, nausea, HA




Calcium Channel Blockers: Nifedipine, verapamil, diltiazem


Mech: Block voltage-dependent L-type Ca++ channels of cardiac and smooth muscle so reduce muscle contractility.  AV nodal cells primarily. Decrease cond. velocity, increase ERP, PR.

Vascular smooth muscle: nifedipine>diltiazem>verapamil

Heart: verapamil>diltiazem>nifedipine

Clinical: Class IV antiarrhythmic, nodal arrhythmias (SVT), HTN, angina

Toxicity: Cardiac depression (CHF, AV block, sinus node depression), peripheral edema, flushing, dizziness, constipation, torsades de pointes.




Mech: blocks catecholamine release and causes depletion


Clinical: antihypertensive


Toxicity: Orthostatic and exercise hypotension, sexual dysfunction, diarrhea







Mech: Blocks catecholamine uptake into storage granules leading to depletion


Clinical: Hypertension,


Toxicity: sedation, depression, nasal stuffiness, diarrhea







Mech: a2-adrenergic agonist, centrally acting decreasing adrenergic outflow from CNS


Clinical: Hypertension, esp renal insufficiency since it doesn’t block renal blood flow


Toxicity: sedation, positive Coomb’s test






Mech: causes vasodilation via release of Nitrous oxide


Clinical: Malignant hypertension


Toxicity: Cyanide poisoning (can be metabolized to cyanide)






ACE Inhibitors: Captopril, enalapril, lisinopril


Mech: Inhibit ACE, reducing levels of ATII and preventing inactivation of bradykinin, a potent vasodilator. Renin release increased due to loss of feedback inhib.


Clinical: Hypertension, CHF, diabetic renal disease


Toxicity: Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower ATII, hyperkalemia. CAPTOPRIL




Mech: ATII receptor antagonist.


Clinical: Hypertension


Toxicity: Fetal renal toxicity, hyperkalemia, does not cause cough






Acetazolamide, dorzolamide, brinzolamide


Mech: Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total body HCO3- stores. Acts at proximal convoluted tubule.

Clinical: Diuretic. Glaucoma – decrease aqueous humor secretion due to decreased HCO3-. Urinary alkalinization, metabolic alkalosis, altitude sickness.


Toxicity: No pupillary or vision changes. Hyperchloremic metabolic acidosis (normal anion gap), neuropathy, ammonia toxicity, sulfa allergy.

Ethacrynic Acid


Mech: Phenoxyacetic acid derivative (not a sulfonamide). Same action as furosemide.


Clinical: Diuresis in patients allergic to sulfa drugs


Toxicity: similar to furosemide, except no hyperuricemia, no sulfa allergy






Mech: Thiazide diuretic. Inhibits NaCl cotransport in early distal tubule, reducing diluting capacity of the nephron. Decreases Ca++ excretion.


Clinical: Hypertension, CHF, calcium stones, nephrogenic DI


Toxicity: hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, slight hyperLipidemia, hyperUricemia, lassitude, hyperCalcemia




Mech: K+ sparing diuretic:  competitive aldosterone receptor antagonist in cortical collecting tubule.


Clinical: Hyperaldosteronism, K+ depletion, CHF


Toxicity: hyperkalemia, endocrine effects (gynecomastia, antiandrogen)




Triamterene, Amiloride


Mech: K+ sparing diuretics: Block sodium channels in the CCT.


Clinical: Hyperaldosteronism, K+ depletion, CHF


Toxicity: Hyperkalemia, no endocrine effects








Mech: Osmotic diuretic, increases tubular fluid osmolarity producing increased urine flow


Clinical: Acute renal failure, drug overdose, decrease intracranial/intraocular pressure


Toxicity: pulmonary edema, dehydration. Contraindicated in anuria, CHF



Electrolyte changes with Diuretics:


Urine NaCl: increase (all diuretics)

Urine K+: increase (all diuretics except spironolactone, triamterene, amiloride)

Blood pH:  Acidosis (carbonic anhydrase inhib, K+ sparing) Alkalosis (loop diuretics, thiazides)

Urine Ca++:  increased (loop diuretics, spironolactone), decreased (thiazides, amiloride)




What is the effect of Nitrates on the heart?


Affect Preload

Decrease EDV, BP, Ejection time, MVO2

Increase Contractility (reflex), HR (reflex)








What is the effect of Beta Blockers on the heart?


Affect afterload

Decrease BP, Contractility, HR, MVO2

Increase EDV, Ejection time








What is the effect of Nitrates plus Beta Blockers on the heart?


No effect or decrease EDV

Little/no effect on Contractility and Ejection time

Decrease BP, HR, MVO2








Nitroglycerin, isosorbide dinitrate


Mech: Vasodilate by releasing nitric oxide in smooth muscle, causing increase in cGMP and smooth muscle relaxation. Dilate veins >> arteries


Clinical: Angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer.

Toxicity: Tachycardia (reflex), hypotension, HA, “Monday disease” in industrial exposure, development of tolerance for vasodilating action during work week and loss of tolerance over weekend, resulting in tachy, dizziness and HA.

Digoxin (Cardiac Glycoside)

Mech: Inhibit Na-K-ATPase of cell membrane causing increase in intracellular Na. Na-Ca antiport does not function as well causing increased Ca inside; leads to positive inotropy. May cause increased PR, decreased QT, scooping of ST segment, T wave inversion on EKG.

Clinical: 75% bioavailability, 20-40% protein bound, T1/2 40 hrs, urinary excretion.  CHF, atrial fibrillation.

Toxicity: Nausea, vomiting, diarrhea, blurry yellow vision (Van Gogh), Arrhythmias. Toxicities increased in renal failure, hypokalemia (potentiates drug effects), and quinidine (decreases clearance, displaces digoxin from tissue binding sites). Antidote: Normalize K+ slowly, lidocaine, cardiac pacer, anti-dig Fab (digibind)

Quinidine, Amiodarone, Procainamide, Disopyramide

Na Channel blockers - Class Ia Antiarrhythmics 


Mech: Increased AP duration, increased ERP, increased QT. Decrease slope of phase 4 depolarization and increase threshold for firing in abnormal pacemaker cells. Are state dependent (fast tachy).


Clinical: Affect both atrial and ventricular arrhythmias.


Toxicity: Quinidine (cinchonism: HA, tinnitus; thrombocytopenia; torsades de pointes due to increased QT interval); Procainamide (reversible SLE-like syndrome)




Lidocaine, mexiletine, tocainide

Na Channel Blockers - Class Ib Antiarrhythmics 

Mech: Decreased AP duration. Affect ischemic or depolarized Purkinje and ventricular tissue. Decrease slope of phase 4 depolarization and increase threshold for firing in abnormal pacemaker cells. Are state dependent (fast tachy).

Clinical: Used in ventricular arrhythmias (esp. post-MI) and in digitalis-induced arrhythmias.

Toxicity: Local anesthetic. CNS stimulation/depression, CV depression

Flecainide, encainide, propafenone

Na Channel Blockers – Class Ic Antiarrhythmics


Mech: No effect on AP duration. Decrease slope of phase 4 depolarization and increase threshold for firing in abnormal pacemaker cells. Are state dependent (fast tachy).

Clinical: Useful in V-tachs that progress to VF and in intractable SVT. Are used as a last resort in refractory tachyarrhythmias because of toxicities.

Toxicity: proarrhythmic



Class II Antiarrhythmics: Beta-blockers: Propranolol, esmolol, metoprolol, atenolol, timolol


Mech: Decrease cAMP, Ca currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive: increased PR. Esmolol is very short acting.


Toxicity: Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask signs of hypoglycemia.



Class III Antiarrhythmics: K+ Channel blockers: Sotalol, ibutilide, bretylium, amiodarone


Mech: Increase AP, ERP, QT.

Clinical: Used when other antiarrhythmics fail.


Toxicity: Sotalol – torsades de pointes, excessive beta-block; Ibutilide – torsades; Bretylium – new arrhythmias, hypotension; Amiodarone – Pulmonary fibrosis, corneal deposits, Hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF), hyper/hypothyroidism.

Check PFTs, LFTs, TFTs with amiodarone.

Class IV Antiarrhythmics: Ca++ Channel blockers: Verapamil, diltiazem


Mech: Primarily effects AV nodal cells. Decrease conduction velocity, increase ERP, PR.


Clinical: Used in preventing nodal arrhythmias (SVT).


Toxicity:  Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression); torsades de pointes (bepridil)





Drug of choice for diagnosing/abolishing AV nodal arrhythmias.












Depresses ectopic pacemakers, especially in digoxin toxicity.












Effective in torsades de pointes and digoxin toxicity










Cholestyramine, colestipol


Mech: Bile acid resins block reabsorption of bile acids. Decrease LDL, no effect on HDL, slight increase in triglycerides.


Clinical: Hypercholesterolemia


Toxicity: Patients hate it. Tastes bad and causes GI discomfort.





Lovastatin, pravastatin, simvastatin, atorvastatin


Mech: HMG-CoA Reductase inhibitors.  Significantly decrease LDL. Small increase in HDL, small decrease in triglycerides.


Clinical: Hypercholesterolemia


Toxicity: Myositis (muscle pain/weakness), reversible increase in LFT’s, expensive






Mech: block cholesterol transport into VLDL particles. Moderate decrease in LDL, Moderate increase in HDL, small decrease in TG.


Clinical: Hypercholesterolemia


Toxicity: Red, flushed face, which is decreased by aspirin or long-term use.




Gemfibrozil, clofibrate


Mech: Lipoprotein lipase stimulators: stimulates conversion of VLDL to IDL. Small decrease in LDL, small increase in HDL, Large decrease in TG’s.


Clinical: Hypercholesterolemia


Toxicity: Myositis, increased LFT’s






Mech: S-phase specific antimetabolite. Folic acid analog that inhibits dihydrofolate reductase, resulting in decreased dTMP and thus decreased DNA and protein synthesis.


Clinical: Leukemias, lymphomas, choriocarcinoma, sarcoma. Abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis.


Toxicity: Myelosuppression, which is reversible with leucovorin (folinic acid) rescue. Macrovesicular fatty change in liver.


5-Fluorouracil (5-FU)


Mech: S-phase specific antimetabolite. Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase, resulting in decreased dTMP and same effects as methotrexate.


Clinical: Colon ca. and other solid tumors, basal cell carcinoma (topical). Synergy with methotrexate.


Toxicity: Myelosuppression which is not reversible with leucovorin; photosensitivity

6-Mercaptopurine (6-MP)


Mech: Blocks purine synthesis


Clinical: Leukemias, lymphomas (not CLL or Hodgkins)


Toxicity: Bone marrow, GI, liver. Metabolized to xanthine oxidase, thus increases toxicity with allopurinol







Mech: Alkylates DNA


Clinical: CML


Toxicity: Pulmonary fibrosis, hyperpigmentation.








Mech: Alkylating agent; covalently x-links (interstrand) DNA at guanine N-7. Requires bioactivation by liver.


Clinical: NHL, breast and ovarian ca. Also an immunosuppressant.


Toxicity: Myelosuppression, hemorrhagic cystitis





Nitrosureas: carmustine, lomustine, semustine, streptozocin


Mech: Alkylates DNA. Requires bioactivation. Crosses BBB to CNS.


Clinical: Brain tumors (including glioblastoma multiforme)


Toxicity: CNS toxicity (dizziness, ataxia)








Mech: Acts like an alkylating agent. X-links via hydrolysis of Cl- groups and reaction with platinum.


Clinical: Testicular, bladder, ovary, and lung ca.


Toxicity: Nephrotoxicity and acoustic nerve damage





Doxorubicin (adriamycin)


Mech: Noncovalently intercalates in DNA, creating breaks to decrease replication and transcription and generate free radicals. Anthracycline antibiotic.


Clinical: Part of AVBD combination regimen for Hodgkins and for myelomas, sarcomas, and solid tumors (breast, ovary, lung).


Toxicity: Cardiotoxicity; also myelosuppression and marked alopecia. Toxic extravasation.




Mech: Intercalates DNA strands and induces free radical formation, causing strand breaks.


Clinical: Testicular ca, lymphomas.


Toxicity: Pulmonary fibrosis, skin changes, minimal myelosuppression







Mech: G2-phase specific inhibits topoisomerase II so that double strand breaks remain in DNA following replication, with subsequent DNA degradation.


Clinical: Oat cell carcinoma of the lung and prostate, testicular ca.


Toxicity: Myelosuppression, GI irritation, alopecia






Mech: May trigger apoptosis. May even work on non-dividing cells. Phospholipase A2 and COX-2 Inhibitor.


Clinical: Most commonly used glucocorticoid in cancer chemotherapy. Used in CLL, Hodgkins lymphomas (part of MOPP, CHOP). Also an immunosuppressant used in autoimmune disease. Asthma.


Toxicity: Cushing-like symptoms; immunosuppression, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis.




Mech: Estrogen receptor mixed agonist/antagonists that block the binding of estrogen to ER+ cells.


Clinical: Breast ca.


Toxicity: Tamoxifen may increase the risk of endometrial ca. via partial agonist effects; hot flashes






Mech: M-phase specific alkaloids that bind to tubulin and block polymerization of microtubules so that mitotic spindle can’t form.


Clinical: Part of MOPP/CHOP regimens for Hodkins/NHL lymphomas, Wilms tumor, choriocarcinoma


Toxicity: Vincristine – neurotoxicity (areflexia, peripheral neuritis), paralytic ileus. Vinblastine – blasts bone marrow (myelosuppression)





Mech: M-phase specific agent obtained from yew tree that binds to tubulin and hyperstabilizes polymerized microtubules so that mitotic spindle can’t break down (anaphase cannot occur)


Clinical: Ovarian and breast ca.


Toxicity: Myelosuppression, hypersensitivity




Lead Poisoning


Lead lines on gingivae and on epiphyses of long bones on x-ray.

Encephalopathy and Erythrocyte basophilic stippling

Abdominal Colic and sideroblastic Anemia

Drops: wrist and foot drop. Dimercaprol and EDTA are first line tx


LEAD – high risk in houses with chipped paint





Drugs that cause SLE-like syndrome:












Drugs that cause Stevens-Johnson Syndrome












Drugs that induce P450:


Barbiturates, phenytoin, carbamazepine, rifampin, griseofulvin, quinidine









Drugs that Inhibit P450:


Cimetidine, ketoconazole, grapefruit, erythromycin, INH, sulfonamides












Mech: Inhibits cGMP phosphodiesterase, causing increased cGMP, smooth muscle relaxation in the corpus cavernosum, increased blood flow, and penile erection


Clinical: Tx of erectile dysfunction


Toxicity: HA, flushing, dyspepsia, blue-green color vision, risk of life-threatening hypotension in patients taking nitrates.





Mech: Partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition and increases release of LH and FSH from pituitary, which stimulates ovulation.


Clinical: Tx of infertility


Toxicity: Hot flashes, ovarian enlargement, multiple spontaneous pregnancies, visual disturbances.



Mifepristone (RU486)


Mech: Competitive inhibitor of progestins at progesterone receptors.


Clinical: Abortificant


Toxicity: Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain





H2-Blockers: Cimetidine, ranitidine, famotidine, nizatidine


Mech: Reversible block of histamine H2 receptors.


Clinical: Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.


Toxicity: Cimetidine is a potent inhibitor of P450; it also has an antiandrogenic effect and decreases renal excretion of creatinine. Other H2 blockers are relatively free of these effects.



Omeprazole, lansoprazole


Mech: Irreversible inhibits H+/K+ ATPase in stomach parietal cells.


Clinical: Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.









Mech: Aluminum sucrose sulfate polymerizes in the acid environment of the stomach and selectively binds necrotic peptic ulcer tissue. Acts as a barrier to acid, pepsin, and bile. Sucralfate cannot work in the presence of antacids or H2 blocers (requires acidic pH to polymerize)


Clinical: Peptic ulcer disease.







Mech: A PGE1 analog. Increases production and secretion of gastric mucous barrier.


Clinical: Prevention of NSAID-induced peptic ulcers, maintains a patent PDA.


Toxicity: Diarrhea. Contraindicated in women of childbearing age (abortificant)



Signs/Symptoms of Antacid overuse:

Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying. Overuse can cause:

1. Aluminum hydroxide: constipation and hypophosphatemia

2. Magnesium hydroxide: diarrhea

3. Calcium carbonate: hypercalcemia, rebound acid increase

All can cause hypokalemia







Mech: Catalyzes the activation of antithromin III. Short half-life. Check aPTT.

Clinical: Immediate anticoagulation for PE, stroke, angina, MI, DVT. Used during pregnancy (does not cross placenta). Follow PTT.

Toxicity: Bleeding, thrombocytopenia, drug-drug interactions. Use protamine sulfate for rapid reversal of heparinization (positively charged molecule that acts by binding negatively charged heparin)

Note: Newer low molec. wt heparins (enoxaparin) have better bioavailability and 2-4 times longer half life. Admin. SQ and w/o PTT.


Warfarin (Coumadin)


Mech: Interferes with normal synthesis and gamma carboxylation of vit-K dependent clotting factors II, VII, IX, X, Protein S and C via vit. K antagonism. Long half-life, slow onset.


Clinical: Chronic anticoagulation. Not used in pregnant women (does cross placenta). Follow PT.

WEPT:  Warfarin affects Extrinsic pathway and prolongs PT


Toxicity: Bleeding, teratogenic, drug-drug interactions


Thrombolytics: Streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)


Mech: Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. It is claimed that tPA specifically converts fibrin-bound plasminogen to plasmin


Clinical: Early MI


Toxicity: Bleeding, hypersensitivity


Aminocaproic acid inhibits Plasminogen activation to Plasmin

Clopidogrel, Ticlopidine


Mech: Inhibits platelet aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen.


Clinical: Actue coronary syndrome; coronary stenting. Decreases the incidence of recurrence of thrombotic stroke. Secondary stroke prevention.


Toxicity: Neutropenia (ticlopidine); reserved for those who cannot tolerate aspirin.




Mech: Selective and specific inhibitor of 5-lipoxygenase preventing formation of both LTB4 and the cysteinyl leukotrienes.


Clinical: Asthma


Toxicity: Liver, Churg-Strauss syndrome (eosinophilic vasculitis), inhibit P450.






Mech: Selective, reversible inhibitors of the cysteinyl leukotriene-1 receptor


Clinical: Asthma


Toxicity: Liver, Churg-Strauss syndrome (eosinophilic vasculitis), inhibit P450.






Mech: Acetylates and irreversibly inhibits cyclooxygenase (1 & 2) to prevent coversion of arachidonic acid to prostaglandins


Clinical: Antipyretic, analgesic, anti-inflammatory, anti-platelet


Toxicity: Gastric ulceration, bleeding, hyperventilation, Reye’s syndrome, tinnitus (CN VIII), renal toxicity




NSAIDS: Ibuprofen, naproxen, indomethacin


Mech: Reversibly inhibit cyclooxygenase (1 & 2).  Block prostaglandin synthesis.


Clinical: Antipyretic, analgesic, anti-inflammatory. Indomethacin used to close a PDA.


Toxicity: Renal damage, aplastic anemia, GI distress




COX-2 Inhibitors: Celecoxib, rofecoxib


Mech: Selectively inhibit cyclooxygenase isoform 2, which is found in inflammatory cells and mediates inflammation and pain; spares COX-1, which helps maintain the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDS on the GI lining.


Clinical: Rheumatoid and osteoarthritis


Toxicity: Similar to other NSAIDS; may have less toxicity to the GI mucosa (lower incidence of ulcers and bleeding)




Mech: Reversibly inhibits COX-1 and 2, mostly in CNS. Inactivated peripherally.


Clinical: Antipyretic, analgesic, but lacking anti-inflammatory properties.


Toxicity: Overdose produces hepatic necrosis; acetominophen metabolite depletes glutathione and forms toxic tissue adducts in liver. Give Mucomyst (N-acetylcysteine) for overdose – replenishes glutathione.

Glucocorticoids: Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone


Mech: Decrease the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2.


Clinical: Addison’s disease, inflammation, immune suppression, cancer therapy, asthma (drug of choice in status asthmaticus along with albuterol)

Toxicity: Iatrogenic Cushing’s syndrome: buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruising, osteoporosis, adrenocortical atrophy, peptic ulcers



Mech: b2 agonist. Relaxes bronchial smooth muscle.


Clinical: Asthma – use during acute exacerbation










Mech: b2 agonist. Long-acting agent for prophylaxis.


Clinical: Asthma.  Controller


Toxicity: tremor and arrhythmia








Mech: Methylxanthine. Bronchodilation mechanism unclear – may cause bronchodilation by inhibiting phosphodiesterase, enzyme involved in degrading cAMP (controversial)


Clinical: Asthma


Toxicities: Seizures, arrhythmias, drug-drug interactions






Mech: Prevents release of mediators from mast cells.


Clinical: Prophylaxis of asthma only. Not effective in an acute attack.


Toxicity: rare








Mech: Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.


Clinical: Acute gout


Toxicity: GI, esp. orally. Indomethacin is less toxic and more commonly used.






Mech: Inhibits reabsorption of uric acid (also inhibits secretion of penicillin)


Clinical: Chronic gout.









Mech: Xanthine oxidase inhibitor, decreases conversion of xanthine to uric acid


Clinical: Chronic gout


Toxicity: increased with 6-mercaptopurine







Mech: Binds insulin receptor, which has tyrosine kinase activity. In liver, increases storage of glucose as glycogen. In muscle, stimulates glycogen and protein synthesis, and K+ uptake. In adipose tissue, facilitates triglyceride storage.


Clinical: Diabetes mellitus.  Life-threatening hyperkalemia, stress-induced hyperglycemia.


Toxicity: hypoglycemia, hypersensitivity (rare)


Sulfonylureas: Tolbutamide, chlorpropamide, glyburide, glipizide


Mech: Oral hypoglycemics used to stimulate release of endogenous insulin in NIDDM. Close K+ channels in b-cell membrane – cell depolarizes – insulin release triggered owing to an increase in Ca++ influx


Clinical: NIDDM. Inactive in IDDM because requires islet fxn


Toxicity: hypoglycemia (more common with 2nd generation: glyburide, glipizide) and disulfuram-like effects (not seen with 2nd gen)




Mech: Unknown. Possibly inhibits gluconeogenesis and increases glycolysis; decreases serum glucose levels.


Clinical: Used as oral hypoglycemic. Can be used in both IDDM/NIDDM


Toxicity: most grave effect is lactic acidosis




Glitazones: Pioglitazone, rosiglitazone


Mech: Increase target cell response to insulin.


Clinical: Used as monotherapy for NIDDM or in combination with above agents.


Toxicity:  Weight gain, hepatotoxic (troglitazone)





a-glucosidase inhibitors: Acarbose, miglitol


Mech: Inhibits intestinal brush border enzymes; delayed hydrolysis of sugars and absorption of glucose leads to decreased post-prandial hyperglycemia.


Clinical: Used as monotherapy in NIDDM or in combination with above agents


Toxicity: GI disturbances





Mech: GnRH analog with agonist properties when used in pulsatile fashion and antagonist properties when used continuously (but causes transient initial burst of LH/FSH)


Clinical: Infertility (pulsatile), prostate cancer (continuous, use with flutamide), uterine fibroids


Toxicity: Antiandrogen, nausea, vomiting





Mech: Inhibits organification and coupling of thyroid hormone synthesis. Also decreases peripheral conversion of T4 to T3.


Clinical: Hyperthyroidism


Toxicity: Skin rash, agranulocytosis, aplastic anemia







Mech: 5a-reductase inhibitor (decreases conversion of testosterone to dihydrotestosterone)


Clinical: BPH









Mech: Non-steroidal competitive inhibitor of androgens at the testosterone receptor.


Clinical: Prostate cancer







Ketoconazole, spironolactone


Mech: Inhibit steroid synthesis


Clinical: Used in treatment of polycystic ovarian syndrome to prevent hirsutism









Mech: Binds to cyclophilins (peptide proline cis-trans isomerase), blocking differentiation and activation of T cells mainly by inhibiting the production of IL-2 and its receptor.


Clinical: Suppresses organ rejection after transplantation; selected autoimmune disorders.


Toxicity: Predisposes patients to viral infections and lymphoma; nephrotoxic (preventable with mannitol diuresis)




Mech: Antimetabolite derivative of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acid.


Clinical: Kidney transplantation, autoimmune disorders (including glomerulonephritis and hemolytic anemia)


Toxicity: Toxic to proliferating lymphocytes after antigenic stimulus.




Tacrolimus (FK506)


Mech: Similar to cyclosporine; binds to FK binding protein, inhibiting secretion of IL-2 and other cytokines


Clinical: Potent immunosuppressive used in organ transplant


Toxicity: Significant: nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia