First Aid 2008 Pharmacology

(A loving compilation by the University of Maryland class of 2010)

NB:
SE = side effect
C/I = contraindication
There are graphics in FA that have not been included in this document

Participants:
Eddie Ahn, Tala Al-Talib, Mona Bahouth, Richie Bryson, Sarah Bui, Niloo Ghassemzadeh, Nidhi Goel, Jen Han, Kyle Hatten, Ashley Huber, Anita Katikineni,
Jessica Lue, Thom Reznik, Justin Waltrous, Felicia Washington, Melissa Wisner, Danielle York, Zombor Zoltani
 ANTIBACTERIAL THERAPY (pp 176-183)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Bacteriostatic vs Bacteriostatic Erythromycin, Clindamycin, Sulfamethoxazole, Trimethoprim, Tetracyclines, Chloramphenicol
bactericidal antibiotics ("We're ECSTaTiC about bacteriostatics")
Bactericidal Vancomycin, Fluoroquinolones, Penicillin, Aminoglycosides, Cephalosporins, Metronidazole
("Very Finely Proficient At Cell Murder")

Penicillin G (IV) -Bactericidal for gram-positive
Penicillin V (oral) cocci, gram-positive rods,
gram-negative cocci, and
spirochetes.
Penicillinase-resistant -S. aureus
penicillins (except MRSA; resistant
Methicillin because of altered pencillin-
Nafcillin binding protein target site)
Dicloxacillin ("Use naf (nafcillin) for staph")
Aminopenicillins -Extended spectrum penicillin:
Ampicillin certain gram-positive bacteria
Amoxicillin and gram-negative rods
(Haemophilus influenzae, E. coli,
Listeria monocytogenes,
Proteus mirabilis, Salmonella,
enterococci)
(Coverage: ampicillin/amoxicillin
HELPS kill enterococci)
Antipseudomonals -Pseudomonas spp. and
Ticarcillin gram-negative rods
Carbenicillin
Piperacillin
(TCP: Takes Care of
Pseudomonas)
1. Bind penicillin-binding proteins -Prototype β-lactam antibiotics
2. Block transpeptidase cross-linking of cell wall -Not penicillinase resistant
3. Activate autolytic enzymes -SE: hypersensitivity reactions, hemolytic anemia
-Same as penicillin -Penicillinase-resistant
-Narrow spectrum -Penicillinase resistant because of bulkier R group
-SE: hypersensitivity reactions;
methicillin - interstitial nephritis
-Same as penicillin -Penicillinase-sensitive
-Wider spectrum -Also combine with clavulanic acid (penicillinase inhibitor)
to enhance spectrum.
-amOxicillin has greater Oral bioavailability than ampicillin
-SE: hypersensitivity reactions; ampicillin rash;
pseudomembranous colitis
-Same as penicillin -Susceptible to penicillinase; use with clavulanic acid
-Extended spectrum -SE: hypersensitivity reactions
Cephalosporins -β-lactam drugs that inhibit cell wall synthesis -Bactericidal
but are less susceptible to penicillinases -SE:
-hypersensitivity reactions
-cross-hypersensitivity with penicillins occurs in
5-10% of patients
-↑ nephrotoxicity of aminoglycosides
-disulfiram-like reaction with ethanol (in cephalosporins
with a methylthiotetrazole group, e.g. cefamandole)
1st generation -Gram-positive cocci,
Cefazolin Proteus mirabilis, E. coli,
Cephalexin Klebsiella pneumoniae
(PEcK)
2nd generation -Gram-positive cocci,
Cefoxitin Haemophilus influenzae,
Cefaclor Enterobacter aerogenes,
Cefuroxime Neisseria spp.,
Proteus mirabilis,
E. coli, Klebsiella pneumoniae,
Serratia marcescens
(HEN PEcKS)
3rd generation -Serious gram-negative infections
Ceftriaxone resistant to other β-lactams
Cefotaxime -Meningitis (most penetrate the
Ceftazidime blood-brain barrier)
-Examples
-ceftazidime for Pseudomonas
-ceftriaxone for gonorrhea
4th generation - ↑ activity against Pseudomonas
Cefepime and gram-positive organisms
Aztreonam -Gram-negative rods:
Klebsiella spp.
Pseudomonas spp.
Serratia spp.
-No activity against
gram-positives or anaerobes.
-Use for penicillin-allergic patients
and those with renal
insufficiency who cannot
tolerate aminoglycosides
Imipenem / cilastatin, -Gram-positive cocci,
Meropenem gram-negative rods, and
anaerobes.
-Drug of choice for Enterobacter
Vancomycin -Used for serious, gram-positive
multidrug-resistant organisms,
including S. aureus and
Clostridium difficile
(pseudomembranous colitis)
-A monobactam resistant to β-lactamases
-Inhibits cell wall synthesis (binds to PBP3)
-Imipenem is a broad-spectrum,
β-lactamase-resistant carbapenem
-Inhibits cell wall mucopeptide formation by
binding D-ala D-ala portion of cell wall
precursors
-Synergistic with aminoglycosides
-No cross-allergenicity with penicillins
-No cross-sensitivity with penicillins or cephalosporins
-SE: usually nontoxic; occasional GI upset
-Always administered with cilastatin (inhibitor of renal
dihydropeptidase I) to ↓ inactivation in renal tubules
(With imipenem, "the kill is LASTIN' with ciLASTATIN")
-The significant side effects limit use to life-threatening
infections, or after other drugs have failed. Meropenem,
however, has a reduced risk of seizures and is stable to
dihydropeptidase I.
-SE: GI distress, skin rash, and CNS toxicity (seizures)
at high plasma levels.
-Bactericidal
-Resistance occurs with amino acid change of
D-ala D-ala to D-ala D-lac
-SE: Nephrotoxicity, Ototoxicity, Thrombophlebitis,
diffuse flushing - "red man syndrome" (can largely
prevent by pretreatment with antihistamines and
slow infusion rate).
(Well tolerated in general - does NOT have many
problems)
Aminoglycosides -Severe gram-negative rod -Inhibit formation of initiation complex and -Bactericidal
Gentamicin, infections cause misreading of mRNA -AminO2glycosides require O2 for uptake; therefore
Neomycin, -Synergistic with β-lactam ineffective against anaerobes
Amikacin, antibiotics -SE:
Tobramycin, -Neomycin for bowel surgery Nephrotoxicity (esp. when used with cephalosporins),
Streptomycin Ototoxicity (esp. when used with loop diuretics),
("Mean" GNATS Teratogen
canNOT kill anaerobes)
Tetracyclines Vibrio cholerae, Acne, Chlamydia, -Bind to 30S and prevent attachment of -Bacteriostatic
Tetracycline, Ureaplasma Urealyticum, aminoacyl-tRNA -Limited CNS penetration
Doxycycline, Mycoplasma pneumoniae, -Doxycycline is fecally eliminated and can be used in
Demeclocycline, Tularemia, H. pylori, Borrelia patients with renal failure
Minocycline burgdorferi (Lyme disease), -Demeclocycline - ADH antagonist; acts as a Diuretic
Rickettsia in SIADH
-Must NOT take with milk, antacids, or iron-containing
(VACCUUM THe BedRoom) preparations because divalent cations inhibit its
absorption in the gut
-SE: GI distress, discoloration of teeth and inhibition of
bone growth in children, photosensitivity
-C/I: pregnancy
Macrolides -URIs, pneumonias, STDs - -Inhibit protein synthesis by blocking -Bacteriostatic
Erythromycin gram-positive cocci translocation -SE: GI discomfort (most common cause of
Azithromycin (streptococcal infections in -Bind to the 23S rRNA of the 50S ribosomal noncompliance), acute cholestatic hepatitis,
Clarithromycin patients allergic to penicillin), subunit eosinophilia, skin rashes. Increases serum
Mycoplasma, Legionella, concentration of theophyllines, oral anticoagulants.
Chlamydia, Neisseria
Chloramphenicol -Meningitis -Inhibits 50S peptidyltransferase activity -Bacteriostatic
(Haemophilus influenzae, -Conservative use owing to toxicities
Neisseria meningitidis, -SE: anemia (dose dependent), aplastic anemia (dose
Streptococcus pneumoniae) independent), gray baby syndrome (in premature
infants because they lack liver UDP-glucuronyl
transferase)
Clindamycin -Treat anaerobic infections -Blocks peptide bond formation at 50S -Bacteriostatic
(e.g. Bacteroides fragilis, ribosomal subunit -SE: pseudomembranous colitis (C. difficile overgrowth),
Clostridium perfringens) fever, diarrhea
-Treats anaerobes above the
diaphragm
Sulfonamides -Gram-positive, gram-negative, -PABA antimetabolites inhibit -Bacteriostatic
Sulfamethoxazole Nocardia, Chlamydia dihydropteroate synthetase -SE: hypersensitivity reactions, hemolysis if
(SMX), -Use triple sulfas or SMX for G6PD deficient, nephrotoxicity (tubulointerstitial
Sulfisoxazole, simple UTI nephritis), photosensitivity, kernicterus in infants,
Triple sulfas, displace other drugs from albumin (e.g. warfarin)
Sulfadiazine,
Trimethoprim -Used in combination with -Inhibits bacterial dihydrofolate reductase -Bacteriostatic
sulfonamides (trimethoprim- -SE: Megaloblastic anemia, leukopenia,
sulfamethoxazole (TMP-SMX)), granulocytopenia. (May alleviate with supplemental
causing sequential block of folic acid)
folate synthesis. ( Trimethoprim = TMP : "Treats Marrow Poorly )
-Combination used for recurrent
UTIs, Shigella, Salmonella,
Pneumocystis jiroveci
pneumonia

Sulfa drug allergies -Patients who do not tolerate sulfa drugs should not be given sulfonamides or other sulfa drugs, such as sulfasalazine, sulfonylureas,
thiazide diuretics, acetazolamide, or furosemide

Fluoroquinolones -Gram-negative rods of urinary -Inhibit DNA gyrase (topoisomerase II) -Bactericidal
Ciprofloxacin, and GI tracts (including -Must not be taken with antacids
Norfloxacin, Pseudomonas), Neisseria, -SE: GI upset, superinfections, skin rashes, headache,
Ofloxacin, some gram-positive organisms dizziness.
Sparfloxacin, In adults, tendonitis and tendon rupture.
Moxifloxacin, In kids, leg cramps and myalgias
Gatifloxacin, -C/I: pregnant women, and in children because animal
Enoxacin, studies show damage to cartilage
(fluoroquinolones), (FluoroquinoLONES hurt attachment to your BONES)
Nalidixic acid (a
quinolone)
Metronidazole -Antiprotozoal. Giardia, -Forms toxic metabolites in the bacterial cell -Bactericidal
Entamoeba, Trichomonas, that damage DNA -SE: Disulfiram-like reaction with alcohol; headache,
Gardnerella vaginalis, metallic taste
Anaerobes (Bacteroides,
Clostridium).
-Used with bismuth and
amoxicillin (or tetracycline) for
"triple therapy" against H. pylori
(GET GAP on the Metro!)
-Treats anaerobes below the
diaphragm
Polymyxins -Resistant gram-negative -Bind to cell membranes of bacteria and -SE: Neurotoxicity, acute renal tubular necrosis
Polymyxin B, infections disrupt their osmotic properties
Polymyxin E -Polymyxins are cationic, basic proteins that
act like detergents
('MYXins MIX up membranes)

Antimycobacterial drugs M. tuberculosis -prophylaxis: Isoniazid

-treatment: Isoniazid, rifampin, ethambutol, pyrazinamide
M. avium-intracellulare -prophylaxis: Azithromycin
-treatment: Azithromycin, rifampin, ethambutol, streptomycin
M. leprae -prophylaxis: N/A
-treatment: Dapsone, rifampin, clofazimine
Anti-TB drugs -important SE of ethambutol is
Streptomycin, optic neuropathy (red-green color blindness).
Pyrazinamide, -for other drugs, hepatotoxicity
Isoniazid (INH),
Rifampin,
Ethambutol
(INH-SPIRE (inspire))
Cycloserine (2nd-line
therapy)
Isoniazid (INH) -Mycobacterium tuberculosis - ↓synthesis of mycolic acids -Different INH half-lives in fast vs slow acetylators.
-The only agent used as solo -SE: Hemolysis if G6PD deficient, neurotoxicity,
prophylaxis against TB hepatotoxicity, SLE-like syndrome.
Pyridoxine (vitamin B6) can prevent neurotoxicity.
(INH Injures Neurons and Hepatocytes)

Rifampin -Mycobacterium tuberculosis
-Delays resistance to dapsone
when used for leprosy
-Used for meningococcal
prophylaxis and
chemoprophylaxis in contacts
of children with Haemophilus
influenzae type B
-Inhibits DNA-dependent RNA polymerase -SE: Minor hepatotoxicity and drug interactions (↑P450);
orange body fluids (nonhazardous side effect).
(Rifampin's 4 R's:
RNA polymerase inhibitor
Revs up microsomal P450
Red/orange body fluids
Rapid resistance if used alone)
Resistance mechanisms Penicillins / cephalosporins β-lactamase cleavage of β-lactam ring, or altered PBP in case of MRSA
for various antibiotics Aminoglycosides Modification via acetylation, adenylation, or phosphorylation
Vancomycin Terminal D-ala of cell wall component replaced with D-lac; ↓ affinity
Chloramphenicol Modification via acetylation
Macrolides Methylation of rRNA near erythromycin's ribosome-binding site
Tetracycline ↓ uptake or ↑ transport out of cell
Sulfonamides Altered enzyme (bacterial dihydropteroate synthetase), ↓ uptake, or ↑ PABA synthesis
Quinolones Altered gyrase or reduced uptake
Nonsurgical Meningococcal infection Rifampin (drug of choice), minocycline
antimicrobial prophylaxis Gonorrhea Ceftriaxone
Syphilis Benzathine penicillin G
History of recurrent UTIs TMP-SMX
Pneumocystis jiroveci pneumonia TMP-SMX (drug of choice), aerosolized pentamidine
Endocarditis with surgical or dental Penicillins
procedures
Treatment of highly MRSA Vancomycin
resistant bacteria VRE Linezolid and streptogramins (quinupristin / dalfopristin)
 ANTIFUNGAL THERAPY (p 184)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Amphotericin B -Used for wide spectrum of -Binds ergosterol (unique to fungi); -SE: Fever/chills ("shake and bake"), hypotension,
systemic mycoses. forms membrane pores that allow leakage of nephrotoxicity, arrhythmias, anemia, IV phlebitis
-Cryptococcus, Blastomyces, electrolytes ("amphoterrible"). Hydration reduces nephrotoxicity.
Coccidioides, Aspergillus, Liposomal amphotericin reduces toxicity.
Histoplasma, Candida, Mucor -Misc. notes: Amphotericin "tears" holes in the fungal
(systemic mycoses). membrane by forming pores.
-Intrathecally for fungal
meningitis; does not cross
blood brain barrier.
Nystatin "Swish and swallow" for oral -Binds to ergosterol, disrupting fungal Misc. notes: Too toxic for systemic use.
candidiasis (thrush); topical for membranes.
diaper rash or vaginal
candidiasis.
Azoles -Systemic mycoses. -Inhibit fungal steroid (ergosterol) synthesis. -SE: Hormone synthesis inhibition (gynecomastia),
Fluconazole, -Fluconazole for cryptococcal liver dysfunction (inhibits cytochrome P-450), fever,
Ketoconazole, meningitis in AIDS patients chills.
Clotrimazole, (because it can cross the
Miconazole, blood-brain barrier) and
Itraconazole, candidal infections of all types
Voriconazole (i.e., yeast infections).
-Ketoconazole for Blastomyces,
Coccidioides, Histoplasma,
Candida albicans ;
hypercortisolism.
-Clotrimazole and miconazole for
topical fungal infections.

Flucytosine -Used in systemic fungal
infections (e.g., Candida,
Cryptococcus ) in combination
with amphotericin B.
Caspofungin -Invasive aspergillosis
Terbinafine -Used to treat dermatophytoses
(especially onychomycosis)
-Inhibits DNA synthesis by conversion to -SE: Nausea, vomiting, diarrhea, bone marrow
fluorouracil, which competes with uracil. suppression.
-Inhibits cell wall synthesis. -SE: GI upset, flushing
-Inhibits the fungal enzyme squalene
epoxidase.

Griseofulvin -Oral treatment of superficial -Interferes with microtubule function; -SE: Teratogenic, carcinogenic, confusion, headaches,
infections; inhibits growth of disrupts mitosis ↑ P-450 and warfarin metabolism.
dermatophytes (tinea, -Deposits in keratin-containing tissues
ringworm). (e.g., nails).
 ANTIVIRAL THERAPY (pp 185-187)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Amantadine -Prophylaxis and treatment for -Blocks viral penetration / uncoating -Mechanism of resistance:
influenza A (M2 protein); Mutated M2 protein. 90% of all influenza A strains
-Parkinson's disease -May buffer pH of endosome. are resistant to amantidine, so not used.
-Also causes the release of dopamine from -Amantadine blocks influenza A and rubellA and causes
intact nerve terminals. problems with the cerebellA
("A man to dine" takes off his coat) -SE: Ataxia, dizziness, slurred speech.
Rimantidine -Rimantidine is a derivative of amantadine with fewer
CNS side effects. Does not cross the blood-brain barrier
Zanamivir -Both influenza A and B -Inhibit influenza neuraminidase, decreasing
Oseltamivir the release of progeny virus.
Ribavirin -RSV, chronic hepatitis C -Inhibits synthesis of guanine nucleotides by -SE: Hemolytic anemia. Severe teratogen.
competitively inhibiting IMP dehydrogenase.
Acyclovir -HSV, VZV, EBV -Monophosphorylated by HSV/VZV thymidine -Mechanism of resistance:
-HSV induced mucocutaneous kinase. Lack of thymidine kinase.
and genital lesions, and -Triphosphate formed by cellular enzymes. -SE: Generally well tolerated
encephalitis -Preferentially inhibits viral DNA polymerase by
-Prophylaxis in chain termination.
immunocompromised pts.
-For herpes zoster- use related
agent famciclovir.
-No effect on latent forms of HSV
and VZV.
Ganciclovir -CMV, especially in -5`-monophosphate formed by CMV viral -Mechanism of resistance:
immunocompromised. kinase or HSV/VZV thyrmidine kinase. Mutated CMV DNA polymerase or lack of viral kinase.
-Triphosphate formed by cellular kinases. -SE: Leukopenia, neutropenia, thrombocytopenia,
-Preferentially inhibits viral DNA polymerase. renal toxicity. More toxic to host enzymes than
acyclovir.
Foscarnet -CMV retinitis in -Viral DNA polymerase inhibitor that binds to -Mechanism of resistance:
immunocompromised patients the pyrophosphate binding site of enzyme Mutated DNA polymerase
when ganciclovir fails. -Does not require activation by viral kinase. -SE: Nephrotoxicity
-Acyclovir resistant HSV. (FOScarnet=pyroFOSphate analog)
Interferons -IFN-α : -Glycoproteins from human leukocytes that -SE: Neutropenia.
chronic hepatitis B, C, block various stage of viral RNA and DNA
Karposi's sarcoma synthesis
-IFN-β : -Induce ribonuclease that degrades viral
MS mRNA.
-IFN-γ :
NADPH oxidase deficiency.
 HIV THERAPY
Protease Inhibitors -HIV -Inhibit assembly of new virus by blocking -SE: GI intolerance (nausea, diarrhea), hyperglycemia,
Saqunavir, protease in progeny virions. lipodystrophy, thrombocytopenia (indinavir)
Ritonavir,
Indinavir,
Nelfinavir,
Amprenavir
-all end in -navir
(NAVIR (never) TEASE
a proTEASE)
Reverse -HIV -Preferentially inhibit reverse transcriptase of -SE:
Transcriptase -HAART (highly active HIV. -Bone marrow suppression (neutropenia, anemia)
Inhibitors antiretroviral therapy) usually a -Prevent incorporation of DNA copy of viral (give GM-CSF + Erythropoetin to reduce marrow
protease inhibitor + RT genome into host DNA. suppression)
Nucleosides inhibitor. Initiated when patients -Peripheral neuropathy
Zidovudine (ZDV have low CD4 (<500) or high -Nucleosides: lactic acidosis
formerly AZT), viral load. -Non-nucleosides: rash
Didanosine (ddI), -ZDV is used for general -ZDV: megaloblastic anemia.
Zalcitabine (ddC), prophylaxis and during
Stavidine (d4T), pregnancy to reduce risk of
Lamivudine (3TC), fetal transmission.
Abacavir

Non-Nucleosides
Nevirapine,
Efavirenz,
Delaviridine.
(Never Ever Deliver
nucleosides)
Fusion Inhibitors -HIV -Bind viral gp41 subunit; inhibit conformational -SE:
Enfuvirtide -In patients with persistent viral change required for fusion with CD4 cells. -Hypersensitivity reactions
replication in spite of -Therefore block entry and subsequent -Reactions at subcutaneous injection site
antiretroviral therapy. replication. -↑ risk of bacterial pneumonia
-Use in combo with other drugs.
 IMMUNOLOGY (pp 204-205)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Immunosuppressants
Cyclosporine -Suppresses organ rejection after -Binds to cyclophilins -SE:
transplantation -The resulting complex blocks the -predisposes patients to viral infections and lymphoma
-Selected autoimmune disorders differentiation and activation of T cells by -nephrotoxic (preventable with mannitol diuresis)
inhibiting calcineurin, preventing the
production of IL-2 and its receptor

Tacrolimus (FK506) -Potent immunosuppressive used -Similar to cyclosporine -SE: Significant-nephrotoxicity, peripheral neuropathy,
in organ transplant recipients -Binds to FK-binding protein, hypertension, pleural effusion, hyperglycemia.
inhibiting secretion of IL-2 and other
cytokines
Azathioprine -Kidney transplantation -Antimetabolite precursor of 6-mercatopurine -SE:
-Autoimmune disorders that interferes with the metabolism and -Bone marrow suppression
(including glomerulonephritis synthesis of nucleic acids. Toxic to -Active metabolite mercaptopurine is metabolized by
and hemolytic anemia) proliferating lymphocytes. xanthine oxidase; thus, toxic effects may be ↑ by
allopurinol
Muromonab-CD3 -Immunosuppression after kidney -Monoclonal Ab that binds to CD3 (epsilon -SE: Cytokine release syndrome,
(OKT3) transplantation chain) on the surface of T cells. hypersensitivity reaction
Blocks cell interaction with CD3 protein
responsible for T cell signal transduction.
Sirolimus (rapamycin) -Immunosuppression after kidney -Binds to mTOR (molecular target of -SE: Hyperlipidemia, thrombocytopenia, leukopenia
transplantation in combo with rapamycin).
cyclosporine and corticosteroids -Inhibits T cell proliferation in response to IL-2
Mycophenolate mofetil -Inhibits de novo guanine synthesis and
blocks lymphocyte production.
Daclizumab -Monoclonal Ab with high affinity for the
IL-2 receptor on activated T cells.
Recombinant
cytokines
Aldesleukin (IL-2) -Renal cell carcinoma
-Metastatic melanoma
Erythropoietin (epoetin) -Anemias (esp in renal failure)
Filgrastim -Recovery of bone marrow
(granulocyte colony-
stimulating factor)
Sargramostim -Recovery of bone marrow
(granulocyte-
macrophage colony-
stimulating factor)

α-interferon -Hepatitis B and C

-Kaposi's sarcoma
-Leukemias
Malignant melanoma
β-interferon -Multiple sclerosis
γ-interferon -Chronic granulomatous disease
Oprelvekin (IL-11) -Thrombocytopenia
Thrombopoietin -Thrombocytopenia

CLASS/NAME CLINICAL USE
Cholinergic agents
(DIRECT, INDIRECT)
Direct agonists
Bethanechol -Postoperative and neurogenic
ileus and urinary retention
Carbachol -Glaucoma
-Pupilary contraction
-↓ Intraocular pressure
Pilocarpine -Potent stimulator of
sweat, tears, saliva
-Emergency treatment for
open and narrow glaucoma
-Contracts ciliary muscle of eye
(open angle), pupillary
sphincter (narrow angle)
Methacholine -Challenge test to diagnose
asthma
Indirect agonists
(anticholinesterases)
Neostigmine -Postoperative and neurogenic
ileus and urinary retention
-Myasthenia gravis
-Reversal of neuromuscular
junction blockade (postop)
Pyridostigmine -Myasthenia gravis (long acting)
Edrophonium -Diagnosis of myasthenia gravis
Physostigmine -Glaucoma (b/c crosses BBB)
-Atropine overdose
Ecothiophate -Glaucoma
PHARMACOLOGY (pp 227-232)
MECHANISM SIDE EFFECTS / MISC
-Direct cholinergic agonist -Resistant to AChE
-Activates Bowel and Bladder smooth muscle (Beth Anne, call (bethanechol) me if you want to
activate your bowels and bladder)
-Direct cholinergic agonist
(muscarinic and nicotinic agonist)
Direct cholinergic agonist -Resistant to AchE
(Pile on the sweat and tears)
-Direct cholinergic agonist
-Stimulates muscarininc receptors in airway
when inhaled
-(Indirect agonist (anticholinesterase)) = -Shorter acting than pyridostigmine
-↑ endogenous Ach
-No CNS penetration (NEO CNS = NO CNS)
-↑ endogenous Ach therefore -Long acting
increases strength
-No CNS penetration
-↑ endogenous Ach -Extremely short acting
-↑ endogenous Ach (PHYS is for EYES)
-Crosses the BBB to CNS
-↑ endogenous Ach

Cholinesterase inhibitor -Causes: Parathion and other organophosphates. Irreversible inhibitors.

poisoning -Symptoms: (DUMBBELSS)
-Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation skeletal muscle and CNS; Lacrimation, Sweating, Salivation (also
abdominal cramping)
-Antidote: Atropine (muscarinic antagonist) plus pralidoxime (chemical antagonist used to regenerate active cholinesterase)
Muscarinic
antagonists
Atropine, -Produce mydriasis and -(Organ system) =
Homatropine, cycloplegia -Eyes
Tropicamide
Benztropine -Parkinson's disease -CNS
(PARK my BENZ)
Scopolamine -Motion sickness -CNS
Ipratropium -Asthma, COPD -Respiratory
Methoscopolamine, -Reduce urgency in mild cystitis -Genitourinary
Oxybutynin, and reduces bladder spasms
Glycopyrrolate

Pirenzepine, -Peptic ulcer treatment -Gastrointestinal

Propantheline

Glaucoma drugs
Epinephrine -Glaucoma -α-agonist -SE: Mydriasis; stinging
-↓ aqueous humor synthesis due to -C/I: Do not use in closed angle glaucoma
vasoconstriction
Brimonidine -Glaucoma -α-agonist -No pupillary or vision changes
-↓ aqueous humor synthesis
Timolol, -Glaucoma -β-blockers -No pupillary or vision changes
Betaxolol, -↓ aqueous humor synthesis
Carteolol
Acetazolamide -Glaucoma -Diuretic -No pupillary or vision changes
-↓ aqueous humor secretion due to
↓HCO3 (via inhibition of carbonic anhydrase)
Pilocarpine, -Glaucoma -Cholinomimetics -SE: Miosis; cyclospasm
Carbachol, -↑ outflow of aqueous humor
Physostigmine, -Contract ciliary muscle and
Echothiophate opens trabecular meshwork
-Use pilocarpine in emergencies
-Very effective at opening the
canal of Schlemm
Latanoprost -Glaucoma -Prostaglandin -SE: Darkens color of iris (browning)
(PGF 2-α) -↑ outflow of aqueous humor
Atropine (Blocks DUMBBELLS) Muscarinic antagonist -SE:
-Eye: -↑ body temp, rapid pulse, dry mouth, dry flushed skin,
-pupil dilation, cycloplegia cycloplegia, constipation, disorientation
-Airway -(Hot as a hare, dry as a bone, red as a beet, blind as a
-↓ secretions bat, mad as a hatter)
-Stomach -Acute angle-closure glaucoma in elderly
-↓ acid secretions -Urinary retention in men with prostatic hypertrophy
-Gut -Hyperthermia in infants
-↓ motility
-Bladder
-↓ urgency in cystitis
Hexamethonium -Ganglionic blocker - used in Nicotinic antagonist -SE: Severe orthostatic hypotension, blurred vision,
experimental models to prevent constipation, sexual dysfunction
vagal reflex responses to
changes in blood pressure
(e.g. prevents reflex
bradycardia caused by NE)
Sympathomimetics
(DIRECT, INDIRECT,
SYMPATHOPLEGICS)

Direct
sympathomimetics
Epinephrine -Anaphylaxis, glaucoma (open α1, α2, β1, β2, low doses selective for β1
angle), asthma, hypotension
NE -Hypotension (but ↓ renal α1, α2 > β1
perfusion)
Isoproterenol -AV block (rare) β1 = β2
Dopamine -Shock (↑ renal perfusion), D1 = D2 > β > α -Inotropic and chronotropic
heart failure
Dobutamine -Shock, heart failure, cardiac β1 > β2 -Inotropic but not chronotropic
stress testing
Phenylephrine -Pupillary dilation, α1 > α2
vasoconstriction,
nasal decongestion
Albuterol, -Albuterol for acute asthma β2 > β1
Terbutaline -Terbutaline reduces premature
uterine contractions
Ritodrine -Reduces premature uterine β2
contractions
Indirect
sympathomimetics
Amphetamine -Narcolepsy, obesity, attention -Indirect general agonist,
deficit disorder releases stored catecholamines
Ephedrine -Nasal decongestion, urinary -Indirect general agonist,
incontinence, hypotension releases stored catecholamines
Cocaine -Causes vasoconstriction and -Indirect general agonist,
local anesthesia uptake inhibitor
Sympathoplegics
Clonidine, -Hypertension, especially with -Centrally acting α2-agonist,
α-methyldopa renal disease (no ↓ in blood ↓ central adrenergic outflow
flow to kidney)

Selective β2-agonists β2-agonist MAST: Metaproterenol, Albuterol, Salmeterol, Terbutaline

Metaproterenol,
Albuterol,
Salmeterol,
Terbutaline
α-blockers
(NONSELECTIVE,
α1 SELECTIVE,
α2 SELECTIVE)

Nonselective -Pheochromocytoma Nonselective α-blocker -SE: Orthostatic hypotension, reflex tachycardia

Phenoxybenzamine (use phenoxybenzamine before
(irreversible) and removing tumor, since high
Phentolamine levels of released
(reversible) catecholamines will not be able
to overcome blockage)

α1-selective -Hypertension, α1 selective α-blocker -SE: 1st-dose orthostatic hypotension, dizziness,

Prazosin, urinary retention in BPH headache
Terazosin,
Doxazosin

α2-selective -Depression α2 selective α-blocker -SE: Sedation, ↑ serum cholesterol, ↑ appetite

Mirtazapine

β-blockers -Hypertension -Nonselective antagonists (β1 = β2) -SE:

Propranolol, ↓ cardiac output, propranolol, timolol, nadolol, pindolol, and -impotence
Metoprolol, ↓ renin secretion labetalol -exacerbation of asthma
Atenolol, -Angina pectoris -β1-selective antagonists (β1 > β2) -cardiovascular adverse effects
Nadolol, ↓ heart rate and contractility, Acebutolol (partial agonist), Betaxolol, (bradycardia, AV block, CHF)
Timolol, resulting in ↓ O2 consumption Esmolol (short acting), Atenolol, Metoprolol -CNS adverse effects
Pindolol, -MI (A BEAM of β1-blockers) (sedation, sleep alterations)
Esmolol, β-blockers ↓ mortality -Nonselective α- and β- antagonists -use with caution in diabetics
Labetalol -SVT (propranolol, esmolol) carvedilol, labetalol
↓ AV conduction velocity (class -Partial β-agonists
II antiarrhythmic) acebutolol, pindolol
-CHF
Slows progression of chronic
failure
-Glaucoma (timolol)
↓ secretion of aqueous humor
 CARDIOVASCULAR (pp 266-272)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Antihypertensives
Hydrochlorothiazide -Hypertension -Thiazide diuretic -SE:
(HCTZ) (prevents NaCl resorption in early DCT) Hypokalemia, mild hyperlipidemia, hyperuricemia,
lassitude, hypercalcemia, hyperglycemia
Loop Diuretics -Hypertension -Loop diuretic -SE:
(blocks NKCC channel in TALH) Potassium wasting, metabolic alkalosis, hypotension,
ototoxicity
Clonidine -Hypertension -Sympathoplegic -SE:
Dry mouth, sedation, severe rebound HTN

Methyldopa -Hypertension -Sympathoplegic -SE:

Sedation, positive Coomb's test

Hexamethonium -Hypertension -Sympathoplegic -SE:

Severe orthostatic hypotension, blurred vision,
constipation, sexual dysfunction
Reserpine -Hypertension -Sympathoplegic -SE:
Sedation, depression, nasal stuffiness, diarrhea

Guanethidine -Hypertension -Sympathoplegic -SE:

Orthostatic and exercise hypotension, sexual
dysfunction, diarrhea
Prazosin -Hypertension -Sympathoplegic -SE:
1st dose orthostatic hypotension, dizziness,
headache
β Blockers -Hypertension -Sympathoplegic -SE:
Impotence, flushing,
Cardiovascular effects (bradycardia, CHF, AV block),
CNS effects (sedation, sleep alterations)
Hydralazine -Severe hypertension -Vasodilator -SE: Nausea, headache, lupus-like syndrome,
-CHF - ↑ cGMP → smooth muscle relaxation. reflex tachycardia, angina, salt/fluid retention.
-First-line therapy for HTN in -Vasodilates arterioles > veins; ↓afterload -C/I: angina/CAD
pregnancy, with methyldopa
-Use with β blockers to prevent reflex tachycardia,
diuretic to block salt retention
Minoxidil -Severe hypertension -Vasodilator -SE: Hypertrichosis, pericardial effusion,
-K+ channel opener - hyperpolarizes and reflex tachycardia, angina, salt retention
relaxes vascular smooth muscle
-Use with β blockers to prevent reflex tachycardia,
diuretic to block salt retention
Nifedipine -Hypertension -Vasodilator -SE:
Verapamil -Angina -Block voltage-dependent L-type Ca channels Dizziness, nausea, flushing,
Diltiazem -Arrhythmias (not nifedipine) of cardiac and smooth muscle and thereby constipation (verapamil), AV Block (verapamil),
-Prinzmetal's angina reduce muscle contractility cardiac depression, peripheral edema
-Raynaud's -Vascular smooth muscle:
Nifed > Dilt > Verap
-Heart:
Verap > Dilt > Nifed
Nitroprusside -Hypertension -Vasodilator -SE:
-Malignant HTN (see below) -Short acting; ↑cGMP via direct release of NO Cyanide toxicity (releases CN)

Diazoxide -Hypertension -Vasodilator -SE: HypER*glycemia (reduces insulin release),

-Malignant HTN (see below) -K+ channel opener - hyperpolarizes and hypotension
relaxes vascular smooth muscle
*Annotate your FA- this is on the errata list
Captopril -Hypertension -ACE Inhibitor -SE:
Enalapril Hyperkalemia, cough, angioedema, taste changes,
Fosinopril hypotension, pregnancy problems (fetal renal damage),
rash, ↑ renin
Losartan -Hypertension Angiotensin II Receptor Inhibitor (ARB) -SE:
Fetal renal toxicity, hyperkalemia
Nitroglycerin, -Hypertension -Vasodilate by releasing nitric oxide in -SE:
Isosorbide dinatrate -Angina smooth muscle, causing ↑ in cGMP and -Tachycardia, hypotension, flushing, headache,
-Pulmonary edema smooth muscle relaxation. -"Monday Disease" in industrial exposure - development
-Also used as an aphrodesiac -Vasodilates veins >> arteries; ↓preload of tolerance for the vasodilating action during the work
and erection enhancer week and loss of tolerance over the weekend,
resulting in tachycardia, dizziness, and headache on
re-exposure.
Malignant HTN
treatment
Nitroprusside Malignant HTN -Vasodilator -SE: Cyanide toxicity (releases CN)
-Short acting; ↑cGMP via direct release of NO
Fenoldopam Malignant HTN -Vasodilator
-Dopamine D1 receptor agonist - relaxes renal
vasuclar smooth muscle
Diazoxide Malignant HTN -Vasodilator -SE: HypER*glycemia (reduces insulin release),
-K+ channel opener - hyperpolarizes and hypotension
relaxes vascular smooth muscle
*Annotate your FA- this is on the errata list
Antianginal therapy -Goal = reduction of myocardial O2 consumption (MVO2) by decreasing 1 or more of the determinants of MVO2: end diastolic volume,
blood pressure, heart rate, contractility, ejection time
-Calcium channel blockers:
Nifedipine is similar to Nitrates in effect;
Verapamil is similar to β blockers in effect.
-Labetalol, pindolol, and acebutolol are partial agonists- CONTRAINDICATED in angina
Component Nitrates (affect preload) β Blockers (affect afterload) Nitrates + β Blockers
EDV ↓ ↑ No effect or ↓
BP ↓ ↓ ↓
Contractility ↑ (Reflex response) ↓ Little/No Effect
HR ↑ (Reflex response) ↓ ↓
Ejection time ↓ ↑ Little/No Effect
MVO2 ↓ ↓ ↓↓
Lipid lowering agents -LDL "bad cholesterol"
-HDL "good cholesterol
-triglycerides = TG
HMG-CoA reductase LDL HDL TG -Inhibit cholesterol precursor, mevalonate -SE: expensive, reversible ↑ LFTs, myositis
inhibitors ↓↓↓ ↑ ↓
Lovastatin
Pravastatin
Simvastatin Atorvastatin

Niacin ↓↓ ↑↑ ↓ -Inhibits lipolysis in adipose tissue; -SE: red, flushed face, which is reduced by aspirin or
reduces hepatic VLDL secretion into long-term use
circulation
Bile acid resins ↓↓ slightly ↑ slightly ↑ -Prevent intestinal reabsorption of bile acids; -SE: pts hate it (tastes bad and causes GI discomfort),
Cholestyramine liver must use cholesterol to make more ↓ absorption of fat-soluble vitamins
Colestipol
Cholesterol absorption ↓↓ -- -- -Prevent cholesterol reabsorption at -SE: rare, ↑LFTs
blockers small intestine brush border
Ezetimibe
"Fibrates" ↓ ↑ ↓↓↓ -Upregulate LPL → ↑ TG clearance -SE: myositis, ↑LFTs
Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate

Cardiac glycosides
Digoxin -CHF (increase contractility)
-Atrial fibrillation (↓conduction at
AV node and depression of SA
node)
-Direct inhibition of Na/K ATPase leads to
indirect inhibition of Na/Ca exchanger/antiport
→ ↑[Ca] → positive inotropy
-Misc: 75% bioavailability
20-40% protein bound
t1/2 = 40 hrs
urinary excretion
-SE:
-cardiac: may cause ↑PR, ↓QT, scooping of ST
segment, T-wave inversion of ECG, arrhythmia
-↑parasympathetic activity - nausea, vomiting, diarrhea,
blurry yellow vision (think Van Gogh)
-↑ toxicity if :
-Renal failure (↓excretion) or
-Hypokalemic (potentiates drug effects) or
-Quinidine (↓digoxin clearance; displaces drug from
tissue binding)
-Antidote: Slowly normalize K+, lidocaine, cardiac paper,
anti-dig Fab fragments, Mg2+
ANTIARRHYTHMICS -Block Na channel -These are local anesthetics
Na+ channel blockers -Slow or block (↓) conduction (esp in -Are state dependent - selectively depress tissue that is
(Class I) depolarized cells) frequently depolarized, eg fast tachycardia
- ↓ slope of phase 4 depolarization, -Hyperkalemia ↑ toxicity for all class I drugs
- ↑ threshold for firing in abnormal
pacemaker cells
Class IA -Affect both atrial and ventricular - ↑ AP duration -SE:
Quinidine arrhythmias, especially - ↑ effective refractory period (ERP) -quinidine
Amiodarone reentrant and ectopic - ↑QT interval -cinchonism (headache, tinnitus, thrombocytopenia)
Procainamide supraventricular and ventricular -torsades de pointes due to ↑ QT interval;
Disopyramide tachycardia -procainamide
-reversible SLE-like syndrome
(Queen Amy
Proclaims Diso's
pyramid)
Class IB -Affect ischemic or depolarized - ↓ AP duration -SE:
Lidocaine Purkinje and ventricular tissue Local anesthetic, CNS stimulation/depression,
Mexiletine -Useful in acute ventricular cardiovascular depression
Tocainide arrhythmias (esp. post-MI) and
in digitalis-induced arrhythmias -phenytoin can also fall into the IB category
(I'd Buy Lidy's
Mexican Tacos)
Class IC -Useful in V-tachs that progess to -No effect on AP duration -SE: proarrhythmic, especially post MI (contraindicated),
Flecainide VF and in intractible SVT significantly prolongs refractory period in AV node
Encainide -Usually used only as last resort
Propafenone in refractory tachyarrhythmias

ANTIARRHYTHMICS
Beta-blockers
(Class II)
Propanolol -V-tach -↓cAMP, ↓Ca currents -Esomolol is very short acting
Esmolol -SVT -Suppress abnormal pacemakers by -SE: Impotence, exacerbation of asthma,
Metoprolol -Slowing ventricular rate during ↓ slope of phase 4 cardiovascular effects (bradycardia, AV block, CHF),
Atenolol atrial fibrillation and atrial flutter -AV node particularly sensitive: ↑ PR interval CNS effects (sedation, sleep alterations);
Timolol May mask signs of hypoglycemia;
Metoprolol can cause dyslipidemia
ANTIARRHYTHMICS -Used when other antiarrhythmics - ↑ AP duration,
K+ channel blockers fail - ↑ effective refractory period
(Class III) - ↑QT interval
Sotalol -SE: torsades des pointes, excesssive β block
Ibutilide -SE: torsades des pointes
Bretylium -SE: new arrhythmias, hypotension
Amiodarone -Safe to use in -SE:
Wolff-Parkinson-White Syndrome -pulmonary fibrosis, corneal deposits,
hepatotoxicity, skin deposits resulting in
photodermatitis, neurologic effects, constipation,
cardiovascular effects (bradycardia, heart block, CHF),
hypothyroidism/hyperthyroidism
(Remember to check PFTs, LFTs, and TFTs when using
amiodarone)

ANTIARRHYTHMICS
Ca2+ channel blocker
(Class IV)

Verapamil -Primarily affect AV nodal cells - ↓ conduction velocity -SE: constipation, flushing, edema,
Diltiazem -Used in prevention of nodal - ↑ effective refractory period CV effects (CHF, AV block, sinus node depression),
arrhythmias (eg SVT) - ↑ PR interval torsades de pointes (bepridil)

OTHER
ANTIARRHYTHMICS
Adenosine -Drug of choice in - ↑K+ out of cells → hyperpolarizing the cell -Very short acting (~15 sec)
diagnosis/abolishment of -SE: Flushing, hypotension, chest pain
AV nodal arrhythmias
K+ -Depresses ectopic pacemakers
in hypokalemia
(e.g. digoxin toxicity)
Mg+ -Effective in torsades de pointes
and digoxin toxicity
 ENDOCRINE (pp 287-288)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Diabetic drugs
Insulins -Type 1 DM -Bind insulin receptor -SE: hypoglycemia, hypersensitivity reaction (very rare)
Lispro (short-acting) -Also: (tyrosine kinase activity)
Aspart (short-acting) life-threatening hyperkalemia & -Liver: ↑ glucose stored as glycogen
NPH (intermediate) stress-induced hyperglycemia -Muscle: ↑ glycogen & protein synthesis,
Lente (long-acting) K+ uptake
Ultralente (long-acting) -Fat: aids TG storage
Sulfonylureas -Stimulate release of endogenous -Close K+ channel in β-cell membrane, so -SE:
insulin in type 2 DM. cell depolarizes → triggering of insulin -1st gen: disulfiram-like effects.
First generation -Require some islet function, so release via ↑ Ca2+ intake -2nd gen: hypoglycemia.
Tolbutamide useless in type 1 DM.
Chlorpropamide

Second generation
Glyburide
Glimepiride
Glipizide
Biguanides -Used as oral hypoglycemic -Exact mechanism is unknown -SE: Most grave adverse effect is lactic acidosis.
Metformin -Can be used in patients without -Possibly:
islet function ↓ gluconeogenesis
↑ glycolysis
↓ serum glucose levels.
Glitazone -Used as monotherapy in - ↑ target cell response to insulin -SE: Weight gain, edema, hepatotoxicity, CV toxicity
Pioglitazone type 2 DM or combined with
Rosiglitazone above agents.
α-glucosidase -Used as monotherapy in -Inhibit intestinal brush-border -SE: GI disturbances
inhibitors type 2 DM or combined with α-glucosidases
Acarbose above agents. -Delayed sugar hydrolysis & glucose
Miglitol absorption lead to ↓ postprandial
hyperglycemia.
Misc endocrine drugs
Orlistat -Long-term obesity management -Alters fat metabolism by inhibiting pancreatic -SE: Steatorrhea, GI discomfort, reduced absorption of
(in conjunction with modified diet) lipases. fat-soluble vitamins, headache.
Sibutramine -Short-term & long-term obesity -Sympathomimetic serotonin & norepinephrine -SE: Hypertension, tachycardia.
management reupake inhibitor.
Propylthiouracil, -Hyperthyroidism -Inhibit organification and coupling of thyroid -SE: Skin rash, agranulocytosis (rare), aplastic anemia.
Methimazole hormone synthesis.
-Propylthiouracil also ↓ peripheral conversion
of T4 to T3
Levothyroxine, -Hypothyroidism, myxedema. -Thyroxine replacement. -SE: Tachycardia, heat intolerance, tremors, arrhythmias
Triiodothyronine

Hypothalamic /
pituitary drugs
GH -GH deficiency
-Turner's syndrome
Somatostatin -Acromegaly
(octreotide) -Carcinoid
-Gastrinoma
-Glucagonoma
Oxytocin -Stimulates labor, uterine
contractions, milk let-down
-Controls uterine hemorrhage
ADH -Pituitary DI
(desmopressin) (central, not nephrogenic)

Glucocorticoids
Hydrocortisone -Addison's disease - ↓ the production of leukotrienes and -SE: Iatrogenic Cushing's syndrome - buffalo hump, moon
Prednisone -Inflammation prostaglandins by inhibiting facies, truncal obesity, muscle wasting, thin skin,
Triamcinolone -Immune suppression phospholipase A2 and expression of COX-2 easy bruisability, osteoporosis, adrenocortical atrophy,
Dexamethasone -Asthma peptic ulcers, diabetes (if chronic).
Beclomethasone
 GASTROINTESTINAL (pp 317-318)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
H2 blockers -Peptic ulcer -Reversible block of histamine H2 receptors -SE of cimetidine:
Cimetidine -Gastritis causing ↓secretion of H+ from parietal cells -Cimetidine is a potent inhibitor of P-450
Ranitidine -Mild esophageal reflux -it also has antiandrogenic effects (prolactin release,
Famotidine gynecomastia, impotence)
Nizatidine -can cross BBB (confusion, dizziness, headaches)
and placenta
(take H2 blockers before -SE of cimetidine & ranitidine:
you DINE) -↓ renal excretion of creatinine
-Other H2 blockers are relatively free of these effects
Proton pump -Peptic ulcer -Irreversibly inhibit H+/K+ ATPase in
inhibitors -Gastritis stomach parietal cells
Omeprazole, -Esophageal reflux
Lansoprazole -ZES

Mucosal protectants
Bismuth, -Improve ulcer healing
Sucralfate -Traveler's diarrhea
Misoprotol -Prevention of NSAID-induced
peptic ulcers
-Maintenance of a patent ductus
arteriosus.
-Induction of labor
-Bind to ulcer base, providing physical
protection, and allow HCO3- secretion to
reestablish pH gradient in the mucous layer
-a PGE1 analog
- ↑production and secretion of gastric
mucous barrier
- ↓acid production
-Triple therapy for H. Pylori ulcers :
Metronidazole, Amoxicillin (or Tetracycline), Bismuth.
-Can also use a PPI
(Please MAke Tummy Better)
-SE: Diarrhea
-C/I: contraindicated in women of childbearing potential
(abortifacient)

Muscarinic antagonist -Peptic ulcer -Block M1 receptors on ECL cells -SE: Tachycardia, dry mouth, difficulty focusing eyes
Pirenzepine, (↓ histamine secretion)
Propantheline -Block M3 receptors on parietal cells
(↓ H+ secretion)

Antacid use -SE of all:

-Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
-All cause hypokalemia
Alumninum hydroxide -SE: Constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures
(AlOH3) (Aluminimum amount of feces)
Magnesium hydroxide -SE: Diarrhea, hyporeflexia, hypotension, cardiac arrest
(Mg = Must go to the bathroom)
Calcium carbonate -SE: Hypercalcemia, rebound acid ↑; can chelate and ↓ effectiveness of other drugs (e.g. tetracycline)
Infliximab -Crohn's disease -A monoclonal antibody to TNF, which is a -SE: Respiratory infection, fever, hypotension
-Rheumatoid arthritis proinflammatory cytokine
(INFLIXimab INFLIX pain on TNF)
Sulfasalazine -Ulcerative colitis -A combination fo sulfapyridine (antibacterial) -SE: Malaise, nausea, sulfonamide toxicity,
-Crohn's disease and mesalamine (anti-inflammatory) reversible oligospermia
-Activated by colonic bacteria
Ondansetron -Control vomiting postoperatively -5-HT3 antagonist -SE: Headache, constipation
and in patients undergoing -(Powerful central-acting antiemetic)
cancer chemotherapy (You will not vomit with ONDANSetron, so you can go ON DANCing)

Prokinetic agents
Cisapride -Acts through 5HT receptors to ↑ACh release -No longer used
at the myenteric plexus. -SE: Serious interactions (torsades des pointes) with
-↑ esophageal tone Erythromycin, Ketoconazole, Nefazodone, Fluconazole
-↑ gastric and duodenal contractility,
improving transit time (including through
the colon)
Metoclopramide -Diabetic and post-surgery -D2 receptor antagonist -SE:
gastroparesis -↑ resting tone, contractility, LES tone, motility -↑ Parksonian Effects.
-Does not influence colon transport time -Restlessness, drowsiness, fatigue, depression,
nausea, diarrhea.
-Drug interaction with digoxin and diabetic agents
-C/I: pts with small bowel obstruction

CLASS/NAME CLINICAL USE
Heparin -Immediate anticoagulation for
pulmonary embolism,
stroke, angina, MI, DVT
-Used during pregnancy
(does not cross placenta)
Lepirudin, -Used as an alternative to
Bivalirudin heparin for anticoagulating
patients with HIT
Warfarin (Coumadin) -Chronic anticoagulant
-Not used in pregnant women
(because warfarin, unlike
heparin, can cross the
placenta)
HEMATOLOGY AND ONCOLOGY (pp 336-340)
MECHANISM SIDE EFFECTS / MISC
-Catalyzes activation of antithrombin III,
↓thrombin and Xa
-Short half-life
-Directly inhibit thrombin
-Interferes with normal synthesis and
γ-carboxylation of vitamin K-dependant
clotting factors (II, VII, IX, X, protein C & S)
-Affects Extrinsic pathway and ↑PT
-Long half-life
(The EX-PaTriot went to WAR(farin))
-Follow patient's PTT when on heparin
-Newer low-molecular-weight heparins (enoxaparin)
act more on Xa, have better bioavailability and
2-4 times longer half-life. Can be administered
subcutaneously and without laboratory monitoring.
Not easily reversible.
-SE:
-bleeding
-osteoporosis
-drug-drug interactions,
-heparin-induced thrombocytopenia (HIT): heparin binds
platelets, causing autoantibody production that
destroys platelets and overactivates the remaining
ones, resulting in a thrombocytopenic,
hypercoagulable state.
-for rapid reversal of heparinization, use
protamine sulfate (positively charged molecule
that acts by binding negatively charged heparin)
-Hirudin derivatives
-Follow patient's PT/INR values when on warfarin
-Metabolized by cytochrome P450
-SE: bleeding, teratogenic, skin/tissue necrosis,
drug-drug interactions
Heparin vs. warfarin
Structure
Route of administration
Site of action
Onset of action
Mechanism of action
Duration of action
Inhibits coagulation in vitro
Treatment of acute OD
Monitoring
Crosses placenta
Thrombolytics
Streptokinase,
Urokinase,
tPA (alteplase),
APSAC (anistreplase)
Heparin Warfarin
Large anionic polymer, acidic Small lipid-soluble molecule
Parenteral (IV, SC) Oral
Blood Liver
Rapid (seconds) Slow, limited by half-lives of normal clotting factors
Activates antithrombin III, which ↓ the action of IIa (thrombin) and Xa Impairs the synthesis of vitamin K-dependent clotting
factors II, VII, IX, and X (vitamin K antagonist)
Acute (hours Chronic (days)
Yes No
Protamine sulfate IV vitamin K and fresh frozen plasma
PTT (intrinsic pathway) PT/INR (extrinsic pathway)
No Yes (teratogenic)
-Early MI -Directly or indirectly aids conversion of -SE: bleeding
-Early ischemic stroke plasminogen to plasmin, which is the -C/I: Patients with active bleeding, history of intracranial
major fibrinolytic enzyme that cleaves bleeding, recent surgery, known bleeding diatheses, or
thrombin and fibrin clots. severe hypertension
-↑PT, ↑PTT, no change in platelet count -Treatment of toxicity is with aminocaproic acid, an
inhibitor of fibrinolysis
Antiplatelet drugs
Aspirin (ASA) -Antipyretic
-Analgesic
-Anti-inflammatory
-Antiplatelet drug
Clopidogrel, -Acute coronary syndrome
Ticlopidine -Coronary stenting
-↓ incidence or recurrence of
thrombotic stroke
Abciximab -Acute coronary syndromes
-Percutaneous transluminal
coronary angioplasty
-Acetylates and irreversibly inhibits -↑ bleeding time.
cyclooxygenase (both COX-1 and COX-2) -No effect on PT, PTT.
to prevent conversion of arachidonic acid to -SE: Gastric ulceration, bleeding, hyperventilation,
thromboxane A2. Reye's syndrome, tinnitus (CN VIII)
-Inhibit platelet aggregation by -SE: Neutropenia (ticlopidine)
irreversibly blocking ADP receptors.
-Inhibit fibrinogen binding by
preventing glycoprotein IIb/IIIa expression.
-Monoclonal antibody that binds to the -SE: bleeding, thrombocytopenia
glycoprotein receptor IIb/IIIa on
activated platelets, preventing aggregation.
Cancer drugs
Methotrexate (MTX) -Leukemias -S-phase-specific antimetabolite. -SE:
-Lymphomas -Folic acid analog that inhibits -Myelosuppression, which is reversible with leucovorin
-Choriocarcinoma dihydrofolate reductase, resulting in (folinic acid) "rescue."
-Sarcoma ↓ dTMP and therefore ↓ DNA and protein -Macrovesicular fatty change in liver
-Abortion synthesis. -Mucositis
-Ectopic pregnancy
-Rheumatoid arthritis
-Psoriasis
5-Fluorouracil (5-FU) -Colon cancer and other solid -S-phase-specific anti-metabolite -SE:
tumors -Pyrimidine analog bioactivated to 5F-dUMP, -Myelosuppression (NOT reversible with leucovorin).
-Basal cell carcinoma (topical) which covalently complexes folic acid. This Can "rescue" with thymidine
-Synergy with MTX complex inhibits thmidylate synthetase, -Photosensitivity
resulting in ↓dTMP and same effects as MTX
6-mercaptopurine -Leukemias -Blocks de novo purine synthesis -Metabolized by xanthine oxidase; thus ↑ toxicity with
(6-MP) -Lymphomas (not CLL or -Activated by HGPRATase allopurinol
Hodgkin's) -SE: Bone marrow, GI, liver
Cytarabine (ara-C) -AML -Inhibit DNA polymerase -SE: Leukopenia, thrombocytopenia, megaloblastic
anemia
Cyclophosphamide, -Non-Hodgkin's lymphoma -Alkylating agent -Requires bioactivation in liver
Ifosfamide -Breast and ovarian carcinoma '-Covalently cross-link (interstrand) DNA at -SE: Myelosuppression; hemorrhagic cystitis.
-Immunosuppressant guanine N-7 Hemorrhagic cystitis can be partially prevented with
mesna
Nitrosoureas -Brain tumors (including -Alkylate DNA -Requires bioactivation
Carmustine glioblastoma multiforme) -Crosses blood-brain barrier → CNS
Lomustine -SE: CNS toxicity (dizziness, ataxia)
Semustine
Streptozocin
Cisplatin, -Testicular, bladder, ovary, and -Act like alkylating agent -SE: Nephrotoxicity, acoustic nerve damage
Carboplatin lung carcinomas
Busulfan -CML -Alkylates DNA -SE: Pulmonary fibrosis, hyperpigmentation
Doxorubicin -Part of ABVD combo for -Generate free radicals and noncovalently -SE: Cardiotoxic, myelosuppression,
(adriamycin), Hodgkin's and for myelomas, intercalate in DNA (creating breaks in marked alopecia, toxic extravasation
Daunorubicine sarcomas, solid tumors DNA strand to ↓ replication)
(breast, ovary, lung)
Dactinomycin -Wilm's tumor -Intercalates in DNA -SE: Myelosuppression
(actinomycin D) -Ewing's sarcoma
-Rhabdomyosarcoma
(ACTinomycin D is used for
childhood tumors (children ACT
out)
Bleomycin -Testicular cancer -Induces free radical formation, which causes -SE: Pulmonary fibrosis, skin changes, but
-Lymphoma (part of ABVD breaks in DNA strands minimal myelosuppression
regimen for Hodgkin's)
Hydroxyurea -Melanoma -Inhibits Ribonucleotide Reductase -SE: Bone marrow suppression, GI upset
-CML → ↓DNA Synthesis (S-phase specific)
-Sickle cell disease
Etoposide (VP-16) -Small cell carcinoma of -G2-phase-specific agent -SE: Myelosuppression, GI irritation, alopecia
lung and prostate -Inhibits topoisomerase II and
-Testicular carcinoma ↑ DNA degradation
Prednisone -Most commonly used -May trigger apoptosis -SE: Cushing-like symptoms, immunosuppression,
glucocorticoid in cancer therapy -May even work on dividing cells cataracts, acne, osteoporosis, hypertension,
-CLL peptic ulcers, hyperglycemia, psychosis
-Hodgkin's lymphoma (part of the
MOPP regimin)
-Immunosuppressant used in
autoimmune disease
Tamoxifen, -Breast cancer -Estrogen receptor antagonist in breast -SE:
Raloxifene -Osteoporosis prevention -Agonist in bone -Tamoxifen may ↑ risk of endometrial carcinoma via
-Block the binding of estrogen to partial agonist effects;
estrogen receptor-positive cells -Roloxifen does not cause endometrial carcinoma
because it is an endometrial antagonist
-"Hot flashes"
Trastuzumab -Metastatic breast cancer -Monoclonal antibody against HER-2 (erb-2) -SE: Cardiotoxic
(Herceptin) -Helps kill breast cancer cells expressing
HER-2 possibly through antibody-dependent
cytotoxicity
Imatinib (Gleevec) -CML -Philadelphia chromosome (bcr-abl) tyrosine -SE: Fluid retention
-GI stromal tumors kinase inhibitor
Vincristine, -Part of MOPP (Oncovin = -M-phase specific alkaloids -SE:
Vinblastine vincristine) regimen for -Bind to tubulin and block polymerization of -Vincristine :
lymphoma microtubules so mitotic spindle cannot form -Neurotoxicity (areflexia, peripheral neuritis),
-Wilm's tumor (Microtubules are the vines of your cells) -Paralytic ileus
-Choriocarcinoma -VinBLASTine : BLASTs Bone marrow (suppression)
Paclitaxel, -Ovarian and breast carcinoma -M-phase specific agents -SE: Myelosuppression and hypersensitivity
other taxols -Bind to tubulin and hyperstabilize polymerized
microtubules so mitotic spindle cannot break
down (anaphase cannot occur)
 MUSCULOSKELETAL (pp 358-359)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
NSAIDs -Antipyretic -Reversibly inhibit cyclooxygenase -SE: Renal damage, aplastic anemia, GI distress, ulcers
Ibuprofen -Analgesic (both COX-1 & COX-2)
Naproxen -Anti-inflammatory -Block prostaglandin synthesis
Indomethacin -Indomethacin: closure of PDA
Ketorolac
COX-2 inhibitor -Rheumatoid and osteoarthritis -Reversibly inhibit specifically the -SE:
Celecoxib cyclooxygenase (COX) isoform 2, -↑ risk of thrombosis
which is found in inflammatory cells and -Sulfa allergy.
mediates inflammation and pain -Less toxicity to GI mucosa (lower incidence of ulcers,
-Spares COX-1, which helps maintain the bleeding).
gastric mucosa. Thus, should not have the
corrosive effects of other NSAIDs on the GI
lining.
Gout drugs -Do not give salicylates
Colchicine -Acute gout -Depolymerizes microtubules, impairing -SE: GI side effects, especially if given orally.
leukocyte chemotaxis & degranulation (Indomethacin is less toxic, more commonly used in
acute gout).
Probenecid -Chronic gout -Inhibits reabsorption of uric acid in PCT -C/I: should not be used to treat an acute episode of gout
(also inhibits secretion of penicillin)
Allopurinol -Chronic gout -Inhibits xanthine oxidase, ↓ conversion of -Interacts with azathioprine & 6-MP
-Also used in lymphoma & xanthine to uric acid. -C/I: should not be used to treat an acute episode of gout
leukemia to prevent
tumor lysis-associated urate
nephropathy

Misc drugs
Acetaminophen -Antipyretic -Reversibly inhibits cyclooxygenase, mostly in -SE: Overdose produces hepatic necrosis;
-Analgesic CNS. acetaminophen metabolite depletes glutathione and
-Lacks anti-inflammatory -Inactivated peripherally. forms toxic tissue adducts in liver.
properties N-acetylcysteine is antidote - regenerates glutathione.
Etanercept -Rheumatoid arthritis -Recombinant form of human TNF receptor
-Psoriasis that binds TNF
-Ankylosing spondylitis.
(EtanerCEPT is a TNF decoy reCEPTor)
Infliximab -Crohn's disease -Anti-TNF antibody -SE: Predisposes to infections (reactivation of latent TB)
-Rheumatoid arthritis
-Ankylosing spondylitis (INFLIXimab INFLIX pain on TNF)
 NEUROLOGY (pp 394-399)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Opioid Analgesics -Pain -Acts as agonist at opioid receptors -SE:
Morphine -Cough suppression (mu=morphine, delta= enkephalin, -Addiction, respiratory depression, constipation,
Fentanyl (dextromethorphan) kappa=dynorphin) to modulate synaptic miosis (pinpoint pupils), additive CNS depression
Codeine -Diarrhea transmission with other drugs
Heroin (loperamide and diphenoxylate) -Tolerance does not develop to miosis and constipation.
Methadone -Acute pulmonary edema, -Toxicity treated with naloxone (opioid receptor
Meperidine -Maintenance programs for antagonist).
Dextromethorphan addicts (methadone)
Note: There is a table on p. 395 of First Aid 2008 detailing the specific usage of epilepsy drugs
Benzodiazepines -Anxiety -Facilitate GABAA action by -Most have long half-lives and active metabolites
Diazepam -Spasticity ↑ frequency of Cl- channel opening -Short acting= TOM Thumb
Lorazepam -Status epilepticus (Triazolam, Oxazepam, Midazolam)
Triazolam (lorazepam and diazepam) (FREnzodiazepines= ↑ FREquency) -SE:
Temazepan -Detoxification -Sedation, tolerance, dependence,
Oxazepam (esp. alocohol withdraw- DTs) addictive CNS depression effects with alcohol
Midazolam -Night tremors -Less risk of respiratory depression and coma than with
Chlordiazepoxide -Sleepwalking barbiturates
Alprazolam -Treat overdose with flumazenil (competitive antagonist
at GABA receptor)
Carbamazepine -Epilepsy -SE: Diplopia, ataxia, blood dyscrasis (agranulocytocic,
aplastic anemia), liver toxicity, teratogenesis,
induction of cytochrome P-450
Ethosuximide -Epilepsy -SE:
-GI distress, fatigue, headache, urticaria
-Stevens-Johnson syndrome
-Prodrome of malaise and fever followed by rapid
onset of erythematous/purpuric macules (oral,
ocular, genital). Skin lesions progress to epidermal
necrosis and sloughing.
(EFGH- Ethosuximide, Fatigue, GI, Headache)
Barbiturates -Sedative for anxiety -Facilitate GABAA action by -SE:
Phenobarbital -Epilepsy ↑ duration of Cl- channel opening, -Sedation, tolerance, dependence
Pentobarbital -Seizures thus ↓ neuron firing -Induction of cytochrome P-450;
Thiopental -Insomnia -Addictive CNS effects with alcohol,
Secobarbital -Induction of anesthesia (BarbiDURATe (↑ DURATion)) -Respiratory or cardiovascular depression
(thiopental) (can lead to death)
-Treat overdose with symptom management
(assist respiration, ↑BP)
-C/I: Porphyria
Phenytoin -Epilepsy -Use-dependent blockade of Na+ channels -SE:
-Tonic-clonic seizures -Inhibition of glutamate release from -Nystagmus, diplopia, ataxia, sedation,
-Also a class IB antiarrhythmic excitatory presynaptic neuron gingival hyperplasia, hirsutism, megablastic anemia,
teratogenesis, SLE-like syndrome,
induction of cytochrome P-450
-Chronic use produced gingival hyperplasia in children,
peripheral neuropathy, hirsutism,
megaloblastic anemia (↓ folate absorption), and
malignant hyperthermia (rare)
-Teratogenic (fetal hydantoin syndrome).
Valproic acid -Epilepsy -SE:
-GI distress, tremor, weight gain
-Rare but fatal hepatotoxicity (measure LFTs)
-Neural tube defects in fetus (spina bifida)
-C/I: Pregnancy
Lamotrigine -Epilepsy -SE: Stevens-Johnson syndrome
Gabapentin -Epilepsy -SE: Sedation, ataxia.
Topiramate -Epilepsy -SE: Sedation, mental dulling, kidney stones, weight loss
Anesthetics - -CNS drugs must be lipid soluble (cross blood-brain barrier) or actively transported
general principles -Drugs with ↓ solubility in blood = rapid induction and recovery times
-Drugs with ↑ solubility in lipids = ↑ potency = 1/MAC (minimal alveolar concentration)
-Examples:
-N2O has low blood and lipid soluble, and thus fast induction and low potency
-Halothane, in contrast, has ↑ lipid and blood solubility and thus slow induction and high potency
Inhaled anesthetics -Anesthesia: -Unknown -SE:
Halothane myocardial depression, -malignant hyperthermia (rare)
Enflurane respiratory depression, -halothane: hepatotoxicity
Isoflurane nausea/emesis, -methoxyflurane: nephrotoxicity
Sevoflurane ↑ cerebral blood flow -enflurane: proconvulsant
Methoxyflurane ↓ cerebral metabolic demand
Nitrous oxide
IV anesthetics B. B. King on Opiates Proposes Foolishly
Barbituates -Induction of anesthesia -↓ cerebral blood flow
(Thiopental) -Short surgical procedures. -High potency, high lipid solubility, rapid entry into brain.
-Effect terminated by redistribution from the brain.
Benzodiazepines -Endoscopy -SE:
(Midazolam) -used in adjunct with gaseous -May cause severe postoperative respiratory
anesthetics and narcotics depression, ↓BP, and amnesia
-Treat overdose with flumazenil
Arylcyclohexylamines -Act as dissociative anesthetics -PCP analogs -↑ cerebral blood flow
(Ketamine) -SE:
-Cardiovascular stimulants
-Cause disorientation, hallucination, and bad dreams
Opiates -Used with other CNS
(Morphine, depressants during general
Fentanyl) anesthesia
Propofol -Rapid anesthesia induction -SE: Less postoperative nausea then thiopental
-Short procedures
Local anesthetics -Minor surgical procedures -Block Na channels by binding to specific -Principles:
-Spinal anesthesia receptors on inner portion of channel. -In infected (acidic) tissue, alkaline anesthetics are
Esters -Give amides if allergic to esters -Preferentially bind to active Na channels, so charged and cannot penetrate membrane effectively.
Procaine most effective in rapidly firing neurons. Therefore, more anesthetic is needed in these cases.
Cocaine -3° amine local anesthetics penetrate the -Order of nerve block:
Tetracaine membrane in uncharged form, then bind to - small-diameter fibers > large diameter
ion channels as charged form. - myelinated fibers > unmyelinated fibers
Amides - Overall, size factor predominates over myelination
Lidocaine such that
Mepivacaine small myelinated > small unmyelinated >
Bupivacaine > large myelinated > large unmyelinated
-Order of loss:
(AmIdes have 2 letter I's - pain (first) > temperature > touch > pressure (last)
in the name) -Except with cocaine, given with vasoconstrictors
(epinepherine) to enhance local action -
↓ bleeding, ↑ anesthesia by ↓ systemic concentration
-SE:
-CNS excitation, severe cardiovascular toxicity
(bupivacaine), hypertension, hypotension, and
arrhythmias (cocaine)

Neuromuscular Used for muscle paralysis in Selective for motor (vs. autonomic) nicotinic
blocking drugs surgery or mechanical ventilation receptor
Depolarizing -Phase 1 - prolonged depolarization -SE: Hypercalemia and hyperkalemia
Succinylcholine -No antidote
-Block potentiated by cholinesterase
inhibitors
-Phase 2 - repolarized but blocked
-Antidote is cholinesterase inhibitors
(e.g. neostigmine)
Nondepolarizing -Competitive
Tubocurarine -complete with Ach for receptors
Atracurium -Reversal of blockade via:
Mivacurium -Neostigmine, edrophonium, and other
Pancuronium cholinesterase inhibitors
Vecuronium
Rocuronium
Dantrolene -Malignant hyperthermia -Prevents the release of Ca2+ from the -Malignant hyperthermia is caused by concomitant
sarcoplasmic reticulum of skeletal muscle use of inhalation anesthetic (except nitrous oxide
(N2O)) and succinylcholine.
-Neuroleptic malignant -Neuroleptic malignant syndrome is a toxicity of
syndrome antipsychotic drugs
Parkinson's disease -Strategies to treat Parkinson's are to -Parkinsonism is due to loss of dopaminergic neurons
drugs -Agonize dopamine receptors and excess cholinergic activity
-↑ dopamine -For essential or familial tremors, use β-blockers
Bromocriptine -Prevent dopamine breakdown
Amantadine -Curb excess cholinergic activity
Levodopa (with
carbidopa)
Selegiline (and
COMT inhibitors)
Antimuscarinics
(BALSA)
Bromocriptine -Parkinsons -Agonize dopamine receptors
Pramipexole -Bromocriptine is an ergot alkaloid and
Ropinirole partial dopamine agonist
Amantadine -Parkinsons -↑ dopamine release -SE: ataxia
-Antiviral (influenza A and rubella)
L-dopa (levodopa) with -Parkinsonism -↑ level of dopamine in the brain -Carbidopa is given with L-dopa in order to
carbidopa -Carbidopa increases -L-dopa, unlike dopamine, can cross the blood ↑ the bioavailability of L-dopa and
bioavailability of L-dopa and brain barrier and is converted into dopamine limit peripheral side effects
limits peripheral side effects in the CNS by dopa decarboxylase -SE:
-Carbidopa is a peripheral decarboxylase -Arrhythmias from peripheral conversion to dopamine
inhibitor -Long-term use → dyskinesia following administration
and akinesia between doses
Selegiline -Parkinsons (is an adjunctive -Prevent dopamine breakdown -SE: May enhance adverse effects of L-dopa
agent to L-dopa for Parkinson's) -Selectively inhibits MAO-B, thereby
↑ the availability of dopamine.
Entacarpone, -Parkinsons -Prevent dopamine breakdown
Tolcapone -COMT inhibitors
Benztropine -Improves tremor and rigidity -Antimuscarinic - curb excess cholinergic "↓ your tremor before you drive your Mercedes-BENZ"
-Little effect on bradykinesia activity

Sumatriptan -Acute migraine -5-HT1D agonist -Half-life < 2 hrs

-Cluster headache attacks -Causes vasoconstriction -SE: Coronary vasospasm, mild tingling,
hypertensive emergencies.
-C/I: patients with CAD or Prinzmetal's angina
 PSYCHIATRY (pp 415-417)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Psychiatric condition Drug used
Alcohol withdrawal BZD
Anorexia/bulimia SSRIs
Anxiety Barbiturates
BZD
Buspirone
MAOI
ADHD Methylphenidate (Ritalin)
Amphetamine
Atypical Depression MAOI
Bipolar Disorder Mood stabilizers:
Lithium
Valproic acid
Carbamazepine
Depression SSRI
TCA
Depression w/ insomnia Trazodone
Mirtazapine
OCD SSRIs
Panic D/O TCAs
Buspirone
Schizophrenia Antipsychotics
Tourette's Syndrome Antipsychotics (haloperidol)
Antipsychotics -Schizophrenia -Block dopamine D2 receptors -Excess dopamine effects connected with schizophrenia
(neuroleptics) -Psychosis -DA = dopamine; DA-R = dopamine receptor
-Acute mania
(Haloperidol + '-azine's) -Tourette's syndrome
High potency -SE: (Neurologic side effects)
Haloperidol, -Extrapyramidal system (EPS) effects:
Trifluoperazine -dystonia (muscle spasm, stiffness)
-akinesia (parkinsonian sx)
-akathisia (restlessness)
-tardive dyskinesia (stereotypic oral-facial
movements due to DA-R sensitization; due to
long-term antipsychotic use)
-Evolution of EPS SEs:
-4 h acute dystonia
-4 d akinesia
-4 wk akathisia
-4 mo tardive dyskinesia (often irreversible)
-Neuroleptic malignant syndrome:
-rigidity
-myoglobinuria
-autonomic instability
-hyperpyrexia
-(treat w/ dantrolene and DA agonists)
Low potency -SE: (Non-neurologic side effects)
Thioridazine -endocrine:
Chlorpromazine - DA-R antagonism → hyperPRL → galactorrhea
-muscarinic block: dry mouth, constipation
-α-block: hypotension
-histamine-R block: sedation
Unspecified
Fluphenazine
Atypical -Schizophrenia, for positive and -Block 5-HT2 and dopamine receptors -SE: Fewer EPS and anticholinergic SE than other
antipsychotics negative symptoms antipsychotics
Clozapine
Olanzapine
Risperidone
Quetiapine
Aripiprazole
Ziprasidone

(It's not atypical for old

closets to risper)
Olanzapine -Schizophrenia
-OCD
-Anxiety
-Depression
-Mania
-Tourette's syndrome
Clozapine -Schizophrenia -SE: agranulocytosis (requires weekly WBC monitoring)

Lithium -Mood stabilizer for
bipolar affective disorder
-Blocks relapse and
acute manic events
Buspirone -Anxiolytic for generalized
anxiety disorder (GAD)
-Unknown
-Possibly related to inhibition of
phosphoinositol cascade
-Stimulates 5-HT1A receptors
-narrow therapeutic window, so requires close monitoring
of serum lvls
-SE:
-tremor
-polyuria (ADH antagonist => nephrogenic diabetes
insipidus)
-hypothyroidism
-teratogenesis
(LMNOP: Lithium side effects - Movement (tremor),
Nephrogenic DI, HypOthyroidism, Pregnancy problems)
-Does not cause addiction or sedation
-No interaction w/ EtOH
ANTIDEPRESSANTS -It normally takes 2-3 weeks for anti-dep to have an effect
SSRIs -Endogenous depression -Serotonin-specific reuptake inhibitors -SE: (Fewer than TCAs)
Fluoxetine -OCD -GI distress
Sertraline -Anorexia/bulimia -sexual dysfunction (anorgasmia)
Paroxetine -"serotonin syndrome" w/ MAOI: hyperthermia,
Citalopram muscle rigidity, cardiovascular collapse
Tricyclic -Major depression -Block reuptake of NE and serotonin -SE:
antidepressants (TCA) -sedation (desipramine is the least sedating)
Imipramine -α-blocking effects
Amitriptyline -atropine-like (anticholinergic) side effects (tachycardia,
Desipramine urinary retention)
Nortriptyline -3° (amitriptyline) have more anticholinergic effects than
Clomipramine 2° (nortriptyline)
Doxepin -at toxic levels, Tri-C's: Convulsions, Coma,
Amoxapine Cardiotoxicity (arrhythmias); respiratory depression,
hyperpyrexia. In elderly, confusion and
hallucinations due to anticholinergic side effects (use
nortriptyline)
Imipramine -Major depression
-Bedwetting
Clomipramine -Major depression
-OCD
Monoamine oxidase -Atypical depression (i.e. w/ -Nonselective MAO inhibition => -SE:
inhibitors (MAOI) mood reactivity, sensitivity to ↑ levels of amine neurotransmitters -hypertensive crisis w/ tyramine ingestion (in many
Phenelzine rejection, hypersomnia) foods, e.g. cheese) and β-agonists
Tranylcypromine -Anxiety -CNS stimulation
-Hypochondriasis -C/I: SSRIs or meperidine (prevent serotonin syndrome)
OTHER
ANTIDEPRESSANTS
You need Butane in
your VEINs to MURder
for a MAP of AlcaTRAZ.

Bupropion (Wellbutrin) -Depression -Not well known - SE:

-Smoking cessation -stimulant effects (tachycardia, insomnia)
-headache
-seizure in bulimic patients
-does not cause sexual SE
Venlafaxine -Depression -Inhibits serotonin, NE, DA reuptake -SE:
-Generalized anxiety disorder -stimulant effects
-increased BP
-sedation
-nausea, constipation
Mirtazapine -Depression -α2 antagonist (↑ release of NE and serotonin) -SE:
-Potent 5-HT2 and 5-HT3 receptor antagonist -sedation
-↑ appetite
-weight gain
-dry mouth
Maprotiline -Depression -Blocks NE reuptake -SE:
-sedation
-orthostatic hypotension
Trazodone -Depression -Inhibits serotonin reuptake -SE:
-sedation
-postural hypotension
-nausea
-priapism

Methylphenidate -ADHD -↑ presynaptic NE vesicular release (like

(Ritalin) amphetamines)
-Mechanism for relief of ADHD symptoms
is unknown
 RENAL (pp 435-436)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Mannitol -Shock -Osmotic diuretic. -SE: pulmonary edema, dehydration
-Drug overdose -↑ tubular fluid osmolarity, -C/I: anuria, CHF
-↓intracranial/intraocular pressure producing ↑ urine flow
Acetazolamide -Glaucoma -Carbonic anhydrase inhibitor. (ACIDazolamide causes ACIDosis)
-Urinary alkalinization -Causes self-limited NaHCO3 diuresis -SE: Hyperchloremic metabolic acidosis, neuropathy,
-Metabolic alkalosis and reduction in total-body HCO3 stores NH3 toxicity, sulfa allergy
-Altitude sickness
Furosemide -Edematous states -Loop diuretic (Sulfonamide) - ↑Ca2+ excretion (Loops Lose calcium)
(CHF, cirrhosis, nephrotic -Inhibits cotransport system (NKCC) of -SE: (OH DANG!)
syndrome, pulmonary edema) thick ascending limb of loop of Henle. Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa)
-Hypertension -Abolishes hypertonicity of medulla, Nephritis (interstitial), Gout
-Hypercalcemia preventing concentration of urine

Ethacrynic acid -Diuresis in patients allergic to -Loop diuretic (NOT a sulfonamide) -Phenoxyacetic acid derivative
sulfa drugs -Essentially same action as furosemide -SE: similar to furosemide,
can be used in hyperuricemia, acute gout (never used
to treat gout)

Hydrochlorothiazide -Hypertension -Thiazide diuretic -↓Ca2+ excretion

(HCTZ) -CHF -Inhibits NaCl reabsorption in the early distal -SE: (hyperGLUC)
-Idiopathic hypercalciuria tubule, reducing diluting capacity of nephron Sulfa allergy.
-Nephrogenic diabetes insipidus Hypokalemic metabolic alkalosis, hyponatremia,
hyperGlycemia, hyperLipidemia, hyperUricemia,
hyperCalcemia.
K+-sparing diuretics (the K+ STAys)
Spironolactone -Hyperaldosteronism -Competitive aldosterone receptor antagonist -SE:
Eplerenone -K+ depletion in the cortical collecting tubule (CCT) Hyperkalemia,
-CHF endocrine effects (gynecomastia, antiandrogen effects)
Triamterene -Hyperaldosteronism -Block Na+ channels in the CCT -SE:
Amiloride -K+ depletion hyperkalemia
-CHF
ACE inhibitors -Hypertension -Inhibit angiotensin-converting enzyme, -Renin release is ↑ due to loss of feedback inhibition
Captopril -CHF reducing levels of angiotensin-II and -SE: (CAPTOPRIL)
Enalapril -diabetic renal disease preventing inactivation of bradykinin, Cough, Angioedema, Proteinuria, Taste changes,
Lisinopril which is a potent vasodilator hypOtension, Pregnancy problems (fetal renal
damage), Rash, Increased renin, Lower angiotensin II.
Hyperkalemia.
-C/I: bilateral renal artery stenosis
Losartan -Angiotensin-II receptor antagonist -It is not an ACE inhibitor and does not cause cough
 REPRODUCTIVE (pp 453-454)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
Antiandrogens (5-alpha reductase)
- Testosterone -----------------------> DHT (more potent)
Finasteride (propecia) -Useful in BPH -5-alpha reductase inhibitor (↓ conversion of -To prevent male-pattern hair loss, give a drug that will
-Promotes hair growth - used to testosterone to dihydrotestosterone) encourage female breast growth)
treat male pattern baldness
Flutamide -Prostate carcinoma -Nonsteroidal competitive inhibitor of
androgens at the testosterone receptor
Ketoconazole -Used in the treatment of -Inhibits steroid synthesis -SE: gynecomastia and amenorrhea
polycystic ovarian syndrome to
prevent hirsutism
Spironolactone -Used in the treatment of -Inhibits steroid binding -SE: gynecomastia and amenorrhea
polycystic ovarian syndrome to
prevent hirsutism
Leuprolide -Infertility (pulsatile) -GnRH analog with… -SE: Antiandrogen, nausea, vomiting
-Prostate cancer (continuous - -agonist properties when used in
use with flutamide) pulsatile fashion
-Uterine fibroids -antagonist properties when used in
continuous fashion.
(Leuprolide can be used in lieu of GnRH)
Sildenafil, -Erectile dysfunction -Inhibits cGMP phosphodiestersase, causing -SE: headache, flushing, dyspepsia, impaired blue-green
Vardenafil ↑cGMP, smooth muscle relaxation in the color vision.
(Sildenafil and vardenafil fill the corpus cavernosum, ↑ blood flow, and -C/I: Risk of life threatening hypotension in patients taking
penis) penile erection nitrates
Mifepristone (RU-486) -Termination of pregnancy -Competitive inhibitor of progestins at -SE:
-administered with progesterone receptors -heavy bleeding
misoprostol (PGE1) -GI effects (nausea, vomiting, anorexia)
-abdominal pain
Oral contraception Advantages
(synthetic progestins, -Reliable (<1% failure)
estrogen) -↓Risk of endometrial and
ovarian cancer
-↓Incidence of ectopic pregnancy
-↓Pelvic infections
-Regulation of menses
Hormone replacement -Used for relief or prevention of
therapy (HRT) menopausal symptoms
(eg. hot flashes, vaginal
atrophy)
-Osteoporosis (due to diminished
estrogen levels)
Dinoprostone -Cervical dilation and
uterine contraction to
induce labor
Ritodrine, -Relax the uterus
Terbutaline
Anastrozole -Breast cancer in
postmenopausal women
Testosterone -Treat hypogonadism and
(methyltestosterone) promote development of
secondary sex characteristics
-Stimulation of anabolism to
promote recovery after burn or
injury
-Treat ER-positive breast cancer
(exemestane)
Estrogens -Hypogonadism or ovarian failure
Ethinyl estradiol -Menstrual abnormalities
DES -HRT in postmenopausal women
Mestranol -Use in men with androgen-
dependent prostate cancer
Progestins -Used in oral contraceptives
-Endometrial cancer
-Abnormal uterine bleeding
Disadvantages
-Taken daily
-No protection against STDs
-↑Triglycerides
-Depression, weight gain, nausea,
hypertension
-Hypercoagulable state
-SE:
-unopposed estrogen replacement therapy (ERT) ↑ the
risk of endometrial cancer, so progesterone is added
-possible ↑ CV risk
-PGE2 analog
-β2 agonist
-Aromatase inhibitor
-Agonist at androgen receptors -SE:
-masculinization in females
-reduces intratesticular testosterone in males by
inhibiting Leydig cells; leads to gonadal atrophy
-premature closure of epiphyseal plates
-↑ LDL, ↓HDL.
-Bind estrogen receptors -SE:
-↑ risk of endometrial cancer
-bleeding in postmenopausal women
-clear cell adenocarcinoma of vagina in females
exposed to DES in utero
-↑ risk of thrombi.
'-C/I: ER-positive breast cancer
-Bind progesterone receptors, reduce growth,
and ↑ vascularization of endometrium
Estrogen partial
agonists
(selective estrogen
receptor modulators-
SERMs)
Clomiphene -Treat infertility and PCOS -Partial agonist at estrogen receptors in -SE:
pituitary gland -hot flashes
-Prevents normal feedback inhibition, and -ovarian enlargement,
↑ release of LH and FSH from pituitary, -multiple simultaneous pregnancies
which stimulates ovulation -visual disturbances
Tamoxifen -Treat and prevent recurrence of -Antagonist on breast tissue
ER-positive breast cancer
Raloxifene -Treat osteoporosis -Agonist on bone; ↓reabsorption of bone
 RESPIRATORY (pp 468-470)
CLASS/NAME CLINICAL USE MECHANISM SIDE EFFECTS / MISC
H1 Blockers
1st generation -Allergy -Reversible inhibitors of -SE: Sedation, antimuscarinic, anti-α-adrenergic
Diphenhydramine, -Motion sickness H1 histamine receptors
Dimenhydrinate, -Sleep aid
Chlorpheniramine

2nd generation -Allergy relief, non-sedating -Reversible inhibitors of -SE: Far less sedating than 1st generation because of
Loratadine, H1 histamine receptors ↓entry into CNS
Fexofenadine,
Desloratadine,
Cetirizine
Asthma drugs
Isoproterenol -non-specific β-agonist -SE: Tachycardia (β1)
-Relaxes bronchial smooth muscle (β2)
Albuterol -Use during acute exacerbation -β2 agonist
of asthma -Relaxes bronchial smooth muscle (β2).
Salmeterol -β2 agonist -SE: Tremor, arrhythmia
-Long acting agent for prophylaxis
Theophylline -Methylxanthine -Metabolized by P450
-Likely causes bronchodilation by inhibiting -Usage is limited because of narrow therapeutic index.
phosphodiesterase, thereby -SE: Narrow therapeutic range (cardiotoxicity,
↓ cAMP hydrolysis neurotoxicity)
Ipratropium -Asthma -Muscarinic antagonist -Also used for COPD
-COPD -Competitive block of muscarinic receptors,
preventing bronchoconstriction

Cromolyn -Asthma prophylaxis -Prevents release of mediators from -Effective only for prophylaxis of asthma. Not effective
mast cells during acute asthma attack.
-SE: Rare
Corticosteroids -1st line therapy for chronic -Inhibit the synthesis of virtually all cytokines.
Prednisone asthma -Inactivate NF-κB, the transcription factor that
Beclomethasone induces the production of TNF-α, among
other inflammatory agents.
Zileuton -Antileukotriene
-5-lipoxygenase pathway inhibitor.
-Blocks conversion of arachidonic acid to
leukotrienes
Zafirlukast -Especially good for -Antileukotriene
aspirin-induced asthma -Blocks leukotriene receptors
Montelukast -Especially good for -Antileukotriene
aspirin-induced asthma -Blocks leukotriene receptors
Expectorants
Guaifenesin (Robitussin) -Removes excess sputum but large doses
necessary; does not suppress cough reflex.
N-acetylcysteine -Mucolytic -Can loosen mucous plugs in CF patients
-Acetaminophen overdose -Also used as an antidote in
acetaminophen overdose.