Complete Drug List

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jknell
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Complete Drug List
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2013-04-01 00:39:35
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  1. Penicillin
    • G: IV and IM
    • V: oral

    • MOA:
    • -Cell Wall Synthesis Inhibitors
    • -bind PBPs (transpeptidases) → prevent cross linking of peptidoglycan

    • Clinical Uses:
    • -GP organisms (bactericidal)
    • -Neisseria meningitidis
    • -Ternponema pallidum
    • -syphilis

    • Toxicity:
    • -hypersensitivity
    • -hemolytic anemia
  2. Second Generation Penicillins
    • Oxacillin
    • Nafcillin (Use Naf for staph)
    • Dicloxacillin

    **penicillnase-resistant penicillins

    • MOA:
    • -Cell Wall Synthesis Inhibitors
    • -bind PBPs (transpeptidases) → prevent cross linking of peptidoglycan
    • *penicillinase resistant b/c of bulky R group

    • Clinical Uses:
    • -MSSA

    • Toxicity:
    • -hypersensitivity
    • -interstitial nephritis
  3. Third Generation Penicillins
    • Ampicillin
    • Amoxicillin

    **Aminopenicillins

    • MOA:
    • -Cell Wall Synthesis Inhibitors
    • -bind PBPs (transpeptidases) → prevent cross linking of peptidoglycan
    • -extended spectrum

    • Clinical Uses:
    • -H flu
    • -E coli
    • -Listeria
    • -Proteus
    • -Salmonella
    • -Shigella
    • -Enterococci
    • (HELPSS kill enterococci)

    • Toxicity:
    • -hypersensitivity reactions
    • -ampicillin rash
    • -pseudomembranous colitis (C. diff!)
  4. Fourth Generation Penicillins
    • Ticarcillin
    • Piperacillin

    **antipseudomonals

    • MOA:
    • -Cell Wall Synthesis Inhibitors
    • -bind PBPs (transpeptidases) → prevent cross linking of peptidoglycan
    • -Extended spectrum
    • -susceptible to penicillinase (use with clavulanic acid)

    • Clinical Use:
    • -Pseudomonas
    • -GNRs

    • Toxicity:
    • -hypersensitivity reactions
  5. β-Lactamase Inhibitors
    • Clavulanic Acid
    • Sulbactam
    • Tazobactam

    "CAST"
  6. First Generation Cephalosporins
    • Cefazolin
    • Cephalexin

    • MOA:
    • -β-lactam drugs
    • -inhibit cell wall synthesis
    • -less susceptible to penicillinases than penicllin
    • -bactericidal

    • Clinical Uses:
    • -GP cocci
    • -Proteus
    • -E Coli
    • -Klebsiella

    "PEcK"

    • Toxicity:
    • -hypersensitivity
    • -vitamin K deficieny
    • -low cross-reactivity with penicillins
    • -increase nephrotoxicity of aminoglycosides
  7. Second Generation Cephalosporins
    • Cefoxitin
    • Cefaclor
    • Cefuroxime

    • MOA:
    • -β-lactam drugs
    • -inhibit cell wall synthesis
    • -less susceptible to penicillinases than penicllin

    • Clinical Uses:
    • -GP cocci
    • -H flu
    • -Enterobacter
    • -Neisseria
    • -Proteus
    • -E coli
    • -Klebsiella
    • -Serrtia

    "HEN PEcKS"

    • Toxicity:
    • -hypersensitivity
    • -vitamin K deficiency
    • -low cross-reactivity with penicillins
    • -increase nephrotoxicity of aminoglycosides
  8. Third Generation Cephalosporins
    • Ceftriaxone
    • Cefotaxime
    • Ceftazidime

    • MOA:
    • -β-lactam drugs
    • -inhibit cell wall synthesis
    • -less susceptible to penicillinases than penicllin

    • Clinical Uses:
    • -Serious GN infections resistant to other β-lactams
    • -Ceftriaxone: meningitis and gonorrhea
    • -Ceftazidine: Pseudomonas

    • Toxicity:
    • -hypersensitivity
    • -vitamin K deficiency
    • -low cross-reactivity with penicillins
    • -increase nephrotoxicity of aminoglycosides
  9. Fourth Generation Cephalosporin
    Cefepime

    • MOA:
    • -β-lactam drugs
    • -inhibit cell wall synthesis
    • -less susceptible to penicillinases than penicllin

    • Clinical Uses:
    • -increased activity against Pseudomonas
    • -increased activity against GP organisms

    • Toxicity:
    • -hypersensitivity
    • -vitamin K deficiency
    • -low cross-reactivity with penicillins
    • -increase nephrotoxicity of aminoglycosides
  10. Aztreonam
    • MOA:
    • -monobactam
    • -resistant to β-lactam
    • -binds PBP3 and prevents peptidoglycan cross-linking
    • -synergistic with aminoglycosides

    • Clinical Uses:
    • -GNRs only
    • *penicillin-allergic patients
    • *renal insufficiency who can't tolerate aminoglycosides

    • Toxicity:
    • -usually non-toxic
    • -occaisional GI upset
  11. Carbapenems
    • Imipenem/cilastatin
    • Meropenem

    • MOA:
    • -broad spectrum, β-lactamaxe resistant
    • -cilastatin decreases inactivation of drug in renal tubules

    • Clinical Uses:
    • -GP cocci
    • -GNRs
    • -limited to life threatening infections or after other drugs have failed

    • Toxicity:
    • -GI distress
    • -skin rash
    • -CNS toxicity (seizures)
  12. Vancomycin
    • MOA:
    • -inhibits cell wall peptidoglycan formation by binding D-ala D-ala
    • -bactericidal

    • Clinical Uses:
    • -GP only!
    • -serious amultidrug-resistant organsims
    • -MRSA
    • -enterococci
    • -C diff

    • Toxicity:
    • -Nephrotoxicity
    • -Otoxtoxicity
    • -Thrombophlebitis
    • -Red Man Syndrome (pre-tx with antihistamines)
    • -"does NOT have many problems"

    • Resistance:
    • -mutation of D-ala D-ala to D-ala D-lac
  13. Antimicrobials: Protein Synthesis Inhibitors
    "Buy AT 30, CCEL at 50"

    • 30S Inhibitors:
    • -Aminoglycosides (cidal)
    • -Tetracyclines (static)

    • 50S Inhibitors:
    • -Chloramphenicol, Clindamycin (static)
    • -Erythromycin (static)
    • -Linezolid (variable
  14. Aminoglycosides
    • Gentamicin
    • Neomycin
    • Amikacin
    • Tobramicin
    • Streptomycin

    • MOA:
    • -bactericidial
    • -inhibit formation of initiation complex
    • -block translocation
    • -require O2 for uptake (ineffective against anaerobes)

    • Clinical Use:
    • -severe GNR infections
    • -synergistic with β-lactam antibiotics

    • Toxicity:
    • -nephrotoxicity
    • -neuromuscular blockade
    • -ototoxicity
    • -teratogen
  15. Tetracyclines
    • Tetracycline
    • Doxycycline
    • Demeclocycline (also ADH antagonist)
    • Minocycline

    • MOA:-bacteriostatic
    • -bind 30S ribosome and prevent attachment of tRNA
    • -limited CNS penetration
    • *do not take with milk, antacids or iron (inhibit absorption)

    • Clinical Use:
    • -Borrelia burgdorferi
    • -M pneumoniae
    • -Rickettsia
    • -Chlamydia
    • *effect against intracellular bugs

    • Toxicity:
    • -GI distress
    • -teeth discoloration
    • -inhibition of bone growth in children
    • -photosensitivity
    • -CI in pregnancy
  16. Macrolides
    • Azithromycin
    • Clarithromycin
    • Erythromycin

    • MOA:
    • -block 50S ribosome
    • -block translocation

    • Clinical Use:
    • -atypical pneumonias (mycoplasma, chlamydia, legionella)
    • -STDs (chlamydia)
    • -GP cocci (strep in pts allergic to penicillins)

    • Toxicity:
    • -Motility issues
    • -Arrhythmia (prolonged QT)
    • -Cholestatic hepatitis
    • -Rash
    • -eOsinophilia
    • "MACRO"
  17. Chloramphenicol
    • MOA:
    • -blocks peptidyltransferase at 50S ribosome

    • Clinical Use:
    • -Meningitis (H flu, N meningitidis, S pneumo)
    • -conservative use (toxicities)

    • Toxicity:
    • -anemia
    • -aplastic anemia
    • -gray baby syndrome (in preemies, low UDP glucuronyl transferase)

    • Resistance:
    • -plasmid encoded acetyltransferase
  18. Clindamycin
    • MOA:
    • -blocks transpeptidation at 50S ribosome
    • -bacteriostatic

    • Clinical Use:
    • -anaerobic infections (B. fragilis, C. perfringens) in aspiration pneumonia or lung abscesses
    • -oral infections with mouth anaerobes

    • Toxicity:
    • -Pseudomembranous colitis (C. diff!!!)
    • -fever
    • -diarrhea

    "Treat anaerobes above the diaphragm with clindamycin, treat anaerobes below the diaphragm with metronidazole"
  19. Sulfonamides
    • Sulfamethoxazole
    • Slufisoxazole
    • Sulfadiazine

    • MOA:
    • -block nucleotide synthesis by inhibiting folic acid synthesis
    • -bacteriostatic

    • Clinical Use:
    • -GP
    • -GN
    • -Nocardia
    • -Chlamydia
    • -SMX for simple UTI

    • Toxicity:
    • -hypersensitivity
    • -hemolysis in G6PD deficiency
    • -nephrotoxicity
    • -photosensitivity
    • -kernicterus (infants)
    • -displace other drugs from albumin (eg: warfarin)

    • Resistance:
    • -altered enzyme
    • -decreased uptake
    • -increased PABA synthesis
  20. Trimethoprim
    • MOA:
    • -block nucleotide synthesis by inhibiting folic acid synthesis (inhibit bacterial DHFR)
    • -bacteriostatic

    • Clinical Use:
    • -TMP-SMX
    • -UTIs
    • -Shigella
    • -Salmonella
    • -PCP

    • Toxicity:
    • -megaloblastic anemia
    • -leukopenia
    • -granulocytopenia
    • *leucovorin rescue (supplemental folinic acid)

    "TMP: Treats Marrow Poorly"
  21. Fluoroquinolones
    • Ciprofloxacin
    • Norfloxacin
    • Levofloxacin
    • Ofloxacin
    • Sparfloxacin
    • Moxifloxacin
    • Gatifloxacin
    • Enoxacin

    • MOA:
    • -inhibit DNA gyrase (topo II)
    • -bactericidal
    • -must NOT be taken with antacids

    • Clinical Use:
    • -GNR of GU tract (including Pseudomonas)
    • -Neisseria
    • -some GP organisms

    • Toxicity:
    • -GI upsets
    • -superinfections
    • -skin rashes
    • -HA-dizziness
    • -tendon rupture! (>60, or taking prednisone)
    • -CI: in pregnancy

    • Resistance:
    • -chromosome-encoded mutation in DNA gyrase
    • -plasmid-mediated resistance
    • -efflux pumps
  22. Metronidazole
    • MOA:
    • -damages DNA
    • -forms free radical toxic metabolites
    • -bactericidal
    • -antiprotozoal

    • Clinical Use:
    • -Giardia
    • -Entamoeba
    • -Trichomonas
    • -Gardnerella vaginalis
    • -Anaerobes (Bacteroides, C. diff)
    • -H Pylori (triple therapy)
    • "GET GAP"

    • Toxicity:
    • -disulfram-like reaction with alcohol
    • -HA
    • -metallic taste

    "Treat anaerobes above the diaphragm with clindamycin, treat anaerobes below the diaphragm with metronidazole"
  23. Antimycobacterial drugs
    • M. tuberculosis
    • -Prophylaxis: Isoniazid
    • -Tx: RIPE

    • M. avium-intracellulare
    • -Prophylaxis: Azithromycin
    • -Tx: Azithromycin, rifampin, ethambutol, streptomycin

    • M. leprae
    • -Tx: dapsone and rifampin (+clofazimine for lepromatous)
  24. Isoniazid (INH)
    • MOA:-decreased synthesis of mycolic acids
    • -need bacterial catalase-peroxidase

    • Clinical Use:
    • -M. tuberculosis

    • Toxicity:
    • -nephrotoxicity
    • -hepatotoxicity
    • -pyridoxine can prevent neurotox

    "INH Injures Neurons and Hepatocytes"
  25. Rifampin
    • MOA:
    • -blocks mRNA synthesis
    • -inhibits DNA-dependent RNA polymerase

    • Clinical Use:
    • -M. tuberculosis
    • -meningococcal prophylaxis
    • -chemoprophylaxis in contacts of children with HIB

    • Toxicity:
    • -minor hepatotoxicity
    • -drug interactions (increases P450)
    • -orange body fluids

    • 4R's:
    • -RNA polymerase inhibitor
    • -Revs up microsomal P450
    • -Red/orange body fluids
    • -Rapid resistance if used alone
  26. Pyrazinamide
    • MOA:
    • -mechanism uncertain
    • -may acidify cellular environment
    • -effective in acidic pH of phagolysosomes (where TB engulfed by MP is found)

    • Clinical Use:
    • -M. tuberculosis

    • Toxicity:
    • -hyperuricemia
    • -hepatotoxicity
  27. Ethambutol
    • MOA:
    • -decrease carbohydrate polymerization of mycobacterium cell wall

    • Clinical Use:
    • -M tuberculosis

    • Toxicity:
    • -optic neuropathy (red-green colorblindness)
  28. Amphotericin B
    • MOA:
    • -binds ergosterol (unique to fungi)
    • -forms membrane pores that allow leakage of electrolytes

    • Clinical Use:
    • -serious, systemic mycoses
    • -Cryptococcus
    • -Blastomyces
    • -Coccidioides
    • -Histoplasma
    • -Candida
    • -Mucor

    • Toxicity:
    • -fever/chills ("shake and bake")
    • -hypotension
    • -nephrotoxicity
    • -arrhythmias
    • -anemia
    • -IV phlebitis

    "amphoterrible"
  29. Nystatin
    • MOA:
    • -forms membrane pores that allow leakage of electrolytes
    • -topical b/c too toxic for systemic use

    • Clinical Use:
    • -oral candidiasis (thrush)
    • -diaper rash or vaginal candidiasis
  30. Azoles
    • Fluconazole
    • Ketoconazole
    • Clotrimazole
    • Miconazole
    • Itraconazole
    • Voriconazole

    • MOA:
    • -inhibit fungal sterol synthesis by inhibiting the involved P-450 enzyme

    • Clinical Use:
    • -local and less serious systemic mycoses
    • -Fluconazole: chronic suppression of crypto meningitis in AIDS
    • -Itraconazole: blasto, cocci, histo
    • -Clotrimazole/Miconazole: topical fungal infections

    • Toxicity:
    • -inhibits testosterone synthesis (gynecomastia)
    • -liver dysfunction (inhibits P-450)
  31. Flucytosine
    • MOA:
    • -inhibits DNA and RNA biosynthesis by conversion to 5-FU by cytosine deaminase

    • Clinical Use:
    • -systemic fungal infections (crypto meningitis)
    • -in combo with amphotericin B

    • Toxicity:
    • -BM suppression
  32. Caspofungin, Micafungin
    • MOA:
    • -inhibit cell wall synthesis by inhibiting synthesis of β-glucan

    • Clinical Use:
    • -invasive aspergillosis
    • -Candida

    • Toxicity:
    • -GI upset
    • -flushing
  33. Terbinafine
    MOA:-inhibits fungal enzyme squalene epoxidase

    • Clinical Use:
    • -dermatophytoses (esp onychomycosis)

    • Toxicity:
    • -abnormal LFTs
    • -visual disturbances
  34. Griseofulvin
    • MOA:
    • -interferes with microtubule function
    • -disrupts mitosis
    • -deposits in keratin tissues

    • Clinical Use:
    • -oral tx of superficial infections
    • -inhibits growth of dermatophytes

    • Toxicity:
    • -teratogenic
    • -carcinogenic
    • -confusion
    • -HA
    • -increase P450 and warfarin metabolism
  35. Chloroquine
    • MOA:
    • -blocks detoxification of heme into hemozoin
    • -heme accumulates and is toxic to plasmodia

    • Clinical Use:
    • -treat plasmodium other than P. falciparum (too much resistance)

    • Toxicity:
    • -retinopathy
  36. Zanamivir
    Oseltamivir
    • MOA:
    • -inhibit influenza neuraminidase
    • -decrease the release of progeny virus

    • Clinical Use:
    • -treatment and prevention of influenza A and B
  37. Ribavirin
    • MOA:
    • -inhibits synthesis of guanine nucleotides

    • Clinical Use:
    • -RSV
    • -chronic Hep C

    • Toxicity:
    • -hemolytic anemia
    • -severe teratogen
  38. Acyclovir
    Famciclovir
    Valacyclovir
    • MOA:
    • -guanosine analog
    • -monophosphorylated by HSV/VZV thymidine kinase
    • -preferentially inhibits viral DNA polymerase

    • Clinical Use:
    • -HSV
    • -VZV
    • -weak activity against EBV
    • -Famciclovir: herpes zoster
    • -Valacyclovir has better oral bioavailibility

    • Toxicity:
    • -few serious adverse effects

    • Resistance:
    • -mutated viral thymidine kinase
  39. Ganciclovir
    • MOA:
    • -5'-monophosphate formed by a CMV viral kinase
    • -guanosine analog
    • -triphosphate formed by cellular kinases
    • -preferentially inhibits DNA polymerase

    • Clinical Use:
    • -CMV (esp immunocompromised)

    • Toxicity:
    • -leukopenia
    • -neutropenia
    • -thrombocytopenia
    • -renal toxicity
    • -more toxic to host enzymes than acyclovir

    • Resistance:
    • -mutated CMV DNA polymerase or lack of a viral kinase
  40. Foscarnet
    • MOA:
    • -viral DNA polymerase inhibitor
    • -does not require activation by viral kinase

    • Clinical Use:
    • -CMV retinitis in immunocompromised patients when ganciclovir fials
    • -acyclovir-resistant HSV

    • Toxicity:
    • -nephrotoxicity

    • Resistance:
    • -mutated DNA polymerase
  41. Cidofovir
    • MOA:
    • -preferentially inhibits viral DNA polymerase
    • -does not require phosphorylation by viral kinase

    • Clinical Use:
    • -CMV retinitis in immunocompromised patients
    • -acyclovir resistant HSV

    • Toxicity:
    • -nephrotoxicity
  42. HAART
    • Initiation:
    • -when patients present with AIDS defining illnesses
    • -Low CD4 counts (<500)
    • -high viral load

    • Regimen:
    • -3 drugs (prevent resistance)
    • -2 NRTIs + 1 NNRTI OR 1 Protease Inhibitor OR 1 integrase inhibitor
  43. Protease Inhibitors (-navirs)
    • Lopinavir
    • Atazanavir
    • Darunavir
    • FOsemprenavir
    • Saquinavir
    • Ritonavir
    • Indinavir

    • MOA:
    • -inhibits protease necessary to cleave polypeptide mRNA
    • -prevents maturation of new virusus

    • Clinical Use:
    • -HIV

    • Toxicity:
    • -hyperglycemia
    • -GI intolerance
    • -Lipodystrophy
    • -Nephropathy
    • -Hematuria
  44. NRTIs
    **Nucleoside reverse transcriptase inhibitors

    • Tenofovir
    • Emtricitabine
    • Abacavir
    • Lamivudine
    • Zidovudine (formerly AZT)
    • Didanosine
    • Stavudine

    • MOA:
    • -inhibit nucleotide binding to RTase and terminate DNA chain

    • Clinical Use:
    • -HIV
    • -ZDV used for general prophylaxis and during pregnancy

    • Toxicity:
    • -BM suppression (reversed with G-CSF and EPO)
    • -peripheral neuropathy
    • -lactic acidosis
    • -rash
    • -anemia
  45. NNRTIs
    **non-nucleoside reverse transcriptase inhibitor

    • Nevirapine
    • Efavirenz
    • Delavirdine

    • MOA:
    • -bind to RTase at different site than NRTIs

    • Clinical Use:
    • -HIV

    • Toxicity:
    • -BM suppression (reversed with G-CSF and EPO)
    • -peripheral neuropathy
    • -lactic acidosis
    • -rash
    • -anemia
  46. Integrase Inhibitors
    Raltegravir

    MOA:-inhibits HIV genome integration into host cell chromosome

    • Clinical Use:
    • -HIV

    • Toxicity:
    • -hypercholesterolemia
  47. Interferons
    • MOA:
    • -glycoproteins synthesized by virus infected cells
    • -block replication of both RNA and DNA viruses

    • Clinical Use:
    • -IFNα: chronic hep B and C, Kaposi's sarcoma
    • -IFNβ: MS
    • -IFNγ: NADPH oxidase deficiency

    • Toxicity:
    • -neutropenia
    • -myopathy
  48. Cyclosporine
    • MOA:
    • -blocks the differentiation and activation of T cells by inhibiting calcineurin
    • -prevents production of IL2 and its receptor

    • Clinical Use:
    • -suppresses organ rejection after transplantation
    • -selected autoimmune disorders

    • Toxicity:
    • -nephrotoxicity
    • -hypertension
    • -hyperlipidemia
    • -hyperglycemia
    • -tremor
    • -gingival hyperplasia
    • -hirsutism
  49. Tacrolimus
    • MOA:
    • -similar to cyclosporine
    • -inhibits calcineurin and secretion of IL2

    • Clinical Use:
    • -potent immunosuppressive (organ transplant)

    • Toxicity:
    • -nephrotoxicity
    • -hypertension
    • -hyperlipidemia
    • -hyperglycemia
    • -tremor
  50. Sirolimus (rapamycin)
    • MOA:
    • -inhibits mTOR
    • -inhibits T cell proliferation in response to IL2

    • Clinical Use:
    • -immunosuppression after kidney transplantation
    • -drug-eluting stents

    • Toxicity:
    • -hyperlipidemia
    • -thrombocytopenia
    • -leukopenia
  51. Azathioprine
    • MOA:
    • -interferes with the metabolism and synthesis of NAs
    • -toxic to proliferating lymphocytes

    • Clinical Use:
    • -kidney transplant
    • -autoimmune disorders (glomerulonephritis and hemolytic anemia)

    • Toxicity:
    • -BM suppression
    • -toxic effects may be increased by allopurinol
  52. Muromonad-CD3
    • MOA:
    • -anti-CD3
    • -blocks T cell transduction

    • Clinical Use:
    • -prevent acute transplant rejection
    • -immunosuppression after kidney transplant

    • Toxicity:
    • -cytokine release syndrome
    • -hypersensitivity
  53. Aldesleukin
    • MOA:
    • -recombinant IL2

    • Clinical Uses:
    • -RCC
    • -metastatic melanoma
  54. Epoetin alfa
    • MOA:
    • -recombinant EPO

    • Clinical Uses:
    • -anemias
    • -especially in renal failure
  55. Filgrastim
    • MOA:
    • -recombinant G-CSF

    • Clinical Uses:
    • -recovery of BM
  56. Sargramostim
    • MOA:
    • -GM-CSF

    • Clinical Uses:
    • -recovery of BM
  57. α-Interferon
    • Clinical Uses:
    • -Hep B and C
    • -Kaposi's sarcoma
    • -leukemias
    • -malignant melanoma
  58. β-Interferon
    • Clinical Uses:
    • -MS
  59. γ-Interferon
    • Clinical Uses:
    • -chronic granulomatous disease
  60. Oprelvekin
    • MOA:
    • -IL-11

    • Clinical Uses:
    • -thrombocytopenia
  61. Thrombopoietin
    • Clinical Uses:
    • -thrombocytopenia
  62. Digoxin Immune Fab
    • Clinical Use:
    • -antidote for digoxin intoxication
  63. Infliximab
    • MOA:
    • -anti-TNFa

    • Clinical Uses:
    • -Crohn's
    • -RA
    • -Psoriatic arthritis
    • -ankylosing spondylitis

    • Toxicity:
    • -predispose to infection
    • -reactivation of latent TB
  64. Adalimumab
    MOA:-anti-TNFa

    • Clinical Uses:
    • -Crohn's
    • -RA
    • -Psoriatic arthritis

    • Toxicity:
    • -predispose to infection
    • -reactivation of latent TB
  65. Abciximab
    • MOA:
    • -anti-glycoprotein IIb/IIIa

    • Clinical Uses:
    • -prevent cardiac ischemia in unstable angina and patients treated with percutaneous coronary intervention
  66. Trastuzumab (Herceptin)
    MOA:-anti-HER2

    • Clinical Uses:
    • -HER2-overexpressing breast cancer
  67. Rituximab
    • MOA:
    • -anti-CD20

    • Clinical Uses:
    • -B-cell non-Hodgkin's lymphoma
  68. Omalizumab
    • MOA:
    • -anti-IgE

    • Clinical Uses:
    • -additional line of treatment for severe asthma
  69. Etanercept
    • Mechanism:
    • -fusion protein (TNFa receptor + IgG Fc)

    • Clinical Use:
    • -RA
    • -psoriasis
    • -ankylosing spondylitis

    • Toxicity:
    • -predispose to infection
    • -reactivation of latent TB
  70. Bethanechol
    • MOA:
    • -direct cholinomimetic agonist
    • -activates bowel and bladder smooth muscle

    • Clinical Uses:
    • -postoperative ileus
    • -neurogenic ileus
    • -urinary retention
  71. Carbachol
    • MOA:
    • -carbon copy of acetylcholine
    • -direct cholinomimetic agonist

    • Clinical Uses:
    • -glaucoma
    • -pupillary contraction
    • -relief of intraoccular pressure
  72. Pilocarpine
    • MOA:
    • -direct cholinomimetic agonist
    • -contracts ciliary muscle of eye, pupillary sphincter
    • -potent stimulator of sweat, tears and saliva

    • Clinical Uses:
    • -open angle glaucoma
    • -closed angle glaucoma
  73. Methacholine
    • MOA:
    • -direct cholinomimetic agonist
    • -stimulates muscarinic receptors in airways

    • Clinical Uses:
    • -challenge test for diagnosis of asthma
  74. Neostigmine
    • MOA:
    • -indirect cholinomimetic agonist
    • -anticholinesterase
    • -increases endogenous ACh
    • -no CNS penetration

    • Clinical Uses:
    • -postoperative and neurogenic ileus and urinary retention
    • -myasthenia gravis
    • -reversal of NMJ blockade
  75. Pyridostigmine
    • MOA:
    • -indirect cholinomimetic agonist
    • -anticholinesterase
    • -increases endogenous ACh
    • -increases strength

    • Clinical Uses:
    • -myasthenia gravis
  76. Edrophonium
    • MOA:
    • -indirect cholinomimetic agonist
    • -anticholinesterase
    • -increases endogenous ACh

    • Clinical Uses:
    • -diagnosis of myasthenia gravis
  77. Physostigmine
    • MOA:
    • -indirect cholinomimetic agonist
    • -anticholinesterase
    • -increases endogenous ACh

    • Clinical Uses:
    • -anticholinergic toxicity (can cross BBB)
    • -reverses atropine OD
  78. Donepezil
    • MOA:
    • -indirect cholinomimetic agonist
    • -anticholinesterase
    • -increases endogenous ACh

    • Clinical Uses:
    • -Alzheimer's disease
  79. Atropine
    Homatropine
    Tropicamide
    • MOA:
    • -muscarinic antagonist

    • Clinical Uses:
    • -produces mydriasis and cycloplegia in the eye
  80. Benztropine
    • MOA:
    • -muscarinic antagonist (CNS)

    • Clinical Uses:
    • -Parkinson's Disease
  81. Scopolamine
    • MOA:
    • -muscarinic antagonist (CNS)

    • Clinical Uses:
    • -Motion sickness
  82. Ipratropium
    Tiotropium
    • MOA:
    • -muscarinic antagonist (respiratory)
    • -competitive block of muscarinic receptors

    • Clinical Uses:
    • -COPD
    • -asthma
  83. Oxybutynin
    • MOA:
    • -muscarinic antagonist (GU)

    • Clinical Uses:
    • -reduce urinary urgency in mild cystitis and reduce bladder spasms
  84. Glycopyrrolate
    • MOA:
    • -muscarinic antagonist (GI, respiratory)

    • Clinical Uses:
    • -Parenteral: Preop to reduce airway secretions
    • -Oral: drooling, peptic ulcer
  85. Atropine
    • MOA:
    • -muscarinic antagonist
    • -↑ pupil dilation, cycloplegia
    • -↓ airway secretions
    • -↓ acid secretion in stomach
    • -↓ gut motility
    • -↓ bladder urgency in cystitis

    • Clinical Uses:
    • -bradycardia
    • -ophthalmic applications

    • Toxicity:
    • -Hot as a hare (increase body temp)
    • -Dry as a bone (dry mouth, skin)
    • -Red as a beet (flushed skin)
    • -Blind as a bat (cycloplegia)
    • -Mad as a hatter (disorientation)
    • -acute angle closure glaucoma in elderly
    • -urinary retention in men with BPH
    • -hyperthermia in infants
  86. Epinephrine
    • MOA:
    • -direct sympathomimetic
    • -α1 +++
    • -α2 +++
    • -β1 ++++
    • -β2 ++++
    • -D1 0

    • Clinical Uses:
    • -anaphylaxis
    • -glaucoma (open angle)
    • -asthma
    • -hypotension
  87. Norepinephrine
    • MOA:
    • -direct sympathomimetic
    • -α1 ++++
    • -α2 ++++
    • -β1 ++++
    • -β2 0
    • -D1 0

    • Clinical Uses:
    • -hypotension

    • Toxicity:
    • -decreases renal perfusion
  88. Isoproterenol
    • MOA:
    • -direct sympathomimetic
    • -α1 0
    • -α2 0
    • -β1 ++++
    • -β2 ++++
    • -D1 0

    • Clinical Uses:
    • -Torsade de pointes
    • -bradyarrhythmias (but can worsen ischemia)
  89. Dopamine
    • MOA:
    • -direct sympathomimetic
    • -α1 +++
    • -α2 +++
    • -β1 +++
    • -β2 ++
    • -D1 +++

    • Clinical Uses:
    • -shock (renal perfusion)
    • -heart failure (ionotropic and chronotropic)
  90. Dobutamine
    • MOA:
    • -direct sympathomimetic
    • -α1 +
    • -α2 +
    • -β1 ++++
    • -β2 +
    • -D1 0

    • Clinical Uses:
    • -heart failure
    • -cardiac stress testing (ionotropic and chronotropic)
  91. Phenylephrine
    • MOA:
    • -direct sympathomimetic
    • -α1 +++
    • -α2 ++
    • -β1 0
    • -β2 0
    • -D1 0

    • Clinical Uses:
    • -hypotension (vasoconstrictor)
    • -ocular procedures (mydriatic)
    • -rhinitis (decongestant)
  92. Albuterol
    Salmeterol
    Terbutaline
    • MOA:
    • -direct sympathomimetic
    • -α1 0
    • -α2 0
    • -β1 ++
    • -β2 ++++
    • -D1 0

    • Clinical Uses:
    • -acute asthma
    • -long term asthma
    • -COPD
    • -terbutaline to reduce premature uterine contractions
  93. Ritodrine
    • MOA:
    • -direct sympathomimetic
    • -α1 0
    • -α2 0
    • -β1 0
    • -β2 ++++
    • -D1 0

    • Clinical Uses:
    • -reduces premature uterine contractions
  94. Amphetamine
    • MOA:
    • -indirect sympathomimetic
    • -indirect general agonist
    • -releases stored catecholamines

    • Clinical Uses:
    • -narcolepsy
    • -obesity
    • -ADD
  95. Ephedrine
    • MOA:
    • -indirect sympathomimetics
    • -indirect general agonist
    • -releases stored catecholamines

    • Clinical Uses:
    • -nasal decongestion
    • -urinary incontinence
    • -hypotension
  96. Cocaine
    • MOA:
    • -indirect sympathomimetic
    • -indirect general agonist
    • -reuptake inhibitor

    • Clinical Uses:
    • -causes vasoconstriction and local anesthesia
    • -never give with beta-blockers! (unopposed α1 activation and extreme hypertension)
  97. Phenoxybenzamine
    • MOA:
    • -non-selective α blocker
    • -irreversible

    • Clinical Uses:
    • -pheochromocytoma (before removing tumor since high levels of release catecholamines will not be able to overcome blockage)

    • Toxicity:
    • -orthostatic hypotension
    • -reflex tachycardia
  98. Phentolamine
    • MOA:
    • -non-selective α-blocker
    • -reversible

    • Clinical Uses:
    • -give to patients on MAO inhibitors that eat tyramine-containing foods
  99. Prazosin
    Terazosin
    Doxazosin
    Tamsulosin
    • MOA:
    • -α1 selective blocker

    • Clinical Uses:
    • -hypertension
    • -BPH urinary retention

    • Toxicity:
    • -orthostatic hypotension
    • -dizziness
    • -HA
  100. Mirtazapine
    • MOA:
    • -α1 selective blocker

    • Clinical Uses:
    • -depression

    • Toxicity:
    • -sedation
    • -increased serum XOL
    • -increased appetite
  101. Acebutolol
    Betaxolol
    Esmolol
    Atenolol
    Metoprolol
    • MOA:
    • -β-1 selective antagonist

    • Clinical Uses:
    • -good in patients with comorbid pulmonary disease
    • -Angina pectoris (↓HR and IS)
    • -MI (↓ mortality)
    • -SVT (↓ AV conduction velocity)
    • -HTN (↓ CO/renin secretion)
    • -CHF (slows progression of chronic failure)

    • Toxicity:
    • -impotence
    • -exacerbation of asthma
    • -CV adverse effects (bradycardia, AV block, CHF)
    • -CNS adverse effects (seizures, sedation)
  102. Propanolol
    Timolol
    Nadolol
    Pinodolol
    • MOA:
    • -Nonselective β antagonist

    • Clinical Uses:
    • -Angina pectoris (↓HR and IS)
    • -MI (↓ mortality)
    • -SVT (↓ AV conduction velocity)
    • -HTN (↓ CO/renin secretion)
    • -CHF (slows progression of chronic failure)

    • Toxicity:
    • -impotence
    • -exacerbation of asthma
    • -CV adverse effects (bradycardia, AV block, CHF)
    • -CNS adverse effects (seizures, sedation)
  103. Non-selective α and β Antagonist
    • Carvedilol
    • Labetalol
  104. Partial β Agonists
    • Pindolol
    • Acebutolol
  105. Calcium Channel Blockers
    • Nifedipine
    • Amlodipine
    • Diltiazem
    • Verapamil

    • MOA:
    • -block voltage dependent L type calcium channels or cardiac and smooth muscle
    • -reduce muscle contractility
    • -Vascular SM: amlodipine = nifedipine > diltiazem > verapamil
    • -Heart: verapamil > diltiazem > amlodipine = nifedipine

    • Clinical Uses:
    • -HTN
    • -angina
    • -arrhythmias
    • -Prinzmetal angina
    • -Raynaud's

    • Toxicity:
    • -cardiac depression
    • -AV block
    • -peripheral edema
    • -flushing
    • -dizziness
    • -constipation
  106. Hydralazine
    • MOA:
    • -increase cGMP causing smooth muscle relaxation
    • -vasodilates arterioles > veins
    • -afterload reduction

    • Clinical Uses:
    • -severe HTN
    • -CHF-pregnancy!

    • Toxicity:
    • -compensatory tachycardia
    • -fluid retention
    • -nausea
    • -HA
    • -angia
    • -lupus-like syndrome
  107. Nitroprusside
    • MOA:
    • -short acting
    • -increases cGMP via direct release of NO

    • Clinical Uses:
    • -malignant hypertension

    • Toxicity:
    • -cyanide toxicity
  108. Fenoldopam
    • MOA:
    • -D1 receptor agonist
    • -coronary, peripheral, renal and splanchnic vasodilation
    • -decrease BP
    • -increase natriuresis

    • Clinical Uses:
    • -malignant HTN
  109. Nitroglycerin
    Isosorbide Dinitrate
    • MOA:
    • -vasodilate by releasing NO in smooth muscle
    • -cause increase in cGMP and smooth muscle relaxation
    • -dilates veins > arteries
    • -decrease preload

    • Clinical Uses:
    • -angina
    • -pulmonary edema

    • Toxicity:
    • -reflex tachycardia
    • -hypotension
    • -flushing
    • -HA
    • -"monday disease"
  110. HMG-CoA Reductase Inhibitors
    • Lovastatin
    • Pravastatin
    • Simvastatin
    • Atorvastatin
    • Rosuvastatin

    • MOA:
    • -inhibits conversion of HMG-CoA to mevalonate (XOL precursor)
    • -decreases LDL and TGs
    • -increases HDL

    • Clinical Uses:
    • -lipid lowering

    • Toxicity:
    • -hepatotoxicity (LFTs)
    • -rhabdomyolysis
  111. Niacin (B3)
    • MOA:
    • -inhibits lipolysis in adipose tissues
    • -reduces hepatic vLDL secretion into circulation
    • -decreases LDL and TGs
    • -increases HDL

    • Clinical Uses:
    • -lipid lowering

    • Toxicity:
    • -red, flushed face
    • -hyperglycemia (acanthosis nigricans)
    • -hyperuricemia (exacerbates gout)
  112. Bile Acid Resins
    • Cholestyramine
    • Colestipol
    • Colesevelam

    • MOA:
    • -prevent intestinal reabsorption of bile acids
    • -liver must use XOL to make more
    • -decreases LD-slightly increases HDL

    • Clinical Uses:
    • -lipid lowering

    • Toxicity:
    • -patients hate it
    • -tastes bad
    • -GI discomfort
    • -decrease absorption of fat soluble vitamins
    • -XOL gallstones
  113. Ezetimibe
    • MOA:
    • -prevents XOL reabsorption at small intestine brush border
    • -decreases LDL

    • Clinical Uses:
    • -lipid lowering

    • Toxicity:
    • -rare increase in LFTs
    • -diarrhea
  114. Fibrates
    • Gemfibrozil
    • Clofibrate
    • Bezafibrate
    • Fenofibrate

    • MOA:
    • -upregulate LPL increasing TG clearance
    • -slightly decreases LDL
    • -increases HDL
    • -significantly decreases TGs

    • Clinical Uses:
    • -lipid lowering

    • Toxicity:
    • -myositis
    • -hepatotoxicity
    • -XOL gallstones
  115. Digoxin
    • MOA:
    • -direct inhibition of Na/K ATPase
    • -leads to indirect inhibition of Na/Ca exchanger
    • -increase intracellular Ca (↑ IS)
    • -stimulate vagus nerve (↓ HR)

    • Clinical Uses:
    • -CHF (increase contractility)
    • -atrial fibrillation

    • Toxicity:
    • -nausea/vomiting/diarrhea
    • -blurry yellow vision
    • -fatigue
    • -HA
    • -dizziness
    • -confusion
    • -bradycardia (can lead to JER and Vfib)
    • -arrhythmia
    • -AV block
    • -hyperkalemia
  116. Class IA Antiarrhythmics
    • Quinidine
    • Procainamide
    • Dispyramide

    • MOA:
    • -Na+ channel blockers
    • -↑ APD
    • -↑ ERP
    • -↑ QT interval

    • Clinical Uses:
    • -atrial and ventricular arrhythmias
    • -reentrant and ectopic supraventricular and ventricular tachycardias

    • Toxicity:
    • -thrombocytopenia
    • -torsades de pointes (↑ QT interval)
    • -Q: HA, tinnitus
    • -P: reversible SLE-like syndrome
    • -D: HF
  117. Class IB Antiarrhythmics
    • Lidocaine
    • Mexiletine
    • Tocainide

    • MOA:
    • -Na+ channel blockers
    • -↓ APD
    • -preferentially affect ischemic or depolarized Purkinje and ventricular tissue

    • Clinical Uses:
    • -acute ventricular arrhythmias (esp post-MI)
    • -digitalis-induced arrhythmias

    • Toxicity:
    • -local anesthetic
    • -CNS stimulation/depression
    • -CV depression
  118. Class IC Antiarrhythmics
    • Flecainide
    • Propafenone

    • MOA:
    • -Na+ Channel blockers
    • -no effect on APD

    • Clinical Uses:
    • -ventricular tachycardias that progress to VF
    • -intractable SVT
    • -usually only last resort in refractory tachyarrhythmias
    • -CI in patients post MI

    • Toxicity:
    • -proarrhythmic, especially post-MI (contraindicated)
    • -significantly prolongs refractory period in AV node
  119. Class II Antiarrhythmics
    • Metoprolol
    • Propanolol
    • Esmolol
    • Atenolol
    • Timolol

    • MOA:
    • -decreases cAMP, Ca currents → decrease in SA and AV nodal activity
    • -suppress abnormal pacemakers by decreasing phase 4 slope
    • -AV node particularly sensitive

    • Clinical Use:
    • -ventricular tachycardia
    • -SVT
    • -slowing ventricular rate during Afib and Aflutter

    • Toxicity:
    • -impotence
    • -exacerbation of asthma
    • -CV effects (bradycardia, AV block, CHF)
    • -CNS effects (sedation, sleep alteration)
    • -M: dyslipidemia
    • -P: aggravate Prinzmetal angina
  120. Class III Antiarrhythmics
    • Amiodarone
    • Ibutilide
    • Dofetilide
    • Sotalol

    "AIDS"

    • Mechanism:
    • -increase AP duration
    • -increase ERP
    • -increase QT interval

    • Clinical Use:
    • -when other antiarrhythmics fail

    • Toxicity:
    • 1. Sotalol:
    • -torsades de pointes
    • -excessive β block

    • 2. Amiodarone:
    • -pulmonary fibrosis
    • -hepatotoxicity
    • -hypo/hyperthyroidism (amiodarone is 40% iodine)
    • -corneal deposits
    • -skin deposits (blue/gray) resulting in photodermatitis
    • -neurologic effects
    • -constipation
    • -CV effects (bradycardia, heart block, CHF)

    **Amiodarone has class I, II, III and IV effects b/c it alters the lipid membrane

    Remember to check PFTs, LFTs and TFTs when using amiodarone
  121. Class IV Antiarrhythmics
    • Verapamil
    • Diltiazem

    • Mechanism:
    • -decrease conduction velocity
    • -increase ERP
    • -increase PR interval

    • Clinical Use:
    • -prevention of nodal arrhythmias (SVT)

    • Toxicity:
    • -constipation
    • -flushing
    • -edema
    • -CV effects (CHF, AV block, SA depression)
  122. Other Antiarrhythmics
    • Adenosine
    • Mg2+
  123. Adenosine
    • Mechanism:
    • -increase K+ out of cells → hyperpolarizing cell and decrease ICa
    • -very short acting (~15 sec)

    • Clinical Use:
    • -drug of choice in diagnosing/abolishing supraventricular tachycardia

    • Toxicity:
    • -flushing
    • -hypotension
    • -chest pain

    Effects blocked by theophyline and caffeine
  124. Mg2+
    • Effective in:
    • -Torsades de pointes
    • -digoxin toxicity
  125. Diabetes drugs
    strategies for DM1/2; Rx classes (mechanisms)
    • -DM 1: low-sugar diet, insulin replacement
    • -DM 2: dietary modification and exercise for wieght loss; oral hypoglycemics and insulin replacements

    • Drug classes:
    • -Insulin: short/rapid-acting, long acting
    • -Biguanides: Metformin (mechanism unknown; ↓gluconeogenesis, ↑ glycolysis, ↑ peripheral glucose uptake)
    • -Sulfonylureas: Glipizide (mechanism: close K+ channels in β-cell membrane → depolarizes cell membrane → triggering insulin release via ↑ Ca2+ influx)
    • -Glitazones/thiazolidinediones: "-glitazones" (↑ insulin sensitivity)
    • -α-glucoside inhibitors: Acarbose (inhibit intestinal brush-border α-glucosidases)
    • -Amylin analogs: Pramlintide (↓ glucagon)
    • -GLP-1 analogs: Exenatide (↑ insulin, ↓ glucagon release)
    • -DPP-4 inhibitors: linagliptin (↑ insulin, ↓ glucagon release)
  126. Insulin
    Mechanism, clinical use, toxicities
    • Lispro (rapid-acting)
    • Aspart (rapid-acting)
    • Glulisine (rapid-acting)
    • Regular (short-acting)
    • NPH (intermediate)
    • Glargine (long-acting)
    • Detemir (long acting)

    • Action: bind insulin receptor (tyrosine kinase activity)
    • -Liver: ↑ glucose stored as glycogen
    • -Muscle: ↑ glycogen and protein synthesis, K+ uptake
    • -Fat: aids TG storage

    Clinical use: Type 1 DM, type 2 DM, gestational diabetes, life-threatening hyperkalemia, and stress-induced hyperglycemia

    Toxicity: hypoglycemia, very rarely hypersensitivity reaction
  127. Biguanides
    Mechanism, clinical use, toxicities
    Metformine

    • Action: Exact mechanism unknown
    • -↓ gluconeogenesis
    • -↑ glycolysis
    • -↑ peripheral glucose uptake (insulin sensitivity)

    • Clinical use: oral
    • -First line therapy in DM2
    • -Can be used in pts without islet function

    • Toxicities: GI upset
    • -Lactic acidosis (*contraindicated in renal failure)
  128. Sulfonylureas
    Mechanism, clinical use, toxicities
    • Fist generation: Tolbutamide, chlorpropamide
    • Second generation: Glyburide, glimepiride, glipizide

    • Mechanism:
    • -Close K+ channel in β-cell membrane, so cell depolarizes
    • -leads to ↑Ca2+influx which triggers release of insulin

    • Clinical use: stimulates release of endogenous insulin in type 2 DM
    • -Require some islet cell function, useless in DM1

    • Toxicities:
    • -First gen: disulfiram-like effects
    • -Second gen: hypoglycemia
  129. Glitazones/thiazolidinediones
    Mechanism, clinical use, toxicities
    Pioglitazone, Rosiglitazone

    • Mechanism:
    • -↑ insulin sensitivity in peripheral tissue
    • -binds to PPAR-γ nuclear transcription regulator

    • Clinical use:
    • -Used as monotherapy in type 2 DM, or in combination

    • Toxicities:
    • -Weight gain
    • -Edema
    • -Hepatotoxicity
    • -Heart failure
  130. α-glucosidase inhibitors
    Mechanism, clinical use, toxicities
    Acarbose, Miglitol

    • Mechanism:
    • -Inhibit intestinal brush-border α-glucosidases
    • -Delayed sugar hydrolysis and glucose absorption → ↓ postprandial hyperglycemia

    Clinical use: Monotherapy in type 2 DM, or combination

    Toxicities: GI disturbances
  131. Amylin analogs
    Mechanism, clinical use, toxicities
    Pramlintide

    Mechanism:↓ glucagon

    Clinical use: type 1 or 2 DM

    • Toxicities:
    • -Hypoglycemia
    • -Nausea
    • -Diarrhea
  132. GLP-1 analogs
    Mechanism, clinical use, toxicities
    Exenatide, Liraglutide

    • Mechanism:
    • ↑ insulin, ↓ glucagon release

    Clinical use: Type 2 DM

    Toxicities:

    • -Naus/Vom
    • -pancreatitis
  133. DPP-4 inhibitors
    Mechanism, clinical use, toxicities
    Linagliptin, saxagliptin, sitagliptin

    • Mechanism:
    • -↑ insulin, ↓ glucagon release

    Clinical use: Type 2 DM

    Toxicities: mild urinary or respiratory infections
  134. Propylthiouracil, methimazole
    Mechanism, clinical use, toxicities
    • Mechanism:
    • -Block peroxidase, inhibiting organification of iodide and coupling of thyroid hormone synthesis
    • -Propylthiouracil also blocks 5'-deiodinase, decreasing peripheral conversion of T4 to T3

    Clinical use: Hyperthyroidism

    • Toxicity:
    • -Skin rash
    • -agranulocytosis (rare)
    • -aplastic anemia
    • -hepatotoxicity (propylthiouracil)
    • -Methimazole is a possible teratogen
  135. Levothyroxine, triiodothyronine
    Mechanism, clinical use, toxicities
    • Mechanism: Thyroxine replacement
    • Clinical use: hypothyroidism, myxedema
    • Toxicity: Tachycardia, heat intolerance, tremors, arrhythmias
  136. Hypothalamic/pituitary drugs
    Drug and clinical use
    • GH → GH deficiency, Turner syndrome
    • Somatostatin (octreotide) → Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices
    • Oxytocin → Stimulates labor, uterine contraction, milk let-down; controls uterine hemorrhage
    • ADH (desmporessin) → Pituitary (central) DI
  137. Demeclocycline
    Mechanism, clinical use, toxicity
    • Mechanism: ADH antagonist (member of the tetracycline family)
    • Clinical use: SIADH
    • Toxicity: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth
  138. Glucocorticoids
    Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone
    Mechanism, clinical use, toxicity
    • Mechanism: ↓ production of leukotrienes and PGs by inhibiting phospholipase A2 and expression of COX-2
    • Clinical use: Addison's disease, inflammation, immune suppression, asthma
    • Toxicity: Iatrogenic Cushing's syndrome → buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruising, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic). Adrenal insufficiency when stopping drug abruptly after chronic use
  139. H2 Blockers
    • Cimetidine
    • Ranitidine
    • Famotidine
    • Nizatidine

    "Take H2 blockers before you dine. Think Table 2"

    • Mechanism:
    • -Reversible block of histamine H2 receptors
    • -decreases H+ secretion by parietal cells

    • Clinical Use:
    • -Peptic ulcer
    • -gastritis
    • -mild esophageal reflux

    • Toxicity (Cimetidine):
    • -potent inhibitor of cytochrome P450 (multiple drug interactions
    • -antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males)
    • -can cross BBB (confusion, dizziness, HA) and placenta
    • -decreased renal excretion of Cr (Ranitidine as well)

    **other H2 blockers are relatively free of these effects
  140. Proton Pump Inhibitors
    • Omeprazole
    • Lansoprazole
    • Esomeprazole
    • Pantoprazole
    • Dexlansoprazole

    • Mechanism:
    • -irreversibly inhibit H+/K+ ATPase in stomach parietal cells

    • Clinical Use:
    • -peptic ulcer
    • -gastritis
    • -esophageal reflux
    • -Zollinger-Ellison syndrome

    • Toxicity:
    • -increased risk of C. difficile infection and pneumonia
    • -Hip fractures
    • -Decrease serum Mg2+ with long term use
  141. Bismuth, sucralfate
    • Mechanism:
    • -bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer

    • Clinical Use:
    • -increase ulcer healing
    • -traveler's diarrhea
  142. Misoprostol
    • Mechanism:
    • -PGE1 analog
    • -increases production and secretion of gastric mucous barrier
    • -decrease acid production

    • Clinical Use:
    • -prevention of NSAID-induced peptic ulcers
    • -maintenance of patent ductus arteriosus
    • -also used to induce labor (ripens cervix)

    • Toxicity:
    • -diarrhea
    • -CI in women of child bearing potential (abortifactant)
  143. Octreatide
    • Mechanism:
    • -long-acting somatostatin analog

    • Clinical use:
    • -acute variceal bleeds
    • -acromegaly
    • -VIPoma
    • -carcinoid tumors

    • Toxicity:
    • -Nausea
    • -Cramps
    • -Steatorrhea
  144. Antacid use
    -can affect absorption, bioavailability or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying

    -all can cause hypokalemia

    -overuse can cause specific problems
  145. Aluminum hydroxide
    Hypokalemia

    • Toxicity:
    • -constipation
    • -hypophosphatemia
    • -proximal muscle weakness
    • -osteodystrophy
    • -seizures

    "Aluminimum amount of feces"
  146. Magnesium hydroxide
    Hypokalemia

    • Toxicity:
    • -diarrhea
    • -hyporeflexia
    • -hypotension
    • -cardiac arrest

    "Mg = Must go to the bathroom"
  147. Calcium Carbonate
    Hypokalemia

    • Toxicity:
    • -hypercalcemia
    • -rebound increase in acid
    • -can chelate and decrease the effectiveness of other drugs (tetracycline)
  148. Osmotic Laxatives
    • Magnesium hydroxide
    • Magnesium citrate
    • Polyethylene glycol
    • Lactulose

    • Mechanism:
    • -provide osmotic load to draw water out
    • -lactulose: also treats hepatic encephalopathy (gut flora degrade it into metabolites that promote nitrogen excretion as NH4+)

    • Clinical use:
    • -constipation

    • Toxicity:
    • -diarrhea
    • -dehydration
    • -may be abused by bulimics
  149. Infliximab
    • Mechanism:
    • -monoclonal antibody to TNFa

    • Clinical Use:
    • -Crohn's disease
    • -ulcerative colitis
    • -rheumatoid arthritis

    • Toxicity:
    • -infection (including reactivation of latent TB)
    • -fever
    • -hypotension
  150. Sulfasalazine
    • Mechanism:
    • -combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
    • -activated by colonic bacteria

    • Clinical use:
    • -ulcerative colitis
    • -Crohn's disease

    • Toxicity:
    • -malaise
    • -nausea
    • -sulfa toxicity
    • -reversible oligospermia
  151. Ondansetron
    • Mechanism:
    • -5HT3 antagonist
    • -powerful central acting anti-emetic

    • Clinical use:
    • -control vomiting post-op and in patients with cancer chemotherapy

    • Toxicity:
    • -HA
    • -constipation

    "At a party but feeling queasy? Keep on dancing with ondansetron!"
  152. Metoclopramide
    • Mechanism:
    • -D2 receptor antagonist
    • -increases resting tone, contractility, LES tone, motility
    • -does not influence colon transport time

    • Clinical use:
    • -diabetic and post-surgery gastroparesis
    • -antiemetic

    • Toxicity:
    • -increased parkinsonian effects
    • -restlessness
    • -drowsiness
    • -fatigue
    • -depression
    • -nausea
    • -diarrhea
    • -drug interaction with digoxin and diabetic agents
    • -CI: patients with small bowel obstruction or Parkinson's Disease
  153. Heparin
    • Mechanism:
    • -cofactor for activation of antithrombin
    • -decreases thrombin and factor Xa
    • -short half life

    • Clinical Use:
    • -PE
    • -acute coronary syndrome
    • -MI
    • -DVT

    • Toxicity:
    • -bleeding
    • -Heparin induced thrombocytopenia
    • -osteoporosis
    • -drug-drug interactions
    • *antidote = protamine sulfate

    • Notes:
    • -LMWH: act more on factor Xa and have longer half life, not easily reversible
    • -follow PTT
  154. Lepirudin
    Bivalirudin
    • Mechanism:
    • -derivatives of leech anticoagulant
    • -inhibit thrombin

    • Clinical Uses:
    • -alternative to heparin for patients with HIT
  155. Warfarin (Coumadin)
    • Mechanism:
    • -interferes with synthesis and carboxylation of vitamin K dependent clotting factors (II, VII, IX, X, protein C and S)

    • Clinical Use:
    • -chronic anticoagulation
    • -STEMI
    • -venous thromboembolism prophylaxis
    • -prevent of stroke in AFib

    • Toxicity:
    • -bleeding
    • -teratogenic (CI in pregnancy)
    • -skin/tissue necrosis
    • -drug-drug interactions

    • Notes:
    • -reverse with vitamin K or fresh frozen plasma
    • -follow PT

    "The EX-PresidenT went to war(farin)"
  156. Thrombolytics
    • Ateplase (tPA)
    • Reteplase (rPA)
    • Tenecteplase (TNK-tPA)

    • Mechanism:
    • -aid conversion of plasminogen to plasmin (cleaves thrombin and fibrin clots)
    • -increase PT and PTT, no change in platelet count

    • Clinical Use:
    • -early MI
    • -early ischemic stroke
    • -direct thrombolysis of severe PE

    • Toxicity:
    • -bleeding
    • -CI: active bleeding, hx of intracranial bleeding, recent surgery, severe HTN
    • -tx toxicity with aminocaproic acid
  157. Aspirin
    • Mechanism:
    • -irreversibly binds COX (1 and 2)
    • -platelets cannot synthesize new enzymes (effects last until new platelets are produced)
    • -decrease TXA2 and PG formation
    • -increase bleeding time, no effect on PT/PTT

    • Clinical Uses:
    • -antipyretic (intermediate dose)
    • -analgesic (intermediate dose)
    • -anti-inflammatory (high dose)
    • -antiplatelet (low dose)

    • Toxicity:
    • -gastric ulceration
    • -tinnitus
    • -chronic use: renal failure, interstitial nephritis, GI bleeding
    • -Reye's syndrome in children with viral infection
    • -OD: metabolic acidosis and respiratory alkalosis
  158. ADP Receptor Inhibitors
    • Clopidogrel
    • Ticlopidine
    • Prasugrel
    • Ticagrelor

    • Mechanism:
    • -inhibit platelet aggregation by irreversibly blocking ADP receptors
    • -inhibit fibrinogen binding (block GpIIb/IIIa)

    • Clinical Use:
    • -acute coronary syndrome
    • -coronary stenting
    • -decrease incidence or recurrence of thrombotic stroke

    • Toxicity:
    • -neutropenia
  159. Cilostazol
    Dipyridamole
    • Mechanism:
    • -Phosphodiesterase III inhibitor
    • -increase cAMP in platelets (inhibiting aggregation)
    • -vasodilators

    • Clinical Uses:
    • -intermittent claudication
    • -coronary vasodilation
    • -prevention of stroke or TIA (combined with ASA)
    • -angina prophylaxis

    • Toxicity:
    • -Nausea
    • -HA
    • -facial flushing
    • -hypotension
    • -abdominal pain
  160. Gp IIb/IIIa Inhibitors
    • Abciximab
    • Eptifibatide
    • Tirofiban

    • Mechanism:
    • -bind GpIIb/IIIa and prevent platelet aggregation

    • Clinical Use:
    • -acute coronary syndrome
    • -percutaneous transluminal coronary angioplasty

    • Toxicity:
    • -bleeding
    • -thrombocytopenia
  161. Methotrexate
    • Mechanism:
    • -folic acid analog that inhibits DHFR
    • -decrease DNA and protein synthesis

    • Clinical Use:
    • -leukemias
    • -lymphomas
    • -choriocarcinoma
    • -sarcomas
    • -abortion
    • -ectopic pregnancy
    • -RA-psoriasis

    • Toxicity:
    • -myelosuppression (leucovorin rescue)
    • -macrovesicular fatty change in liver
    • -mucositis
    • -teratogenic
  162. 5-FU
    • Mechanism:
    • -pyrimidine analog
    • -inhibits DNA and protein synthesis

    • Clinical Use:
    • -colon cancer
    • -basal cell carcinoma

    • Toxicity:
    • -myelosuppression (not reversible)
    • -OD: rescue with thymidine
    • -photosensitivity
  163. Cytarabine
    • Mechanism:
    • -pyrimidine analog
    • -inhibition of DNA polymerase

    • Clinical Use:
    • -leukemias
    • -lymphomas

    • Toxicity:
    • -Leukopenia
    • -thrombocytopenia
    • -megaloblastic anemia
  164. Azathioprine
    6-MP
    6-TG
    • Mechanism:
    • -purine analogs
    • -decrease de novo purine synthesis
    • -activated by HGPRT

    • Clinical Use:
    • -leukemias

    • Toxicity:
    • -BM
    • -GI
    • -Liver
    • -increase toxicity with allopurinol
  165. Dactinomycin
    • Mechanism:
    • -antitumor antibiotics
    • -intercalates in DNA

    • Clinical Use:
    • -Wilm's tumor
    • -Ewing's sarcoma
    • -Rhabdomyosarcoma
    • -childhood tumors
    • "Children act out"

    • Toxicity:
    • -myelosuppression
  166. Doxorubicin (Adriamycin)
    Daunorubicin
    • Mechanism:
    • -antitumor antibiotics
    • -generate free radicals
    • -intercalate in DNA and generate breaks
    • -reduces replication

    • Clinical Use:
    • -solid tumors
    • -leukemias
    • -lymphomas

    • Toxicity:
    • -cardiotoxicity (dilated cardiomyopathy)
    • -myelosuppressive
    • -alopecia
    • -toxic to tissues following extravasation
    • -dexrazoxane used to prevent cardiotoxicity
  167. Bleomycin
    • Mechanism:
    • -antitumor antibiotic
    • -induces free radical formation causing breaks in DNA strands

    • Clinical Use:
    • -testicular cancer
    • -Hodgkin's lymphoma

    • Toxicity:
    • -pulmonary fibrosis
    • -skin changes
    • -minimal myelosuppression
  168. Cyclophosphamide
    • Mechanism:
    • -alkylating agent
    • -cross linked into DNA
    • -requires bioactivation by liver

    • Clinical Use:
    • -solid tumors
    • -leukemias
    • -lympomas
    • -some brain cancers

    • Toxicity:
    • -myelosuppression
    • -hemorrhagic cystitis
    • -partially prevented with mensa
  169. Nitrosoureas
    • Carmustine
    • Lomustine
    • Semustine
    • Streptozocin

    • Mechanism:
    • -alkylating agents
    • -require bioactivation
    • -cross BBB

    • Clinical Use:
    • -brain tumors (glioblastoma multiforme)

    • Toxicity:
    • -CNS toxicity (dizziness, ataxia)
  170. Busulfan
    • Mechanism:
    • -alkylates DNA

    • Clinical Use:
    • -CML
    • -ablate marrow before HSCT

    • Toxicity:
    • -pulmonary fibrosis
    • -hyperpigmentation
  171. Vincristine
    Vinblastine
    • Mechanism:
    • -microtubule inhibitors
    • -prevent mitotic spindle formation in M phase

    • Clinical Use:
    • -solid tumors
    • -leukemias
    • -lymphomas

    • Toxicity:
    • -Vincristine: neurotoxic, paralytic ileus
    • -Vinblastine: blasts BM
  172. Paclitaxel
    • Mechanism:
    • -microtubule inhibitor
    • -prevent mitotic spindle breakdown in M phase
    • "it's taxing to stay polymerized"

    • Clinical Use:
    • -ovarian carcinoma
    • -breast carcinoma

    • Toxicity:
    • -myelosuppression
    • -hypersensitivity
  173. Cisplatin
    Carboplatin
    • Mechanism:
    • -crosslink DNA

    • Clinical Use:
    • -testicular carcinoma
    • -bladder carcinoma
    • -ovary carcinoma
    • -lung carcinoma

    • Toxicity:
    • -nephrotoxicity (prevent with amifostine and chloride diuresis)
    • -acoustic nerve damage
  174. Etoposide
    Teniposide
    • Mechanism:
    • -inhibit topoisomerase II
    • -increased DNA degradation

    • Clinical Use:
    • -solid tumors
    • -leukemias
    • -lymphomas

    • Toxicity:
    • -myelosuppression
    • -GI irritation
    • -alopecia
  175. Hydroxyurea
    • Mechanism:
    • -inhibits ribonucleotide reductase
    • -decreases DNA Synthesis (S phase specific)

    • Clinical Use:
    • -Melanoma
    • -CML
    • -Sickle cell disease (increase HbF)

    • Toxicity:
    • -BM suppression
    • -GI upset
  176. Prednisone
    Prednisolone
    • Mechanism:
    • -may trigger apoptosis
    • -may even work on non-dividing cells

    • Clinical Use:
    • -most commonly used GC in cancer chemotherapy
    • -CLL
    • -non-Hodgkin's lymphoma
    • -immunosuppressant (autoimmune diseases)

    • Toxicity:
    • -Cushing like sx
    • -immunosuppression
    • -cataracts
    • -acne
    • -osteoporosis
    • -HTN
    • -Peptic ulcers
    • -hyperglycemia
    • -psychosis
  177. Tamoxifen
    Raloxifene
    • Mechanism:
    • -SERMs
    • -Estrogen R antagonists in breast
    • -Estrogen R agonists in bone

    • Clinical Use:
    • -breast cancer treatment and prevention
    • -prevent osteoporosis

    • Toxicity:
    • -T: partial agonist in endometrium (increased risk of endometrial cancer), hot flashes
    • -R: no increased risk of endometrial cancer
  178. Trastuzumab (Herceptin)
    • Mechanism:
    • -anti-HER2
    • -may cause antibody-dependent cytotoxicity of Her2+ cells

    • Clinical Use:
    • -HER2+ breast cancer

    • Toxicity:
    • -cardiotoxicity
  179. Imatinib (Gleevac)
    • Mechanism:
    • -philadelphia chromosome bcr-abl inhibitor

    • Clinical Use:
    • -CML
    • -GI stromal tumors

    • Toxicity:
    • -fluid retention
  180. Rituximab
    • Mechanism:
    • -anti-CD20

    • Clinical Use:
    • -Non-Hodgkin's lymphoma
    • -RA (with methotrexate)
  181. Vemurafenib
    • Mechanism:
    • -small molecule inhibitor of B-Raf with V600E mutation

    • Clinical Use:
    • -metastatic melanoma
  182. Bevacizumab
    • Mechanism:
    • -anti-VEGF
    • -inhibits angiogenesis

    • Clinical Use:
    • -solid tumors
  183. NSAIDs
    • Ibuprofen
    • Naproxen
    • Indomethacin
    • Ketorolac
    • Diclofenac

    • Mechanism:
    • -reversibly inhibit COX (1 and 2)
    • -block PG synthesis

    • Clinical Use:
    • -antipyretic
    • -analgesic
    • -anti-inflammatory
    • -Indomethacin: close PDA

    • Toxicity:
    • -interstitial nephritis
    • -gastric ulcer
    • -renal ischemia (PGs vasodilate afferent arteriole)
  184. Celecoxib
    • Mechanism:
    • -selective Cox-2 inhibitor
    • -COX2 found in inflammatory cells and vascular endothelium
    • -spares GI and platelet function

    • Clinical Use:
    • -RA
    • -osteoarthritis
    • -patients with gastritis or ulcers

    • Toxicity:
    • -increased risk of thrombosis
    • -sulfa allergy
  185. Acetaminophen
    • Mechanism:
    • -reversibly inhibits COX
    • -mostly in CNS, inactivated peripherally

    • Clinical Use:
    • -antipyretic
    • -analgesic
    • -NOT ANTI-INFLAMMATORY
    • *used in children instead of ASA to avoid Reye's syndrome

    • Toxicity:
    • -OD produces hepatic necrosis (depletes glutathione and forms toxic tissue adducts)
    • -antidote = N- acetylcysteine
  186. Bisphosphonates
    • Alendronate
    • -dronates

    • Mechanism:
    • -pyrophosphate analogs
    • -bind hydroxyapatite in bone
    • -inhibit osteoclast activity

    • Clinical Use:
    • -Osteoporosis
    • -Hypercalcemia
    • -Paget's disease of bone

    • Toxicity:
    • -corrosive esophagitis
    • -osteonecrosis of jaw
  187. Allopurinol
    • Mechanism:
    • -inhibits xanthine oxidase
    • -decreases generation of uric acid

    • Clinical Use:
    • -chronic gout
    • -prevents tumor lysis-associated urate nephropathy (leukemia and lymphoma)

    • Toxicity:
    • -increases azathioprine and 6-MP
    • -do not give salicylates
  188. Febuxostat
    • Mechanism:
    • -inhibits Xanthine oxidase

    • Clinical Use:
    • -chronic gout
  189. Probenecid
    • Mechanism:
    • -inhibits reabsorption of uric acid in CPT

    • Clinical Use:
    • -chronic gout

    • Toxicity:
    • -inhibits secretion of PCN
  190. Colchicine
    • Mechanism:
    • -binds and stabilizes tubulin → inhibits polymerization
    • -impairs leukocyte chemotaxis and degranulation

    • Clinical Use:
    • -chronic gout

    • Toxicity:
    • -GI side effects (esp if give orally)
  191. Epinephrine
    • Mechanism:
    • -α-agonist
    • -decreased aqueous humor synthesis via vasoconstriction

    • Clinical Uses:
    • -glaucoma

    • Adverse Effects:
    • -mydriasis
    • -do not use in closed-angle glaucoma
  192. Brimonidine
    • Mechanism:
    • -α2 agonist
    • -decrease aqueous humor synthesis

    • Clinical Uses:
    • -glaucoma

    • Adverse Effects:
    • -blurry vision
    • -ocular hyperemia
    • -foreign body sensation
    • -ocular allergic reactions
    • -ocular pruritus
  193. β-Blockers
    • Timolol
    • Betaxolol
    • Carteolol

    • Mechanism:
    • -β antagonist
    • -decrease aqueous humor synthesis

    • Clinical Uses:
    • -glaucoma

    • Adverse Effects:
    • -no pupillary or vision changes
  194. Acetazolamide
    • Mechanism:
    • -diuretic
    • -decrease aqueous humor synthesis via inhibition of carbonic anhydrase

    • Clinical Uses:
    • -glaucoma

    • Adverse Effects:
    • -no pupillary or vision changes
  195. Cholinomimetics
    • Direct:
    • -Pilocarpine
    • -Carbachol

    • Indirect:
    • -Physostigmine
    • -Echothiophate
    • Mechanism:
    • - increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

    • Clinical Uses:
    • -glaucoma
    • *use pilocarpine in emergencies: very effective at opening meshwork into canal of Schlemm

    • Adverse Effects:
    • -miosis
    • -cyclospasm (contraction of ciliary muscle)
  196. Latanoprost
    • Mechanism:
    • -prostaglandin analog (PGF2a)
    • -increase outflow of aqueous humor

    • Clinical Uses:
    • -glaucoma

    • Adverse Effects:
    • -darkens color of iris (browning)
  197. Opioid Analgesics
    • Morphine
    • Fentanyl
    • Codeine
    • Heroin
    • Methadone
    • Merperidine
    • Dextromethorphan
    • Diphenoxylate

    • Mechanism:
    • -agonists at opioid receptors
    • -mu → morphine
    • -delta → enkephalin
    • -kappa → dynorphin
    • -modulate synaptic transmission: opens K+ channels, closes Ca2+ channels
    • -decreases synaptic transmission
    • -inhibits release of ACh, NE, 5-HT, glutamate, substanceP

    • Clinical Use:
    • -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 with other drugs
    • -tolerance does not develop to miosis and constipation
    • -toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
  198. Butorphanol
    • Mechanism:
    • -mu opioid receptor partial agonist and kappa opioid receptor agonist
    • -produces analgesia

    • Clinical Use:
    • -severe pain (migraine, labor etc)
    • -causes less respiratory depression than full opioid agonist

    • Toxicity:
    • -can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors)
    • -OD not easily reversed with naloxone
  199. Tramadol
    • Mechanism:
    • -very weak opioid agonist
    • -also inhibits serotonin and NE reuptake
    • "Works with multiple NTs: "tram it all" in with tramadol"

    • Clinical Use:
    • -chronic pain

    • Toxicity:
    • -similar to opioids
    • -decreases seizure threshold
  200. Phenytoin (Seizures)
    • Mechanism:
    • -increase Na+ channel inactivation

    • Clinical Use:
    • -simple partial seizures
    • -complex partial seizures
    • -First line for tonic-clonic seizures
    • -First line for prophylaxis of status epilepticus

    • Toxicity:
    • -nystagmus
    • -diplopia
    • -ataxia
    • -sedation
    • -gingival hyperplasia
    • -hirsutism
    • -megaloblastic anemia
    • -teratogenesis (fetal hydantoin syndrome)
    • -SLE-like syndrome
    • -induction of cytochrome P-450
    • -lymphadenopathy
    • -Stevens-Johnson Syndrome
    • -osteopenia

    • Notes:
    • -Fosphenytoin for parenteral use
  201. Carbamazepine
    • Mechanism:
    • -increase Na+ channel inactivation

    • Clinical Use:
    • -first line for simple partial seizures
    • -first line for complex partial seizures
    • -first line for tonic-clonic seizures
    • -first line for Trigeminal Neuralgia

    • Toxicity:
    • -diplopia
    • -ataxia
    • -blood dyscrasias (agranulocytosis, aplastic anemia)
    • -liver toxicity
    • -teratogenesis
    • -induction of cytochrome P-450
    • -SIADH
    • -Stevens-Johnson syndrome
  202. Lamotrigine
    • Mechanism:
    • -blocks voltage gated Na+ channels

    • Clinical Use:
    • -simple partial seizures
    • -simple complex seizures
    • -tonic-clonic seizures

    • Toxicity:
    • -Stevens-Johnson Syndrome
  203. Gabapentin
    • Mechanism:
    • -designed as a GABA analog
    • -primarily inhibits high voltage activated Ca2+ channels

    • Clinical Use:
    • -simple partial seizures
    • -simple complex seizures
    • -tonic-clonic seizures
    • -peripheral neuropathy
    • -postherpetic neuralgia
    • -migraine prophylaxis
    • -bipolar disorder

    • Toxicity:
    • -sedation
    • -ataxia
  204. Topiramate
    • Mechanism:
    • -blocks Na+ channels
    • -increases GABA action

    • Clinical Use:
    • -simple partial seizures
    • -complex partial seizures
    • -tonic-clonic seizures
    • -migraine prevention

    • Toxicity:
    • -sedation
    • -mental dulling
    • -kidney stones
    • -weight loss
  205. Phenobarbital
    • Mechanism:
    • -increase GABAA action

    • Clinical Use:
    • -simple partial seizures
    • -simple complex seizures
    • -tonic-clonic seizures
    • **first line in children

    • Toxicity:
    • -sedation
    • -tolerance
    • -dependence
    • -induction of cytochrome P-450
  206. Valproic Acid
    • Mechanism:
    • -increase Na+ channel inactivation
    • -increase GABA concentration

    • Clinical Use:
    • -simple partial seizures
    • -simple complex seizures
    • -first line for tonic-clonic seizures
    • -absence seizures
    • -myoclonic seizures

    • Toxicity:
    • -GI distress
    • -rare but fatal hepatotoxicity (measure LFTs)
    • -neural tube defects in fetus (spina bifida)
    • -tremor
    • -weight gain
    • -CI in pregnancy
  207. Ethosuximide
    • Mechanism:
    • -blocks thalamic T-type Ca2+ channels

    • Clinical Use:
    • -first line for absence seizures

    • Toxicity:
    • -GI distress
    • -fatigue
    • -headache
    • -urticaria
    • -Stevens-Johnson syndrome

    • EFGH
    • -Ethosuximide
    • -Fatigue
    • -GI
    • -Headache
  208. Benzodiazepines
    • Diazepam
    • Lorazepam

    • Mechanism:
    • -increase GABAA action

    • Clinical Use:
    • -first line for acute status epilepticus
    • -seizures of eclampsia (first line is MgSO4)

    • Toxicity:
    • -sedation
    • -tolerance
    • -dependence
  209. Tiagabine
    • Mechanism:
    • -inhibits GABA reuptake

    • Clinical Use:
    • -simple partial seizures
    • -simple complex seizures
  210. Vigabatrin
    • Mechanism:
    • -irreversibly binds GABA transaminase
    • -increases GABA

    • Clinical Use:
    • -simple partial seizures
    • -simple complex seizures
  211. Levetiracetam
    • Mechanism:
    • -unknown
    • -may modulate GABA and glutamate release

    • Clinical Use:
    • -simple partial seizures
    • -simple complex seizures
    • -tonic-clonic seizures
  212. CNS Stimulants
    • Methylphenidate
    • Dextroamphetamine
    • Methamphetamine

    • Mechanism:
    • -increase catecholamines at the synaptic cleft, especially NE and DA

    • Clinical Use:
    • -ADHD
    • -Narcolepsy
    • -Appetite control
  213. First Generation Antipsychotics
    • Haloperidol
    • Trifluperazine
    • Fluphenazine
    • Thioridazine
    • Chlorpromazine

    • Mechanism:
    • -block D2 receptors (increase cAMP)

    • Clinical Uses:
    • -Schizophrenia (positive sx)
    • -psychosis
    • -acute mania
    • -Tourette's

    • Toxicity:
    • -stored in fat (slow removal)
    • -EPS (dyskinesias)
    • -Endocrine AE (hyperPRL, galactorrhea)
    • -muscarnic blockade (dry mouth, constipation)
    • -alpha blockade (hypotension)
    • -histamine blockade (sedation)
    • -Neuroleptic Malignant Syndrome (Fever, Encephalopathy, Vitals unstable, Elevated enzymes, Rigid muscles)
    • -Tardive dyskinesia
  214. Second Generation Antipsychotics
    • Olanzapine
    • Clozapine
    • Quetiapine
    • Risperidone
    • Aripiprazole
    • Ziprasidone

    "It's atypical for old closets to quietly risper from A to Z"

    • Mechanism:
    • -not completely understood
    • -varied effects on 5HT2, DA, α and H1 receptors

    • Clinical Use:
    • -schizophrenia (positive and negative sx)
    • -bipolar disorder
    • -OCD
    • -Anxiety disorder
    • -depression
    • -mania
    • -Tourette's

    • Toxicity:
    • -fewer EPS and anticholinergic side effects
    • -Metabolic syndrome
    • -C: agranulocytosis and seizure
  215. Lithium
    • Mechanism:
    • -unknown

    • Clinical Use:
    • -mood stabilizer for bipolar disorder
    • -blocks relapse and acute manic events
    • -SIADH

    • Toxicity:
    • -tremor
    • -sedation
    • -edema
    • -heart block
    • -hypothyroidism
    • -polyuria (NDI)
    • -teratogen
    • *narrow therapeutic window (close monitoring)

    • LMNOP
    • Lithium Side Effects
    • Movement (tremor)
    • Nephrogenic diabetes insipidus
    • hypOthyroidism
    • Pregnancy problems
  216. Buspirone
    • Mechanism:
    • -stimulates 5HT receptors

    • Clinical Uses:
    • -generalized anxiety disorder

    • Toxicity:
    • -1-2 weeks to take effect

    • Notes:
    • -no sedation, addiction, or tolerance
    • -doesn't interact with alcohol (vs benzos and barbs)
  217. SSRIs
    • Fluoxetine
    • Paroxetine
    • Sertraline
    • Citalopram

    • Mechanism:
    • -serotonin-specific reuptake inhibitors

    • Clinical Use:
    • -depression
    • -GAD
    • -panic disorder
    • -OCD
    • -bulemia
    • -social phobias
    • -PTSD

    • Toxicity:
    • -fewer than TCAs
    • -GI distress
    • -sexual dysfunction
    • -Serotonin Syndrome (when combined with any drug that increase serotonin: MAOIs, SNRIs, TCAs)
    • -takes 4-8 weeks to have an effect
  218. SNRIs
    • Venlafaxine
    • Duloxetine

    • Mechanism:
    • -inhibit serotonin and NE reuptake

    • Clinical Use:
    • -depression
    • -V: GAD, panic disorder
    • -D: peripheral diabetic neuropathy

    • Toxicity:
    • -hypertension most common
    • -stimulant effects
    • -sedation
    • -nausea
  219. TCAs
    • Amitriptyline
    • Nortriptyline
    • Imipramine
    • Desipramine
    • Clomipramine
    • Doxepin
    • Amozapine

    • Mechanism:
    • -block reuptake of NE and serotonin

    • Clinical Use:
    • -major depression
    • -bedwetting
    • -OCD
    • -fibromyalgia

    • Toxicity:
    • -sedation
    • -α1 blocker effects (postural hypotension)
    • -anticholinergic side effects (tachycardia, urinary retention, dry mouth)
    • -respiratory depression
    • -hyperpyrexia
    • -confusions and hallucinations in elderly

    • Tri-Cs
    • -Convulsions
    • -Coma
    • -Cardiotoxicity (arrhythmias
  220. MAOIs
    • Tranylcypromine
    • Phenelzine
    • Isocarboxazid
    • Selegiline

    • Mechanism:
    • -non-selective MAO inhibition
    • -increase levels of amine NTs (NE, 5HT, DA)

    • Clinical Use:
    • -atypical depression
    • -anxiety
    • -hypochondriasis

    • Toxicity:
    • -hypertensive crisis (with ingestion of tyramine: wine and cheese)
    • -CNS stimulation
    • -CI: SSRIs, TCAs, St John's Wart, dextromethorphan (prevent serotonin syndrome)
  221. Bupropion
    • Mechanism:
    • -increases NE and DA via unknown mechanism

    • Clinical Use:
    • -atypical antidepressant
    • -smoking cessation

    • Toxicity:
    • -stimulant effects (tachycardia, insomnia)
    • -HA
    • -seizure in bulimic patients
    • -No sexual side effects
  222. Mirtazapine
    • Mechanism:
    • -α2-antagonist
    • -increased release of NE and 5HT
    • -potent 5HT receptor antagonist

    • Clinical Use:
    • -atypical antidepressant

    • Toxicity:
    • -sedation (may be desirable)
    • -increased appetite
    • -weight gain (may be desirable)
    • -dry mouth
  223. Maprotiline
    • Mechanism:
    • -blocks NE reuptake

    • Clinical Use:
    • -atypical depression

    • Toxicity:
    • -sedation
    • -orthostatic hypotension
  224. Trazodone
    • Mechanism:
    • -primarily inhibits 5HT reuptake

    • Clinical Use:
    • -insomnia primarily (high doses needed for antidepressant effect)
    • -atypical antidepressant

    • Toxicity:
    • -sedation
    • -nausea
    • -priapism ("Trazobone")
    • -postural hypotension
  225. Mannitol
    • MOA:
    • -osmotic diuretic
    • -↑ tubular fluid osmolarity producing ↑ urine flow
    • -↓ Intracranial/intraocular pressure
    • -functions at proximal tubule

    • Clinical Use:
    • -drug OD
    • -elevated intracranial/intraocular pressure

    • Toxicity:
    • -pulmonary edema
    • -dehydration

    • Contraindications:
    • -anuria
    • -CHF
  226. Ethacrynic Acid
    • Mechanism:
    • -phenoxyacetic acid derivative (NOT a sulfonamide)
    • -essentially same action as furosemide

    • Clinical Use:
    • -diuresis in patients allergic to sulfa drugs

    • Toxicity:
    • -similar to furosemide
    • -can cause hyperuricemia (NEVER USE TO TX GOUT!)
  227. Hydrochlorothiazide
    Thiazide diuretic

    • Mechanism:
    • -inhibits NaCl reabsorption in early distal tubule (inhibits NCC)
    • -reduces diluting capacity of the nephron
    • -decreases Ca2+ excretion

    • Clinical Use:
    • -Hypertension
    • -CHF
    • -Idiopathic hypercalciuria
    • -nephrogenic diabetes insipidus

    • Toxicity:
    • -hypokalemic metabolic alkalosis
    • -hyponatremia
    • -hyperGlycemia
    • -hyperLipidemia
    • -hyperUricemia
    • -hyperCalcemia
    • -Sulfa allergy

    "hyperGLUC"
  228. K+ Sparing Diuretics
    • Spironolactone and eplerenone
    • Triamterene and Amiloride

    "The K+ STAys"

    • Mechanism:
    • -Spironolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule
    • -Triamterene and Amiloride act at CCT to block ENaC

    • Clinical Use:
    • -hyperaldosteronism
    • -K+ depletion
    • -CHF

    • Toxicity:
    • -hyperkalemia (arrhythmias)
    • -endocrine effects with spironolactone (gynecomastia and antiandrogen effects)
  229. ACE Inhibitors/ARBs
    Captopril, Enalapril, Lisinopril

    • Mechanism:
    • -inhibit ACE
    • -decrease generation of ATII → ↓GFR by preventing constriction of efferent arterioles
    • -increased levels of renin due to loss of feedback inhibition
    • -also prevents inactivation of bradykinin (vasodilator)

    • Clinical Uses:
    • -hypertension
    • -CHF
    • -proteinuria
    • -diabetic renal disease
    • *prevent unfavorable heart remodeling as a result of chronic HTN

    • Toxicity:
    • -Cough
    • -Angioedema
    • -Teratogen (fetal renal malformation)
    • -Cr increase (decrease GFR)
    • -Hyperkalemia
    • -Hypotension

    "Captopril's CATCHH"

    • Contraindicated:
    • -bilateral renal artery stenosis b/c ACEI further decrease GFR → renal failure

    ARBs (-sartans) have effects similar to ACE inhibitors but do not increase bradykinin (no cough or angioedema)
  230. Leuprolide
    • Mechanism:
    • -GnRH analog
    • -agonist properties when used in a pulsatile fashion
    • -antagonist properties when used in continuous fashion (↓FSH, LH)

    • Clinical Use:
    • -infertility (pulsatile)
    • -prostate cancer (continuous - use with flutamide)
    • -uterine fibroids (continuous)
    • -precocious puberty (continuous)

    • Toxicity:
    • -antiandrogen
    • -nausea
    • -vomiting

    "Leuprolide can be used in lieu of GnRH"
  231. Testosterone, Methyltestosterone
    • Mechanism:
    • -agonist at androgen receptors

    • Clinical Use:
    • -hypogonadism
    • -promotes development of secondary sex characteristics
    • -stimulate anabolism to promote recovery after burn or injury

    • Toxicity:
    • -causes masculinization in females
    • -reduces intratesticular testosterone in males by inhibiting release of LH → gonadal atrophy
    • -premature closure of epiphyseal plates
    • -↑ LDL
    • -↓ HDL
  232. Finasteride
    • Mechanism:
    • -a 5α-reductase inhibitor (decreased conversion of testosterone to DHT)

    • Clinical Use:
    • -BPH
    • -Male Pattern Baldness

    To prevent male-pattern hair loss, give a drug that will encourage female breast growth
  233. Flutamide
    • Mechanism:
    • -nonsteroidal competitive inhibitor of androgens at the testosterone receptor

    • Clinical Use:
    • -prostate carcinoma
  234. Ketoconazole
    • Mechanism:
    • -inhibits steroids synthesis (inhibits 17,20 desmolase)

    • Clinical Use:
    • -PCOS (prevent hirsutism)

    • Toxicity:
    • -gynecomastia
    • -amenorrhea
  235. Spironolactone
    • Mechanism:
    • -inhibits steroids binding (MC R antagonist that also affects androgen receptor)

    • Clinical Use:
    • -PCOS (prevent hirsutism)

    • Toxicity:
    • -gynecomastia
    • -amenorrhea
  236. Estrogens (ethinyl estradiol, DES, mestranol)
    • Mechanism:
    • -bind estrogen receptors

    • Clinical Use:
    • -hypogonadism
    • -ovarian failure
    • -menstrual abnormalities
    • -HRT in postmenopausal women
    • -in men with androgen-dependent prostate cancer

    • Toxicity:
    • -increased risk of endometrial cancer
    • -bleeding in postmenopausal women
    • -vaginal clear cell adenocarcinoma in women exposed to DES in utero
    • -increased risk of thrombi

    • Contraindications:
    • -ER positive breast cancer
    • -history DVTs
  237. Selective Estrogen Receptor Modulators (SERMs)
    • Clomiphene
    • Tamoxifen
    • Raloxifene
  238. Clomiphene
    • Mechanism:
    • -partial agonist at estrogen receptors in hypothalamus
    • -prevents normal feedback inhibition and increased release of LH and FSH from pituitary, which stimulates ovulation

    • Clinical Use:
    • -infertility
    • -PCOS

    • Toxicity:
    • -hot flashes
    • -ovarian enlargement
    • -multiple simultaneous pregnancies
    • -visual disturbances
  239. Tamoxifen
    • Mechanism:
    • -estrogen receptor antagonist on breast tissue

    • Clinical Uses:
    • -treat and prevent recurrence of ER-positive breast cancer
  240. Raloxifene
    • Mechanism:
    • -estrogen agonist on bone
    • -reduces reabsorption of bone

    • Clinical Uses:
    • -osteoporosis
  241. Hormone Replacement Therapy
    • Clinical Uses:
    • -relief or prevention of menopausal symptoms (hot flashes, vaginal atrophy)
    • -osteoporosis (increased estrogen decreases osteoclast activity)

    • Toxicity:
    • -unopposed ERT increases the risk of endometrial cancer (add progesterone)
    • -possible increased cardiovascular risk
  242. Anastrozole/Exemestane
    • Mechanism:
    • -aromatase inhibitors

    • Clinical Uses:
    • -used in postmenopausal women with breast cancer
  243. Progestins
    • Mechanism:
    • -bind progesterone receptors
    • -reduce growth and increase vascularization of endometrium

    • Clinical Use:
    • -used in OCPs
    • -used in the treatment of endometrial cancer and abnormal uterine bleeding
  244. Mifepristone (RU-486)
    • Mechanism:
    • -competitive inhibitor of progestins and progesterone receptor

    • Clinical Use:
    • -termination of pregnancy
    • -administered with misoprostol (PGE1)

    • Toxicity:
    • -heavy bleeding
    • -GI effects (N/V, anorexia)
    • -abdominal pain
  245. Oral Contraception (synthetic progestins, estrogen)
    • Mechanism:
    • -estrogen and progestins inhibit LH/FSH and thus prevent estrogen surge
    • -no estrogen surge → no LH surge → no ovulation
    • -progestins cause thickening of cervical mucus (limits access of sperm to uterus)
    • -progestins also inhibits endometrial proliferation (makes it less suitable for implantation)

    • Clinical Use:
    • -contraception

    • Contraindications:
    • -smokers > 35 years (increased risk of CV events)
    • -hx of thromboembolism and stroke
    • -hx of estrogen dependent tumor
  246. Terbutaline
    • Mechanism:
    • -β2 agonist
    • -relaxes uterus

    • Clinical Use:
    • -reduce premature uterine contractions
  247. Tamsulosin
    • Mechanism:
    • -α1-antagonist
    • -inhibits smooth muscle contraction
    • -selective for α1AD receptors on prostate (not vascular receptors)

    • Clinical Use:
    • -BPH
  248. Sildenafil, Vardenafil
    • Mechanism:
    • -inhibit PDE5
    • -causes increased cGMP → smooth muscle relaxation in corpus cavernosum
    • -increases blood flow and penil erection

    • Clinical Use:
    • -erectile dysfunction

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

    "Sildenafil and vardenafil fill the penis"

    "Hot and sweaty" but then Headache, Heartburn and Hypotension"
  249. Danazol
    • Mechanism:
    • -synthetic androgen that acts as partial agonist at androgen receptors

    • Clinical Use:
    • -endometriosis
    • -hereditary angioedema

    • Toxicity:
    • -weight gain
    • -edema
    • -acne
    • -hirsutism
    • -masculinization
    • -decreased HDL levels
    • -hepatotoxicity
  250. First Generation H1 Blockers
    • Diphenhydramine
    • Dimenhydrinate
    • Chlorpheniramine

    • Mechanism:
    • -reversible inhibitors of H1 receptors

    • Clinical Use:
    • -allergy
    • -motion sickness
    • -sleep aid

    • Toxicity:
    • -sedation
    • -antimuscarinic
    • -anti-α-adrenergic
  251. Second Generation H1 Blockers
    • Loratadine
    • Fexofenadine
    • Desloratadine
    • Cetirizine

    • Mechanism:
    • -reversible inhibition of H1 receptors
    • -decreased entry into CNS

    • Clinical Use:
    • -allergy

    • Toxicity:
    • -far less sedating than first generation
  252. β2 Agonists
    • Albuterol:
    • -relaxes bronchial smooht muscle
    • -use during acute exacerbation

    • Salmeterol, Formoterol:
    • -long-acting agents for prophylaxis
    • -toxicity: tremor, arrhythmia
  253. Methylxanthines
    Theopylline

    • Mechanism:
    • -inhibits phosphodiesterase → decrease cAMP hydrolysis → bronchodilation

    • Clinical Use:
    • -asthma
    • -limited due to narrow therapeutic index

    • Toxicity:
    • -cardiotoxicity
    • -neurotoxicity
    • -blocks actions of adenosine
  254. Corticosteroids
    • Beclomethasone
    • Fluticasone

    • Mechanism:
    • -inhibit the synthesis of virtually all cytokines
    • -inactivate NFkB (decrease TNFa transcription)

    • Clinical Use:
    • -first line therapy for chronic asthma
  255. Antileukotrienes
    • Montelukast, Zafirlukast:
    • -MOA: block LT receptors
    • -Clinical Use: esp good for ASA-induced asthma

    • Zileuton:
    • -MOA: 5-lipoxygenase pathway inhibitor, blocks conversion of AA to LTs
  256. Omalizumab
    • Mechanism:
    • -monoclonal anti-IgE antibody
    • -binds mostly unbound serum IgE

    • Clinical Use:
    • -allergic asthma resistant to inhaled steroids and long-acting β-agonists
  257. Guaifenesin
    • Mechanism:
    • -expectorant
    • -thins respiratory secretions
    • -does not suppress cough reflex
  258. N-acetylcysteine
    • Mechanism:
    • -mucolytic

    • Clinical Use:
    • -can loosen mucus plugs in CF patients
    • -antidote for acetaminophen OD
  259. Bosentan
    • Mechanism:
    • -competitive antagonist of endothelin-1 receptors
    • -decreases PVR

    • Clinical Use:
    • -Pulmonary arterial HTN
  260. Dextromethorphan
    • Mechanism:
    • -antitussive (antagonizes NMDA glutamate Rs)
    • -synthetic codeine analog
    • -mild opioid effect when used in excess

    • Clinical Use:
    • -cough suppressant?

    • Toxicity:
    • -naloxone can be given for OD
    • -mild abuse potential
  261. Pseudoephedrine
    Phenylephrine
    • Mechanism:
    • -sympathomimetic alpha agonist

    • Clinical Use:
    • -reduce hyperemia, edema and nasal congestion
    • -open obstructed eustachian tubes

    • Toxicity:
    • -hypertension
    • -can also cause CNS stimulation/anxiety

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