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31 Cards in this Set

  • Front
  • Back
Albuterol
- (Proventil®, Ventolin®)

Indication – reversible airway obstruction (asthma)
MOA - 2 agonist at bronchial smooth muscle
Triamcinolone
(Azmacort®)

Indication – reversible airway obstruction (asthma)

– decreased mediator synthesis, release, and infiltration of inflammatory cells
Hydrocortisone
(Cortef®, SoluCortef®)

Indication – adrenocortical insufficiency, other uses

– glucocorticoid > mineralocorticoid
Cyclosporine
(Sandimmune®, GenGraf®, Neoral®)

Indication – immunosuppression s/p transplantation

Mechanism – binds cyclophilin, then inhibits calcineurin required for IL-2 production and T-cell proliferation
Tacrolimus
(ProGraf®)

Indication – immunosuppression s/p transplantation

Mechanism – binds FKBP12, then inhibits calcineurin required for IL-2 production and T-cell proliferation
Aspirin
Indication – pain associated with inflammation

Mechanism – inhibits cyclo-oxygenase (COX)
Ibuprofen
(Motrin®, Advil®, others)

Indication – pain associated with inflammation

Mechanism – inhibits cyclo-oxygenase
Celecoxib
(Celebrex®)

Indication – acute pain, dysmenorrhea, arthritis

Mechanism – inhibits COX-2
Penicillin G + Penicillin V
G - given IV; V - given PO

Indication – infections caused by susceptible strains of bacteria including Streptococci and Neisseria

MOA – PBP binding  cell lysis and death
Cephalexin
(Keflex®, Keftab®)

Indication – infections caused by susceptible strains of bacteria including Staphylococci and Streptococci

MOA – PBP (penicillin binding protein) binding - causes cell wall lysis and dea
Cefotaxime
(Claforan®)

Indication – infections caused by susceptible strains of GN bacteria including Neisseria, Hemophilus, Proteus, Salmonella, Klebsiella, and Serratia

MOA – PBP binding  cell lysis and death
Imipenem
(Primaxin®)

- a prototype for the carbapenems

Indication – infections caused by susceptible strains of GP cocci, GN bacilli and cocci, and mixed aerobic/anaerobic infections - (can treat gram + gram -, mixed, etc, so it was touted as the most amazing drug, when first reteased); great for at first, when you don’t know what is causing the infection, but n

MOA – PBP binding causing cell lysis and death
Vancomycin
(Vancocin®, Vancoled®)

Indication – serious infections caused by MRSA or MRSE, or infections caused by susceptible strains of GP bacteria in patients with beta-lactam allergy

MOA – binding to cell wall precursor molecules  cell lysis and death
Gentamicin
(Garamycin®)

Indication – serious infections caused by susceptible strains of GN (gram negative) bacilli; it’s the high conc. that kills the drug

MOA – binding to 30-S ribosomal subunit to disrupt bacterial protein synthesis
Daptomycin
Indication - infections by suceptible GP bacteria

MOA - inserts into cell membrane to form a channel that allows K efflux which depolarizes cell and reduces protein synthesis
Erythromycin
Indication – infections caused by susceptible strains of GP and some GN bacteria

MOA – binding to 50-S ribosomal subunit to disrupt bacterial protein synthesis
Tetracycline
ndication – infections caused by susceptible strains of GP and GN organisms including Rickettsia, spirochetes, Chlamydia, Mycloplasma, and Vibrio

MOA – binding to 30-S ribosomal subunit to disrupt bacterial protein synthesis
Clindamycin
(Cleocin®)

Indication – infections caused by susceptible anaerobes and some strains of GP aerobes

MOA – binding to 50-S ribosomal subunit to disrupt bacterial protein synthesis (overlaps macrolide site)
Linezolid
(Zyvox®)

Indication – severe infections caused by multi-drug resistant strains of GP organisms (e.g., VRE, MRSA); usually in pts who can’t take vanco or b-lactam drugs

MOA – binding to 50-S ribosomal subunit (23-S portion) to disrupt bacterial protein synthesis
Ciprofloxacin
Cipro®)

Indication – infections caused by susceptible GN and some GP organisms

MOA – inhibits DNA gyrase, preventing DNA supercoiling
Metronidazole
(Flagyl®)

Indication – infections caused by susceptible anaerobes including B. fragilis, C. difficile, and strains of Fusobacterium, Peptococcus, and Peptostreptococcus

MOA – causes strand breaks in DNA structure
Sulfamethoxazole
- a sulfonamide

Indication – infections caused by susceptible GP cocci, GN bacilli

MOA – inhibits folic acid synthesis required for growth; but at a different step in the process than trimethoprim does
Trimethoprim
(Proloprim®)

Indication – infections caused by susceptible GP bacilli and GN bacilli and some protozoa

MOA – inhibits folic acid synthesis required for growth; but at a different step in the process than sulfamethoxazole does
Co-trimoxazole
(Bactrim®, Cotrim®, Septra®)

Indication – infections caused by susceptible organisms

(from E. coli to Yersinia pestis)

MOA – synergistic effect on folic acid metabolism
Isoniazid
(Nydrazid®)

Indication – infections caused by susceptible strains of Mycobacterium including M. tuberculosis

MOA – inhibits mycolic acid needed for cell wall (bactericidal in dividing cells, bacteriostatic in dormant cells)
Rifampin
(Rifadin®)

Indication – infections caused by susceptible strains of Mycobacterium including M. tuberculosis; also some GN

MOA – inhibits bacterial DNA-dependent RNA-polymerase to decrease RNA and protein synthesis (bactericidal)
Ethambutol
(Myambutol®)

Indication – infections caused by susceptible strains of Mycobacterium including M. tuberculosis

MOA – inhibits mycolic acid for cell wall (bacteriostatic)
Pyrazinamide
Indication – infections caused by susceptible strains of Mycobacterium including M. tuberculosis

MOA – (bactericidal)
Amphotericin B deoxycholate
(Fungizone®)

- untill the last 10 years, was the only systemic anti-fungal that we had

Indication – severe systemic infections caused by susceptible strains of pathogenic fungi

MOA – binds to cell membrane ergosterol to increase permeability  fungicidal or fungistatic
Ketoconazole
(Nizoral®)

- fluconozole is the one you see used most often b/c its the most well absorbed in the mouth

Indication – systemic (and superficial) infections caused by susceptible strains of pathogenic fungi

MOA – inhibits fungal CYP-dependent enzymes in ergosterol synthesis, thereby increasing cell permeability (fungistatic -> fungicidal); so any drug which is cleared bia CYP, will be cleared much much much more slowly
Clotrimazole
(Lotrimin®, Gyne-Lotrimin®, Mycelex®)

Indication – superficial infections caused by susceptible strains of pathogenic fungi

MOA – inhibits fungal CYP-dependent enzymes in ergosterol synthesis