Flashcards in Antibiotics (17) Deck (86):
Why is penicillin G not a good drug?
Not stable in stomach pH
Pen V instead
What are the properties of ideal antibacterials?
1. Stable in body
2. Water soluble
3. Diffusible across junctions
4. Slow excretion
5. Large therapuetic index
What could cause sulfonamides to cause crystalluria?
Lack of hydration
_________ has an effect on the choice of drug, how much drug, and drug combinations.
What are the two ways in which microbes will respond to drugs?
2. Secondary products of bacterial destruction (esp gram -)
T/F: Vancomycin is strictly a bactericidal drug.
Bactericidal mechanism, but due to resistance has become functionally static
T/F: Gram positive bacteria have a thick cell wall.
T/F: Gram positive bacteria stain dark purple.
Thick dark cell wall
T/F: Vancomycin is effective on both gram- and gram+ bacteria.
Cannot get through pores of gram-
T/F: Resistance of gram- bacteria to ciprofloxacin is an intrinsic method of resistance.
Pores are changed so it cannot enter - acquired resistance
T/F: Resistance of gram- bacteria to vancomycin is an intrinsic method of resistance.
Pores are naturally too small
T/F: The gold standard of testing antibiotic activity is the broth dilution assay.
T/F: MIC values increase as resistance increases.
How do penicillin and aminoglycosides use synergism to fight bacteria?
Penicillin breaks cell wall, Aminoglycoside gets in cell and does damage
T/F: Sulfonamids and penicillins work well together.
Sulfonamids stop cell from growing -> penicillin cannot work
T/F: Sulfonamides are bacteriocidal.
Bacteriostatic - stop cell growth
Sulfonamides act as competitive inhibitors for which enzyme?
Result is inhibition of folate (and DNA) synthesis
What is the spectrum for sulfonamides?
Gram+ and gram- but relatively narrow
What is the mechanism of resistance to sulfonamides?
targeted enzyme is altered to avoid drug
What are three clinical uses for sulfonamides?
2. P. jiroveccii in HIV/AIDS
3. Prophylaxis (burns, wounds)
T/F: Sulfonamides are safe for new borns (neonates).
Can cause kernicterus
What drug other than sulfonamides alters folic acid production?
Alters dihydrofolate reductase
T/F: Trimethoprim works downstream from sulfonamides in the production of folic acids.
T/F: Trimethoprim has a broader spectrum than sulfonamides.
What is the mechanism of resistance to trimethoprim?
More enzyme is produced
Trimethoprim is commonly combined with what other drug?
T/F: Combo of trimethoprim and sulfamethoxazole is useful in treating MRSA and SSTIs.
T/F: Trimethoprim is extremely effective against P. aeruginosa.
Low MIC for many pathogens
Ineffective for P. aeruginosa
What is the first line for tuberculosis?
T/F: Rifampin is bactericidal.
What enzyme is inhibited by rifampin?
What is the resistance mechanism for rifampin?
altered binding to RNA polymerase
Why would you not give rifampin to a patient with HIV/AIDS?
Will induce p450 de-acetylation of other drugs
Give Rifabutin instead
What is the mechanism of quinolones?
inhibit DNA gyrase and DNA topoisomerase IV
T/F: Quinolones are bacteristatic.
What is the spectrum of quinolones?
Which quinolones are anti-pseudomonal?
Cipro and levofloxacin
T/F: Quinolones are second line of defense for tuberculosis.
Rifampin is first
Which antibiotic is used to treat anthrax?
What are the mechanisms of resistance to quinolones?
1. Mutated enzymes
2. Efflux of enzymes
3. Altered porins in cells
T/F: Quinolones can cause tendon ruptures and peripheral neuropathy
What is special about the third and fourth classes of quinolones?
Levofloxacin and moxifloxacin
Good against gram +/- (class 1 and 2 only gam-)
What drugs should be used to target respiratory bacteria (S. pneumoniae) that are resistant to penicillin?
3rd and 4th generation quinolones (levo and moxifloxacin)
T/F: Levofloxacin is not cleared by the kidney and is low in the urine.
_________ is primarily used for treating anaerobic bacteria.
What is the mechanism of action of metronidazole?
Reduced to metabolites that will alter DNA function
What is the mechanism of resistance to metronidazole?
Drug will not be reduced to metabolites
What are some toxic effects of metronidazole?
1. Metalic taste
2. Nausea and vomiting (disulfiram effect)
3. Central neurotoxicity
What will be the negative effect of drinking alcohol with metronidazole?
Disulfiram effect will result in vomiting/nausea
*Which type of bacteria will not be effected by cell wall inhibitors?
How does cycloserine inhibit cell wall synthesis?
Inhibits L-ala -> D-ala
How does vancomycin inhibit cell wall synthesis?
Inhibits peptidoglycan synthase
What are four cell wall inhibitors?
3. Fosfomycin (UTIs)
How will the cells eventually die from cell wall inhibitors?
Cell wall will not keep growing, pressure in cell will build up -> osmotic lysis
T/F: Penicillins will normally cross the BBB?
Will during meningitis because cells are inflamed
How do penecillins work?
They mimic D-ala-D-ala, so penicillin binding proteins bind penicillin instead of the proper amino acids -> disrupt cell wall crosslinking
What is Beta-lactamase?
A resistance factor to penicillin
Will cleave beta-lactan ring turning penicillin into benzylpenicilloic acid
Which two drugs damage the cell membranes of bacteria?
Polymyxins and Daptomycin
Which cell membrane damaging drug has a rapid action and is concentration dependent?
*T/F: Polymyxins are effective against Gram+ only.
Polymyxens = gram-
Daptomycin = gram+
Which drug can be used against multi-drug resistant pseudomonal infections via IV?
Esp against Acinetobacter
T/F: Resistance to polymyxins is very common.
T/F: Daptomycin is often used to treat lung infections.
It will inactivate surfactant
T/F: Daptomycin will have a post antibiotic effect.
What are the four major mechanisms of resistance to Beta-Lactams (penecillin)?
2. Altered PBPs (MRSA)
3. Altered porins (gram-)
4. Increased efflux (gram-)
T/F: The majority of protein synthesis inhibitors are bacteriostatic.
Aminoglycosides are cidal
T/F: Drugs used to inhibit bacterial protein synthesis will bind to 40s and 60s subunits.
50s (most) and 30s (tetracyclines)
T/F: Aminoglycosides are mainly effective against gram- bacteria.
What is the major resistance mechanism for aminoglycosides?
Transferase enzymes in bacteria change the drugs structure
Which drug is often used against endocarditis?
Mostly gram-, some gram+
T/F: Kanamycin is a commonly used aminoglycoside.
It has developed resistance so others are used
T/F: Aminoglycosides are concentration-dependent drugs with post-antibiotic effects.
What four drugs are concentration-dependent and will therefore have post-Antibiotic effects?
What three drugs are time-dependent?
1. Beta lactams
T/F: Many beta-lactams will begin with Cep- or Ceph-.
Which types of drugs end in -floxacin?
Cell wall inhibitors would not work against mycoplasma. What agent would be effective?
T/F: Tetracyclines have a broad spectrum.
Gray baby syndrome is due to high concentrations of which drug?
What is the prototype macrolide?
T/F: Macrolides are bactericidal.
What types of infection are most often fought with macrolides (erythromycin)?
Respiratory infections (C. pneumoniae)
T/F: Ketolides (telithromycin) is a commonly used drug.
_________ is a protein synthesis inhibitor often used for anaerobic infection of penecillin resistant bacteria.
What is a negative of Clindomycin?
Can become susceptible to C. dif -> Pseudomembranous colitis