Term
| What are some beta-lactams and what is their mode of action? What can they be used with? What is the trend going from first to third gen? |
|
Definition
-Penicillin and cephalosporins
-Inhibits *cell wall at level of **transpeptidase enzymes (penicillin binding proteins); do cross-linking
-Mainly for gram+ bacteria
-Only active on replicating bacteria (synthesizing wall)
-Can be used used with *clavulanic acid and *sulbactam (B-lactamase inhibitors)
-Cephalosporin goes from first to third generation with activity for gram+ decreasing, and for gram- increasing
-Cephalosporins are mainly second line drugs for seriously ill patients |
|
|
Term
| What is cycloserine? What does it inhibit |
|
Definition
-An **alanine analog
-Inhibits *cell wall at level of *alanine racemase and *D-alanyl-D-alanine synthetase
-Alanine racemase makes L-->D-ala while DaDa makes a D-ala dipeptide (for peptidoglycan)
-It is broad spectrum |
|
|
Term
| What is the mode of action of vancomycin? |
|
Definition
-Inhibits *cell well synth
-It binds to that *terminal D-ala on the peptidoglycan dimer pentapeptide and inhibits **translocation to the exterior
-Used often when resistance to other drugs is present |
|
|
Term
|
Definition
-Inhibits *cell wall by inhibiting the dephosphorylation of a **phospholipid carrier outside the membrane so that it can't react with the incoming *UDP-MurNAc
-For gram+ |
|
|
Term
| So again, what are the major cell wall inhibitors? |
|
Definition
-Penicillins & cephalosporins (B-lactams),
-Cycloserine
-Vancomycin
-Bacitracin |
|
|
Term
| What is the action of polymyxins? What type are used? What is it used for? What is a side effect? |
|
Definition
-They act on the *cell membrane
-Basically act as **detergents and may *bind LPS
-Only polymyxin B & E are used
-Used for gram- (esp. P. aeroginosa infections)
-Nephrotoxic |
|
|
Term
| What are the polyene agents? How do they work? |
|
Definition
-*Antifungal agents that binds to the **ergosterols of fungi membranes (preferentially over cholesterol) and disrupts the membrane
-**Amphotericin B is used mostly for systemic infections, while **nystatin is more topical
-Amphotericin can be *nephrotoxic (binds chol. some)
-(also in mycology cards) |
|
|
Term
| What are azoles? Give two examples? |
|
Definition
-Azoles are *antifungals that inhibit **ergosterol synthesis by inhibiting **cytochrome P-450 (membrane inhibition)
-All of the names end in "azole"; such as *imidazoles and *bistriazoles |
|
|
Term
| What is the action of flucytosine? What do we use it for and with? Side effects? |
|
Definition
-5-Fluorocytosine acts as a **nucleoside analogue which will be incorporated into fungal RNA and inhibit protein production
-We often use it in conjunction with *amphotericin B for systemic infections (meningitis, candidiasis, etc.)
-It is toxic and patients may become leukopenic
-Note; it is not the same 5-Flu for cancer treatment which is 5-fluroURACIL |
|
|
Term
| What is the action of griseofulvin? What is it used for and how is it taken? |
|
Definition
-It given orally and over time is incorporated into keratin layers of skin where it interferes with **DNA replication by blocking with **microtubule assembly
-Targets fungi with chitin in cell wall
-Used for *dermatophytosis (ring worm)
-Has little to no side effects |
|
|
Term
| What were those antifungals again? |
|
Definition
1. Polyene compounds (Nystatin & Amphotericin B)
-Bind ergosterol
2. Azoles
-Bolock ergosterol synth
3. Flucytosine
-Blocks DNA synth
4. Griseofulvin
-Blocks microtubule polymerization (mitosis) |
|
|
Term
| GIve the four inhibitors of nucleic acid function in bacteria? |
|
Definition
1. Quinolones (nalidixic acid, fluroquinolones [ciprofloxacin and norfloxacin])
2. Nitrofurantoin
3. Nitroimidazoles (metronidazole)
4. Rifamycins (Rifampin) |
|
|
Term
| Give the mechanism for Quinolones? What are the two major kinds? What do they effect, for both? |
|
Definition
-They inhibit the **A subunit of both **DNA gyrase and **topoisomerase II
-Nalidixic acid is for *aerobic gram- bac
-Fluroquinolones are more *broad spectrum (like ciprofloxacin and norfloxacin) |
|
|
Term
| What are the two fluoroquinolones again? What is special about them? |
|
Definition
-Ciprofloxacin and norfloxacin
-Remember, these are broader spectrum |
|
|
Term
| What is the action of nitrofurantoin? Spectrum? |
|
Definition
-**Reduced in the bacteria, producing toxic product that will cause **DNA breaks
-Broad spectrum |
|
|
Term
| What is the action for nitroimidazoles? What is the main one? What does it act on? |
|
Definition
-**Metronidazole is reduced in the bacteria, producing **free radicals that damage DNA** and other components
-Acts on ***anaerobic bacteria (and some parasites) |
|
|
Term
| What is the action of rifampin? Spectrum? |
|
Definition
-Inhibits bacterial **DNA-dependant RNA-polymerase (i.e. transcription)
-Broad spectrum (including *mycobacteria) |
|
|
Term
| What are the inhibitors of the 30S subunit (3)? |
|
Definition
1. Aminoglycosides (streptomycin, kanamycin, etc.)
2. Tetracycline
3. Spectinomycin (aminocyclitol) |
|
|
Term
| What is the action of aminoglycosides? Give two examples of them? Give an example of how it can be used synergistically? Side effects? Spectrum? |
|
Definition
-Bind to the **30S subunit at P site blocking entry of fMet and cause **misreading
-Examples are *kanamycin and **streptomycin
-Aminoglycosides have slow entry into bacteria, so we can pair it with a cell wall targeting antibiotic to increase permeability
-Broad spectrum for aerobic bacteria |
|
|
Term
| What is the mechanism of tetracycline? Side effects and contraindication? Spectrum? |
|
Definition
-Binds reversibly to the 30S subunit near the A site, blocking incoming tRNA
-Can stain teeth during development, so contraindicated for children under 8 and during pregnancy
-Broad spectrum |
|
|
Term
| What is the action of spectinomycin? What is the specific use? |
|
Definition
-An **aminocyclitol antibiotic that binds to the **30S subunit and interferes with **mRNA binding
-Used to treat *gonorrhea |
|
|
Term
| What are the inhibitors of the 50S subunit (3)? |
|
Definition
1. Chloramphenicol
2. Macrolides (erythromycin)
3. Lincosamides (lincomycin) |
|
|
Term
| What is the activity of chloramphenicol? Spectrum? |
|
Definition
-It binds to the **50S subunit and inhibits peptide bond formation (**peptidyl transferase reaction)
-Broad spectrum |
|
|
Term
| What is the mechanism of action of erythromyosin and lincomycin? Why types are they? |
|
Definition
-They both bind to the *50S and inhibit **translocation
-Erythromycin is a macrolide
-Lincomycin is a lincosamide |
|
|
Term
| What are the inhibitors of metabolic pathways (2)? How do they inhibit? |
|
Definition
1. Sulfonamides
2. Trimethoprim
-Both are anti-folate drugs
-Note; these can also be called antimetabolites, which are metabolite analogues |
|
|
Term
| What is the action of sulfonamides? Spectrum? |
|
Definition
-They are *p-aminobenzoid acid analogues that interfere with **tetrahydrofolic acid production by binding to and inhibiting **dihyropteroate synthetase (Our folate comes from diet)
-Tetrahydrofolic acid is a one-carbon donor
-Broad spectrum? |
|
|
Term
| What is the action of trimethoprim? Toxicity? |
|
Definition
-Another *folic acid inhibitor, but this one inhibits at the level of **dihydrofolate reductase
-May cause folate deficiency |
|
|
Term
| What are some drugs effective against mycobacteria (3) and the main drug in that class (first two)? What kinds of compounds are these? What one did we learn already that also can inhibit mycobacteria? |
|
Definition
1. Isoniazid (Isonicotinic acid hydrazine; INH)
2. Sulfones (Dapsone)
3. p-Aminosalicylic acid (PAS)
-These are all antimetabolites, but specific to mycobateria
-Remember *rifampin is one that works also |
|
|
Term
| What is the mechanism of INH? What does it stand for again? What does it target? What do we see in toxicity? |
|
Definition
-Isonicotinic acid hydrazide is thought to inhibit synthesis of **mycolic acid (in cell wall of *mycobacteria)
-See **B6 def. in toxicity |
|
|
Term
| What is the mechanism of dapsone? What class is it again? What is the specific disease of treatment? |
|
Definition
-This *sulfone has the same action as the sulfonamides with blocking early **folate metabolism at the level of **dihydropteroate synthetase
-Because of toxicity, it is used only for **leprosy |
|
|
Term
| What is the mechanism of PAS? What is it used to treat mainly? |
|
Definition
-*p-Aminosalicylic acid has the same mech as the sulfonamides (**early folate blockage)
-Used mainly as second line for M. tuberculosis (drug resistant)
-It is also pretty toxic, but not as bad as dapsone |
|
|
Term
| What are MIC and MBC? What is the Kirby-Bauer technique? |
|
Definition
-Minimum inhibitory & bactericidal concentrations
-Measures potency
-Use broth to measure (*quantitative)
-In the Kirby-Bauer technique, infectious agent is spread on agar, and discs of antimicrobials are added to see effect (*qualitative) |
|
|
Term
| What is the difference between antibiotics and chemotherapuetics? What is the one between the two? |
|
Definition
-Both are toxic to some microorganism
-Antibiotics are produced by a microorganism
-Chemotherapuedics are man-made
-*Semisynthetic antibiotic are antibiotics that have been reacted to get a different structure |
|
|
Term
|
Definition
-Just halts growth
-In contrast, bactericidal kills |
|
|
