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I&I - M1T1 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What are the 5 catergories of antibiotics?

A
  1. Inhibition of cell wall synthesis
  2. Inhibition of protein synthesis
  3. Inhibition of DNA synthesis
  4. Inhibition of RNA synthesis
  5. Inhibitors of metabolites (metabolism)
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2
Q

Bacteriocidal antibiotics

A

target cell wall causing lysis (ex. beta lactams)

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3
Q

Bacteriostatic antibiotics

A

inhibit growth or replication by targeting rna synthesis, protein synthesis, dna synthesis, prevent cell wall synthesis, and antimetabolites

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4
Q

MIC/MBC determination

A

Used to find how much of a drug you need to inhibit or kill microorganism. Minimal Inhibitory Concentration = lowest concentration that results in inhibition of visible growth. Minimal bactericidal concentration = lowest concentration that kills 99.9% of inoculum (ug/ml)

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5
Q

What are 3 types of antibiotic spectrums?

A

Spectrum matters because if you don’t know what’s up you might start with something broad, and switch to something narrow. Broad = acts on gram + or gram -, often used whe bacteria unknown.
Extended = moderately broad, usually penicillin based.
Narrow = kill limited, and may not harm normal flora or less resistance

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6
Q

synergy

A

combined drugs that result in enhancement of over antimicrobial activity. Opposite of indifference (nothing happens) and antagonism (not good)

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7
Q

How do bacteria cause antibiotic resistance

A
  1. Produce enzymes that destroy antibiotics
  2. Synthesis of modified targets, if it does get in
  3. decreased permeability
  4. or export it as it comes in
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8
Q

Intrinsic resistance

A
  1. some live intracellularly
  2. some lack a cell wall
  3. naturally resistance via capsule/biofilm ex. mycobacteria has mycolic acid that prevents antibiotics
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9
Q

Antibiotics that inhibit cell wall synthesis

A

Beta lactam based: penicillins, cephalosporins, carbapenems, monobactams. Non beta lactams: Vancomycin, Daptomycin, Isoniazid, Ethambutol, Pyrazinamide

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10
Q

What’s mechanism of beta lactams

A

The peptidoglycan is cross-linked by transpeptidase during cell wall synthesis. Transpeptidase is a penicillin binding proteins. Beta lactams like, Penicillin can bind to this group of enzymes; the natural substrate is the D-alanyl-D-alanine residues of the peptidoglycan to be cross-linked. Penicillins inhibit cross-linking by irreversibly binding to these enzymes, causing lysis

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11
Q

Beta lacamase decoys plus beta lactam

A

Makes drug more effective because bacteria will try and secrete lactamases, but they will be caught up with the decoys

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12
Q

What is Natural Penicillin useful against and not useful against?

A

It can be served orally (V) or IV (G). Used against a lot of gram positive and a few gram negative. Not useful against S. aureus, S. epidermis, or intracellular bacteria. S. aureus and S. epidermis have penicillinases that break beta lactam ring. Luckily thats why we got penicillinase resistant penicillins that can resist the pencillinases (exps. nafcillin, oxacillin (only in lab), flucloxacillin, dicloxacillin)

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13
Q

Anti-Staphylococcal (natural penicillin)

A

Methicillin drugs used against organisms that are penicillin resistant and methicillin sensitive. Examples: Naficillin, Oxacillin (used in lab to see if methicillin resistant), and Flucloxicillin (oral). Also Dicloxacillin, and Flucoxicillin (parenteral). these drugs used on staph aureus, EXCEPT MRSA and MRSE.

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14
Q

How is MRSA and MRSE reistant against methicillin?

A

Changes the target of the methicillin drugs by altering the PBP

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15
Q

Which are aminopenicillins (natural penicillin) and how do they get in?

A

Ampicillin (oral/parenteral), amoxicillin, has addition of amino group to R that helps it enter through porins of some gram negatives. They work best in intestine; not useful against S. aureus, S. epidermis

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16
Q

What are 3 natural extended penicillins that are a little better than aminopenicillins?

A

Piperacillin (parenteral), ticarcillin (parenteral), and carbenicillin (oral)

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17
Q

Beta lactamases

A

include penicillinase, extended spectrum beta lactamases, and cephalosporinase. Those decoys or beta lactamase inhibitors prevent lactamases by combine with normal drugs are: clavulanic acid, sulbactam, tazobactam. Some common combos: Amoxicillin/clavulanate, Ampicillin/Sulbactam, piperacillin/Tazobactam, Ticarcillin/Clavulanate. > create broad spectrum

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18
Q

Hypersensitivities to Penicillin

A

Type 1: skin rash, anaphylaxis
Type 2: hemolytic anemia, metabolite can bind to RBC and cause lysis

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19
Q

Cephalosporins and Cephamycins

A

Have two R groups, R1 modifications affect antibiotic activity, adn R2 modifications affect pharmacokineitc properties . These are more resistant than natural penicillins to beta lactamases

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20
Q

Carbapenems

A

broad “the hail mary drug”, all parental. Inlcudes: imipenem, meropenem, ertapenem, doripenem. Have enhanced binding to PBP, resistance to Beta lactamases, and porin activity. Spooky resistance of Enterobacteriaceae

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21
Q

Vanomycin

A

glycopeptide (not beta lactam), inhibits cell wall by binding to the building blocks of peptidoglycan. Narrow spectrum against gram positive. Some enterococci can be resistant due to Lac in building block sequence.

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22
Q

Daptomycin

A

cyclic lipopetide (not beta lactam). Lipid portion inserts into bacterial membrane causing lysis. Active on gram positive. Used for MRSA, invasive S. pneumoniae, and vancomycin resistant enterococci. Poor activity in lungs

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23
Q

How are bacteria Macrolide resistant?

A

Efflux pump like in in Strep pneumoniae, or enzyme mediated methylation of 23S can render bacteria resistant to all macrolides.

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24
Q

Clindamycin

A

targets 50S to inhibit protein synthesis, active against gram positive and MRSA and strep pneumo, some anaerobes, and protozoa (toxoplasma/plasmodium). Not useful against aerobic gram negatives and 23S methylated

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25
Q

DNA gyrase Inhibitors

A

Quinolone (not used), and Fluoroquinolones: ciprofloxacin, gatifloxacin, levofloxacin, oflaxacin, moxifloxacin. The fluoroquinolones are broad and used against aerobic gram negatives, some atypical, and some staph.strep. Used to treat UTI, diarrhea, pneumonia

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26
Q

RNA polymerase inhibitors

A

Block mRNA elongation, treat tuberculosis, and includes: rifampinm rifabutin, rifapentine

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27
Q

Anti folate drugs: TMP/SMX

A

sulfonamides, trimethoprim; broad spectrum: aerobic gram pos, MRSA, aerobic gram neg, protozoa (toxoplasma/pneumocytsis); treats UTIs, RTIs; bad side effects against normal flora, rash, NO alcohol

28
Q

Metronidazole (antimetabolite)

A

best against anaerobics, acts by becoming free radical and destroying bacterial DNA

29
Q

Anti Tuberculosis Drugs

A

Treated with 4 drugs: first two = Isoniazid and ethambutol ehich blocks mycolic acid synthesis. Then pyrazinamide inhibits membrane fatty acid synthesis, and Rifampin inhibits RNA synthesis by binding to RNA polymerase.(latent TB only isoniazid/rifampin)

30
Q

Acquired resistance

A
  1. chromosomal mutation = mutation in gene that codes for drug target
  2. acquisition of plasmid or transposon = resistance plasmid that has genes to degrade antibiotics
  3. Transposons = genes transferred within or between larger pieces of DNA. Drug resistant transposon consists of resistant genes flanked by insertions that code for transposase.
31
Q

How do bacteria resist Penicillin and Cephalosporin?

A

Cleavage of Beta lactam ring by penicillin binding lactamases, modifications to penicillin binding proteins in membrane, and poor permeability to drug.

32
Q

How do bacteria resist Vancomycin?

A

Change in peptide component of peptidoglycan from D- alanine-D-alanine to D-alanine-D-lactam.

33
Q

How do bacteria resist Aminoglycosides?

A

Modify the drugs by phosphorylation, adenylation and acetylation, alter the ribosomal binding site, decrease permeability to drug, or efflux pumps.

34
Q

How do bacteria resist tetracyclines?

A

decrease levels of drug accumulation due to plasmid encoded processes, mutations on small ribosome prevents binding, and genes that protect bacterial ribosomes from tetracycline.

35
Q

How do bacteria resist chloramphenicol?

A

due to plasmid encoded acetyltransferase that inactivates the drug, and efflux pumps

36
Q

How do bacteria resist erythromycin

A

inactivation by methylation of adenine residue of small ribosome.

37
Q

Which cephalosporins are parenteral?

A

cefazolin, cefuroxime, ceftriaxone, cefepime, and ceftaroline (1st to 5th generation)

38
Q

Which cephalosporins are oral?

A

cephalexin, cefuroxime, and cefixime

39
Q

What are the two parenteral cephamycins?

A

cefotetan and cefoxitin

40
Q

What do generations mean in Cephalosporins/cephamycins?

A

Generalization: with increasing “generation” activity in vitro against aerobic Gram positive organisms decreases while activity against aerobic Gram negatives increases; exceptions are anaerobes and intracellulars because they don’t work against those, or patients with allergies should not receive cephalosporins.

41
Q

What are first generation cephalosporins for?

A

They are Cefazolin, Cefadroxil, cephalexin (penicillinase resistants) and used for Minor skin infections, and UTIs

42
Q

Second generation cephalosporins and cephamycins

A

Cephasporins = example is cefuroxime same activity as first generation for aerobic gram positives, but also against some gram negatives. Cephamycin = examples: cefotetan and cefoxitin which slightly act on aerobic gram positives and anaerobes

43
Q

Third generation cephalosporins

A

All third gen can moderately act on aerobic gram pos, and there’s increased activity against aerobic gram negatives. Examples cefotaxime and ceftriaxone (cross BBB), cefitzoxime (against anaerobes), and ceftazidime (against pseudomonas)

44
Q

Fourth generation

A

can still affect some gram pos (MSSA) with increased activity against gram negatives including some pseudomonas and enterobacteriaceae ex. cefepime

45
Q

Fifth generation

A

The toughest… activity against MRSA and strep pneumoniae. Also against many gram negatives rods (ones that don’t make lactamases), example is ceftaroline and ceftolozane

46
Q

What is the only licensed monobactam?

A

Aztreonam, which can bind to gram negative PBP

47
Q

Vancomycin

A

glycopeptide antibiotic that can either be IV or oral. It’s mechanism is cell wall inhibitor, and is considered narrow for MRSA, penicillin resistant S. pneumo, and possible enterococcal infections. Only thing that inhibits it is if there D-Ala to D-Lac

48
Q

Daptomycin

A

a cyclic lipopeptide antibiotic, that facilitates bacterial lysis (bacteriocidal) by inserting lipids into membrane. Active against aerobic gram positive (narrow).

49
Q

Which antibiotics bind to 50S and which bind to 30S

A

50S are Oxazolidinones, Macrolides, Clindmycin, StrepGramins, and Chloramphenicol
30S are Aminoglycosides and Tetracyclines

50
Q

Aminoglycosides

A

Types are Streptomycin, Gentamicin, Amikacin, Tobramycin, Neomycin, Kanamycin. They are used for serious aerobic (only aerobic because they O2 dependent mechanism) gram neg infection. Bind to 30S to inhibit protein synthesis.

51
Q

How can bacteria resist Aminoglycosides?

A

Resistance is not common, but bacteria can produce an enzyme that modifies aminoglycoside so it can’t bind or efflux pump

52
Q

Tetracyclines

A

Inlude Doxycyline, Minocycline, Glycylcycline. They act by binding to 30s to block tRNAs from coming in. Acts on aerobic Gram +, aerobic Gram -, Anaerobes, atypical bacteria (used especially for these!), and Some protozoan parasites. resistance only from efflux pump

53
Q

Macrolides

A

Includes: erythromycin, clarithromycin, and azithromycin. Given oral/IV and binds to rRNA of 50S the prevent elongation. Given orally or IV

54
Q

Ketolides

A

includes Telithromycin which binds to two sites.Enhanced activty against strep pneumo that is resistant to penicillin and macrolides.

55
Q

What are some differentials and similarities between erythromycin, clarithromycin, and Azithromycin?

A

Erythromycin is less tolerated in GI, while Clarithromycin and Azithromycin are better for oral consumption, and has increased activity against actypical bacteria and protozoa. All 3 macrolides are resisted from efflux pumps, enzyme methylation of 23S

56
Q

Clindamycin

A

a lincosamide that binds to 50S ribosome. Acts against aerobic gram +, some Strep pneumo, gram + or gram - anaerobes, some protozoa. Clinically used in skin, RT stomach, gynecology, acne, and osteomyelitis

57
Q

Oxazolidinones

A

linezolid that binds to 50S, narrow but acts against the really resistant hoes like MRSA, strep pneumo, and entercocci

58
Q

DNA gyrase inhibitors

A

Quinolone (not used) and Fluoroquinolones: Ciprofloxacin, Gatifloxacin, Levofloxacin, Oflaxacin, Moxifloxacin

59
Q

Fluoroquinolones

A

Broad spectrum, important against aerobic gram negative, atypicals, and some staph and strep. The most famous we’ve heard in like 5 other lectures is Ciprofloxacin, which is for UTI, RTI, skin infections, and diarrhea. However these drugs can cause cartilage and aorta growth.

60
Q

RNA polymerases

A

Block elongation and are specifically used to treat TB. Includes: Rifampin, Rifabutin, Rifapentine

61
Q

Anti-folate Drugs: TMP/SMX

A

Anti folate drugs include sulfonamides and trimethoprim (with sulfamethoxazole = TMP/SMX). Stops nucleic acid synthesis, but this can have bad side effects: GI upsets. (think of how folate was sooo important for neural tube formation). Targets some gram + aerobic, some aerobic gram neg, and some protozoa. Treats prostate and vaginal infections

62
Q

Metronidazole

A

anaerobic, once activated it acts as free radical and breaks bacterial DNA. Targets gram neg anaerobes, gram pos anaerobes, usually for C. diff

63
Q

Anti TB drugs

A

There’s two drugs that block mycolic acid synthesis: Isoniazid, and Ethambutol. Then there’s Pyrazinamide that inhibts membrane synthesis of fatty acids, and rifampin which inhibits RNA synthesis. (Latent TB = isoniazid + rifapentine)

64
Q

Summary of Drug inhibitions

A
65
Q

Some common resistance mechanisms

A

I&I - M1T1 (36 decks)

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