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0. Step Ib > Antibiotics - Synthesis inhibitors > Flashcards

Antibiotics - Synthesis inhibitors Flashcards

1
Q

Why are synthesis inhibitors have a broader spectrum compared to ß lactams?How are our own cells protected from these synthesis inhibitors?

A

all bacteria need protein synthesis to grow

ribosomes in eukaryotic cells sufficiently different from bacterial to provide selectivity

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2
Q

Difference between Concentration vs. time-dependent killing (CDK vs. TDK)?

A

CDK - exposure to higher concentration of the drug is more efficient (even if it is short); there is no benefit of longer exposure TDK - need longer exposure (e.g., frequent dosing)

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3
Q

mnemonic that you should always remember for these synthesis inhibitors

A

Buy AT 30, CCEL for 50” can think of “for” as “four” drugs

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4
Q

Of ALL the drugs that we’ve learned, which ones are the only ones that are bactericidal?

A

Aminoglycosides

  • Gentamicin
  • Amikacin
  • Tobramycin
  • Streptomycin
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5
Q 
Drugs under the class of aminoglycoside?
*ONLY GENERAL CLASS NAME IS USED IN SUBSEQUENT F.C.*
A
  • Gentamicin
  • Amikacin
  • Tobramycin
  • Streptomycin
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6
Q

Aminoglycosides MoA?

A

binds 30S and inhibits formation of initiation complex, cause misreading of mRNA (blocks translocation), and inhibits recycling of ribosomes

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7
Q

Why are aminoglycosides ineffective against anaerobes?

A

requires O2 for uptake (ineffective against anaerobes)

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8
Q

What must you consider when giving aminoglycosides to?

A

renal excretion (adjust dose in patients w/ renal dysfunction)

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9
Q

How are aminoglycosides administered?

A

parenteral administration (poor oral absorption)

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10
Q

Aminoglycosides indications?

A

GNR

GP - synergistic with ß-lactam antibiotics (??dblck)

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11
Q

Mechanism of resistance in aminoglycosides?

A

bacterial transferase enzymes inactivate the drug via acetylation, phosphorylation, or adenylation

(also altered membrane permeability, mutation of binding sites, methylation of rRNA)

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12
Q

Side effects of aminoglycosides? must know

A

Nephrotoxicity /ATN (esp when used with cephalosporin)
Neuromuscular blockade /muscle weakness
Ototoxicity (esp w/ loop diuretics)
Teratogen / Bone marrow suppression

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13
Q

Drugs under the class of Tetracycline?

A

Doxycycline
Tetracycline
Minocycline

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14
Q

is tetracycline bacteriostatic or bacteriocidial?

A

Bacteriostatic

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15
Q

Mechanism of action for tetracycline?

A

30S – prevents attachment of amino-acyl tRNA (prevents elongation)

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16
Q

What should patients avoid if they’re on tetracyclines?

A

Divalent cations can inhibits absorption in the gut (avoid milk, antacids, or Fe-preps)

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17
Q

Which tetracycline is the only one that can be used in renal failure patients, and why?

A

Dox: fecal elimination (only tetracycline that can be used in patients with renal failure)

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18
Q

Indications for tetracycline?

A 
Borrelia burgdorferi
Rickettsia (Rocky MTN fever)
M. pneumoniae
S. pneumoniae 
Chlamydia 
Legionella
Acne Vulgaris (T = T zone)
Anti-parasites malarial
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19
Q

Mechanisms of tetracycline resistance?

A

Plasma encoded transport pumps result in decr. uptake/incr. efflux
(also reduced binding to ribosomal binding site, enzymatic inactivation)

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20
Q

Why are tetracyclines rarely used in the US?

A

resistance

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21
Q

Side effect of tetracyclines?

A

GI distress (N/V/D, hepatotoxicity)
Teeth discoloration Inhibition of bone growth in children
Photosensitivity
Contraindicated in pregnancy, neonates, children – Rx deposits in enamel of teeth and bone

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22
Q

Drugs under the class of Macrolides

A

Azithromycin

Erythromycin

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23
Q

mechanism of action for Macrolides?

A

50S – blocks translocation (macro“slides”)

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24
Q

How often should macrolides be dosed? why?

A

very long t½ = 68 hrs (once-daily dosing)

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25
Q

Indications of Macrolides?

A

GPC
Atypical pneumonias (Mycoplasma, Chlamydia, Legionella, H influenza)
STD – chlamydia
Pen-allergic patients

S. pneumoniae, S. aureus are often resistant

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26
Q

Mechanisms of resistance in Macrolides?

A

Methylation of 23S rRNA-binding site prevents binding of drug (also efflux or reduced permeability, mutation or modification of binding site, production of esterase by enteriobacteriaceae)

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27
Q

Side effect of macrolides?

A 
C – cholestatic hepatitis 
R – rash 
A – arrhythmias/prolonged QT
M – motility issues (GI)
Eosinophilia or Ototoxicity (in elderly)
GI upsets

incr. theophyllines and oral anticoagulants bioavailability

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28
Q

mechanism of action of Chloramphenicol?

A

50S – blocks peptidyltransferase at 50S ribosomal subunit

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29
Q

is chloramphenicol bacteriostatic or bacteriocidial?

A

bacteriostatic

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30
Q

indications for chloramphenicol?

A

Meningitis (h. influenza, Neisseria meningitides, Strep. pneumoniae)
Rickettsia (Rocky MTN fever)

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31
Q

mechanism of resistance for Chloramphenicol?

A

Plasma-encoded acetyltransferase inactivates the drug

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32
Q

side effects of Chloramphenicol?

A

Aplastic anemia

Gray baby syndrome (because they lack liver UDP glucuronyl transferase)

33
Q

What are some drugs under the class of Lincosamide

A

Clindamycin

34
Q

Mechanism of action of Lincosamide?

A

50s - blocks translocation

35
Q

is Lincosamide bacteriostatic or bactericidal?

A

bacteriostatic

36
Q

Indications for Lincosamide?

A 
Narrow spectrum
GPC (Staph, Strep/GAS)
Aspiration pneumonia (Bacteriodes, Clostridium perfringens)
Lung abscess
Oral infections (dental prophylaxis)
37
Q

Mechanism of resistance for Lincosamide

A

Methylation of 23S rRNA-binding site prevents binding of drugCan interfere with macrolide action if co-prescribed (binding site partially overlaps with macrolides)

(also efflux or reduced permeability, mutation or modification of binding site, production of esterase by enteriobacteriaceae)

38
Q

Side effect of Lincosamide?

A 
Pseudomembranous colitis (C. diff)
Fever
GI intolerance (N/V/D)
Bone marrow suppression 
Hepatotoxic 
Hypersensitivity: rash
39
Q

drugs under the class of Oxazolidenone?

A

Linezolid (synthetic)

40
Q

Mechanism of action for Oxazolidenone?

A

50S – blocks formation of the initiation complex

41
Q

Oral bioavailability for Oxazolidenone? How often should it be dosed?

A

100% oral bioavailability

t½ = 5hrs (twice daily dosing)

42
Q

Indications for Oxazolidenone?

A 
GP
Bacteriostatic: staph, enterococci
Bacteriocidal: strep
VRE
VRSA
MRSA
43
Q

Mechanism of resistance for Oxazolidenone?

A

23S rRNA alterations

44
Q

Side effects of Oxazolidenone

A

Leukopenia, anemia, thrombocytopenia
GI intolerance (N/V/D)
Hepatitis
Weak drug interaction with MAOi

45
Q

what’s the difference btwn clindamycin and metronidazole in terms of indications?

A

clindamycin is used to treat anaerobes ABOVE the diaphragm, metronidazole is used to treat anaerobes BELOW the diaphragm

46
Q

T/F both eukaryotes and prokaryotes RNA/DNA synthesis need folate synthesis

A

F. prokaryotes RNA/DNA synthesis does NOT need folate synthesis, while eukaryotes do!

47
Q

Topoisomerases of eukaryotes?prokaryotes?

A

prokaryotic DNA replication requires Topo II/IVeukaryotic DNA replication requires I/II

48
Q

Anti-folate drug?

A

TrimethoprimSulfamethoxazole (TMP/SMX)

49
Q

MoA for TMP/SMX?

A

combination therapy causes sequential block of folate synthesis, resulting in decr. synthesis of Thymidine, Methionine, Purines (TMP)

50
Q

what is SMX?

A

SMP – analog of PABA; competitively inhibits DHPS (dihydropterorate synthase)

51
Q

What is TMP

A

TMP competitively inhibits DHFR (dihydrofolate reductase); 50,000x more active against bacterial DHFR

52
Q

TMP bacteriostatic or bactericidal?

A

bacteriostatic

53
Q

indications for TMP/SMX?

A 
SMX
*GP
GN
Nocardia
Chlamdia
TMP/SMX
UTI
Shigella
Salmonella
Pneumocystis jirovecii (trmt/prophylaxis)
Toxoplasmosis (prophylaxis)

Clinical uses: respiratory tract infections, otitis, UTIs, prostatitis, MRSA skin and soft tissue infections

54
Q

Mechanism of resistance for TMP? SMX?

A

TMP - decr. DHFR binding affinity, overexpression of enzyme, reduce bacterial permeability to TMP SMX – altered enzyme

(bacterial dihydropteroate synthase, decr. uptake, or incr. PABA endogenous synthesis

55
Q

Side effects of TMP?

A

TMP = Treats Marrow Poorly
Megaloblastic anemia
Leukopenia Granulocytopenia

56
Q

Side effects of SMX?

A

SMX
Hypersensitivity
Hemolysis (if G6PD deficient)
Nephrotoxicity (tubulointerstitial nephritis)
Photosensitivity
Kernicterus in infants
Displaces drugs from albumin (ie warfarin)

57
Q

Side effect of TMP/SMX?

A 
Erythema Multiforme
Hepatitis
Hyperkalemia 
Bone marrow suppression
GI upsets (N/V)
Avoid in the 1st trimester of pregnancy
58
Q

Drugs under the class of Fluoroquinolones?

A

Ciprofloxacin
Levofloxacin
Moxifloxacin

59
Q

MoA of Fluoroquinolones?

A

inhibits DNA Gyrase (Topo II) and DNA Topo IV

impt in alleviating supercoiling that occurs during DNA replication

60
Q

Fluoroquinolones bacteriostatic or bactericidal?

A

bactericidal

61
Q

distribution of Fluoroquinolones?

A

wide distribution, high concentration in tissues and CSF
cipro – hepatic + renal clearance
moxi/levo – mostly hepatically cleared

62
Q

what should you avoid if you’re on Fluoroquinolones?

A

antacids

63
Q

indications for ciprofloxacin?

A

UTI, STD

64
Q

indications for Levofloxacin/Moxifloxacin?

A

GP
GN
Chlamydia

Clinical uses:
Moxi/Levo-: pneumonia
Levo: UTI

65
Q

MoA for Fluoroquinolones?

A

Mutation in DNA gyrase efflux pumps plasma -mediated resistance via Qnr proteins

66
Q

Side effects of Fluoroquinolones?

A 
GI upset (N/V/D)
Superinfections
Skin rashes
CNS: HA, dizziness, seizures
Less common: tendon inflammation, rupture (esp. in elderly >60 and those on prednisone Rx), leg cramps, myalgias “-lones” hurt attachments to your bonesA

rthralgia, joint swelling in children
CI in pregnant patients due to possible damage to cartilage
Ciprofloxacin - inhibits hepatic CYP450 (Moxi/Levo do not)
rare: bone marrow failure, hemolytic anemia, nephrotoxicity, arthropathy in CF patients

67
Q

DNA Alkylator

A

Metronidazole

68
Q

Mechanism of action of Metronidazole?

A

forms a reactive nitro-anion and free radical toxic metabolites that damage DNA, mainly at the AT base pairs (may also damage proteins, lipids)

69
Q

Metronidazole - bacteriostatic or bactericidal?

A

bactericidal and anti-protozoal

70
Q

Metronidazole absorption and distribution?

A

well absorbed in the GI tract, but food delays its absorption widely distributes; enters CSF well

71
Q

Indications for Metronidazole?

A

Protozoa (Giardia Lamblia, Entamoeba Histolytica, Trichomonas,)
Gardnerella vaginalis
Anaerobes (Bacteroides , C. difficile)
Pylori (use with PPI and clarithromycin, “triple therapy”)

72
Q

Side effects of Metronidazole?

A

Inhibits CYP3A4 and aldehyde dehydrogenase (-> acetaldehyde accumulates), resulting in a disulfram-like rxn (flushing, tachycardia, hypotension with OH intake “instant hangover”)
HAGI upsets
Metallic taste

CNS effects: ataxia, vertigoNeutropenia
Dark urine
Teratogenic

73
Q

Drugs under the class of Rifamycins?

A

Rifampin (semi-synthetic derivative of rifamycin B)

74
Q

MoA of Rifamycins?

A

RNA Polymerase Inhibitors (does not inhibit mammalian nuclear RNA polymerase but does inhibit mammalian mitochondrial RNA polymerase at high concentrations)

75
Q

Rifamycins - bacteriostatic or bactericidal?

A

bacteriostatic and bactericidal

76
Q

absorption and distribution of Rifamycins?

A

good oral absorption, but impaired by food enters CSF well

77
Q

indications of Rifamycins?

A 
Mycoplasma 
Tuberculosis and other mycobacteria 
Most GP, many GN (broad spectrum)
Staph Aureus
Legionella
Neisseria meningitides prophylaxis in children with H. influenza type B/post-exposure prophylaxis
78
Q

Mechanism of reaction for rifamycin?

A

Mutations in RNA polymerase (rpoB)

Never use alone in TB therapy due to increasing problems with Mycoplasma TB resistance

79
Q

side effects of Rifamycins?

A 
Red orange body fluids
Rapid resistance if used alone
Ramps up cytochrome P450, creating multiple drug interactions (rifabutin does not and is preferred in HIV patients)
GI intolerance: N/V
Hepatitis

0. Step Ib (19 decks)

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