Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q 
Drugs under the class of aminoglycoside?
*ONLY GENERAL CLASS NAME IS USED IN SUBSEQUENT F.C.*
A
  • Gentamicin
  • Amikacin
  • Tobramycin
  • Streptomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Aminoglycosides MoA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why are aminoglycosides ineffective against anaerobes?

A

requires O2 for uptake (ineffective against anaerobes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What must you consider when giving aminoglycosides to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are aminoglycosides administered?

A

parenteral administration (poor oral absorption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aminoglycosides indications?

A

GNR

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Drugs under the class of Tetracycline?

A

Doxycycline
Tetracycline
Minocycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

is tetracycline bacteriostatic or bacteriocidial?

A

Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mechanism of action for tetracycline?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why are tetracyclines rarely used in the US?

A

resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Drugs under the class of Macrolides

A

Azithromycin

Erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

mechanism of action for Macrolides?

A

50S – blocks translocation (macro“slides”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How often should macrolides be dosed? why?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Indications of Macrolides?
GPC Atypical pneumonias (Mycoplasma, Chlamydia, Legionella, H influenza) STD – chlamydia Pen-allergic patients S. pneumoniae, S. aureus are often resistant
26
Mechanisms of resistance in Macrolides?
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)
27
Side effect of macrolides?
``` 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
28
mechanism of action of Chloramphenicol?
50S – blocks peptidyltransferase at 50S ribosomal subunit
29
is chloramphenicol bacteriostatic or bacteriocidial?
bacteriostatic
30
indications for chloramphenicol?
Meningitis (h. influenza, Neisseria meningitides, Strep. pneumoniae) Rickettsia (Rocky MTN fever)
31
mechanism of resistance for Chloramphenicol?
Plasma-encoded acetyltransferase inactivates the drug
32
side effects of Chloramphenicol?
Aplastic anemia | Gray baby syndrome (because they lack liver UDP glucuronyl transferase)
33
What are some drugs under the class of Lincosamide
Clindamycin
34
Mechanism of action of Lincosamide?
50s - blocks translocation
35
is Lincosamide bacteriostatic or bactericidal?
bacteriostatic
36
Indications for Lincosamide?
``` Narrow spectrum GPC (Staph, Strep/GAS) Aspiration pneumonia (Bacteriodes, Clostridium perfringens) Lung abscess Oral infections (dental prophylaxis) ```
37
Mechanism of resistance for Lincosamide
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
Side effect of Lincosamide?
``` Pseudomembranous colitis (C. diff) Fever GI intolerance (N/V/D) Bone marrow suppression Hepatotoxic Hypersensitivity: rash ```
39
drugs under the class of Oxazolidenone?
Linezolid (synthetic)
40
Mechanism of action for Oxazolidenone?
50S – blocks formation of the initiation complex
41
Oral bioavailability for Oxazolidenone? How often should it be dosed?
100% oral bioavailability | t½ = 5hrs (twice daily dosing)
42
Indications for Oxazolidenone?
``` GP Bacteriostatic: staph, enterococci Bacteriocidal: strep VRE VRSA MRSA ```
43
Mechanism of resistance for Oxazolidenone?
23S rRNA alterations
44
Side effects of Oxazolidenone
Leukopenia, anemia, thrombocytopenia GI intolerance (N/V/D) Hepatitis Weak drug interaction with MAOi
45
what's the difference btwn clindamycin and metronidazole in terms of indications?
**clindamycin is used to treat anaerobes ABOVE the diaphragm, metronidazole is used to treat anaerobes BELOW the diaphragm**
46
T/F both eukaryotes and prokaryotes RNA/DNA synthesis need folate synthesis
F. prokaryotes RNA/DNA synthesis does NOT need folate synthesis, while eukaryotes do!
47
Topoisomerases of eukaryotes?prokaryotes?
prokaryotic DNA replication requires Topo II/IVeukaryotic DNA replication requires I/II
48
Anti-folate drug?
TrimethoprimSulfamethoxazole (TMP/SMX)
49
MoA for TMP/SMX?
combination therapy causes sequential block of folate synthesis, resulting in decr. synthesis of Thymidine, Methionine, Purines (TMP)
50
what is SMX?
SMP – analog of PABA; competitively inhibits DHPS (dihydropterorate synthase)
51
What is TMP
TMP competitively inhibits DHFR (dihydrofolate reductase); 50,000x more active against bacterial DHFR
52
TMP bacteriostatic or bactericidal?
bacteriostatic
53
indications for TMP/SMX?
``` 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
Mechanism of resistance for TMP? SMX?
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
Side effects of TMP?
TMP = Treats Marrow Poorly Megaloblastic anemia Leukopenia Granulocytopenia
56
Side effects of SMX?
SMX Hypersensitivity Hemolysis (if G6PD deficient) Nephrotoxicity (tubulointerstitial nephritis) Photosensitivity Kernicterus in infants Displaces drugs from albumin (ie warfarin)
57
Side effect of TMP/SMX?
``` Erythema Multiforme Hepatitis Hyperkalemia Bone marrow suppression GI upsets (N/V) Avoid in the 1st trimester of pregnancy ```
58
Drugs under the class of Fluoroquinolones?
Ciprofloxacin Levofloxacin Moxifloxacin
59
MoA of Fluoroquinolones?
inhibits DNA Gyrase (Topo II) and DNA Topo IV | impt in alleviating supercoiling that occurs during DNA replication
60
Fluoroquinolones bacteriostatic or bactericidal?
bactericidal
61
distribution of Fluoroquinolones?
wide distribution, high concentration in tissues and CSF cipro – hepatic + renal clearance moxi/levo – mostly hepatically cleared
62
what should you avoid if you're on Fluoroquinolones?
antacids
63
indications for ciprofloxacin?
UTI, STD
64
indications for Levofloxacin/Moxifloxacin?
GP GN Chlamydia Clinical uses: Moxi/Levo-: pneumonia Levo: UTI
65
MoA for Fluoroquinolones?
Mutation in DNA gyrase efflux pumps plasma -mediated resistance via Qnr proteins
66
Side effects of Fluoroquinolones?
``` 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
DNA Alkylator
Metronidazole
68
Mechanism of action of Metronidazole?
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
Metronidazole - bacteriostatic or bactericidal?
bactericidal and anti-protozoal
70
Metronidazole absorption and distribution?
well absorbed in the GI tract, but food delays its absorption widely distributes; enters CSF well
71
Indications for Metronidazole?
Protozoa (Giardia Lamblia, Entamoeba Histolytica, Trichomonas,) Gardnerella vaginalis Anaerobes (Bacteroides , C. difficile) Pylori (use with PPI and clarithromycin, “triple therapy”)
72
Side effects of Metronidazole?
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
Drugs under the class of Rifamycins?
Rifampin (semi-synthetic derivative of rifamycin B)
74
MoA of Rifamycins?
RNA Polymerase Inhibitors (does not inhibit mammalian nuclear RNA polymerase but does inhibit mammalian mitochondrial RNA polymerase at high concentrations)
75
Rifamycins - bacteriostatic or bactericidal?
bacteriostatic and bactericidal
76
absorption and distribution of Rifamycins?
good oral absorption, but impaired by food enters CSF well
77
indications of Rifamycins?
``` 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
Mechanism of reaction for rifamycin?
Mutations in RNA polymerase (rpoB) | Never use alone in TB therapy due to increasing problems with Mycoplasma TB resistance
79
side effects of Rifamycins?
``` 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions