Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > FA - Micro - Antimicrobials > Flashcards

FA - Micro - Antimicrobials Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
0
Q

Antimicrobials - DNA topoisomerases?

A 
Fluoroquinolones:
1. Ciprofloxacin
2. Levofloxacin
Quinolone
1. Nalidixic acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Antimicrobials - Folic acid synthesis (DNA methylation)?

A 
Sulfonamides:
1. Sulfamethoxazole
2. Sulfisoxazole
3. Sulfadiazine
\+ Trimethoprim.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Antimicrobials - Damages DNA?

A

Metronidazole

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

Antimicrobials - mRNA synthesis (RNA pol)?

A

Rifampin

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

Antimicrobials - Protein Synthesis - 50S subunit?

A
  1. Chloramphenicol
  2. Clindamycin
  3. Linezolid
    Macrolides:
  4. Azithromycin
  5. Clarithromycin
  6. Erythromycin
    Streptogramins
  7. Quinupristin
  8. Dalfopristin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antimicrobials - Protein synthesis - 30S subunit?

A 
Aminoglycosides
1. Gentamicin
2. Neomycin
3. Amikacin
4. Tobramycin
5. Streptomycin 
Tetracyclines:
1. Tetracycline
2. Doxycycline 
3. Minocycline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Antimicrobials - Cell wall synthesis - Peptidoglycan synthesis - Glycopeptides?

A
  1. Vancomycin

2. Bacitracin

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

Antimicrobials - Peptidoglycan cross-linking - Penicillinase-sensitive penicillins?

A
  1. Penicillins G, V
  2. Ampicillin
  3. Amoxicillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Antimicrobials - Cell wall synthesis - Peptidoglycan cross-linking - Penicillinase-resistant penicillins?

A
  1. Oxacillin
  2. Nafcillin
  3. Dicloxacillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Antimicrobials - Cell wall synthesis - Peptidoglycan cross linking - Antipseudomonals?

A
  1. Ticarcillin

2. Piperacillin

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

Antimicrobials - Cell wall synthesis - peptidoglycan cross-linking Cephalosporins?

A 
1st - Cephazolin
2nd - Cefoxitin
3rd - Ceftriaxone 
4th - Cefipime
5th - Ceftaroline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Antimicrobials - Cell wall synthesis - Peptidoglycan cross-linking Carbapenems?

A
  1. Imipenem
  2. Meropenem
  3. Ertapenem
  4. Doripenem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Antimicrobials - Cell wall synthesis - Peptidoglycan cross-linking - monobactams?

A

Aztreonam

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

Penicillin G route?

A

IV, IM

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

Penicillin V route?

A

Oral

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

Penicillin G, V - Mechanism?

A
  1. Bind penicillin-binding proteins (transpeptidases)
  2. Block transpeptidase cross-linking of peptidoglycan.
  3. Activate autolytic enzymes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Penicillin G, V - Clinical use?

A
  1. Mostly for Gram(+) - S.pneumoniae, S.pyogenes, Actinomyces.
  2. Also for N.meningitidis, T.pallidum.
  3. Bactericidal for gram(+) cocci, gram(+) rods, gram(-) cocci, spirochetes.
  4. Penicillinase sensitive.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Penicillin G,V - Toxicity?

A
  1. HSR

2. DIRECT COOMBS (+) Hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Penicillin G, V - Resistance?

A

Penicillinase in bacteria (a type of beta-lactamase) cleaves beta-lactam ring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ampicillin, amoxicillin - Mechanism?

A

Same as penicillin. Wider spectrum + Penicillinase SENSITIVE.
–> Combine with clavulanic acid to protect against beta-lactamase.

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

Ampicillin vs Amoxicillin - Bioavailability?

A

Amoxil > Ampicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ampicillin/Amoxicillin - Clinical use?

A

Extended-spectrum penicillin:

  1. H.influenza
  2. E.coli
  3. L.monocytogenes
  4. P.mirabilis
  5. Salmonella
  6. Shigella
  7. Enterococci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ampicillin/Amoxicillin - Toxicity?

A
  1. HSR
  2. Rash
  3. Pseudomembranous colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ampicillin/Amoxicillin - Mechanism of resistance?

A

Penicillinase in bacteria (a type of beta-lactamase) cleaves beta-lactam ring.

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

Oxacillin/Nafcillin/Dicloxacillin - Mechanism?

A

Same as penicillin. Narrow spectrum - Penicillinase-RESISTANT because bulky R group blocks access of beta-lactamase to beta-lactam ring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Oxacillin/Nafcillin/Dicloxacillin - Clinical use?

A

S.aureus - except MRSA - resistant because of altered penicillin-binding protein target site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Oxacillin/Nafcillin/Dicloxacillin - Toxicity?

A
  1. HSR

2. Interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ticarcillin/Piperacillin (antipseudomonals) - Mechanism?

A

Same as penicillin. Extended spectrum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Ticarcillin/Piperacillin (antipseudomonals) - Clinical use?

A
  1. Pseudomonas spp.
  2. Gram(-) rods
  3. Susceptible to penicillinase
  4. Use with beta-lactamase inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Ticarcillin/Piperacillin (antipseudomonals) - Tox?

A

HSR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Mention beta-lactamase inhibitors?

A
  1. Clavulanic acid
  2. Sulbactam
  3. Tazobactam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Cephalosporins - Mechanism?

A
  1. Beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.
  2. Bactericidal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Organisms typically NOT covered by cephalosporins?

A

LAME:

Listeria
Atypicals (Chlamydia, Mycoplasma)
MRSA
Enterococci

Exception: Ceftaroline covers MRSA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

1st Gen cephalosporins - Clinical use?

A

Cefazolin, cephalexin.

  1. Gram(+) cocci
  2. P.mirabilis
  3. E.coli
  4. K.pneumoniae
  5. Cefazolin used prior to surgery to prevent S.aureus wound infections.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

2nd gen cephalosporins - Clinical use?

A

Cefoxitin, cefaclor, cefuroxime:

  1. Gram(+) cocci
  2. H.influenza
  3. Enterobacter aerogenes
  4. Neisseria spp.
  5. P.mirabilis
  6. E.coli
  7. K.pneumoniae
  8. S.marcescens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

3rd gen cephalosporins - Clinical use?

A

Ceftriaxone, cefotaxime, ceftazidime.
Serious gram(-) infections resistants to other beta-lactams.
Ceftriaxone –> Meningitis + Gonorrhoeae + Disseminated LYME.
Ceftazidime –> Pseudomonas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

4th gen cephalosporins - clinical use?

A

Cefepime.

Incr. activity against pseudomonas + gram(+) organisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

5th gen cephalosporins - clinical use?

A 
Ceftaroline.
Broad gram(+) and gram(-) organism coverage, incl. MRSA.
Does NOT cover Pseudomonas.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Cephalosporins toxicity?

A
  1. HSR.
  2. Autoimmune hemolytic anemia.
  3. Disulfiram-like reaction.
  4. VitK def.
  5. Low cross-reactivity with penicillins.
  6. Increase nephrotoxicity of aminoglycosides.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Aztreonam - Mechanism?

A
  1. Monobactam - resistant to beta-lactamases.
  2. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3.
  3. Synergistic with aminoglycosides.
  4. No cross-allergenicity with penicillins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Aztreonam - Clinical use?

A
  1. Gram(-) rods only.
  2. No activity against gram(+) or anaerobes.
  3. For penicillin allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Aztreonam - toxicity?

A

Usually nontoxic - occasional GI upset.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Aminoglycosides - Mechanism?

A
  1. Bactericidal
  2. Inhibit formation of initiation complex and cause misreading of mRNA.
  3. Also block translocation.
  4. Require O2 for uptake - therefore ineffective against anaerobes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Aminoglycosides - Clinical use?

A
  1. Severe gram(-) rods.
  2. Synergistic with beta-lactams
  3. Neomycin for bowel surgery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Aminoglycosides toxicity?

A
  1. Nephrotoxicity (especially when used with cephalosporins)
  2. Neuromuscular blockade
  3. Ototoxicity (especially when used with loop diuretics)
  4. Teratogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Aminoglycosides - Mechanism of resistance?

A

Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Tetracyclines - mechanism?

A
  1. Bacteriostatic
  2. Bind to 30S and prevent attachment of aminoacyl-tRNA.
  3. Limited CNS penetration.
  4. Doxycycline is fecally eliminated and can be used in patients with renal failure.
  5. Do NOT take with milk (Ca), antacids (Ca, Mg), or iron-containing preparations because divalent cations inhibit its absorption in the gut.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Tetracyclines - Clinical use?

A
  1. Borrelia burgdorferi
  2. M.pneumoniae
  3. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia/Chlamydia.
  4. Also used to treat acne.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Tetracyclines - Toxicity?

A
  1. GI distress
  2. Discoloration of teeth and inhibition of bone growth in children
  3. Photosensitivity
  4. Contraindicated in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Tetracyclines - Mechanism of resistance?

A
  1. Decr. UPTAKE

2. Incr. EFFLUX out of bacterial cells by plasmid-encoded transport pumps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Macrolides - Mechanism?

A
  1. Inhibits protein synthesis by blocking TRANSLOCATION (macroslides).
  2. Bind to the 23S rRNA of the 50S subunit.
  3. Bacteriostatic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Macrolides - Clinical use?

A
  1. Atypical pneumonias
  2. STDs (Chlamydia)
  3. Gram(+) cocci (strep infections in patients allergic to penicillin).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Macrolides - toxicity?

A
  1. GI motility issues
  2. Arrhythmia caused by prolonged QT
  3. Acute cholestatic hepatitis
  4. Rash
  5. Eosinophilia
  6. Incr. serum concentration of theophyllines + Oral anticoagulants.
  7. Erythro + Clarithro INHIBIT CYP450.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Macrolides - mechanism of resistance?

A

Methylation of 23S rRNA-binding site prevents binding of drug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Chloramphenicol - Mechanism?

A

Blocks peptidyltransferase at 50S ribosomal subunit - Bacteriostatic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Chloramphenicol - Clinical use?

A
  1. Meningitis (H.influenza, N.meningitidis, S.pneumoniae).
  2. RM spotted fever - R.rickettsii
  3. Limited use due to toxicity but often still in developing countries because of low cost.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Chloramphenicol - Toxicity?

A
  1. Anemia - DOSE-dependent.
  2. Aplastic anemia - DOSE-dependent.
  3. Gray baby syndrome - in premature infants because they lack liver UDP-glucuronyl transferase.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Chloramphenicol - Mechanism of resistance?

A

Plasmid-encoded acetyltransferase inactivates the drug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Clindamycin - Mechanism?

A

Blocks peptide transfer (translocation) at 50S - Bacteriostatic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Clindamycin - Clinical use?

A
  1. Anaerobic infections (e.g., Bacteroides spp., C.perfringens) in aspiration pneumonia, lung abscesses, oral infections.
  2. Also effective against invasive Group A strep infection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Clindamycin vs Metronidazole?

A

Treats anaerobes ABOVE the diaphragm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Clindamycin - toxicity?

A
  1. Pseudomembranous colitis (C.difficile overgrowth)
  2. Fever
  3. Diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Sulfonamides - Mechanism?

A
  1. Inhibit folate synthesis.
  2. Para-aminobenzoic acid (PABA)
  3. Antimetabolites inhibit dihydropteroate synthase.
  4. Bacteriostatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Sulfonamides - Clinical use?

A
  1. Gram(+)
  2. Gram(-)
  3. Nocardia
  4. Chlamydia
  5. Triple sulfas or SMX for simple UTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Sulfonamides - Toxicity?

A
  1. HSR
  2. Hemolysis if G6PD deficient
  3. Nephrotoxicity (tubulointerstitial nephritis)
  4. Photosensitivity
  5. Kernicterus in infants
  6. Displace other drugs from albumin (e.g., warfarin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Mechanism of resistance - Sulfonamides?

A
  1. Altered enzyme (bacterial dihydropteroate synthase)
  2. Decr. UPTAKE
  3. Incr. PABA synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Trimethoprim - mechanism?

A

Inhibits bacterial dihydrofolate REDUCTASE - Bacteriostatic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Trimethoprim - Clinical use?

A
  1. Used in combination with sulfonamides (TMP-SMX)
  2. Cause sequential block of folate synthesis.
  3. Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis.
  4. Toxo prophylaxis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Trimethoprim - Toxicity?

A
  1. Megaloblastic anemia
  2. Leukopenia
  3. Granulocytopenia
    May alleviate with supplemental folinic acid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Fluoroquinolones - mechanism?

A
  1. Inhibits DNA gyrase (topoiso II) + topoiso IV.
  2. Bactericidal.
  3. Must not be taken with antacids.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Fluoroquinolones - Clinical use?

A

Gram(-) rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram(+) organisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Fluoroquinolones - Toxicity?

A
  1. GI upset
  2. Superinfections
  3. Skin rashes
  4. Headaches
  5. Dizziness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Fluoroquinolones - Less common toxicity?

A
  1. Tendonitis
  2. Tendon rupture
  3. Leg cramps
  4. Myalgias
  5. Contra in pregnancy, nursing mothers , and children under 18yrs due to possible damage to cartilage.
  6. May prolong QT syndrome
  7. May cause tendon rupture in people >60 and in patients taking prednisone.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Fluoroquinolones - Mechanism of resistance?

A

Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Metronidazole - mechanism?

A

Forms free radical toxic metabolites in the bacterial cell that damages DNA. Bactericidal, antiprotozoal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Metronidazole - Clinical use?

A
  1. Giardia
  2. Entamoeba
  3. Trichomonas
  4. G.vaginalis
  5. Anaerobes (bacteroides, C.difficile)
  6. H.pylori + clarithromycin + PPI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Metronidazole - Disulfiram-like toxicity?

A
  1. Disulfiram-like reaction - severe flushing, tachycardia, hypotension with alcohol.
  2. Headache
  3. Metallic taste
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

M.tuberculosis - prophylaxis?

A

Isoniazid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

M.tuberculosis - Treatment?

A
  1. Rifampin
  2. Isoniazid
  3. Pyrazinamide
  4. Ethambutol (RIPE for treatment)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

M.avium-intracellulare - Prophylaxis?

A
  1. Azithromycin

2. Rifabutin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

M.avium-intracellulare - treatment?

A
  1. More drug resistant than M.tuberculosis.
  2. Azithromycin or clarithromycin + ethambutol
  3. Can add rifabutin or ciprofloxacin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

M.leprae - prophylaxis?

A

No prophylaxis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

M.leprae - Treatment?

A
  1. Long-term treatment with dapsone + rifampin for TUBERCULOID FORM.
  2. Add clofazimine for LEPROMATOUS form.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Isoniazid - Mechanism?

A
  1. Decr. synthesis of mycolic acids.

2. Bacterial catalase-peroxidase (encoded by katG) needed to convert INH to active metabolite.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Isoniazid - Clinical use?

A

M.tuberculosis - the ONLY agent used as solo prophylaxis against TB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Isoniazid - fast vs slow acetylators?

A

Different half-lives.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Isoniazid - toxicity?

A
  1. Neurotoxicity
  2. Hepatotoxicity
  3. Pyridoxin (B6) can prevent neurotoxicity, lupus
87
Q

Rifamycins (Rifampin, rifabutin) - mechanism?

A

Inhibits DNA-dependent RNA polymerase.

88
Q

Rifamycins - clinical use?

A
  1. M.tuberculosis.
  2. Delays resistance to dapsone when used for leprosy.
  3. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H.influenza B.
89
Q

Rifamycins - Toxicity?

A
  1. Minor hepatotoxicity and drug interactions (Incr. P-450).
  2. Orange body fluids (non hazardous side effect).
  3. Rifabutin favored over rifampin in patients with HIV infection due to less CYP450 stimulation.
90
Q

Rifampin’s 4 R’s?

A 
RNA polymerase inhibitor
Ramps up microsomal CYP450
Red/orange body fluids
Rapid resistance if used alone
Rifampin ramps up CYP450, but rifabutin does not.
91
Q

Pyrazinamide - mechanism?

A
  1. Uncertain
  2. Thought to acidify intracellular environment via conversion to pyrazinoic acid.
  3. Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found.
92
Q

Pyrazinamide - clinical use?

A

M.tuberculosis

93
Q

Pyrazinamide - Tox?

A
  1. HYPERURICEMIA

2. Hepatotoxicity

94
Q

Ethambutol - mechanism?

A

DECREASED carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

95
Q

Ethambutol - Clinical use?

A

M.tuberculosis.

96
Q

Ethambutol - toxicity?

A

Optic neuropathy - red/green color blindness.

97
Q

High risk for endocarditis and undergoing surgical or dental procedures - Prophylaxis?

A

Amoxicillin.

98
Q

Gonorrhea - Prophylaxis?

A

Ceftriaxone

99
Q

History of recurrent UTIs - proph?

A

TMP-SMX

100
Q

Exposure to meningococcal infection - proph?

A
  1. Ceftriaxone.
  2. Ciprofloxacin.
  3. Rifampin.
101
Q

Pregnant women carrying GBS - Proph?

A
  1. Intrapartum penicillin G.

2. Ampicillin.

102
Q

Prevention of gonococcal or chlamydial conjunctivitis in newborn?

A

Erythromycin ointment on eyes.

103
Q

Prevention of postsurgical infection due to S.aureus?

A

Cefazolin

104
Q

Prophylaxis of strep pharyngitis in child with prior RF?

A
  1. Benzathine penicillin G.

2. Oral penicillin V.

105
Q

Syphilis proph?

A

Benzathine penicillin G.

106
Q

Proph in HIV - CD4<200?

A

TMP-SMX –> Pneumocystis pneumonia.

107
Q

Proph in HIV - CD4<100?

A

TMP-SMX –> Pneumocystis pneumonia and toxoplasmosis.

108
Q

Proph in HIV patients - CD4

A

Azithromycin or Clarithromycin –> MAC complex.

109
Q

Treatment of MRSA?

A
  1. Vancomycin
  2. Daptomycin
  3. Linezolid (can cause serotonin syndrome)
  4. Tigecycline
  5. Ceftaroline
110
Q

Treatment of VRE?

A
  1. Linezolid

2. Streptogramins (quinupristin/dalfopristin)

111
Q

Antifungal therapy - Lanosterol synthesis?

A

Terbinafine

112
Q

Antifungal therapy - Cell wall synthesis?

A

Echinocandins:

  1. Caspofungin
  2. Micafungin
  3. Anidulafungin
113
Q

Antifungal therapy - Forms membrane pores?

A

Polyenes:

  1. Amphotericin B
  2. Nystatin
114
Q

Antifungal therapy - Nucleic acid synthesis?

A

5-flucytosine

115
Q

Antifungal therapy - Ergosterol synthesis?

A

Azoles:

  1. Fluconazoles
  2. Ketoconazole
  3. Clotrimazole
  4. Miconazole
  5. Itraconazole
  6. Voriconazole
116
Q

Amphotericin B - mechanism?

A
  1. Binds ergosterol (unique to fungi)

2. Forms membrane pores that allow leakage of electrolytes

117
Q

Amphotericin B - Clinical use?

A
  1. Serious, systemic mycoses.
  2. Cryptococcus - ampho B +/- flucytosine for cryptococcal meningitis.
  3. Blastomyces
  4. Coccidioides
  5. Histoplasma
  6. Candida
  7. Mucor
118
Q

Amphotericin B - route for fungal meningitis?

A

Intrathecally

119
Q

Amphotericin B - Supplements?

A

K and Mg because of altered renal tubule permeability.

120
Q

Amphotericin B - toxicity?

A
  1. Fever/chills (shake and bake)
  2. Hypotension
  3. Nephrotoxicity
  4. Arrhythmias
  5. Anemia
  6. IV phlebitis
121
Q

Amphotericin B - what to reduce toxicity?

A
  1. Hydration reduces nephrotoxicity.

2. Liposomal amphotericin decreases toxicity.

122
Q

Nystatin - Mechanism?

A

Same as amphotericin B.

123
Q

Nystatin - route?

A

Topical form because too toxic for systemic use.

124
Q

Nystatin - clinical use?

A
  1. “Swish and shallow” for oral candidiasis.

2. Topical for diaper rash or vaginal candidiasis.

125
Q

Azoles - mechanism?

A

Inhibit fungal sterol (ergosterol) synthesis, by inhibiting CYP450 that converts lanosterol to ergosterol.

126
Q

Azoles - Clinical use?

A
  1. Local and less serious systemic mycoses.
  2. FLUCONAZOLE for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types.
  3. ITRACONAZOLE –> Blasto + Coccidioides + Histoplasma.
  4. CLOTRIMAZOLE/MICONAZOLE –> Topical fungal infections.
127
Q

Azoles - Toxicity?

A
  1. Testosterone synthesis inhibition –> gynecomastia esp. with ketoconazole.
  2. Liver dysfunction (inhibits CYP450).
128
Q

Flucytosine - Mechanism?

A

Inhibits DNA/RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase.

129
Q

Flucytosine - clinical use?

A

Systemic fungal infections (esp.meningitis caused by Cryptococcus) in combination with amphotericin B.

130
Q

Flucytosine - toxicity?

A

Bone marrow suppression.

131
Q

Echinocandins - mechanism?

A

Inhibit cell wall synthesis by inhibiting synthesis of β-glucan.

132
Q

Echinocandins - clinical use?

A
  1. Invasive aspergillosis

2. Candida

133
Q

Echinocandins - toxicity?

A
  1. GI upset

2. Flushing (histamine release)

134
Q

Terbinafine - mechanism?

A

Inhibits the fungal enzyme squalene epoxidase.

135
Q

Terbinafine - clinical use?

A

Dermatophytoses (especially onychomycosis - fungal infection of finger or toe nails).

136
Q

Terbinafine - toxicity?

A
  1. GI upset
  2. Headaches
  3. Hepatotoxicity
  4. Taste disturbance
137
Q

Griseofulvin - Mechanism?

A
  1. Interferes with microtubule function - Disrupts mitosis.

2. Deposits in keratin-containing tissues (e.g. nails).

138
Q

Griseofulvin - clinical use?

A
  1. Oral treatment of superficial infections.

2. Inhibits growth of dermatophytes (tinea, ,ringworm).

139
Q

Griseofulvin - Toxicity?

A
  1. Teratogenic
  2. Carcinogenic
  3. Confusion
  4. Headaches
  5. Incr. P450 + warfarin metabolism
140
Q

Antiprotozoan therapy - Toxoplasmosis?

A

Pyrimethamine

141
Q

Antiprotozoan therapy - T.bruceii?

A

Suramin and melarsoprol.

142
Q

Antiprotozoan therapy - T.cruzi?

A

Nifurtimox

143
Q

Antiprotozoan therapy - Leishmaniasis?

A

Sodium stibogluconate.

144
Q

Chloroquine - mechanism?

A

Blocks detoxification of heme into hemozoin –> Heme accumulates and is toxic to plasmodia.

145
Q

Chloroquine - Clinical use?

A

Treatment of plasmodial species other than P.falciparum - frequeency of resistance in P.falciparum is too high.

146
Q

P.falciparum - mechanism of resistance to chloroquine?

A

Resistance due to membrane pump that decreases intracellular concentration of drug.

147
Q

How to treat P.falciparum?

A

Artemether/Lumefantrine or atorvaquone/proguanil.

148
Q

What to give for life-threatening malaria?

A

Use quinidine in US (quinine elsewhere) or artesunate.

149
Q

Chloroquine toxicity?

A
  1. Retinopathy

2. Pruritus - esp. in dark skinned.

150
Q

Antihelminthic therapy - main agents?

A
  1. Mebendazole
  2. Pyrantel pamoate
  3. Ivermectin
  4. Diethylcarbamazine
  5. Praziquantel
    immobilize helminths.
151
Q

Praziquantel - clinical use?

A

Against flukes (trematodes) such as Schistosoma.

152
Q

Antiviral therapy - HIV - Fusion?

A

Attachment –> Maraviroc

Penetration –> Enfuvirtide

153
Q

Antiviral therapy - HIV - Integrase inhibitors?

A
  1. Raltegravir.
  2. Dolutegravir.
  3. Elvitegravir.
154
Q

Antiviral therapy - HIV antiviral therapy - reverse transcriptase inhibitors - NRTIs?

A
  1. Tenofovir (TDF)
  2. Emtricitabine (FTC)
  3. Abacavir (ABC)
  4. Lamivudine (3TC)
  5. Zidovudine (ZDV, formerly AZT)
  6. Didanosine (ddl)
  7. Stavudine (d4T)
155
Q

Antiviral therapy - HIV - RTI - NNRTIs?

A
  1. Nevirapine
  2. Efavirenz
  3. Delavirdine
156
Q

Antiviral therapy - HIV - PIs?

A
  1. Lopinavir
  2. Atazanavir
  3. Darunavir
  4. Fosamprenavir
  5. Saquinavir
  6. Ritonavir
  7. Indinavir
157
Q

Other antiviral therapy - protein synthesis?

A

IFN-α (HBV, HCV).

158
Q

Other antiviral therapy - Uncoating?

A
  1. Amantadine
  2. Rimantadine
    no longer useful for influenza due to incr. resistance.
159
Q

Antiviral therapy - Nucleic acid synthesis - Guanine nucleotide synthesis?

A

Ribavirin –> RSV, HCV.

160
Q

Antiviral therapy - Nucleic acid synthesis - Viral DNA polymerase inhibitors?

A
  1. Foscarnet
  2. Cidofovir
    - -> CMV, HSV (acyclovir-resistant)
161
Q

Antiviral therapy - Guanosine analogs?

A
  1. Acyclovir –> HSV, VZV.

2. Ganciclovir –> CMV.

162
Q

Antiviral therapy - release of progeny virus?

A

Neuraminidase inhibitors:
1. Zanamivir
2. Oseltamivir
influenza A, B.

163
Q

Zanamivir/Oseltamivir - mechanism?

A

Inhibit influenza neuraminidase –> Decr. RELEASE of progeny virus.

164
Q

Zanamivir/Oseltamivir - Clinical use?

A

Treatment and prevention of both influenza A and B.

165
Q

Ribavirin - Mechanism?

A

Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase.

166
Q

Ribavirin - Clinical use?

A

RSV (palivizumab preferred in children).

Chronic Hep C.

167
Q

Ribavirin - toxicity?

A
  1. Hemolytic anemia

2. Severe teratogen

168
Q

Acyclovir/Famciclovir/Valacyclovir - mechanism?

A
  1. Monophosphorylated by HSV/VZV thymidine kinase and NOT phosphorylated in uninfected cells –> Few adverse effects.
  2. Guanosine anagog
  3. Triphosphate formed by cellular enzymes.
  4. Preferentially inhibits viral DNA polymerase by chain termination.
169
Q

Acyclovir/Famciclovir/Valacyclovir - clinical use?

A
  1. HSV/VZV
  2. Weak activity against EBV.
  3. No activity against CMV.
  4. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis.
  5. Prophylaxis in immunocompromised patients.
  6. No effect on LATENR forms of HSV, VZV.
  7. For herpes zoster use Famciclovir.
170
Q

Valacyclovir?

A

Prodrug of acyclovir –> better ORAL bioavailability.

171
Q

Acyclovir/Famciclovir/Valacyclovir - Toxicity?

A
  1. Obstructive crystalline nephropathy

2. Acute renal failure if not adequately hydrated.

172
Q

Acyclovir/Famciclovir/Valacyclovir - Mechanism of resistance?

A

Mutated viral thymidine kinase.

173
Q

Ganciclovir - mechanism?

A

5-monophosphate formed by a CMV viral kinase –> Guanosine analog –> Triphosphate formed by cellular kinases –> Preferentially inhibits viral DNA poly.

174
Q

Ganciclovir - Clinical use?

A

CMV especially in immunocompromised.

175
Q

Valganciclovir?

A

Prodrug of ganciclovir - better ORAL bioavailability.

176
Q

Ganciclovir toxicity?

A
  1. Leukopenia
  2. Neutropenia
  3. Thrombocytopenia
  4. Renal toxicity
  5. More toxic to host enzymes than acyclovir
177
Q

Ganciclovir - mechanism of resistance?

A

Mutated viral kinase.

178
Q

Foscarnet - mechanism?

A

Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme.
Does NOT require activation by viral kinase.

179
Q

Foscarnet - clinical use?

A
  1. CMV retinitis in immunocompromised when ganciclovir fails.
  2. Acyclovir-resistant HSV.
180
Q

Foscarnet - toxicity?

A
  1. Nephrotoxicity.
  2. Electrolyte abnormalities = Hypo/hyperCALCEMIA + Hypo/hyperPHOSPHATEMIA + HYPOkalemia + HYPOmagnesemia –> Can lead to SEIZURES.
181
Q

Foscarnet mechanism of resistance?

A

Mutated DNA polymerase.

182
Q

Cidofovir - mechanism?

A

Preferentially inhibits viral DNA poly - does NOT require phosphorylation by viral kinase.

183
Q

Cidofovir - clinical use?

A

CMV retinitis in immunocompromised patients - acyclovir resistant HSV - Long half-life.

184
Q

Cidofvir - toxicity?

A

Nephrotoxicity –> Coadminister with probenecid and IV saline to decrease toxicity.

185
Q

HAART - when to initiate?

A

Often initiated AT THE TIME OF DIAGNOSIS - When patients present with AIDS-defining illness –> Low CD4 cell counts (

186
Q

HAART regimen?

A

3 drugs to prevent resistance:

2 NRTIs + preferrably an integrase inhibitor.

187
Q

PIs - mechanism?

A

Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts.
–> PIs prevent MATURATION of new viruses.

188
Q

Important about ritonavir?

A

Can “boost” other drug concentrations by inhibiting CYP450.

189
Q

PIs - toxicity?

A
  1. Hyperglycemia
  2. GI intolerance (nausea, diarrhea)
  3. Lipodystrophy (Cushing-like syndrome)
  4. Nephropathy (indinavir)
  5. Hematuria (indinavir)
190
Q

NRTIs - Mechanism?

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3-OH group).

191
Q

Important about tenofovir?

A

The only NRTI that is a nucleoTide - others are nucleoSides and need to be phosphorylated to be active.

192
Q

ZDV - clinical use?

A

It is used for general prophylaxis and during pregnancy to decr. risk of fetal transmission.

193
Q

NRTIs - Toxicity?

A
  1. Bone marrow suppression (reversed with G-CSF, erythropoietin)
  2. Peripheral neuropathy
  3. Lactic acidosis (nucleosides)
  4. Anemia (ZDV)
  5. Pancreatitis (Didanosine)
194
Q

NNRTIs - mechanism?

A

Bind to reverse transcriptase at site different from NRTIs.

Do NOT require phosphorylation to be active or compete with nucleotides.

195
Q

NNRTIs toxicity?

A
  1. Rash + hepatotoxicity –> Common to ALL NNRTIs.
  2. Vivid dreams and CNS symptoms –> common to efavirenz.
  3. Delavirdine + Efavirenz –> Contra in pregnancy.
196
Q

Raltegravir - mechanism?

A

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase.

197
Q

Raltegravir toxicity?

A

UP Creatine kinase.

198
Q

Efuvirtide - mechanism?

A

Binds gp41 - inhibiting viral entry.

199
Q

Maraviroc - mechanism?

A

Binds CCR5 on surface of T-cells/monocytes, inhibiting interaction with gp120.

200
Q

Enfuvirtide - toxicity?

A

Skin reaction at injection sites.

201
Q

Interferons - mechanism?

A

Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties.

202
Q

Interferons - IFN-alpha - clinical use?

A
  1. Chronic hep B/C
  2. Kaposi sarcoma
  3. Hairy cell leukemia
  4. Condyloma acuminatum
  5. Renal cell carcinoma
  6. Melanoma
203
Q

IFN-beta - clinical use?

A

MS

204
Q

IFN-gamma - clinical use?

A

Chronic granulomatous disease.

205
Q

Interferons - Toxicity?

A
  1. Neutropenia.
  2. Myopathy.
  3. Flu-like symptoms.
  4. Depression.
206
Q

Antibiotics to AVOID IN PREGNANCY:

A
  1. Sulfonamides
  2. Aminoglycosides
  3. Fluoroquinolones
  4. Clarithromycin
  5. Tetracyclines
  6. Ribavirin
  7. Griseofulvin
  8. Chloramphenicol

SAFe Children Take Really Good Care

207
Q

Sulfonamides in pregnancy?

A

Kernicterus

208
Q

Aminoglycosides in pregnancy?

A

Ototoxicity

209
Q

Fluoroquinolones in pregnancy?

A

Cartilage damage

210
Q

Clarithromycin in pregnancy?

A

Embryotoxic

211
Q

Tetracyclines in pregnancy?

A

Discolored teeth + inhibition of bone growth.

212
Q

Ribavirin in pregnancy?

A

Teratogenic

213
Q

Griseofulvin in pregnancy?

A

Teratogenic

214
Q

Chloramphenicol in pregnancy?

A

“Gray baby”

Microbiology (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions