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USMLE > Antibiotics First Aid > Flashcards

Antibiotics First Aid Flashcards

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USMLE® Step 1 flashcards
1
Q

What drugs have the mechanism of action to block cell wall synthesis by inhibition of peptidoglycan cross linking?

A

Penicillin, Methicillin, Ampicillin, Piperacillin, Cephalosporins, Aztreonam, imipenam

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2
Q

What drugs have the mechanism of action to block peptidoglycan synthesis?

A

Bacitracin

Vancomycin

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3
Q

What drugs have the mechanism of action to block nucleotide synthesis?

A

Sulfonamides

Trimethoprim

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4
Q

What drugs have the mechanism of action to block DNA topoisomerases?

A

Fluoroquinolones

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5
Q

What drugs have the mechanism of action to block mRNA synthesis?

A

Rifampin

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6
Q

What drugs have the mechanism of action to damage DNA?

A

Metronidazole

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7
Q

What drugs have the mechanism of action to block protein synthesis at 50S ribosomal subunit?

A

Choramphenicol, macrolides, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid

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8
Q

What drugs have the mechanism of action to block protein sysnthesis at 30S ribosomal subunit?

A

Aminoglysosides

Tetracyclines

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9
Q

Mechanism of Penicillin?

A
  1. Bind penicillin-binding proteins
  2. Block transpeptidase cross-linking of peptidoglycan
  3. Activate autolytic enzymes
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10
Q

Clinical use of Penicillin

A

Mostly for gram-pos organisms (S. pneumoniae, S. pyogenes, Actinomyces) and syphilis.

Bactericidal for gram-pos cocci, gram-pos rods, gram (-) cocci, and spirochetes.

Not penicillinase resistant

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11
Q

Penicillin toxicity?

A

Hypersensitivy reactions

Hemolytic anemia

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12
Q

What causes penicillin resistance?

A

B-lactamases cleaving B-lactan ring

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13
Q

Drugs that are penicillinase-resistant penicillins?

A

Methicillin

Nafcillin

Dicloxacillin

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14
Q

Mechanism for penicillin-resistant penicillins

A

Same as penicillin. Narrow spectrum; penicillinase resistant because of bulkier R group.

“Use naf (nafcillin) for staph”

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15
Q

Clinical use for penicillinase-resistant penicillins

A

S. aureus (except MRSA; resistant because of altered PBP protein target site)

“Use naf (nafcillin) for staph”

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16
Q

Toxicity of penicillinase-resistant penicillins

A

Hypersensitivity reactions

Methicillin –> interstitial nephritis

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17
Q

Ampicillin and amoxicillin are what type of penicillin?

A

Aminopenicillins

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18
Q

Mechanism for aminopenicillin

A

Same as penicillin

Wider spectrum; penicillinase sensitive

Also combine with clavulanic acid to protect against B-lactamase.

Amoxicillin has greater oral bioavailability than ampicillin

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19
Q

Clinical use of aminopenicillins

A

Extended-spectrum penicillin - H. influenzae, E.coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci.

“Ampicillin/amoxicillin HELPSS kill enterococci”

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20
Q

Toxicity of aminopenicillins

A

Hypersensitivy reactions

Ampicillin rash

Pseudomembranous colitis

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21
Q

What causes resistance to aminopenicillins (amoxicillin/ampicillin)?

A

B-lactamases

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22
Q

What drugs are antipseudomonals?

A

Ticarcillin

Carbenicillin

Piperacillin

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23
Q

Mechanism of action of ticaricillin, carbenicillin, peperacillin?

A

Same as penicillin

Extended spectrum

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24
Q

Clinical use of antipseudomonals

A

Pseudomonas species and gram (-) rods; susceptible to penicillinase; use with clavulanic acid

TCP: Takes Care of Pseudomonas

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25
Q

Toxicity of antipseudomonals

A

Hypersensitivy reactions

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26
Q

What are the B-lactamse inhibitors?

A

Clavulonic Acid, Sulbactam, Tazobactam.

Often added to penicillin abx to protect the abx from destruction by B-lactamase (penicillinase)

CAST

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27
Q

Mechanism of Cephalosporins

A

B-lactam drugs that inhibit cell wall synthesis

BUT less susceptible to penicillinase.

Bactericidal

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28
Q

What are the organisms not covered by cephalosporins?

A

Listeria, Atypicals (Chlamydia and Mycoplasma), MRSA, and Enterococci

LAME

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29
Q

Clinical use for 1st generation cephalosporins and drugs of 1st gen?

A

Cefazolin and cephalexin

Gram (+) cocci, Proteus mirabilis, E. coli, Klebsiella pneumonia

PEcK

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30
Q

Clinical use for 2nd gen cephalosporins and the drugs for it

A

Cefoxitin, Cefaclor, cefuroxime

Gram (+) cocci, H. influenzae, Enterobacter aerogenes, Neisseria spp, Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescans.

HEN PEcKS

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31
Q

Clinical use for 3rd gen cephalosporins and the drugs for it

A

Ceftriaxone, cefotaxime, ceftazidime

Serious gram (-) infections resistant to other B-lactams

Ceftriaxone: meningitis and gonorrhea

Ceftazidime: Pseudomonas

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32
Q

Clinical use for 4th gen cephalosporins and drugs for it

A

Cefepime

Increased activity against Pseudomonas and gram (+) organisms

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33
Q

Cephalosporin toxicity

A

Hypersensitivy reactions, vit K deficiency.

Cross-hypersensitivy with penicillin occurs in 5-10% of patients.

Increased nephrotoxicity of aminoglycosides; disulfiram-like reaction with ethanol (in cephalosporins with a methltheitetrazole group, eg cefamandole)

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34
Q

Mechanism of action for Aztreonam

A

A monobactam resistant to B-lactamases.

Inhibits cell wall synthesis (binds to PBP3).

Synergistic with aminoglycosides.

No cross-allergenicity with penicillins

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35
Q

Clinical use for Aztreonam

A

Gram-negative rods only

No activity against gram (+) or anaerobes.

For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides

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36
Q

Toxicity of Aztreonam

A

Usually nontoxic; occasional GI upset.

No cross-sensitivity with penicillins or cephalosporins

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37
Q

Mechanism of action for Imipenem/cilastatin and meropenem

A

Imipenem is a broad-spectrum, B-lactamase resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules

With imipenem, “the kill is LASTIN’ with ciLASTATIN”

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38
Q

Clinical use for imipenem/cilastatin and meropenem

A

Gram (+) cocci, gram (-) rods, and anaerobes.

Wide spectrum, but significant side effects limit use to life-threatening infections, or after other drugs have failed.

Meropenem, however, has a reduced risk of sezures and is table to dehydropeptidase I.

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39
Q

Toxicity of imipenem/cilastatin and meropenem

A

GI distress

Skin rash

CNS toxicity (seizures) at high plasma level

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40
Q

Mechanism of Vancomycin

A

Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors.

Bactericidal

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41
Q

Clinical use for Vancomycin

A

Gram-positive only - serious, multidrug-resistant organisms, including S. aureus, enterococci, and C.difficile (oral dose for pseudomembranous colitis)

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42
Q

Toxicity for Vancomycin

A

Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing - “red man syndrome” (can largely prevent by pretreatment with antihistamines and slow infusion rate). Well tolerated in general - does NOT have many problems

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43
Q

What causes resistance to Vancomycin?

A

Occurs with amino acid change of D-ala D-ala to D-ala D-lac.

“Pay back 2 D-alas (dollars) for vandalizing”

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44
Q

What antibiotic drugs are 30S inhibitors?

A

Aminoglycosides

Tetracyclines

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45
Q

What antibiotics are 50S inhibitors?

A

Chloramphenicol

Clindamycin [bacteriostatic]

Erythromycin (macrolides) [bacteriostatic]

Liniezolid (variable)

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46
Q

What drugs are aminoglycosides?

A

Gentamycin, Neomycin, Amikacin, Tobramycin, Streptomycin

“Mean” GNATS canNOT kill anaerobes

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47
Q

Mechanism of aminoglycosides

A

Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA.

Require O2 for uptake; therefore ineffective against anerobes.

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48
Q

Clinical use of aminoglycosides

A

Severe gram (-) rod infections.

Synergistic with B-lactam abx

Neomycin for bowel surgery.

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49
Q

Toxicity of aminoglycosides

A

Nephrotoxicity (especially when used with cephalosporins)

Ototoxicity (especially when used with loop diuretics)

Teratogen

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50
Q

How is resistance to aminoglycosides developed?

A

Transferase enzymes that inactivate the drug by:

Acetylation

Phosphorylation

Adenylation

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51
Q

What drugs are tetracylines?

A

Tetracyline, doxycycline, demeclocycline, minocycline

“Demeclocycline - ADH antagonist; acts as a Diuretic in SIADH”

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52
Q

Mechanism of Tetracyclines

A

Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration

Doxycycline is fecally eliminated and can be used in patients with renal failure.

Must NOT take with milk, antacids, or iron-containing preparatins because divalent cations inhibit absorption in the gut.

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53
Q

Clinical use of Tetracyclines

A

Borrelia burgdorferi, M. pneumoniae.

Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia

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54
Q

Toxicity of Tetracycline

A

GI distress

Discoloration of teeth and inhibition of bone growth in children

Photosensitivity

Contraindicated in pregnancy

55
Q

How is resistance to tetracyclines developed?

A

Decrease uptake into cells or increase efflux out of cell by plasmid0encoded transport pumps

56
Q

What drugs are macrolides?

A

Azithromycin

Clarithromycin

Erythromycin

“ACE”

57
Q

Mechanism of macrolides

A

Inhibit protein synthesis by blocking translocation (“macroSlides”)

Bind to 23S rRNA of the 50S ribosomal subunit

Bacteriostatic

58
Q

Clinical use of Macrolides

A

Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), URIs, STDs, gram (+) cocci (streptococcal infections in patients allergic to penicillin, and Neisseria

59
Q

Toxicity of Macrolides

A

Prolonged QT interval (especially erythromycin), GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis, eosinophila, skin rashes.

Increases serum concentration of theophyllines, oral anticoagulants

60
Q

How is resistance to macrolides developed?

A

Methylation of 23S rRNA binding site

61
Q

Mechanism of Chloramphenicol

A

Blocks peptide bond formation at 50S

Bacteriostatic

62
Q

Clinical use of Chloramphenicol

A

Meningitis (H. influenzae, Neisseria meningitidis, S. pneumoniae)

63
Q

Toxicity of Chloramphenicol

A

Anemia, anaplastic anemia (both dose dependent)

Gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase)

64
Q

How is resistance to Chloramphenicol developed?

A

Plasmid-encoded acetyltransferase that inactivates drug

65
Q

Mechanism of Clindamycin

A

Blocks peptide formation at 50S

Bacteriostatic

66
Q
A
66
Q

Clinical use of Clindamycin

A

Anaerobic infections (e.g Bacteroides fragilis, Clostridium perfringens) in aspiration pneumonia or lung abscesses

Treats anaerobes above the diaphragm vs metronidazole (anaerobic infections below diaphragm)

67
Q

Toxicity of Clindamycin

A

Pseudomonas colitis (C. difficile overgrowth)

Fever

Diarrhea

68
Q

What drugs are Sulfonamides?

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

69
Q

Mechanism of sulfonamides

A

PABA antibmetabolites inhibit dihydropteroate synthase.

Bacteriostatic

70
Q

Clinical use of Sulfonamides

A

Gram (+), gram (+), Nocardia, Chlamydia.

Triple sulfas or SMX for simple UTI

71
Q

Toxicity of sulfonamides

A

Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (eg warfarin)

72
Q

How is resistance to sulfonamides developed?

A

Altered enzyme (bacterial dihydropteroate synthase), decrease uptake, or increased PABA synthesis

73
Q

Mechanism of Trimethoprim

A

Inhibits bacterial dihydrofolate reductase

Bacteriostatic

Trimethoprim = TMP: “Treats Marrow Poorly”

74
Q

Clinical use of Trimethoprim

A

Used in combo with sulfonamides (TMP-SMX) causing sequential block of folate synthesis.

Combination used for UTIs, Shigella, Salmonella, Pneumosystis jiroveci pneumonia

75
Q

Toxicity of Trimethoprim

A

Megaloblastic anemia, leukopenia, granulocytopenia

May alleviate with supplemental folinic acid (leucovorin rescue)

76
Q

What drugs are fluoroquinolones?

A

Ciprofloxacin, norfloxacin, levofloxacin, moxifloxacin, enoxacin, nalidixic acid (a quinolone)

“-floxacin”

77
Q

Mechanism of fluroquinolones

A

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

78
Q

Toxicity of Fluoroquinolones

A

GI upset, superinfections, skin rashes, headache, dizziness.

Contraindicated in pregnant women and in children because animal studies show dmg to cartilage.

Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids

“FluoroquinoLONES hurt attachments to your BONES”

79
Q

Resistance mechanism to fluoroquinolones

A

Chromosome-encoded mutation in DNA gyrase

80
Q

Mechanism of Metrodinazole

A

Forms free radical toxic metabolites in the bacterial cell that damage DNA.

Bactericidal, antiprotazoal

81
Q

Clinical use of Metrodinazole

A

Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. difficile).

Used with bismuth and amoxicillin (or tetracycline) for “triple therapy” against H. Pylori

“GET GAP on the METRO!”

Anaerobic infection below the diaphragm

82
Q

Toxicity of Metronidazole

A

Disulfiram-like reaction with alcohol; headache, metallic taste

83
Q

Prophylaxis for M. tuberculosis

A

Isoniazid

84
Q

Treatment for M. tuberculosis

A

Rifampin, Isoniazid, Pyrazinamide, Ethambutol

RIPE

85
Q

Prophylaxis for M. avium-intracellulare

A

Azithromycin

86
Q

Treatment for M. avium intracellulare

A

Azithromycin, rifampin, ethambutol, streptomycin

87
Q

Treatment for M. leprae

A

Dapsone, rifampin, clofazimine

88
Q

Mechanism of INH

A

Decrease synthesis of mycolic acids.

Bacterial catalase peroxidase (KatG) needed to convert INH to active metabolite

89
Q

Clinical use of INH

A

M. tuberculosis. Only agent used as solo prophylaxis against TB

90
Q

Toxicity of INH

A

Neurotoxicity, hepatoxicity, lupus.

Pyridozine (vitamine B6) can prevent neurotoxicity, lupus

“INH Injures Neurons and Hepatocytes”

91
Q

Mechanism of rifampin

A

Inhibits DNA-dependent RNA polymerase

Rifampin 4 R’s:

RNA polymerase inhibitor

Revs up microsomal P450

Red/orange bloody fluids

Rapid resistance if used alone

92
Q

Clinical use of rifampin

A

M. tuberculosis

Delays resistance to dapsone when used for leprosy.

Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H. influenzae type B

93
Q

Toxiciy of rifampin

A

Minor hepatotoxicity and drug interactions (increase P450)

Orange body fluids (nonhazardous)

94
Q

Mechanism and clinical use of Pyrazinamide

A

Inhibits mycolic acid production by pyrazinamidase

Effective in acidic pH of phyagolysosomes, where TB engulfed by macrophages is found

M. tuberculosis

95
Q

Toxicity of Pyrazinamide

A

Hyperuricemia

Hepatoxicity

96
Q

Mechanism and clinical use of Ethambutol

A

Decrease carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

M. tuberculosis

97
Q

Toxicity of Ethambutol

A

Optic neuropathy (red-green color blindness)

98
Q

Meningococcal infection prophylaxis

A

Ciprofloxacin (DOC)

Rifampin

Minocycline

99
Q

Prophylaxis for gonorrhea

A

Ceftriaxone

100
Q

Prophylaxis for syphillis

A

Benzathine penicillin G

101
Q

Propylaxis for recurrent UTIs

A

TMP-SMX

102
Q

Prophylaxis for Endocarditis with surgery/dental procedures

A

Penicillins

103
Q

Treatment for MRSA

A

vancomycin

104
Q

Treatment for VRE

A

Linezolid and streptogramins (quinupristin/dalfopristin)

105
Q

Empiric therapy for CAP in outpatient setting

A

Macrolides

106
Q

Empiric therapy for CAP in inpatient setting

A

Fluoroquinolones

107
Q

Empiric therapy for CAP in ICU setting

A

B-lactam + fluoroquinolone/azithromycin

108
Q

Mechanism of Amphotericin B

A

Binds ergosterol (unique to fungi)

Forms membrane pores that allow leakage of electrolytes

Disrupts membrane function

109
Q

Clinical use for Amphotericin B

A

Serious, systemic mycoses

Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses).

1st line treatment for cryptococcal meningitis

Intrathecally for fungal meningitis

Supplement K and Mg because of altered renal tubule permeability

110
Q

Toxicity of Amphotericin B

A

Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmieas, anemia, IV phlebitis (“amphoterrible”).

Hydration reduces nephrotoxicity

Liposomal amphotericin reduces toxicity

111
Q

Mechanism of Nystatin

A

Same as amphotericin B. Topical form because too toxic for systemic use

112
Q

Clinical use for Nystatin

A

“Swish and swallow” for oral candidiasis (thrush)

Topical for diaper rash and vaginal candidiasis

113
Q

Name a couple -azoles

A

Fluconazole

ketoconazole

miconazole

itraconazole

114
Q

Mechanism of “-azoles”

A

Inhibit fungal sterol (ergosterol) synthesis, by inhibiting the P450 enzyme that converts lanosterol to ergosterol

115
Q

Clinical use of “-azoles”

A

Systemic mycoses

Fluconazole for cryptococcal meningitis in AIDS and candidal infections of all types

Ketoconazole for Blastomyces, Coccidioides, Histoplasma, Candida albicans; hypercortisolism

Clotrimazole and miconazole for topical fungal infections

116
Q

Toxicity of “-azoles”

A

Hormone synthesis inhibition (gynecomastia), liver dysfucntion (inhibits P450), fever, chills

117
Q

Mechanism of Flucytosine

A

Inhibits DNA synthesis by conversion to 5-FU by cytosine deaminase

118
Q

Clinical use of Flucytosine

A

Used in systemic fungal infections (e.g Cryptococcus) in combination with amphotericin B

119
Q

Toxicity of Flucystosine

A

Nausea, vomiting, diarrhea, bone marrow suppression

120
Q

Mechanism of Caspofungin

A

Inhibits cell wall synthesis by inhibiting synthesis of B-glucan

121
Q

Clinical use of Caspofungin

A

Invasive aspergillosis, Candida

122
Q

Toxicity of Caspofungin

A

GI upset

Flushing

123
Q

Mechanism of Terbinafine

A

Inhibits fungal enzyme squalene epoxidase; inhibits ergosterol synthesis

124
Q

Clinical use of Terbinafine

A

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

125
Q

Toxicity of Terbinafine

A

Abnormal LFTs

Visual disturbances

126
Q

Mechanism of Griseofulvin

A

Interferes with microtubule function; disrupts mitosis

Deposits in keratin containing tissues (eg nails)

127
Q

Clinical use of Griseofulvin

A

Oral treatment of superficial infections

Inhibits growth of dermatophytes (tinea, ringworm)

128
Q

Toxicity of Griseofulvin

A

Teratogenic, carcinogenic, confusion, headaches, increase P450 and warfarin metabolism

129
Q

What is the antiprotozoan therapy?

A

Pyrimethane: toxoplasmosis or Plasmodium falciparum

Suramin and melarsoprol: Trypanosoma brucei

Nifurtimox: T. cruzi

Sodium stibogluconate: leshmaniasis

130
Q

Mechanism of Chloroquine

A

Blocks plasmodium heme polymerase

131
Q

Clinical use for Chloroquine

A

Plasmodium species

Also mefloquine (for treatment/ppx)

Quinine for resistant species in combination with pyrimethamine/sulfonamide

132
Q

Toxicity of Chloroquine

A

Retinopathy

G6PD hemolysis

133
Q

What is the antihelminthic therapy?

A

Mebendazole

Pyrantel pamoate

Ivermectin

Diethylcarbamazine

Praziquantel

(Immobilize helminths)

USMLE (2 decks)

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