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USMLE Step I > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Sulfonamides

  1. Mechanism
  2. Resistance
A

Bacteriostatic (Bactericidal when administered with Trimethoprim)

PABA analog that acts as a competitive antagonist against dihydrojpterate synthase. Inhibitor of folic acid biosynthesis which inhibits nucleic acid biosynthesis.

Resistance: mutations that result in alterations of target enzyme, decreased uptake, or increased PABA synthesis

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2
Q

Trimethoprim (Benzylpyrimidine)

  1. Mechanism
  2. Resistance
A

Bacteriostatic (Bactericidal when administered with Sulfonamides)

Inhibits dihydrofolate reductase. Inhibitor of folic acid biosynthesis which inhibits nucleic acid biosynthesis

Resistance: decreased influx, increased production of dihydrofolate reductase, decreased antibiotic binding affinity to dihydrofolate reductase

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3
Q

Fluoroquinolones

  1. Mechanism
  2. Resistance
A

Bactericidal

Inhibits DNA Gyrase (DNA Topoisomerase II) in gram negative bacteria → Prevents relaxation of the DNA strand as it is unwound by helicase

Inhibits DNA Topoisomerase IV in gram positive bacteria → Prevents separation of the replicated chromosomal DNA into daughter cells during cell division

Resistance: chromosome-encoded mutation in DNA gyrate which decreases the binding affinity of the antibiotic, plasmid mediated resistance, efflux pumps, decreased influx

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4
Q

Metronidazole

  1. Mechanism
  2. Resistance
A

Bactericidal

Pro-drug → the nitro group is chemically reduced by bacterial oxidoreductases to become active (mammalian cells lack the enzymes that reduce the pro-drug)

The reduced form of the drug causes damage to DNA strands

Resistance: observed but unknown

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5
Q

Rifamycins

  1. Mechanism
  2. Resistance
A

Bactericidal

Binds non-covalently to the β-subunit of DNA dependent RNA polymerase. Inhibits the initiation of transcription but does not inhibit transcription already in progress

Resistance: mutations that reduce drug binding to RNA polymerase.
Monotherapy rapidly leads to resistance

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6
Q

Chloramphenicol

  1. Mechanism
  2. Resistance
A

Bacteriostatic for most organisms
Bactericidal for H. influenzae, S. Pneumoniae, N. meningitidis

Inhibits elongation of the peptide chain during translation by inhibiting peptidyltransferase (forms peptide bonds between adjacent amino acids) in the 23S component of the 50S subunit

Resistance: decreased influx, plasmid-encoded acetyl transferase inactivates the drug

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7
Q

Clindamycin (Lincosamides)

  1. Mechanism
  2. Resistance
A

Bacteriostatic

Inhibits translocation (peptide transfer) during translation by binding to the P and A sites in the 50S subunit

Resistance: production of a methylase that modifies the ribosomal target and leads to decreased drug binding (ribosomal methylation)

Expression of MLS-B resistance can be constitutive or inducible. In inducible resistance, the bacteria produce inactive mRNA that is unable to encode methylase. The mRNA becomes active only in the presence of a macrolide inducer. By contrast, in constitutive expression, active methylase mRNA is produced in the absence of an inducer.

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8
Q

Linezoid (Oxazolidinones)

  1. Mechanism
  2. Resistance
A

Bacteriostatic (sometimes bactericidal)

Prevents initiation of translation by binding to the 50S ribosomal subunit and inhibiting the formation of the 70S ribosomal initiation complex

Resistance: point mutations of the 23 S rRNA component prevent binding of the drug

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9
Q

Macrolides

  1. Mechanism
  2. Resistance
A

Bacteriostatic

Inhibits translocation during translation by binding to the 23S rRNA component of the 50S subunit

Resistance: efflux via an ATP-dependent pump, production of a methylase that modifies the ribosomal target and leads to decreased drug binding (ribosomal methylation), hydrolysis by esterases, mutation of the 23S rRNA component of the 50S ribosomal subunit

Expression of MLS-B resistance can be constitutive or inducible. In inducible resistance, the bacteria produce inactive mRNA that is unable to encode methylase. The mRNA becomes active only in the presence of a macrolide inducer. By contrast, in constitutive expression, active methylase mRNA is produced in the absence of an inducer.

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10
Q

Streptogramins

  1. Mechanism
  2. Resistance
A

Bactericidal

Streptogramin A (Dalfopristin): binds to the 50S subunit and induces a conformational change in the subunit which enhances the binding of streptogramin B (quinupristin)

Streptogramin B (Quinupristin): inhibits translocation during translation by binding to 23S rRNA of the 50S subunit (occupies the same location as macrolides)

Resistance: production of a methylase that modifies the ribosomal target and leads to decreased drug binding (ribosomal methylation)
Active transport efflux and acetyltransferases are the mechanisms for resistance against Streptogramin A

Expression of MLS-B resistance can be constitutive or inducible. In inducible resistance, the bacteria produce inactive mRNA that is unable to encode methylase. The mRNA becomes active only in the presence of a macrolide inducer. By contrast, in constitutive expression, active methylase mRNA is produced in the absence of an inducer.

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11
Q

Aminoglycosides

  1. Mechanism
  2. Resistance
A

Bactericidal

Inhibits the initiation and translocation steps of translation and causes misreading of the mRNA.
Covalently binds to the 30S subunit to prevent formation of the initiation complex.

Resistance: acquisition of plasmid encoded inactivating enzymes - acetylases, adenylases, phosphorylases
decreased drug permeability / influx

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12
Q

Tetracyclines and Tigecycline

  1. Mechanism
  2. Resistance
A

Bacteriostatic

Inhibits elongation of the peptide chain during translation by preventing aminoacyl-tRNA from binding the A site of the ribosome.
Binds to the 30S subunit

Resistance: decreased intracellular accumulation due to decreased influx or acquisition of an energy dependent efflux mechanism, decreased access to the ribosome due to ribosome protecting proteins encoded by the TetO genes, enzymatic inactivation of the drug (TetX modification)

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13
Q

β-lactam antibiotics
(Penicillins, Cephalosporins, Carbapenems, Monobactams)
1. Mechanism
2. Resistance

A

Bactericidal

Structural analogs of D-alanyl-D-alanine that covalently (irreversibly) bind to transpeptidases (penicillin binding proteins) and prevent transpeptidase cross-linking of the peptidoglycan in the cell wall

Resistance: β-lactamase (penicillinase) inactivates the antibiotic, decreased drug permeability / influx, ATP-dependent efflux pumps, decreased binding affinity of the antibiotic to penicillin binding proteins (transpeptidases) through mutation or recombination

**Carbapenems are resistant to β-lactamases

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14
Q

β-lactamase-resistant antibiotics
(Nafcillin, Oxacillin, Methicillin, Flucloxacillin, Cloxacillin, Dicloxacillin)
1. Mechanism
2. Resistance

A

Bactericidal

Same mechanism of action as other β-lactam antibiotics, but they are resistant to β-lactamase because they have a bulky R group that blocks access of β-lactamase to the β-lactam ring

Resistance: decreased binding affinity of the antibiotic to penicillin binding proteins (transpeptidases) through mutation or recombination

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15
Q

Mechanism: β-lactamase inhibitors

A

Protect β-lactam antibiotics from destruction by β-lactamase (penicillinase)

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16
Q

Vancomycin

  1. Mechanism
  2. Resistance
A

Bactericidal for gram positive rods
Bacteriostatic for gram positive cocci

Binds the D-ala-D-ala terminus of the muerin monomer of cell wall precursors which inhibits the attachment of disaccharide subunits to the pre-existing cell wall

Resistance: acquisition of the vancomycin HAX genes - replace the terminal D-ala-D-ala normally found at the end of the pentapeptide chain (where vancomycin binds) with D-lactate

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17
Q

Mechanism: Polymyxins

A

Bactericidal

Cationic detergents that disrupt the membranes of gram negative bacteria

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18
Q

Mechanism: Daptomycin

A

Bactericidal: VRE
Bacteriostatic: S. pneumoniae, S. aureus

Lipopeptide that disrupts the cell membrane of gram positive cocci. It inserts into the cell membrane and aggregates which creates holes in the membrane that leak ions. This causes rapid depolarization resulting in a loss of membrane potential which inhibits protein, DNA, and RNA synthesis and leads to cell death.

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19
Q

Isoniazid (INH)

  1. Mechanism:
  2. Resistance:
  3. Toxicity:
  4. Pharmacokinetics
A

Bacteriostatic

Inhibits the synthesis of mycolic acids which are essential components of the mycobacterial cell wall and are unique to mycobacteria

Resistance: mutations leading to the under expression of KatG

Toxicity: neurotoxicity and hepatotoxicity
Pyridoxine (vitamin B6) can prevent neurotoxicity

Pharmacokinetics: inactivated by acetylation
The rate of acetylation (different for each patient) determines the drug’s effectiveness

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20
Q

Ethambutol (EMB)

  1. Mechanism:
  2. Toxicity:
A

Bacteriostatic
Only effective aganist mycobacteria

Inhibits the polymerization of arabinogalactan in the cell wall by inhibiting arabinosyltransferase

Toxicity: optic neuropathy (red-green color blindness)

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21
Q

Pyrazinamide (PZA)

  1. Mechanism:
  2. Toxicity:
A

Bacteriostatic

Prodrug → converted into the active compound pyrazinoic acid by pyrazinamidase in tuberculosis.
Unknown mechanism - maybe inhibits mycobacterial fatty acid synthase I (FAS-I) gene involved in mycolic acid biosynthesis

Toxicity: hyperuricemia, hepatotoxicity

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22
Q

Dapsone

  1. Mechanism
  2. Toxicity:
  3. Pharmacokinetics
A

Bacteriostatic

Inhibits folate synthesis (same mechanism as sulfonamides)

Toxicity: hemolysis at doses >200mg/day, GI intolerance, fever, pruritus, erythema nodosum leprosum may develop during therapy

Pharmacokinetics: acetylated in the liver by the same enzymes as INH, 70-80% is excreted in the urine

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23
Q

Clinical Use: Sulfonamides

A

Broad spectrum

Nocarida, Chlamydia

Combination therapy with TMP (TMP-SMX):
Urinary tract infections
Cellulitis
Pneumocystis jirovecii pneumonia or toxoplasmosis prophylaxis in HIV patients
Shigella, Salmonella
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24
Q

Clinical Use: Trimethoprim

A

Broad spectrum

Combination therapy with TMP (TMP-SMX):
Urinary tract infections
Cellulitis
Pneumocystis jirovecii pneumonia or toxoplasmosis prophylaxis in HIV patients
Shigella, Salmonella
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25
Clinical Use: Fluoroquinolones
Gram-negative rods of the urinary and GI tracts including Pseudomonas and Neisseria
26
Clinical Use: Metronidazole
Treats anaerobic infections below the diaphragm (ex: C. difficile) Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis Used with a proton pump inhibit and clarithromycin for "triple therapy" against H. pylori
27
Clinical Use: Rifamycins
Mycobacterium tuberculosis, Neisseria Used in combination with Dapsone for Leprosy Prophylaxis for meningitis from meningococci and H. influenzae
28
Clinical Use: Chloramphenicol
Meningitis: H. influenzae, Neisseria meningitidis, S. pneumoniae Rocky Mountain Spotted Fever (Rickettsia rickettsii)
29
Clinical Use: Clindamycin
Treats anaerobic infections above the diaphragm (aspiration pneumonia, lung abscess, oral infections)
30
Clinical Use: Linezoid
Treats MRSA, VRE | Gram positive organisms
31
Clinical Use: Macrolides
Atypical pneumonias (Mycoplasma, Chlamydia, Legionella) STI (Chlamydia) B. pertussis Gram positive cocci
32
Clinical Use: Streptogramins
VRE
33
Clinical Use: Aminoglycosides
Severe gram negative rod infections Synergistic with β-lactam antibiotics Pseudomonas aeruginosa
34
Clinical Use: Tetracyclines
Drug is able to accumulate intracellularly - effective against Rickettsia and Chlamydia Borrelia burgdorferi, M. pneumoniae Treats acne Tigecycline: MRSA
35
Clinical Use: Penicillin G, V
Gram positive cocci, gram positive rods, gram negative cocci, and spirochetes (T. pallidum)
36
Clinical Use: Amoxicillin, ampicillin
Wider spectrum than penicillin | H. pylori, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, and enterococci
37
Clinical Use: β-lactamase-resistant antibiotics | Nafcillin, Oxacillin, Methicillin, Flucloxacillin, Cloxacillin, Dicloxacillin
Narrow spectrum | S. aureus
38
Clinical Use: Anti-pseudomonals | Piperacillin, Ticarcillin
Pseudomonas aeruginosa | Gram negative rods
39
Clinical Use: Cephalosporins (I) | Cefazolin, Cephalexin
Narrow spectrum Gram positive cocci (staphylococci and streptococci) Proteus mirabilis, E. coli, Klebsiella pneumoniae Cefazolin: Antibiotic prophylaxis against S. aureus for surgical procedures Cephalexin: recommended for mild foot infections in diabetics
40
Clinical Use: Cephalosporins (II) | Cefoxitin, Cefaclor, Cefuroxime
Gram positive cocci | H. influenzae, Enterobacter aerogenes, Neisseria, Proteus mirabilis, E. coli, Klebsiella pneumoniae, Sebratia marcescens
41
Clinical Use: Cephalosporins (III) | Ceftriaxone, Cefotaxime, Ceftazidime
Serious gram negative organisms resistant to other β-lactams Ceftriaxone: meningitis, gonorrhea, disseminated lyme disease. Primary choice for Neisseria gonorrhea and Neisseria meningitis Ceftazidime: Pseudomonas aeruginosa
42
Clinical Use: Cephalosporins (IV) | Cefepime
Broad spectrum | Increased activity against Pseudomonas aeruginosa
43
Clinical Use: Cephalosporins (V) | Ceftaroline
Broad spectrum MRSA Does not cover Pseudomonas aeruginosa
44
Clinical Use: Carbapenems | Imipenem, Meropenem, ertapenem, Doripenem
Wide spectrum | Gram positive cocci, gram negative rods, anaerobes
45
Clinical Use: Monobactams | Aztreonam
Gram negative rods only No activity against gram positive organisms or anaerobes Used for patients allergic to PCN (no cross-allergenicity with PCN) or for patients with severe renal insufficiency who cannot tolerate aminoglycosides
46
Clinical Use: Vancomycin
Gram positive organisms only | C. difficile, MRSA, S. epidermis, sensitive enterococcus species
47
Clinical Use: Daptomycin
MRSA VRE (not first choice) Cases of bacteremia or endocarditis
48
Treatment of MRSA
``` Ceftaroline (5th Gen Cephalosporin) Clindamycin Daptomycin Linezolid Tigecycline Vancomycin ```
49
Treatment of VRE
Linezolid | Streptogramins
50
Treatment of Pseudomonas aeruginosa
``` Aminoglycosides Carbapenems (ertapenem) Piperacillin Ticarcillin Fluoroquinolones Ceftazidime (3rd Gen) Cefepime (4th Gen) ``` For multi-drug resistant strains: polymyxins B and E (colistin)
51
Treatment of Mycoplasma tuberculosis
Prophylaxis: Isoniazid Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol
52
Treatment of Mycoplasma avium
Prophylaxis: Azithromycin, Rifabutin Treatment: Azithromycin or clarithromycin with ethambutol. Can add rifabutin or ciprofloxacin
53
Treatment of Mycoplasma leprae
Tuberculoid form: dapsone and rifampin | Lepromatous form: dapsone, rifampin, and clofazimine
54
β-lactam antibiotics: Penicillin 1. Toxicity 2. Pharmacokinetics
Toxicity: hypersensitivity reactions, hemolytic anemia, diarrhea (infants) Pharmacokinetics: renal secretion Route: G = IV, IM; V = PO Amoxicillin is more completely absorbed after oral administration than ampicillin
55
β-lactam antibiotics: Cephalosporins 1. Toxicity 2. Pharmacokinetics
Toxicity: hypersensitivity reactions (do not use in patients allergic to penicillin), autoimmune hemolytic anemia, vitamin K deficiency (bleeding) Bleeding: Hypoprothrombinemia, thrombocytopenia, and/or platelet dysfunction Nephrotoxicity: especially when used in combination with aminoglycosides Disulfiram-like alcohol reaction: flushing, hypotension, tachycardia, dyspnea, nausea, vomiting Pharmacokinetics: first generation drugs do not cross the BBB
56
β-lactam antibiotics: Carbapenems 1. Toxicity 2. Pharmacokinetics 3. Unique feature of Meropenem
Toxicity: GI distress, skin rash, and seizures Pharmacokinetics: rapidly hydrolyzed (inactivated) by renal tubule dipeptidase *Given in combination with cilastatian (a renal dehydropeptidase inhibitor) as Primaxin Route: IV only 3. Meropenem is structurally related to imipenem, but is less susceptible to hydrolysis by renal tubule dipeptidase. Does not require cilastatian to achieve therapeutic concentrations and is less nephrotoxic than imipenem
57
Vancomycin 1. Toxicity 2. Pharmacokinetics
Toxicity: nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing (redman syndrome), tissue necrosis if given IM, and neutropenia Pharmacokinetics: Renal elimination Route: administer IV; poorly absorbed from the GI tract
58
Daptomycin 1. Toxicity 2. Pharmacokinetics
Toxicity: rhabdomyolysis (increase in CPK), myopathy, nephrotoxicity Pharmacokinetics: primarily renal elimination Does not cross the BBB Route: IV injection only Do not administer IM because there is a toxic effect on muscles
59
Polymyxins 1. Toxicity 2. Pharmacokinetics
Toxicity: associated with severe nephrotoxicity Pharmacokinetics: often used topically or in ophthalmic and otic drops
60
Aminoglycosides 1. Toxicity 2. Pharmacokinetics
Toxicity: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogen Pharmacokinetics: rapid renal excretion
61
Tetracyclines 1. Toxicity 2. Pharmacokinetics
Toxicity: GI distress, IV administration can lead to venous thrombosis, IM administration causes painful local irritation, Renal and hepatic toxicity, photosensitivity Teratogen: treatment of pregnant women or children less than 8 can result in permanent tooth discoloration, bone deformation, and growth retardation in the child Pharmacokinetics: Tetracycline: absorption is impaired by food, diary products, antacids, and supplements containing divalent and multivalent cations, and by alkaline pH. This is not a problem for doxycycline or minocycline All penetrates the CNS Doxycycline is primarily eliminated through the feces Tetracycline and minocycline is primarily eliminated by the kidneys
62
Chloramphenicol 1. Toxicity 2. Pharmacokinetics
Toxicity: Normocytic Anemia due to erythroid suppression of the bone marrow (dose dependent), aplastic anemia (dose independent) Gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase - inadequate metabolism): presents as vomiting, flaccidity, hypothermia, respiratory distress, gray pallor, and shock. Drug interactions: Inhibits CYP3A4 May prolong the T-1/2 of drugs normally metabolized by these enzymes Competitively antagonizes the effects of macrolides and clindamycin because chloramphenicol binds to a similar position in the ribosome Pharmacokinetics: penetrates the CNS
63
Clindamycin 1. Toxicity 2. Pharmacokinetics
Toxicity: pseudomembranous colitis, fever, diarrhea Pharmacokinetics: does not penetrate the BBB
64
Oxazolidinones (Linezolid) 1. Toxicity 2. Pharmacokinetics
Toxicity: Serotonin syndrome - inhibits monamine oxidase (MAO) GI: nausea, vomiting, diarrhea Thrombocytopenia, anemia, myelosuppression
65
Macrolides 1. Toxicity 2. Pharmacokinetics
Toxicity: Gastrointestinal Motility issues, Arrhythmia caused by prolonged QT interval, acute cholestatic hepatitis, Rash, eosinophilia. Increases serum concentration of theophyllines, oral anticoagulants. Clarithromycin and erythromycin inhibit cytochrome P-450 Pharmacokinetics: Elimination: erythromycin and azithromycin primarily liver; clarithromycin renal and non-renal Erythromycin is inactivated by gastric acid, but is absorbed in upper small intestine
66
Trimethoprim 1. Toxicity 2. Pharmacokinetics
Toxicity: Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid)
67
Sulfonamides 1. Toxicity 2. Pharmacokinetics
Toxicity: Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g., warfarin)
68
Fluoroquinolones 1. Toxicity 2. Pharmacokinetics
Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Less commonly, can cause leg cramps and myalgias. Contraindicated in pregnant women, nursing mothers, and children Contraindicated in patients >60 taking prednisone
69
Metronidazole | 1. Toxicity
Toxicity: headache, metallic taste | Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol
70
Rifamycins 1. Toxicity 2. Pharmacokinetics
Toxicity: Minor hepatotoxicity and drug interactions (􏰊cytochrome P-450); orange body fluids (nonhazardous side effect). Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation **Rifampin ramps up cytochrome P-450, but rifabutin does not**

USMLE Step I (4 decks)

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