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Step 1 Pharmacology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are Penicillin G and V?

A

Penicillin G (IV and IM form), penicillin V (oral). Prototype β-lactam antibiotics.

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2
Q

What is the mechanism of Penicillin G and V?

A

▪ Bind penicillin-binding proteins (transpeptidases).
▪ Block transpeptidase cross-linking of peptidoglycan.
▪ Activate autolytic enzymes.

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3
Q

What are the clinical uses of Penicillin G and V?

A

Mostly used for gram-positive organisms (S. pneumoniae, S. pyogenes, Actinomyces). Also used for N. meningitidis and T. pallidum. Bactericidal for gram-positive cocci, gram-positive rods, gram-negative cocci, and spirochetes. Penicillinase sensitive.

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4
Q

What are the toxicities of Penicillin G and V?

A

Hypersensitivity reactions, hemolytic anemia.

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5
Q

What are the resistances of Penicillin G and V?

A

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

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6
Q

What is the mechanism of Ampicillin and amoxicillin (aminopenicillins, penicillinase-sensitive penicillins)?

A

Same as penicillin. Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against β-lactamase.

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7
Q

What are the clinical uses of Ampicillin and amoxicillin (aminopenicillins, penicillinase-sensitive penicillins)?

A

Extended-spectrum penicillin—Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci. (HELPSS kill enterococci)

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8
Q

What are the toxicities of Ampicillin and amoxicillin (aminopenicillins, penicillinase-sensitive penicillins)?

A

Hypersensitivity reactions; rash; pseudomembranous colitis.

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9
Q

What is the mechanism of resistance of Ampicillin and amoxicillin (aminopenicillins, penicillinase-sensitive penicillins)?

A

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

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10
Q

What is a major difference between Ampicillin and amoxicillin?

A

Amoxicillin has greater Oral bioavailability

than ampicillin.

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11
Q

What is the mechanism of Oxacillin, nafcillin, and dicloxacillin (penicillinase-resistant penicillins)?

A

Same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.

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12
Q

What is the clinical use of Oxacillin, nafcillin, and dicloxacillin (penicillinase-resistant penicillins)?

A

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

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13
Q

What is the toxicity of Oxacillin, nafcillin, and dicloxacillin (penicillinase-resistant penicillins)?

A

Hypersensitivity reactions, interstitial nephritis.

Ticarcillin,

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14
Q

What is the mechanism of Ticarcillin and piperacillin (antipseudomonals)?

A

Same as penicillin. Extended spectrum.

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15
Q

What is the clinical use of Ticarcillin and piperacillin (antipseudomonals)?

A

Pseudomonas spp. and gram-negative rods; susceptible to penicillinase; use with β-lactamase inhibitors.

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16
Q

What is the toxicity of Ticarcillin and piperacillin (antipseudomonals)?

A

Hypersensitivity reactions

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17
Q

What are the β-lactamase inhibitors?

A

CAST - Include Clavulanic Acid, Sulbactam, Tazobactam. Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase).

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18
Q

What is the mechanism of Cephalosporins (generations I, II, III, IV, V)?

A

β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

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19
Q

What organism are not covered by Cephalosporins?

A

LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci. Exception: ceftaroline covers MRSA.

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20
Q

What is the clinical use of 1st generation Cephalosporins (cefazolin, cephalexin)?

A

1st generation—PEcK.
Gram-positive cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections.

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21
Q

What is the clinical use of 2nd generation Cephalosporins (cefoxitin, cefaclor, cefuroxime)?

A 
2nd generation—HEN PEcKS.
2nd generation (cefoxitin, cefaclor, cefuroxime)—gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens.
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22
Q

What is the clinical use of 3rd generation Cephalosporins (ceftriaxone, cefotaxime, ceftazidime)?

A

Serious gram-negative infections resistant to other β-lactams.
Ceftriaxone—meningitis and gonorrhea.
Ceftazidime—Pseudomonas.

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23
Q

What is the clinical use of 4th generation Cephalosporins (cefepime)?

A

↑ activity against Pseudomonas and gram-positive organisms.

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24
Q

What is the clinical use of 5th generation Cephalosporins (ceftaroline)?

A

Broad gram-positive and gram-negative organism coverage, including MRSA; does not cover Pseudomonas.

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25
Q

What are the toxicities of Cephalosporins?

A

Hypersensitivity reactions, vitamin K deficiency. Low cross-reactivity with penicillins. ↑ nephrotoxicity of aminoglycosides.

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26
Q

What is the mechanism of Aztreonam?

A

A monobactam; resistant to β-lactamases. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins.

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27
Q

What are the clinical uses of Aztreonam?

A

Gram-negative rods only—no activity against gram-positives or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

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28
Q

What are the toxicities of Aztreonam?

A

Usually nontoxic; occasional GI upset.

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29
Q

What are the Carbapenems?

A

Imipenem, meropenem, ertapenem (new; limited Pseudomonas coverage), doripenem (new).

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30
Q

What is the mechanism of Carbapenems?

A

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

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31
Q

What is the clinical use of Carbapenems?

A

Gram-positive cocci, gram-negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed. Meropenem has a ↓ risk of seizures and is stable to dehydropeptidase I.

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32
Q

What are the toxicities of Carbapenems?

A

GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.

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33
Q

What is the mechanism of Vancomycin?

A

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

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34
Q

What are the clinical uses of Vancomycin?

A

Gram positive only—serious, multidrug-resistant organisms, including MRSA, enterococci, and Clostridium difficile (oral dose for pseudomembranous colitis).

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35
Q

What are the toxicities of Vancomycin?

A

Well tolerated in general—but NOT trouble free. Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing—red man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate).

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36
Q

What is the mechanism of resistance of Vancomycin?

A

Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac.

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37
Q

How do the protein synthesis inhibitors work?

A

Specifically target smaller bacterial ribosome (70S, made of 30S and 50S subunits), leaving human ribosome (80S) unaffected.

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38
Q

What are the 30S inhibitors?

A 
A = Aminoglycosides [bactericidal]
T = Tetracyclines [bacteriostatic]
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39
Q

What are the 50S inhibitors?

A 
C = Chloramphenicol, Clindamycin [bacteriostatic]
E = Erythromycin (macrolides) [bacteriostatic]
L = Linezolid [variable]
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40
Q

What is the mechanism of Linezolid (50S inhibitor)?

A

Prevents formation of initiation complex

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41
Q

What are the Aminoglycosides?

A

GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.

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42
Q

What is the mechanism of Aminoglycosides?

A

Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Also block translocation. Require O2 for uptake; therefore ineffective against anaerobes.

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43
Q

What are the clinical uses of Aminoglycosides?

A

Severe gram-negative rod infections. Synergistic with β-lactam antibiotics.
Neomycin for bowel surgery.

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44
Q

What are the toxicities of Aminoglycosides?

A

Nephrotoxicity (especially when used with cephalosporins), Neuromuscular blockade, Ototoxicity (especially when used with loop diuretics). Teratogen.

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45
Q

What is the mechanism of resistance of Aminoglycosides?

A

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

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46
Q

What are the Tetracyclines?

A

Tetracycline, doxycycline, minocycline

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47
Q

What is the 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. Do not take with milk (Ca2+), antacids (Ca2+ or Mg2+), or iron-containing preparations because divalent cations inhibit its absorption in the gut.

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48
Q

What are the clinical uses of Tetracyclines?

A

Borrelia burgdorferi, M. pneumoniae. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne.

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49
Q

What are the toxicities of Tetracyclines?

A

GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.

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50
Q

What is the mechanism of resistance of Tetracyclines?

A

↓ uptake or ↑ efflux out of bacterial cells by plasmid-encoded transport pumps.

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51
Q

What are the Macrolides?

A

Azithromycin, clarithromycin, erythromycin

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52
Q

What is the mechanism of Macrolides?

A

Inhibit protein synthesis by blocking translocation (“macroslides”); bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.

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53
Q

What are the clinical uses of Macrolides?

A

Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STDs (for Chlamydia), and gram-positive cocci (streptococcal infections in patients allergic to penicillin).

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54
Q

What are the toxicities of Macrolides?

A

MACRO: Gastrointestinal Motility issues, Arrhythmia caused by prolonged QT, acute Cholestatic hepatitis, Rash, eOsinophilia. Increases serum concentration of theophyllines, oral anticoagulants.

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55
Q

What are is the mechanism of resistance of Macrolides?

A

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

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56
Q

What is the mechanism of Chloramphenicol?

A

Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic.

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57
Q

What are the clinical uses of Chloramphenicol?

A

Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and Rocky Mountain spotted fever (Rickettsia rickettsii).
Limited use owing to toxicities but often still used in developing countries because of low cost.

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58
Q

What are the toxicities of Chloramphenicol?

A

Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase).

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59
Q

What are is the mechanism of resistance of Chloramphenicol?

A

Plasmid-encoded acetyltransferase inactivates the drug.

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60
Q

What is the mechanism of Clindamycin?

A

Blocks peptide transfer (translocation) at 50S ribosomal subunit. Bacteriostatic.

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61
Q

What are the clinical uses of Clindamycin?

A

Anaerobic infections (e.g., Bacteroides spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections. Also effective against invasive Group A streptococcal (GAS) infection.

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62
Q

What are the toxicities of Clindamycin?

A

Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea.

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63
Q

What is one major difference between Clindamycin and Metronidazole?

A

Clindamycin treats anaerobes above the diaphragm vs. metronidazole (anaerobic infections below diaphragm).

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64
Q

What are the Sulfonamides?

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

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65
Q

What is the mechanism of Sulfonamides?

A

Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic.

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66
Q

What are the clinical uses of Sulfonamides?

A

Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

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67
Q

What are the toxicities of Sulfonamides?

A

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

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68
Q

What is the mechanism of resistance of Sulfonamides?

A

Altered enzyme (bacterial dihydropteroate synthase), ↓ uptake, or ↑ PABA synthesis.

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69
Q

What is the mechanism of Trimethoprim?

A

Inhibits bacterial dihydrofolate reductase. Bacteriostatic.

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70
Q

What are the clinical uses of Trimethoprim?

A

Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMPSMX]), causing sequential block of folate synthesis. Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis.

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71
Q

What are the toxicities of Trimethoprim?

A

Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid).

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72
Q

What are the Fluoroquinolones?

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gemifloxacin, enoxacin (fluoroquinolones), nalidixic acid (a quinolone).

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73
Q

What is the mechanism of Fluoroquinolones?

A

Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV. Bactericidal. Must not be taken with antacids.

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74
Q

What are the clinical uses of Fluoroquinolones?

A

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

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75
Q

What are the toxicities of Fluoroquinolones?

A

GI upset, superinfections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnant women, nursing mothers, and children under 18 years old due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people > 60 years old and in patients taking prednisone.

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76
Q

What is the mechanism of resistance of Fluoroquinolones?

A

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

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77
Q

What is the mechanism of Metronidazole?

A

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

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78
Q

What are the clinical uses of Metronidazole?

A

Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. difficile). Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori.

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79
Q

What are the toxicities of Metronidazole?

A

Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol; headache, metallic taste.

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80
Q

What Antimycobacterial drug is used for M. tuberculosis prophylaxis?

A

Isoniazid

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81
Q

What Antimycobacterial drug is used to treat M. tuberculosis?

A

Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE for treatment)

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82
Q

What Antimycobacterial drug is used for M. avium–intracellulare prophylaxis?

A

Azithromycin, rifabutin

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83
Q

What Antimycobacterial drug is used to treat M. avium–intracellulare?

A

More drug resistant than M. tuberculosis. Azithromycin or clarithromycin + ethambutol. Can add rifabutin or ciprofloxacin.

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84
Q

What Antimycobacterial drug is used for M. leprae prophylaxis?

A

N/A

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85
Q

What Antimycobacterial drug is used to treat M. leprae?

A

Long-term treatment with dapsone and rifampin for tuberculoid form. Add clofazimine for lepromatous form.

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86
Q

What is the mechanism of Isoniazid (INH)?

A

↓ synthesis of mycolic acids. Bacterial catalaseperoxidase (encoded by KatG) needed to convert INH to active metabolite.

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87
Q

What are the clinical uses of Isoniazid (INH)?

A

Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB.

88
Q

What are the toxicities of Isoniazid (INH)?

A

Neurotoxicity, hepatotoxicity. Pyridoxine (vitamin B6) can prevent neurotoxicity, lupus.

89
Q

What is an additional important fact about Isoniazid (INH)?

A

Different INH half-lives in different people (fast vs. slow acetylators).

90
Q

What are the Rifamycins?

A

Rifampin and rifabutin

91
Q

What is the mechanism of Rifamycins?

A

Inhibits DNA-dependent RNA polymerase.

92
Q

What are the clinical uses of Rifamycins?

A

Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B.

93
Q

What are the toxicities of Rifamycins?

A

Minor hepatotoxicity and drug interactions (↑ P-450); orange body fluids (nonhazardous side effect). Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.

94
Q

What are the 4 R’s of Rifampin?

A 
RNA polymerase inhibitor
Ramps up microsomal cytochrome P-450
Red/orange body fluids
Rapid resistance if used alone
Rifampin ramps up cytochrome P-450, but
rifabutin does not
95
Q

What is the mechanism of Pyrazinamide?

A

Mechanism uncertain. Thought to acidify intracellular environment via conversion to pyrazinoic acid. Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found.

96
Q

What are the clinical uses of Pyrazinamide?

A

Mycobacterium tuberculosis

97
Q

What are the toxicities of Pyrazinamide?

A

Hyperuricemia and hepatotoxicity

98
Q

What is the mechanism of Ethambutol?

A

↓ carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

99
Q

What are the clinical uses of Ethambutol?

A

Mycobacterium tuberculosis

100
Q

What are the toxicities of Ethambutol?

A

Optic neuropathy (red-green color blindness)

101
Q

What prophylaxis is used for Endocarditis with surgical or dental procedures?

A

Penicillins

102
Q

What prophylaxis is used for Gonorrhea?

A

Ceftriaxone

103
Q

What prophylaxis is used for History of recurrent UTIs?

A

TMP-SMX

104
Q

What prophylaxis is used for Meningococcal infection?

A

Ciprofloxacin (drug of choice), rifampin for children

105
Q

What prophylaxis is used for Pregnant woman carrying group B strep?

A

Ampicillin

106
Q

What prophylaxis is used for Prevention of gonococcal or chlamydial conjunctivitis in newborn?

A

Erythromycin ointment

107
Q

What prophylaxis is used for Prevention of postsurgical infection due to S. aureus?

A

Cefazolin

108
Q

What prophylaxis is used for Prophylaxis of strep pharyngitis in child with prior rheumatic fever?

A

Oral penicillin

109
Q

What prophylaxis is used for Syphilis?

A

Benzathine penicillin G

110
Q

What prophylaxis is used for HIV patients with CD4 < 200 cells/mm3 and for what infection?

A

TMP-SMX; Pneumocystis pneumonia

111
Q

What prophylaxis is used for HIV patients with CD4 < 100 cells/mm3 and for what infection?

A

TMP-SMXl Pneumocystis pneumonia and toxoplasmosis

112
Q

What prophylaxis is used for HIV patients with CD4 < 50 cells/mm3 and for what infection?

A

Azithromycin; Mycobacterium avium complex

113
Q

In regards to prophylaxis in HIV patients, what can a patient use if he or she is unable to tolerate TMP-SMX?

A

Aerosolized pentamidine may be used if patient is unable to tolerate TMP-SMX, but this may not prevent toxoplasmosis infection concurrently.

114
Q

What do you treat Methicillin-resistant Staphylococcus aureus (MRSA) with?

A

Vancomycin, daptomycin, linezolid (can cause serotonin syndrome), tigecycline, ceftaroline.

115
Q

What do you treat Vancomycin-Resistant Enterococci (VRE) with?

A

Linezolid and streptogramins (quinupristin/dalfopristin)

116
Q

What are the polyenes?

A

Amphotericin B and Nystatin

117
Q

What is the mechanism of Amphotericin B?

A

Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes.

118
Q

What are the clinical uses of Amphotericin B?

A

Serious, systemic mycoses. Cryptococcus (amphotericin B with/without flucytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor. Intrathecally for fungal meningitis. Supplement K+ and Mg2+ because of altered renal tubule permeability.

119
Q

What are the toxicities of Amphotericin B?

A

Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (“amphoterrible”). Hydration ↓ nephrotoxicity. Liposomal amphotericin ↓ toxicity.

120
Q

What is the mechanism of Nystatin?

A

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

121
Q

What are the clinical uses of Nystatin?

A

“Swish and swallow” for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.

122
Q

What are the Azoles?

A

Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.

123
Q

What is the mechanism of Azoles?

A

Inhibit fungal sterol (ergosterol) synthesis, by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol.

124
Q

What are the clinical uses of Azoles?

A

Local and less serious systemic mycoses. Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

125
Q

What are the toxicities of Azoles?

A

Testosterone synthesis inhibition (gynecomastia, esp. with ketoconazole), liver dysfunction (inhibits cytochrome P-450).

126
Q

What is the mechanism of Flucytosine?

A

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

127
Q

What are the clinical uses of Flucytosine?

A

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

128
Q

What are the toxicities of Flucytosine?

A

Bone marrow suppression

129
Q

What are the Echinocandins?

A

Caspofungin, micafungin, anidulafungin

130
Q

What is the mechanism of Echinocandins?

A

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

131
Q

What are the clinical uses of Echinocandins?

A

Invasive aspergillosis, Candida.

132
Q

What are the toxicities of Echinocandins?

A

GI upset, flushing (by histamine release).

133
Q

What is the mechanism of Terbinafine?

A

Inhibits the fungal enzyme squalene epoxidase

134
Q

What are the clinical uses of Terbinafine?

A

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

135
Q

What are the toxicities of Terbinafine?

A

GI upset, headaches, hepatotoxicity, taste disturbance

136
Q

What is the mechanism of Griseofulvin?

A

Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (e.g., nails).

137
Q

What are the clinical uses of Griseofulvin?

A

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).

138
Q

What are the toxicities of Griseofulvin?

A

Teratogenic, carcinogenic, confusion, headaches, ↑ P-450 and warfarin metabolism.

139
Q

What are the Anti-protozoan therapies?

A

Pyrimethamine - toxoplasmosis
Suramin and melarsoprol - Trypanosoma brucei
Nifurtimox - T. cruzi
Sodium stibogluconate - leishmaniasis

140
Q

What is the mechanism of Chloroquine?

A

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

141
Q

What are the clinical uses of Chloroquine?

A

Treatment of plasmodial species other than P. falciparum (frequency of resistance in P. falciparum is too high). Resistance due to membrane pump that ↓ intracellular concentration of drug. Treat P. falciparum with artemether/lumefantrine or atovaquone/proguanil. For life-threatening malaria, use quinidine in U.S. (quinine elsewhere) or artesunate.

142
Q

What are the toxicities of Chloroquine?

A

Retinopathy; pruritus (especially in dark-skinned individuals).

143
Q

What are the anti-helminthic therapies?

A

Mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel; immobilize helminths. Use praziquantel against flukes (trematodes) such as Schistosoma.

144
Q

What is the mechanism of Zanamivir and oseltamivir?

A

Inhibit influenza neuraminidase → ↓ the release of progeny virus.

145
Q

What are the clinical uses of Zanamivir and oseltamivir?

A

Treatment and prevention of both influenza A and B.

146
Q

What is the mechanism of Ribavirin?

A

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

147
Q

What are the clinical uses of Ribavirin?

A

RSV, chronic hepatitis C

148
Q

What are the toxicities of Ribavirin?

A

Hemolytic anemia. Severe teratogen.

149
Q

What is the mechanism of Acyclovir, famciclovir, and valacyclovir?

A

Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells → few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.

150
Q

What is the clinical use of Acyclovir, famciclovir, and valacyclovir?

A

HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
For herpes zoster, use a related agent, famciclovir.

151
Q

What are the toxicities of Acyclovir, famciclovir, and valacyclovir?

A

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated.

152
Q

What is the mechanism of resistance of Acyclovir, famciclovir, and valacyclovir?

A

Mutated viral thymidine kinase

153
Q

What is the mechanism of Ganciclovir?

A

5′-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.

154
Q

What is the clinical use of Ganciclovir?

A

CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability.

155
Q

What are the toxicities of Ganciclovir?

A

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

156
Q

What is the mechanism of resistance of Ganciclovir?

A

Mutated CMV DNA polymerase or lack of viral kinase.

157
Q

What is the mechanism of Foscarnet?

A

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

158
Q

What is the clinical use of Foscarnet?

A

CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV.

159
Q

What are the toxicities of Foscarnet?

A

Nephrotoxicity.

160
Q

What is the mechanism of resistance of Foscarnet?

A

Mutated DNA polymerase

161
Q

What is the mechanism of Cidofovir?

A

Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase.

162
Q

What is the clinical use of Cidofovir?

A

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

163
Q

What are the toxicities of Cidofovir?

A

Nephrotoxicity (coadminister with probenecid and IV saline to ↓ toxicity).

164
Q

Describe HIV therapy.

A

Highly active antiretroviral therapy (HAART): initiated when patients present with AIDS-defining illness, low CD4 cell counts (< 500 cells/mm3), or high viral load. Regimen consists of 3 drugs to prevent resistance:
[2 nucleoside reverse transcriptase inhibitors (NRTIs)] + [1 non-nucleoside reverse transcriptase inhibitor (NNRTI) OR 1 protease inhibitor OR 1 integrase inhibitor]

165
Q

What are the Protease inhibitors?

A 
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir
Ritonavir
Saquinavir
166
Q

What is the mechanism of Protease inhibitors?

A

Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
Ritonavir can “boost” other drug concentrations by inhibiting cytochrome P-450.

167
Q

What are the toxicities of Protease inhibitors?

A

Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy.
Nephropathy, hematuria (indinavir).

168
Q

What is the mechanism of Chloroquine?

A

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

169
Q

What are the clinical uses of Chloroquine?

A

Treatment of plasmodial species other than P. falciparum (frequency of resistance in P. falciparum is too high). Resistance due to membrane pump that ↓ intracellular concentration of drug. Treat P. falciparum with artemether/lumefantrine or atovaquone/proguanil. For life-threatening malaria, use quinidine in U.S. (quinine elsewhere) or artesunate.

170
Q

What are the toxicities of Chloroquine?

A

Retinopathy; pruritus (especially in dark-skinned individuals).

171
Q

What are the anti-helminthic therapies?

A

Mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel; immobilize helminths. Use praziquantel against flukes (trematodes) such as Schistosoma.

172
Q

What is the mechanism of Zanamivir and oseltamivir?

A

Inhibit influenza neuraminidase → ↓ the release of progeny virus.

173
Q

What are the clinical uses of Zanamivir and oseltamivir?

A

Treatment and prevention of both influenza A and B.

174
Q

What is the mechanism of Ribavirin?

A

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

175
Q

What are the clinical uses of Ribavirin?

A

RSV, chronic hepatitis C

176
Q

What are the toxicities of Ribavirin?

A

Hemolytic anemia. Severe teratogen.

177
Q

What is the mechanism of Acyclovir, famciclovir, and valacyclovir?

A

Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells → few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.

178
Q

What is the clinical use of Acyclovir, famciclovir, and valacyclovir?

A

HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
For herpes zoster, use a related agent, famciclovir.

179
Q

What are the toxicities of Acyclovir, famciclovir, and valacyclovir?

A

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated.

180
Q

What is the mechanism of resistance of Acyclovir, famciclovir, and valacyclovir?

A

Mutated viral thymidine kinase

181
Q

What is the mechanism of Ganciclovir?

A

5′-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.

182
Q

What is the clinical use of Ganciclovir?

A

CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability.

183
Q

What are the toxicities of Ganciclovir?

A

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

184
Q

What is the mechanism of resistance of Ganciclovir?

A

Mutated CMV DNA polymerase or lack of viral kinase.

185
Q

What is the mechanism of Foscarnet?

A

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

186
Q

What is the clinical use of Foscarnet?

A

CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV.

187
Q

What are the toxicities of Foscarnet?

A

Nephrotoxicity.

188
Q

What is the mechanism of resistance of Foscarnet?

A

Mutated DNA polymerase

189
Q

What is the mechanism of Cidofovir?

A

Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase.

190
Q

What is the clinical use of Cidofovir?

A

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

191
Q

What are the toxicities of Cidofovir?

A

Nephrotoxicity (coadminister with probenecid and IV saline to ↓ toxicity).

192
Q

Describe HIV therapy.

A

Highly active antiretroviral therapy (HAART): initiated when patients present with AIDS-defining illness, low CD4 cell counts (< 500 cells/mm3), or high viral load. Regimen consists of 3 drugs to prevent resistance:
[2 nucleoside reverse transcriptase inhibitors (NRTIs)] + [1 non-nucleoside reverse transcriptase inhibitor (NNRTI) OR 1 protease inhibitor OR 1 integrase inhibitor]

193
Q

What are the Protease inhibitors?

A 
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir
Ritonavir
Saquinavir
194
Q

What is the mechanism of Protease inhibitors?

A

Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
Ritonavir can “boost” other drug concentrations by inhibiting cytochrome P-450.

195
Q

What are the toxicities of Protease inhibitors?

A

Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy.
Nephropathy, hematuria (indinavir).

196
Q

What are the NRTIs?

A 
Abacavir (ABC)
Didanosine (ddI)
Emtricitabine (FTC)
Lamivudine (3TC)
Stavudine (d4T)
Tenofovir (TDF)
Zidovudine (ZDV, formerly AZT)
197
Q

What is the mechanism of NRTIs?

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3′ OH group). Tenofovir is a nucleoTide; the others are nucleosides and need to be phosphorylated to be active.
ZDV is used for general prophylaxis and during pregnancy to ↓ risk of fetal transmission.

198
Q

What are the toxicities of NRTIs?

A

Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), anemia (ZDV), pancreatitis (didanosine).

199
Q

What are the NNRTIs?

A

Efavirenz
Nevirapine
Delavirdine

200
Q

What is the mechanism of NNRTIs?

A

Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.

201
Q

What are the toxicities of NNRTIs?

A

Rash and hepatotoxicity are common to all NNRTIs. Vivid dreams and CNS symptoms are common with efavirenz. Delavirdine and efavirenz are contraindicated in pregnancy.

202
Q

What is the mechanism of Integrase inhibitors (Raltegravir)?

A

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

203
Q

What is the toxicity of Integrase inhibitors (Raltegravir)?

A

Hypercholesterolemia.

204
Q

What is the mechanism of Enfuvirtide (fusion inhibitor)?

A

Binds gp41, inhibiting viral entry.

205
Q

What is the toxicity of Enfuvirtide (fusion inhibitor)?

A

Skin reaction at injection sites.

206
Q

What is the mechanism of Maraviroc (fusion inhibitor)?

A

Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120.

207
Q

What is the mechanism of Interferons?

A

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

208
Q

What are the clinical uses of Interferons?

A

IFN-α: chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma
IFN-β: multiple sclerosis
IFN-γ: chronic granulomatous disease

209
Q

What are the toxicities of Interferons?

A

Neutropenia and myopathy

210
Q

What is the adverse effect of Sulfonamides in pregnancy?

A

Kernicterus

211
Q

What is the adverse effect of Aminoglycosides in pregnancy?

A

Ototoxicity

212
Q

What is the adverse effect of Fluoroquinolones in pregnancy?

A

Cartilage damage

213
Q

What is the adverse effect of Clarithromycin in pregnancy?

A

Embryotoxic

214
Q

What is the adverse effect of Tetracyclines in pregnancy?

A

Discolored teeth, inhibition of bone growth

215
Q

What is the adverse effect of Ribavirin (antiviral) in pregnancy?

A

Teratogenic

216
Q

What is the adverse effect of Griseofulvin (antifungal) in pregnancy?

A

Teratogenic

217
Q

What is the adverse effect of Chloramphenicol in pregnancy?

A

“Gray baby”

Step 1 Pharmacology (18 decks)

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