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Microbiology > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Penicillin G,V: Clinical use

A

Mostly used for gram + organisms (S.pneumo, S.pyogenes, Actinomyces
Also used for gram - cocci (N.meningitidis) and spirochetes (T.pallidum)
Bacteriocidal for Gram + cocci, Gram + rods, Gram - cocci and spirochetes
Penicillinase sensitive

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2
Q

Penicillin G,V: Adverse effects

A

Hypersensitivity reactions

direct Coomb’s positive hemolytic anemia

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3
Q

Penicillin G,V: resistance

A

Penicillinase in bacteria (a type of beta-lactimase) cleaves the beta-lactam ring

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4
Q

Penicillin G,V: Mechanism

A

D-Ala-D-Ala structural analog. Binds penicillin binding protein (PBP) a transpeptidase
Blocks transpeptidase cross-linking of peptidoglycan in cell wall
Activates autolytic enzymes

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5
Q

Penicillinase-sensitive penicillins: Mechanism

A

Amoxicillin, ampicillin, aminopenicillins
Same as penicillin (PBP protein blocking transpeptidation)
Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against destruction by beta-lactamases
AMinoPenicillins are AMPed-up penicillin. AmOxicillin has greater Oral bioavailability than ampicillin

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6
Q

Penicillinase-sensitive penicillins: Clinical Use

A

Amoxicillin, ampicillin, aminopenicillins
Extended spectrum penicillin - H.influenzae, H.pylori, E.coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci
Coverage: ampicillin/amoxicillin HHELPSS kill enterococci

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7
Q

Penicillinase-sensitive penicillins: Adverse Effects

A

Amoxicillin, ampicillin, aminopenicillins

Hypersensitivity reactions, rash, pseudomembrane colitis

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8
Q

Penicillinase-sensitive penicillins: Resistance

A

Amoxicillin, ampicillin, aminopenicillins

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

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9
Q

Penicillinase-resistant penicillins: Mechanism

A

Dicloxacillin, nafcillin, oxacillin
Same as penicillin (PBP binding so transpeptidation cannot occur)
Narrow spectrum; penicillinase resistant because of bulky R group which blocks access of beta-lactamase to beta-lactam ring

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10
Q

Penicillinase-resistant penicillins: Clinical Use

A

Dicloxacillin, nafcillin, oxacillin
S.aureus (except MRSA; resistant because of altered PBP target site)
Use naf for staph

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11
Q

Penicillinase-resistant penicillins: adverse effects

A

Dicloxacillin, nafcillin, oxacillin

Hypersensitivity reactions; interstitial nephritis

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12
Q

Antipseudomonal penicillins

A

Piperacillin, ticarcillin
MOA: same as penicillin but extended spectrum
Clinical use: pseudomonas spp. And gram - rods; susceptible to penicillinase; used with beta lactamase inhibitors
SEs: hypersensitivity reactions

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13
Q

Beta-lactamase inhibitors

A

Include Clavulanic Acid, Sulbactam and Tazobactam

Often added to penicillin antibiotics to protect from antibiotic destruction

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14
Q

Cephalosporins: Mechanism

A

Beta lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases
Bactericidal
Organisms typically not covered by 1-4th generation are LAME
-Listeria, Atypicals (chlamydia, mycoplasma), MRSA, and Enterococci
Exception is ceftaroline (5th gen)

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15
Q

Clinical use of 1st gen cephalosporins

A

Cefazolin, cephalexin
Gram + cocci
PEcK
Proteus mirabilis, E.coli, Klebsiella pneumoniae
Cefazolin used prior to surgery to prevent S.aureus wound infections

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16
Q

Clinical use of 2nd gen cephalosporins

A

Cefaclor, cefoxitin, cefuroxime (Fake fox fur)
Gram + cocci
HENS PEcK
H.influenzae, Enterobacter aerogenes, Neisseria spp, Serratia marcescens, Proteus mirabilis, E.coli, Klebsiella pneumoniae

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17
Q

Clinical use for 3rd gen cephalosporins

A

Ceftriaxone, cefotaxime, ceftazidime
Serious gram - infections resistant to other beta lactams
Ceftriaxone - meningitis, gonorrhea, disseminated Lyme disease
Ceftazidime - pseudomonas

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18
Q

Clinical use of 4th gen cephalosporins

A

Cefepime

Gram - organisms with increased activity against pseudomonas and gram + organisms

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19
Q

Clinical use for 5th gen cephalosporins

A

Ceftaroline
Broad gram + and gram - organism coverage, including MRSA
Does not cover pseudomonas

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20
Q

Cephalosporins: adverse effects

A

Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency, Exhibit cross reactivity with penicillins, increased nephrotoxicity of aminoglycosides

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21
Q

Cephalosporins: resistance

A

Structural change in PBP (transpeptidases)

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22
Q

Carbapenems: Mechanism

A

Imipenem, meropenem, ertapenem, doripenem
Imipenem- broad spectrum, beta-lactamase resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules (the kill is lastin’ with cilastatin)

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23
Q

Carbapenems: clinical use

A

Imipenem, meropenem, ertapenem, doripenem
Gram + cocci, gram - rods and anaerobes
Wide spectrum, but significant SEs limit use to life-threatening infections or after other drugs that have failed.
Meropenem has a decreased risk of seizures and is stable to dehydropeptidase

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24
Q

Carbapenems: Adverse Effects

A

Imipenem, meropenem, ertapenem, doripenem

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

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25
Q

Monobactams: Aztreonam

A

MOA: less susceptible to beta-lactamases. Prevents peptidoglycan cross-linking by binding PBP 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins
Clinical Use: gram - rods only, no activity against gram + rods or anaerobes. For penicillin-allergic pts and those with renal insufficiency who cannot tolerate aminoglycosides
SEs: usually non-toxic, occasional GI upset

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26
Q

Vancomycin: Mechanism

A

Inhibits cell wall peptidoglycan from forming by binding D-ala-D-aka portion of cell wall precursors.
Bactericidal against most bacteria (bacteriostatic against C.difficile)
Not susceptible to beta-lactamases

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27
Q

Vancomycin: Clinical Use

A

Gram + bugs only
Serious, mutlidrug resistant organisms, including MRSA, S.epidermidis, sensitive Enterococci species, and Clostridium difficile (oral dose for pseudomembranous colitis)

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28
Q

Vancomycin: Adverse Effects

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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29
Q

Vancomycin: resistance

A

Occurs in bacteria via amino acid modification
D-ala-D-ala to D-ala-D-lac
Pay back 2 D-alas (dollars) for vandalizing (vancomycin)

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30
Q

Protein synthesis inhibitors

A

Specifically target smaller bacterial ribosomes (70S=30S+50S) leaving the human ribosome (80S) unaffected
30S inhibitors: Aminoglycosides and Tetracyclines
50S inhibitors: chloramphenicol, Clindamycin, Erythromycin (macrolides), Linezolid
Buy AT 30, CCEL at 50

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31
Q

Aminoglycosides: Mechanism

A

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin
Mean (aMINoglycosides) GNATs caNNOT kill anaerobes
Bactericidal; irreversible inhibition of initiation complex through binding of the 30S subunit
Can cause misreading of mRNA. Also block translocation. Require O2 for uptake therefore are ineffective against anaerobes

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32
Q

Aminoglycosides: Clinical Use

A

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin
Severe gram - rod infections. Synergistic with beta-lactam antibiotics
Neomycin for bowel surgery

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33
Q

Aminoglycosides: Adverse effects

A

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

Nephrotoxicity, Neuromuscular blockade, Ototoxicity (esp. When used with loop diuretics), Teratogen

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34
Q

Aminoglycosides: Resistance

A

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

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35
Q

Tetracyclines: Mechanism

A

Tetracycline, doxycycline, minocycline
Bacteriostatic
Bind to 30S and prevent attachment of aminoacyl tRNA; limited CNS penetration.
Doxycycline is recalls eliminated and can be used in pts with renal failure. Do not take tetracyclines with milk (Ca2+), antacids (Ca2+ or Mg2+), or iron-containing preparations because diva lent cations inhibit drugs absorption in the gut

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36
Q

Tetracyclines: Clinical use

A

Tetracycline, doxycycline, minocycline
Borrelia burgodorferi, M.pneumoniae
Drugs’ ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia
Also used to treat acne

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37
Q

Tetracylcines: Adverse Effects

A

Tetracycline, doxycycline, minocycline
GI distress, discoloration of tweet and inhibition of bone growth in children, photosensitivity
Contraindicated in pregnancy

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38
Q

Tetracyclines: Resitance

A

Decreased uptake or increased efflux out of bacterial cells by plasmid encoded transport pumps

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39
Q

Chloramphenicol: mechanism

A

Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic

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40
Q

Chloramphenicol: Clinical Use

A

Meningitis (H.influenzae, Neisseria meningitidis, S.pneumoniae) and RMSF (rickettsia rickettsii)
Limited use owing to toxicities but often used in developing countries due to lost cost

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41
Q

Chloramphenicol: Adverse Effects

A

Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in premature infants because they lack liver UDP-glucoronyl transferase

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42
Q

Chloramphenicol: resistance

A

Plasmid encoded acayltransferases inactivate drugs

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43
Q

Clindamycin: Mechanism

A

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

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44
Q

Clindamycin: Clinical use

A

Anaerobic infections (Bacteroides spp, Clostridium perfringens) in aspiration pneumonia, lung abscesses and oral infections
Also effective against invasive group A strep infection
Treats anaerobic infections ABOVE the diaphragm vs. metronidazole (anaerobic infections BELOW diaphragm)

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45
Q

Oxazollidinones (Linezolid)

A

MOA: inhibit protein synthesis by binding to the 50S subunit and preventing formation of the initiation complex
Clinical use: gram + species including MRSA and VRE
SEs: BM suppression (esp thrombocytopenia), peripheral neuropathy, 5HT syndrome
Resistance: point mutation of ribosomal RNA

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46
Q

Macrolides: Mechanism

A

Azithromycin, clarithromycin, erythromycin
Inhibit protein synthesis by blocking translocation (macroSLIDES)
Bind to the 23S rRNA of the 50S subunit
Bacteriostatic

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47
Q

Macrolides: Clinical use

A

Atypical pneumoniae (mycoplasma, chlamydia, legionella), STIs (chlamydia), gram + cocci (strep infections in pts allergic to penicillin) and B.pertussis

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48
Q

Macrolides: Adverse Effects

A

Azithromycin, clarithromycin, erythromycin
MACRO: gastrointestinal Motility issues, Arrhythmia caused by prolonged QT interval, acute Cholestatic hepatitis, Rash, eOsiniophilia.
Increases serum concentration of theophylline, oral anticoagulants. Clarithromycin and erythromycin inhibit CYP450

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49
Q

Macrolides: Resistance

A

Azithromycin, clarithromycin, erythromycin

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

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50
Q

Sulfonamides: mechanism

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine
Inhibit dihyrdopteroate synthase, thus inhibiting folate synthesis
Bacteriostatic (bactericidal when combined with trimethoprim)

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51
Q

Sulfonamides: Clinical use

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

Gram +, gram -, nocardia, chlamydia, SMX for simple UTI

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52
Q

Sulfonamides: Adverse effects

A

Hypersensitivity reaction, hemolysis of G6PD deficient, nephrotoxicity (tubulointersitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (eg warfarin)

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53
Q

Sulfonamides: resistance

A 
Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine
Altered enzyme (bacterial dihyrdopteroate synthase), decreased uptake or increased PAABA synthesis
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54
Q

Dapsone

A

MOA: similar to Sulfonamides, but structurally distinct
Clinical use: leprosy (lepromatous, tuberculoid), pneumocystis jirovecci prophylaxis
SEs: hemolysis if G6PD deficient

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55
Q

Trimethoprim

A

MOA: inhibits bacterial dihydrofolate reductase. Bacteriostatic
Clinical use: used in combo with sulfonamides (TMP-SMX) causing sequential block of folate synthesis; combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis
SEs: megaloblastic anemia, leukopenia, granulocytopenia (may alleviate with supplemental folinic acid)
TMP Treats Marrow Poorly

56
Q

Fluroquinolones: Mechanism

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enoxacin
Inhibit prokaryotic enzymes topoisomerase II (DNA grade) and topoisomerase IV
Bactericidal
Must not be taken with antacids

57
Q

Fluoroquinolones: Clinical use

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enoxacin
Gram - rods of urinary and GI tracts (including pseudomonas), Neisseria, some gram + organisms

58
Q

Fluoroquinolones: Adverse Effects

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enoxacin
GI upset, superinfections, skin rashes, HA, dizziness
Less commonly: leg cramps and myalgias
Contraindicated in pregnant women, nursing mothers, children

59
Q

Fluoroquinolones: Resistance

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enoxacin
Chromosome encoded mutation in DNA grade, plasmid mediated resistance, efflux pumps

60
Q

Daptomycin

A

Mechanism: lipopeptide that disrupts cell membrane of gram + cocci
Clinical use: S.aureus skin infections (esp MRSA), bacteremia, endocarditis, VRE
Not used for pneumonia (avidly binds and inactivates surfactant)
SEs: myopathy, rhabdomyolysis

61
Q

Metronidazole: Mechanism

A

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

62
Q

Metronidazole: Clinical Use

A

Treats Giardiasis, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C.difficile)
Used with PPI and Clarithromycin for “triple therapy” against H.pylori
GET GAP on Metro with metronidazole
Treat infections below the diaphragm

63
Q

Antimicrobial drugs: for M.tuberculosis

A

Prophylaxis: Isoniazid
Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE)

64
Q

Antimicrobial drugs: for M.avium-intracellular even

A

Prophylaxis: Azithromycin, rifabutin
Treatment: more drug resistant that M.tb - Azithromycin or Clarithromycin + ethambutol (can add rifabutin or ciprofloxacin)

65
Q

Antimicrobial drugs: for M.leprae

A

no prophylaxis

Treatment: long term with dapsone and rifampin for tuberculoid form, add clofazimine for lepromatous form

66
Q

Rifamycins (Rifampin, Rifabutin): mechanism

A 
Inhibit DNA-dependent RNA polymerase 
*4 Rs of Rifampin*
RNA polymerase inhibitors
Ramps up microsomal CYP450 (not rifabutin)
Red/Orange body fluid
Rapid resistance if used alone
67
Q

Rifamycins (Rifampin, Rifabutin): clinical use

A

Mycobacterium tuberculosis; delay resistance to dapsone when used for leprosy
Used for meningococcal prophylaxis and chemoprophylaxis in contact of children with HiB

68
Q

Rifamycins (Rifampin, Rifabutin): adverse effects

A

Minor hepatotoxicity and drug interactions (increases CYP450)
Orange body fluids (nonhazardous)
Rifabutin favored over rifampin in pts with HIV infection due to les CYP450 stimulation

69
Q

Isoniazid: Mechanism

A

Decreased synthesis of mycolic acids. Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolite

70
Q

Isoniazid: clinical use

A

Mycobacterium tuberculosis
The only agent used as solo prophylaxis against TB. Also used as monotherapy for latent TB
Different INH half lives in fast vs slow acetylators

71
Q

Isoniazid: adverse effects

A

Hepatoxicity, P450 inhibition, drug induced SLE, Vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia). Administer with pyridoxine (B6)
INH: Injures Neurons and Hepatocytes

72
Q

Isoniazid: resistance

A

Mutations leading to underexpression of KatG

73
Q

Pyrazinamide

A

MOA: uncertain, Pyrazinamide is a prodrug that is converted to the active compound pyrazinoic acid. Works best at acidic pH (host phagolysosomes)
Clinical: mycobacterium tuberculosis
SEs: hyperuricemia, hepatotoxicity

74
Q

Ethambutol

A

MOA: decreased carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase
Clinical use: mycobacterium tuberculosis
SEs: optic neuropathy (red-green color blindness) (EYEthambutol)

75
Q

Streptomycin

A

MOA: interferes with 30S component of ribosome
Clinical use: mycobacterium tuberculosis (second line)
SEs: tinnitus, vertigo, ataxia, nephrotoxicity

76
Q

Antimicrobial prophylaxis: amoxicillin

A

High risk for endocarditis and undergoing surgical or dental procedures

77
Q

Antimicrobial prophylaxis: Ceftriaxone

A

Exposure to gonorrhea

78
Q

Antimicrobial prophylaxis: TMP-SMX

A

History of recurrent UTIs

79
Q

Antimicrobial prophylaxis: Ceftriaxone, ciprofloxacin or rifampin

A

Exposure to meningococcal infection

80
Q

Antimicrobial prophylaxis: intrapartum penicillin G or ampicillin

A

Pregnant woman carry group B strep

81
Q

Antimicrobial prophylaxis: erythromycin ointment of eyes

A

Prevention of gonococcal conjunctivitis in newborn

82
Q

Antimicrobial prophylaxis: Cefazolin

A

Prevention of post-surgical infection due to S.aureus

83
Q

Antimicrobial prophylaxis: benthazine penicillin G or oral penicillin V

A

Strep pharyngitis in a child with prior rheumatic fever

84
Q

Antimicrobial prophylaxis: benzathine penicillin G

A

Exposure to syphilis

85
Q

Prophylaxis in HIV pts: CD4

A

TMP-SMX

For pneumocystis pneumonia

86
Q

Prophylaxis in HIV pts: CD4

A

TMP-SMX

Pneumocystis pneumonia and toxoplasmosis

87
Q

Prophylaxis in HIV pts: CD4

A

Azithromycin or Clarithromycin

Mycobacterium avium complex

88
Q

Treatment for MRSA

A

Vancomycin, daptomycin, Linezolid, tigecycline, ceftaroline

89
Q

Treatment for VRE

A

Linezolid and streptogramins (quinipristin, dalfopristin)

90
Q

Treatment of multidrug resistant P aeruginosa & acinetobacter

A

Polymixins B & E (colistin)

91
Q

Amphotericin B: mechanism

A 
Binds ergosterol (unique to fungi) and forms membrane pores that allow leakage of electrolytes
*amphoTERicin "TEARs" holes in the fungi membrane
92
Q

Amphotericin B: Clinical use

A

Serious, systemic mycoses
Cryptococcus (+/- flu cytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor
Intrathecally for fungal meningitis
Supplement K+ & Mg2+ because of altered renal tubule permeability

93
Q

Amphotericin B: Adverse effects

A

Fevers/chills (shake and bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (amphoterrible).
Hydration decreases nephrotoxicity
Liposomal amphotericin decreases toxicity

94
Q

Nystatin

A

MOA: same as amphotericin B (pokes holes in membrane)

Clinical use: swish and swallow for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis

95
Q

Flucytosine

A

MOA: inhibits DNA and RNA biosynthesis by conversion to 5-FU by cytosine deaminase
Clinical use: systemic fungal infections (esp meningitis caused by Cryptococcus) in combo with amphotericin B
SEs: BM suppression

96
Q

Azoles

A

MOA: inhibit fungal sterol (ergosterol) synthesis by inhibiting CYP450 enzyme that converts lanosterol to ergosterol
Clinical use: local and less serious systemic mycoses
-fluconazole from chronic suppression of cryptococcal meningitis in AIDS pts and candidal infections of all types
-Itraconazole for Blastomyces, Coccidioides, Histoplasma
-Clotrimazole and miconazole for all types of fungal infections
SEs: testosterone synthesis inhibition (gynecomastia esp in ketoconazole) liver dysfunction (inhibits CYP450)

97
Q

Terbinafine

A

MOA: inhibits fungal enzyme squalene epoxidase
Clinical use: dermatophytoses (esp onychomycosis -fungal infection of finger or toenail)
SEs: GI upset, HA, hepatotoxicity, taste disturbance

98
Q

Enchinocandins

A

Anidulafungin, caspofungin, micafungin
MOA: inhibit cell wall synthesis by inhibiting synthesis of beta-glucan
Clinical use: invasive aspergillosis, Candida
SEs: GI upset, flushing (by histamine release)

99
Q

Griseofulvin

A

MOA: interferes with microtubule function; disrupts mitosis. Deposits in keratin containing tissues (nails)
Clinical use: oral treatment of superficial infections, inhibits growth of dermatophytes (tinea, ringworm)
SEs: teratogenic, carcinogenic, confusion, HA, increased CYP450 and warfarin metabolism

100
Q

Antiprotozoan therapy

A

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

101
Q

Chloroquine

A

MOA: blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia
Clinical use: treatment of plasmodial species other than P.falciparum (frequency of resistance is too high); resistance due to membrane pump that decrease intracellular concentration of drug.
-treat P.falciparum with artemether/lumefantrine or atovaquone/proguanil
-for life threading malaria use quinidine in USA (quinine elsewhere) or artesunate
SEs: retinopathy, pruritis (esp in dark skinned individuals)

102
Q

Antihelminthic therapy

A

Mebendazole (microtubule inhibitor), pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel

103
Q

Oseltamivir, zanamivir

A

MOA: inhibit influenza neuraminidase to decrease release of progeny virus
Clinical use: treatment and prevention of both influenza A & B

104
Q

Acyclovir, famciclovir, valcyclovir: Mechanism

A

Guanosine analogs
Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells (fewer SEs)
Triphosphate formed by cellular enzymes
Preferentially inhibit viral DNA polymerase by chain termination

105
Q

Acyclovir, famciclovir, valacyclovir: clinical use

A 
HSV & VZV
-mucocutaneous and genital lesions as well as for encephalitis 
-no effect on latent forms
Weak activity agains EBV
No activity against CMV
Prophylaxis in immunocompromised pts
Valacyclovir: prodrug of acyclovir, better bioavailability 
herpes zoster - famciclovir
106
Q

Acyclovir, famciclovir, valacyclovir: adverse effects

A

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated

107
Q

Acyclovir, famciclovir, valacyclovir: Resistance

A

Mutated viral thymidine kinase

108
Q

Ganciclovir

A

MOA: 5’-monophosphate formed by a CMV viral kinase; guanosine analog, triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase
Clinical use: CMV, esp immunocompromised pts (Valganicilovir - prodrug - has better bioavailability)
SEs: BM suppression (leukopenia, neutropenia, thrombocytopenia), renal toxicity
-more toxic to host enzymes than acyclovir
Resistance: mutated viral kinase

109
Q

Foscarnet

A

MOA: viral DNA/RNA polymerase inhibitor and HIV RT inhibitor; binds to pyrophosphate-binding site of enzyme; does not require kinase activation
Clinical use: CMV retinitis in immunocompromised pts when ganciclovir fails; acyclovir resistant HSV
SEs: nephrotoxicity, electrolyte abnormalities which can lead to seizures
Resistance: mutated DNA polymerase

110
Q

Cidofovir

A

MOA: preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase
Clinical use: CMV retinitis in immunocompromised pts; acyclovir resistant HSV. Long half-life
SEs: nephrotoxicity (coadminister with probenecid and IV saline to decrease toxicity)

111
Q

HIV therapy

A

Highly active antiretroviral therapy (HAART): often initiated at the time of HIV diagnosis
Strongest indication for pts presenting with AIDS-defining illness, low CD4 count (

112
Q

NTRIs

A

Abacavir (ABC), didanosine (ddl), Emtricitabine (FTC), Lamivudine (3TC), Stavudine (d4T), Tenofovir (TDF), Zidovudine (ZDV, formally AZT)

113
Q

NTRIs: mechanism

A

Competitively inhibit nucleotide binding to RT and terminate the DNA chain (lack a 3’OH group)
Tenofovir is an nucleoTide; the others are nucleosides and need to be phosphorylated to be active
ZDZ can be used for general prophylaxis and during pregnancy to decrease risk of fetal transmission
HaVE YOU DINED (vudine) with my nuclear (nucleosides) family?

114
Q

NTRIs: toxicity

A 
BM suppression (can be reversed with G-CSF and EPO), peripheral neuropathy, lactic acidosis (nucleosides), anemia (ZDV), pancreatitis (didanosine)
Abacavir contraindicated if pt has HLA-B5701 mutation
115
Q

NNTRIs

A

Delavirdine
Efavirenz
Nevirapine

116
Q

NNTRIs: mechanism

A

Bind to RT at site different from NTRIs

Do not require phosphorylation to be active or compete with nucelotides

117
Q

NNTRIs: toxicity

A

Rash and hepatotoxicity are common to all NNTRIs
efavirenz- vivid dreams and CNS symptoms
Delavirdine and efavirenz are contraindicated in pregnancy

118
Q

Protease inhibitors

A

Atazanavir, Darunavir, Fosamprenavir, Indinavir, Lopinavir, Ritonavir, Saquinavir
Navir (never) tease a protease

119
Q

Protease inhibitors: mechanism

A

Assembly of visions depends on HIV-1 protease (pol gene) which cleaves the polypeptide products of HIV mRNA into their functional maturation of new viruses
Ritonavir can boost other drugs concentrations by inhibiting CYP450

120
Q

Protease inhibitors: toxicity

A

hyperglycemia, GI intolerance (nausea/diarrhea), lipodystrophy (Cushing-like syndrome)
Nephropathy, hematuria (Indinavir)
Rifampin (a potent CYP/UGT inducer) contraindicated with protease inhibitors because it can decrease the protease concentration

121
Q

Integrase inhibitors

A

Raltegravir
Elvitegravir
Dolutegravir
tegra in common

122
Q

Integrase inhibitors: mechanism

A

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

123
Q

Integrase inhibitors: toxicity

A

Increased creatine kinase

124
Q

Fusion inhibitors: Enfuvirtide

A

MOA: binds gp41, inhibiting viral entry
SEs:: skin reaction at injection sites

125
Q

Fusion inhibitors: maraviroc

A

Binds CCR-5 on surface of Tcells/monocytes, inhibiting interaction with gp120

126
Q

Interferons: Mechanism

A

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

127
Q

Interferons: clinical use

A

IFN-alpha: chronic hepatitis B&C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma and malignant melanoma
IFN-beta: MS
IFN-gamma: chronic granulomatous disease

128
Q

Interferons: Adverse Effects

A

Flu-like symptoms, depression, neutropenia, myopathy

129
Q

HepC therapy: Ribavirin

A

MOA: inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate hydrogenated
Clinical use: chronic HCV, also used in RSV (palivizumab preferred in children)

130
Q

HepC therapy: Sofosbuvir

A

MOA: inhibits HCV RNA-dependent RNA polymerase acting as a chain terminator
Clinical Use: chronic HCV in combo with Ribavirin +/- peginterferon alpha
-do not use as monotherapy
SEs: fatigue, HA, nausea

131
Q

HepC therapy: SImeprevir

A

MOA: HCV protease inhibitor; prevents viral replication
Clinical use: chronic HCV in combo with ledipasvir (NS5A inhibitor)
-do not use as monotherapy
SEs: photosensitivity reactions, rash

132
Q

Autoclave

A

Pressurized steam at >120 degrees C

May be sporicidal

133
Q

Alcohols

A

Denature proteins and disrupt cell membrane

Not sporicidal

134
Q

Chlorhexidine

A

Denatures proteins and disrupts cell membranes

Not sporicidal

135
Q

Hydrogen peroxide

A

Free radical oxidation

Sporicidal

136
Q

Iodine and iodophors

A

Halogenation of DNA, RNA & proteins

May be sporicidal

137
Q

Antimicrobials to avoid in pregnancy

A 
*SAFe Children Take Really Good Care*
Sulfonamides - kernicterus 
Aminoglycosides - Ototoxicity 
Fluoroquinolones - cartilage damage
Clarithromycin - embryotoxic
Tetracyclines - Discolored teeth, inhibition of bone growth
Ribavirin - teratogenic 
Griseofulvin - teratogenic
Chloramphenicol - gray baby syndrome

Microbiology (8 decks)

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