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Pharm2Exam3 Flashcards

1
Q

Beta Lactams

A 
Penicillins
Cephalosporins
Carbapenems
Monobactams
Beta-Lactamase Inhibitors
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2
Q

Penicillins (drugs)

A 
Penicillin G (IV)
Penicillin V (PO)
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3
Q

Penicillin Coverage

A

Streptococcus

Syphilis

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4
Q

Aminopenicillins (drugs)

A

Amoxicillin

Ampicillin

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5
Q

Penicillin Pharm

A

Protein bound
low BV (poor diffusion) low CSF, brain, prostate, eye, etc. concentration
Little hepatic metabolism
Eliminated renally

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6
Q

Amoxicillin Spectrum

A

Strep, no staph, Enterococcus faecalis, no MRSA, no G-, Haemophilius influenzae (G-)

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7
Q

Ampicillin Spectrum

A

Strep, no staph, Enterococcus faecalis, Listeria, no G-, Haemophilius influenzae (G-)

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8
Q

Anti-staphylococcal Penicillins (drugs)

A

Methicillin
Nafcillin
Oxacillin
Dicloxacillin

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9
Q

Anti-staph penicillin coverage

A

Staph, strep, no Enterococcus, No MRSA, little G-

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10
Q

Extended Spectrum penicillins

A

Piperacillin

Ticarcillin

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11
Q

Extended Spectrum penicillin coverage

A

Streph, minimal staph, Enterococcus faecalis, No MRSA, G- coverage**, Pseudomonas, some anaerobes

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12
Q

Beta-lactamase inhibitors (drugs)

A

Amoxicillin/Clavulanate
Ampicillin/Sulbactam
Pipercillin/Tazobactam
Ticarcillin/Clavulanate

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13
Q

Amoxicillin/Clavulanate

A

Staph, strep, E. facealis, G-! Neisseria, E coli, Proteus, Morexella, Hemophilus influenzae, Klebsiella, and anaerobes

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14
Q

Amoxicillin/Clavulanate

A

Staph, strep, E. facealis, G-! Neisseria, E coli, Proteus, Morexella, Hemophilus influenzae, Klebsiella, and anaerobes

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15
Q

Ampicillin/Sulbactam

A

Similar to amoxicillin/clavulanate + acinetobacter

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16
Q

Piperacillin/Tazobactam

A

Beta-lactamase inhibitor

Staph. strep, E faecalis, no MRSA, broad G-***, pseudomonas, anaerobes

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17
Q

Ticarcillin/clavulanate

A

Same as pipercillin/tazobactam

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18
Q

Penicillin Tox

A 
Mainly tolerable
*Allergies - anaphylaxis, urticaria, fever, swelling, hemolytic anemia, vasculitis
Penicillin: Seizures*
Nafcillin: Myelosuppression
Oxacillin: Hepatitis
*Large PO doses = GI tox
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19
Q

Beta-lactam Resistance Mech.

A

Altered PBPs, reduced permeability, Beta-lactamases

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20
Q

Type 1 Beta Lactamase

A

Cephalosporinase
Hydrolyzes: beta-lactamase inhibitor/beta-lactam combo drugs, penicillins, 1/2/3 gen cephalosporins, monobactams
Treatments: Imipenem, fluoroquinolones, and cefepime

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21
Q

Type II Beta Lactamase

A

Extended Spectrum Beta-lactamases
Hydrolyzes: cephalosporins (except cefoxitin, cefmetazole, and cefotetan), Aztreonam, Extended spectrum penicillins!, combo penicillins kind of work
Treatment: Carbapenems, Non-beta lactams, Cephamycins

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22
Q

Type III Beta Lactamases

A

Metallo-beta-lactamases
Hydrolyzes: Carbapenems!!, older penicillins, cefotaxime, ceftriaxone
Treatment: Piperacillin, ceftazidime, some combo penicillins

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23
Q

1st Gen cephalosporins

A

Cefazolin
cephalexin
Cefadroxil

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24
Q

1st Gen cephalo Spectrum

A

NO ENTERO, staph, strep, NO MRSA, G-: proteus, e coli, klebsiella

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25
Q

1st Gen cephalo Spectrum

A

NO ENTERO, staph, strep, NO MRSA, G-: proteus, e coli, klebsiella

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26
Q

2nd Gen Cephalosporins

A 
Cefuroxime
Cefaclor
Cefprozil
Cefoxitin
Cefotetan
Cefmetazole
Cefimandole
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27
Q

2nd gen Cephalo spectrum

A

staph, strep, no entero, less G+ that 1st gen, no MRSA, G-: HENPEK

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28
Q

3rd gen Cephalosporins

A 
Ceftriaxone
Ceftazidime*
Cefoperazone*
Cefixime
Cefdinir
Cefpodoxime
Ceftibuten
* Pseudomonas
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29
Q

3rd gen cephalos spectrum

A

Steph, strep, no entero, less than 1st or 2nd gen (G+), G-: HENPEK + Serratia, Citrobacter, Acinetobacter, Morganella, Providencia

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30
Q

4th generation Cephalosporin

A

Cefepime (broadest spectrum cephalo)

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31
Q

Cefepime

A

4th gen cephalo

Staph, Strep, no Entero, G-: broad G-, +pseudomonas

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32
Q

5th generation Cephalosporin

A

Ceftaroline

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33
Q

Ceftaroline

A

Staph, MRSA**, Strep, Entero (minimal)

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34
Q

Cephalosporin Tox

A

Mostly tolerated
Most common = allergy: anaphylaxis, urticaria, fever, swelling, etc.
Hemolytic anema, interstitial nephritis, vasculitis
Long term = myelosupression, large PO = GI tox
Cefotetan, Cefmetazole, and Cefimandole = antabuse reaction, platelet dysfunction (bleeding)

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35
Q

Carbapenem Pharm

A

All eliminated in the urine (Imipenem: brush border dihydropeptidase to inactive metabolite)
Some liver metabolism (meropenem and Doripenem)
Good CSF penetration with meropenem
Otherwise similar to penicillins

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36
Q

Carbapenems (drugs)

A 
Imipenem/Cilastatin*
Meropenem*+
Doripenem*+
Ertapenem - no pseudomonas or entero
*Pseudomonas
\+minimal E. Faecalis
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37
Q

Carbapenem spectrum

A

Staph, Strep, no MRSA, no E faecium, no VRE

G- = broad spectrum, + pseudomonas, anaerobes

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38
Q

Carbapenem Tox

A

mostly tolerable
Seizures (neurotox)
most common = allergy (anaphylaxis, urticaria, fever, swelling)

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39
Q

Aztreonam

A

Monobactam
metabolism via liver, and renal exclusion. CSF penetration.
No IgE mediated cross-reactivity with beta-lactams except Ceftazidime.

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40
Q

Aztreonam spectrum

A

Similar to aminoglycosides
No G+
Broad G- coverage, pseudomonas

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41
Q

Aztreonam Tox

A

No penicillin allergy reaction
Well tolerated
Hepatoxicity
Allergy non-related to penicillin allergy

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42
Q

Glycopeptides

A

Vancomycin

Teicoplanin

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43
Q

Vancomycin/Telavancin MOA

A

MOA: inhibits transglycosylases preventing peptidoglycan cross linking, disrupts cell membrane resulting in loss of membrane potential
Pharm: No PO, IV only. Poor penetration CSF, brain, eye, prostate, lung, etc. Almost 100% renal eliminated

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44
Q

Glycopeptide Spectrum

A

G+: Staph, MRSA! Strep, Entero, no VRE, Clostridium difficile
NO G-

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45
Q

Glycopeptide Spectrum

A

G+: Staph, MRSA! Strep, Entero, no VRE, Clostridium difficile
NO G-

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46
Q

Lipoglycopeptides

A

Telavancin

Dalbavancin

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47
Q

Glycopeptide Resistance

A

Alteration in peptidoglycan target

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48
Q

Glycopeptide TOX

A

Tissue irritation, infusion related rxn Collitis, Rare: nephrotoxicity, ototoxicity

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49
Q

Polymyxins (drugs)

A

Polymyxin B
Polymyxin E
Colistimethate (prodrug)

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50
Q

Polymyxins MOA

A

Cationic detergent disrupts PM

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51
Q

Polymyxins Pharm

A

No PO, Renally eliminated

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52
Q

Polymyxins Spectrum

A

Broad G-, no Proteus (slimey membrane)

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53
Q

Polymyxins Resistance

A

Cell wall alterations (Thickening), PM alterations (slimey), Cell envelope protection by PM.

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54
Q

Polymyxins TOX

A

Nephrotoxicity, Neurotoxicity

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55
Q

Cyclic lipopeptides

A

Daptomycin

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56
Q

Daptomycin

A

Cyclic lipopeptides
MOA: Ca dependent insertion into PM = K+ efflux resulting in loss of membrane potential.
Pharm: no PO, renal elimination

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57
Q

Daptomycin Spectrum

A

G+: MSSA, MRSA, Staph, Strep, Entero, VRE!!!

NO G-

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58
Q

Daptomycin resistance

A

Alteration to reduce binding to PM

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59
Q

Daptomycin TOX

A

Muscle tox - rare Rabhdomyolysis (monitor CDK)

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60
Q

Aminoglycosides MOA

A

Binds 30S ribosomal subunit and prevents binding of 50S, inhibiting initiation of coding or miscoding effecting translocation.

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61
Q

Aminoglycoside pharm

A

Hexose ring, streptidine - streptomycin
more active in alkaline environments
Post-antibiotic effect! (bacteriocidal even under MIC)
O2 dependent
No PO, hydrophilic, poor penetration: CSF, brain, eye, prostate, lung, etc.
Eliminated via urine

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62
Q

Aminoglycoside Agents

A 
Streptomycin
Gentamicin
Tobramycin
Netilmicin
Amikacin
Spectinomycin
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63
Q

Aminoglycoside Spectrum

A

G+ = minimal staph, synergy with beta-lactams and vanco against strep, staph, and entero, synergy against listeria (thick CW no PM penetration to get to ribosome)
G-: broad coverage, pseudomonas
Atypical: Nocardia, tuberculosis, Neisseria

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64
Q

Aminoglycoside Resistance

A

Modifying enzyme inactivation, reduced permeability, altered ribosome to prevent binding
1,2,3 acetyltransferase
4 phosphotransferase
5 adenylyltransferase
*Amikacin is resistant to modification at 2, 3, 4, 5 (only susceptible at 1 and enzyme that modifies is less common)

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65
Q

Aminoglycoside TOX

A

Hypersensitivity (rare) - except topical neomycin
Nephrotoxicity
Ototoxicity - auditory and vestibular (balance loss)
At high dose: neuromuscular blockade

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66
Q

Tetracycline MOA

A

Binds to 30S ribosomal subunit with inhibits protein synthesis (similar to aminoglycosides)

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67
Q

Tetracycline pharm

A

well absorbed PO, short half-life, PM permeable, penetrate most tissues well

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68
Q

Tetracycline drugs

A

Tetracycline
Doxycycline
Minocycline
Demeclocycline

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69
Q

Tetracycline Spectrum

A

Strep, Staph, NO entero, Listeria, Neisseria, Moraxella, Hemophilus, Atypical: Legionella, mycoplasma, chlamydia, Rickettsia

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70
Q

Tigecycline

A

Glycylcycline
G+: Strep, Staph, Entero, VRE, Listeria
G-: broad coverage, except the 3 P’s: Pseudomonas, Proteus, Providencia
Atypicals: Legionella, Mycoplasma, chlamydia, Rickettsia

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71
Q

Tetracycline Resistance

A

Altered permeability, Altered ribosomal binding, Enzymatic inactivation of tetracycline

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72
Q

Tetracycline TOX

A

rare hypersensitivity, GI tox, tetra teeth, bone deformities (kids), hepatoxicity, nephrotoxicity, photosensitivity, vestibular tox (NR), tissue injury (IV infusion)

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73
Q

Chloramphenicol

A

MOA: Different! Reversibly binds the 50S subunit of the 70S ribosome inhibiting protein synthesis
Pharm: absorbed PO, high levels orally lipophilic does not solublize well. Metabolized by liver, no renal. Penetrates CSF well

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74
Q

Chloramphenicol Spectrum

A

Broad G+, poor staph coverage, broad G- poor pseudomonas coverage, anaerobes, atypicals: rickettsia

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75
Q

Chloramphenicol Resistance

A

Alterations in PM permeability, Enzymatic inactivation of drug - chloramphenicol acetyltranferase

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76
Q

Chloramphenicol Tox

A

A LOT
GI, Hematologic**, myelosuppression, aplastic anemia (irreversible and idosyncratic)
Gray syndrome (neonates can not glucuronidate drug)
Optic neuritis: visual issues both reversible and irreversible.

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77
Q

Macrolides

A

MOA: lipophilic = good penetration but no IV formula
binds the 23S ribosomal subunit on 50S ribosome inhibiting protein synthesis
Pharm: water insoluble, Erythromicin is acid labile (unstable in stomach acid). Crosses BBB

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78
Q

Macrolides drugs

A

Erythromycin
Azithromycin
Clarithromycin
Dirithromycin

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79
Q

Macrolide spectrum

A

G+: strep, staph, no VRE, Listeria, some MRSA
G-: Morexella, Hemophilus
Atypical: mycoplasma, legionella, chlamydia, rickettsia, syphilis
Strep/staph: Clarithro>erythro>azithro

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80
Q

Macrolide Resistance

A

Alteration of the ribosome (methylation of RNA target)
Efflux pumps
Enzymatic inactivation of drug

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81
Q

Macrolide Tox

A

Hypersensitivity - uncommon
GI**
Hepatotoxicity = ^^ liver metabolites

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82
Q

Ketolides

A

Semi-synthetic 14-member macrolides
Increased stability to acid
Similar spectrum to macrolides
Similar macrolide tox - higher hepatotoxicity

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83
Q

Lincosamides

A

Clindamycin

MOA: bind the 50S subunit of the 70S ribosome inhibits protein synthesis

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84
Q

Clindamycin Pharm

A

Well absorbed PO, poor CSF/brain penetration, metabolized by the liver* (= hepatotox)

85
Q

Clindamycin spectrum

A

G+: Strep, staph, no entero

Anaerobes

86
Q

Clindamycin Resistance

A

Enzymatic inactivation of the drug

Alteration of the ribosome (mutation of receptor site or methylation of the ribosome to prevent drug binding)

87
Q

Clindamycin Tox

A

Hypersensitivity (not adverse)
GI
Hepatotoxicity
myelosuppression (chronic use) neutropenia

88
Q

Oxazolidinones

89
Q

Linezolid

A

Oxazolidinone
MOA: inhibits protein synthesis by binding 23S subunit
Pharm: well absorbed PO, hepatic metabolism, almost 100% BA

90
Q

Linezolid spectrum

A

MSSA, MRSA, coagulase (-) staph, strep, entero, VRE

NO G-

91
Q

Linezolid Resistance

A

Mutation in 23S binding site

92
Q

Linezolid Tox

A

myelosuppression (reversible), optic neuritis, peripheral neuropathy (Irreversible), lactic acidosis (mitochondrial tox)

93
Q

Protein synthesis inhibitors

A

Aminoglycosides: Streptomycin, Gentamicin, Tobramycin, Netilmicin, Neomycin, Amikacin, Spectinomycin
Tetracyclines: Tetracycline, Doxycycline, Minocycline, Demeclocycline
Glycylcyclines: Tigecycline
Chloramphenicol
Macrolides: Erythromycin, Azithromycin, Clarithromycin, Dirithromycin
Ketolides
Lincosamides: Clindamycin
Oxazolidinones: Linezolid

94
Q

30S binding - protein synth inhibitors

A

Aminoglycosides

Tetracyclines

95
Q

50S binding - protein synth inhibitors

A

Chloramphenicol

Lincosamides

96
Q

23S binding - protein synth inhibitors

A

Macrolides
ketolides
Oxazolidinones

97
Q

23S binding - protein synth inhibitors

A

Macrolides
ketolides
Oxazolidinones

98
Q

Sulfonamides

A

MOA: inhibit the conversion of PABA to dihydrofolic acid by inhibiting the enzyme dihydropteroate synthase
Pharm: Well absorbed orally, highly lipophilic. Penetrates tissues well including brain and CSF
Acetylated and glucuronidated in the liver (increased water solubility) then excreted in urine

99
Q

Sulfonamides drugs

A 
Sulfacytine
Sulfisoxazole
Sulfamethizole
Sulfadiazine*
Sulfamethoxazole* (SMX)
Sulfapyridine
Sulfadoxine
100
Q

Pyrimidines (Sulfonamides)

A

Trimethoprim

101
Q

Trimethoprim (TMP)

A

Inhibits conversion from dihydrofolic acid to trihydrofolic acid via enzyme dihydrofolate reductase
Synergistic effect with sulfonamides – they inhibit PABA conversion via different MOA

102
Q

Sulfonamide Resistance

A

Altered enzymes
Overproduction of PABA (overcome inhibition)
Alteration in permeability

103
Q

Sulfonamide TOX

A

Hypersensitivity (2nd most common)
Photosensitivity, Nephrotox: allergic nephritis, Precipitation in urine (hematuria, crystalluria, renal damage), anemia (hemolytic, aplastic), Kernicterus, GI, Hepatotox

104
Q

TMP/SMX spectrum

A

G+: minimal strep, staph, some MRSA, Listeria, no Entero
G-: Nieserria, morexella, hemophilus, E coli, Klebsiella, Stenotrophomonas maltophilia, Yersinia, F tularensis, Brucella
Atypical: PCP, Nocardia
*Niche or uncommon pathogens

105
Q

Trimethoprim resistance

A

Alterations in permeability, overproduction of dihydrofolate reductase, alterations in dihydrofolate reductase

106
Q

TMP/SMX tox

A

Same as sulfonamide tox except more anemia, including megaloblastic

107
Q

Fluoroquinolones

A

MOA: effects topoisomerase I and II, inhibit nicking and closing activity
Pharm: absorbed PO, absorption decreased when given with cations (Ca, Mg, Fe, Cu, etc)
penetrates well

108
Q

Fluoroquinolones

A

MOA: effects topoisomerase I and II, inhibit nicking and closing activity
Pharm: absorbed PO, absorption decreased when given with cations (Ca, Mg, Fe, Cu, etc)
penetrates well

109
Q

Fluoroquinolones (drugs)

A 
Ciprofloxacin
Gatifloxacin
Gemifloxacin
Levofloxacin
Moxifloxacin
Norfloxacin
Ofloxacin
Lomefloxacin
110
Q

Fluoroquinolones spectrum

A

G+: staph, strep, no entero (except Cipro)
G-: good coverage, +pseudomonas
Anaerobic in Gati and Moxi only
Atypical: mycoplasma, legionella, chlamydia, mycobacterium

111
Q

Fluoroquinolone Resistance

A

Altered DNA gyrase target

Efflux pump or reduced PM permeability

112
Q

Fluoroquinolone Tox

A

Hypersensitivity, GI, CNS tox (more in elderly), hepatox (uncommon), alterations in glucose (Gatifloxacin), QTc prolongation, tendon rupture (athletes), arthropathy

113
Q

Sulfonamides drugs

A 
Sulfacytine
Sulfisoxazole
Sulfamethizole
Sulfadiazine*
Sulfamethoxazole* (SMX)
Sulfapyridine
Sulfadoxine
114
Q

Fluoroquinolones (drugs)

A 
Ciprofloxacin
Gatifloxacin
Gemifloxacin
Levofloxacin
Moxifloxacin
Norfloxacin
Ofloxacin
Lomefloxacin
115
Q

Nucleic Acid Inhibitors

A

Sulfonamides: Sulfacytine, Sulfisoxazole, Sulfamethizole, Sulfadiazine, Sulfamethoxazole (SMX), Sulfapyridine, Sulfadoxine
Trimethoprim
Fluoroquinolones: Ciprofloxacin, Gatifloxacin, Gemifloxacin, Levofloxacin, Moxifloxacin, Norfloxacin, Ofloxacin, Lomefloxacin

116
Q

Anti-Fungals

A

Polyenes: Amphotericin B, Nystatin (not systemic)
Flucytosine
Azoles: Fluconazole, Itraconazole, Voriconazole, Posaconazole
Echinocandins: Capsofungin, Micafungin, Anidulafungin
Griseofulvin
Terbinafine
Tolnaftate
Saturated Solution of Potassium Iodide (SSKI)

117
Q

Polyenes MOA

A

Bind ergosterol in fungal PM. A potassium channel is formed causing an efflux of K and loss of PM potential
Ergosterol is inhibited (PM instability)

118
Q

Polyenes Pharm

A

Not absorbed well PO, and insoluble in water. Must be complexed in colloidal suspension with bile acid salt to make water soluble for IV use.
Hepatic and renal elimination
Penetrates tissues well, concentrates in liver, spleen and kidney
Long 1/2 life, once/day dose (can accumulate in bone)

119
Q

Amphotericin B agents/spectrum

A

Liposomal and lipid complex Amph. B have decreases nephrotoxicity and side effects.
Spec: Candida (minus lusitaniae), Aspergillus, Histoplasma, Blastomyces, Coccidioides, Zygomycetes

120
Q

Lipid Amphotericin B

A

Lower toxicity, but less evidence
*Used in patient that won’t tolerate regular Amph-B, or those at high risk for adverse events (renal compromised patients!!)

121
Q

Amph-B resistance

A

Impaired Ergosterol binding:

decreasing ergosterol in PM or altered ergosterol target

122
Q

Amph-B tox

A

**Nephrotoxicity! (long term use)– electrolyte wasting (K and Mg need to supplement) and bicarbonate wasting
Need to monitor renal fxn and electrolytes
Renal vasospasm: ischemia, decrease GFR and increased creatinine (duration and dose dependent, reversible)
Infusion reactions
Anemia

123
Q

Nystatin

A

Polyene

Very high nephrotoxicity, only use PO and topical, not systemic

124
Q

Flucytosine MOA

A

MOA: converted to 5-FU, and then FdUMP and FUTP which inhibit DNA and RNA synthesis respectively

125
Q

Flucytosine Pharm

A

absorbed PO, renal elimination, penetrate tissue well CSF/brain

126
Q

Flucytosine Spectrum

A

Cryptococcus neoformans

Candida (not often used)

127
Q

Flucytosine Resistance

A

Can develop quickly– often used with other anti-fungal drugs
Altered metabolism of flucytosine (must become triphosphorylated)

128
Q

Azoles MOA

A

imidazoles have only 2 N groups, triazoles have 3 N groups
Imidazoles are less fungal selective and cause more tox
Triazoles are more selective with less tox
Azole work by inhibiting lanosterol 14-a-demethylase = decreases ergosterol synthesis
Decreased ergosterol = unstable PM
*decreases efficacy of Amph-B

129
Q

Azole Pharm

A

Triazoles have greater affinity for fungal cells than mammalian cells = less tox
Drug intxns! - induction or inhibition of drug metabolism thru CYP450 enzymes

130
Q

Azole drugs

A

Fluconazole
Itraconazole
Voriconazole
Posaconazole

131
Q

Azole drugs

A

Fluconazole
Itraconazole
Voriconazole
Posaconazole

132
Q

Fluconazole

A

Azole anti-fungal
IV and PO
Hepatic metabolism, renal elimination (only 10% is metabolites, 90% unchanged drug in kidney BAD, requires adjustment in renally compromised patients)
Penetrate CSF/tissues
USE: Dermatophytes, cryptococosis, candidiasis, coccidiodes
Tox: GI, hepatotox, alopecia*

133
Q

Itraconazole

A

Azole anti-fungal
IV and PO decreased oral absorption with increased stomach pH - don’t use PPI’s or antacids before use
metabolized in liver
good tissue/CSF penetration
USE: dermophytes, onychomycosis, blastomycosis, histoplasmosis
Tox: GI, Hepatotox, mineral corticoid excess, negative inotropy* (low EF and heart fxn, can increase BP with fluids)

134
Q

Voriconazole

A

Azole anti-fungal
IV and PO
Long 1/2 life
Metabolized hepatically
penetrate tissue/CSF well
USE: aspergillus, candidiasis, blastomycosis, histoplasmosis
TOX: GI, hepatotox, visual changes* (rule of 30s), photosensitivity*

135
Q

Posaconazole

A 
azole anti-fungal
PO only
liver metabolized
penetrates well
USE: "BAD molds": aspergillus, candidiasis, blastomycosis, histoplasmosis, zygomycectes
TOX: no significant, GI, and hepatotox
136
Q

Posaconazole

A 
azole anti-fungal
PO only
liver metabolized
penetrates well
USE: "BAD molds": aspergillus, candidiasis, blastomycosis, histoplasmosis, zygomycectes
TOX: no significant, GI, and hepatotox
137
Q

Azole resistance

A

Increased efflux of azole
Over expression of lanosterol 14-a-demethylase (overcomes inhibition of ergosterol synthesis)
point mutation leading to decreases affinity of azoles for lanosterol

138
Q

Echinocandin MOA

A

inhibit beta-glucan synthase preventing synthesis of beta-glucan resulting in weak cell wall and structural instability

139
Q

Echinocandin pharm

A

Not absorbed orally, IV only (large cyclic peptides)
metabolized in situ
Hepatic metabolism (capsofungin and Micafungin)

140
Q

Echinocandin Spectrum

A

Candidas and Aspergillus ONLY

minus C. parapsilosis due to high MIC required

141
Q

Echinocandin Resistance

A

Mutation at Beta-(1,3)-glucan preventing synth inhibition

Up-regulation of chitin synthesis, makes up for beta-glucan loss.

142
Q

Echinocandin Tox

A

Histamine release during infusion
hypersensitivity
hypokalemia
hepatotoxicity (increase ALT/AST with cyclosporines)

143
Q

Echinocandin drugs

A

Capsofungin
Micafungin
Anidulafungin

144
Q

Griseofulvin

A

anti-fungal
MOA: inhibits fungal mitosis by binding microtubules disrupting mitotic spindle
binds keratin precursor cells, preventing new nails from infection
Tox: GI, (not as used due to replacement therapy)

145
Q

Terbinafine

A

Anti-fungal
MOA: Allylamine inhibits ergosterol synthesis (enzyme squalene epoxidase)
Topical and oral only
Use: skin/nail infections, athletes foot/ skin-skin infections
Tox: hepatitis, and hepatotoxicity

146
Q

Tolnaftate

A

Anti-fungal
MOA: thiocarbamate, topical
USE: limited spectrum, Tinea infections
-don’t need to know much

147
Q

Saturated Solution of Potassium Iodide (SSKI)

A

Anti-fungal
Oral solution
TOX: nausea, bitter emesis, hypersalivation
USE: former treatment of Sporotrichosis (now itraconazole)

148
Q

Anti-Herpes agents

A 
Acyclovir
Valacyclovir
Famciclovir
Penciclovir
Docosanol
Trifluridine
149
Q

Anti-herpes agents MOA

A

*Must be triphosporylated to work (to look like NTPs)
Acyclovir and Penciclovir require all 3 phosphorylations, first by virus-specific enzymes, thymidine kinase, (point of resistance) and the 2nd and 3rd phosphorylation are by mammalian enzymes
Trifluridine, cidofovir, and foscarnet already have 1st phosphate, so they can bypass the viral kinase step directly phophorylated by mammalian kinases.
After activation, drug is either directly bound to DNA polymerase to prevent replication or incorporated into DNA resulting in early termination.

150
Q

Acyclovir

A 
Anti-herpes
Acyclic guanosine derivative
HSV-1 HSV-2 and VZV
MOA: requires 3 phosphorylations, prevents or terminates DNA synthesis
IV and PO
Renal elimination, minimal hepatic
Penetrates most tissues
151
Q

Acyclovir Resistance

A

Alteration of thymidine kinase

Alteration in DNA polymerase

152
Q

Acyclovir TOX

A

GI
nephrotox - must be renally adjusted
Neurotox - tremors, delirium, seizures, AMS

153
Q

Famciclovir

A 
Anti-herpes
Prodrug of penciclovir
Hepatically metabolized 
HSV-1 HSV-2 and VZV
MOA: requires 3 phosphorylation to inhibit DNA synthesis
154
Q

Famciclovir Resistance

A

Alteration in thymidine Kinase

155
Q

Famciclovir TOX

A

GI, less nephro- and neurotox

concentration dependent

156
Q

Valacyclovir

A

Anti-herpes
Prodrug of acyclovir - hydrolyzed to acyclovir in liver/intestine
improved PO absorbance
Same resistance/tox as acyclovir

157
Q

Penciclovir

A

Anti-herpes agent
Active metabolite of famciclovir
Topical only
treatment of oral herpes

158
Q

Docosanol

A 
Anti-herpes agent
USE: HSV-1 and HSV-2
MOA: inhibits fusion of PM and viral envelope
Topical 
Tox: minimal
159
Q

Trifluridine

A

Fluorinated pyrimidine nucleoside
Use: HSV-1, HSV-2, CMV
MOA: phosphorylated intracellularly by host enzymes, then competes with thymidine triphosphate for incorporation by viral DNA polymerase

160
Q

Cytomegalovirus agents

A

Ganciclovir
Valganciclovir
Foscarnet
Cidofovir

161
Q

Cytomegalovirus agents MOA

A

Same as anti-herpes agents
Ganciclovir needs all 3 phosphorylations, relies on protein kinase phosphotransferase (UL97).
Cidofovir and Foscarnet come with 1 phosphate group, do not rely on thimidine kinase and are directly phosphorylated by host enzymes

162
Q

Ganciclovir

A 
CMV agent
acyclic guanosine derivative 
Use: CMV, HSV1, HSV2 and VZV
MOA: requires 3 phosphorylations to be active and inhibit DNA synthesis (protein kinase UL97)
IV and PO, poor oral absorption
Renally eliminated
Penetrates most tissues
163
Q

Ganciclovir Resistance

A

Alterations in protein kinase (UL97)

Alteration in DNA polymerase (UL54)

164
Q

Ganciclovir TOX

A 
GI
myelosuppression - leukopenia
hepatotoxicity
Teratogenic**
Neurotox - (more without renal adjustment)
165
Q

Valganciclovir

A

CMV agent
Ganciclovir plus valine group (improved BA)
acyclic guanosine derivative
USE: CMV, HSV1, HSV2, VZV
100x more active against CMV than acyclovir
MOA: Requires 3 phosphorylation steps to be active
1st phosphate group added by protein kinase phosphotransferase UL97
Only PO renally eliminated
Penetrates most tissue - no CNS

166
Q

Valganciclovir Resistance

A

Alteration of UL97

Alteration in DNA polymerase (UL54)

167
Q

Valganciclovir TOX

A 
GI
Myelosuppression
hepatotox
teratogenic
neurotox 
Same as ganciclocvir
168
Q

Foscarnet

A 
CMV agent
MOA: does not require viral enzyme for 1st phosphorylation, inhibits DNA polymerase, RNA polymerase, HIV reverse transcriptase
Use: HSV1, HSV2, VZV, CMV, EBV, HIV-1
IV only
penetrate +CNS
Renal elimination
169
Q

Foscarnet Resistance

A

Point mutation in DNA polymerase and HIV reverse transcriptase

170
Q

Foscarnet Tox

A 
Nephrotox - serum creatinine and must monitor electrolytes
Electrolyte disturbances
GI
Hepatotox
CNS
Infusion arrhythmias, numbness, tingling
171
Q

Cidofovir

A

CMV agent
HIGHLY NEPHROTOXIC
acyclic cytosine analog
MOA: does not require first phosphorylation, independent of protein kinase. Inhibits DNA polymerase, or incorporated into DNA.
Use: CMV, HSV1, HSV2, VZV, EBV, polyomavirus
Poor CNS penetration
Renally eliminated

172
Q

Cidofovir Resistance

A

Point mutation in DNA polymerase (no UL97)
*Cidofovir resistance isolates are usually also resistant to ganciclovir, but susceptible to foscarnet
Cidofovir resistance predicts foscarnet resistance but not the other way around!

173
Q

Cidofovir Tox

A

Nephrotox!!
Ocular tox
neutropenia
Mutagenic, gonadotoxic, and embryotoxic (infertility)

174
Q

NRTI drugs

A 
HIV agents
Abacavir
Didanosine
Emtricitabine
Lamivudine
Stavudine
Tenofovir
Zidovudine
175
Q

NNRTI drugs

A 
HIV agents
Nevirapine
Delavirdine
Efavirenz
Etravirine
Rilpivirine
176
Q

NRTIs

A

Looks like nucleoside/nucleotides
Need to be triphosphorylated to be active
Same as guanaline analogs
= early termination or direct inhibition of enzymes

177
Q

NRTIs

A

Looks like nucleoside/nucleotides
Need to be triphosphorylated to be active
Same as guanaline analogs
= early termination or direct inhibition of enzymes
MOA: competitive inhibition of HIV-1 reverse transcriptase, incorporation into growing viral DNA chain = termination
Hepatic and renal elimination

178
Q

NRTIs TOX

A

Mitochondrial tox (inhibits mitochondrial DNA polymerase gamma), lactic acidosis, hepatotoxicity

179
Q

NNRTIs

A

Bind directly to HIV-1 reverse transcriptase, DO NOT require phosphorylation
Hepatically metabolized

180
Q

NNRTI tox

A

GI, skin rash

Liver enzyme induced drug interactions! CYP450

181
Q

Protease Inhibitors

A 
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir/ritonavir
Nelfinavir
Ritonavir
Saquinavir
Tipranavir
182
Q

Protease Inhibitor MOA

A

Prevents post-translational cleavage of the Gag-Pol polyprotein = prevents processing of viral proteins into functional conformations, or results in production of immature/non-infectious particles
Do not require intracellular activation
Hepatic metabolism

183
Q

Protease Inhibitor Tox

A 
Redistribution of body fat - peripheral and facial fat wasting, central obesity, buffalo hump, breast enlargement
Hyperlipidemia
Hyperglycemia, diabetes
Osteoporosis
Live enzyme drug interactions, CYP450
184
Q

Entry inhibitors

A

HIV agent
CCR5 Antagonist: Maraviroc
Fusion inhibitor: Enfuvirtide

185
Q

Maraviroc MOA

A

Binds CCR5 entry of CCR5 tropic HIV
Co-receptors are necessary for the entrance of HIV into CD4 cells: CCR5 CXCR4
HIV has 2 receptors, one of each, or both or one or the other
**Only active against CCR5 + CCR5 HIV
Hepatically metabolized
Not 1st line, only for resistance HIV with CCR5/CCR5 receptors

186
Q

Maraviroc Resistance

A

Mutation in CCR5 receptor

Presence of non-CCR5 tropic HIV

187
Q

Maraviroc TOX

A 
Cough
Respiratory problems
Muscle/joint pain
Diarrhea
Sleep disturbances**
Hepatotox
188
Q

Enfuvirtide

A

MOA: inhibits HIV entry into cell by binding gp41
metabolized via proteolytic hydrolysis
Resistance: mutations in gp41 codon, no cross-resistance
TOX: injection site reactions, hypersensitivity

189
Q

Intergrase Inhibitor

A

Raltegravir
Dolutegravir
Elvitegravir

190
Q

Intergrase Inhibitors

A

HIV agents
Pyrimidinone analog
MOA: binds intergrase which inhibits strand transfer thus interfering with integration of reverse transcribed viral DNA into the chromosome of the host cell
Drug is glucuronidated, liver metabolism but not CYP450.
Glucuronidated = increased water solubility.

191
Q

Intergrase Inhibitors

A

HIV agents
Pyrimidinone analog
MOA: binds intergrase which inhibits strand transfer thus interfering with integration of reverse transcribed viral DNA into the chromosome of the host cell
Drug is glucuronidated, liver metabolism but not CYP450.
Glucuronidated = increased water solubility.

192
Q

Intergrase Inhibitors Resistance

A

Mutations in intergrase

193
Q

Intergrase Inhibitors Resistance

A

Mutations in intergrase

194
Q

1st line Anti-mycobacterials

A 
Isoniazid
Rifampin
Ethambutol
Pyrazinamide
Streptomycin
195
Q

2nd line Anti-mycobacterials

A 
Amikacin
Aminosalicylic Acid
Capreomycin
Ciprofloxacin
Clofazamine
Cycloserine
Ethionamide
Levofloxacin
Rifabutin
Rifapentine
196
Q

Isoniazid

A 
Anti-mycobacterial
Prodrug
MOA: most active against M tuberculosis. Inhibits the synthesis of mycolic acid
Bactericidal
Hepatically metabolized
197
Q

Isoniazid Resistance

A

Point mutations in katG (low level - effective at higher doses)
Large mutation or deletion in katG (high level - no efficacy)
Mutations in inhA (low level resistance)

198
Q

Isoniazid Toxicity

A

Hepatotox** significant drug interactions, minor increases in liver enzymes, hepatitis/liver failure
Neurotox - peripheral neuropathy due to clearance of pyridoxine (usually supplemented)
Hypersensitivity rxn

199
Q

Isoniazid OD

A

Large doses = metabolic acidosis, hyperglycemia, Seizures, coma

200
Q

Rifampin

A 
Anti-mycobacterial
MOA: binds to beta subunit of bacterial DNA dependent RNA polymerase and inhibits RNA synthesis
Bactericidal
Penetrates tissues
Hepatically metabolized
201
Q

Rifampin Resistance

A

Mutations in rpoB - gene for beta subunit of RNA polymerase.

202
Q

Rifampin TOX

A

Hepatotox - hepatitis, drug interactions*, failure (fatal)
Nephrotox - nephritis, acute tubular necrosis (rare)
Hypersensitivity
Orange body fluid discoloration
Flu-like symptoms - more common with high dose/intermittent therapy

203
Q

Ethambutol

A

Anti-mycobacterial
MOA: inhibits arabinosyl transferase enzyme involved in arabinogalactan biosynthesis within cell wall, = instability
*bacteriostatic
Hepatically metabolized

204
Q

Ethambutol Resistance

A

The embCAB operon codes for synthesis of arabinogalactan and lipoarabinogalactan (overcomes inhibition of enzymes)
Mutations in emb = loss of ethambutol activity

205
Q

Ethambutol TOX

A 
Optic Neuritis (larger doses)
Hypersensitivity rxn
206
Q

Pyrazinamide

A

Anti-microbacterial
MOA: synthetic analog of nicotinamide. prodrug- must be converted to pyrazanoic acid to be active. MOA unknown
Bactericidal
Hepatically metabolized

207
Q

Pyrazinamide Resistance

A

Mutations in pncA (codes for pyrazinamidase) = decreased activation of pyrazinamide into pyrazanoic acid = decreased concentration)

208
Q

Pyrazinamide TOX

A 
Hepatotox
N/V
Polyarthalgias* (joint pain)
Nephrotoxicity
Hypersensitivity
Urate retention (exacerbates gout)
Photosensitivity

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