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Winter 2021 Finals > Pharm - Antibiotics, Antifungals, Antivirals > Flashcards

Pharm - Antibiotics, Antifungals, Antivirals Flashcards

1
Q

Antimicrobial drugs do not readily enter

A

CNS, bone, prostate, eye

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2
Q

Narrow spectrum penicillin exemplar

A

Penicillin V

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3
Q

Penicillin V coverage

A

non-beta lactamase producing gram+ve cocci, treponema pallidum

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4
Q

Extended spectrum penicillin exemplar

A

Amoxicillin

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5
Q

Amoxicillin coverage

A

non-beta lactamase producing gram +ve cocci, gram -ve

Common bacterial infections - OM, strep, second line for UTI

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6
Q

Amoxicillin resistance

A
  • Escherichia d/t upregulation of beta-lactamases
  • S pneumoniae - overcome by dose
  • Moraxella, haemophilus - overcome by adding beta lactamase inhibitor
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7
Q

Monobactam exemplar

A

Aztreonam

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8
Q

Aztreonam coverage/ use

A
  • Enhanced against gram -ve bacili, none against gram +ve

- For serious infections w/ resistant bacteria incld. pseudomonas (IV)

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9
Q

Carbapenem exemplar

A

Meropenem

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10
Q

Meropenem coverage/ use

A
  • Similar to penicillins, larger spectrum of gram +ve and -ve
  • resistance is growing
  • systemic infections and multidrug resistant (IV)
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11
Q

Cephalosporins coverage

A

1st gen primarily against gram +ve, later increased gram -ve and decreased gram +ve

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12
Q

First gen cephalosporin exemplar

A

Cephalexin

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13
Q

Cephalexin use

A

prior to surgery to eliminate skin flora

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14
Q

Second gen cephalosporin exemplar

A

Cefuroxime

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15
Q

Third gen cephalosporin exemplar

A

Ceftriaxone

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16
Q

Ceftriaxone uses

A
  • hospital acquired infections
  • can enter CNS - meningitis
  • gonorrhea
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17
Q

Fourth gen cephalosporin exemplar

A

Cefepine

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18
Q

Cefepime uses and drawbacks

A
  • treatment of multi-drug resistant

- associated with higher all cause mortality d/t encephalopathy

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19
Q

Beta lactam adverse effects

A
  • common: N/V, diarrhea, rash, urticaria, superinfections (candida)
  • less common: fever, vomiting, erythema, dermatitis, angioedema
  • Pseudomembranous colitis d/t c difficile
  • allergy/ anaphylaxis/ hypersensitivity
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20
Q

Beta lactam classes

A

Pencillins, monobactam, carbapenems, cephalosporins

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21
Q

Other cell wall inhibitor classes

A

UDP-MurNAc inhibitor, Glycopeptide, Beta lactamase inhibitor

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22
Q

Fosfomycin mechanism

A
  • interferes with synthesis of UDP-NAM near the beginning of the peptidoglycan synthesis pathway
  • rapidly excreted which creates effectively high urinary levels
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23
Q

Fosfomycin dosing

A

One large dose as resistance rapidly emerges

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24
Q

Vancomycin mechanism

A

Binding to end of peptidoglycan and interfering with crosslinking

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25
Q

Vancomycin uses

A
  • serious infections caused by gram +ve drug resistant (IV)
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26
Q

Vancomycin adverse effect

A
  • can cause diffuse flushing and pruritis d/t histamine release (red man syndrome)
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27
Q

Beta lactamase inhibitors exemplar

A

Clavulanic acid aka clavulanate

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28
Q

Clavulanate mechanism

A
  • inhibits class-A beta lactamases
  • No intrinsic antimicrobial activity, but serves as surrogate beta-lactamase substrate when given with another beta lactam antibiotic and protects it from destruction
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29
Q

Common bacterial resistance mechanisms

A
  • production of various classes of beta lactamases
  • alteration of structure of penicillin-binding proteins
  • changes to porins in outer membrane of gram -ve bacteria
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30
Q

Inhibitors of bacterial protein synthesis classes

A
  • Affect 30s - aminoglycosides, tetracyclines

- Affect 50S - macrolides, other

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31
Q

Aminoglycosides exemplar

A

Gentamicin

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32
Q

Aminoglycoside mechanism

A

Bind the 30S subunit and interfere with reading of mRNA code –> insertion of wrong amino acid in peptide chain
irreversible

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33
Q

Gentamicin usage

A
  • active against wide range of grame -ve
  • used in combination with penicillin to treat serious infection (bacterial endocarditis)
  • IV or topical, measure plasma concentration
  • has long post-antibiotic effect
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34
Q

Gentamicin adverse effects

A
  • Nephrotoxicity, ototoxicity (more commonly vestibular)
  • irreversible toxicity can occur even after drug is discontinued
  • one of the most common causes of drug-indcued renal failure
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35
Q

Tetracyclines mechanism

A

Competitively blocks tRNA binding to the 30S subunit , preventing the addition of a new amino acid
Reversible (bacteriostatic)

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36
Q

Tetracycline dosing info

A
  • oral

- reduce bioavailability if taken w/ mineral supplements, antacids, bismuth salicylate products, dairy

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37
Q

Tetracycline coverage

A
  • Broad spectrum bacteriostatic
  • includes rickettsia, spirochetes, mycoplasma, chlamydia
  • many common pathogens have developed resistance
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38
Q

Tetracycline adverse effects

A
  • CI in pregnancy, children <8 d/t it concentrating in growing bones and teeth
  • permanent tooth discoloration and hypoplasia of enamel
  • nephrotoxicity rare - increased risk close to expiration date, w/ other nephrotoxic drugs
  • hepatoxicity, esp in pregnancy
  • photosensitivity
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39
Q

Macrolides exemplar

A

Azithromycin

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40
Q

Macrolides mechanism

A
  • Affect 50S subunit
  • inhibit peptidyl transferase which links amino acids in growing peptide chain
  • interferes with translocation
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41
Q

Macrolides usage

A
  • covers many of the bacteria that cause respiratory tract infections and CAP
  • pts with penicillin allergy
  • pneumonia in pregnancy
  • pts taking other CYP3A4 drugs
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42
Q

Azithromycin use

A
  • reserved for pts w/ penicillin allergies d/t rising resistance and treatment failure
  • pneumoniae in pregnancy
  • may be preferred for pts taking other CYP3A4 drugs (little effect on this system)
43
Q

Azithromycin adverse effects

A
  • Common: stomatitis, heartburn, nausea, anorexia, abdominal pain, diarrhea
  • Less affinity for motilin receptor and less GI side effects
  • Potential cardiac conduction issuse
44
Q

“Other” 50S affecting exemplar

A

Clindamycin

45
Q

Clindamycin mechanism

A

Interferes with translocation

46
Q

Clindamycin usage

A
  • Resistant infections like MRSA

- Skin infections in pencillin allergic pts

47
Q

Clindamycin adverse effects

A
  • Higher rates of GI superinfections than other antibiotics
48
Q

Antifolate drugs exemplar

A

Trimethoprim-Sulfamethoxazole

49
Q

TMP-SMX mechanism

A
  • Synergistic effect by sequential blockade of folate synthesis
  • [SMX] 20: [TMP] 1
50
Q

TMP-SMX usages

A
  • Bacterial prostatitis, vaginitis

- UTI

51
Q

TMP-SMX adverse effects

A
  • N/V, diarrhea, rash, renal impairment, thrombocytopenia, anemia, agranulocytosis
  • May cause false elevation in creatine, hypoglycemia w/ sulfonylureas
  • Hypersensitivity reaction, CI in pts with sulfa allergy
  • Megaloblastic anemia if dietary folate is low
52
Q

Fluoroquinolone exemplar

A

Ciprofloxacin

53
Q

Fluoroquinolone mechanism

A

Inhibit the A subunit of DNA gyrase –> inhibits genetic replication d/t accumulation of double stranded breaks

54
Q

Ciprofloxacin usage

A
  • Second line for UTI, prostatitis, PID
  • Should be reserved for serious UTI, when others are not effective
  • Resistance increasing through efflux pumps and change to porins
55
Q

Ciprofloxacin dosing

A

Absorption decreased if taken w/ mineral supplements, antacids, bismuth salicylate products

56
Q

Ciprofloxacin adverse effects

A
  • Tendonitis, tendon rupture (high risk in pts >60, concomitant steroid use, transplant pts)
  • May cause permanent peripheral neuropathy, alterations in blood glucose
  • Seizures, phototoxicity, prolonged QT interval
  • Restlessness/ anxiety/ insomnia/ confusion
57
Q

“Other” Nucleic acid disruptor exemplar

A

Nitrofurantoin

58
Q

Nitrofurantoin mechanism

A

Reduced by bacterial flavoproteins to reactive intermediates which inactivate or alter bacterial ribosomal proteins and other macromolecules

59
Q

Nitrofurantoin usages

A

UTI, not pyelonephritis

D/t very short elimination half life, does not persist long enough to be systemically used

60
Q

Nitrofurantoin adverse effects

A
  • HA, GI (reduced when used in monohydrate/ macrocrystal formulation)
  • Long term may cause hepatic toxicity, rarely pulmonary
61
Q

Clostridium difficile risk

A

Highest - fluoroquinolones, cephalosporins, aztreonam, carbapenems
Moderate - macrolides, TMP-SMX, Penicillins

62
Q

Antifungal classes

A

Polyene, Azole derivatives, allylamines, echinocandins. other

63
Q

Polyene exemplar

64
Q

Nystatin uses

A
  • Often used in suspension (“swish and swallow”), available in various
  • prophylactic prevention of oral candidiasis in immunocompromise
  • Topical not routinely recommended
65
Q

Polyene mechanism

A

Selectively binds to ergosterol in membrane, is incorporated, and forms micropores

66
Q

Azole derivates mechanism

A
  • Inhibit ergosterol biosynthesis via 14 alpha-demethylase –> disrupted membrane structure and function
67
Q

Azole derivates exemplar

A

Fluconazole

68
Q

Fluconazole usage

A
  • Drug of choice for prophylaxis and treatment of common fungal infections, oral and vulvovaginal candidiasis
  • only azole derivative that concentrates in CSF - meningitis
69
Q

Fluconazole adverse effects

A
  • Less affinity for CYP450s, so fewer drug interactions
  • systemic administration can cause skin rash, hepatic injury, hematopoietic toxicity, GI distress
  • Birth defects with chronic use in doses >400 mg during first trimester
70
Q

Allylamine mechanism

A
  • Similarly to azole derivatives

- inhibits squalene epoxidase –> disrupts biosynthesis of ergosterol, results in accumulation of toxic squalene

71
Q

Allylamine exemplar

A

Terbinafine

72
Q

Terbinafine usage

A

Oral drug of choice for fungal nail infections (preferred d/t higher tolerability, efficacy, lower drug interactions)

73
Q

Terbinafine adverse effects

A
  • GI upset, HA, rash, sensory loss

- rarely severe hepatotoxicity

74
Q

Other antifungal exemplar

A

Flucytosine

75
Q

Flucytosine mechanism

A
  • Pyrimidine analog accumulated by fungal cells –> acts as false nucleotide
  • mammalian cells unable to activate drug
  • always given with amphotericin B d/t rapid development of resistance
76
Q

Flucytosine usage

A

-Cryptococcus neoformans meningitis in advanced HIV/ AIDS

77
Q

HIV treatment classes

A

NRTI, NNRTI, Protease inhibitor, fusion/ entry inhibitor, integrase strand transfer inhibitor

78
Q

Attachment/ entry inhibitor exemplar

79
Q

Maraviroc mechanism

A

Targets host chemokine receptor CCR5

80
Q

Maraviroc usages

A
  • treatment of HIV when other drugs are ineffective or resistance is high to other drugs
  • only effective if pt is infected with HIV that only uses CCR5
  • metabolized by CYP3A4 so combination therapy used
81
Q

NRTI exemplar

A

Emtricitabine/ Tenofovir

82
Q

Emtricitabine/ Tenofovir usages

A
  • Treatment of established HIB, pre-exposure prophylaxis
  • One of the preferred combinations during pregnancy
  • Common backbone to all three common HIV treatment regimes
83
Q

NRTI mechanism

A
  • Converted to nucleotides by host cell

- Compete with endogenous nucleotides for incorporation into viral DNA, causing chain termination

84
Q

Emtricitabine/ Tenofovir adverse effects

A
  • Renal, liver toxicity
  • Lactic acidosis
  • Decreased bone density and risk of fracture
  • Lipodystrophy
  • HA, nausea, diarrhea, fatigue, depression, insomnia
85
Q

NNRTI mechanism

A
  • Do not require metabolic activation and directly inhibit reverse transcription
  • act synergistically with NRTs and are never used alone
86
Q

NNRTI exemplar

87
Q

Efavirenz usages

A
  • Addition to NRTIs is 1 common regime

- NNRTI of choice when viral load is <100,000

88
Q

Efavirenz adverse effects

A
  • CNS toxicity - sleep disturbances, abnormal dreams, depression
  • Avoid in pts with history of anxiety, depression, psychosis
  • Rash
  • CI in 1st trimester of pregnancy
  • many serious interactions with NNRTIs
89
Q

HIV Protease inhibitors mechanism

A
  • Inhibits protease activity –> production of immature, non-infectious viral particles
  • Synergistic with NRTIs
90
Q

HIV Protease inhibitor exemplar

A

Atazanavir

91
Q

Atazanavir usage

A
  • Combination with NRTIs one of the common regimes

- Given alongside other drugs (boosted therapy) Ritonavir or Cobicistat

92
Q

Protease inhibitor adverse effects

A

-Lipodystrophy, hyperlipidemia, insulin resistance and diabetes, liver damage, prolongation of PR interval

93
Q

HIV integrase inhibitor mechanism

A

Inhibits integrase, which incorporates viral DNA into DNA of CD4+ cells

94
Q

HIV integrase inhibitor exemplar

A

Raltegravir

95
Q

Raltegravir usage

A
  • Combination with NRTIs one of common regimes
96
Q

Raltegravir adverse effects

A
  • Cause far fewer as a class
  • HA, diarrhea, nausea
  • less commonly, neuropsych
  • Rarely life threatening skin and hypersensitivity reactions
97
Q

Herpes DNA polymerase inhibitor mechanism

A
  • Similar to NRTIs

- viral and host kinases must activate

98
Q

Herpes DNA polymerase inhibitor exemplar

99
Q

Acyclovir usage

A
  • Treatment of HSV 1 or 2
  • Must be started w/ in 1 hr for orolabial and 7 days for genital
  • IV for serious infection
  • Suppressive for people who experience 4+ recurrences per year
100
Q

Acyclovir adverse effects

A
  • Not many - GI, HA, rash most common
101
Q

Influenza neuraminidase inhibitor exemplar

A

Oseltamivir

102
Q

Neuraminidase inhibitor mechanism

A
  • Neuraminidase cannot cleave sialic acid from membrane glycoproteins –> virus remains tethered
103
Q

Oseltamivir useage

A
  • Chemoprophylaxis and treatment of flu A and B during outbreaks
  • dosing dependent on renal function
  • Treatment best initiated w/in 48 hours of sx onset
  • reduces complications influenza
104
Q

Oseltamivir adverse effects

Winter 2021 Finals (6 decks)

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