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PLAB Pharmacology > Anti-Microbials Part 2 > Flashcards

Anti-Microbials Part 2 Flashcards

1
Q

what is the prophylaxis if patient is at high risk for endocarditis and undergoing surgical or dental procedures?

A
  • amoxicillin
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2
Q

what is the prophylaxis for exposure to gonorrhea?

A
  • ceftriaxone
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3
Q

what is the prophylaxis for history of recurrent UTIs?

A
  • TMP-SMX
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4
Q

what is the prophylaxis to exposure to meningococcal infections?

A
  • ceftriaxone
  • ciprofloxacin
  • rifampin
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5
Q

what is the prophylaxis for a pregnant woman carrying gruop B strep?

A
  • intrapartum penicillin G
  • ampicillin
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6
Q

what is the prophylaxis for prevention of gonococcal conjunctivitis in newborns?

A
  • erythromycin ointment on eyes
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7
Q

what is the prophylaxis for prevention of postsurgical infection due to S. aureus?

A
  • Cefazolin
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8
Q

what is the prophylaxis for strep pharyngitis in child with prior rheumatic fever?

A
  • benzathine penicillin G
  • oral penicillin V
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9
Q

what is the prophylaxis for exposure to syphilis?

A
  • benzathine penicillin G
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10
Q

HIV infection for cell count of CD4 < 200 cells/mm3

A

Pneumocystis pneumonia

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11
Q

prophylaxis for HIV patients with cell count CD4 < 200 cells/mm3

A

TMP-SMX

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12
Q

HIV infection for cell count of CD4 < 100 cells/mm3

A

Pneumocystis pneumonia and toxoplasmosis

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13
Q

prophylaxis for HIV patients with cell count CD4 < 100 cells/mm3

A

TMP-SMX

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14
Q

HIV infection for cell count of CD4 < 50 cells/mm3

A

Mycobacterium avium complex

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15
Q

prophylaxis for HIV patients with cell count CD4 < 50 cells/mm3

A

azithromycin or clarithromycin

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16
Q

what are the treatments for MRSA?

A
  • vancomycin
  • daptomycin
  • linezolid
  • tigecycline
  • ceftaroline
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17
Q

what are the treatments for VRE?

A
  • linezolid and streptogramins (quinupristin, dalfopristin)
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18
Q

what are the treatments for multidrug resistant P. aeruginosa, multidrug resistant Acinebacter baumannii?

A
  • polymyxins B and E (colistin)
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19
Q

antifungal drugs that disrupt cell membrane integrity

A
  • amphotericin B
  • nystatin
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20
Q

antifungal drugs that inhibit nucleic acid synthesis

A
  • flucytosine
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21
Q

antifungal drugs that inhibit cell wall synthesis

A
  • echinocandins
    • anidulafungin
    • caspofungin
    • micafungin
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22
Q

antifungal drugs that inhibit lanosterol synthesis

A
  • terbinafine
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23
Q

antifungal drugs that inhibit ergosterol synthesis

A
  • azoles
    • clotrimazole
    • fluconazole
    • itraconazole
    • ketoconazole
    • miconazole
    • voriconazole
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24
Q

amphotericin B–mechanism

A
  • binds ergosterol (unique to fungi)
  • forms membrane pores that allow leakage of electrolytes
    • “amphotericin “tears” holes in the fungal membrane by forming pores”
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25
Q

amphotericin B–use

A
  • serious, systemic mycoses
  • Cryptococcus
    • amphotericin B with or without flucytosine for cryptococcal meningitis
  • Blastomyces
  • Coccidioides
  • Histoplasma
  • Candida
  • Mucor
  • intrathecally for fungal meningitis
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26
Q

what should you supplement amphotericin B use with and why?

A
  • K+ and Mg+ b/c of altered renal tubule permeability
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27
Q

amphotericin B–toxicity

A
  • fever/chills–“shake and bake”
  • hypotension
  • nephrotoxicity
  • arrhythmias
  • anemia
  • IV phlebitis–“amphloterrible”
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28
Q

what decreases the risk of nephrotoxicity from taking amphotericin B?

A
  • hydration
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29
Q

what decreases toxicity from taking amphotericin B?

A
  • liposomal amphotericin
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30
Q

nystatin–mechanism

A
  • same as amphotericin B
    • binds ergosterol (unique to fungi)
    • forms membrane pores that allow leakage of electrolytes
  • topical use only as too toxic for systemic use
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31
Q

nystatin–use

A
  • “swish and swallow” for oral candidiasis (thrush)
  • topical for diaper rash or vaginal candidiasis
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32
Q

flucytosine–mechanism

A
  • inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase
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33
Q

flucytosine–use

A
  • systemic fungal infections (especially meningitis caused by Cryptococcus) in combination with amphotericin B
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34
Q

flucytosine–toxicity

A
  • bone marrow suppression
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35
Q

name the azoles

A
  • clotrimazole
  • fluconazole
  • itraconazole
  • ketoconazole
  • miconazole
  • voriconazole
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36
Q

azoles–mechanism

A
  • inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol
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37
Q

azoles–use

A
  • local and less serious systemic mycoses
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38
Q

fluconazole–use

A
  • (azole)
  • chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types
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39
Q

itraconazole–use

A
  • (azole)
  • Blastomyces
  • Coccidioides
  • Histoplasma
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40
Q

clotrimazole and miconazole–use

A
  • (azole)
  • for topical fungal infections
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41
Q

azoles–toxicity

A
  • testosterone synthesis inhibition
    • gynecomastia, especially with ketoconazole
  • liver dysfunction
    • inhibits cytochrome P-450
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42
Q

terbinafine–mechanism

A
  • inhibits the fungal enzyme squalene epoxidase
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43
Q

terbinafine–use

A
  • dermatophytoses
    • especially onychomycosis–fungal infection of finger or toe nails
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44
Q

terbinafine–toxicity

A
  • GI upset
  • headaches
  • hepatotoxicity
  • taste disturbance
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45
Q

name the echinocandins

A
  • anidulafungin
  • caspofungin
  • micafungin
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46
Q

echinocandins–mechanism

A
  • inhibit cell wall synthesis by inhibiting synthesis of beta glucan
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47
Q

echinocandins–use

A
  • invasive aspergillosis
  • Candida
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48
Q

echinocandins–toxicity

A
  • GI upset
  • flushing (by histamine release)
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49
Q

griseofulvin–mechanism

A
  • interferes with microtubule function
    • disrupts mitosis
  • deposits in keratin containing tissues
    • ie. nails
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50
Q

griseofulvin–use

A
  • oral treatment of superficial infections
  • inhibits growth of dermatophytes (tinea, ringworm)
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51
Q

griseofulvin–toxicity

A
  • teratogenic
  • carcinogenic
  • confusion
  • headaches
  • inc cytochrome P-450
  • inc warfarin metabolism
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52
Q

antiprotozoan therapy

A
  • pyrimethamine–toxoplasmosis
  • suramin and melarsoprol–Trypanosoma brucei
  • nifurtimox–T. cruzi
  • sodium stibogluconate–leishmaniasis
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53
Q

anti mite/louse therapy

A
  • permethrin
  • malathion
  • lindane
    • used to treat scabies (Sarcoptes scabei) and lice (Pediculus and Pthirus)
    • “treat PML (Pesty Mites and Lice) with PML (Permethrin, Malathion, Lindane), b/c they NAG you (Na, AChE, GABA blockade)”
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54
Q

permethrin–mechanism

A
  • (anti-mite/louse therapy)
  • blocks Na+ channels –> neurotoxicity
    • “treat PML (Pesty Mites and Lice) with PML (Permethrin, Malathion, Lindane), b/c they NAG you (Na, AChE, GABA blockade)”
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55
Q

malathion–mechanism

A
  • (anti mite/louse therapy)
  • acetylcholinesterase inhibitor
    • “treat PML (Pesty Mites and Lice) with PML (Permethrin, Malathion, Lindane), b/c they NAG you (Na, AChE, GABA blockade)”
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56
Q

lindane–mechanism

A
  • (anti mite/louse therapy)
  • blocks GABA channels –> neurotoxicity
    • “treat PML (Pesty Mites and Lice) with PML (Permethrin, Malathion, Lindane), b/c they NAG you (Na, AChE, GABA blockade)”
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57
Q

chloroquine–mechanism

A
  • blocks detoxification of heme into hemozoin
  • heme accumulates and is toxic to plasmodia
58
Q

chloroquine–use

A
  • treatment of plasmodial species other than P. falciparum
    • frequency of resistance in P falciparum is too high
59
Q

why does P. falciparum have high resistance to chloroquine and how should you treat it?

A
  • resistance due to membrane pump that dec intracellular concentration of drug
  • treat with artemether/lumefantrine or atovaquone/proguanil
60
Q

how should you treat malaria?

A
  • quinidine in US (quinine elsewhere)
  • artesunate
61
Q

chloroquine–toxicity

A
  • retinopathy
  • pruritis–especially in dark skinned individuals
62
Q

antihelminthic therapy

A
  • Mebendazole–microtubule inhibitor
  • pyrantel pamoate
  • ivermectin
  • diethylcarbamazine
  • praziquantel
63
Q

oseltamivir, zanamivir–mechanism

A
  • inhibit influenze neuroaminidase –> dec release of progeny virus
64
Q

oseltamivir, zanamivir–use

A
  • treatment and prevention of both influenza A and B
65
Q

acyclovir, famciclovir, valacyclovir–mechanism

A
  • guanosine analogs
  • monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells –> few adverse effects
  • triphosphate formed by cellular enzymes
  • preferentially inhibit viral DNA Polymerase by chain termination
66
Q

acyclovir, famciclovir, valacyclovir–use

A
  • HSZ 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
67
Q

valacyclovir vs. acyclovir

A
  • valacyclovir is a prodrug of acyclovir
  • valacyclovir has better oral availability
68
Q

acyclovir, famciclovir, valacyclovir–toxicity

A
  • obstructive crystalline nephropathy
  • acute renal failure
    • both may occur if not adequately hydrated
69
Q

acyclovir, famciclovir, valacyclovir–mechanism of resistance

A
  • mutated viral thymidine kinase
70
Q

ganciclovir–mechanism

A
  • 5’ monophosphate formed by a CMV viral kinase
  • guanosine analog
  • triphosphate formed by cellular kinases
  • preferentially inhibits viral DNA polymerase
71
Q

ganciclovir–use

A
  • CMV–especially in immunocompromised patients
72
Q

vanganciclovir vs. ganciclovir

A
  • vanganciclovir is a prodrug of ganciclovir
  • vanganciclovir has better oral availability
73
Q

ganciclovir–toxicity

A
  • bone marrow suppression–leukopenia, neutropenia, thrombocytopenia
  • renal toxicity
  • more toxic to host enzymes than acyclovir
74
Q

ganciclovir–mechanism of resistance

A
  • mutated viral kinase
75
Q

foscarnet–mechanism

A
  • viral DNA/RNA polymerase inhibitor
  • HIV reverse transcriptase inhibitor
  • binds to pyrophosphate binding site of enzyme
  • does not require any kinase activity
  • “foscarnet = pyrofosphate analog”
76
Q

foscarnet–use

A
  • CMV retinitis in immunosompromised patients when ganciclovir fails
  • acyclovir resistant HSV
77
Q

foscarnet–toxicity

A
  • nephrotoxicity
  • electrolyte abnormalities can lead to seizures
    • hypo/hypercalcemia
    • hypo/hyperphosphatemia
    • hypokalemia
    • hypomagnesemia
78
Q

foscarnet–mechanism of resistance

A
  • mutated DNA polymerase
79
Q

cidofovir–mechanism

A
  • preferentially inhibits viral DNA polymerase
  • does not require phosphorylation by virla kinase
80
Q

cidofovir–use

A
  • CMV retinitis in immunocompromised patients
  • acyclovir resistant HSV
  • long half life
81
Q

cidofovir–toxicity

A
  • nephrotoxicity
82
Q

how to decrease possible toxicity of cidofovir?

A
  • coadminister with probenecid and IV saline
83
Q

HIV therapy

A
  • highly active antiretroviral therapy (HAART)
  • often initiated at the time of HIV diagnosis
84
Q

what does the highly active antiretroviral therapy for HIV consist of?

A
  • 3 drugs to prevent resistance
    • 2 NRTIS
    • 2 integrase inhibitor
85
Q

what are the strongest indications for patients to receive HAART?

A
  • AIDS defining illness
  • low CD4+ cell counts (<500 cells/mm3)
  • high viral load
86
Q

what are the 5 classes of HIV therapy drugs?

A
  • NRTIs
  • NNRTIs
  • protease inhibitors
  • integrase inhibitors
  • fusion inhibitors
87
Q

name the NRTIs

A
  • Abacavir (ABC)
  • DIdanosine (ddl)
  • Emtricitabine (FTC)
  • Lamivudine (3TC)
  • Stavudine (d4T)
  • Tenofovir (TDF)
  • Zidovudine (ZDV, formerly AZT)
88
Q

NRTIs–mechanism

A
  • competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group)
89
Q

which of the NRTIs are nucleotides? which are nucleosides?

A
  • Tenofovir is a nucleoTide
  • the others are nucleosides and nee to be phosphorylated to be active
    • “Have you dined (vudine) with my nuclear (nucleosides) family?”
90
Q

what is special about Zidovudine (ZDV)?

A
  • can be used as a general prophylaxis
  • can be used during pregnancy to dec risk of fetal transmission
91
Q

when is Abacavir (ABC) contraindicated?

A
  • when the patient has an HLA-B*5701 mutation
92
Q

NRTIs–toxicity

A
  • bone marrow suppression–can be reversed with granulocyte colony stimulating factor (G-CSF) and erythropoietin
  • peripheral neuropathy
  • lactic acidosis–nucleosides
  • anemia–ZDV
  • pancreatitis–didanosine
93
Q

name the 3 NNRTIS

A
  • delavirdine
  • efavirenz
  • nevirapine
94
Q

NNRTIs–mechanism

A
  • bind to reverse transcriptase at site different from NRTIs
  • do not require phosphorylation to be active or compete with nucleotides
95
Q

what are common toxicity signs for all NNRTIs?

A
  • rash
  • hepatotoxicity
96
Q

efavirenz–toxicity

A
  • (NNRTI)
  • vivid dreams
  • CNS symptoms
97
Q

what is a contraindication for delavirdine and efavirenz?

A
  • (NNRTI)
  • pregnancy
98
Q

name the protease inhibitors

A
  • atazanavir
  • darunavir
  • fosamprenavir
  • indinavir
  • lopinavir
  • ritonavir
  • saquinavir
    • ​“Navir (never) tease a protease”
99
Q

protease inhibitors–mechanism

A
  • assembly of virions depends on HIV-1 protease (pol gene) which cleaves the polypeptide products of HIV mRNA into their functional parts
    • so, pretease inhibitors prevent maturation of new viruses
100
Q

what is important about ritonavir?

A
  • (protease inhibitor)
  • can “boost” other drug concentrations by inhibiting cytochrome P-450
101
Q

protease inhibitors–toxicity

A
  • hyperglycemia
  • GI intolerance–nausea, diarrhea
  • lipodystrophy–Cushing like syndrome
102
Q

indinavir–toxicity

A
  • (protease inhibitor)
  • nephropathy
  • hematuria
103
Q

why is rifampin contraindicated with protease inhibitors?

A
  • rifampin is a potent CYP/UGT inducer
  • contraindicated with protease inhibitors b/c it can decrease protease inhibitor concentration
104
Q

name the integrase inhibitors

A
  • raltegravir
  • elvitegravir
  • dolutegravir
105
Q

integrase inhibitors–mechanism

A
  • inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase
106
Q

integrease inhibitors–toxicity

A
  • inc creatine kinase
107
Q

name the fusion inhibitors

A
  • enfuvirtide
  • maraviroc
108
Q

enfurvirtide–mechanism

A
  • (fusion inhibitor)
  • binds gp41 to inhibit viral entry
109
Q

enfurvirtide–toxicity

A
  • skin rxn at injection site
110
Q

maraviroc–mechanism

A
  • (fusion inhibitor)
  • binds CCR-5 on surface of T cells/monocytes which inhibit interaction with gp120
111
Q

interferons–mechanism

A
  • glycoproteins normally synthesized by virus-infected cells
  • exhibit a wide range of antiviral and antitumoral properties
112
Q

INF alpha–use

A
  • chronic hepatitis B and C
  • Kaposi sarcoma
  • hairy cell leukemia
  • condyloma acuminatum
  • renal cell carcinoma
  • malignant melanoma
113
Q

IFN beta–use

A
  • multiple sclerosis
114
Q

IFN gamma–use

A
  • chronic granulomatous dz
115
Q

interferon–toxicity

A
  • flu like symptoms
  • depression
  • neutropenia
  • myopathy
116
Q

name the hepatitis C therapy drugs

A
  • ribavirin
  • sofosbuvir
  • simeprevir
117
Q

ribavirin–mechanism

A
  • inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase
118
Q

ribavirin–use

A
  • chronic HCV
  • also used in RSV
    • palivizumab preffered in children
119
Q

ribavirin–toxicity

A
  • hemolytic anemia
  • severe teratogen
120
Q

sofosbuvir–mechanism

A
  • inhibits HCV RNA dependent RNA polymerase acting as a chain terminator
121
Q

sofosbuvir–use

A
  • chronic HCV in combination with ribavirin
    • +/- peginterferon alfa
  • do not use as monotherapy
122
Q

sofosbuvir–toxicity

A
  • fatigue
  • headache
  • nausea
123
Q

simeprevir–mechanism

A
  • HCV protease inhibitor
  • prevent viral replication
124
Q

simeprevir–use

A
  • chronic HCV in combination with ledipasvir (NS5A inhibitor)
  • do not use as monotherapy
125
Q

simeprevir–toxicity

A
  • photosensitivity rxns
  • rash
126
Q

what is the goal of infection control techniques?

A
  • reduction of pathogenic organism counts to safe levels–disinfection
  • inactivation of self propagating biological entities–sterilization
127
Q

list 5 infection control techniques

A
  • autoclave
  • alcohols
  • chlorhexidine
  • hydrogen peroxide
  • iodine and iodophors
128
Q

explain autoclave

A
  • pressurized steam at > 120 deg C
  • may be sporicidal
129
Q

explain alcohols (as an infection control technique)

A
  • denature proteins and disrupt cell membranes
  • not sporicidal
130
Q

explain chlorhexidine

A
  • denatures proteins and disrupts cell membranes
  • not sporicidal
131
Q

explain hydrogen peroxide as an infection control technique

A
  • free radical oxidation
  • sporicidal
132
Q

explain iodine and iodophors as an infection control technique

A
  • halogenation of DNA, RNA, and proteins
  • may be sporicidal
133
Q

name tha antimicrobials to avoid during pregnancy

A
  • Sulfonamides
  • Aminoglycosides
  • Fluoroquinolones
  • Clarithromycin
  • Tetracyclines
  • Ribavirin
  • Griseofluvin
  • Chloramphenicol
    • “SAFe Children Take Really Good Care”
134
Q

what is the adverse effec tof sulfonamides during pregnancy?

A

kernicterus

135
Q

what is the adverse effect of aminoglycosides during pregnancy?

A

ototoxicity

136
Q

what is the adverse effect of fluoroquinolones during pregnancy?

A

cartilage damage

137
Q

what is the adverse effect of clarithromycin during pregnancy?

A

embryotoxic

138
Q

what is the adverse effect of tetracyclines during pregnancy?

A
  • discolored teeth
  • inhibition of bone growth
139
Q

what is the adverse effect of ribavirin during pregnancy?

A

teratogenic

140
Q

what is the adverse effect of griseofulvin during pregnancy?

A

teratogenic

141
Q

what is the adverse effect of chloramphenicol during pregnancy?

A

Gray baby syndrome

PLAB Pharmacology (17 decks)

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