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Step One > Pharm antimicrobials > Flashcards

Pharm antimicrobials Flashcards

1
Q

What is used for prophylaxis in:

High risk for endocarditis and undergoing surgical or dental procedures:

Exposure to gonorrhea:

History of recurrent UTIs:

Exposure to meningococcal infection:

Pregnant woman carrying group B strep:

Prevention of gonococcal conjuctivitis in newborn

Prevention of postsurgical infection due to S. aureus

Prophylaxis of strep pharyngitis in child with prior rheumatic fever:

Exposure to syphilis:

A

High risk for endocarditis and undergoing surgical or dental procedures: Amoxicillin

Exposure to gonorrhea: Ceftriaxone

History of recurrent UTIs: TMP-SMX

Exposure to meningococcal infection: Ceftriaxone, ciprofloxacin, rifampin

Pregnant woman carrying group B strep: penicillin G

Prevention of gonococcal conjuctivitis in newborn: Erythromycin ointment

Prevention of postsurgical infection due to S. aureus: cefazolin

Prophylaxis of strep pharyngitis in child with prior rheumatic fever: Penicillin

Exposure to syphilis: Penicillin

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2
Q

What is used for prophylaxis in:

High risk for endocarditis and undergoing surgical or dental procedures:

Exposure to gonorrhea:

History of recurrent UTIs:

Exposure to meningococcal infection:

Pregnant woman carrying group B strep:

Prevention of gonococcal conjuctivitis in newborn

Prevention of postsurgical infection due to S. aureus

Prophylaxis of strep pharyngitis in child with prior rheumatic fever:

Exposure to syphilis:

A

High risk for endocarditis and undergoing surgical or dental procedures: Amoxicillin

Exposure to gonorrhea: Ceftriaxone

History of recurrent UTIs: TMP-SMX

Exposure to meningococcal infection: Ceftriaxone, ciprofloxacin, rifampin

Pregnant woman carrying group B strep: penicillin G

Prevention of gonococcal conjuctivitis in newborn: Erythromycin ointment

Prevention of postsurgical infection due to S. aureus: cefazolin

Prophylaxis of strep pharyngitis in child with prior rheumatic fever: Penicillin

Exposure to syphilis: Penicillin

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3
Q

What prophylactic antimicrobes are given to HIV patients when they reach CD4

A

200=TMP-SMX=PCP
100=TMP-SMX=PCP and toxo
50=azithromycin or clarithromycin=MAC

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4
Q

What is used to treat MRSA? VRE? Mutil drug resistant P. aeruginosa?

A

MRSA: Vanco, daptomycin, linezolid, tigecycline, ceftaroline

VRE: Linezolid and streptogramins (quinuprastin, dalfopristin)

Pseudomonas: Polymixins B and E (colistin)

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5
Q

Which antifungals inhibit

lanosterol synth? 
Ergosterol synth? 
Nucleic acid synth? 
Forms membrane pores? 
Cell wall synth?
A 
lanosterol synth? terbinafine
Ergosterol synth? Azoles
Nucleic acid synth? flucytosine
Forms membrane pores? amphoterecin B and nystatin
Cell wall synth? Echinocandins
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6
Q

What is the mechanism of amphoterecin B? Clinical use? What should it be given with? Why? Toxicity? Prevention?

A

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

Serious systemic mycoses
Cryptococcus w/w/o flucytosine for cryptococcal meningitis
Blasto, coccid, histoplasma, candida, mucor
Intrathecally for fungal meningitis

Supplement K and MG b/c of altered renal tubule permeabililty

Fever/chills
Hypotnesion
nephrotoxicity
arrhythmias
anemia
IV phlebitis

Hydration decr. nephrotoxicity
Liposomal amphoterecin decr. toxicity

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7
Q

What is the mechanism of Nystatin? Clinical use?

A 
Binds to ergosterol. membrane pores
Topical use (too toxic)

Swish and swallow for oral candidiasis (thrush)
topical for diaper rash and vulvovaginal candidiasis

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8
Q

What is the mechanism of flucytosine? Clincal use/organisms? Toxicity?

A

Inhibits DNA and RNA biosynth by conversion to 5 FU by cytosine deaminase

Systemic fungal infections (especially crypto meningitis) in combo with ampho B

Bone marrow suppression

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9
Q

What type of drugs are clotrimazole (3), fluconazole (1), itraconazole (2), ketoconazole (5), miconazole (4), voriconazole? Mechanism? Clinical use generally? Of 1? Of 2? Of 3/4? Toxicity? Of 5 especially?

A

Azoles

Inhibit fungal ergosterol synth by inhibiting the cytochrome P450 enzyme that converts lanosterol to ergosterol

Local and less serious systemic mycoses
1-chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types
2-blasto, histo, coccidio
3/4=topical fungal infections

Testosterone synth inhibition (especially 5)
liver dysfunction

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10
Q

What is the mechanism of terbenafine? Clinical use? Toxicity?

A

Inhibits the fungal enzyme squalene epoxidase (prevents lanosterol/ergosterol production)

Dermatophytoses (especially onychomycosis)

GI upset
headaches
hepatotoxicity
taste disturbance

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11
Q

What type of drugs are anidulafungin, caspofungin, and micafungin? Mechanism? Clinical use? Toxicity?

A

Echinocandins

Inhibit cell wall synth by inhibiting synth of beta glucan

Invasive aspergillosis, candida

GI upset, flushing (histamine)

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12
Q

What is the mech of griseofulvin? Clincal use? Toxicity?

A

Interferes with microtubule formation; disrupts mitosis
Deposits in keratin containing tissues (nails)

Oral treatment of superficial infections
Inhibits growht of dermatophytes

Teratogenic, carcinogenic, confusion, headaches, incr. P450 and warfarin metabolism

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13
Q

What is used to treat toxo? Trypanosoma brucei? T. cruzi? leishmaniasis?

A

Toxo=Pyrimethamine
T. brucei=suramin and melarsoprol
T. cruzi=nifurtimox
Leish=sodium stibogluconate

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14
Q

What is used to treat scabies and lice? Other names for scabies and lice? Mechanism of scabies and lice treatments?

A

Scabies=sarcoptes scabiei
Lice=Pediculus and pthirus

Permethrin (blocks na+ channels leading to neurotoxicity)
malathion (AChE inhibitor)
Lindane (blocks GABA channels leading to neurotoxicity)

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15
Q

What is the mechanism of chloroquine? Clincal uses/organisms? Toxicity? Method of resistance?

A

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

Treatment of plasmodial species other than P. falciparum (frequency of resistance is too high)

Retinopathy; pruritus (especially in dark skinned)

Membrane pump that decr. intracellular conc. of drug

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16
Q

What should be used to treat P. falciparum? Life threatening malaria?

A

Artemether/lumefantrine or atovaquone/proguanil

Quinidine or artesunate

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17
Q

What should be used to treat P. falciparum? Life threatening malaria?

A

Artemether/lumefantrine or atovaquone/proguanil

Quinidine or artesunate

18
Q

What is used to treat helminths?

A

Mebendazole, pyrantel pomoate, ivermectin, diethylcarbamazine, praziquantel

19
Q

What is used to treat helminths?

A

Mebendazole, pyrantel pomoate, ivermectin, diethylcarbamazine, praziquantel

20
Q

Concerning HIV drugs, which type/class:

prevent attachment:
Prevent penetration:
Inhibit integration:
Inhibit reverse transcriptase: 
Inhibit proteolytic processing:
A

prevent attachment: Maraviroc
Prevent penetration: Enfurvitide
Inhibit integration: Raltegravir
Inhibit reverse transcriptase: NRTIs and NNRTIs
Inhibit proteolytic processing: Protease inhibitors

21
Q

Concerning non HIV antivirals, which type/class

Affect protein synth:
Inhibit uncoating:
inhibit nucleic acid synth:
affect release of progeny viruses:

A

Affect protein synth: Interferon alpha
Inhibit uncoating: amantidine, rimantidine
inhibit nucleic acid synth: guanosine analogs, viral DNA polymerase inhibitors, Guanosine nucleotide synth
affect release of progeny viruses: NA inhibitors

22
Q

Concerning non HIV antivirals, which type/class

Affect protein synth:
Inhibit uncoating:
inhibit nucleic acid synth:
affect release of progeny viruses:

A

Affect protein synth: Interferon alpha
Inhibit uncoating: amantidine, rimantidine
inhibit nucleic acid synth: guanosine analogs, viral DNA polymerase inhibitors, Guanosine nucleotide synth
affect release of progeny viruses: NA inhibitors

23
Q

What is the mechanism of oseltamavir and zanamivir? Clinical use?

A

Inhibit influenza NA leading to decr. release of progeny

Treatment and prevention and influenza A and B

24
Q

What type of drug are acyclovir (1), famciclovir (2), and valacyclovir (3)? Mechanism of action? Clinical use? How do 1 and 3 differ? What is used to treat herpes zoster (shingles)? Toxicity? Prevention? Mechanism of resistance?

A

Guanosine analogs

Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells leading to few adverse effects.
Triphosphate formed by cellular enzymes
Preferentially inhibit viral DNA polymerase by chain termination.

HSV and VZV
WEak EBV, no CMV.
HSV induced mucocutaneous and genital lesions as well as for encephalitis
Prophylaxis in immunocompr.
No effect on latent infection

3 is prodrug of 1 with more bioavailability
Herpes zoster=2

Obstructive crystalline nephropathy and acute renal failure
Hydrate!

Mutated viral thymidine kinase

25
Q

What is the mechanism of ganciclovir (1)? Clinical use? What is valganciclovir (2)? Toxicity? Mechanism of resistance?

A

Guanosine analog

5’ monophosphate formed by CMV viral kinase
Triphosphate formed by cellular kinases
Preferentially inhibits viral DNAP by chain termination

CMV, especially immunocompromised

2 is prodrug of 1 with greater bioavail.

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

Mutated viral kinase

26
Q

What is the mechanism of Foscarnet? Clinical use? Toxicity? Mechanism of resistance?

A

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor.
Binds to pyrophosphate binding site of enzyme
Does not require activation by viral kinase

CMV retinitis in immunocompromised pts when gancyclovir doesn’t work.
Acyclovir resistant HSV

Nephrotoxicity, electrolyte abnormalities can lead to seizures

Mutated DNAP

27
Q

What is the mechanism of Foscarnet? Clinical use? Toxicity? Mechanism of resistance?

A

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor.
Binds to pyrophosphate binding site of enzyme
Does not require activation by viral kinase

CMV retinitis in immunocompromised pts when gancyclovir doesn’t work.
Acyclovir resistant HSV

Nephrotoxicity, electrolyte abnormalities can lead to seizures

Mutated DNAP

28
Q

What is the mechanism of cidofovir? Clinical use? Toxicity? Prevent?

A

Preferentially inhibits viral DNAP
Does not require phosphorylation by viral kinase

CMV retinitis in imunocompromised
acyclovir resist HSV
Long half life

Nephrotoxicity (coadminister with probenecid and IV saline)

29
Q

What is HAART? When is it started? When is it most strongly indicated? What does it consist of?

A

Highly active retroviral therapy

Often initiated at time of diagnosis of HIV

AIDS defining illness
CD4

30
Q

What type of drugs are atazanavir, darunavir, fosamprenavir, indinavir, lopinavir, ritonavir, and saquinavir? Mechanism? Toxicity? CIs? Clinical use?

A

Inhibit HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts; prevent maturation of new viruses.

Hyperglycemia, GI intolerance, lipodystrophy

CI use with rifampin (CYP inducer=derease protease inhibitor concentration).

HAART

31
Q

What type of drugs are abacavir, didanosine, emtricitabine, lamivudine, stavudine, tenofovir (1), zidovudine (2)? Mechanism? Of 1? Clinical use? of 2? Toxicity? Reversal?

A

NRTIs

Competetively inhibit NT binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group)
Nucleosides=must be phosphorylated
1=NT

HAART
2=general prophylaxis and during pregnancy to reduce risk of fetal transmission.

Bone marrow suppression (reversed with G-CSF and EPO)
Periph neuro
lactic acidosis

no vir in the middle of the word

32
Q

What type of drugs are delavirdine (1), efavirenz (2), nevirapine? Mechanism? Toxicity? Of 2? CI of 1/2? Use?

A

NNRTIs

Bind to RT at site different than NRTIs
Do not require phosphorylation
Do not compete with NTs

Rash and hepatotoxicity
2=vivid dreams and CNS symptoms
1/2=CI in pregnancy

HAART

‘vir in middle of name

33
Q

What type of drug is raltegravir? Mechanism? Toxicity? Use?

A

Integrase Inhibitor

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

Incr. CK

“tegra”=tegrase

34
Q

What type of drugs are enfuvirtide (1) and maraviroc (2)? Mechanism of 1? Of 2? Toxicity of 1?

A

Fusion inhibitors

1=Binds gp41, inhibits viral entry
“enfu”=envelope, fusion

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

“Mar” = mare = knight =t cell

1=skin reaction at injection sites

35
Q

What is the mechanism of interferons? Clinical use of alpha (1) ? beta (2) ? Gamma (3)? Toxicity?

A

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

Alpha: chronic hep B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell CA, malignant melanoma

Beta: multiple sclerosis

Gamma: chronic granulomatous disease

Neutropenia, myopathy

36
Q

What is the treatment of Hep C?

A

Ribavirin, simeprevir, and sofosbuvir

37
Q

What is the mechanism of Ribavirin? Clinical use? Toxicity?

A

Inhibits synth of guanine NT by competetively inhibiting inosine monophosphate dehydrogenase

Chronic HCV, also used in RSV (in children palivizumab is preferred)

Hemolytic anemia
Severe teratogen

38
Q

What is the mechanism of simepravir? Clinical use? Toxicity?

A

HCV protease inhibitor; prevents viral replication

Chronic HCV in combination with ribavirin and peginterferon alpha, never alone.

Photosensitivity, rash

39
Q

What is the mechanism of Sofosbuvir? use? Toxicity?

A

Inhibits HCV RNA-dependent RNAP acting as a chain terminator.

Chronic HCV in combo with ribavirin, +/- peginterferon alpha, never alone

Fatigue, headache, nausea

40
Q

What are the goals of infection control? What does the autoclave do? Alcohols? Chlorhexedine? Hydrogen peroxide? Iodine and iodophors?

A

Disinfection (reduction of pathogenic organism to safe level)

Sterilization (inactivation of self propagating bio entities)

Autoclave: pressurized steam at > 120 C. maybe sporicidal.

Alcohols: Denatures proteins and disrupts cell membranes. Not sporicidal

Chlorhexidine: denatures proteins and disrupts cell membranes. Not sporicidal

H2O2: Free radical oxidation. Sporicidal

Iodine: Halogenation of DNA, RNA, and proteins. May be sporicidal.

41
Q

What are the goals of infection control? What does the autoclave do? Alcohols? Chlorhexedine? Hydrogen peroxide? Iodine and iodophors?

A

Disinfection (reduction of pathogenic organism to safe level)

Sterilization (inactivation of self propagating bio entities)

Autoclave: pressurized steam at > 120 C. maybe sporicidal.

Alcohols: Denatures proteins and disrupts cell membranes. Not sporicidal

Chlorhexidine: denatures proteins and disrupts cell membranes. Not sporicidal

H2O2: Free radical oxidation. Sporicidal

Iodine: Halogenation of DNA, RNA, and proteins. May be sporicidal.

42
Q

What are some antibiotics that should not be taken in pregnancy? Why?

A

SAFe Children Take Really Good Care

Sulfonamides: kernicterus
Aminoglycosides: ototoxicity
Flouroquinolones: Cartilage damage
Clarithromycin: Embryotoxic
Tetracyclines: Discolored teeth, inhibition of bone growth
Ribavirin (antiviral): teratogenic
Griseofulvin: teratogenic
Chloramphenicol: gray baby syndrome

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