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USMLE 1 > Microbiology- Antimicrobials (Micobacterium, HIV and Micosis) > Flashcards

Microbiology- Antimicrobials (Micobacterium, HIV and Micosis) Flashcards

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USMLE® Step 1 flashcards
1
Q

Antifungal therapy Imagen

A

pag 198

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2
Q

Amphotericin B

  • Mechanism
  • Adverse effects
A

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

Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (“amphoterrible”). Hydration lowers nephrotoxicity. Liposomal amphotericin lowers toxicity.

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3
Q

Amphotericin B

- Clinical Uses

A

Serious, systemic mycoses. Cryptococcus (amphotericin B with/without flucytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida,
Mucor. Intrathecally for fungal meningitis. Supplement K+ and Mg2+ because of altered renal tubule permeability.

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4
Q

Nystatin

  • Mechanism
  • Clinical Uses
A

Same as amphotericin B. Topical use only as too toxic for systemic use.

“Swish and swallow” for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.

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5
Q

Flucytosine

  • Mechanism
  • Clinical Uses
  • Adverse effects
A

Inhibits DNA and RNA biosynthesis by conversion to 5 fluorouracil by cytosine deaminase.

Systemic fungal infections (especially meningitis caused by Cryptococcus) in combination with amphotericin B.

Bone marrow suppression.

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6
Q

Azoles

  • Names
  • Mechanism
  • Adverse effects
A

Clotrimazole, fluconazole, isavuconazole, itraconazole, ketoconazole, miconazole, voriconazole.

Inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol.

Testosterone synthesis inhibition (gynecomastia, especially with ketoconazole), liver dysfunction (inhibits cytochrome P-450).

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7
Q

Azoles

- Clinical use

A

Local and less serious systemic mycoses. Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types.

Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

Voriconazole for Aspergillus and some Candida. Isavuconazole for serious Aspergillus and Mucor
infections

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8
Q

Terbinafine

  • Mechanism
  • Clinical Uses
  • Adverse effects
A

Inhibits the fungal enzyme squalene epoxidase

Dermatophytoses (especially onychomycosis—fungal infection of finger or toe nails).

GI upset, headaches, hepatotoxicity, taste disturbance.

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9
Q

Echinocandins

  • Names
  • Mechanism
  • Clinical Uses
  • Adverse effects
A

Anidulafungin, caspofungin, micafungin

Inhibit cell wall synthesis by inhibiting synthesis of β-glucan.

Invasive aspergillosis, Candida.

GI upset, flushing (by histamine release).

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10
Q

Griseofulvin

  • Mechanism
  • Clinical Uses
  • Adverse effects
A

Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (eg, nails).

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm)

Teratogenic, carcinogenic, confusion, headaches, disulfiram-like reaction, High cytochrome P-450 and
warfarin metabolism.

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11
Q

Antiprotozoal therapy

A

Pyrimethamine (toxoplasmosis), suramin and melarsoprol (Trypanosoma brucei), nifurtimox (T cruzi), sodium stibogluconate (leishmaniasis).

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12
Q

Anti-mite/louse therapy

A

Permethrin (inhibits Na+ channel deactivation, neuronal membrane depolarization), malathion (acetylcholinesterase inhibitor), lindane (blocks GABA channels, neurotoxicity).

Used to treat scabies (Sarcoptes scabiei) and lice (Pediculus and Pthirus).

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13
Q

Chloroquine

  • Mechanism
  • Clinical Uses
  • Adverse effects
A

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

Treatment of plasmodial species other than P falciparum. Resistance due to membrane pump that lowers intracellular concentration of drug.

Treat P falciparum with artemether/lumefantrine or atovaquone/proguanil. For life-threatening malaria,
use quinidine in US (quinine elsewhere) or artesunate.

Retinopathy; pruritus (especially in dark-skinned individuals).

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14
Q

Antihelminthic therapy

A

Pyrantel pamoate, Ivermectin, Mebendazole (microtubule inhibitor), Praziquantel, Diethylcarbamazine.

Helminths get PIMP’D.

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15
Q

Oseltamivir, zanamivir

  • Mechanism
  • Clinical Uses
A

Inhibit influenza neuraminidase, lowers release of progeny virus.

Treatment and prevention of both influenza A and B. Beginning therapy within 48 hours of symptom onset may shorten duration of illness.

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16
Q

Acyclovir, famciclovir, valacyclovir

  • Mechanism
  • Adverse effects
  • Resistance
A

Guanosine analogs. Monophosphorylated by HSV/VZV thymidine kinase. Triphosphate formed by cellular enzymes. Preferentially inhibit viral DNA polymerase by chain termination.

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated.

Mutated viral thymidine kinase.

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17
Q

Acyclovir, famciclovir, valacyclovir

- Clinical use

A

HSV and VZV. Weak activity against EBV. No activity against CMV.

Used for HSVinduced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in
immunocompromised patients. No effect on latent forms of HSV and VZV.

Valacyclovir, a prodrug of acyclovir, has better oral bioavailability. For herpes zoster, use famciclovir.

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18
Q

Ganciclovir

  • Mechanism
  • Adverse effects
  • Resistance
A

5′-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.

Bone marrow suppression, renal toxicity. More toxic
to host enzymes than acyclovir.

Mutated viral kinase.

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19
Q

Ganciclovir

- Clinical use

A

CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability.

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20
Q

Foscarnet

  • Mechanism
  • Adverse effects
  • Resistance
A

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

Nephrotoxicity, electrolyte abnormalities (hypo- or hypercalcemia, hypo- or hyperphosphatemia, hypokalemia, hypomagnesemia) can lead to seizures.

Mutated DNA polymerase.

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21
Q

Foscarnet

- Clinical use

A

CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV.

22
Q

Cidofovir

A

Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase.

CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half-life.

Nephrotoxicity (coadminister with probenecid and IV saline to reduce toxicity).

23
Q

HIV therapy

A

Highly active antiretroviral therapy (HAART): often initiated at the time of HIV diagnosis.

Strongest indication for patients presenting with AIDS-defining illness, low CD4+ cell counts (< 500 cells/mm3), or high viral load.

Regimen consists of 3 drugs to prevent resistance:
2 NRTIs and preferably an integrase inhibitor

24
Q

NRTIs

- Mechanism

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3′ OH group). All need to be phosphorylated to be active.

ZDV can be used for general prophylaxis and during pregnancy to reduce risk of fetal transmission.

25
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).

Abacavir contraindicated if patient has HLA-B*5701 mutation due to risk of hypersensitivity.

26
Q

NRTIs

- Names

A 
Abacavir (ABC)
Didanosine (ddI)
Emtricitabine (FTC)
Lamivudine (3TC)
Stavudine (d4T)
Tenofovir (TDF)
Zidovudine (ZDV,cformerly AZT)
27
Q

NNRTIs

  • Names
  • Mechanism
A

Delavirdine, Efavirenz, Nevirapine

Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.

28
Q

NNRTIs

- Toxicity

A

Rash and hepatotoxicity are common to all NNRTIs. Vivid dreams and CNS symptoms are common with efavirenz. Delavirdine and efavirenz are contraindicated in pregnancy.

29
Q

Protease inhibitors

- names

A 
Atazanavir
Darunavir
Fosamprenavir
Indinavir
Lopinavir
Ritonavir
Saquinavir
30
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

Ritonavir can “boost” other drug concentrations by inhibiting cytochrome P-450.

31
Q

Protease inhibitors

- Toxicity

A

Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy (Cushing-like syndrome).

Nephropathy, hematuria, thrombocytopenia (indinavir).

Rifampin (potent CYP/UGT inducer) reduces protease inhibitor concentrations; use rifabutin instead

32
Q

Integrase inhibitors

  • Names
  • Mechanism
  • Toxicity
A

Dolutegravir, Elvitegravir, Raltegravir

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

High creatine kinase

33
Q

Fusion inhibitors

  • Enfuvirtide
  • Maraviroc
A
  • Binds gp41, inhibiting viral entry. Skin reaction at injection sites.
  • Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120.
34
Q

Interferons

  • Mechanism
  • Adverse effects
A

exhibiting a wide range of antiviral and antitumoral properties.

Flu-like symptoms, depression, neutropenia, myopathy.

35
Q

Interferons

- Clinical use

A

Chronic HBV and HVC, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell
carcinoma, malignant melanoma, multiple sclerosis, chronic granulomatous disease.

36
Q

Hepatitis C therapy

A

Chronic HCV infection is treated with different combinations of the following drugs; none is approved as monotherapy. Ribavirin also used to treat RSV (palivizumab preferred in children).

  • Ledipasvir, Ribavirin, Simeprevir, Sofosbuvir
37
Q

Ledipasvir

A

Viral phosphoprotein (NS5A) inhibitor; NS5A plays important role in replication.

38
Q

Ribavirin

  • Mechanism
  • Adverse effects
A

Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase.

Hemolytic anemia, severe teratogen.

39
Q

Simeprevir

  • Mechanism
  • Adverse effects
A

HCV protease (NS3/4A); prevents viral replication.

Photosensitivity reactions, rash

40
Q

Sofosbuvir

  • Mechanism
  • Adverse effects
A

Inhibits HCV RNA-dependent RNA polymerase (NS5B) acting as a chain terminator.

Fatigue, headache, nausea.

41
Q

Antimicrobials to avoid in pregnancy

A

SAFe Children Take Really Good Care.

Sulfonamides
Aminoglucosidos
Fluoroquinolone
Claritromicina
Tetraciclina
Ribavirin
Griseofulvin
Cloranfenicol
42
Q

Disinfection and

sterilization

A

Pag 204

43
Q

Antimycobacterial drugs

M tuberculosis

A

RIPE: Rifampin, Isoniazid, Pyrazinamide, Ethambutol

Profilaxis: Isoniazid

44
Q

Antimycobacterial drugs

M avium–intracellulare

A

More drug resistant than M tuberculosis. Azithromycin or clarithromycin + ethambutol. Can add rifabutin or ciprofloxacin.

Profilaxis: Azithromycin, rifabutin

45
Q

Antimycobacterial drugs

M leprae

A

Long-term treatment with dapsone and rifampin for tuberculoid form. Add clofazimine for lepromatous form.

46
Q

Rifamycins (Rifampin, rifabutin.)

  • Mechanism
  • Clinical use
A

Inhibit DNA-dependent RNA polymerase.

Mycobacterium tuberculosis; delay resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H influenzae type b.

47
Q

Rifamycins (Rifampin, rifabutin)

  • Adverse effects
  • Resistance
A

Minor hepatotoxicity and drug interactions (Enhance cytochrome P-450); orange body fluids (nonhazardous side effect). Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.

Mutations reduce drug binding to RNA polymerase. Monotherapy rapidly leads to resistance.

Rifampin’s 4 R’s:
RNA polymerase inhibitor
Ramps up microsomal cytochrome P-450
Red/orange body fluids
Rapid resistance if used alone
48
Q

Isoniazid

  • Mechanism
  • Clinical use
A

Lowers synthesis of mycolic acids. Bacterial catalaseperoxidase (encoded by KatG) needed to convert INH to active metabolite.

Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB. Also used as monotherapy for latent TB.

49
Q

Isoniazid

  • Adverse effects
  • Resistance
A

Hepatotoxicity, P-450 inhibition, drug-induced SLE, anion gap metabolic acidosis, vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia). Administer with pyridoxine (B6).

INH Injures Neurons and Hepatocytes.

Mutations leading to underexpression of KatG.

50
Q

Pyrazinamide

  • Mechanism
  • Clinical use
  • Adverse effects
A

Mechanism uncertain. Pyrazinamide is a prodrug that is converted to the active compound pyrazinoic acid. Works best at acidic pH.

Mycobacterium tuberculosis

Hyperuricemia, hepatotoxicity.

51
Q

Ethambutol

  • Mechanism
  • Clinical use
  • Adverse effects
A

lowers carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

Mycobacterium tuberculosis

Optic neuropathy (red-green color blindness). Pronounce “eyethambutol.”

52
Q

Streptomycin

  • Mechanism
  • Clinical use
  • Adverse effects
A

Interferes with 30S component of ribosome

Mycobacterium tuberculosis (2nd line).

Tinnitus, vertigo, ataxia, nephrotoxicity

USMLE 1 (73 decks)

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