Pharmacology animicrobial Q&a

[Anonymous]

Q: A common side effects of INF treatment is?
A: Neutropenia

Q: Antimicrobial prophylaxis for a history of recurrent UTIs
A: TMP-SMZ

Q: Antimicrobial prophylaxis for Gonorrhea
A: Ceftriaxone

Q: Antimicrobial prophylaxis for Meningococcal infection
A: Rifampin (DOC), minocycline

Q: Antimicrobial prophylaxis for PCP
A: TMP-SMZ (DOC), aerosolized pentamidine

Q: Antimicrobial prophylaxis for Syphilis
A: Benzathine penicillin G

Q: Are Aminoglycosides Teratogenic?
A: Yes

Q: Are Ampicillin and Amoxicillin penicillinase resistant?
A: No

Q: Are Carbenicillin, Piperacillin, and Ticarcillin penicillinase resistant?
A: No

Q: Are Cephalosporins resistant to penicillinase?
A: No, but they are less susceptible than the other Beta lactams

Q: Are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant?
A: Yes

Q: Clinical use of Isoniazid (INH)?
A: Mycobacterium tuberculosis, the only agent used as solo prophylaxis against TB

Q: Common side effects associated with Clindamycin include?
A: Pseudomembranous colitis (C. difficile), fever, diarrhea

Q: Common toxicities associated with Fluoroquinolones?
A: GI upset, Superinfections, Skin rashes, Headache, Dizziness

Q: Common toxicities associated with Griseofulvin are…...?
A: Teratogenic, Carcinogenic, Confusion, Headaches

Q: Describe the MOA of Interferons (INF)
A: Glycoproteins from leukocytes that block various stages of viral RNA and DNA synthesis

Q: Do Tetracyclines penetrate the CNS?
A: Only in limited amounts

Q: Does Ampicillin or Amoxicillin have a greater oral bioavailability?
A: AmOxicillin has greater Oral bioavailability

Q: Does Amprotericin B cross the BBB?
A: No

Q: Does Foscarnet require activation by a viral kinase?
A: No

Q: Foscarnet toxicity?
A: Nephrotoxicity

Q: Ganciclovir associated toxicities?
A: Leukopenia, Neutropenia, Thrombocytopenia, Renal toxicity

Q: How are INFs used clinically?
A: Chronic Hepatitis A and B, Kaposi's Sarcoma

Q: How are Sulfonamides employed clinically?
A: Gram +, Gram -, Norcardia, Chlamydia

Q: How are the HIV drugs used clinically?
A: Triple Therapy' 2 Nucleoside RT Inhibitors with a Protease Inhibitor

Q: How are the Latent Hypnozoite (Liver) forms of Malaria (P. vivax, P.ovale) treated?
A: Primaquine

Q: How can Isoniazid (INH)-induced neurotoxicity be prevented?
A: Pyridoxine (B6) administration

Q: How can the t1/2 of INH be altered?
A: Fast vs. Slow Acetylators

Q: How can the toxic effects fo TMP be ameliorated?
A: With supplemental Folic Acid

Q: How can Vancomycin-induced 'Red Man Syndrome' be prevented?
A: Pretreat with antihistamines and a slow infusion rate

Q: How do Sulfonamides act on bacteria?
A: As PABA antimetabolites that inhibit Dihydropteroate Synthase, Bacteriostatic

Q: How do the Protease Inhibitors work?
A: Inhibt Assembly of new virus by Blocking Protease Enzyme

Q: How does Ganciclovir's toxicity relate to that of Acyclovir?
A: Ganciclovir is more toxic to host enzymes

Q: How does resistance to Vancomycin occur?
A: With an amino acid change of D-ala D-ala to D-ala D-lac

Q: How is Acyclovir used clinically?
A: HSV, VZV, EBV, Mucocutaneous and Genital Herpes Lesions, Prophylaxis in Immunocompromised pts

Q: How is Amantadine used clinically?
A: Prophylaxis for Influenza A, Rubella ; Parkinson's disease

Q: How is Amphotericin B administered for fungal meningitis?
A: Intrathecally

Q: How is Amphotericin B used clinically?
A: Wide spectrum of systemic mycoses: Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor

Q: How is Chloramphenical used clinically?
A: Meningitis (H. influenza, N. meningitidis, S. pneumoniae), Conserative treatment due to toxicities

Q: How is Foscarnet used clinically?
A: CMV Retinitis in IC pts when Ganciclovir fails

Q: How is Ganciclovir activated?
A: Phosphorylation by a Viral Kinase

Q: How is Ganciclovir used clinically?
A: CMV, esp in Immunocompromised patients

Q: How is Griseofulvin used clinically?
A: Oral treatment of superficial infections

Q: How is Leishmaniasis treated?
A: Pentavalent Antimony

Q: How is Ribavirin used clinically?
A: for RSV

Q: How is Rifampin used clinically?
A: 1. Mycobacterium tuberculosis
A: 2. Delays resistance to Dapsone when used of Leprosy
A: 3. Used in combination with other drugs

Q: How is Trimethoprim used clinically?
A: Used in combination therapy with SMZ to sequentially block folate synthesis

Q: How is Vancomycin used clinically?
A: For serious, Gram + multidrug-resistant organisms

Q: How would you treat African Trypanosomiasis (sleeping sickness)?
A: Suramin

Q: In what population does Gray Baby Syndrome occur? Why?
A: Premature infants, because they lack UDP-glucuronyl transferase

Q: Is Aztreonam cross-allergenic with penicillins?
A: No

Q: Is Aztreonam resistant to penicillinase?
A: Yes

Q: Is Aztreonam usually toxic?
A: No

Q: Is Imipenem resistant to penicillinase?
A: Yes

Q: Is Penicillin penicillinase resistant?
A: No - duh

Q: IV Penicillin
A: G

Q: Mnemonic for Foscarnet?
A: Foscarnet = pyroFosphate analog

Q: MOA for Penicillin (3 answers)?
A: 1)Binds penicillin-binding proteins
A: 2) Blocks transpeptidase cross- linking of cell wall
A: 3) Activates autolytic enzymes

Q: MOA: Bactericidal antibiotics
A: Penicillin, Cephalosporins, Vancomycin, Aminoglycosides, Fluoroquinolones, Metronidazole

Q: MOA: Block cell wall synthesis by inhib. Peptidoglycan cross-linking (7)
A: Penicillin, Ampicillin, Ticarcillin, Pipercillin, Imipenem, Aztreonam, Cephalosporins

Q: MOA: Block DNA topoisomerases
A: Quinolones

Q: MOA: Block mRNA synthesis
A: Rifampin

Q: MOA: Block nucleotide synthesis
A: Sulfonamides, Trimethoprim

Q: MOA: Block peptidoglycan synthesis
A: Bacitracin, Vancomycin

Q: MOA: Block protein synthesis at 30s subunit
A: Aminoglycosides, Tetracyclines

Q: MOA: Block protein synthesis at 50s subunit
A: Chloramphenicol, Erythromycin/macrolides, Lincomycin, Clindamycin, Streptogramins (quinupristin, dalfopristin)

Q: MOA: Disrupt bacterial/fungal cell membranes
A: Polymyxins

Q: MOA: Unkown
A: Pentamidine

Q: MOAisrupt fungal cell membranes
A: Amphotericin B, Nystatin, Fluconazole/azoles

Q: Name common Polymyxins
A: Polymyxin B, Polymyxin E

Q: Name several common Macrolides (3)
A: Erythromycin, Azithromycin, Clarithromycin

Q: Name some common Sulfonamides (4)
A: Sulfamethoxazole (SMZ), Sulfisoxazole, Triple sulfas, Sulfadiazine

Q: Name some common Tetracyclines (4)
A: Tetracycline, Doxycycline, Demeclocycline, Minocycline

Q: Name the common Aminoglycosides (5)
A: Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

Q: Name the common Azoles
A: Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole

Q: Name the common Fluoroquinolones (6)
A: Ciprofloxacin, Norfloxacin, Ofloxacin, Grepafloxacin, Enoxacin, Nalidixic acid

Q: Name the common Non-Nucleoside Reverse Transcriptase Inhibitors
A: Nevirapine, Delavirdine

Q: Name the common Nucleoside Reverse Transcriptase Inhibitors
A: Zidovudine (AZT), Didanosine (ddI), Zalcitabine (ddC), Stavudine (d4T), Lamivudine (3TC)

Q: Name the Protease Inhibitors (4)
A: Saquinavir, Ritonavir, Indinavir, Nelfinavir

Q: Name two classes of drugs for HIV therapy
A: Protease Inhibitors and Reverse Transcriptase Inhibitors

Q: Name two organisms Vancomycin is commonly used for?
A: Staphlococcus aureus and Clostridium difficile (pseudomembranous colitis)

Q: Oral Penicillin
A: V

Q: Resistance mechanisms for Aminoglycosides
A: Modification via Acetylation, Adenylation, or Phosphorylation

Q: Resistance mechanisms for Cephalosporins/Penicillins
A: Beta-lactamase cleavage of Beta-lactam ring

Q: Resistance mechanisms for Chloramphenicol
A: Modification via Acetylation

Q: Resistance mechanisms for Macrolides
A: Methylation of rRNA near Erythromycin's ribosome binding site

Q: Resistance mechanisms for Sulfonamides
A: Altered bacterial Dihydropteroate Synthetase, Decreased uptake, or Increased PABA synthesis

Q: Resistance mechanisms for Tetracycline
A: Decreased uptake or Increased transport out of cell

Q: Resistance mechanisms for Vancomycin
A: Terminal D-ala of cell wall replaced with D-lac; Decreased affinity

Q: Side effects of Isoniazid (INH)?
A: Hemolysis (if G6PD deficient), Neurotoxicity, Hepatotoxicity, SLE-like syndrome

Q: Specifically, how does Foscarnet inhibit viral DNA pol?
A: Binds to the Pyrophosphate Binding Site of the enzyme

Q: The MOA for Chloramphenicol is ……………..?
A: Inhibition of 50S peptidyl transferase, Bacteriostatic

Q: Toxic effects of TMP include………?
A: Megaloblastic anemia, Leukopenia, Granulocytopenia

Q: Toxic side effects of the Azoles?
A: Hormone synthesis inhibition (Gynecomastia), Liver dysfunction (Inhibits CYP450), Fever, Chills

Q: Toxicities associated with Acyclovir?
A: Delirium, Tremor, Nephrotoxicity

Q: What additional side effects exist for Ampicillin?
A: Rash, Pseudomembranous colitis

Q: What antimicrobial class is Aztreonam syngergestic with?
A: Aminoglycosides

Q: What are Amantadine-associated side effects?
A: Ataxia, Dizziness, Slurred speech

Q: What are Aminoglycosides synergistic with?
A: Beta-lactam antibiotics

Q: What are Aminoglycosides used for clinically?
A: Severe Gram - rod infections.

Q: What are common serious side effects of Aminoglycosides and what are these associated with?
A: Nephrotoxicity (esp. with Cephalosporins), Ototoxicity (esp. with Loop Diuretics)

Q: What are common side effects of Amphotericin B?
A: Fever/Chills, Hypotension, Nephrotoxicity, Arrhythmias

Q: What are common side effects of Protease Inhibitors?
A: GI intolerance (nausea, diarrhea), Hyperglycemia, Lipid abnormalities, Thrombocytopenia (Indinavir)

Q: What are common side effects of RT Inhibitors?
A: BM suppression (neutropenia, anemia), Peripheral neuropathy

Q: What are common toxic side effects of Sulfonamides? (5)
A: -Hypersensitivity reactions
A: -Hemolysis
A: -Nephrotoxicity (tubulointerstitial nephritis)
A: -Kernicterus in infants
A: Displace other drugs from albumin (e.g., warfarin)

Q: What are common toxicities associated with Macrolides? (4)
A: GI discomfort, Acute cholestatic hepatitis, Eosinophilia, Skin rashes

Q: What are common toxicities associated with Tetracyclines?
A: GI distress, Tooth discoloration and Inhibition of bone growth in children, Fanconi's syndrome, Photosensitivity

Q: What are common toxicities related to Vancomycin therapy?
A: Well tolerated in general but occasionally, Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing='Red Man Syndrome'

Q: What are Fluoroquinolones indicated for? (3)
A: 1.Gram - rods of the Urinary and GI tracts (including Pseudomonas)
A: 2.Neisseria
A: 3. Some Gram + organisms

Q: What are major side effects of Methicillin, Nafcillin, and Dicloxacillin?
A: Hypersensitivity reactions

Q: What are Methicillin, Nafcillin, and Dicloxacillin used for clinically?
A: Staphlococcus aureus

Q: What are Polymyxins used for?
A: Resistant Gram - infections

Q: What are the Anti-TB drugs?
A: Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH)

Q: What are the clinical indications for Azole therapy?
A: Systemic mycoses

Q: What are the clinical uses for 1st Generation Cephalosporins?
A: Gram + cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae (PEcK)

Q: What are the clinical uses for 2nd Generation Cephalosporins?
A: Gram + cocci, Haemophilus influenza, Enterobacter aerogenes, Neisseria species, P. mirabilis, E. coli, K. pneumoniae, Serratia marcescens ( HEN PEcKS )

Q: What are the clinical uses for 3rd Generation Cephalosporins?
A: 1) Serious Gram - infections resistant to other Beta lactams
A: 2) Meningitis (most penetrate the BBB)

Q: What are the clinical uses for Aztreonam?
A: Gram - rods: Klebsiella species, Pseudomonas species, Serratia species

Q: What are the clinical uses for Imipenem/cilastatin?
A: Gram + cocci, Gram - rods, and Anerobes

Q: What are the Macrolides used for clinically?
A: -Upper respiratory tract infections
A: -pneumonias
A: -STDs: Gram+ cocci (streptococcal infect in pts allergic to penicillin)
A: -Mycoplasma, Legionella,Chlamydia, Neisseria

Q: What are the major structural differences between Penicillin and Cephalosporin?
A: Cephalosporin: 1) has a 6 member ring attached to the Beta lactam instead of a 5 member ring
A: 2)has an extra functional group ( attached to the 6 member ring)

Q: What are the major toxic side effects of Imipenem/cilastatin?
A: GI distress, Skin rash, and Seizures at high plasma levels

Q: What are the major toxic side effects of the Cephalosporins?
A: 1) Hypersensitivity reactions
A: 2) Increased nephrotoxicity of Aminoglycosides
A: 3) Disulfiram-like reaction with ethanol (those with a methylthiotetrazole group, e.g., cefamandole)

Q: What are the side effects of Polymyxins?
A: Neurotoxicity, Acute renal tubular necrosis

Q: What are the side effects of Rifampin?
A: Minor hepatotoxicity, Drug interactions (activates P450)

Q: What are toxic side effects for Metronidazole?
A: Disulfiram-like reaction with EtOH, Headache

Q: What are toxicities associated with Chloramphenicol?
A: Aplastic anemia (dose independent), Gray Baby Syndrome

Q: What conditions are treated with Metronidazole?
A: Giardiasis, Amoebic dysentery (E. histolytica), Bacterial vaginitis (Gardnerella vaginalis), Trichomonas

Q: What do Aminoglycosides require for uptake?
A: Oxygen

Q: What do you treat Nematode/roundworm (pinworm, whipworm) infections with?
A: Mebendazole/Thiabendazole, Pyrantel Pamoate

Q: What drug is given for Pneumocystis carinii prophylaxis?
A: Pentamidine

Q: What drug is used during the pregnancy of an HIV + mother?, Why?
A: AZT, to reduce risk of Fetal Transmission

Q: What drug is used to treat Trematode/fluke (e.g., Schistosomes, Paragonimus, Clonorchis) or Cysticercosis
A: Praziquantel

Q: What is a common drug interaction associated with Griseofulvin?
A: Increases coumadin metabolism

Q: What is a mnemonic to remember Amantadine's function?
A: Blocks Influenza A and RubellA; causes problems with the cerebellA

Q: What is a prerequisite for Acyclovir activation?
A: It must be Phosphorylated by Viral Thymidine Kinase

Q: What is a Ribavirin toxicity?
A: Hemolytic anemia

Q: What is an acronym to remember Anti-TB drugs?
A: RESPIre

Q: What is an additional side effect of Methicillin?
A: Interstitial nephritis

Q: What is an occasional side effect of Aztreonam?
A: GI upset

Q: What is Clindamycin used for clinically?
A: Anaerobic infections (e.g., B. fragilis, C. perfringens)

Q: What is clinical use for Carbenicillin, Piperacillin, and Ticarcillin?
A: Pseudomonas species and Gram - rods

Q: What is combination TMP-SMZ used to treat?
A: Recurrent UTIs, Shigella, Salmonella, Pneumocystis carinii pneumonia

Q: What is combined with Ampicillin, Amoxicillin, Carbenicillin, Piperacillin, and Ticarcillin to enhance their spectrum?
A: Clavulanic acid

Q: What is Fluconazole specifically used for?
A: Cryptococcal meningitis in AIDS patients and Candidal infections of all types

Q: What is Imipenem always administered with?
A: Cilastatin

Q: What is Ketoconazole specifically used for?
A: Blastomyces, Coccidioides, Histoplasma, C. albicans; Hypercortisolism

Q: What is Metronidazole combined with for 'triple therapy'? Against what organism?
A: Bismuth and Amoxicillin or Tetracycline; against Helobacter pylori

Q: What is Metronidazole used for clinically?
A: Antiprotozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis
A: Anaerobes: Bacteroides, Clostridium

Q: What is Niclosamide used for?
A: Cestode/tapeworm (e.g., D. latum, Taenia species Except Cysticercosis

Q: What is Nifurtimox administered for?
A: Chagas' disease, American Trypanosomiasis (Trypanosoma cruzi)

Q: What is the chemical name for Ganciclovir?
A: DHPG (dihydroxy-2-propoxymethyl guanine)

Q: What is the clinical use for Ampicillin and Amoxicillin?
A: Extended spectrum penicillin: certain Gram + bacteria and Gram - rods

Q: What is the clinical use for Nystatin?
A: Topical and Oral, for Oral Candidiasis (Thrush)

Q: What is the clinical use for Penicillin?
A: Bactericidal for: Gram + rod and cocci, Gram - cocci, and Spirochetes

Q: What is the major side effect for Ampicillin and Amoxicillin?
A: Hypersensitivity reactions

Q: What is the major side effect for Carbenicillin, Piperacillin, and Ticarcillin?
A: Hypersensitivity reactions

Q: What is the major toxic side effect of Penicillin?
A: Hypersensitivity reactions

Q: What is the memory aid for subunit distribution of ribosomal inhibitors?
A: Buy AT 30, CELL at 50'

Q: What is the memory key for Isoniazid (INH) toxicity?
A: INH: Injures Neurons and Hepatocytes

Q: What is the memory key for Metronidazole's clinical uses?
A: GET on the Metro

Q: What is the memory key for organisms treated with Tetracyclines?
A: VACUUM your Bed Room'

Q: What is the memory key involving the Ɗ R's of Rifampin?'
A: 1. RNA pol inhibitor
A: 2. Revs up P450
A: 3. Red/orange body fluids
A: 4. Rapid resistance if used alone

Q: What is the MOA for Acyclovir?
A: Inhibit viral DNA polymerase

Q: What is the MOA for Amphotericin B?
A: Binds Ergosterol, forms Membrane Pores that Disrupt Homeostatis

Q: What is the MOA for Ampicillin and Amoxicillin?
A: Same as penicillin. Extended spectrum antibiotics

Q: What is the MOA for Carbenicillin, Piperacillin, and Ticarcillin?
A: Same as penicillin. Extended spectrum antibiotics

Q: What is the MOA for Clindamycin?
A: Blocks Peptide Bond formation at the 50S subunit, Bacteriostatic

Q: What is the MOA for Methicillin, Nafcillin, and Dicloxacillin?
A: Same as penicillin. Act as narrow spectrum antibiotics

Q: What is the MOA for Metronidazole?
A: Forms toxic metabolites in the bacterial cell, Bactericidal

Q: What is the MOA for Nystatin?
A: Binds ergosterol, Disrupts fungal membranes

Q: What is the MOA for Rifampin?
A: Inhibits DNA dependent RNA polymerase

Q: What is the MOA for the Aminoglycosides?
A: Inhibits formation of Initiation Complex, causes misreading of mRNA, Bactericidal

Q: What is the MOA for the Azoles?
A: Inhibit Ergosterol synthesis

Q: What is the MOA for the Cephalosporins?
A: Beta lactams - inhibit cell wall synthesis, Bactericidal

Q: What is the MOA for the Fluoroquinolones?
A: Inhibit DNA Gyrase (topoisomerase II), Bactericidal

Q: What is the MOA for the Macrolides?
A: Blocks translocation, binds to the 23S rRNA of the 50S subunit, Bacteriostatic

Q: What is the MOA for the Tetracyclines?
A: Binds 30S subunit and prevents attachment of aminoacyl-tRNA, Bacteriostatic

Q: What is the MOA for Trimethoprim (TMP)?
A: Inhibits bacterial Dihydrofolate Reductase, Bacteriostatic

Q: What is the MOA for Vancomycin?
A: Inhibits cell wall mucopeptide formation, Bactericidal

Q: What is the MOA of Amantadine?
A: Blocks viral penetration/uncoating; may act to buffer the pH of the endosome

Q: What is the MOA of Aztreonam?
A: Inhibits cell wall synthesis ( binds to PBP3). A monobactam

Q: What is the MOA of Foscarnet?
A: Inhibits Viral DNA polymerase

Q: What is the MOA of Ganciclovir?
A: Inhibits CMV DNA polymerase

Q: What is the MOA of Griseofulvin?
A: Interferes with microtubule function, disrupts mitosis, inhibits growth

Q: What is the MOA of Imipenem?
A: Acts as a wide spectrum carbapenem

Q: What is the MOA of Isoniazid (INH)?
A: Decreases synthesis of Mycolic Acid

Q: What is the MOA of Polymyxins?
A: Bind cell membrane, disrupt osmotic properties, Are Cationc, Basic and act as detergents

Q: What is the MOA of Ribavirin?
A: Inhibits IMP Dehydrogenase (competitively), and therefore blocks Guanine Nucleotide synthesis

Q: What is the MOA of the RT Inhibitors?
A: Inhibit RT of HIV and prevent the incorporation of viral genome into the host DNA

Q: What is the most common cause of Pt noncompliance with Macrolides?
A: GI discomfort

Q: What is treated with Chloroquine, Quinine, Mefloquine?
A: Malaria (P. falciparum)

Q: What microorganisms are Aminoglycosides ineffective against?
A: Anaerobes

Q: What microorganisms are clinical indications for Tetracycline therapy?
A: Vibrio cholerae
A: Acne
A: Chlamydia
A: Ureaplasma
A: Urealyticum
A: Mycoplasma pneumoniae
A: Borrelia burgdorferi (Lyme's)
A: Rickettsia
A: Tularemia

Q: What microorganisms is Aztreonam not effective against?
A: Gram + and Anerobes

Q: What musculo-skeletal side effects in Adults are associated with Floroquinolones?
A: Tendonitis and Tendon rupture

Q: What neurotransmitter does Amantadine affect? How does it influence this NT?
A: Dopamine; causes its release from intact nerve terminals

Q: What organism is Imipenem/cilastatin the Drug of Choice for?
A: Enterobacter

Q: What organisms does Griseofulvin target?
A: Dermatophytes (tinea, ringworm)

Q: What parasites are treated with Pyrantel Pamoate (more specific)?
A: Giant Roundworm (Ascaris), Hookworm (Necator/Ancylostoma), Pinworm (Enterobius)

Q: What parasitic condition is treated with Ivermectin?
A: Onchocerciasis ('river blindness'--rIVER-mectin)

Q: What populations are Floroquinolones contraindicated in? Why?
A: Pregnant women, Children; because animal studies show Damage to Cartilage

Q: What should not be taken with Tetracyclines? / Why?
A: Milk or Antacids, because divalent cations inhibit Tetracycline absorption in the gut

Q: What Sulfonamides are used for simple UTIs?
A: Triple sulfas or SMZ

Q: When is HIV therapy initiated?
A: When pts have Low CD4+ (< 500 cells/cubic mm) or a High Viral Load

Q: When is Rifampin not used in combination with other drugs?
A: 1. Meningococcal carrier state
A: 2. Chemoprophylaxis in contacts of children with H. influenzae type B

Q: Where does Griseofulvin deposit?
A: Keratin containing tissues, e.g., nails

Q: Which Aminoglycoside is used for Bowel Surgery ?
A: Neomycin

Q: Which antimicrobial classes inhibit protein synthesis at the 30S subunit? (2)
A: 1) Aminoglycosides = bactericidal
A: 2) Tetracyclines = bacteriostatic

Q: Which antimicrobials inhibit protein synthesis at the 50S subunit? (4)
A: 1) Chloramphenical = bacteriostatic
A: 2) Erythromycin = bacteriostatic
A: 3) Lincomycin = bacteriostatic
A: 4)cLindamycin = bacteriostatic

Q: Which individuals are predisposed to Sulfonamide-induced hemolysis?
A: G6PD deficient individuals

Q: Which RT inhibitor causes Megaloblastic Anemia?
A: AZT

Q: Which RT inhibitors cause a Rash?
A: Non-Nucleosides

Q: Which RT inhibitors cause Lactic Acidosis?
A: Nucleosides

Q: Which Tetracycline is used in patients with renal failure? / Why?
A: Doxycycline, because it is fecally eliminated

Q: Why are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant?
A: Due to the presence of a bulkier R group

Q: Why is Cilastatin administered with Imipenem?
A: To inhibit renal Dihydropeptidase I and decrease Imipenem inactivation in the renal tubules