Pharmacology animicrobial Q&a
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 anti****bolites 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: MOA isrupt 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 Tran******ase Inhibitors
A: Nevirapine, Delavirdine
Q: Name the common Nucleoside Reverse Tran******ase 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 Tran******ase 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
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