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الموضوع: pharmacology Q & A

  1. #1
    كبار الشخصيات
    عضو مؤسس
    الصورة الرمزية الوسادة
    تاريخ التسجيل
    Feb 2010
    الدولة
    (Jordan ( Amman
    العمر
    32
    المشاركات
    3,989

    Icon14 pharmacology Q & A

    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




    يتبع ......

  2. #2
    كبار الشخصيات
    عضو مؤسس
    الصورة الرمزية الوسادة
    تاريخ التسجيل
    Feb 2010
    الدولة
    (Jordan ( Amman
    العمر
    32
    المشاركات
    3,989

    افتراضي رد: pharmacology Q & A

    [align=left]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 ****bolism

    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 ***394; 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 ****bolites 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 trans********, 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


    [/align]

  3. #3
    كبار الشخصيات
    عضو مؤسس
    الصورة الرمزية الوسادة
    تاريخ التسجيل
    Feb 2010
    الدولة
    (Jordan ( Amman
    العمر
    32
    المشاركات
    3,989

    افتراضي رد: pharmacology Q & A

    [align=left]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
    Pharmacology toxicology Q&a
    Q: Acetaldehyde is ****bolized by Acetaldehyde dehydrogenase, which drug inhibs this enzyme?
    A: -Disulfram & also sulfonylureas, metronidazole

    Q: Explain pH dependent urinary drug elimination?
    A: -Weak Acids>Alkinalize urine(CO3) to remove more -Weak ****s>acidify urine to remove more

    Q: How do you treat coma in the ER (4)?
    A: -Airway -Breathing -Circulation -Dextrose(thiamine &narcan) -ABCD

    Q: In coma situations you rule out what (7)?
    A: -Infections -Trauma -Seizures -CO -Overdose -****bolic -Alcohol (IT'S COMA)

    Q: List some specifics of lead poisoning(4)?
    A: -A57Blue lines in gingiva& long bones -Encephalopathy & Foot drop -Abdominal colic / -Sideroblastic anemia

    Q: List the specific antidote for this toxin: Acetaminophen
    A: -N-acetylcystine

    Q: List the specific antidote for this toxin: Amphetamine
    A: -Ammonium Chloride

    Q: List the specific antidote for this toxin: Anticholinesterases (organophosphate.)
    A: -Atropine & pralidoxime

    Q: List the specific antidote for this toxin: Antimuscarinic (anticholinergic)
    A: -Physostigmine salicylate

    Q: List the specific antidote for this toxin: Arsenic (all heavy ****ls)
    A: -Dimercaprol, succimer

    Q: List the specific antidote for this toxin: Benzodiazepines
    A: -Flumazenil

    Q: List the specific antidote for this toxin: Beta Blockers
    A: -Glucagon

    Q: List the specific antidote for this toxin: Carbon monoxide
    A: -100% oxygen, hyperbaric

    Q: List the specific antidote for this toxin: Copper
    A: -Penicillamine

    Q: List the specific antidote for this toxin: Cyanide
    A: -Nitrate, hydroxocobalamin thiosulfate

    Q: List the specific antidote for this toxin: Digitalis
    A: -Normalize K+, Lidocaine, & Anti-dig Mab

    Q: List the specific antidote for this toxin: Heparin
    A: -Protamine

    Q: List the specific antidote for this toxin: Iron
    A: -Deferoxamine

    Q: List the specific antidote for this toxin: Lead
    A: -EDTA, dimercaprol, succimer, & penicillamine

    Q: List the specific antidote for this toxin: Methanol & Ethylene glycol
    A: -Ethanol, dialysis, & fomepizole

    Q: List the specific antidote for this toxin: Methemoglobin
    A: -Methylene blue

    Q: List the specific antidote for this toxin: Opioids
    A: -B51Naloxone / naltrexone (Narcan)

    Q: List the specific antidote for this toxin: Salicylates
    A: -Alkalinize urine & dialysis

    Q: List the specific antidote for this toxin: TPA & Streptokinase
    A: -Aminocaproic acid

    Q: List the specific antidote for this toxin: Tricyclic antidepressants
    A: -NaHCO3

    Q: List the specific antidote for this toxin: Warfarin
    A: -Vitamin K & fresh frozen plasma

    Q: What are the products and their toxicities of the ****bolism of ethanol by / alcohol dehydrogenase?
    A: -Acetaldehyde -Nausea, vomiting, headache, & hypotension

    Q: What are the products and their toxicities of the ****bolism of Ethylene Glycol by / alcohol dehydrogenase?
    A: -Oxalic acid -Acidosis & nephrotoxicity

    Q: What are the products and their toxicities of the ****bolism of Methanol by / alcohol dehydrogenase?
    A: -Formaldehyde & formic acid -severe acidosis & retinal damage

    Q: Which drug(s) cause this reaction: Adrenocortical Insufficiency
    A: -Glucocorticoid withdrawal

    Q: Which drug(s) cause this reaction: Agranulocytosis (3)?
    A: -Cloazapine -carbamazapine -colchicine -PTU

    Q: Which drug(s) cause this reaction: Anaphylaxis?
    A: -Penicillin

    Q: Which drug(s) cause this reaction: Aplastic anemia (5)?
    A: -Chloramphenicol -benzene -NSAIDS -PTU -phenytoin

    Q: Which drug(s) cause this reaction: Atropine-like side effects?
    A: -Tricyclic antidepressants

    Q: Which drug(s) cause this reaction: Cardiac toxicity?
    A: -Daunorubicin & Doxorubicin

    Q: Which drug(s) cause this reaction: Cinchonism (2)?
    A: -Quinidine -quinine

    Q: Which drug(s) cause this reaction: Cough?
    A: -ACE inhibitors (Losartan>no cough)

    Q: Which drug(s) cause this reaction: Cutaneous flushing (4)?
    A: -Niacin -Ca++ channel blockers -adenosine -vancomycin

    Q: Which drug(s) cause this reaction: Diabetes insipidus?
    A: -Lithium

    Q: Which drug(s) cause this reaction: Disulfram-like reaction (4) ?
    A: -Metronidazole -certain cephalosporins -procarbazine -sulfonylureas

    Q: Which drug(s) cause this reaction: Drug induced Parkinson's (4) ?
    A: -Haloperidol -chlorpromazine -reserpine -MPTP

    Q: Which drug(s) cause this reaction: Extrapyramidal side effects (3)?
    A: -Chlorpromazine -thioridazine -haloperidol

    Q: Which drug(s) cause this reaction: Fanconi's syndrome?
    A: -Tetracycline

    Q: Which drug(s) cause this reaction: Focal to massive hepatic necrosis (4)?
    A: -Halothane -Valproic acid -acetaminophen -Amantia phalloides

    Q: Which drug(s) cause this reaction: G6PD hemolysis(8)?
    A: -Sulfonamides -INH -ASA -Ibuprofen -primaquine -nitrofurantoin /-pyrimethamine -chloramphenicol

    Q: Which drug(s) cause this reaction: Gingival hyperplasia?
    A: -Phenytoin

    Q: Which drug(s) cause this reaction: Gray baby syndrome?
    A: -Chloramphenicol

    Q: Which drug(s) cause this reaction: Gynecomastia (6) ?
    A: -Cimetidine -ketoconazole -spironolactone -digitalis -EtOH -estrogens

    Q: Which drug(s) cause this reaction: Hepatitis?
    A: -Isoniazid

    Q: Which drug(s) cause this reaction: Hot flashes?
    A: -Tamoxifen

    Q: Which drug(s) cause this reaction: Neuro and Nephrotoxic?
    A: -polymyxins

    Q: Which drug(s) cause this reaction: Osteoporosis (2)?
    A: -Corticosteroids -heparin

    Q: Which drug(s) cause this reaction: Oto and Nephrotoxicity (3)?
    A: -aminoglycosides -loop diuretics -cisplatin

    Q: Which drug(s) cause this reaction: P450 induction(6)?
    A: -Barbiturates -phenytoin -carbamazipine -rifampin -griseofulvin -quinidine

    Q: Which drug(s) cause this reaction: P450 inhibition(6)?
    A: -Cimetidine -ketoconazole -grapefruit juice -erythromycin -INH -sulfonamides

    Q: Which drug(s) cause this reaction: Photosensitivity(3)?
    A: -Tetracycline -amiodarone -sulfonamides

    Q: Which drug(s) cause this reaction: Pseudomembranous colitis?
    A: -Clindamycin

    Q: Which drug(s) cause this reaction: Pulmonary fibrosis(3)?
    A: -Bleomycin -amiodarone -busulfan

    Q: Which drug(s) cause this reaction: SLE-like syndrome
    A: -Hydralazine -Procainamide -INH -phenytoin

    Q: Which drug(s) cause this reaction: *******-Johnson syn. (3) ?
    A: -Ethosuxamide -sulfonamides -lamotrigine

    Q: Which drug(s) cause this reaction: Tardive dyskinesia?
    A: -Antipsychotics

    Q: Which drug(s) cause this reaction: Tendonitis and rupture?
    A: -Fluoroquinolones

    Q: Which drug(s) cause this reaction: Thrombotic complications?
    A: -Oral Contraceptives

    Q: Which drug(s) cause this reaction: Torsade de pointes (2) ?
    A: -Class III antiarrhythmics (sotalol) -class IA (quinidine)

    Q: Which drug(s) cause this reaction: Tubulointerstitial Nephritis (5)?
    A: -Sulfonamides -furosemide -methicillin -rifampin -NSAIDS (ex. ASA)
    Pharmacology general Q&a
    Q: Describe first-order kinetics?
    A: Constant FRACTION eliminated per unit time.(exponential)

    Q: Describe Phase I ****bolism in liver(3)?
    A: -reduction, oxy, & hydrolysis -H2O sol. Polar product -P450

    Q: Describe Phase II ****bolism in liver(3)?
    A: -acetylation, glucuron.,& sulfation -Conjugation -Polar product

    Q: Explain differences between full and partial agonists(2).
    A: - Act on same receptor - Full has greater efficacy

    Q: Explain potency in relation to full and partial agonists(2).
    A: - partial agonist can have increased, decreased, /A21or equal potency as full agonist. - Potency is an independent factor.

    Q: How do spare receptors effect the Km?
    A: - ED 50 is less than the Km (less than 50% of receptors)

    Q: How do you calculate maintenance dose?
    A: Md= (CpxCL)/F Cp= plas. Conc. CL=clear. F=bioaval.

    Q: How does a competitive antagonist effect an agonist?
    A: -Shifts the curve to the right -increases Km

    Q: How does a noncompetitive antagonist effect an agonist?
    A: - Shifts the curve down -reduces Vmax

    Q: Name the steps in drug approval(4)?
    A: -Phase I (clinical tests) -Phase II -Phase III -PhaseIV (surveillance)

    Q: Steady state concentration is reached in __#half-lifes
    A: In 4 half-lifes= (94%) T1/2 = (0.7x Vd)/CL

    Q: What is the definition of zero-order kinetics? Example?
    A: -Constant AMOUNT eliminated per unit time. -Etoh &ASA

    Q: What is the formula for Clearance (CL)
    A: CL= (rate of elimination of drug/ Plasma drug conc.)

    Q: What is the formula for Volume of distribution (Vd)
    A: Vd= (Amt. of drug in body/ Plasma drug conc.)

    Q: What is the loading dose formula?
    A: Ld= (CpxVd)/F Cp=plasma conc. F= Bioaval.
    Pharmacology (from old Usmle tests)
    Q: Acetaminophen has what two clinical uses and lacks what one clinical use of the NSAIDs?
    A: Acetaminophen has antipyretic and analgesic properties, but lacks anti-inflammatory properties.

    Q: Can Heparin be used during pregnancy?
    A: Yes, it does not cross the placenta.

    Q: Can Warfarin be used during pregnancy?
    A: No, warfarin, unlike heparin, can cross the placenta.

    Q: Does Heparin have a long, medium, or short half life?
    A: Short.

    Q: Does Warfarin have a long, medium, or short half life?
    A: Long.

    Q: For Heparin what is the 1. Structure 2. Route of administration 3. Onset of action 4. Mechanism of action
    A: 1. Structure - Large anionic polymer, acidic
    A: 2. Route of administration - Paranteral (IV, SC)
    A: 3. Onset of action - Rapid (seconds)
    A: 4. Mechanism of action - Activates antithrombin III

    Q: Heparin continued: 5. Duration of action 6. Ability to inhibit coagulation in vitro 7. Treatment for overdose 8. Lab value to monitor 9. Site of action
    A: 5. Duration of action - Acute (hours)
    A: 6. Ability to inhibit coagulation in vitro - Yes
    A: 7. Treatment for overdose - Protamine sulfate
    A: 8. Lab value to monitor - aPTT (intrinsic pathway)
    A: 9. Site of action - Blood

    Q: For Warfarin what is the 1. Structure 2. Route of administration 3. Onset of action 4. Mechanism of action
    A: 1. Structure - Small lipid-soluble molecule
    A: 2. Route of administration -Oral
    A: 3. Onset of action - Slow, limited by half lives of clotting factors
    A: 4. Mechanism of action - Impairs the synthesis of vitamin K-dependent clotting factors

    Q: Warfarin continued 5. Duration of action 6. Ability to inhibit coagulation in vitro 7. Treatment for overdose 8. Lab value to monitor 9. Site of action
    A: 5. Duration of action - Chronic (weeks or months)
    A: 6. Ability to inhibit coagulation in vitro - No
    A: 7. Treatment for overdose - IV vitamin K and fresh frozen plasma
    A: 8. Lab value to monitor - PT
    A: 9. Site of action - Liver

    Q: Is toxicity rare or common whith Cromolyn used in Asthma prevention?
    A: Rare.

    Q: List five common glucocorticoids.
    A: 1. Hydrocortisone
    A: 2. Predisone
    A: 3. Triamcinolone
    A: 4. Dexamethasone
    A: 5. Beclomethasone

    Q: Of the following: 1. Antigen recognition, 2. Proliferation, 3. Differentiation synthesis,
    Q: 5. Tissue injury; Which sites do each of the following act upon?
    Q: 1. Prednisone 2. Cyclosporine 3. Azathioprine 4. Methotrexate
    A: 1. Prednisone - 2. Proliferation, 5. Tissue injury
    A: 2. Cyclosporine - 2. Proliferation, 3. Differentiation synthesis
    A: 3. Azathioprine - 2. Proliferation
    A: 4. Methotrexate - 2. Proliferation

    Q: Sites continued: 5. Dactinomycin 6. Cyclophosphamide
    A: 5. Dactinomycin - 2. Proliferation, 3. Differentiation synthesis
    A: 6. Cyclophosphamide - 2. Proliferation

    Q: Sites continued: 7. Antilymphocytic globulin and monoclonal anti-T-cell antibodies 8. Rh3(D) Immune globulin 9. Tacrolimus
    A: 7. Antilymphocytic globulin and monoclonal anti-T-cell antibodies - 1. Antigen recognition, 2. Proliferation, 3. Differentiation synthesis
    A: 8. Rh3(D) Immune globulin - 1. Antigen recognition
    A: 9. Tacrolimus - 4. Cytokine secretion.

    Q: Secretion of what drug is inhibited by Probenacid used to treat chronic gout?
    A: Penicillin.

    Q: The COX-2 inhibitors (celecoxib, rofecoxib) have similar side effects to the NSAIDs with what one exception?
    A: The COX-2 inhibitors should not have the corrosive effects of other NSAIDs on the gastrointestinal lining.

    Q: What are are the Sulfonylureas (general de******ion) and what is their use?
    A: Sulfonylureas are oral hypoglycemic agents, they are used to stimulate release of endogenous insulin in NIDDM (type-2).

    Q: What are five advantages of Oral Contraceptives (synthetic progestins, estrogen)?
    A: 1. Reliable (<1% failure)
    A: 2. Lowers risk of endometrial and ovarian cancer
    A: 3. Decreased incidence of ectopic pregnancy
    A: 4. Lower risk of pelvic infections
    A: 5. Regulation of menses

    Q: What are five disadvantages of Oral Contraceptives (synthetic progestins, estrogen)?
    A: 1. Taken daily
    A: 2. No protection against STDs
    A: 3. Raises triglycerides
    A: 4. Depression, weight gain, nausea, HTN
    A: 5. Hypercoagulable state

    Q: What are five possible toxic effects of Aspirin therapy?
    A: 1. Gastric ulceration
    A: 2. Bleeding
    A: 3. Hyperventilation
    A: 4. Reye's syndrome
    A: 5. Tinnitus (CN VIII)

    Q: What are five toxicities associated with Tacrolimus (FK506)?
    A: 1. Significant: nephrotoxicity
    A: 2. Peripheral neuropathy
    A: 3. Hypertension
    A: 4. Pleural effusion
    A: 5. Hyperglycemia.

    Q: What are four advantages of newer low-molecular-weight heparins (Enoxaparin)?
    A: 1. Better bioavailability
    A: 2. 2 to 4 times longer half life
    A: 3. Can be administered subcutaneously
    A: 4. Does not require laboratory monitoring

    Q: What are four clinical activities of Aspirin?
    A: 1. Antipyretic
    A: 2. Analgesic
    A: 3. Anti-inflammatory
    A: 4. Antiplatelet drug.

    Q: What are four clinical uses of glucocorticoids?
    A: 1. Addison's disease
    A: 2. Inflammation
    A: 3. Immune suppression
    A: 4. Asthma

    Q: What are four conditions in which H2 Blockers are used clinically?
    A: 1. Peptic ulcer
    A: 2. Gastritis
    A: 3. Esophageal reflux
    A: 4. Zollinger-Ellison syndrome

    Q: What are four H2 Blockers?
    A: 1. Ci****dine
    A: 2. Ranitidine
    A: 3. Famotidine
    A: 4. Nizatidine

    Q: What are four Sulfonylureas?
    A: 1. Tolbutamide
    A: 2. Chlorpropamide
    A: 3. Glyburide
    A: 4. Glipizide

    Q: What are four thrombolytics?
    A: 1. Streptokinase
    A: 2. Urokinase
    A: 3. tPA (alteplase), APSAC (anistreplase)

    Q: What are four unwanted effects of Clomiphene use?
    A: 1. Hot flashes
    A: 2. Ovarian enlargement
    A: 3. Multiple simultaneous pregnancies
    A: 4. Visual disturbances

    Q: What are nine findings of Iatrogenic Cushing's syndrome caused by glucocorticoid therapy?
    A: 1. Buffalo hump
    A: 2. Moon facies
    A: 3. Truncal obesity
    A: 4. Muscle wasting
    A: 5. Thin skin
    A: 6. Easy bruisability
    A: 7. Osteoporosis
    A: 8. Adrenocortical atrophy
    A: 9. Peptic ulcers

    Q: What are signs of Sildenafil (Viagra) toxicity?
    A: Headache, flushing , dyspepsia, blue-green color vision.

    Q: What are the clinical uses for Ticlopidine, Clopidogrel?
    A: Acute coronary syndrome; coronary stenting. Decreases the incidence or recurrence of thrombotic stroke.

    Q: What are the four conditions in which Omeprazole, Lansoprazole is used?
    A: 1. Peptic ulcer
    A: 2. Gastritis
    A: 3. Esophageal reflux
    A: 4. Zollinger-Ellison syndrome

    Q: What are three clinical uses of the Leuprolide?
    A: 1. Infertility (pulsatile)
    A: 2. Prostate cancer (continuous: use with flutamide)
    A: 3. Uterine fibroids

    Q: What are three clinical uses of the NSAIDs?
    A: 1. Antipyretic
    A: 2. Analgesic
    A: 3. Anti-inflammatory

    Q: What are three common NSAIDS other than Aspirin?
    A: Ibuprofen, Naproxen, and Indomethacin

    Q: What are three complications of Warfarin usage?
    A: 1. Bleeding
    A: 2. Teratogenicity
    A: 3. Drug-drug interactions

    Q: What are three possible complications of Heparin therapy?
    A: 1. Bleeding
    A: 2. Thrombocytopenia
    A: 3. Drug-drug interactions

    Q: What are three possible toxicities of NSAID usage?
    A: 1. Renal damage
    A: 2. Aplastic anemia
    A: 3. GI distress

    Q: What are three toxicities of Leuprolied?
    A: 1. Antiandrogen
    A: 2. Nausea
    A: 3. Vomiting

    Q: What are three toxicities of Propylthiouracil?
    A: 1. Skin rash
    A: 2. Agranulocytosis (rare)
    A: 3. Aplastic anemia

    Q: What are three types of antacids and the problems that can result from their overuse?
    A: 1. Aluminum hydroxide: constipation and hypophosphatemia
    A: 2. Magnesium hydroxide: diarrhea
    A: 3. Calcium carbonate: Hypercalcemia, rebound acid increase
    A: - All may cause hypokalemia

    Q: What are three unwanted effects of Mifepristone?
    A: 1. Heavy bleeding
    A: 2. GI effects (n/v, anorexia)
    A: 3. Abdominal pain

    Q: What are two Alpha-glucosidase inhibitors?
    A: 1. Acarbose
    A: 2. Miglitol

    Q: What are two clinical uses of Azathioprine?
    A: 1. Kidney transplantation
    A: 2. Autoimmune disorders (including glomerulonephritis and hemolytic anemia)

    Q: What are two conditions in which COX-2 inhibitors might be used?
    A: Rheumatoid and osteoarthritis.

    Q: What are two Glitazones?
    A: 1. Pioglitazone
    A: 2. Rosiglitazone.

    Q: What are two mechanisms of action of Propythiouracil?
    A: Inhibits organification and coupling of thyroid hormone synthesis. Also decreases peripheral conversion of T4 to T3.

    Q: What are two processes Corticosteroids inhibit leading to decreased inflammation?
    A: 1. Phospholipase A2 is prevented from releasing arachidonic acid



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