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Thread: Student Note Book: Pharmacology (Q & A)

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    Arrow Student Note Book: Pharmacology (Q & A)

    Student Note Book: Pharmacology (Q & A)

    1 A common side effects of Infection treatment is?

    Neutropenia

    Neutropenia: a condition of the blood, in which your white blood cells have a low count of neutrophils. Neutrophils, a type of white blood cell, is part of your bodys immune system, and it helps fight off bacterial infections. When you have neutropenia, you are at greater risk of infections, and your body is not well-equipped to fight back.


    Neutropenia is a common side effect of chemotherapy and radiation for breast cancer. Because both kinds of treatment can destroy white and red blood cells, it is important to take a Complete Blood Count test (CBC) often during your treatment. A CBC will reveal the count of different kinds of blood cells.


    Treatments include Neulasta or Neupogen (filgrastim), both of which can stimulate white blood cell production. When the injections are working, you may experience bone pain, which can be alleviated by a soak in a hot bath, or by taking Tylenol.


    2 Antimicrobial prophylaxis for a history of recurrent UTIs


    TMP-SMZ

    Oral antibiotics for prophylaxis of urinary tract infections in children

    Antimicrobial: Trimethoprim/sulfamethoxazole (TMP/SMX) (Bactrim, Septra)

    Prophylaxis dosage: 2 mg of TMP, 10 mg of SMX per kg as single bedtime or 5 mg of TMP, 25 mg of SMX per kg twice per week

    Antimicrobial: Nitrofurantoin (Macrodantin)

    Prophylaxis dosage : 12 mg/kg as single daily dose

    Antimicrobial: Cephalexin (Keflex)

    Prophylaxis dosage: 10 mg/kg as single daily dose


    Antimicrobial : Amoxicillin

    Prophylaxis dosage:10 mg/kg as single daily dose

    Antimicrobial:Sulfisoxazole (Gantrisin Pedatric)

    Prophylaxis dosage:1020 mg/kg divided every 12h



    3 Antimicrobial prophylaxis for Gonorrhea


    Ceftriaxone



    4 Antimicrobial prophylaxis for Meningococcal infection
    Rifampin (DOC), minocycline


    5 Antimicrobial prophylaxis for PCP
    TMP-SMZ (DOC), aerosolized pentamidine


    6 Antimicrobial prophylaxis for Syphilis
    Benzathine penicillin G


    7 Are Aminoglycosides Teratogenic?
    Yes


    8 Are Ampicillin and Amoxicillin penicillinase resistant?
    No


    9 Are Carbenicillin, Piperacillin, and Ticarcillin penicillinase resistant?
    No


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


    11 Are Methicillin, Nafcillin, and Dicloxacillin penicillinase resistant?
    Yes


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


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


    14 Common toxicities associated with Fluoroquinolones?
    GI upset, Superinfections, Skin rashes, Headache, Dizziness


    15 Common toxicities associated with Griseofulvin are…...?
    Teratogenic, Carcinogenic, Confusion, Headaches


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


    17 Do Tetracyclines penetrate the CNS?
    Only in limited amounts


    18 Does Ampicillin or Amoxicillin have a greater oral bioavailability?
    AmOxicillin has greater Oral bioavailability


    19 Does Amprotericin B cross the BBB?
    No


    20 Does Foscarnet require activation by a viral kinase?
    No


    21 Foscarnet toxicity?
    Nephrotoxicity


    22 Ganciclovir associated toxicities?
    Leukopenia, Neutropenia, Thrombocytopenia, Renal toxicity


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


    24 How are Sulfonamides employed clinically?
    Gram +, Gram -, Norcardia, Chlamydia


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


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


    27 How can Isoniazid (INH)-induced neurotoxicity be prevented?
    Pyridoxine (B6) administration


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


    29 How can the toxic effects fo TMP be ameliorated?
    With supplemental Folic Acid


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


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


    32 How do the Protease Inhibitors work?
    Inhibt Assembly of new virus by Blocking Protease Enzyme


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

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


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


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


    37 How is Amphotericin B administered for fungal meningitis?
    Intrathecally


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


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


    40 How is Foscarnet used clinically?
    CMV Retinitis in IC pts when Ganciclovir fails


    41 How is Ganciclovir activated?
    Phosphorylation by a Viral Kinase


    42 How is Ganciclovir used clinically?
    CMV, esp in Immunocompromised patients


    43 How is Griseofulvin used clinically?
    Oral treatment of superficial infections


    44 How is Leishmaniasis treated?
    Pentavalent Antimony


    45 How is Ribavirin used clinically?
    for RSV


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


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


    48 How is Vancomycin used clinically?
    For serious, Gram + multidrug-resistant organisms


    49 How would you treat African Trypanosomiasis (sleeping sickness)?
    Suramin


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


    51 Is Aztreonam cross-allergenic with penicillins?
    No


    52 Is Aztreonam resistant to penicillinase?
    Yes

    53 Is Aztreonam usually toxic?
    No

    54 Is Imipenem resistant to penicillinase?
    Yes

    55 Is Penicillin penicillinase resistant?
    No - duh

    56 IV Penicillin
    G

    57 Mnemonic for Foscarnet?
    Foscarnet = pyroFosphate analog


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


    59 MOA: Bactericidal antibiotics
    Penicillin, Cephalosporins, Vancomycin, Aminoglycosides, Fluoroquinolones, Metronidazole


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


    61 MOA: Block DNA topoisomerases
    Quinolones


    62 MOA: Block mRNA synthesis
    Rifampin


    63 MOA: Block nucleotide synthesis
    Sulfonamides, Trimethoprim


    64 MOA: Block peptidoglycan synthesis
    Bacitracin, Vancomycin


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

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


    67 MOA: Disrupt bacterial/fungal cell membranes
    Polymyxins
    68 MOA: Unkown
    Pentamidine

    69 MOA : Disrupt fungal cell membranes
    Amphotericin B, Nystatin, Fluconazole/azoles


    70 Name common Polymyxins
    Polymyxin B, Polymyxin E


    71 Name several common Macrolides (3)
    Erythromycin, Azithromycin, Clarithromycin


    72 Name some common Sulfonamides (4)
    Sulfamethoxazole (SMZ), Sulfisoxazole, Triple sulfas, Sulfadiazine


    73 Name some common Tetracyclines (4)
    Tetracycline, Doxycycline, Demeclocycline, Minocycline


    74 Name the common Aminoglycosides (5)
    Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin


    75 Name the common Azoles
    Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole


    76 Name the common Fluoroquinolones (6)
    Ciprofloxacin, Norfloxacin, Ofloxacin, Grepafloxacin, Enoxacin, Nalidixic acid


    77 Name the common Non-Nucleoside Reverse Transcriptase Inhibitors
    Nevirapine, Delavirdine


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


    79 Name the Protease Inhibitors (4)
    Saquinavir, Ritonavir, Indinavir, Nelfinavir


    80 Name two classes of drugs for HIV therapy
    Protease Inhibitors and Reverse Transcriptase Inhibitors


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


    82 Oral Penicillin
    V


    83 Resistance mechanisms for Aminoglycosides
    Modification via Acetylation, Adenylation, or Phosphorylation


    84 Resistance mechanisms for Cephalosporins/Penicillins
    Beta-lactamase cleavage of Beta-lactam ring


    85 Resistance mechanisms for Chloramphenicol
    Modification via Acetylation


    86 Resistance mechanisms for Macrolides
    Methylation of rRNA near Erythromycin's ribosome binding site


    87 Resistance mechanisms for Sulfonamides
    Altered bacterial Dihydropteroate Synthetase, Decreased uptake, or Increased PABA synthesis


    88 Resistance mechanisms for Tetracycline
    Decreased uptake or Increased transport out of cell


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


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


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


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


    93 Toxic effects of TMP include………?
    Megaloblastic anemia, Leukopenia, Granulocytopenia


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


    95 Toxicities associated with Acyclovir?
    Delirium, Tremor, Nephrotoxicity


    96 What additional side effects exist for Ampicillin?
    Rash, Pseudomembranous colitis


    97 What antimicrobial class is Aztreonam syngergestic with?
    Aminoglycosides


    98 What are Amantadine-associated side effects?
    Ataxia, Dizziness, Slurred speech


    99 What are Aminoglycosides synergistic with?
    Beta-lactam antibiotics


    100 What are Aminoglycosides used for clinically?
    Severe Gram - rod infections.


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


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


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


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


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


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


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


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


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


    110 What are major side effects of Methicillin, Nafcillin, and Dicloxacillin?
    Hypersensitivity reactions


    111 What are Methicillin, Nafcillin, and Dicloxacillin used for clinically?
    Staphlococcus aureus


    112 What are Polymyxins used for?
    Resistant Gram - infections


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


    114 What are the clinical indications for Azole therapy?
    Systemic mycoses


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


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


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


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


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


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


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


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


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


    124 What are the side effects of Polymyxins?
    Neurotoxicity, Acute renal tubular necrosis


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


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

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


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


    129 What do Aminoglycosides require for uptake?
    Oxygen


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


    131 What drug is given for Pneumocystis carinii prophylaxis?
    Pentamidine


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


    133 What drug is used to treat Trematode/fluke (e.g., Schistosomes, Paragonimus, Clonorchis) or Cysticercosis
    Praziquantel
    134 What is a common drug interaction associated with Griseofulvin?
    Increases coumadin metabolism


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


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


    137 What is a Ribavirin toxicity?
    Hemolytic anemia


    138 What is an acronym to remember Anti-TB drugs?
    RESPIre


    139 What is an additional side effect of Methicillin?
    Interstitial nephritis


    140 What is an occasional side effect of Aztreonam?
    GI upset


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


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


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


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


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


    146 What is Imipenem always administered with?
    Cilastatin


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


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


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


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


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


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


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


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


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


    156 What is the major side effect for Ampicillin and Amoxicillin?
    Hypersensitivity reactions


    157 What is the major side effect for Carbenicillin, Piperacillin, and Ticarcillin?
    Hypersensitivity reactions


    158 What is the major toxic side effect of Penicillin?
    Hypersensitivity reactions


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


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


    161 What is the memory key for Metronidazole's clinical uses?
    GET on the Metro


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


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


    164 What is the MOA for Acyclovir?
    Inhibit viral DNA polymerase


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


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


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


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


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


    170 What is the MOA for Metronidazole?
    Forms toxic metabolites in the bacterial cell, Bactericidal


    171 What is the MOA for Nystatin?
    Binds ergosterol, Disrupts fungal membranes


    172 What is the MOA for Rifampin?
    Inhibits DNA dependent RNA polymerase


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


    174 What is the MOA for the Azoles?
    Inhibit Ergosterol synthesis


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


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


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


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


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


    180 What is the MOA for Vancomycin?
    Inhibits cell wall mucopeptide formation, Bactericidal


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


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


    183 What is the MOA of Foscarnet?
    Inhibits Viral DNA polymerase


    184 What is the MOA of Ganciclovir?
    Inhibits CMV DNA polymerase


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


    186 What is the MOA of Imipenem?
    Acts as a wide spectrum carbapenem


    187 What is the MOA of Isoniazid (INH)?
    Decreases synthesis of Mycolic Acid


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


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


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


    191 What is the most common cause of Pt noncompliance with Macrolides?
    GI discomfort


    192 What is treated with Chloroquine, Quinine, Mefloquine?
    Malaria (P. falciparum)


    193 What microorganisms are Aminoglycosides ineffective against?
    Anaerobes


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


    195 What microorganisms is Aztreonam not effective against?
    Gram + and Anerobes


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


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


    198 What organism is Imipenem/cilastatin the Drug of Choice for?
    Enterobacter


    199 What organisms does Griseofulvin target?
    Dermatophytes (tinea, ringworm)


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


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


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


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


    204 What Sulfonamides are used for simple UTIs?
    Triple sulfas or SMZ


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

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


    207 Where does Griseofulvin deposit?
    Keratin containing tissues, e.g., nails

    208 Which Aminoglycoside is used for Bowel Surgery ?
    Neomycin


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


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


    211 Which individuals are predisposed to Sulfonamide-induced hemolysis?
    G6PD deficient individuals


    212 Which RT inhibitor causes Megaloblastic Anemia?
    AZT


    213 Which RT inhibitors cause a Rash?
    Non-Nucleosides


    214 Which RT inhibitors cause Lactic Acidosis?
    Nucleosides


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


    216 Who's your daddy?
    B.W. !!!, Ha. Good Luck on Boards


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


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


    219 List the mechanism, clinical use, & toxicity of 5 FU.
    -S-phase anti-metabolite Pyr analogue -Colon, solid tumors, & BCC/ -Irreversible myelosuppression


    220 List the mechanism, clinical use, & toxicity of 6 MP.
    -inhibits HGPRT (pur. Syn.) - Luk, Lymph,


    221 List the mechanism, clinical use, & toxicity of Bleomycin.
    -DNA intercalator -testicular & lymphomas -Pulmonary fibrosis mild myelosuppression.


    222 List the mechanism, clinical use, & toxicity of Busulfan.
    -Alkalates DNA -CML -Pulmonary fibrosis hyperpigmentation


    223 List the mechanism, clinical use, & toxicity of Cisplatin.
    -Alkalating agent -testicular,bladder,ovary,&lung -Nephrotoxicity & CN VIII damage.


    224 List the mechanism, clinical use, & toxicity of Cyclophosphamide.
    -Alkalating agent -NHL, Breast, ovary, & lung. - Myelosuppression, & hemorrhagic cystitis.


    225 List the mechanism, clinical use, & toxicity of Doxorubicin.
    -DNA intercalator -Hodgkin's, myeloma, sarcoma, and solid tumors -Cardiotoxicity & alopecia


    226 List the mechanism, clinical use, & toxicity of Etoposide.
    -Topo II inhibitor(GII specific) -Oat cell of Lung & prostate, & testicular -Myelosuppression & GI irritation.


    227 List the mechanism, clinical use, & toxicity of Methotrexate.
    -S-phase anti-metabolite folate analogue -Luk, Lymp, sarc, RA, &psoriasis / -Reversible myelosuppression


    228 List the mechanism, clinical use, & toxicity of Nitrosureas.
    -Alkalate DNA -Brain tumors -CNS toxicity


    229 List the mechanism, clinical use, & toxicity of Paclitaxel.
    -MT polymerization stabilizer -Ovarian & breast CA -Myelosupperession & hypersensitivity.


    230 List the mechanism, clinical use, & toxicity of Prednisone.
    -Triggers apoptosis -CLL, Hodgkin's in MOPP -Cushing-like syndrome


    231 List the mechanism, clinical use, & toxicity of Tamoxifen.
    -Estrogen receptor antagonist -Breast CA -increased endometrial CA risk


    232 List the mechanism, clinical use, & toxicity of Vincristine.
    -MT polymerization inhibitor(M phase) -MOPP, lymphoma, Willm's & choriocarcinoma -neurotoxicity and myelosuppression

    233 Which cancer drugs effect nuclear DNA (4)?
    -Alkalating agents+cisplatin -Doxorubicin+Dactinomycin -Bleomycin -Etoposide


    234 Which cancer drugs inhibit nucleotide synthesis(3)?
    - Methotrexate - 5 FU - 6 mercaptopurine


    235 Which cancer drugs work at the level of mRNA(2)?
    -Steroids -Tamoxifen


    236 Which cancer drugs work at the level of proteins(2)?
    -Vinca alkaloids(inhibit MT) -Paclitaxel


    237 ACE inhibitors- clinical use?
    hypertension, CHF, diabetic renal disease


    238 ACE inhibitors- mechanism?
    reduce levels of Angiotensin II, thereby preventing the inactivation of bradykinin (a potent vasodilator); renin level is increased


    239 ACE inhibitors- toxicity?
    fetal renal damage, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)


    240 Acetazolamide- clinical uses?
    glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness


    241 Acetazolamide- mechanism?
    acts at the proximal convoluted tubule to inhibit carbonic anhydrase. Causes self-limited sodium bicarb diuresis and reduction of total body bicarb stores.


    242 acetazolamide- site of action?
    proximal convoluted tubule


    243 Acetazolamide- toxicity?
    hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy


    244 Acetazolamide causesأ?
    ACIDazolamide' causes acidosis


    245 Adenosine- clinical use?
    DOC in diagnosing and abolishing AV nodal arrhythmias


    246 ADH antagonists- site of action?
    collecting ducts


    247 adverse effect of Nitroprusside?
    cyanide toxicity (releases CN)


    248 adverse effects of beta-blockers?
    impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations)


    249 adverse effects of Captopril?
    fetal renal toxicity, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)


    250 adverse effects of Clonidine?
    dry mouth, sedation, severe rebound hypertension


    251 adverse effects of ganglionic blockers?
    severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction


    252 adverse effects of Guanethidine?
    orthostatic and exercise hypotension, sexual dysfunction, diarrhea


    253 adverse effects of Hydralazine?
    nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retention


    254 adverse effects of Hydrochlorothiazide?
    hypokalemia, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia


    255 adverse effects of Loop Diuretics?
    K+ wasting, metabolic alkalosis, hypotension, ototoxicity


    256 adverse effects of Losartan?
    fetal renal toxicity, hyperkalemia


    257 adverse effects of Methyldopa?
    sedation, positive Coombs' test


    258 adverse effects of Minoxidil?
    hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention


    259 adverse effects of Nifedipine, verapamil?
    dizziness, flushing, constipation (verapamil), nausea


    260 adverse effects of Prazosin?
    first dose orthostatic hypotension, dizziness, headache


    261 adverse effects of Reserpine?
    sedation, depression, nasal stuffiness, diarrhea


    262 Amiodarone- toxicity?
    pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, consitpation, CV (bradycardia, heart block, CHF), and hypo- or hyperthyroidism.


    263 antidote?
    slowly normalize K+, lidocaine, cardiac pacer, and anti-Dig Fab fragments


    264 Beta Blockers- CNS toxicity?
    sedation, sleep alterations
    265 Beta Blockers- CV toxicity?
    bradycardia, AV block, CHF


    266 Beta Blockers- site of action?
    Beta adrenergic receptors and Ca2+ channels (stimulatory)


    267 BP?
    decrease


    268 BP?
    decrease


    269 Bretyllium- toxicity?
    new arrhythmias, hypotension


    270 Ca2+ channel blockers- clinical use?
    hypertension, angina, arrhythmias


    271 Ca2+ channel blockers- mechanism?
    block voltage dependent L-type Ca2+ channels of cardiac and smooth muscle- decreasing contractility


    272 Ca2+ channel blockers- site of action?
    Cell membrane Ca2+ channels of cardiac sarcomere


    273 Ca2+ channel blockers- toxicity?
    cardiac depression, peripheral edema, flushing, dizziness, constipation


    274 Ca2+ sensitizers'- site of action?


    troponin-tropomyosin system
    275 Cautions when using Amiodarone?
    check PFTs, LFTs, and TFTs


    276 class IA effects?
    increased AP duration, increased ERP increased QT interval. Atrial and ventricular.


    277 class IB- clinical uses?
    post MI and digitalis induced arrhythmias


    278 class IB- effects?
    decrease AP duration, affects ischemic or depolarized Purkinje and ventricular system


    279 class IB- toxicity?
    local anesthetic. CNS stimulation or depression. CV depression.


    280 class IC- effects?
    NO AP duration effect. useful in V-tach that progresses to V-fib and in intractable SVT LAST RESORT


    281 class IC- toxicity?
    proarrhythmic


    282 class II- effects?
    decrease the slope of phase 4, increase PR interval (the AV node is particularly sensitive)


    283 class II- mechanism?
    blocking the beta adrenergic receptor leads to decreased cAMP, and decreased Ca2+ flux


    284 class II- toxicity?
    impotence, exacerbation of asthma, CV effects, CNS effects, may mask hypoclycemia


    285 Class III- effects?
    increase AP duration, increase ERP, increase QT interval, for use when other arrhythmics fail


    286 class IV- clinical use?
    prevention of nodal arrhythmias (SVT)


    287 class IV- effects?
    decrease conduction velocity, increase ERP, increase PR interval


    288 class IV- primary site of action?
    AV nodal cells


    289 class IV- toxicity?
    constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression), and torsade de pointes (Bepridil)


    290 classes of antihypertensive drugs?
    diuretics, sympathoplegics, vasodilators, ACE inhibitors, Angiotensin II receptor inhibitors


    291 clinical use?
    angina, pulmonary edema (also, erection enhancer)


    292 clinical use?
    CHF, atrial fibrillation


    293 contractility?
    increase (reflex response)


    294 contractility?
    decrease


    295 contraindications?
    renal failure, hypokalemia, pt on quinidine


    296 decrease Digitoxin dose in renal failure?
    NO


    297 decrease Digoxin dose in renal failure?
    YES


    298 Digitalis- site of action?


    Na/K ATPase
    299 Digoxin v. Digitoxin: bioavailability?
    Digitoxin>95% Digoxin 75%


    300 Digoxin v. Digitoxin: excretion?

    ----------Digoxin=urinary Digitoxin=biliary

    Last edited by trimurtulu; 04-16-2009 at 10:18 PM.

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    Pharmacology : Question & Answers




    1. Generic names ending with ...azole = acid reducers


    2. Generic names ending with ...azone and ...ride = diabetes


    3. Generic names ending with ...acin and mycin = anti-infective


    4. Generic names ending with ...statin and ...or = cholesterol


    5. Generic names ending with ...pril = blood pressure


    6. Generic names ending with ...olol, artan, and dipine = cardiac


    7. Generic names ending with ...one = hormone


    8. Generic names ending with ...pam, pram, tine = psychological


    9. Generic names ending with ...fil = reproduction


    10.Generic names ending with ...coxib = arthritis .





    Question 1 :

    Drugs that block cell wall synthesis by inhibiting peptidoglycan x-linking

    Answer 1

    PCN, Ampicillin, Ticarcillin, Piperacillin, Imipenem, Aztreonam, Cephalosporins

    Question 2

    Drugs that block peptidoglycan synthesis

    Answer 2

    Bacitracin, Vancomycin, Cycloserine

    Question 3

    Drugs that block protein synthesis at 50S ribosomal subunit

    Answer 3

    Chloramphenicol, Erythromycin/Macrolides, Lincomycin, Clindamycin, Streptogramins (Quinupristin, Dalfopristin), Linezolid


    Question 4

    Drugs that block protein synthesis at 30S ribosomal subunit

    Answer 4

    Aminoglycosides, Tetracyclines

    Question 5

    Drugs that block nucleotide synthesis

    Question 6

    Drugs that block DNA topoisomerases

    Answer 6

    Quinolones

    Question 7

    Drugs that block mRNA synthesis

    Answer 7

    Rifampin

    Question 8

    Bactericidal antibiotics

    Answer 8

    Penicillin, Cephalosporins, Vancomycin, Aminoglycosides, Fluoroquinolones, Metronidazole

    Question 9

    Drugs that disrupt bacterial/fungal cell wall membranes

    Answer 9

    Polymyxins

    Question 10

    Drugs that disrupt fungal cell wall membranes

    Question 11

    PCN (G = IV, V = oral); hypersensitivity rxn and hemolytic anemia

    Answer 11

    Bactericidal for G+ cocci (1st line for Pneumococcal Pneumonia); G+ rods, G- cocci, Spirochetes (syphilis, lyme dz)

    Question 12

    Methicillin, Nafcillin, Dicloxacillin (hypersensitivity rxn; meth = interstitial nephritis)

    Answer 12

    Narrow spectrum Abx; Penicillinase Resistant d/t bulkier R group; use for Staph aureus

    Question 13

    Ampicillin, AmOxicillin (better oral availability); (hypersensitivity, amp rash, pseudomembranous colitis)

    Answer 13

    Wider spectrum HELPS kill enterococci (Haemophilus, E. coli, Listeria, Proteus, Salmonella, enterococcus); sensitive to penicillinase, but can combine with Clavulanic Acid (inhibitor);

    Question 14

    Carbenicillin, Piperacillin, Ticarcillin (hypersensitivity)

    Answer 14

    Extented spectrum (Pseudomonas, G- rods); use with Clavulanic acid

    Question 15

    Cephalosporins

    Answer 15

    b-lactam drugs inhibit cell wall synthesis but are less susceptible to penicillinases; bactericidal

    Question 16

    1st generation cephalosporins (Cephalexin, Cefadroxil, Cefazolin): PEcK



    Answer 16

    Proteus, E. coli, Klebsiella

    Question 17

    2nd generation cephalosporins (Loracarbef, Cefprozil, Cefuroxime, Cefaclor): HEN PEcKS

    Answer 17

    Haemophilus, Enterobacter, Neisseria, Proteus, E. coli, Klebsiella, Serratia

    Question 18

    3rd generation cephalosporins (Ceftazidime, Ceftriaxone)


    Answer 18

    great G- coverage; Tx meningitis, Pseudomonas, Gonorrhea

    Question 19

    4th generation cephalosporins

    Answer 19

    increased activity against Pseudomonas and G+ bugs

    Question 20

    Cefoperazone

    Answer 20

    2nd generation cephalosporin; use in pts with decreased renal failure; HEN PEcKS

    Question 21

    Ceftazidime

    Answer 21

    3rd generation cephalosporin; use for Pseudomonas (and other G-s)

    Question 22

    Ceftriaxone

    Answer 22

    3rd generation cephalosporin; use for GONORRHEA (and other G-s)

    Question 23

    Cephalosproin toxicity

    Answer 23

    Disulfiram-like rxn w/ethanol (ex: Cefamandole d/t methylthiotetrazole grp); hypersensitivity rxns d/t x-reactivity w/PCNs in some pts; They increase nephrotoxicity of aminoglycosides

    Question 24

    Aztreonam

    Answer 24

    G- rods ONLY: Klebsiella, Pseudomonas, Serratia; Good for RENAL PTs who can't tolerate aminoglycosides; resistant to b-lactamase; no PCN x-allergenicity

    Question 25

    Imipenem/Cilastatin (imipenem is renally longer LASTIN' with ciLASTIN)


    Answer 25

    #1 for ENTEROBACTER; Broad spectrum (G+ cocci, G- rods, Anaerobes); can cause seizures

    Question 26

    Vancomycin (nephrotoxic, ototoxic, thrombophlebitis, "red man syndrome" from fast infusion)

    Answer 26

    Save for SERIOUS G+ MULTI-DRUG RESISTANT bugs: S. aureus and Clostridium difficile; changes AAs from D-ala to D-lac;

    Question 27

    Protein Synthesis Inhibitors: "Buy AT 30, CELL at 50"

    Answer 27

    30s (Aminoglycosides - bactericidal, Tetracyclines); 50S (Chloramphenicol, Erythromycin, Lincomycin, cLindamycin); all except aminoglycosides are bacteriostatic

    Question 28

    Gentamicin, Neomycin, Tobramycin, Streptomycin, Amikacin

    Answer 28

    Aminoglycosides; Good for SEVERE G- Rod infxns; bactericidal - no initiation complex/misread mRNA; synergistic with b-lactams; requires O2 for uptake (no anaerobic coverage);

    Question 29

    Neomycin

    Answer 29

    used for bowel surgery

    Question 30

    Toxicity of Aminoglycosides + Cephalosporins

    Answer 30

    Nephrotoxicity

    Question 31

    Toxicity of Aminoglycosides + Loop diuretics

    Answer 31

    Ototoxicity

    Question 32

    Tetracycline, Doxycycline, Demeclocycline (VACUUM your BedRoom Tonight)

    Answer 32

    Vibrio, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia, Rickettsia, Tularemia; Bacteriostatic; bind 30S/prevent tRNA attachment; don't take with Ca or Fe b/c divalent cations bind in gut

    Question 33

    Doxycycline

    Answer 33

    safe to use in renal patients

    Question 34

    Toxicity of Tetracycline, doxycycline, demeclocycline

    Answer 34

    discoloration of teeth and inhibition of bone growth in kids; photosensitivity; GI distress

    Question 35

    Erythromycin, Azithromycin, Clarithromycin (GI discomfort is bad; acute cholestatic hepatitis, eosinophilia, rash)

    Answer 35

    URIs, Pneumonias, STDs, Strep infxns in PCN-allergies; Mycoplasma, Legionella, Chlamydia, Neisseria; Macrolides; block protein translocation (23S rRNA of 50S subunit); Bacteriostatic

    Question 36

    Chloramphenicol (anemia, aplastic anemia, gray baby d/t lack of liver UDP-glucuronyl transferase)

    Answer 36

    Meningitis (H. influenza, N. menigitidis, S. pneumoniae); Bacteriostatic; inhibits 50S peptidyltransferase; Toxicity = use conservatively

    Question 37

    Clindamycin (causes C. difficile overgrowth)

    Answer 37

    blocks 50S peptide bond; bacteriostatic; Tx ANAEROBIC infxns above diaphragm (Bacteriodes fragilis, Clostridium perfringens

    Question 38

    Sulfamthoxazole (SMX), Sulfisoxazole, Triple Sulfas, Sulfadiazine

    Answer 38

    G+, G-, Nocardia, Chlamydia coverage; UTI; bacteriostatic; sulfonamides; PABA-antimetabolites inhibit dihydropteroate synth; hemolysis in G6PD deficiency; nephrotoxic, kernicterus infant, diplaces warfarin from albumin

    Question 39

    Trimethoprim

    Answer 39

    Treat recurrent UTIs, Shigella, Salmonella, Pneumocystis carinii; bacteriostatic; inhibits bacterial dihydrofolate reductase; use in combo w/SMX to block folate synth; may cause marrow suppression

    Question 40

    Ciprofloxacin, Norfloxacin, Ofloxacin, Sparfloxacin, Moxifloxacin, Gatifloxacin, Enoxacin, Nalidixic acid

    Answer 40

    Treat G- rods in UTI, GI infxns; PSEUDOMONAS, Neisseria, some G+s; Bactericidal; inhibit DNA gyrase (topoisomerase II); Fluoroquinolones; contra in pregnancy; may cause Tendonitis/rupture

    Question 41

    Metronidazole: GETon the metro!

    Answer 41

    Antiprotozoal: Giardia, Entamoeba, Trichomonas, Gardernela vaginalis, ANAEROBES (Bacterioides, Clostridium); Use as part of triple therapy for H.pylori (w/bismuth, amoxicillin or tetracycline); Disulfiram-like rxn w/alcohol, HA

    Question 42

    Polymyxin B, Polymyxin E

    Answer 42

    Use for resistant G- infections; alter osmotic properties in bacterial membrane; cationic basic ptns that act as detergents; can be neurotoxic, nephrotoxic

    Question 44

    Isoniazid

    Answer 44

    Can solely prophylax against TB; decreases mycolic acid synthesis; "INH" = injures neurons and hepatocytes; also causes hemolysis in G6PD deficiency; B6/pyridoxine can prevent neurotoxicity

    Question 45

    Rifampin

    Answer 45

    Treats TB; delays dapsone resistance in leprosy; Meningococcal prophylaxis for Hib; "4 Rs" = RNA polymerase inhibitor, revs up P450; Red/orange body fluids, Rapid resistance if used alone

    Question 46

    Penicillin/cephalosporin resistance mechanism

    Answer 46

    b-lactamase cleavage of b-lactam ring

    Question 47

    Aminoglycoside resistance mechanism

    Answer 47

    modification via acetylation, adenylation, or phosphorylation

    Question 48

    Vancomycin resistance mechanism

    Answer 48

    terminal D-ala of cell wall replaced with D-lac; decreases affinity

    Question 49

    Chloramphenicol resistance mechanism

    Answer 49

    modification via acetylation

    Question 50

    Macrolide resistance mechanism

    Answer 50

    methylation of rRNA near erythromycin's ribosomal binding site

    Question 51

    Tetracycline resistance mechanism

    Answer 51

    decreased or increased transport out of cell

    Question 52

    Sulfonamide resistance mechanism

    Answer 52

    altered enzyme (bacterial dihydropteroate synthase); dec uptake or inc PABA synthesis

    Question 53

    Nonsurgical antimicrobial prophylaxis for Meningococcal infection

    Answer 53

    Rifampin (drug of choice), minocycline

    Question 54

    Nonsurgical antimicrobial prophylaxis for Gonorrhea

    Answer 54

    Ceftriaxone

    Question 55

    Nonsurgical antimicrobial prophylaxis for Syphilis

    Answer 55

    Benzathine PCN-G (IV)

    Question 56

    Nonsurgical antimicrobial prophylaxis for h/o recurrent UTIs

    Answer 56

    TMP-SMX

    Question 57

    Nonsurgical antimicrobial prophylaxis for Pneumocystic carinii pneumonia

    Answer 57

    TMP-SMX (drug of choice), aerosolized pentamidine

    Question 58

    Amphotericin B

    Answer 58

    Treat systemic mycoses: Cryptococcus, Blastomycoses, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor; binds ergosterol, "tears" pores in membrane; fever/chills, hypotension, nephrotoxic, Arrhythmias

    Question 59

    Nystatin

    Answer 59

    "swish and swallow" for oral candidiasis; binds ergosterol disrupting fungal membranes

    Question 60

    Fluconazole, Ketoconazole, Clotrimazole, Miconazole, Itraconazole, Voriconazole

    Answer 60

    Treat Systemic mycoses and hypercortisolism: inhibit ergosterol synthesi

    Question 61

    Fluconazole

    Answer 61

    Treat cryptococcal meningitis in AIDS and all candidiasis infxns (except yeast)

    Question 62

    Ketoconazle

    Answer 62

    Treat Blastomyces, Coccidioides, Histoplasma, Candida albicans, hy.


    .
    Last edited by trimurtulu; 04-16-2009 at 08:50 PM.

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    Question 1

    antacids

    Answer 1

    relieves gastritis, ulcer pain, indigestion heart burn

    Question 2

    antianginals

    Answer 2

    relieves heart pain

    Question 3

    anticoagulant

    Answer 3

    dissolves or prevents blood clots

    Question 4

    anticonvulsants

    Answer 4

    prevents seizures

    Question 5

    antidepressants

    Answer 5

    prevents depression

    Question 6

    antidiarrheals

    Answer 6

    stops diarrhea

    Question 7

    antiemetics

    Answer 7

    prevents nausea and vomiting



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    .



    Question 1

    DNS

    Answer 1

    do not substitute

    Question 2

    opium

    Answer 2

    an analgesic made from poppy plant

    Question 3

    medication errors

    Answer 3

    preventable event that cause or leads to inappropriate medication use or patient harm

    Question 4

    OBRA 90

    Answer 4

    Omnibus Budget Reconciliation Act: law that requires pharmacy to consel patients on new prescriptions

    Question 5

    AAA

    Answer 5

    Apply to Affected Area

    Question 6

    DEA

    Answer 6

    Drug Enforcement Administration

    Question 7

    Dual Marketing

    Answer 7

    status of medication like PlanB that are classified as both prescription drugs and OTC drugs

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    .


    Question 1 - methylphenidate

    Answer 1 - concerta, ritalin

    Question 2 - cozaar

    Answer 2 - losartan

    Question 3 - quetiapine


    Answer 3 - seroquel

    Question 4 - coreg

    Answer 4 - carvedilol

    Question 5 - tenormin

    Answer 5 - atenolol

    Question 6 - indication for mobic

    Answer 6 - NSAID

    Question 7 - promethazine

    Answer 7 - phenergan

    .

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    .

    Question 1

    DNA contains what sugar?

    Answer 1

    2-deoxyribose

    Question 2

    Purines. Contains ______ rings in their structure

    Answer 2

    Adenine and guanine. 2 rings

    Question 3

    Pyrimidines. Contain ______ rings in their structure

    Answer 3

    Cytosine, Uracil, Thymine. 1 ring

    Question 4

    A nucleoside is made up of:

    Question 5

    The 5' carbon of the sugar residue attaches to:

    Answer 5

    phosphate group

    Question 6

    List what attaches to the 1' carbon in DNA

    Answer 6

    1' - glycosidic bond,

    Question 7

    List what attaches to the 2' carbon in DNA

    Answer 7

    2' - no hydroxy group,

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    .

    Question 1

    DNA contains what sugar?

    Answer 1

    2-deoxyribose

    Question 2

    Purines. Contains ______ rings in their structure

    Answer 2

    Adenine and guanine. 2 rings

    Question 3

    Pyrimidines. Contain ______ rings in their structure

    Answer 3

    Cytosine, Uracil, Thymine. 1 ring

    Question 4

    A nucleoside is made up of:

    Question 5

    The 5' carbon of the sugar residue attaches to:

    Answer 5

    phosphate group

    Question 6

    List what attaches to the 1' carbon in DNA

    Answer 6

    1' - glycosidic bond,

    Question 7

    List what attaches to the 2' carbon in DNA

    Answer 7

    2' - no hydroxy group,


    Biochem - Protein and AA Metabolism and The Urea Cycle


    Question 1

    AA catabolism produces what toxic product?

    Answer 1

    Ammonia

    Question 2

    What are the essential amino acids?

    Answer 2

    PVT TIM HALL(phenylalanine, valine, tryptophan, threonine, isoleucine, methionine, histidine, arginine, lysine, leucine)

    Question 3

    What are the two possible sources of essential amino acids?

    Answer 3

    diet, protein turnover

    Question 4

    What are some products that are made from amino acids?

    Answer 4

    Carbon (synthesis of glucose, fatty acids, ketones and energy)Nitrogen (urea)Synthesis of other N-containing molecules (purines, pyrimidines, porphyrine (bilirubin), neurotransmitters)

    Question 5

    What is negative nitrogen balance?

    Answer 5

    When input is less than output. Endogenous amino acids are being broken down, thus "excreting" and is more than is being taken in.

    Question 6

    When does negative nitrogen balance occur?

    Answer 6

    Dietary Deficiency (starvation)Catabolic stress (ex. infection)

    Question 7

    What is positive nitrogen balance?

    Answer 7

    When input is greater than output. You are taking in more nitrogen than you are excreting.


    Question 1

    in the MEOS system, what enzyme is used?

    Answer 1

    cytochrome p450 enzyme cyp2e1

    Question 2

    what is the cofactor in the meos system? is this molecule oxidized or reduced?

    Answer 2

    nadph; oxidized

    Question 3

    what can the liver make out of acetyl coa?

    Question 4

    how can nadh make energy?

    Answer 4

    ox phos, various dehydrogenases

    Question 5

    what tissues aside from liver can use acetate?

    Answer 5

    kidney, heart, skeletal muscle

    Question 6

    which adh isoenzyme has highest km in liver

    Answer 6

    adh2

    Question 7

    excessive nadh increases what reactions?

    Answer 7

    g-3-p production, lactate production, and malate production

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    .

    The management of patients with STD who are coinfected with HIV presents complex clinical and behavioral issues. Because of its effect on the immune system, HIV may alter the natural histories of many STD, as well as the effect of antimicrobial therapy. Close clinical follow-up is imperative. STD infection in patients with and without HIV is a sentinel event, often indicating continued unprotected sexual activity. Further patient counseling is indicated in these situations. STD Reporting and Confidentiality

    Disease surveillance activities, which include the accurate identification and timely reporting of STD, form an integral part of successful disease control. Reporting assists local health authorities in identifying sexual contacts who may be infected (see next section). Reporting is also important for assessing morbidity trends.

    Reporting may be provider- and/or laboratory-based. Cases should be reported in accordance with local statutory requirements and in as timely a manner as possible. Clinicians who are unsure of local reporting requirements are encouraged to seek advice through their local health departments or state STD programs.

    STD reports are held in strictest confidence and in many jurisdictions are protected by statute from subpoena. Before any follow-up of a positive STD test is conducted by STD program representatives, these personnel consult with the provider to verify the diagnosis and treatment. Most local health departments offer STD partner notification and follow-up services for selected STD. Management of Sex Partners and Partner Notification

    Clinical guidelines for management of sex partners are included in each disease section.

    Breaking the chain of transmission is crucial to STD control. Further transmission and reinfection are prevented by referral of sex partners for diagnosis and treatment. Patients should ensure that their sex partners, including those without symptoms, are referred for evaluation. Partners of patients with STD should be examined; treatment should not be provided for partners who are not examined, except in rare instances such as when the partner is at a site remote from medical care. Appropriate referral for sex partners should be provided if care will not or cannot be provided by the initial health-care provider. Disease Intervention Specialists (DIS), i.e., public health professionals trained in STD management, can assist patients and practitioners in this process through interviewing and confidential field outreach procedures. Local and state health departments offer DIS referral services. Physicians and other community health personnel are encouraged to use DIS services to ensure complete case management. Health department managers should allocate DIS resources based on local morbidity patterns, outbreak situations, and available resources. Medical Resources

    Health-care providers caring for STD patients should ensure that medical resources for the following are available either on site or through referral: --Medical evaluation and treatment facilities for HIV-infected patients --Hospitalization facilities for patients with complicated STD infection, such as pelvic inflammatory disease (PID) and disseminated gonococcal infection (DGI) --Medical, pediatric, infectious disease, dermatologic, and gynecological/obstetrical referral services --Family planning services --Substance abuse treatment services AIDS and HIV Infection in The General STD Setting

    The acquired immunodeficiency syndrome (AIDS) is a late manifestation of infection with human immunodeficiency virus (HIV). Most people infected with HIV remain asymptomatic for long periods. HIV infection is most often diagnosed by using HIV antibody tests. Detectable antibody usually develops within 3 months after infection. A confirmed positive antibody test means that a person is infected with HIV and is capable of transmitting the virus to others. Although a negative antibody test usually means a person is not infected, antibody tests cannot rule out infection from a recent exposure. If antibody testing is related to a specific exposure, the test should be repeated 3 and 6 months after the exposure.

    Antibody testing for HIV begins with a screening test, usually an enzyme-linked immunosorbent assay (ELISA). If the screening test is positive, it is followed by a more specific confirmatory test, most commonly the Western blot assay. New antibody tests are being developed and licensed that are either easier to perform or more accurate. Positive results from screening tests must be confirmed before being considered definitive.

    The time between infection with HIV and development of AIDS ranges from a few months to greater than or equal to 10 years. Most people who are infected with HIV will eventually have some symptoms related to that infection. In one cohort study, AIDS developed in 48% of a group of gay men less than or equal to 10 years after infection; but additional AIDS cases are expected among those who have remained AIDS-free for greater than 10 years.

    Therapy with zidovudine (ZDV--previously known as azidothymidine) has been shown to benefit persons in the later stages of disease (AIDS or AIDS-related conditions along with a CD4 (T4) lymphocyte count less than 200/mm3). Serious side effects, usually anemias and cytopenias, have been common during therapy with ZDV; therefore, patients taking ZDV require careful follow-up in consultation with physicians who are familiar with ZDV therapy. Clinical trials are currently evaluating ZDV therapy for persons with asymptomatic HIV infection to see if it decreases the rate of progression to AIDS. Other trials are evaluating new drugs or combinations of drugs for persons with different stages of HIV infection, including asymptomatic infections. The complete therapeutic management of HIV infection is beyond the scope of this document. Preventing the Sexual Transmission of HIV

    The only way to prevent AIDS is to prevent the initial infection with HIV. Prevention of sexual transmission of HIV can be ensured in only two situations: 1) sexual abstinence or 2) choosing only sex partners who are not infected with HIV.

    Many HIV-infected persons are asymptomatic and are unaware that they are infected. Therefore, without an antibody test, infected persons are difficult to identify. AIDS case surveillance and HIV seroprevalence studies allow estimation of risk for persons in different areas; however, these population estimates may have a limited impact on an individual's sexual decisions. Although knowledge of antibody status is desirable before a sexual relationship is initiated, this information may not be available. Therefore, individuals should be counseled that when they initiate a sexual relationship they should use sexual practices that reduce the risk of HIV transmission.

    Sexual practices may influence the likelihood of HIV transmission during sexual contact with an infected partner. Women who practice anal intercourse with an infected partner are more likely to acquire infection than women who have only vaginal intercourse. The relative risk of transmission by oral-genital contact is probably somewhat lower than the risk of transmission by vaginal intercourse. Other STD or local trauma that breaks down the mucosal barrier to infection would be expected to increase the risk of HIV transmission. Condoms supplement natural barriers to infection and therefore reduce the risk of HIV transmission (see "Clinician Guidelines and Public Health Considerations"). When to Test for HIV

    Voluntary, confidential, HIV antibody testing should be done routinely when the results may contribute either to the medical management of the person being tested or to the prevention of further transmission.

    Testing is important for persons with symptoms of HIV-related illnesses or with diseases such as syphilis, chancroid, herpes, or tuberculosis, for which a positive test result might affect the recommended diagnostic evaluation, treatment, or follow-up. HIV counseling and testing for persons with STD is a particularly important part of an HIV prevention program, because patients who have acquired an STD have demonstrated their potential risk for acquiring HIV.

    Because no vaccine or cure is available, HIV prevention requires changes in behavior by people at risk for transmitting or acquiring infection. Therefore, patient counseling must be an integral part of any HIV testing program in an STD clinic. Counseling should be done both before and after HIV testing. Pretest Counseling

    Pretest counseling should include assessment of the patient's risk for HIV infection and measures to reduce that risk.

    Intravenous (IV) drug users should be advised to stop using drugs. If they do not stop, they should not share needles. If needle-sharing continues, injection equipment should be cleaned with bleach between uses. Sexually active persons who have multiple partners should be advised to consider sexual abstinence or to enter a mutually monogamous relationship with a partner who has also been tested for HIV. Condoms should be used consistently if either or both partners are infected or have other partners. Similarly, heterosexuals with STD other than HIV should be encouraged to bring their partners in for HIV testing and to use condoms if they are not in a mutually monogamous relationship with an uninfected partner. Posttest Counseling and Evaluation

    Persons who have negative HIV antibody tests should be told their test result by a person who understands the need to reduce unsafe sexual behaviors and can explain ways to modify sexual practices to reduce risks.

    Antibody tests cannot detect infections that occurred in the several weeks before the test (see above). Persons who have negative tests should understand that the negative test result does not signify protection from acquiring infection. They should be advised about the ways the virus is transmitted and how to avoid infection. Their partners' risks for HIV infection should be discussed, and partners at risk should be encouraged to be tested for HIV.

    Persons who test positive for HIV antibody should be told their test result by a person who is able to discuss the medical, psychological, and social implications of HIV infection. Routes of HIV transmission and methods to prevent further transmission should be emphasized.

    Risks to past sexual and needle-sharing partners of HIV antibody-positive patients should be discussed, and they should be instructed in how to notify their partners and to refer them for counseling and testing. If they are unable to notify their partners or they are not sure that their partners will seek counseling, physicians or health department personnel should assist, using confidential procedures, to ensure that the partners are notified. Infected women should be advised of the risk of perinatal transmission (see below), and methods of contraception should be discussed and provided. Additional follow-up, counseling, and support systems should be available to facilitate psychosocial adjustment and changes in behavior among HIV antibody-positive persons. Perinatal Infections

    Infants born to women with HIV infection may also be infected with HIV; this risk is estimated to be 30%-40%. The mother in such a case may be asymptomatic and her HIV infection not recognized at delivery. Infected neonates are usually asymptomatic, and currently HIV infection cannot be readily or easily diagnosed at birth. (A positive antibody test may reflect passively transferred maternal antibodies, and the infant must be observed over time to determine if neonatal infection is present.) Infection may not become evident until the child is 12-18 months of age. All pregnant women with a history of STD should be offered HIV counseling and testing. Recognition of HIV infection in pregnancy permits health-care workers to inform patients about the risks of transmission to the infant and the risks of continuing pregnancy. Asymptomatic HIV Infections

    As more HIV-infected persons are identified, primary health-care providers will need to assume increased responsibility for these patients. Most internists, pediatricians, family practitioners, and gynecologists should be qualified to provide initial evaluation of HIV-infected individuals and follow-up of those with uncomplicated HIV infection. These services should be available in all public health clinics.

    Health-care professionals who identify HIV-positive patients should provide posttest counseling; medical evaluation (either on site or by referral)--including a physical examination, complete blood count, lymphocyte subset analysis, syphilis serology, and a purified protein derivative (PPD) skin test for tuberculosis. Psychosocial counseling resources should also be available.

    All clinics and providers should establish and maintain contacts with resources in their regions for persons concerned about HIV infection, and they should refer patients when necessary. Possible resources for referral include counseling services, support groups, social workers, physicians, and clinics. Diseases Characterized by Genital Ulcers or Inguinal Lymphadenopathy

    In the United States, most patients with genital ulcers have genital herpes, syphilis, or chancroid. Inguinal lymphadenopathy is common in these infections. More than one of these diseases may be present in a patient. Patients who have genital ulcers may be at increased risk for HIV infection.

    Diagnosis based only on history and physical examination is often inaccurate. Thus, evaluation of most persons with genital ulcers should include one or more of the following: --Dark-field examination or direct immunofluorescence test for T. pallidum --Serologic test(s) for syphilis --Culture or antigen test for HSV --Culture for Haemophilus ducreyi Chancroid

    Because of recent spread of H. ducreyi, chancroid has become an important STD in the United States. Its importance is enhanced by the knowledge that outside the United States chancroid has been associated with increased infection rates for HIV. Chancroid must be considered in the differential diagnosis of any patient with a painful genital ulcer. Painful inguinal lymphadenopathy is present in about half of all chancroid cases. Recommended Regimen Erythromycin base 500 mg orally 4 times a day for 7 days, or Ceftriaxone 250 mg intramuscularly (IM) in a single dose. Alternative Regimen Trimethoprim/sulfamethoxazole 160/800 mg (one double-strength tablet) orally 2 times a day for 7 days. Comment: The susceptibility of H. ducreyi to this combination of antimicrobial agents varies throughout the world; clinical efficacy should be monitored, preferably in conjunction with monitoring of susceptibility patterns. or Amoxicillin 500 mg plus clavulanic acid 125 mg orally 3 times a day for 7 days. Comment: Not evaluated in the United States. or Ciprofloxacin 500 mg orally 2 times a day for 3 days. Comment: Although a regimen of 500 mg orally once was effective outside the United States, based on pharmacokinetics and susceptibility data, 2- or 3-day regimens of the same dose may be prudent, especially for patients coinfected with HIV. Quinolones, such as ciprofloxacin, are contraindicated during pregnancy and in children 16 years of age or younger. Management of Sex Partners

    Sex partners, within the 10 days preceding onset of symptoms in an infected patient, whether symptomatic or not, should be examined and treated with a recommended regimen. Follow-Up

    If treatment is successful, ulcers due to chancroid symptomatically improve within 3 days and objectively improve (evidenced by resolution of lesions and clearing of exudate) within 7 days after institution of therapy. Clinical resolution of lymphadenopathy is slower than that of ulcers and may require needle aspiration (through healthy, adjacent skin), even during successful therapy. Patients should be observed until the ulcer is completely healed. Because of the epidemiologic association with syphilis, serological testing for syphilis should be considered within 3 months after therapy. Treatment Failures

    If no clinical improvement is evident by 7 days after therapy, the clinician should consider whether 1) antimicrobials were taken as prescribed, 2) the H. ducreyi causing infection is resistant to the prescribed antimicrobial, 3) the diagnosis is correct, 4) coinfection with another STD agent exists, or 5) the patient is also infected with HIV. Preliminary information indicates that patients coinfected with HIV do not respond to antimicrobial therapy as well as patients not infected with HIV, especially when single-dose treatment is used. Antimicrobial susceptibility testing should be performed on H. ducreyi isolated from patients who do not respond to recommended therapies. Syphilis General principles Serologic Tests

    Dark-field examinations and direct fluorescent antibody tests on lesions or tissue are the definitive methods for diagnosing early syphilis. Presumptive diagnosis is possible by using two types of serologic tests for syphilis: 1) treponemal (e.g., fluorescent treponemal antibody absorbed (FTA-ABS), microhemagglutination assay for antibody to T. pallidum (MHATP)) and 2) nontreponemal (e.g., Venereal Disease Research Laboratory (VDRL), rapid plasma reagin (RPR)). Neither test alone is sufficient for diagnosis. Treponemal antibody tests, once positive, usually remain so for life, regardless of treatment or disease activity. Treponemal antibody titers do not correlate with disease activity and should be reported as positive or negative. Nontreponemal antibody titers do tend to correlate with disease activity, usually rising with new infection and falling after treatment. Nontreponemal antibody test results should be reported quantitatively and titered out to a final end point rather than reported as greater than an arbitrary cutoff (e.g., greater than 1:512). With regard to changes in nontreponemal test results, a fourfold change in titers is equivalent to a two-dilution change--e.g., from 1:16 to 1:4, or from 1:8 to 1:32.
    Last edited by trimurtulu; 04-16-2009 at 10:29 PM.

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