# منتديات طلاب الجامعات الأردنية > منتدى طلاب الطب والصيدلة والتخصصات الطبية >  pharmacology Q & A

## الوسادة

Pharmacology animicrobial Q&a
Q: A common side effects of INF treatment is?
A: Neutropenia

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

Q: Antimicrobial prophylaxis for Gonorrhea
A: Ceftriaxone

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

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

Q: Antimicrobial prophylaxis for Syphilis
A: Benzathine penicillin G

Q: Are Aminoglycosides Teratogenic?
A: Yes

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: Foscarnet toxicity?
A: Nephrotoxicity 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: How is Leishmaniasis treated?
A: Pentavalent Antimony

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

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

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

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

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

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

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

Q: Is Aztreonam resistant to penicillinase?
A: Yes

Q: Is Aztreonam usually toxic?
A: No

Q: Is Imipenem resistant to penicillinase?
A: Yes

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

Q: IV Penicillin
A: G

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

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

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

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

Q: MOA: Block DNA topoisomerases
A: Quinolones

Q: MOA: Block mRNA synthesis
A: Rifampin

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

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

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

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

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

Q: MOA: Unkown
A: Pentamidine

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

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

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

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

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

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

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

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

Q: Name the common Non-Nucleoside Reverse Tran******ase Inhibitors
A: Nevirapine, Delavirdine

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

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

Q: Name two classes of drugs for HIV therapy
A: Protease Inhibitors and Reverse Tran******ase Inhibitors

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

Q: Oral Penicillin
A: V

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

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

Q: Resistance mechanisms for Chloramphenicol
A: Modification via Acetylation

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

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

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

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

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

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

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

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

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

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

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

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




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## الوسادة

[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


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## الوسادة

[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+ (&lt; 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 (&lt;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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