Thread: 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 body’s 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 : 1–2 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:10–20 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

thanks you.....

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.


.

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



.

.



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

.


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

.

.

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,

.

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

.

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.

thank u soooooooooooooooooo much...................