Term
| What is Selective Toxicity? |
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Definition
| Selective toxicity is defined as the ability of a drug to injure a target cell or target organism without injuring other cells or organisms that re in intimate contact with the target. |
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Term
| What are the three ways that selective toxicity can be achieved? |
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Definition
| Disruption of a bacterial cell wall, Inhibition of an enzyme unique to bacteria, disruption of bacterial protein synthesis. |
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Term
| How can an organism develop tolerance to a drug? |
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Definition
| Microbes may elaborate drug-metabolizing enzymes, microbes may cease active uptake of certain drugs, microbial drug receptors may undergo change resulting in decreased antibiotic binding and action and microbes may synthesize compounds that antagonize drug actions. |
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Term
| What is a suprainfection? |
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Definition
| A suprainfection is simply a special example of the emergence of drug resistance. This happens when antibiotics kill off normal flora and allow more dangerous |
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Term
| What is the mechanism of action on penicillin based drugs? |
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Definition
| Penicillins weaken teh cell wall, causing bacteria to take up excessive amounts of water and rupture. They work by two actions. Inhibition of transpeptidases and disinhibition of autolysins. |
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Term
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Definition
| penicillin-binding proteins. They are named as such because pen. must bind to them to produce antibacterial effects. |
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Term
| What is the difference in gram positive and gram negative binding for penicillin? |
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Definition
| Penicillin effectivley attacks gram positive bacteria but cannot penetrate the outer membrane of gram negative cells. |
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Term
| What do Beta-lactamases do? |
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Definition
| They cleave the beta-lactam ring in penicillin rendering it ineffective. |
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Term
| How do gram positive and gram negative bacteria treat beta-lactamases differently? |
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Definition
| The g+ bacteria produce large amounts of B-L and discharge it in to the local medium. G- produce small amounts and secrete them into the periplasmic space. |
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Term
| Where are penicillins derived from? |
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Definition
| 6-aminopenicillanic acid. |
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Term
| What are the three salts of penicillin G? |
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Definition
| Potassium penicillin G, Procain Penicillin G, and benzathine penicillin G |
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Term
| T/F If and individual is allergic to Penicillin G they will in 5% to 10% of cases be allergic to cephalosporins and carbapenems. |
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Definition
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Term
| What is the allergen in Penicillin? |
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Definition
| Penicillin iteslf is not an allergen, however with degradation the small molecules form haptens with proteins and this can cause a reaction. |
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Term
| What is the major antigenic determinant reagent? |
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Definition
| benzypenicilloyl-polylysine |
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Term
| What does the minor determinant mixture detect? |
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Definition
| It detects antibodies that mediate immediate allergic responses (anaphylaxis) |
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Term
| How do aminoglycosides and pen. work together and against each other? |
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Definition
| They work because Pen. defeats the cell wall allowing aminoglycosides to get inside the cell. They work against each other because they two can react in solution. The solution to this problem is to administer them in seperate IV solutions so that the reaction doesn't occur. |
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Term
| What are the 3 agents that are penicillinase-resistance?What are they used against? (ONLY) |
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Definition
nafcillin, oxacillin, dicloxacillin.
Staph. aureus and staph. epidermis |
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Term
| What are the two broad-spectrum penicillins? |
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Definition
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Term
| What are extended-spectrum penicillins used for? |
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Definition
| Primarily for infections with P. aeruginosa. These infections often occur in the immunocompromised host and can be very difficult to eradicate. |
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Term
| What 3 drugs are appropriate for use with patients that are allergic to Pen.? |
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Definition
| Vancomycin, erythromycin, and clindamycin. |
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Term
| How are penicillins eliminated? |
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Definition
|
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Term
| Can Pen. G be adminstered orally? |
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Definition
| NO. It is unstable in the stomach, IM injection or IV. |
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Term
| What is the active area of a cephalosporin? |
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Definition
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Term
| How do cephalosprins work? |
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Definition
| They act by binding to penicillin-binding proteins and disrupt cell wall synthesis and activate autolysins. Death is caused by autolysis. |
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Term
| In order what is the least to most resistant to betalactamases? |
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Definition
| 1st gen 2nd gen and then finally 3rd and 4th gen are most resistant. |
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Term
| What happens from 1st gen to 4th gen cephalosprins? |
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Definition
| Increasing activity against gram-negative bacteria and anaerobes, increasing resistance to destruction by beta lactamases and increasing ability to reach the CSF. |
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Term
| t/f cephalosporins are absorbed by the GI tract well. |
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Definition
| False, they must be given parenterally. |
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Term
| What two cephalosporins are not eliminated by nonrenal routes? |
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Definition
| cefoperazone and cefriaxone. |
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Term
| What three cephalorpsorings can NOT be taken with alcohol? |
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Definition
| cefmetazole, cefoperazone, cefotetan. They result in a disulfuram like reaction causing intense sickness. |
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Term
| What are carbapenems? What are the 3 drugs? |
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Definition
| Beta-lactam antibiotics that have very broad antimicrobial spectra. imipenem, meropenem, and ertapenem. |
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Term
| What is the mechanism for imipenem? |
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Definition
| imipenem binds to two pbps (pbp1 and pbp2) causing lysis. It is resistant to almost all beta-lactamases. |
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Term
| What is the primary introduction route and how does the body eliminate imipenem? |
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Definition
| Parenterally, and it is primarily renal. it is inactivted by depeptidase. |
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Term
| What are teh adverse effects of imipenem? |
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Definition
| Gastrointestinal effects are most common with hypersensitivy reactions that have also occur. |
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Term
| How does Vancomycin work? |
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Definition
| inhibits cell wlal synthesis and thereby promotes bacterial lysis and death. it however does not interact with PBPs |
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Term
| T/F Vanco. is a wide spectrum drug. |
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Definition
| False, it is only active acainst gram positive bacteria. Staph aureus and staph epdiermidis. |
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Term
| What is the most serious effect of vanco? |
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Definition
| ototoxicity. Hearing impairment can be reversible but not always. risk is increased by high doses and longterm treatment. Rapid infusion can cause rash, pruritus, urticaria, tachycardia, and hypotension. |
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Term
| How do tetracyclines suppress bacterial growth? |
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Definition
| by binding to the 30s ribosomal subunit and thereby inhibit binding of transfer RNA to the messenger RNA-ribosome complex. PRotein synth is then halted. |
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Term
| What diseases are tetracyclines 1st line for? |
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Definition
| rickettsial diseases chlamydia trachomatis brucellosis cholera pneumonia by mycoplasma pneumoniea lyme disease anthrax and gastric infection with h. pylori. |
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Term
| T/F tetracyclines are used to treat acne? |
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Definition
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Term
| What two tetracylcines are used to treat peridontal disease? Which is used in pill form and which is topical? |
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Definition
| doxycycline is in 20 mg twic daily pills and minocycline is topical. |
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Term
| What should tetracyclines not be administerd with? |
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Definition
| calcium supplements, milk products, iron supplements, magnesium containing laxatives, and most antacids. This is because it is a chelating agent. |
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Term
| How are tetracyclines elimnted? |
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Definition
| Kidneys and liver. All tetracyclines are excreteed by the liver into the bile. After the bile enters the intestine most tetracyclines are reabsorbed. Ultimate elimination of short and intermediate acting tets is in urine. Long acting tets are eliminated by the liver as metabolies. |
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Term
| What are the effects on bones and teeth by teterocyclins? |
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Definition
| Teterocyclins bind to calcium in developing teeth resultin gi n yellow or brown discoloration. Hypoplasia of thee namel may also occur. |
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Term
| What is the minimal inhibitory concentration? |
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Definition
| concentration of antimicrobial that inhibits growth in 18-24 hours. |
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Term
| What is minimal bacterialcidal concentration? |
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Definition
| minimum concentration that kills 99.9% of the cells. |
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Term
| What are bacteriostatic agents best used for? |
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Definition
| uncomplicated host infections that the host body can take care of if just kept in check. NOT FOR NEUTROPENIA in patients. If they have no immune system slowing down the bug will not help. |
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Term
| Tetreacyclines can cause what in the liver and kidneys? |
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Definition
| Fatty infilltration and can exacerbate renal impairment in patients with pre existing kidney disease. |
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Term
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Definition
| broad spectrum antibiotics that inhibit bacterial protein synthesis. They are called macrolides because they are large molecules. |
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Term
| Where does erythromycin bind to? |
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Definition
| 50s subunit on the ribosome to block addition of new amino acids to the growing peptide chain. |
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Term
| What two ways can bacteria become resistant to erythromycin? |
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Definition
1L production of a pump that exports the drug
2: modifications (by methylation) of target ribosomes so that binding of erythromycin is impaired. |
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Term
| What is erythromyacin a possible replacement for? |
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Definition
| Pen. G as it doesn't ignite the typical allergy |
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Term
| What are the first line treatment uses for erthromycin? |
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Definition
| Legionella pneumophillia (legionnaires' disease, bordetella pertussis, whooping cough. Diptheria, urethritis, cervicitis, streptococus pyrogenes and streptococcus pneumoniae. |
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Term
| What are the adverse effects of erythromycin? |
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Definition
| Gastrointestinal effects, Liver injury form the erythromycin estolate version. QT prolongation and sudden cardiac death |
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Term
| What are drug interactions with erythromycin? |
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Definition
| By inhibition of hepatic P450 enzymes elevated levels of all drugs can occur. Theophylline, carbamazepine, and warfarin are of particular importance. Erythromycin should not be combined with drugs that inhibit erythro. metabolism. These are verapamil, diltiazem, HIV protease inhibitors and azole antifungal drugs. |
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Term
| Clindamycin can cause what problems? |
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Definition
| it can promote secere antibiotic associated pseudomembranous colitis. This condition can be fatal. |
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Term
| How does clindamycin work? |
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Definition
| it acts by binding to the 50s subunit of bacterial ribosomes. It is the same site as erythromycin and so they can antagonize each other. |
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Term
| What is clindamycins antimicrobial spectrum? |
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Definition
| It is active against most anerobic bacteria (G+ and G-) and most areobic G+ microbes. |
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Term
| What is AAPMC and what does Clindamycin do to make it worse? |
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Definition
| Antibiotic-associated pseudomemembranous colitis. It is caused by a suprainfecton of the bowel by C. difficile. It is characterized by profuse, watery diarrhea, abdominal pain, fever and leukocytosis. Left untreated it could be fatal. |
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Term
| What is linezolid a first class member of? |
|
Definition
|
|
Term
|
Definition
| it is useful because it has activity against multidrug reistant gram positive pathogens, including vancomycin resistant enterocci and methicillin-resistant staph. aureus (MRSA) |
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|
Term
| What is the mechanism of linezolid? |
|
Definition
| It binds to the 23S portion of the 50S ribosomal subunit. |
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|
Term
| What are aminoglycosides composed of? |
|
Definition
| two ore more amino sugars connected by a glycoside linkage. |
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Term
| What is the mechanism of action for aminoglycosides? |
|
Definition
| They bind to the 30s ribosomal subunit, and thereby cause protein synthesis inhibition, premature terminatino of protein synthesis, and production of abnormal proteins |
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Term
| What are aminoglycosides limited to attacking? |
|
Definition
| aerobic gram negative bacilli. Escherchia colik, Lebsiella pneumoniae, serratia marcescens, proteus mriabilis, and psudomans aeruginosa. |
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|
Term
| How well and what types of administration of aminoglycosides are used? |
|
Definition
|
|
Term
| How are aminiglycosides eliminated? |
|
Definition
| primarily by the kidney, they are not metabolized. |
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|
Term
| What can cause interpatient variation in absorption of aminoglycosides? |
|
Definition
| age,m percent, pahtophysiology. |
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|
Term
| What are adverse effects of aminoglycosides? |
|
Definition
| ototoxicity, nephrotoxicity,neuromuscular blockade and hypersensitivity |
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Term
| Why do aminoglycosides cause ototoxicity? |
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Definition
| They can accumulate within the inner ear causing cellular injury. The risk of ototoxicity is related primariliy to excessive trough levels. |
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Term
| Why is ototoxicity caused by high trough levels of aminoglycosides? |
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Definition
| This is because when trough levels remain persistently elevated, aminoglycosides are unable to diffuse out of inner ear cells and hence the cells are exposed to the drug continuously. |
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Term
| How is nephrotoxicity related to dosage? |
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Definition
| Total cumulative dose of aminoglycosides. it typically results in acute tubular necrosis. |
|
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Term
| t/f penicillins and aminoglycosides are frequently employeed together. |
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Definition
| True, pen. breaks down the cell wall and aminoglycosides kill the cell. |
|
|
Term
| What is the dosing schedule of aminoglycosides? |
|
Definition
| one large dose once a day in modern applications. |
|
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Term
| What are the outstanding features of amikacin? |
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Definition
| it has the broadest spectrum of action against gram-negative bacilli and all of the aminoglycosides, amikacin is the least vulnerable to inactivation by bacterial enzymes. |
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Term
| What are sulfonamides structureal analogs of? |
|
Definition
|
|
Term
| What is the mechanism of sulfonamides? |
|
Definition
| they hnhibit synthesis of folic acid. |
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Term
| What are the therapeutic uses of sulfonamides? |
|
Definition
| urinary tract infections (sulfamethoxazole) |
|
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Term
| What are the adverse effects of sulfonamides? |
|
Definition
| hypersensitivity reactions, blood dyscrasias, kernicterus, and renal damage. |
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Term
| What is the most severe hypersensitivity reaction of sulfonamides? |
|
Definition
| stevens-johnson syndrome, a rare reaction that has a mortality rate of about 25%. Symptoms include widespread lesions of the skin and mucous membranes, together with fever, malaise, and toxemia. |
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Term
| What are the hematologic effects of sulfonamides? |
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Definition
| hemolytic anemia in patients whose red blood cells have a genetically determined deficiency in glucose-6-phosphate dyhydrogenase. Most common in African Americans and people of mediterranean origin. |
|
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Term
|
Definition
| it is a disorder in newborns caused by deposition of bilirubin in the brain. B. is neurotoxic and can cause severe neurologic deficits and even death. |
|
|
Term
|
Definition
| because of low soluability sulfonamides can cause crystalline aggregates that can cause irritation and obstruction sometimes resulting in anuria and even death. |
|
|
Term
| What is sulfamethoxazole combined with? is it an intermediate or short acting sulfonamide? |
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Definition
| Trimethoprim, intermediate. |
|
|
Term
| How does trimethoprim work? |
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Definition
| it inhibits dihydrofolate reductase from working. |
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Term
| What are adverse affects of trimethoprim? |
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Definition
| megaoblastic anemia, thrombocytopenia, and neutropenia can occur in individuals with pre-existing folic acid deficiency. pregnancy useage can cause fetal malformations in animals but no cases observed in humans. |
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Term
| How does the trimethoprim/sulfamethoxazole combination work? |
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Definition
| they work by inhibiting consecutive steps in the synthesis of tetahydrofolic acid. SMZ acts first to inhibit paba incorperation. TMP then inhibits dihydrofolate reductase. |
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Term
| What are the side effects of trimethoprim+sulfamethoxazole? |
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Definition
| Hypersensitivty, stevens-johnson syndrome (with long-acting agents) hematological reactions, incerased serum creatinine concnetration and drug interactions with protein binding displacement and competition for metabolizing enzymes. |
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Term
| What is the clinical manifestation of acute cystitis? |
|
Definition
| dysuria, urinary urgency, urinary frequency, suprapubic discomfort, pyuria, and bacteriuia. |
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