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96 Cards in this Set

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As far as pharmacokinetics go, how is the systemic route of administration different from Parenteral?
Parenteral?
What are the pharmacokinetic considerations dealing when dealing with antibacterials?
Access of antibiotics to the site of infection, route of administration, Absoption, and Distribution.
What does penetration rely on?
Lipid and water solubility and protein biding. Lipophilic antibiotics (like tetracycline, macrolides) diffuse better than hydrophilics (B-lactams)
How does protein binding affect drug penetration?
If they are tightly bound in the plasma they won’t diffuse through capillary walls.
What are GI absorption, Permeability, Protein binding, Lipophilicity and the effects of dietary factors like for tetracycline?
GI absorption is 77-88%, Permability is low, protein binding is 55-64%, lipophilicity is low and absorption is inhibited by food, Ca, Fe…peanutbutter.
How does doxycycline compare to tetracycline in the above areas?
It is higher in all areas except dietary factors don’t affect absorption as much.
How does liver function relate to drug metabolism?
Some antibiotics are metabolized here and you can have drug toxicity if the pt has liver insufficiency, or in underdeveloped liver of the very young or w/reduced rates in the elderly.
How are most antibiotics excreted?
Via the urine in their active forms, so lower doses are needed to treat a UTI as the drug is very targeted/concentrated in these areas.
What is the therapeutic index?
The ratio of toxic dosage to the effective dosage (LD50/ED50)
What is the therapeutic range?
It falls between the toxic dose and the effective dose
What does the therapeutic index indicate?
The greater the ratio the easier it is to find a dosage that kills the bug but doesn’t harm the host.
What are the adverse effects of antibacterials?
GI disturbances (most common), Allergy (penecillins, sulfonamides, and cephalosporins), superinfections(Candida, antibiotic-associated colitis), and teratogenicity.
What are the 6 targets of antibacterial agents?
Cell wall synthesis, DNA replication, RNA synthesis, Folic Acid Synthesis, Protein synthesis 30s, and Protein synthesis 50s.
How do Penicillin and cephalosporins and vancomycin work?
They inhibibit petidoglycan synthesis by binding and inhibiting transpeptidase, so the bacteria can’t for a cell wall and they die => bactericidal.
What might enhance the effectiveness of Beta Lactams like penicillin or cephalosporin?
The use of beta-lactamase inhibitors like Clavulanic acid, Sulbactam, and Tazobactam.
Which beta lactamase inhibitor is most commonly used?
Clavulanic acid is used with amoxicillin as Augmentin.
What is the primary cause of antibiotic allergies?
Penicillin …note that 10% of patients with penicillin allergies show cross reactivity to cephalosporins.
What are three general types of penicillin?
There are narrow spectrum types like penicillin G and procaine penicillin that target most oral anaerobes, There are broad spectrum types like ampicillin or amoxicillin, and there are penicillinase/ beta-lactamase resistant penicillins like Methicillin.
What are the newer cephalosporin generations working to improve?
Increased spectrum, beta-lactamase resistance, and CNS penetrance
What is ceftriaxone?
The DOC for N. gonorrhea…a third generation cephalosporine.
What are the pharmacokinetics like for penicillin?
They are poorly lipid soluble, and don’t cross the BBB unless inflames as in meningitis, excreted by the kidney in active form so dose should be reduced in renal failure.
What are the pharmacokinetics of cephalosporins like?
Lipophilic, well aborbed w/good distribution, newer agents penetrate the CSF.
How do Vancomycin, Bacitracin, and Cycloserine work?
They interrupt petidoglycan synthesis.
How is Bacitracin taken?
Topical use only.
What is cycloserine?
A TB drug that works by inhibiting peptidoglycan synthesis.
What is Vancomycin like?
It is a hospital drug that is broad spectrum with high toxicity, can cause direct histamine release from mast cells to give Red Man syndrome. (looks like an allergic reaction, but isn’t)
What are the 30s protein synthesis inhibitors?
Aminoglycosides and Tetracyclines
What are some common aminoglycosides and what can they cause?
Streptomycin, Neomycin, gentamycin can cause Ear or Kidney issues.
What are tetracycline and doxycycline?
30s protein synthesis inhibitors that bind reversibly (bacteriostatic) can cause tooth staining and are used for Chlamydia, Rickettsia, and Mycoplasma.
What are the drugs that bind the 50s subunit to inhibit protein synthesis?
Macrolides (Erythromycin, azythromycin) and Chloramphenicol….these all bind reversibly and are bacteriostatic.
What is the first choice for penicillin allergic patients?
Erythromycin
What can Chlorampheicol cause and what is it used for?
It is used for Typhoid and could cause Aplastic Anemia or Gray Baby syndrome.
What are the pharmacokinetics of aminoglycosides?
Poorly lipid soluble, not absorbed orally so they must be injected, excreted in active form by the kidneys and can cause toxic tubular damage.
What are the pharmacokinetics like for tetracyclines?
Bind heavy metal ions, absorption is greatly reduced if taken with food, milk, antacids, or Fe tablets.
What are the pharmacokinetics like for macrolides?
Erythromycin is acid labile and so it is given as an enteric coated tablet.
What is unique about Linezolid?
It binds the 50s and inhibits the binding of 30s subunits, it can be bacteriostatic vs. enterococci and staph or bactericidal vs. strept, can have adverse side effects, used in serious infections (MRSA)
Are Fusidic Acid and Liconsamides (clindamycin) bactericidal or bacteristatic?
They are bacteriostatic
What side effect is clinamycin associated with?
It is broad spectrum and can cause psuedomembranous colitis via a superinfection with C. difficile.
What mechanism do quinolones, Rifampin, and Daptomycin use?
They are nucleic acid inhibitors and are all bactericidal.
What is the number one drug for uncomplicated UTI’s?
Septra
Which drugs are DNA gyrase inhibitors?
Quinolones
What is Rifampin used for?
TB and prophylaxis for N. meningitides
What is Daptomycin like?
It inhibits everything and is used for MRSA and VRSA skin infections and is bacticidal vs. enterococcus faecalis.
What is Metronidazole?
It is a DNA synthesis inhibitor that is bactericidal and is the DOC for ANUG and for Mild antimicrobial-induced enterocolitis.
What is unique about Metronidazole?
It can be used to treat mild antimicrobial-induced enterocolitis, but it can also cause that disorder. It also creates a state of alcohol intolerance and so can be used to help alcoholics quit.
What would you treat a severe case of antimicrobial-induced enterocolitis with?
Vancomycin.
What type of drugs are sulfonamides and trimethoprim?
They inhibit folic acid synthesis.
What is Septra the DOC for?
Pneumocystis jiroveci pneumonia, and most UTI’s (E. coli)
What is the second most common cause of antibiotic allergy?
The sulfonamides….they can also cause blood dyscrasias.
How does dapsone work and what is it used for?
It competes with PABA to inhibit folic acid synthesis and is used to tx leprocy…and brown recluse spider bites.
What are the 1st line drugs you would take if you seroconvert on your TB test?
1st Isoniazid (INH) that inhibits the synthesis of Mycolic acid
What is para-aminosalicylic acid (PAS)?
Works like sulfonamides and are bacteriostatic
What is the anti-leprosy drug?
Moxifloxacine
What are three possible interactions between antibacterials?
Additive, Synergistic, and Antagonistic
What are the indications for combining drugs?
Prevent resistant strains, treat polymicrobial infections, empirical therapy (just throw everything you have at it), and due to proven synergy of combo drugs.
When should we use antibacterials to manage an odontogenic infections?
Acute onset of fever or chills, spreading abscess, diffuse swelling or cellulitis, involvement of fascial spaces, or immunodeficient.
When don’t you need an antibiotic for an odontogenic infection?
In a chronic well localized abscess or in a minor vestibular abscess.
Which drugs would you usually prescribe for odontogenic management?
Penicillin or amoxicillin…if no improvement in 48-72 hours then metronidazole. Give clindamycin if allergic to penicillin….this is different than infections in the rest of the body where erythromycin is the DOC for penicillin allergic patients.
Who should get antibiotics before dental tx?
Prosthetic cardiac valves, Previous infective endocarditis, surgically placed shunts or implanted devices, and cardiac transplants with valve regurgitation.
Who doesn’t need antibiotic coverage for dental tx?
Rheumatic heart disease, mitral valve prolapsed, mitral or aortic valve stenosis, and congenital heart conditions n/c VSD or ASD.
If a patient requires antibiotic coverage what is usually prescribed?
A single dose of 2gm Amoxicillin for adults or 50mg Amoxicillin for kids 30-60 minutes prior to procedure.
As of 2009, what are the AAOS recommendations on antibiotic prophylaxis for those with joint replacements?
We are to administer a cephalosporin or amoxicillin 2 g orally 1 hour prior to procedure and they started a study in 2010 but there is still no change to this recommendation.
What is the difference between cross resistance and multiple resistance?
Cross resistance is via a single mechanism with other closely related drugs (same class), multiple resistance is due to multiple mechanisms by unrelated antibiotics.
What can cause antimicrobial resistance?
Misuse and overuse.
Which type of bacteria are famous for acquired resistance?
S. Aureus.
What are 4 types of antimicrobial resistance?
Natural or intrinsic due to structure: eg. Gram-negative anaerobes w/erythromycin, 2. Mutational: chromosomal changes, 3. Acquired: extrachromosomal via transformation, transduction, like with beta-lactamase., 4. Biofilm bacteria may be 1000X more resistant.
How do organisms develop beta lactamase resistance mechanisms?
They are acquired via transformation, transduction, or conjugation
What are 4 mechanisms of resistance?
1. Blocking entry, 2. Inactivating enzymes, 3. Alteration of target molecules, and 4. Efflux of antibiotic.
What are the two methods for antibiotic susceptibility testing in vitro?
MIC/ minimum inhibitory concentration (the lowest concentration that results in inhibition of visible growth) and MBC/ minimum bactericidal concentration (min concentration that kills 99.9 % of the original inoculums)
What is the Disk Diffusion test?
It Is the current way of testing antibiotic susceptibility via MIC. Different concentrations of antibiotic on disks dropped onto an agar plate and then the radius of inhibited growth is measured….<6mm: resistant, >6mm: susceptible.
What do most antivirals aim to do?
Act on nucleic acid synthesis
What are the 4 mechanisms of nucleic acid synthesis?
Nucleoside analogs, Nucleotide analogs, non-nucleoside analogs and Protease inhibitors.
What is the DOC for HSV 1?
Acyclovir
What is the DOC for HSV-2?
Valacyclovir
What is the DOC for CMV?
Gancyclovir
Why is acyclovir the perfect antiviral?
It is inactive (prodrug) in the body until it encounters the virus and then it becomes active via phosporylation by the herpes thymidine kinase…the viral enzymes have a broader specificity than human kinases so the human kinases don’t recognize acyclovir. Low toxicity.
What drugs do we use for seasonal flu and what do they do?
Zanamivir and Oseltamivir are antivirals for respiratory viruses that block viral release.
What is Ribavirin used for?
It is used for HCV with IFN or for RSV….not proven conclusively to work for RSV…it can be toxic causing hemolytic anemia or teratogens.
How does IFN-alpha work?
It is produced by infected cells to protect other cells by inhibiting protein synthesis, causes flu-like toxicity and depression/psychological issues, it is used to treat hairy cell leukemia, KS, Melanoma, and Hep C. (w/ribavirin)
What can you prevent by using more than one type of drug?
Emergence of resistant forms.
What are the 4 types of anti-retroviral tx?
Reverse Transcriptase inhibitors like NRTIs and NNRTIs, Protease inhibitors, Fusion/entry inhibitors, and Integrase inhibitors
What are two common side effets of NRTIs/ anti-HIV drugs?
Neuropathy and marrow suppression.
What are some side effects of Protease inhibitors?
Glucose Intolerance, Hyperlipidemia, Lipodystrophy, and breast hypertrophy….metabolic affects.
What are 4 characteristics of lipodystrophy?
Fat buildup, fat loss, increase in blood levels of triglycerides/cholesterol, and increase in blood sugar/diabetes.
What are 5 categories of anti-fungal agents?
Polyenes (Nystatin, amp B), Azoles: Ergosterol synthesis inhibitors (Ketoconazole, fluconazole) , Neucleic acid synthesis inhibitors (Flucytosine), Cell wall synthesis inhibitors (Echinocandins), and treatment of dermatophytes(Griseofulvin and naftifine)
How do Polyenes work?
They bind ergosterol and form porescell leakage/death.
What are two common polyenes?
Amphotericin B for sever systemic fungal diseases and Nystatin…given topically.
What are the drawbacks to Amphotericin B?
Nephrotoxic and marrow suppression.
What do Azoles do and what are they used for?
They inhibit ergosterol synthesis and are used for mucocutaneous and systemic infections that aren’t too severe.
What are two groups of azoles?
Imidazoles (Clotrimazole, and ketoconazole) and Triazoles (fluconazole, itraconazole and the new posaconazole)…they are broad spectrum and may help prevent candida and aspergillosis in the immunocompromised.
What is flucytosine?
A nucleic acid synthesis inhibitor that is a nucleotide analog that is converted in fungal cells to inhibit DNA and RNA synthesis…used for Cryptococcosis but causes liver and marrow toxicity.
What does micafungin do to candida and aspergillus?
It is fungicidal vs. candida and fungistatic vs. Aspergillus.. It is used for systematic candidiasis in HIV patient or for fungal infections in neutropenic person or vs. invasive aspergillosis in pts. Who can’t take ampotericin B.
What type of drug is micafungin?
Echinocandin that inhibits cell wall synthesis.
What are dermatophytes treated with?
Griseofulvin, Naftifine, Tolnaftate, and Terbinafine
How does griseofulvin work?
It inhibits mitosis in fungi…not effective vs. candida and ugly side effects.
How do Naftifine, Tolnaftate and Terbinafine work?
Terbinafine is taken orally and the others are topical and they inhibit ergosterol synthesis in nail infections.