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213 Cards in this Set
- Front
- Back
Characteristics of tumor cells (5)?
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1.derive from our cells (normal)
2. Aberrant (abnormal) 3. Clonal (from 1 cell) 4. Hyperproliferative: no controls 5. Can be metastatic |
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Cancer is ___highest cause of death?
what % of people develop cancer? |
second
30% |
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etiology for cancer?
contributing factors? |
80% unknown.
viruses, environmental, radiation, life style |
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what percentage of tumors has tx been effective on mortality?
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less than 20%
|
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Grade vs stage?
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Grade: histology (biopsy) or blood smear
stage: whole organ level (single mass or metastasis) |
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failure of chemotherapy usually do to ?
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80% due to resistance
|
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types of chemotherapy resistance?
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single agent: resist build to only 1 agent
multidrug resist: to many |
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Combination chemo is based on?
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side effects of drugs (most are myelosuppressive at 28 days so cycle 1 month)
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Why do combination chemo?
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overcome resistance
enhance anti-tumor effect rescue normal cells |
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CR for chemo is? PR?
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Complete response: no disease left
Partial: greater than 50% size reduction |
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what are teh 3 major classes of chemotherapeutic agents?
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1. Alkylating agents
2.Antimetabolites 3 Plant alkaloids |
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Alkylating agents do?
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bind covalenty to dna (stop cell growth)
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alkylating agents derived from?
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chemical war fare agents
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alkylating agents exs?
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Cyclophosphamide
carmustine |
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Antimetabolites do?
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block biosynthesis/use of cellular metabolites
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how do antimetabolites differ from alkylating agents?
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better for slower growing tumors
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exs of antimetabolites ?
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methotrexate and 5-fluorouracil
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Plant alkaloids exs?
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vincas: vinblasting, vinorelbine, vindesine
taxenes |
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how do the vincas work?
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arrest cell division by stoping mitotic spindle
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how do taxenes work?
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stabilize microtubules to inhibit mitotic spindle assembly (stop cell division)
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what are the 3 major toxicities of chemotherapeutic agents?
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1. myelosuppression (bone marrow)
2. dermatologic 3. GI |
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dose limiting is due to
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myelosuppression (b/c makes pts susceptible to infections
|
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Dermatologic toxicity ex is?
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alopecia (hair loss)
2. extravasation necrosis: if administered outside vein, tissue dies 3. oral mucositis |
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how treat oral mucosits?
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saline/bicarbonate rinse
2. mucosal coating 3. lubricating agents topical anesthetics 5. film forming agents |
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types of nausea and vomiting? time/cause?
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acute: within minutes of drug injection
chronic: hours/days anticipatory: smells, colors, places, etc. |
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subdivisions of chemotherapeutic agents are?
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anti cancer and anti infective
|
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disinfectant vs antiseptic?
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dis: remove microbes
anti: skin use |
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Selective toxicity is? is related to?
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harms only invading microbe
mechanism of action |
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drugs that attack cell walls?
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penecillin
cephalosporins vancomycin |
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drugs that attack protein synthesi/
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macrolides
tetracycline clindamycin |
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drugs that destroy cell membrane function?
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fungal membranes: polyene, azole
|
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altered nucleic acid synthesis?
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fluoroquinolones
sulfonamides and trimethoprim (thymidine synthesis) |
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metronidazole does?
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is metabolized by anaerobic bacteria or amebas (metabolite kills organism)
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antibiotic-associated colitis is ex of?
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overgrowth of non-susceptible organisms
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antibacterial spectrum is?
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type of bacteria that a drug is usually effective against
|
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extended spectrum drugs means?
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intermediate between narrow spectrum and broad spectrum
|
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exs of narrow spectrum antibiotics?
Extended? broad? |
pen g and v
amoxicillin and cephalexin tetracyclines, sulfonamides, ciprofloxacin |
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drugs for anaerobic bacteria
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clindamycin and metronidazole
|
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exs of problem bacteria?
what does "problem" mean? |
m. tuberculosis
s. aureus pseudomonas aeruginosa resist normal antibiotics |
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MIC is?
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minimum inhibitory concentration: amount to achieve inhibition
|
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what are the drug types that inhibit cell wall synthesis?
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Pens, cephalosporins, (Beta lactam antibiotics)
|
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what is clavulanic acid?
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a beta lactamase inhibitor given with amoxicillin to increase its effectiveness
|
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Macrolide antibiotics do? first drug of this type was?
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inhibit 50 s ribosome
erythromycin |
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are they broad or narrow spectrum?
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extended spectrum
|
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Most widely used macrolide?
another ex? |
azithromycin
clarithromycin |
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Tetracyclines MOA?
ex? |
inhibit bacterial protein synthesis (30 s)
dyxycycline |
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adverse effects of tetracyclines?
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high concentrations in skin and salive
deposite with Ca in teeth and bones. |
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tetracycline absorption can be prevented by?
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dairy, antacids
|
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MOA of fluoroquinolones?
cidal or static? |
altered nucleic acid metabolism (inhibit DNA gyrase) (bacterialcidal)
|
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Ex of fluoroquinolones?
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ciprofloxacin, levofloxacin (improved against gram+)
|
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MOA of Sulfonamides and trimethoprim?
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inhibit bacterial folic acid synthesis and recycling
|
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why is trimethoprim included?
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adminstered with sulfamethoxazole (effects the same pathway)
|
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Why fungi are important even though not as common?
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b/c candida is 4th most common cause of hospital-acquired bloodstream infections
|
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most common fungal pathogens effecting humans?
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A. fumigatus
C. albicans C. glabrata, parasilosis, tropicalis, krusei, cryptococcus neoformans |
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Fungal drugs discussed? MOA?
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amphotericin B: binds ergosterol (in cell wall)
Azoles: inhibit ergosterol biosynthesis |
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downside to amphotericin B?
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IV, side effects: kidney
|
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ex of azole ?
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fluconazole (oral med)
|
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how do antivirals usually work?
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attack early stages of viral DNA replication with antiviral nucleoside analogs
|
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ex. of antivirals?
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acyclovir: herpes
Zidovudine: reverse transcriptase inhibitors |
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most common antiparasitic drug?
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metronidazole
|
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gut parasites?
intestinal parasite common in USA? |
round/flat worms
pinworm |
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drugs for malaria?
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chloroquine
Mefloquine (for chloroquine resistant strains) some sulfa drugs (folic acid inhibition) |
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what are the types of oral infections?
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1. chronic
2. Chronic-subacute with acute exacerbations 3. Intensely acute |
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ex. of chronic infection?
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periodontisis
|
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ex of chronic-subacute infections?
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percoronitis, periodontal abscess
|
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ex of intensely acute infections?
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necrotizing gingivitis, pa abscess, cellulitis,
|
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how many microbes usually in orofacial infections?
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2-8 (polymicrobial)
|
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why do orofacial pathogens become pathogenic?
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local variables change
|
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orofacial infections have ___ onset?
can usually be treated with? |
rapid (so quick cure too)
incision and drainage (not antibiotics) |
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why not just use antibiotics instead of incision and drainage?
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1. antibiotics do not diffuse well in infected areas
2. inactive antibiotics by pH 3. abscess microbes not alwasy dividing (low metabolic state) 4. high levels of antibiotic inhibitors |
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periodontal abscesses are due to
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breakdown of periodontum within gingival wall of pocket (purulence accumulation)
|
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predominant microflora in periodontal abscess?
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74% anaerobes
67% gram - rods |
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what are the beta lactam antibiotics reserved for hospital aquired infections (serious ones)
|
cabapenems, monobactams
|
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penicillins effect better gram ___?
what % of bacteria from mouth are sensitive to one of the penicillins? |
+.
90% |
|
Pen G is good b/c?
downside? |
most active form
narrow spectrum, not stable in acid (not orally admin), short half life |
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how overcome short half life of Pen g?
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Procain and benzathine pen G are insoluble salts. IM injection
|
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what is Pen V?
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same as G, but stable in acid
|
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Penicillinase-resistant Penicillins aka?
exs? |
anti-staphylococcal penicillins
best is Dicloxacillin for oral cloxacillin, oxacillin, nafcillin, methicillin |
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penicillinase resistant pens are ___spectrum?
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narrow
|
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exs of extended spectrum penicillins?
which is prototype and which is better taken orally? |
ampicillin and amoxicillin
ampicillin |
|
broad spectrum penicillins exs?
|
piperacillin and mezlocillin. not used b/c not orally effective
|
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beta-lactamase inhibitors exs?
|
clavulanic acid
|
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what are the initial drugs of choice in orofacial infections?
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Pen V and amoxicillin
|
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when use parental pen G?
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sever infection
oral route compromised |
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how do pen allergies manifest?
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maculopapular or urticarial skin reactions
|
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which types of allergic reactions are most life threatening?
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immediate: seconds to 1 hour after exposure
|
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what is an accelerated allergic reaction?
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urticaria and angioedema 1-72 hrs post exposure
|
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most common cause of antibiotic induced diarrhea/colitis?
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amoxicillin
|
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NSAIDS and penicillins? and probenecid?
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both increase half life of penicillins by decreasing renal excretion
|
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what is different about cephalosporins?
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more diverse group (2 spots for substitutions)
|
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how are cephalosporins grouped?
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4 generations
|
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first generation cephalosporins are?
exs or oral and parenteral drugs? |
older, extended spectrum antibiotics
oral: cephalexin Parenteral: cefazolin |
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uses of first generation cephalosporins?
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tx staphlococcal and streptococcal infections
surgical and endocarditis prophylaxis |
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how do 2nd generation cephalosporins differ from 1st?
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more stable against beta lactamases (thus increased activity)
|
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major use of 2nd gen cephalosporins?
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tx respiratory infections
|
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third generation cephalosporins are ___ spectrum?
differ by? |
broad
used against gram - (improbed antibacterial effects), resistant to most beta lactamases |
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3rd generation cephalosporins used for?
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serious gram - infections
meningitis, pneumonia, gonorrhea, sepsis |
|
4th generation cephalosporins differ by?
ex? |
more resistant to beta lactamases, more active against gram + bacteria.
cefepime |
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cephalosporins uses in dentistry?
|
against orofacial pathogens but not oral anaerobes
|
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cephalosporins adverse effects?
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cross allergy with penicillins (rare that is serious or has anaphylaxis)
|
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drug interactions of cephalosporins?
|
antacids decrease plama concentration
|
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ex of carbapenems?
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meropenem, ertapenem, imipenem (ME I)
|
|
carbapenems ___ spectrum?
beta lactamases effect by? pregnancy rating? |
wide
not hydrolyzed by most b or c |
|
carbapenems can raise serum levels of ?
can cause? |
liver transaminases
colitis, skin rash |
|
first carbapenem?
|
imipenim/cilastatin
|
|
imipenem is metabolized in?
|
kidney (but found to be toxic to kidney)
|
|
why are meropenem and ertapenem not administered with cilistatin?
|
not nephrotoxic
|
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ex of monobactams?
|
aztreonam
|
|
aztreonam spectrum?
|
narrow (gram -)
|
|
drugs used if oral infection is mix of gram + and -?
|
amoxicillin or ampicillin (if beta lactamase producer, add in clavulanic acid)
|
|
most important glycopeptide antibiotic?
does? |
vancomycin
cell wall inhibition |
|
vancomycin spectrum?
|
narrow, gram +
|
|
uses of vancomycin?
|
for resistant strains
|
|
vancomycin is given?
|
IV (not well absorbed)
|
|
adverse effects of vancomycin are?
|
pain at injection site, histamine release (from high blood levels), nephrotoxicity
ototoxicity, skin rash (red man syndrome) |
|
what drugs bind the 50s subunite?
|
macrolides, lincomycin, clindamycin, chloramphenicol
|
|
exs of macrolides?
aka? |
erythromycin, clarithromycin, azithromycin
large ring antibiotics |
|
are macrolides cidal or static
spectrum? |
static
extended (effective especially for gram +) |
|
absorption of macrolides?
|
via salts derivatives b/c by themselves are not acid stable
|
|
adverse effects of erythromycin?
|
10-20% get GI symptoms
reversible liver injury (occasionally) Deafness torsades de points (long QT interval) arrythmias metabolized in liver, drug interactions (inhibits their metabolism) |
|
how does clarithromycin differ from erythromycin?
|
same spectrum,
longer half life, acid stability, better absorption |
|
Azithromycin differs b/c has ?
how differ? |
additional nitrogen atom in ring
spectrum includes more gram - than erythromycin |
|
azithromycin distribution?
|
more in tissues very quickly so little in blood (so longer half life,68 hrs)
|
|
macrolides in dentistry?
|
against acute orofacial infections (if beta lactam allergy)
not good against gram - endocarditis (clari, azithromycin) |
|
most common mechanism of bacterial resistance for macrolides?
|
erythromycin resistant methylase:
|
|
when take erythromycin?
|
1 hr before
2 hrs after meal |
|
what is done to macrolides to increase absorption?
|
salts, enteric coating
|
|
erythro and clarithro and azithro excreted by?
|
urine
azi: bile |
|
max adult does of macrolides?
if renal impaired? |
4g/day
1.5g/day |
|
macrolide drug interactions?
|
inhibit metabolism of other drugs
can decrease cardiac glycoside metabolism if co administration with oral contraceptive, can increase hepatic cholestasis likelihood |
|
contraindications of macrolides?
|
pts with allergies
pts with history of cholestatic hepatitis pts taking other drugs that together can lead to torsades de pointe |
|
exs of lincosamides?
|
lincomycin and clindamycin
|
|
clindamycin differs from loncomycin by?
|
is chlorinated, giving increased antimicrobial potency and better absorption from GI
|
|
lincosamides spectrum
|
narrow: gram + but good against anaerobes (static)
|
|
lincosamides metabolized in?
excreted in? taken via? |
liver
biles and urine oral |
|
adverse effects of lincosamides?
|
may mild GI
metallic taste sensation |
|
clindamycin is drug most often associated with ?
|
antibiotic associated colitis
|
|
contraindications for lincosamides?
|
do not co administer with neuromuscular blocking drugs
|
|
dental indications for clindamycin?
|
purulent osteitis (bacteroides infections)
if conditions do not respond to other drugs prophylaxis in pts allergic to pen |
|
Tetracyclines effect?
|
30s ribosome subunit
|
|
what do the tetracycline derivatives differ by?
|
duration/rate of excretion/metabolism
|
|
tetracycline derivatives:
short acting medium long acting? |
short: tetracycline
Med: methacycline long: doxycycline |
|
tetracycline spectrum?
static of cidal? |
broad (includes rickettsia)
static? |
|
used for?
|
tx of serious nosocmial infections for highly resitant strains (although there are resistant forms of tetracycline)
maleria |
|
tetracycline distribution?
|
high in skin and saliva, well distributed
can deposite in developing teeth and bones |
|
absorption of tetracycline? % absorbed?
prevented by? |
incompletely absorbed (doxy better)
tetra: 60-80 doxy: 95-100% dairy, antacids |
|
tetracyclines metabolized by? excreted by?
|
met: liver
exc: kidney |
|
Adverse reaction and contraindications to tetracyclines?
|
C. albicans superinfections,
phototoxicity GI difficulties do not take before 8 pregnancy (preg D)/breast feeding |
|
drug interactions for tetracyclines?
|
reduce efficacy of cell wall inhibitors
reduce insulin requirements increase serum blood levels of digoxin increase coumarin effects |
|
tetracyclines used in dentistry for?
|
alternative to pens,
acute necrotizing ulcerative gingivitis, perio disease |
|
aminoglycosides act on?
static or cidal? |
30s subunit (some act on both)
cidal |
|
ex of an aminoglycoside?
|
gentamicin
|
|
Gentamicin is used for?
|
serious infections by gram -s.
|
|
gentamicin spectrum?
|
extended
|
|
absorption of aminoglocosides?
excretion? |
not orally
in urine |
|
adveres effects of aminoglycosides?
|
8th CN toxicity, (hearing and vestibular function of innner ear)
toxic to kidney |
|
chlorampheniol does?
|
inhibits bacterial protein synthesis
first discovered! |
|
absorption of chloramphenicol?
|
complete orally and crosses BBB (use for meningitis)
|
|
why is chloramphenicol not used?
|
anemia, "grey baby syndrome",
not used in orofacial infections |
|
mupirocin is a ?
used for? |
topical antibiotic that inhibits Bacterial RNA/protein synthesis.
impetigo, or nasal cavity to control staph infections |
|
streptogramins are like/do?
|
macrolides (block protein synthesis
|
|
oxazolidinones are?
|
newest
|
|
classes of drugs that inhibit bacterial NA sythesis?
|
Quinolones
Sulfonamides and trimethoprim |
|
Quinolones exs?
|
older ones for UTI: nalidixic acid, cinoxacin
Fluoroquinolones; ciprofloxacin, levofloxacin |
|
what do fluoroquinolones do?
|
inhibit dna gyrase.
|
|
how does levofloxacin differ from ciprofloxacin?
|
improved against gram+
|
|
quinolones spectrum?
|
gen 1: limited
gen 2: broad spectrum gen 3: better when broader spectrum needed gen 4: broad, plus anaerobes |
|
absorption of quinolones?
half-life? excretion? |
good orally
long half-lives (gen 3,4) kidneys |
|
Adverse effects of quinolones?
|
mild. cartilage damage if growing (do not take under 18 yrs)
intereacts with antacids, phototoxicity, arrythmias, |
|
sulfonamides are derived from ?
|
p-aminobenenesulfonamide
|
|
solubility of sulfonamides?
|
low, especially in low pH (they are weak acids)
|
|
how do sulfonamides work
|
inhibit dihydropteroate synthetase (stop folic acid synthesis)
|
|
trimethoprim does?
|
inhibits step in folic acid synthesis
|
|
what does folic acid do?
|
used for synthesis step in nucleotide synthesis
|
|
sulfonamides used to tx?
|
respiratory, urinary and GI infections
(nothing orally) |
|
absorption of sulfonamides?
metabolized by? excreted by? |
penetrate CNS !
liver kidney |
|
side effects of sulfonamides?
|
GI problems:8%
3-5% skin rash |
|
drug interactions of sulfonamides?
|
can increase oral anticoagulants
stuff with PABA (sunscreens, health foods) contraindicated |
|
how does metronidazole work?
|
metabolized by bacteroides to products that damage NA
(also for protozoans) |
|
if someone is at rist for mycobacterial infection, first step is?
|
prophylaxis, preventative
|
|
first line anti-tubicular drugs (less toxic) ex?
|
isoniazid
|
|
Isoniazid is used for?
|
prophylaxis and tx
|
|
isoniazid does?
|
inhigits synthesis of mycolic acids in cell wall, bactericidal (only against active bacteria)
|
|
side effects?
|
older pts: hepatic damage
nervous system toxicity (prevent by b6 vitamin) |
|
second line antitubicular drugs?
aka? |
capreomycin and cycloserine
retreatment agents |
|
downsides to capreomycin and cycloserine?
|
cap: injection
cyclo:1% of pts psychosis (must be monitored for CNS effects) |
|
what is MAC?
what is it? |
mycobacterium avium complex
for pts with AIDS, is clarithromycin, or azithromycind plus rifabutin to treat tb infection by m. avium |
|
what heart conditions warrant prophylaxis for IE?
|
Prosthetic valve, previous IE, congential heart disease (CHD), repaired heart with prosthetic material/devise, repaired CHD with residual defects, transplants with valvulopathy
|
|
malaria is caused by?
most dangerous cause? |
4 species of plasmodia
p. falciparum |
|
how get malaria/ stages?
|
infected bite: sporozoites into blood-->liver-->tissue schizont which then rupture and merozoites enter circulation enter erythrocytes and begin cycle again
|
|
antimalarial drugs active against?
aka? |
erythrocytic forms
schizontocides |
|
what does malaria rely on in humans?
|
proteins form erythrocytes. (this is what the schizontocides probably interfiere with
|
|
how does the accumulation of p. falciparum and p. malariae differ from ovale and vivax?
|
falciparum and malariae leave no residual merozoites in the liver and thus cannot have recurrent episodes later on
|
|
what is the drug of choice to tx liver for malaria?
|
primaquine
|
|
drug to tx malaria in the blood?
|
chloroquine
|
|
chloroquine absorptions?
excreted by? half life? |
good orally. accumulates in liver
kidneys. 7 days |
|
side effects of chloroquine?
|
at prophylaxis levels, none.
dizzy, headache, GI upset/vomit, skin rashes, itching and blurring of vision at high doses, can cause retinopathy *bulls eye), lupus like skin, cardiovascular toxicity |
|
chloroquine effects on body tissues?
|
relaxes smooth muscle, antiarrhythmic, antiinflammatory action
|
|
what is the chloroquine drug that is save during pregnancy?
|
chloroquine phosphate
|
|
Mefloquine is for?
half life? |
strains of P. falciparum ( a single dose can be curative)
14 days (efective levels for up to 30 days) |
|
mefloquine side effects?
|
GI upset, sometimes serious psychiatric effects
|
|
quinine is used for?
absorption? half life? |
erythrocytic forms
orally (half life of less than 5 hours) |
|
quinine as IV?
|
can be, but hazardous due to cardiotoxid effects,
|
|
toxicity with quinine causes?
|
cinchonism: headache, etc
|
|
atovaquone is good as a ?
|
blood schizotocide: inhibits electron transport
|
|
Proquanil does?
|
inhibits plasmodial dihydrofolate reductaase activity
|
|
what is artimesinin for?
|
erythrocitic stages of P. vivax/falciparum
|
|
Halofantrine is for?
|
blood schizontocide (alternative to quinine)
|
|
what are the antimarlarials for exoerythrocytic forms (outside blood)?
(kill liver forms) |
primaquine, pyrimethamine, sulfonamides, tetracyclines
|
|
What is the prototype of the 8-aminoquinoline compouds?
|
primaquine
|
|
Primaquine absorption?
|
rapidly absorbed orally and then rapidly converted to quinone
|
|
primaquine does?
|
interfere with ubiquinone in mitochondria
|
|
downside to primaquine?
|
hemolytic anemia, methemoglobinemia (with persons with glucose 6 p dehydrogenase deficiencies)
|