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ME Pharm test 7
| Question | Answer |
|---|---|
| aerobic | organism lives only in presence of oxygen |
| anaerobic | organism that can live in absence of oxygen |
| antibacterial | drug used to kill/suppress growth of bacteria |
| antibiotic | used to treat bacteria, viruses, fungus |
| antibiotic drug resistance | acquired through genetic mutation or acquisition of genetic material from other organisms |
| autogenous infection | caused by normal flora bacteria |
| bactericidal | kills bacteria |
| bacteriostatic | suppresses growth of bacteria |
| facultative | organisms able to live in presence or absence of oxygen |
| loading dose | initial dose of drug (large) used to achieve therapeutic levels quickly |
| suprainfection | opportunistic infection caused by overgrowth of microorganisms that aren't susceptible to antibacterial therapy |
| IE | infective endocarditis |
| TJR | total joint replacement |
| commensal agents | agents that live in an environment without causing harm |
| mycotic infection | caused by fungi or molds |
| neonate | infant younger than 1 month |
| parasitism | evolution from commensal status to causing disease |
| saprophytic | ability to live on decaying organic matter |
| subacute | disease development without overt clinical signs and symptoms |
| HIV | human immunodeficiency virus |
| HIVD | human immunodeficiency viral disease |
| HSV | herpes simplex virus |
| antibacterial agent | destructive to or prevents growth of bacteria |
| antibacterial agents are used to | treat infection (usually odontogenic) and antibiotic prophylaxis (to prevent bacteremia) |
| adult body harbors an indigenous flora that includes | bacteria, viruses, fungi, protozoa |
| infection | invasion and multiplication of microorganisms in body tissues, resulting in local cellular injury |
| cross-infection | obtained from other humans, animals, environment |
| the strategy in treating bacterial infections is to | target differences between bacterial (prokaryotic) and host/body (eukaryotic) cells |
| drugs have the least toxicity to host when | have more unique pathways |
| drugs have more toxicity to host when | target shared pathways |
| when you have to use a drug that may injure host cells, you take _________ into account | therapeutic index |
| in TI, a higher number means the drug is | safer |
| what is essential for resolution of an infection | debridement and host immune response |
| debridement removes | infection debris |
| for a compromised immune response you would use what kind of drug | bactericidal |
| when a broad spectrum antibacterial is used it can | kill/inhibit harmless bacteria in normal flora |
| use of a broad spectrum antibacterial can result in | suprainfection |
| oral infections are caused by | gram+ facultative cocci gram- bacilla (strict anaerobes) |
| by the time a antibacterial is indicated (fever, lymphadenopathy) what bacteria dominates | anaerobic gram- bacilli |
| spectrum | relative range of drug's antibacterial action |
| narrow spectrum | effective in limited bacterial species |
| extended | effective on greater number of microorganisms |
| broad | can kill/suppress growth of wide variety (most) |
| narrow, extended, and broad spectrum antibacterials are effective on | gram+, gram-, aerobic, facultative, anaerobic organisms |
| most odontogenic infections are | polymicrobial (mixed) |
| most common organism responsible for odontogenic infections include | viridians streptococci |
| what organisms predominate in odontogenic infections | facultative gram+ cocci anaerobic gram+ cocci gram-bacilli |
| what effects plasma concentration | absorption, distribution, elimination of agents |
| what happens to bacteria in a more acidic enviornment | number of species declines, is an increase in number of ones left |
| as an infection matures it becomes | acute or chronic |
| acute infection | spreads |
| chronic infection | localized |
| what infections can become "walled-off" by fibrous connective tissue | low-grade chronic infections |
| to make it easier for antibacterials to reach a "walled-off" infection, you must | remove infected fibrous tissue through debridement |
| debridement often... | eliminates the need for antibacterial agents |
| antibacterial can't destroy all bacteria, they | enhance the immune response |
| host defense mechanism can be adversely affected by | some diseases and medications |
| in a suppressed immune system, use | bactericidal drugs |
| antibacterials work in what ways | 1. interrupt bacterial wall synthesis (cidal) 2. interrupt bacterial DNA replication/repair (cidal) 3. interrupt protein (RNA) synthesis (static) |
| Antibacterials that inhibit cell wall synthesis: | penicillins cephalosporins bacitracin vancomycin |
| antibacterials that inhibit protein synthesis | macrolides clindamycin tetracyclines (doxycycline, minocycline) neomycin |
| antibacterials that inhibit DNA synthesis | metronidazole fluoroquinolones |
| what kind ofdrug do you use with an immunocompromised patient | bactericidal |
| combining a static and cidal can result in | antagonistic effects |
| which kind of drug works best in rapid cell growth | bactericidal |
| if given and cidal and a static it will | slow growth of cell and impede cidal drug effects |
| pencillins (narrow spectrum - pen VK) are beta-lactamase | susceptible |
| penicillinase-resistant penicillins (dicloxacillin) are beta-lactamase | resistent |
| broader-spectrum penecillins (ampicillin, amoxicillin, amoxicillin with clavulanic acid) are beta-lactamase | susceptible - with clavulanic adic, mostly resistant |
| cephalosporins first generation are beta-lactamase | susceptible |
| cephalosporins second generation are beta-lactamase | resistant(some) |
| cephalosporins third generation are beta-lactamase | resistant (Greater) |
| beta-lactam antibiotics interfere with... | cell wall synthesis (repair of cell) |
| most common penicillin used it | pen VK |
| pencillin is a prototype drug of | beta-lactamase |
| penicillinase | enzyme that degrades penicillin molecule, eliminated therapeutic effect |
| dicloxacillin is | prototype penicillinase-resistant agent |
| clavulanic acid | added to some penicillins (ex. amoxicillin) to make penicillin combo penicillinase-resistant |
| Cephalosporins cause an allergic reaction to | 10% of people with penicillin allergies |
| oral dose forms of cephalosporin are resistant to | penicillinase |
| oral dose forms of cephalosporin are destroyed by | cephalosporinase |
| antibiotic drug resistance can be | genetic or nongenetic, natural or intrinsic, arise from chromosomal mutations |
| vertical transmission - | (daughter cells) of genes that effect altered drug: targets, transport, metabolic pathways |
| horizontal transmission | gaining genetic material from other bacteria |
| #1 reason for development of antibiotic resistance is | indiscriminate use |
| indiscriminate use causes | mutation of chromosomes of bacteria |
| indiscriminate use is ______________ transmission | vertical |
| genetic drug resistance | organisms with natural or intrinsic resistance |
| acquired drug resistance | acquire resistance by gaining genetic material from other bacteria |
| acquired drug resistance is ___________ transmission | horizontal |
| what is the main mode of drug resistance? | acquired drug resistance |
| biolfilm-related drug resistance | bacteria that are stacked and encased in hydrated mix of polysaccharides and protein, form towerlike structures |
| once in a biofilm, bacteria are protected from | antibodies and leukocyte phagocytosis |
| pharmokinetic condiserations refer to | issues related to absorption, distribution, bioavailability, metabolism, elimination of drugs |
| access of antibiotics to site of infection depends on: | 1. route of administration 2. degree of plasma protein-binding in circulation 3. concentration of free drug in plasma/extracellular fluid 4. passive diffusion into area of infection |
| periodontal infections are... | polymicrobial |
| what organisms predominate in a periodontal infection | gram- and anaerobic |
| odontogenic infections are usually... | autogenous |
| odontogenic infections primarily affect | teeth (caries), pulpal, periodontal, pericoronal tissues |
| formation of purulent exudate can... | block antibacterials from reaching infection |
| antibiotics are indicated when patient presents with | malaise, chills (fever), trismus, lymphadenopathy, swelling or if they are compromised |
| DOC for uncomplicated odontogenic infection is | pen VK |
| if no improvement in infection after 2-3 days | empirical addition of metronidazole (7 days) while continuing penicillin |
| empirical | affects most bugs so is prescribed |
| many gram- anaerobes have natural/intrinsic resistance to | erythromycin |
| if resistant to erythromycin, will also be resistant to | clindamycin |
| clindamycin is associated with | pseudomembranous collitis |
| pseudomembranous collitis | caused by C.difficle liberating toxins that desquamate epithelial lining of intestines, causing bloody diarrhea and systemic infection |
| Treatment of odontogenic infection: primary line | pen VK, 500mg |
| Treatment of odontogenic infection: secondary | metronidazole or azithromycin 250mg |
| Treatment of odontogenic infection: tertiary | clindamycin 300mg |
| antibacterial agent should be taken ______ before treatment | 30 minutes to 1 hour |
| premed: if patient forgets to take premed, can be taken | up to 2 hours after |
| premed: if patient is already on an antibiotic, give | drug from different class, unless it has been 10 days (then can use same) |
| premed: if patient is taking anticoagulants | don't give IM or IV, only oral meds |
| premed: coronary artery bypass grafts/stents | after initial 3 months of healing, don't need premed |
| premed: removal of spleen | may need to premed if done in last 2 years or is a child |
| premed: uncontrolled diabetes | refer for med consult, don't treat |
| premed: end-stage renal disease | premed patients with underlying cardiac risk (check with doc about cleaning before or after dialysis) |
| premed: HIV | considered if <500PMN/mm3 (delay elective treatment) |
| premed: organ transplant | check with doctor |
| premed: hydrocephalus shunt | yes if drains into heart |
| metronidazole interacts with ___________ and produces what adverse effect | alcohol, antabuse effect: nausea, vomiting, abdominal cramps |
| oral antibacterial agents, especially ______________ often cause nausea, vomiting, retching, diarrhea | macrolides |
| metronidazole causes | reddish color in urine |
| tetracycline causes | intrinsic tooth staining (if taking during pregnancy or under 9 years old) |
| minocycline causes | black pigmentation in mucosa and bone |
| superinfections with _________________ commonly occur in association with antibacterial chemotherapy | c. albicans |
| in immunocompromised patients, oral candidiasis may | spread systemically via bloodstream |
| oral candidiasis is treated with | antifungals |
| most allergenic drug is | penicillin |
| are ___________ fungal species | 100,000 |
| ______ fungal species are pathogenic to humans | a few |
| commensals | obtain benefit without causing harm |
| commensals are found on | oral, vaginal, GI mucosa, harmless residents of skin, respiratory epithelium |
| paratism/superfection | overgrowth of numbers of commensal organisms, disease develops |
| mycotic infections are associated with | opportunistic infection due to impaired immune system |
| mycotic infections usually affect people with compromised immune system, such as | hiv, use of immunosuppression drugs, treatment of malignant disease (oncology treatment) |
| mycotic infections present as | superficial, cutaneous (skin, mucosa), subcutaneous, systemic |
| most common fungal infections | candida albicans (candidiasis, thrush) and tinea |
| amphotericin B and nystatin are | ergosterol binding |
| amphotericin B treats | systemic fungal infections, fungal meningitis, fungal UTIs |
| nystatin treats | oral and intestinal candidiasis, thrush |
| fluconazole treats | systemic histoplasmosis, opportunistic candidiasis |
| antifungal agents work by | inhibiting ergosterol synthesis, disrupting plasma membrane by binding to ergosterol |
| ergosterol is synthesized within | fungal cells |
| ergosterol is necessary for | cellular activity |
| ergosterol blocks | cytochrome P450 (CYP450)enzyme |
| major adverse effect of all systemic azole antifungals? | hepatotoxicity |
| nystatin is an antifungal that | binds to ergosterol in fungal plasma membrane |
| nystatin increases | membrane permeability, resulting in leakage of cellular components, leading to cell death |
| nystatin use is limited to treatment of | superficial candidial infections of skin, oral, vaginal mucosa with topicals |
| nystatin must stay in contact with skin for | 5-7 minutes |
| the most common fungal infection is by | candida species |
| oral candidial infections: presence of blastosphores without hyphae is | commonsal |
| oral candidial infections: presence of blastosphores with hyphae is | opportunistic infection |
| C. albicans is an | opportunistic organism |
| Oral candidiasis is a __________ infection with potential for_______________ | localized, systemic dissemation |
| pseudomembranous candidiasis is a | white psuedomembrane, can be wiped away, leaves painful, red, sometimes bleeding area |
| pseudomembranous candidiasis can be | acute or chronic |
| pseudomembranous candidiasis is observed in | neonates (thrush) and immunosuppressed patients |
| Erythematous Candidiasis is a | red patch, usually on palate or dorsum of tongue |
| Erythematous Candidiasis symptoms | loss of filiform papilla, burning sensation |
| Erythematous Candidiasis can be | acute or chronic |
| hyperplastic candidiasis is also known as | candida leukoplakia |
| hyperplastic candidiasis is a | persistent (chronic)white plaque |
| hyperplastic candidiasis is _______ common | least |
| denture stomatitis is | erythematous area beneath denture, can get into acrylic of denture |
| when treating denture stomatitis | treat person and denture with nystatin |
| median rhomboid glossitis is | erythematous patch with loss of filiform papilla on dorsum of tongue |
| angular chelitis is | erythematous fissures at commissures of lips |
| angular chelitis is an infection of | c. albicans and staphylococcus aureus |
| angular chelitis is caused by | poor OH, decrease in intermaxillary space, nutritional deficiencies |
| diagnosis of oral candidiasis is based on | clinical signs and symptoms |
| additional test to diagnose oral candidiasis are | exfoliative cytology, culture, biopsy |
| exfoliative cytology | scraping suspected lesion with sterile instrument/tongue blade, smearing on glass slide |
| primary line of antifungal therapy includes | topicals: nystatin, clotrimazole |
| nystatin in DOC for treatment of | oral candidiasis |
| nystatin comes in what forms | pastilles or rinses |
| treatment with nystatin should continue for how long after elimination of signs/symptoms? | at least 48 hours |
| is nystatin absorbed in GI tract? | no |
| what form of nystatin doesn't contain sucrose? | vaginal tablets |
| when would you use nystatin vaginal tablets as oral lozenges? | with caries-prone patients |
| does nystatin have side effects? | no |
| clotrimazole is not recommended for treatment of candidiasis in | pregnant, children under 3 |
| secondary line of antifungal therapy includes | systemic, fluconazole |
| adverse effect of systemic azoles and warfarin is? | may increase blood levels of warfarin, increasing risk of bleeding |
| antiviral agents are likely to be toxic to | host cells as well as virus |
| most common viral infection? | HSV-1 |
| transmission of HSV-1&2 occurs via | direct contact with contaminated secretion of infected person |
| HSV-1 in transmitted by | contact with oral secretions, vesicular fluid |
| HSV-2 transmitted | sexually, can be translocated to oral cavity |
| to differentiate between HSV-1&2 you need an | antigen-specific test |
| primary infections of HSV-1 occur primarily in | children between 2-3 |
| prodromal stage | tingling felt before lesion erupts |
| primary line of HSV-1 antifungals include | topicals: penciclovir (Rx), docosanol (OTC) |
| in cases of complicated primary herpetic gingivostomatitis and immunocompromised patients ____________ should be added to primary line of treatment | systemic antivirals, such as acyclovir |
| topical antifungals are most effective if applied | during prodromal stage |
| penciclovir | reduces duration, pain. speeds healing |
| docosanol | shortens healing time, reduces symptoms and pain |
| docosanol is not indicated for | intraoral use |
| infection begins when | a virion attaches to a host cell |
| most common hepatitis infections are | B and C |
| hepatitis infection results in | reduced liver function |
| reduced liver function results in | increased bleeding due to reduction of vitamin K clotting factors |
| manifestation of hepatitis? | jaundice |
| enfuvirtide inhibits | viral entry into host cells |
| HIV is a ______ | retrovirus |
| what is essential for HIV replication? | reverse transcriptase |
| HIV is treated with a | multi-drug regime |
| hepatitis: delay elective procedure if _______ | <50,000 platelets mm3 |
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mnerion
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