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