Download B250C MODULE 3 EXAM PREP PRACTICE SET 2026 FULL SOLUTION and more Exams Electrical and Electronics Engineering in PDF only on Docsity!
B250C MODULE 3 EXAM PREP PRACTICE SET
2026 FULL SOLUTION
◉ common alkylating agents. Answer: formaldehyde, glutaraldehyde, ethylene oxide, o-phthaldehyde ◉ peroxygens are _______ that can be used as disinfectants or antiseptics. Answer: strong oxidizing agents ◉ how does h2o2 work?. Answer: - produces free radicals that damage cellular macromolecules
- broad spectrum (against gram - and gram +) ◉ how does the disk-diffusion method test effectiveness of chemicals?. Answer: a larger zone of inhibition after placing disks on lawn of bacteria correlates with increased efficacy ◉ how does the phenol coefficient test the effectiveness of chemicals?. Answer: - compares a chemical's antimicrobic properties to those of phenol
- no longer used
- PC of 1 = same efficacy as phenol ◉ how does the use-dilution test determine the effectiveness of chemicals?. Answer: (on inanimate surface) cylinder dipped in bacteria - > dipped in disinfectant solutions - > cylinder transferred to tube with sterile medium bacterial survival indicated by turbidity in medium ◉ how does the in-use test determine the effectiveness of chemicals?. Answer: determines if an actively used solution of disinfectant in a clinical setting is microbially contaminated ◉ how do dilution methods test the effectiveness of chemicals?. Answer: measure minimum inhibitory concentration, contamination of agent, or degradation ◉ Which antimicrobial was found in the remains of ancient Nubians?. Answer: tetracycline, most likely from beer ◉ When was the introduction of modern drugs that caused the "medical revolution?". Answer: the 1930s
◉ what is semisynthetic antimicrobial?. Answer: chemically modified derivative of a natural antibiotic the chemical changes increase the range of target bacteria and stability, and decrease toxicity ◉ What are examples of natural antimicrobials, and where are they commonly found found?. Answer: - actinomycin, streptomycin, neomycin
- bacteria in Actinomycetes (genus Streptomyces) and genus bacillus
- molds in genera Penicillium and Cephalosporium ◉ prophylaxis. Answer: use of a drug to prevent imminent infection of a person at risk ◉ antimicrobial chemotheraphy. Answer: the use of chemotherapeutic drugs to control infection ◉ antibiotics. Answer: substances produced by the natural metabolic processes of some microorganisms that can inhibit or destroy other microorganisms
◉ narrow/limited spectrum antibiotics. Answer: antimicrobials effective against a limited array of microbial types (ex, only targets gram neg) ◉ broad/extended spectrum antibiotics. Answer: - effective against a wide variety of microbial types (ex, targets both gram negative and gram positive)
- important for acute life-threatening disease
- kill polymicrobial infections ◉ would a person who is immunocompromised need a bacteriostatic or bactericidal drug?. Answer: bactericidal ◉ when is it best to use a narrow-spectrum antibiotic?. Answer: when a pathogen causing an infection has been identified, that way collateral damage to normal microbiota is minimized ◉ when are broad-spectrum antibiotics most often used?. Answer: polymicrobic infections (multiple bacterial species) or prophylactic prevention of infections from surgery, or when narrow-spectrum drug encounters resistance
◉ why are most antimicrobial drugs currently in use antibacterial?. Answer: the prokaryotic cell provides greater variety of unique targets for selective toxicity ◉ Kirby-Bauer Test. Answer: - determine drug susceptibility and/or antibiotic resistance
- agar diffusion test
- cannot tell bacteriostatic v. bactericidal
- small discs with antibiotic placed on plate
- zone of inhibition surrounding discs measured and compared to standards for susceptibility or resistance ◉ E-test. Answer: - determine drug susceptibility
- combo of Kirby-Bauer and dilution
- uses gradient of dilution on plastic strips placed on agar
- determines the minimal inhibitory concentration (MIC - lowest antibiotic concentration preventing bacterial growth) ◉ tube dilution tests. Answer: - determine drug susceptibility, MBC, and MIC
- more sensitive and quantitative than Kirby-Bauer
- antimicrobial diluted serially in tubes of broth
- each tube inoculated with small uniform sample of pure culture (broth with no visible growth) ◉ Minimum inhibitory concentration (MIC). Answer: - smallest concentration (highest dilution) of drug that visibly inhibits growth
- useful for determining effective dosage and providing index against other microbials ◉ what are some causes of failure of an antimicrobial treatment?. Answer: - inability of drug to diffuse into body compartment
- resistant microbes in infection that were not in sample collected for testing
- side chains modified to make derivatives (increased activity, longer half-life, better dosing)
- penicillin, cephalosporins, monobactams, carbapenems ◉ how are cephalosporins different than penicillins?. Answer: they are more resistant to enzymatic inactivation by B-lactamases than other B-lactams also have an additional R group ◉ How do glycopeptides work?. Answer: - inhibit cell wall synthesis
- bind to NAM AA side chain to block peptidoglycan synthesis
- usually IV administered
- treat gram + and C. difficile
- last resort drug, resistance is an issue
- vancomycin
◉ How does bacitracin work?. Answer: - inhibits cell wall synthesis
- interferes with peptidoglycan precursor transport across cytoplasmic membrane
- common in first aid ointments
- topical application because toxic to kidneys ◉ inhibitors of protein synthesis. Answer: - exploit prokaryotic and eukaryotic differences
- some bind to 30S subunit, others bind to 50S subunit ◉ how do aminoglycosides work?. Answer: - bind to 30S subunit to impair proofreading
- produce faulty proteins (bactericidal)
- toxic to kidneys, NS, and ears
- daptomycin inserts into cytoplasmic membrane of Gram + organisms
- does not work against Gram - ◉ how do polymyxins work?. Answer: - inhibits membrane function
- interacts with LPS in outer membrane of Gram - cells
- binds to eukaryotic cells (limits usefulness to topical applications)
- used intravenously because of multi-drug resistant bacteria (last resort)
- colistin ◉ How do fluoroquinolones work?. Answer: - inhibit bacterial DNA synthesis
- inhibit topoisomerases (DNA gyrase)
- broad-spectrum activity
- possible systemic and skin infections as side effects ◉ How do rifamycins work?. Answer: - block prokaryotic RNA pol
- prevents initiation of transcription
- selective toxicity
- bactericidal against Gram + and some Gram - (M. tuberculosis) ◉ how does metronidazole work?. Answer: - binds to DNA and interferes with synthesis
- causes DNA breaks
- only functions in reduced env'ts
- toxic only in anaerobic organisms
- they hijack host cellular machinery - not possible to target ◉ how do antiviral drugs work?. Answer: - inhibit viral replication by acting as nucleoside analogs, non-nucleoside pol inhibitors, or non-nucleoside RT inhibitors
- inhibit viral entry
- inhibit integrase
- inhibit assembly and release of viral particles ◉ Drug modification or inactivation. Answer: - mechanism of drug resistance
- chemical modification/inactivation/death of antimicrobial
- resistance to B-lactams, aminoglycosides, macrolides, rifamycins ◉ prevention of cellular uptake or efflux. Answer: - mechanism of drug resistance
- inhibit accumulation of antimicrobial
- prevents drug from reaching target
- common in Gram - pathogens
- resistance to fluoroquinolones, aminoglycosides, tetracyclines, B- lactams, macrolides ◉ target modification. Answer: - mechanism of drug resistance
- structural changes to targets (RNA and ribosomal subunits) prevents drug binding, making it ineffective (ex: binding site of PBP)
- common in S. pneumoniae and S. aureus
- resistance to fluoroquinolones, rifamycins, vancomycin, B-lactams, macrolides, aminoglycosides ◉ multidrug-resistance microbes (MDRs). Answer: - carry one or more resistance mechanisms to make them resistant to multiple antimicrobials
◉ how does spontaneous mutation cause drug resistance?. Answer:
- nucleotide changes alter promoter activity and amino acid composition
- may cause slight changes in drug sensitivity that can be overcome with larger doses ◉ how does horizontal gene transfer cause drug resistance?. Answer: - conjugation, transformation, transduction
- effected genes could encode antibiotic resistance proteins (efflux pumps, enzymes, etc) ◉ superinfection examples. Answer: - lactobacilli in the female vagina are killed by broad-spectrum cephalosporin used to treat UTI, overgrowth of Candida albicans occurs, causing a vaginal yeast infection or oral thrush
- oral therapy with tetracyclines, clindamycin, and broad-spectrum penicillins kills of normal biota of the colon; overgrowth of Clostridium difficile invades the intestinal lining and releases toxins that cause diarrhea, fever, and abdominal pain ◉ Colonization vs. Infection. Answer: colonization - microbe establishing itself on body surface
infection - successful colonization of host by microorganism ◉ nosocomial disease. Answer: acquired in hospital settings ◉ iatrogenic disease. Answer: condition caused by medical procedure ◉ 5 phases of disease. Answer: 1. incubation period
- prodromal period
- period of illness
- period of decline
- period of convalescence ◉ incubation period. Answer: - pathogen enters hose and begins multiplying at portal of entry
- not enough damage to cause symptoms
- varies according to host resistance and degree of virulence
