INF Flashcards
what are the 2 classes of azole antifungals?
- triazoles
- imidazoles
what are the 2 examples of polyene antifungals?
- amphotericin B
- nystatin
how are immunocompromised patients treated with regard to fungal infections?
- at particular risk = antifungal drugs prophylactically
- oral triazole antifungals = 1st line
- micafungin = prophylaxis of candidiasis
what are the side effects of macrolides?
- QT prolongation
- hepatotoxicity
- ototoxicity
what are the side effects for tetracyclines?
- hepatotoxicity
- photosensitivity
- GI distress
what are the side effects for cephalosporins?
- GI distress = gut flora = increase diarrhoea
- cross-sensitivity
- nephrotoxicity
- CNS toxicity
- alcohol = disulfiram-like reaction
what are the side effects of penicillins?
- cross-sensitivity/hypersensitivity
- skin reactions
- CI hepatotoxicity
- GI disturbances
what are the side effects of trimethoprim & sulfonamides?
- risk folate deficiency
- hyperkalaemia
- hypersensitivity
- CI 1st trimester
what are the side effects of quinolones?
- QT prolongation
- GI disturbances
- seizures & tendonitis
what are the side effects of rifampicin?
- GI distress
- hepatotoxicity
- discolouration body fluids
what are the side effects of metronidazole?
- GI disturbances
- discolouration body fluids
- skin reactions
- peripheral neuropathy
- metallic taste
what are the side effects of nitrofurantoin?
- GI disturbances
- discolouration body fluids
- blood disorders
- pulmonary toxicity
what is the mechanism for penicillins/cephalosporins/carbapenems/monobactams & vancomycin?
- bind to & block transpeptidase enzyme by mimicking substrate D-Ala-D-Ala
- inhibit final cross-linking
- block & prevent synthesis new cell wall = bacterial lysis
which ones target 30s ribosomes?
- tetracyclines = prevent t-RNA from binding
- gentamicin
which ones target 50s ribosomes?
- clindamycin
- macrolides
- oxazolidinones
which ones target folic acid metabolism?
- trimethoprim = dihydrofolate reductase
- sulfonamides = sulfamethoxazole = PABA
- sequential blocking = synergic effect
what do quinolones target?
- DNA gyrase = gram -
- DNA topoisomerase = gram +
which ones target RNA polymerase?
- rifampin
- streptovaricins
what is the mechanism for metronidazole & nitrofurantoin?
- generate free radicals
- nitro group reduced on cell entry
- generate unstable reactions O2 species = DNA fragmentation
- bactericidal & active against anaerobes
what are the drugs that target protein synthesis?
- lincosamines = clindamycin
- oxazolidinone = linezolid
what is the Pro-Tide approach?
- added to anti-viral prodrugs
- needed so antiviral drugs can enter the cell
- have phosphate groups that need to be protected
- pro-tide drug broken down after antiviral enter
what are the advantages Pro-Tide approach?
- protect phosphate group of prodrugs
- slow step = phosphorylation not needed if phosphate group = bypassing
- increase passive diffusion
- products of Pro-tide drugs = not toxic
what’s the difference between nucleoside inhibitors & non-nucleoside inhibitors?
nucleoside = aciclovir
- compete natural substrate
- incorporated into the growing nucleic acid chain to terminate polymerase elongation
- must be activated = triphosphate
- phosphorylation thymidine kinase
non-nucleoside
- doesn’t resemble nucleosides
- allosteric binding inhibition
- indirectly inhibit DNA polymerase
- no activation or phosphorylation
what 2 drugs stop viral binding?
- fostemsavir = target virus protein = HIV gp120
- maraviroc = target host cell protein = CCR5 antagonise
what are the advantages & disadvantages host cell/virus targets?
[ virus ] = sofosbuvir = HCV
- selective & reduced toxicity
- risk drug resistance
[ cell host ] = maraviroc = HIV
- reduced drug resistance
- broad spectrum
- less specific
what does enfuvirtide target?
- inhibit fusion virus to host cell membrane
- binds to GP41 protein
what do amantadine & rimantadine target?
- prevent virus uncoating
- block proton influx
which drugs are non-nucleoside & nucleoside?
- acyclovir, sofosbuvir & ribavirin = NI
- nucleoside inhibitors = raltegravir
how do integrase inhibitors like raltegravir work?
- block stand transfer step HIV DNA integration into human chromosomal DNA
- chelating Mg2+ in catalytic site
how do viral protease inhibitors work?
- protease = maturation of proteins
- inhibit protease by binding to viral protease & reversibly block proteolytic cleavage of polyprotein precursor
- atazanavir = -navir HIV only
- glecaprevir = -previr HCV only
what are the 3 tests for antibiotics?
- Disk diffusion test = qualitative = most clear zone
- dilution susceptibility test = lowest antibiotic conc.
- E-test = quantitative = lowest antibiotic conc.
= both e test & dilution = MIC factored & quantitative
what are the types of microbiology testing?
- rapid tests & immunoassays
- molecular testing
- culture
- microscocopy
what are the types of drug resistance?
- alteration drug target site = acquired
- drug inactivation & drug efflux= both
- reduced drug intake into cell = intrinsic
what are the types of acquired drug resistance?
- mutation
- vertical transfer = parent to offspring
- horizontal = bacterium to bacterium/environment
what are the types of horizontal transfer?
- conjugation = direct physical contact = pili
- transduction = transfer by viruses/no direct contact
- transformation = DNA from environment
how do you reduce drug resistance?
- develop new antibiotics & vaccines
- sustain effectiveness existing antibiotics
- use antibiotics when necessary
- educate pts finish course
- improve diagnostics precision & rapid tests
- alternative therapies
- start smart, then focus
what are the responsibilities of devolved authorities?
- organisational control and funding of NHS systems
- family planning
- provision of health services
- prevention, treatment and alleviation of disease, illness, injury, disability and mental disorder
what are the 3 further NHS trusts that provide services on All Wales basis?
- Public Health Wales NHS Trust
- Velindre NHS Trust
- Welsh Ambulance Services NHS Trust
what is the difference between bacteriostatic & bactericidal?
[ bacteriostatic ]
- prevent bacterial growth
- reversible effect
- bacterial clearance depend immune system
[ bactericidal ]
- kill target bacteria
- irreversible effect
- appropriate in poor immunity
what is the mechanism of action for sulfonamides?
- folic acid need to produce DNA
- sulfonamides vs PABA = substrate dihydropteroate synthase
what is the mechanism of action for trimethoprim?
- dihydrofolate reductase (DHFR) = target
- reduce folic acid = active
- selective bacteria
what is the mechanism of action for fluoroquinolones?
- inhibit DNA replication = interfere bacterial topoisomerases
- block bacterial DNA replication & make DNA inaccessible = cell death
- levofloxacin & ciprofloxacin
what is the mechanism for rifamycins?
- inhibit initiation bacterial DNA transcription
- block activity of β-subunit bacterial RNA polymerase
- rifampicin
why is mycobacterium tuberculosis particularly hard to get rid of?
- complex & unique cell wall = thick & hydrophobic
- can survive phagocytosis of macrophages
- can replicate inside & kill it
what is the treatment for newly diagnosed TB?
[ 2 months ]
- Rifampicin = RNA polymerase inhibitor
- Isoniazid = inhibitor mycolic acid synthesis
- Pyrazinamide = interferes fatty acid synthesis
- Ethambutol = interferes synthesis arabinogalactans
- last 3 all in cell wall
[ 4 months ]
- Rifampicin
- Isoniazid
what is the treatment for the re-treatment of TB?
[ 2 months ]
- RIPE & streptomycin
[ 5 months ]
- RIE
what are the HEIW’s contributions to NHS Wales?
- address strategic & specialist workforce issues
- make Wales a great place to train & work for health & care staff
- maximise contribution of professions and occupations through statutory functions
what are the 3 things necessary for an infection to occur?
- a source = surfaces, sinks…
- susceptible person
- transmission
what are the different diseases transmitted and how?
- contact = c. diff & mrsa
- droplet respiratory = covid
- aerosol respiratory = TB
what is a bacteria that causes infection in healthcare settings?
- c. diff = toxin damage colon lining
- gut normal flora disrupted/immunocompromised pts
- risk factors = antibiotic treatment
- mild diarrhoea to colon perforation & death
- infection reoccur & spores survive alcohol gel so wash hands w/ soap & water
what are 3 resistant infections?
- MRSA infections
- glycopeptide resistant enterococci
- carbapenemase-producing organisms
how are patients decolonised for MRSA?
- nasal decolonisation w/ antibiotic or antiseptic nasal cream
- disinfectant skin/hair washes
- for 5 days
what are the 5 reasons for inappropriate antibiotics prescribing?
- time constraints
- decision fatigue
- uncertain diagnoses
- assuming other prescribers = problem
- patient satisfaction & pressure
what are the 5 main mechanisms to fight bacterial infections?
- inhibit metabolism
- inhibit cell wall synthesis
- disrupt protein synthesis
- inhibit nucleic acid transcription/replication
- alter plasma membrane permeability
what are the requirements for the Pro-Tide approach?
- lipophilic
- stable in plasma
- hydrolyses in cells
- byproducts non-toxic
