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Pharmacy 201 > INF > Flashcards

INF Flashcards

1
Q

what are the 2 classes of azole antifungals?

A
  • triazoles
  • imidazoles
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2
Q

what are the 2 examples of polyene antifungals?

A
  • amphotericin B
  • nystatin
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3
Q

how are immunocompromised patients treated with regard to fungal infections?

A
  • at particular risk = antifungal drugs prophylactically
  • oral triazole antifungals = 1st line
  • micafungin = prophylaxis of candidiasis
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4
Q

what are the side effects of macrolides?

A
  • QT prolongation
  • hepatotoxicity
  • ototoxicity
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5
Q

what are the side effects for tetracyclines?

A
  • hepatotoxicity
  • photosensitivity
  • GI distress
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6
Q

what are the side effects for cephalosporins?

A
  • GI distress = gut flora = increase diarrhoea
  • cross-sensitivity
  • nephrotoxicity
  • CNS toxicity
  • alcohol = disulfiram-like reaction
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7
Q

what are the side effects of penicillins?

A
  • cross-sensitivity/hypersensitivity
  • skin reactions
  • CI hepatotoxicity
  • GI disturbances
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8
Q

what are the side effects of trimethoprim & sulfonamides?

A
  • risk folate deficiency
  • hyperkalaemia
  • hypersensitivity
  • CI 1st trimester
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9
Q

what are the side effects of quinolones?

A
  • QT prolongation
  • GI disturbances
  • seizures & tendonitis
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10
Q

what are the side effects of rifampicin?

A
  • GI distress
  • hepatotoxicity
  • discolouration body fluids
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11
Q

what are the side effects of metronidazole?

A
  • GI disturbances
  • discolouration body fluids
  • skin reactions
  • peripheral neuropathy
  • metallic taste
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12
Q

what are the side effects of nitrofurantoin?

A
  • GI disturbances
  • discolouration body fluids
  • blood disorders
  • pulmonary toxicity
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13
Q

what is the mechanism for penicillins/cephalosporins/carbapenems/monobactams & vancomycin?

A
  • bind to & block transpeptidase enzyme by mimicking substrate D-Ala-D-Ala
  • inhibit final cross-linking
  • block & prevent synthesis new cell wall = bacterial lysis
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14
Q

which ones target 30s ribosomes?

A
  • tetracyclines = prevent t-RNA from binding
  • gentamicin
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15
Q

which ones target 50s ribosomes?

A
  • clindamycin
  • macrolides
  • oxazolidinones
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16
Q

which ones target folic acid metabolism?

A
  • trimethoprim = dihydrofolate reductase
  • sulfonamides = sulfamethoxazole = PABA
  • sequential blocking = synergic effect
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17
Q

what do quinolones target?

A
  • DNA gyrase = gram -
  • DNA topoisomerase = gram +
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18
Q

which ones target RNA polymerase?

A
  • rifampin
  • streptovaricins
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19
Q

what is the mechanism for metronidazole & nitrofurantoin?

A
  • generate free radicals
  • nitro group reduced on cell entry
  • generate unstable reactions O2 species = DNA fragmentation
  • bactericidal & active against anaerobes
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20
Q

what are the drugs that target protein synthesis?

A
  • lincosamines = clindamycin
  • oxazolidinone = linezolid
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21
Q

what is the Pro-Tide approach?

A
  • 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
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22
Q

what are the advantages Pro-Tide approach?

A
  • protect phosphate group of prodrugs
  • slow step = phosphorylation not needed if phosphate group = bypassing
  • increase passive diffusion
  • products of Pro-tide drugs = not toxic
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23
Q

what’s the difference between nucleoside inhibitors & non-nucleoside inhibitors?

A

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

24
Q

what 2 drugs stop viral binding?

A
  • fostemsavir = target virus protein = HIV gp120
  • maraviroc = target host cell protein = CCR5 antagonise
25
Q

what are the advantages & disadvantages host cell/virus targets?

A

[ virus ] = sofosbuvir = HCV
- selective & reduced toxicity
- risk drug resistance

[ cell host ] = maraviroc = HIV
- reduced drug resistance
- broad spectrum
- less specific

25
Q

what does enfuvirtide target?

A
  • inhibit fusion virus to host cell membrane
  • binds to GP41 protein
26
Q

what do amantadine & rimantadine target?

A
  • prevent virus uncoating
  • block proton influx
27
Q

which drugs are non-nucleoside & nucleoside?

A
  • acyclovir, sofosbuvir & ribavirin = NI
  • nucleoside inhibitors = raltegravir
28
Q

how do integrase inhibitors like raltegravir work?

A
  • block stand transfer step HIV DNA integration into human chromosomal DNA
  • chelating Mg2+ in catalytic site
29
Q

how do viral protease inhibitors work?

A
  • 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
30
Q

what are the 3 tests for antibiotics?

A
  • 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
31
Q

what are the types of microbiology testing?

A
  • rapid tests & immunoassays
  • molecular testing
  • culture
  • microscocopy
32
Q

what are the types of drug resistance?

A
  • alteration drug target site = acquired
  • drug inactivation & drug efflux= both
  • reduced drug intake into cell = intrinsic
33
Q

what are the types of acquired drug resistance?

A
  • mutation
  • vertical transfer = parent to offspring
  • horizontal = bacterium to bacterium/environment
34
Q

what are the types of horizontal transfer?

A
  • conjugation = direct physical contact = pili
  • transduction = transfer by viruses/no direct contact
  • transformation = DNA from environment
35
Q

how do you reduce drug resistance?

A
  • 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
36
Q

what are the responsibilities of devolved authorities?

A
  • 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
37
Q

what are the 3 further NHS trusts that provide services on All Wales basis?

A
  • Public Health Wales NHS Trust
  • Velindre NHS Trust
  • Welsh Ambulance Services NHS Trust
38
Q

what is the difference between bacteriostatic & bactericidal?

A

[ bacteriostatic ]
- prevent bacterial growth
- reversible effect
- bacterial clearance depend immune system

[ bactericidal ]
- kill target bacteria
- irreversible effect
- appropriate in poor immunity

39
Q

what is the mechanism of action for sulfonamides?

A
  • folic acid need to produce DNA
  • sulfonamides vs PABA = substrate dihydropteroate synthase
40
Q

what is the mechanism of action for trimethoprim?

A
  • dihydrofolate reductase (DHFR) = target
  • reduce folic acid = active
  • selective bacteria
41
Q

what is the mechanism of action for fluoroquinolones?

A
  • inhibit DNA replication = interfere bacterial topoisomerases
  • block bacterial DNA replication & make DNA inaccessible = cell death
  • levofloxacin & ciprofloxacin
42
Q

what is the mechanism for rifamycins?

A
  • inhibit initiation bacterial DNA transcription
  • block activity of β-subunit bacterial RNA polymerase
  • rifampicin
43
Q

why is mycobacterium tuberculosis particularly hard to get rid of?

A
  • complex & unique cell wall = thick & hydrophobic
  • can survive phagocytosis of macrophages
  • can replicate inside & kill it
44
Q

what is the treatment for newly diagnosed TB?

A

[ 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

45
Q

what is the treatment for the re-treatment of TB?

A

[ 2 months ]
- RIPE & streptomycin

[ 5 months ]
- RIE

46
Q

what are the HEIW’s contributions to NHS Wales?

A
  • 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
47
Q

what are the 3 things necessary for an infection to occur?

A
  • a source = surfaces, sinks…
  • susceptible person
  • transmission
48
Q

what are the different diseases transmitted and how?

A
  • contact = c. diff & mrsa
  • droplet respiratory = covid
  • aerosol respiratory = TB
49
Q

what is a bacteria that causes infection in healthcare settings?

A
  • 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
50
Q

what are 3 resistant infections?

A
  • MRSA infections
  • glycopeptide resistant enterococci
  • carbapenemase-producing organisms
51
Q

how are patients decolonised for MRSA?

A
  • nasal decolonisation w/ antibiotic or antiseptic nasal cream
  • disinfectant skin/hair washes
  • for 5 days
52
Q

what are the 5 reasons for inappropriate antibiotics prescribing?

A
  • time constraints
  • decision fatigue
  • uncertain diagnoses
  • assuming other prescribers = problem
  • patient satisfaction & pressure
53
Q

what are the 5 main mechanisms to fight bacterial infections?

A
  • inhibit metabolism
  • inhibit cell wall synthesis
  • disrupt protein synthesis
  • inhibit nucleic acid transcription/replication
  • alter plasma membrane permeability
54
Q

what are the requirements for the Pro-Tide approach?

A
  • lipophilic
  • stable in plasma
  • hydrolyses in cells
  • byproducts non-toxic

Pharmacy 201 (4 decks)

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