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Medical Pharmacology > DNA and Antimetabolites > Flashcards

DNA and Antimetabolites Flashcards

1
Q

what does DNA gyrase do

A

relieves supercoiling of prokaryotic DNA

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2
Q

what does topoisomerase IV do

A

decatenation (unlinking) of interlinked chromosomes

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3
Q

how to quinolones or fluoroquinolones work?

A

inhibit DNA gyrase and topoisomerase IV to kill prokaryotes

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4
Q

how do quinolones enter

A

porin! gram -

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5
Q

what is more important in gram-?

A

DNA gyrase

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6
Q

what is more important in gram +

A

topoisomerase IV

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7
Q

what are the respiratory fluoroquinolones?

A
  1. levofloxacin

2. moxifloxacin

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8
Q

what fluroquinolones cover pseudomonas?

A
  1. ciprofloxacin

2. levofloxacin (has some)

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9
Q

what is nalidixic acid?

A

fluoroquinolone that is not used clinically because it doesn’t reach systemic levels. only covers gram- in urine.

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10
Q

nalidixic acid and resistance

A

if cultures reveal resistance to this, it is a short step to resistance to ciprofloxacin

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11
Q

characteristic of ciprofloxacin

A

achieves systemic levels and covers gram- aerobes including pseudomonas

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12
Q

what does levofloxacin cover

A 
respiratory FQ so:
s. pneumoniae
m. pneumoniae  
c. pneumoniae 
l. pneumoniae 
some pseudomonas
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13
Q

what does moxifloxacin cover

A 
respiratory FQ so:
s. pneumoniae
m. pneumoniae  
c. pneumoniae 
l. pneumoniae 
some anaerobes (bacteroides) 
NO PSEUDOMONAS
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14
Q

what is ciprofloxacin used for

A

gram- only for complicated UTI, prostatitis, anthrax, gram- ostomyelitis, pseudomonas

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15
Q

why can moxifloxacin not be used for UTI?

A

it doesn’t accumulate in the urine, so not used for UTI

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16
Q

what can moxifloxacin be used for?

A

ob/gyn/GI surgeries since it covers bacteroides

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17
Q

what can levofloxacin, gemifloxacin and moxifloxacin be used for?

A

empirically as monotherapy for CAP, skin and soft tissue infections because cover gram- to varying degrees
can also be used for UTI (except not moxifloxacin)

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18
Q

fluoroquinolones MOA

A

inhibition of topoisomerase leading to cleavage of DNA and cell death

are concentration dependent killers

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19
Q

resistance against FQ

A

cross resistance among FQ

  1. mutations in topoisomerase (GyrA and GyrB genes)
  2. efflux pumps
  3. altered porin channels
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20
Q

which FQ are available PO or IV?

A
  1. ciprofloxacin
  2. levofloxacin
  3. ofloxacin
  4. moxifloxacin
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21
Q

kinetics of FQ

A

achieves high concentrations in most compartments except CNS (moxifloxacin has limited in urine)

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22
Q

FQ and other cells

A

penetrates microphages and PMNs

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23
Q

what limits absorption of FQ

A

chelation with dairy, antacids, iron formulations and Mg.

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24
Q

which meds are you not to take with dairy

A

tetracyclines and FQ

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25
Q

ADE of FQ

A
  1. chelation so don’t use in pregnancy or children
  2. photosensitivity
  3. QTc prolongation
  4. tendinitis
  5. inhibition of CYP450
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26
Q

what does FQ inhibit

A

CYP450

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27
Q

why can FQ cause tendinitis

A

breaks down collagen and inhibits collagen repair processes. so could cause aortic dissection and ruptures too.

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28
Q

safety alerts for FQ

A

aortic dissection and rupture, hypoglycemia, mental disturbances

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29
Q

box alerts for FQ

A

tendinitis, exacerbation of myasthenia gravis, peripheral neuropathy and CNS effects

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30
Q

what do drugs that interfere with bacterial folate do?

A

bacteriostatic

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31
Q

what drugs interfere with bacterial folate?

A
  1. sulfonamides and sulfones

2. trimethoprim and pyrimethamine

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32
Q

what folate inhibitors are usually combined?

A

SMX/TMP sulfamethoxazole/trimethoprim

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33
Q

which drugs are PABA analogs?

A

sulfonamides

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34
Q

what are the sulfonamides

A

sulfamethoxazole, sulfadiazine, sulfadoxine, sulfone

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35
Q

what drugs are dihydropteroate synthase inhibitors?

A

sulfonamides (this is a bacterial mechanism)

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36
Q

what drugs are dihydrofolate reductase inhibitors?

A

pyrimethamine, trimethoprim (this is a human mechanism)

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37
Q

spectrum of TMP/SMX

A
  1. pneumocystic jiroveci
  2. nocardia
  3. enterobacteriacae like ecoli, klebsiella, enterobacter, proteus (important)
  4. moraxella
  5. hemophilus
  6. community acquired MRSA (important)
  7. c trachomatis
  8. protozoa
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38
Q

what are the folate antagonists used for

A

UTI, pneumonia in immunocompromised, burns (topical), conjunctivitis (topical), leprosy (dapsone), malaria (pyrimethamine)

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39
Q

resistance of sulfonamides

A

cross resistance (if resistant to one of them, resistant to them all)

  1. increased production of PABA (outcompetes)
  2. alteration in dihydropteroate synthetase
  3. decreased cellular permeability
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40
Q

resistance of trimethoprim

A
  1. altered bacterial DHFR

2. increased bacterial expression of DHFR (makes its own not humans)

41
Q

kinetics of sulfonamides

A

highly plasma protein bound which could cause kernicterus in neonates and pass into placenta

42
Q

absorption of sulfonamides

A

sulfasalazine has poor absorption, used for GI

43
Q

what do sulfonamides pass into

A

CNS, prostate, placenta

44
Q

how are sulfonamides eliminated?

A

N-acetylation and renal elimination

45
Q

where does trimethoprim accumulate

A

weak base so accumulates in prostate and vaginal fluids

46
Q

trimethoprim elimination

A

renally (primary)

47
Q

what occurs with hypersensitivity reaction to sulfonamides

A

steven johnson syndrome (slough of skin)

48
Q

what other sulfonamides are cross sensitive with SMX and SSD

A
  1. diuretics (loop, thiazides, carbonic anhydrase inhibitors)
  2. oral hypoglycemic sulfonylureas
  3. celecoxib
  4. bacitracin
49
Q

ADE of sulfonamides

A
  1. rash
  2. crystalluria (drink a lot of fluid)
  3. photosensitivity
50
Q

what happens in neonates with sulfonamides

A

kernicterus – displacement of bilirubin from albumin (jaundice)

51
Q

what is stevens johnson syndrome

A

immune complex mediated hypersensitivity (type III but follows type IV)

52
Q

when is steven johnson syndrome a risk

A

with slow acetylators, immunocompromised and pt with brain tumors/undergoing radiotherapy/with antiepileptics

53
Q

what does steven johnson syndrome entail

A

skin and mucous membranes where apoptosis of keratinocytes cause separation of epidermis from the dermis. fas and Fas L, activated T cells.

54
Q

area of SJS

A

minor form of toxic epidermal necrolysis (TEN) with less than 10% body surface area detachment

55
Q

what is TEN

A

detachment of more than 30% of body surface area

56
Q

what is a major problem for sulfonamides and sulfone?

A

hemolytic anemia in G6PD deficiency

57
Q

ADE of trimethoprim

A

leukopenia and macrocytic anemia if chronic use since inhibiting mammalian DHFR

58
Q

what drugs interfere with RNA polymerase

A

rifamycins

59
Q

what is needed for bacterial transcription initiation

A

RNA polymerase

60
Q

what is needed for bacterial transcription elongation

A

adding bases to chain via RNA polymerase

61
Q

what is needed for termination?

A

dissociation of the DNA, RNA polymerase, and newly formed RNA

62
Q

what do rifamycins do?

A

bind to beta subunit of RNA polymerase, which blocks elongation of the nascent RNA chain

63
Q

what are the rifamycins

A

rifampin, rifabutin, rifapentine

64
Q

MOA rifamycins

A

form very stable complex with RNA polymerase (very low affinity for human, even mitochondrial) to prevent elongation

65
Q

rifamycin spectrum

A

love to kill bacteria in the phagosome, very broad including mycobacteria

66
Q

what do rifamycin not cover

A

enterobacteraceae

67
Q

resistance against rifamycin

A

spontaneous mutation of rpoB gene that is rapid and predictable

68
Q

use of rifamycins (monotherapy)

A

monotherapy only in the prophylaxis of neisseria meningitidis or H influenzae meningitis

69
Q

use of rifamycins (combination treatment)

A

TB, leprosy, bone infections, endocarditis

70
Q

adverse effects of rifamycins

A
  1. stains body fluids orange/red
  2. powerful enzyme inducer (many drug interactions, decrease effects of other drugs)
  3. hepatotoxic (hepatitis)
  4. flu like hypersensitivity
71
Q

MOA of rifamixin

A

inhibits DNA dependent RNA polymerase

72
Q

spectrum of rifamixin

A

ecoli, possibly other enterobacteriaeceae and possibly e coli (narrow)

73
Q

use of rifamixin

A

uncomplicated travelers diarrhea bc does not achieve therapeutic levels systemically

74
Q

SE of rifamixin

A

not absorbed systemically, so minimal or local SE

75
Q

which drugs generate ROS

A

metronidazole, nitazoxanide

76
Q

MOA metronidazole

A

activated by pyruvate-ferredoxin oxireductase (PFOR) to its active reduced form, which is thought to bind DNA and proteins, leading to microbial death

77
Q

spectrum of metronidazole

A

protozoa (giardia, trichomonas), anaerobes, H pylori

78
Q

use of metronidazole

A

C diff except now use oral vancomycin 1st then a macrolide then metronidazole.

amoebic dyssenterty, amoebiasis, below the belt anaerobes

79
Q

ADE of metronidazole with alcohol

A

inhibits aldehyde dehydrogenase making a disulfram reaction that makes you sick when you drink alcohol

80
Q

ADE of metronidazole

A

leukopenia, thrombocytopenia, metallic taste, neurotoxic, ototoxic, neuopathy, inhibits warfarin metabolism

81
Q

MOA nitazoxanide

A

activate by pyruvate ferredoxin oxidoreductase leads to formation of free radicals and ROS

82
Q

SE nitazoxanide

A

very few SE or drug interactions

83
Q

spectrum nitazoxanide

A

adjunct to antiretroviral therapy in cryptosporidium and giardia in kids

84
Q

urinary tract drugs are

A

nitrofurantoin, methenamine, cranberry, phenazopyridine (AZO, pyridium)

85
Q

MOA methenamine

A

forms formaldehyde at acidic pH so acts as antiseptic

86
Q

MOA cranberry

A

inhibits adherence of uropathogens to uroepithelial cells (no real data)

87
Q

contraindications for AZO/pyridium/phenazopyridine_

A

pt with creatine clearance less than 50

88
Q

caution for AZO

A

max of 2 days of therapy or else causes hemolytic anemia leading to acute renal failure

89
Q

what does AZO do to urine

A

changes urine from orange to red

90
Q

MOA nitrofurantoin

A

reduced form damages DNA

91
Q

spectrum of nitrofurantoin

A

e coli, enterococci

92
Q

uses for nitrofurantoin

A

urinary tract only

93
Q

what is best for nitrofurantoin

A

acidic urine is better effect for treatment and prophylaxis of uncomplicated UTI

94
Q

ADE of nitrofurantoin

A

issue in G6PD!! causes anemia, hepatotoxic, neurologic disturbances

95
Q

what drugs are issues in G6PD ?

A

sulfonamides and nitrofurantoin

96
Q

what are the GI antibiotics?

A
  1. neomycin
  2. vancomycin (oral)
  3. metronidazole (but will have systemic absorption)
  4. rifamixin
  5. fidoxamicin
  6. bacitracin
  7. some sulfonamides like sulfadiazine
97
Q

what drugs should not be used in children for risk of discoloration of teeth and remodeling of bone?

A

tetracyclines and fluoroquinolones (both cause chelation)

98
Q

what carbapenem has little activity against pseudomonas?

A

ertapenem

Medical Pharmacology (13 decks)

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