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pr3151 > quinolones, folic acid antagonists and urinary antiseptics > Flashcards

quinolones, folic acid antagonists and urinary antiseptics Flashcards

1
Q

what compound was the structure of fluroquinolones derived from

A

nalidixic acid

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2
Q

draw structure of nalidixic acid

A
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3
Q

what is the infection that is most commonly associated with fluoroquinolones

A

c. difficile and abx resistance

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4
Q

what are the examples of fluoroquinolones

A

ciprofloxacin, levofloxacin, moxifloxacin, nalidixic acid, norfloxacin, ofloxacin

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5
Q

what is the moa of fluoroquinolones

A

target primarily DNA gyrase in gram neg bacteria and topoisomerase IV in gram pos bacteria to inhibit DNA replication

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6
Q

do eukaryotic cells (human) contain DNA gyrase

A

no, have topoisomerase II which works mechanistically similar to DNA gyrase and will be inhibited by fluoroquinolones at high conc

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7
Q

what are the routes for fluoroquinolones

A

IV, PO, ophthalmic

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8
Q

what is the absorption, distribution and excretion of fluoroquinolones

A

well absorbed after taking orally, best on empty stomach, to take 2h before or 6h after if ingesting with potential fdi

well distributed in bone, urine (except moxifloxacin), kidney and prostatic tissue

renally cleared for all except moxifloxacin which is hepatically metabolised

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9
Q

what are the indications for ciprofloxacin

A

gram neg incl penicillin cephalosporin and aminoglycoside resistant strains, only PO agent for pseudomonas, food poisoning caused by enterobacteriae (salmonella, shigella, e coli) and campylobacter, traveller’s diarrhoea caused by e coli, typhoid fever caused by salmonella and anthrax

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10
Q

what conditions of ciprofloxacin not used for

A

simple uti and MRSA

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11
Q

why is ciprofloxacin not used for MRSA

A

ineffective against anaerobes and is highly resistant to staphylococcus

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12
Q

what is levofloxacin and mixofloxacin known as

A

respiratory quinolones

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13
Q

what are the indications of respiratory quinolones

A

better coverage against gram pos, atypicals and mycobacterium

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13
Q

what are the indications of respiratory quinolones

A

better coverage against gram pos, atypicals and mycobacterium

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14
Q

what are the adverse effects of fluoroquinolones

A
  1. GI
  2. risk of dysglycemia
  3. aortic dissections or rupture of aortic aneurysm
  4. increase risk of c. difficile due to clearing of bowel flora esp with ciprofloxacin
  5. phototoxicity
  6. light headedness, dizziness and headache
  7. joint problems (not for <18yo)
  8. increase risk of tendonitis or tendon rupture due to systemic use
  9. peripheral neuropathy (affect tendon, muscle, joints, nerves and can occur any time and last for months or even permanent even after stopping)
  10. QT prolongation (third gen esp)
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15
Q

can fluoroquinolones be used in pregnancy

A

category C due to atropathy (fetal cartilage development disorders) and ciprofloxacin detected in breast milk

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16
Q

what are the c/i of fluoroquinolone

A

myasthenia gravis, muscle weakness, g6pd deficiency

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17
Q

what are the fdi of fluoroquinolone

A

ingestion with Ca or other divalent or trivalent cations can reduce absorption (Al, Fe, Mg, Zn)

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18
Q

what are the ddi of fluoroquinolone

A

raise serum level of warfarin and cyclosporin

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19
Q

what is folic acid

A

vitamin B that helps make RBC

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20
Q

what is the folic acid synthesis pathway

A

pteridine and PABA -> dihydropteroic acid [dihydropteroate synthease] -> dihydrofolic acid [dihydrofolate synthase] -> tetrahydrofolic acid [dihydrofolate reductase with NADH] -> AA, purine, thymine synthesis

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21
Q

what are the drugs that are anti folate drugs

A

sulfonamides and trimethoprim

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22
Q

what is the moa of sulfonamides

A

competitive inhibitor of dihydropteroate synthase enzyme upstream which is the bacterial enzyme that incorporates para-aminobenzoic acid (PABA) into dihydropteroic acid which is the immediate precursor of folic acid

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23
Q

what type of activity does sulfonamides have

A

bacteriostatic

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24
Q

are mammalian cells affected by the mechanism of sulfonamides

A

no, we require preformed folic acid (only have step from conversion of dihydrofolic acid into tetrahydrofolic acid)

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25
Q

what is the moa of trimeptoprime

A

potent inhibitor of dihydrofolate reductase enzyme which inhibits the reduction of dihydrofolic acid into tetrahydrofolic acid which leads to a decreased availability of tetrahydrofolate cofactors required for AA, purine and thymine synthesis which will affect DNA synthesis as a whole

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26
Q

what is the benefit of coadministering sulfonamides and trimeptoprime

A

introduces sequential blocks in biosynthetic pathway for tetrahydrofolate which allows for synergistic effect

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27
Q

what are the types of sulfonamides and examples of drugs of each type

A

short acting - sulfisoxazole
intermediate acting - sulfadiazine, sulfamethoxazole
poorly absorbed (active in bowel lumen) - sulfasalazine
topically applied - silver sulfadiazine, sulfacetamide
long acting - sulfadoxine

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28
Q

what are the absorption, distribution, metabolism and excretion characteristics of sulfonamides

A

absorption: well absorbed after oral administration

distribution: bound to serum albumin and can displace other things bound to serum albumin, distribute throughout bodily fluids and can penetrate into csf even without inflamm, pass placenta barrier and enter fetal tissues

metabolism: acetylation and conjugation occur in liver, byproducts are devoid of antimicrobial activity but has the potential to cause toxicity as it can precipitate in neutral or acidic pH and cause crystaluria which can damage the kidney

excreted by glomerular filtration and secretion, renal dose adjustments needed, may be secreted into breast milk

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29
Q

what are the indications for sulfonamides

A

pneumocystis (cotrimoxazole), drug resistant malaria and toxoplasmosis (with pyrimethamine), ibs (sulfasalazine), infected burns (topical silver sulfadiazine), STI, respiratory tract infections, acute UTI

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29
Q

what are the indications for sulfonamides

A

pneumocystis (cotrimoxazole), drug resistant malaria and toxoplasmosis (with pyrimethamine), ibs (sulfasalazine), infected burns (topical silver sulfadiazine), STI, respiratory tract infections, acute UTI

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30
Q

what are the adverse effects of sulfonamides

A
  1. crystalluria
  2. hypersensitivity
  3. hematopoietic disturbances (hemolytic anemia and thrombocytopenia)
  4. kernicterus
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31
Q

what is the ddi for sulfonamides

A

warfarin with sulfamethoxazole

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32
Q

what is the c/i for sulfonamides

A

newborns, infants <2m, pregnant at term

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33
Q

in which special population might hemolytic anemia occur and what drug is it

A

sulfonamides can cause hemolytic anemia in g6pd deficient as sulfa drugs produces alot of ROS/ free radicals which will not be removed if deficient

34
Q

which drug can cause kernicterus and why

A

sulfonamides can cause kernicterus in newborns as sulfa drugs can displace bilirubin from serum albumin which results in free bilirubin that can cross into cns as bbb is not fully developed and not very effective liver function thus leading to neurodamage and affect brain development

35
Q

what are the indications for trimethoprim

A

enterobacter species (ecoli, klebsiella), monoagent for UTI and bacteria prostatitis but fluoroquinolones preferred

36
Q

what are the mechanisms of resistance for trimethoprim

A
  1. altered dihydrofolate reductase which has lower affinity for trimeptoprim
  2. presence of efflux pumps and decreased permeability to drug
37
Q

absorption, distribution and excretion of trimethoprim

A

absorption: rapidly absorbed after oral adminstration, weak base so higher conc achieved in relatively acidic prostatic and vaginal fluids

distribution: widely distributed to bodily tissues and fluids, good penetration into csf

excretion: 60-80% unchanged renally, renal dose adjustments required

38
Q

what are the adverse effects of trimethoprim

A
  1. folic acid deficiency (megaloblastic anemia, leukopenia, granulocytopenia in pregnant and those with very poor diets)
39
Q

what might trimethoprim cause in pregnant patients

A

folic acid deficiency

40
Q

which drug causes folic acid deficiency and how to manage

A

trimethoprim and manage by simultaneously administering folinic acid

41
Q

what is folinic acid and how does it help reverse folic acid deficiency

A

is a 5-formyl derivative of tetrahydrofolic acid which readily converts to tetrahydrofolic acid which is required for important cellular metabolic functions, does not enter bacteria and is not dihydrofolic acid which requires to be reduced into active form

42
Q

what is cotrimoxazole

A

1:5 ratio of trimethoprime and sulfamethoxazole

43
Q

what is the moa of cotrimoxazole

A

synergistic antimicrobial activity derived from inhibiting two sequential steps in synthesis of tetrahydrofolic acid

44
Q

what are the indications for cotrimoxazole

A

UTI, e coli, prophylaxis for recurrent UTI, RTI (klebsiella, moraxella catarrhalis, haemophilus), MRSA, community acquired skin and soft tissue infections, pneumocystis pneumonia

45
Q

absorption, distribution and excretion of cotrimoxazole

A

absorption: PO with full cup of water, IV for severe pneumonia or UTI if unable take by mouth

distribution: both distribute well throughout body, trimethoprim conc in relative acidic fluids, good csf penetration

excretion: parent and metabolites excreted in urine

46
Q

what are the ddi of cotrimoxazole

A

increases half life of phenytoin, enhances effect of warfarin

47
Q

what are the adverse effects of cotrimoxazole

A
  1. skin rash
  2. photosensitivity
  3. GI (N, V)
  4. glossitis, stomatitis (hemolytic anemia in g6pd deficient due to sulfamethoxazole, megaloblastic anemia/ leukopenia/ thrombocytopenia due to trimethoprim)
  5. folic acid deficiency (caution in pregnancy)
48
Q

what special population to take note of for cotrimoxazole

A

g6pd deficient and pregnancy

49
Q

which trimesters should cotrimoxazole especially not be used in

A

first trimester as pregnancy very sensitive to folate levels, third trimester not sure if child is g6pd deficient

50
Q

what class of drug is nitrofurantoin

A

urinary antiseptic

51
Q

what is the moa of nitrofurantoin

A

nitrofurantoin sensitive bacteria reduces the drug to a highly active intermediate that inhibits various enzymes and disrupts the synthesis of DNA, RNA and proteins, and metabolic processes

52
Q

what are the indications for nitrofurantoin

A

acute lower UTI, prophylaxis for recurrent UTI

53
Q

what is the spectrum of activity of nitrofurantoin

A

e coli, enterococci

54
Q

what bacteria is resistant to nitrofurantoin

A

klebsiella, pseudomonas, proteus, enterobacter

55
Q

what pH does nitrofurantoin work best in

A

activity higher in acidic urine pH <5.5

56
Q

does nitrofurantoin colour urine

A

yes colours it brown

57
Q

absorption, distribution and excretion of nitrofurantoin

A

absorption: PO absorbed rapidly from GIT

distribution: achieves high urinary conc while limiting systemic exposure due to rapid clearance

excretion: 40% excreted unchanged in urine, rate of excretion linearly related to CrCl so decrease efficacy and increase toxicity if impaired glomerular function

58
Q

is macrocrystalline form of nitrofurantoin absorbed more rapidly or more slowly

A

absorbed and excreted more slowly than nitrofurantoin

59
Q

what are the adverse effects of nitrofurantoin

A
  1. GI (N,V,D) -> macrocrystalline preparation better tolerated
  2. hypersensitivity
  3. cholestatic jaundice and hepatocellular damage
  4. pulmonary toxicity esp in older adults
  5. peripheral neuropathy in impaired renal function and long treatment
  6. prolonged incubation period to onset of liver injury
60
Q

how does nitrofurantoin cause cholestatic jaundice and hepatocellular damage

A

nitro reductive metabolism produces injurious oxidative free radicals which damages hepatocytes

61
Q

what are the c/i of nitrofurantoin

A
  1. renal impairment (CrCl <40ml/min)
  2. pregnant (38-42w gestation), during labour and delivery as unsure if child is g6pd deficient
62
Q

what are the types of UTI

A

nephritis and pyelonephritis

63
Q

what is nephritis

A

bladder infection

64
Q

what is pyelonephritis

A

kidney infection

65
Q

what are the symptoms of nephritis

A

increased urinary frequency, urgency, dysuria (painful urination), pain above pubic region, WBC and bacteria in urine, possible hematuria, more common in women

66
Q

what are the symptoms of pyelonephritis

A

flank pain, high fever, malaise, WBC ans bacteria in urine, urinary symptoms similar to nephritis

67
Q

what is the first line drug for nephritis and pyelonephritis

A

nephritis: nitrofurantoin
pyelonephritis: IV ceftriaxone

68
Q

what is the first lie drug for ESBL

A

carbapenems

69
Q

what is a anti-protazoal agent

A

metronidazole

70
Q

where are protozoal infections common in

A

underdeveloped tropical and subtropical countries

71
Q

what is the characteristics of protozoal cells

A

protozoal cells are unicellular eukaryotic cells with a clearly defined nucleus and has metabolic processes that are similar to those of human host than to prokaryotic bacterial pathogens

72
Q

what is amebiasis

A

an infection of the intestinal tract caused by entamoeba histolytica

73
Q

what are the types of agents used for amebiasis

A

luminal, systemic and mixed amebicides chemotherapeutic agents

74
Q

what does luminal chemotherapeutic agents act on

A

act on parasite in bowel lumen

75
Q

what does systemic chemotherapeutic agents act on

A

act on amoebas in intestinal wall and liver after being absorbed

76
Q

what are mixed amebicides used for

A

effective against both luminal and systemic although luminal conc not high enough for single drug treatment

77
Q

what is an example of a mixed amebicide agent

A

metronidazole

78
Q

is metronidazole safe in pregnancy

A

category B, avoid use in first trimester, not proven safe and crosses placental barrier and enters fetal circulation rapidly

79
Q

what is the moa of metronidazole

A

amoebas possess an electron transport protein that participate in metabolic electron removal reactions and since metronidazole has a nitro group it can serve as an electron acceptor to form cytotoxic free radicals which causes protein and DNA damage and leads to cell death

80
Q

what are the conditions for reduction of metronidazole to exert its moa

A

anaerobic conditions as anaerobes have better reducing potential than aerobes

81
Q

what are the indications for metronidazole

A
  1. amebic infections caused by protozoa
  2. anaerobes like bacteriodes, c. difficile
  3. h pylori
  4. surgical prophylaxis
82
Q

absorption, distribution, metabolism and excretion of metronidazole

A

absorption: completely and rapidly absorbed after oral administration

distribution: well distributed throughout bodily tissues and fluids (vaginal, seminal fluid, saliva, breast milk), good csf penetration

metabolism: hepatic metabolism (drug accumulates in severe hepatic disease, concomitant administration of cyp inhibitors or inducers can affect rate of drug metabolism)

excretion: parent and metabolites excreted in urine

83
Q

what are the adverse effects of metronidazole

A
  1. GI
  2. unpleasant metallic taste
  3. oral moniliasis (yeast infection of mouth)
  4. central and peripheral nervous system effects (convulsive seizures, optic and peripheral neuropathy)

pr3151 (12 decks)

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