Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

draw structure of nalidixic acid

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the infection that is most commonly associated with fluoroquinolones

A

c. difficile and abx resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the examples of fluoroquinolones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the routes for fluoroquinolones

A

IV, PO, ophthalmic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what conditions of ciprofloxacin not used for

A

simple uti and MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

why is ciprofloxacin not used for MRSA

A

ineffective against anaerobes and is highly resistant to staphylococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is levofloxacin and mixofloxacin known as

A

respiratory quinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the indications of respiratory quinolones

A

better coverage against gram pos, atypicals and mycobacterium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the indications of respiratory quinolones

A

better coverage against gram pos, atypicals and mycobacterium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

can fluoroquinolones be used in pregnancy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the c/i of fluoroquinolone

A

myasthenia gravis, muscle weakness, g6pd deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the ddi of fluoroquinolone

A

raise serum level of warfarin and cyclosporin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is folic acid

A

vitamin B that helps make RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the drugs that are anti folate drugs

A

sulfonamides and trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what type of activity does sulfonamides have

A

bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
are mammalian cells affected by the mechanism of sulfonamides
no, we require preformed folic acid (only have step from conversion of dihydrofolic acid into tetrahydrofolic acid)
25
what is the moa of trimeptoprime
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
26
what is the benefit of coadministering sulfonamides and trimeptoprime
introduces sequential blocks in biosynthetic pathway for tetrahydrofolate which allows for synergistic effect
27
what are the types of sulfonamides and examples of drugs of each type
short acting - sulfisoxazole intermediate acting - sulfadiazine, sulfamethoxazole poorly absorbed (active in bowel lumen) - sulfasalazine topically applied - silver sulfadiazine, sulfacetamide long acting - sulfadoxine
28
what are the absorption, distribution, metabolism and excretion characteristics of sulfonamides
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
29
what are the indications for sulfonamides
pneumocystis (cotrimoxazole), drug resistant malaria and toxoplasmosis (with pyrimethamine), ibs (sulfasalazine), infected burns (topical silver sulfadiazine), STI, respiratory tract infections, acute UTI
29
what are the indications for sulfonamides
pneumocystis (cotrimoxazole), drug resistant malaria and toxoplasmosis (with pyrimethamine), ibs (sulfasalazine), infected burns (topical silver sulfadiazine), STI, respiratory tract infections, acute UTI
30
what are the adverse effects of sulfonamides
1. crystalluria 2. hypersensitivity 3. hematopoietic disturbances (hemolytic anemia and thrombocytopenia) 4. kernicterus
31
what is the ddi for sulfonamides
warfarin with sulfamethoxazole
32
what is the c/i for sulfonamides
newborns, infants <2m, pregnant at term
33
in which special population might hemolytic anemia occur and what drug is it
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
which drug can cause kernicterus and why
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
what are the indications for trimethoprim
enterobacter species (ecoli, klebsiella), monoagent for UTI and bacteria prostatitis but fluoroquinolones preferred
36
what are the mechanisms of resistance for trimethoprim
1. altered dihydrofolate reductase which has lower affinity for trimeptoprim 2. presence of efflux pumps and decreased permeability to drug
37
absorption, distribution and excretion of trimethoprim
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
what are the adverse effects of trimethoprim
1. folic acid deficiency (megaloblastic anemia, leukopenia, granulocytopenia in pregnant and those with very poor diets)
39
what might trimethoprim cause in pregnant patients
folic acid deficiency
40
which drug causes folic acid deficiency and how to manage
trimethoprim and manage by simultaneously administering folinic acid
41
what is folinic acid and how does it help reverse folic acid deficiency
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
what is cotrimoxazole
1:5 ratio of trimethoprime and sulfamethoxazole
43
what is the moa of cotrimoxazole
synergistic antimicrobial activity derived from inhibiting two sequential steps in synthesis of tetrahydrofolic acid
44
what are the indications for cotrimoxazole
UTI, e coli, prophylaxis for recurrent UTI, RTI (klebsiella, moraxella catarrhalis, haemophilus), MRSA, community acquired skin and soft tissue infections, pneumocystis pneumonia
45
absorption, distribution and excretion of cotrimoxazole
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
what are the ddi of cotrimoxazole
increases half life of phenytoin, enhances effect of warfarin
47
what are the adverse effects of cotrimoxazole
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
what special population to take note of for cotrimoxazole
g6pd deficient and pregnancy
49
which trimesters should cotrimoxazole especially not be used in
first trimester as pregnancy very sensitive to folate levels, third trimester not sure if child is g6pd deficient
50
what class of drug is nitrofurantoin
urinary antiseptic
51
what is the moa of nitrofurantoin
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
what are the indications for nitrofurantoin
acute lower UTI, prophylaxis for recurrent UTI
53
what is the spectrum of activity of nitrofurantoin
e coli, enterococci
54
what bacteria is resistant to nitrofurantoin
klebsiella, pseudomonas, proteus, enterobacter
55
what pH does nitrofurantoin work best in
activity higher in acidic urine pH <5.5
56
does nitrofurantoin colour urine
yes colours it brown
57
absorption, distribution and excretion of nitrofurantoin
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
is macrocrystalline form of nitrofurantoin absorbed more rapidly or more slowly
absorbed and excreted more slowly than nitrofurantoin
59
what are the adverse effects of nitrofurantoin
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
how does nitrofurantoin cause cholestatic jaundice and hepatocellular damage
nitro reductive metabolism produces injurious oxidative free radicals which damages hepatocytes
61
what are the c/i of nitrofurantoin
1. renal impairment (CrCl <40ml/min) 2. pregnant (38-42w gestation), during labour and delivery as unsure if child is g6pd deficient
62
what are the types of UTI
nephritis and pyelonephritis
63
what is nephritis
bladder infection
64
what is pyelonephritis
kidney infection
65
what are the symptoms of nephritis
increased urinary frequency, urgency, dysuria (painful urination), pain above pubic region, WBC and bacteria in urine, possible hematuria, more common in women
66
what are the symptoms of pyelonephritis
flank pain, high fever, malaise, WBC ans bacteria in urine, urinary symptoms similar to nephritis
67
what is the first line drug for nephritis and pyelonephritis
nephritis: nitrofurantoin pyelonephritis: IV ceftriaxone
68
what is the first lie drug for ESBL
carbapenems
69
what is a anti-protazoal agent
metronidazole
70
where are protozoal infections common in
underdeveloped tropical and subtropical countries
71
what is the characteristics of protozoal cells
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
what is amebiasis
an infection of the intestinal tract caused by entamoeba histolytica
73
what are the types of agents used for amebiasis
luminal, systemic and mixed amebicides chemotherapeutic agents
74
what does luminal chemotherapeutic agents act on
act on parasite in bowel lumen
75
what does systemic chemotherapeutic agents act on
act on amoebas in intestinal wall and liver after being absorbed
76
what are mixed amebicides used for
effective against both luminal and systemic although luminal conc not high enough for single drug treatment
77
what is an example of a mixed amebicide agent
metronidazole
78
is metronidazole safe in pregnancy
category B, avoid use in first trimester, not proven safe and crosses placental barrier and enters fetal circulation rapidly
79
what is the moa of metronidazole
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
what are the conditions for reduction of metronidazole to exert its moa
anaerobic conditions as anaerobes have better reducing potential than aerobes
81
what are the indications for metronidazole
1. amebic infections caused by protozoa 2. anaerobes like bacteriodes, c. difficile 3. h pylori 4. surgical prophylaxis
82
absorption, distribution, metabolism and excretion of metronidazole
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
what are the adverse effects of metronidazole
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions