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pharmaco > quinolones, folic acid ant urinary antiseptics > Flashcards

quinolones, folic acid ant urinary antiseptics Flashcards

1
Q

what kind of microbial activity does fluroquinolones have

A

broad spectrum

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2
Q

what is bad about fluroquinolone

A

tied to clostridium difficile infection and spread of antimicrobial resistance in many organisms

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3
Q

what does DNA gyrase do?

A

introduce negative supercoils into the DNA, to prevent excessive supercoiling, allows DNA to replicate

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4
Q

what does topoisomerase IV do

A

promotes seperation of chromosomal DNA into daughter cells

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5
Q

What does fluoroquinolones target

A

targets DNA gyrase primarily in gram negative bacteria

targets topoisomerase IV in gram positive bacteria to inhibit DNA replication

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6
Q

what are the types of fluoroquinolones

A

ciprofloxacin
levofloxacin
moxifloxacin

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7
Q

What kind of administration are there for fluoroquinolones

A

oral, IV, ophthalmic

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8
Q

What can you say about the absorption of fluoroquinolones

A

generally well absorbed after oral but should take on empty stomach as if ingested with calcium or other divalent cations, like aluminium or magnesium containing antacids, or dietary supplements that has iron or zinc can reduce absorption

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9
Q

how is the distribution of fluoroquinolones

A

high in bones , urine ( except moxifloxacin), kidney, prostatic tissues and concentration in lungs exceed those in serum

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10
Q

what is the primary route of clearance of quinolones

A

renal. Thus dose adjustment necessary for patients with renal failure

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11
Q

Where is moxifloxacin metabolised, when will dose adjustment be needed?

A

mainly in liver, when patients have hepatic failure

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12
Q

what is ciprofloxacin most active against

A

gram negative strains and enteric coliform

highly active against P. aeruginosa

Travellers diarrhoea caused by ecoli. food poisoning caused by enterobacteriaceae and campylobacter jejuni

typhoid fever caused by salmonella typhi

used as anthrax caused by bacillus anthracis

prostatitis

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13
Q

What has increased resistance against fluoroquinolones

A

UTI

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14
Q

which infection should you avoid using ciprofloxacin? why?

A

MRSA infections, associated with high incidence of staphylococcal resistance. Ineffective against anaerobes

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15
Q

what type of fluoroquinolones have better coverage against gram positive organisms and anaerobes?

A

third gen- levo and moxifloxacin

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16
Q

what is levo and moxifloxacin used for

A

prostatitis due to E coli

CAP, nosocomial pneumonia

Excellent activity against S. pneumoniae, and mycobacterium tuberculosis

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17
Q

What are some adverse effects of quinolones

A

○ GI related most common: nausea, vomiting and diarrhoea
○ Risk of dysglycaemia especially in diabetic patients
○ Aortic dissections or ruptures of an aortic aneurysm. Rare but serious events of ruptures or tears in aorta
§ Can lead to dangerous bleeding or even death
○ Increased risk of C. diff colitis as they clear the bowel flora, especially with ciprofloxacin
○ Headache and dizziness or light headedness. Patients with CNS like epilepsy should be treated cautiously
○ Fluroquinolones can cause phototoxicity. Avoid excess exposure to sunlight, use sunscreen
○ May have an increased risk of tendinitis or tendon rupture
○ May cause joint problems in young animals, not recommended for infants or children below 18 years of age
○ Fluoroquinolones may prolong the QTc interval (cardiac)
§ Thus should not be used in patients predisposed to arrhythmias or other medications that can cause QT prolongation
Peripheral neuropathy with systemic use

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18
Q

should fluoroquinolone be used as a first line drug?

A

No, because it can cause potentially many side effects

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19
Q

What are some contraindications of using fluoroquinolones

A

during breast feeding should not use ciprofloxacin

avoid in patients with myasthenia gravis as it may exacerbate muscle weakness

avoid in patients with g6pd deficiency

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20
Q

what are some drug interactions of quinolones

A

may raise serum levels of warfarin and cyclosporine

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21
Q

what does folic acid do

A

is a B vitamin, helps body make red blood cells

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22
Q

what are some examples of folic acid inhibitors

A

trimethoprim, sulfonamides, cotrimoxazole

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23
Q

how does sulfonamides work

A

competitive inhibitors of dihydropteroate synthase

24
Q

what does dihydropteroate synthase do

A

resposible for the incorporation of para-aminobenzoic acid into dihydropteroic acid, the immediate precursor of folic acid

25
Q

how is sulfonamides administered

A

oral administration

26
Q

how is sulfonamides distributed

A

sulfa drugs bound to serum albumin, penetrates well into CSF even without inflammation. Can pass placenta barrier to enter fetal tissue

distributes well in bodily fluids

27
Q

How is sulfonamides metabolised

A

acetylated and conjugated primarily in liver

has potential to precipitate at acidic or neutral pH

28
Q

what adverse effect can sulfonamide cause?

A

crystallruia due to precipitation of acetylated product at neutral or acidic pH that can cause potential damage to kidney

hypersensitivity like rashes or SJ syndrome

Hematopoietic disturbance
- hemolytic anemia in patients with G6PD deficiency, can also cause thrombocytopenia

Kernicterus which can occur in newborns when sulfa drugs taken in late pregnancy can displace billirubin from binding sites on serum albumin. Bilirubin then can pass into the CNS as BBB is not fully developed

can have drug potentiation, anti coagulant effect of warfarin results from the displacement from binding sites on serum albumin in patients receiving sulfamethoxazole and warfarin

29
Q

How are sulfa drugs eliminated, and do they need dose adjustments

A

by glomerular filtration and secretion, and require dose adjustments for renal dysfunctions

30
Q

What are the contraindications of sulfonamides

A

avoid in newborn and infants less than 2 months of age and pregnant women in term

31
Q

What is trimethoprim function

A

inhibits bacterial dihydrofolate reductase Decreases availability of tetrahydrofolate cofactors required for purine, pyrimidine and a.a synthesis

32
Q

what are the clinical uses of trimethoprim

A

anti bacterial spectrum similar to sulfamethoxazole

may be used laone to treat UTI and bacterial prostatitis

33
Q

What bacteria is resistant to trimethoprim and why

A

gram negative bacteria, because there exists altered dihydrofolate reductase that has a lower affinity for trimethoprim

34
Q

How is the absorption of trimethoprim

A

orally, rapidly absorbed

High concentrations are achieved in relatively aciic prostatic and vaginal fluids, due to it being a weak base

35
Q

Hows the distribution of trimethoprim

A

widely distributed into CSF and tissues and fluids

36
Q

how is trimethoprim excreted

A

60-80% excreted renally, unchanged

37
Q

what are some adverse effects of using trimethoprim

A

can produce the effects of folic acid deficiency

  1. megaloblastic anemia
  2. leukopenia
  3. granulocytopenia
38
Q

What category of pregnancy is trimethoprim

A

Cat C

39
Q

How to manage folic acid deficiency with trimethoprim

A

simultaneous administration of folinic acid which interconverts to tetrahydrofolic acid

40
Q

What is cotrimoxazole comprised of

A

trimethoprime compounded with sulfamethoxazole 1:5 ratio

41
Q

What is the mechanism of action of cotrimoxazole

A

synergistic antimicrobial activity from

  1. sulfamethoxazole inhibits incorporation of PABA into dihydrofolic acid precursors
  2. trimethoprim prevents reduction of dihydrofolate to tetrahydrofolate
42
Q

How is cotrimoxazole administered

A

orally with water

IV may be used in patient with severe pneumonia, UTI if patient cannot take orally

43
Q

what are the clinical indications of sulfonamide drugs

A

pneumocystis carinii

for drug resistant malaria and for toxoplasmosis

In IBD

for infected burns

for STI like chlamydia

44
Q

how is the distribution of cotrimoxazole

A

concentrates in relatively acidic milieu of prostatic fluids, can treat prostatitis.

Has good CSF penetration, can readily cross BBB

45
Q

How is cotrimoxazole excreted

A

in urine

46
Q

What are the clinical uses of cotrimoxazole

A

treat UTI, E coli

Respiratory tract infection by haemophilus, klebsiella pneumonia

MRSA and community acquired skin and soft tissue infections

Pneumocystis pneumonia caused by pneumocystis jiroveci

47
Q

What are some adverse effect of cotrimoxazole

A

rashes

photosensitivity
nausea vomitting
stomatitis, glossitis
hemolytic anemia in patients with g6pd deficiency

megaloblastic anemia, leukopenia, thrombocytopenia ( can be reversed with concurrent administration of folinic acid)

48
Q

What is nitrofurantoin used for

A

treatment and prevention of lower UTI

49
Q

How does nitrofurantoin act

A

nitrofurantoin sensitive bacteria reduce drug to highly active intermediate that inhibits various enzymes disrupts the syntehsis

50
Q

what is the antimicrobial effect of nitrofurantoin

A

against many strains of e.coli and enterococci

51
Q

what is resistant against nitrofurantoin

A

most species of proteus and pseudomonas and many species of klebsiella and enterobacteria are resistant

52
Q

how is administration of nitrofurantoin

A

oral

53
Q

what form of nitrofurantoin is absorbed and excreted slower

A

macrocrystalline form

54
Q

How is nitrofurantoin distributed

A

achieves high urinary concentration while limiting systemic exposure due to rapid clearance

55
Q

how is nitrofurantoin eliminated

A

40% excreted unchanged into urine

colours urine brown

56
Q

adverse effects of nitrofurantoin

A

nausea, vomiting, diarrhea

hypersensitivity reactions

hemolytic anemia with g6pd deficiency as nitrofurantoin produces a lot of freee radicals

hepatocellular damage, cholestatic jaundice

peripheral neuropathy in patients renally impaired or on long treatment

57
Q

Contraindications of nitrofurantoin

A

indiv with impaired renal function

pregnant women (38-42 weeks gestation )or when labor is imminent

infants <1 month of age

pharmaco (19 decks)

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