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Pharma 3 > Sulphonamides and Trimethoprim. Fluoroquinolones > Flashcards

Sulphonamides and Trimethoprim. Fluoroquinolones Flashcards

1
Q

General Background Info On Sulphonamides and Trimethoprim

A

Are folate antagonists–> inhibit folic acid metabolism

Are Antimetabolites–> inhibits cell growth by competing with/substituting for a natural substrate

Folate
Cofactor as methyl group donor in synth of purines and
pyrimidines–> req. for DNA and RNA synth
Humans can’t synthesise, need to absorb
Bacteria can synthesise, can’t absorb
Active in THF form; both humans and bacteria need to
activate it

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2
Q

Synthesis and Activation of Folate

3 Steps

A

p Aminobenzoic Acid via Dihydropteroayte synthase–>

Dihydrofolic Acid via Dihydrofolate reductase–>

Tetrahydrofolic Acid

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3
Q

Point of Action: Sulphonamides and Trimethoprim in Folic Acid Synthesis

A

Sulphonamides: Dihydropteroate Synthase
do so as they have similar structure to PABA

Trimethoprim: Dihydrofolate Reductase

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4
Q

Toxicity of Sulphonamides and Trimethoprim

A

Class II of selective toxicity meaning
block synth of simple block of cell (NA/AA/sugar)

Inhibition of folate metabolism is bacteriostatic effect

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5
Q

General Information of Sulphonamides

A

Synthetic structural analoges of PABA

Compete with PABA for dihydropteroate synthase
as the enzyme is dominant in bacteria–> selective toxicity

Counteract the effect of sulphonamides by adding PABA

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6
Q

Sulphonamides

Pharmacokinetics
Spectrum
MoR

A

Good oral bioavail.–> per os
Distributes if total water space
Crosses BBB and placenta
Strong PPB–> displacement

Elimination
Biotransformation (acetylation)
Excreted into urine and milk

Spectrum
G+: Streptococci, Staph
G-: E. Coli, Shigella, Salmonella
Chlamydia, Nocardia

MoR
Anaerobic bacteria show natural resistance
Overproduction or mutation of enzyme–> resistance

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7
Q

Sulphonamides

Uses
SE

A

Not given topically –> risk of allergic reactions

Nocardiosis
Travellers Diarrhoea
Toxoplasmosis
UTI and upper resp. infections

SE
Allergies: skin
Metabolites may precipitate in kidney failure
–>crystalluria
Anaemia, haemolysis
ICTERUS (bilirubin displaced from albumin)

Can be avoided by stimulating elimination: alkalising
urine–> ionisation–> elimination
Admin of diuretics

STIMULATE GROWTH OF RICKETTSIA

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8
Q

Sulphonamides

Interactions

A

Local Anaesthetics ex. procain can antagonise effect
as procaine is a PABA ester

Kernicterus due to displacement of bilirubin from PP

Comb with dihydrofolate reductase inhibitors
Decreases resistance
Synergism

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9
Q

Sulphonamides

Drug Groups

A

Short Acting

Intermediate Acting

Long Acting

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10
Q

Sulphonamides

Short Acting

A

Sulfadiazine and Sulfadimidine

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11
Q

Sulphonamides

Intermediate Acting

A

Sulfamethoxazole

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12
Q

Sulphonamides

Long Acting

A

Sulfadimethoxine Sulfadoxine

Long acting due to strong PPB or renal reabsorption

Sulfadoxine can also be used in malaria prophylaxis

OTHER: sulfasalazine
also used in RA, UC

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13
Q

Trimethoprim

General
MoA

A

Chemically related to pyrimthamine (sulfonamide)

MoA
structural folate analogue: competitively inhibits
dihydrofolate reductase –> bacteriostatic

Also affects DNA and RNA synthesis of humans but has
a much stronger affinity to bacterial dihydrofolate
reductase

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14
Q

Trimethoprim

Pharmacokinetics
Resistance
Use
SE

A

Good oral bioavailability–> per os
Distributed throughout; passes BBB
Excreted renally

Resistance by mutation and overprod. of enzyme

Uses: UTI and Resp Infection

SE
folate deficiency–> megaloblastic anaemia
nausea vomiting

SHOULD BE GIVEN WITH FOLIC ACID (same with sulphonamides)

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15
Q

Combination: Sulphonamides and dihydrofolate reductase inhibitor

A

Trimethoprim and Sulfamethaxazole= CO TRIMOXAZOLE

Potentiate each other
Wider spectrum; decreased resistance

Drugs have similar half life

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16
Q

MIC

A

Minimal Inhibitor Concentration–> bacteriostatic

Conc which inhibits bacterial division in std test

17
Q

Fluoroquinolones

General Background

A

DNA inhibitor: Topoisomerase II and Topoisomerase IV

Topoisomerase II: DNA gyrase (unwinding)
Topoisomerase IV: resp. for separation of replicated DNA

Time and conc. dep. killing: parabola

Bactericidal

18
Q

Fluoroquinolones

Resistace
Spectrum

A

Resistance
Mutation of topoisomerase II
Decreased permeability
Plasmid mediated resistance

Spectrum
G-: E. Coli, Klebsiella, Proteus, Pseudomonas
G+: gen not that sensitive; some Ste. pneu., anthrax
IC pathogens: Chlamydia, mycoplasma

19
Q

Fluoroquinolones

Pharmacokinetics
Uses

A

Excellent bioavailability; iron/Ca limit absorption
Mainly eliminated via kidney: filtration and active
secretion
–> must reduce dose in renal dysfunction

Uses
   UTIs
   STDs/PIDs: chlamydia, gonorrhoea 
   Travellers diarrhoea 
   Drug resistant pneumonia 
   Mixed tissue infections; penetrating wound body 
         cavities
20
Q

Fluoroquinolones

SE

A

CNS (activating): tremor, agitation, headache, seizures

GIT: Nausea, vomiting, abdominal discomfort

Phototoxicity

Damages growing cartilage: CI in preggos and kiddies

21
Q

Fluoroquinolones

Drug Grouping

A

Generation 0-4

22
Q

Fluoroquinolones

Generation 0

A

Oxolinic Acid

Only used orally
Only reaches effective level in GIT and UT

Th of UTIs
Active against G- enteric pathogens

23
Q

Fluoroquinolones

Generation I

A

Norfloxacin

Orally used
Doesn’t produce systemic plasma level

Used in UTIs
Active against G- enteric pathogens

24
Q

Fluoroquinolones

Generation II

A

Ciprofloxacin Ofloxacin

Cipro has best G- activity out of all fluoroqui.

Given mainly per os, IV possible

25
Q

Fluoroquinolones

Generation III

A

Levofloxacin

Better coverage G+ and IC; less G-

per os, IV also possible

26
Q

Fluoroquinolones

Generation IV

A

Moxifloxacin

superior G+ acitivity

!Biliary excretion!
!!!Not suitable for UITS!!!

27
Q

MBC

A

Minimal Bacteriocidal Concentration

conc. that kills 99.9% of bacteria in standard test

Pharma 3 (14 decks)

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