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26 Cards in this Set

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  • Back
Sulfonamides mechanism
- anaoug of PABA
- block formation of folate by competitively inhibiting the formation of DHT from PABA catalyzed by DHTS -> inhibition of DNA, RNA, and protein synthesis
– bacteriostatic
Sulfonamides antimicrobal spectrum
- can act on both (-) and (+)
- chlamydia and some protozoa
- but many strains resistant
– Rickettsiae are naturally resistant
Sulfonamides Pharmacokinetics
- given orally
- variable amount is bound
– well distributed and will cross BBB and placental B
- acetylated in liver and eliminated renally
Sulfonamides adverse effects
- Hypersensitivity and GI most common
- kernicterus in newborns
- crystalluria
- Blood dyscrasias are rare
Sulfonamides drug interactions
will potentiate warfarin by interfering with metabolism by P450
Sulfonamides uses
- limited as a single agent
2) Toxoplasmosis
3) Uncomplicated, acute UTIs
Sulfonamides resistance
1) altered DHTS w/ lower affinity
2) redueced uptake
3) ↑ PABA
Trimethoprim mechanism
- potent inhibitor of DHFR
– further down the same pathway than sulfonamides
– usually used w/ sulfamethoxazole synergistically
Trimethoprim pharmokinetics
- penetrates most tissues, including brain
– excreted via the kidney
– accumulates in prostatic and vaginal fluids
Trimethoprim Antimicrobial spectrum
the combo is broad spectrum
Trimethoprim uses
1) UTIs
2) Shigella enteritis
3) P. carinii pneumonia Alternative for
1) OM and RTI’s from H. flu or Strep pneumoniae
2) Chloroquine-resistant malaria
3) Nocardia infection
4) (-) bacilli
Trimethoprim adverse effects
- Combo is the same as sulfa
- difficult for pts with FA def and AIDS pts w/ PCP
- they get rash, fever, leukopenia, and hepatitis
- Pentamidine is alternative
Trimethoprim resistance
1) production of DHFR w/ reduced affinity for trimethoprim
2) overproduction
Fluoroquinolones mechanism
- inhibit DNA gyrase, preventing unwinding
– often bactericidal
Fluoroquinolones antimicrobial spectrum
- best for (-) rods
- (+) and IC (legionella) ok
– wont work w/ anaerobes
- used with B-lactams for broad spectrum in life-threatening infections
Fluoroquinolones pharmokinetics
oral administration, distributed widely in tissues and body fluids - excreted unmodified via the kidney - Penetration into the CNS is unreliable - Antacids can interfere with oral administration
Fluoroquinolones clinical use
1) UTIs (inc P. aeruginosa) 2) N. gonorrhoeae
3) any enteritis, salmonella
4) V. cholerae or S. marcescens
5) wierd infections in normal and neutropenic pts
Fluoroquinolones adverse effects
usually well-tolerated
1) NandV, and diarrhea
2) CNS effects
3) may damage cartilage -> an arthropathy (no kids, pregnant, nursing)
- Interferes w/ theophylline and caffeine metabolism
Fluoroquinolones Resistance
1) prod of altered DNA gyrase w/ a lower affinity
2) decreased uptake
Nitrofurantoin Mechamism
is reduced by the bacteria to a reactive species that reacts with DNA
Nitrofurantoin antimicrobial spectrum
- taken orally
- accumulates in the urine to bacteriostatic or bactericidal levels
Nitrofurantoin clnical use
1) uncomplicated UTI’s with common (-)
2) for chronic therapy of recurring infections
Nitrofurantoin adverse effects
- common are anorexia, nausea, hypersensitivity reactions
- CNS disturbances more rare
Nitrofurantoin drug interactions
w/ naladixic acid and nitrofurantoin it is antagonistic