Resp Pharm 3

Front 1

Sulfonamides mechanism

Back 1

- 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

Front 2

Sulfonamides antimicrobal spectrum

Back 2

- can act on both (-) and (+)
- chlamydia and some protozoa
- but many strains resistant
– Rickettsiae are naturally resistant

Front 3

Sulfonamides Pharmacokinetics

Back 3

- given orally
- variable amount is bound
– well distributed and will cross BBB and placental B
- acetylated in liver and eliminated renally

Front 4

Sulfonamides adverse effects

Back 4

- Hypersensitivity and GI most common
- kernicterus in newborns
- crystalluria
- Blood dyscrasias are rare

Front 5

Sulfonamides drug interactions

Back 5

will potentiate warfarin by interfering with metabolism by P450

Front 6

Sulfonamides uses

Back 6

- limited as a single agent
1)Nocardiosis
2) Toxoplasmosis
3) Uncomplicated, acute UTIs

Front 7

Sulfonamides resistance

Back 7

1) altered DHTS w/ lower affinity
2) redueced uptake
3) ↑ PABA

Front 8

Trimethoprim mechanism

Back 8

- potent inhibitor of DHFR
– further down the same pathway than sulfonamides
– usually used w/ sulfamethoxazole synergistically

Front 9

Trimethoprim pharmokinetics

Back 9

- penetrates most tissues, including brain
– excreted via the kidney
– accumulates in prostatic and vaginal fluids

Front 10

Trimethoprim Antimicrobial spectrum

Back 10

the combo is broad spectrum

Front 11

Trimethoprim uses

Back 11

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

Front 12

Trimethoprim adverse effects

Back 12

- 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

Front 13

Trimethoprim resistance

Back 13

1) production of DHFR w/ reduced affinity for trimethoprim
2) overproduction

Front 14

floxacin

Back 14

Fluoroquinolone

Front 15

ciprofloxacin

Back 15

Fluoroquinolone

Front 16

Fluoroquinolones mechanism

Back 16

- inhibit DNA gyrase, preventing unwinding
– often bactericidal

Front 17

Fluoroquinolones antimicrobial spectrum

Back 17

- best for (-) rods
- (+) and IC (legionella) ok
– wont work w/ anaerobes
- used with B-lactams for broad spectrum in life-threatening infections

Front 18

Fluoroquinolones pharmokinetics

Back 18

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

Front 19

Fluoroquinolones clinical use

Back 19

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

Front 20

Fluoroquinolones adverse effects

Back 20

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

Front 21

Fluoroquinolones Resistance

Back 21

1) prod of altered DNA gyrase w/ a lower affinity
2) decreased uptake

Front 22

Nitrofurantoin Mechamism

Back 22

is reduced by the bacteria to a reactive species that reacts with DNA

Front 23

Nitrofurantoin antimicrobial spectrum

Back 23

- taken orally
- accumulates in the urine to bacteriostatic or bactericidal levels

Front 24

Nitrofurantoin clnical use

Back 24

1) uncomplicated UTI’s with common (-)
2) for chronic therapy of recurring infections

Front 25

Nitrofurantoin adverse effects

Back 25

- common are anorexia, nausea, hypersensitivity reactions
- CNS disturbances more rare

Front 26

Nitrofurantoin drug interactions

Back 26

w/ naladixic acid and nitrofurantoin it is antagonistic