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Pharm 2 Part 3: Chemotherapy and Antibiotics and Antifungals > Pharm: L29: Fluoroquinolones and Sulfonamides > Flashcards

Pharm: L29: Fluoroquinolones and Sulfonamides Flashcards

1
Q

Fluoroquinolones (-oxacin)

  1. What 7
A
  1. CIPROFLOXACIN (P. AERUGINOSA!)
  2. Ofloxacin
  3. Norfloxacin
  4. Levofloxacin
  5. Moxifloxacin (Penicillin resistant S. Pneumoniae and ANAEROBES!)
  6. Gatifloxacin
  7. Gemifloxacin (Active against Penicillin Resistant S. Pneumoniae, ANAEROBES, and CAP)
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2
Q

Fluoroquinolones

  1. Medically important ones are SYNTHETIC FLUORINATED ANAOLOGS of what Acid?
A
  1. NALADIXIC ACID!
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3
Q

Fluoroquinolones: MOA

  1. What do they INHIBIT?
    a. What does this prevent happening?
  2. What else do they inhibit?
    a. What does this interfere with?
A
  1. DNA GYRASE
    a. Prevents relaxation of Positively Supercoiled DNA that’s needed for NORMAL TRANSCRIPTION and REPLICATION
  2. TOPO IV
    a. Separation of replicated chromosomes to Daughter cells
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4
Q

Fluoroquinolones: MOA (2)

  1. Bacteriostatic/cidal?
A
  1. Bactericidal!
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5
Q

Fluoroquinolones: Spectrum

  1. Work BEST against what?
    a. They also have good coverage for what?
  2. Antipseudomonal?
  3. It’s really good as a PROPHYLACTIC AGENT AGAINS WHAT?
    a. Which is the DOC?
  4. Not effective against what type of infections?
A
  1. AEROBIC G- RODS!
    a. GOOD G+ (includes MRSA and Penicillin Resistant S. Pneumoniae (Moxi and Gemi-)
  2. YES (Cipro-)
  3. ANTHRAX
    a. CIPRO
  4. ANAEROBIC INFECTIONS (except for Gemi-, Moxi-, and Trova- Floxacin)
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6
Q

Fluoroquinolones: Pharmacokinetics

  1. How do we take them?
    a. Decreased absorption with what 3 minerals?

b. Distribution?
2. CNS Penetration?

  1. How does the body get rid of them?
    a. Can be BLOCKED by what drug?
A
  1. ORAL
    a. Calcium, Magnesium, Iron (DONT TAKE WITH FOOD!)

b. Wide. Good Tissue Penetration. (PROSTATITIS: NORFLOX/OFLOX)
2. POOR

  1. KIDNEY
    a. by PROBENECID
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7
Q

Fluoroquinolones: Resistance

  1. Big thing (Think of mechanism)
  2. What else can happen?
A
  1. MUTATION (in DNA GYRASE Enzyme)

2. Decreased permeability of the Bacteria; Antibiotic Modification (Ciprofloxacin)

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8
Q

Fluoroquinolones: Adverse Effects

  1. BIG THING?
  2. What other 2 things are important to remember?
  3. CI in what?
A
  1. GI DISTURBANCES
  2. CARTILAGE EROSIONS, TENDON RUPTURE
  3. PREGGERS and CHILDREN (CARTILAGE DAMAGE) < 18 YEARS
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9
Q

Metronidazole: MOA

  1. Prodrug: What happens?
    a. Only found in whom?
  2. Metronidazole metabolites are taken up into what?
    a. Bacteriostatic/cidal?
A
  1. Non-enzymatically reduced by reacting with REDUCED FERREDOXIN
    a. FERREDOXIN only found in ANAEROBES!
  2. BACTERIAL DNA (make unstable molecules)
    a. Bacteriocidal!
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10
Q

Metronidazole: Spectrum

  1. WORKS REALLY WELL AGAINST WHAT type of Bacteria (aerobes or Anaerobes)?
    a. What specifically?
  2. Used best for Treatment of what?
  3. What else?
A
  1. ANAEROBES
    a. G- and G+ BACILLI (anaerobes)
  2. PSEUDOMEMBRANOUS COLITIS, abdominal infections (anaerobic or MIXED infections)
  3. H. Pylori eradication w/a multi-drug regimen
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11
Q

Metronidazole: Pharmacokinetics

  1. How is it taken?
  2. How does the body get rid of it?
A
  1. Oral, IV, Topical

2. Liver metabolism and Eliminated in the Urine

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12
Q

Metronidazole: Adverse RxNs

  1. What SUPERINFECTION?
  2. What else?
A
  1. Candida Superinfection!

2. GI, CNS and PNS toxicity, Hypersensitivity

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13
Q

Sulfonamides

  1. Oral, Parenteral drug?
  2. Topical? **
A
  1. Sulfamethoxazole + Trimethoprim, Co-trimoxazole, TMP-SMX (Bactrim)
  2. Silver Sulfadiazine (Burns) (Silvadene) (*JUST KNOW THAT ITS TOPICAL)
    * Trimethoprim is not a sulfonamide.
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14
Q

Sulfonamides: (Antimetabolite)

  1. They’re Antimetabolites: They compete with what?
    a. This is for incorporation into what?
    b. Bacteriostatic/Cidal?
A
  1. PABA
    a. into FOLIC ACID
    b. Bacteriostatic
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15
Q

Sulfonamides:

  1. Sulfamethoxazole
    a. What does it do?
  2. Trimethoprim
    a. Prevents REDUCTION of what?
    b. It’s essential for what?
  3. What’s the purpose of these 2 molecules?
A
  1. a. Competes with PABA in making Bacterial FOLIC ACID (unique step for BACTERIA)…we as humans have to get Folic Acid from our Diet
  2. a. of Dihydrofolate to Tetrahydrofolate
    b. It’s ESSENTIAL for 1 Carbon Transfer
  3. They have a SYNERGISTIC RELATIONSHIP!!
    a. Sulfonamides Compete with PABA at Dihydropteroate Synthase

b. Triethoprim inhibits Dihydrofolate Reductase (or competes there to prevent Dihydrofolic Acid from being converted to Tetrahydrofolic Acid)

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16
Q

Sulfamethoxazole + Trimethoprim, Co-trimoxazole, TMP-SMX (Bactrim) : SPECTRUM

  1. Bacteristatic or cidal?
    a. When is it the other one?
  2. What do Sulfa Drugs INHIBIT (What organisms)
A
  1. generally BACTERIOSTATIC
    a. In the URINARY TRACT, a BACTERICIDAL CONCENTRATION can be reached!
  2. G+ AND G-!
17
Q

Sulfamethoxazole + Trimethoprim, Co-trimoxazole, TMP-SMX (Bactrim)

  1. DOC for what INFECTIONS?
  2. Prophylaxis Tx for what?
A
  1. for UTI INFECTIONS (first attack) (Co-trimoxazole)

2. PNEUMOCYSTIS JIROVECI infections in CHILDREN and in AIDS Pts.

18
Q

Sulfamethoxazole + Trimethoprim, Co-trimoxazole, TMP-SMX (Bactrim): PHARMACOKINETICS

  1. How is it taken?
  2. Metabolized where?
  3. Freely cross what?
A
  1. ORAL (absorption is FAST). (Co-Trimoxazole is available for IV use but ONLY use in EXTREME SITUATIONS!)
  2. MAINLY in the LIVER as ACETYLATED PRODUCTS and Excreted mainly thru the KIDNEY!
  3. the Placenta and BBB
19
Q

Toxicities of SULFA Drugs!

  1. High rate of what? (2nd to what class of drugs)?
  2. Other MAJOR SIDE EFFECT?
  3. SULFA DRUGS SHOULD NOT be GIVEN to whom?!
    a. WHY?
A
  1. DRUG SENSITIVITY!: so ALLERGY. (PENICILLINS)
  2. STEVENS-JOHNSON SYNDROME
  3. to INFANTS less than 2 MONTHS of AGE; AVOID use near term or in nursing premature or jaundiced infants!
    a. Due to KERNICTERUS (Sulfonamides compete w/binding of BILIRUBIN to PLASMA PROTEINS)
    * NEONATES/Newborns: Dont use this and Phenicol (carbphenicol??maybe..)
20
Q

Sulfamethoxazole + Trimethoprim, Co-trimoxazole, TMP-SMX (Bactrim)

RESISTANCE

  1. 3 places (think of mechanisms)
A
  1. Increased production of essential Metabolite or Drug Antagonist (PABA)
  2. Active Efflux or Decreased permeability
  3. Alternate Metabolic Pathway for Synthesis of Essential Metabolite (PLASMID)
21
Q

Lipopeptide Antibiotics

  1. DAPTOMYCIN (CUBICIN)
    a. Type of Protein?
    b. Do they penetrate the BACTERIAL CYTOPLASM?

c. What does it do? (MOA)

A
  1. a. CYCLIC Lipoprotein
    b. NO!

c. Binds to BACTERIAL MEMBRANES and CAUSE a RAPID DEPOLARIZATION of the MEMBRANE POTENTIAL (leads to loss of membrane potential causing inhibition of Protein, DNA, and RNA synthesis –> Cell Death)

22
Q

Lipopeptide Antibiotics

  1. Daptomycin (Cubicin)
    a. Forms what kind of channels?
    b. What does this do?
A
  1. a. Transmembrane Channels

b. Leaks intracellular Ions and Depolarization to inhibit DNA, RNA, and Protein Synthesis!

23
Q

Lipopeptide Antibiotics

  1. Daptomycin: SPECTRUM
    a. Bacteriostatic or Cidal?
    b. Work against what bacteria types?
    c. Does resistance occur?
  2. Drugs of first choice before using Daptomycin?
A
  1. a. Bactericidal
    b. G+ (MRSA and MSSA: Concentration dependent); AEROBIC and ANAEROBIC
    c. RARE. No mechanism of resistance to Daptomycin has been identified.
    * NEVER A DRUG OF FIRST CHOICE due to its effects against MRSA and MSSA
  2. Penicillin (ase resistance) for STAPH, if that doesnt work, then Vancomycin, if that doesnt work, then Ceptaroline, Benozalid (sp? last lecture) and Daptomycin
24
Q

Lipopeptide Antibiotics

  1. Daptomycin: Pharmacokinetics
    a. How is it given?

b. Half Life?
c. How does the body get rid of it?
2. Use is suitable when?

A
  1. a. IV
    b. 8-9 hrs so only need ONCE DAILY DOSING!
    c. Kidneys.
  2. for EMPIRIC THERAPY in patients with SERIOUS G+ INFECTIONS (alternate to Vancomycin!)
25
Q

Lipopeptide Antibiotics: Mupirocin (Bactroban)

  1. Made from what?

a. What does it INHIBIT?
b. How?

  1. When is it given frequently?
A
  1. Pseudomonas Fluorescens
    a. PROTEIN and RNA SYNTHESIS!
    b. Reversible binding to Bacterial Isoleucyl-t-RNA SYNTHETASE! (Affecting TRANSLATION!!)
  2. BEFORE SURGERY (20% of peeps carry MRSA in their nose)
26
Q

Lipopeptide Antibiotics: Mupirocin (Bactroban)

  1. Spectrum
    a. Good against what?
    b. Bacteriostatic/cidal?
    c. How is it GIVEN?
A
  1. a. Good against G+ and some G-
    b. Bacteriostatic at LOW CONCENTRATIONS and Bactericidal at HIGH CONCENTRATIONS
    c. TOPICALLY to the skin or the nares
27
Q

Lipopeptide Antibiotics: Mupirocin (Bactroban)

  1. Tx
    a. Tx of what? This is caused by what?

b. INTRANASAL APPLICATION to patients who carry what?
c. Unique Mechanism, so it has little chance for what?

A
  1. a. IMPETIGO: S. Aureus, B-hemolytic Streptococci (including Streptococcus Pyogenes)
    b. MRSA
    c. for Cross-resistance with other Antibiotics
28
Q

Polypeptide Antibiotics

  1. What 2 did we talk about?
  2. They’re MOSTLY USED for what infections?
  3. MOA
    a. Polymyxin B binds to what? This binding does what?

b. Is it Bacteriostatic/cidal?
i. Exceptions?

c. NO EFFECT on what?

A
  1. Polymyxin B (know!) and Polymixin E
  2. G- INFECTIONS
  3. a. G- Bacterial CELL MEMBRANE PHOSPHOLIPIDS (Lipid A of ENDOTOXIN); it INCREASES permeability of the cell membrane causing LOSS of metabolites needed for bacterial existence
    b. Bactericidal against MOST G- BACILLI!
    i. Proteus and Neisseria Species
    c. in G+ (dont have ENDOTOXIN)
29
Q

Polypeptide Antibiotics

  1. Pharmacokinetics
    a. No use how?
    b. Binds very well to what?
    c. Excretion thru Kidney is what?
  2. Toxicity:
    a. BIG ONE!
  3. Use: How?
A
  1. a. No GI absorption (no oral use); Poor Parenteral use
    b. to Plasma Proteins
    c. SLOW
  2. a. NEPHROTOXICITY: so ONLY USE it TOPICALLY!!
  3. Topical in combination with Neomycin and Bacitracin; and topical application to Wounds, burns, etc (Pseudomonas Infections) and the Eye.

Pharm 2 Part 3: Chemotherapy and Antibiotics and Antifungals (7 decks)

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