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Pharm 2 Part 3: Chemotherapy and Antibiotics and Antifungals > Pharm: L28: Aminoglycosides & Broad Spectrum Antibiotics > Flashcards

Pharm: L28: Aminoglycosides & Broad Spectrum Antibiotics Flashcards

1
Q
  1. Aminoglycosides: Do what?
  2. Tetracyclines: Do what?
  3. Chloramphenicol: Does what?
A
  1. Blocks Initiation of TRANSLATION and causes the misreading of mRNA
  2. Blocks the Attachment of tRNA to the Ribosome
  3. Prevents Peptide Bonds from being formed
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2
Q

AMINOGLYCOSIDES

  1. What are the 5? (STANG)
A
  1. STREPTOMYCIN
  2. Tobramycin
  3. Amikacin
  4. Neomycin
  5. Gentamicin
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3
Q

AMINOGLYCOSIDES

  1. Streptomycin: What does it do?
  2. Tobramycin: What does it do?
  3. Amikacin: What does it do?
  4. Neomycin: What does it do?
  5. Gentamicin: What does it do?
A
  1. Tuberculosis, 2nd Line Agent: IV/IM
  2. G-, Combo, IV/IM, Topical
  3. G-, Combo, IV/IM
  4. Oral, Topical-Oral, Topical
  5. G-, Combo, IV/IM, Topical
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4
Q

AMINOGLYCOSIDES (2)

  1. What do all of these Antibiotics contain?
    a. Their POLARITY is RESPONSIBLE for what?
A
  1. Amino Sugars in Glycosidic Linkage (Aminoglycosidic Antibiotics)
    a. for their PHARMACOKINETIC PROPERTIES (Absorption, distribution, etc)
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5
Q

AMINOGLYCOSIDES (3): MOA

  1. How do they work?
  2. Bacteriostatic/-cidal?
A
  1. IRREVERSIBLY INHIBIT PROTEIN SYNTHESIS (inhibit 30S) **KNOW THIS (It will be ON THE TEST!!!) (it’s a very important feature…only one that Irreversibly binds)
  2. BACTERICIDAL
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6
Q

AMINOGLYCOSIDES: Active Transport and O2

  1. To be effective, Aminoglycosides first must be what?
    a. Under what conditions are aminoglycosides BACTERICIDAL?
A
  1. ACTIVELY TRANSPORTED (O2 requiring process) into susceptible bacteria and bind to the Bacterial 30S subunit to produce non-functional 30S initiation complex
    a. Under AEROBIC CONDITIONS. (not effective against anaerobic species)
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7
Q

AMINOGLYCOSIDES: Spectrum and Use

  1. What spectrum is it?
  2. Uses
    a. Streptomycin
    b. Gentamicin/Tobramycin/Amikacin
    c. Neomycin and Gentamicin
  3. Enterococci (Gram+ Cocci): DOC? (NEED TO KNOW)
  4. P. Aeruginosa: DOC? (NEED TO KNOW)
A
  1. AEROBIC G- ENTERIC BACTERIA (RODS) (usually combined w/beta-lactam antibiotics), or when there’s a SUSPICION OF SEPSIS OR ENDOCARDITIS
  2. a. Tb, Bubonic Plague, Tularemia, and Endocarditis (when given along w/other agents: Combined therapy)
    b. Effective against P. AERUGINOSA
    c. Topical application of Wounds and Burns caused by Gram-Negative Organisms
  3. AMINOGLYCOSIDE + PENICILLIN (why? Cuz Aminoglycoside can’t get in w/o Penicillin)
  4. AMINOGLYCOSIDE + ANTIPSEUDOMONAL PENICILLIN
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8
Q

AMINOGLYCOSIDES

  1. Concentration-Dependent Killing: What does this mean?
A
  1. Increasing Concentrations Kill an increasing population of Bacteria, and at a More Rapid Rate (MIC: b/w 4 and 63. By 64 MIC, it takes under 2 hrs)
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9
Q

AMINOGLYCOSIDES

  1. Post-Antibiotic Effect
    a. They have a Significant what?

b. Antibacterial Activity Persists beyond the time of what?
c. What is more effective: SINGLE LARGE DOSE or MULTIPLE SMALLER DOSES and why?

A
  1. a. PAE
    b. that the Antibiotic is Measurable
    c. SINGLE LARGE DOSE cuz it REDUCES the TOXIC SIDE EFFECTS
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10
Q

AMINOGLYCOSIDES: Toxicity

  1. What are the 2 MAJOR TOXIC EFFECTS?
A
  1. OTOTOXICITY and NEPHROTOXICITY!
    * VERY Toxic, Need a High Concentration to be effective, but because the have a PAE (Post something Effect) you can use them ONCE DAILY at a safe dose, and may still see side effects but not anything that will be killing.
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11
Q

AMINOGLYCOSIDES: Pharmacokinetics

  1. How are they given?
  2. None is absorbed adequately after what?
  3. None Penetrates what readily?
  4. Normal kidney does what?
A
  1. IM or IV, and Topical
  2. after Oral Administration (not absorbed thru GI tract; 3% for Neomycin)
  3. CSF
  4. rapidly excretes all.
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12
Q

AMINOGLYCOSIDES

  1. CROSS RESISTANCE
    a. Bacteria that ACQUIRE RESISTANCE to one Aminoglycoside may EXHIBIT what?
  2. RESISTANCE
    a. Deficiency of what?
    b. Lack of Permeability of what?
    c. Enzymatic Modification by what?
  3. AMINOGLYCOSIDES are USED MOSTLY in what?
A
  1. a. CROSS-RESISTANCE to the other Aminoglycosides
  2. a. of Ribosomal Receptors
    b. of the drug molecule into the bacteria
    c. by the bacteria
  3. in COMBINATION with other Antibiotics
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13
Q

Broad Spectrum Antibiotics

  1. What 3 are there?
A
  1. Chloramphenicol
  2. Tetracyclines
  3. Glycylcyclines
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14
Q

Broad Spectrum Antibiotics

  1. Chloramphenicol
    a. Isolated from what?

b. It has the distinction of being the first and probably the only commercially successful synthetic antibiotic of Major Significance. However, IT’s ASSOCIATED WITH What?

A
  1. a. from Streptomyces Venezuelae in 1947 (soil sample)

b. FATAL APLASTIC ANEMIA, and OTHER SERIOUS and POTENTIALLY FATAL SIDE EFFECTS

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15
Q

Broad Spectrum Antibiotics

  1. Chloramphenicol (MOA)
    a. What does it do?

b. Bacteriostatic/-cidal?
2. Chloramphenicol can also INHIBIT what?
3. Many of the Adverse Effects of Chloramphenicol, including Dose Dependent Bone Marrow Depression and Gray Baby Syndrome Appear to be a result from INHIBITION of what?

A
  1. a. reversibly binds the 50S Subunit and prevents attachment of the AA containing end of the Aminoacyl-tRNA to the acceptor site on the ribosome. Thus, PROTEIN SYNTHESIS IS INHBITIED
    b. BACTERIOSTATIC (but it can be bacteriocidal against certain common meningeal pathogens like H. Influenzae, N. Meningitidis, Streptococcus Pneumoniae at therapeutic concentrations
  2. MITOCHONDRIAL PROTEIN SYNTHESIS IN MAMMALIAN CELLS (perhaps cuz mitochondrial ribosomes resemble bacterial ribosomes (both are 70 S) more than they do the 80 S Cytoplasmic Ribosomes of Mammalian Cells
  3. of PROTEIN SYNTHESIS in HOST MITOCHONDRIA
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16
Q

Broad Spectrum Antibiotics

  1. Chloramphenicol: Spectrum
    a. What is it?
  2. Therapeutic Use
    a. First choice? Why?

b. Main use?

A
  1. BROAD: Gram -, Gram +, Anaerobes, Aerobes, Atypicals (spirochetes, rickettsiae, chlamydiae)
  2. a. NO!. Restricted to Life Threatening Infections!
    b. BACTERIAL CONJUNCTIVITIS (TOPICAL)
    * Typhoid Fever, Meningitis, Ricksettsia, Brucellosis, Rocky Mountain Spotted Fever, Melioidosis
17
Q

Broad Spectrum Antibiotics

  1. Chloramphenicol: Pharmacokinetics
    a. Route once used in the US?
    b. Current Route?

c. Distribution? (KNOW THIS!!)
d. Metabolized in what?
e. Metabolite Excreted in what?

A
  1. a. Oral (No longer available due to APLASTIC ANEMIA)
    b. PARENTERAL ADMINISTRATION currently used
    c. Distributed widely in the body, to all tissues including EYES AND CNS (BEST CNS PENETRATION)!!!!
    d. in the LIVER (90%): CONJUGATED with GLUCURONIC ACID to form Chloramphenicol Glucuronate, an inactive metabolite
    e. in the KIDNEY
18
Q

Broad Spectrum Antibiotics

  1. Chloramphenicol: Toxicities

a. Hematopoietic Problems:
i. Dose Dependent?
ii. Dose Independent?

b. Gray Baby SYNDROME in infants?
c. What else?

A
  1. a. i. BONE MARROW SUPPRESSION: Anemia, leukopenia, thrombocytopenia; Reversible upon discontinuation of Chloramphenicol
    ii. FATAL APLASTIC ANEMIA (rare cases)
    b. Inadequate activity of Glucuronyl Transferase in the newborn liver
    c. Rash, angioedema, Urticaria, but rarely anaphylactic reactions
19
Q

Broad Spectrum Antibiotics

  1. Chloramphenicol: Resistance
    a. What is significant?

b. What enzyme is produced by the resistant organisms? What does it do?
c. Binding site may be what?
d. What else?

A
  1. a. Bacterial Resistance
    b. ACETYL TRANSFERASE; Acetylates and Inactivates Chloramphenicol
    c. Modified (Acetylated)
    d. Efflux Pumps
20
Q

Tetracyclines

  1. What 3 drugs are there?
A
  1. TETRACYCLINE
  2. Doxycycline
  3. Minocycline
21
Q

Tetracyclines

  1. At this time, how many are marketed in the US?
  2. Type of antibiotic?
A
  1. 5 Tetracyclines

2. BROAD SPECTRUM w/common chemical structure, mechanism of action, antibacterial activity and toxicity

22
Q

Tetracyclines: MOA

  1. INHIBITION of what?
  2. Bacteriostatic/-Cidic?
  3. Bind REVERSIBLY to what?
A
  1. of BACTERIAL PROTEIN SYNTHESIS
  2. Bacteriostatic
  3. to 30S RIBOSOMES
23
Q

Tetracyclines

  1. Spectrum: What is it?
  2. What 3 Organisms are Resistant to Tetracyclines
A
  1. Broad Spectrum: Gram -, Gram +, anaerobes, Aerobes, Atypicals (Spirochetes, Rickettsiae, Mycoplasma)
  2. B. Fragilis, Proteus (most strains); Pseudomonas (most strains)
24
Q

Tetracyclines: Therapeutic Use

  1. What is the Major DOC?
A
  1. Infections with CHLAMYDIA (as well as Azithromycin and Erythromycin)
25
Q

Tetracyclines: Resistance

  1. Resistance to tetracycline usually conferred by what?
  2. Tetracycline resistant strains may be susceptible to what 3 things?
A
  1. EFFLUX PUMPS

2. Doxycycline, Minocycline and Tigecycline: All of which are poor substrates for the Efflux Pumps

26
Q

Tetracyclines: Pharmacokinetics

  1. Absorption after what route of administration?
  2. Main thing: THEY CHELATE WHAT?
  3. Distribution is wide in all tissues EXCEPT?
  4. Tetracyclines DEPOSIT THEMSELVES in what?
  5. How does the body get rid of them?
    a. What about Doxycycline?
  6. Long Acting Tetracyclines (Doxycycline, and Minocycline) are what?
A
  1. After ORAL use is adequate but INCOMPLETE (D and M are much better)
  2. Ca2+ mainly.. (also Iron, Aluminum)
  3. CNS and Joints
  4. in BONE AND TEETH (chelate Ca2+)
  5. Liver metabolizes, and excreted primarily thru Urine and some thru bile
    a. not hepatically metabolized; Major route of Doxycycline excretion is via the FECES
  6. SLOWLY EXCRETED: Therefore have longer plasma half-life and require less frequent administration
27
Q

Tetracyclines: Adverse Reactions

  1. Changes?
  2. What 2 bad things?
  3. Tetracyclines SHOULD NOT BE GIVEN TO whom?
A
  1. NORMAL FLORA CHANGES (GI effects)
  2. BONE and TEETH
  3. PREGNANT WOMEN OR CHILDREN BELOW THE AGE OF 8 YEARS (Can cross the placenta to reach fetus and are also excreted in Breast Milk)
28
Q

Glycycyclines

  1. What drug?
  2. Route of administration?
  3. Binds to what?
  4. Bacteriostatic/-cidic?
  5. Spectrum of Activity of Tigecycline is what?
A
  1. Tigecycline
  2. IV ONLY
  3. 30S ribosomal subunits
  4. BACTERIOSTATIC
  5. SIMILAR to that of TETRACYCLINE, Doxycycline, and Minocycline; However, Tigecycline SHOWS ACTIVITY AGAINST TETRACYCLINE-RESISTANT ORGANISMS
29
Q

Glycycyclines

  1. Tigecycline has activity against a wide variety of RESISTANT PATHOGENS: What ones?
  2. How does the body get rid of it?
  3. Adverse Effects?
    a. MAIN ADVERSE EFFECT?
A
  1. MRSA, MRSE, PRSP, and VRE
  2. 2/3 of the dose is eliminated by Fecal; 1/3 by Renal Excretion
  3. Similar to Tetracyclines
    a. Nausea and Vomiting
30
Q

Clinical Use

  1. Adult Chlamydia: What drugs
  2. Neonate Chlamydia?
  3. Inflammatory Cojunctivitis w/Blepharitis?
A
  1. Doxycycline or Azithromycin
  2. Erythromycin
  3. Tetracycline or Doxycycline

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

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