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PHRM 865: Theraputics V > Lecture 11: Clindamycin, Tetracycline, Quinolones > Flashcards

Lecture 11: Clindamycin, Tetracycline, Quinolones Flashcards

Cushman's Section

1
Q

What is the Mechanism of action for clindamycin and compare it to erythromycin?

A
  • Similar to Erythromycin; Inhibits protein synthesis by binding to 50s - preventing movement to the A-site
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2
Q

What is the main clinical use of Clindamycin?

A
  • Gram (+): Strep & Staph
  • Gram (-): Bcteroides & Fusobacterium
  • TREATS bone infections with SA, Severe ance, vaginosis
  • IV Clinda with pyrimethamine Treats AIDS by Toxoplama gondii
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3
Q

What is the Main Side Effect that limits the its clinical use of Clindamycin?

A
  • Pseudomembranous Colitis and Diarrhea
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4
Q

What is the metabolic pathway of clindamycin and state the effects of metabolism on biological activity?

A
  • By CYP450 in the liver to Sulfoxide & N-demethylated Derivative
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5
Q

What is the absorption, distribution, and elimination of clindamycin?

A
  • Absorption: GI tract
  • Distribution: widely even in CNS
  • Elimination: Urine & Bile

Half Life of 1.5-5 h
May need to dose adjust

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6
Q

What are some of the adverse effects of clindamycin?

A
  • Diarrheaa, C. Diff, Nausea, Vomiting, Stomach Cramps, Rash
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7
Q

What is Psudomembranous Colitis and its signifiances?

A
  • Potentially Lethal Condition
  • An overgrowth of C. Diff in the colon that SHOULD be treated with Metro or Vanco
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8
Q

What is the reason that Tetracyclines SHOULD NOT be given with food that are rich in Calcium, or with other drugs that are rich in Calcium, or other heavy metals?

A
  • Tetracyclines WONT be absorbed with Calcium products
  • Should be given 1 hour before or 2 hours after
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9
Q

What is the preferred route of administration of the Tetracyclines?

A
  • ORAL
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10
Q

What is the reason that Children SHOULD NOT take Tetracycline during the period of permanent teeth formation?

A
  • Stain the Teeth –> Brown or Grey
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11
Q

What is Epimerization and what effect does it have on bioloigcal activity?

A
  • There is an elongation [amide group] that makes it inactive
  • Slow in steady state & rapid at pH4
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12
Q

What is the pH that tetracycline epimerization is most rapid and the relative rate of epmierizatin in the sild state vs in solution?

A
  • pH 4 = most rapid
  • SLOW in solid state [capsules]
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12
Q

What is Tetracycline Dehydration?

A
  • C-6 Group is antiperiplaner so a H- at C-5a kicks it off making a Methyl
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12
Q

What is the toxicity of Epianhydrotetracycline?

A
  • Toxic to kidneys
  • Produces Fanconi syndrome [failure of reabsorption in kidneys = malabsorption] which is FATAL
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13
Q

What is the why that there is selective toxicity of tetracyclines to bacteria BUT not the host?

A
  • Eukaryotic cells DONT have uptake mechanisms
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13
Q

What is the reason that Minocycline and Doxycycline lack the renal toxicity of Tetracycline?

A
  • Lack C-6 hydroxyl group
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13
Q

What is the way that the Tetracycline are cleaved under basic conditions?

A
  • Cleave at pH <8.5; lactone is inactive
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14
Q

What is the mechanism of action for the Tetracyclines?

A
  • Bind to 30s and inhibit synthesis by blocking tRNA to A-site = termination of chain growth
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15
Q

What is the Main Theraputic Use for Tetracyclines?

A
  • ACNE
  • Chlamydia, Rickettsia, Brucellosis
  • Anthrax, Plague, Tularemia, Leginonnarries
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16
Q

What is the main advantage of using tetracycline itself rather than on of the other antibiotics in the tetracycline class?

A
  • Generic and Inexpensive
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17
Q

What is the way that Demeclocycloine is more stable to dehydration than tetracycline?

A
  • Hydroxyl group at C-6 instead of tertiary hydroxyl group
  • Dehydrates slow because of secondary cation
18
Q

What is the reason that Minocycline and Doxycyline do not undergo dehydration?

A
  • Lacks C-6 hydroxyl group
19
Q

What is a unique toxicity for Minocycline in comparsion to the other Tetracyclines?

A
  • Vistibular Toxicities [Vertigo, Axtaxia, Nausea]
20
Q

What is the reason that Doxycycline is widely considered the Tetracycline of Choice?

A
  • NO 4 -epianhydrotetracycline toxicity AND fewer GI issues
21
Q

What is the reason that Tigecycline has no potential for 4-epianhydrotetracycline-mediated toxicity?

A
  • NO C-6 hydroxyl group
22
Q

What is the main theraputic use of Sarecycline and Omadacycline?

A
  • Mod to severe Acne
23
Q

Why sarecycline and omadacycline should not be given to pregnant woman and are not recommended during breast feeding?

A
  • Fetal harm
24
Q

What is the mechanism of action for Chlorapmhenicol?

A
  • Binds to 50s that is near for erythromycin and clindamycin
  • Inhibits the peptidyl transferase activity - blocking the action between P-site & A-site
25
Q

What is the relationship between Chlorampheicol sodium succinate and chloramphenicol?

A
  • Cholrampheicol sodium succinate is a PRODRUG for IV or IM that becomes Chloramphicol
26
Q

What is the main therpautic use of Cholrampheicol sodium succinate?

A
  • Meningitis, typhoid fever, rickettsial infections…
27
Q

What is the metabolism of chooramphenicol sodium succinate?

A
  • Hydrolyed in the liver??
28
Q

What is the solubility characteristics and ditribution of chlorapmphenicol?

A
  • Lipid soluble; remain unbound
  • Penetrates all tissues of the body even the brain
29
Q

What are the mechanism of resistance for chloramphenicol?

A
  • Reduced permeability
  • Mutation of 50s
  • Increase of Chloramphenicol Asetyltransferase
30
Q

What are some of the more serious toxicities of chloramphenicol and how it limits the use of it?

A
  • Aplastic Anemia; can be fatal
  • High risk with oral and low risk with eye drops
31
Q

How does the risk factor of Aplastic Anemia compare between Chloramphenicol Eye drop vs oral?

A
  • HIGHEST RISK orally and LOWEST RISK eye droply
32
Q

Is Chloramphenicol Bone Marrow Suppression a predictor for Aplastic Anemia?

A
  • NO
33
Q

What is the relationship between Chloramphenicol bone marrow suppression and cumulative dose?

A
  • Predictable once the cumulative does of 20g is given
34
Q

What is the relationship of Chloramphenicol-induced childhood leukemia and length of treatment with chloramphenicol?

A
  • Increased risk and Increased Length
35
Q

What are the drug interactions with Chloramphenicol?

A
  • Inhibits CYP450
36
Q

What is the effect that inflammation of the meninges has on the brain concentrations of Chloramphenicol?

A
  • Conc. are about 30-50% when NOT inflammed AND about 89% WHEN inflammed
37
Q

What is the core structure of the Quinolones?

A
  • Two 6 membered rings connected with a N at C-1
38
Q

What are some general characteristics of the 1st, 2nd, and 3rd generation Quinolones?

A
  • 1st: Good Gram (-); UTI [D/Cd]
  • 2nd: F at C-6 & Piperazine at C-7; Good Gram (+)
  • 3rd: Good Gram (+), even S. Pneumoniae
39
Q

What is the function of the Gyrases and Topoisomerases?

A
  • Untangling DNA by cutting ONE or TWO strands; passing them through
40
Q

What are the differences between topoisomerase I and II?

A
  • Topo I: Cuts ONE strand
  • Topo II: Cuts TWO strands
41
Q

What is the common mechanism for DNA Gyrase, Bacterial Topoisomerase IV and Mammalian Topoisomerase II?

A
  • G-segment binds to CAP region; T-segment comes into OPEN ATPase domain; ATP will CLOSE domain BREAKING the G-segment; passing T-segment through; Reconnecting G-segment; repeat
42
Q

What is the unwinding by the strand passage mechanism by DNA Gyrase, Bacterial Topoisomerase IV and Mammalian Topoisomerase II?

A
  • Basically grab open part and twist it 360 degress
43
Q

What is the theraputics uses of the Quinolones?

A
  • UTI [Cipro], Prostatitis [Cipro & Oflox], STI, GI infections [Cipro], Respiratory Tract…
44
Q

What is the main bacterial resistance mechansim to the Quinolones?

A
  • Decreased Permeability
  • Efflux pumps
  • Mutation of target enzymes
45
Q

What are the main features of Quinolones absorption, distribution and elimination?

A
  • Absorption: Readly absorb orally
  • Distribution: Widely
  • Elimination: Renally and Hepatically
46
Q

How is Ciprofloxacin metabolized?

A
  • Glucuronide at the 3-carboxyl position in the urine
47
Q

What are the main adverse effects of the Quinolones?

A
  • Nausea, Vomiting, Diarrhea
  • Headache, Dizziness
  • Rash

PHRM 865: Theraputics V (42 decks)

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