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GS Pharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

Antibiotic Mechanisms of Action

A
  1. Distruption of bacterial cell walls
  2. Interference with cell membrane
  3. Inhibition of protein synthesis
  4. Agent that binds to 30S ribosomal subunit
  5. Agent that affects nucleic acid metabolism
  6. Antimetabolites
  7. Nucleic acid which binds viral enzyme
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2
Q

Bacteriostatic

A

temporarily inhibits growth of microorganism

allows body’s immune system to build up and fight for itself

can often be bacteriocidal when two are combined, but a bacteriocidal and bacteriostatic together tend to antagonism each other

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3
Q

Bacteriocidial

A

causes death of microorganism

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4
Q

Narrow Spectrum

A

acts on only a single or limited group

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5
Q

Extended Spectrum

A

are effective against gram positive and a significant number of gram negative bacteria

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6
Q

Broad Spectrum

A

affect a wide variety of species, usually a 3rd or 4th generation antibiotic

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7
Q

Antibiotic Resistance Mechanisms

A
  1. Mutation
  2. Transduction
  3. Transformation
  4. Conjugation
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8
Q

Host Factors

A
  1. Age
  2. Genetic factors
  3. Pregnancy
  4. Drug allergies
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9
Q

Common Misuses of Antibiotics

A
  1. tx of untxable infection
  2. therapy of fever of unknown origin
  3. improper dosages
  4. reliance on drugs w/o surgical drain
    • i.e. not draining an abcess
  5. lack of adequate bacteriological info
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10
Q

DNA replication antibiotic inhibitors

A
  • nalidixic acid
  • quinolones
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11
Q

DNA-dependent RNA polymerase antibiotic inhibitors

A

Rifampin

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12
Q

Protein Synthesis Antibiotic Inhibitors (50S)

A
  • Erythromycin
  • Chloramphenicol
  • Clindamycin
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13
Q

Protein Synthesis Antibiotic Inhibitors (30S)

A
  • Tetracycline
  • Spectinomycin
  • Streptomycin
  • Gentamicin
  • Tobramycin
  • Amikacin
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14
Q

Cell Membrane Antibiotic Antagonists

A

polymyxins

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15
Q

Folic Acid Metabolism Antibiotic Inhibitors

A
  • Trimethoprim
  • Sulfonamides
  • PABA
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16
Q

Cell Wall Synthesis Antibiotic Inhibitors

A
  • Cycloserine
  • Vancomycin
  • Bacitracin
  • Fosfomycin
  • Penicillins
  • Cephalosporins
  • Monobactams
  • Carbapenems
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17
Q

Stepromycin Mechanism of Action

A

changes shape of the 30S rRNA & causes mRNA to be read incorrectly

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18
Q

Chloramphenicol Mechanism of Action

A

binds to 50S of rRNA & inhibits formation of peptide bonds

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19
Q

Erythromycin Mechanism of Action

A

binds to 50S rRNA & prevents movement along mRNA

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20
Q

Tetracycline Mechanism of Action

A

interfers with tRNA anticodon reading of mRNA

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21
Q

Aminoglycoside Structure

A

compounds containing amino sugars joined to a hexose nucleus in glycosidic linkage

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22
Q

Members of Aminoglycoside Class

A
  • Streptomycin
  • Neomycin
  • Gentamycin
  • Tobramycin
  • Amikacin
  • Netilmicin
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23
Q

Streptomycin

A
  1. tx of TB: po with Isoniazid
  2. tx of plague (Yersinia pestis): alone
  3. tx of tularemia (Franscisiella tularensis): alone
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24
Q

Neomycin

A

usually topical in dermatological or opthalmic preparations

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25
Gentamycin
commonly used for treating Proteus (probacteria, usually causes UTI), Pseudomonas, and Serratia (gram- GI bacteria)
26
Tobramycin
similar spectrum to Gentamycin, but more effective against Pseudomonas
27
Amikacin
semi synthetic similar to Gentamycin used for resistant cases of Serratia
28
Netilmicin
semisynthetic newest to class (1983!!!) broad spectrum
29
Aminoglycoside Mechanism of Action
inhibit protein biosynthesis irrevesibly bind to 30S subunit of rRNA and induce misreading of mRNA the wrong amino acids get incorporated into proteins rapidly BACTERIOCIDAL
30
Aminoglycoside Spectrum of Activity
* effective against most gram negative aerobic bacteria * anaerobic bacteria are generally resistant * transport across membrane is oxygen dependent * Resistance: * failure to permeate membrane * low affinity to rRNA * inactivation by microbial enzyme
31
Aminoglycoside Pharmacokinetics
poorly absorbed in GI tract due to polycationic structure usually administered IV or IM largely excluded from most cells do not penetrate CNS high levels found in kidneys more active in alkaline environments
32
Aminoglycoside Toxicity
* hypersenitivity is not common * Neuromuscular blockade * ralated to rapid administration of high doses * more common in Parkinsons, MS, uremic, & those on tubourarine * acute muscular paralysis & apnea * reversed w/Ca or neostigimine * Ototoxicity * sustained blood levels \>2 weeks * Kanamycin, Amikacin, & Tobramycin are cochleotoxic * Streptomycin & Gentamycin are vestibulotoxic * IRREVERSIBLE * Nephrotoxicity * Gentamycin most so * increased when also given cephalosporins * REVERSIBLE
33
Chloramphenicol
* no longer used due to toxicity * Mechanism: BACTERIOSTATIC, reversibly binds to 50S rRNA, suppresses peptidyl transferase activity * \*\*also inihibts mitochondrial protein synthesis in mammalian cells, esp. blood * variable activity against gram + & - aerobic bacteria & most anaerobic bacteria * Resistance through plasmid * good distribution, crosses to CNS & placenta * metabolized in liver, excreted in urine * TOXICITY: aplastic anemia, Gray baby syndrome (cardiovascular colapse-\>death), neurological damage if long term use
34
Eythromycin Chemistry
lactone ring and 1 or more deoxy sugars macrolide antibiotic isolated from Streptomyces erytheus
35
Erythromycin Mechanism
inhibits bacterial protein synthesis at 50S subunit BACTERIOSTATIC small peptides are produced normally, but highly polymerised homopepetides are suppressed high doses are BATERIOCIDAL
36
Erythromycin Pharmakinetics
* po administration in stearate or succinate salt form * passes to all but CNS * metabolized in liver through cytochrome p-450 system * interfers w/ secondary metabolism * grapefruit juice also activates pathway and will slow metabolism of drug * half-life= 1.6 hours
37
Erythromycin Spectrum
* gram + bacteria, including soem of those resistant to PCN * safe for those allergic to PCN
38
Erythromycin Toxicity
* GI disturbances * allergic rxn, including jaundice * increased levels of SGOT, SGPT, alkaline phosphatase & bilirrubin * Eosinophilia
39
Clindamycin Chemistry
derivative of amino acid trans-L-4-n-propylhygrinic acid attached to a sulfur containing derivative of an octose derivative of lincomycin, less side effects
40
Clindamycin Mechanism
inhibits protein synthesis by binding to 50S rRNA blocks peptide synthesis same as Erythromycin BACTERIOSTATIC
41
Clindamycin Pharmacokinetics
* po or parenteral * rapidly & completely absorded * widely distributed * does not penetrate CNS * excreted in urine & bile * metabolized in liver to inactive sulfoxide
42
Clindamycin Specrum
* anaerobic infections in combo w/ aerobic bacteria * gram+ coccal infections * all aerobis gram - are resistant
43
Clindamycin Toxicity
* pseudomembraneous colitis * hepatotoxicity: elevated SGOT & SGPT * Stevens-Johnson Syndrome * severe skin & mucous membrane rxn * treated w/ corticosteriods
44
Spectinomycin Chemistry
produced by Streptomyces spectabilis
45
Spectinomycin Mechanism
inhibition of protein synthesis binds to 30S rRNA BACTERIOSTATIC
46
Spectinomycin Pharmacokinetics
IM administration urine excretion complete in 48 hours
47
Spectinomycin Spectrum
active against Gram - bacteria less effective than other agents readily inhibits gonococcal organisms usually given to those that do not respond to PCN G
48
Spectinomycin Toxicity
none really hives, chills, fever, nausea, insomnia, or dizziness
49
Dalfopristin/ Quinupristin (Synercid)
* 70:30 (D:Q) mix of two streptogramin antibiotics * Mechanism: 50S rRNA binding, alters the exit site, inhibits tRNA synthetase * each are BACTERIOSTATIC, but together are BACTERIOCIDAL * Spectrum: gram + organisms resistant to Vancomycin (VRE) * 0.8 hour half-life * hepatic elimination * toxicity: rare hepatotoxicity, hyperbilirubinemia, GI, pseudomembraneous colitis * interacts w/ CYP3A4 * use ONLY for Enterococcus faecium VRE
50
Linezolid (Zyvox)
* OXAZOLIDINONE * totally synthetic * Mechanism: binds to 50S rRNA, interferes w/ assembly of the P site * Spectrum: Gram + (0.5-4mg/L), Gram - (2-26mg/L), Legionella * absorbed completely & rapidly w/ good distribution including CNS * metabolism: slow, non-enzymatic, no interactions, produces 2 inactive carboxylic acid derviatives * 35% cleared by kidneys, 10% in feces * half-life= 5 hours * Adverse effects: GI, MAO inhibition
51
Tetrahydrofolic acid
coenzyme in the synthesis of purine bases & thymidine needed for cell growth & replication
52
Sulfonamide Chemistry
* first effective antibacterial, before 1940 * contain a derivative of sulfanilamide * p-amino group is essential for antibacterial activity
53
Sulfonamide Mechanism
competitive antagonism between p-ABA & sulfonamide prevent normal utilization of p-ABA by bacterial Bacterial cells are impermeable to folic acid & synthesize it from p-ABA
54
Sulfonamide Spectrum
broad spectrum gram + cocci & bacilli a few gram - topical sulfonamides are used for conjunctivitis due to gram + cocci today, generally limited to UTI
55
Sulfonamide Pharmacokinetics
po administration metabolized in liver potential for kidney stone formation wide distribution, including CNS, pleural, peritoneal, synovial, & ocular cavities
56
Sulfonamide Toxicity
* drug fever * hypersensitivity rxns * blood dyscrasis, agranulocytosis, aplastic anemia, hemolytic anemia, granulocytopenia * jaundice * renal damage due to stones * photosensitivity
57
Trimethoprim Chemistry
a trimethoxybenzylpyrimidine
58
Trimethoprim Mechanism
inhibits dihydrofolate (DHF) reductase, used for the conversion of folic acid to folinic acid 10,000 times more effective on bacterial enzyme than human enzyme Synergistic effect with sulfonamides
59
Trimethoprim Pharmacokinetics
usually given po combo w/ sulfamethoxazole cen be IV high absorbance in gut wide distributiuon including CNS excreted in urine within 24 hours
60
Trimethoprim Spectrum
UTI
61
Trimethoprim Toxicity
* megaloblastic anemia, leukopenia, granulocytopenia due to folic acid interference * GI disturbances * drug fever * renal damage * CNS disturbances
62
Co-Trimoxazole
combination of trimethoprim & sulfamethoxazole w/ similar action to sulonamides but with a broader spectrum
63
Sulfasalazine
used for treatment of IBD (UC or Crohn's) Gut bacteria split this compound into sulfapyridine & 5-amino-salicylic acid
64
Quinolone Members
* Nalidixic acid * Norfloxacin * Ciprofloxacin * Levofloxacin * Gatifloxacin * Mxifloxacin * Gemifloxacin
65
Quinolone Mechanism
DNA gyrase inhibitors prevent the resealing of opened strands of DNA BACTERIOCIDAL do NOT affect human/host cells
66
Quinolone Pharmacokinetics
variably absorbed after po administration food delays absorption Mg & Al decrease extent of absorption eliminated through renal & biliary excretion 30-45% excreted by urine within 24-48 hours
67
Quinolone Spectrum
* very high activity against Gram - pathogens * good against Staph & moderate against Strep * no activity against gram+ bacteria * majority of pathogens resistant to beta-lactams can be treated with fluoroquinolones * reccomended for lower RTI, UTI, skin, bone and joint infections * do NOT use during pregnancy, lactation, or periods of growth
68
Quinolone Toxicity
Gi disturbances rarely hypersensitivity

GS Pharmacology (4 decks)

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