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GS Pharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

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
Q

Gentamycin

A

commonly used for treating Proteus (probacteria, usually causes UTI), Pseudomonas, and Serratia (gram- GI bacteria)

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26
Q

Tobramycin

A

similar spectrum to Gentamycin, but more effective against Pseudomonas

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27
Q

Amikacin

A

semi synthetic

similar to Gentamycin

used for resistant cases of Serratia

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28
Q

Netilmicin

A

semisynthetic

newest to class (1983!!!)

broad spectrum

29
Q

Aminoglycoside Mechanism of Action

A

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
Q

Aminoglycoside Spectrum of Activity

A
  • 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
Q

Aminoglycoside Pharmacokinetics

A

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
Q

Aminoglycoside Toxicity

A
  • 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
Q

Chloramphenicol

A
  • 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
Q

Eythromycin Chemistry

A

lactone ring and 1 or more deoxy sugars

macrolide antibiotic

isolated from Streptomyces erytheus

35
Q

Erythromycin Mechanism

A

inhibits bacterial protein synthesis at 50S subunit

BACTERIOSTATIC

small peptides are produced normally, but highly polymerised homopepetides are suppressed

high doses are BATERIOCIDAL

36
Q

Erythromycin Pharmakinetics

A
  • 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
Q

Erythromycin Spectrum

A
  • gram + bacteria, including soem of those resistant to PCN
  • safe for those allergic to PCN
38
Q

Erythromycin Toxicity

A
  • GI disturbances
  • allergic rxn, including jaundice
  • increased levels of SGOT, SGPT, alkaline phosphatase & bilirrubin
  • Eosinophilia
39
Q

Clindamycin Chemistry

A

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
Q

Clindamycin Mechanism

A

inhibits protein synthesis by binding to 50S rRNA

blocks peptide synthesis

same as Erythromycin

BACTERIOSTATIC

41
Q

Clindamycin Pharmacokinetics

A
  • po or parenteral
  • rapidly & completely absorded
  • widely distributed
  • does not penetrate CNS
  • excreted in urine & bile
  • metabolized in liver to inactive sulfoxide
42
Q

Clindamycin Specrum

A
  • anaerobic infections in combo w/ aerobic bacteria
  • gram+ coccal infections
  • all aerobis gram - are resistant
43
Q

Clindamycin Toxicity

A
  • pseudomembraneous colitis
  • hepatotoxicity: elevated SGOT & SGPT
  • Stevens-Johnson Syndrome
    • severe skin & mucous membrane rxn
    • treated w/ corticosteriods
44
Q

Spectinomycin Chemistry

A

produced by Streptomyces spectabilis

45
Q

Spectinomycin Mechanism

A

inhibition of protein synthesis

binds to 30S rRNA

BACTERIOSTATIC

46
Q

Spectinomycin Pharmacokinetics

A

IM administration

urine excretion complete in 48 hours

47
Q

Spectinomycin Spectrum

A

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
Q

Spectinomycin Toxicity

A

none really

hives, chills, fever, nausea, insomnia, or dizziness

49
Q

Dalfopristin/ Quinupristin (Synercid)

A
  • 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
Q

Linezolid (Zyvox)

A
  • 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
Q

Tetrahydrofolic acid

A

coenzyme in the synthesis of purine bases & thymidine needed for cell growth & replication

52
Q

Sulfonamide Chemistry

A
  • first effective antibacterial, before 1940
  • contain a derivative of sulfanilamide
  • p-amino group is essential for antibacterial activity
53
Q

Sulfonamide Mechanism

A

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
Q

Sulfonamide Spectrum

A

broad spectrum

gram + cocci & bacilli

a few gram -

topical sulfonamides are used for conjunctivitis due to gram + cocci

today, generally limited to UTI

55
Q

Sulfonamide Pharmacokinetics

A

po administration

metabolized in liver

potential for kidney stone formation

wide distribution, including CNS, pleural, peritoneal, synovial, & ocular cavities

56
Q

Sulfonamide Toxicity

A
  • drug fever
  • hypersensitivity rxns
  • blood dyscrasis, agranulocytosis, aplastic anemia, hemolytic anemia, granulocytopenia
  • jaundice
  • renal damage due to stones
  • photosensitivity
57
Q

Trimethoprim Chemistry

A

a trimethoxybenzylpyrimidine

58
Q

Trimethoprim Mechanism

A

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
Q

Trimethoprim Pharmacokinetics

A

usually given po

combo w/ sulfamethoxazole cen be IV

high absorbance in gut

wide distributiuon including CNS

excreted in urine within 24 hours

60
Q

Trimethoprim Spectrum

A

UTI

61
Q

Trimethoprim Toxicity

A
  • megaloblastic anemia, leukopenia, granulocytopenia due to folic acid interference
  • GI disturbances
  • drug fever
  • renal damage
  • CNS disturbances
62
Q

Co-Trimoxazole

A

combination of trimethoprim & sulfamethoxazole w/ similar action to sulonamides but with a broader spectrum

63
Q

Sulfasalazine

A

used for treatment of IBD (UC or Crohn’s)

Gut bacteria split this compound into sulfapyridine & 5-amino-salicylic acid

64
Q

Quinolone Members

A
  • Nalidixic acid
  • Norfloxacin
  • Ciprofloxacin
  • Levofloxacin
  • Gatifloxacin
  • Mxifloxacin
  • Gemifloxacin
65
Q

Quinolone Mechanism

A

DNA gyrase inhibitors

prevent the resealing of opened strands of DNA

BACTERIOCIDAL

do NOT affect human/host cells

66
Q

Quinolone Pharmacokinetics

A

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
Q

Quinolone Spectrum

A
  • 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
Q

Quinolone Toxicity

A

Gi disturbances

rarely hypersensitivity

GS Pharmacology (4 decks)

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