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Antibiotics > Antibiotics1 > Flashcards

Antibiotics1 Flashcards

1
Q

Penicillin

A

AB altering cell wall synthesis of bacteria

  • Bactericidal
  • Nautral: penicillin G,V
  • Penicillinase-restistant penicillin: oxacillin
  • Broad spectrum penicillins: aminopenicillins

Penetrate through cell wall of G+

  • G(-) could alter their porins –> resistance
  • Alter molecular structure of transpeptidase, impossible for B-lactam ring to bind = MRSA

Given with B-lactamase inhibitors, as the bacteria have B-lactamase which will cleave the B-lactam ring and inhibit the AB

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2
Q

Carbapenems

A

Altering cell wall synthesis of bacterie

  • Broad spectrum, against multiresistant bacteria
  • Anaerobic bacteria
  • Highly resistant against most B-lactamases

Imipenem, meropenem

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3
Q

Cephalosporins

A

Altering the cell wall synthesis of bacteria

B-lactam ring and a 6-member ring, the latter makes it more resistant to B-lactamases.

I: bactericide against most G+ cocci = Cefazolin

II: increased activity against G(-) rods, but are active against some G+ bacteria too = cefuroxim

III: used against MDR aerobic G(-) organisms causing pneumonia, meningitis, sepsis and UTI = Ceftriaxone

IV: extended spectrum 3 genereation = Cefepime

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4
Q

Monobactams

A

Altering the cell wall synthesis of bacterie

  • Aztreonam
  • Limited application: G-
  • B-lactam ring is alone
  • Binding to the PBP-3 receptor of G(-) bacteria
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5
Q

Bactericin polypeptide

A

inhibits transfer of NAG-NAM

  • Mainly G+
  • Local infections as they are quite toxic
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6
Q

Tetracyclin

A

Altering the protein synthesis of bacteria
- Bacteriostatic
- Inhibit binding of aminoacyl-tRNA to the 30S subunit of the ribosome
- Doxocyclin: broad spectrum
- Toxicity: deposition in developing teeth –> discoloration
- effective treatment against Chlamydia, mycoplasma and Rickettsia
Form complexes with Ca2+ –> dont drink milk

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7
Q

Aminiglycosides

A

Altering the protein synthesis of bacteria

  • Bactericidal
  • inhibit protein synthesis by effecting the translocation
  • streptomycin and gentamycin
  • need to diffuse across the cell wall and is therefore used together with penicillin
  • toxic effect on the kidney
  • ineffective against anaerobes because their transport into the bacteria require O2
  • useful for G+ infections
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8
Q

Chloramphenicol

A

Altering the protein synthesis of bacteria
- Bacteristatic
- Act on the 50S R
- inhibit peptidyl transferase and thereby block the attatchment of AA to the nascent peptide chain
Has rare, but severe side effects (BM toxicity)

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9
Q

Macrolides

A

Altering the protein synthesis of bacteria

  • Bacteriostatic
  • Inhibition of the binding of tRNA by binding of 23S rRNA blocking polypeptide elongation (EF-2)
  • Erythromycin, clintamycin
  • Most G(-) bacteria are resistant
  • Little toxicity
  • Effective against i.c. living bacteria, anaerobic streptococci and campylobacter
  • Also: mycoplasma and Legionella
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10
Q

Lincosamides

A

Altering the protein synthesis of bacteria

  • Block protein elongation by inhibition of the binding of tRNA
  • CLINDAMYCIN
  • useful against G(-) and g+ bacteria
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11
Q

Linezolid

A

Altering the protein synthesis of bacteria
- Bacteriostatic
- Inhibit formation of the 70S initiation complex
- Against G+ cocci
Works against MRSA and VRE

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12
Q

Streptogramins

A

Altering the protein synthesis of bacteria

  • Bactericidal
  • inhibit peptidyl transferase on 50S
  • Quentipristin + dalfopristin –> act synergistically
  • Works against gram + cocci and MRSA
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13
Q

Glycopeptides

A

AB drugs altering the membrane functions

  • Site of action: membranes, periplasmic space
  • Target: permeability, cell wall
  • Mechanism: inhibit peptidoglycan synthesis by binding to D-Ala-D-Ala preventing the binding of enzyme (transpeptidase), thereby preventing the addition of new unit to the peptidoglycan (inhibit cross-linking)
  • Bactericidal
  • Only for G+ bacteria
  • MRSA therapy
  • VANcomycin and Teicoplasmin

VRE: have D-ala-D-lactate = vancomycin cant bind

VRSA

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14
Q

Polypeptides

A

AB drugs altering the membrane functions
- Site of action: membranes, periplasmic space
- Target: permases, peptidases
- Mechanism: binding to membrane protein enzymes (i.e. PL) procuding increased permeability of the cell and eventually cell death
- Bactericidal
- Against G- rods
Capable of causing serious nephrotoxicity so their use is limited to external treatment of localized infections e.g. external otitis, eye infections and skin infections

  • POLYMYXIN/Colistrin: used in life-threatening conditition
  • BACITRACIN: superficial skin infections
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15
Q

Daptomycin

A

AB drugs altering the membrane functions

  • depolarizes the cell membrane
  • Against G+ bacteria, as G(-) are naturally resistant
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16
Q

Quinolones and Fluoroquinolones

A

Alter the DNA synthesis of bacteria

  • Site of action: cell nucleoid
  • Mechanism: inhibition of bacterial DNA topoisomerase II (gyrase) or topoisomerase IV which are required for DNA replication, recombination and repair
  • Quinolones (O.generation) highly protein bound, bacteristatic moisstly used in UTIs against Gram (-) bacteria
  • Fluoroquinolones: not highly proteins bound
  • Bacteriostatic
    1st gen: NORFLOXACIN: g-, enteric tract bacteria, UTI and enteritis

2nd gen: CIPROFLOXAciN: G- bacteria. Against pseudomonas. UTI, gI and resp infections

3rd gen: gram - and +
- Good tissue penetration –> systemic infections
LEVOFLOXACIN

4th gen: MAXIFLOXACIN - gram + and -, anaerobic, good tissue penetration

Resistance by mutation of the gyrase enzyme
Damage the liver
Should not be given to children or pregnant –> can damage growing bone and cartilage

17
Q

Rifampicin

A

Alter the DNA synthesis of bacteria

  • site of action: mesosom-ribosome complexes
  • mechanism: inhibitiron of RNA synthesis by inhibiting the DNAdep. RNA polymerase
  • Bactericidal for mycobacterium
  • Active against gram + cocci
  • used for treatment and prevention of meningococcus
  • Broad spectrum
18
Q

Metronidazole

A

Alter the DNA synthesis of bacteria

  • Also against anaerobes and fungi
  • Activated in the host cells where cytotoxic substances will disrupt the host DNA
  • Bactericidal
  • higher concentration or longer treatment is toxic
19
Q

Sulphonamide (PABA)

A

Alter the DNA synthesis of bacteria

  • Target: folic acid synthesis
  • Mechanism: competitive inhibition of para-amino-benoic acid utilization
  • Bacteriostatic
20
Q

Trimethoprim

A

Alter the DNA synthesis of bacteria

  • Target: folic acid synthesis
    Mechanism: inhibit dihydrofolate reductase
  • Bactericidal
21
Q

Combination of trimethoprim and sulphonamide

A

Alter the DNA synthesis of bacteria

  • good activity against g- and g+ bacteria
  • 2 drugs act synergistically
  • MRSA
  • toxicity: upset GI, hemopoietic disorder, rash
  • SMX: TMP -> 5:1 ration

Antibiotics (5 decks)

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