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Pharmacology > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Selective Toxicity

A
  • using toxic drugs as long as they are more toxic to your target than to normal tissues
    1. antimicrobial drugs
    2. anticancer drugs
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2
Q

Bactericidal vs Bacteriostatic Drugs

A
  • growth is arrested (e.g.. sulfonamides), success depends on an effective immune response
  • bacteria is killed (e.g. penicillins), use if the patient is immunosuppressed
  • explain in terms of eggs vs milk
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3
Q

Draw the structure of gram negative and gram positive cells, highlighting important features

A

-see antimicrobial lecture

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4
Q

Penicillin binding proteins catalyze which step of cell wall formation?

A

-transpeptidation-the creation of links between glycine and alanine

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5
Q

Transpeptidation inhibitors include… (3)

A
  • penicillins
  • carbapanems
  • cephalosporins
  • all beta lactams
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6
Q

What is the ‘attack strategy’ of penicillins?

A
  • bacteria have a rigid cell wall
  • they need this to survive and grow
  • its made up of a fibrous scaffold
  • the scaffold is assembled using enzymes
  • block the enzymes so the cell wall cannot be made properly (binds to the PBPs)
  • bacteria will not survive
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7
Q

What are the 2 potential problems of penicillin use?

A
  1. getting across the outer lipid membrane in gram neg bacteria –>porins
  2. interference by beta lactamases, cleave the beta lactam ring
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8
Q

There are different penicillins which differ in their…

A

-sensitivity to beta lactamases ‘
-pharmacokinetics
-spectrum of action
narrow spectrum-penicillin V
extended spectrum-amoxicillin

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9
Q

What can we do about beta lactamases?

A
  1. use a beta lactamase resistant antibiotic (eg. Nafcillin, penicillinase resistant)
  2. combine with a beta lactamase inhibitor (e.g. clavulanate, clavulin-amoxicillin and clavulanate)
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10
Q

Why are 4th gen cephalosporins better than 1st gen?

A
  • better activity against gram neg bacteria
  • better ability to cross into tissue spaces
  • generally more resistance to beta lactamases
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11
Q

Carbapanems

A
  • eg. Imipenem
  • penicillin like antibiotics in which the S atom is replaced with C
  • altered spectrum
  • resistant to beta lactamases
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12
Q

What are the 2 other major cell wall inhibitors besides penicillin?

A

Vancomycin-binds to the growing peptide chain, prevents subsequent ability to cross link
Bacitracin-a mixture of cyclic peptides, works inside the cell to block cell wall synthesis

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13
Q

What are the 4 different classes of drugs that block protein synthesis?

A
  1. chloramphenicol
  2. macrolides (erythromycin)
  3. aminoglycosides (gentamicin)
  4. tetracyclines (tetracycline)
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14
Q

Chloramphenicol

A

-binds to the 50s subunit and inhibits formation of peptide bond
-broad spectrum, active against many types of bacteria
-bacteriostatic
Problems:
-bone marrow disturbances
-common interactions with other drugs
-gray baby syndrome

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15
Q

Macrolides (‘omycin’)

A
  • work best against gram positive bacteria

- bacteriostatic

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16
Q

Erythromycin

A
  • binds to 50s portion
  • prevents translocation-movement of ribosome along mRNA
  • unstable in acid conditions
  • food reduces absorption
  • useful in penicillin resistant infections
17
Q

Clarithromycin

A
  • has an additional methyl group compared to erythromycin
  • improved acid stability
  • improved oral absorption
18
Q

Azithromycin

A
  • has an additional lactone ring compared to erythromycin
  • excellent tissue penetration
  • longer half life
  • best activity against gram neg anaerobes
  • also acts against spirochetes
  • less likely to be involved in drug interactions
19
Q

Aminoglycosides (streptomycin and gentamicin)

A
  • changes shape of 30s
  • used against gram negative enteric bacteria
  • oral doses poorly absorbed (given intramuscularly, by IV)
  • ototoxic and nephrotoxic
  • have a hexose ring
20
Q

Aminoglycosides cause (3)…

A
  1. block formation of initiation complex
  2. miscoding
  3. block of translocation
21
Q

Tetracyclines

A
  • broad spectrum
  • bacteriostatic
  • resistance is common
  • chelate divalent cations (Ca)
  • cause GI irritation
22
Q

What is the MOA of tetracyclines?

A

-interfere with attachment of tRNA to mRNA ribosome complex

23
Q

If macrolides, tetracyclines and aminoglycosides all block protein synthesis in bacteria, why are they different in use? (2)

A
  1. Different chemically -affects stability and absorption

2. Interfere at different sites on the ribosome-different therapeutic actions

24
Q

Draw the folic acid synthesis pathway with the drugs that effects the pathway

A

-antimicrobial drugs

25
Q

Fluoroquinolones

A

eg ciproflaxin

-inhibition of DNA gyrase (topo II), needed for uncoiling DNA

26
Q

Polymyxins

A
  • molecule has detergent like properties
  • binds to PE in cell membrane
  • causes disruption of the bacterial cell membrane
27
Q

What are the advantages and disadvantages of polymyxins?

A

Disadvantages-human cells have PE, toxic if given systemically
-used topically
Advantages-resistance rarely develops, hypersensitivity is rare

28
Q

What are the advantages of using antimicrobial drugs in combinations? (3)

A
  • wider spectrum
  • reduced dose
  • synergism
29
Q

What are the disadvantages of using antimicrobial drugs in combinations?

A
  • increased possibility of adverse reactions
  • antagonism between antibiotics
  • greater risk of antibiotic resistance
30
Q

Septra

A
  • sulfamethoxazole=bacteriostatic
  • trimethoprim-bacteriostatic
  • synergistic
  • septra=bactericidal
31
Q

What are 4 mechanisms of antibiotic resistance?

A
  1. altered site
  2. enzymatic degradation
  3. bypass pathway
  4. decreased entry
  5. efflux pump
32
Q

Sulfonamide resistance

A
  1. decreased permeability of the cell membrane
  2. the bacteria produce a form of dihydropteroate synthetase that binds the sulfonamide poorly
  3. increased production of PABA by the bacteria (increase the amnt of substrate)
33
Q

Trimethoprim resistance

A
  1. deceased permeability of the cell membrane
  2. the bacteria produce a form of DHFR that binds trimethoprim poorly
  3. the bacteria produces more DHFR
34
Q

How do antifungals work?

A
  • mostly target ergosterol
  • form pores
  • inhibit enzymes important in making ergosterol
35
Q

Amphotericin B

A
  • polyene macrolide antibiotics
  • lipophillic on one side
  • hydrophillic on the other side
  • aggregates and forms pores in lipid membranes
  • may be some toxicity (nephrotoxicity) due to cholesterol binding
36
Q

Fluconazole

A
  • an azole anti fungal drug
  • inhibits fungal cyto P450
  • lower affinity for human P450
  • works through ergosterol

Pharmacology (9 decks)

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