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Semester 1 > Pharm 4 Exam I > Flashcards

Pharm 4 Exam I Flashcards

1
Q

Define MIC

A

Minimum Inhibitory Concentration- Minimum concentration of a drug that will inhibit the growth of a pathogen after 18-24 hours of incubation in vitro.

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2
Q

When is a pathogen considered sensitive to a drug?

A

If the concentration of the drug that will inhibit the growth of a pathogen is low

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3
Q

When is a pathogen considered resistant to a drug?

A

If the minimum concentration of drug needed to inhibit the growth of the pathogen is high.

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4
Q

Define time dependent bactericidal agents

A

Drugs that exhibit a constant rate of killing independent of its concentration as long the drug concentration is greater than the MBC. Ex Beta lactam

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5
Q

Define concentration dependent bactericidal agents

A

Drugs that exhibit rate of killing that increases with the concentration of the drug as long as the drug concentration is greater than the MBC. Ex. Vancomycin and Aminoglycosides

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6
Q

Define MBC

A

Minimum Bactericidal Concentration - The lowest drug level at which 99.9% of a culture of bacteria or other microorganisms is killed after 18-24 hours incubation in vitro.

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7
Q

Why do bacteriostatic drugs require an intact immune system?

A

Because they do not kill the existing microorganism only prevent multiplication.

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8
Q

Characteristics of the GN cell wall

A
  • Second lipid bilayer called the outer membrane which hinders hydrophilic molecules
  • Has Porin pores that transverse the outer membrane
  • The murein layer is porous enough to allow hydrophilic molecules to pass through
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9
Q

What is important pharmacologically about the Porin pores?

A

Through them hydrophilic abx can gain access to the murein layer of GN bacteria

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10
Q

Characteristics of GP cell wall

A
  • Cell wall is a thick coat of murein which is porous.
  • Murein layer is thicker than GN
  • No outer membrane
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11
Q

Three major phases of bacterial cell wall synthesis

A
    1. Synthesis of murein monomers from amino acids
    1. Polymerization of the murein monomers into peptidoglycan polymers
    1. Crosslinking of the polymers
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12
Q

Describe the first step in bacterial cell wall synthesis. Synthesis of murein monomers.

A
  • Synthesis of murein monomers from amino acids
  • Takes place in the cytoplasm
  • Begins with the modification of glucose into NAG and NAM
  • Next the peptide component is added by a series of peptide transferases
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13
Q

Describe the second step in bacterial cell wall synthesis. Polymerization.

A
  • Polymerization of the murein monomers into peptidoglycan polymers
  • Occurs in the cytoplasmic membrane
  • murein monomers are ferried across the lipid bilayer, assisted by phosphorylated bactoprenol
  • In the periplasmic space the monomer is attached to the chain via bonds between NAM and NAG
  • This is catalyzed by transglycosydase
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14
Q

Describe the third step in bacterial was synthesis. Crosslinking of the polymers.

A
  • Crosslinking of the polymers occurs in the paraplasmic space (between the cytoplasmic membrane and the murein layer)
  • Murein chains are crosslinked to one another by transpeptidease enzymes
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15
Q

What is another name for transpeptidase?

A

Penicillin binding proteins (PBP)

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16
Q

What do transpeptidases

A

Form an intermediate that can attach and form a crosslink.

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17
Q

What do autolysins do?

A

They punch small holes in the peptidoglycan wall which allow for remodeling to occur

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18
Q

If murein synthesis is blocked then what else is blocked

A

Mediated autolysis and cell wall synthesis

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19
Q

Compare the bacterial RNA polymerase to that of human cells

A
  • Bacteria only 1 RNA polymerase is present which has 5 subunits
  • Humans have 3 RNA polymerases which are much more complex
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20
Q

Which two enzymes are required for bacterial gene expression?

A
  • RNA polymerase

- DNA topoisomerase

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21
Q

What is the function of DNA topoisomerase?

A
  • To regulate the coiling of DNA. Thus bacterial ribosomes can be targets for selective abx.
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22
Q

What are the stages of bacterial transcription?

A
    1. Initiation - RNA polymerase separates a section of DNA
    1. Elongation - RNA polymerase synthesizes complementary DNA strand
    1. Termination - A termination sequence is reached on the mRNA
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23
Q

What are the subunits of 70S ribosomes and their functions?

A
  • 30S subunit is responsible for decoding the mRNA

- 50S subunit catalyzes the peptide bond formation.

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24
Q

Define bacterial resistance

A

Bacterial growth is not halted by the maximum abx that can be tolerated

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25
Q

Methods of bacteria developing resistance

A
  • Spontaneous mutations of DNA
  • DNA transfers from one bacterium to another
  • Resistance encoded R factors (resistance plasmids)
  • Efflux pumps
  • Enzyme inactivation
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26
Q

Which drugs are inhibitors of topoisomerase

A

Floroquinolones

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27
Q

MOA of flouroquinolones

A

GN - Eliminate DNA gyrase

GP - Eliminate topoisomerase IV

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28
Q

Contraindications of flouroquinolones

A
  • Pregnancy

- Children - causes joint pain

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29
Q

Side effects of flouroquinolones

A
  • Well tolerated

- Tendon rupture

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30
Q

How do flouroquinolones enter the cell?

A

By passive diffusion through the pores of the outer membrane

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31
Q

What is the function of the topoisomerases

A

They change the configuration of DNA by cutting, passing through and the resealing DNA

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32
Q

Which drugs are inhibitors of bacterial RNA synthesis?

A

Rifamycins

33
Q

MOA of Rifamycins

A
  • They form a complex with bacterial DNA independent of RNA polymerase
  • This prevents initiation of RNA synthesis (not elongation)
34
Q

Contraindications of Rifamycins

35
Q

Side effects of rifamycins

A
  • Discoloration of secretions

- Cholestatic jaundice and hepatitis

36
Q

Which antibiotics are inhibitors of translocation?

A

Lincosamides

37
Q

MOA of Lincosomides

A
  • Bind to 23S rRNA molecule of the 50S subunit
  • Inhibit peptidyl transferase
  • Blocks elongation, meaning it blocks the transfer of amino acids to the peptide chain
38
Q

Contraindications of Liconsamides

39
Q

Side effects of lincosamides

A
  • Pseudomembranous colitis

- They can wipe out normal flora allowing pathogenic flora to grow

40
Q

Which drugs target the 30S RSU?

A
  • Aminoglycosides

- Tetracyclines

41
Q

MOA of Aminoglycosides

A
  • Create pores in the outer membrane
  • Bind irreversibly to the 30S RSU
  • Interferes with the function of the ribosome causing the 30S RSU to misread mRNA
42
Q

Contraindications for Aminoglycosides

A

Renal dysfunction

43
Q

Side effects of aminoglycosides

A
  • Ototoxicity

- Nephrotoxicity

44
Q

MOA of tetracyclines

A
  • Bind reversibly to 16S subunit of the 30S RSU
  • Inhibits translation by blocking tRNA to the A site of mRNA
  • Weakens ribosome tRNA interaction
45
Q

Contraindications of tetracyclines

A
  • Pregnancy, lactation

- Children under 8 because of tooth discoloration

46
Q

Side effects

A
  • GI nausea and vomiting

- Mottling of teeth because of calcium binding

47
Q

Which drugs target the 50S RSU?

A
  • Macrolides

- Oxazolidinodes

48
Q

MOA of Oxazolidinones

A
  • Inhibits the formation of the 70S RSU
  • Bind to the 23 rRNA site on the 50S RSU near the interface with the 30S
  • Inhibits translocation/ protein synthesis
49
Q

Contraindications of oxazolidinones

50
Q

Side effects of Oxazolidinones

A
  • Serotonin syndrome

- Hyperlactemia and metabolic acidosis

51
Q

MOA of macrolides

A
  • Bind reversibly to the 23S subunit on the 50S RSU
  • Inhibit peptidyl transferase which blocks the binding of amino acids onto the peptide chain
  • Inhibits translocation
52
Q

Contraindications of macrolides

A

Hepatic dysfunction

53
Q

Side effects of macrolides

A
  • Significant increase in gut motility

- Acute cholestatic hepatitis

54
Q

Which genetic inhibitors are bacteriostatic?

A
  • Tetracycline
  • Lincosamides
  • Macrolides
  • Oxazolidinones
55
Q

Which genetic inhibitors are bactericidal?

A
  • Fluroquinolones
  • Rifamycins
  • Aminoglycosides
56
Q

What are the subclasses of Beta Lactams

A
  • Penicillins
  • Cephalosporins
  • Monobactam
  • Carbapenem
57
Q

Beta lactams are effective only against organisms which are doing what?

A

Actively proliferating

58
Q

MOA of beta lactams

A
  • Interfere with the last step in bacterial wall synthesis (crosslinking)
  • Bind to PBP’s (transpeptidases)
  • Expose the membrane to autolysins
59
Q

Beta lactams are effective on GN or GP?

A

GP because they have a thick peptidoglycan layer. GN are protected by the liposaccharide layer

60
Q

Contraindications of penicillins

A

Hypersensitivity allergy

61
Q

Side effects of penicillins

A

Hypersensitivity rash

62
Q

What are beta lactamases?

A

Antibiotic inactivating enzymes

63
Q

MOA of beta lactamases?

A

Hydolytically inactivate beta lactam rings of penicillins and cephalosporins

64
Q

How are cephalosporins different chemically from penicillins?

A

They have a 6 member core instead of a 5 member core

65
Q

How are cephalosporins classified?

A

1st - 4th generation based on susceptibility to beta lactamases. 1st is narrow spectrum 4th is broad spectrum (IV only)

66
Q

Contraindications for cephalosporins

A

Anaphylaxis to penicillin

67
Q

Side effects of cephalosporins

A
  • Bone marrow suppression
  • Nephrotoxicity
  • Pseudomembranous toxicity
68
Q

Contraindications of carbapenems

A 
Seizure activity
(Imipenum)
69
Q

Side effects of Carbapenems

A
  • N/V
  • Neurotoxicity
  • Fever
70
Q

Which drugs are inhibitors of murein polymer synthesis?

A

Glycopeptides

71
Q

MOA of glycopeptides

A
  • Bind to the D-ALA-D-ALA terminus of the murein monomer
  • Inhibit transglycosidase
  • Block the action of murein units
72
Q

Contraindications of Glycopeptides

73
Q

Side Effects of glycopeptides

A
  • Flushing

- Ototoxicity

74
Q

Which type of bacteria are glycopeptides effective against, GN or GP?

A

GP because GN have a liposaccaride layer that covers and protects the peptidoglycan layer

75
Q

MOA of Sulfonamides

A
  • Compete with the substrate for the bacterial enzyme dihydropteroate synthase
  • Inhibits the synthesis of tetrhydrofolte (THF)
76
Q

Contraindications of Sulfonamides

A

Allergy to sulfa antibiotics

77
Q

Side effects of Folate Sulfonamides

A
  • Precipitate urine
  • N/V/D
  • Photosensitivity
78
Q

Which drugs are Folate Synthesis Inhibitors?

A

Sulfonamides

Semester 1 (15 decks)

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