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AU 15 - Pharm Final > Antibacterial drugs - Part 1 (Intro - Inhibitors of Cell Wall Synthesis) > Flashcards

Antibacterial drugs - Part 1 (Intro - Inhibitors of Cell Wall Synthesis) Flashcards

1
Q

Antibiotics definition

A

Substances produced by micro-organisms to kill other micro-organisms or to protect them from toxins produced by other microorganisms

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2
Q

“Antibiosis”

A

Life destroys life amongst lower species

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3
Q

What are desirable pharmacologic properties of ideal Antibacterial Drugs

A 
Stability
Solubility
Diffusability
Slow Excretion
Large Theraputic index - Selective
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4
Q

In response to a pathogen, a host may respond with what?

A

Active Immunity
Passive Immunity
Overt Disease

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5
Q

In response to a drug, a host may respond with what?

A

Allergy

Toxicity

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6
Q

What effects may drugs have on a host?

A

Selective toxicity

Effects on non-pathogenic flora

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7
Q

Microbes may respond to drugs with what?

A

Resistance

Secondary products of bacterial destruction

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8
Q

Prophylaxis

A

Temporarily decreases most likely pathogens below critical level required to cause infection
One-quarter to one-half of antibacterial drug use is for prophylaxis

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9
Q

What might prophylaxis drugs be useful for?

A

Prevent epidemic meningitis, bacterial endocarditis
Prosthetics - artificial valves, arteries
Transplants
Surgery

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10
Q

Empiric Therapy

A

Initiation of treatment before etiology of infection is known with agents known to be effective against the most likely pathogen acquired (suspected from source of infection)

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11
Q

Pathogen-directed Therapy

A

Identify bacterial species, and then treat

Identify via staining with crystal violet (gram stain)

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12
Q

Drug resistance is a determinant of what?

A

Choice of drug
How much drug
Drug combinations

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13
Q

Gram+ bacteria will stain what color?

A

Purple

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14
Q

Gram- bacteria will stain what color

A

Pink

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15
Q

How does the cell wall of a gram+ bacteria compare to gram-

A

Gram+ = Thick Peptidoglycan layer (50-100 cells thick) outside the plasma membrane

Gram- = Thin Peptidoglycan layer (1-2 cells thick), then wide Periplasmic space, then the plasma membrane

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16
Q

What can be used to determine Antibiotic sensitivity

A

Minimum inhibitory concentration (MIC)
Minimum bactericidal concentration (MBC)
Disk diffusion Assays and E-test

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17
Q

Minimum inhibitory concentration

A

Lowest concentration of drug which completely inhibits growth at 24 hrs

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18
Q

What are we able to do once we know the antibiotic sensitivity profile?

A

Select effective drugs with the narrowest spectrum of activity in order to avoid emergence of resistant micro-organisms

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19
Q

Why is it important to know the location of an infection?

A

Many agents don’t cross the blood brain barrier

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20
Q

Pharmacokinetics

A

Route and time course of…

  • Absorption
  • Metabolism
  • Excretion
  • Toxicity
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21
Q

Emergence of different resistant strains in different locales is depndent on what?

A

Clinical use and/or natural selection

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22
Q

What are some host factors to keep in mind when selecting a drug?

A 
Age
Allergy history
Food/hydration effects on pharmacokinetics, absorption, solubility, and renal function
Hepatic funciton
Pharmacogenetics
Pregnancy status
Immune status
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23
Q

Antibiotic combinations are helpful for what?

A

Empiric Therapy
Mixed Infections
Synergism
Antagonism

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24
Q

What are the different mechanisms of action of antibacterial drugs?

A 
Inhibition of Nucleic Acid Synthesis
DNA Damaging Agents
Inhibition of Cell wall synthesis
Damage of Cell Membranes
Inhibitors of Protein Synthesis
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25
Q

What drugs Inhibit Nucleic Acid Synthesis

A

Sulfonamides, Trimethoprim (Antifolates)

Rifampin

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26
Q

What drugs are DNA damaging agents?

A

Quinolones
Nitrofurantoin
Metronidazole
Methenamine

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27
Q

What drugs inhibit cell wall synthesis?

A

Beta-lactams
Vancomycin
Bacitracin

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28
Q

What drugs damage cell membranes?

A

Polymyxins

Daptomycin

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29
Q

What drugs inhibit protein synthesis?

A 
Aminoglycosides
Tetracyclines
Tigecycline
Macrolides (Erythromycin, Clarithromycis, Azithromycin)
Clindamycin
Linezolid
Quinupristin/Dalfopristin
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30
Q

Sulfonamides mechanism

A

Competitive inhibitor of Dihydropteroate synthase - which is required for synthesis of folic acid
Bacteriostatic

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31
Q

Sulfonamides selectivity

A

Selective because bacteria must synthesize their own folate, while humans utilize dietary folate

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32
Q

Sulfonamides Antibacterial spectrum

A

Inhibits growth of gram positive and gram negative organisms

Resistant strains are numerous

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33
Q

Sulfonamides clinical uses

A

Uncomplicated UTIs
Toxoplasmosis - a parasite infection
Malaria
Prophylactic - topical for burn patients, and in AIDS patients to prevent P. jirovecii

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34
Q

Sulfonamide Absorption

A

Good oral absorption

Poorly absorbed forms are used to decrease colonization density before surgery

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35
Q

Sulfonamide Distribution

A

Widely distributed including penetration into the CSF

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36
Q

Sulfonamide Excretion

A

Renal

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37
Q

Sulfonamide Toxicity

A

Dose related

  • Crystalluria (that’s why you should take it with lots of water)
  • Hemolytic anemia
  • GI upset
  • Kernicterus (sulfa drug displaces albumin bound bilirubin - which can then pass BBB in newborns. CNS deposition leads to encephalopathy)

Dose unrelated

  • Hypersensitvity (mild rash to Stevens-Johnson syndrome)
  • Photosensitivity
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38
Q

Trimethoprim Mechanism

A

Inhibitor of Dihydrofolate reductase (DHDR) - required for folic acid synthesis
Structural analog of pteridine
Bacteriostatic

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39
Q

Trimethoprim Selectivity

A

Need much higher concentration to inhibit human DHFR compared to bacterial DHFR

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40
Q

Trimethoprim Antibacterial Spectrum

A

Broader spectrum of activity against both gram+ and gram- compared to sulfonamides
Resistance is associated with alterations in DHFR

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41
Q

Trimethoprim Clinical Uses

A

Usually used in combination with Sulfamethoxazole (5:1 ratio of Sulfa to Trimeth) -becomes bacteriocidal
UTI treatment
Intestinal infections
Community acquired MRSA treatment
P. jarovecii treatment and prevention in AIDS pts

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42
Q

Trimethoprim Absorption

A

Oral

GI absorption is also good

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43
Q

Trimethoprim Distribution

A

Wide

penetrates into CNS

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44
Q

Trimethoprim Excretion

A

Renal

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45
Q

Trimethoprim Toxicity

A

Slight blood dyscrasias - Usuually associated with sulfa combination
Anemias in patients that are already folate deficient

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46
Q

Rifampin Mechanism

A

Binds to an inhibits RNA polymerase

Bactericidal

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47
Q

Rifampin Resistance

A

Induction of resistance is rapid

Not usually used as monotherapy because of this

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48
Q

Rifampin Selectivity

A

Doesn’t bind to human RNA polymerase - bacteria only

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49
Q

Rifampin Antibacterial Spectrum

A

Potent against M. tuberculosis at both intracellular and extracellular sites
Some activity against staphylococci

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50
Q

Rifampin Clinical uses

A

First-line antituberculosis drug
Used in combination with other first-line anti-tubercular drugs
Some use in combination with other agents for treatment of prosthetic valve endocarditis, resistant staph infections
Prophylaxis against meningococcal disease and meningitis

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51
Q

Rifampin Absorption

A

Oral - peak levels within 2-4 hours

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52
Q

Rifampin Distribution

A

Widely distributed to organs, tissues, and body fluids (including CSF)
Can impart red-orange color to urine, feces, saliva, tears - so just inform patient so they don’t go ape-shit

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53
Q

Rifampin Metabolism

A

In the liver via P450 enzyme-mediated deacetylation

Metabolite remains full antibacterial activity, but intestinal reabsorption is diminshed

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54
Q

Why is a Rifampin-substitute given to HIV+ patients with tuberculosis?

A

It is a potent inducer of hepatic microsomal enzymes, and can therefore increase metabolism and decrese the half-lifke of HIV proteases and nonnucleoside reverse transcriptase inhibitors

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55
Q

Rifampin Excretion

A

Rapid elimination in bile as parent and as deacetylated metabolite - so daily dosing is encouraged

56
Q

Rifampin Toxicity

A

Liver damage - jaundice

57
Q

Quinolones Mechanism

A

Inhibit DNA replication through “poisoning” of DNA Gyrase A
Specifically, they inhibit the uncoiling funciton of DNA gyrase ahead of the replication fork
Alo inhibit the separation of newly replicated sstrands of DNA (decatenation) through the inhibition of DNA topoisomerase IV
Bacteriocidal

58
Q

Quinolones Selectivity

A

Mammalian DNA topoisomerase II is not inhibited to the same extent as DNA gyrase and DNA topoisomerase IV in bacteria

59
Q

Quinolones Antibacterial Spectrum

A

A variety of analogs are effective against either gram- or gram+ bacteria

60
Q

Quinolones Clinical Uses

A

UTI
RTI
Anti-tubercular (when there’s resistant to other anti-tubercular drugs)
Ciprofloxacin & Levofloxacin are effective against P. aeruginosa

61
Q

Quinolone Drug resistance mechanisms

A

1) Mutations in Gyrase or Topoisomerase target
2) Increased Efflux pumps
3) Altered porins (gram-)

62
Q

1st Generation Quinolones

A

Nalidixic acid (Historical)

63
Q

2nd Generation Quinolones

A

Ciprofloxacin
Ofloxacin
Norfloxacin

64
Q

3rd Generation Quinolones

A

Levofloxacin - for gram+ bacteria

65
Q

4th Generation Quinolones

A

Moxifloxacin - for gram- abcteria

66
Q

Quinolone Absorption

A

Rapid absorption after oral administration

Cations can chelate Quinolones and limit absorption

67
Q

Quinolone Excretion

A

Rapid renal elimination

68
Q

Quinolone Distribution

A

High concentrations in kidney and urine
Except Moxifloxacin, which is not cleared by the kidney
Ciprofloxacin penetrates into prostatic fluid - good for prostatitis

69
Q

Quinolone Toxicity

A

Generally well tolerated
Ciprofloxacin can rupture tendons in children
Can lead to GI intolerance/nausea

70
Q

Nitrofurans Mechanism

A

DNA damage caused by the formation of O2 free radicals subsequent to reduction of nitro group

71
Q

Nitrofurans Selectivity

A

High concentrations in urine and renal interstitial fluid
Bacteria cause reductive activation more extensively than mammalian cells
Low serum concentrations prohibits use for systemic infections

72
Q

Nitrofurans Antibacterial Spectrum

A

Broad spectrum against gram+ and gran- strains

Not effective against P. aerudinosa

73
Q

Nitrofurans Clinical uses

A

Only for treatment of UTIs

74
Q

Nitrofurans Pharmacokinetics

A

Well absorbed orally
Rapidly metabolized
Renal excretion
High concentrations in urine achieved - good for treatment of UTIs

75
Q

Nitrofurans Contraindications

A

Low creatinine clearance (Poor renal function)

76
Q

Nitrofurans Toxicity

A

Toxicity includes acute fever, rashes, urticaria
Possible pleural effusions
Chronic toxicity is associated with pulmonary fibrosis (often reversible)

77
Q

Methenamine Mechanism

A

Hydrolyzed at acid pH to form formaldehyde
Acidify urine to increase selectivity
Denature proteins
In addition, formaldehyde has been shown to damage DNA
Bacteriocidal

78
Q

Methenamine Clinical Uses

A

Only for prophylaxis for lower UTIs

79
Q

Methenamine Antibacterial Spectrum

A

Gram-

80
Q

Methenamine Pharmacokinetics

A

Oral administration
Well distributed into total body water
Stomach hydrolysis is 10-30% unless tablets enterically coated

81
Q

Methenamine Toxicity

A

Include gastric distress, bladder irritation, crystalluria due to precipitation of acidifying agents if there’s inadequate urine flow

82
Q

Metronidazole Mechanism

A

Reductive activation of nitro group specifically in anaerobic bacteria leads to free radical species and reactive intermediates that bind to and affect DNA function
Also activation and DNA damage activity in some protozoa
Therefore, it is a pro-drug that requires metabolic activation

83
Q

Metronidazole Antibacterial Spectrum

A

Bactericidal against most obligate anaerobic gram+ and gram- bacteria
Not active against aerobes or facultative anaerobes
Active against some protozoa

84
Q

Metronidazole Clinical Uses

A

Anaerobic and some protozoal infections

85
Q

Metronidazole Resistance

A

Due to reduced activation

86
Q

Metronidazole Absorption

A

Well absorbed orally

87
Q

Metronidazole Distribution

A

Widely distributed into fluid compartments

Penetrates into the CNS

88
Q

Metronidazole Excretion

A

Renal –> metabolites

89
Q

Metronidazole Toxicity

A

Mild nausea and vomitting
Metallic taste
Can have disulfiram-like effect where complete metabolism of alcohol is prevented, leading to nausea, vomiting, GI distress if alcohol is consumed

90
Q

Bactericidal Effects of Inhibition of Cell Wall Synthesis

A

High internal osmotic pressure of bacteria requires a rigid cell wall to maintain integrity and shape.
During growth and division, bacteria require new cell wall synthesis, and therefore, inhibitors render growing bacteria susceptible to osmotic rupture, with no effect on mammalian cells which do not contain cell walls

91
Q

T/F - Bactericidal effects of Cell wall synthesis inhibitors only occur when cells are growing

A

True

92
Q

What bacteria are resistant to drugs that Inhibit Cell wall synthesis? Why?

A

Mycoplasma - lack cell walls, so intrinsically resistant
L-forms of bacteria - lack cell walls
The kidney is also a sanctuary for bacteria against these drugs, because osmotic pressure is high

93
Q

Cell wall synthesis

A

1) Linkage of L-ala to D-ala OR Linkage of two D-ala peptides
2) Linkage of D-ala dipeptide to three other amino acids and N-acetylmuramic acid to form a pentapeptide with a UDP-carrier + isoprene
3) Coupling to N-acetylglucosamine
4) Sugar-peptide structure linked to isoprenyl-phosphate lipid carrier is transported to exterior of cell membrane
5) Sugar-peptide added to polymer via Peptidoglycan synthase
6) Transpeptidation reaction cross-linking peptidoglycan strands by connecting penultimate D-ala from one strand to a diaminopimelic acid unit in a sugar-peptide of an adjacent strand

94
Q

What are the different types of Beta-Lactams?

A 
Penicillins
Cephalosporins
Monobactams
Carbapenems
B-Lactamase Inhibitors
95
Q

Penicillin Mechanism

A

Miminx D-ala-D-ala structure of pentapeptide on peptidoglycan and ties up transpeptidase
Bacteriocidal

96
Q

Penicillin Selectivity

A

Penicillins and all B-lactams work to inhibit cell wall synthesis
Since eukaryotic cells do not contain cell walls, there are no direct cytotoxic effects in the host

97
Q

What are the different types of Penicillin Classifications?

A

Natrually Occuring Penicillins
Anti-staphlococcal (B-lactamase resistant) Penicillins
Amino-penicillins
Anti-Pseudomonal Penicillins

98
Q

What is the spectrum of Naturally Occurring Penicillins?

A

Narrow spectrum -

effective against streptococci, many anaerobes, enterococcus, and a few gram- organisms

99
Q

What is the spectrum of Anti-staphylococcal Penicillins?

A

Narrow spectrum -

effective against infections caused by staphylococci and streptococci

100
Q

What is the spectrum of Amino-penicillins

A

Broader spectrum

  • effective against streptococci, entrococci, and some gram- organisms
  • not effective against P. aeruginosa
101
Q

What is the spectrum of Anti-pseudomonal penicillins?

A

Extended spectrum

-effective against streptococci and many gram- bacteria including various Enterobacteriae and Pseudomonas

102
Q

What are clinical uses of Penicillins?

A

Streptococcus pneumoniae (pneumonia, meningitis, ottis media, bacteremia)
Haemophilus influenza (Meningitis, epiglotitis)
STDs (syphilis)
UTIs

103
Q

What are the mechanisms of Drug resistance to Penicillins and B-Lactams?

A

1) B-lactamases
2) Altered Penicillin Binding Proteins
3) Altered porins (doesn’t allow B-lactams in)
4) Increased efflux (enhanced efflux pump mechanisms)

104
Q

Penicillin Absorption

A

Poor oral absorption (only ~50%) - food intake will decrease absorption (so take before eating)
Acid destruction is a factor and therefor give an acid stable drug such as Pen-V
Short blood or plasma half life after reaching max level within 2 hours

105
Q

Penicillin Distribution

A

Varies
Lipid insoluble and therefore no good penetration of the BBB
CSF entry is increased with inflammation of meninges
Protein binding varies
Distribution can be affected by pathology of infection

106
Q

Penicillin Excretion

A

Renal - by glomerular and tubular secretion

107
Q

Penicillin Toxicity

A

Relatively nontoxic but direct toxic effects in the kidney are noted as well as hypersensitivity reactions

108
Q

Why are Penicillins “time-dependent” drugs?

A

Since concentrations in the blood must be maintained for a sufficient period to inhibit cell wall synthesis and kill all bacteria

109
Q

Cephalosporins Mechanism

A

Same as for Penicillins - Mimics D-ala-D-ala structure of pentapeptide on peptidoglycan and ties up transpeptidase
Bacteriocidal

110
Q

First Generation Cephalosporins Selectivity

A

Penicillin alternative
Effective against gram positive organisms
Added activity against E. coli

111
Q

Second Generation Cephalosporins Selectivity

A

Increased activity against gram- bacteria compared to first generation

112
Q

3rd Generation Cephalosporin Selectivity

A

Even grater activity against gram- bacteria

113
Q

4th Generation Cephalosporin Selectivity

A

Effective against Pseudomonas
More resistant to B-lactamase breakdown
Only administered via IV

114
Q

Cephalosporins Absorption

A

Oral and Parenteral

115
Q

Cephalosporins Distribution

A

Wide

3rd and 4th can cross BBB and penetrate CSF

116
Q

Cephalosporins Metabolism

A

Not extensively metabolized

117
Q

Cephalosporins Excretion

A

Similar to penicillins

Renal elimination via filtration and tubular excretion

118
Q

Cephalosporins Toxicity

A

Relatively non-toxic and better tolerated than penicillins

Hypersensitivity and cross-sensiticiy (1-10%) in patients who have allergic reactions to penicillin

119
Q

Carbapenems Spectrum

A

Broad/Extended spectrum against gram- and gram+ bacteria

Resistant to B-lactamases

120
Q

Carbapenems Absorption

A

IV only

121
Q

Carbapenems Excretion/Metabolism

A

Undergoes hydrolysis in renal system

122
Q

Carbapenems Clinical Uses

A

Use reserves for serious noscomial infections

123
Q

Carbapenems Toxicity

A

Can be limiting (Seizures)

124
Q

Monobactams Spectrum and Use

A

Effective against aerobic gram- organisms (including P. aeruginosa)
Essentially no activity against gram+ organisms because of poor binding to PBPs in gram+ organisms

125
Q

Monobactams Pharmacokinetics

A

Given only IV or IM injection
Elimination same as penicillins
Hypersensitivity reactions are rare

126
Q

B-lactamase Inhibitors Mechanism

A

Inhibits B-lactamase
Binds irreversibly to serine at active site of lactamase
Suicide inactivator

127
Q

B-lactamase Inhibitor Clinical uses

A

Used in combination with beta-lactam antibiotics to extend the spectrum

128
Q

Vancomyocin Mechanism

A

Binds to carboxyl terminus of D-ala-D-ala and therby…
1) Inhibits Peptidoglycan synthase
2) Inhibits transpeptidation reaction
Bactericidal

129
Q

What is a major problem with Vancomyocin?

A

Resistance - due to altered D-ala-D-ala peptide structures so Vancomyocin doesn’t bind as readily
Strains of Enterococcus faecium and Staphylococcus aureus are becoming vancomyocin resistant (VRE-type resistance)

130
Q

Vancomyocin Spectrum

A

Active against gram+ staphylococci and streptococci

Large size means it can’t penetrate the outer membrane of gram- bacteria

131
Q

Vancomyocin Absorption

A

Given IV
Not absorbed form GI
Can be used orally to trat C. difficle, but results in rapid emergence of resistant enterococci

132
Q

Vancomyocin Metabolism/Excretion

A

Not metabolized
Renal excretion
Half-life = 6-9 hours

133
Q

Vancomyocin Toxicity

A

Hearing loss is dose-related and often related to an underlying renal imapirment which leads to slower excretion
Rash can occur if Vancomyocin is infused too quickly

134
Q

Bacitracin Mechanism

A

Binds to isoprenyl-phosphate lipid carrrier, inhibiting dephosphorylaiton and utlization

135
Q

Bacitracin Spectrum

A

Inhibits gram+ cocci

Some activity against gram-

136
Q

Bacitracin Clinical Uses

A

Superficial skin infections, opthalmic infections

Used in creams and ointments

137
Q

Bacitracin Pharmacokinetics

A

Poorly absorbed - only administered topically

If given IV, then can cause renal damage

AU 15 - Pharm Final (7 decks)

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