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Pharmacology - Fall > Lecture 14 - Antibiotics > Flashcards

Lecture 14 - Antibiotics Flashcards

1
Q

What are some common diseases caused by pathogenic bacteria?

A
  • Bacteremia
  • Pneumonia
  • Meningitis
  • Tuberculosis
  • Epiglottitis
  • Gonorrhoeae
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2
Q

What are some factors that influence development of infection?

A
  • Systemic – disease and drugs
  • Local – cleaning, closure of wound, contraction of vessels
  • Virulence, number, host resistance
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3
Q

What determines the selection of antibiotic?

A
  • Identification of organism
  • Susceptibility of organism to a particular agent
  • Site of infection
  • Drug characteristics (lipid solubility, molecular weight, protein binding)
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4
Q

___ soluble antibiotics penetrate the lung tissue better

A

Lipid

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5
Q

What is an advantage and disadvantage to protein binding?

A
  • Can increase half-life

- More protein binding means less efficient diffusion

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6
Q

When is the oral route chosen for antibiotics?

A

Infections that are mild and can be treated on an outpatient basis

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7
Q

When is the intravenous route chosen for antibiotics?

A

Most serious infections

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8
Q

What is an example of an antibiotic that is poorly absorbed by the intestine?

A

Vancomycin

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9
Q

What patient factors affect selection of antimicrobial agent?

A
  • Immune system
  • Renal function
  • Hepatic function
  • Poor perfusion
  • Age
  • Pregnancy/lactation
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10
Q

What is empiric therapy?

A
  • Initiation of treatment before a firm diagnosis

- Usually use broad spectrum antibiotics

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11
Q

What is directed therapy?

A

Choose treatment based on knowledge of the organism that is the cause of the infection

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12
Q

What factors influence the choice of empiric therapy?

A
  • Site of infection
  • Immunocompromised
  • Neutropenia
  • Community vs. hospital acquired infection
  • Age
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13
Q

What is neutropenia?

A

Low levels of neutrophils

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14
Q

When would antibiotics be used for suppression?

A

Px may have a chronic bacterial infection in a place of the body that is hard for antibiotics to penetrate, so would use antibiotics to prevent a systemic infection

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15
Q

What does bactericidal mean?

A

Kills bacteria at concentrations achievable in the patient

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16
Q

What does bacteriostatic mean?

A

Arrests the growth and replication of organisms, limiting the spread of infection

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17
Q

What is concentration-dependent killing?

A

Significant increase in the rate of bacterial killing w/ higher concentrations of the drug

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18
Q

When is concentration-dependent killing useful?

A

Rapid killing of infective pathogens

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19
Q

What are narrow spectrum antimicrobial agents?

A

Act on a limited group of microorganisms

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20
Q

What are extended spectrum antimicrobial agents?

A

Effective against one class of organisms as well as a significant number in a different class

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21
Q

What are broad spectrum antimicrobial agents?

A

Kill a range of antimicrobial species

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22
Q

When are antimicrobial combinations used?

A
  • Unknown organism
  • Polymicrobial infection
  • Antibiotic synergy
  • Patient/population factors
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23
Q

What are disadvantages to antimicrobial combinations?

A
  • Superinfection
  • Eradication of normal microflora
  • Resistance
  • Adverse effects (greater toxicity)
  • Patient adherence to therapy
  • Increased cost
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24
Q

Define antibiotic synergism

A

When the effect of 2 drugs in combination is greater than the sum of the effect when 2 drugs are administered independently

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25
Q

Define antibiotic antagonism

A

When the effect of 2 drugs in combination is less than the sum of the effect when 2 drugs are administered independently

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26
Q

What are the mechanisms of antibiotic synergy?

A
  • One drug enhances uptake of the second
  • One drug enhances the metabolic effect of the other
  • Drugs act sequentially in a common pathway
  • Drugs inhibit the same target but in different ways
  • 2 or more drugs inhibit targets in different pathways
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27
Q

What are mechanisms of antibiotic antagonism?

A

Not well studied b/c disadvantageous for clinical therapy

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28
Q

What is one of the most widely effective and least toxic antibiotic strategies?

A

Targeting synthesis of bacterial cell walls

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29
Q

Cell wall inhibitors are only effective against _____

A

Actively growing bacteria

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30
Q

What is the mechanism of penicillin?

A
  • Blocks last step of bacterial cell wall synthesis
  • Inhibits transpeptidases
  • Causes osmotic pressure on cells, resulting in cell lysis
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31
Q

What do transpeptidases do?

A

Form cross-links between peptidoglycan chains that are essential for cell wall integrity

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32
Q

What enzymes do gram positive bacteria produce and why is this important to cell walls?

A
  • Autolysins, which break down the cell wall

- Without active cell wall synthesis autolysins can damage the cell

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33
Q

What are 2 examples of penicillinase-resistant penicillins?

A

Methicillin and cloxacillin

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34
Q

What are 2 examples of extended spectrum penicillins?

A

Ampicillin and amoxicillin

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35
Q

Which portion of penicillin is critical to inhibit the transpeptidase enzyme?

A

Beta lactam ring

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36
Q

What type of side effects will all antibiotics that are administered orally have?

A

GI effects

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37
Q

What is needed to be considered bacteriocidal?

A

At least 3log10 killing

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38
Q

What are some adverse effects of penicillins?

A
  • GI effects
  • Allergy to metabolites
  • Cross allergy w/in penicillin class
  • Reduced coagulation for px receiving anticoagulants
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39
Q

Is penicillin safe for pregnant and breastfeeding women?

A

Yes

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40
Q

Cephalosporins are structurally similar to _____

A

Penicillins

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41
Q

What are some adverse effects of cephalosporins?

A
  • Cross resistance and cross allergic potential w/ each other and w/ penicillins
  • Allergy and GI effects less common than w/ penicillins
42
Q

What is the mechanism of protein synthesis inhibitors?

A

Bind to 70S ribosomes, which are only found in bacteria

43
Q

Which microorganisms are protein synthesis inhibitors effective against?

A

Gram positive and gram negative

44
Q

What are examples of protein synthesis inhibitors?

A
  • Tetracyclines
  • Aminoglycosides
  • Macrolides
  • Chloramphenicol
  • Clindamycin
45
Q

What is the mechanism of tetracyclines?

A
  • Bind irreversibly to 30S ribosome

- Blocks acyl-tRNA access to the ribosome

46
Q

Tetracyclines are _____ spectrum

A

Broad

47
Q

Are tetracyclines bacteriostatic or bactericidal?

A

Bacteriostatic

48
Q

What are some adverse effects of tetracyclines?

A
  • GI discomfort
  • Deposition in bones and teeth of growing children
  • Hepatotoxicity
  • Increased UV sensitivity
  • Dizziness, nausea, vomiting
  • Resistance is common
49
Q

Which patients shouldn’t get tetracyclines?

A
  • Kidney/liver disease

- Pregnant/lactating

50
Q

What is the mechanism of aminoglycosides?

A
  • Bind irreversibly to 30S ribosome

- Blocks functional assembly of ribosome

51
Q

Which bacteria are aminoglycosides effective against?

A

Aerobic gram negative bacteria

52
Q

Are aminoglycosides bactericidal or bacteriostatic?

A

Bactericidal

53
Q

Which aminoglycosides are derived from streptomyces?

A

Streptomycin and kanamycin

54
Q

Which aminoglycosides derived from micromonospora?

A

Gentamicin and amikacin

55
Q

What are some adverse effects of aminoglycosides?

A
  • Nephrotoxicity
  • Ototoxicity (deafness)
  • Neuromuscular paralysis
  • Allergic reactions (contact dermatitis)
56
Q

What is the mechanism of macrolides?

A
  • Bind irreversibly to 50S ribosome

- Block peptidyl transfer

57
Q

Are macrolides broad or narrow spectrum and which bacteria are they effective against?

A
  • Broad spectrum

- Gram positive

58
Q

Are macrolides bacteriostatic or bactericidal?

A

Bacteriostatic, but bactericidal at high doses

59
Q

Which macrolides are derived from streptomyces?

A

Erythromycin, clarithromycin, and azithromycin

60
Q

What are some adverse effects of macrolides?

A
  • GI problems
  • Jaundice
  • Ototoxicity
  • Prolonged QTc interval in px w/ existing arrythmias
  • Myopathy (interactions w/ statins)
61
Q

When is quinupristin/dalfopristin used?

A

For treatment of vancomycin resistant enterococcus

62
Q

What is quinupristin/dalfopristin?

A

Mixture of 2 drugs in a ratio of 70:30

63
Q

What is the mechanism of quinupristin?

A

Binds to 50S subunit preventing peptide elongation

64
Q

What is the mechanism of dalfopristin?

A

Binds to 23S subunit preventing peptidyl transfer

65
Q

Is quinupristin/dalfopristin bacteriostatic or bactericidal?

A

Bactericidal w/ long post-antibiotic effect

66
Q

What are some adverse effects of quinupristin/dalfopristin?

A
  • Venous irritation when given IV
  • Joint/muscle ache in px w/ high doses
  • Hyperbilirubinemia
  • Inhibits cytochrome P450
67
Q

What is the mechanism of DNA/RNA synthesis inhibitors?

A
  • Inhibit enzymes required for bacterial DNA synthesis
  • Inhibit bacterial topoisomerase or DNA gyrase
  • Block synthesis of DNA/RNA and growth of cells
68
Q

DNA/RNA synthesis inhibitors are only effective against _____

A

Actively growing bacteria

69
Q

What are 2 examples of DNA/RNA synthesis inhibitors?

A

Fluoroquinolones and rifamycin

70
Q

What is the mechanism of fluoroquinolones?

A

1) Inhibit DNA gyrase
2) Prevent DNA replication
3) Bactericidal

71
Q

What are some adverse effects of fluoroquinolones?

A
  • GI (nausea, vomiting, diarrhea)
  • CNS (dizziness)
  • Phototoxicity
  • Cartilage erosion
72
Q

Are fluoroquinolones safe to use in pregnant or nursing women?

A

No

73
Q

What is the most commonly prescribed fluoroquinolone?

A

Ciprofloxacin

74
Q

Which infections is ciprofloxacin used for?

A
  • Bones/joints
  • Respiratory tract
  • Urinary tract
75
Q

What are some interactions w/ ciprofloxacin and levofloxacin?

A
  • Alters levels of drugs metabolized by CYP 1A2
  • Warfarin levels increased
  • Increased seizure risk when used w/ NSAIDs
76
Q

Which infections is moxifloxacin used for?

A
  • Respiratory tract and tuberculosis
  • Endocarditis
  • Meningitis
  • Conjunctivitis
77
Q

What is the most common adverse effect of moxifloxacin?

A

May prolong QTc interval

78
Q

What does moxifloxacin interact w/?

A

Warfarin

79
Q

What is the mechanism of metabolite synthesis inhibitors?

A
  • Competitive inhibitors of essential metabolites

- Structurally similar to metabolite but doesn’t fulfill its metabolic function w/in the bacteria

80
Q

What are 2 examples of metabolite synthesis inhibitors?

A

Sulfonamides and trimethoprim

81
Q

What is the mechanism of sulfonamides?

A

Inhibit synthesis of bacterial dihydrofolic acid

82
Q

Are sulfonamides broad or narrow spectrum and which bacteria are they effective against?

A
  • Broad spectrum

- Effective against more gram positive and many gram negative bacteria

83
Q

Which bacteria are resistant to sulfonamides?

A

Bacteria that obtain folates from the environment

84
Q

What are some short acting sulfonamides?

A

Sulfamethoxazole and sulfadiazine

85
Q

What is a long acting sulfonamide?

A

Sulfadimethoxine

86
Q

What are common adverse effects of sulfonamides?

A
  • Allergies (rashes)
  • Kernicterus, especially newborns (bilirubin-induced brain dysfunction)
  • Nephrotoxicity
  • Hemolytic anemia
87
Q

What is the mechanism of trimethoprim?

A

Inhibit synthesis of bacterial tetrahydrofolic acid

88
Q

Is trimethoprim broad or narrow spectrum and which bacteria is it effective against?

A
  • Broad spectrum

- Effective against most gram positive and many gram negative

89
Q

Is trimethoprim bacteriostatic or bactericidal?

A

Bacteriostatic

90
Q

What infections is trimethoprim used for?

A
  • UTI’s
  • Vaginal infections
  • Bacterial prostatitis
  • Prophylaxis
91
Q

Can trimethoprim be used in pregnant women?

A

No

92
Q

What does trimethoprim interact with?

A

Warfarin

93
Q

What is cotrimoxazole composed of?

A

Trimethoprim:sulfonamethoxazole in 1:5 ratio

94
Q

What is cotrimoxazole used for?

A

Inhibition of folate synthesis

95
Q

What is cotrimoxazole used for?

A
  • UTI’s
  • Respiratory tract infections
  • Kidney infections
  • GI tract infections
  • Septicemia
  • Prophylaxis in HIV px
96
Q

Is cotrimoxazole widely used? Why or why not?

A

No b/c of high level of adverse reactions

97
Q

Can cotrimoxazole be used in pregnant women?

A

No

98
Q

What are some adverse effects of cotrimoxazole?

A
  • Skin rashes
  • Nausea, vomiting
  • Jaundice, renal damage/failure
99
Q

How long does it take for relief of symptoms when taking antibiotics?

A

Usually 48-72 hours

100
Q

What is the common duration of antibiotic therapy?

A

7-14 days, but longer for tuberculosis (months)

101
Q

Why does the full course of antibiotics need to be finished even if the px is feeling better?

A

Reduce the risk of developing a secondary infection and reduces selection of resistant bacteria

102
Q

How can GI and vaginal side effects be minimized or prevented?

A

Take oral antibiotics w/ food

Pharmacology - Fall (15 decks)

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