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Pharmacology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What are the factors influencing infection?

A

Virulence, number of organisms and host resistance
Host resistance can be local (cleaning, closure, contraction-ability for organism to enter host) or systemic (disease or drug suppressing immune system).

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2
Q

What are the drug characteristics that must be taken into consideration during antimicrobial agent selection?

A

Lipid solubility (more means better lung penetration), molecular weight and protein binding (less means more efficient diffusion, more means longer half life)

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3
Q

What would affect the route of administration of an antibiotic?

A

Oral for mild infections that can be treated on an outpatient basis
Intravenous for more serious infections
Intramuscular for rapid action
Topical for infections on the skin surface

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4
Q

What would the choice of empiric therapy depend on?

A

Site of infection (polymicrobial), immunocompromised, neutropenia (low levels of neutrophils), age (very young or old), hospital acquired infection

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5
Q

What are antibiotics used for?

A

Prophylaxis (surgery, rheumatic fever, meninges, endocarditis), therapy and suppression

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6
Q

How can we identify the infecting organism?

A

Culture and identification, gram stain, antigen detection, DNA or RNA detection and immune response.

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7
Q

What does it mean to be bactericidal?

A

Kill bacteria at concentrations achievable in the patient

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8
Q

What does it mean to be bacteriostatic?

A

Arrest the growth and replication of organisms, limiting the spread of infection.

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9
Q

What is minimum inhibitory concentration (MIC)?

A

The lowest concentration of drug that inhibits bacterial growth. For clinical therapy, antibiotic concentration must be greater than MIC.

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10
Q

What is minimum bactericidal concentration (MBC)?

A

Minimum concentration of antibiotic that kills bacteria (99.9% fewer bacteria after 24 hours)

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11
Q

What is concentration-dependent killing?

A

A significant increase in the rate of bacterial killing with higher concentrations of the drug.
Useful for rapid killing

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12
Q

What is time-dependent killing?

A

Drugs that require time to achieve effective killing. Higher concentrations of drug do not increase rate of killing

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13
Q

What is the post-antibiotic effect?

A

The suppression of microbial growth even after levels of antibiotic have fallen below MIC. Length of time following removal of antimicrobial drug to reach log-phase growth.

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14
Q

What are narrow spectrum antibiotics? Give an example.

A

Antibiotics that act on a limited group of microorganisms.

Isoniazid on mycobacteria

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15
Q

What are extended spectrum antibiotics? Give an example.

A 
Antibiotics that are effective against one class of organisms as well as a significant number in a different class.
Ampicillin in gram + bacilli and gram - rods
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16
Q

What are broad spectrum antibiotics? Give an example.

A

Antibiotics that act to kill a range of antimicrobial species.

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17
Q

When are antibiotic combinations used?

A

When there is an unknown organism, polymicrobial infection, to achieve antibiotic synergy or when there are patient/population factors

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18
Q

Why would antibiotic combinations be used?

A

What is known in the hospital and dose related toxicity.

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19
Q

What are some disadvantages of antibiotic combinations?

A

Superinfection, eradication of normal microflora, resistance, adverse effects (greater toxicity), patient adherence to therapy and increased cost

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20
Q

What is drug synergism?

A

When the effect of two drugs in combination is greater than the sum of the effect when two drugs are administered independently.
Enhancing uptake of other, enhancing metabolic effect of other, inhibit same target in different ways, inhibit targets in different pathways

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21
Q

What is drug antagonism?

A

When the effects of two drugs in combination is less than the sum of the effect when two drugs are administered independently.

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22
Q

What type of testing is the checkerboard method?

A

Bacteriostatic because the bacteria has not yet grown.

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23
Q

What type of testing is the disk diffusion method?

A

Bactercidal because it is killing off the bacteria that has already grown.

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24
Q

What are gram positive bacteria?

A

Have a thick outer cell wall composed of peptidoglycans. Purple in gram stain
Staph. aureus

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25
Q

What are gram negative bacteria?

A

Have an outer membrane containing lipopolysaccharides and a thin inner peptidoglycan cell wall. Pink in gram stain
E. coli

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26
Q

How does a gram stain work?

A

Crystal violet, iodine, decolorizer (alcohol or acetone) and safarin red

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27
Q

What are examples of cell wall inhibitors?

A

Penicillins and cephalosporins

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28
Q

How do cell wall inhibitors work?

A

Only effective against actively growing bacteria. Beta-lactam ring inhibits transpeptidases that form cross links between peptidoglycan chains essential for cell wall integrity. Creates osmotic pressure on cells, resulting in cell lysis. Autolysins from gram + bacteria can damage cell.

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29
Q

What are the types of penicillins?

A

Penicillin G (original), penicillin V
Penicillinase-resistant penicillins (methicillin, cloxacillin)
Extended spectrum penicillins (ampicillin, amoxicillin)
Bactericidal, cross resistance, cross allergic potential

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30
Q

What is the administration route of antibiotics determined by?

A

The stability of the medication to gastric acid and the severity of infection.

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31
Q

How are penicillins absorbed?

A

Most are incompletely absorbed so they affect the composition of the intestinal flora
Must be administered before a meal or 2-3 hours after.

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32
Q

How are penicillins distributed in the body?

A

Throughout the body, crosses the placenta but doesn’t penetrate bone or CNS

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33
Q

What are some adverse effects of penicillins?

A

GI effects (lessened due to microflora)
Allergy, cross allergy within penicillin class
Reduced coagulation
No teratogenicity

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34
Q

What are some examples of cephalosporins?

A

Cephalexin, Cephalothin, Cepazolin, Cefepin (similar mechanism and structure to penicillins)

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35
Q

How are cephalosporins distributed?

A

Throughout the body

cefazolin penetrates bone, cefuroxime crosses BBB, cefotaxime penetrates cerebrospinal fluid

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36
Q

What are the adverse effects/problems with cephalosporins?

A

Cross resistance and cross allergic potential with each other and other penicillins
Allergy and GI effects less common than penicillins

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37
Q

What is vancomycin? How does it work?

A

A tricyclic glycopeptide that binds to D-Ala-D-Ala side chain of the precursor pentapeptide and prevents transglycosylation step in peptidoglycan polymerization

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38
Q

What are some adverse effects of vancomycin?

A

Fever, chills or phlebitis
Rapid infusion causes shock due to histamine release
Hearing loss in patients with kidney disease
Toxicity when given with aminoglycosides

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39
Q

How do protein synthesis inhibitors work?

A

Bind to the 70S ribosomes (only found in bacteria and composed of 50S and 30S subunits, 80S are in bacteria) and stop the synthesis of protein

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40
Q

What are protein synthesis inhibitors effective against?

A

Gram positive and gram negative bacteria as well as other microorganisms

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41
Q

What are some examples of protein synthesis inhibitors?

A

Tetracyclines (doxycycline, minocycline), chloramphenicol, aminoglycosides (gentamicin, streptomycin), macrolides (clarithromycin, azithromycin), clindamycin, erythromycin

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42
Q

How do tetracyclines work?

A

Bind irreversibly to the 30S ribosome subunit and blocks acyl-tRNA access to the ribosome.
Broad spectrum, bacteriostatic

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43
Q

How are tetracyclines absorbed?

A

Adequately but incompletely absorbed orally.

Reduced by dairy foods and antacids

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44
Q

What are the adverse effects of tetracyclines?

A 
GI discomfort (take with food)
Deposition in bones and teeth of children, sunburn, dizziness, nausea, headache, superinfections (resistance is common)
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45
Q

What are contraindications for tetracyclines?

A

Patients with kidney/liver disease or pregnant/lactating women

46
Q

How do aminoglycosides work?

A

Binds irreversibly to the 30S ribosome subunit and blocks functional assembly of the ribosome
Effective against aerobic gram negative bacteria

47
Q

What are some adverse effects of aminoglycosides?

A

Nephrotoxicity, ototoxicity, neuromuscular paralysis (high dose), allergic reactions (contact dermatitis)

48
Q

How do macrolides work?

A

Bind irreversibly to the 50S ribosome subunit and blocks peptidyl transfer
Broad spectrum, bacteriostatic, bactericidal at high doses
Effective against gram positive

49
Q

What are some adverse effects of macrolides?

A

GI problems, jaundice (CI in liver disease), ototoxicity, prolonged QTc interval in those with existing arrythmias, myopathy when given with statins

50
Q

How does clindamycin work?

A

Binds irreversibly to the 50S ribosome subunit and blocks peptidyl transfer.
Effective against anaerobic bacteria and aerobic gram positive cocci
Bacteriostatic

51
Q

How is clindamycin distributed?

A

Throughout body, concentrates in liver, does not penetrate cerebrospinal fluid or brain

52
Q

How does chloramphenicol work?

A

Binds irreversibly to the 50S ribosome and blocks peptidyl transfer
Broad spectrum, bacteriostatic, bactericidal at high doses

53
Q

How is chloramphenicol absorbed?

A

Adequate, food interferes

54
Q

What are some adverse effects of chloramphenicol?

A 
Hemolytic anemia (rare), gray baby syndrome, myopathy when taken with statins
Other drug interactions
55
Q

How does synercid work?

A

Binds to separate sites on the ribosome
Quinupristin bind to 50S subunit preventing peptide elongation
Dalfopristin bind to 30S subunit preventing peptidyl transfer

56
Q

What is synercid used for?

A

Treatment of vancomycin resistant enterococcus (gram positive cocci)
Bactericidal with long post-antibiotic effect

57
Q

How is synercid distributed?

A

Penetrates macrophages and polymorphonucleosites

Low levels in CSF

58
Q

What are some adverse effects of synercid?

A

Venous irritation, joint/muscle ache (high doses), hyperbilirubinemia, inhibition of cytochrom P450

59
Q

What is a DNA/RNA synthesis inhibitor? How does it work?

A

Inhibits enzymes required for bacterial DNA synthesis (bacterial topoisomerase, DNA gyrase) and thus cell growth
Only effective for actively growing cells
Fluoroquinolones

60
Q

How do flouroquinolones work? What are some examples?

A

Interferes with DNA gyrase (topoisomerase II, IV), blocks DNA replication and induces DNA clearing
Bactericidal
Ciprofloxacin, levofloxacin

61
Q

How are flouroquinolones absorbed?

A

85-95% absorbed (interfered by calcium, magnesium, zinc, antacids)

62
Q

What are some risks for flouroquinolones?

A

Nausea, vomiting, dizziness, phototoxicity, cartilage erosion (CI in pregnant or nursing women)

63
Q

What is ciprofloxacin used for?

A

Most common.

Infections of bones/joint, respiratory tract, urinary tract

64
Q

What are some of the flouroquinolone drug interactions?

A

Alters levels of drugs metabolized by the cytochrome P450 enzyme CYP1A2
Warfarin increased, seizure risk with NSAIDS, renal clearance of methotrexate affected, drugs that prolong QT, corticosteroids (tendon rupture)

65
Q

What is levofloxacin used for?

A

Respiratory infections (pneumonia, bronchitis), urinary tract infections, skin infections

66
Q

What is moxifloxacin used for?

A

Respiratory tract infection, TB, endocarditis, meningitis, conjuctivitis

67
Q

How do metabolite synthesis inhibitors work? What are some examples?

A

Competitive inhibitor of essential metabolites (structurally similar but does not fulfill metabolic function)
Sulfonamides, trimethoprim

68
Q

How do sulfonamides work?

A

Inhibit synthesis of bacterial dihydrofolic acid
Broad spectrum, effective against most gram positive and some gram negative bacteria
Bacteriostatic
Sulfamethoxazole is short acting

69
Q

What are some adverse effects of sulfonamides?

A

Allergies (rashes), kernicterus (newborns), nephrotoxicity, hemolytic anemia

70
Q

What are drug interactions with sulfonamides?

A

Tolbutamide, warfarin

71
Q

How does trimethoprim work?

A

Inhibit synthesis of bacterial tetrahydrofolic acid

Broad spectrum, bacteriostatic

72
Q

What is trimethoprim used for?

A

Urinary tract infection, vaginal infections, bacterial prostatitis, prophylaxis

73
Q

What are some problems with trimethoprim?

A

CI in pregnancy
Thrombocytopenia
Interacts with warfarin

74
Q

What is cotrimoxazole?

A

A 1:5 ratio of trimethoprim: sulfonamethoxazole. Synergistic activity from sequential inhibition of folate synthesis.
Broader spectrum than sulfonamides, bacteriostatic

75
Q

What is cotrimoxazole used for?

A

Urinary tract infection, respiratory tract infections, kidney infection, GI tract infection, septicemia, prophylaxis in HIV patients

76
Q

What are some problems with cotrimoxazole?

A

Usage is restricted
CI in pregnant women
Thrombocytopenia, anemia, leukopenia, skin rash, nausea, jaundice, diarrhea
Interacts with warfarin, methotrexate

77
Q

How does metronidazole work?

A

A bactericidal that prevents DNA replication and fragments the DNA
No resistance

78
Q

What is metronidazole used for?

A

Amebic infections, anaerobic cocci, anaerobic gram negative bacteria
Colitis, brain abscess, periodontal abscess, bone/joint infection, diabetic foot ulcer, endometritis, endocarditis, septicemia

79
Q

What are some adverse effects of metronidazole?

A

Skin irritation, nausea, abdominal cramps, metallic taste in mouth, dizziness, potential carcinogen

80
Q

What are some interactions with metronidazole?

A

Alcohol and mebendazole

81
Q

What is a medication that interacts with antibiotics?

A

Oral contraceptive steroids will be decreased

82
Q

What are some patient related factors that increase the risk of antibiotic resistance infections?

A

Increasing age and increasing severity of underlying disease

83
Q

What are some hospital related factors that increase the risk of antibiotic resistance infections?

A

Increasing length of stay, admission to ICU, proximity to infected patients

84
Q

What are some treatment related factors that increase the risk of antibiotic resistance infections?

A

Prolonged use of broad spectrum antibiotics and contaminated devices or procedures

85
Q

How do antibiotics promote resistance?

A

Selection of resistant bacteria, societal effects and global spread

86
Q

What are some causes of antibiotic resistance?

A

Overuse of antibiotics in humans and non-humans, developing countries, world travel, critically ill patients and industry advertising/promoting

87
Q

When should antibiotics not be prescribed?

A

For viral infections and bronchitis

88
Q

How can antibiotic resistance occur in developing countries?

A

Available OTC, poor patient compliance, cost causing a subtherapeutic course, quality is low (counterfeit, adulterated, poor potency)

89
Q

How does inherent antibiotic resistance occur?

A

A natural resistance by microbes to an antibiotic.
Growth of organism doesn’t have a target for the antibiotic, organism doesn’t have a transport system for the antibiotic, organism is resistant to antibiotics they produce (streptomycete resistant to streptomycin)

90
Q

How does vertical evolution antibiotic resistance occur?

A

Driven by natural selection. Non-mutants are killed, resistant mutants grow and flourish

91
Q

How does horizontal evolution antibiotic resistance occur?

A

Acquisition of genes from other organisms by genetic transfer between bacteria or from virus to bacteria

92
Q

How can DNA transformation cause antibiotic resistance?

A

DNA comes from the environment after being released by another cell (plasmid DNA)

93
Q

How can DNA transduction cause antibiotic resistance?

A

Virus transfers DNA between bacteria

94
Q

How can DNA conjugation cause antibiotic resistance?

A

Contact between cells as DNA crosses from donor to recipient

95
Q

What are some mechanisms of acquired antibiotic resistance?

A

Alteration in target site (MRSA), decreased uptake (P.aeruginosa), increased drug efflux (S.aureus, fluoroquinolones), inactivation of antibiotic (beta-lactamases)

96
Q

How was resistance to penicillins formed?

A

S. aureus developed beta-lactamases which inactivate beta-lactam drugs through cleavage of the central ring

97
Q

How can penicillin resistance be overcome?

A

Develop inhibitors of beta-lactamases, combine penicillin with other antibiotics, add bulkier side chains to basic penicillin structure (hinder enzyme access)

98
Q

How can synergy be used to overcome penicillin resistance?

A

Combine beta-lactamase inhibitor with beta-lactam antibiotics (clavulanic acid with amoxicillin)

99
Q

How can vancomycin resistant enterococci (VRE) occur?

A

Enterococcus faecium

Prior use of broad spectrum beta-lactam antibiotics with poor activity predisposes VRE colonization

100
Q

How can VRE be overcome?

A

Prevention, syndercid, linezolid (reserve antibiotic, protein synthesis inhibitor, toxic to mitochondria, short term use)

101
Q

How does resistance to tetracyclines occur?

A

Mg-dependent active efflux mediated by the TetA gene, enezymes inactivate antibiotics or expression of bacterial proteins that inhibit binding of tetracycline to the ribosome.
Bacteria usually have cross resistance

102
Q

How does resistance to aminoglycosides occur?

A

Decreased uptake of the drug by absence or porin channels or oxygen-dependent transport system
Enzymes that inactivate aminoglycosides (acetyltransferases, nucleotidytransferases, phosphotransferases)
Cross resistance is rare

103
Q

How does resistance to macrolides occur?

A

Decreased uptake of drug, increased efflux of drug, reduced affinity for 50S subunit (methylation of adenine), erythromycin esterase inactivating drug, cross resistance

104
Q

How does resistance to clindamycin occur?

A

Increased efflux of drug, reduced affinity to 50S subunit (methylation of adenine) and cross resistance with macrolides

105
Q

How does resistance to chloramphenicol occur?

A

Decreased uptake of drug due to reduced permeability, reduced affinity for 50S subunit, inactivation enzymes

106
Q

How does resistance to fluoroquinolones occur?

A

Evolves rapidly during treatment

Alterations to DNA gyrase, decreased uptake, increased efflux, cross resistance

107
Q

In which organisms does resistance to ciprofloxacin occur?

A

In S. aureus, S. pyogenes, enterococci, K. penumoniae

108
Q

How does resistances to sulfonamides and trimethoprim occur?

A

Bacteria which obtain folate from the environment, altered diihydropteroate synthase or reductase, reduced permeability to drugs, enhanced folate production

109
Q

What are some examples of organisms with multi drug resistance?

A

MRSA, VRE, gram negative bacteria producing extended spectrum beta-lactamases (ESBL)

110
Q

What are extended spectrum beta-lactamases (ESBL)?

A

CTX-M, TEM, SHV
Plasmid mediated, highly mobile
Inhibited by beta-lactamase inhibitors

111
Q

What can community associated MRSA do?

A

Cause severe, life-threatening soft tissue infections in healthy adults

112
Q

Who usually obtains community-associated MRSA?

A

Injection drug addicts, homeless shelters, nursing homes

Epidemic outbreaks in day care centers, prison inmates, ships, military, contact sports

Pharmacology (11 decks)

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