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Pharmacotherapeutics I > Introduction to Antibiotics > Flashcards

Introduction to Antibiotics Flashcards

1
Q

Antibiotics- definition

A

Substances produced by various species of microorganisms that surpress growth or destroy microorganisms. Including fungi, bacteria, and actinomyces

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2
Q

Bactericidal

A

Directly kill bacteria
Inhibitors of cell wall synthesis, cell membrane distributors, aminoglycosides, DNA gyrase inhibitors
Does not require functioning immune system

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3
Q

Bacteriostatic

A

Arrest growth or replication of bacteria. Host immune system then eliminates the pathogens.
Must have a functioning immune system

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4
Q

Bactericidal with a bacteriostatic antibiotic?

A

NEVER

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5
Q

General characteristics of ABX

A

All antibiotics can ellicit allergic response
Cross-sensitivity between agents in different classes
Target normal body flora in addition to pathogens

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6
Q

Classifications of ABX- Agents that inhibit cell wall synthesis

A 
Penicillins
Cephalosporins
Cycloserine
Vancomycin
Bacitracin
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7
Q

Classifications of ABX- Agents that act directly on the cell membrane of the microorganism affecting permeability and leading to leakage of intracellular compounds

A

Detergents

- polymyxin

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8
Q

Classifications of ABX- Agents that interfere with protein synthesis by interaction with bacterial ribosomes

A 
Chloramphenicol
Tertracyclines
Macrolides
Clindamycin
Streptogramins
Ketolides
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9
Q

Classifications of ABX- Agents that interfere with protein synthesis by blocking initiation

A

Oxazolidinoses (linezolid)

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10
Q

Classifications of ABX- Agents that interfere with protein synthesis by inhibition of tRNA synthesis

A

Mupirocin

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11
Q

Classifications of ABX- Agents that interfere with protein synthesis by multiple mechanisms leading to disruption of RNA processing

A

Aminoglycosides

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12
Q

Classifications of ABX- Agents that inhibit DNA processing by

A

Inhibition of DNA topoisonerases
Quinolones
Inhibition of DNA-dependent RNA polymerase (Directly-rifampin and indirectly- nitrofurantoin)

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13
Q

Classifications of ABX- The antimetabolites- blocking bacterial folic acid pathway

A

Trimethoprim

Sulfonamides

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14
Q

Two ways antibiotics are used

A

As emperical therapy- before lab results and dx (broad spectrum)
As definitive therapy- after lab results and dx
Goal is to choose a therapy most selectively active for the organism, with the least potential for toxicity

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15
Q

Selecting an Antimicrobial agent

A

Decide if ABX if truly needed

Evaluation is necessary before administration of ABX since diagnosis may be masked w/out appropriate culture.

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16
Q

Host defenses

A

Low immune respsonses may result in therapeutic failure despite the use of appropriate and effective therapy.

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17
Q

Humoral immunity

A

Inadequacy in the immunoglobulins

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18
Q

Cellular immunity

A

Inadequacy in the phagocytic cells

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19
Q

Host factors- Age

A

Renal and hepatic metabolism can be affected by infants and elderly

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20
Q

Host factors- genetic factors

A

In patients w/ glucose-6-phosphate deficiency certain drugs can cause acute hemolysis

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21
Q

Host factors- disorders of the nervous system

A

Patients w/ seizure disorder usually occurs with high doses of PCN G
Patients w/ myasthenia gravis- susceptible to neuromusular blocking effects of certain antibiotics.

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22
Q

Host factors

A 
Host defenses
Age
Genetic factors
Pregnancy
Drug allergy
Disorders of the nervous system
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23
Q

Pharmacokinetic factors

A

Infection in the CSF-drug must cross the BBB
Penetration of the drug into the local area since many antibiotics are highly protein bound.
Knowledge of the pts kidney and liver status.

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24
Q

Resistance of microogranisms to antimicrobial agents

A

If the concentration of the drug required to inhibit or kill the microorganism is greater than the concentration that can be safely achieved then its resistant.

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25
Q

Resistance occurs becasue?

A

Drug fails to read target (Decreased intracellular concentration)
Drug is inactivated
Target is altered (change in binding site)
Adaptations that bypass need for binding sites

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26
Q

Antibiotic resistance-Drug fails to read target

A

Change in cell wall to increase efflux- TCN and quinolone resistance
Decreased cell membrane permeability-beta lactam and quinolone resistance
Decrease cytoplasmic membrane transport aminoglycosides

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27
Q

Antibiotic resistance- Drugs inactivated

A

Lactamases deactivate beta-lactams

Phosphotransferases and acetyltransferases deactivate amino glycosides

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28
Q

Antibiotic resistance- Target is altered

A

DNA gyrase prevents quinolone binding

Methylation of rRNA prevents macrolide binding

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29
Q

Antibiotic resistance- Adaptations that bypass need for binding site

A

Use alternative metabolic route in folate synthesis avoiding effects of trimethoprim

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30
Q

Resistance- antibiotic use

A

Exerts selective pressure on bacteria to acquire resistance to survive

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31
Q

Resistance- innate resistance

A

a long-standing characteristic of a particular species of bacteria

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32
Q

Resistance- Acquired resistance

A

Mutations-random events that confer a selective advantage to the bacterium
Transfer or plasmids-transduction, transformation, conjugation

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33
Q

Transduction

A

The intervention of a bacteriophage (a virus that infects bacteria)
Contains bacterial DNA which may contain a gene resistant to antibacterial agents
Resistance can be passed down to progeny

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34
Q

Transformation

A

Incorporates DNA from the environment into bacteria
Penicillin resistance in pneumococci and Neisseria
PBPs and DNA pieces probably from closely related species of streptococcus

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35
Q

Conjugation

A

Passage of genes from cell to cell by direct contact through a bridge
Conjugation occurs primarily among gram-negative bacilli.

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36
Q

Multiple drug-resistance bacteria

A

Methicillin-resistant Staphylococcus aureus (MRSA) and Mycobacteria tuberculosis

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37
Q

Inhibitors of cell wall synthesis

A

Mammalian cells lack cell walls
Cell wall inhibitors require actively proliferating microorganisms for maximal effect
B-lactam ABX, vancomycin, bacitracin are major members of this class

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38
Q

Consequences of Cell wall inhibition

A

Lytic death- cell wall breaks down cell and cell is destroyed
Non-lytic death- dissolve the cell inside out
Tolerance-inhibition of growth becoming bacteriostatic (Cell shuts down to survive) instead of -cidal.

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39
Q

Beta Lactam Compounds

A 
Penicillins
Cephalosporins
Cabapenems
Monobactams
Beta lactamase inhibitors
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40
Q

Beta Lactam Compounds- Penicillins

A

Natural penicillin
Aminopenicillins
Penicillinase Resistanct Penicillins
Extended spectrum penicillins (Anti-psuedomonal)

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41
Q

Beta Lactam Compounds- Cephalosporin

A

First generation- fifth generation

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42
Q

Beta-lactam drugs

A

Defined by beta-lactam ring in chemical structure.
Inherently the beta-lactam ring is unstable to pH and beta-lactamases
Drugs undergo acylation; form covalent bond with trans-peptidase

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43
Q

Modifications of the beta-lactam ring define subclasses

A

Penicillins- thiazolidine ring
Cephalosporins- dihydrothiazine ring
Monobactam- no additional ring
Cabapenems- unsaturated ring with no sulfur external to ring

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44
Q

Beta-lactam ABX

A

Generally bactericidal
Most active against growing organisms
Many have gram-positive and gram-negative activity

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45
Q

Penicillins-Introduction

A

1928 discovery by Alexander Fleming
Widely used and relatively safe (Class B in pregnancy)
Beta-lactam ring (a thiazolidine ring) with side chains

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46
Q

What was the name of the original penicillin

A

Penicillin G

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47
Q

Penicillins Mechanism of Action

A

Interfere with the last step in bacterial cell wall growth
Works best on rapidly proliferating organisms
No effect on organisms without a cell wall (protozoa, mycoplasma, mycobacteria, fungi, and viruses)

48
Q

Penicillin resistance

A

Inactivated by beta-lactamase
Modification of PBP target (mechanisms of MRSA and penicillin resistant to pneumococci)
Impaired penetration of drug to target PBP

49
Q

Penicillin classification- Natural Penicillins

A

Penicilling G or V
Narrow spectrum, PCN G acid labile, penicillinase sensitive.
Highly active against sensitive stains of gram positive cocci (Not staphylococcus)
Anaerobes
Some gram negative

50
Q

Penicillin G or V

A

Tx infections of upper and lower respiratory tract, throat, skin, and GU tract.
Prophylaxis in rheumatic fever, dental procedure for those at risk of endocarditis, gonorrhea or syphilis expose.

51
Q

Penicillin G or V- gram positive cocci

A

Streptococcus, enterococcus faecalis, listeria morlocytogenes

52
Q

Penicillin G or V- Anaerobes

A

Bacteroides species and fusebacterium species

53
Q

Penicillin G or V- gram negative

A

E. coli, H. influenzae, N. gonorrhoeae, Treponema be, and suspectible psuedomonas species.

54
Q

Amniopenicillins

A

Ampicillin and amoxicillin

55
Q

Ampicillin and Amoxicillin

A

Activity of PCN G plus improved coverage of gram negative cocci adn Enterobacteriaceae
Not active against treponema or actinomyces

56
Q

Ampicillin and Amoxicillin- therapeutic uses

A

URI (Otitis, sinusitis), uncomplicated UTI, meningitis, salmonella infections

57
Q

Ampicillin and amoxicillin- resistance leading to combinatins with beta-lactamase inhibitors

A

Augmentin = Amoxicillin + Clavulanic acid
Ampicillin + sulbactam (unasyn)
Better coverage against H. Influenzae and Klebsiella sp.

58
Q

Penicillinase-Resistance Penicillins (antistaphylococcal penicillins)

A

Nafcillin, oxacillin, dicloxacillin
Methicillin and cloxacillin no longer available in US
Penicillinase resistance, narrow spectrum
Staph resistant to this class is called MRSA

59
Q

Penicillinase-Resistance Penicillins (antistaphylococcal penicillins)- tx

A

Used in treatment of staphylococcal infection with high beta-lactamase production (cellulitis and endocarditis)
Not active against gram-negative or anaerobic organisms

60
Q

Antipseudomonal penicillins

A

Piperacillin, ticarcillin, carbenicillin (PO)
Maintains activity of PCN G but gain great gram negative coverage including psuedomonas
Coverage against H. influenzae and kelbsiella sp
No coverage against treponema palladium or actinomyces
Gram negative infections in combo with aminoglycosides (bacteremias, pneumonias, resistant UTIs, infections in burn patients)

61
Q

Antipseudomonal penicillins- resistance issues and are paired with beta-lactamase inhibitors

A

Piperacillin + tazobactam = zosyn

Ticarcillin + clavulanic acid= timentin

62
Q

Beta-lactamase inhibitors

A

Clavulanic acid, sulbactam, tazobactam
Structurally similar but lack antibacterial activity
Act as suicide inhibitors -> potent, irreversible inhibitors of many lactamases.
Extends the spectrum of the ABX its paired with

63
Q

Addition of Beta-lacamase inhibitors- Aminopenicillins

A

Amoxicillin + clavulanic acid (augementen)

Ampicillin + sulbactam (unasyn)

64
Q

Addition of Beta-lacamase inhibitors- Antipseudomonal penicillins

A

Piperacillin + tazobactam (Zosyn)

65
Q

Addition of Beta-lacamase inhibitors

A

Increased coverage against H. flu, staph, moraxella catarrhailis
Variable coverage against gram (-) bacteria- pseudomonas, enterobacter, E. coli, klebsiella, serratia due to resistance to these beta-lactamase inhibitors.

66
Q

Penicillin administration- oral only

A

Penicillin V, amoxicillon w/ or w/out clavulanic acid

67
Q

Penicillin administration- Oral and IV

A

Nafcillin, ampicillin

68
Q

Penicillin administration- IV only

A

Antipseudomonal penicillins = piperacillin w/ or w/out tazobactam

69
Q

Penicillin administration- depot forms

A

procain and bensathine PCN G

70
Q

Penicillin pharmacokinetics-absorption

A

Many cannot be administered orally (due to destruction in acid)
Food may decrease the absorption of available oral penicillins
IV route bypasses absorption considerations and is preferred for serious infections.

71
Q

Penicillin pharmacokinetics- Distribution

A

Widely distributed with tissue level=to serum
Poorly penetrate the eyes, CNS, and prostate
ONLY PENETRATE THE CNS WHEN MENINGES ARE INFLAMED.

72
Q

Penicillin pharmacokinetics- metabolism

A

Most penicillins are not metabolized by dependent on the kidney for elimination

73
Q

Penicillin pharmacokinetics- elimination

A

Kidney excretion is the main route of elimination (except antipseudomonal PCN and nafcillin via billiary excretion)
Penicillins are filtered (10%) and actively secreted (90%) into the urine
Active secretion can be blocked by probenecid
Doses need to be adjusted in renal insufficiency

74
Q

Penicillins Adverse Effects

A

Hypersensitivity
Allergic responses develop in respinse to beta-lactam ring and derivatives (Cross rxn)
Anaphylactic shock is rare
Serum sickness- urticaria, rash, fever, angioedema
Interstitial nephritis and hemolytic anemia
Desensitization protocols are available.

75
Q

Penicillins adverse effects

A

GI upset with oral agents
Diarrhea
Secondary infections- vaginal candidiasis
Hepatitis w/ oxacillin
Neutropenia w/ nafcillin
Abnormal platelet aggregation with ticarcillin and carbenicillin

76
Q

PCN drug interactions

A

Don’t give concurrently with TCN or other bacteriostatic agents
Anti-pseudomonal PCN affect warfarin metabolism

77
Q

Cephalosporins Intro

A

Discovered 1948 by Guisepee Brotzu
Similar to penicillins chemically, MOA, and toxicity
Bactericidal
Inhibit bacterial-cell wall synthesis similar to PCNS
Structurally contain a dihydrothiazine ring connected to the B-lactam ring making them more resistant to hydrolysis by B-lactamase (Broader spectrum of activity)
Classified by 5 generations
Category B in pregnancy

78
Q

Cephalosporin Resistance

A

Mutations or carried on plasmids
Mutations in PBP
Production of Beta-lactamases
Alteration in cell-membrane porins in gram negative bacteria

79
Q

1st Generation Cephalosporins Spectrum

A

Good aerobic gram-positive, above the diaphragm anaerobes and community acquired gram negative coverage.
Stable against staph produced penicillinase
IV= Cefazolin (Ancef)
PO= Cephalexin (keflex)

80
Q

1st Generation Cephalosporins - Use

A

Used for septic arthritis in adults, skin infections, acute otitis media, prophylaxis for clean surgeries, and gram (+) infections in pts that cannot take penicillin

81
Q

2nd Generation Cephalosporins- Spectrum

A 
Two classes w/in second generation
Added gram (-) coverage (ie moraxella, neisseria, salmonella, shigella, haemophilus influenzae)
IV and PO= cefuroxime (zinacef, ceftin)
Added anaerobic coverage (especially B. Fragilis)
IV= cefotetan (cefotan)
82
Q

2nd Generation Cephalosporins- Use

A 
Added gram (-)
IV and  PO= cefuroxime (zinacef, ceftin)
Useful for sinusitis, otitis, CAP
Added anaerobic coverage
IV- cefotetan (cefotan)
Useful for tx of abd and gynecological infections
83
Q

Summary of 2nd generation cephalosporins

A

Gram (+): 2nd generation < 1st generation (somewhat)

Gram (-): 2nd generation > 1st generation (Significantly)

84
Q

3rd Generation Cephalosporins- Spectrum

A

Expanded gram-negative coverage and penetration of BBB
Cefpodoximine (Vantin), cefdinir (omnicef), cefixime (suprax)=oral
Cefotaxime (claforan)
Ceftriaxone (rocephin) = IV and IM
Ceftazidime (fortaz) distinguishes itself w/ increased anti-pseudomonal coverage.

85
Q

3rd Generation Cephalosporins- clinical use

A

Used to tx a wide variety of serious infections caused by organism that may be resistant to other antimicrobial agents
Drugs of first choice in tx of meningitis, pneumonia in children and adults, sepsis, peritonitis
Tx of UTI, skin infections, and oesteomyelitis, Neisseria gonorrhea infections

86
Q

Summary of 3rd generations cephalosporins

A

Gram (+): 1st generations > 2nd generation or 3rd generation

Gram (-): 3rd generation= 2nd generation > 1st generation

87
Q

4th Generation Cephalosporins- Spectrum

A

Cefepime (maxipime) IM/IV

Good activity against both gram(+) and gram (-) bacteria; ALSO ANAEROBIC COVERAGE

88
Q

4th Generation Cephalosporins- coverage

A

P. aeruginosa, H. influenzae, N. meningitidis, N. gonorrhoeae
Enterobacteriasceae that are resistant to other cephalosporins

89
Q

4th Generation Cephalosporins- clinical use

A

Intra-abdominal infections, respiratory tract infections, skin infections

90
Q

Summary of 4th generation cephalosporins

A 
Improved gram (+) compared to 2nd and 3rd generations (Closer to 1st generation)
Retain gram (-) = or > 2nd and 3rd generations
91
Q

5th Generation Cephalosporin

A

Ceftobiprole medocaril
Approved March 2008
Tx of complicated skin and skin structure infections (MRSA)
Inhibits PBPs involved in cell wall synthesis
Well tolerated-nausea and taste disturbances
IV form only

92
Q

Cephalosporins Pharmacokinetics

A

Orally administered absorbed rapidly
Presence of food may increase, decrease, or not affect absorption
Extensive distribution (most don’t cross CSF except cefuroxime, cefotaxime, ceftriaxone, cefepime)
Most eliminated via kidneys

93
Q

Cephalosporins toxicities/ side effects

A

Hypersensitivity same spectrum as PCN
Structure is structurally different allowing use in PCN allergy pts
5-10% cross sensitivity
Pts w/ anaphylaxis or angioedema with PCN should not recive
Suprainfection- resistant organism and fungi may proliferate.

94
Q

Cephalosporins toxicities/ side effects (2)

A

GI upset- N/V/D
1-3% allergic rxn - rash, fever, eosinophilia, urticaria
Cholelithiasis
Blood dyscrasias- eosinophilia, thrombocytopenia, leukopenia
Methylthiotetrazole side chains

95
Q

Cephalosporin drug interactions

A

Increased serum levels if co-administered with probencecid

Increased effects of warfarin- cefotetan, cefazollin, cefoxitin, ceftriaxone

96
Q

Carbapenems (the most broad spectrum)

A

Resistant to many beta-lactamases, most broad spectrum of beta-lactam class of ABX (gram + and gram - coverage)
Ertapenem (Ivanz), and imipenem-cilastin (primaxin)
Meropenem (merrem)

97
Q

Carbapenems- Ertapenem (Ivanz), and imipenem-cilastin (primaxin)

A

Coverage included resistant gram (-) bacilli (P. aeruginosa), gram (+) bacteria (MRSA, enterococcus), and anaerobes (bacteroides)
Tx of UTI, pneumonia, intra-abdominal infections, skin and soft tissue infections

98
Q

Carbapenems- meropenem (Merrem)

A

Greater activity against gram-negative
Intra-abdominal infections
Meningitis > 3 mo. of age

99
Q

Carbapenems- Pharmacokinetics

A

Given parenterally-> unstable in stomach acid
Cilastin inhibits dehydropeptidase I which inhibits imipenem by breaking beta-lactam ring
Well distributed in the body
Renal excretion

100
Q

Carbapenems- toxicities

A

Well tolerated- N/V, phlebitis at infusion site, leukopenia, elevated LFTs
Seizures in pts w/ renal failure
High degree of cross-sensitivity with PCN

101
Q

Carbapenems- Drug interactions

A

Ertapenem cant be infused w/ dextrose or other medications
Meropenem reduces valproic acid levels
Meropenem and ertapenem category B- safe
Imipenem/cilatin category C- not removed from option when considering risk vs. benefit

102
Q

Monobactams

A

Aztreonam (Azactam) the only monbactam available in the US
Spectrum of activity is purely gram-negative rods (inihibits mucopeptide synthesis in cell wall by binding to PBP, resistant to most beta lactamases)
No cross reactivity with PCN or cephalosporin allergic pts

103
Q

Monobactams- pharmacokinetics

A

Tx of gram (-) infections- pneumonia, soft-tissue infections, UTI, intra-abdominal and pelvis infections
Acid Labile
Widely distributed including inflames meningeal tissue
Excreted in urine unchanged

104
Q

Monobactams- Toxicity

A

No major toxicity- rash, N/V, elevated LFT, transient eosinophilia
No reported drug interations
Special populations- category B in pregnancy and safe in kids over 9 mo.

105
Q

Cycloserine

A

Inhibition that ultimately disrupts assembly of cell wall synthesis.
HIghly susceptible to resistance

106
Q

Cycloserine- indications

A

restricted for use as a secondary anti-tubercular drug

107
Q

Cycloserine- ADRs- very toxic

A

CNS toxicity-reversible w/pyridoxine

Renal impairment will accelerate toxicity

108
Q

Vancomycin Mechanism and Spectrum

A

Acts on diff binding site than beta-lactamase but has the same effect on cell wall synthesis.
Bactericidal

109
Q

Vancomycin Mechanism and Spectrum- mechanism of resistance

A

Acquired (plasmid born)- VanA phenotypes. A component of the peptidoglycan has modified so that vancomycin can not bind.
Innate resistance- most gram negatives-outer membrane resistance penetration

110
Q

Vancomycin

A

Active against gram positive organisms only.
Including beta-lactamase producing varieties
Reserved for pts allergic to B-lactams with serious gram (+) infections, infections resulting from MRSA, and used in antibiotic associated enterocolitis.

111
Q

Vancomycin Pharmacokinetics

A

Not absorbed when given orally and used orally in tx of C. Diff.
Given IV to maintain levels in a range that enhances outcome and avoids toxicity.
Widely distributed including CNS when meninges are inflamed.
Not metabolized by 90% renally excreted.

112
Q

Vancomycin clinical use

A

Main indication for parenteral vancomycin is for methicillin resistant staph aureus or staph epu
Used for penicillin resistant pnemococcus pneumonia

113
Q

Vancomycin-adverse effects

A

Local and infusion related reactions- red man syndrome (very flushed, hot, and itchy); phlebitis
Ototoxicity- irreversible hearing damage
Nephrotoxicity- reversible damage to the kidneys

114
Q

Bacitracin-MOA

A

Polypeptide compound
Interferes w/ recycling steps of the phospholipid carrier of petidoglycan synthesis
Not a very specific target (membrane lipid)

115
Q

Bacitracin- clinical use

A

Very nephrotoxic, so limited to topical use
Most gram (+) cocci and bacilli are sensitive
Often combined with neomycin or polymyxin or both

Pharmacotherapeutics I (23 decks)

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