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Pharm - Drugs > Antibacterial Drugs > Flashcards

Antibacterial Drugs Flashcards

1
Q

What are the factors to consider when selecting an anti-infective?

A
  • Microorganism factor
  • Host factors
  • Drug factors
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2
Q

What are examples of microorganism factors to consider when selecting an anti-infective?

A
  • Identification of organism
  • susceptibility
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3
Q

What are examples of host factors to consider when selecting an anti-infective?

A
  • Drug allergies
  • PK variables
  • Drug Absorption (food, diseases, other drugs)
  • Renal / hepatic function
  • Pregnancy / lactation
  • Site of infection
  • Signs and symptoms
  • Fever, malaise, leukocytosis, purulent drainage
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4
Q

What are examples of drug factors to consider when selecting an anti-infective?

A
  • economics
  • Can the patient afford the drug?
  • tissue penetration
  • drug toxicity
  • preventing resistance
  • are combination of drugs indicated?
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5
Q

Name 4 possible ways to get antibacterial resistance.

A
  • Alteration in receptor targets
  • decrease entry or efflux of drug out of the microorganism
  • alteration in metabolic pathway
  • drug is inactive
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6
Q

Antibacterial agents work by 4 distinct mechanism of action. Name the 4

A
  • inhibition of cell way synthesis
  • inhibition of protein synthesis
  • inhibition of folic acid biosynthetic pathway
  • inhibition of DNA/RNA synthesis
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7
Q

What is minimal inhibitory concentration?

A

lowest concentration of an antibiotic that inhibits microorganism growth in liquid culture

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8
Q

What is minimal bactericidal concentration?

A

the lowest concentration of antibiotics that induces bacterial cell death

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9
Q

Why would you want to combine drugs?

A

To achieve synergistic killing effect by use of drugs that work by different mechanism

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10
Q

Name 4 drugs that work by inhibiting cell wall synthesis

A

-penicillin, - cephalosporins -carbapenem - monobactam

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11
Q

Is penicillin bacteriostatic or bactericidal?

A

bactericidal

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12
Q

What enzyme does penicillin bind to?

A

transpeptidase enzyme

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13
Q

what does transpeptidase enzyme do?

A

to crosslink NAM and NAGs; crosslink provides structural stability.

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14
Q

How does penicillin inhibit cell wall synthesis (in general)?

A

interfere with formation of peptidoglycan layer

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15
Q

What is penicillin binding proteins?

A

group of proteins that penicillin binds to and autolysins that hydrolyze and destroy components of the cell

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16
Q

What is the general targets of PBP?

A

transpeptidase

carboxypeptidase - break peptide bonds

endopeptidases - break peptide bonds

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17
Q

True or false, penicillin need to gain access to microbial cell?

A

True

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18
Q

Name 4 ways bacteria may become resistance to penicillin

A
  • modification of their PBPs - active pumping of the drugs back out of the cell - cleavage of B-lactam ring structure of penicillin via B-lactamases (also called penicillinases) within the periplasmic spaces, rendering the drug inactive - Altered porin (gram-neg only) that prevents drugs from reaching the PBP targets.
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19
Q

What are some adverse effects of penicillin?

A

hypersensitivity. Type 2

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20
Q

Do most penicillin when excreted are in the changed or unchanged form?

A

unchanged

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21
Q

High IV doses of penicillin may cause what?

A

seizures or antiplatelet effects

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22
Q

Penicillin binding to PBPs do 2 things.

A

1) inhibits cell wall synthesis by blocking transpeptidation of peptidoglycan 2) activate autolytic enzymes in the cell wall that cause lesions resulting in bacterial death.

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23
Q

Where are B-lactamases found?

A

periplasmic space

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24
Q

What must happen in bacteria for penicillin to be effective inhibitors of cell wall synthesis?

A

microorganism must be actively growing and dividing

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25
Q

What do pharmacologic antagonism occur with penicillin?

A

combined with drugs that are bacteriostatic like tetracycline.

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26
Q

Would combination of tetracycline and penicillin produce synergistic actions?

A

NO!

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27
Q

Do combining penicillin or any antibiotic with oral contraceptive lessen the efficacy of the oral conceptive? If so, why and how?

A

Yes, because estrogens are recycled via the enterohepatic recirculation pathway. But what does antibiotic do to the normal flora… Go to the next card to find out

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28
Q

True or false, normally gut flora cleave estrogen-glucuronide conjugates?

A

True

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29
Q

What happens when antibiotic are given to the normal GI flora?

A

disrupted the flora… kill them?

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30
Q

What happens to estrogen in the enterohepatic circulation when gut flora are disrupted?

A

impair the recirculation, thus diminishing their half life. Thus, you should warn women who are relying on contraceptive for pregnancy prevention that a backup method should be considered when taking antibiotics… and for 7 days after.

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31
Q

what are the 4 distinct categories of penicillin?

A

-natural - aminopenicillin - penicillinase-resistant - antipseudomonal

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32
Q

What can you coadminister with penicillin if you know the bacteria has B-lactamase enzyme?

A

coadminister with irreversible inhibitors of B-lactamase

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33
Q

General rule, what type of penicillin are used to treat gram +? which are used to treat gram -?

A

Gram +: natural & penicillinase Gram - : aminopenicilins and antipseudomonal

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34
Q

What are some examples of natural penicillin?

A

Penicillin G and Penicillin V

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35
Q

What are the PK of penicillin G?

A
  • readily destroyed in acidic environment. - must be administered IV or IM -long acting IM used to prevent rheumatic fever and to treat syphillis
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36
Q

What are the PK of pencillin V?

A

more stable than penicillin G in acidic environment. - administered orally -must be taken on empty stomach 1 hr before meal or 2/3 hours after for maximal efficacy

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37
Q

FYK: what are natural penicillin used to treat? Not on the test

A

Gram + Pencillin G = serious strep; neurosyphilis, endocarditis. Penicillin V= strep pharyngitis. Both inactivated by B-lactamases.

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38
Q

Ampicillin and amoxicillin are what type of penicillins?

A

aminopenicillins.

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39
Q

What are the PK of synthetic ampicillin?

A
  • administered enterally or parenterally - prescribed orally but must be taken on empty stomach.
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40
Q

What are the PK of amoxicillin?

A
  • taken with or w/o food because it is stable in the presence of gastric acid.
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41
Q

What is the purpose of taking with or without food? How does eating affect pH or absorption?

A

Eating food slows down gastric emptying, thus drugs that are unstable in acidic environment like the stomach should not be administered with food.

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42
Q

Which is most stable in the stomach, amoxicillin or ampicillin?

A

amoxicillin

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43
Q

FYK: what do aminopenicillin usually treat?

A

commonly treat ENT, lower respiratory tract. Ineffective against bacteria with B-lactamases, thus coadministered with B-lactamases inhibitor.

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44
Q

What are some drugs of the penicillinase-resistant penicillin?

A

Dicloxacillin, methicillin, oxacillin, nafcillin

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45
Q

What is special about the mechanism of action of penicillinase-resistant penicillin?

A

it contains side groups that protect the drug from being inactivated by bacterial B-lactamases

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46
Q

PK of penicillinase-resistant penicillin?

A
  • Methicillin, oxacillin, and nafcillin are given parenterally. - MNO = Parenterally Dicloxacillin is given orally.
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47
Q

FYK: Clinical Use of Pencillinase-resistant penicillin?

A

treat B-lactamases producing Staphylococci. - Tx and prevention of upper/lower respiratiory, skin, bone, joints. Tx meningitis, septicemia, endocarditis Assume all Staph synthesize B-lactamases. MRSA: resistant to all penicillin and cephalosporin.

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48
Q

What are examples of antipseduomonal penicillins (extended spectrum penicillins)?

A
  • carbenicillin - ticarcillin - mezlocillin - piperacillin
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49
Q

PK of antipseudomonal penicillins?

A

All are given parenterally. - carbenicillin is the only drug given orally, but therapeutic levels are then found only in urinary tract; limiting its enteral utility to treating UTI and prostatic infection.

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50
Q

What are some drugs that are Irreversible inhibitors of B-lactamases?

A

-Clavulanic acid - sulbactam - tazobactam

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51
Q

What are some clinical uses of Irreversible inhibitors of B-lactamases?

A

No antimicrobial activity themselves. - when combined with penicillin, expanded coverage against B-lactamases producing microorganisms.

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52
Q

Describe the structure and PK of cephalosporin?

A

structurally resemble pencillin and posses a B-lactam chemical backbone. - stable to pH changes - taken with or w/o food -alternative to patients with penicillin allergy.

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53
Q

What is the drug of choice to treat Klebsiella?

A

Cephalosporins

54
Q

What are other clinical utilities of cephalosporin?

A
  • treat 3 microorganisms that causes pediatric meningitis (H. influenza, Strep. Pneumonae, Neissera meningitis)
55
Q

Mechanism of action of Cephalosporin.

A

Same as penicillin.

56
Q

What are some mechanism of resistance of these (Cephalosporin) drugs?

A

porin alternation (prevent entry; especially in gram -) mutation in PBP - lack of PBP

57
Q

What are the possible adverse effects of Cephalosporin drugs, based on structure?

A

There is a possibility for penicillin-allergic patients to be hypersensitive to cephalosporins. Recent data suggest lower cross-reactivity, but rule of thumb, refrain from prescribing cephalosporin with document history of anaphylatic reactions to penicillin.

58
Q

Name one adverse effect common with oral cephalosporin.

A

GI irritation; taking with food may prevent this.

59
Q

What is a side effect of administering cephalosporing parenterally?

A

Local irritation @ site of injection

60
Q

What are other side effects of cephalosporin?

A
  • renal toxicity, b/c excreted by the kidney -2nd/ 3rd generation may cause disulfiram-like reaction and hypoprothrmobinemia. - newer cephalosporin, when administered parenterally may cause seizures. (usually found in individuals with impaired kidney function b/c of drug accumulation) - may cause 2ndary infection b/c it disrupts the normal flora (pseudomembranous colitis and vaginal yeast infection)
61
Q

What are some drugs in the carbapenems’ family?

A

imipenem/ cilastatin, doripenem, ertapenem, and meropenem.

62
Q

What is the mechanism of action of carbapenems?

A

Bactericidal inhibit cell wall synthesis. - different stereochemical structure in their B-lactam ring that prevents them to be degrade from B-lactamases. - administer parenterally

63
Q

What are some other antibiotics that disrupt cell walls other than penicillin, cephalosporin and carbanems?

A

vancomycin telavancin

64
Q

What are the mechanism of action for vancomycin and telavancin?

A

interfere with cell wall by blocking polymerization and crosslinking of peptidoglycan by binding to D-Ala- D-Ala portion of the cell wall. Telavancin also disrupt the membrane potential and changes the cell permeability because of the lipophilic side chain moiety. - only effective against Gram +.

65
Q

What is the mechanism of action of cycloserine?

A

-inhibits cell wall synthesis in gram + and gram - microorganisms. - reserved for treating TB infection that are resistant to anti-TV drugs.

66
Q

What is the mechanism of action of Polymyxin B?

A
  • bactericidal to nearly all Gram - bacilli, except Proteus - cationic detergent that disrupts lipoprotein in bacterial cell wall, increasing membrane permeability.
67
Q

True or False, Protein synthesis inhibitors are not bactericidal?

A

False

68
Q

How do protein synthesis inhibitors exert their effects?

A
  • at different location along the protein synthesis pathway. - directly interferes with initiation phase of protein synthesis - binding of tRNA - activity of peptidyl transferase - inappropriate AA insertion, which interferes with protein function
69
Q

What are some examples of aminoglycosides?

A

Amikacin Gentamicin Kanamycin Netilmicin Streptomycin Tobramycin Neomycin

70
Q

What are the mechanism of action of aminoglycosides?

A
  • binding to the bacterial 30S ribosomal subunit. - aminoglycosides interfere with formation of the initiation complex - misread mRNA and miscode AA into the growing peptide chain - cause ribosomes to separate from mRNA.
71
Q

What is a monosome?

A

Blockade of movement of the ribosome that may occur after formation of a single initiation complex, resulting in a mRNA chain with a single ribosome. (key ribosome) - causes inefficient protein synthesis b/c polysomes typically work together during protein translation.

72
Q

What are the PK of aminoglycosides?

A
  • too water soluble to be given orally. - given parenterally - exhibits marginal penetration of the CNS b/c of high degree of hydophillicity, except in neonates. - short half life in the systemic circulation; accumulates in inner ear and renal cortex, causing nephrotoxic and ototoxic side effects. - exhibits postantibiotic effect due to translational mechanism of action.
73
Q

What is postantibiotic effect?

A

Micoorganism continue to die even as plasma level of drug decline.

74
Q

What ways of resistance to aminoglycoside drugs?

A
  • used only in treating Gram - - anaerobes have resistance by alteration of proteins on their ribosomes, preventing aminoglycosides from binding. - bacteria may alter the drug via phosphorylation, acetylation, or adenylation, interfering with the drug’s ability to bind efficiently to ribosomal units.
75
Q

What are examples of drugs in the tetracycline family?

A
  • tetracycline - minocycline, - doxycycline - demeclocycline - oxytetracycline - tigecycline (all ending with cycline)
76
Q

What is the mechanism of action for tetracyclines?

A

Inhibit protein synthesis through REVERSIBLE binding of 30S ribosomal subunts, preventing amino-acyl-tRNA to attach new AA to the growing peptide.

77
Q

What is special about tigecycline?

A
  • 1st glycylcycline antibiotic
78
Q

What are glycycyclines?

A
  • antibiotics derived from tetracycline that have 2 mechanism to overcome resistance. - resistance mediated efflux pump - ribosomal protection - closely structured to minocycline.
79
Q

True or false, tetracycline are bactiostatic against Gram + and Gram -?

A

True - passive diffusion in gram - - active transport in gram +

80
Q

What are the PK of tetracyclines?

A
  • gastric absorption may be inhibited by chelation to divalent cation (Fe, Mg, Ca-antacids, milk) and bile acid resins - administer on empty stomach - doxycycline is metabolized hepatically an excreted in feces (safest option in pt with renal dysfunction)
81
Q

What are pathways of resistance to Tetracyclines?

A
  • Gram +: active pumping of drug out of the cell via efflux pump Gram -: alteration in their outer membrane protein that prevent entry - tigecycline is not affected by tetracycline resistance mechanisms and cross-resistance between it and other drugs are not observed.
82
Q

What is Cloramphenicol mechanism of action?

A
  • bacteriostatic - binds to 50S ribosomal subunit and block linkage of incoming AA to the growing peptide chain by interfering with peptidyl transferase.
83
Q

What is the PK of chloramphenicol?

A

it is metabolized via glucuronidation - can result in “gray baby” or ‘gray adult’ syndrome in patients with hepatic disease because infant fail to eat, fail to thrive, become pale and cyanotic, have abdominal distention, and may die of respiratory or vasomotor collapse. - if signs or symptom arise, discont. drug ASAP

84
Q

What is the common drug of lincosamine?

A

clindamycin

85
Q

How does clindamycin work?

A

prevent protein synthesis by binding to 50S and prevent translocation of incoming AA from ribosomal A site to P site.

86
Q

What are examples of macrolides drugs?

A
  • Erythomycin base: estolate, stearate, ethylsuccinate - clarithromycin - azithromycin
87
Q

How do macrolides work?

A
  • bind to 50S ribosome subunit like clindamycin and cholramphenicol.
  • prevent translocation of AA from A site to P site.
  • because of same mechanism of action as clindamycin and chloramphenicol, they may interfere with one another and cross-resistance may develop.
  • bacteriostatic or bactericidal depending on concentration.
88
Q

What are pathways of resistance for macrolides?

A
  • permeability to drug is altered.
  • methylation of 50S ribosome
  • bacteria develop mechanism to enzymatically destroy the drug.
89
Q

What are some adverse effects of erythromycins?

A
  • GI distress; minimized when taken with food - estolate salt may cause cholestatic hepatitis –> elevated liver enzymes, maliase, nausea, vomitting, abdominal cramps, jaundice, fever - may potentiate other drugs by inhibiting microsomal P450 3A4, leading to toxicity of other drugs. - prolong QT interval –> leading to torsades de pointes, fatal cardiac arrhythmia, (especially when combined with meds that also prolong QT intervals).
90
Q

What are the adverse effects of clarithomycin?

A
  • prolong QT intervals - inhibits P450 3A4; - unlike erythromycin, less GI distress
91
Q

What are the adverse effects of azithromycin?

A
  • do not prolong QT interval - do not inhibit hepatic microsomal P450 enzymes. - minimal incidence of diarrhea
92
Q

What are examples of ketolides?

A
  • telithromycin
93
Q

What is the mechanism of action of telithromycin?

A
  • inhibits 50S ribosomal subunits - bind to 2 separate domains - need 2 diff. mutation to develop resistance - poor substance for efflux pump - these characteristics contribute to its effectiveness.
94
Q

What is Retapamulin MOA?

A
  • topical ointment - structurally, pleuromutilin antibiotic - interfere with peptidyl transferase - bind to unique site on 50S, prevent formation of active 50S - inhibits peptidyl transferase - block P-site interaction - used to treat skin infection (staph, strep)
95
Q

What is Mupirocin MOA?

A
  • topical cream or ointment - result in no cross resistance - inhibits tRNA that transport Isoleucine.
96
Q

What is Linezolid MOA?

A
  • interferes by binding to unique RNA site on 50S subunit, preventing formation of 70S complex - bacteriostatic against enterococci and Staph - bacteriocidal to Strep. - oral tablet with 100% F - tx: vancomycin-resistant Enterococcus faecium; MRSA and community acquired Staph Pneumoniae
97
Q

What is Streptogramins?

A
  • combination of quinupristin and dalfopristin
98
Q

What is Streptogramin MOA?

A
  • combination acts on bacterial ribosome and interferes with protein synthesis - Quinupristin irreversiblely blocks ribosome and inhibit late phase of protein synthesis. - Dalfopristin inhibits early phase of protein synthesis. - tx: life-threatening infection caused by vancomycin-resistant enterococci and skin infection caused by MRSA.
99
Q

What does folic acid synthesis inhibitors target?

A

synthesis of critical bacterial metabolites, in specific, inhibiting the bacterial folic acid synthesis. - bacteria can synthesize their own folic acid, humans cannot and obtain them from vit. B in the diet. - However, bacteria cannot use folic acid from the environment.

100
Q

Name the sulfoamides drugs.

A

sulfadizine silver “ ‘’’’’ sulfisoxazole sulfamethoxazole sulfacetamide sulfasalazine

101
Q

What are the MOA of sulfonamides?

A

Compete with parabenzoic acids at the first biosynthetic step of the folic acid pathway

102
Q

What is the PK of sulfonamides?

A
  • highly protein bound - drug interaction, if sulfonamides are displaced from the plasma protein-binding site. - adverse effects with warfarin, NSAID, sulfonylureas. - not used in pregnant women near term and kids <2 m/o b/c drugs displace bilirubin - hyperbilirubinemia in neonates may cause kernicterus (CNS disorder caused by elevated bilirubin)
103
Q

What are mechanisms of resistance of sulfonamides?

A
  • reduce bacterial uptake of the drug - develop alternative metabolic pathway to synthesize folic acid - production of excess para-aminobenzoic acid to compete with sulfonamides - alteration or mutation in dihydropteroate synthesis (enzyme in the rate limiting step of folate synthesis)
104
Q

What are the metabolic PK of sulfonamides?

A
  • hepatically acetylation, oxidation, and/or glucuronidation. - slower acetylators may be at risk for hypersensitivity - oxidation of sulfonamides likely responsible adverse effects. - metabolites are excreted renally
105
Q

What is the MOA of trimethoprim?

A

inhibits dihydrofolate reductase, last step of folic acid synthesis.

  • nearly always used in combination with sulfamethoxazole for synergic effect.
  • possess antimalarial properties
  • alone: bacteriostatic - combo with sulfonamides: bactericidal.
106
Q

What are the resistance mechanism of trimethoprim?

A
  • reduce bacterial uptake - alteration or mutation in dihydrofolate reductase - overproduction of dihydrofolate reductase
107
Q

What kind of inhibitor is fluoroquinolones

A

DNA/RNA synthesis inhibitor

108
Q

Name the drugs in the fluroquinolones family.

A
  • besifloxacin - ciprofloxacin - gatifloxacin - gemifloxican - levofloxacin - moxifloxican - norfloxacin - ofloxacin (all ending in -floxacin)
109
Q

What is the MOA of fluoroquinolones?

A
  • bactericidal - interferes with DNA synthesis by inhibiting one of 2 enzymes. - inhibits DNA gyrase (relax supercoil DNA, responsible for replication and transcription, and DNA repair) - can also inhibit topoisomerase IV (enzyme used in separating DNA into daughter cells during replication) - gemifloxican: both mechanisms, thus resistance req. 2 mutations.
110
Q

what is the PK for fluroquionolones?

A
  • Food, cation (Ca, Fe, Al, Mg, Zn) impair absorption of fluoroquinolones. - drug penetration to CNS is low, it distributes to all body compartments.
111
Q

Resistance for Fluroquinolones are by:

A
  • altered membrane permeability or mutation in the DNA binding region
112
Q

Adverse effects of fluroquinolones:

A
  • photosensitivity, rash, and rarely Stevens-Johnson syndrome. - dysgeusia: bad taste in the mouth - prolong QT (cautious)
113
Q

What is the name of the drug in the lipopeptide family?

A

daptomycin

114
Q

What is the MOA of daptomycin?

A
  • differs from all other antimicrobial
  • binds to bacterial membrane, causing rapid depolarization
  • loss of membrane potential brings DNA, RNA and protein synthesis to a halt, cell death.
  • no known cross-resistance - excreted unchanged in urine
115
Q

What are the 3 drugs with distinct mechanisms?

A
  • Metronidazole - Nitrazoxanide - Tinidazole - these drugs may be mutagenic and possibly carcinogenic. - tinidazole and metronidazole are contraindicated during the 1st trimester of pregnancy.
116
Q

What is Metronidazole MOA?

A
  • selectively absorbed by anaerobic bacteria and sensitive protozoa - nonenzymatically reduced by reacting with reduced ferredoxin… generating pyruvate/ferredoxin oxido-reductase that is toxic to the cell. This result in inhibition of DNA synthesis, degradation of DNA, breaking of DNA, and inhibition of nucleotide synthesis.
117
Q

How does Nitazoxanide work?

A
  • interferes with pyruvate / ferredoxin oxidoreductase enzyme electron transfer, a reaction essential in anaerobes.
118
Q

How does Tinidazole work?

A
  • cause cytotoxicity by damaging DNA and inhibiting further DNA synthesis.
119
Q

What is the PK of metronidazole?

A
  • penetrates the CNS and used to treat meningitis and brain abscesses caused by anaerobes. - absorption through skin or mucus membrane is low when used topically. - used topically to treat acne or rosacea
120
Q

What is Rifaximin MOA?

A

a rifampin derivative that inhibits bacterial RNA synthesis by binding to bacterial DNA-dependent RNA polymerase

121
Q

What is the PK of rifaximin?

A
  • not absorbed from GI tract - excreted unchanged in feces - does not intefere with cyto P450 like rifampin
122
Q

What are mycobacteria?

A
  • gram +, rodlike aerobic bacteria that form filamentous branching structures.
123
Q

Why are mycobacteria hard to treat?

A
  • grow slowly (18 hrs to divide) - can lie dormant - cell wall are thick and impermeable (hard to get in) - reside inside host cells (hard for get to therapeutic index) - become resistant to quickly Thus, need to treat for long period, with several different antibiotic simulataneously. - current tx: isoniazid, rifampin, pyrazinamide, ethambutol, and clofazimine
124
Q

What is Isoniazid MOA?

A
  • inhibit the synthesis of mycolic acid (essential part of mycobacterial cell wall)
125
Q

What is the PK of Isoniazid?

A
  • diffuse throughout the body water (include CNS) - metabolized by acetylation - fast acetylators may not reach therapeutic level and will have short plasma half life. - slow acetylators are at great risk for drug-related toxicity because of long half life.
126
Q

What is the MOA of rifampin?

A
  • inhibits bacterial RNA polymerase (prevent transcription by suppressing initation of RNA chain formation)
127
Q

What is the PK of rifampin?

A
  • potent inducer of drug metabolism and alter plasma level of other drugs. - watch for drug-drug interaction - drug of choice for meningococcal meningitis
128
Q

What is the MOA of pyrazinamide?

A
  • unclear - lowers pH in the tubercle cavity and inhibits growth of mycobacterium
129
Q

What is the MOA of ethambutol?

A
  • inhibits RNA synthesis and decrease replication of tubercle bacilli
130
Q

What is the MOA of clofazimine

A
  • binds to mycobacterial DNA and inhibits RNA polymerase actions. - activity of this drug is slow - pt treated for at least 2 years or life.

Pharm - Drugs (9 decks)

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