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Bugs and Drugs > Antibacterial Drugs > Flashcards

Antibacterial Drugs Flashcards

1
Q

What are the four main antibiotic antimetabolites and nucleic acid inhibitors ?

A
  1. Sulfonamides
  2. Fluoroquinolones
  3. Other (for UTI)
  4. Rifamycins
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2
Q

What are the 2 major sulfonamides?

A
  1. Sulfisoxazole

2. sulfamethoxazole-trimethoprim (co-trimoxazole)

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3
Q

What are the 2 major fluoroquinolones?

A
  1. ciprofloxacin

2. levofloxacin

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4
Q

What drugs are used as antimetabolite/nucleic acid inhibitors for UTI?

A
  1. nitrofurantoin

2. metronidazole

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5
Q

What rifamycin drugs are we responsible for?

A
  1. rifampin

2. rifabutin

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6
Q

What are the major categories of antibiotics used as cell wall inhibitors?

A
  1. B-lactams
  2. glyopeptides
  3. “Other”- bacitracin, cycloserine, fosfomycin
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7
Q

What are 3 categories of B- lactams we are responsible for?

A
  1. penecillins
  2. cephalosporin
  3. “other”
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8
Q

What are the major penecillins? (8)

A
  1. Pen G
  2. Pen G- benzathine
  3. nafcillin
  4. oxacillin
  5. ampicillin
  6. amoxicillin
  7. ticarcillin
  8. piperacillin
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9
Q

What are the major cephalosporins?

A
  1. cefazolin
  2. cephalexin
  3. cefuroxime
  4. cefoxitin
  5. cefotaxime
  6. ceftriaxone
  7. ceftazidime
  8. cefepime
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10
Q

What two b-lactams are NOT penecillins or cephalosporins?

A

Clavulanic acid

imipenem (+cilastatin)

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11
Q

What is the major glycopeptide bacterial cell wall inhibitor?

A

vancomycin

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12
Q

What are the four types of ribosome binder antibiotics?

A
  1. aminoglycosides
  2. tetracyclines
  3. MLSK drugs
  4. Linezolid
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13
Q

What are the major aminoglycosides?

A
  1. streptomycin
  2. gentamycin
  3. tobramycin
  4. amikacin
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14
Q

What are the major tetracyclines?

A
  1. tetracycline
  2. doxycycline
  3. minocycline
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15
Q

What are the three classes of MSLK drugs we are responsible for?

A
  1. Macrolides (erythromycin, clarithromycin, azithromycin)
  2. Lincosamide (clindamycin)
  3. Streptogramin (Quinupristin-dalfopristin)
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16
Q

What are the three macrolides we are responsible for?

A
  1. erythromycin
  2. clarithromycin
  3. azithromycin
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17
Q

What is the major lincosamide we are responsible for?

A

clindamycin

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18
Q

What is the major streptogramin we are responsible for?

A

quinupristin-dalfopristin

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19
Q

What antimicrobial drug is a lipopeptide?

A

daptomycin

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20
Q

What antimicrobials are anti-leprosy drugs?

A
  1. dapsone

2. rifampin

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21
Q

Are sulfonamide drugs bacteria static or bactericidal?

A

static

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22
Q

All cells require ______ acid to grow, divide and sustain metabolism.
The active form is ____________ which must transfer carbons to synthesize purines, pyrimidines and several AA.

A

folic acid.

The active form is tetrahydrofolate

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23
Q

What is different about mammalian cells and microbes in regard to folic acid acquisition?

A

Mammalian cells take folic acid in as a vitamin through folic acid receptors
Microbes synthesize folic acid

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24
Q

What are the three moieties of folic acid?

A
  1. pABA
  2. dihydropteridine
  3. glutamate
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25
Q

What is the first step in the microbial synthesis of folate?

A

pABA and dihydropteridine condense to make dihydropteroic acid.

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26
Q

What is the mchanism of action of sulfonamide drugs?

A

They are pABA analogs and act as competitive inhibitors for dihydropteroic acid synthase

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27
Q

What antagonizes the function of sulfonamide drugs?

A

Tissue break down products because microbes can import purines, pyrimidines and AA from the pus bypassing the need to synthesize their own

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28
Q

What are the steps of folic acid synthesis in microbes?

What drugs inhibit steps in this pathway?

A
  1. pABA + dihydropteredine–>DAS–> dihydropteroic acid
  2. dihydropteroic acid + 1 to 6 glutamic acids–> dihydrofolate
  3. dihydrofolate–> DHFR–> tetrafolate

Sulfonamides are competitive inhibitors for DAS by mimicking pABA

Trimethaprim inhibits DHFR

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29
Q

What are two mechanisms of resistance to sulfonamides?

A
  1. excess pABA concentration in the microbe cytoplasm

2. altered DAS that does not bind sulfonamides

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30
Q

How are sulfonamides:

  1. absorbed
  2. distributed
  3. Metabolized
  4. excreted
A
  1. orally
  2. distribute to all tissues including CNS
  3. metabolized via acetylation in the liver
  4. glomerular filtration
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31
Q

In a patient with what deficiency would the use of sulfonamide be contraindicated?

A

In patients with G6PD deficiency (lacking G6phosphate dehydrogenase).
If they lack G6PD they will not make glutathione reductase which is necessary to reduce oxidative substances.

Sulfonamides make a lot of oxidized species

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32
Q

What are the therapeutic uses for sulfonamides alone?

A
  1. Nocardia infections

2. Minor UTI because G- and chlamydia respond

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33
Q

What are the therapeutic uses for sulfamethoxazole-trimethaprim (cotrimoxazole)?

What bacterial species is it effective against?
What bacterial species is it ineffective against?

A

This would inhibit two steps in folic acid biosythesis and act synergistically –> bactericidal

  • UTI
  • Respiratory
  • Shigella, typhoid fever, salmonella, p. jirovecii
  • ear infections

This gives protection against G+, G-, MRSA and fungi.
NOT protective against anaerobes

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34
Q

What is the most popular sulfonamide for single-drug therapy? Why?

A

Sulfisoxazole

  1. free and acetylated are both soluble
  2. practically no side effects
  3. good CNS distribution
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35
Q

Which sulfonamide is typically used with trimethaprim? Why?

A

sulfamethoxazole because it has a longer half life than sulfisoxazole so it is more matched to the half life of trimethaprim

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36
Q

What bacteria are fluoroquinolones used against?
What bacteria are they not effective against?
Are they bactericidal or bacteristatic?

A

G+, G- and other infections (broad spectrum)
They are only effective against aerobes
They are bactericidal

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37
Q

What is the mechanism of fluroquinolone action?

A

They bind prokaryotic topoisomeraseIV or gyrase-DNA complexes inactivating the enzymes.
This makes them no longer able to relieve supercoil of the DNA and inhibits transcription and replication

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38
Q

_____________________ is the major target for fluoroquinolones in G+ bacteria while ________ is the target in G- bacteria.

A

Topoisomerase IV= G+ target

Gyrase = G- target

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39
Q

Describe the pharmokinetics of fluoroquinolines.

  1. Absorption
  2. distribution
  3. metabolism
  4. excretion
A
  1. absorbed orally (but inhibited by cations like milk, antacids, Fe and Ca)
  2. NO CNS penetration
    3/4- depends. some enter bile and enterohepatic circulation while others are eliminated by the kidney
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40
Q

Who would the use of fluoroquinolines be contraindicated in?

A
  1. children under 18 and women because it weakens cartilage

2. Skin sensitive because it causes phototoxicity

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41
Q

How is resistance to fluoroquinolines achieved?

A

due to its widespread use in animal feed, resistance is now due to

  1. altered topoisomerase target
  2. increased efflux and decreased influx mechanisms
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42
Q

What are the two major fluoroquinolones and what is the difference between the two?

A
  1. Ciprofloxacin- used widespread but not respiratory because it is weakly active against Strep pneumonia
  2. Levofloxacin- Active against strep pneumonia, staph, G+ and G-
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43
Q

What is nitrofurantoin used to treat?
What is the mechanism of action?
Is it static or cidal?
Who cannot use it?

A

It is used to treat UTI
It is reduced within bacterial cells and makes toxic intermediates to damage DNA
It is both static and cidal.
Pregnant women can’t use it because it causes hemolytic anemia in newborns

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44
Q

What is metronidazole used to treat?

How is it different from the other anti-metabolite/nucleic acid inhibitor drugs?

A

UTI and is active against protozoal and anaerobic bacteria

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45
Q 
What is the mechanism of action of rifamycin?
Is this class of drugs bacteriostatic or bactericidal?
A

They bind to DNA-directed RNA polymerase to inhibit it. This blocks initiation of transcription.

Bactericidal

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46
Q

What are the two main rifamycin drugs?

What infections are they used against?

A
  1. Rifampin- TB, prophylaxis of meningococcal meningitis, Legionella,hat leprosy in dapsone-resistant populations
  2. Rifabutin- TB and Mycobacterium avium (MAC infection common in AIDs patients)
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47
Q

How do b-lactams inhibit bacterial growth in general?

A

They inhibit cell wall production and remodelling and activate autolysin.

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48
Q

What are the steps in bacterial cell wall synthesis?

A
  1. disaccharide pentapeptide is synthesized
  2. It binds to an isoprenoid lipid and flips across the membrane
  3. Attachment of the disaccharide to the growing polysaccharide chain is established
  4. Pentapeptides are crosslinked by transpeptidase which binds to the terminal D-ala-D-ala
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49
Q

What is different structurally between penecillins, cephalosporins and carbopenems (imipenem)

A

They all have the same b-lactam structure (cyclic structure with 4 sides and a nitrogen amide in the ring)
They differ in the second ring adjacent to the b-lactam.
Penicillin- five member ring with a S group
Cephalosporin- six member ring with a S group
Carbopenem- five member ring with no sulfur

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50
Q

What is the mechanism of action that B-lactams work?

Is the effect bacteriostatic or bactericidal?

A
  1. They resemble D-ala-D-ala so transpeptidase will bind irreversible to the b-lactam and will be inactivated.
    The bacteria will not be able to synthesize the cell wall (or remodel it) and thus will cease growing.
    This effect is bacteriostatic.
  2. Once cell wall synthesis is stopped by B-lactam, autolysins will degrade the cell wall and the cell will lyse
    This is bactericidal
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51
Q

What must the cell be doing for a b-lactam to be an effective drug?

A

The cell must be growing to be killed by penicillin. The more vigorous the growth, the stronger the effect

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52
Q

What are the two main mechanisms of bacterial resistance to beta-lactams?

A
  1. Inherent resistance-
    * porins of G- and b-lactamase concentration in G- periplasm
  2. Acquired resistance
    * beta-lactamases break the unstable 90 degree bonds of the b-lactam
    * transpeptidases have altered structure
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53
Q

B- lactams are great drugs for ________ infections but are less effective against ______ because______.

A

They are great with G+ but are less good at G- due to inability to come through porins and b-lactamase concentrated in the periplasm

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54
Q

What drug is a suicide inhibitor of b-lactamases, encouraging its use with penicillin or cephalosporin resistant bacteria?

A

Clavulanic acid

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55
Q

Describe the pharmacokinetics of beta-lactams.

  1. absorption
  2. distribution
  3. elimination
A
  1. They are acid labile so NOT delivered orally (exceptions: PenV, ampicillin/amoxicillin)
  2. Widely distributed but not CNS or eyes unless there is meningitis. Low half life (hours, penG 30min)
  3. Renal- glom filtration and organic acid pump
56
Q

Why is penicillin able to be used for meningitis?

A

Because inflamed tissue allow penicillin past the BBB.

Drawback- relapses can occur one the BBB reseals

57
Q

Why is the half life of penicillins so short?

What drug can lengthen the half life?

A

PenG (30min) to a few hours for the others.
The half life is short because renal elimination uses glomerular filtration and an organic acid pump in the kidney secreting it in the urine.

Probenecid is used blocks the organic acid pump in the kidneys

58
Q

What is the function of probenecid?

What is the drawback of using it?

A

It is used to block the organic acid pump in the kidney that excretes penicillin so it prolongs the half life.
The drawback is that it inhibits the organic pump in the choroid plexus that eliminates the drug from the brain. This can lead to build up and seizure

59
Q

When referring to penicillin allergies, what is meant by major and minor?
What causes the sensitivity in each?
Which is more severe?

A

The frequency of the allergy NOT the severity

Major- penicillin molecules covalently linked to lysine of serum proteins. Determined with a skin test. Seldom life threatening

Minor- breakdown products of penicillin and penicillin itself that can lead to life-threatening reactions.

60
Q

If a patient is mildly allergic to a penicillin, administering a ____________ would probably be safe and vice versa.

A

Cephalosporin

61
Q

How can you elicit a subclinical mast cell response when a patient has a penicillin allergy?

A

Give minute doses and slowly increase. This may desensitize but is also very dangerous and usually avoided

62
Q

Aside from allergies, what are the adverse effects of using beta lactams?

A
  1. large amount of sodium
  2. seizures when accumulated in the brain (exacerbated by probenecid)
  3. broad spectrum (cephalosporin) can lead to superinfections
63
Q

What type of infection would you use a B-lactam against?

A

Most effective against G+ and spirochetes

Antipseudomonal b-lactams (ticarcillin and piperacillin)

3rd and 4th generation cephalosporins G- (but then become less good at G+ so its a trade off)

64
Q

What are the two major narrow spectrum penicillins and what is the difference?

A

Pen G= acid labile but more potent

Pen V= acid stable (oral) but less potent

65
Q

What is Pen G-benzathine?

A

a form of penicillin G that has a 1 to 2 week half life (much much longer than the normal 30-60 minutes)
It has a much lower serum concentration though

66
Q

______________________ are inversely related to the half life when discussion penicillins.

A

Serum concentrations

67
Q

What are the therapeutic uses for Pen G?

Which strains are usually resistant

A

G+ cocci and bacilli (but not enterococcus)
N. gonorrhea
Spirochetes
VERY LOW MIC

S aureus and N. gonnorhea are mostly resistant
Strep faecalis is less sensitive

68
Q

What are oxacillin and nafcillin used against?

What is the difference?

A

Nafcillin is the new “methicillin” and is used on staph that is resistant to pen G. ACID LABILE

Oxacillin is for less severe staph. ACID STABLE

69
Q

What have MRSA strains acquired that make them resistant ?

A

MecA transpeptidase that is resistant to binding of beta-lactams

70
Q

What are the broader spectrum penicillins?

A

Ampicillin
Amoxacillin
Both are acid stable and orally prescribed
They are broader spectrum because in addition to G+, they are effective against:
1. H infleunza
2. E coli
3. proteus

71
Q

Ticarcillin and piperacillin are used against what pathogens?
Why are they often prescribed with aminoglycosides?

A

They are anti-pseudomonal against P. aeruginosa as well as G- like Klebsiella and Serratia

They are frequently prescribed with aminoglycosides (that are effective against G-) because MIC for ticarcillin and piperacillin are too close to the therapeutic index

72
Q

What are 4 reasons that cephalosporins are considered to be improved over some penicillins?

A
  1. They can be used in pen allergic patients
  2. Less sensitive to b-lactamases (including S aureus lactamase)
  3. 2nd to 4th generation can penetrate CSF
  4. Prophylaxis for surgery bc some can be useful against G- and anaerobes
73
Q

What is the spectrum for first generation cephalosporin?

What are 2 examples of a first generation?

A

Similar to ampicillin. It covers G+, and a few G- (klebsiella, e coli, proteus)
Great against penicillinase staph strains

Parenteral = cefazolihat 
Oral= cephalexin
74
Q

What is the spectrum for 2nd generation cephalosporin?

What are 2 examples and what is the benefit of each?

A

Increased G- spread to include H influenza, enterobacter, neisseria
More effective at anaerobes

Cefuroxime- crosses BBB

Cefoxitin- good at anaerobes

75
Q

What is the spectrum of 3rd generation cephalosporin?
What problem is encountered with third generation?
What are 3 examples?

A

Broader spectrum G-, pseudomonas, gets into CSF.
Problem is this increases superinfection risk.
1. cefotaxime
2. ceftriaxone
3. ceftazidime

76
Q

What are the three 3rd generation cephalosporin and what is unique to each?

A
  1. Cefotaxime- resistant to beta-lactamases, good for meningitis
  2. Ceftriaxone- longest half life; gonorrhea (1st choice), meningitis, lyme disease
  3. Ceftazidime- antipseudomonal
77
Q

What is the difference between third and fourth/fifth spectrum cephalosporins?

A

Broader spectrum, greater resistance to beta-lactamases, greatest potency

78
Q

What is the major 4th/5th generation cephalosporin?

A

Cefepime- better against staph, more b-lactamase resistant, great CSF penetration

79
Q

What is the spectrum of Imipenem?

A

EXTREMELY broad spectrum

  1. G+
  2. G-
  3. aerobes AND anaerobes

Resistant to most b-lactamases BUT in the last few years carbopenem-resistant enterobacteriacaeae have been developing

80
Q

What is CRE?

A

carbopenem resistant enterobacteriaceae that is resistant to all drugs and the broadest spectrum drug imipenem

81
Q

What is imipenem usually given in combination with? Why?

A

It is usually inactivated in the renal tubules by dihydropeptidases.

Cilastatin inactivates these enzymes

82
Q

What does clavulanic acid do?

A

Inactivates beta-lactamases
Usual combos:
1. amoxacillin-clavulanic acid
2. piperacillin-tazobactam

83
Q

What is the mechanism of action of vancomycin? What is the spectrum?
Is it bactericidal or bacteriostatic?

A

Instead of resembling D-ala-D-ala and binding to the transpeptidase like B-lactam drugs do, Vanco binds to the D-ala-D-ala shielding it from the transpeptidase

It works on G+ only
It is bactericidal (for the same reason as b-lactams. disrupt cell wall-> autolysin)

84
Q

Vancomycin is the drug of last resort for what bacteria?

What bacteria has been gaining vanco-resistance?

A

It is a drug of last resort for MRSA

It is also used for E. faecalis, C. dificil and S. viridians (endocarditis)

Enterococci have been gaining resistance by substituting D-ala-D-lactate

85
Q

What is the pharmacokinetics of Vanco?

  1. absorption
  2. distribution
  3. excretion
A
  1. poorly absorbed orally
  2. good penetration, not CSF unless meninges are inflamed
  3. glom filtration
86
Q

What are the three major adverse effects of vanco?

A
  1. red neck syndrome b/c it releases histamine
  2. ototoxic- hearing AND balance
  3. nephrotoxic (usually due to impurities in old preparations)
87
Q

What should you NEVER give vancomycin with?

A

Aminoglycosides because they are both ototoxic and nephrotoxic

88
Q

Vancomycin can be used to treat C. dificil, but what drug is preferred for this superinfection?

A

Metronidazole

89
Q

What are the ribosome binding drug classes?

Which bind 30S and which bind 50S?

A
  1. Aminoglycosides (30S)
  2. Tetracycline (30S)
  3. MSLK (50S)
  4. Linezolid (both)
90
Q

What is the spectrum of aminoglycosides?
What are they often used in combination with?
Are they bacteriostatic or bactericidal?

A

They are mainline drugs for G-.
They are given with penicillin or cephalosporin (never vanco) for eterococcal endocarditis
They are bactericidal

91
Q

What is the structure of aminoglycosides?

Why does this restrict how they must be administered?

A

They have 3 or 4 amino sugars.
One of them lacks an oxygen in the ring (cyclohexitol).
The amino groups off the sugar rings will be charged at neutral pH and have poor membrane penetration so they cannot be taken orally

92
Q

What is the mechanism of action of aminoglycosides?

bacteriostatic and bactericidal effects

A

They inhibit protein synthesis by blocking initiation and elongation–> static

They also cause mRNA misreading- the acceptor site on the 30S subunit binds and activates tRNA leading to proteins with AA substitutions that incorporate into the membrame causing leakage and cell lysis –>cidal

93
Q

How do aminoglycosides gain access to the ribosome structures to kill bacteria?

How does this affect what bacteria are naturally resistant to aminoglycosides?

A
  1. Diffuse through G- porins
  2. Actively pumped over cell membrane (dependent on O2, neutral/high pH, normal osmolarity)

Aminoglycosides thus are not good at treating:

  1. anaerobes
  2. bacteria in low pH (UTI)
94
Q

What are the mechanisms of resistance to aminoglycosides?

A
  1. altered ribosomal subunit by adding carbohydrate groups

2. Transferase enzymes (phospho, acetyl, adenyl) rendering the drug unable to bind the ribosome

95
Q

How is resistance to b-lactams different in mechanism from resistance to aminoglycosides?

A

b-lactams are inactivated by the b-lactamases

Aminoglycosides are not hydrolyzed, they are just blocked from binding the ribosome

96
Q

What is the pharmokinetics of aminoglycosides?

  1. absorption
  2. distribution
  3. elimination
A
  1. polar so not absorbed well from GI.
  2. limited to extracellular fluids and poor CSF and eye distribution. Over concentrate in the ear and renal cortex
  3. glom filtration
97
Q

What are the adverse effects of aminoglycosides?

How are these effects reduced?

A
  1. ototoxic and nephrotoxic
  2. neuromuscular blockade
  3. damage to optic nerve

Aminoglycosides have a post-antibiotic effect so they are given one or two times a day and bacteria continue to be killed after the removal of the drug

98
Q

What are the four aminoglycosides we are responsible for?

A
  1. streptomycin
  2. gentamicin and tobramycin
  3. Amikacin
  4. Neomycin
99
Q

What specifically would streptomycin be used to treat?

A
  1. Drug resistant TB
  2. combined w/ b-lactam for enterococcus endocarditis

(minor for tularemia and plague)

100
Q

What are gentamicin and tobramycin used to treat?

A 
Gram neg bacteria specifically:
Klebsiella
Pseudomonas aeruginosa
enterobacter
serratia
101
Q

What is the benefit of using Amikacin?

A

it is resistant to a lot of the inactivation transferase enzymes so it works on drug resistant strains

102
Q

What is neomycin used for ?

A

prepare the bowel for surgery

103
Q

What is the spectrum of tetracycline?

Are they bacteriostatic or bactericidal?

A

They are broad spectrum for many G+ and G- and are bacteriostatic

104
Q

What is the mechanism of action for tetracycline?

A

It binds to the 30S subunit of bacteria inhibiting tRNA from getting to the acceptor site inhibiting initiation and elongation

105
Q

How has resistance to tetracycline developed?

A

To gain access to the 30S subunit tetracycline must enter G- porins.
Resistant strains still allow the drug to enter, but they have developed efflux pumps to get the drug back out (the pump is induced by tetracycline)

106
Q

How do tetracycline, doxycycline and minocycline differ in their hydrophobicity?
Which are long lasting and which are short acting?

A

The hydrophobicity depends on substitutions of 5. 6 and 7 on the rings.

Tetracycline is short-acting and 40% absorbed
Doxy and minocycline are long-lasting and >90% absorbed)

107
Q

Which tetracycline drug has the longest half life? How is it eliminated?

A

Doxycycline has the longest half life and is hepatically excreted

108
Q

How is tetracycline excreted?
Doxycycline?
Minocycline?

A 
Tetra= renally
Doxy= hepatically
Mino= mainly hepatic, a little renal
109
Q

What kind of tetracycline drug would you use for a patient that has kidney failure?

A

doxy because its excreted mainly hepatically

110
Q

What two drugs are poorly absorbed in the presence of cations (milk, antacids, etc)

A

Tetracyclines and Fluroquinolones

111
Q

What are the adverse effects of using tetracycline?

A
  1. broad spectrum = superinfection
  2. Binds to Caphosphate in teeth.bones causing discoloration if taken during 1st or 2nd dentation
  3. hepatotoxic especially in pregnancy
  4. photooxidize in UV so avoid bright sunlight
112
Q

When would superinfection be likely when using tetracycline?

What would be a sign that superinfection was occuring?

A

If the patient had been taking it for over 2 weeks

C dificile overgrowth would cause diarrhea

113
Q

What is tetracycline the drug of first choice for?

What else is it used to treat?

A

Rickettsia infections like RMSF

It is also used to treat:

  1. MRSA
  2. mycoplasma and chlamydia
  3. gonorrhea and syphilis in pen allergic
114
Q

What are the major macrolides?

Which are 14-membered and which are 15?

A 
14 = erythromycin and clarithromycin
15= azithromycin
115
Q

What is the spectrum for macrolides? Are they bacteriostatic or bactericidal?

A

They work on G+ and are static.

They sub for b-lactams in allergic patients

116
Q

What is the mechanism of action for macrolides?

A

They bind to the 23S RNA in the 50S subunit inhibiting peptidyl transferase (which adds AA to a peptide chain)

117
Q

Which macrolide is acid labile?

How is it given orally?

A

erythromycin but it can be given orally with enteric coated prep

118
Q

What is unusual about the distribution of azithromycin?

A

It binds avidly to tissue as is released over weeks (5 day z-pack)

119
Q

How are macrolides eliminated?

A

Hepatically through the bile

120
Q

What are the adverse effects of macrolides?

A

They can cause epigastic distress, hepatotoxicity, drug-drug interactions

121
Q

What specific bacteria are macrolides used against?

What is it the drug of first choice for?

A

Strep
Listeria in patients allergic to B-lactams
chlamydia & mycoplasma
Drug of first choice for Legionella

122
Q

What differentiates clarithromycin from the other macrolides?

A
  1. better bioavailability

2. M. Avium

123
Q

What is clindamycin active against?

A

G+ infections but especially:

  1. anaerobes
  2. B. fragilis, C. perfringens
124
Q

What is the mechanism of action of clindamycin?

A

It binds 50S ribosomal subunit and is antagonized by the macrolides (erythro, clarithromycin and azithromycin)

125
Q

What is the mechanism of action of quinupristin and dalforpristin?

A

they binds 50S and cause release of incomplete chains of peptide.
When used together = bactericidal

126
Q

What is the adverse reaction of quinupristin-dalforpristin?

A

It inhibits p450 so there are drug interactions esp. with cyclosporine

127
Q

What is quinupristion-dalfopristin used to treat?

A
  1. MRSA

2. VRE (faecalis is resistant)

128
Q

What is the mechanism of action of Linezolid?

What are the adverse reactions?

A

It binds 23S RNA subunit of the 50S ribosomal subunit (30S and 50S) and prevents initiation and binding of tRNA

It is a mild MAOI so avoid aged cheese and wine

129
Q

What is linezolid used to treat?

A

multidrug resistant G+

VRE, MRSA, pneumonias, skin infections

130
Q

What is Daptomycin used to treat?

When can it not be used?

A

VRE and MRSA
LIFE THREATENING INFECTIONS ONLY

It can’t be used in pulmonary infections because it can’t bind surfactant

131
Q

What is the mechanism of action of Daptomycin?

A

binds phosphatidyl glycerol in bacterial membranes and depolarizes

132
Q

What is metronidazole used to treat?

A
  1. anaerobic- b. fragilis, C. dificil, C. perfringens

2. protozoa- T vaginalis, G lamblia, E. histolytica

133
Q

What is drug has a similar mechanism of action to metronizadole?

A

nitrofurantoin because they both get into cells, are reduced and cause toxic intermediates to destroy the cell

134
Q

What is bacitracin used to treat?

A

Topical for G+ and G- infections like eczema/ulcers

Orally for C. dificile in GI

135
Q

What is the mechanism of dapsone? What does it treat?

What drug is it used in combo with?

A

It treats leprosy and acts like sulfonamide (blocks purine, pyrimidine synthesis)
It is used with Rifampin

Bugs and Drugs (21 decks)

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