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Pharmacology > Antibacterials 5 > Flashcards

Antibacterials 5 Flashcards

1
Q

Name 2 Streptogramins?

A

Quinupristin, Dalfopristin

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2
Q

Describe Streptogramins and MOA?

A

• Given as a combination (act synergistically to have
bactericidal action)
• Long postantibiotic effect
Mechanism of action
• Bind to separate sites on 50S bacterial ribosome
• Resistance is uncommon

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3
Q

Streptogramins Antibacterial Spectrum?

A

• Gram-positive cocci
• Multi-drug resistant bacteria (streptococci, PRSP(penicilin resistant S pneumoniae),
MRSA, E.faecium)

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4
Q

Streptogramins Clinical Applications?

A

• Restricted to treatment of infections caused by drug resistant Staphylococci or VRE

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5
Q

Streptogramins PK?

A
  • IV only
  • Penetrates macrophages & polymorphonucleocytes
  • Inhibitors of CYP 3A4
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6
Q

Streptogramins AE?

A
  • Infusion related (venous irritation, arthralgia & myalgia)
  • GI effects
  • CNS effects (headache, pain)
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7
Q

Linezolid MOA and Describe?

A

• Bacteriostatic (cidal against streptococci & Clostridium
perfringens)
Mechanism of action
• Inhibits formation of 70S initiation complex
• Binds to unique site on 23S ribosomal RNA of 50S
subunit

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8
Q

Linezeolid Resistance?

A
  • Decreased binding to target site
  • Point mutation of ribosomal RNA
  • No cross-resistance with other drug classes
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9
Q

Linezolid Antibacterial Spectrum?

A

• Most Gram-positive organisms (staphylococci,
streptococci, enterococci, Corynebacterium, Listeria
monocytogenes) including MRSA and VRE
• Moderate activity against mycobacterium tuberculosis

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10
Q

Linezolid Clinical Applications and PK?

A 
• Treatment of multi-drug resistant infections
PK:
• Oral (100% bioavailable) & IV
• Widely distributed (including CSF)
• Weak reversible inhibitor of MAO
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11
Q

Linezolid AE and Contraindications?

A

• Well tolerated for short admin. (GI, nausea, diarrhea,
headaches, rash)
Long-term admin. can cause:
• Bone marrow suppression, esp. thrombocytopenia
• Optic & peripheral neuropathy, & lactic acidosis
• Serotonin syndrome

Contraindication:
• Reversible, nonselective inhibitor of MAO
-> potential
to interact with adrenergic and serotonergic

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12
Q

Describe Fidaxomicin activity and spectrum?

A

• Narrow spectrum macrocyclic antibiotic
• Activity against Gram-positive aerobes and
anaerobes especially Clostridia
• No activity against Gram-negative bacteria

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13
Q

Fidaxomicin MOA??

PK?

A

• Inhibits bacterial protein synthesis by binding to RNA
polymerase
PK:
• When administered orally, systemic absorption is
negligible but fecal concentrations are high

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14
Q

Fidaxomicin AE?

A
  • Main effects appear to be gastrointestinal disorders

* The safety and effectiveness of fidaxomicin in patients < 18 years of age have not been established.

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15
Q

Describe Mupirocin?

A

• Antibiotic belonging to monoxycarbolic acid class
• Activity against most Gram-positive cocci, including
MRSA and most streptococci (but not enterococci)
• Only topical/intranasal agent with activity against
MRSA

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16
Q

Mupirocin MOA and AE?

A

MOA:
• Binds to bacterial isoleucyl transfer-RNA synthetase
resulting in the inhibition of protein synthesis
AE:
• Resistance develops if used for long periods of time
• Mainly local and dermatologic effects (eg, burning,
edema, tenderness, dry skin, pruritus)

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17
Q

Mupirocin Clinical Applications?

A

• Intranasal:
• Eradication of nasal colonization with MRSA in
adult patients and healthcare workers
• Topically:
• Treatment of impetigo or secondary infected
traumatic skin lesions

18
Q

Which 3 drugs affects nucleic acid synthesis?

A
  • Fluoroquinolones
  • Sulfonamides
  • Trimethoprim
19
Q

List the Fluoroquinolones by generation?

A 
First generation-
Nalidixic Acid (quinolone)
Second generation-
Ciprofloxacin
Third generation-
Levofloxacin
Fourth generation-
Gemifloxacin, Moxifloxacin
20
Q

Fluoroquinolones MOA?

A
  • Broad spectrum, bactericidal drugs
  • Enter bacterium via porins
  • Inhibit bacterial DNA replication via interference with topoisomerase II (DNA gyrase) & IV
21
Q

Fluoroquinolones Resistance?

A
  • Emerged rapidly in 2nd generation
  • Due to chromosomal mutations that:
  • encode subunits of DNA gyrase and topo IV
  • regulate expression of efflux pumps
  • Cross-resistance between drugs occurs
22
Q

Describe antibacterial spectrum of fluoroquinolones?

A
  • Classified into generations
  • Lower generations have excellent Gram-negative activity
  • Higher generations have improved activity against Grampositives
23
Q

Antimicrobial spectrum of 1st and 2nd generation fluoroquinolone?

A

1st Nalidixic acid Moderate Gram -ve activity

2nd Ciprofloxacin Expanded Gram -ve activity
Some activity against Gram +ve and atypical organisms.
Synergistic with
beta-lactams

24
Q

Antimicrobial spectrum of 3rd and 4th generation fluoroquinolone?

A

3rd Levofloxacin Expanded Gram -ve activity
Improved activity against Gram +ve and atypical organisms.
Excellent activity against
S.pneumoniae

4th Moxifloxacin,
Gemifloxacin
Improved Gram +ve activity and
anaerobic activity

25
Q

Clinical Applications of 3rd and 4th generation fluoroquinolone?

A 
3rd Levofloxacin Prostatitis
STD’s (not syphilis)
Skin infections
Acute sinusitis, bronchitis, TB
Community acquired pneumonia

4th Moxifloxacin,
Gemifloxacin
Community acquired pneumonia

26
Q

Clinical Applications of 1st and 2nd generation fluoroquinolone?

A

1st Nalidixic acid Uncomplicated UTI’s

2nd Ciprofloxacin Travelers diarrhea
P.aeruginosa (CF patients)
Prophylaxis against meningitis
(alternative to ceftriaxone & rifampin)

27
Q

Describe Respiratory Fluoroquinolones?

A

Levofloxacin, moxifloxacin & gemifloxacin (excellent
activity against most common causes of pneumonia)
Used in treatment of pneumonia when:
• First-line agents have failed
• In the presence of comorbidities
• Patient is an inpatient

28
Q

Fluoroquinolones PK?

A

• Good oral bioavailability
• Well distributed into all tissues and fluids (including
bones)
• Iron, zinc, calcium (divalent cations) interfere with
absorption
• Dosage adjustments required in renal dysfunction (except
moxifloxacin)

29
Q

Fluoroquinolones AE?

A

• GI distress
• CNS, rash, photosensitivity
• Connective tissue problems (avoid in pregnancy,
nursing mother, under 18’s) – Black Box Warning!
• Peripheral neuropathy (FDA warning)
• QT prolongation (moxifloxacin, gemifloxacin,
levofloxacin)
• High risk of causing superinfections (C.difficile, C
albicans, streptococci)

30
Q

Contraindications and Interactions with Fluoroquinolones?

A

Interactions:
• Theophylline, NSAIDs & corticosteroids = enhance
toxicity of fluoroquinolones
• 3rd & 4th generation = raise serum levels of warfarin,
caffeine & cyclosporine
Contrainidications:
• Pregnancy & nursing mothers
• Children < 18y (unless benefits outweigh risks)

31
Q

Name the 3 Sulfonamides?

A

Sulfamethoxazole, Sulfadiazine, Sulfasalazine

32
Q

Describe Sulfonamides?

A

• Structural analogs of p-aminobenzoic acid (PABA)
• Bacteriostatic against Gram-positive & Gram-negative
organisms

33
Q

Sulfonamides MOA?

A

• Inhibit bacterial folic acid synthesis
• Synthetic analogs of PABA (p-amino-benzoic acid)
• Competitive inhibitors (& substrate) of dihydropteroate
synthase

34
Q

Sulfonamide resistance?

A

Plasmid transfers / random mutations that:
• Altered dihydropteroate synthase
• Decreased cellular permeability
• Enhanced PABA production
• Decreased intracellular drug accumulation

35
Q

Sulfonamide Clinical Applications?

A

Infrequently used as single agents (resistance)
• Topical agents (ocular, burn infections)
• Oral agents (simple UTI’s)
• Sulfasalazine (oral) = ulcerative colitis, enteritis, IBD

36
Q

Sulfonamide PK?

A

• Oral or topical
• Can accumulate in renal failure
• Acetylated in liver. Can precipitate at neutral or acidic pH
-> kidney damage

37
Q

Sulfonamide AE?

A

• GI distress, fever, rashes, photosensitivity are common
• Crystalluria (nephrotoxicity)
• Hypersensitivity reactions
• Hematopoietic disturbances (esp. patients with G6PD
deficiency)
• Kernicterus (in newborns and infants <2 months)

38
Q

Sulfonamide Drug Interactions? Contraindication?

A

• Can displace other drugs from albumin eg, warfarin,
phenytoin and methotrexate
• Newborns & infants < 2 months (kernicterus) – drugs
compete with bilirubin for binding sites on albumin

39
Q

Describe Trimethoprim and MOA?

A

• Structurally similar to folic acid
• Bacteriostatic against Gram-positive & Gram-negative
organisms
MOA:
• Potent inhibitor of bacterial dihydrofolate reductase
• Inhibits purine, pyrimidine & amino acid synthesis

40
Q

Trimethoprim Clinical Applications?

A
  • UTI’s
  • Bacterial prostatitis
  • Bacterial vaginitis
41
Q

Trimethoprim PK?

A
  • Mostly (80-90%) excreted unchanged through kidney

* Reaches high concentrations in prostatic & vaginal fluids

42
Q

Trimethoprim AE?

A
  • Antifolate effects (contraindicated in pregnancy)

* Skin rash, pruritus

Pharmacology (49 decks)

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