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Pharmacology (Fall) > Antibiotics IV: NN > Flashcards

Antibiotics IV: NN Flashcards

1
Q

What are examples of Fluroquinolones?

A
  • Levofloxacin, moxifloxacin, ciprofloxacin, ofloxacin – IV, PO, topical
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2
Q

What is the target of Fluroquinolones?

A
  • DNA gyrase inhibitor
    (respon. For making spiral/coil) – INHIBITS RELAXATION of supercoiled DNA and PROMOTES BREAKAGE of DNA strands
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3
Q

What are the features of Fluroquinolones?

A
  • Levofloxacin and ciprofloxacin-adjust dose in renal impairment (not moxi)
  • Distributes widely into body tissues and fluids (moxi not for kidney infections)
  • BacterioCIDAL
  • CONCENTRATION DEPENDENT (want to get good concentrations), post-antibiotic effect
  • *EXCELLENT PO absorption (can switch from IV as long as they are okay to swallow pills)
  • Absorption affected by DIVALENT cations, metal cations (Fe)-separate in time
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4
Q

What is the Spectrum of Activity of Fluroquinolones?

A
  • Variable gram positive coverage, good gram negative coverage, good atypical coverage, tuberculosis (cipro has unreliable strep pneumo coverage, but covers pseudomonas
  • (can add to list of what we can use for CAP)
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5
Q

What are the adverse effects of Fluroquinolones?

A
  • US boxed warning re: tendinitis, tendon rupture, peripheral neuropathy, CNS effects; also QTc prolongation, dysglycemia (unpredictable – sometimes goes up or down) , photosensitivity, increased risk of aortic dissection or rupture
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6
Q

What are examples of Trimethoprim/Sulfamethoxazole?

A
  • Trimethoprim/Sulfamethoxazole – IV, PO (combo)
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7
Q

What is the target of Trimethoprim/Sulfamethoxazole?

A
  • Both interfere with bacterial folic acid synthesis
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8
Q

What are the features of Trimethoprim/Sulfamethoxazole?

A
  • Sulfamethoxazole is a PABA analog & inhibits the synthesis of dihydrofolic acid
  • Trimethoprim inhibits later in the pathway by binding to bacterial dihydrofolate reductase (& prevents formation of tetrahydrofolic acid)
  • Synergistic combination
  • Bactericidal/static
  • Time/concentration dependent
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9
Q

What is the Spectrum of Activity of Trimethoprim/Sulfamethoxazole?

A

BROAD
* Gram + (incl. MRSA), gram -, Pneumocystis jirovecii, NOT anaerobes

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10
Q

What are the adverse effects of Trimethoprim/Sulfamethoxazole?

A
  • Cystalluria, rashes can be severe (SJS, TEN rare but serious), photosensitivity (careful when in summer – use sunscreen), hyperkalemia, increased serum creatinine, renal failure
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11
Q

What is the target of Nitrofurantoin?

A
  • Reduced by bacterial flavoproteins to reactive intermediates that inactivate/alter ribosomal proteins
  • *This results in numerous effects incl. impaired protein synthesis, aerobic energy metabolism, DNA, RNA & cell wall synthesis
  • Used for uncomplicated UTIs but kidney function must be good enough otherwise drug will not get into the urine in high enough concentrations. *CANNOT use for pyelonephritis
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12
Q

What are the features of Nitrofurantoin?

A
  • Bacteriocidal
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13
Q

What is the Spectrum of Activity of Nitrofurantoin?

A
  • Gram + incl. MRSA, few gram –‘s, NOT anaerobes
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14
Q

What are the adverse effects of Nitrofurantoin?

A
  • Hepatotoxicity (prolonged use), pulmonary fibrosis (prolonged use), hematologic toxicity (elderly?)
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15
Q

What is the target of Metronidazole?

A
  • Disrupts DNA which inhibits nucleic acid synthesis
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16
Q

What are the features of Metronidazole?

A
  • Bacteriocidal
  • Concentration dependent
17
Q

What is the Spectrum of Activity of Metronidazole?

A

NARROW
* Anaerobes incl. c. difficile, protozoa, amoeba

18
Q

What are the adverse effects of Metronidazole

A
  • Metallic taste (makes everything taste a bit off)
  • Disulfiram like rxn
  • Headache
19
Q

What are Anti-Tubercular Drugs used for?

A

M. tuberculosis
* Acid fast bacillus
* Very slow growing
* Resistant to most antibiotics
* Resistant to host defences
* Spread via inhaled droplet nuclei

(diff. to treat b/c grows slowly & resistant)

20
Q

What are the Anti-Tubercular Drugs?

A

1st line drugs RIPE, must use combo therapy due to drug resistance
1. Rifampin
2. Isoniazid
3. Pyrazinamide
4. Ethambutol

  • Direct Observed Therapy
    o Public health nurse will come & observe you taking it for like 9 months (v. serious)
    o Follow all protocols if TB is in hospital
21
Q

What is the target of Rifampin?

A

Also rifabutin

*Used for both in initial & continuation phase of treatment

  • Binds to beta subunit of DNA-dependent RNA polymerase thereby blocking RNA transcription & inhibiting bacterial RNA synthesis
22
Q

What are the features of Rifampin?

A
  • Bacteriocidal
  • *Body fluids (tears, urine, sweat etc.) may turn red-orange, hepatitis
  • Induces many CYP P450 enzymes incl. being a strong inducer of 3A4 & 2C19 (cause other drugs to be cleared quickly & if you stop it the enzyme will dose down & you can end up with an overdose)
    o lots of drug interactions (careful when starting & stopping it – BIG inducer)
23
Q

What is the Spectrum of Activity of Rifampin?

A
  • Gram + & some gram -, M. tuberculosis
24
Q

What is the target of Isoniazid?

A

*Used for both initial & continuation phase of treatment

  • Inhibits mycolic acid synthesis (required for cell wall) resulting in mycobacterial cell death
25
Q

What is the Adverse Effects of Isoniazid?

A
  • Hepatotoxicity, peripheral neuropathy (give in combo with pyridoxine), rash (baseline before treatment)
  • Bacteriocidal against actively growing M. tuberculosis
26
Q

What is the target of Pyrazinamide?

A
  • Converted to pyrazinoic acid – inhibits mycolic acid synthesis which results in mycobacterial cell death
27
Q

What are the features of Pyrazinamide?

A

Bactericidal

Typically used for 1st 2 months of tx

Adjust interval in renal impairment

28
Q

What is the Adverse Effects of Pyrazinamide?

A
  • Anorexia, muscle aches, rash, hepatotoxicity, gout, photosensitivity (some don’t feel great with this, take baseline)
29
Q

What is the target of Ethambutol?

A
  • Impairs mycobacterial wall synthesis by inhibiting arabinosyl transferase
30
Q

What is the Adverse Effects of Ethambutol?

A
  • Bacteriostatic
  • Initial therapy, may be discontinued if no drug resistance to isoniazid (typ. dropped quite quickly)
  • Adjust interval in renal impairment
  • Optic neuritis, loss of central vision (baseline eye exam & monitor throughout therapy)

Pharmacology (Fall) (28 decks)

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