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Pharmacology > Aminoglycosides > Flashcards

Aminoglycosides Flashcards

0
Q

What are the 5 aminoglycosides?

A
  1. streptomycin
  2. tobramycin
  3. gentamicin
  4. amikacin
  5. neomycin
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1
Q

What do aminoglycosides do?

A

Aminoglycosides inhibit protein synthesis by binding to the 30s ribosomal subunit

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2
Q

What is the mode of administration for streptomycin and what does it treat?

A

IV/IM

second line TB drug

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3
Q

what is the mode of administration for gentamicin?

A

IV/IM/Topical

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4
Q

what is the mode of administration for Tobramycin?

A

IV/IM/topical

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5
Q

what is the mode of administration for amikacin?

A

IV/IM

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6
Q

what is the mode of administration for neomycin?

A

topical/PO

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7
Q

Describe the structure of aminoglycosides and how this affects their pharmacokinetics?

A

Aminoglycosides are amino sugars in glycosidic linkage. They are polycations. Their polarity affects their absorption and distribution (it explains why they must be taken in combination with inhibitors of cell wall synthesis)

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8
Q

What do aminoglycosides do to the 30s ribosomal subunit?

A

They irreversibly bind to the 30s ribosomal subunit and block its activity. Because this binding is irreversible, aminoglycosides are bacteriocidal!

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9
Q

What requirements must be met for aminoglycosides to be functional?

A

Aminoglycosides must be actively transported into the bacterial cells which involves the use of O2. Therefore, aminoglycosides are only useful against aerobic and not anaerobic bacteria

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10
Q

In general, when are aminoglycosides used?

A

They are used to specifically treat aerobic G- enteric (rods) bacteria. They are also used when sepsis or endocarditis is suspected.

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11
Q

Streptomycin uses:

A
  1. tularemia
  2. bubonic plague
  3. TB
  4. endocarditis (part of combination therapy)
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12
Q

which aminoglycosides are effective against P. aeruginosa?

A

gentamicin, tobramycin, amikacin

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13
Q

Neomycin and gentamicin uses:

A

topical application of wounds and burns caused by aerobic G- bacteria

gentamicin is also active against P. aeruginosa

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14
Q

What is the DOC for enterococcus species?

A

penicillin + aminoglycosides

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15
Q

Explain resistance and synergism when it comes to aminoglycosides and ICWS:

A

Aminoglycosides are too large and polar to enter the cells on their own. They are unable to cross the membrane. ICWS have a hard time completely breaking down the walls of G- bacteria but they are able to weaken it. ICWS weaken the cell walls of G- bacteria enough to allow the aminoglycosides to enter the cells and bind to the 30s ribosomal subunit irreversibly, where the inhibit protein synthesis and cause the cell to die.

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16
Q

What is the DOC for P. aeruginosa?

A

antipseudomonal penicillin + aminoglycosides

17
Q

Do aminoglycosides fall under concentration dependent killing or time dependent killing?

A

Aminoglycosides are concentration dependent killing antibiotics. Increasing the concentration of aminoglycosides increases the number of susceptible bacteria they are able to kill and the rate at which they kill the bacteria

18
Q

Explain the post antibiotic effect (PAE) of aminoglycosides:

A

Aminoglycosides exhibit a PAE. That is, antibacterial activity persists even when you can no longer detect the antibiotics. This means that a single large dose is more effective than multiple small doses which allows for decreased toxicity b/c toxicity is based on number of repeat exposure and total time the drug is detectable in the body

19
Q

Aminoglycoside toxicity:

A
  1. Ototoxicity and Nephrotoxicity
  2. GI (N/V)
  3. Superinfections
  4. Allergies
20
Q

which types of drugs should not be administered with aminoglycosides and why?

A
  1. loop diuretics should not be administered with aminoglycosides b/c it increases the risk of ototoxicity (synergism)
  2. cephalosporins, vancomycin, cisplatin, and cidofovir should not be given with aminoglycosides bc they act synergistically and cause nephrotoxicity
21
Q

Aminoglycosides pharmacokinetics:

A
  1. IV/IM/Topical (PO neomycin - 3% absorption)
  2. renal excretion
  3. poor CNS penetration
22
Q

Resistance and aminoglycosides:

A

If a bacteria develops resistance to one aminoglycoside it might be resistant to other aminoglycosides. This phenomenon is known as cross resistance.
Bacteria can develop resistance to aminoglycosides a few ways:
1. deficiency of ribosomal receptor
2. lack of permeability to drug
3. enzymatic modification of aminoglycoside

23
Q

What are the three broad spectrum antibiotics?

A
  1. chloramphenicol
  2. tetracyclines
  3. glycylcyclines
24
Q

What side effects is chloramphenicol associated with?

A

It is associated with fetal aplastic anemia and other fatal side effects.

25
Q

Describe the mechanism of action for chloramphenicol:

A
  1. chloramphenicol reversibly binds the 50s subunit.
  2. it is bacteriostatic.
  3. it inhibits protein synthesis
26
Q

Chloramphenicol and mitochondrial ribosomes:

A

Mitochondrial ribosomes are slightly more similar to prokaryotic ribosomes and chloramphenicol is able to take advantage of this and inhibit mitochondrial protein synthesis in humans. This can have many adverse side effects

a. dose dependent bone marrow depression
b. gray baby syndrome

27
Q

Spectrum of Chloramphenicol vs. use:

A

Chloramphenicol is active against G+/G-, anaerobes, aerobes and atypicals. However it is only used for life threatening conditions:

  1. Typhoid Fever
  2. Meningitis
  3. Rickettsia, Brucellosis, Rocky Mountain Spotted Fever, and Meliodosis
  4. Bacterial Conjunctivitis (topical)
28
Q

Chloramphenicol pharmacokinetics:

A
  1. Oral administration: complete absorption, no longer used (aplastic anemia)
  2. parenteral administration
  3. good tissue penetration (including eyes)
  4. good CNS penetration
  5. 90% metabolized in the liver. conjugated with glucuronic acid
  6. metabolite excreted renally
29
Q

chloramphenicol resistance development:

A
  1. inactivation by acetyl transferase
  2. modify the binding site
  3. efflux pumps
30
Q

What are the three tetracyclines and their modes of administration?

A
  1. tetracycline: PO/topical
  2. doxycycline: oral
  3. minocycline: oral
31
Q

Tetracycline mechanism of action:

A

bind reversibly to 30s ribosomal subunit.
bacteriostatic
prevent protein synthesis

32
Q

Tetracycline spectrum:

A

G+/G-
anaerobes/aerobes
atypicals

33
Q

List the organisms that are resistant to tetracyclines:

A
  1. B. fragilis
  2. proteus
  3. pseudomonas
34
Q

Therapeutic use for tetracyclines:

A 
H. pylori infection
cholera
mycoplasma pneumonia
chlamydia
Rickettsia (rocky mountain spotted fever)
amebiasis, acne, gonorrhea (acute)
brucellosis
Early Lyme disease
plague 
vibrio species
35
Q

Tetracyclines are the DOC for what types of infections:

A
  1. cholera
  2. Rocky Mountain spotted fever
  3. Early Lyme Disease
  4. Mycoplasma Pneumonia
  5. Chlamydia
36
Q

How do bacteria develop resistance to tetracyclines?

A
  1. efflux pumps

2. doxycycline and minocycline may still be effective b/c they are poor substrates for the efflux pumps

37
Q

Tetracycline pharmacokinetics

A
  1. PO
  2. chelation with Ca, Fe, and Al
  3. all tissues except CNS and joints
  4. deposit themselves in bone
  5. liver metabolism
  6. renal excretion
  7. doxycycline is not metabolized by the liver and it is excreted in the feces
  8. long acting tetracyclines are slowly excreted, longer t1/2 and less frequent dosing
38
Q

Tetracycline toxicity:

A
  1. normal flora changes
  2. prevents growth of long bones
  3. teeth discoloration

** do not give to pregnant woman or children under 8 yo

39
Q

What is a glycylcycline?

A
  1. synthetic minocycline derivative
  2. IV administration only
  3. complicated skin/skin-structure and complicated intra-abdominal infections
  4. bind 30s ribosomal subunit - bacteriostatic
  5. similar to tetracyclines but also has activity against tetracycline resistant organisms
  6. 2/3 fecal elimination and 1/3 renal elimination
  7. side effects similar to tetracycline
  8. MRSA, MRSE, PRSP and VRE

Pharmacology (7 decks)

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