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Cology 2 Exam 2 > Aminoglycosides > Flashcards

Aminoglycosides Flashcards

1
Q

What are aminoglycosides’ MOA for protein synthesis inhibition?

A

There are 3:

  • Bind the 30s ribosome, preventing the initiation of meth-tRNA from biding to the P site
  • Enhances early breakdown of the ribosomal subunit (Binds to the interface between the 30 and 50s subunit)
  • Interferes with reading/distorts codons
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2
Q

Name the aminoglycosides (6)

A 
Amikacin
Gentamicin
Kanamycin
Neomycin
Tobramycin
Streptomycin
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3
Q

Why is the naming of aminoglycosides important?

A
  • micin means it was obtained from Streptomyces griseus from soil sample
  • mycin means it was obtained from Actinomycete Micromonospora

Note: Tobramycin was obtained from S. tenebrarius!

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4
Q

Which aminoglycosides are semisynthetic?

A

Kanamycin

Amikacin

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5
Q

What do aminoglycosides target?

A

Gram - bacilli

Aerobic bacteria

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6
Q

Are aminoglycosides bacteriostatic or bacteriocidal?

A

Bacteriocidal

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7
Q

How do aminoglycosides kill the cell?

A

They enter the bacteria through porins (ENERGY DEPENDENT transport), inhibit protein synthesis

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8
Q

Are aminoglycosides time dependent or concentration dependent?

A

They are CONCENTRATION dependent
Once they are in the cell, they stay there
Do NOT need to maintain certain concentrations - this makes adverse effects more likely

Also have post antibiotic effect! Still see effect when levels are low because the aminoglycosides are INSIDE the cell

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9
Q

How are aminoglycosides administered? Why?

A

Injection only (IM, IV)

Because they are ionized in body fluids and not readily absorbed

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10
Q

How are aminoglycoside eliminated?

A

Eliminated by glomerular filtration

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11
Q

When are aminoglycosides used in combination?

A

Serious infection
Sepsis
Pneumonia
Endocarditis

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12
Q

Aminoglycosides can be combined with _______. Why?

A

Beta lactams
They break down the cell wall, allow the aminoglycosides to get into the cell easier
Can decrease dose of aminoglycoside needed when we do this`

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13
Q

What are the major toxicity concerns with aminoglycosides?

A

Nephrotoxicity
Ototoxicity
Neuromuscular blockade
Hypersensitivity reactions (rare)

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14
Q

What is the incidence of nephrotoxicity with aminoglycoside use?

A

8-25%

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15
Q

What is the most toxic aminoglycoside? Least toxic?

A

Most toxic: Neomycin

Least toxic: Streptomycin

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16
Q

What causes nephrotoxicity with aminoglycoside use?

A

The aminoglycoside accumulates in the proximal tubule, inhibiting prostaglandin synthesis.
This causes damage to brush border cells

17
Q

Incidence of nephrotoxicity increases with what?

A

Age (poor renal function?)
Total dose (increases in dose = increases in incidence)
Females at higher risk than males
Duration of treatment
Multiple daily dosing more than single dosing
When you try to maintain certain plasma levels

18
Q

Nephrotoxity risk is additive with what agents?

A

Cisplatin
Cyclosporine
Furosemide
(and other nephrotoxins)

19
Q

True or False: If you d/c aminoglycosides, hearing will come back

A

False - it may be permanent

20
Q

Describe the ototoxicity caused by aminoglycosides

A

Accumulation of aminoglycosides in fluid of the cochlea can lead to both auditory and vestibular dysfunction

(Hearing and balance affected)

21
Q

True or false: Ototoxicity from aminoglycosides is dose related

A

True

Continued loss occurs with repeated dosing

22
Q

What agents can enhance ototoxicity from aminoglycosides?

A

Ethacrynic acid, furosemide, cisplatin, and other ototoxins

23
Q

What can increase sensitivity of ototoxicity from aminoglycosides?

A

Genetic mutations in microsomal RNA (3 different point mutations in RNA)

24
Q

What cells are most sensitive to ototoxicity?

A

Outer hair cells are lost before inner hair cells

25
Q

What is thought to be the mechanism of hearing loss in aminoglycoside toxicity?

A 
3 major hypotheses:
Calcium hypothesis (interferes with calcium channels in hair cells)
Free radical hypothesis (interact with iron to form superoxide and hydroxyl free radicals, can poke holes in membrane and damage DNA)
NMDA hypothesis (Interact with NMDA receptors and glutamate to cause excitotoxicity)
26
Q

Which agents have the highest incidence of auditory toxicity?

A

Amikacin
Kanamycin
Neomycin

27
Q

Which agents have the highest incidence of vestibular toxicity?

A

Gentamycin

Streptomycin

28
Q

Which agent has equal effect on auditory and vestibular?

A

Tobramycin

29
Q

Recovery from aminoglycoside toxicity can take how long?

A

12-18 months

Some residual damage persists

30
Q

Are there treatments for aminoglycoside toxicity?

A

No treatment except to stop drug as early as possible

31
Q

What causes neuromuscular blockade with aminoglycoside use?

A

Blocks presynaptic release of calcium

32
Q

What is the order of neuromuscular blocking potency for the aminoglycosides?

A 
(Highest) Neomycin
Kanamycin
Amikacin
Gentamicin
Tobramicin (Lowest)
33
Q

How do you treat neuromuscular blockade in aminoglycoside toxicity?

A

IV calcium salt

34
Q

What are the contraindications for aminoglycoside use?

A

Myasthenia gravis
(Neuromuscular blockade can occur)

Can also enhance neuromuscular blockade in surgery

35
Q

What causes aminoglycoside resistance?

A

Plasmid acquired aminoglycoside modifying enzymes (can increase metabolism)

Altered porins can alter transport into the bacteria

Altered ribosomes

36
Q

Which aminoglycoside is used for nosocomial infections?

A

Amikacin

37
Q

Which aminoglycoside is used for the plague?

A

Streptomycin

38
Q

Which aminoglycoside is used for Tularemia?

A

Streptomycin

39
Q

Which aminoglycoside is used for Tuberculosis?

A

Streptomycin

Cology 2 Exam 2 (18 decks)

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