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Antimicorbial: protein synthesis inhibitors Flashcards

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1
Q

What is selective toxicity?

A

the drug blocks a reaction that is vital to both

the microbe and host but has greater impact on the microbe

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2
Q

do humans hav e a 70s ribosome?

A

yes, mitochondrial

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3
Q

What is the one drugs that attaches tRNA synthetas?

A

mupirocin

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4
Q 
What protein subunit doe each of the following drugs affect?
1.Tetracycline
2 aminoglycosides
3spectinomycin
4macrolides
5chloramphenicol
6streptogramins
7oxazolidinones
8lincosamides?
A
  1. 30
  2. 30
  3. 30
  4. 50
  5. 50
  6. 50
  7. 50
  8. 50
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5
Q

What is the selective toxicity of tetracyclines? static or cidal?

A
  1. 70s mitoch. ribosomes, not cytoplasmic ribosomes

2. static

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6
Q

How is resistance incurred against tetracyclines?

A
  1. decreased intracellular levels
    a. decreased influx
    b. increased efflux
  2. enzymatic inactivation of drug
  3. expression of proteins that
    protect ribosomes from drug
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7
Q

What are key points about tetracyclines absorption?

A

oral is variable

  • decreased by divalent and trivalent cations found in dairy and iron supplements
  • decreased when gastric pH is elevated
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8
Q

Is the distribution of tetracyclines wide or narrow?

A

Very wide- accumulation in spleen, bone marrow, bone, dentine, enamel of teeth, crosses BBB and placenta

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9
Q

Where is excretion of most tetracyclines? what are the two exceptions

A
  1. most through kidneys with some bile/reabsorbed
  2. a. doxycycline- inactive chelate/conjugate in feces
    b. minocycline-metab. by liver and passed in feces.
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10
Q

What are the two most common things treated with tetracyclines?

A

Acne

Riskettsial diseases

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11
Q

Who should tetracyclines absolutely not be given to?

A

pregnant women and children under 8—>discoloration of teeth

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12
Q

What type of superinfection is common with the use of tetracyclines?

A

pseudomembranous colitis

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13
Q

Tetracyclines especially effects which drugs?

A 
bactericidal antibiotics (penicillins)
- digoxin, oral anticoagulants, oral hypoglycemics do to effects on liver and kidney
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14
Q

Tigecycline is especially effective against what>

A
  • strains that are get-resistant

- hershey isolate of MRSA

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15
Q

What gourd of drugs should we think if we see it end with acin or micin or mycin? are they static or tidal? irreversible or reversible binding to 30S?

A
  1. aminoglycosides
  2. bactericidal
  3. irreversible
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16
Q

T-F- aminoglycosides have concentration dependent killing with significant PAE?

A

True

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17
Q

What accumulates when using amino glycosides?

A

streptomycin monosomes–>blocks further translation of messages

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18
Q

What spectrum of bacteria are aminoglucosides? combination with what?

A
  1. Gm- aerobes

2. penicillin or vancomycin

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19
Q

How is resistance incurred with amino glycosides?

A
  1. mutant bacterial ribosome
  2. decreased uptake or efflux
  3. enzymatic inactivation of the drug
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20
Q

How are aminglycosides administered? why? clearance?

A
  1. IM or IV
  2. highly polar and poorly absorbed through GI
  3. renal clearance
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21
Q

What is distribution like for the amino glycosides?

A

not well distributed to most cells, eye or CNS

High concentration only in inner ear and renal cortex–> toxicities (reversible)

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22
Q

What limits the use of streptomycin?

A

high resistance

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23
Q

When is gentamicin used topically? how is resistance conferred against gentamicin? is the vestibular ototoxicity reversible?

Study These Flashcards
A
  1. burns, wounds, skin lesions
  2. poor drug uptake
  3. no
24
Q

What is slightly more active against pseudomonas than gentamycin? What else is it often used for?

Study These Flashcards
A
  1. tobramycin

2. P. aeruginosa RTI w/ cystic fibrosis

25
What is the semisynthetic derivative of kanamycin and has reduced toxicity? what does it treat?
1. amikacin | 2. Bugs resistant to gentamicin, treats M. tuberculosis
26
Widespread use of what during bowel surgeries led to resistance and enter colitis outbreaks? what does this mean>
1. neomycin/kanamycin | 2. limited to topical and oral use
27
Is spectinomycin an aminoglycoside? how do we administer?
1. NO!!! aminocyclitol | 2. IM
28
What type of antibiotics should we think when we see romycin or domycin?
macrolides
29
Are macrocodes static or cidal? because of proximity of their sites of action, they competitively inhibit what? G+ or G- more?
1. static 2. ribosome binding of streptogramins, clindamycin, chloramphenicol 3. G+
30
is erythromycin more effective against anaerobes than clarithromycin and azithromycin?
No
31
Can resistance to macrolides develop rapidly?
yes
32
What are the 3 mechanisms of macrolides resistance?
1. Efflux pump 2.methylase modifies the bacterial ribosome so unable to bind drug 3. hydrolysis of macrolides by esterases produced by Enterobacteriaceae
33
What macrolide is unstable in acid?
erythromycin- use with stearate salts or estolate esters coating
34
Do macrolides penetrate the CNS well? what penetrates abcesses well?
1. no 2. erythromycin
35
How is erythromycin secreted? clarithromycin?
1. bile | 2. met. by liver, secreted by kidney
36
Does azithromycin inhibit CYP3A4?
No- erythromycin, clarithromycin, and | troleandomycin-->potentiate the effects of other drugs
37
Is telithromycin a macrolide?
No ketolide- semi-synthetic derivative of erythromycin [* increased acid stability * increased affinity for bacterial 50S ribosome * reduced induction of bacterial resistance]
38
How is telithromycin administered? metabolized? excreted
1. orally 2. hepatic 3. hepatic and renal
39
T-F--telithromycin does not induce cross-R via methyl's expression, but S. aureus and S. pyogenes with MLSB R are resistant to telithromycin?
True
40
Does telithromycin increase levels of other CYP3A4 substrates?
Yes- cisapride, simvastatin
41
What drugs is the binding site of chloramphenicol close to? is it static or cidal?
1. clindamycin and macrolides | 2. static
42
How does resistance occur with chloramphenicol?
acetyltransferases that modify the drug
43
Does chloramphenicol oral or parenteral? cross placenta? penetrate CNS? metabolize by what? secreted by what?
1. both 2. yes 3. yes 4. liver 5. urine
44
What is grey baby syndrome from chloramphenicol?
``` a. inadequate levels of liver glucuronyl transferase=> can’t metabolize the drug b. vomiting, cyanosis, loose green stools, ashen color, flaccid, hypothermic; death of 40% of patients within 2 days ```
45
T-F--chloramphenicol does not prolong the half life of CYP drugs?
False- they do
46
T-F-- quiupristin/dalfopristin individually are static, but combined are cidal? main use?
1. True- they are synergistic | 2. MRSA, VREF, VRSA, Strep pneumoniae
47
How do we get resistance to quinupristin?
a. erm-encoded methylases (50S rib) | b. vgb-encoded lactonases (drug)
48
How do we get resistance to dalfopristin?
``` a. vat- or sat-encoded acetyltransferases (drug) b. vga-/vgb-encoded ATPbinding efflux proteins to transport the drug out of the cell ```
49
Is oxazolidinones static or tidal? linezolid
static
50
Do Oxazolidinones have x-resistance with other synthesis inhibitors?
No and this is a main point
51
What group of drugs is clindamycin?
lincosamide
52
Is clindamycin static or cidal?
mainly static but can be cidal in some
53
How is bacterial resistance conferred?
ribosomal methylase- slow and stepwise- it does not induce the methylase to do this
54
What is distribution like for clindamycin? how is it administered?
1. wide including bone, but not in CNS | 2. oral and parenteral
55
T-F clindamycin is metabolized by the liver and excreted in urine and bile?
yes
56
How is mupirocin administered? what is it useful for? is resistance to mupirocin common?
1. topical use only 2. treating impetigo caused by MRSA or Group A Streptococci 3. No very rare

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