Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

4 Pharm Self > Antimicorbial: protein synthesis inhibitors > Flashcards

Antimicorbial: protein synthesis inhibitors Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

do humans hav e a 70s ribosome?

A

yes, mitochondrial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the one drugs that attaches tRNA synthetas?

A

mupirocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

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

2. static

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two most common things treated with tetracyclines?

A

Acne

Riskettsial diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Who should tetracyclines absolutely not be given to?

A

pregnant women and children under 8—>discoloration of teeth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tetracyclines especially effects which drugs?

A 
bactericidal antibiotics (penicillins)
- digoxin, oral anticoagulants, oral hypoglycemics do to effects on liver and kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tigecycline is especially effective against what>

A
  • strains that are get-resistant

- hershey isolate of MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What accumulates when using amino glycosides?

A

streptomycin monosomes–>blocks further translation of messages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What spectrum of bacteria are aminoglucosides? combination with what?

A
  1. Gm- aerobes

2. penicillin or vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How are aminglycosides administered? why? clearance?

A
  1. IM or IV
  2. highly polar and poorly absorbed through GI
  3. renal clearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What limits the use of streptomycin?

A

high resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

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?

A
  1. tobramycin

2. P. aeruginosa RTI w/ cystic fibrosis

25
Q

What is the semisynthetic derivative of kanamycin and has reduced toxicity? what does it treat?

A
  1. amikacin

2. Bugs resistant to gentamicin, treats M. tuberculosis

26
Q

Widespread use of what during bowel surgeries led to resistance and enter colitis outbreaks? what does this mean>

A
  1. neomycin/kanamycin

2. limited to topical and oral use

27
Q

Is spectinomycin an aminoglycoside? how do we administer?

A
  1. NO!!! aminocyclitol

2. IM

28
Q

What type of antibiotics should we think when we see romycin or domycin?

A

macrolides

29
Q

Are macrocodes static or cidal? because of proximity of their sites of action, they competitively inhibit what? G+ or G- more?

A
  1. static
  2. ribosome binding of
    streptogramins, clindamycin,
    chloramphenicol
  3. G+
30
Q

is erythromycin more effective against anaerobes than clarithromycin and azithromycin?

A

No

31
Q

Can resistance to macrolides develop rapidly?

A

yes

32
Q

What are the 3 mechanisms of macrolides resistance?

A
  1. Efflux pump
    2.methylase modifies the bacterial
    ribosome so unable to bind drug
  2. hydrolysis of macrolides by esterases
    produced by Enterobacteriaceae
33
Q

What macrolide is unstable in acid?

A

erythromycin- use with stearate salts or estolate esters coating

34
Q

Do macrolides penetrate the CNS well? what penetrates abcesses well?

A
  1. no 2. erythromycin
35
Q

How is erythromycin secreted? clarithromycin?

A
  1. bile

2. met. by liver, secreted by kidney

36
Q

Does azithromycin inhibit CYP3A4?

A

No- erythromycin, clarithromycin, and

troleandomycin–>potentiate the effects of other drugs

37
Q

Is telithromycin a macrolide?

A

No ketolide- semi-synthetic derivative of erythromycin
[* increased acid stability
* increased affinity for bacterial 50S ribosome
* reduced induction of bacterial resistance]

38
Q

How is telithromycin administered? metabolized? excreted

A
  1. orally
  2. hepatic
  3. hepatic and renal
39
Q

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?

A

True

40
Q

Does telithromycin increase levels of other CYP3A4 substrates?

A

Yes- cisapride, simvastatin

41
Q

What drugs is the binding site of chloramphenicol close to? is it static or cidal?

A
  1. clindamycin and macrolides

2. static

42
Q

How does resistance occur with chloramphenicol?

A

acetyltransferases that modify the drug

43
Q

Does chloramphenicol oral or parenteral? cross placenta? penetrate CNS? metabolize by what? secreted by what?

A
  1. both
  2. yes
  3. yes
  4. liver
  5. urine
44
Q

What is grey baby syndrome from chloramphenicol?

A 
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
Q

T-F–chloramphenicol does not prolong the half life of CYP drugs?

A

False- they do

46
Q

T-F– quiupristin/dalfopristin individually are static, but combined are cidal? main use?

A
  1. True- they are synergistic

2. MRSA, VREF, VRSA, Strep pneumoniae

47
Q

How do we get resistance to quinupristin?

A

a. erm-encoded methylases (50S rib)

b. vgb-encoded lactonases (drug)

48
Q

How do we get resistance to dalfopristin?

A 
a. vat- or sat-encoded
acetyltransferases (drug)
b. vga-/vgb-encoded ATPbinding
efflux proteins to
transport the drug out of
the cell
49
Q

Is oxazolidinones static or tidal? linezolid

A

static

50
Q

Do Oxazolidinones have x-resistance with other synthesis inhibitors?

A

No and this is a main point

51
Q

What group of drugs is clindamycin?

A

lincosamide

52
Q

Is clindamycin static or cidal?

A

mainly static but can be cidal in some

53
Q

How is bacterial resistance conferred?

A

ribosomal methylase- slow and stepwise- it does not induce the methylase to do this

54
Q

What is distribution like for clindamycin? how is it administered?

A
  1. wide including bone, but not in CNS

2. oral and parenteral

55
Q

T-F clindamycin is metabolized by the liver and excreted in urine and bile?

A

yes

56
Q

How is mupirocin administered? what is it useful for? is resistance to mupirocin common?

A
  1. topical use only
  2. treating impetigo caused by MRSA or Group A Streptococci
  3. No very rare

4 Pharm Self (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions