Antimicorbial: protein synthesis inhibitors Flashcards Preview

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Flashcards in Antimicorbial: protein synthesis inhibitors Deck (56):
1

What is selective toxicity?

the drug blocks a reaction that is vital to both
the microbe and host but has greater impact on the microbe

2

do humans hav e a 70s ribosome?

yes, mitochondrial

3

What is the one drugs that attaches tRNA synthetas?

mupirocin

4

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

1. 30
2.30
3.30
4.50
5.50
6.50
7.50
8.50

5

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

1. 70s mitoch. ribosomes, not cytoplasmic ribosomes
2. static

6

How is resistance incurred against tetracyclines?

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

7

What are key points about tetracyclines absorption?

oral is variable
-decreased by divalent and trivalent cations found in dairy and iron supplements
- decreased when gastric pH is elevated

8

Is the distribution of tetracyclines wide or narrow?

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

9

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

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.

10

What are the two most common things treated with tetracyclines?

Acne
Riskettsial diseases

11

Who should tetracyclines absolutely not be given to?

pregnant women and children under 8--->discoloration of teeth

12

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

pseudomembranous colitis

13

Tetracyclines especially effects which drugs?

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

14

Tigecycline is especially effective against what>

-strains that are get-resistant
-hershey isolate of MRSA

15

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?

1. aminoglycosides
2. bactericidal
3. irreversible

16

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

True

17

What accumulates when using amino glycosides?

streptomycin monosomes-->blocks further translation of messages

18

What spectrum of bacteria are aminoglucosides? combination with what?

1. Gm- aerobes
2. penicillin or vancomycin

19

How is resistance incurred with amino glycosides?

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

20

How are aminglycosides administered? why? clearance?

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

21

What is distribution like for the amino glycosides?

not well distributed to most cells, eye or CNS

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

22

What limits the use of streptomycin?

high resistance

23

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

1. burns, wounds, skin lesions
2. poor drug uptake
3. no

24

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

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