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Systemic Pharm I > Protein Synthesis Inhibitors > Flashcards

Protein Synthesis Inhibitors Flashcards

1
Q

Tetracylines

A

tetracycline, doxycycline, minocycline, demeclocycline

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2
Q

Aminoglycosides

A

amikacin, gentamicin, neomycin, streptomycin, tobramycin

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3
Q

Macrolides

A

azithromycin, clarithromycin, erythromycin, fidaxomicin

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4
Q

Other synthesis inhibitors

A

clindamycin and linezolid

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5
Q

What subunits does a bacterial ribosome have?

A

50s and 30s

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6
Q

What subunits does a human ribosome have?

A

60s and 40s

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7
Q

What is different about mitochondrial ribosomes?

A

mammalian mitochondrial ribosomes are closer to bacteria, so drugs targeting it may cause toxic effects

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8
Q

Which drugs inhibit protein synthesis at the 30s ribosome?

A

tetracyclines and aminoglycosides

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9
Q

Which drugs inhibit protein synthesis at the 50s ribosome?

A

macrolides and “others” + chloramphenicol

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10
Q

Which group of drugs have adverse effects on the teeth?

A

tetracyclines

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11
Q

What is the tetracycline MOA?

A

reversibly bind the 30s subunit to prevent binding of tRNA which prevents the addition of new amino acids to the growing peptide chain

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12
Q

Are tetracyclines bacteriostatic or bactericidal?

A

bacteriostatic

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13
Q

Which two tetracyclines are longer lasting?

A

doxycycline and minocycline

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14
Q

What do tetracyclines treat?

A

broad spectrum, gram - and , chlamydia!

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15
Q

How does resistance to tetracyclines come about?

A

mutation preventing organism from taking in the drug, plasma encoded efflux of drug, enzymatic inactivation, or producing proteins that prevent binding to ribosome

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16
Q

What does tetracycline bind to?

A

calcium, aluminum, iron, magnesium

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17
Q

What reduces the bioavailability of tetracycline?

A

dairy products– avoid antacids and iron supplements as well

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18
Q

What tissues does tetracycline bind to?

A

tissues undergoing calcification

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19
Q

Which tetracycline can penetrate CSF but is not effective for CNS infections?

A

minocycline

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20
Q

T/F tetracyclines cross the placenta and bind fetal bones and teeth

A

true– contraindication!

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21
Q

Who should you not prescribe tetracycline to?

A

pregnant/breastfeeding women

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22
Q

Describe the elimination of tetracycline

A

gets concentrated in the liver, secreted into bile, reabsorbed into the intestine and excreted in urine

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23
Q

T/F doxycycline is excreted by the kidney

A

false, good for patients with renal disease

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24
Q

What are the adverse effects of tetracycline?

A

gastric discomfort, effects on calcified tissues, photo-toxicity, vestibular issues, and pseudotumor cerebri

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25
Q

What are tetracyclines effects on calcified tissue?

A

discoloration and hypoplasia of teeth in children, can stunt growth, avoided in children under 12

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26
Q

What are tetracyclines effects on the vestibular system?

A

it concentrates in endolymph in the ear and can cause vertigo

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27
Q

What is pseudotumor cerebri?

A

effect of tetracycline, idiopathic intracranial hypertension, pt symptoms are headache and blurred vision with a swollen appearance to the optic nerve (bilaterally)

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28
Q

What are three superinfections that can result from tetracyclines?

A

candida (yeast), resistant staph, colitis

29
Q

Summarize the four main contraindications of tetracyclines

A

only doxycycline for those with kidney problems, NO pregnant women, no children under 12, inhibits warfarin (blood thinner) clearance

30
Q

What is a 50 mg or less dose of doxycycline for?

A

anti-inflammatory effects that work on soft tissue inflammation and do not encourage bacterial resistance to larger dose

31
Q

What is the MOA of aminoglycosides?

A

bind 30s ribosome proteins and interfere with initiation complex by causing misreading of mRNA

32
Q

Are aminoglycosides bacteriostatic or bactericidal?

A

bactericidal

33
Q

Which two aminoglycosides often cause allergies?

A

gentamicin and neomycin

34
Q

What is true of the absorption of aminoglycosides?

A

oral absorption is inadequate because of highly polar structure

35
Q

How are aminoglycosides administered?

A

IV, IM, topically

36
Q

What are aminoglycosides used against?

A

gram - including pseudomonas, with some gram +

37
Q

What can an aminoglycoside be combined with to improve the spectrum?

A

b-lactam or vancomycin

38
Q

What are two causes of aminoglycoside resistance?

A

decreased uptake of drug, plasmid associated synthesis of enzyme

39
Q

Describe the aminoglycoside distribution?

A

inadequate CSF penetration, low tissue penetration, high concentration in renal cortex and inner ear, all cross the placenta

40
Q

What is the elimination of aminoglycosides?

A

no host metabolism, rapidly excreted into urine

41
Q

What are four main adverse effects of aminoglycosides?

A

ototoxicity, nephrotoxicity, neuromuscular paralysis, allergic reactions

42
Q

What is ototoxicity?

A

an adverse effect of aminoglycosides with deafness that may be irreversible, orally will affect the fetus

43
Q

How does aminoglycoside neuromuscular paralysis occur?

A

after very large doses it causes decrease in acetylcholine release and in post-synaptic sensitivity to acetylcholine

44
Q

Are topical aminoglycosides likely to become resistant?

A

no

45
Q

What is the MOA of macrolides?

A

bind to the 50s ribosomal subunit to block peptidyltransferase center and prevent amino acid chain elongation… can also inhibit formation of 50s

46
Q

What is a good macrolide alternative to PCN?

A

erythromycin

47
Q

Which macrolide is effective against H. influenzae

A

clarithromycin

48
Q

Which macrolide is best for respiratory infections and chlamydia?

A

azithromycin (1000 mg once)

49
Q

What are three mechanisms of macrolide resistance?

A

inability to take up antibiotic/efflux pump, decreased affinity of 50s subunit, and presence of plasmid associated enzyme

50
Q

T/F macrolides are well absorbed orally

A

true

51
Q

Which macrolide should not be given via IV for thrombophlebitis risk?

A

erythromycin

52
Q

T/F macrolides only diffuse into one tissue type

A

false, distributes well into fluids and tissues

53
Q

Which macrolide has a long half life and high V?

A

azithromycin

54
Q

What is true of erythromycin and telithromycin metabolism?

A

extensively metabolized and inhibit oxidation of many drugs, interact with P450

55
Q

Which organ excretes macrolides?

A

kidney

56
Q

What are three macrolide adverse effects?

A

GI problems, acute hepatitis with jaundice, ototoxicity

57
Q

Which macrolide primarily produces ototoxicity in high doses?

A

erythromycin

58
Q

What are two contraindications of macrolides?

A

hepatic dysfunction, arrhythmia

59
Q

T/F macrolides inhibit hepatic metabolism of many drugs

A

true via P450

60
Q

What is the MOA of clindamycin?

A

same as erythromycin, bind 50s

61
Q

What is clindamycin used to treat?

A

MRSA, abdominal anaerobic infections

62
Q

T/F clindamycin has poor absorption to CSF

A

true

63
Q

What is linezolid used to treat?

A

resistant gram + organisms like MRSA

64
Q

What is the MOA of linezolid?

A

inhibits formation of ribosomal complex by binding 50s subunit near the interface with 30s

65
Q

T/F linezolid has no cross-resistance with other drug classes

A

true

66
Q

Linezolid vs vancomycin for MRSA

A

linezolid is noninferior to vancomycin for MRSA pneumonia but is not used for MRSA bacteremia

67
Q

What are important pharmacokinetic principles of linezolid?

A

completely absorbed orally, high V, no interaction with P450, renal and nonrenal excretion

68
Q

What are three adverse effects of linezolid?

A

thrombocytopenia, anemia, optic and peripheral neuropathy

69
Q

What are contraindications for linezolid?

A

caution with MAOIs and SSRIs due to case reports of serotonin syndrome

Systemic Pharm I (13 decks)

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