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ID > tetracyclines and lincosamides > Flashcards

tetracyclines and lincosamides Flashcards

1
Q

tetracyclines and lincosamides inhibit ____

A

protein synthesis

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2
Q

what is the structure of a tetracycline

A

4 rings, parent aromatic compound is naphthacene

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3
Q

what color are tetracyclines

A

yellow

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4
Q

other chemistry characteristics of tetracyclines

A

bitter, crystalline, strong yellow fluorescence under UV light, amphoteric, form crystalline water soluble salts with strong acids and bases

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5
Q

what 3 substitutions for tetracyclines result in variable PK and antimicrobial activity

A

C5, C6, C7

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6
Q

tetracyclines have increased lipophilicity with ____ at C_

A

absence of hydroxylation at C6

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7
Q

what does the absence of hydroxylation at C6 with doxy, mino, and tige lead to

A

increased stability to degradation, increased fluid and tissue penetration, longer t1/2, enhanced antibacterial activity, higher fraction of plasma protein binding, higher volume of distribution and lower renal clearance

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8
Q

alterations at which faces of the tetracycline molecule lead to improved antimicrobial activity and PK properties

A

northern and western faces

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9
Q

alterations at which faces of the tetracycline molecule produce a considerable loss in antimicrobial activity

A

southern and eastern

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10
Q

tetracyclines inhibit bacterial protein synthesis by reversibly binding to the ___ ribosomal subunit of the 70S ribosome

A

30S

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11
Q

tetracyclines are _______ (bacteriostatic or bactericidal)

A

bacteriostatic; they inhibit organism growth rather than directly kill

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12
Q

spectrum of tetracyclines

A

broad spectrum: gram +, gram -, anaerobes, atypical bacteria, spirochete bacteria, some protozoa

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13
Q

what are two broad bacterial resistance mechanisms?

A

decreased accumulation of the drug within the cell, inhibition of drug binding to the target site of action

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14
Q

what are 3 ways of decreasing accumulation of the drug within the cell by bacterial resistance

A

decreased influx, increased outflux/efflux pumps, drug inactivation

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15
Q

how do bacteria resist by inhibiting drug binding to the target site of action

A

target site modification: ribosomal protection proteins alter the confirmation of the ribosome to prevent drug binding.

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16
Q

what mechanisms do tetracyclines use to resist?

A

efflux pumps and target site modification

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17
Q

a _____ contains loops of DNA with genes that encode for resistance and are easily shared between various bacteria

A

plasmid

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18
Q

a ______ contains loops of DNA with genes that encode for resistance and are easily shared within the chromosome of a given bacteria

A

transposon

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19
Q

in short, plasmids are ____

A

exogenous

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20
Q

in short, transposons are ___

A

internal

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21
Q

efflux pumps and target site modification are typically acquired via __

A

plasmids or transposons that encode the resistance; often inducible

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22
Q

resistance to tetracycline via efflux pumps typically _____ predict resistance to second or third generation

A

doesn’t

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23
Q

resistance to tetracycline via drug inactivation by enzymatic or nonenzymatic mechanisms typically ____ predict resistance to second or third generation

A

does

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24
Q

resistance to tetracycline by target site modification typically predicts ___

A

resistance to second generation but not third

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25
Q

common uses of tetracycline in the community setting

A

CAP, PUD, urethritis (genital), PID, lyme, syphilis, acne, MRSA skin/soft tissue infxn

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26
Q

less common uses of tetracycline in the community setting

A

malaria chemoprophylaxis and treatment, rickettsial infections, animal bites

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27
Q

special uses of doxycycline in the community

A

rosacea, bioterrorism pathogens

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28
Q

what are bioterrorism pathogens

A

anthrax, plague, tularemia, Q fever, brucellosis

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29
Q

special uses of minocycline in the community

A

rosacea, acne

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30
Q

special uses of tetracycline in the community

A

oral infections: recurrent oral aphthous ulcers, canker sores, periodontitis

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31
Q

special use of demeclocycline in the community

A

chronic hyponatremia associated with SIADH

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32
Q

tetracycline absorption

A

60-80%

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33
Q

tetracycline half life

A

6-12h, short acting

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34
Q

doxycycline and minocycline absorption

A

90-100%

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35
Q

doxycycline and minocycline half life

A

18-22h, long acting

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36
Q

tetracycline urinary excretion

A

20-55%: eliminated primarily in the kidneys, thus drug accumulates with renal insufficiency–> avoid

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37
Q

doxycycline urinary excretion

A

40%: fecal excretion is increased in the setting of renal insufficiency so it can be used in renal impairment

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38
Q

minocycline urinary excretion

A

5-10%: less than 20% is eliminated by the kidneys, and 20-34% excreted in the feces: accumulation potential with renal insufficiency may preclude use

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39
Q

food ___ absorption of tetracyclines

A

decreases (significant for tetracycline and demeclocycline)

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40
Q

tetracyclines form stable _____ with divalent and trivalent cations

A

chelates; hinders GI absorption by 50-90%

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41
Q

distribution of tetracyclines

A

lipophilic–> highly diffusible and penetrate hard to reach tissues and fluids (CSF, eye, prostate, sebum, respiratory secretions, dentin, reticuloendothelium, bone)

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42
Q

t/f: tetracycline crosses the placenta

A

true

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43
Q

t/f: tetracycline is excreted in breast milk

A

true

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44
Q

how are tetracyclines generally excreted

A

in the urine and feces mainly as unchanged drug

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45
Q

tetracyclines are concentrated in __

A

liver and bile

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46
Q

tetracyclines undergo ____ via bile

A

enterohepatic recycling

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47
Q

tetracyclines are partially inactivated via ____

A

hepatic metabolism

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48
Q

how can doxycycline be given to patients with renal impairment

A

extrarenal mode of elimination: in renal impairment, it diffuses into the intestinal lumen and chelates with Ca or Mg, the complex is incapable of reabsorption

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49
Q

how is minocycline metabolism an exception

A

metabolized extensively in the liver to at least 6 inactive metabolites

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50
Q

adverse reactions with tetracyclines

A

superinfection, esophageal ulceration, renal, vestibular, deposition in growing teeth, bones, nails, photosensitivity/phototoxicity, intracranial hypertension, papilledema, discoloration of skin/teeth, thyroid

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51
Q

superinfection from tetracycline is due to ___

A

candida albicans (yeast)– due to non-susceptible or resistant organisms

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52
Q

esophageal ulceration with tetracyclines is particularly seen in ___

A

patients with GERD, bedtime dose with little water

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53
Q

counseling to prevent esophageal ulceration from tetracyclines

A

take last dose 1hr before bed or recumbency with 100 mL water, and remain standing for at least 90 seconds

54
Q

renal toxicity from tetracycline is due to ____

A

decomposed nephrotoxic tetracyclines– NEVER DISPENSE DISCOLORED (DARK) TETRACYCLINES

55
Q

renal toxicity from tetracycline causes ___

A

faconi-like syndrome and systemic lupus erythematosus phenomenon

56
Q

brown-to-black colored decomposition products of tetracycline are __ and __

A

anhydrotetracycline and epianhydrotetracycline

57
Q

signs and symptoms of renal toxicity due to tetracyclines

A

nausea and vomiting, proteinuria, acidosis, glycosuria, death

58
Q

vestibular effects are most common with which tetracycline

A

minocycline

59
Q

what are the vestibular effects from tetracyclines

A

dizziness, vertigo, ataxia, nausea, vomiting; occurs in first 2 days and disappears in 48 hours

60
Q

what discoloration does tetracycline cause in teeth, bones, nails

A

yellow, brown, gray (UV fluorescent)

61
Q

deposition in enamel and dentin of permanent teeth and new bone formation is due to ______ complex

A

tetracycline-calcium orthophosphate

62
Q

permanent teeth are affected if tetracyclines are administered to ___

A

children 8 years or younger

63
Q

when is the greatest danger to developing teeth with tetracyclines

A

second trimester of pregnancy to 7 years old, permanent anterior teeth

64
Q

what is nail stain with prolonged treatment with tetracyclines

A

photo-onycholysis

65
Q

which tetracycline is least likely to deposit in teeth/bones/nails

A

doxycycline- less intense chelation

66
Q

what is a phototoxic reaction to tetracycline

A

looks like exaggerated sunburn, appears quickly within minutes to hours of exposure to the sun

67
Q

what is a photoallergic/photosensitivity reaction to tetracycline

A

mimics contact dermatitis, may spread to areas not exposed to the sun, delayed onset over 24 hours after exposure to the sun

68
Q

signs of intracranial hypertension with tetracyclines

A

headache, blurred vision, dipolopia, vision loss

69
Q

avoid concomitant use of _____ with tetracyclines due to intracranial hypertension

A

isotretinoin (accutane)

70
Q

what is papilledema

A

optic disk swelling secondary to elevated intracranial pressure

71
Q

when is there greater risk of developing papilledema from tetracyclines

A

females of childbearing age who are overweight

72
Q

is papilledema reversible

A

usually on drug cessation, but permanent vision loss can occur

73
Q

what are uncommon adverse effects more common with minocycline

A

black discoloration of tongue or thyroid, brown-to-black pigmentation in chronic acne patients, discoloration of soft contact lenses, thyroid cancer

74
Q

contraindications to tetracyclines

A

children 8 years or younger, pregnancy

75
Q

what are the risks to tetracyclines for children 8 years or younger

A

permanent discoloration of the teeth and enamel, hypoplasia, retardation of skeletal development and bone growth

76
Q

what are pregnancy risks with tetracyclines

A

micromelia (disproportionately short limbs), cusp deformities on teeth and discoloration, cataracts (loss of lens transparency), cleft lip, cleft palate

77
Q

what are drug interactions with tetracyclines

A

supplements/vitamins/antacids, warfarin, penicillins and aminoglycosides, oral contraceptives

78
Q

what is the interaction between supplements/vitamins/antacids and tetracyclines

A

decrease absorption of tetracycline drugs

79
Q

what is the mechanism of interaction between supplements/vitamins/antacids and tetracyclines

A

chelation of divalent or trivalent cations by tetracycline drugs

80
Q

how to manage the interaction between supplements/vitamins/antacids and tetracyclines

A

separate administration 1-2 hours ac or 2 hours pc

81
Q

what is the interaction between warfarin and tetracycline

A

depresses plasma prothrombin activity

82
Q

what is the mechanism for interaction between warfarin and tetracycline

A

may increase risk of bleeding

83
Q

management for the interaction between warfarin and tetracycline

A

increase monitoring for bleeding

84
Q

patient counseling for tetracyclines

A

take on empty stomach w/ full glass of water 1 hour before a meal or 2 hours after a meal. avoid simultaneous ingestion of dairy, antacids, iron, mineral supplements. avoid recumbency after ingestion. avoid prolonged exposure to sunlight or sunlamps

85
Q

what are third generation tetracyclines

A

tigecycline, eravacycline, omadacycline, sarecycline

86
Q

substitutions at _____ in 3rd gen tetracyclines have what benefits

A

R9, reduce bacterial resistance, improve PK

87
Q

what mechanisms of tetracycline resistance do the third generations overcome

A

efflux pumps and ribosomal protection proteins

88
Q

why is sarecycline unique

A

R7 substitution leading to unique mechanism at the 50S ribosome A (acceptor) site. not approved for treatment of infections

89
Q

omadacycline is present as its ____ salt

A

monotosylate

90
Q

approved indications for omadacycline

A

CAP, skin/skin structure infxn

91
Q

omadacycline dosage forms

A

po, iv

92
Q

sarecycline is present as its ____ salt

A

monohydrochloride

93
Q

approved indications for sarecycline

A

therapy of inflammatory lesions of non-nodular moderate to severe acne vulgaris in patients 9 years of age or older—- NOT EVALUATED TO TREAT INFECTIONS

94
Q

sarecycline dosage forms

A

po

95
Q

sarecycline adverse effects

A

nausea

96
Q

omadacycline spectrum

A

gram positive, gram negative, atypical

97
Q

sarecycline spectrum

A

LACKS activity against most gram negatives, has activity against gram positive

98
Q

omadacycline with food?

A

food affects rate and extent, administer 4 hours AC or 2 hours PC, avoid dairy, multivitamins or antacids for 4 hours AC

99
Q

sarecycline with food?

A

not significantly affected by food

100
Q

clindamycin is significantly more _____ than lincomycin

A

lipophilic

101
Q

what does the lipophilicity of clindamycin provide advantage for

A

greater oral absorption, better penetration into bacterial cell membranes, higher intracellular concentration, more reliable activity

102
Q

structure of lincosamides

A

amino acid linked to an amino sugar

103
Q

where do clindamycin and lincomycin differ

A

r1 and r2 at c6

104
Q

lincosamides form salts at ____

A

tertiary amine hydrogen

105
Q

lincosamides form esters at ___

A

c2 hydroxy group in amino sugar

106
Q

what is the significance of clindamycin forming an ester

A

it is a biologically inactive prodrug: clindamycin phosphate, clindamycin palmitate hydrochloride, hydrolyzes to the parent base in vivo in the bloodstream

107
Q

mechanism of action of lincosamides

A

bind to 23s rRNA component of the 50S bacterial ribosomal subunit to interrupt the process of peptide chain initiation, bacteriostatic/bactericidal

108
Q

lincosamides spectrum of activity

A

aerobic gram +, anaerobic gram +, anerobic gram -, spore forming protozoa

109
Q

important bacterial resistance mechanisms for lincosamides

A

decreased influx and target site modification

110
Q

what is the significance of limitations to drug uptake by bacterial resistance to lincosamides

A

poor permeability= intrinsic gram negative resistance

111
Q

how do bacteria alter the 23S rRNA of 50S ribosomal subunit to resist lincosamides

A

methylation: plasmid mediated providing MLS(B) resistance (ermA gene) or methytransferse enzyme (cfr gene)

112
Q

_____ and lincosamide binding sites overlap on the 50S subunit so resistance may indicate lincosamide resistance

A

macrolides

113
Q

what is MLS(B)

A

macrolide lincosamide streptogramin(B) resistance: erm gene

114
Q

what is erm gene

A

erythromycin ribosome methylase gene: encodes enzymes that confer inducible or constitutive resistance to MLS agents via methylation of the 23s rRNA binding site

115
Q

what does a positive D test indicate

A

erythromycin has induced clindamycin resistance, do not use clindamycin, presence of an erm gene that could result in clindamycin failure

116
Q

common uses of lincosamides in the community setting

A

skin/soft tissue infections, oral cavity infection, acne vulgaris, bacterial vaginosis, bacterial endocarditis prophylaxis

117
Q

clindamycin is __% bioavailable

A

90

118
Q

lincosamide distribution

A

wide, into most tissues/fluids/bone, does not achieve significant CSF levels

119
Q

lincosamide metabolism

A

hepatic (liver) to active and inactive metabolites; the active metabolite N-demethyl clindamycin is more active than the parent compound

120
Q

lincosamide elimination

A

excreted in urine, to a lesser extent the bile as metabolites

121
Q

adverse effects with lincosamides

A

cutaneous reactions, common cause of antibiotic associated diarrhea, may cause severe or even fatal colitis usually due to overgrowth of C. diff because it is resistant

122
Q

drug interactions with lincosamides

A

CYP3A4 inhibitors/inducers, cyclosporine, macrolides

123
Q

some formulations of clindamycin contain ____

A

tartrazine; aspirin allergy associated

124
Q

patient counseling for clindamycin

A

take capsules with a full glass of water to avoid esophageal irritation

125
Q

what class is mupirocin (bactroban)

A

pseudomonic acid A

126
Q

what is the mechanism of mupirocin

A

inhibits bacterial protein synthesis via a specific and reversible binding to bacterial isoleucyl transfer-RNA synthetase–> prevents incorporation of isoleucine into growing protein chains, bacteriostatic

127
Q

indications for mupirocin

A

topical only: impetigo (ointment) or secondary infected traumatic skin lesions (cream) due to staph/strep, eradication of nasal colonization with MRSA in adult patients and health care workers (nasal ointment)

128
Q

warnings for mupirocin

A

potentially toxic amounts of PEG in the vehicle may be percutaneously absorbed in patients w/ open wounds or extensive burns, not for the treatment of pressure sores, avoid prolonged use may result in the overgrowth of non-susceptible organisms

129
Q

what class is retapamulin (altabax)

A

pleuromutilin

130
Q

retapamulin mechanism

A

interacts at 50S bacterial ribosomal subunit via a mechanism different from any other antibiotic results in inhibition of protein synthesis

131
Q

indications for retapamulin

A

topical treatment of impetigo due to MSSA/strep pyogenes

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