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Pharm Exam 4 > Protein Synthesis Inhibitors > Flashcards

Protein Synthesis Inhibitors Flashcards

1
Q

What is a ribosome?

A

large nucleoprotein complex that catalyzes the ordered polymerization of amino acids

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2
Q

What directs the ribosome to order the amino acids? What is the term for this?

A

mRNA template (mRNA translation)

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3
Q

How can drugs target bacterial ribosomes while not affecting human ribosomes?

A

Structural difference (70s prokaryote vs. 80S Eukaryote)

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4
Q

What are the three steps in protein synthesis?

A

Initiation, Elongation, termination

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5
Q

Which step of protein synthesis do most current protein synthesis inhibitors target?

A

Elongation

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6
Q

How do aminoglycosides inhibit protein synthesis?

A

Promote premature termination

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7
Q

What are the five protein synthesis inhibitors?

A

Aminoglycosides, tetracyclines, chloramphenicol, macrolides and clindamycin

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8
Q

Tetracyclines are named how?

A

number of fused rings: Tetra = 4, Doxy = 2, and Mino = 1

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9
Q

What helps tetracycline’s effect on bacteria?

A

Bacteria concentrate tetracyclines inside the cell, eukaryotes and resistant bacterial do not

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10
Q

How are human and bacterial ribosomes different? Similar?

A

Bac: 70S (30s and 50s)
Human Cytoplasm: 80S (40s and 60s)
Human mito: 70S (30s and 50s)

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11
Q

Describe the process of adding amino acids.

A

Peptidyl site–>AA join in A-site (30s subunit)–> Amino and carboxyl ends react to form bond–> ribosome translates so new peptide is in P-site, A-site now vacant for new AA and process repeats

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12
Q

Are tetracyclines bactericidal?

A

No, bacteria start to grow again once stop taking tetracycline

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13
Q

What is the spectrum of Tetracycline?

A

Broad: G+, G-, aerobe, anaerobe and atypical bacteria

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14
Q

What are atypical bacteria and three examples?

A

No cell wall and may cross human cell membrane; rickettsiae, mycoplasma, & chlamydia

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15
Q

How do tetracyclines inhibit protein synthesis?

A

Bind to the 30S ribosomal subunit and inhibit binding of amino acylated tRNA to A site of ribosome

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16
Q

Basis for selectivity for tetracyclines?

A

Tetracyclines are concentrated inside bacterial cells by an active transporter in bacterial cytoplasmic membrane; human cells do not concentrate the tetracyclines

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17
Q

Of Tetracycline, Doxycycline, and Minocycline: which has the lower bioavailability and higher risk of superinfection in the gut?

A

Tetracyclines

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18
Q

What inhibits the absorption of Tetracyclines?

A

Divalent and trivalent cations (Ca, Mg, Al, Fe). Think of tetracycline binding to bone. Do not take w/ milk, kaopectate, pepto-bismol, iron meds, or Ca2+ supplements. Take 1-2 hrs prior to a meal. Potent chelator

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19
Q

Of tetracycline, doxycycline and minocycline: which are the most lipophilic and are therefore more easily distributed?

A

Tetracycline and doxycycline

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20
Q

What is a characteristic of tetracyclines that is useful in the treatment of adults with periodontal disease?

A

Concentrate in gingival crevicular fluid

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21
Q

What is the distribution of TC’s?

A

Diffuse easily across cell membrane, volume of distribution (everywhere b/c in water), [ ] in CSF is much lower than plasma, excreted in milk, binding to structures actively calcifying and [ ] in skin/GCF

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22
Q

Of Tetracycline, doxycycline, and minocycline: which has the shortest halflife and therefore must be dosed more often during the day?

A

Tetracycline (4/day) and minocycline/doxycycline (1-2/day)

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23
Q

Of tretracycline, doxycycline, and minocycline: which is eliminated unchanged in the urine?

A

Tetracycline
Minocycline and Doxycyclines undergo hepatic
metabolism and excretion and renal excretion

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24
Q

When is tetracycline contraindicated?

A

Pregnant women and children less than 8. Uptake and concentrates in developing bones and teeth

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25
Q

3 common side effects of tetracycline?

A

Staining of teeth and altered rates of bone growth, GI disturbances, & phototoxic skin reactions

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26
Q

Out of the tetracyclines, which two drugs have the lowest risk of pseudomembranous colitis? Which is the DOC for treating PC?

A

Doxycycline and minocycline; vancomycin or metranidazole

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27
Q

What are the two ways GI disturbances can occur via tetracyclines?

A

Direct effect on enterocytes or indirect effect by causing disturbances in GI flora

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28
Q

Teeth staining is reversible/irreversible, dose dependent/non-dose dependent?

A

Irreversible and dose-dependent

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29
Q

What is the superinfection and its symptoms that can be caused by tetracycline (doxycycline has reduced risk)?

A

Pseudomembranous colitis due to superinfection by C. difficile (bloody stools)

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30
Q

What can be a rare side effect from treating a meningococcal infection with minocycline?

A

Vestibular toxicity: dizziness, vertigo

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31
Q

What do doxycycline and minocycline do in the blood and what consideration must be made?

A

Depress plasma prothrombin. If pt on anticoagulation therapy, dosing may need to be reduced

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32
Q

What can outdated tetracyclines cause (rare)?

A

Nephrotoxicity (Fanconi syndrome-proximal tubule toxicity)

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33
Q

What is a rare adverse effect from tetracyclines in pregnant women?

A

Hepatotoxicity (after large oral doses)

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34
Q

Why don’t we use a tetracycline with a penicillin?

A

Tetra is bacteriostatic, so it will reduce the amount of cell wall synthesis penicillin targets (reducing its bacteriocidal effectiveness)

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35
Q

Tetracyclines are DOC for the treatment of what infections (9)?

A

Mycoplasma pneumonia, Rickettsia, Borrelia, Chlamydia, Vibrio, Combo therapy for H. pylori ulcer, acne, and gonorrhea/syphilis in those with penicillin allergies

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36
Q

What drug is commonly used for the eradication of the meningococcal carrier state (treating people who have come in close contact with someone who has meningitis)?

A

Minocycline

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37
Q

What is a dental specific use of tetracycline?

A

Chronic periodontal disease: Systemic or topical

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38
Q

What is Periostat?

A

Doxycycline (20mg tab bid, p.o.). Systemic therapy of advanced periodontal disease for up to 1 year.

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39
Q

What is Arestin?

A

Topical minocycline to be placed in periodontal pocket for up to 3 weeks release

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40
Q

What drug is predominantly used as a collagenase inhibitor?

A

Periostat (doxycycline)

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41
Q

What other periodontal problem can tetracyclines be used to treat (as an alternative to penicillin)

A

ANUG

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42
Q

Protein synthesis inhibitor that is isolated from Streptomyces soil bacteria?

A

Chloramphenicol

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43
Q

What is the major side effect associated with Chloramphenicol?

A

Aplastic anemia

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44
Q

Aplastic anemia associated with Chloramphenicol is an example of …?

A

Idiosyncratic toxicity (characteristic peculiarity)

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45
Q

Though Chloramphenicol is similar to tetracycline in its spectrum of activity, how is it different (mechanism of action)?

A

Binds to 50S bacterial ribosome and inhibits ribosomal peptidyltransferase; blocks “transpeptidation” reaction

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46
Q

What is the antimicrobial spectrum of chloramphenicol?

A

Just like Tetracycline: Broad: Gram +, gram -, anaerobes (excellent), atypical bacteria

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47
Q

What is Gray Baby Syndrome?

A

Neonate symptom that showed infants do not have mature hepatic drug metabolizing system (Chloramphenicol requires hepactic metabolism)

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48
Q

T/F. Chloramphenicol does not cross into the CNS well.

A

False. Reaches therapeutic [ ] in brain, CSF and crosses cell membranes

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49
Q

What character of Chloramphenicol makes it useful in treating bacterial meningitis?

A

Lipophilic and crosses blood brain barrier

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50
Q

2 blood dyscrasias associated with Chloramphenicol?

A
  1. ) predictable, dose dependent depression of bone marrow cell proliferation
  2. ) non-predictable, non-dose dependent risk of aplastic anemia that can occur even months after off Chloramphenicol
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51
Q

What is the good thing about the depressed bone marrow cell depression caused by Chloramphenicol?

A

It goes away once Chloramphenicol is stopped

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52
Q

Why does chloramphenicol cause depressed bone marrow cell depression/

A

Not as selective as tetracyclines and causes mitochondrial protein synthesis problems; also inhibits cytochrome C oxidaase, ubiquinone, cytochrome C reductase and protein translocating ATPase

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53
Q

When is Chloramphenicol indicated for treatment?

A

Severe systemic infections not treatable with less- toxic drugs. E.g. Cephalosporing resistant typhoid (S. typhi) or Meningitis and pneumonia caused by H.influenza or B. fragilis

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54
Q

Aminoglycosides are important for treating what bacteria?

A

G- bacilli aerobes and Pseudomona (P. aeruginosa)

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55
Q

How must aminoglycosides be administered?

A

Parenteral (outside alimentary, normally IV or IM)

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56
Q

Do aminoglycosides have a high or low therapeutic index?

A

Low TI, so require monitoring

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57
Q

Are aminoglycasides bactericidal/static and narrow or wide spectrum?

A

Bactericidal and narrow spectrum

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58
Q

Are aminoglycosides useful against anaerobes?

A

No (don’t affect atypical bacteria either)

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59
Q

Aminoglycoside mechanism of action?

A

Bind bacterial ribosome 30s subunit and inhibit protein synthesis

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60
Q

3 effects caused by aminoglycosides binding the 30S bacterial ribosome?

A
  1. ) Inhibit initiation: accumulation of initiation complexes (streptomycin monosomes)
  2. ) Misincorporation: misread mRNA = wrong amino acid inserted
  3. ) Premature termination: premature protein release from mRNA
61
Q

Why are Aminoglycosides poorly absorbed if taken orally?

A

Large size and charged so can’t cross membrane

62
Q

How are aminoglycosides excreted (2)?

A

Unchanged, rapidly by kidney (glomerular filtration)

63
Q

What is the basis for selectivity of aminoglycosides? What does it depend upon? What inhibits aminoglycosides?

A

[ ] inside bacterial cells by a cytoplasmic membrane transporter; oxygen dependent (anaerobic environment or low pH inhibit)

64
Q

2 toxicities associated with Aminoglycosides?

A

Ototoxicity and nephrotoxicity

65
Q

How are aminoglycoside toxicity avoided (3)?

A

Avoid longer interval, monitored dosing, not in patients with impaired kidney function (elderly/young kids)

66
Q

What makes bacteria resistant to aminoglycosides?

A

Aminoglycoside-metabolizing enzyme acquired from plasmids

67
Q

Systemic infections that are treated by Aminoglycosides (6)?

A

Klebsiella, Proteus, E.coli, Enterobacter, Pseudomonas aeruginosa, Serratia

68
Q

Why are Aminoglycosides NOT used at abscess sites?

A

Abscesses have anaerobes against which Aminoglycosides are ineffective

69
Q

2 infections where aminoglycosides are administered along with penicillin?

A

Meningitis and Enterococcal endocarditis

70
Q

Five uses of aminoglycasides by itself?

A

Pseudomonas aeruginosa, infections caused by gram - enterics, N. gonorrhea, or sterilization of gut prior to sx

71
Q

Prototype aminoglycoside?

A

Gentamicin

72
Q

This aminoglycoside is used in skin ointments or to sterilize bowel prior to GI surgery?

A

Neomycin

73
Q

This aminoglycoside is used in pseudomonal infections?

A

Tobramycin

74
Q

2 aminoglycosides that are back up drugs for Gram negative drug resistant infections?

A

Amikacin, netilimicin

75
Q

Macrolides are what general antibiotic type and for what are they named?

A

Protein synthesis inhibitors and named for large Macrolide ring structure

76
Q

Prototype Macrolide

A

Erythromycin

77
Q

What drug does Erythromycin act like in its antibacterial activity?

A

Penicillin, which is a cell wall inhibitor

78
Q

Name the 2 new macrolides that are semisynthetic with an extended spectrum and improved pharmacokinetics.

A

Azithromycin, clarithromycin

79
Q

What are the 2 new macrolides, Azithromycin and Clarithromycin used for?

A

Alternatives to penicillins for prophylaxis of bacterial endocarditis

80
Q

What structure in the Macrolide makes it easily hydrolyzed in the stomach and thereby inactivating a large part of the drug?

A

The Lactone Ring

81
Q

Erythromycin spectrum of activity, bacteriostatic/cidal, bacteria active against

A

Narrow spectrum, Bacteriostatic, Gram Positive Cocci and bacilli

82
Q

What is the spectrum of activity for Azithromycin and Clarithromycin?

A

Somewhat broader, lower activity against some Gram + (Strep and Staph) but includes activity against Gram negatives like H. influenza

83
Q

What is the Macrolide mechanism of action?

A

Bind to 50S bacterial ribosome subunit to inhibit ribosomal trasnlocase activity

84
Q

What does inhibiting translocase activity of the 50S subunit mean?

A

Stops transfer of nascent peptide from A site to P site which stop the next amino acid from being added

85
Q

Can Erythromycin be bacteriocidal?

A

Yes, dependent on [ ] of developing bad resistance

86
Q

What is good about narrow spectrum in antibiotics?

A

Reduces the risk of developing bacterial resistance

87
Q

What is the drawback of erythromycin method of delivery and how is it avoided?

A

Destroyed by stomach acid so give w/ enteric coating or as ester salt (estolate, state)

88
Q

Major difference in Azithromycin and Clarithromycin from Erythromycin?

A

Azithromycin and Clarithromycin are not sensitive to stomach acid

89
Q

If bacteria are resistant to Erythromycin, Azithromycin, Clarithromycin, what does that mean for other drugs that bind the 50S subunit?

A

Bacteria are most likely resistant to those as well

90
Q

What are the other two 50S subunit binding protein synthesis inhibitor antibiotics?

A

Clindomycin and chloramphenicol

91
Q

Of Eryhtromycin, Azithromycin, and Clarithromycin: which has the longest half-life?

A

Azithromycin (60-70 hrs)

92
Q

Where do macrolides concentrate?

A

Macrophages

93
Q

Azithromycin and Clarithromycin, due to their concentration in Macrophages, are useful against this opportunistic infection in HIV and immunocompromised pts.

A

Mycobacterium avium intracellulaire

94
Q

Where is erythromycin metabolized?

A

Liver

95
Q

What is the positive with the longer half-lives of Azithromycin and Clarithromycin?

A

Requires dosing only 1-2 times/day

96
Q

Most common side effects of Macrolides (erythromycin, azithromycin, clarithromycin)?

A

GI Disturbances

97
Q

What metabolism process do macrolides interfere with leading to their drug interactions?

A

Inhibit cytochrome P450 drug metabolism by liver

98
Q

How is Azithromycin metabolized?

A

In urine and bile, so safe for person with liver disease (also infers why it has a longer half life)

99
Q

Most common mechanism for resistance to Macrolides in bacteria?

A

Plasmids encoding erythromycin efflux transporters or methylation enzymes

100
Q

What is a positive side effect of erythromycin?

A

Increases peristalsis so may help with patients that have problems with stomach emptying

101
Q

What is Macrolide dosing for endocarditis prophylaxis that Dr. Ritter gave?

A

A/C: 500mg, 30-60mins before surgery

102
Q

What is a rare risk factor associated with erythromycin? What pop’n is this important?

A

Cholestatic jaundice from ester salts of erythromycin interrupting bile flow; pregnant women

103
Q

What Penicillin Class is Erythromycin similar to?

A

Penicillin G

104
Q

What are the two ways bacteria gain resistance to macrolides?

A
  1. Acquisition of met gene (erythromycin efflux transporter)

2. Acquisition of arm gene (methylates a base residue in the 23S RNA of the ribosome)

105
Q

When would a macrolide be indicated (2 general)?

A

Pt w/ penicillin allergy or bacteria is penicillin resistant

106
Q

What three infections are macrolides commonly used to treat?

A

Respiratory (pneumonia, sinusitis, and bronchitis), middle ear and skin

107
Q

Prototype Fluoroquinolone?

A

Norfloxacin (limited distribution), then Ciprofloxacin

108
Q

3 major advantages of Fluoroquinolones?

A

Oral effectiveness, Broad spectrum, and Safe

109
Q

Ciprofloxacin (fluoroquinolone) :cidal/static, bacteria effective against?

A

Bactericidal and G+ and G-

110
Q

Fluoroquinolone method of action?

A

Inhibit DNA replication by inhibiting bacterial enzymes topisomerase (Gram +) and DNA gyrase (-) which untwist DNA supercoil

111
Q

Bacterial DNA gyrase is related to what in humans and what are their purposes?

A

Human DNA topoisomerases and relieve buildup of torsional strain during DNA replication

112
Q

What is an administration consideration with fluoroquinolones?

A

Don’t take with dairy or antacids because they bind divalent and trivalent metal cations(like tetracyclines do as well)

113
Q

Which fluoroquinolone is useful for the treatment of UTIs because it does not have as good tissue penetration as Ciprofloxacin and Ofloxacin?

A

Norfloxacin

114
Q

What can block the excretion of fluoroquinolones?

A

Probenecid (used in war to prolong supplies of penicillin)

115
Q

Huge Contraindiction for using fluoroquinolones?

A

Do not use in pregnant/nursing women or children under 18 due to potential to damage growing cartilage (Achilles tendon rupture)

116
Q

Notable drug interaction for fluoroquinolones?

A

They increase plasma levels of warfarin

117
Q

Quinolone (older group) that is used only for UTIs?

A

Nalidixic Acid

118
Q

Large Glycopeptide druge whose most important use is treatment of Methicillin Resistant Staphylococcus infections (MRSA)?

A

Vancomycin

119
Q

How are fluoroquinolones excreted?

A

Excreted unchanged in urine; reduce dose w/ renal insufficiency

120
Q

Vancomycin bactericidal or static?

A

Vancomycin

121
Q

Vancomycin method of action?

A

Inhibit cell wall synthesis but by different mechanism than penicillin

122
Q

Vancomycin is DOC for?

A

Treating pseudomembranous colitis from clindamycin

123
Q

2 methods of administration for Vancomycin and is it absorbed systemically?

A

IV or orally (125 mg 4/day) No systemic absorption

124
Q

Vancomycin excretion?

A

Kidney

125
Q

2 side effect risks from Vancomycin?

A

Ototoxicity, nephrotoxicity, thrombophlebitis and red man syndrome (degranulation)

126
Q

Bacitracin mechanism of action?

A

Inhibit transport of building blocks of cell wall to outside cell membrane

127
Q

Clinical use of Bacitracin?

A

Topical treatment of skin & eye bacterial infections

128
Q

Bacitracin used in combo with what drugs normally?

A

Polymyxin B and Neomycin

129
Q

Clindamycin is an alternative drug for what?

A

Alternative to amoxicillin for endocarditis prophylaxis

130
Q

How is clindamycin similar to erythromycin? Different?

A

Activity against gram +, has high activity towards anaerobes

131
Q

What is the MOA for clindamycin?

A

Protein synthesis inhibitor by binding 50S; same site as macrolides and chloramphenicol

132
Q

T/F. Clindamycin is not absorbed well when taken orally.

A

F. Absorbed almost completely and penetrates deep into soft tissues, including bone

133
Q

Clindamycin is DOC for?

A

Anaerobes and lung/pleural space infections (abscesses)

134
Q

Clindamycin is good against anaerobes which makes it key treatment when?

A

late phase dental infections (bacteroides, prevotella, porphyromonas, fusobacterium)

135
Q

Dosing of Clindamycin before surgery for endocarditis prophylaxis?

A

600 mg 30-60 min before surgery

136
Q

3 protein synthesis inhibitor drugs that are alternatives to amoxicillin for prophylaxis of endocarditis?

A

Azithromycin, clarithromycin and clindamycin

137
Q

Major risk with Clindamycin?

A

Antibiotic associated enterocolitis due to C. diff overgrowth (superinfection); drug can also accumulate in patients with hepatic failure

138
Q

What is the drug used to treat the superinfection caused by Clindamycin?

A

Vancomycin (vancomycin vanquishes the turds)

139
Q

2 drugs other than Nalidixic acid and Norfloxacin for UTIs?

A

Nitrofurantoin and methenamine

140
Q

5 drugs used to treat M. tuberculosum?

A

Isoniazid, Ethambutol, Rifampin/Rifampicin, Pyrazinamide, and Streptomycin

141
Q

3 major agents used to treat M. tuberculosum?

A

Isoniazid, Ethambutol, and Rifampin

142
Q

The major agent used for M. tuberculosum?

A

Isoniazid

143
Q

Isoniazid has hepatotoxicity when paired with what other Tb drug?

A

Rifampin/Rifampicin

144
Q

Ethambutol mechanism of action?

A

Inhibits synthesis of tubercle bacilli cell wall component

145
Q

What combination is used only in hospital settings? How work and how administered?

A

Imipenem-cilastatin; Beta-lactam in the carbapenem subclass, cell wall synthesis inhibitor and Cilastatin inhibits kidney enzyme that metabolizes imipenem; parenteral formulation

146
Q

Rifampin mechanism of action

A

inhibits DNA-dependent RNA polymerase

147
Q

Tb drug that is an inducer of hepatic microsomal drug-metabolizing enzymes leading to many drug-drug interaction?

A

Rifampin

148
Q

Why use drug cocktail on Tb?

A

Tb is slow growing with high mutation and resistant rates

149
Q

What two additional drugs are used for UTI?

A

Nitrofurantoin and methenamine

Pharm Exam 4 (4 decks)

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