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Pharmacology 2nd Sem Prelim > Protein Synthesis Inhibitors > Flashcards

Protein Synthesis Inhibitors Flashcards

1
Q

inhibits subunits of peptidoglycan

A

Cycloserine

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2
Q

hinders the elongation of peptidoglycan

A

Vancomycin

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3
Q

interferes with transport of precursors across plasma membrane

A

Bacitracin

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4
Q

Inhibition of transcription and DNA replication

A

Nucleic acid synthesis

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5
Q

sulfa drugs block PABA to folic acid used to make nucleotides by competitive inhibition of enzyme trimethoprim and sulfamethoxazole SXT

A

Sulfonamides

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6
Q

bind to 30s subunit blocks translation and misreading of mRNA

A

Aminoglycosides - (streptomycin, gentamicin)

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7
Q

bind to 30s subunit and block attachment of tRNA

A

Tetracycline

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8
Q

binds to 50S subunits and prevents peptide bonds from being formed

A

Chloramphenicol

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9
Q
  • bind to 50s subunits and prevents the continuation of protein synthesis - used in many G(+) and walking atypical pneumonia instead of penicillin
A

Macrolides

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10
Q

binds with phospholipids in membrane - not as selectively toxic - topical

A

Polymyxin

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11
Q

•Inhibition of enzymatic activities

A

Like sulfa and PABA blocked to folic acid

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12
Q

Cell membrane

A

Polyxmyxins

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13
Q

Cell wall inhibitors

A 
Bacitracin
Cephalosporin 
Cycloserine 
Fosfomycin
Penicillin
Isoniazid
Vancomycin
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14
Q

Inhibit replication and transcription

Inhibit gyrase

A

Ciprofloxacin ( quinolones )

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15
Q

Inhibit RNA polymerase

A

Rifampin

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16
Q

Protein synthesis inhibitor

Site of action is 50S subunit

A

CECO

Cholorampenicol
Erythromycin
Clindamycin
Oxazolidinones

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17
Q

Protein synthesis inhibitor

30s sub unit is the location

A

ATSA

Aminoglycosides
Tetracycline
Streptomycin
Amikacin

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18
Q

Blocked pathways and inhibit metabolism

A

Sulfonamides

Trimethoprim

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19
Q

Protein synthesis inhibitor

Usually act at the _________ level, taking advantage of the major differences between prokaryotic and eukaryotic ribosome structures

A

ribosome

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20
Q

the point of entry for the aminoacyl tRNA

A

A site

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21
Q

where the peptidyl tRNA is formed in the ribosome.

A

P site

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22
Q

the exit site of the now uncharged tRNA after it gives its amino acid to the growing peptide chain.

A

E site

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23
Q

Initiation

involves formation of an initiation complex that contains

A

mRNA,
both subunits of ribosomes and
the first aminoacyl-tRNA (formyl-methionyl tRNA)

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24
Q

synthesis of the first peptide bond to addition of the last amino acid.

A

Elongation

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25
Q

polypeptide is transferred from peptidyl-tRNA in the P site to aminoacyl-tRNA in the A site

A

Peptide bond formation

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26
Q

moves ribosome one codon; places peptidyl-tRNA in the P site; deacylated tRNA leaves via the E site; A site is empty for next aa-tRNA

A

Translocation

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27
Q

•encompasses the release of the completed polypeptide chain and dissociation of the ribosome from the mRNA.

A

Termination

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28
Q

the charged tRNA unit carrying amino acid 6 binds to the acceptor site on the 70S ribosome.

A

Step 1

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29
Q

The peptidyl tRNA at the donor site, with amino acids 1 through 5, then binds the growing amino acid chain to amino acid 6 (peptide bond formation)

A

Step 2

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30
Q

The uncharged tRNA left at the donor site is released

A

Step 3

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31
Q

the new 6-amino acid chain with its tRNA shifts to the peptidyl site (translocation)

A

Step 4

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32
Q

bind to the 50S subunit and block peptide bond formation (step 2).

A

Chloramphenicol (C) and macrolides (M)

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33
Q

bind to the 30S subunit and prevent binding of the incoming charged tRNA unit (step 1).

A

Tetracycline

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34
Q

50 S INHIBITORS

A 
●Chloramphenicol
●Macrolides (Erythromycin)
●Clindamycin
●Oxazoladinones (linozelid)
●Streptogramins
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35
Q

30 s inhibitors

A

Aminoglycosides

Tetracycline

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36
Q

Older Aminoglycosides

A
  • Streptomycin

* Kanamycin

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37
Q

Newer Aminoglycosides:

A 
●Gentamicin    
● Netilmicin
●Tobramycin
●Sisomicin
●Neomycin
●Paromomycin
●Amikacin
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38
Q

Aminoglycosides

Antimicrobial spectrum

A 
•Gram (-) Aerobic Bacilli
•Beta-lactamase producers:
            Staph. aureus
            N. gonorrhea
•Mycobacteria
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39
Q

Aminoglycosides MOA

A
  • Irreversible inhibitors of protein synthesis

* Exact mechanism for bactericidal activity unknown

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40
Q

used to achieve bactericidal activity in treatment of enterococcal endocarditis

A

Penicillin plus aminoglycosides

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41
Q

Penicillin plus aminoglycosides

to shorten duration of therapy for

A

viridans streptococcal & staphylococcal endocarditis

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42
Q

AMINOGLYCOSIDES ADVERSE EFFECTS

A

All are ototoxic & nephrotoxic

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43
Q

Aminoglycosides that can cause ototoxicity

A

Neomycin, Kanamycin & Amikacin

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44
Q

Aminoglycosides that cause nephrotoxicity

A

vancomycin & amphotericin

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45
Q

Aminoglycosides

Most nephrotoxic

A

Neomycin, Tobramycin, Gentamicin

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46
Q

Aminoglycosides that can causes most ototoxic

A

Neomycin, Kanamycin, Amikacin

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47
Q

Aminoglycosides

•Respiratory Paralysis
–In very high doses, can produce a curarelike effect with neuromuscular blockade

Reversed by

A

Ca gluconate or neostigmine

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48
Q

•Mainly used as 2nd line agent for the treatment of TB at 0.5-1 g/d , IM or IV.

A

Streptomycin

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49
Q

In plague, tularemia and sometimes brucellosis:

A

Streptomycin

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50
Q

Streptomycin + penicillin

A

for enterococcal endocarditis and 2 week therapy of viridans streptococcal endocarditis

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51
Q

Streptomycin + penicillin can cause

A

pain at the injection site, fever, skin rashes and other allergic reactions

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52
Q

Streptomycin + penicillin most serious toxic effect

A

Vestibular dysfunction

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53
Q

Streptomycin + penicillin if given during pregnancy, can cause

A

deafness in the newborn

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54
Q

•effective against both gram –positive and gram-negative organisms

A

Gentamycin

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55
Q

very similar to the C1a component of gentamicin

A

Sisomicin

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56
Q

Gentamycin –inhibits in vitro many strains of

A

staphylococci and coliforms and other gram-negative bacteria

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57
Q

active alone, but also as a synergistic companion with β-lactam antibiotics

Gentamycin

A 
Escherichia coli , 
Proteus , 
Klebsiella pneumoniae, 
Enterobacter, 
Serratia , 
Stenotrophomonas , 
and other gram-negative rods that may be resistant to multiple other antibiotics.
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58
Q

Gentamycin Like all aminoglycosides, it has no activity against

A

anaerobes

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59
Q

relatively resistant to gentamicin

A

Streptococci and entero cocci

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60
Q

Gentamycin in combination with Nafcillin in

A

selected cases of staphylococcal endocarditis

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61
Q

Neither gentamicin nor any other aminoglycosides should be used for single agent therapy of

A

pneumonia

62
Q

–treatment of infected burns, wounds, or skin lesions

–prevention of intravenous catheter infections.

A

Gentamicin sulfate 0.1% - 0.3% cream, ointment

63
Q

Gentamicin

partly inactivated by purulent exudates

A

Topical gentamicin

64
Q

Gentamicin Intrathecal:

A

obsolete

65
Q

Gentamicin adverse effect

A
  • Nephrotoxicity is reversible and usually mild
  • Ototoxicity is Irreversible manifested as vestibular dysfunction
  • hypersensitivity reactions are uncommon
66
Q

Antimicrobrial spectrum and pharmacokinetic properties identical to gentamicin

A

Tobramycin

67
Q

Tobramycin Slightly more active against pseudomonas but not to

A

E. faecium

68
Q

Tobramycin AE

A

Ototoxicity

Nephrotoxicity

69
Q
  • semisynthetic derivative of kanamycin

* resistant to many inactivating enzymes

A

Amikacin

70
Q

Strains of multiple drug resistant tuberculosis, including Streptomycin resistant are usually susceptible

A

Amikacin

71
Q

Amikacin AE

A

Nephrotoxic and ototoxic (auditory portion of CN VIII)

72
Q

shares many characteristics with gentamicin and tobramycin

A

Netilmicin

73
Q
  • Also Paromomycin

* Used for bowel preparation for elective surgery

A

Kanamycin and neomycin

74
Q

Too toxic for parenteral use, now limited to topical and oral use

A

Kanamycin and neomycin

75
Q

applied on infected surfaces or injected into joints, pleural cavity, tissue spaces or abscess cavities where infection is present.

A

K and N

76
Q

–applied to infected skin lesions or in the nares for suppression of staphylococci

A

Ointments (Neomycin-Polymyxin-Bacitracin combination)

77
Q

K and N AE

A

Nephrotoxic and ototoxic ( Auditory dysfunction)

78
Q

Sudden absorption of postoperatively instilled kanamycin from the peritoneal cavity (3-5 g) has resulted in

A

curare-like neuromuscular blockade and respiratory arrest

–Calcium gluconate and neostigmine can act as antidotes

79
Q
  • chemically related to the aminoglycosides
  • binds at the 30 S subunit (bacteriostatic)
  • dispensed as the dihydrochloride pentahydrate for IM injection
A

Spectinomycin

80
Q

•used solely as an alternative treatment for gonorrhea in patients who are allergic to penicillin or whose gonococci are resistant to other drugs

A

Spectinomycin

81
Q

Short acting tetracycline

A

Tetracyline, Oxytetracycline, Chlortetracycline

82
Q

Intermediate acting tetracycline

A

Demeclocycline, Methacycline

83
Q

Long acting tetracycline

A

Doxycycline, Minocycline

84
Q

– – carrier state of Meningococcal infections, N. asteroides, N. gonnorhea

A

Minocycline

85
Q

Tetracycline MOA

A
  • binds to 30 S and prevents attachment of aminoacyl tRNA, prevents the addition of amino acids to the growing peptide
  • Bacteriostatic
86
Q

–Must not be taken with dairy products or antacids

–Cross placenta, excreted in milk

A

Tetracycline

87
Q

Tetracycline DOC

A

M. pneumoniae, Chlamydia, ricketssiae, spirochetes

88
Q

Tetracycline No longer use in

A

gonococcal dse. (resistance)

89
Q

Tetracycline In combination regimens for

A

gastric & duodenal ulcer due to H. pylori

90
Q

Other clinical use of tetracycline

A

•Borrelia burgdorfi (Lyme disease), Ureaplasma, Acne, Tularemia, Cholera, Leptospirosis, Protozoal infections

91
Q

200 mg orally daily for 5 days – can eradicate the meningococcal carrier state

A

Minocycline

92
Q
  • – inhibits the action of ADH in the renal tubule

* treatment of inappropriate secretion of ADH or similar peptides by certain tumors

A

Demeclocycline

93
Q

Tetracycline toxicity

A
  • Renal toxicity
  • local tissue toxicity, photosensitization, GI distress, discolors teeth,
  • inhibits bone growth in children, potentially teratogenic, hepatotoxicity,
  • vestibular toxicity
94
Q

50s inhibitors

A
  • CHLORAMPHENICOL
  • MACROLIDES
  • CLINDAMYCIN/LINCOMYCIN
  • STREPTOGRAMINS
  • OXAZOLADINONES
95
Q

Chloramphenicol •Bactericidal

–

A

H. influenzae, N. meningitides, B. fragilis

96
Q

Chloramphenicol MOA

A
  • attaches at P sites of 50 S subunit of microbial ribosomes
  • inhibits functional attachment of amino-acyl end of AA-t-RNA to 50 S subunit
  • inhibits peptidyl transferase step
97
Q

Choramphenicol more effective than Tetracyclines against

A

Typhoid Fever and other Salmonella infections

98
Q

Chloramphenicol AE

A

•GIT, oral or vaginal candidiasis, irreversible aplastic anemia, reversible bone marrow depression, Gray Baby Syndrome

99
Q

Old gen macrolides

A

Erythromycin

100
Q

New generation macrolides

A

, , Clarithromycin, Azithromycin, , Ketolides

101
Q

has a narrow Gram (+) spectrum similar to Pen. G.

A

Erythromycin

102
Q

Erythromycin •Also active against

A

Chlamydia and Legionella organisms

103
Q

Macrolides MOA

A

binds to the P site of the 50 S bacterial ribosomal subunit.

104
Q

poor CSF penetration

Macrolides

A

Erythromycin

105
Q

Erithromycin AE

A

GIT dysfunction, intrahepatic cholestatic jaundice

106
Q

Erthromycin erythromycin metabolites can inhibit

A

cytochrome p450 enzymes

107
Q
  • hydroxylated derivative of erythromycin
  • more active against Gram (+) pathogens, Legionella and Chlamydia than Erythromycin
  • lower frequency of GIT effects, less frequent dosing
A

Clarithromycin

108
Q
  • more active than erythromycin against several Gram (-) pathogens
  • maintains high concentrations for prolonged periods into a number of tissues (lungs, tonsils, cervix)
A

Azithromycin

109
Q

Community acquired pneumonia –

A

Azithromycin

110
Q

Azithromycin

A

does not inactivate cytochrome p450 enzymes and free of the drug interactions that occur with erythromycin and clarithromycin

111
Q

•: A is the 1st letter, thus aminoglycosides inhibit Initiation (the first step of translation) by preventing formation of the initiation complex.

A

Aminoglycosides

112
Q

: the only one with a “P”, thus the only one inhibiting Peptide bond formation (by peptidyltransferase)

A

ChloramPhenicol

113
Q

: prevent the Movement of ribosomes (translocation)

A

Macrolides

114
Q

: makes ribosomes Cling to mRNA (prevents translocation)

A

Clindamycin

115
Q

(TTC): tRNA Tries but Can’t (prevents the aminoacyl-tRNA from attaching to the A site of the ribosome)

A

Tetracyclines

116
Q

: Like erythromycin (prevents translocation)

A

Lincomycin

117
Q

: Like an aminoglycoside (prevents initiation)

A

Linezolid

118
Q

react with enzymes in formation of cross links

A

lactams like Penicillins and cephalosporin

119
Q

Clindamycin and lincomycin MOA

A
  • attach to 50 S ribosomal subunit

* inhibits protein synthesis by interfering with the formation of initiation complexes and translocation reaction

119
Q

Clindamycin spectrum

A

•Narrow Gram (+) spectrum, excellent activity against anaerobic bacteria; strep, pneumococci, staphylococci

120
Q

•prophylaxis of endocarditis in patients with valvular heart disease for dental procedures

A

Clindamycin

121
Q

Clindamycin most important indication

A

severe anaerobic infection

122
Q

Clindamycin plus what?

used to treat penetrating wounds of the abdomen & gut

A

aminoglycoside or cephalosporin-

123
Q

Clindamycin plus what?

effective alternative to trimethoprim sulfamethoxazole for moderate to moderately severe Pneumocystis carinii pneumonia in AIDS patients

A

Primaquine

124
Q

Clindamycin plus what?

for AIDS – related toxoplasmosis of the brain.

A

Pyrimethamine

125
Q

Clindamycin

A

septic abortion,
pelvic abscesses,
aspiration pneumonia

126
Q

Clindamycin adverse effect

A

•Antibiotic associated colitis caused by toxigenic C. difficile.

127
Q
  • action is similar to macrolides except bactericidal for staph and most organisms except Enterococcus faecium
  • prolonged postantibiotic effect up to 10 h for Staph. aureus
A

Streptogamins

128
Q

•inhibits CYP 3A4, which metabolizes warfarin, diazepam, astemizole, terfenadine, cisapride, nonnucleoside reverse transcriptase inhibitors and cyclosporine.

A

Streptogamins

129
Q

•infections caused by Vancomycin resistant strains of E faecium but not E. faecalis, bacteremia or respiratory tract infections caused by methicillin-resistant staphylococci and penicillin susceptible and resistant strains of S. pneumonia

A

Streptogamins

130
Q

Streptogamins toxicity imes

A

infusion related events, pain at the injection site, arthralgia, myalgia

131
Q
  • (-) protein synthesis by preventing formation of the ribosome complex that initiated protein synthesis.
  • Its unique binding site located on 23 S ribosomal RNA of the 50 S subunit, results in no cross resistance with other drug classes
A

Linezolid

132
Q
  • structural analogs of PABA (paraaminobenzoic acid)
  • competitively inhibit dihydropteroate synthase (catalyzed the synthesis dihydropteroic acid)
  • inhibits growth by reversibly blocking folic acid synthesis
A

Sulfonamides

133
Q

Sulfonamide spectrum

A
  • Inhibit the growth both Gm (+) and Gm (-) bacteria, Nocardia, Chlamydia trachomatis & some protozoa
  • Enteric bacteria such as E.coli,klebsiella, salmonella,shigella, and enterobacter are also inhibited
  • Rickettsia – not inhibited but growth stimulated by sulfas
134
Q

Sulfonamides topical

A

a. Sodium sulfacetamide ophthalmic sol’n or ointment – for bacterial conjunctivitis
b. Mafenide acetate- prevent bacterial colonization and infection of burn wounds
c. Silver sulfadiazine –prevent of infection in burn wounds

135
Q

Sulfonamide plus what?

• Toxoplasmosis
Malaria

A

With pyrimethamine:

136
Q

Sulfonamides AE

A

Hemolytic anemia

Kernicterus in new born

137
Q

Co trimoxazole

Combination causes

A
  1. INCREASE POTENCY
  2. INCREASE SPECTRUM
  3. DECREASE INCIDENCE OF RESISTANCE
138
Q

Co trimoxazole

MOA

A

MOA: blocks the sequential steps in the obligate enzymatic reaction in bacteria preventing formation of nucleotide

139
Q

Co trimoxazole spectrum

A

broad gm + & gm –

140
Q

for leishmaniasis & toxoplasmosis

A

Sulfadiazine plus Pyrimethamine

141
Q

2.

for Falciparum malaria

A

Sulfadoxime + pyrimethamine

142
Q

Nucleic acid inhibitors

first generation

A

Nalidixic Acid

143
Q

Nucleic acid synthesis inhibitor or gyrase inhibitor

2nd gen

A

•Second Generation: Ciprofloxacin, Norfloxacin, Ofloxacin, Levofloxacin, Enoxaxin, Lomefloxacin

144
Q

Nucleic acid synthesis inhibitor or gyrase inhibitor

3rd gen

A
  • Third Generation: Gatifloxin, Moxifloxacin,

* Gemfloxaxin

145
Q
  • Inhibits DNA Gyrase or Topoisomerase II - Block the relaxation of supercoiled DNA that is catalyzed by DNA gyrase
  • Inhibits Topoisomerase IV – interferes with the separation of replicated chromosomal DNA during cell division
A

Fluoroquinolones

146
Q

Fluoroquinolones spectrum

A

broad ; aerobic gm (+) & gm (-) but not anaerobes

147
Q

Fluoroquinolones clinical uses

A
  • UTI
  • Sexually transmitted diseases : Gonorrhea, Chlamydia, chacroid, Prostatitis
  • Respiratory infection due to H. influenza, M. catarrhalis, Strep pneumoniae, M. pneumoniae
148
Q
  • Most widely used
  • DOC for anthrax
  • Most potent for P. aeroginosa
  • Synergistic with beta lactams
  • M. tuberculosis
A

Ciprofloxacin

149
Q

Not effective in systemic infection

A

Norfloxacin

150
Q
  • Prostatitis ,E. coli
  • Urethritis, cervicitis
  • Skin infections
  • S. pneumoniae
A

Levofloxacin

Pharmacology 2nd Sem Prelim (7 decks)

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