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2nd Year 2nd Term > MT6314 PROTEIN SYNTHESIS INHIBITORS AND AMINOGLYCOSIDES > Flashcards

MT6314 PROTEIN SYNTHESIS INHIBITORS AND AMINOGLYCOSIDES Flashcards

1
Q

T or F: Protein synthesis in microorganisms is identical to mammalian cells

A

F, NOT identical

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2
Q

How many S ribosomal units are in bacteria and what are the subunits?

A

70S (50S and 30S)

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3
Q

How many S ribosomal units are in mammalians and what are the subunits?

A

80S (40S and 60S)

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4
Q

Protein Synthesis Inhibitors have a basis for (WHAT) against microorganisms without causing major effects on mammalian cells?

A

selective toxicity

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5
Q

Differences in protein synthesis inhibitors are based on?

A

Chemical composition
Ribosomal subunits
Functional specificities of component nucleic acids and proteins

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6
Q

What are the types of MOAs in protein synthesis inhibitors?

A

Bacteriostatic
Bactericidal

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7
Q

What protein synthesis inhibitors are under the bactericidal MOA?

A

Oxazolidinones and Pleuromutilins

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8
Q

All have a 50S ribosomal unit except?

A

Tetracycline

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9
Q

A normal bacterial ribosomal complex is composed of what ribosomal units?

A

Entire structure - 70S
Larger - 50S
Smaller - 30S

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10
Q

Can inhibit transpeptidation (part of the bacterial MOA structure) – acting on the cell wall

A

Chloramphenicol

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11
Q

Blocks translocation of peptide tRNA from acceptor site

A

Macrolides

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12
Q

Where are the tetracyclines located: 30S or 50S?

A

30S

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13
Q

Blocks the binding of the charged tRNA to the acceptor site

A

Tetracyclines

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14
Q

Constricts the channel and inhibits the entrance of other molecules which created a steric effect on the growing peptide chain

A

Streptogramins

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15
Q

What protein synthesis inhibitors are under the broad spectrum?

A

Chloramphenicol and Tetracyclines

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16
Q

What protein synthesis inhibitors are under the moderate spectrum?

A

Macrolides and Ketolides

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17
Q

What protein synthesis inhibitors are under the narrow spectrum?

A

Lincosamides
Streptogramins
Linezolid

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18
Q

Disadvantage of broad spectrum inhibitors?

A

Affect normal flora

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19
Q

ROA of chloramphenicols?

A

Parenteral and oral

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20
Q

MOA of chloramphenicols?

A

inhibits microbial protein synthesis
bacteriostatic against most susceptible organisms
binds reversibly to the 50S subunit of the bacterial ribosome and inhibits peptide bond formation

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21
Q

Chloramphenicols readily cross the?

A

BBB
Placenta

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22
Q

T or F: Chloramphenicols can be used in pregnant patients and NOT in patients with meningitis and encephalopathy.

A

F, CANNOT in pregnant and CAN in meningitis and encephalopathy

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23
Q

Chloramphenicols under go ___ cycling

A

Enterohepatic

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24
Q

T or F: Some fraction of chloramphenicols remains unchanged in the urine

A

T

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25
Q

The enterohepatic cycling of chloramphenicols is inhibited by?

A

Glucuronosyltransferase

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26
Q

Chloramphenicol’s are active against?

A

G(+) nand G(-) bacteria

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27
Q

Bactericidal antimicrobial activity of chloramphenicols are effective against strains of?

A

H. influenzae
N. meningitidis
Some strains of Bacteroides

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28
Q

Chloramphenicols are NOT effective against?

A

Chlamydia

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29
Q

Resistance to chloramphenicols are ___ mediated through the formation of _______

A

Plasmid
Chloramphenicol acetyltransferases

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30
Q

Clinical Uses of chloramphenicols?

A
  • Rickettsial infections: typhus and Rocky Mountain spotted
  • Alternative to a β-lactam antibiotic for bacterial meningitis in patients who have major hypersensitivity reactions to penicillin
  • Severe infections - Salmonella spp.
  • Alternative to pneumococcal and meningococcal meningitis
  • Anaerobic - B. fragilis
  • Topical antimicrobial
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31
Q

IV formulation of chloramphenicol involves the hydrolysis of what component to form what component?

A

chloramphenicol succinate (prodrug) -> hydrolyzed to yield free chloramphenicol

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32
Q

Chloramphenicol is widely distributed, including?

A

CNA and CSF

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33
Q

T or F: Concentrations of chloramphenicol in the brain tissue may be equal to that in serum

A

T

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34
Q

Chloramphenicols are inactivated by?

A

(1) conjugation with glucuronic acid or
(2) reduction to inactive aryl amines

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35
Q

Excretion of chloramphenicols

A

Active chloramphenicol + inactive degradation products = urine
Small amount of active drug - bile and feces

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36
Q

Toxicity of chloramphenicols

A
  1. Gastrointestinal disturbances
  2. Oral or vaginal candidiasis due to alteration of normal flora
  3. Bone marrow
  4. Gray baby syndrome
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37
Q

What is a rare idiosyncratic reaction in the toxicity of chloramphenicols?

A

Aplastic anemia

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38
Q

T or F: Aplastic anemia is reversible

A

F, irreversible nad fatal

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39
Q

In gray baby syndrome, the baby lacks what?

A

Effective glucuronic acid conjugation mechanism for degradation and detoxification

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40
Q

T or F: Neonates and premature babies are more sensitive to the dosages of chloramphenicols to older infants

A

T

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41
Q

What are the drug interactions of chloramphenicols?

A
  • Inhibits hepatic drug-metabolizing enzymes
  • Increasing the elimination half-lives of drugs
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42
Q

Chloramphenicol increases the half life of what drugs?

A

Warfarin
Tolbutamide
Chlorpropamide
Phenytoin

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43
Q

What are the kinds of tetracyclines?

A

Tetracycline
Doxycycline
Minocycline
Tigecycline
Eravacycline
Omadacycline

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44
Q

Tetracyclines are bacteriostatic or bactericidal?

A

Bacteriostatic

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45
Q

MOA of tetracyclines?

A

bind reversibly to the 30S subunit of the bacterial ribosome, blocking the binding of aminoacyl-tRNA to the acceptor site on the mRNA-ribosome complex and prevents addition of amino acids to the growing peptide

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46
Q

Oral absorption for tetracyclines include which kinds?

A
  • 60–70% for tetracycline and demeclocycline
  • 95–100% for doxycycline and minocycline
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47
Q

Which tetracyclines are exempt from being taken on an empty stomach?

A

Doxycycline and Minocycline

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48
Q

Tetracyclines which are taken intravenously

A

Tigecycline and eravacycline

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49
Q

Tetracycline is excreted in?

A

Feces

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50
Q

Tetracyclines absorption occurs mainly in the?

A

Upper small int.

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51
Q

Tetracycline absorption is impaired by?

A

Food, multivalent cations (Ca2+, Mg2+, Fe2+, Al3+); dairy products and antacids, and by alkaline pH

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52
Q

T or F: Tetracyclines cross the placenta

A

T

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53
Q

Tetracyclines have wide tissue distribution except in the?

A

CSF

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54
Q

Tetracyclines cross the placental barrier and excreted in?

A

breast milk

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55
Q

Tetracyclines excreted mainly in?

A

bile and urine
Except : Doxycycline and tigecycline (eliminated by nonrenal mechanisms and do not accumulate significantly in renal failure, requiring no dosage adjustment)

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56
Q

T or F: Tetracyclines also undergo enterohepatic cycling

A

T

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57
Q

Doxycycline and Tigecyclines are excreted in?

A

Feces/ fecal extraction

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58
Q

t1/2 of Tetracycline?

A

6-11h

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59
Q

t1/2 of doxycycline and minocycline?

A

15-23h

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60
Q

t1/2 of tigecycline?

A

30-36h

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61
Q

Shortest acting tetracycline?

A

tetracycline (oral)

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62
Q

Intermediate acting tetracycline?

A

demeclocycline (oral)

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63
Q

Long acting oral and IV tetracyclines?

A

doxycycline and minocycline

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64
Q

Tetracyclines with long half lives?

A

Tigecycline (IV),
Eravacycline (IV),
Omadacycline (oral and IV)

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65
Q

Antibacterial Activity of tetracyclines?

A

Active against gram-positive and gram-negative bacteria - certain anaerobes, rickettsiae, chlamydiae, and mycoplasmas (CRAM)

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66
Q

Resistance mechanisms for tetracyclines?

A

(1) impaired influx or increased efflux by an active transport protein pump
(2) ribosome protection due to production of proteins that interfere with tetracycline binding to the ribosome
(3) enzymatic inactivation

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67
Q

Primary clinical uses of tetracyclines?

A

Mycoplasma pneumoniae (in adults)
Chlamydiae
Rickettsiae*
Borrelia sp.*
Vibrios
Spirochetes
Anaplasma phagocytophilum
Ehrlichia sp
(CREAMBVS)

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68
Q

Secondary uses for tetracyclines include its use an alternative to treat?

A

CAP
Syphilis
Chronic bronchitis
Leptospirosis
Acne
(SLACC)

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69
Q

Selective use of tetracycline includes treating?

A

GI ulcers in H. pylori

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70
Q

Doxycycline selective uses includes treatment for?

A

Lyme disease

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71
Q

Minocycline includes selective use against?

A

meningococcal carrier state

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72
Q

Selective use of doxycycline is used for?

A
  • Malaria prophylaxis
  • Treat ameobiasis
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73
Q

Demeclocycline selective use is to?

A
  • inhibits the renal actions of antidiuretic hormone (ADH)
  • ADH-secreting tumors
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74
Q

Selective use includes Coagulase-negative staphylococci (CoNS), gram-positive cocci resistant to methicillin (MRSA strains) and vancomycin (VRE strains)

A

Tigecycline, eravacycline and omadacycline

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75
Q

Tigecycline, eravacycline and omadacycline has selective uses against?

A

Streptococci,
enterococci,
G(+) rods,
Enterobacteriaceae,
Acinetobacter sp,
anaerobes,
rickettsiae,
Chlamydia sp,
L. pneumophila; and
rapidly growing mycobacteria

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76
Q

Tetracyclines toxicity includes?

A
  1. Gastrointestinal disturbances
  2. Bony structures and teeth
  3. Hepatic toxicity
  4. Renal toxicity
  5. Photosensitivity
  6. Vestibular toxicity
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77
Q

Fetal exposure to tetracycline will cause?

A
  • irregularities in bone growth
  • tooth enamel dysplasia
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78
Q

Toxicities of tetracycline seen in the Bony structures and teeth in children are due to?

A
  • enamel dysplasia
  • crown deformation (permanent teeth)
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79
Q

Photosensitivity toxicity seen in tetracyclines is seen in?

A

demeclocycline

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80
Q

Vestibular toxicity in tetracyclines is prominent in?

A

Doxycycline and minocycline

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81
Q

Vestibular toxicity in tetracyclines is characterized by?

A

Dose-dependent reversible dizziness and vertigo

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82
Q

Macrolides includes?

A

Erythromycin
Azithromycin
Clarithromycin
(ACE)

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83
Q

Macrolides have what structure?

A

lactone ring with attached sugars

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84
Q

Prototype macrolide is?

A

Erythromycin (1952)

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85
Q

Semisynthetic derivatives of erythromycin include?

A

Clarithromycin and azithromycin

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86
Q

Macrolides MOA?

A

Inhibition of protein synthesis occurs via binding to the 50S ribosomal RNA

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87
Q

Macrolide antibiotics prolong the _______________ due to an effect on ________ channels: _______________

A

electrocardiographic QT interval
potassium channels
torsades de pointes arrhythmia

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88
Q

Macrolides has (good/bad) oral F

A

Good

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89
Q

Azithromycin absorption impeded by?

A

Food

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90
Q

Azithromycin is distributed mainly where?

A

tissues and phagocytes > plasma

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91
Q

T or F: Macrolides are distributed mainly in most body tissues

A

T

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92
Q
  • Erythromycin (oral and IV) half-life: _____
  • Clarithromycin (oral) half-life: ______
  • Azithromycin (oral and IV) half-life: ______
A

2 hours
6 hours
2 to 4 days

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93
Q

Antibacterial activity of erythromycin includes?

A

Campylobacter
Chlamydia
Mycoplasma
Legionella
G(+) cocci and some G(-) organisms

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94
Q

Azithromycin and Clarithromycin antibacterial activity?

A

Greater activity against Chlamydia, Mycobacterium avian complex and Toxoplasma

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95
Q

Azithromycin is used as an alternative drug against?

A

Gonorrhea

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96
Q

Resistance in gram-positive bacteria in macrocodes are due to?

A
  • efflux pump mechanisms
  • production of a methylase
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97
Q

T or F: There is complete cross resistance between macrolides

A

T

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98
Q

In macrolide antibacterial activity, there is partial cross resistance between?

A

clindamycin and streptogramins.

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99
Q

Resistance in Enterobacteriaceae is caused by?

A

drug-metabolizing esterases.

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100
Q

Erythromycin is effective against G(+) cocci except?

A

penicillin-resistant Streptococcus pneumoniae [PRSP] strains

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101
Q

Erythromycin is effective against G(-) cocci except?

A

MRSA strains

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102
Q

Azithromycin more active against what bacterial infections?

A
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Neisseria.
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103
Q

A single dose of azithromycin is useful against?

A

genitourinary infections - C trachomatis

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104
Q

A 4-day course of treatment by azithromycin is useful against?

A

CAP

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105
Q

What macrolide has the same spectrum as erythromycin?

A

Clarithromycin

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106
Q

Clarithromycin and erythromycin are used for what clinical uses?

A
  • prophylaxis and treatment of M avium complex
  • drug regimens for ulcers caused by H pylori.
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107
Q

What is a narrow-spectrum macrolide example and its uses?

A

Fidaxomicin used for gram-positive aerobes and anaerobes.

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108
Q

Fidaxomicin is as effective as what drug for what infection?

A

effective as vancomycin vs difficile colitis

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109
Q

Toxicity to erythromycin includes?

A

GI irritation
Skin rashes
Eosinophila

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110
Q

Acute cholestatic hepatitis is caused by?

A

Erythromycin estolate

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111
Q

Erythromycin estimate causes what condition?

A

Acute cholestatic hepatitis

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112
Q

T or F: Hepatic toxicity in erythromycin is common in children

A

F, rare

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113
Q

Who is at higher risk of erythromycin estolate?

A

pregnant women

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114
Q

Inhibits cytochrome p450

A

Erythromycin

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115
Q

T or F: Azithromycin inhibits cytochrome P450

A

F, does not

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116
Q

With the inhibition of cytochrome P450, erythromycin increases plasma levels of?

A

Anticoagulants, cisapride, carbamezapine, digoxin

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117
Q

Ketolide structurally related to macrolides.

A

Telithromycin

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118
Q

Telithromycin has the same spectrum and MOA as?

A

erythromycin

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119
Q

Telithrmycin is usually used to treat?

A

Community acquired bacterial pneumonia

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120
Q

What strains are susceptible to telithromycin?

A

Macrolide-resistant strains

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121
Q

Telithromycin is metabolized in?

122
Q

Telithromycin is excreted in?

A

Bile and urine

123
Q

How often is the dosing of telithromycin?

A

Once daily, 800mg

124
Q

Telithromycin reversibly inhibits what in the enzyme system?

125
Q

T or F: Telithromycin also prolongs the QTc intervals

126
Q

Telithromycin is only used for the treatment of?

A

Community acquired bacterial pneumonia

127
Q

Telithromycin can also cause what kind of toxicity?

A

Hepatitis and liver failure

128
Q

Telithromycin contraindicated in patients with?

A

Myasthenia gravis

129
Q

A fluoroketolide

A

Solithromycin

130
Q

Solithromycin showed noninferiority with ______ in the treatment of ______

A

Moxifloxacin
Community acquired bacterial pneumonia

131
Q

Solithromycin has in vitro activity against?

A

Macrolide resistant bacteria
Staphylococci, S. pneumoniae, Neisseria, Enterococci, Chlamydia

132
Q

Solithromycin lacks what side chain group?

A

Pyridine imidazole

133
Q

What is the role of pyridine-imidazole side chain to telithromycin?

A

Contributes to its hepatotoxicity

134
Q

Solithromycin is also used against what infections?

135
Q

What is still the DOC for STIs?

A

Ceftrizxone and Azithromycin

136
Q

Gram-negative organisms erythromycin is effective against include?

A

Neisseria sp,
Bordetella pertussis,
Bartonella spp.
Rickettsia species
Treponema pallidum,
Campylobacter species

137
Q

Erythromycin resistance mechanisms include?

A

(1) Reduced permeability of the cell membrane or active efflux
(2) Production (by Enterobacteriaceae) of esterases that hydrolyze macrolides
(3) Modification of the ribosomal binding site (so-called ribosomal protection) by chromosomal mutation or by a macrolide-inducible or constitutive methylase.

138
Q

T or F: Food interferes with absorption in Erythromycin

139
Q

Erythromycin is excreted mainly in?

A

bile (only 5% in the urine)

140
Q

Erythromycin is distributed widely except to the?

A

Brain and CSF

141
Q

Erythromycin is mainly taken up by what cells?

A

polymorphonuclear leukocytes and macrophages

142
Q

Erythromycin also traverses the?

A

placenta and reaches the fetus

143
Q

What is the main adverse reaction seen in Erythromycin?

A

Cholestatic hepatitis

144
Q

Erythromycin has drug interactions with?

A

theophylline
warfarin
cyclosporine
methylprednisolone
digoxin
(MTW-DC)

145
Q

Useful as a penicillin substitute in penicillin-allergic individuals with infections caused by staphylococci and streptococci

A

Erythromycin

146
Q

Clarithromycin is more active against what strains of bacteria?

A

Mycobacterium avium complex
M leprae, T gondii, H influenzae.

147
Q

Where is Clarithromycin metabolized mainly?

148
Q

Where is Clarithromycin excreted mainly?

A

Partially in the urine, mainly in bile

149
Q

What is the major metabolite seen in Clarithromycin that confers its antibacterial activity?

A

14-hydroxyclarithromycin

150
Q

Where is 14-hydroxyclarithromycin eliminated?

151
Q

What is the adverse reaction observed in Clarithromycin?

A

lower incidence of gastrointestinal intolerance

152
Q

Clarithromycin has similar drug interactions with?

A

Erythromycin

153
Q

Dosage reduction for Clarithromycin is recommended in patients with?

A

creatinine clearances less than 30 mL/min

154
Q

Azithromycin penetrates into _____ and ______ really well

A

most tissues (except cerebrospinal fluid) and phagocytic cells extremely well

155
Q

Azithromycin is rapidly absorbed and tolerated well in what ROA?

156
Q

When taken with Azithromycin, these substances do not alter bioavailability but delay absorption and reduce peak serum concentrations

A

Aluminum and magnesium antacids

157
Q

What are the effects of Aluminum and magnesium antacids on the absorption of Azithromycin?

A

do not alter bioavailability but delay
absorption and reduce peak serum concentrations

158
Q

T or F: Azithromycin has drug interactions

159
Q

What is the drug under Lincosamide?

A

Clindamycin

160
Q

Clindamycin has similar MOA with?

A

Macrolides

161
Q

T or F: Clindamycin is chemically related to Macrolides

162
Q

Clindamycin is useful against?

A
  • Streptococci, staphylococci, and pneumococci
  • Bacteroides sp and other anaerobes
163
Q

What strains are intrinsically resistant to Clindamycin?

A

Gram-negative aerobes due to poor penetration through the outer membrane.

164
Q

MOA of Clindamycin

A

Oral and IV

165
Q

When does good tissue penetration of Clindamycin occur?

A

after oral absorption

166
Q

Mode of metabolism of Clindamycin?

A

Hepatic metabolism

167
Q

Half life of Clindamycin?

168
Q

Excretion of Clindamycin happens through?

A

renal and biliary excretion

169
Q

Clinical Use of Clindamycin includes?

A
  • Severe anaerobic infections: Bacteroides, Fusobacterium, and Prevotella (BFP)
  • Backup for gram-positive cocci: Community-acquired strains of MRSA
  • Toxic shock syndrome (with penicillin G) or necrotizing fasciitis
  • Penetrating wounds of the abdomen and gut (combined with aminoglycoside or cephalosporin)
  • Septic abortion, pelvic abscesses, or pelvic inflammatory disease; and lung and periodontal abscesses
  • Prophylaxis of endocarditis in valvular disease (patients allergic to penicillin)
  • In combination with primaquine alternative vs P. jiroveci pneumonia in AIDS
    patients
  • In combination with pyrimethamine for AIDS-related toxoplasmosis
170
Q

Toxicities commonly seen in Clindamycin include?

A
  • GI irritation
  • Skin rashes
  • Neutropenia
  • Hepatic dysfunction
  • Superinfections C. difficile- pseudomembranous colitis
171
Q

Dalfopristin is to streptogramin (A/B)?

172
Q

Quinupristin is to streptogramin (A/B)?

173
Q

Quinupristin-dalfopristin have the same ribosomal binding site as?

A

macrolides and clindamycin

174
Q

Quinupristin-dalfopristin are bacteriostatic or bactericidal?

A

Bactericidal

175
Q

T or F: Quinupristin-dalfopristin have post-antibiotic effects, wherein the effects still linger long after the serum concentrations have gone down

176
Q

Quinupristin-dalfopristin are all bactericidal except combating which bacteria?

A

Enterococcus faecium

177
Q

Quinupristin-dalfopristin is active against what bacterium?

A

Active against gram-positive cocci (multidrug-resistant strains of streptococci, PRSPs, methicillin-susceptible and resistant strains of staphylococci, and E faecium)
VRSA

178
Q

What bacterium is intrinsically resistant via efflux transport system in Quinupristin-dalfopristin?

A

E faecialis

179
Q

Resistance of Quinupristin-dalfopristin methods include?

A
  • Modification of the quinupristin binding site (MLS-B type resistance)
  • Enzymatic inactivation of dalfopristin
  • Efflux
180
Q

ROA of streptogramins?

181
Q

Which has a faster metabolism activity/more rapidly metabolized: Quinupristin or Dalfopristin?

A

Dalfopristin t1/2 = 0.7 hours

182
Q

Elimination of Quinupristin-dalfopristin?

A

fecal route

183
Q

Side effects of the IV ROA of Quinupristin-dalfopristin?

A

Pain
Arthralgia Myalgia syndrome

184
Q

T or F: Dose adjustment for Quinupristin-dalfopristin is necessary for renal failure, peritoneal dialysis, or hemodialysis

A

F, not necessary

185
Q

Quinupristin-dalfopristin has drug interactions with what substances due to the inhibition of what substance?

A

due to inhibition of CYP3A4:
warfarin, diazepam, quetiapine, simvastatin, and cyclosporine

186
Q

Clinical uses of Quinupristin-dalfopristin include?

A

Infections caused by staphylococci or by vancomycin-resistant strains of E faecium

187
Q

Adverse effects of Quinupristin-dalfopristin include?

A

Pain at infusion site and arthralgia-myalgia syndrome

188
Q

Oxazolidinones include?

A

Linezolid
Tedizolid

189
Q

Linezolid is active against?

A

Active against gram-positive organisms including staphylococci, streptococci, enterococci, anaerobics, corynebacteria, Nocardia sp, L monocytogenes, and Mycobacterium tuberculosis

190
Q

Linezolids are mainly bacteriostatic or bactericidal?

A

Bacteriostatic but bactericidal against streptococci

191
Q

MOA of Linezolid

A

preventing formation of the ribosome complex that initiates protein synthesis.

192
Q

Where is the binding site of Linezolid?

A

23S ribosomal RNA of the 50S subunit

193
Q

Resistance of Linezolid

A

mutation of the linezolid binding site on 23S ribosomal RNA

194
Q

T or F: There is rare resistance with Linezolid

195
Q

T or F: There is cross resistance between Linezolid and other protein synthesis inhibitors

196
Q

Rare resistance in Linezolid involves a (decreased/increased) affinity to its binding site

197
Q

MOA of Linezolid

A

Oral and IV

198
Q

t1/2 of Linezolid

199
Q

Method of metabolism of Linezolid

A

oxidative metabolism to form inactive metabolites

200
Q

Linezolid is usually reserved for what kind of bacteria?

A

Multidrug resistant G(+) bacteria

201
Q

Linezolid is mainly metabolized by what organ?

202
Q

Clinical uses of Linezolid

A

vancomycin-resistant E faecium infections, HCAP, CAP, skin and soft tissue infections (gram-positive bacteria).

203
Q

Off-label uses of Linezolid

A

treatment of MDR-TB and Nocardia infections

204
Q

Adverse effects of Linezolid

A

thrombocytopenia, anemia, neutropenia; optic and peripheral neuropathy and lactic acidosis; serotonin syndrome

205
Q

Tedizolid is an active prodrug against?

A

tedizolid phosphate

206
Q

High potency against G(+) or G(-) bacteria?

A

G(+) - (MRSA, VRE, streptococci, gram-positive
anaerobes)

207
Q

Bioavailability and t1/2 of Tedizolid

A

91% bioavailability; t1/2: 12 hours

208
Q

T or F: Tedizolid is higher protein binding than Linezolid

A

T; Higher protein-binding (70–90%) than linezolid (31%)

209
Q

Tedizolid penetrates well into?

A

muscle, adipose, and pulmonary tissues

210
Q

T or F: Tedizolid requires no dose adjustment for renal or hepatic impairment

211
Q

Clinical use of Tedizolid

A

skin and soft tissue infection

212
Q

Adverse effects of Tedizolid

A

Lower risk of bone marrow suppression, lower risk of serotonergic toxicity

213
Q

Pleuromutilins includes?

214
Q

MOA of Lefamulin

A

binding the 50S ribosome and inhibits bacterial protein synthesis; binding pocket closes around the drug molecule, preventing bacterial transfer RNA from binding appropriately

215
Q

Is Lefamulin bactericidal or bacteriostatic?

A

Bactericidal

216
Q

Lefamulin is Bactericidal against what infections?

A

lower respiratory tract infections (S. pneumoniae, H. influenzae)

atypical pathogens (L. pneumophila, M. pneumoniae, and C. pneumoniae)

aerobic gram-positive organisms (S. pyogenes, S. aureus, and E. faecium)

STIs (M. genitalium, N. gonorrhoeae, and C. trachomatis)

217
Q

Lefamulin lacks activity against?

A

E. faecalis, P. aeruginosa, A. baumannii, and the Enterobacteriaceae group of gram-negative organisms (EPEA)

218
Q

Mechanisms for resistance in Lefamulin

A

ribosomal target site alteration and active efflux from the site of action

219
Q

Clinical use of Lefamulin

220
Q

ROA of Lefamulin

A

Oral and IV

221
Q

Bioavailability and protein binding availability of Lefamulin

A

25% bioavailability; 95-97%-protein bound

222
Q

t1/2 of Lefamulin

A

T1/2: 8 hours

223
Q

Method of excretion of Lefamulin

A

Excreted by hepatic metabolism (CYP3A4)

224
Q

T or F: Dose adjustment for severe hepatic impairment is needed in Lefamulin

225
Q

Adverse effects of Lefamulin includes?

A

infusion-site reactions, GI disturbances, congenital malformations

226
Q

Aminoglycosides are used in the treatment of microbial infection with?

A

Antibiotics

227
Q

The serum concentration levels of Aminoglycosides must be (above/below) the MIC

228
Q

As the plasma level of ahminoglycosides is increased (above/below) the MIC, the drug kills an (increasing/decreasing) proportion of bacteria at a more (rapid/slow) rate

A

Above
Increasing
Rapid

229
Q

What antibiotics are time dependent?

A

Penicillin and Cephalosporins

230
Q

Time is (directly/indirectly) related to the MIC

231
Q

T or F: The duration of the antibiotic is independent of the concentration once MIC is reached

232
Q

Event whenreim aminoglycosidesʼ killing action continues when the plasma levels have declined below measurable levels

A

POSTANTIBIOTIC EFFECT

233
Q

Aminoglycosides have a greater efficacy when administered how often?

A

SINGLE LARGE DOSE than when given as multiple smaller doses

234
Q

Toxicity of ahminoglycosides (in contrast to antibacterial activity) depends on?

A

critical plasma concentration and on that time such a level is exceeded

235
Q

Time (above/below) such threshold of MIC is shorter with single large dose

236
Q

Aminoglycosides are structurally related to _______ attached by ______

A

amino sugars
glycosidic linkages

237
Q

Aminoglycosides are polar or non polar?

238
Q

Are aminoglycosides absorbed orally?

239
Q

ROA of aminoglycosides

A

IM or IV for systemic effects

240
Q

Penetration of Aminoglycosides: Widely distributed or limited

241
Q

Do aminoglycosides cross the BBB?

242
Q

Major mode of excretion of aminoglycosides

A

Glomerular filtration

243
Q

Aminoglycoside plasma levels are affected by changes
in?

A

renal function

244
Q

Aminoglycoside excretion is (directly/indirectly) proportional to?

A

Directly
creatinine clearance

245
Q

With normal renal function, elimination of aminoglycosides is how long?

246
Q

Needed for safe and effective dosage selection and adjustment in aminoglycosides

A

Monitoring plasma levels

247
Q

How often should aminolgycosides be given daily?

A

2-3x / day

248
Q

When should peak serum levels for aminoglycosides be measured?

A

30-60 minutes after administration

249
Q

When should trough serum levels for aminoglycosides be measured?

A

Measured just before the next dose

250
Q

MOA of aminoglycosides

A

Bactericidal (irreversible) inhibitors of protein synthesis

251
Q

Aminoglycoside penetration of bacterial cell wall is partly dependent on?

A

O2-dependent active transport

252
Q

Aminoglycosides have minimal activity against?

A

strict anaerobes

253
Q

Aminoglycoside transport is enhanced by?

A

cell wall synthesis inhibitors via antimicrobial synergism

254
Q

Aminoglycosides bind to what ribosomal unit?

255
Q

How do aminoglycosides interfere with protein synthesis?

A
  1. Block formation of initiation complex
  2. Cause misreading of the code on the mRNA template
  3. Inhibit translocation
256
Q

Aminoglycosides are resistant to what bacterium?

A
  • Streptococci, including S. pneumoniae
  • Enterococci
257
Q

Why are aminoglycosides resistant to Streptococci and Enterococci?

A

due to failure to penetrate into the cell

258
Q

Aminoglycoside primary mechanism of resistance

A

Plasmid-mediated formation of inactivating enzymes

259
Q

Catalyze the acetylation of amine functions

A

Group transferases

260
Q

Transfer of phosphoryl or adenyl groups to the O2 atoms of hydroxyl groups on the aminoglycoside

A

Group transferases

261
Q

Transferases produced by enterococci can inactivate what molecules?

A

Amikacin
Gentamicin
Tobramycin
(TAG)

262
Q

Transferases produced by enterococci CANNOT inactivate what molecules?

A

streptomycin

263
Q

Less susceptible to plasmid-mediated formation of inactivating enzymes and is active against more strains of organisms

A

Netilmicin

264
Q

Receptor protein on the 30S ribosomal subunit may be deleted or altered as a result of?

A

a mutation

265
Q

What are the different aminoglycosides and spectinomycins?

A

Gentamicin
Tobramycin
Amikacin
Streptomycin
Neomycin
Spectinomycin

266
Q

MOA of aminoglycosides and spectinomycins

A

Bactericidal, inhibiting protein synthesis by binding to 30S ribosomal unit, concentration dependent action with post antibiotic effect

267
Q

Aminoglycoside with least resistance

268
Q

Aminoglycosides and spectinomycin are used against?

A

Aerobic G(-) - H. influenzar, M catarrhalis, Shigella
Can be used with beta lactase for gonorrhea (spectinomycin; IM) and TB (spectromycin; IM)

269
Q

Main ROA of aminoglycosides and spectinomycins

A

IV with renal clearance
Once daily dosing

270
Q

Oral and topical examples of aminoglycosides and spectinomycins

A

Neomycin and gentamicin

271
Q

Toxicities of aminoglycosides and spectinomycins

A

Nephrotoxicity (reversible)
Ototoxicity (irreversible)
Neuromuscular blockade

272
Q

CLINICAL USES of GENTAMICIN, TOBRAMYCIN, AMIKACIN

A

Serious infections caused by aerobic gram (-) bacteria (SKEEPPP)

Used for the following but is not DOC
H. influenzae
M. catarrhalis
Shigella species

273
Q

Aminoglycosides and spectinomycins are not effective for G (+/-) cocci when used alone

274
Q

Aminoglycosides are combined with _______ in the treatment of Pseudomonas, Listeria and Enterococcus

A

penicillin

275
Q

Aminoglycosides are combined with penicillins to treat what conditions?

A

Pseudomonas, Listeria and Enterococcus

276
Q

STREPTOMYCIN clinical uses

A

Tuberculosis
Plague
Tularemia

277
Q

Multi-drug-resistant (MDR) strains of TB resistant to streptomycin maybe susceptible to?

278
Q

NEOMYCIN, KANAMYCIN, PAROMOMYCIN clinical uses

A

Neomycin – topical
Kanamycin and paromomycin – IM/IV/PO
* Active against: Gram-positive bacteria, Gram-negative bacteria, some mycobacteria

279
Q

Kanamycin and paromomycin are resistant against?

A

P aeruginosa, Streptococci

280
Q

NETILMICIN ROA

A

IM/IV/Topical/Ocular/Intrathecal

281
Q

Netilmicin clinical uses

A

serious infections resistant to other aminoglycosides

282
Q

SPECTINOMYCIN is a ____ related to aminoglycosides

A

Aminocylitol

283
Q

T or F: Spectinomycin is a back up drug

284
Q

SPECTINOMYCIN as a single dose is useful against?

A

Gonorrhea but NOT recommended for treatment of pharyngeal gonococcal infections

285
Q

TOXICITY of AMINOGLYCOSIDES includes

A

OTOTOXICITY
NEPHROTOXICITY
NEUROMUSCULAR BLOCKADE
SKIN REACTIONS

286
Q

Auditory impairment is caused by which aminoglycosides?

A

Amikacin and kanamycin

287
Q

Vestibular dysfunction is caused by which aminoglycosides?

A

Gentamicin and tobramycin

288
Q

Ototoxicity risk is (proportionate/disproportionate) to plasma levels

A

Proportionate

289
Q

Ototoxicity is increased with the use of?

A

loop diuretics

290
Q

Ototoxicity is contraindicated in?

291
Q

NEPHROTOXICITY includes what condition?

A

Acute tubular necrosis

292
Q

Is nephrotoxicity in aminoglycosides reversible?

293
Q

Most nephrotoxic AMINOGLYCOSIDES

A

 Gentamicin
 Tobramycin

294
Q

Nephrotoxicity is common in which demographic?

A

 More common in elderly patients

 Patients concurrently receiving
 Amphotericin B
 Cephalosporins
 Vancomycin

295
Q

T or F: NEUROMUSCULAR BLOCKADE is a common toxicity in AMINOGLYCOSIDES

296
Q

High doses of aminoglycosides can cause what blockade subsequently causing what condition?

A

Curare-like block may occur at high doses
Respiratory paralysis

297
Q

Is Neuromuscular blockade reversible?

298
Q

Treatment for neuromuscular blockade

A

 Calcium
 Neostigmine
 Ventilatory support

299
Q

SKIN REACTIONS are caused by?

300
Q

AMINOGLYCOSIDES can cause allergic skin reactions like?

A

contact dermatitis

2nd Year 2nd Term (38 decks)

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